Lesson 1

HEALTH CARE SERVICES I

PUBLIC HEALTH
The term “public health” came into general use around 1840. It arose from the need to
protect “the public” from the spread of communicable diseases. Later, it appeared in 1848 in the
name of a law, the Public Health Act in England to crystallize the efforts organized by society
to protect, promote and restore the people’s health.
In 1920, C.E.A. Winslow, a former professor of public health at Yale University, gave the
oft-quoted definition of public health. The WHO Expert Committee on Public Health
Administration, adapting Winslow’s earlier definition has defined it as :
“the science and art of preventing disease, prolonging life, and promoting health and
efficiency through organized community efforts for the sanitation of the environment,
the control of communicable infections, the education of the individual in personal
hygiene, the organization of medical and nursing services for early diagnosis and
preventive treatment of disease, and the development of social machinery to ensure
for every individual a standard of living adequate for the maintenance of health, so
organizing these benefits as to enable every citizen to realize his birthright of health
and longevity”.
Whereas in developing countries such as India, public health has not made much headway
in terms of sanitary reforms and control of communicable diseases, it has made tremendous
strides in the industrialized western countries resulting in longer expectation of life and significant
decline in death rates. As a result of improvements in public health during the past 50 or 60 years,
public health in the developed countries has moved from sanitation and control of communicable
diseases (which have been largely controlled) to preventive, therapeutic and rehabilitative aspects
of chronic diseases and behavioural disorders.
A EURO symposium in 1966 suggested that the definition of public health should be
expanded to include the organization of medical care services. This was endorsed by another
Expert Committee of WHO in 1973. Thus modern public health also includes organization of
medical care, as a means of protecting and improving the health of people. Since the organization
of public health tends to be determined by cultural, political and administrative patterns of the
countries, there is a wide mosaic of organizational arrangements.
Public health, in its present form, is a combination of scientific discipliness (e.g., epidemiology
biostatistics, laboratory sciences, social sciences, demography) and skills and strategies (e.g.
epidemiological investigations, planning and management, interventions, surveillance, evaluation)
that are directed to the maintenance and improvement of the health of the people.
Health
Health is a state of complete physical, mental and social well-being which is essential for
leading a productive life, and is not merely the absence of disease or infirmity. Provision for
health should be considered a fundamental human right and attainment of highest level of health
is a most important social goal.

1
Concept of Health Care
Since health is influenced by a number of factors such as adequate food, housing, basic
sanitation, healthy life styles, protection against environmental hazards and communicable diseases;
the frontiers of health extend beyond the narrow limits of medical care. It is thus clear that
“health care” is not synonymous with “medical care”. Health care covers a broad spectrum of
personal health services ranging from health education and information through prevention of
disease, early diagnosis and treatment and rehabilitation.
This health care services may be defined as “all those personal and community health
services, including medical care and related education and research directed towards the protection
and promotion of the health of the community.”
The term “health services” implies organization, delivery, staffing.
The major themes have emerged in the recent years in the delivery of health services :
(a) First, that health services should be organised to meet the needs of entire population and not
merely selected groups. Health services should cover the full range of preventive, curative and
rehabilitation services. Health services are now seen as part of the basic social services of the
community; (b) secondly, it is now fully realised that the best way to provide health care to the
vast majority of underserved rural people and urban poor is to develop effective “primary health
care” services supported by an appropriate referral system. The current social policy throughout
the world is to build up health systems based on primary health care, towards the policy objective
of Health for All by 2000AD.
Basis for Health Care in India in Modern Time
India gained independence in August, 1947, after a long colonial rule. Although, the National
Health Policy in India was not framed and announced until 1983. The basis for organisation of
health services in India through the primary health care approach in modern time was laid by
recommendations and guidance provided by the ‘Health Survey and Development Committee’
(Bhore Committee) in 1946. The community development was launched in October 1952, as the
first integrated all round rural development programme. It was proposed to establish one primary
health centre (PHC) for each community development block. At that time, the operational
responsibilties of the PHC were to cover medical care, control of communicable diseases, maternal
and child health (MCH), nutrition, health education, school health, environmental sanitation and
the collection of vital statistics. Each PHC had three sub-centres, being looked after by a trained
midwife for providing MCH services.
Subsequently, over the past decades the health services organization and infrastructure have
undergone extensive changes and expansion in stages following a review by a number of expert
committees, namely the Mudaliar Committee (1961), the Mukherjee Committee (1966), the
Kartar Singh Committee (1974), and the Srivastava Committee (1975). Progressive changes have
been introducted into the programme over the six five-year plan periods. The first five-year plan
(1951-56) initiated a process of all-round balanced development to ensure a steady improvement
in the living standard over a period of time. New programmes for control of communicable
diseases such as Malaria, filaria, tuberculosis, leprosy etc. was instituted. Health and medical care
infrastructure and facilities, and water supply and sanitation were expanded with a view to
improve the accessibility and availability of services.
The subsequent five-year plans aimed at expanding health and family planning services to
bring these services within the reach of all people for improving their health status. During the

2
fifth plan (1974-80), removal of poverty and achievement of self-reliance on the part of the
community were given emphasis. For preventing and correcting nutritional deficiencies,
supplementary feeding programmes for children and expectant mothers were initiated on a country-
wide basis. The family planning programme was integrated with the MCH and Nutrition
programmes.
India is a signatory to the Alma Ata Declaration of 1978, as is committed to attaining the
goals of “Heath for All” (HFA) by the year 2000 A.D., through the primary health care approach.
Consequently, while formulating the sixth five-year plan (1980-85), a critical review was made
of the approaches in the first five-year plans. Based on these, a long term perspective plan was
outlined by the Government for achieving the HFA goals. Also efforts were initiated for the
formulation of the National Health Policy keeping in view the HFA principles and strategies.
HEALTH FOR ALL
Since 1975, the WHO has been developing the concept of achieving health for all by 2000
AD. In the 30th World Assembly in 1977, it was decided that the main social goal of the
governments and the WHO should be “the attainment by all the people of the world by the year
2000, of a level of health that will permit them to work productively and to participate actively
in the social life of their community.” This was popularly known as “Health for All (HFA) by
2000 AD.”
In the International Conference on Primary Health Care, jointly organised by WHO and
UNICEF in Alma Ata, USSR in 1978, this concept of HFA by 2000 AD was endorsed and it was
further stated that primary health care would be the key to attaining this target. These also spelt
out the minimum essential components of primary health care and the supportive activities
needed for their successful implementation.
To achieve the goal of Health for All, a number of immediate goals or milestones had been
planned in between as below:
1985— Providing right kind of food for all
1986— Providing essential drugs for all
1990— (a) Providing basic sanitation for all
(b) Providing adequate supply of drinking water for all
(c) Immunization of children against six common diseases, viz. measles,
whooping cough, tetanus, diptheria, polio and tuberculosis.
Besides the above, a number of indicators (e.g. health status indicators, health care indicators,
social and economic indicators and health policy indicators) have also been developed to enable
countries to measure and monitor as they work towards the goal. However, it was left to each
country to decide its own norms, while suggesting a minimum life expectancy of 60 years and
maximum infant mortality rate of 50 per 1000 live births.
Most recent estimates indicate that some 83% habitations are ‘fully covered’, 15% are
‘partially covered’ and only 2% of habitations are not covered.
There has been marked impovement in the health status of the people in the country. Life
expectancy has increased to 64.6 years during 2000. Crude birth rate has reduced to 26.1 during
1999. Crude death rate has declined to 8.7 and infact mortality rate to 70 during the same period.
Planned initiatives taken in the public health field have also resulted in improvement in
epidemiological scenario in the country. Small pox and Guinea worm diseases have been eradicated,
Polio is on the verge of eradication, Leprosy, Kala-Azar and Filariasis can be expected to the

3
eliminated in the foreseeables future. Incidence of malaria which showed resergence during early
seventies has reduced to 2.2 million cases during 2000.
Primary Heath Care
The term “primary health care” was first used to mean the care given to the patient by the
health worker who saw him first. It was also called FIRST CONTACT CARE. If the patient was
referred to the hospital, it was called “secondly care.” More recently, the Alma Ata Conference
in 1978 gave primary health care a wider meaning. The Alma Ata Conference defined primary
health care as follows:
“Primary health care is essential health care made universally accessible to individual and
acceptable to them, through their full participation and at a cost the community and country
can afford.”
For achieving success in HFA development at least eight components of primary health care
need to be properly implemented. For this, the cooperation and support of other social and
economic development sectors, such as education, social and women’s welfare, food and agriculture,
animal husbandry, water resources, housing, rural development, energy, environmental protection,
industry, communication, etc. would be vital.
Level of Care
Health services are usually organised at various levels (a) Primary level: The first level is
the point of contact between individuals and the health system, where primary health care is
delivered. The primary health centres and their sub-centres constitute this level of care in India,
(b) Intermediate level: At this level, more complex problems are dealt with. The sub-divisional/
district hospitals usually constitute the second level. They provide support to the primary health
care institutions, (c) Central level: The central level institutions (viz. Regional hospitals, Medical
College Hospitals, specialised Hospitals) not only provide highly specialised care but, also to
sustain primary health care as part of comprehensive national health system.
Principle underlying Primary Health Care
Primary health care is based on four principles:
1. Equitable distribution: Health service should be accessible to all the sections of the
society with special attention to the needy and vulnerable groups. It is well known, that
rural population, in most developed countries, are widely scattered and do not have
adequate transportation facilities. City hospitals are beyond the reach of most rural
people and are usually patronised by those in their immediate vicinity. Primary health
care aims to correct this imbalance and bring health services as near people’s home as
possible and is supported by a higher level of health care, to which the patient can be
referred.
2. Community participation: The involvement of individual families and communities
in promotion of their health and welfare, including self-care, is an essential ingredient
of primary health care. Community involvement also implies that the community should
participate in the planning, implementation and maintenance of health services.
3. Multisectorial approach: Joint effort of the health sector and other health related
sectors viz. education, food and agriculture, social welfare, animal husbandry, housing
and public works, rural reconstruction etc. are needed for attainment of health.
4. Appropriate technology: Appropriate technology is not cheap primitive technology
for poor, primitive people. It calls instead for scientifically sound materials and methods
that are socially acceptable, directed against relevant health problems.

4
Health System Infrastructure
The country is divided into 22 major States and 9 smaller union territories, which in turn
are divided into administrative districts. At present, there are 431 districts. Each district is divided
into sub-districts or talukas, under which are situated the community development blocks. There
are about 6,000 community development blocks in the country.
As mentioned earlier, over the past three decades the health services infrastructure and
health care facilities have been expanded considerably. It is aimed to further improve the facilities
as noted below:
Facilities at Village Level : In a village, for about 1,000 population, there will be one health
guide and one trained dai or traditional birth attendant (TBA), both will be selected from the
community. They will be trained at the level of the primary health centre (PHC) and the sub-
centre. These two village level functionaries are to receive technical support and continuing
education from the multi-purpose health workers (male and female) posted at the sub-centre.
Other administrative control and supervision should ideally be carried out by the village health
committee or the village panchayat.
Facilities at Sub-centre Level : The most peripheral health institutional facility will be at
the sub-centre, manned by one male and one female multi-purpose health workers. At present,
in most places there is one sub-centre for about 10,000 population. It is, however, aimed to have
one sub-centre per 5,000 population (3,000 population in hilly and desert areas, and difficult
terrain) by the end of the Seventh Five Year Plan i.e. 1990. To date, about 83,000 sub-centre (both
on the old and new patterns mentioned above) have been established.
Facilities at PHC Level : At present there is one PHC in each community development
block, which covers about 1,00,000 or more population. It was aimed to establish one PHC for
every 30,000 population by the year 1990. Many rural dispensaries are being upgraded to create
the subsidiary health centres or these new PHCs. Each new PHC will have one medical officer,
two health assistants—one male and one female, and the health workers and other supporting
staff. For strengthening preventive and promotive aspects of health care, a new non-medical post
called community health officer (CHO) will be provided at each new PHC. To date, there are
about 11,000 PHCs (both old and new combined).
Facilities at Community Health Centre : For a successful primary health care programme,
effective referral support to be provided. For this purpose one community health centre (CHC)
will be established for every 1,00,000 population, and this centre will provide the main specialist
services. The CHCs will be established either by upgrading the sub-district/taluka hospitals or
some of the block level PHCs, or by creating a new centre wherever absolutely needed.
Facilities at District Level : District health organisation is to be appropriately strengthened to
cater to the needs of the expanding rural health and family welfare programmes. Not only the
planning and implementation and monitoring of health and family welfare programmes are to be
carried out at the district level (preferably on a decentralised basis), all the referral services from
the periphery i.e. PHCs, community health centres and taluka hospitals, are to be attended to
satisfactorily.
The primary contact care will be provided by the health functionaries at the village level and
by the multipurpose workers at the sub-centres level. The cases needing further help will be dealt

5
with at the PHC, and those needing referral support by the specialist would be referred to the
community health centre. The second and third level referral supports will be provided at the
district hospital and the medical college/specialised hospitals respectively.
Organisation at State Level
Under the Ministry of Health and Family Welfare in each State, there is one technical
directorate functioning under the Director(s) of Health Services, and one executive wing headed
by the Health Secretary, who has also the overall administrative control.
Organisation at National Level
Under the Union Ministry of Health and Family Welfare, there are two technical
departments— the Health Department is headed by the Director General of Health Services and
Family Welfare Department is headed by the Commissioner, Family Welfare. The executive wing
as well as the technical departments are under the overall administrative control of the Secretary
to the Government of India.

6
 Lesson 2

HEALTH CARE SERVICES-II

ESSENTIAL COMPONENTS OF PRIMARY HEALTH CARE

In the Alma Ata Declaration, it was stated that at least the following components should be
included in primary health care:
1. Education of people about prevailing health problems and methods of preventing and
controlling them.
2. Promotion of food supply and proper nutrition.
3. Adequate supply of safe water and basic sanitation.
4. Maternal and child health care and family planning.
5. Immunization against major infectious diseases.
6. Prevention and control of major endemic diseases.
7. Appropriate treatment of common diseases and injuries.
8. Provision of essential drugs.
Current Status of Various Components of Primary Health Care in India and Remedial
Measures
1. Education of people about Health Matters
Problems—People in general, particularly in rural areas and urban slums are not
knowledgeable about health matters, such as what are the prevailing health problems in the
community and how to prevent and control these; what are the needs for the maintenance and
promotion of health; what are the resources available and how and when to utilise these etc.
Socio-economic backwardness, ignorance, traditions and superstitions had been acting as blocks
to progressive thinking including development of the concept of positive health. Health education
efforts have been very inadequate. Illiteracy, particularly of the women, has acted as barriers to
communication in health and related matters.
Remedial measures—Appropriate educational programmes are to be organised for different
groups of people. Health education to the community should be a prime function of health
workers and village level functionaries. In this endeavour, functionaries of other sectors such as
social and women’s welfare, education, agriculture and youth clubs can contribute very significantly.
Health education in schools and adult education sessions should incorporate various health
problems, and the methods for their prevention and control.
2. Promotion of Food Supply and Proper Nutrition
Problems—Nutritional deficiency states of varying degrees in regard to protein-calorie
malnutritional, vitamin A and iodine deficiency and nutritional anaemia are prevalent in a wide
section of population. Nutritional deficiency states are particularly noticeable among pregnant
and nursing mothers, and in infants and children. Available statistics indicate that of the deaths
occuring among the age group of 0 to 5 years, in 7 per cent of deaths, malnutrition is the
causative factor and in another 46 per cent, it is an associated factor.
Remedial measures—This dismal condition can be substantially improved by organizing
and conducting nutrition education in the community and in the schools; encouraging people to

7
make kitchen gardens and community gardens; and educating the people on food hygiene. Steps
also need to be taken to encourage growing locally more foods such as cereals, pulses, vegetables,
fruits, milk, fish and poultry products through cooperative and other efforts so as to make these
easily accessible and affordable to the people. Simultaneously, the purchasing capacity of the
families might be improved through a variety of income generating schemes. In addition, for the
moderately and severely malnourished groups, special nutrition programmes are to be organised.
In these endeavours, functionaries from other sectors such as agriculture, animal husbandary,
irrigation, banks and cooperatives, social and women’s welfare, panchayat and voluntary
organisations can play a very significant role.
3. Supply of Safe Water and Basic Sanitation Measures
Problems—Many health problems have their roots in various aspects of community life and
cannot be influenced by medical or health interventions alone. Safe and potable water is not
available to a majority section of the population. Many of the water borne diseases prevalent in
the country are preventable, but the importance of the use of pure and safe water as well as the
personal hygiene are not properly appreciated. Environmental sanitation is very poor, particularly
in rural areas and in urban slums. In most of the places, there are no proper arrangements for
disposal of human and animal wastes, sewage and sullage etc.
Remedial measures—Systematic approach should be made to survey and identify resources
of safe water and to carry out proper analysis of the water. Arrangements should be made for
regular purification of water through chlorination etc. before using for drinking and other household
purposes. People at all levels including the village leaders, women, and children at schools
should be educated on continuous basis about the importance of proper maintenance of water
resources, simple means of purification of water and the use of safe water. Observation of
personal hygienic practices should be emphasised.
It would be important to organise the people and the resources for constructing household
and community latrines, and making arrangements for collecting and disposal of human and
animal wastes. Proper and imaginative disposal of waste water is also very important. Construction
of composting facilities, soakage pits and use of some of the waste water in kitchen gardens
should be encouraged and helped. Educating the women about the proper maintenance of water
sources and the importance of kitchen garden would be helpful. Proper educational programmes
on all these aspects for the children, youths, adults and the mothers should be organised in a
systematic manner.
4. Maternal and Child Health Care
Maternal Care
Problems—In India, the Maternal Mortality Rate (MMR) which is calculated as the number
of maternal deaths per 1,00,000 live births is among the highest in the world and has worsened
in the recent years. It has gone from 424 in 1992-93 to 407 in 1998. (source SRS 1998). No valid
information of morbidity data on mothers is available. Maternal care—antenatal, natal and post-
natal, in rural areas and urban slums, is totally inadequate. In rural areas, majority (about 80 per
cent) of births-are occurring outside the institutions, and are being attended by untrained birth
attendants.
In India most deliveries take place at home without professional assistance under unhygienic
surroundings. In 1998-99, 42% deliveries were assisted by a health professional and only 34%
of births took place in a medical institution. The performance of Kerela and Goa surpass all other

8
states in terms of deliveries taking place in medical institutions with a similarly high percentage
of births being assisted by a health professional. By contrast in Nagaland, Bihar and Uttar
Pradesh only 12-16 percent of births are in medical institutions and in Meghalaya, Assam, Uttar
Pradesh and Bihar only 21-23% deliveries are assisted by a health professional.
Some of the important causes of maternal mortality are sepsis, haemmorhage, toxaemia,
illegal abortion and malnutrition. Liberalisation of abortion laws and enactment of medical
termination of pregnancy (MTP) act in 1971 were the direct outcome of the realization of the fact
that induced abortion performed by unqualified persons under unhygienic conditions significantly
increased maternal mortality and morbidity.
Remedial measures—Systematic efforts are to be made to progressively increase antenatal
registration and care of pregnant women from the present level of 35 to 50 per cent to 100 per
cent. It is also to be ensured that progressively almost all deliveries are conducted under aseptic
conditions by trained health personnel i.e. the dais or female multi-purpose workers. Pregnant
and nursing mothers should get prophylactially two to three doses of tetanus toxoid, and iron and
folic acid supplement for nutritional anaemia. During post-natal checkups, mothers are to be
educated on breast feeding, growth monitoring, proper weaning practice and immunization of the
child; and on personal hygiene, exercises, proper diet and family planning.
Facilities for MTP services by properly trained and skilled doctors are to be provided,
wherever needed, in rural areas and urban slums.
Infant Care
Problems—India has established a reliable system for reporting infant mortality rate (IMR)
which is the number of infant deaths per 1,000 live births. Latest data for 1999 reveal an IMR
of 70 deaths per 1,000 live births — down from 129 in 1971 and 80 in 1990. An IMR of 70
inplies that of the 27 million children born every years in India, close to 1.7 million die before
celebrating their first birthday. About 50 to 60 per cent of this is caused by mortality during the
neonatal period (0-28 days) and particularly in the first week of life. Several factors contribute
to this mortality and these include poor maternal health during pregnancy, frequent child births,
inadequate care of mothers at risk, poor infrastructure facilities, lack of care of new born at birth
and practically no facilities for new bom care from primary to tertiary levels.
Low-birth-weight infants, either due to prematurity or due to infra-uterine growth retardation,
result from various factors such as how maternal weight and height, frequent pregnancies, maternal
malnutrition and anaemia, chronic maternal diseases and pregnany complications. Low birth
weight if particularly associated with pre-maturity is a major underlying factor for neonatal or
infant mortality. Non-immunization of pregnant women with tetanus toxoid may result in death
due to tetanus neonatorum.
Remedial measures—For dealing with these problems, the dais and female health workers
and health assistants have to be properly trained in perinatal and neonatal are adopting a high-
risk approach. Proper facilities for referrals to the secondary and tertiary levels are also to be
developed and organised. Communities are to be properly educated about the importance of
antenatal and neonatal care, and be encouraged to actively participate in these programmes.
Care of Young Children
Problems—Among the children aged 0-5 years i.e. the pre-school children, the major problems
are the morbidity and mortality due to malnutrition, diarrhoeal diseases—respiratory infections

9
(three accounts for 30% under 5 deaths) and other preventable infections. Malnutrition predisposes
the children to infection, the morbidity rates being three times higher in malnourished children.
Remedial measures—Two types of intervention programmes would be needed (a) prevention
and treatment of malnutrition, and (b) reduction of mortality due to diarrhoea accounts for 20%
under 5 deaths respiratory infections and other infections preventable by immunization.
The strategies for reduction of prevalence rate of malnutrition in pre-school children would
be: (a) to provide nutrition education to the mothers; (b) to detect the cases of malnutrition and
to grade them; (c) to rehabilitate moderately/severally malnourished cases by supplementary
feeding from home resources; (d) supplementary feeding at sub-centres; and (e) referral grade III
cases associated with diarrhoea or infection to secondary level of care i.e. the community health
centres or district or taluka level hospitals.
The strategies for reduction in infant mortality due to diarrhoeal diseases and respiratory
infections would be (a) to educate the mothers how to prevent and treat diarrhoeal and respiratory
diseases; (b) to train the health functionaries about how to recognise and treat these disorders,
and to judge which patients would need referral to higher levels of health service(b) and
cotrimoxagole is distributed through all health outlets (c) to create facilities for secondary level
care to referred cases; and (d) to provide drugs, oral rehydration salts (ORS) and other supportive
measures. The government has launched the Oral Dehydration Therapy Programme to prevent
death due to dehydration. In 1998-99, 62% of the mothers knew about ORS packets—an increase
from 42% in 1992-93.
All children, preferably at the age of under one year must be immunised against tuberculosis,
poliomyelitis, diphtheria, tetanus, whooping cough, and measles (where feasible).
Family Planning
Problems—Even though India was the first country in the world to take up family planning
as an official programme in 1952, achievements over the past 33 years have not been as good
as would be desirable. Currently 1996 the crude birth rate is around 27.5 per 1000 population.
For reducing the birth rate to 25 per 1000 population and to achieve a net reproduction rate
(NRR) of unity by 2000 A.D., 60 per cent of the eligible couples in the reproductive are to be
effectively protected through contraceptive practice. It is estimated that about 32 per cent of the
couples in the reproductive age group have been protected by contraceptive measures. Out of this
nearly 27 per cent have been protected by sterilization alone, and only 5 per cent have been using
spacing methods. More than 80 per cent of the acceptors of sterilization had three or more living
children. Obviously, we may not expect the desired demographic gain from such contraceptive
measures.
Remedial Measures—Now more concentrated attention has to be given to younger couples
with low parity—i.e. the newly married couples, and one-child and two-child families for
contraceptive protection with spacing methods.
The acceptance and continued use of contraceptives are influenced by several factors such
as the character of the method including its advantages and disadvantages; individual and social
acceptability; provider’s knowledge, skill and attitude; effective communication, motivation, and
counselling; the nature and quality of delivery services including supply logistics and follow up
care; and the cost.

10
 Small family norm has to become a way of life; for this purpose, organisation of population
education in the schools and colleges, for the out of school youths and in adult education
programmes would be most vital.
5. Immunization Against Major Infectious Diseases
Immunization of the children and pregnant mothers has already been referred to earlier.
India has a long history of vaccination programmes. In the sixties vaccination against smallpox
and tuberculosis was started, and in mid-seventies vaccination against diphtheria, pertusis and
tetanus was taken up. Polio vaccination was initiated in 1980 and, in a limited scale, the measles
vaccination in 1985. Presently, the package of immunization services for infants includes vaccination
against tuberculosis, diphtheria, pertusis, tetanus, poliomyelitis and measles. Expectant mothers are to
be given two doses or one booster dose of tetanus toxoid. In some endemic areas immunization
against cholera and typhoid has also to be considered.
The immunization schedule presently being followed in the country is given below:
Beneficiaries Age Vaccine Doses
Pregnant women 16-26 weeks TT 2*
Infants 3-12 months DPT 3
Polio 3
BCG 1
9-15 months Measles 1
18-24 months DPT 1
Polio 1
Children 5-6 years DT 1**
Typhoid 2
10 years TT 1**
10 years TT 1**
Typhoid 1**
16 years TT 1**
Typhoid 1**
* One booster only if vaccinated previously.
** Two doses if not vaccinated previously.
The vaccination of children against 6 serious but preventable diseases (diptheria, pertusis,
polio, measles, tetanus and tuberculosis) has been a cornerstone of the child care system in India.
The Universal Immunization Programme (UIP) was launched in 1985-86 specifically for this
purpose. By 1998-99, 42% of children aged 12-23 months were fully vaccinated (as against 36%
in 1992-93).
With the help of Pulse Polio Immunization Programme (PPI) launched in 1996, India has
achieved considerable success in its campaign to eradicate polio.
6. Prevention and Control of Locally Endemic Diseases
Although the prevalence of endemic diseases will vary from one region to another, some of
the important ones are: tuberculosis, malaria, leprosy, filaria, scabies, guinea-worm infestation,
rabies, iodine deficiency goitre etc. People are to be educated for their early diagnosis and

11
treatment health functionaries are to be trained for early detection and the services and follow up
care to be organized.
7. Appropriate Treatment of Common Diseases and Injuries
Treatment of minor ailments and first-aids may be given at village level. Treatment of
common diseases and injuries are to be provided at the sub-centres and PHCs, and appropriate
referral services are to be organized. People need to be educated about the availability of local
remedies and other facilities to meet these needs. Other sectors such as Education, Social and
Women’s Welfare, Panchayat, Voluntary Organizations can play an important role in educating
the people and school teachers etc. and in organization of resources.
8. Provision of Essential Drugs
For local health care and treatment of common diseases and disorders, at least 20 drugs
should be available within one hour’s walk and travel. Utilising locally available remedies and
using indigenous system of medicines should be considered. Considering the financial constraints
from Government sources, community’s participation through cooperative functioning etc. may
be explored.
References
1. Primary health care in India, Technical Paper 5, National Institute of Health and
Family welfare.
2. Social and Preventive Medicine, Park and Park, 16th Edition.

12
 Lesson 3

PROTEIN—ENERGY MALNUTRITION
Protein energy malnutrition (PEM) is the most widespread form of malnutrition, especially
among infants and children between 1-3 years of age. PEM is largely responsible for the fact that
in many areas particularly in the developing countries like India, South East Asia and Africa up
to half the children born, do not survive to the age of 5 years, those children who do survive,
live with permanent impairement of physical and possibly mental growth.
PEM describes a spectrum of clinical disorders, ranging from mild to moderate deficiency
as well as its most serious forms, which are Kwashiorkar and Marasmus. These two serious
forms are the extremes and in between are a great number of intermediate case which often go
unrecognised. Until recently, PEM was referred to as protein caloric malnutrition, but this
nomenclature has been changed, as it has been argued that malnutrition occurs more due to a
“food gap” rather than a specific calorie deficit. Moreover, the term protein calorie malnutrition,
is too narrow a concept, as malnutrition may not be just a deficiency of calorie and protein, but
other nutrient deficiencies may be involved.
Kwashiorkar was first described in 1995 by Dr Cicely Williams. She referred to it as a
“disease the child gets when the next baby is born.” the disease develops due to ignorance
regarding the best weaning foods to be given to a child or due to an inability to provide these
foods to the child for some reason or the other. The older child gets displaced from the breast
and has to subsit on largely carbohydrate diets, which are low in protein i.e. an imbalance
between protein and carbohydrate.
Kwashiorkar is due to a quantitative and qualitative deficiency of protein, but in which
energy intake may be adequate. But a diet deficient in calories, but in which protein may be
adequate leads to marasmus. Marasmus is derived from the greek word, meaning “to waste”.
Nutritional marasmus is the childhood equivalent of starvation in adults. The marasmus form of
protein energy malnutrition occurs mostly in infants under one year of age, occuring due to early
weaning, replaced by inadequate, dilute milk. This condition arises due to a continued restriction
of both dietary energy and protein, as well as other nutrients.
The acute form of protein energy malnutrition is often precipitated due to inability on the
part of the mother to supply proper nutrients to the foetus and later inability on her part to lactate.
Marasmus is most common in infants and children below the age of 15 month, and is most
frequently found in twins; whereas kwashiorkor occurs most often among children beyond this
age. The degree of severity of protein energy malnutrition is related to the extent of growth
failure. It is expressed by the weight loss per age as compared to the weight of normal children.
Loss of weight by 11-25% is classified as grade 1, weight loss by 26.40% as grade II and weight
loss by more than 40% as grade III in protein energy malnutrition.
Causes of Protein-Energy Malnutrition (PEM)
PEM occurs characteristically in children under 5 years, whenever the diet is poor in protein
and energy. No age is immune to this, but in the older persons the disease is much less frequent
and the clinical manifestations are less obvious and severe, as both protein and energy requirements
are relatively reduced as the age advances. The main factors are discussed below:
1. Age group of sufferer: PEM is found exclusively in children under 5 years and over 1
year—the pre-school group. It is uncommon under 1 year in countries where prolonged breast

13
feeding is the common practice. Similarly those children who have escaped PEM and reached the
age group of 5 or 6 years can be regarded as “out of danger”. Recent studies in many countries
have revealed that the most vulnerable age group can be narrowed down to the period between
1 to 3 years of age.
Nutritionally this is the most dangerous age-period when the majority of young children do
not get mothcr’s milk in adequate amounts even when prolonged breast feeding is practised, at
the same time, according to usual dietary practice in most countries, solid foods are also not
given in appreciable amounts to meet the ever increasing demand of calories, proteins and other
nutrients. Besides, the child also starts getting all types of infections cither by feeding by bottle
or by picking things from outside and this age group therefore gets all stypes of infections and
infestation along with dietary defecieney.
2. Birth order of the child: Commonly, the sufferer belongs to a family with large number
of children and has a relatively high birth-order. There are several studies on correlation between
malnutrition of family size, which confirms that a mother with a large number of children is
herself malnourished and sick, does not have time and energy for child care. On top of this, she
gradually loses her ability of lactation. With each addition of a child, the total condition worsens.
A child with fifth or sixth birth order in a poor or even middle class family groups up in
situations favourable for the developments of PEM.
3. Unavailablity of Protein rich foods: Weaning period in topical countries is often
characterised by a shortage of suitable, easily digestible foods, containing protein of good quality.
All over the world, the animal origin foods are in short supply and expensive; thus unavailable
as weaning food.
Due to industrialization, there is a tendency to abandon breast feeding and return to work;
leading to deficiency of protein and in some cases, of protein as well as energy in the young
infants.
Finally the advertising of tinned milk preparation, which can never be afforded in adequate
‘quantities, resulting in over dilution, thus the diet of the child deficit in protein.
4. Ignorance and Poverty: Unawareness regarding the needs of the child and available
resources is one of the foremost important cause of PEM. The mother may be ignorant about the
cheap available food sources of good protein. The child is given milk with no supplementation,
leading to gross deficiency of protein. Many a times, due to high cost of food, proper
supplementation is not started.
5. Beliefs Taboos and Customs: Beliefs and customs regarding the requirements of the
child may lead to malnutrition. Some of the examples are a prejudice against giving eggs to
infants, prolonged restriction or use of purges in diarrhoeal disease, the habit of reserving animal
protein for the males, breast feeding the infant and the sibling at the same time and overvaluation
of the largely carbohydrate foods as “superfood” for the infants. Citrus fruits are believed to cause
for common cold & cough.
6. Infection: In developing countries, major factor in PEM is the effect of frequent infections
experienced by children in the first few years of life. Infections adversly effect the nutritional
status; decreased appetide leads to reduced food intake, deminished absorption when diarrhoea
is present. Even the slightest infection increases the loss of nitrogen through urine. Infection
increases the need for energy, vitamin A and C and some other nutrients. There is enough

14
evidence showing that PEM increases the susceptibility to infections, specially diarrhoeal and
respiratiory diseases.
7. Premature Weaning: PEM is recent times has shown a tendency to occur at an earlier
age due to several reasons. The period of breast feeding is becoming shorter in towns and cities
of the developing countries. In circumstances where mothers work away from home, resorting to
artifical feeds is a necessity. The duration of breast feeding is shortened sometimes in response
to advertisement, in the mistaken belief that it is good for infants, or a desire to imitate the better
educated affluent section of society. Artificial feeds is unsatisfactory for a number of reasons. The
fomulations may be wrong, and unhygienic methods used, predisposing the infants to attacks of
gastroenteritis and hence to early PEM. It has thus been recommended that every effort, should
be made to encourage mothers, particularly in the developing countries to breast feed at least
throughout the first year of life.
Marasmus: The predisposing factors leading to the marasmic condition are a rapid succession
of pregnancies and early, abrupt weaning. This is followed by duly and unsound artificial feeding
of the infants with very dilute milk or milk products given in inadequate amounts to avoid
expense. Thus, diet is low in both proteins as well as energy. In such circumstances, in poor
house the preparation of clean food is almost impossible, resulting in repeated infections, especially
of the gastro intestinal tract. The mother often treats this condition by “starvation therapy”.
Typically the marasmic from of the syndrome occurs in infants under 1 year and is more frequently
found in towns. In marasmus, weaning is often early, the mother being induced to stop breast
feeding for various reasons. The reasons could be an influence of advertisements advocating the
use of articial food products, or presence of infection in herself or in the infant. Quite often poor,
uneducated mothers stop breast feeding when another pregnancy begins. There is a widespread
belief that the milk of a pregnant mother is bad for her child. In towns, the necessity to return
to paid work is another factor leading to the stoppage of breast feeding in early infancy.
Kwashiorkar: This condition arises when after a prolonged period on the breast, the child
is weaned to the traditional family diet, which is often low in protein because of poverty. Most
often there is no supplement of milk available to the child. Kwashiorkar is frequently precipitated
by the outbreak of illnesses such as malaria, measles or gastroenteritis. The presence of the
infection raises the requirement of protein and energy in the body, which are already limiting in
the child’s body.
Both marasmus and kwashiorkar arise as a result of poverty and ignorance. Even when food
is available, customs and food taboos restrict the use of certain foods, Unsuitable commercial
food preparations may be purchased or good preparation misused from a failure to understand
how to use them, when the elementary rules of food hygiene are not followed. The incidence of
marasmus in the underdeveloped countries is on the increase as a consequence of a decline in
breast feeding, urbanisation of uneducated families in need of jobs, who live in poor unsanitary
houses with insufficient money.

15
 Chart below shows the factors leading to the development of Marasmus and Kwashiosrkar:
BIRTH—
œ œ
Repeated Pregnancies Continued breast feeding till one year or later
œ œ
Breast feeding only upto 5 months or so Late gradual weaning
œ œ
Early, abrupt weaning Starchy family diet fed to the child.
œ œ
Dilute Dietary formulae Acute infections
œ œ
Repeated infections esp. Gastroentertis Kwashiorkar
œ
Starvation therapy
œ
Nutritional Marasmic
Marasmus Kwashiorkar
Identification of PEM
The manifestations of PEM vary widely, according to the nature of the causative factors, the
age of the patient, the time for which they operate etc. two severe clinical forms are recognized:
Kwashiorkar and nutritional marasmus. The protein deficiency in adult may show itself in the
form of loss of weight, reduced subcuanous fat, anaemia, great susceptibility to infection, frequent
loose stoolsol, general lethargy, inability to do substantial hard work, delay in healing of wounds
and oedema. Thc clinical features of marasmus and Kwashiorkar will be dealt separately.
Marasmus
The symptoms of marasmus are as follows (fig. 1) :
(1) The child is reduced to mere skin and bone due to diminution of muscle mass.
(2) He has a shrunken, shrivelled skin and a monkey like face.
(3) There is usually watery diarrhoea or acidic bulky stools.
(4) Dehydration may occur due to watery diarrhoea.
(5) The weight of the child is much below the standard.
(6) The temperature is usually subnormal and the pulse rate low.
(7) The hair is dull and dry.
(8) The abdomen way be shrunken or distended with gas.
(9) The eyes become large in size due to shrunken face and gives the appearance, of
staring.
(10) There may be a continued feeling of hunger.

16
 Fig. 1 : Clinical photograph of a child suffering from marasmus
Kwashiorkar
The physical features characteristics of Kwashiorkar can be classified as follows:
(a) Constant (b) Usual (c) Occassional
(a) Constant Features (fig. 2)
(1) Psychmotor changes: The child becomes extremely apethetic, with no interest in his
surroundings. He is cheerless, miserable with no appetite. He remains seated where he
is put down.
(2) Growth retardation: The supply of protein is limited and whatever is there, is used for
energy, resulting in failure of growth. Body weight is reduced, but it may be covered
by the presence of subcutaneous fat and oedema.
(3) Oedema: It occurs when there is excessive loss of nitrogen and the body tries to retain
a state of normalcy by transfusion of extracellular fluid to the intracellular space of the
cells. Oedema first occures on the feet and lower legs and then involves the back of
hands, the thighs, the sacrum, the back arms and the face.
(4) Muscle wasting with retention of some subcutaneous fat: Muscle wasting is a constant
feature of Kwashiorkar with a reduction in the circumference of the upper arm. This
is due to muscle wasting. The relative thick layer of subcutaneous fat can also be
observed both on the body and the limb.
(b) Usual Features
(1) Hair Changes : The hair is often sparse, soft and thin & can be pulled out easily
causing pain. The characteristic curl in negro children is lost, loss of hair results in
patchy alopecia. Their may be changes in pigmentation of hair, with streaks of blond
and grey hair called ‘flag sign’.
(2) Skin Changes: The skin changes observed are areas of pigmenation and depigmentation.
It is dry, and rough. The peeling of the pigmented areas gives the appearance of flaked
paint. Patches of skin become inflammed and is called ‘crazy pavement dermatosis’.

17
 (3) Moon Face: Oedema leads to a full, well rounded face with sagging cheeks and swollens
eye lids.

Fig. 2 : Photograph of a child suffering from kwashiorkor

(4) Anorexia and Diarrhoea: Watery stools or large semisold acid stools are present. Poor
sanitation is likely to be the cause of diarrhoea, which in turn rapidly advances the child
to severe Kwashiorkar.
(5) Abdomen: distended but ascites is rare.
(c) Occassional Features
(1) Fatty Liver: Due to fat deposition inside the liver cells, the liver gets considerably
enlarged down to the level of umbilicus.
(2) Associated vitamins deficiency: Vitamin A defeciency at times have been associated
with PEM with manifestation of keratomalacia. Also angular stomatitis and glossitis
may be observed due to riboflavin deficiency. Associated Fe (iron) and folate deficiency
leads to anaemia.
(3) Susceptibility to infection: Children become prone to infectious desease.
The Principal Features of PEM
Features Marasmus Kwashiorkar
Essential features
(1) Oedema None Lower Legs, face or may
be generalised.
(2) Wasting Marked. The childs appears Less Obvious
to be skin and bones
(3) Muscle Wasting Severe Sometimes
(4) Growth retardation Severe Less than in marasmus
in terms for body
weight
(5) Mental Changes Usually Usually mental changes

18
Variable features
(1) Appetite Usually good Usualy poor
(2) Diarrhoea Often Often
(3) Skin Change Usually none Often pigmentation observed.
(4) Hair changes Texture may be modified, Sparse, straight, silky hair
rough dispigmented often.
(5) Moon face None Often
(6) Liver enlargement None Often
The terms Kwashiorkar and nutritional marasmus are of little relevance in field studies, as
the number of frank cases of either condition is always small compared to the total number of
children who are malnourished. The original classification of PEM by Gomez into 3 degrees of
malnutrition based on weight deficit takes into account the age of the child and the severity, but
not the type or duration of the condition. It has also been suggested by some workers that cases
with oedema be classified as 3rd degree malnutrition, regardless of the weight loss or extent of
the growth failure. This implies that a child who is 50% of standard weight without oedema and
a child who is 80% of standard weight with oedema are in the same category as regards the
severity of their conditon. It has been realized that the measurement of deficit in height or body
length gives valuable information about the chronicity of malnutrition, complementary to that
given by the measurement of weight deficit. A reduction of stunting of height is evidence of past
malnutrition; a low body weight in relation to height is evidence of present malnutrition,
complementary to that given by the measurement of weight deficit. It is thus important to take
into account both height and weight.
Treatment of PFM
The principles of treatment are :
(1) Adequate diet: The aim is to supply the lacking nutrients in the diet which are calories
and proteins.
(2) Treatment of infections.
(3) Health education of parents, taking care of the children on how to prevent a relapse of
the case.
A suitable diet is the main stay of treatment. The basic principle of treatment is to raise the
child’s nutritional status as quickly as possible, by providing sufficient calories and high quality
protein. The child may have to be tube fed in the begining, which calls for a liquid diet. It is
generally agreed that a daily intake of 170—200 Kcal per Kg. body weight and 3-4 gms of good
quality protein per kg. body weight are sufficient to cover the child’s needs. The protien used in
treatment will depend on the local resources that are available. Whole milk is generally considered
to be one of the best sources of protein being easy to administer as well as assimilate. A seriously
ill child cannot tolerate whole milk and should be provided with skimmed milk or preprations
of casein and mashed bananas. Gradually when the condition improves, whole milk can be
resorted to alongwith vegetable protein multi mixes. The lack of Vitamin A is overcome by
adding it to milk or giving a supplement. It is better to use milk and milk powders alongwith
cereals, as excessive use of milk may cause diarrhoea. Once the milk toleration is better, the child
can be put on other vegetable protein also. Vegetable proteins if carefully selected can be satisfactory
if supplementing the cereals with dals, beans, peas in the ratio of 2:1 which can be a substitute
for milk protein.

19
 However, it should be borne in mind that the utilisation of protein depends on an adquate
dietary supply of energy. Recovery and weight gain are not accelerated by intakes of over
3-5g Kg/day. Infants who have impaired digestive functions and are seriously ill, improve with
an intake of 1g/kg/day, although larger amount are necessary at a slightly later stage for full
recovery. It has been found that diets based on natural foods are better than protein concentrates
and hydrolysates used.
Once the child is one the pathway of recovery, the metabolism is speeded up and the
demand for vitamins and minerals is greater, thus the vitamin deficiencies may become more
marked. Five or six small meals can alternate with snacks or beverages. Fish, egg, milk can be
included in generous amounts. The same kind of diet should be continued at home, even after
the patient is discharged from the hospital, which means education of the mother in terms of
nutritional care is very important.
The importance of observing strict hygienic conditions while preperation of food is essential
for successful treatment. Care should be taken to reconstitute milk powers with boiled water and
use contamination free feeding bottles. It is safer to use the milk power by sprinkling it on the
cereal or any other part of the child’s meal.
In severe cases, when the child is hospitalised and is dehydrated, it is necessary to correct
the water-electrolyte imbalance before starting the dietetic treatment. A. solution made of glucose,
sodium, potassium, chloride and lactate can be given by mouth in small doses, upto a total of
100-200ml/Kg/ 24 hours. If vomiting continues, larger amounts may continue for 2-3 days if the
diarrhoea and vomiting are severe. Once diet therapy begins, potassium, magnesium and iron are
given as mineral supplements to make up the depletion in the body. For the first ten days in the
hospital a multi vitamin preparation is given. Large doses are not required unless there is clinical
evidence of a specific vitamin deficiency such as retinal if xeropthalmia is present or folic acid
if megaloblastic anaemia is observed. Daily supplements of iron (60mg/day) and folic acid (100
mg/day) should be given to correct anaemia. When the child’s apetite returns to normal it is best
to meet the vitamin requirement through natural foods.
As PEM is frequently associated with infections, antibiotic therapy is required.
Amongst the general measures in the treatment of PEM-are keeping the child in a heated
room as the body temperature is sub-normal. Education of the mother keeping in mind her
economic position, education, experience and locally available foods is essential. Children can
effectively be rehabilitated at home by convincing the mother that the cure can be effected by
simple modifications of the diet within the economic reach of the family. The National Institute
of Nutrition, has formulated an energy protein rich mixture to treat PEM at home level. It
consists of
Whole wheat roasted 40 gms
Bengal gram roasted 15 gms
Groundnut 10 gms
Jaggery 20 gms
The energy value of this mixture is. 330 Kcalories and the protein content is 113 grams.
Many children with PEM were cured within 3 months when treated with this food mixture.
Similar mixtures based on cereals and legumes have been formulated. Incaparaina, Pronutro, AK-
100 and Supramine arc available in some countries. India, Balamlul, Bal-Ahar, Pronurto, Protinex,
protinules and Threptin biscuits are available.

20
Prevention of PEM
There is no simple solution to the problem of PEM. Many kinds of Inter-disciplinary action
may be required. The following approach can be used for the prevention of PEM in the community.
(a) Health Promotion
It includes
1. Education of pregnant and lactating women. Distribution of supplements.
2. Promotion of breast feeding.
3. Development of low cost weaning foods.
4. Methods to improve the family diet.
5. Nutrition education regarding promotion of correct feeding practices.
6. Family planning.
7. Improving the family environment and sanitation.
(b) Specific Protection for Children
1. The child’s diet must contain adequate calories and proteins. Foods rich in both
should be used based on locally available foods like cereals and pulses.
2. Immunization programme should be intensified.
3. Food fortification.
4. Addition of fat to increase calorie density of food.
5. Amylase—rich foods prepared from wheat / maize to reduce bulk of weaning
foods.
(c) Early Diagnosis and Treatment
1. Periodic surveillance of the population at risk.
2. Early diagnosis of any lag in growth by use of growth charts.
3. Early diagnosis and treatment of infections and diarrhoea.
4. Programmes for early rehydration in diarrhoea cases.
5. Supplementary feeding programmes during epidemics.
6. Deworming of heavily infested children.
(d) Rehabilitation
1. Provision of nutritional rehabilitation services for moderate cases.
2. Hospital treatment for severe cases.
3. Follow up care through supplementary feeding and nutrition education to prevent
relapses of PEM.
Ignorance and poverty are the two main causes of PEM. Education in nutrition is necessary
not only for mothers and potential mothers but for the whole community, including doctors and
nurses. Recipies for weaning foods which are well within the reach of the family in agriculture,
fertilisers and improved varieties of seeds are required. Only a system which provides employment
and fair wages for all, linked with an educational system can prevent children dying from
malnutrition. Family planning should be integrated with child health, both in the health centres
as well as in the minds of the mothers. PEM has adverse effects on survival, health performance
and the progress of population groups, therefore preventive action on a world wide basis is
urgently needed.

21
Refrences
(1) Normal and Therapeutic Nutrition, Robinson and Lawler,
(2) Applied Nutrition (Third Edition), Rajalakshmi.
(3) An advanced Textbook on Food & Nutrition, Vol. II, Dr. M Swaminathan.
(4) Food and Nutrition (for Senior Students), Education Planning Group.
(5) Fundamentals of Food and Nutrition, Mudambi & Rajagopal.

22
 Lesson 4
VITAMIN A DEFICIENCY
Night blindness as a result of Vitamin A deficiency has been mentioned in Egyptian and
Chinese, writings way back in 1500. A global survey sponsored by WHO in 1964 showed that
Xeropthalmia i.e. all ocular manifestations due to Vitamin A deficiency is common in South and East
Asia, many parts of Africa and Latin America. Vitamin A deficiency is closely associated with
protein energy malnutrition. The peak age of its occurencc is between 2-5 years, when Kwashiorkar
is very common. According to rough estimates 50,000 children may lose their eye sight every
year due to vitamin A deficiency in India. Globally, it is estimated that every year about 7,00,000
children are likely to develop corneal lesions due to vitamin A deficiency and 20-40 million
children are estimated to have mild vitamin A deficiency at any point of time.
Vitamin A plays an important part in many body functions and one of them is vision.
Vitamin A is a component of visual purple, a pigment found in the retina of the eye.. When light
strikes the retina, the visual purple changes into another pigment called visual yellow. In the dark
the visual yellow again turns back into visual purple. However, this process is not 100% efficiency
and a small amount of visual purple is always lost in the transformation. Thus, it must constantly
be renewed from a steady source of vitamin A. When the nutrient is not present, vision is
impaired and night blindness occurs, which is one of the first signs of vitamin A deficiency. In
fact, the quickness of the eyes ability to adapt to darkness is sometimes used to measure the
supply of vitamin A in the person’s body.
INCIDENCE
1. Age : Vitamin A deficiency is preponderant in children. There is a progressive increase
in the prevalance up to the age of 12-13 years. The corneal lesions, however, are rarely
seen in the children about the age of 6 years. A great majority of the cases of careal
xerophtholuia occur between 1 & 3 years.
2. Sex : Xerophthalmia is more frequent in boys than in girls though the incidence of
kerotomalacia is similar in both sexes.
3. Socio-economic factors : Children from rural and tribal families belonging to low income
group are more vulnerable to vitamin A deficiency. Families cannot afford animal foods
which are rich in preformed VTA because of their poverty.
4. Seasonal effects : The seasonal charges in vitamin A deficiency are related to times of
harvest. Studies indicate that the highest prevalance is observed in the months of May-
June. There appears to be another peak in November and December. The peaks appear
to be associated with total food intake and the consequent variation in the growth of the
children.
5. Drought : The extent of vitamin A deficiency is more during drought due to non-
availability of leafy regetables because of shortage of rainfall. The prevalance is higher
in areas which are chronically drought prone.
6. Regional Differences : National Nutrition Monitoring Bureau (NNMB) surveys indicate
that in the states of Andhra Pradesh, Gujarat, Karnataka, Orissa, Uttar Pradesh and West
Bengal, the prevalance of xerophthalmia is higher.

23
Causes of Vitamin A Deficiency
1. Inadequacy of the diet or a low dietary intake of vitamin A or its precursors, the
caroteniods—Deficiency occurs when the intake of Vitamin A or its precursor, carotene
is poor. Sometimes food taboos and ignorance also leads to avoidance of certain
beneficial foods.
2. Impaired absorption of vitamin A—It can be a major cause of deficiency. Failure
to convert dietary carotene into biologically active vitamin can take place as a result
of severe liver disease, diabetes, hypertension and body reserve may be depleted, as
during pregnancy and lactation.
Absorption is also impaired in a condition where a major portion of the instestines has been
surgically removed or in a condition called steatorrhea. Excessive intake of mineral oil is another
cause of malabsorption of vitamins A, as much of it gets excerted in the faeces.
Lack of fat in the diet leads to impair absorption of fat soluble vitamins in the diet. Bile
helps In the absorption of vitamin A and carotene. When there is an abstruction in the bile duct
or low fat intake, absorption of vitamin A is seriously impaired, the conversion of carotene into
vitamin A in the intestinal mucosa is helped in the presence of insulin and thyroxine. An absence
of these harmones can be detrimental to vitamin A production in the body.
When the absorption of vitamin A is poor, the reserve in the liver is used up which in turn
can lead to a deficiency.
3. Infections—It has been confirmed that the lowering of serum Vitamin A levels is
directly related to infections. The drop in the vitamin A level is further aggravated if
the infection is febrile. The degree of fever being directly proportional to the decrease
in the Vitamin A level. Certain parasites e.g. Ascaris lumbrioides consumes a large
amount of this Vitamin.
4. Deficiency of Proteins and relationship with Protein Energy Malnutrition—For
the efficient coversion of carotene to vitamin A, and for the absorption, storage,
transport and utilisation of Vitamin A certain amount of protein supply is essential.
Protein metabolisin has a bearing on the transport of Vitamin A as this Vitamin is
transported in serum in combination with a protein known as retinal bound protein (RBP).
The synthesis of this protein is lowered in protein deprivation.
Foods which provide proteins also provide Vitamin A. Thus there is a direct relationship
between PEM and Vitamin A decifiency. Children suffering from Kwashiorkar may fail to
absorb Vitamin A given orally unless their protein status is improved.
5. Poor Maternal Nutritional Status—The maternal nutritional status directly affects
the foetal stores as well as the amount of vitamin A that is secreted in breast milk.
The foetal stores of babies belonging to mothers with poor nutritional status is much
lower than their counterparts belonging to mothers having adequate nutrition.
6. Poor Weaning Practices—Delayed weaning with little or absolute non inclusion of
green leafy vegetables can lead to Viamin A deficiency.
7. Lack of awareness—Due to lack of awareness, the community does not make use of
the primary health care services like diarrhoea - control, immunization, vitamin A
supplementation and other basic health services.
8. Low purchasing power : Low purchasing power of the communities and their inability
to meet the dietary requirements ever after spending 80-90% of their income on food

24
 is an important factor for vitamin A deficiency. Animal foods like eggs, milk & liver
provide preformed vitamin A, but these cannot be afforded by poor communities and
they rely on plant foods which provide only provitamin A.
Indentification of Deficiency
Vitamin A has several functions in the body. These are
1. It plays a crucial role in normal vision.
2. It is needed for the health of the epithelial celis viz. mucous membranes, skin.
3. It is connected with growth especially skeletal growth.
4. It is anti-infective i.e. protects the body against microbial infections.
It is thus obvious that a deficiency of vitamin A will hinder any one or all the processes
mentioned above. The commonly affected part of the body as a result of Vitamin A deficiency
are the eyes. Night blindness (fig 1) or inability to see in dimlight is the earliest symptom of
Vitamin A deficiency. It is noticed that the child, stumbles or gropes for objects in dim light.
Xeropthalmia literally means “dry eyes”. The term is now used as a descriptive term for the
ocular manifestations of Vitamin A deficiency in man. The presence of one or more of the
following eye changes should be considered as incidence of Xeropthalmia.
(a) Conjuctival Xerosis—The Conjunctiva appears muddy and wrinkled instead of the
usual transparent and clear. It becomes dry and unwettable. This is the first clinical sign
of vitamin A deficiency.
(b) ‘Bitot’s Spots—There are extension of the xerotic process. These are greyish, triangular,
foamy, rough and raised patches on the conjunctiva. They are frequently bilateral.
When Bitot spots are observed along with conjunctial xerosis, they are regarded as
indicative or Vitamin A deficiency (fig. 2)
(c) Carneal Xerosis—This stage usually follows conjunctival Xerosis. The corneal surface also
becomes dry and hazy, similar to ground glass. Corneal involvement should be considered
a medical emergency.
(d) Corneal ulceration with Xerosis—If the ulcer progresses, there may be perforation of
the cornea along with iris (eye muscles) prolapse. These unless are characteristically
circular and sharply demarcated.
(e) Keratomalacia (fig. 3)—It consists of softening of the entire thickness or a part of the
cornea. This process is rapid and if not treated promptly, it may lead to necrosis (scar
formation) and destruction of the eye ball resulting in blindness.
The WHO reports the clinical symptoms of vitamin A deficiency affecting the eye and classifies
the signs into primary and secondary signs.

25
Fig. 1 : Blindness due to vitamin A deficiency.

26
Fig. 2 : Photograph of an eye with Bitot spot on the Conjunctiva

Fig. 3 : Photograph of an eye with keratomalacia

27
 Theprimary signs according to increasing order of severity include:
X1A Conjunctival Xerosis.
X1B Conjunctival Xerosis with Bitot Spot.
X2 Corneal Xerosis.
X3 Corneal Ulceration.
X3B Keratomalacia.
Uptodate the X3A stage there are possibilities of reversing the damage caused by administering
massive doses of vitamin A. However, once the X3B stage sets in, irreversible changes occur.
The Secondary signs include:
X1N Night Blindness
XB Bitot Spot only
XF Typical fundus changes in the eye
XS Corneal scars attributed to Xeropthalmia.
The Secondary signs are not pathognomonic signs of vitamin A deficiency i.e. there is no
direct cause and effect relationship. Only when the secondary signs are observed in association
with the primary signs, are they indicative of Vitamin A deficiency.
Besides affecting the eyes, in Vitamin A deficiency the mucous memberances of the nose,
throat, trachea and bronchi become rough and dry resulting in bacterial infections.
In the alimentary canal, there is thickening and dryness of the tract resulting in diminished
secretion of digestive juices, impaired absorption and increased liabilities to infections and
diarrhoea. Due to changes in the epithelium, the skin becomes dry and scaly, the condition is
known as follicular Keratosis, toad skin or Phynoderma.
Growth and reproduction affected by various forms of Vitamin A has been confirmed in
animals studies. ‘Bone development may be showed if the vitamin is lacking during the rapid
growth period. A liberal, apply of this vitamin, especially during prenatal life and childhood is
important. Vitamin A is important for tooth formation. Like other epithelial cells, the enemel
forming cells are affected by the lack of the vitamin. Fissures may be present on the enamel layer
and the teeth tend to decay.
It has been shown in human beings that in acute infections, the serum levels of vitamin A
and liver reserves decrease. This has been demonstrated in patients with pneumonia, tonsilitis and
other febrile diseases. This indicates an increased need for the vitamin during infections or
possibly increased destruction of the vitamin. A correlation between the amount of Vitamin A in
the diet and the prevalence tuberculosis has been noted in human beings. Kidney and bladder
disorders also arise as a result of epithelium abnormalities.
Identification of Vitamin A deficiency is also done by the biochemical criteria. Plasma levels
if Vitamin A are indicative of the deficiency. 30 mcg to 50 mcg retional per 100 ml serum are
considered acceptable, 20-30 mcg retinal/100 ml are indicative of deficiency and values below
10 mcg, 100 ml serum are considered very low. Plasma levels of<10 mcg/100 ml in more than
5% of the population at risk which is 0-5 years has been suggested for the community diagnosis
of Xeropthalmia and vitamin A deficiency. Similarly if more than 2% of the children between
0-5 years show Bitot’s spots Conjunctal Xerosis, it is regarded as a criterion for community
diagnosis of Vitamin A deficiency.

28
Treatment
The oral administration of large doses of vitamin A is recommended method of treating of
all stages of xerophthalia including corneal lesons. Immediately on diagnosis, an oral doses
2,00,000 I.U. of oil miscible vitamin A should be given to children in the age group of 1-6 years.
In case of those with persistent vomiting and diarrhoea, an intramuscular injection of 1,00,000
IU of water miscible vitamin A can be substituted for the oral dose. This is followed by another
dose of 2,00,000 IU one to four weeks later. In case of infants under the age of 12 months, half
the dose of vitamin A is given.
For the prevention and treatment of secondary infections, antibiotics are of great value.
Prevention
The prevention and control of this deficiency can be done through the following methods
(1) Improving the dietary intake
The regular intake of green ieafy vegetables like spinach, methi, amaranth, cabbage; colored
vegetables like carrots and pumpkin; fruits like mango and papaya, improves the serum vitamin
A levels. These plant products contain Beta-carotene, the precursor of Vitamin A. The carotenes
are converted to retinol mainly in the walls of the small intestine. Animal foods such as milk,
egg yolk, butter, cheese, whole milk, fish are direct sources of retinol, but are relatively expensive.
A daily intake of 100 gm leafy vegetables is practical way of meeting the daily adult requirement.
Feeding children with 30 gms green vegetables for 12 weeks maintains adequate serum levels of
the next 24 weeks period. The use of red palm oil should be encouraged wherever available. Red
palm oil besides being rich in carotene pigments, the fat aids the carotene absorption in the diet.
Breast feeding including feeding of colostrum must be encouraged. However, improvement in the
dietary intake involves intensive nutrition education and is a long term approach.
(2) Administration of a single prophylactic dose of Vitamin A
The administration of 2 lakh IU of retinyl palmitate in oil by mouth every 6 months to pre-
school children (1 to 5 years of age) has been found to be effective in reducing the incidence of
ocular signs in preschool children by about 70-75%. A fat soluble preparation of the vitamin
given orally is recommended rather than parenteral injection in oil, as the injected carrier fat is
poorly absorbed. For injections, a water soluble preparation is preferred. The National Programme
is now extended to cover children 6-11 months and a priority is now being given for children
6 months to 3 years. For 6-11 months infants one dose of 1 lakh IU is administered orally at the
time of measles immunization.
(3) Fortification
Fortification with Vitamin A has been used as a technique to prevent blindness. Mother
diary fortifies milk with vitamin A. Certain oils and Vanaspati are also fortified with this vitamin.
Some countries like Guatemala, Panama, Costa Rica are using sugar fortified with vitamin A to
prevent blindness. Trials have shown that tea leaves can be fortified with vitamin A and it is
stable. Similarly, salt can also be used as a vehicle for fortification.
(4) Dose for Lactating mothers
To improve the quality of breast milk, 1 lakh I.U of water soluble Vitnmin A is given to the
mother as soon as the baby is born. However, this method is not in practice and may not be very
helpful too, as the Vilamin A may be all used up to replenish the mothers stores.

29
 Lesson 5
ANAEMIA
Anaemia is said to be present when the concentration of haemoglobin (Hb) in the blood fails
below the normal level. Hb is a vital biomolecule for the maintenance of normal health of an
individual. Normal Hb levels vary with age, sex and physiological status. The WHO scientific
group defined Nutritional anaemia as a condition in which the Hb content of blood is lower than
normal, as a result of a deficiency of one or more essential nutrients, regardless of the cause of
such deficiency. It is theoretically possible for anaemia to occur when there is a deficiency of any
one of the substances which are known to be essential for red blood cell production i.e. proteins,
amino acids, ascorbic acid, iron, folic acid, vitamin B]2, riboflavin, nicotinic acid, pyridoxine,
pantothenic acid, copper and cobalt. Yet, it has been observed that deficiency of iron plays role
in precipitating the anaemic condition followed by the nutrients like folate and vitamine B12.
In India and other developing countries nutritional anaemia is primarily due to iron deficiency.
It is a major public health problem involving hundreds of millions of people throughout the
world. Anaemia occurs with greatest frequency at the peak periods of iron requirement which are
infancy, menstruating females and during pregnancy. During these crucial periods the requirement
for iron is increased.
Studies conducted by the National Institute of Nutrition have shown that 63 per cent of
India’s children below three years and 45 per cent from three to five years suffer from iron
deficiency anaemia-moderate or severe in 10 to 15 percent cases.
There are wide ranges of Hb concentrates in healthy persons and adult men have slightly
higher values than adult women and children. The table gives figures below which the anaemic
condition is said to exist. (WHO, 1972).
Age Hb (g/100 ml)
Children 6 months—6 years 11
6 years—14 years 12
Adults Men 12
Women 12
Pregnant women 11
Lactating women 12
There are three main causes of anaemia :
1. Reduced production of erythrocytes (red blood cells) and Hb.
2. Loss of blood from the circulation, due to internal or external haemorrhage.
3. Haemolysis i.e., increased destruction of the red blood cells.
We will deal primarily with the first category of anaemias which is Nutritional Anaemia. In
nutritional anaemias, the activity of the bone marrow which is the production site for the red
blood cells is limited. The life of a red blood cell is 120 days. The bone marrow replaces them
at such a rate that their number remains constant. When there is a deficiency of one or more
essential nutrients involved in erythropoiesis (red blood cell production), the Hb concentration
cannot be maintained and anaemia results. Nutritional anaemia is broadly classified into 2 types:

30
 Nutritional Anaemia
œ
œ œ
Microcytic Macrocytic
hypochromic
œ œ
(due to iron (due to folate or
deficiency) B deficiency)
12

Folate B Deficiency
12
Deficiency (pernicious
anaemia)
Causes of Anaemia
Iron Deficiency Anaemia
Iron deficiency anaemia is prevalent throughout the world. The incidence of anaemia is
quite high in this country even in the upper classes, particularly among young children and
women during their reproductive period. Anaemia is highly prevalent even among the men in
rural areas because of hookworm infestations. The Bhils subsisting on maize are found to show
a higher incidence, perhaps because of the low iron content of maize as compared to other grains.
Although the infant at birth is born with adequate stores of iron, these are largely used up in the
first six months and thereafter the child becomes anaemic, if the diet does not include enough
iron. Infants born of anaemic mothers are found to become anaemic much earlier. Breast milk
contains twice as much iron as bottle milk, so that bottle-fed infants need even more of supplements.
Causes of Iron deficiency Anaemia
1. Low dietary intake
The consumption of a merger diet is an important cause of anaemia, particularly where the
economy is restricted. Quite often ignorance may lead to iron rich foods not being included in
the diet.
II. Low availability of Iron
It also happens that even when the dietary intake of iron is adequate, anaemia exists. This
is due to the poor absorption of iron from the diet. The cereal based diets, consumed in India
contain high amounts of phosphates, phytatcs, oxalates. These from insoluble salts with iron and
thus depress its absorption. Tea drinking also inhibits iron absorption in the body. Iron from
animal foods, which is in the form of haem iron is better absorbed man non-haem iron from
vegetarian sources. There are some nutrients which favour the absorption of iron like calcium,
vitamin C and proteins, but their quantities are limited in the Indian diet. These nutrients increase
the availability of non-haem iron in the diet. In some persons gastric secretions of hydrochloric
acid are absent which favours iron liberation. This condition may also lead to anaemia.
III. Increased Losses from the body:
(a) Menstrual losses
(b) Pregnancy and lactation
(c) Haemorrhages

31
 (d) Sweat losses
(e) Parasitic infestation
(f) Malabsorption syndrome.
(a) Menstrual losses—The menstrual blood loss varies between 10-151 ml of blood per
period. The amount of Iron lost from the body is about 30 mg. and to meet this loss,
1.0 mg of iron has to be absorbed daily.
(b) ‘Pregnancy and Lactation—The loss of iron involved in a normal pregnancy, delivery
and lactation for six months is approximately 900 mg. iron. Basal iron requirement is
280 mg., expansion of red cell mass is 570 mg., transfer to foetus 200-370 mg, iron
content of placenta and cord, 34-170 mg, blood loss at delivery — 100-250 mg.
Overall 500-600 mg of additional iron is required during entire pregnancy—daily
requirement of 4-6 mg. of iron. Plus breast feeding also results in loss of another 100-
180 mg of iron.
(c) Haemorrhages could be acute or chronic. There may be sudden loss of large volume
of blood or there may be repeated loss of small amounts of blood like in peptic ulcers,
haemorrhoids etc.
(d) Sweat losses of iron are particularly significant in the tropical climates, especially
when muscular work is performed.
(e) Parasitic infestation—Hook worm infestation is an important cause of anaemia,
particularly in the tropics. Blood loss through this parasite ranges from .03 ml to. 2ml/
day/worm. Malaria parasite also destroys the red blood cells leading to the anaemic
condition and later also lowers the iron absorpfon in the body.
(f) Malabsorption syndrome—Diseases of the gastro-intestinal tract like tropical sprue,
coelic disease result in the anaemic state, gasitis. Gastric surgery, myxoedema and
acute infections also result in the anaemic state.
Folic Acid Deficiency
Folate deficiency is observed in large sections of the population. It may occur at any age
but pregnant women, infants and young children are affected more frequency. A high incidence
of folic acid deficiency has been noted in elderly patients, correlated with poor intake of milk,
fresh fruits and vegetables.
The causes of folate deficiency in man are:
(1) Destruction of the vitamin during processing and cooking—These procedures may
bring about as much as 95% loss in the folate content. Pasteurisation of milk also
destroys the folate to some extent. Storage of milk in transparent glass bottles leads
to loss of folic acid, therefore, milk should be stored in opaque bottles.
(2) Insufficient absorption of folate: This arises as a result of a failure to absorb folic acid
in certain gastro-intestinal disorders. Moreover adequate amounts of vitamin B12 is
also required for the absorption of folate. For folate metabolism, certain vitamin B12
dependent enzymes are required. Therefore, it could be an indirect lack of vitamin B12.
(3) Drugs: Certain group of drugs used for epileptics e.g. primidone, phenylhydraintone,
phenobarbitones lead to increased folate excretion and megaloblastic anaemia. Alcohol
and oral contraceptives also impair folate absorption.
(4) Promature Children: As the foetus acquires the folate from the mother only in the last
term of pregnancy, premature children have a very low folate nutritional status.

32
Vitamin B12 Deficiency
Vitamin B12 must be bound to intrinsic factor, produced by parietal cells of the stomach
before it is absorbed in the terminal ileum. Inability to produce intrinsic factor results in pernicious
anaemia. The red cell count is often less than 2.5 million and a large proportion of the cells are
macrocytic. The anaemia occurs chiefly in middle aged and elderly persons and may be a genetic
defect.
Vitamin B12 is found only in foods of animal origin therefore strict vegetarians who avoid
dairy products, eggs, meat, are at a risk of developing this deficiency. However, the vegetarian
population derives their supply of vitamin B12 is uncommon.
The causes of vitamin B12 deficiency are:
(1) failure in secretion of intrinsic factor by the stomach—This is often a congenital
defect in which condition the parietal cells of the stomach do not secrete the intrinsic
factor leading to pernicious anaemia. Extreme cases of ulcers, where the stomach
lining gets erroded also leads to mis condition. Coeliac disease, tropical sprue, other
mal-absorption syndromes precipitate vitamin B12 deficiency.
(2) Parasites—Fish tape worm known as Diphyllobothrium latum is selective in drawing
only vitamin B12 from the body.
(3) Poor foetal stores—Vitamin B12 is similar to the fact soluble vitamins, as it can be
stored in the liver. When an infant is born with poor foetal stores, the risk of developing
this deficiency is greater.
Identification of Anaemia
Anaemia give rise to the same general features whatever the cause. Anaemia often develops
slowly. The patient may unknowingly reduce his physical activity. Lowered haemoglobin levels
result in decreased ability to carry oxygen to the cells and to return carbon dioxide to the lungs
for exhalation, (haemoglobin acts as a carrier of oxygen from lungs to tissues and of carbon
dioxide from tissues to lungs or exhalation). With less oxygen and more carbon dioxide in the
cells, body processes become sluggish and efficiency is lowered. A person in this condition is
usually listless and dispirited. The severity of clinical features are dependent not only on the
degree of anaemia, but on the rapidity of development.
The common symptoms are general fatigue, breathlessness on exertion, giddiness, headache,
sleeplessness, the skin becomes pale, palpitations are felt, there is anorexia, a tingling sensation
is felt in (the fingers and toes (paraesthesia). In addition to these, general features, signs of
nutritional deficiency are seen. The tongue has a smooth glazed appearance due to the atrophy
of the papillae and mucous membrance. Changes in the nails are observed. First, there is brittleness
and dryness, later there is fattening and thinning, and finally spoon shaped nails (koilonychia)
result. In general there is loss of efficiency and impaired general health. Psychiatric symptons are
associated with low levels of vitamin B12 only.
The deleterious effects of anaemia are observed in (a) Pregnancy (b) work capacity of the
individual (c) Resistance to infections.
The public healths importance of severe anaemia in a pregnant, woman is an increased
maternal morbidity (sickness) and mortality (death) rate and increased risk for the foetus, as Hb
concentration is definitely correlated with the birth weight of the infant. Anaemia lowers the
capacity to do work, especially sustained physical activity for a continous period. This occurs as

33
Hb, the Oxygen carrier in blood is reduced. Iron deficiency anaemia in particular lowers the
resistance to infections; as certain iron containing enzymes are reduced in the body.
The blood picture in the anaemic state gives indication as to the type of anaemia. In iron
deficiency anaemia, the red blood cells are pale (hypochromic) and small (microcyctic) as there
is insufficient iron for the formation of Hb. If the maturation of the red cells in the bone marrow
is impaired due to the lack of folatc or vitamin B12, the cells which enter the blood stream are
irregular in shape and size but on an average, larger than normal (macrocytic). However, this is
usually referred to as megaloblastic anaemia after the immature precursor of the red blood cells,
the megaloblast. A measurement of Hb does not distinguish between these types of anaemias. For
this two additional measurements are required. The first is to the packed cell volume (PCV)
obtained by centrifuging blood and reading the height of the column of packed cells. The ratio
of Hb/PCV gives the mean corpuscular Hb concentration (MCHC) in gms/100 ml. If the value
is below 30, the red cells are lacking in Hb and the anaemia is hypochromic i.e., iron therapy
is required. The ratio of PCV/RBC count gives the mean corpuscular volume (MCV). A value
of 95 indicates the larger than normal size of the erythrocytes, suggesting either folate or B12,
deficiency.
Treatment
Iron deficiency anaemia—Once anaemia has developed, it is both unwise and uneconomic
to try and correct it by dietary means alone. The administration of one 200 mg tablet of ferrous
sulphate thrice daily for 30 days brings about a mean rise in Hb of 4 grns/100 ml. i.e., a rise of
1 g/100 ml/week. Ferrous sulphate is the iron preparation of choice. Ferrous gluconate, ferrous
succinate and ferrous fumarate are equally effective but more expensive. Treatment should be
continued for approximately 2 months after the Hb level has returned to normal in order to
restock to body’s depleted iron stores.
Parenteral iron therapy — this is often used when iron deficiency anaemia is detected in
the last trimester of pregnancy or when patient does not take oral iron preparation and anaemia
is serve. The advantages of parentical iron therapy are :
a. minimisation of hospital stay.
b. total amount of iron needed can be adnisitered in a short time.
c. no problem of Gastro Intestinel intolerance.
Folate deficiency anaemia—Folic acid in a dose of 5-10 mg daily is effective. Patients
with Hb<5g/100 ml need blood transfusions to tide them over until the folic acid has acted. The
patient should be given a well balanced diet and continue on it. The diet should include some
good sources of folate every day.
Vitamin B12 deficiency anaemia (Pernicious anaemia)—Cyanocobalamine should be given
in a dosage of 1000 mcg intramuscularly twice during the 1st week, then 250 mcg weekly until
the blood count is normal. Folic acid should never be used for the treatment of pernicious
anaemia, as it does not prevent the development of neurological complications but may precipitate
them. Within 48 hours of the first injection of Cyanocobalamine, the bone marrow shows a
striking change from megaloblastic to normal size of the red blood cells. Regular dose of
cobalamine should be continued for life. A dose of 1000 mcg given every 4-6 weeks maintains
the Hb level. The diet should be light, easily digested, rich in proteins, iron and vitamin C.

34
Prevention of Nutritional Anaemias
Iron Deficiency
Prevention of anaemia solely depends on a satisfactory diet giving an adequate supply of
iron for the normal expansion of the tissue mass and blood volume. Of all nutrients, it is the most
difficult to provide in diet. The anaemia is better understood if we know the individual iron
requirements and the sources supplying it. Protein foods are concentrated sources of iron. Organ
meats such as liver, lean muscle meat of all kinds and dried legumes, dark green leafy vegetables,
dried fruits, egg yolk, whole grain enriched cereals and breads and jaggery are all goods sources
of iron. Milk, cheese and ice-cream are poor sources of iron. In general fresh fruits and vegetables
are of great value because of their vitamin C content which facilitates iron absorption. Cereals
do not contribute much to the iron intake because of the phytates and phosphates. Thus education
regarding the good sources of iron which can be afforded as well, is essential. Regular consumption
of vitamin C to promote iron absorption & discouraging the consumption of foods like tea &
tamarind that inhibit Fe absorption.
Besides, the incidence of anaemia can be reduced by the use of iron supplements, especially
for the vulnerable groups. Research work carried out at the National Institute of Nutrition,
Hyderabad, has shown that in pregnancy anaemia can be prevented by intake of iron tablets
during the last 100 days of pregancy. Distributions of tables containing iron and folic acid to
pregnant woman was, therefore, included as a preventive programme by the Government of
India.
According to the supplementation programme, people found to have no iron stores in the
body are given tablets. For pregnent women tablets containing 60 mg/100mg of elemental iron
500µg of folic acid is given daily for 100 days. The same is given to talking mothers and I.U.D.
accepters and preschool children receive 20 mg. elemental iron + 100 mg folic acid daily.
Another method would be of foods with iron. The type of iron used for fortification must
be one that is readily assimilated, does not cause undesirable changes in the vehicle or the food,
and is stable under locally prevailing storage conditions. At present ferrous sulphate, ferrous
ortho-phosphate, iron sodium pyrophosphate are the most commonly used forms for fortification.
The vehicle of fortification should be one that is already being consumed in adequate amounts
by the people in need. Salt is a likely substance for iron fortification. Besides salt in other
countries cereals, sugar, infant foods have .aso been fortified.
Besides this, removal of parasites from the body needs immediate attention and an integrated
approach is required so that repeated infestation does not occur from the environment.
In general the preventive measures should be such as to increase the absorption of iron from
the diet and at the same time reduce the losses from the body.
Folate Deficiency
(1) “Education regarding the folale rich foods such as green leafy vegetables, yeast, foods
of animal origin. Education in connection with the cooking methods which should be
followed in order to retain the folate is important. Most baby foods available in the
market are low in folate, therefore specific education should be given as how to
improve it.
(2) Supplementation—500 µg of folate should be given to all pregnant women from the
2nd trimester of pregnancy and continued upto 6 months of lactation.
(3) Combat associated problems—Tackling the problem of malaria help in the prevention
of folate deficiency.

35
Anaemia in infancy
Most of the time the anaemia is due to iron deficiency. The following factors explain the
of anaemia in early life.
(1) Prolonged milk, feeding — Milk is a poor source of iron and without supplements of
iron containing foods, anaemia develops.
(2) Low Birth weight—At full term the baby has a Hb of 20 g/100 ml. After birth hemolysis
(red cell break-down) occurs and by the 8-10 week the Hb drops to 10 gms/100 ml.
The iron is set free and is stored in the liver, to be utilised during milk feeding.
Premature infants have a small blood volume and hence smaller stores of iron to tide
them through milk feeding period. Moreover, their rate of growth is greater and hence
the requirement of iron in increased, making them prone to anaemia.
(3) Nutritional anaemia in the mother — As a result of the mother’s anaemic condition,
the child’s stores of iron are inadequate.
(4) Infection — Common infections depress the bone marrow function of producing red
blood cells.
(5) Malabsorption may sometimes cause anaemia.
Treatment—Medicinal iron, in a dose of 6 mg/kg is required. Ferrous sulphate mixture for
infants diluted with water 3 times a day is the usual dose, depending on the age.
Prevention
(1) Prevention and treatment of anaemia in pregnant women.
(2) Treatment of infections in infants.
(3) Provision of supplementary foods rich in iron from 4-6 months onwards.
(4) Administering prophylactic doses of iron to low birth weight infants from the 3rd
month onwards. One paediatric tablet contains 20 mg iron and 100 mg folic acid is to
be given daily for 100 days every year.
References
(1) Normal and Therapeutic Nutrition, Robinson and Lawler.
(2) Applied Nutrition (Third Edition), Rajalakshmi.
(3) An Advanced Textbook on Food & Nutrition, Vol. II, Dr. M. Swaminathan.
(4) Food and Nutrition (for Senior Students), Education Planning Group.
(5) Fundamentals of Foods and Nutrition, Mudambi & Rajagopal.

36
 Lesson 6
IODINE AND FLUORINE DEFICIENCY DISORDERS

Iodine Deficiency Disorders

The term ‘goitre’ is used to denote enlargement of the thyroid gland of whatever kind.
Simple goitre is said to be present when the gland is visible and palpable, but no symptoms of
either hypothyroidism or hyperthyroidism are felt by the subject. Goitre is endemic in many parts
of the world. When goitre occurs in a significant number of people living in a particular area,
it is considered endemic. If the prevalence of goitre is found in more than 2% of the population,
the area is considered as goitre region. Prevalence of goitre in more than 5% is very young girls
calls for public health intervention, as the area is considered as endemic goitre region. Simple
goitres do not usually affect health, but they sometimes result in complications which may have
serious consequences such as hypothyroidism, cretinism or deaf mutism. The complications
rarely occur and more likely to be encountered in-regions where endemic goitre is prevalent.
There is no doubt that environmental rather than hereditary factors determine the prevalence of
most simple goitres-especially dietary factors, of which iodine deficiency is the major one.
The most obvious consequence of iodine deficiency is goitre, but recent studies have indicated
that there is a much wider spectrum of disorders, some of them so severe as to be disabling. They
include:
a) hypothyroidism
b) retarted physical development and impaired mental function
c) increased rate of spontaneous abortion and still birth
d) neurological cretinism, including deaf-mutism; and
e) myxoedematous critinism, including dwarfism and severe mental relardation
To express it more clearly, the term “endemic goitre” is now replaced by the term Iodine
Deficiency Disorders (IDD) to refer to all the effects of iodine deficiency on human growth arid
development which can be prevented by the correction of iodine deficiency.
Causes of Deficiency
1. Lack of Iodine
The lack of iodine in the diet is the major causative factor leading to goitre. Ocean foods
such as sea-weeds, sea fish, shell fish are very good sources of iodine. Fresh river water fish are
poor in iodine. Water and soil contain some amount of iodine. Most green leafy vegetables
especially spinach contains a fair amount of iodine. Tea is also a good source of iodine.
2. Presence of goitrogenic substances in food
The identification of natural inhibitors of the thyroid gland in the causation of goitre is also
well established. The goitrogenic properties are found in cabbage, turnips, seeds of cabbage,
brassica seeds, groundnuts, cassava, soyabeans. The goitrogenic substances can be divided into
3 classes
Class-I These substances inhibit the uptake of iodine by the thyroid gland. eg. : Throcyanate,
Isothipaganate cyanogenic glysosides.
Class II These substances interfere with organification of iodine molecule. An example such
as inhibitor is thiooxazolidone (commonly called goitrin) which is activated by the
enzyme thio glucosidase. Cooking and boiling destroys the goitrogenic substance.

37
Hardness of Water
Certain minerals like calcium, magnesium, flourine found in hand water effects the functioning
of the thyroid gland and may lead to goitre.
4. Dirty Water
Certain observation led to thinking that faecal bacteria can produce a goitrogenic substance.
Eight villages on the foot hills of the Himalayas deriving their water supply from a single source
was studied. The incidence of goitre was highest in the lowest village where the pollution in the
water progressively increased. The neighbouring villages were entirely free from goitre as it had
an independent water supply. However, the correlation between goitre and bacterial counts in
water have not been confirmed.
5. Genetic basis of goitre
In areas where endemic goitre exists, endemic cretinism is also present. There is some
evidence, though not with certainly that, parents with goitre give birth to children who also suffer
from goitre.
Identification
The problem of IDD is far more greater than that of goitre (fig : 1) and critinism.
It is a national problem with grave socio-economic consequences.
It has always been thought in India that goitre and cretinism were only found to a significant
extent in the “Himalaya Goitre belt” which is the world’s biggest goitre belt. It stretches from
Kashmir to Naga Hills in the east, extending about 2400 km and effecting the northern states of
Jammu and Kashmir, Himachal Pradesh, Punjab, Haryana, Delhi, Uttar Pradesh, Bihar, West
Bengal, Sikkim, Assam, Arunachal Pradesh, Nagaland, Mizoram, Meghalaya, Tripura and Manipur.
In recent years renewed surveys outside the conventional goitre belt have identified endemic of
iodine deficiency and the associated IDD in parts of Madhya Pradesh, Gujarat, Maharashtra,
Andhra Pradesh, Kerala and Tamil Nadu. More and more new areas are being identified. Even
areas near the sea coast like Bharuch district in Gujarat and Ernaculum district in Kerala are
found goitre affected. In short no slate in India can be said to be entirely free from goitre. About
140 million people are estimated to be living in goitre endemic regions of the country. In the sub-
Himalayan goitre belt of India done, nearly 55 million are estimated to be suffering from endemic
goitre, with an average goitre prevalence rate of about 36 per cent. The spectrum of IDD is shown
in Table I.
Table 1
The spectrum of iodine-deficiency disorders in approximate order of increasing severity.
Disorders Levels of Severity
Goitre — Grade I
— Grade II
— Grade III
— Multinodular
Hypothyroidism — Varying combination of clinical signs
Subnormal intelligence
Delayed motor mile stones

38
Mental deficiency variable security
Hearing defects
Speech defects
Strabismus (squint) — Unilateral
— Bilateral
Neuron-muscular weakness — muscle weakness in legs, arms, truck
— Spastic diplegia
— Spastic quadralagia
Endemic cretinism — Hypothyroid cretinism
— Neurological cretinism
Intrauterine death
(Spontaneous abortion, miscarriage)

Fig. : 1 Photograph of a man suffering from goitre.

39
Treatment
A simple goitre in a non endemic area already requires treatment. If the goitre becomes
disfiguring, iodine therapy is seldom effective but thyroxine 0.2-0.3 mg. per day may be given.
This inhibits the production of the thyroid stimulating hormone secreted by the pituitary gland
and so, reduces this size of the thyroid gland. If there is no response to thyroxine and the goitre
continues to be disfiguring, thyroidectomy (partial removal of thyroid gland) should be considered,
especially if the size of the goitre obstruct the trachea.
Results of studies show that sodium iodide is effective in both prevention and cure of
endemic goitre. When iodine is taken in forms other than food, careful supervision is essential.
In goitrous regions, periodic checking of thyroid gland by physical examination is helpful so that
curative treatment may be started before the goitre develops to any extent.
Prevention
There is evidence to show that iodine supplementation is effective as a means of eradicating
endemic goitre and its complications.
1. Iodised Salt i.e., common salt fortified with small quantities of sodium or potassium
iodate has been widely used in reducing the prevalence of goitre. The range of iodization
depends on the degree of relative stability of salt, the amount of salt consumed by the
population and the degree of goitre.
The range of iodisation varies between one part of potasium iodide added to 1,000
to 130,000 of sodium chloride (common salt). The normal level of iodisalion is 1 part
potassium iodide in 25,000 to 50,000 parts of salt. It was observed that there was
49.90% reduction in goitre due to iodisation of salt. The choice of iodine salt varied
in different parts of the world. Potassium iodide is used in America and Western
countries. Potassium iodate, is found to be better adapted for fortification in our country
than iodide since it is a more stable compound, especially in areas where moisture and
high temperatures prevail. Daily consumption of 10g of iodised salt (25 ppm KI)
provides about 150µg of iodine consumption.
2. Iodised oil—In areas where salt Iodization cannot be employed, intramuscular injection
of iodised oil has been used for preventisng endemic goitre. It is cheap, long acting and
relatively free from side effects. Iodized poppyseed oil for injection (Lipiodol) as well
as for oral administration (Oriodol) containing 37% of iodine has been successfully
used. The dose recommended is 1.2 ml for adults and smaller doses for infants and
children to be given once in every 3 years.
3. Iodised bread—Potassium iodate was added to bread with successful results. The
prevalence of goitre in schoolchildrcn decreased.
4. Iodine Tablets—Sodium and potassium iodide tablets were distributed amongst children
in Ohio with encouraging results.

40
 FLUROSIS
Flurosis is a condition caused by an excess intake of flourine. Flourine is often called a two-
edged sword. Ingestion of large amounts is associated with dental and skeletal flurosis and
indequate amount with dental caries. Minute quantities of fluoride protect the teeth and even
slightly raised levels produce harmful effects.
The main source of fluoride to man is drinking water, which is about 0.5 mg/litre in this
country. In flurosis-endemic areas, the natural wastes have been found to contain as much as
3-12 mg of fluoride per litre.
Causes
The main cause of fluorsis is high fluoride content of drinking water. It has been found that
flurosis occur only in areas with drinking water fluorid content about 1-2 ppm. With a longer
time of exposure, these is likely to be greater accumulation of fluoride. Males are predominantly
affected. The disease is more common in farmers and heavy manual workers especially those
who carry heavy loads on their heads.
Areas where fluorosis is found are by and large rocky and sandy ones with hot and dry
ultimate and low rainful. Further, the disease does not involve wide zones and has a patchy
distribution. The villages affected often depend on well water for drinking purposes.
Villages with deeper wells are less severely affected.
Considerable amount of fluorides may be taken in with foods grown on fluoride rich soil.
Similarly sea food, tea and cheese are rich in its fluoride content. Sorghum based diets have been
found to result in higher retention of fluoride as compared to rice based diets.
In India fluorosis was initially seen in the Southern States & later in North Indian district
of Bhatinda and Raibarily. Recently a new syndrome known as ‘Genu Velgum’ was discoursed
in the areas of endemic fluorosis. It has been reported to occur in certain villages of Andhra
Pradesh.
Nutrition plays a crucial role in susceptibility of persons chronically exposed to excessive
intakes of flouride to its toxic effects. The effects of protein, calcium and vitamin C undenutrition
have been stressed. Protective actions of the above nutrients on toxic manifestations of flouride
ingestion has been reported.
The intake of certain other elements might either mitigate or potentiate the manifestations
of chronic flouride toxicity. Silicon is essential for normal metabolism of bone & connective
tissues. But its excessive intake can be deleterious to health. High intake of silicate aggravates
the severity of dental and skeletal flourosis & enhances the retention of flouride in these tissues.
Molybdenum—High intake of molybdenum has been found to promote the retention of
flouride in the bones of animals.
Copper—Copper deficiency can aggravate some clinical signs of flurosis. In endenic zones
of flourosis, a primary deficiency of this element can exist due to its suboptimal intake. In
addition, secondary deficiency of copper can also occur due to exessive intake of both flouride
& molybdenum. The latter elements are known to deplete the copper pools of the body.
Dietary practices also can add to the fluoride intake. Parboiling of paddy enhences the
fluoride content of rice significantly, the increase being directly proportional to the flouride
content of the water used.

41
Clinical features or Symptoms
In milder from there is involvement of teeth only—dental fluorosis, while in severe cases,
the entire skeleton is involved-skeletal fluorosis.
1) Dental fluorosis : It is the earliest and the most sensitive index of fluoride over
intake during the period of teeth eruption. Usually the teeth of secondary dentition are
involved, but in very severe cases, those of primary dentition may also be affected.
The teeth loose their shiny appearance and chalkwhile patches appear on them. This
is known as “mottled enamel” and is an early sign of dental fluorosis. The white
patches later become yellow and sometimes brown or black. In severe cases, loss of
enamel is accompanied by ‘pitting’ which gives the tooth a corroded a appearance.
Mottling is best seen on the incisors of the upper jaw. Dental motting is an irreversible
change and both boys and girls are equally affected.
2) Skeletal fluorosis : In older people, the disease affects the bones, tendons and
ligaments. This is known as ‘skeletal fluorosis’. This is followed by pain and stiffness
of the back and later of joints of both limbs and limitation of neck movements. This
loss of movements is because of the calcification of inverteberal, which renders the
vertebral column rigid. This abnormal calcification also results in narrowing of inverted
foramena and spinal canal and compression of vertebral disc. Skeletal fluorosis has
been reported to be a public health problem of considerable magnitude in several
districts of Andhra Pradesh, Haryana, Karnataka, Kerala, Punjab, Rajasthan and Tamil
Nadu.
3) Genu Velgum (or knocked knee syndrome) : Recently scientists working at National
Institute of Nutrition. Hyderabad found a new form of fluorosis called Genu velgum.
Young and adobscent people were found to be the chief victims of the syndrome with
higher preponderance in boys. These subjects exhibit typical signs of dental and
skeletal fluorosis. In addition, they suffer from extensive osteoporosis of the limb
bones. It is found in districts of Andhra Pradesh & Tamil Nadu. It was observed that
this syndrome was seen among people where staple diet was sorghum.
Prevention & Control
The tolal amount of fluoride ingested determines the development of fluorosis. Therefore,
it has been suggested that nutritional factors may modify the clinical course and severity of the
disease. This also means that curtailment (reduction) in some way of the total fluoride intake may
modify the severity of the clinical manifestations. Dietary survey carried out in Audhra Pradesh
where fluorosis is endemic suggests that inadequate intakes of nutrients like proteins, ascorbic
acid and calcium may aggravate the disease. In order to reduce the severity, these nutrients should
be in sufficient amounts in the diet. Foods high in fluoride content should be avided by the
population at risk. Communities need to be educated against indiscriminate use of fluoride rich
pesticides and fertilizers, which are known to cause substantial increase in fluoride levels of
foods. Paddy should be parboiled, if necessary in safe water only. It is also necessary to enlighten
the people about the inherent risk of using fluoridated dental preparations newly dentrifices,
mouthrinses, gels & tablets without adequate supervision.
Among the public health approaches suggested to control the problem are:
1) Defluoridation: Defluoridation using defluoridation agents to bring down the fluoride
levels drinking water. The National Environment Engineering Research Institute, Nagpur

42
 has developed a simple technique known as ‘Nalgonda Technique’ for defluoridation of
water. 1st involves additions of two readily available chemicals, vis. lime and alum in
sequence followed by flocculation, sedimentation and filtration. Lime powder is added
first (30 mg/1) and mixed well with water. Generally the lime dose is l/20th of the alum
dose. Alum (500 mg/1) is then added and the water is stirred for 10 minutes. The
contents are allowed to settle for one hour. The settled water will contain fluoride within
permissible limits. The technique is suitable for both domestic and community water
treatment.
2) Deep Wells : Replacement of present wells with deep bore wells because in lower
levels the fluoride content of water is lower. Deep drinking of wells may even give
fluoride free water.
3) Use of canal & dam water : In Andhra Pradesh analysis of water smaples collected
from dams and canals showed that their fluoride contents were much lower than that
seen in well water which is presently being used for drinking purposes.
References
(1) Normal and Therapeutic Nutrition, Robinson and Lawler.
(2) Applied Nutrition (Third Edition), Rajalakshmi.
(3) An Advanced Textbook on Food & Nutrition, Vol. II, Dr. M. Swaminathan.
(4) Food and Nutrition (for senior Students), Education Planning group.
(5) Fundamentals of Food and Nutrition, Mudambi & Rajagopal.

43
 Lesson 7
DIET IN FEVERS
Fever is an elevation of body temperature above normal which results from an imbalance
between the heat produced and eliminated from the body. Fever may occur in response to an
infection, inflammation or a number of other causes brought about by exogenous agents like
bacteria or fungi or endogenous factors like antigen-antibody reaction, malignancy or graft rejection.
Fevers may be classified as acute or chronic.
• Acute fevers: Acute fevers are of short duration but the body temperature may rise to
even above 104° F. Fevers accompanying infections like chicken pox, tonsilitis, influenza,
pneumonia, typhoid, malaria are few examples of acute fevers. Malaria, though an acute
fever is also called a recurrent fever because of repeated episodes of high fever.
• Chronic fever: These are of long duration. The temperature may remain low but fever
continues for a longer period of time, even several months as in the case of tuberculosis.
Thus, chronic fever is one which has slow, gradual onset and is low in severity.
Metabolism in fevers
With a rise in body temperature above normal (98.4° F or 37° C), the following metabolic
changes occur inside the body. These changes are in proportion to the elevaton of body temperature
above normal and the duration of fever.
(i) There is a 7% increase in BMR with every 1° F increase in body temperature or 13%
increase with every 1° C rise in body temperature true. This change is more significant
in patients suffering from acute fever.
(ii) Glycogen and adipose tissue stores decrease significantly because of increased energy
expenditure. Thus more energy is required.
(iii) The rate of protein catabolism increases depending upon severity of infection and
duration of fever. There are increased losses in long continuous fever than in short
duration fevers. Protein breakdown is especially marked in fevers such as typhoid,
malaria, poliomyelitis and tuberculosis. This leads to increased nitrogen wastes and
places an additional burden on the kidneys.
(iv) There is loss of body fluid in the form of excessive sweat and urine formation.
(v) There is increased loss of minerals like sodium, potassium, chloride etc. through sweat,
urine and vomiting leading to electrolyte imbalance.
(vi) The absorption of nutrients like protein, minerals and vitamins decreases.
(vii) The above changes are accompanied by a loss of appetite resulting in low intake of
food which leads to loss of weight.
Acute fever - Typhoid
Typhoid fever is an infectious disease caused by a bacteria Salmonella typhi. The infection
is transmitted through the faecal-oral route i.e. by consumption of food, water or milk contaminated
with intestinal contents. It may affect all age groups but commonly occurs in children.
Body Changes in Typhoid Fever
There is loss of tissue protein which may amount to as much as 250-500g of muscle tissue
a day. Body stores of glycogen are quickly depleted and the water electrolyte balance is disturbed.

44
The intestinal tract is highly inflamed and irritable and diarrhoea is, therefore, a frequent
complication which interferes with the absorption of nutrients. Ulceration in the intestines, i.e.,
Peyer’s patches may be so severe that haemorrhage and even perforation of intestine may occur.
Treatment
Treatment of typhoid involves:
(i) Rest in the bed is mandatory for all patients
(ii) At all times patient should be kept warm
(iii) Antibiotics are given to cure the infection
(iv) Diet is modified to bring the patient to eat food and recover the losses and maintain
thereafter.
Dietary Management
During high fever, there is an aversion towards foods in the form of anorexia, nausea and
vomiting. The diet should be planned with the following objectives:
i) to maintain adequate nutrition
ii) to restore positive nitrogen balance and reduce the burden on kidneys
iii) to provide relief to symptoms as and when present.
iv) to correct and maintain water and electrolyte balance
v) to avoid irritation of intestinal tract as may occur in typhoid.
To achieve the above objectives, the nutrient intake may be modified as follows :
Energy
Since, there is a rise in body temperature, BMR may be increased by as much as 50%.
Therefore, it is recommended to increase the energy intake by 10-20%. Initially, during the acute
stage, a patient may be able to consume only 600-1200 kcal/day, but the energy intake should be
gradually increased with recovery and improved tolerance.
Protein
Since there is excessive destruction of tissues, the protein intake should be increased to
11/2 to 2 times the normal, i.e. 1.5 to 2 g protein/kg body wt/day. For efficient utilization of
protein, energy intake should be adequate. To minimize the tissue loss, protein foods of high
biologic value such as milk and eggs should be used liberally as they are most easily digested
and absorbed.
Carbohydrates
A liberal intake of carbohydrates is suggested to replenish the depleted glycogen stores of
the body. Well cooked, easily digestible carbohydrates like simple starches, glucose, honey, cane
sugar etc. should be included as they require much less digestion and are well assimilated.
Fats
Fats are required mainly to increase the energy intake. However, due to the presence of
diarrhoea, fats only in the emulsified form like cream, butter, whole milk, egg yolk should be
included in the diet, as they are easily digested and well tolerated by patients. Fried food which
are difficult to digest should be avoided.

45
Minerals
There is excessive loss of electrolytes like sodium, potassium, and chloride due to increased
perspiration. Salty soups broths fruit juices, milk etc. should be included to compensate for the
loss of electrolytes.
Vitamins
As infections increase the requirement for vitamin A and deplete tissue stores of vitamin C,
there is a need to increase the intake of both these vitamins. With the increase in energy requirements
the need of B group vitamins also increases. So, vitamin supplements may have to be given for
some time.
Dietary fibre
The symptoms of typhoid include diarrhoea and lesions in the intestinal tract, all forms of
irritants have to be eliminated from the diet. All harsh, irritating fibre should, therefore, be
avoided in the diet, as it is a mechanical irritant.
Fluid
In order to compensate for the losses through the skin and sweat and also for ensuring
adequate volume of urine for excreting waste, a liberal intake of fluids is very essential. A daily
fluid intake for 2.5 to 5 litres is desirable. Fluids may be included in the form of beverages,
soups, juices, plain water etc.
Consistency
A high energy, high protein, full fluid diet is recommended in the beginning. Small meals
are given at frequent intervals of 2-3 hours. Sufficient intake of fluids and salt should be ensured.
As soon as the fever comes down, a bland, low fibre, soft diet, which is easily digested
and absorbed should be given to the patient. Well cooked, well mashed, sieved, bland, semisolid
foods like khichdi, rice with curd, kheers, custard may be given. Bland, readily digested food
affords physiological rest to the alimentary tract. In the beginning, small quantities of food at
2-3 hours interval will provide adequate nutrition without overtaxing the digestives system at any
one time.
Foods to be used in restricted amount or avoided
• High fibre foods like whole grain cereals and their products e.g. whole wheat flour and
cracked wheat, whole pulses and pulses with husk,
• All raw vegetables and fruits excluding papaya and banana.
• Fried fatty foods such as samosas, pakoras, halwas, ladoos etc.
• Chemical irritants such as condiments, spices, pickles, relishes, chutneys and strongly
flavoured vegetables like cabbage, capsicum, turnip, raddish, onion and garlic.
Foods to be included
• Plenty of fluids like juices and soups.
• Milk and milk based beverages.
• Low fibre foods such as refined cereals and their products, dehusked pulses, well
cooked fruits, vegetables in soft and puree form and potatoes.
• Foods providing proteins of high biologic value e.g. eggs, soft cheeses, tender meats,
fish, poultry etc.
• Plain gelatin based desserts, sugars, honey, jam.

46
A Day’s Sample Diet Plan for a Typhoid Patient
Personal Data
Age 8 years
Socio-economic MIG
Food habits Non-vegetarian
Recommended Dietary Allowances (ICMR, 1990)
Normal Modified
Energy 2190 kcal +10% = 2,420 kcal
Protein 54 g +50%=81g
Vitamin A 600 mg retinol
Vitamin C 40 mg.
Chronic fever—tuberculosis
Tuberculosis is a chronic infectious disease and is one of the major causes of illness and
death in the underdeveloped countries as well as the deprived sections of developed countries.
Malnutrition resulting from poverty and ignorance combined with unhygienic living conditions
and poor sanitation makes an individual susceptible to the infection. It is caused by a bacteria
Mycobacterium tuberculosis. The bacteria most often affect the lungs, leading to pulmonary
tuberculosis.
Body Changes in Tuberculosis
Pulmonary tuberculosis is accompanied by wasting of tissues, exhaustion, cough, expectoration
and fever. It is characterized in the early stage by a marked rise in body temperature, flushed face,
increased circulation and respiration, constant fatigue, loss of weight, cough and a general run
down condition. If the temperature rises above 39% C, the metabolic rate may increase 20-30%
above normal. In the acute stage, the disease is quite similar to that of acute fevers. The chronic
phase is accompanied by low grade fever and therefore, increase in metabolic rate is not marked
as in typhoid. However, due to the long duration of illness, wasting of body tissues may be
considerable and there is a noticeable loss of muscle tissues.
Treatment
Rest, antibiotic therapy and fresh air along with nourishing food are the four factors necessary
to provide recovery from tuberculosis.
Dietary Treatment
Chronic fever leads to increased tissue breakdown and malnutrition. Therefore, the objectives
of dietary treatment are:
i) to reduce mortality by providing nutrients required by body’s immune mechanism,
ii) to prevent or control weakness and loss of weight, and
iii) to accelerate convalescence.
To achieve the above objectives, the following nutrient modifications are made.
Energy
As the patient with chronic tuberculosis is undernourished and underweight, energy needs
are increased in order to minimize weight loss and achieve desirable weight. Therefore, energy
intake needs to be increased by 300-500 kcal/day above the normal intake.

47
Protein
In fevers of prolonged duration like tuberculosis, there is a considerable wasting of body
tissues. Serum albumin level is often low. Therefore, it is essential to increase the protein intake.
Protein foods of high biological value should be included in the diet. About 1.2 to 1.5g of protein
per kg body weight per day must be given.
Carbohydrates and Fats
Enough carbohydrates should be included in the diet to meet the increased energy requirement.
An abundant amount of carbohydrate helps in sparing proteins for tissue building. Too much fat
should be avoided as it frequently causes gastric upsets and diarrhoea.
Minerals
A liberal amount of calcium should be included in the diet to promote the healing of
tuberculin lesions. Therefore, some amount of milk should be included in the daily diet. Iron
supplementation may be necessary, if the patient suffers from haemorrhages.
Vitamins
The diet should provide liberal amounts of all vitamins. Since the conversion of Beta
carotene to retinol in the intestinal mucosa is a adversely affected, the diet should provide as
much ratinal as possible by giving some amount of milk and milk products, eggs and meat.
Tuberculosis being an infectious disease results in increased urinary loss of ascorbic acid. As
ascorbic acid helps in healing, additional amounts of ascorbic acid are therefore, recommended
in the diet.
For proper absorption of calcium, enough of vitamin D should be included, as the energy
needs increase. In addition, prolonged use of chemotherapeutic agents used in treatment of
tuberculosis may have an adverse effect on the utilization of certain B-group vitamins.
Consistency and Feeding Pattern
During the acute stage of illness when fever is high, a high protein, high energy full fluid
diet as used for acute fevers is given. As improvement occurs, this diet is progressed to a soft
and then a regular diet. Most patients have a poor appetite. Meals should be made simple, easily
digestible, well prepared and tempting to encourage the patient to eat. All meals should have
cereal-pulse combination with some amount of animal protein e.g. khichdi with curd, sweet dalia
with milk, Pushtik roti and curd etc. Cheap sources of vitamin C, such as guavava, and sprouted
pulses must be given. Seasonal vegetables must be simply provided.
A Day’s Sample Diet Plan for a Tuberculosis Patient
Personal Data
Age : 28 years
Sex : Female
Socio-economic status : Low middle income group
Food habits : Non-vegetarian
Recommended Dietary Allowances (ICMR 1990)
Normal Modified
Energy 2225 kcal: + 25-50% = 62 - 75g
Protein 50 g :
Vitamin A 600 mg retinol
Calcium 400 mg
48
Meal Menu Amount
Early morning Tea 1 cup
Breakfast Buttered Toast 2
Boiled egg 2
Milk 1 cup
Orange 1
Mid-morning Milk 1 glass
Poha 1 Bowl
Lunch Vegetable Khichiri 1 Bowl
Curds 1 medium bowl
Mix Vegetable 1 medium bowl
Fruit cream 1 medium Bowl
Tea Tea 1 cup
Paneer sandwich 2 slices with paneer & tomato
Dinner Idli Sambhar Sambhar with 2 idlis
Curd Fruit 1 medium bowl
Boiled Potatoes 1 larges

49
 Lesson 8
DIET DURING DIARRHOEA
Diarrhoea is a common illness and a leading cause of death in young children. In developing
countries, children suffer an average of three episodes per year during the first five years of life.
An estimated 4 million diarrhoea related deaths occur annually among young children throughout
the world.
What is diarrhoea?
The number of stools normally passed in a day varies with diet and age of the person. In
diarrhoea, the stool contains more water than normal. They may also contain blood and mucous,
in which case the diarrhoea is called dysentery. Therefore, we can say that diarrhoea is the
frequent passage of loose watery and informed stools which may also contain blood or mucous.
It occurs due to an abnormally rapid passage of food along the alimentary tract, preventing
complete digestion and absorption. The number of stools may vary from several per day to one
every few minutes. The affected individual becomes weak and malnourished. His body capacity
to work as well as the resistance to disease is lowered considerably. In children physical and
mental state may also be affected. Diarrhoea, if neglected can lead to dehydration due to excess
loss of water and electrolytes from the body. This may prove fatal, particularly in infants and
young children.
Etiology
Diarrhoea is generally not a disease by itself but symptom of an underlying functional or
organic disease.
In organic diarrhoea, there are lesions in the mucosal linning of the intestines. It can be
caused by
• Bacterial infection as in typhoid and Bacillary dysentery continued through food or
water.
• Parasitic or Protozoal infection like amoebiasis.
• Malabsorption syndrome like celiac disease.
• Other diseases like viral hepatitis, tuberculosis, liver, cirrhosis etc.
• Carcinoma of the intestine.
Functional Diarrhoea results from an increase in the neuromuscular activity which may be
brought about by any of the following :
• Inflammation of mucous membrane by physical, chemical or bacterial agents as in food
poisoning.
• Sensitivity to a particular food as in allergies.
• In nutritional deficiencies such as PEM, Vitamin A deficiencies, pellagra etc.
• In emotional disturbed state as in fear, anxiety or tension.
Diarrhoea may be either acute or chronic in nature.
Acute Diarrhoea
Acute Diarrhoea is characterized by sudden onset and frequent passage of watery and
unformed stools. The patient may even pass several stools in an hour. Other symptoms include

50
abdominal pain, cramps, weakness and sometime fever and vomiting. Acute diarrhoea lasts for
only 24-48 hours. Due to danger of dehydration, replacement of water and electrolytes is of prime
importance and meeting the nutritional requirements become secondary.
Chronic Diarrhoea
Chronic diarrhoea persists for a longer time even several weeks and the patient may pass
4-5 unformed stools in a day. The rapid passage of food through the intestines does not allow
sufficient time for absorption of nutrients and thus nutritional deficiency symptoms may develop.
Therefore, meeting the nutritional needs and providing an extra allowance to compensate for the
nutrient losses becomes the major objective of the treatment.
How does diarrhoea cause dehydration ?
The body normally takes in water and salts it needs through drinks and food (input). It
normally loses water and salt through stools, urine and sweat (output).
When the bowel is healthy, water and salts pass from the bowel into the blood. The water
and salts can then be used again by the body. When there is diarrhoea, the bowel does not work
normally. Less water and less salts pass into the bowel. Thus, more than the normal amount of
water and salts is passed out of the body, in the stools. This large than normal loss of water and
salts from the body results in dehydration. The more diarrhoea stools a person passes, the more
water and salts he or she loses.
Dehydration occurs faster in infants and young children, in hot chimates and when a person
has fever.
Treating a child who has Acute diarrhoea
In acute diarrhoea emphasis is laid on restoration of lost fluid and electrolytes.
The most important factors in the treatment of diarrhoea are :
• To prevent dehydration from occurring, if possible
• To treat dehydration quickly and well if it does occur; and
• To feed the child
Dehydration can usually be prevented in the home if the child drinks more fluids than usual
as soon as the diarrhoea starts. A child should be given one of the fluids recommended for home
treatment. Food-based fluids, for example gruel, soup, rice, water can be used.
Treatment of dehydration - Oral rehydration therapy (ORT)
If dehydration occurs, the child should be taken to community health worker or health centre
for the treatment. The best treatment for dehydration is Oral Rehydration Therapy (ORT) with
a solution made with rehydration salts (ORS). It is a simple, inexpensive and effective treatment.
The composition of oral rehydration salts (ORS) which are available in a dry packed form, as per
the standard WHO/UNICEF formula is given in Table I.
Table 1
Formula of Oral Rehydration Salt
Salt Amount
Sodium Chloride 3.5 g
Sodium Hydrogen Carbonate 2.5 g
Potassium Chloride 1.5 g
Glucose 20 g
To be dissolved in 1 litre of clean drinking water

51
 The oral rehydration should be started as the child passes even one watery stool, and should
be given as frequently as possible.
Other fluids which may be given along with ORS are coconut water, whey water. Cereal/
rice konjee, weak tea. barley water and pulse water.
While the child is ill with diarrhoea, he or she should be frequently offered small amount
of nutritious easily digestible foods. Feeding during diarrhoea episode provide nutrients the child
needs to be strong and to grow, and helps prevent weight loss. The extra fluids given to the child
do not replace the need for food. After the diarrhoea has stopped an extra meal each day for a
week will help the child regain the weight loss during the illness.
What foods to be given ?
1. Fluids - Give the recommended home fluid or food based fluids such as gruel, soup,
or rice water.
If an infant is breast-fed and try to do so more often than normal (at last every 3 hours).
If the infant is not breast-fed than diluted milk is the ratio of 1:1 is given every 3 hours.
2. Foods - Weaning starts when the child is 4-6 months old. Give a child of above this
age foods with highest amount of nutrients and calories. Fresh fruit juice and banana
are useful as they help replace potassium.
Dietary Management of chronic Diarrhoea
The objectives of dietary treatment in chronic diarrhoea are
• to meet the nutritional requirements.
• to replenish water & electrolyte losses.
• to provide extra nutrients to compensate for losses, and
• to reduce residue to minimum levels.
The dietary modifications in chronic diarrhoea are :
Energy - Energy requirements are increased by 10-20% to meet the losses during diarrhoea
as well as overcome weakness and loss of weight.
Protein - An increase of 50% in protein intake is essential to build up body tissues and
replace the tissue breakdown which has occurred.
Carbohydrates - The intake of carbohydrates should be increased to meet the high energy
requirement. However, the fibre intake is kept to a minimum (l-2g/day), to give rest to the
intestines.
Fats - Due to increased mobility of the intestines, fats are not completely digested and
therefore their intake needs to be restricted. At the same time, some amount of fat is essential
to meet the increased energy needs. Emulsified fats like butter and whole milk may be given as
they are easy to digest. Coconut oil may also be include in the diet.
Minerals - The absorption of calcium and iron is lowered during diarrhoea. Therefore,
calcium and iron rich foods should be included in the diet.
Vitamins - In areas where vitamin A deficiency is common, foods that are rich in Vitamin
A are recommended. In any case the absorption of all vitamins is affected during diarrhoea.
Vitamin B should also be given in good amount as they are not synthesied immediately after
diarrhoea.

52
 Fibre - Low fibre foods should be given, as high fibre diet will irritate the intestine. Some
low and high fibre foods are mentioned below.
High fibre food - Whole pulses and cereals, green leafy vegetables and other vegetables
like beans, drumsticks, lotus stem, fruits like apple, guava, peas, cherries etc.
Low fibre food - Refined cereals like bread, semolina, washed pulses, vegetables like
potato, pumpkin, bottle gourd, fruit juices and fruit like banana and papaya, sugar & oils.
Foods allowed in Restricted Amounts or Avoided
Whole cereals and pulses, raw vegetables and fruits, fried foods nuts, milk & milk based
beverages, foods with lots of sugar.
Foods Allowed
Washed pulses and refined cereal, well cooked vegetables, banana, papaya, milk products
such as curd, paneer, egg, chicken, fish.
Prevention of Diarrhoea
1) Breast feeding should be encouraged as it is clean and contains substances that protects
against diarrhoea. Besides, unhygienic bottles and teets are a source of contamination
with microorganisms causing diarrhoea.
2) For weaning purposes, fresh utensils and fresh and properly washed vegetables should
be used.
3) Drinking water should be clean with a covered container. It possible, water can be
boiled.
4) Mothers hand should be washed after defecation, after cleaning a child who has defecated,
after disposing of an infants faeces, before preparing food and before feeding the child.
5) Children’s hand should be washed after they defecate and before they eat.
6) Pet and other animals should be kept in pens or otherwise prevented from entering the
house, areas where food and water are kept or places where children play.
7) Infants and young children cannot use a latrine. Their faeces should be promptly collected
and placed in latrine of buried.
8) Careful attention should be given to hygiene, which includes the building, maintenance
and consistent use of latrine by all members of the family.
A Day’s Sample Diet Plan for a Chronic Diarrhoea Patient
Personal Data :
Age : 5 Years
Sex : Male
Socio-economic Status : MIG
Food habits : Non-vegetarian
Pathological Condition : Chronic Diarrhoea

53
Menu Plan
MEAL MENU
Breakfast Semolina Porridge
Boiled egg
Bread and butter
Mid- Morning Orange juice
Biscuits
Lunch Spinach Khichdi
Curd
Mid-afternoon Banana custard
Evening Tea Paneer & Tomato Sandwich
Dinner Lentil & Tomato soup
Moong Dal & Rice
Bed - Time Phirni

54
 Lesson 9
DIET IN CONSTIPATION
Constipation is a physiological disosder of alimentary canal. It may be defined as the
retention of the faeces in the colon beyond the normal length of emptying time. It is characterised
by infrequent, incomplete and difficult evacuation of hard, dry stools. Infrequent or insufficient
emptying of the bowel may lead to malaise, headache, coated tongue, foul breath and lack of
appetite. These symptoms disappear after satisfactory evacuation.
Causes of Constipation. A number of factor leads to constipation,
i. Irregular eating time practices
ii. Change in ones usual routine due to illness, in travel, nervous tension, depression,
anxiety, worry or excitement
iii. Faulty dietary habits like inadequate intake of water or fluids, use of highly refined
foods,
iv. Lack of sufficient rest
v. Poor muscle tone of small intesline due to lack of exercise and sedentary lifestyles.
vi. Difficult or painful evacuation due to fissures or haemorrhoids
vii. Intake of drugs or medicine
viii. Poor personal hygiene - urge to defecate may be neglected leading to irregular times
of evacuation
ix. Excessive and continuous use of laxatives and regular enemas
There are three types of Constipation
i. Atonic constipation
ii. Spastic constipation
iii. Obstructive constipation
(ii) Atonic Constipation is more common. The main reason for atonic constipation are lack
of fluids in the body, especially after perspiration, lack of roughage which contributes to the lack
of cellulose, deficiency of vitamin B, which produces poor muscle tone, irregular evacuation
habits and use of purgative agents. Due to any of the above causes muscular tone of the intestine
is affected and peristaltic action is reduced. Bacterial action on stagnated food is more and
symptoms of constipation develops.
(ii) Spastic Constipation, on the contrary, occurs due to excessive muscle tone of the
colonic muscles. The movement of the food is very irregular and often causes pain in the lower
abdomen. Irritating foods, excessive use of purgatives and mental stress produce this type of
constipation. Spastic constipation occurs as a complication of some other disease. Excessive use
of alcohal, tea or coffee also produce this.
(iii) Obstrutive Constipation is due to maliganancy or stricture of the colon.
Use of castor oil or other purgatives in infancy is a common practice in our country. It
contributes to constipation in later life.

55
 Treatment Should attempt at the following
1 Correction of faulty food habits.
2 One should follow regular bowel movements habits
3 The patient should be advised to take exercise for the development of abdominal
muscles. Regular physical exercise is beneficial especially for sedentary workers.
4 Mental worry and anxiety should be avoided.
5 Consume a high fibre diet.
6 Ensure an adequate intake of fluids.
Modification of Diet
A well balanced diet with B group vitamins and liberal fluid intake is recommended. Fibre
or cellulose content of the diet must be high. High fibre foods like whole grain cereals &
legumes, green leafy vegetables and other vegetables and other fibres foods should be eaten is
large amounts. Bland cooking is preferred. In spastic constipation high roughage is harmful. Fat
containing foods are useful for some because of their lubricating effect and stimulating action of
the fatty acids on the mucous membrane. A normal diet with light mental attitude and proper
exercise or physical activity is recommended for a constipation patient.
For spastic constipation, a soft bland diet is recommended. Small meals prevent stagnation
of food mass in intestine. Vitamin B supplements are essential. Daily 8 to 10 glasses of water
must be ingested to help stool formation.
Foods to be Included : Whole cereals, whole legumes, fruits like guava, apple, oranges,
bananas, grapes and green vegetables.
Foods to be Avoided : Highly refined foods and foods which leave very little residue such
as maida, meat, rice and candies.
Constipation among children :
Continuous usage of castor oil or purgatives by infants and children to clean the bowels
affect the muscle tone of the intestine. This leads to constipation and interfere seriously with the
absorption of fat soluble vitamins - vit A & K. Instead of purgatives lots of water, fruit juices
and fruits like banana, apple or guava or other fibrous fruits are better.
In cases of chronic constipation, inert laxatives like hydrophilic colloids i.e. isabgol & agar
agar may be helpful, because in the presence of water they swell up ands increase feacal volume.
A Day’s sample Diet plan for a constipation Patient
Personal Data
Age - 42 Yrs
Activity - Sedantry
Socio-economic status - Middle income group
Food habits - Non Vegetarian
Pathological Condition - Constipation

56
Menu Plan
Meal MENU
Early Morning Hot water with lemon juice.
Breakfast Wheat dalia
Omelette
Brown bread
Tea
Mid Morning Apple
Lunch Chapati
Rajma Curry
Carrots & Pea subzi
Spinach Raita
Cucumber & tomato salad
Evening Tea Coffee
Guava, papaya, sweet potato & cucumber
chaat
Dinner Sweet corn chicken soup
Vegetable noodles
Sweet & sour paneer & vegetables
Orange and Cabbage and salad greens
Bed Time Milk

57
 Lesson 10

OBESITY

Obesity is the most common nutritional disorders of the affluent countries as well as the
high socio-economic groups of our country. Obesity can be defined as generalized accumulation
of excess fat in the body. In clinical learns, it is defined as a condition of excess body weight
i.e. when a person is 20% or more above the ideal weight. Overweight term is at times used to
refer to individuals with body weight 16-20% an excess of ideal body weight.
Excess of fat is as much a hindrance as carrying a load of the same weight day and night.
It gives rise to breathlessness on moderate exertion. Obesity predisposes to diseases like angina
pectoris, coronary thrombosis, high blood pressure, diabetes, gall bladder diseases and osteoarthritis
of weight bearing joints. Surgery life expectancy dismisses with excess weight.
Assessment of obesity
(i) Standard Weight for Height Measures: These are based on weight ranges associated
with least mortality rates and serve as only a rough guide for estimating desirable
weight. They may not be the representative of the total population and so must be used
with discretion.
(ii) Body Mass Index: This is a measure of relative body fatness to evaluate the risk factors
associated with obesity. It is based on weight (in Kg) and height (in meters) with
minimum clothing and no shoes.
BMI = Wt (kg)
Ht. (Mt)2
BMI value indicative of Obesity are given in Table 1
Table 1
Grading of Obesity by BMI
Grade BMI (kg/m2)
Not obese 25
Grade I 25-29.9
Grade II 30-40
Grade III >40
(iii) Skin Fold Thickness: Measurement of skin fold thickness has been frequently used
as a measure fat deposited under the skin. (Sub-cutaneous). As the obesity increases,
the thickness of fat increases. Sub-cutaneous fat is about 14% of body weight in man
and 18% in women. The thickness of fat is measured at various sites with skin calipers.
The limitation of using skin fold measurement is, that, there is no agreement on the
number and sites that best reflect the actual body fat content.
Etiology
Obesity is either due to excessive energy consumption or decreased energy output resulting
in positive energy balance. The main contributing factors can be discussed as follows:

58
1. Physiological Factors
(i) Age and sex: The normal physiology of growth and development during the life cycle
contributes to accumulation of adipose tissue. Critical periods for the onset of obesity
are early childhood and adulthood; when no diet adjustments are made for decreased
activity. In women obesity normally occur during pregnancy and after menopause.
(ii) Endocrinal Factors: Obesity normally occurs at puberty, pregnancy and at menopause.
It clearly suggests the role of harmons for the occurrence of obesity. Obesity is also
associated with hypothyroidism or myxoedema. Crushing syndrome or over creation
of the adrenal gland leads to obesity in which excess fat is laid on the trunk and
usually not on the limbs. Intake of oral contraceptives may lead to obesity, as these
are hormonal in nature. Endocrine factors, however, contribute to less than 5% of the
total cases of obesity.
2. Genetic Factors
The role of genetics in obesity is not will understood, neither the genes responsible for it
have been identified. However, it has been observed that the chance of obesity in a child increases,
if both the parents are obese. However, the dietetic habit of a family rather than hereditary factors
may be responsible for obesity.
3. Psychological factors
These may be the etiological as well as the aggravating factors for obesity. In some cases
eating is a compensatory mechanism to attain self satisfaction, when there has been failure or
frustration is life. Tension, anxiety and the humiliation associated with being obese may further
make a person resort to food for emotional satisfaction.
4. Eating Habits
Over eating is the prime factor in obesity. Any excess of ingested calories over energy
expenditure is stored as fat. Nibbling in between meals, eating at night due to insomnia and
consumption of refined, starchy and fatty foods contribute to a high energy intake. An extra slice
of bread or a banana provides 50-100 calories and such slight excess, amounts to a considerable
accumulation in the course of time. From a variety of foods, an obese person usually chooses
fried potatoes, while a thin person prayers vegetable salad.
5. Physical Activity
Obesity is most common after the age of 35 years. Most of us do more physical work and
also take more exercise before this age than, in later life. With the proceed of middle age,
promotion to executive jobs involves longer hours at the desk with less physical work. Food
consumption either remains the same or may even increase with the improved economic status.
6. Social factors
Social pressures and need for eating out and attending parties is a common cause of excessive
intake of food and energy.
Consequences of Obesity
As already discussed obesity leads to mechanical disabilities, predisposes to renal, metabolic
and cardiovascular diseases and reduces life expecting, as well as psychological factors.

59
a) Psychological Factor
These may be the etiological as well as the aggravating factors of obesity obese people after
feel humiliated and unhappy. This further leads to eating for solution. Thus it’s a vicious cycle
where psychological factors leading to obesity and obesity leading to psychological factors.
b) Mechanical disabilities
The extra load of the body may cause flat feet and arthritis leading to pain in hips, knees
and spine. It also results in varicose veins and abdominal hernias. Fat is deposited under the
diaphragm and on the chest. This interferes with the normal respiration and predispose to bronchitis.
It also causes carbon dioxide retention and drowsiness.
Predisposes to other diseases
Obesity contributes to a number of health related problems namely hyperlipidemia,
hypertension, diabetes, pulmonary and renal problems and pregnancy complications. Alteration
in lipoprotein levels have been observed in obese people, which in turn is related to increased
risk of developing coronary atherosclerosis. Certain cancers such as cancer of gall bladder, biliary
tract, ovary, breast and cervix cancer in women and cancer of colon and prostate in men have
been associated with obesity.
Obesity is also associated with complications in pregnancy. The frequency of toxemia and
hypertension has been shown to be greatly increased and duration of labour is usually longer in
overweight women. The chances of caesarean delivery are increased with increased body weight.
Reduced Life Expletory
Obesity, because of its association with several other diseases and risk factors decreases life
expectancy.
Treatment
Successful weight loss can be brought about through a combined nutrition and behavioral
approach. The food plan should be well balanced and suited to the particular needs of the
individual, together with constant exercise for effective results.
Dietary Management: The objective of the dietary modification in the treatment of obesity ares
a) to bring about a gradual weight loss. A low calorie diet is designed to reduce the weight
by 3-4 Kg per month till the ideal body weight is reached.
b) To main a desirable weight and a good nutritional status. A moderate diet is designed
to maintain the ideal weight for the three to six months.
c) To control faulty food habits - A revision to the usual diet with such a mental reorientation
that foods of high calorie value are taken in small judicious helpings
Energy
The level of energy is adjusted to individual weight reduction requirements. A decrease of
1000 Kcals daily is required to lose about 1 kg a week and reduction of 500 Kcals brings about
a weight loss of about 1/2 kg. a week.
An average low calorie diet prescribed for women is 1000-1200 K cals. and for men is
1500-1800 Kcals. per day. A drastic restriction of energy is not advisable as it leads to hunger,
nervous exhaustion, weakness and inadequacy of other nutrients. The patient is checked every
week for weight loss and a weight loss of 3-4 kg is expected by the end of the month. Table 2
gives the value of energy needs per kg IBW based on activity. It can be used for energy intake
of any individual.

60
 Table 2
Energy requirement (Kcals/kg Ideal Body wt./day)
Activity Obese Normal Under Weight
Sedentary 20-25 30 35
Moderate 30 35 40
Heavy 35 40 45-50
Protein: Normally a slightly higher protein diet gives a feeling of satiety and also helps to
maintain a good nutritional status. Approximately 20% of the total energy must be provided from
protein. These should include good dietary protein in the form of low fat milk, lean meats and
whole pulses.
Fat: Energy provided by the fat should be 20% or less. Fat used should be unsaturated to
avoid heart related ailments. Fried foods are strictly prohibited.
Carbohydrates: Carbohydrates should provide about 60% of the energy. These should
mainly be complex carbohydrates like starches and dietary fibes. Use of simple carbohydrates
like glucose and sugar should be avoided
Minerals and Vitamins: Adequate minerals and vitamins should be provided by the diet.
The diet should include ample fruits and vegetables as they are low in energy, but a good some
of vitamins and minerals.
Fibre: To avoid constipation, the diet should have enough fibre by taking bulk producing
vegetable and fruits.
Fluids: Enough fluid in the form of water and other liquids should be given to avoid
constipation. It also gives a fuller stomach feeling.
Foods to be used in restricted amounts or avoided
1. High carbohydrate foods such as bread, cakes, cookies, dried fruits, rich pulses, potato,
sweet, honey, syrups, jams, puddings, chocolates, sugar etc.
2. Carbonated and matted beverages, alcoholic drinks and sweetened fruit juices.
3. High Fat foods like butter, ghee, fried foods, ice-creams, processed cheese, potato chips,
nuts, pastries, rich salad dressings etc.
Exercise: Aerobic exercise consists of activities that are sustained long enough to draw on
body’s fat reserve for fuel while increasing oxygen intake. Lean body mass burns fat in presence
of oxygen. Aerobic exercise helps in reducing weight by suppressing appetite and thus reducing
food intake and by increasing BMR and hence energy expenditure. It also lowers set point and
reduces body fat while retaining lean body mass.

61
 A sample Diet
A Day’s sample Diet for An obese female aged 39 years having a sedately life style with
a weight 65 kg and height 5’ 3”.
Menu :
Meal Menu Amount
Early Morning Tea without sugar 1 cup
Break fast Skimmed Milk, 1 cup
Boiled egg. 1
Toast without butter 1
Mid-day Watermelon 1 cup
Lunch Chappati 1
3
Thin Arhar Dal /4 katori
Skimmed milk curd 1 katori
Salad without dressing 1 plate
Tea Tea without sugar 1 cup
3
Sprouted Moong /4 katori
Early Dinner Chappati 1
Chana Dal with 1 katori
Bottle ground
Fruit salad 1 plate
Kheer with sugar free 1 katori

62
 Lesson 11
DIABETES MELLITUS
Diabetes Mellitus is a chronic disease that has affected mankind thoughout the world. The
records of the ancient civilization of Egypt, India, Japan, Greece and Rome describe the symptoms
of this disease.
It is a metabolic disorder characterised by the decreased ability or complete inability of the
tissues to utilize carbohydrates, accompanied by changes in the metabolism of fat, protein, water
and electrolytes. This defect is due to deficiency or diminished effectiveness of hormone insulin.
The insulin affect may be a failure in its formation, liberation, or action since insulin is produced
by the B-cells of the Islets of Langerhans in pancreas, any reduction in the number of functioning
cells, will decrease the amount of insulin that can be synthesized.
Prevalence:
Diabetes Mellitus is an important public health problem all over the world. In India the
prevalence of diabetes in India is about 2.1% in the urban population and 1.5% in the rural
population. This is about 2% of the total population in our country. Besides, there is an equal
number having undetected diabetes. Urbanisation and increasing prosperity have raised the
prevalence rates.
Type of Diabetes
Diabetes Mellitus (DM) is of there types:
i) Insulin Dependent Diabetes Mellitus (1DDM) or Type I : It usually occurs is much
younger adults, normally prior to the age of 20 yrs. This disease usually has an abrupt
onset and the abnormality of carbohydrate metabolism is severe due to lack of endogenous
insulin to control blood glucose levels. Insulin therapy is a must for these patients. The
patients are usually obese and may even be wasted and underweight. This type is
difficult to manage.
ii) Non-Insulin Dependent Diabetes Mellitus (NIDDM) or Type II : This type normally
occurs in middle mostly after 4 yrs. of age, but may occur before also. The onset is
gradual and there is some amount of endogenous insulin. Majority of the patients are
obese, and improve on weight loss and can be maintained on diet therapy. The treatment
is usually assisted by oral hypoglycemic drugs.
iii) Malnutrition Related Diabetes Mellitus (MRDM) : In this case Diabetes Mellitus is
secondary to other conditions such as pancreatic disorder, protein deficiency in early
years etc.
AT RISK OF DIABETES MELLITUS
Besides the known cases of DH, there are others who may be at risk of developing DM.
Some of these risk factors are discussed below:
(i) Impaired Glucose Tolerance (IGT) : Patients suffering from impaired glucoses
tolerance are regarded as ‘at risk’. Risk factor should, therefore, be minimlised in such
patients to prevent development of diabetes.
(ii) Gestational Diabetes Mellitus (GDM) : It is diagnosed when glucose intolerance is
detected for the first time during pregnancy. It does not apply to women known to be
diabetic before conception.

63
 (iii) Latent Diabetes : Subjects who have normal glucose tolerance but had a temporary
period of abnormal glucose tolerance earlier. Such a period of glucose intolerance
might have been precipitated by stressful situation like infection or trauma.
(iv) Potential Diabetes : Subjects with potential abnormality of glucose tolerance like
children, twins, siblings of known diabetics; women with bad obstetric history or with
a history of having delivered infants of high birth weight; ethnic groups with a high
predisposition for diabetes and obese subjects with a strong family history. These
subjects have a potential abnormality of glucose tolerance and therefore, are at a risk
of developing diabetes.
Etiology
The Main causes are:
(i) Heredity: There is a familial tendency to develop diabetes but the specific biochemical
defect and the mode of inheritance has not been identified. The tendency of diabetes
is believed to be inherited as a Mendelian recessive, characteristic. If both parents are
diabetic, all their children will be diabetic. If one parent is a diabetic and the other is
a diabetic carrier, half of their children will be potential diabetics. If one parent is a
diabetic and the other a non-diabetic and also a non-carrier, none of their children will
be diabetic, but they all will be carriers. If these children and their children consistently
marry non diabetics, the carrier tendency will eventually disappear. However,
environmental and other factors play a role in unmasking an underlying diabetics
genotype and determine whether a person with a genetic predisposition actually develops
the disease or not.
(ii) Age: The disease may occur at any age but about 80% of the cases occur after the age
of 50. Diabetes is thus mainly a disease of the middle aged and elderly.
(iii) Sex: In the younger age groups, diabetes is more commonly seen in males than in
females. In middle age, women are more affected and the chances increase with
pregnancy.
(iv) Obesity: There is a strong association between diabetes and obesity but it is uncertain
whether obesity is the result or the cause of diabetes. The majority of middle-aged
diabetics are obese, while only a minority of obese people develop diabetes. Whether
an obese individual develops diabetes or not is probably dependent on genetic factors.
Obese people are also less physically active than normal weight individuals which
increase the risk of diabetes.
(v) Dietary factors: A high intake of sugar has been related to obesity and may predispose
to diabetes as seen in Indians in South Africa. A low intake of fibre due to consumption
of refined foods is associated with high prevalence of diabetes in prosperous
communities. The specific effect of fibre in reducing the risk of diabetes is, however,
not clearly defined.
(vi) Infections: Infections, particularly staphylococcal, may unmask latent diabetes due to
production of hormones that are antagonist to insulin. There is increasing evidence of
Type I diabetes following viral infection, which brings about an autoimmune reaction
that destroy the B-cells of pancreas and impairs insulin secretion.
(vii) Stress: Physical injury or emotional stress may be a cause of unmasking latent diabetes
by eliciting Adrenocortical response. Surgical operation and severe infections may,
therefore, be contributing factors in precipitating the disorder.

64
 Secondary Diabetes- A minority of diabetes occur as secondary to some other disorders.
These are due to diseases (i) which destroy pancreas and lead to impaired secretions and release
of insulin or (ii) Abnormal concentration of certain hormones in the circulation which are insulin
antagonist e.g. Growth Harmone, Adrenocortical, Hormone, Adrenaline, Thyroid Hormone.
Clinical Pathology
The normal blood glucose level is 70 to 120 mg/100 ml. when this level is lowered, the cells
starve and die due to lack of energy while in case of hyperglycemia, the body’s life sustaining
water, electrolyte and acid base balances are disturbed. To maintain a normal blood sugar level,
a balance is kept between the
- entry of blood glucose from dietary carbohydrates, protein, fat and liver glycogen, and
- removal of blood glucose to prevent a rise above 120 mg/100 ml.
Insulin, The hormone secreted by the Beta-cells of the Islets of Langerhans of the pancreas helps
in regulating blood glucose in the following way :
- Insulin facilitates transport of glucose across the cell membranes through specialized
insulin receptors, which are located on insulin-sensitive cells in the adipose tissue. The
receptors have been found to be fewer in obese diabetics and their number increases with
exercise and weight loss.
- Insulin brings about glycogenesis i.e. conversion of glucose to glycogen for storage in the
liver.
- Insulin brings about conversion of glucose to fat (lipogenesis)
- Insulin inhibits lipolysis and breakdown of protein.
- Insulin increase protein synthesis by promoting uptake of amino acids.
- Insulin brings about glycolysis i.e. oxidation of glucose for release of energy.
Metabolic Changes in Diabetes Mellitus
In diabetes, insulin secreted by the pancreas is either insufficient or ineffective. This may
be due to a primary disorder of insulin secretion or due to insulin resistance because of a receptor
defect in the target tissues. As a result, glucose cannot be oxidized propertly through the main
glycolytic pathways in the cells to furnish energy and its leveling in the blood rises, leading to
hyperglycemia.
When the glucose concentration in the blood exceeds the renal threshold or the capacity of
renal tubules to reabsorb glucose from the glomerular filtrate, glocosuria i.e. presence of glucose
is the urine, occurs. In most of the people this occurs when blood glucose level is about 180mg/
100 ml. Increased concentration of glucose increases the osmolarity of the glomerular tubules.
This increases the volume of urine causing polymeric and nocturia. Loss of water lead to excessive
thirst i.e. polydipsia. Due to high blood glucose levels, the extra cellular fluid becomes hypertonic
and water comes out of the cells ultimately leading to dehydration.
Impaired utilization of carbohydrates leads to intra-cellular lack of glucose. This brings into
effect two compensatory reactions so as to provide metabolic substrate. Both lead to loss of body
tissue and wasting despite of food intake being normal or even increased.
Symptoms
Onset of diabetes or an uncontrolled state, the following symptoms observed
1. Polyuria or increased urination

65
 2. Polydipsia or increased thirst as a result of excessive water loss.
3. Polyphagia or increased hunger due to a failure to utilize food for nourishment of the
body.
4. General weakness.
5. Decreased resistance to infection especially staphylococcal infection and T.B.
6. Deceased ability of wound healing due to a high blood sugar and poor fluid balance.
7. Dehydration as a result of excessive water and electrolyte loss from the body, causing
dry furred tongue and cracked lips.
8. Vulvitis or balnitis due to an infection of the external genitalia by a fungus (Candida)
which flourishes on skin and mucous membranes having a high concentration of glucose.
9. Ketosis or ketoacidosis i.e. accumulation of ketone bodies in the blood as a result of
increased lipolysis. Breathing may be deep and rapid and the breath has acetone smell.
Ketosis, if not controlled, may lead to coma and finally death.
10. Degenerative changes in advanced cases include peripheral neuritis, retinitis,
atherosclerosis with associated diseases of coronary arteries and vascular changes in
kidneys causing nephropathy. Associated symptoms are failing or blured vision, pain,
numbness of the limbs and proteinuria.
Biochemical Changes
Laboratory tests show:
(i) Hyperglycemia or elvated blood sugar levels
(ii) Glycosuria or presence of sugar in the urine as a consequence to hyperglycemia
(iii) Ketonemia or elevated levels of ketone bodies in the blood
(iv) Abnormal glucose tolerance tests.
Dietary Management
Basic objective in the care of a diabetic person is to maintain and prolong a healthy and
productive life. The aims are:
• To maintain optimal nutrition so as to provide for adequate growth development and
maintenance;
• To achieve and maintain a desirable body weight;
• To provide relief from symptoms;
• To maintain normal blood sugar levels and
• To prevent, delay or minimize the onset of chronic degenerative complications.
Diet therapy has a major important role to play in realising these aims. Success or failure
of the treatment depends to very large extent on patient. Self-discipline and self-control under the
guidance of the doctor and nutritionist are needed for sound management. The patients have to
ultimately treat themselves and therefore, educating them on the objectives of treatment is extremely
important. Counseling the patient so as to make him understand the problem, reassurance, proper
instructions teaching means of self-care and monitoring go a long way in controlling the disorder.
A therapeutic diet plays an important role in the treatment of diabetes. The diet may be used
alone or in combination with insulin injections or oral hypoglycemic drugs.

66
 The diet plan of an individual is based on height, weight, age, sex, physical activity and
nature of diabetes. The following are the essential considerations:
1. Determining energy requirements.
2. Distribution of energy in terms of carbohydrate, fat and protein.
3. Determining the type of carbohydrate, fibre and type of preparations.
4. Distribution of carbohydrate.
Determining energy requirements
The energy value of the diet and its proportionate distribution needs to be calculated for
each diabetic patient individually. In case of IDDM or Type 1, the kilocalories prescribed are
based on needs for normal growth and development, physical activity and maintenance of desirable
body weight.
In case of NIDDM or Type II, as the majority of cases are obese, the kilocalories adjustment
is made to achieve weight loss.
This can be done in the following way:
a) Calculation of ideal body weight (IBW) on the basis of weight and Height.
b) Determining energy intake on the basis of kcal prescribed per kg IBW according to
activity and whether the individual is normal weight, obese or underweight.
Distribution of energy in terms of carbohydrate, fat and protein
The ratio of carbohydrate, protein and fat in the diet should be such that it maintains blood
glucose and reduces the risk of cardiovascular diseases.
a) The protein allowance is essentially the same as that for a normal individual and may
vary from 1.0 to 1.5 g/kg of desirable body weight. Proteins should provide about
15-20% of the total energy in the diet as compared to proteins providing normally about
10% of total energy. Slightly higher than normal protein are given, as in poorly regulated
diabetes large quantities of nitrogen are excreted in the urine. Another reason for
prescribing higher protein is that the metabolism of protein to glucose is slower and
hence there is less available glucose. Children require enough protein to meet growth
and development needs.
b) The carbohydrate allowance is estimated on the basis of the patient’s bloods sugar,
urine analysis, and available insulin. A moderate restriction of carbohydrate calories is
made to about 55-70% of total calories. An amount less than 100g carbohydrate per day
is not advisable as it leads to ketosis. On the other hand, more than 300g carbohydrate
per day may overburden the metabolic capacity. Not only the total amount of carbohydrate
but the type of carbohydrate and its distribution between different meals is extremely
important and depends on the type of treatment being followed.
c) The fat allowance of the diet is calculated so as to provide the rest of energy. Total fat
intake is lowered to 20% or less of the day’s energy intake in case of obese, adult
diabetics. As diabetic patients have an increases risk of atherosclerosis, the total amount
of fat must be restricted. At the same time, polyunsaturated fats should be given rather
than saturated ones.
d) Mineral and vitamin requirements of patients with well controlled diabetes do not
differ much from those of normal subjects. Neuritis, a frequent complication in diabetic
patient is prevented by liberal intakes of B-group vitamins especially thiamine; Vitamin

67
 and mineral supplements are not needed if the diet is well planned and nutritionally
adequate. Alcohol may be allowed only in moderation at the same time, its energy value
and the carbohydrate content must be taken into account. Beer contains about 20 to 60g
of carbohydrate per litre. Sweet wines and cider have a high sugar content, while
whisky and gin although free of carbohydrates, provide about 70 kcals for every 30ml.
Type of carbohydrate and amount of fibre and types of preparations
More of carbohydrate must be given as complex starches rather than simple sugars as they
breakdown more slowly to releases glucose. The presence of fibre in complex carbohydrate like
grains, vegetables and other starches increases intestinal transmit time, delays gastric emptying
and slow glucose absorption. Soluble fibre present in oats, barley, fruits and legumes has been
shown to lower fasting blood sugar and glycosuria and improve sensitivity to insulin. Some of
the high fibre foods are whole cereals like buck wheat (kootu), barley, ragi and oats, leafy
vegetable, beans whole pulses and legumes. Refined foods like maida, suji arrowroot, sago,
juices, etc. are low in fibre and should be avoided. Supplementation or cereals with gram is
beneficial. For example using three part of whole wheat flour with one part of gram flour in
making of chapattis; one part rice with one part whole pulse to make idli, dosa, khichri and two
part suji with one part of pulse to make upma. The rise of blood sugar after a meal does not
merely depend upon the amount of carbohydrate ingested but also on the rapidity of absorption
which varies with the fibre content, phylate, lactins and enzyme inhibitors.
Meal Intervals
In all diabetics, the amount and the time of food intake particularly the carbohydrate, should
be conferred to prevent fluctuations.
Foods not Allowed
Glucose, sugar, honey, all sweets, chocolates and candies.
Foods to be avoided or restricted
Potato, yam, arbi, sweet potatoes, Mangoes, grapes, bananas, alcoholic beverages, fried
goods, poories, pakoras, dalmoth, mathris, deep fried vegetable, dry fruits, rich salad dressings
cakes and pastries
Foods to be used freely
Green leafy vegetables, tomatoes, cucumber, reddish lenous, clear soups, black coffee and
tea without sugar, butter milk, pickles without oil.
A Day’s sample Diet for a Patient with NIDDM
Plan a day’s diet/menu for a 49 years old men, this built 5’7" weighing 64 kg and suffering
from Type II DM. He is a sedentary worker and a vegetarian.
Personal Data
Age - 49 years
Sex - Male
Work - Sedentary
Eating Habits - Vegetarian
Physiological condition - Diabetic Mellitus Type II

68
Recommended Dietary Allowances
Energy
i) Estimate IBW for heigh = 48 kg + (2.7 x 7 kg)
= 48 + 18.9
= 67 kg.
ii) For IBW estimate energy = 67 x 30
for Normal adult = 1910 cals.
The patient’s weight is 3 kg less than required but for a diabetic patient 10% less weight
is preferable. There for no adjustment for weight gain will be made.
Protein 20% of energy = 0.2 x 1910 = 95g
Fats 20% of energy = 0.2 x 1910 = 45.5g
Carbohydrates 60% of energy = 0.6 x 1910 = 285 g
Calcium = 400 mg
Thiamine = 0.95 mg
Menu Plan
Menu Food stuff Amount
Early Morning Tea without sugar 1 cup
Breakfast Cracked wheat porridge 1 medium bowl
Boiled egg 1
Toast with Paneer 1
And tomato
Tea without sugar 1 cup
Mid Morning Guava/Apple 1
Lunch Chappati 3
3
Arhar Dal /4 katori
Bottle gourd vegetable 1 katori
Salad cucumber, tomatoes. 1 plate
onion, raddish
Mid day Tea without sugar 1 cup
Idli/sandwich 2
Dinner Chappati 2
Cauliflower 1 katori
Spinach & Paneer 1 katori
Curds 1 katori
Salad, cucumber, corn. 1 plate
Tomato
Before Bed Milk without sugar

69
 LESSON 12
HYPERTENSION

Hypertension or elevation of blood pressure above normal is a symptom that accompanies

may cardiovascular and renal diseases. It can involve many organs and systems including the
heart, endocrine glands, kidney and central and autonomic nervous system. It has been clearly
shown to increase the risk of developing stroke, coronary heart disease, congestive heat failure,
peripheral vascular disease and nephrosclerosis.
Blood pressure is a continuous or graded phenomenon and the risk of hypertension increases
speedily with blood pressure level - either systolic blood pressure (SBP) or diastolic blood
pressure (DBF). Therefore, any definition of elevated blood pressure is arbitrary and serves to
classify people into risk categories. Table I shows the classification of blood pressure in adults-
18 years & above.
Table 1
Classification of Blood Pressure in Adults 18 Yrs. & Older*
Blood Pressure Range Classification
Diastolic Blood Pressure
< 85 Normal Blood Pressure
85 to 89 High Normal Blood Pressure
90 - 104 Mild Hypertension
105 - 114 Moderate Hypertension
> 115 Severe Hypertension
Systolic Blood Pressure (when DBP > 90)
140 Normal Blood Pressure
140 - 159 Borderline isolated systolic hypertension
> 160 Isolated systolic hypertension

*Adopted from JNC (1988)

Etiology
More than 90 percent of the people do not have identifiable cause of elevated blood pressure
and are said to have ‘Primary’, or ‘essential’ hypertension. Rest of the people with hypertension
do have an identifiable cause and are said to have ‘secondary’ hypertension. Secondary hypertension
may be due to
• Renal diseases
• Use of oral contraceptives in women
• Endocrine diseases such as hypothyroidism, hyperaldosteronism. Factors responsible
for primary hypertension are diet related or lifestyle related and can be linked as risk
factors, which are discussed below.
1) Age : Systolic blood pressure rises steeply from infancy to adulthood and levels off once
adult height is reached. Studies have shown that SBP increases on an average by about

70
 20mm Hg between ages 20 and 60 an additional 20mm Hg between the age of 60 and 80.
Diastolic blood pressure rises approximately 10 mm Hg between the age of 20 and 60 and
gradually declines thereafter.
2) Sex : Higher prevalence of hypertension has been found among males from adolescence till
45 years of age. After this age, mean blood pressure values are higher in women.
3) Heredity : A genetic predisposition to hypertension is generally there for humans, although
it has not been determined whether it is via a single gene or is a polygenic inheritance.
4) Social and Cultural Influences : People moving from rural to more urbanised way of live
usually show an increase in blood pressure. Little is known how these factors influence.
5) Exercise & Activity : Some studies suggest that increase physical activity and exercise have
a long term hypertensive effect, either independently or in association with diet. However,
the data is not very conclusive.
6) Dietary Factors : Some of the dietary factors such as total energy, dietary fat, dietry fibre,
sodium, potassium, alcohol and caffeine have been linked with high blood pressure.
a) Energy: Increased energy intake has been associated with increase blood pressure.
b) Dietary Fat: The ratio of polyunsaturated to saturated fat (P/S ratio) in the diet may
affect blood pressure. Increasing the P/S ratio to 1 or more with app. 25% of energy as
fat, has been associated with lowering blood pressure in hypertensive patients. This
effect is independent of sodium balance or body weight.
c) Dietary Fibre: Several studies have suggested that increased dietary fibre intake may
lower blood pressure. Vegetarians who diet are usually high in fibre generally have
lower blood pressure but a number of other differences in vegetarian and non-vegetarian
diets may also account for this variation.
d) Sodium: Since 1920, studies of isolated populations have suggested an association
between sodium chloride intake and blood pressure. Deprivation of sodium has led to
fall in blood pressure in hypertensives.
e) Potassium: It has been suggested that potassium salt supplementation in hypertensive
subjects lowered their blood pressure, especially the ones sensitive to sodium chloride.
f) Calcium & Magnesium: High dietary calcium intake has been associated with lower
blood pressure in men. A number of studies have also suggested that low dietary
magnesium level may be associated with higher blood pressure and large doses of
magnesium salts may lower blood pressure.
Alcohol: A strong association exists between moderate to heavy alcohol consumption and
hypertension. The effect of alcohol consumption on blood pressure appears to be more pronounced
in the elderly compared to the young.
Caffeine: Caffeine present in coffee can produce a short term significant increase in both
SBP and DBF, but its long term affect is not clear.
Symptoms
Most patients with hypertension have no symptoms and the condition is discovered in the
course of a routine medical examinations. Common symptoms observed are the headache, dizziness,
impaired vision, failing memory, shortness of breath, pain and gastrointestinal disturbances.
Extent of the symptoms depend on the elevation of the blood pressure and the length of the time
it has been present.

71
Treatment
Patients suffering from secondary hypertension should be treated for the underlying cause.
Patients suffering from primary hypertension generally do not have any overt symptoms and
continue to lead a normal life. Hypertension is a chronic, life long condition and may lead to the
development of CHD and stroke. Therefore, the treatment is directed towards controlling the
blood pressure within the normal limits by, the use of drugs diet and behavior modification. In
mild to moderate hypertension, this may be achieved by the diet restriction, controlling weight,
cessation of smoking, alcohol restriction, regular physical activity and moderation in life.
However in serve hypertension, there is danger of the involvement of other vital organs,
therefore, drugs such as diuretics and Beta blockers are used along with the above measures to
reduce the elevated blood pressure.
Dietary Management
Objectives of Diet Management are
i) To achieve a gradual weight loss in overweight and obese individuals and maintain their
weight slightly below the normal weight,
ii) To reduce the sodium intake,
iii) To maintain adequate nutrition .
To achieve the above objectives the diet modified is as follows :
i. Energy : Hypertension is often lowered with weight loss in obese patients. Even a
5 to 6% weight loss is sufficient to produce a substantial fall in blood pressure in
overweight persons with mild hypertension. Even normal weight hypertensive persons
benefit with slight reduction in weight. Therefore, energy intake should be adjusted in
such a manner so as to bring about weight loss and maintain it slightly below the normal
level.
ii. Protein: Protein should contribute about 15% to 20% energy in a low energy diet and
thus it is recommended that the diet of a hypertensive patient should have about this
much protein. Vegetable protein from legumes and pulses are high in protein and fibre
and low in sodium, should be included in the diet. Animal protein are rich in protein
as well as fat, therefore, should be used judiciously.
iii. Carbohydrate: Simple Carbohydrates like sugar and glucose should be avoided. Complex
carbohydrate from whole legumes, pulses, vegetable and fruits should be included. As
such, carbohydrate should account for 60-65% of the energy.
iv. Fats: Fats should not provide more than 20% of the energy in the diet. Since it is
important to raise the P/S ratio to 1 or above, saturated fat should be avoided and should
be replaced by unsaturated fat.
v. Sodium: Sodium restriction is affective in lowering blood pressure when used alone.
However, except for the patient with mild hypertension, the level of sodium permitted
is so low as to be impractical for most. The primary means of treating hypertension is
through diuretics and a mild restriction of sodium is recommended.
vi. Potassium & Calcium: An adequate amount of potassium is an essential part of
hypertension treatment. It can be achieved by including sufficient amounts of food rich
in potassium such as milk, fruits and vegetables. Some studies have suggested that

72
 optimum intake of calcium has a beneficial effect in hypertension, hence, calcium rich
food like milk, leafy vegetable should be included in the diet.
A. SAMPLE DIET IN HYPERTENSION
Plan a day’s diet for a hypertension female 50 Years old weighting 65 Kg and is 5’2" tall.
Her blood pressure is 150/90 mm Hg. She has been advised to reduce her weight. She needs a
sedentary life and is a vegetarian.
I. Persona Data
Age : 50 Yrs.
Sex : Female
Weight : 65 Kg
Height : 5’’2’
Activity : Sedentary
Food Preference : Vegetarian
II. Recommended Dietary Allowances
a) Energy Requirement
(i) Estimate IBW for height : 100lbs + (2x5 lbs)
= 110lbs = 52 Kg
(ii) for 1BW, estimate energy = 52x30 K cal/Kg
required = 1560 Keals.
(iii) Estimate weight above 1BW = 65 Kg - 52 Kg
= 13 Kg
(iv) Estimate energy required to = 1560+(8.8 Kcals above 1BW)
maintain present weight = 1560+115 = 1675 Kcals.
(v) Estimate energy required to = 1674 - 500
loose weight = 1174 Kcals
This will result in a weight loss of approximately 1/2 Kg/week.
B) Approximate distribution of energy from Protein, Fats and Carbohydrates
Protein (20% of energy) = 0.2x1174/4 = 59g
Fats (20% of energy) = 0.2x1174/9 = .26g
Carbohydrates (60% of energy) = 0.6x1174/4 = 176 g
C) Sodium = 500mg to 1000mg
Menu
Menu Food Stuff Amount
Early Morning Tea without sugar 1 Cup
Breakfast Wheat Poriddge 1 Bowl
Toast without Butter 1
Tea without Sugar 1 Cup

73
Mid Day Fruit 1 Bowl
Orange/Watermelon
Lunch Chapati 1
3
Chick Pea Curry /4 Katori
Pumpkin Vegetable 1 Katori
Curd from skimmed Milk 1 Katori
Salad (Cucumber, Tomato, 1 Plate
Lemon, Onion)
Evening Tea Tea without sugar 1 Cup
Moong Sprouts 1 Bowl
Dinner Chapati 1
3
Spinach & Paneer Veg /4 Katori
Bottle Gourd Vegetable 1 Katori
Fruit Salad Papaya/Apple

74
 Lesson 13
FOOD ADULTERATION
In any country, the food industry is a major industry with a very large turnover. In India,
except among the very rich, the money spent on food accounts for a large portion of the family
budget. In low income group families, money spent on food may be as high as 80% of the income
and about 55% and 30% in the middle income group and high income respectively. Food supplies
are dwindling in relation to population in the case of pulses, oils, milk, meat and eggs. At the
same, the demand for foods other than foodgrain is increasing with industrialisation. Due to
export possibilities, as in the case of spices, tea and Coffee, home market is at time strained. Thus
in case of both foods, which are in short supply and foods which are abundantly produced, there
is a real or artificial gap between supply and demand. When that happens, there is a great
temptation for the shopkeepers for either adulterating the food sold or selling food of inferior
quality.
What is adulteration?
The word “adulterated” implies an element of deceit. It means according to the definition
in chamber’s Twentieth century Dictionary “to debase, falsify by mixing with something inferior
or spurious.
Any food article is considered to be adulterated if its nature and quality are not upto the,
standards, which it professes to have, implicity of explicitly. Adulteration may be intentional or
incidental, former is a wilful act on the part of the adulterator, intended to increase the margin
of profit, food contamination is usually due to ignorance, negligence or lack of proper facilities.’
A third category is the contamination of food with harmful microorganisms during production,
and handling.
When is food deemed to be adulterated?
In order to protect the health of the consumer, the Govt. of India promulgated the Prevention
of Food Adulteration Act (P.F.A. Act) in 1954. The act prohibits the manufacture, sale and
distribution of not only adulterated foods but also foods contaminated with toxicants and
misbranded foods. A central food laboratory established under the act is located at Calcutta, for
the purpose of reporting on suspected products. More recently, the central Food Technological
Research Institute, Mysore has been recognised as another laboratory for the testing of adulterated
foods for the Southern Regions. “A Central Committee for Food Standards” has been constituted
under the act for the appointment of Food Inspectors by the state governments and their powers
have been defined. The state government will set up food laboratory and will appoint Public
Analyst with adequate staff to report on suspected foods.
In this unless otherwise requires:
(i) “adulterant” means any material which is or could be employed for the purpose of
adulteration.
(ii) “adulterated”—an article of food shall be deemed to be adulterated-
(a) If the article sold by the vendor is not of the nature, substance or quality demanded
by the purchaser and is to his prejudice, or is not of the nature, substance or
quality which it purports or is represented to be;

75
 (b) if the article contains any other substance which affects, or if the the article
processed so as to affect, injuriously the nature, substance or quality thereof;
(c) if any inferior or cheaper substance has been substituted wholly or in part for
article, so as to affect, injuriously the nature, substance or quality thereof;
(d) if any constituent of the article has been wholly or in part abstracted, so as to affect
injuriously the nature, substance or quality thereof;
(e) if the article had been prepared, packed or kept under instanitary conditions, whereby
it has become contaminated or injurious to health;
(f) if the article consists wholly or in part of any filthy, putrid, rotten, decomposed or
diseased animal or vegetable substance or is insect-infested or is otherwise unfit
for human consumption;
(g) if the article is obtained from a diseased animal.
(h) if the article contains any poisonuous or other ingredient which redcrs it injurious
to health;
(i) If the container of the article is composed, whether wholly or in part, of any
poisonous or deleterious substance, which renders it contents injurious to health;
(j) if any coloring matter other than the prescribed in respect thereof is present in the
article, or if the amounts of the prescribed coloring matter which is present in the
article are not within the prescribed limits of variability;
(k) if the article contains any prohibited preservative or permitted preservatives in
excess of the prescribed limits;
(1) if the quality or purity of the article falls below the prescribed standard or its
constituents are present in quantities not within the prescribed limits or variability,
which renders it injurious to health;
(m) if the quality or purity of the article falls below the prescribed standards or its
constituents are present in quantities not within the prescribed limits of variability,
but, which does not render it injurious to health;
Provided that, where the quality or purity of the article, being primary food, has fallen below
the prescribed standards or its constituents are present in quantities not within the prescribed
limits of variability, in either case, solely due to natural causes and beyond the control of human
agency, then, such article shall not be deemed to be adulterated within the meaning of this sub
clause.
This act came into force of 1st June, 1955 and the rules have been amended in 1968, 1973
and 1976. The standard which prescribed the minimum requirements for all types and categories
of foods—are amended when required by the Central Committee of Food Standards (CCFS).
Common Adulterants in Food Material
The prevention of food adulteration act makes it obligatory for merchants and caterers to
distribute foods coming up to specified standards. The term adulteration includes foods of inferior
quality (e.g. grains), food contaminated with other substances (e.g. ghee), as well as those from
which valuable factors have been removed (e.g. milk). It is also obligatory to make specified
addition to certain foods (for example, stabilizers for ice creams and til oil for hydrogenated oil),
and to specify the addition in the case of others (e.g. coloring matter, sweetening agents etc.)

76
 Despite the Act, the adulterated food continue to be sold on a large scale. Housewives and
others, concerned with the purchase of foods must be aware of the qualities expected in different
foods and the ways by which the same can be ascertained.
(i) Cereals and pulses : These being seasonal corps are usually for 6-12 months. During
this period degenerative changes may take place affecting their nutritional value because
of their liability to be subjected to insect infestation. The changes occuring in them
during this process can be summarised as follows:-
1. Loss in weight with decrease in the ratio of weight volume. This happens with insect
infestation.
2. As uric acid is the main end product of protein metabolism in insects, contamination
with uric acid increase proportionately with the storage period and insect infestation.
3. Decrease in organoleptic acceptability.
4. Increase in hydrolytic rancidity due to the deterioration of fat in the grain.
5. Deterioration in the quality of gluten in wheat and its products.
In most cases, the inferior quality of grains is apparent by visual inspection and tasting.
The permitted limit for uric acid is 20 mg. per cent, but market samples often contain more
than this. Uric acid content was found to be as high as 40 mg. per 100 g. In some wheat samples,
64 mg. per 100 g. in maida samples, 50 mg. per 100 g. in bengalgram flour samples and 69 mg.
per 100 g. in backgram dal, samples of balahar used in school lunch programmes have been
found to contain as much as 180 mg. per cent.
The addition of exrantous matter like grains stone, marble chips and other filth to grain is
also widely practised, specially in times of scarcity. These can be seperated by visual inspection
from a known weight of grain and weighed. The permitted limit is less than 4%. Samples of bajra
containing as much as 20-25% of extraneous matter have been found.
fungal and pesticide contamination of grains is also becoming common. Pesticides are
sprayed in high doses and their residues are toxic to man. Sometimes grain is tended for seed
and, therefore, heavily sprayed with pesticide is sold for human consumption resulting in death
and disability.
Wheat flour, suji, and maida are expected to have a gluten content of at least 7%. As wheat
contains 10-12% gluten, the permitted limit gives scope for adulteration.
Suzi is sometimes contaminated with iron fillings which can be detected by combing with
a magnet.
Kesari dal (Lathyrus) is mixed witivoiher pulses. This is a staple food of the low income
group in manys parts of Madhya Pradesh, Uttar Pradesh, Bihar and Bengal. This plant grows with
very little effort and yields abundant crops, even under adverse conditions.
Common pulses adulterated with lathyrus are:
1. The whole pulse like black masoor, black bengal gram with whole kesari dal,
2. Split pulses such as arhar and chana dal with kesari dal.
3. It is mixed with besan, hence in all preparations made out of besan.
Intake of more than 30% of the calories may result in a disease called Lathyrism, P.F.A. has
banned the use of Kesari dal in all form.

77
 (ii) Milk : It is subjected to more adulteration than any other commodity. The readiness
with which water can be added and fat removed, plus the fact that the demand is greater
than supply, encourage adulteration.
The composition of milk is dependent on a number of factors viz. the breed, the season, the
time of the day, the individuality of the cow, age and feed of the cow, estral period, the part of
udder from which milking is done and the period of lactation. Still some reasonable minimum
standards can be expected and have been set.
The adulteration of milk consists of either addition of extra water or the removale fat or
both. Sometimes extraneous substances like groundnut milk are added. The selling of diluted
buffalo milk as cow milk after coloring it, is a common practice (Cow’s milk has a slight
yellowish tinge not found in buffalos milk).
The constituents of milk bear a constant relationship with each other and this has led to the
formulation of standards such as the percentage of dry solids, protein-fat ratio and lactose -
protein ratio, which help in detecting abnormalities in milk sample resulting respectively from
addition of water, removal of fat or addition of extraneous matter like groundnut milk.
Milk has a specific gravity of 1.029 to 1.035, which can be measured by lactometer by the
housewife also. Milk adulterated with water when set as curd, can also be used as a criterion.
Milk adulterated with other substances become yellowish and frothy and does not form good curd
and it forms sour taste.
Khoa may contain maida, which can be detected by testing for the presence of starch.
The following standards have been prescribed by law for milk and milk products.
Milk Product Standards Specified
Skimmed Milk At least 8.5% non-fat milk solids.
Toned Milk 8.5% non-fat solids and 3% fat.
Butter Milk fat not less than 80%.
Condensed skimmed Milk At least 20% milk solids.
Chana At least 15% milk fat.
Cream Not less than 23% milk fat.
Ice-Cream Not less than 36% by weight of milk solids.
Khoya Not more than 10% moisture and not less than 20% fat.
(iii) Salt, Sugar and Jaggery: These may contain extraneous matter (insoluble matter) like
dirt, marble chip, chalk, dust, dirt etc. The same can be measured by dissolving the
substance in water and filtering the solution. The residue can be dried and weighed. By
law, such insoluble matter should be less than 1% in the case of salt 2% in the case
of jaggery and nil in the case of sugar. Sometimes salt and Sugar absorb moisture and
become heavy. According to law, the moisture content of salt and sugar should not
exceed 6.0 and 1.5% respectively. The same can be determined by weighing the sample
before and after drying. Metanil yellow colour is added to jaggery to give it a bright
appearance. This is a non-permitted colour due to its toxic effects on man, Washing
Powder may be added as an adulterant to bura.
(iv) Spices: Turneric and chillies are colored with lead pigments in order to give them a
bright color and the appearance of a product of good quality. Small quantities of lead

78
 are deposited in the skeleton and the progressive accumulation of the same over the
years may result in their release into the blood stream and consequently serious liver
damage etc.
Metanil yellow which is a carcinogenic agent is also used for coloring turmeric powder. It
is sold as Kesar color and used for the coloring of sweets and beverages, very widely and openly,
although it is prohibited by law.
Hing (as afoetida) is adultered with foreign resins. Pure hing dissolves in water to form a
milky white liquid and burns with a bright flame on being ignited.
The essential oils are extracted from cloves and cardamons, leaving behind a product
without its full fragrance. Cinamon powder, which is cheaper, is passed off as nutmeg.
Mustard seed is often adulterated with sand which may be as much as 10% or more in some
sample. Mustard seeds are adulterated with a toxic seed i.e. argemone seed. Argemone seed is
similar to mustard seed, except that it has a tail on one end. These can be identified under a
magnifying glass.
Crops of clay, grit, chaf, straw are found in coriander (whole) and cumins.
Garam masala and other masala’s contain more salt than prescribed. Salt being cheaper than
other expensive spices like black pepper, cinamon etc. leaves a margin for profit. Salt is not
harmful, but the quality of these masalas go down.
(v) Coffee, Tea and Cocoa: The quality of tea is affected by malpractices such as addition
of sawdust, exhausted (leaves, foreign etc. Microscopic example of tea sample discloses
a great deal about its purity. Other estimates which should be made, when a thorough
checkup is desired are moisture, total soluble and insoluble ash and nitrogen. Exhausted
tea leaves when used, are colored to make the appearance acceptable. The coloring
matter used, may be harmful for health.
In case of coffee, the raw seeds do not lend themselves to adulteration, except by way of
mixing inferior seeds with superior ones. But, when roasted and ground, they are liable to
adulteration of various kinds. The most common is the roasted seeds of dates and tamarind.
Other powder which may be added, is chicory powder. The important constituents of coffee are
caffeine, sugar, cellulose, protein and small quantities of fat and essential oils.
The ash content of the powder is used as an index of purity. The ash content of coffee is
less than 4-6%, of which about half is water soluble, while adulterants like chicory contain a
higher amount of insoluble ash.
In the case of cocoa, there is a temptation for the manufacturers to use the finely ground
sell as an adulterant, sago flour or starch coloured with red oxide or iron is also used. Microscopic
examination is useful in selecting the presence of shell.
(vi) Eggs: The shells of fresh egg have a glazed appearance. The air space between the
contents and top of the shell is not more that 1/4" wide. The eggs should feel heavy
for its size. When opened, the white should be clear and yolk, yellow and firm, without
the signs of embryo or a blood spot. Eggs must be discarded, if increase in air space,
unpleasant colour, discoloration of yolk, watery white mould infestation on the shell
and blood stains are evident. Fresh egg sinks in water while spoilt egg floats. This test
of efficiency is improved by using a salt solution containing 2 ozs of salt per pint of
water.

79
 (vii) Meat: The quality of meat is determined by its tenderness, juiciness and palatibility.
It is almost a universal practice to hang the carcass overnight after slaughter of the
animals. Thus meat sold to the public is generally hung for 15-24 hours at room
temperature. The carcasses become rigid a few hours after the slaughter of the animal.
This change is a accompanied by a drop in pH from 6.5 to 5.7 and again increases to
6.1 when stored for 20 hours.
Inspection of the meat is necessary to ensure that the meat is from a healthy animal in a
sound condition at the time of slaughter.
According to the report of the committee appointed by FAO/WHO in 1955, the following
steps should be take to ensure a safe meat supply:
1. Examination of animal before slaughter. ,
2. Examination of carcass and parts of carcass immediately after slaughter.
3. Removal of all unfit and diseased material.
4. Adoption of environmental conditions to prevent the contamination of edible parts.
5. Hygiene of meat handler.
6. Transport and distribution of meat under proper conditions.
Meat from diseased animal or if unfit due to hygienic conditions of improper handling by
the handler, is designated adulterated.
(vii) Vegetables and Fruits: The quality of vegetable varies considerably and although
some variation such as those in tenderness, color and moisture content are of no serious
concern from the stand point view of hygiene, their working quality and acceptibility
are affected. Vegetables are prone to mould and worm infestation. Vegetables and fruits
often contain the eggs of intestinal parasites, if they have been exposed to contaminated
soil and must be thoroughly scrubbed and cleaned before consuming.
(ix) Other Foods: It is particularly important to ensure the purity of prepared foods sold in
restaurants and sweet meat shops and rcady-to-eat foods such as candy, dates, raisins
etc. Sweet-meats may contain non permitted colours like metanil yellow in laddoos and
jalebis. Non-permitted colours are used by ice-cream, ice-ball vendors. The syrup used
for decorating the ice-balls may contain saccharine. Many a times Khoa preparation like
burfi, gulab-jamum contains excess of maida. The aluminium sheets are used to decorate
the sweet-meats in place of silver foil, which may result in poisoning from aluminium.
Food poisoning often results because of the Bacterial contamination, particularly sweets
prepared from milk; copper poisoning may result from the use of insufficiency tinned
copper brass vessels. Milk and prepared foods should be kept in containers made of
galvanised iron. Various preparation like pani-puri, bhel-puri, chaat etc. may contain
harmful Bacteria, resulting in gastro-intestinal infections. A number of snacks bought
by school children may be adulterated. Example of some of them are given in Table I.
Table I
Possible Adulterants in some school snacks
Name of the snack Adulterants
1. Am papad dust, insect exereta, harmful becteria
2. Ice candy (a) Metanil yellow

80
 3. Ice candy (b) Rhodamin ‘B’
4. Karachi Halwa (c) Orange II
5. Rasgulla (d) Blue VRs
6. Colored Sweets (e) Auramine
7. Sugar coated saunf (f) Malachite green
8. Churan Saw-dust, red-poisonous color, excess lead
9. Supari Orange B, Auramine, Dust, Other nuts, fragments of insects
10. Toffee, Biscuits Talc or soap stone, asbestos
11. Groundnuts Fungus & Fungal Toxins
(x) Packed Foods: Many hazards may result from packaging material used for packaging
the foods. Polythylene, polyvinyl chloride and altered compounds are used to produce
flexible packaging material. While this method of packaging is very convenient, it may
contain noxious thermal breakdown products, which could be injurious to health. Further,
temperature used for heat sealing, or sterlisation may result in the formation of toxic
residues. It has been observed sometimes that in foods like pickles, the acid and oil
could attack the plastic packaging material and creates a health hazard.
Tin is used for packaging various materials like oils, fats, beverages, biscuits and all types
of processed foods stuffs, which is normally well tolerated. Yet there are many cases of tin
poisoning due to ingestion of contaminated fruit juices. Tin poisoning may result (a) when the
canned food is acidic; (b) when the food contains nitrates, oxalates copper or certain sulphur
compounds; (c) when moist food is left in the can after opening.
Reference
1. Food and Nutrition by Education Planning Group, Delhi, Arya Publishing House.
2. Fundamentals of Foods & Nutrition; S.R. Mudambi, M.V. Rajagopal; Wiley Eastern
Limited.
3. Applied Nutrition; R. Rajalaxmi: Oxford & BH Publishing.
4. Food and Nutrition, Dr. M. Swaminathan, The Banglore Printing and Publishing Company
limited.

81
 Lesson 14
ILL EFFECTS AND DETECTION
OF SOME COMMON ADULTERANTS
Adulteration of food articles is rampant in the country and has to become a grave menace
lo the health and well being of a community. It makes a heavy dent in the already low nutritional
standards and the benefits of many public health programmes, on which large sums of money are
spent. The consumer is not a producer himself and has to depend upon the market. He is
blissfully ignorant of the insidious hazards of consuming adulterated foods, which may be
adulterated at all stages, from production to retail. Foods of excellent nutritive value to begin
with, may become unfit for human consumption during storage or handling, Insect infested
grains, rancid fats and contaminated milk and sweets are example. An average consumer is
mostly guided by the price, visual appearance and claims of the advertisement. He has still to
grasp the idea of a good quality in his mind.
Ill Efects of Adulteration
Main ill effects of adulteration may be classified into three main categories.
(a) Consumer is penalised by paying for the adulterant along with the food.
(b) Consumer is getting less for his money’s worth i.e. the nutritional content of the
adulterated food may be less than the pure food, as in case of milk adulterated with
water.
(c) Lastly, but not the least, are the numerous health hazards that can adversely affect the
consumer. These are discussed in detail below.
Health hazards: Numerous health hazards may occur due to adulteration, which could be
intentional or incidental. Intentional adulterants are added to increase the margin of profit. These
could also be due to contaminations with bacteria or fungi during storing and handling.
(a) Health Hazards due to Intentional Adulterants:
(i) Sand, Stones, earth, marble chips and otfur fifth may be found in food grain, pulses,
spices etc. Stones and sand if present could have an adverse effect on the teeth and
soft linning of the digestive tract. Filth in any form is a health hazard, as it may contain
millions of disease producing micro-organisms.
(ii) Talc and Chalk power are usually added to wheat flour, powdered spieces which are
white and to other such foods. Being undigestible by the human system, these can
effect the normal digestion.
(iii) Water and excess moisture are added to milk curd, paneer, butter and other products.
It is not a health hazard unless the water is contaminated, and if so, it may result in
gastro-intestinal disturbances.
(iv) Asbestos is often used in filtering fruit juice and soft drinks. It is a natural fibrous
silicate. It has been found that these fibres which are very fine and can only be seen
through an electron microscope, are present in clear juices. These are known to cause
gastro-intestinal cancer.
(v) Sugar and Sweeteners: If sugar is added in pure form to honey, then no health hazard
is involved. Toxic sweeteners like cyclonates, dulcine or saccharine may be present,
where not permitted as in sweetmeats or in excess of the permissible amounts. Fruits
are injected with saccharine to make them more sweet in taste.

82
 Additives are colorings, preservatives, flavourings, anti-toxicants, emulsifying and stabilizing
agents, anti-microbial agents. The amount of these additives, if exceeds the minimum amount
permissible, may have harmful effects, varying from minor gastro-ailment to cancer.
(vi) Mineral oil mixed with edible oil, when taken in sufficient amount may cause gastro-
intestinol disturbances and vomiting. These are petroleum derivates and much cheaper
than edible oils. These have been known to adversely effect the absorption of vitamin-
AO.
(vii) Rancid Oil is sometimes mixed with edible oil for increasing the margin of profit.
Food stuffs cooked in this oil may loose its vitamin content.
(viii) Argemone Seeds: These seeds look very much like mustard seeds and mixed with
mustard seeds as an adulterant. Argemone seed is different from mustard seed by
possessing a little tail at one end. When oil is extracted from adulterated mustard
seeds, it is highly toxic because consumption of argemone oil can lead to loss of eyes
sight, heart disease, epidemic dropsy resembling wet beri-beri.
In 1971 in kagaznagar (West Bengal), hundreds of families including young children, became
victims of epidemic dropsy due to adulteration by argemone oil. Even in 1973, these was a report
from Hari Nagar, New Delhi. This made the Union health Ministry issue a warning to public at
that time, against buying mustard oil from unreliable sources.
(ix) Kesari Dal (Lathyrus) kesari dal would be mixed as an adulterant with the other dals.
(a) The whole pulses like black masoor, black bengal gram with whole Kesari dal.
(b) Split pulses such as arhar and channa dal with kesari dal.
(c) It is mixed in besan, hence all preparations of besan.
When more than 30 per cent of the total calories consumed is contributed by this dal, it can
cause lathyrism, a from of crippling paralysis of both lower limbs, mainly in boys and men in
the age group of 5 to 45 years. If a diet consists of 40% or more of lathyrus, then this disease
manifests itself in 2-4 months. The disease starts with stiffness of the knee joints and legs with
pain around the knee and ankle joints. Within 10 to 30 days of the onset of the symptoms,
paralysis of the lower limbs set in. The patient gradually becomes crippled as his knees are bent
and stiff.
(x) foreign seeds, barks, leaves or other foreign matter:
(a) Foreign seeds may be colored to look like genuine food material. These are added to
increase the bulk, as most of these have no value as condiments. As such they may
not be harmful, but addition of toxic colors to it could be harmful. Cumin seeds,
cardamons, poppy seeds, black pepper etc. are adulterated with these foreign matter,
e.g. the seeds of wild grass which resemble cumin seeds are added to it. Fenugreek
and aniseed may similarly be adulterated with excess of other edible seeds. Black
pepper may contain dry papaya seeds, cardamom may contain damaged seeds or
substitutes.
(b) Roasted tarmarind and date seeds are powdered and mixed with coffee or cocoa.
(c) Chicory seeds are powdered and mixed with coffee powder.
(d) Thick bask of cassia is added to cinamon as an adulterant.
(e) Foreign leaves or exhausted tea leaves are colored. These and saw dust have been
mixed with fresh tea leaves.

83
 (f) Exhausted bark or seeds of coffee or spices are suitably dried and colored and substituted
for fresh ones. In such cases the sample will be deficient in its volatile oil content.
(g) Powdered bran and sawdust are often present in atta, suji and ground spices.
(h) Strips of jute, paper or foreign material may be suitably dyed to pass off as saffron.
(i) Resin or gum is generally used as an adulterant in asafoetida.
(j) Cinamon powder which is cheaper, may be passed of as nutmeg powder.
(k) Refind starch or mashed potato being cheap are used in milk and milk products like
khoya, burfi, ice-cream, rasgulla, butter, ghee, cheese. Rice starch or starch from
tapioca are added to arraroot, turmeric powder, coriander and mixed spice.
(xi) Toxic colorings: Color is added to increase the variety in food and also its acceptibility.
Color is widely used in preperations of ice-creams, dairy products, biscuits,
confectionaires, pastries, fruit products, processed and preserved vegetable, jelly, custard
powder, soup powder, toffee, sweets etc. Many of the colors are not permitted, due to
its harmful effects and addition of these colors is adulteration. The common non-
permitted colours used are mineral pigments like lead chromate, red or yellow earth,
color dyes like metanil yellow, Rhodamine B, orange I and II. Most popular is the
water soluble metanil yellow. It is widely used to color pulses and spices, sweet-meats,
(jelabies, ladoos, karachi halwa) and aerated waters. These colorings are carcinogenic
in effect. Intake of these colors produces various abnormalities of eyes, bone, spin,
lungs, ovaries, testes etc. The non-permitted coal dyes are generally found as adulterants
in the followings foods :
Metanil yellow : Ice Candy, faluda, ice balls, pulses.
Orange II : Karachi Halwa
Rhodamine B : Red Chilly powder and churan
Blue VRS : colored sweets
Auramine : sugar coated saunf and supari
Malachite green : Coconut
(b) Health hazards due to Metal Contaminants:
Most metals are toxic when present beyond a specific concentration. Its poisonous effect is
neutralised in the beginning, when they combine with proteins. With the increase in concentration,
symptoms such as vomiting, nausea, stomachache may arise.
(i) Arsenic: It is present in small amounts in air, water and oil and slowly finds its way
into food. Arsenic pesticides are the main source of arsenic contamination of foods.
For example fruits such as apple and grapes sprayed with lead arsenate, if eaten
without washing, could be harmful. The quantity of arsenic allowed in food products
various from 0.1 p.p.m. (in milk) to 5.0 p.p.m. (in pectins, spices) depending upon the
food. When arsenic concentration is higher than prescribed, it can cause dizziness,
chills, cramps and paralysis.
(ii) Lead: Human system absorbs lead not only from foods, but also from water and dust
in the air. It is absorbed more easily from liquid foods than solid. Lead is present is
varying amounts in food stuffs such as shellfish, herbs, edible gelatin, pectin, food
colorings, tea, baking powder, custard and peaches. In addition to this, food may be
contaminated by.

84
 * Exposure to leaded dust in air.
* Contant with Equipment packing i.e. tin plate containing lead.
* Lead pipe through which drinking water is obtained.
* Use of turmeric powder with lead chromate.
* Spraying and dusting of fruits and vegetables with lead containing pesticide.
* Use of synthetic dyes.
The quantity of lead allowed in food products varies from 0.5 p.p.m. (in concentrated soft
drinks) to 10 p.p.m (in liquid pectin and chemicals not otherwise specified), depending on the
food product. If build up of lead in blood increase beyond the critical blood level of 40 to 80
mg. per 100 ml of blood, mental disturbances and behaviour disorders may be produced followed
by paralysis, convulsions and permanent brain damage. Milk has been recommended as a good
antidote for lead prisoning.
(iii) Mercury: It is present is traces in the form of its compounds in all water and food. The
effluents from many industries now a days have high concentrations of mercury and
human beings and animals consuming crops grown with such water or fish from such
areas could develop mercury poisoning. Intakes of about 0.0033 mg/kg. of mercury and
methylmercury per person are harmful. Such intakes of mercury could affect the brain
with the patient becoming blind or deaf. Convulsions with intense plain is also one of
the symptoms of mercury poisoning.
(iv) Tin: Various kinds of food come in close contact with tin in the process of preperation
and storage. Beverages and canned food stuffs normally contain very small amount of
tin which are well tolerated, yet, there are many cases of tin poisoning due to ingestion
of contaninated fruit juices. A variety of containers made of this plate are also used for
storing oils, fats, beverages, biscuits and all types of proceed foods. Tin poisoning may
result.
* When the canned food is acidic.
* When the food contains nitrates, oxalates, copper or certain sulphur compounds.
* When moist food is left in the can after opening.
The maximum tin content allowed in any canned food stuff is 250 p.p.m. High tin content
in foods (about two to three grams) may cause severe headache, vomiting, vertigo, photophobia,
abdominal pain, dehydration and retention of urine.
(v) Copper: It is normally present in food stuffs in traces, but contaminated food causes
diarrhoea, abdominal pain and vomiting. Acute poisoning by copper salts brings
constriction in throat and an astringent taste with thirst within 5-10 minutes.
(vi) Aluminium: Sweetmeats were generally topped with their silver foil. Now-a-days very
often this aluminium foil is used. This can cause undesirable reactions in the digestive
tract, interfering with the normal functioning.
(vii) Cadmium: It is a silvery soft, white metal, used for plating utensils and electric
cookers. It is resistant to alkalies, but dissolves in the acid present in fruit juices, wines,
soft drinks. The salts of cadmium thus formed, dissolve in food and can be harmful
to health, 15-30 minutes after ingestion of contaminated food.

85
 (c) Health hazards due to Pests, and Pesticides:
Pests such as rodents and insects once get into food, can cause heavy damage due a high
degree of filth in the form of excreta, bodily secretions, insects fragments and hairs as well as
disease bearing and spoilage micro-organisms.
(i) Rodents: They usually include rats and mice. A single rat voids 10,000 dropings and
4 litres of urine annually, besides constantly shedding some of its coat made up of 5
lakh hairs. The kidneys of these rodents have an organism, which causes disease of
liver (spirochaectal jaundice). This is usually transmitted to man through food or water
mixed with rat urine. Some bacterias are found in rat urine, which resist ordinary
cooking temperatures. Rat alone may cause, as many as 35 diseases. Their rate of
reproduction is very high, which creates a major problem.
(ii) Insects: Insects such as beetles, weevils is, bores, enter in foods like cereals, pulses and
their flours, when kept in warm, humid climate. They practically eat up the whole grain
or food and in this process uric acid and a offensive odour and taste develop in the
food.
(iii) Pesticides: At times, food is directly mixed with the pesticides, although it is against
law. Organic pesticides such as DDT/BHC, Malathion, Pyrethrum are used, but these
leave behind a residue (the unchanged chemical or its derivative) on the food. These
are toxic depending on the nature of the pesticide. The maximum concentration of
pesticide residue, that is permitted in or on the food is laid down by PFA. The maximum
permissible residues allowed for DOT, and malathion is 3 p.p.m. For pyrethram it is
10 p.p.m. Many time, pesticides residue could be much higher than this figure and
could the be toxic. Acute poisoning by DDT and BHC are rare, but continued
consumption of these may lead to chronic poisoning.
(d) Health Hazards due to Packaging
The most common packaging material in the food industry is PVC (polyvinylchloride) and
PE (Polyethylene or plastic), to produce flexible packaging material. While this method of
packaging is very convenient, it must not contain any noxious thermal breakdown products,
which could be injurious to health. Furthermore temperature used for heat sealing, or sterlisation
should not result in formation of toxic residues. It has been observed that in foods like pickles,
the acid and oil could attack the plastic packaging material and create a health hazards. To avoid
such incidents, it is essential that only food grade plastic packaging material be use for packaging
foods.
(e) Health Hazards due to Bacterial and Fungal Contamination
Improper and unhygenic methods of storage, handling, and preparation may result in
contamination of food material with numerous bacterias and fungi. This has a direct and immediate
impact on the public health. The foods that are commonly contaminated are milk and milk
products, meat and meat products, poultry, eggs, fish, raw vegetables, cereal-based products.
Food serves as a vehicle to transport these micro-organism to man. In the host, they multiply and
during the process of growth, some microbes produce toxic metabolities, which may remain in
the food even after organism dies. The symptoms of pathogenic bacterial contamination may be
nervous disturbances or gastro-intestinal disorders.
Simple tests for detection of food adulterants
The adulterants used are so similar to natural food-stuffs that it becomes very difficult for
a common man to detect them. A few simple tests can be conducted to detect the presence of
adulterants.

86
(a) Cereals and Pulses
(i) Stone chips in Rice: Place the rice grains on the palm of the hand and gradually
immerse the hand in water. The stone chips will sink.
(ii) Inorganic and Organic Matter: Inorganic matter consists of matter like sand, gravel,
dirt, pebbles, stones, lumps of earth, clay or mud. Organic matter could be chaff, straw,
edible seeds. These may be used as an adulterant in rice, sugar, pulses, wheat, jowar,
mustard, edible seeds etc. Such matter could be observed and removed physically.
Presence of these substances is allowed to the extent of two to five percent, depending
on the food product. Beyond this limit, food is considered adulterated.
(iii) Infested Grain: The grain may become infested by pests and rodents during storage.
These can be observed and removed physically. Presence of infested grain is allowed
upto one percent, beyond which the food produced is considered adulterated.
(iv) Kesari Dal (Lothyrus) in Arhar, Masoor and Ghana Dais: Kesari dal has a
characteristic wedge shape. There are two varieties. One is small and resemble masoor
dal. The larger is the size of arhar. The husked kesari dal is mixed with arhar and
chana dals. The unhusked one is mixed with black masoor or bengal gram. Kesari dal
can be separated by visual examination.
It can be tested chemically also. Add 5 ml. of normal hydrochloric acid to a small quantity
of dal in a glass. Keep the glass in simmering water for 15 minutes. Development of pink colour
indicates the presence of kesari dal.
(v) Ergot in Bajra: Ergot seeds are lighter than bajra seeds. If a small quantity of grains
are put in 20% salt solution of water in a glass, ergot seeds will float to the surface,
while bajra will settle down.
(vi) Argemone seeds with Mustard seeds: Argcmonc seeds are small and black in colour,
resembling mustard but not uniformly smooth and round. They can be identified under
a magnifying glass.
(vii) Coal tar dye in Roasted Gram: This would be detected by visual observation.
(vii) Iron fillings in Suzi/Semolina: By drawing a magnet over the sample, iron fillings
will cling to the magnet, thus revealing their presence.
(b) Milk and Milk Products
(i) Water in Milk: The specific gravity of milk lies between 1.029 to 1.035. With the
increase in fat content, the specific gravity decreases and conversely as the non-fat
solids increase, the specific gravity increases. However, water added may not be detected
by specific gravity, if water is added and the fat is also removed.
(ii) Starches in Milk: Addition of a drop of iodine solution, to starch containg milk, will
turn it blue. Pure milk turn a coffee shade.
(c) Fats and Oils
(i) Vanaspati in Pure Ghee: One teaspoon of pure ghee or butter is mixed with equal
quantity of concentrated hydrochloric acid in a test tube. To this 2 to 3 drops of
furfurol solution is added and the test tube is shakcd well and allowed to stand for
five minutes. Appearance of pink colour in the lower layer of acid means that vanaspati
is present in pure ghee/butter as an adulterant.
(ii) Mashed potatoes, sweet potatoes and other starches in Butter: Iodine test is
performed i.e. addition of a drop of iodine solution turns the butter blue.

87
 (iii) Cheap edible oils in vanaspati: A solution of washing soda is added to the sample
of vanaspati and shaked well. Appearance of a froth on top is taken as an inference
that cheap oil has been added to vanaspati.
(iv) Argemone Oil in Mustard Oil: 5 ml. of test sample is heated with 5 ml. of nitric
acid for two or three minutes. Appearance of red colour is an indicator of the presence
of argemone oil.
(v) Rancidity in Oils: To 5 ml. of sample in a test tube, 5 ml. of hydrochloric acid is
added. Stopper the test tube and shake vigorously for thirty seconds. Add 5 ml. of 0.1
per cent phloroglucinol solution in either. Shake for thirty seconds and allow to stand
for thirty minutes. A pink or red colour in the acid layer indicates that the oil sample
is rancid.
(d) Sugar and Sugar Products
(i) Chalk or any other dust or dirt in Sugar: Dissolve a little of the sample is hot water,
Sugar will dissolve while the impurities will not.
(ii) Jaggery with mctanil yellow: Hydrochloric acid is added to the solutions of jaggery.
Appearance of magenta r«l colour is an indicator of the presence of adulteration with
the meianil yellow colour.
(iii) Bura (Sugar powder) with Washing Soda: With hydrochloric acid, the audlterated
sample give effervescence. If dissolved in water the washing soda will turn red litnus
into blue.
(e) Spices and Condiments
(i) Metanil yellow colouring in Haldi, Haldi Powder: To 2 g. of sample, add 5 ml. of
alcohol. Shake and add a few drops of concentrated hydrochloric acid. A pink coloration
indicates the presence of metanil yellow.
(ii) Artificial colour in Chillies: (i) Rub Ihc outside of a chilli with a cotton soaked in
liquid paraffin. If the cotton extracts the colour and becomes red, it is an indication that
the sample has added colour, (ii) Mix a small quantity or red chilly powder in ether.
Take the extract and add conccnteated hydrochloric acid, A dark pink colour indicates
that ihe sample has added colour.
(iii) Grit, Clay, extraneous matter in common Salt: Dissolve the sample in some water
in a tumbler. Pure salt will completely dissolve in it, while extraneous matter will be
seen in the solution or it will settle down.
(iv) Grit in Spices: Spices can be dissolved in carbon tetrachloride. In water, the sprinking
of small quantity of the samples will result in floating of the spices while grit will settle
down. A tumbler should be used for testing.
(v) Resin or Gum in asafoetida: Pure asafoetida dissolves in water to form a milky
solution. Pure asafoetida burns with a bright flame on ignition. Any deviation will be
the indicator of adulteration.
(f) Beverages
(i) Artificial colourings in tea-leaves: Deposit the tea leaves on a moistened blotting
paper. Artificially dyed tea leaves will impart colour to the moistoned blotting paper
immediately.
(ii) Powdered date seeds or tarmarind Powder in Coffee: Spinkle a little coffee powder
on a piece of blotting paper and spread a few drops of potassium hydroxide solution

88
 over this paper. If a brown colour emerges around the particles of coffee, adulteration
is established.
(iii) Starch in Coffee: Make a decoction of the coffee. Decolorize it by adding potassium
permagnate soludons. Then add a drop of iodine solutions. Blue colour formation
indicates adulteration with starch.
(iv) Chicory in Coffee Powder: Sprinkle a small quantity of coffee powder on the surface
of water in a glass tumbler. Particles of genuine coffee powder will float, but chicory
powders will begin to sink within seconds. They will also leave a stain of colour in
the water.
References
1. Food and Nutrition for senior students, Education Planning Group Arya Publications.
2. Essentials of food and Nutrition, Applied Aspects, Vol II, Dr. M. Swaminathan.

89
 Lesson 15
ACCIDENTAL CONTAMINATION

Food can be contaminated by accident also, through chemicals, the utensils we use or the
packaging we use. It can also occur due to various microbes like bacteria or fungi. At times
certain plants animals have natural poison which are harmful for the human body e.g. certain
mushrooms, favabeans etc. Contamination of food accidently by any of the above mentioned
sources result in food poisoning. This chapter deals with this type of food poisoning and the
remedeal measures.
Food poisioning is defined as illness resulting from ingestion of food containing certain
inorganic chemicals, poisions derived from animals and plants and toxic products produced by
several species of bacteria and fungus. Essentially they are of three types as given in fig.1.
Plants and animals
Chemicals

Food Poisioning

Microbial i.e. bacterial or fungal

Fig. 1: Three types of food poisioning
Food poisioning is characterised by its very explosive nature of illness. The prominent
symptom is gastro-intestinal upset, therefore nausea, diarrhoea, vomiting and abdominal cramping
are seen, it is different from food infections like cholera and typhoid for two reasons. Firstly, the
incubation period of infection is longer than food poisioning and secondly in food poisioning,
the toxin is present in the food itself at the time of consumption and affects immediately; whereas
in infection, food is only a carrier and the bacteria invades the body, grows and multiplies and
leaves toxic products which damages the tissue, e.g. in typhoid there is inflamation and eruptions
in intestine followed by high fever. Similarly, in cholera there may be discharge of mucous and
blood in loose stools due to disruption in the integrity of the gut muscles. There is a possibility
that micro-organisms produce the toxins and escape or are killed on their own or on cooking, but
toxic residues are still present and are potent to cause food poisioning.
Let us now study, the three types of poisioning in detail. These are :
— Chemical poisioning
— Plant and animal poisioning
— Microbial poisioning (both bacterial and fungal)
1. Chemical Poisioning
Incubation period for this is very short. Incubation period, i.e. the time taken for the first
symptom to appear after eating the unacceptable food is 10 min—2 hours.
Alcohol Poisoning—Almost every year it is heard that a group of people became blind
because of unacceptable alcohol consumption due to methyl alcohol (CH3OH) toxicity. The
methyl alcohol toxicity appear when the preparation of alcohol (C2H5OH) is crude. Methyl
alcohol toxicity appears within 18 to 48 hours after consumption. Methyl alcohol is also used to

90
denature alcohol i.e. make ethyl alcohol unfit for human consumption and prevent stealing of
ethy alcohol. Its consumption leads to blindness, abdominal disorder and ultimately death.
Selenium (Se) toxicity : Small amount of selenium is required by the body, but excess leads
to gastro intestinal disturbances, dyspepsia, anorexia, stunted growth, falling of hair. The toxicity
occurs where soil is rich in selenium, therefore, plant and cattle are rich in selenium leading to
exceeding the toxic level in man.
Antimony poisoning: It occurs from eating food which are looked in cheap, grey enamelled
utensils or by consumptions of water rich in industrial wastes.
Cadmium poisoning (Cd): is associated with acidic liquids stored in cadmium plated
metallic utensils or corrosion of water pipes, crops of cadmium rich soil, by industrial waste and
environmental pollution. Also, by cigarette smoking one inhales 0.1 my cigrette. If a 70 kg man
takes 25-60 meg/day toxicity can occur. It competes with zinc in body and affects growth and
leads to stunting. It is a cumulative poison and is reabsorbed by renal tubules leading to renal
failure. It is retained in large amounts in kidney and liver and can therefore also lead to liver
damage (liver cirrhosis). Due to the effect on renal system, it can also cause hypertension and
anaemia.
High calcium and high protein diet protects from cadmium toxicity. Further prevention of
this toxicity requires lowering from environmental pollution and the industrial waste.
Nitrates, Nitramine, and Nitrosamine: Their toxicity leads to digestive problems, cyanosis
in 2-3 days. Cyanosis in small children can lead to death. Nitrates can come from water, fertilisers,
foods like spinach, cured meats. But fortunately, on cooking nitrates are converted to nitrites
which is not harmful. Nitramine and nitrosamine are carcinogenic, but its occurrence has been
reported only from South Africa where plantain and banana is eaten in plenty (40 mg/l00g
banana). It leads to myocardial fibrosis.
Cancer is reported on use of nitrate and nitramines in cured meats.
Lead Poisoning (Pb): Lead salts are sprayed on fruits and unwashed fruits can accidentally
cause lead poisoning. Some of it is received through water from lead pipes. Lead is a cumulative
poison i.e. it takes some time to show signs and symptoms and accumulate in the body till it
reaches toxic levels. Symptoms like anaemia, anorexia, gastroenterities are seen.
Barium carbonate (BaCO3): is also called red poisoning and is accidental when it is used
instead of taking soda accidentally.
Arsenic poisoning: Fruits sprayed by arsenic salts can cause toxicity, if consumed unwashed.
Flouride toxicity : Sodium flouride (NaF)—is used to kill cockroaches, and if mistaken-
for salt or baking powder in the kitchen, it can lead to death. Flouride excess affects teeth and
bones and can cause crippling. Excess flourides can be ingested from crops grown on flouride
rich soil, toohpastes etc.
Zinc poisoning—Zinc is a trace element required in small amounts by the body, but its
excess (which is rare) can cause zinc poisoning. This can occur when acidic fruits (or foods) are
cooked in galvanised containers.
Mercury poisoning—It is very rare and occurs if industrial waste contaminates the water.
The fish in river can get killed, and if it survives, it becomes a carrier of large amounts of
mercury.

91
Symptoms of chemical poisoning
These are nausea, vomitting, general malaise (feeling of not being well), lassitude, abdominal
cramping and in cases like sodium fluride poisoning can cause paralysis of certain muscles or
death.
Safe chemicals—Aluminium, tin, stainles steel, brass (tinned only) chromium, glass are
safe for cooking and storing purposes. Packaging material of aluminium foil or polyethylene
terephthalate (PET) are recommended. Wax coated paper for bread and butter paper for biscuits
are also used.
Prevention of chemical poisoning
Usually cure is very difficult and these usually lead to irreversible changes like paralysis or
death. Precautions should be taken to prevent it—
(1) Safe utensils and storage containers should be used for handling food.
(2) Proper labelling of insecticides should be done and they should not be stored in
kitchen.
(3) Children should be kept away from insecticides.
Effect of other Chemicals
Chemicals poisoning can also take place due to insecticides, fertilisers and its residues,
contaminants, adulterants, preservatives and packaging materials. Artificial colors like coaltar
dyes, some of which are permitted, but most especially in large can cause cancer, paralysis,
indigestion and pathological lesions in vital organs like brain, kidney, liver, spleen. Colors like
metanil yellow, lead chromate, rhodamirie, sudan red are popular but not permitted colors. They
are used for dals, haldi, chillies etc. and can cause cancer, brain damage. Preventive measures are
to give consumer education, buy from reliable shop etc.
Pesticide residue can also be toxic but pesticide benefits are more than harm; therefore their
uses are only encouraged. NaFC (cochroach bait), BaCOS (rat baits) DDT, pyrethum, parathion,
malathion etc. are usual toxicants. DDT, is very popular and is cumulative poison, therefore, even
seen in breast milk. Malathion, parathion etc. (organophosphates) are neurotoxin i.e. affect nervous
system causing anxiety, giddiness, insomnia (lack of sleep) paralysis, mental depression etc.
Food packaging should be very selective. Only materials which are recommended to hold
food should be used. Aluminium foils, polyethylene terephthalate (PET) are recommended instead
of polyvinyl chloride, other plastics, cardboard etc. Recycled dyed polyvinyl chloride decreases
shelf life of food, discharges color in acidic or alkaline foods. Food and Drug Administration in
USA, Japan, UK and West Germany recommended (PET bottles which are tightweight,
unbreakable, and hygienic for packaging food products. Bread is packed in parafin wax coated
paper. Cardboard caused poisoning through noodles stored in it in Japan. Special precautions are
therefore required while tinning the foods, cardboard packaging and not using recycled colored
PVC etc.
II. Plant and animal poisoning
Some plants and animals have natural poisons, which render them unfit for human
consumption. It is for this reason that certain foodstuffs are excluded, like favabeans, snake root,
shubarbs, certain mushrooms, gossypol, green potato, raw soyabean, goitrogens, kesari dal (Lathyras
sativus), argemonc seeds etc. from plant kingdom and shell fish from animal kingdom.

92
 Favabeans (Vicia faba) cause ‘favism’. This is not prevalent in our country. Even smelling
the flowers of this plant can cause poisoning leading to haemolysis of blood, jaundice, blood in
urine haematuria.
Snake root—Usually animal feed on it and milk given by these animals affect us.
Rhubarb is a green leafy vegetable like spinach or lettuce and is rich in ‘oxalic acid’.
Usually its consumption leads to oxalic acid stones, but excess consumption leads to oxalic acid
poisoning.
Mushrooms—Only a few type of mushrooms are edible and usually these are cultivated.
The local Indian name is khumbi (button mushrooms), guchic (morels), dhingri. Some of the
most beautiful varieties in color and size and extremely poisonous and can cause death like
Amanita Muscarin (toxin is an alkaloid—muscarin). Muscarin causes excess salivation, blindness,
anuria (no urine)vomitling, abdominal cramping, diarrhoea, dizziness, confusion, convulsion i.e.
act as neurotoxin. Antidote is atropine and electrolytes and water is given to prevent dehydration.
Gossypol is yellow pigment in cotton seed cake used as protein supplement. ISI has now
laid standards for cake and oil, so gossypol has to be extracted and removed. Gossypol binds with
lysin and reduces protein quality.
Green potato contains solanine which can be harmful apart from giving an off taste.
Salaniane is a glycosidal alkaloid, which is produced when potato is exposed to sun. 8 kg of such
potatoes or 40-50 mg of solanine can lead to poisoning. Thus, its a rare feature. The symptoms
appear in 8 hrs like abdominal pain, vomitting, diarrhoea. Solanine is heat stable but prevention
is possible by discarding the keel and green area.
Soyabean (raw)—Soyabean has been largely advocated by nutritionists for its protein, fat
and fibre content. Soya protein was textured to nutrinuggets or nutrela to give an appearances of
a non-vegetarian dish and provide good amount of protein (42% by weight). Soya oil is also a
good substitute for vegetable oils in the market and is rich in poly unsaturated fatty and, which
is recommended for heart patient. Soya fibre prevents increase in blood cholestrol and blood
sugar and is, therefore, good for heart patients and diabetes patients. But these soyabeen preparations
are processed on cooked. Raw soyabean has trypsin inhibitor, which must be destroyed by
heating (or cooking) so that the soya proteins are better digested. Otherwise, raw soya-diet can
decrease the digestibility of proteins in the diet. Trypsin inhibitor can be destroyed on cooking,
soaking and sprouting the beans.
Goiterogens: Raw cabbage has thiocyanates which can suppress thyroid gland activity, but
cooked cabbage does not have this effect.
Kesari dal (Lathyris Sativus): Increased consumption of this dal can lead to lathyrism
which is characterised by paralysis of limbs, the toxic principle is BOAA i.e. B oxalyl amino
alanine. BOAA is water soluble, heat labile to some extent and varies from one variety to another
of kesari dal (12-20% of total proteins can have BOAA).
Mode of action—It can cross the brain barrier and circulate in the blood supply of brain. It
is a known neurotoxin. In animal studies the toxin had produced damage to heart, liver etc
because it is a deep penetrating toxicant.
Once lathyrism sets in, it is difficult to cure. It is more common in males than females,
especially in productive age group (15-45 years). Therefore, work output decreases and it is a
chronic ailment. It takes 2-4 months for the symptoms to appear when 20% of total energy from
diet is from kesari dal.

93
 Symptoms—It is a neurotoxin which can also affect the skeletal system. It is, therefore,
called neuro-osteo-lathyrism. The first symptom is pain and cramps in legs, (myospasms) numbness
of extremeties, paralysis of limbs and uninary bladder and rectum (i.e. loss of sphincter control),
and finally death. Because skeletal system is affected, walking is improper; thus called “weakling
disease”. Once it sets in, it is incurable, the person ultimately starts walking on four, but it takes
6 months to appear. Therefore, if diagnosed earlier, stop the intake of dal so that disease does
not progress.
Prevention:
1. Identity the dal and discourage its use (looks like arhar dal).
2. Crop variety can be developed which has low BOAA.
3. Parboiling prevents the toxin.
4. Detoxify the dal by procedure given by NIN (National Institute of Nutrition, Hyderabad)
Detoxify at home level by soaking the dal for 24 hours. Decant the water, put seeds in
boiling water, Let it remain for 2 days, decant the water, dry it. The seeds have reduced
amount of toxin. This method should be educated to the related community (mostly in
Madhya Pradesh and Bihar)
Argemone seeds—Argemone is grown along with mustard and colour of the seeds is same
as mustard or rye. The adulteration can be accidental or intentional because, it is very rich in oil
(60.65% by weight of seeds) as compared to mustard (40% by weight of seeds).
The toxin in called “sanguanarian” and results in “Epidemic dropsy.” It occurs in epidemic
because contaminated mustard oil may be consumed by many people in that area. Symptoms are
nausea, vomitting, diarrhoea, swelling of limbs, pitting odema, redening of exposed skin, swelling
of face and eyes and cardiac arrest can take place in uncontrolled cases, leading finally to death.
Occurence of symptoms is so fast that death occurs before any control is possible. In 1973, 172
persons died in West Bengal due to unintentional adulteration of mustard oil.
Prevention of dropsy is possible only by visual inspection of mustard seeds or rye seeds with
argenome. From oil it is difficult to identify the toxin, nor is the toxin destroyed by heat. By
commercial processing the mustard oil, the toxin can be removed (called degumming of oil), but
this is not possible at home level.
Shell fish—Rivers and ponds contaminated with industrial wastes, radioactive wastes etc.
can increase the toxic load of water plants and animals. Water animal like fish, shell fish, prawns
and lobsters can be the carriers of chemical or radioactive toxins. Some marine animals have
toxic acids and phenols which are not edible. Shell fish has saxitoxin which lead to paralysis of
limbs and brain damage.
III. Microbial poisoning
This class of poison is produced by bacteria or fungi. In this class we will give especial
attention to
— Botulism
— Staphylococcal poisons
— Other microbes like Salmonella, Streptococcus fecalis, Clostridium perferinges, E. coli,
B. coli etc.
— Fungal toxins or mycotoxiiis like Ergot poisoning, Aflatoxin.

94
 Sometimes, Nematoda infections like of Trichinella spirialis are also included, only they are
infestation with nematodes (worms). They enter in human body as cysts from an infected food
e. g. pork and the larvae from the cysts affect the intestinal mucosa or they migrate in blood to
affect other tissues. This category is not strictly a poisoning, but is an infection giving similar
symptoms of nausea, anorexia (i.e. lack of apetite) colic pain, vomitting, diarrhoea, sweating and
soreness of infested muscles.
Botulism—It is caused by Clostridium botulinum. It is very rare, but is fatal. Common
foodstuffs which are associated as the carrier of its toxin are sausages and preserved foods which
are not prepared well like caused meat, smoked meat, home or improperly canned foods etc.
Usually in non acidic foods, they grow, multiply and produce toxin.
Symptoms of botulism—First and foremost is the occurrence of dysphagia (i.e. difficulty to
swallow the food). There is double vision, nausea, diarrhoea, fatigue, dizziness, headache, difficulty
in speech, difficulty in breathing and finally death because of the paralysis of the respiratory tract.
The symptoms am produced in 1-3 days (incubation period), and usually by the time the
symptoms appear, the toxin has already caused enough damage which is irrevocable. An antitoxin
therapy becomes ineffective but other people in the community who have consumed the
contaminated product can be saved.
The toxin is a neurotoxin and the bacteria are rod shaped, which can grow even in the
absence of oxygen (anaerobic). Optimum temperature for their growth is 35°C (10-48°C) in 30%
moisture with a pH of 5 or above (i.e. below 4.7 it cannot grow). Destruction of bacteria takes
place at 121°C in 15 minutes. High salt concentration also inhibits their growth. The toxin itself
is heat labile and gets destroyed in 1/2—6 minutes at 80°C.
Treatment—Enema (washing the colon and rectum with soap solution) is given. The patient
cannot tolerate anything and therefore does not eat anything. To prevent dehydration due to loss
of water arid electrolytes in stools, vomits, electrolyte solution (oral rehydration solution, Annexure
1) is given.
Prevention—Even I mcg of toxin can cause poisoning, so it is recommended that a can in
which there are bubbles of gas or have an off odour, should not be even tasted. The toxin is heat
labile and gets destroyed at 80°C, but the spores of bacteria are very resistant. The germination
of spores can however be prevented by keeping the pH below 4.7.
The prevention of the growth of the bacteria or the production of toxin can be ensured—
1. Use of approved heat processes for canning; i.e. pressure cooking for low acid vegetable,
fruits and meats at 115.5°C 10lb pressure for 20-45 minute.
2. Reject all gassy or swollen canned foods, or if the tin is otherwise spoilt or damaged
or give some offensive odour.
3. Refusal to even taste the contents of doubtful food.
4. Consume only freshly cooked food which has gone through good heat treatment.
5. Smoked meat and fish are also important carriers and therefore, sanitation should be
maintained while handling, processing or serving the food. It has to be ensured that
food is heated at least for 30 minutes in the corest part to 82°C. The fish should be
frozen immediately after smoking and packing.
Staphylococcal food poisoning—In the commonest type of microbial food poisoning, usually
type A strain is responsible.

95
 The usual carriers are milk, cheese, cream filled bakery products (like cream rolls, eclairs),
custards, ice creams, sometimes even sausages and cured meats. Usually, starch and protein
encourages the production of the toxin.
The optimum temperature for growth is 98°F, but it can grow in wide range of 40-116°F
(optimum temperature—98°F). The toxin production is maximum between 17—97°F. The optimum
pH for growth of bacteria and toxin production is 5 and below 4.8 growth is retarded. They are
aerobic organisms, thus need oxygen for their growth.
Staphylococci are present in clusters or bunches of grapes which is present in throat, nasal
passages and pimples, boils and wounds etc. Nasal droppings of persons suffering with cold are
rich in this bacteria.
Symptoms—These are vomitting, nausea, salivation, diarrhoea, abdominal cramps, fatigue
and feeling to just lay down. In moderately severe conditions, headache, sweating, muscular
cramping are reported.
The symptoms may appear within 25-30 hrs after taking infected food. Exact incubation
time on susceptibility of the person and amount of food eaten. Unlike the neurotoxin producing
botulism, the toxin here is enterotoxin because it affects the gut. The intestines get inflammed
within hours, provided the conditions are favourable.
Treatment—Recovery is quick i.e. almost 1-2 days. This can be facilitated if the patient is
given electrolyte solution (ORS, Annex. 1) and almost no solids are given. Ispaglula husk has
been recommended by dietitians because this dietary fibre is soft, non irritant and viscous. It acts
as a stool binder and absorbs the toxins. No other medicine should be given because toxin gets
washed out as diarrhoea or vomitting. The only precaution is against dehydration for which ORS
is recommended.
Prevention—To prevent staphyococcal infections, following precautions must be taken-
1. General sanitation-food handling should be done under sanitary conditions especially
in restaurants, hotels, canteens etc.
2. Proper storage-all perishable foods should be stored under refrigeration, otherwise they
make excellent media for the growth of the organisms. Similarly frozen foods should
always be in frozen form.
3. Cooking-foods should be properly heated and cooked before consuming.
4. Personnel management-all the personnel in catering should not have sinus infections
or infected wounds, boils or cold; and people suffering from it should not be allowed
to handle the food.
5. Pasteurization of milk destroys the organism, but if toxins are produced before hand,
than can still cause poisoning as the toxin is not heat labile. To kill toxin, the food
should be boiled for 20-30 minutes or more.
Other bacteria causing food Poisoning are Salmonella, Streptococcus fecalis, Clostirdium
perfringes, E. coli, B. coli etc. Most of these bacteria should be ingested in million to cause
poisoning.
Salmonella—The food poisoning is called salmonellosis. The foods that act as carriers are
meat, sausages, processed meat, eggs of infected poultry,,raw vegetables like salads. The incubation
period is 7-12 hours and the symptoms are nausea, vomitting, diarrhoea, abdominal pain, fever,
muscular weakness which last for 2-3 days. Usually there is complete recovery. Prevention is
same as for other microbial poisoning.

96
 Streptococcus fecalis—Usually animal food are involved like sausages, meat products that
are not properly processed. Incubation period is 5-12 hours. Prevention is same as for other
bacterial poisoning.
Clostridium perfringes is the bacteria that forms spores and is present is soil, water, milk,
sewage and the intestines of man and animal. Foods involved are meat, fish, poultry and milk.
The incubation period is 10-12 hrs. Usually symptoms are nausea, abdominal pain, diarrhoea, but
vomitting is not usual. Although stools are offensive, the recovery is rapid.
Mycotoxins
Aparts from bacteria, the toxins of various fungus are also harmful. These toxins are called
mycotoxins e.g. aflatoxin, ergot toxin etc.
Aflatoxin is produced by the fungus—Aspirgillus flavus. This fungus usually grows in
water (30-37o C), damp (moisture above 16%) conditions on ground nut, maize, cotton seed or
its cake (i.e. defatted cotton seeds), and also on wheat, rice, jowar or soyabeans. Aflatoxin affects
the liver of the animal or human being, it can cause liver cirrhosis marked with jaundice and
ascites followed with cancer and death. If breast milk has aflatoxin, child can have infantile
cirrhosis.
Prevention—Foods should be stored in dry conditions, preferably in tins which can be
fimigated with antifungal agents. Doubtful food articles (i.e. with grey-green fungus) should not
be consumed lasted. Pressure cooking does not destroy the toxin, but heating under alkaline
conditions gets it destroyed Hand-picking and discarding infected seeds (groundnut, maize, rice
etc. in) can reduce the contamination. Now by genetic approach, seeds resisting this fungal
growth are grown.
Ergot toxin—the poisoning is called ergotism. Usually foods like bajra, wheat, Jowar
causes ergotism, because of the fungal growth of ergot on these millets. When the food is
infested, the food poisoning is characterized by diarrhoea, nausea, giddiness, vomitting, abdominal
stress, headache painful cramps; all of these cap become severe.
Summary
Food poisoning occurs from very diverse sources like-chemicals, plant and animal toxins
bacterial toxins and fungal toxins. Prevention is therefore specific for each source. Some toxins
are heat labile, some can be reduced by parboiling (lathyrus toxin-BOAA) and some can be
washed off. Some toxins are very resistent to heating processing or just washing.
General principle of management are:
1. Identify the cause of poisoning and prevent further poisoning. Treat with antidote if
known.
2. Gastroenteritis and other disturbances are usually seen like nausea, vomitting. The
patient requires nourishment, therefore, food should be presented aesthetically to
overcome nausea. Give plenty of water to flush toxin from GIT and overcome nausea.
Water can be substituted with electrolyte mixture (oral rehydration education), so that
water which is lost in vomitting or diarrhoea is compensated. Water absorption is better
in the presence of glucose and salt (sodium chloride); further glucose is absorbed better
in the presence of salt. Therefore ORS is better accepted than plain water.

97
Composition of home made ORS
1 Litre of boiled cooled water (5 glasses)
5 g of sodium chloride (pinch of common salt)
25 g of sugar (handful of table sugar)
1 lemon juice to taste is dissolved and the patient can drink in 5-6 divided dose to
prevent dehydration.
3. Whey, dal water, rice water (kanji) juices etc. can be given, but food should be avoided
because the patient may not tolerate. Fluids as drinks, juices, soups etc. should be given
at 2-hrly intervals, round the clock i.e. 24 hrs day and night in amounts not more than
150 ml per feed.
4. Soft fibre like mucilax or isabghol (ispaghula husk) give bulk to stools, reduce watering
stools. It also absorb the toxin and entangles it and removes it through fcaces, instead
or letting it get absorbed. This removal of toxin by fibre may not be possible for all
types of toxin and by not all types of fibre. Harsh fibres cannot be given, as they can
further irritate GIT.
5. The person must report to the hospital. ORS alone cannot treat or prevent further
damage, some toxins are fatal and needs to be washed off by dialysis or require antidote.
6. If epidemic of adulteration, it should be made public like epidemic dropsy, methyl
alcohol toxicity etc. Mass media are used like radio and televisions to make people
aware within hours of its occurrence.
Selected References:
1. Textbook of Preventive and Social Medicine; Park & Park.
2. Advanced Textbook on Foods & Nutrition; Vol. II: Dr. M. Swaminathan.
3. Foods & Nutrition for Senior Students; Education planning Group; Arya Publications.

98
 Lesson 16
FOOD SAFETY
Food has a well recognised function. It is essential for ‘growth and maintenance of health.
But food can perform this basic function only if, it is safe. It should be safe in nature and free
from toxins and such other components like additives and contaminates which may interfere in
assimilation of nutrients or prove to be potential health hazard.
Every food may not be safe from health point of view. When is food fit to eat? It is fit to
eat, if, it is free from harmful contaminants, toxins, bacteria, etc. and after consumption the
person does not feel sick.
Factors Affecting the Safety of Food
The type of food systems by which food is produced, processed, distributed, prepared and
consumed is related to the stage of development, level of income and socio-culture characteristics
of communities.
The food system can be broadly divided into three important categories namely:
(a) Low income rural system.
(b) Low income urban system.
(c) High income system.
Each system has its own particular food safety problems and require different remedial
approach.
(a) Low income rural system: Since most of the food utilized in this system is produced
locally, the primary areas of concern are:
(i) The frequent contamination of grains and pulses during harvesting by soil borne spores
of organisms such as Bacillus cereus and Clostridium perfringens.
(ii) The contamination of food at the time it enters the home possibly through the use of
non-potable water in growing or washing vegetables and fruits before eating as raw
foods.
(iii) Poor practices in drying, storing, handling and preparing the staple food, and/or use of
non-potable water.
The main food contamination threats appears to be raw food, non-potable water, inadequate
domestic sanitary practices, (practically improper food-handling practices, especially of cooked
food), and in-appropriate storage practices.
(b) Low income urban system: The basic areas of concern of this category are:
(i) The growth of centralized markets as primary distribution points for food supplies
purchased from large number of small farms in the rural areas and transported by
assembly traders to the urban areas.
(ii) The greater tendency for cereal staples to be ground, partially processed or cooked
before the retail stage, and for developing separate marketing channels for these
commodities.
(iii) An increase in the quantity of simple processed or prepared food for consumption
inside or outside the home and mostly produced by relatively small scale processors.

99
 (iv) A retail system consisting of multitude of small scale traders, vendors and retail
outlets, each selling small quantities of raw, processed or ready to-eat foods.
(C) High income systems: As income rises, the percentage of available income spent on
food declines. People can afford a more varied diet and are likely to purchase more
semi-processed or processed foods that incorporate variety and reduce time spent on
food purchase and preparation.
It is because of these reasons that the population failing in this category is more depended
on industrial processing techniques. The potential problem thus arises from failures in the quality
(and safety) control of processed and prepared foods by the industrial food processors or mass
caterers.
Suggested ways to Food safety in General
Food hygiene covers all measures necessary to ensure the safe, whole-someness, soundness
of food at all stages from its growth, production or manufacture, until its final consumption.
Because there are so many sources from which disease agents may be transmitted to food and
because food can become easily contaminated by these organisms, food must be protected at all
points along the food chain, from the time it is produced until it is served to the consumer.
All the measured or precautions practiced in applying the principles of food protection, can
be classified into 4 basic rules:
(i) Keep food clean.
(ii) Store in cool place.
(iii) Serve food hot.
(iv) Don’t keep food in dirty places.
In particular, the following can ensure food safety and prevent food borne illnesses.
A. Personal Hygiene
“Human element” is the single most important factor in the control of food borne illness.
Every individual must follow some routine habits like hand washing throughout the preparation
of meals to avoid possible risks of contamination. Cuts, sores, burns and , boils should always
be covered with water proof bandages because they also carry food poisoning bacteria. Food
service workers in food service establishments must be free from all communicable disease.
B. Food must be secured from Approved Sources
Since food come from different places, one has to ensure that the incoming food is safe for
consumption.
- Water supply/potable water: Water through not considered as food yet, plays an important
role in human nutrition. When contaminated, it transmits disease through the pathogenic
organisms it contains or through the utensils and equipment washed in it. Thus, it is
necessary to use safe water for consumption.
- Safe sources of food: Most foods supports microbiological growth. The consumers
should take particular care to purchase only uncontaminated foods. Milk and milk
products should be pasteurized. Meat and poultry should be slaughtered and processed
in sanitary conditions. It should bear the label of an official inspection agency. Canned
food should be processed in authorised food processing plants.

100
C. Store Foods Properly
Foods are not usually prepared and served just after purchase. It is stored for varying lengths
of time and in a variety of conditions until it is prepared for service. Thus, subjecting to
contamination in a variety of ways.
- Protection during dry storage: Foods placed in a dry storage should be arranged and
stored so that the food placed in first is used before newer incoming supplies, that it,
“First in, First out”. All foods should be stored off floors on pallets and shelves and,
if possible, away from walls thus preventing it from being contaminated by insects or
rodents or from flooding.
- Avoid wet storage of packaged food: Never store packaged foods like cartons or bottles
of milk and juices in iced water to keep them cold. Water in which the container is
stored is contaminated through use and seepage through leaks may aggravate the problem.
- Temperature has relation to food protection: Food, moisture, temperature and time are
some of the requirements for the growth of organisms. There is little opportunity to
control the first two and so prevention of contamination depends on controlling the
temperature of food to control microbial growth.
Temperature Guide (F)
180
To serve hot 170
Foods, store while 160
Serving above 150
o
140 F (soups, gravies
Meats etc.) 140 Some bacterial
130 growth may occur
120
DANGER ZONE 110 Ordinary room
Most bacteria temperatures
including food poi- may fall in this
soning type will 100 range. Do not
grow rapidly 90 store prepared
over this temp. foods at room
range. temperature.
80
70
60
50 Some bacterial
40 Growth may occurs
Refrigerate Pre 30 To serve pre
Pared foods to pared cold dishes
prevent bacterial keep on ice
growth and to while serving
prevent food 20 (Potato salad,
spoilage. 10 Chicken salad etc.
Store frozen 0 Thaw or cook
Foods at this tem- from frozen con-
Perature or be dition when
Low Ready to use.

101
 Microbial organisms grow best at temperature near that of human body or about 100°F
(37°C). Disease organisms grow over a wider range of temperature in the danger zone where the
microbial growth is rapid, i.e. 45°-140°F (4°C-60°C). Therefore food should be stored either
below 45°F (4°C) or above 140°F (60°C) but not for too long.
Keep food cold so that micro-organisms do not grow very well to reproduce in numbers
sufficient to cause illness. This temperature or even freezing and refrigeration does not kill most
micro-organisms but only slow down or halt their growth temporarily. If temperature rises
significantly, any organism present in the food begins to grow.
On the other hand, in case food held is at 140°F (60°C) or above, micro organisms are killed
rapidly but are not readily affected when the temperature goes below 140°F(60°C). So after food
is cooked, it should be kept hot and not just warm, until served. If it is kept “just warm” on the
back of the kitchen range or on the table, rapid microbial growth may occur and outbreak of food
borne illness could result.
D. Practice Proper Preparation of food
- Work with clean hands: Hands must be washed often with warm water and soap to keep
them clean. Though many foods are handled by hands during preparation, practice
using sterilized handling utensils for food like forks or tongs. This is not only appealing
but shows concern about health of the consumer.
- Use clean utensils: Clean contact surfaces of tables and equipments. Prompt and
throughout washing and sanitizing between uses prevent outbreaks from occurring.
- Clean raw fruits and vegetables: Fruits and vegetables are grown and handled in many
different conditions. Soaking followed by throughout washing in running water is usually
sufficient to remove most chemical contaminants or disease organisms.
- Avoid left overs: Food kept for a long time between preparation and serving is more
likely to cause disease. If leftover prepared foods (unserved) are to be kept, adequately
protect and refrigerate them. Serve hot food again by rapidly reheating to above 140°F
(60°C) to boiling temperature.
- Practice healthy habits: Habits of individuals are most important in providing proper
protection during food preparation. Therefore, habits as placing fingers in the hair.
Picking at the nose, or coughing and sneezing are to be avoided when preparing food.
- Cook foods properly: In cooking see that all parts of the food reach the proper
temperature. The principles that apply to cooking foods also apply to reheating of food.
- Store and display food properly: Cold foods on a serving line must be maintained at
a temperature of 45°F (4°C) or below and not that of the ice or cold plate on which
the food is placed. Hot foods on a serving line must be maintained at 140°F (60°C) or
above. This must be the temperature of the heating unit at which the food is held.
Serving of foods should be done with an appropriate utensil.
Pack foods properly. Packaged foods that have been opened once should not be offered
for resale or reservice.
E. Observe Proper Practices for Refrigeration of foods
1. Foods must be refrigerated at all times except during the period of actual preparation
or serving. Hot foods removed from the range should be refrigerated immediately after
cooling to shorten the time it is in the danger zone.

102
 2. Thaw frozen food quickly.
Frozen foods should be kept frozen at all times. They should be kept in the freezer of
the refrigerator until thawed and newer at room temperature.
For quick thawing, place the food in a clean plastic bag and suspend in running 70oF
or less) tap water and cook promptly.
3. Arrange food in containers in refrigerator.
Store foods in shallow pans or in smaller round containers to cool Rapidly. A good rule is
to make certain that the distance to the centre of the food is not more than 2 inches. This means
that shallow pans or even round containers should be filled not more than 4 inches deep.
Stir the food occasionally to bring warmer parts of the food mass closer to the surface to
dissipate heat rapidly.
Place containers in the refrigerator in a manner that permits air circulation around each
container.
Cover all containers in the refrigerator to prevent contamination from the shelves and
among the foods in the refrigerator.
Clean refrigerator thoroughly with a detergent.
F. Practice Hygiene at home and at commercial and Community Feeding
Establishments
Proper ventilation, lighting, floors, adequate supply of safe drinking water and water for
washing drains, surface drainage, regular collection and storage of garbage in covered bins and
removal at least daily, sanitary latrines control measures for flies and rats are pre-requisite and
should invariably be observed.
G. Observe Legislation Procedures
To support proper investigation in matters of food sanitation, ordinances and regulations are
promulgated, which is discussed in the next chapter.

103
 Lesson 17
FOOD STANDARDS
As already discussed in the proceeding chapters, adulteration of food stuffs is on the increase.
It is a menace which saps the vitality of our people. The Indian consumer, in general is blissfully
ignorant of the harmful hazards caused by various adulterants, and is mostly guided by the price,
visual appearance and claims made by the advertisements. To safeguard the people from the
health hazards posed by the practice of adulteration, it is necessary to exercise a strict check and
control over the quality of foods offered for sale in our different markets. As already mentioned,
according to the consumer the most important factors that determine the quality are price, color
and appeal in respect to both appearance, and taste. But what really is quality? It has been stated
to be the product and not the sum of all the variable involved. If any one of the desirable
characteristics approaches zero, the quality and therefore, the product acceptance itself approaches
zero.
To understand the quality features of a certain food stuff, it is essential to know the meaning
of the word “quality”. It is defined as character, kind, property, status grade of goodness, excellence.
The parameters of the quality are the grades, standards and specifications laid down by the
government of expert bodies constituted for the purpose. However, there may be varying and
numerous qualities. An established system of quality control assures uniformity in accepted
standards and thereby ensures that each food stuff is what is purports to be and what its label
claims to be.
Standardization is a method by which quality control can be maintained. This is done to
maintain the minimum standard necessary for foodstuffs. Standard is something that is set up and
established by authority for ensuring quantity, weight, extent, value of quality.
International Food Standards
The International codex Alimentarius Commission is the principal organ of a world-wide
food standards programme, under the joint auspices of FAO (Food Agricultural Organization and
WHO (World Health Organization) two specialized agencies of the United Nations Organizations.
The Commission’s main task is to prepare an international codex alimentations, based on principles
outlined in statement prepared by the commission itself.
General Principles of Codes Alimentarius
Purpose of the Codex Alimentarius
The Codex alimentarius is a collection of internationally adopted food standards presented
in a uniform manner. These food standards aim at protecting consumer’s health and ensuring fair
practices in the food trade. The publication is intended to guide and promote the elaboration and
establishment of definitions and reauirements for foods, to assist in their harmonization and in
so doing to facilitate international trade.
Scope of Codex Alimentarius
The Codex Alimentarius is to include standards for all the principal foods, whether processed,
semi-processed or raw for distribution to the consumer. The Codex Alimentarius is to include
provisions in respect of food additives, pesticides residues, contaminants, labelling and presentation,
methods of analysis and sampling.

104
Nature of Codex Standards
Codex standards contain requirements for food aimed at ensuring for the consumer, a sound,
wholesome food product free from adulteration, correctly labelled and presented. A codex standards
should, therefore, for any food or foods:
1. Incorporate by reference the applicable hygiene, labelling, method of analysis and other
general provisions adopted by the commission; and
2. Specify in whole or in part the following criteria, as appropriate:
(a) Product designation, definition and composition: these should describe and define
the food and cover compositional requirements which may include quality criteria.
(b) Hygiene requirements: These should include such factors as specific sanitary and
other protective measures and safeguards to assure a sound, wholesome and
marketable product.
(c) Weight and measure requirement, such as fill of container, weight, measure, or
count of units based on an appropriate method or criterium.
(d) Labelling requirements: These should include specific requirement for labelling
presentation.
(e) Sampling, testing and analytical methods: These should cover specific sampling,
testing, and analytical procedures.
HACCP
An important guideline of Codex Alimentaries Commission for the food processing companies
is to follow a food quality management systems called HACCP.
HACCP has been defined as systematic approach to be used in food production as the means
to ensure food safety. Seven basic principles underlie the concept and these principle include an
assessment of the inherent risk that may be present from the harvest till ultimate consumption.
These principles are :
1. Assess Hazards and Risks associated with growing, harvesting, raw material and
ingredients, processing, manufacturing, distribution, marketing, preparation and
consumption of food.
2. Determine critical control points required to control the identified hazards.
3. Establish the critical limits that must be met at each identified CCP.
4. Establish procedures to monitor CCP.
5. Establish corrective action to be taken when there is a deviation identified by
monitoring a CCP.
6. Establish effective record keeping system that document the HACCP plan.
7. Establish procedures for verification that HACCP system is working correctly.
Foods Standards in India :
A number of existing food standards in India are based on the international codex alimentarius,
with relevant modifications and additions wherever necessary. The most important of these are:
* Prevention of Food Adulteration Act (PFA)
* ‘Agmark’ Standards (JAGMark)
* Fruit Products Order (FPO)
* Specifications of Indian Standards Institution (ISI)

105
Quality standards are descriptions of commodities in terms of net weight, accurate size, dimensions,
content and other characteristics. The following gives an idea of the kind of specific requirements
laid down as quality standards:
* Establish the minimum and also maximum content of one or more components of food,
e.g. cooking chocolate contains not less than 50% and more than 58% by weight of cocoa
fat.
* Establish the ingredient content of food e.g. jams made of mixtures composed of 45 parts
by weight of fruit constitutent and 55 part by weight of sugar.
* Establish the minimum quality of one or more ingredients of food, e.g. margarine contains
no less than 80% fat.
* Describe processing requirement e.g., sealed in a container and so processed by heat to
prevent spoiling.
* Identify the species of plant that may have been utilized.
* Define packing media of any foods such as water, syrup, juices and oils.
* Prescribe essentials in production e.g., bread is prepared by baking a kneaded yeast
leavened dough made by moistoring flour with water or other specified liquid.
* Require label statement of the use of any food additives with explanation of use.
1. The PFA Standards
These precribe the minimum standards for all types and categories of food. The PFA rules
were fjist introduced in 1955 and have been subsequently amended in 1968, 1973 and 1978 and
this has been reinforced since June 1st 1945. The standards are formulated and revised when
required, by an expert body called the central committee for food standards (CCFS). Only food
does not conform to the minimum standards laid down by the PFA rales, is said to be adulterated,
irrespective of whether anything has been added to or removed from the original food.
The regulation consist of many articles direction towards the protection of food adulteration.
Some of these are discussed below :
1. Section II : This section gives some common definitions like definition of adulteration,
definition of food false labels.
(a) Definition of Food Adulteration : This has been discussed in chapter 13 already.
(b) Definition of Food Stuff: All the liquid and solid products that are ingested (except
water and medicine are termed as food stuffs.
(c) False Label : The following conditions define any product with false label :
(i) If the label is deceptive or not true,
(ii) If the product is sold by some another name.
(iii) If the product is the copy of some other product and the name of the product is
not mentioned on the label.
(iv) If the container is such that is deceives about the amount it contains.
(v) If the lable does not mention the name of the manufacture and the products used
and their standard.
(vi) The lable cannot be read easily.
(vii) If the artificial colors and chemical preservatives used are not mentioned,
(viii) If the standard of the food product is not mentioned.

106
 2. Section (V) : This Section mentions the food products whose sale is prohibited in India
(i) adulterated food stuff: (ii) Food products with false lable; (iii) Import of licenced food stuffs;
(iv) any other food product which is not in this law.
3. Section (X) : This Section mentions the rights and duties of food inspectors (i) Food
Inspectors can take the sample of any food product to sent it for testing and keeping the public
health in mind, he can prohibit the sale of any food product with the prior permission of food
officer (ii) Food Inspector can take the sample from any place of inspection (a) where the food
stuff is produced; where it is stored and (c) where it has been kept for sale. (iii) When the food
adulteration has been certified, food Inspector can assess the seller. He (iv) can take possession
of the adulterated food stuff and send the, same for testing.
4. Articie (XI) : According to this article, when the food inspector takes samples for testing,
then (i) then he will give notice to the seller, then the sample has been sent for testing : (ii) The
sample will be sealed in three different parts : one for seller, one for testing and one for himself.
5. Article (XII) : According to it, any food stuff suspected for adulteration by the consumer,
can be sent by him for testing, and so proved, the testing cost is reimbursed to the consumer and
the seller is taken by the law.
According to PFA act, a person keeping, selling or transporting the adulterated food stuff
may be jailer from three to six months and fined for a sum from Rs. 500 to Rs. 2000. If the same
person is caught again, his name and offence is published in the local newspaper and the
expenses are borne by the same person. If a consumer dies after consuming adulterated food stuff,
then he offencer may he given life imprisonment.
2. Fruit Product Order (F.P.O.)
The Fruit Products Order was promulgated by the Government of India in 1946, under the
Defence India Rules. In 1955, the order was revised and section III of the Essential commodities
Act, which was enacted that year. This order stipulates minimum fruit and vegetable products
manufactured in India. Under this act, every manufacturer for fruit and vegetable products must
obtain a licence before starting production and the products should confirm to the standards
prescribed under the order. The latest amendment was made in 1975.
The Central Fruit Products Advisory Committee constituted under the order is expert body
which advises the Central Government on Standards and policy matters relating to the vegetable
and fruit industry. Any product which deviates from the minimum prescribed standards under the
order is decalred sub-standard and in case the office is repeated, the producer is liable to punishment
under the provision of law. The Main objective of the F.P.O. is to ensure minimum standards for
various fruit and vegetable product. The order specifies standards and sanitation and hygiene to
be followed in the factories besides giving directions regarding packing, marking and labelling
of containers. The inspectors attached to the Deptt. of Agricultural Marketing are empowered to
collect samples and inspect the factory and send the samples to the control testing laboratory
located at Central Food Research Institute, Mysore. The order has further laid down limits for
the presence of poisonous elements, permitted food colors, preservatives and other food additives.

107
 Fig. 1
The following are the products of fruit and vegetables marked with FPO :
(i) Preserved fruit (in cans and bottles)
(ii) Preserved vegetables (in cans and bottles)
(ili) Fruit juice and fruit pulp (in cans, bottles)
(iv) Fruit drinks like Rasika, Mangola etc.
(v) Jam, Jelly and Marmalade.
(vi) Squash, Syrup and Cordial.
(vii) Pickles, Chutneys and Preservers.
(viii) Dried fruit and vegetables.
(ix) Candid and Glazed Fruits
(x) Freezed Fruit, vegetables, fruit, juice and fruit pulp.
(xi) Sherbet and carbonated drinks like Cola drinks etc.
(xii) Synthetic vinegar.
Obviously, the objective of the PFA and FPO standards is to obtain a minimum level of
quality for food stuffs, consistent with the minimum quality attainable under Indian conditions
by the majority of farmers, processors, sales and distribution agencies. Needless to say, these can
never cover excellence nor the zenith of quality. In fact these minimal requirement sometimes act
as a deterrent to improvement of quality above the prescribed minimum.
‘Ag Mark’ Standards
This was set up by the Directorate of marketing and Inspection of the Government of India
to cover the various quality levels of agricultural commodities. The Grading and Marketing of
Agricultural Products Act of 1937, defines standards for the quality of creals, oilseeds, oils,
butter, ghee, legumes, eggs, etc. and provides for the categorisation of commodities into various
grades depending on the degree of purity in each case. The several grades are : (i) Special (Grade
1); (2) Good (Grade 2); (3) Fair (Grade 3); and (4) Ordinary (Grade 4). These standards also
specify the type of packaging to be used for different products.
AgMark specification are mainly formulated on the basis of physical and chemical
characteristics, intrinsic as well as acquired during processing or otherwise. The agricultural
practices prevailing in the country, consumer preferences and availability of the different farm
commodities are taken into consideration while framing these standards.
The benefits of Agmark standardisation are made available to public by providing for
Agmarking of articles of foods such as edible oils, butter, ghee, eggs, etc. The mark gives the
consumer an assurance of quality in accordance with the standards laid down. This system of
grading and marking has made better buying and selling of agricultural produce possible by
establishing regulated markets, the salient features of these markets are healthy market practices,

108
use of standard weights and measures, licencing of market functionaries, arrangement for settling
disputes in regard to quality, weight and discounts.
Ag Mark certification is passed only after elaborate testing. All the Food processing Factories
with Ag Mark certification appoint an expert (chemical) with the permission of Ag Mark Officers,
who checks and controls the raw materials and produced food product for quality control, Ag
Mark inspection can take sample from the factory or open market and can get it analysed in
dependently in their food laboratory. If the testing shows that the product is below the required
standard, then factory’s chemical expert services are terminated and the sale of that batch of food
product is prohibited.
List of Ag Mark certified Food Products :
1. Ghee
2. Butter
3. Edible Oil
4. Honey
5. Pulses
6. Ground spices
7. Wheat Flour
8. Besan
Meat Foods Product order
This makes it illegal to transport meet unless is has been prepared and processed according
to the provisions of the order and carries the make of inspection. It provides for means to:
a. detect and destroy meat of diseased animals
b. ensure that the prepcration and handling of meat and meat products be conducted in a
clean and sanitary manner
c. Prevent the use of harmful substances in meat foods.
d. see that every cut of meat is inspected before sale to ensure its wholesomeness.
The order also lays down rules and conditions for procedures to be adopted for the selection
of disease free animals, slaughter house practices and further treatment of the meat so as to
maintain the meat in a wholesome manner, devoid of pathogens.
BIS (Bureau of Indian Standards)
BIS was found in 1986 under BIS act. It comprises of members representing industries,
consumer organizations, scientific and research institutes, professional bodies and ministries.
Function of BIS is expert promotion of food products which are prepared and processed in safe
hygienic conditions.
So far 15,000 standards have been formulated in different technological areas and these
standards fall in the following categories:
1. Product specification
2. Method of Test
3. Quotes of practices & guidelines
4. Terminologies
5. Basic standard

109
 BIS is founder member of the International Organization for standardization, ISO. It is also
involved in international electro-technical commission and also has a particular status in 46th
technical committee. In addition to the mandatory acts and order, agencies like ISI and Directorate
of Marketing and Inspection have also laid down quality standards of foods. These are refered
to as voluntary standards.
(1) AGMARK
(2) ISI
Indian Standards
Indian Standard Institution was established in 1947. The ISI is the national standards
organisation for India, responsible for laying down standards in consultation with, and with the
active participation of experts drawn from manufacturing units, research and technical institutions
and laboratories, purchase organisations and other parties involved. Following are the objectives
of Indian standards Institution:
1. To formulate standards for commodities, products, materials and processes.
2. To encourage their adoption at National and International level.
3. Certification of Industrial Products.
4. Help in production of Standard Products.
5. Distribution of information regarding standardisation.
The Indian Standards are available for vegetable and fruit products, spices, condiments,
animal products and various processed foods. The standards are formulated and revised from
time to tme by various committees set up by the Indian Standards Institution (1ST) for the
purpose. The standards are evolved on the basis of physical characteristics and chemical as well
as biological assessment as and when required.
The ISI certification Marks Scheme under the Indian Standards Institution (Certification
Marks) Act, 1952, as amended by the Amendment Act of 1961, makes provision for making
quality goods with ISI stamp. The ISI mark on any food article is a guarantee of good quality,
in accordance with the prescribed Indian Standards for that commodity. Licence to use the marks
are granted only to producers following ISI approved methods of production and quality control.
The method of manufacture and the premises as well as the final product are all subject to
inspection by the ISI personnel. For analysis, the samples are sent to the independent laboratories
if the product is found to be of inferior quality, the manufacturer is warned and the sale of the
products of that batch is prohibited. ISI has its own laboratory at I.T.O., New Delhi and Ghaziabad,
where the products of licence demanding applicants (manufacturers) are tested. Other small
laboratories are in Bombay, Calcutta and Madras.

Fig. 3

110
 Agencies of international level like I.S.O. Organization for standardization and I.E.C,
(International Electrotechnical Commission) helps in certification and promote and encourage it.
Following are the eleven departments, under which the cerufication is passed.
1. Agricultural and Food Products
2. Chemicals
3. Civil Engineering
4. Consumer Products and Medical Instruments
5. Electronics and Telecommunication
6. Electro Technical
7. Marine, Cargo movement and Packaging
8. Petroleum, coal and related products
9. Mechanical Engineering
10. Structural and Metals
11. Textile
List of I.S.I. Certified Food Products
1. Edible common salt
2. Arrowroot
3. Custard Powder
4. Biscuits
5. Baking powder
6. Cocoa powder
7. Milk powder
8. Condensed Milk
9. Baker’s yeast
10. Infant Milk Food
11. Vermicelli, Macroni and Sphagetti
12. Besan
13. Cheese
14. Coffee Powder
15. Ice Cream
16. Egg Powder
17. Saccharin
18. Drinking chocolate
19. Rum, Beer, Gin, Whisky, Brandy
List of some domestic Electrical equipments with I.S.I. Mark
1. Electric Iron
2. Electric Fan and Regulator

111
 3. Electric Kettle and Jug
4. Electric Hot Plate
5. Domestic Food Mixers
6. Switches
7. Pressure Cookers (Non Electric)
8. Gas Stove
Export Inspection Council : This council has been constituted to check quantity of
number of food materials meant for export.
Standard for weights and measures Act, 1976 : This act establishes standards for weights
and measures to regulate inter-state trade or commerce of goods which are sold or distributed by
weight, measure or number. This Act aims at the caliberation of the use of weights or measures
as a standard and this is used in case of commodity in packaged forms. It defines the standard
units of weights and measures which are based on metric system. It also quotes the derived unit
which means a unit derived from the base or a supplementary unit or both.
Ecomark : The Government of India has instituted a scheme known as ecomark, for
labelling environment friendly products. This scheme administered by BIS provides labelling of
household and consumer products which meet certain environmental criteria along with the
quality requirement prescribed in ISI.
In 1992, most of the European countries joined and formed European Economic Committee
which at present comprises of 12 member countries namely Belgium, France, Italy, Germany,
Luxemburg, Netherland, Denmark, Ireland, UK, Grace, Portugal and Spain. The 7 of these
members are from European free trade association (EFTA). In this some common standards
dealing with minimum menufacturing practices for quality management and proper inspection
and testing are prescribed and only those products confirming to these standards are allowed to
be marketed. Thus to boost the export of European market it is necessary to confirm to these
standards.
ISO 9000 (International Organization for Standardization) is about corporate white quality
systems. A quality system is designed to ensure the continued repeatability of a set of product
and service characteristics that have been explicitedly & implicitedly agreed to by the customer
and supplier.
ISO 9000 is a series of international standards for total quality systems. The major objective
is :
To facilitate international trade by creating atmosphere of mutual trust with regard to
maintainance of quality of the product. ISO 9000 looks at every aspect of the company’s operations
including :
* Tooling Procedure
* Assembly line Equipment
* Personnel Management
* Accounting Procedures.
The Indian Standards ISO 9000 series clearly describes the quality system models, one of
which can be chosen by the suppliers which is most appropriate to the nature of operation and
the quality requirement of their customer. This series is a set of 5 primary standards namely ISO
9000 I, ISO 9000 II, ISO 9000 III, ISO 9000 IV & ISO 9000.

112
 ISO 9000 and ISO 9000 IV refers to the guidelines framed whereas 9000 I, II and III address
specific quality systems.
ISO 9000 states guidelines for selection and use of quality management and quality assurance
standards.
ISO 9000 I refers to the quality system pertaining to the models for quality, assurance in
design, development and service. ISO 9000 I which refers to the quality assurance in design,
development and service is for use when confirmance to specified needs is to be assured by the
supplier throughout the whole cycle from design to servicing.
ISO 9000 II refers to the quality system pertaining to the models for quality assurance in
production and installation. ISO 9000 II which takes into account production, installation and
servicing is for use when the specified requirement for products are stated in terms of an established
design or specification and the supplier’s capability in only production, installation and servicing
are to be demonstrated.
ISO 9000 III refers to the quality systems pertaining to the model for quality to the model
for quality assurance in final inspection and test. ISO 9000 III appliers to a situation where the
supplier’s capability of only inspection & test conducted on finished products can be satisfactorily
demonstrated.
ISO 9000 IV states quality management and quality systems, elements and their guidelines.
These ISO series are equivalent to the Indian, British & European standards which are ISI
4000, BS 5750, EN 29000.
References
1. Food Adulteration, ThanKamma Jacob, Mc, Millan Publishers.
2. Advanced Text Book on Food & Nutrition, Vol. II, Dr. M. Swaminathan, Bappco.
3. Food & Nutrition for Senior Students, Education Planning Group, Arya Publishers.

113
 Lesson 18
SOCIAL HEALTH PROBLEMS - I

SMOKING
Smoking is a worldwide public health problem. In India, tobacco smoking and chewing is; one
of the principal causes of preventable disease and early death. Though tobacco has been in use for
several centuries, its deleterious effects were increasingly recognised in the 20th century only. Since
then, several harmful effects of tobacco usage have been brought in to focus. The medical community
all over the world is constantly campaigning to cut down tobacco consumption by public at large. As
a result of mass education, tobacco smoking has decreased considerably among the educated people
in the developed countries. No statistics is yet available from India. Systematic studies of the deleterious
consequences of tobacco smoking and chewing are also lacking in this country. Large studies in
western populations have demonstrated that male smokers above 35 years of age have 70% higher
death rate than non smokers.-The maximum risk of death is in 45-55 age group. The risk of excess
death is also evident in females, though not as much as in males. The morbidity and mortality due
to cigarette smoking is directly proportional to the number of cigarettes smoked per day, age of
smoking and the degree or smoke inhalation.
(i) Nicotine: Nicotine is a highly toxic substance which exerts deleterious effects on the
heart, blood vessels and nervous system. It has also several harmful biochemical effects.
(ii) Carbon monoxide: Carbon monoxide is a toxic gas that interferes with oxygen transport
and utilisation in the body and may produce a subtle abnormality of the functioning of
the brain.
(iii) Carcinogens: Carcinogens i.e. cancer producing substances are also present in tobacco
smoke.
(iv) Lung irritants: Cigarette smoke increases respiratory secretions and produces
abnormalities of the lung function.
Harmful effects of cigarette smoking
(i) Diseases of the heart and blood vessels: Heart attack in early life is the most important
consequence of cigarette smoking. Sudden death may be the first manifestation of heart
disease due to cigarette smoking. The risk of sudden death in the middle aged male smokers
is 2 to 3 times more than that of non-smokers. Heavy smokers are more prone to heart
disease than light smokers. Women smokers are also at a high risk of developing heart
attack and the use of both cigarettes and oral contraceptives result in a 10 fold increase in
the risk of heart disease. The risk of heart disease due to smoking decreases considerably,
if smoking is stopped for more than I year. The risk of complications following heart surgery
is more in smokers as compared to non-smokers.
Cigarette smoking is also a strong predisposing factor for poor blood circulatioin in the legs. :
Sometimes the circulation in the lower limbs becomes so poor that gargerine sets in the feet and a
part of lower limb needs amputation. Cigarette smoking also increases the risk of stroke (paralysis).
Smoking does not produce high blood pressure by itself but it accentuates the severity of hypertnsion
which can lead to several complications.
(ii) Cancer: Cigarette smoking is a well documented cause of lung cancer. The risk of lung
cancer is directly proportional to the amount of smoking. On giving up cigarettes, there

114
 is a gradual decline in the risk of lung cancer. Cigarette smoking is also a causative factor
for the cancer of mouth, wind pipe and the food pipe. Cancer of several other regions in
the body may be related to cigarette smoking or chewing.
(iii) Respiratory disease: Cigarette smoking is a major cause of chronic bronchitis and prolonged
respiratory disablity. Patients with chronic bronchitis suffer from frequent cough with
yellow sputum and breathlessness. Ultimately they die of respiratory or heart failure.
Patients with chronic bronchitis are also more prone to develop pneumonia and influenza.
(iv) Disorders of the intestinal tract: Smokers have a higher prevalence of peptic ulcer.
Healing of peptic ulcer is retarded by continued smoking. The risk of recurrence of peptic
ulcer is also increased.
(v) Smoking and pregnancy: Smoking may delay conception. Smoking also results in low
birth weight due to impaired circulation through the placenta. Smoking during pregnancy
increases the risk of miscarriage and foetal death. Pregnancy may also adversly affect the
physical and mental growth of the child after birth.
(vi) Smoking and drug effectiveness: Smoking adversely influences the action of several drugs
including drugs used to treat high blood pressure and bronchial asthma.
Involuntary smoke inhalation: Contamination of atmosphere by cigarette smoke results in
involuntary i.e. inhalation by non-smokers. This is called involuntary or passive smoking. Environmental
contamination by cigarette smoke is now recognised as an important cause of air pollution. Its effects
on non-smokers may be comparable to those occuring in light smokers. Passive smoking may contribute
to development of chronic bronchitis and lung cancer.
Prevention of smoking: Cessation of smoking is primarily achieved by self motivation based
on awareness of ill effects of smoking. Drug therapy plays minimum or no role in stoppage of
smoking.
Alcoholism
Alcoholism has been defined as both a chronic disease and a disorder of behaviour,
characterised by drinking of alcohol to an extent that surpasses the social drinking customs of
the community and that interferes with the drinker’s health, inter-personal relations or means of
earning a livelihood. In other words, it is addiction to alcohol.
The causation of alcoholism is complex. Recent observations point to a genetic influence
on the development of alcoholism especially in males. The incidence is higher in children of
alcoholic parents than in those of non-alcoholic parents. In addition there are psychological
factors, Mental tensions and serious setbacks in personal life drive a person to adopt alcohol as
a means of finding temporary relief from his problems. Besides, the company of alcohol addicts
gradually lures a person into the evil of alcoholism. At times individuals drink excessively with
full knowledge that such a action will result in physical injury to themselves and irrepairable
harm to their families. This represents total psychological dependence on alcohol in which the
individual needs alcohol for adquate functioning and continues drinking despite social or
occupational problems.
The syndrome, of alcoholism consists of two phases: problem drinking means very frequent
use of alcohol, often to alleviate tension or solve other emotional problems. Alcohol addiction
consists of physiologic dependence on alcohol as manifested by evidence of withdrawal symptoms
when intake is interrupted. Continued drinking results in tolerance to effects of alcohol. Prolonged,
regular alcohol intake results in liver and brain damage frequently. Alcohol drinking also results

115
in impairment of social and occupational life. Alcoholics are often simultaneously depedent on
sleeping pills and other drugs. Alcoholics are often depressed. Majority of the people who
commit suicide are alcoholics in the western countries.
Acute-intoxication by alcohol leads to drowsiness, lack of inhibition, slurring of speech,
errors of commission, unstable gait and vomiting. Severe intoxication is marked by
unconsciousness, low blood pressure, respiratory failure and death.
Alcohol withdrawal leads to anxiety, tremors, irritability, hyperreactivity and defective
cognition. Severe alcohol withdrawal (delirium tremens) consists of mental confusion, tremors,
visual hallucinations, sweating, dehydration, fits and low blood pressure. Delirium tremens
culminate in death not too infrequently. It usually manifests 24-72 hrs after the last drink.
Alcoholic hallucinosis either during heavy drinking or on withdrawal. It consists of a major
psychiatric disorder (psychosis) characterised by auditory hallucinations which may provoke the
patient to behave aggressively.
Chronic drinking can also cause brain damage, manifested by erratic behaviour, loss of
memory, emotional instability and defective vision.
Every alcoholic should be carefully screened for an underlying major psychiatric disorder
which may be the cause of alcoholism.
Alcoholism also leads to heart disease (arrhythmias and heart failure) diseases of the nerves
(neuropathy) liver failure (cirrhosis and jaundice). Alcoholism also predisposes to peptic ulcer
and may precipitate bleeding from stomach. Children born of mothers who take alcohol during
pregnancy are likely to have low birth weight, mental retardation and a variety of birth defects
including abnormalities of the heart. Physical and mental growth of these children may also be
impaired.
‘Treatment of the problem of drinking is difficult but by no means impossible. Total abstinence
(not controlled drinking) should be the primary goal. Psychological therapy should include the
help of social agencies and religious counselling. The patient should be seen frequently by the
doctor who is aware of his social and medical problems.
Alcoholics should not be placed in jobs which require working alone e.g. sales executive.
Highly competitive posts should be avoided to minimize the stress and strain of daily life.
Positions that require quick decision making on important matters should also be prohibited.
Hospitalisation is not indicated unless required due to other medical grounds. Cardiac, liver
and neurological problems of alcoholics should be treated adequately.
Unpleasant effects due to alcoholism can be accentuated by intake of a drug called disulfiram.
Intake of this drug may motivate a patient to stop drinking. This drug may have dangerous side
effects and therefore should be taken only under strict medical supervision.
Alcoholic hallucinosis requires hospitalisation and care by an expert psychiatrist. Delirium
tremers also require hospitalisatin, and sedation by sleeping pills till withdrawal syndrome
disappears.
Alcoholics should be advised to take a balanced diet, rich in vitamin B complex and vitamin
C to correct vitamin deficiency.
Drug dependency and drug abuse
Drug dependency means drug under compulsion and includes both drug addiction and habituation.
Drug dependence may be due to one or more of the following:

116
 (i) Psychological depdence i.e. psychological craving for the drug.
(ii) Physiological (physical) dependence i.e. occurance of withdrawal symptoms on
discontinuation of the drug.
(iii) Tolerance i.e. the need to increase the does with continued use to obtain the same desired
effects.
Drug dependency occurs due to frequent use of large amounts of drugs though some drugs
produce dependence after single time use. Dependency increases with the passage of time. Polydrug
usage is very common.
Opiates: The term opiates includes a number of drugs with actions that mimick those of
morphine. The commonly abused opiates are (i) Opium, a crude preparation of the milky juice of
poppy fruit (ii) Morphine, a refined product of the milky juice of poppy fruit. Morphine is used in
treatment of several disease states (iii) heroin, a derivative of morphine which has no known medical
use, (iv) Purify Synthetic Opiates like propoxyphene, pethidind and pentazocine and (v) others including
Codeine. All these drugs share the common effects of damping of pain perception, feeling of drowsiness
and euphoria. Tolerance to any of these drugs is likely to cause tolerance to other drugs of the same
variety (i.e. cross tolerance). Each of these substance is capable of producing a psychological as
well as physical (physiological) dependence and withdrawal syndrome similar to others but the
frequency, amount and duration for which each drug should be taken before addiction occurs varies
from drug to drug.
All the opiate drugs can be taken by mouth or by intravenous or intramuscular injections. Opium
is taken by mouth. Morphine is taken by injection most often. Heroin can be taken by intravenous
injection but most of the crude preparations of herion (e.g. smack/brown sugar) are inhaled as these
drugs can be readily absorbed by lungs too. Street heroin typically contains only 5-10% of pure heroin,
the remainder consists of contaminants such as fruit sugars, quinine, powdered mil, caffeine etc. which
are used to cut the drug and increase the margin of profit.
Opiates cause the following effects on body systems; lack of appetite, constipation, hepatitis,
nausea and vomiting, decreased pain perception, euphoria, drownsiness, decreased sexual drive,
respiratory depression, low blood pressure, infection of the lungs and heart valves. Contaminants may
cause permanent brain damage, loss of vision and brain abscess. A large number of intravenous drug
abusers have required immuno-deficiency syndrome (AIDS) antibodies.
Administration of high doses accidentally or for suicidal purposes may cause severe respiratory
depression, slow pulse, low blood pressure, decrease in body temperature, frothing through mouth and
absence of responsiveness. Death may occur from cardiorespiratory arrest. Effects of opiates on body
can be reversed by a drug called naloxone.
There are 2 categories of opiate abusers (i) medical abuser, who suffers from a chronic painful
condition and misuses the prescribed drug (ii) street abuser. A significant proportion of street abusers
have antisocial personality. However, the majority of street abusers belong to a class with high level
of premorbid functioning. They start taking opiates occasionally, often after experimenting with tobacco,
then alcohol and charas. The outcome is usually serious once opiate addiction is established. At least
25% of opiate addicts die within 10-20 years due to suicide, homicide, accidents, infections or over-
dosage. A large number of opiate addicts also become alcoholics. Another group at high risk is that
of physicians, nurses and pharmacists who have easy access to drugs.
Symptoms of opiate with withdrawal include nausea, diarrhoea, cough, excessive salivation,
running nose, excessive sweating, goose pimples, muscle twitching, tremors, hot and cold flushes,

117
mild fewer, rapid respiration, high blood pressure, fast pulse, diffuse body pain, inability to sleep,
yawning spontaneous ejaculation, orgasm and craving for the drug. Withdrwal symptoms disappear
within 5-8 days but mild symptoms may persist upto 6 months.
Opiate withdrawal can be treated by gradual withdrawal of the drug over 5-10 days. Atternatively,
a long acting opiate like methadone may be administered in tapering doses. Some symptoms of opiate
withdrawal can also be eliminated by clonidine, a drug which does not belong to the class of opiates.
Rehabilitation of the opiate addict requires help by a physician as well as the family of the
addict. The victim should be motivated towards abstinence by counselling arid education. Addicts
often to conceal their dependence on drugs. Intravenous drug abusers can be readily recognised by
multiple puncture marks over the forearm or wrist. Patients should be educated about their responsibility
towards improving their lives and the potential consequences of continued addiction. Group therapy
goes a long way in motivating drug addicts to shed off their dependence. In this type of treatment,
several addicts sit together and discuss and narrate their problems to one another. Besides that an ex-
addict describes his experiences and the way to deaddiction. Nearly one-third addicts become drug
free within one year of such therapies. Another one-third do not use opiates anymore though they may
continue to abuse milder drugs. Well educated addicts and those in job have a better prospect of
getting rid of drug addiction. Persistent and heavy addiction is usually a difficult problem and may
require hospitalisation for several weeks to months. Chronic administration of methadone may be
necessary.
Marijunana (Charas, Hashish, Bhaog and Ganja): Cannabis saltiva, a plant, is the source
of marijuana. Different parts of this plant vary in potency. The derivative of the flowering tops of the
female plant (hashish, charas) is the most potent, followed by the dried leaves and flowering shoots
of the female plant (bhang) and the resinous mass from small leaves of non-flowering shoots (ganja).
The least potent parts are the lower branches and leaves of the female plant and all parts of the
male plant. Hashish, charas and ganja are inhaled by smoking while bhang is taken by mouth. Effects
occur within 10-20 mins and last for 2-3 hours.
The effects of marihuana are mild euphoria followed by sleepiness. In the acue state the user
develops an altered time perception, less inhibited emotions, impaired immediate memory, redness of
eyes and rapid heart rate. High doses produce transient alteration of psyche. Marijhuana frequently
aggravates pre-existing mental illness and slows the learning process in children. Long term
usage adversely affects the nose, larynx (voice box) and the lungs. Electrocardiogram (ECG) may
become abnormal during marihuana intoxication but no long term heart disease is known to occur.
Sperm counts may decrease. Abnormal menstruation and lack of ovulation is also known to occur.
Marihuana abuse during pregnancy may cause impaired growth of foetus. Sudden withdrawal of
marihuana produces lack of sleep, nausea, tremor, bodyache and irritability. The withdrawal symptoms
are milder in comparison to those observed with heavy opiate or alcohol addicts and rarely require
medical therapy. Tolerance to the effects of marihuana develops rapidly.
Other drugs: A large number of drugs are abused all over the world. The pattern of drug
abuse varies in different countries and the pattern in a single country also keeps on changing with
time. Herion was the most commonly abused drug in the western countries till early 1970s, when
marihuana took over. In India, opium, charas and ganja have been the traditionally abused drugs
since the ancient times. At present, crude preparations of herion including brown sugar and
smack top the list at least in the urban areas. Charas, ganja and bhang continue to be popular
among Indians. Cocaine is the most popular drug in America at present, but it is not commonly
abused in India due to its/high cost.

118
Other drugs which are occasionallyjased by habitual drug users are sleeping pittls, L.S.D.
(lysergic acid diethylamide), pheftcyclidine, amphetamines and antihistafninic drugs Sleeping
pills can produce dependency and resemble alcohol in their behavioural manifestations. Acute
intoxication with sleeping pills produces drownsiness, errors of commission, slowed speech and
thinking, impaired memory, disinhibition and unstable gait. Respiratory depression, low blood
pressure, unconsciousness and death may occur. Withdrawal symptoms include’restlessness, tremor,
anxiety, fits weakness, palpitations and delirium. Overdosage with sleeping pills may be complicated
by pneumonia and other serious complications, which may culminate in death. Treatment requires
hospitalisation.
LSD, when ingested, produces a feeling of tension followed by emotional release (laughing
or crying), perceptional distortions such as visual illusions and hallucinations, changes in time
sense and mood lability. Its use during first trimestes of pregnancy commonly leads to abortion
or birth defects. Treatment of LSD addiction includes treatment with antipsychotic drugs.
Phencyclidine has simillar effects. It can be inhaled, injected, swallowed or smoked. Overdosage
may be fatal due to severe elevation of blood pressure, respiratory depression or fits.
Amphetamines are abused because of the ability of these drugs to produce excessive physical
activity and a sense of enhanced mental capacity. Acute intoxication causes excessive sweating,
rapid pulse, high blood pressure, confusion and disorientation. Tolerance develops rapidly.
Continued use may cause mental illness. Sudden withdrawal is characterised by depression and
excessive sleeping and eating.
General treatment of drug addiction: Nearly all drug addicts require psycho-social care.
This is a very time consuming process and should be done with the help of family members as
well as a trained psychologist. For this purpose, all the major psychiatric departments of different
hospitals run a regular ‘de-addiction clinic’ which aims at treating cases of addiction by psycho-
therapy and drug treatment, whichever is appropriate. In some cases who are not likely to give
up drugs at home, a brief period of hospitalisation may also be necessary in order to control the
withdrawal symptoms which may prompt the person fcf resort to drugs again.
AIDS
AIDS, the acquired immuno-deficiency syndrome (sometimes called “slim disease”) is a
fatal illness caused by a retrovirus known as the human immuno-deficiency virus (HIV) which
breaks down the body’s immune system, leaving the victim vulnerable to a host of life-threatening
opportunistic infections, neurological disorders, or unusual malignancies. Among the special
features of HIV infection are that once infected, it is probable that a person will be infected for
life. Strictly speaking, the terms AIDS can be called our modern pandemic, affecting both
industrialized and developing countries.
Public Health Concern
Recognized as an emerging disease only in the early 1980s, AIDS has rapidly established
itself throughout the world and it likely to endure and persist well into the 21st century.
The number of people living with HIV continues to grow, as does the number of deaths due
to AIDS. A total of 39.5 million (34.1 million — 47.1 million estimated) people are living with
HIV in 2006, about 2.6 million more than in 2004. This figure includes the estimated 4.3 million
(3.6 million — 6.6 million) adults and children who were newly infected with HIV in 2006.
The interaction of HIV/AIDS with other infectious diseases is an increasing public health
concern. Tuberculosis, bacterial infection and malaria have been identified as the leading cause

119
of HIV-related morbidity in Sub-Sharan Africa. HIV infection increases the incidence and severity
of clinical malaria in adults.
In India, the early cases of HIV/AIDS were concentrated primarily to Chennai and Mumbai.
The disease soon spread to other parts of the country, often following the path of major highways
and labour migrants. By mid-2003, Tamil Nadu had nearly half of the reported AIDS cases.
Mumbai and rest of Maharashtra now share about 19.74 per cent of the AIDS reported cases. Fig.
1 shows the distribution of reported AIDS cases by states upto August 2006.
Epidemiological Features
1. Agent factors
(a) Agent: When the virus was first identified it was called “lymphadenophathy—associated
virus (LAV)” by the French scientists. Researchers in USA called it “human T-cell
lymphotropic virus III (HTLV-iii)”. In May 1986, the International Committee on the
Taxonomy gave it a new name: Human Immuno-deficiency Virus (HIV).
The virus is 1/10,000th of millimeter in diameter. It is a protein capsule containing two
short stands of genetic material (RNA) and enzymes. The virus replicates in actively
dividing T4 lymphocytes and like other retroviruses can remain in lymphoid cells in a
latent state that can be activated. The virus has the unique ability to destroy human
T4 helper cells, a subset of the human T-lymphocytes. The virus is able to spread
throughout the body. It can pass through the blood-brain barrier and can then destroy
some brain cells.
(b) Reservoir of Infection: These are cases and carriers. Once a person is infected, the
virus remains in the body life-long. The risk of developing AIDS increase with time.
Since HIV infection can take years to manifest itself, the symptomless carrier can
infect other people for years.
(c) Source of Infection: The virus has been found in greatest concentration in blood,
semen and CSF. Lower concentrations have been detected in tears, saliva, breast milk,
urine, and cervical and vaginal secretions. HIV has also been isolated in brain tissue
lymph nodes, bone marrow cells and skin. To date, only blood and semen have been
conclusively shown to transmit the virus.
2. Host factors
(a) Age: Most cases have occurred among sexually active persons aged 20-49 years. This
group represents the most productive members of the society and those responsible for
less than 3 per cent of the cases.
(b) Sex: In North America, Europe and Australia, about 51 per cent of cases are homosexual
or bisexual men.
(c) High Risk Groups: Male homosexuals and bisexuals, heterosexual partners (including
prostitutes), intravenous drug abusers, transfusion recipients of blood and blood products,
haemophiliacs and clients of STD.

120
Mode of transmission
The causative virus is transmitted from person—to—person, most frequently through sexual
activity. The basic modes of transmission are :
(a) Sexual Transmission—AIDS is first and foremost a sexually transmitted disease. In
the USA, over 51 per cent of the cases were in homosexual or bisexual men. In
contrast, in equatorial Africa, AIDS is acquired mainly through heterosexual contact.
(infected man to woman; infected woman to man) from male to female is twice as
likely as from female to male.
(b) Blood contact—AIDS is also transmitted by contaminated blood — transfusion of
whole blood cells, platelets and factors VIII and IX derived from human plasma.
(c) Maternal—foetal transmission: mother-to-child transmission HIV may pass from an
infected mother to her foetus, through the placenta or to her infant during delivery or
by breast-feeding. In the absence of any intervention, rates of this form of transmission
can vary from 15-30 percent without breast feeding.
Incubation period
While the natural history of HIV infection is not yet fully known, current data suggest that
the incubation period is uncertain, (from a few months to 10 years or even more) from HIV
infection to the development of AIDS. The virus can lie silent in the body for many years. The
percentage of people infected with HIV, who will develop clinical disease remains uncertain—
possibly 10-30 per cent will develop AIDS, and another 25-30 per cent will develop AIDS-related
complex. However, it is estimated that 75 per cent of those infected with HIV will develop AIDS
by the end of ten years.
Control of AIDS
Until a vaccine or cure for AIDS is found, the only means at present available is health
education to enable people to make life—saving choices:
(1) Avoiding indiscriminate sex, using condoms. There is, however, no guarantee that the
use of condoms will give full protection.
(2) One should also avoid the use of shared razors and toothbrushes.
(3) Intravenous drug users should be informed that the sharing of needles and syringes
involves special risk.
(4) Women suffering from AIDS or who are at high risk of infection should avoid becoming
pregnant, since infection can be transmitted to the unborn or newborn.
(5) Educational material and guidelines for prevention should be made widely available.
(6) All mass media channels should be involved in educating the people on AIDS.
National AIDS Control Programme
With the spread of AIDS from one country to another it became necessary to initiate a
national control programme. The Govt. of India in 1985 constituted a task force to look into this
matter. It began by pilot screening programme of high-risk population. National AIDS control
Programme was launched in 1987. In the years 1992, the Ministry of Health and Family Welfare
set up a National AIDS Control Organization as a separate wing to implement and closely

121
monitor the various components of the programme. The Government of India launched a 5 year
HIV/AIDS Control Project from September 1992 to September 1997 as 100 per cent centrally
sponsored project for all states/UTs. The project was later on extended upto March 1992.
The Phase II (1999-2006) of the National AIDS Control Programme has become effective
th
from 9 November 1999. It is also a 100% centrally sponsored scheme implemented in 32 States/
UTs and 3 Municipal Corporation namely Ahmedabad, Chennai and Mumbai through AIDS
control Societies. The three new states of Chhattisgarh, Uttaranchal and Jharkhand are in the
process of establishing their State AIDS Control Societies.
The National AIDS Control Programme Phase II has two key objective:
1. To reduce the spread of HIV infection in India; and
2. To strengthen India’s capacity to respond to HIV/AIDS on a long term basis.

122
1st Proof - 1.10.08 Through Bhattacharya Ji

2nd Proof - 23.10.08 Self (Bhattacharyas)

3rd Proof - 24.11.08 Self

123