Dietary Intravention On Cardiac Patients
Dietary Intravention On Cardiac Patients
Dietary Intravention On Cardiac Patients
ABBREVIATIONS
CI confidence interval
HR hazard ratio
MI myocardial infarction
Introduction
Behavior modification is a key strategy that may prevent a large number of
primary and secondary cardiovascular events (1). Suboptimal diet is responsible
for an estimated 1 in 5 premature deaths globally from 1990–2016 (2).
Observational study of human diet and health outcomes are challenging due to
difficulties in measuring dietary intakes (3) and potential problems with
generalizability and confounding (4). While randomized trials provide stronger
potential for causal inference, they typically have small sample sizes, short
durations of follow-up, noncompliance, high attrition rates, and ethical constraints
(5). Thus, current dietary recommendations are based on a combination of human
observational and intervention trial evidence supplemented by findings from
mechanistic studies (6).
In the present review, we first summarize the current state of knowledge regarding
various food groups and nutrients. Subsequent sections explore factors driving
individual food choice, where preventive action can be implemented, and what
potential roadblocks may hinder progress.
High amounts of processed meat, SSB, and refined grain consumption are
associated with greater CVD incidence; moderate coffee and alcohol intake, and
high fruit/vegetable, dairy (low-fat), whole grain, fish, and nut intake are
associated with lower incidence. High adherence to Mediterranean, DASH, AHEI,
and Prudent dietary patterns are significantly predictive of lower CVD incidence.
Abbreviations: AHEI, Alternative Healthy Food Index; CHD, coronary heart
disease; CI, confidence interval; CVD, cardiovascular disease; DASH, Dietary
Approaches to Stop Hypertension; MedDiet, Mediterranean Diet; RR, risk ratio;
SSB, sugar sweetened beverage.
Intake of total fruits and vegetables has been inversely associated with CVD risk
(14). However, benefits for subgroups have been less studied, and may vary
considerably. Various phytochemicals and micronutrients such as folate,
potassium, fiber, and flavonoids found in fruits and vegetables are hypothesized to
be responsible for the observed benefits (15). Potatoes have been viewed with
skepticism due to their high starch content; higher potato intake, especially from
French fries, has been associated with greater risk of hypertension, type 2 diabetes
(T2D), and CHD risk (16–18).
Whole grain intake is associated with a substantially lower risk of CVD whereas
refined grain intake is suggestive of an increased but nonsignificant association
(19). The bran and germ layers, present in whole grains but removed from refined
grains, are rich in fiber, lignans, micronutrients, fatty acids, and other
phytonutrients (20). Depletion of these nutrients during the milling process
partially explains why whole grain consumption is generally related to higher
satiety and a lower glycemic response compared with refined grains (21).
Marine fish is rich in long-chain omega-3 fatty acids, which are thought to reduce
arrhythmias, thrombosis, inflammation, blood pressure, as well as favorably
modify the lipid profile (22). A meta-analysis suggests that a 15g/d increment in
fish intake is associated with a HR = 0.96 (95% CI = 0.90, 0.98) for CHD mortality
(23).
Nuts and legumes are beneficial through their high unsaturated fat, fiber,
micronutrient, and phytochemical content (24). A meta-analysis of 25
observational studies found that a 4 serving/week increase in nut intake was
associated with an HR = 0.76 (95% CI = 0.69, 0.84) for fatal CHD and HR = 0.78
(95% CI = 0.67, 0.92) for nonfatal CHD (24). Small intervention studies have
reported lower total cholesterol, LDL-c, ApoB, and triglycerides among those
randomized to consuming tree nuts compared to the control arms (25).
Dairy products have shown null or weakly inverse associations with CVD. For
example, fermented dairy (i.e. sour milk products, cheese, yogurt) showed a HR
per 20g/d = 0.98 (95% CI = 0.97–0.99) (26) with similar associations observed
across different dairy products. Similar associations have also been observed for
total dairy and T2D (HR per 200g/d = 0.97, 95% CI = 0.95, 1.00), and yogurt (HR
per 80g/d = 0.86, 95% CI = 0.83, 0.90) (27). Potential benefits of fermented dairy
may be due to its probiotics contents (28).
Intake of processed meat (i.e., hamburgers, hot dogs, deli meats) has been shown
to increase the risk of CVD in a robust linear fashion (29,30). Higher consumption
of unprocessed red meat has also been associated with increased risk of CVD
mortality (29). Replacing processed and unprocessed red meat with other sources
of protein such as fish, poultry, and nuts was associated with lower incidence of
coronary heart disease (31). Low carbohydrate diets high in animal protein and fat
were associated with higher risk of total and cardiovascular death among MI
survivors (32). Important bioactive molecules in red meat include heme iron,
sodium, nitrates, and L-carnitine that may lead to significant elevations in blood
pressure, worsening oxidative stress, greater lipid peroxidation, and unfavorable
alterations of the gut microbiome (33,34).
Beverages
Alcohol is related to CVD risk in a U-shaped relationship, with both abstainers and
heavy drinkers having an increased risk compared to moderate drinkers (35). The
exact nadir of risk differs according to age, sex, ethnicity, and baseline disease
(36), but the consistent observation is that individuals who consume 1–2 drinks a
day have the lowest risk (37). Moderate alcohol intake has been shown to increase
HDL-c, apolipoprotein A1, adiponectin, and decrease fibrinogen levels (38,39).
Higher consumption of sugar-sweetened beverages has been associated with risk of
CVD in a dose-dependent relationship (40). This association is partially mediated
by an increase in body weight; high intake of liquid calories does not seem to
reduce later intake of solid foods (41). Independent of weight change, intake of
SSBs increase postprandial blood glucose and insulin concentrations through a
high glycemic load, as well as conferring adverse effects on fat deposition, lipid
metabolism, blood pressure, insulin sensitivity, and lipogenesis (42).
Regular consumption of coffee has been consistently associated with lower risk of
CVD, with the greatest risk reduction occurring at around 3–5 cups per day
conferring an 11% lower risk (43). Biological mechanisms for the cardioprotective
effects of moderate coffee consumption include a high concentration of
chlorogenic acid, micronutrients, lignans, and phytochemicals. Short term trials of
coffee report higher insulin sensitivity and a favorable inflammatory marker
profile, but excess intake (>8 cups/d) may lead to acute elevations in blood
pressure (44).
Tea has likewise been reported to be inversely associated with CVD incidence
(45). Tea flavonoids, specifically flavonols, have received considerable attention
and are themselves independently associated with reduced CVD risk (46).
Dietary patterns and quality are the most comprehensive metrics of assessing
eating habits and include indices based on a priori scoring, such as the Alternative
Mediterranean diet score (aMED), Alternative Healthy Food Index (AHEI), and
Dietary Approaches to Stop Hypertension (DASH) diet score, as well as
exploratory methods including principal component analysis and cluster analysis
(47). Holistic evaluation of the diet is useful because it captures potential food and
nutrient interactions that studies of single nutritional items cannot (48).
Individual diet indices differ in their components and weighting, but most
emphasize high intake of fruits and vegetables, whole grains, nuts; moderate intake
of low/nonfat dairy and alcohol; and low intake of sodium, processed meats, added
sugar, and saturated fat (49). In the Women’s Health Initiative, high HEI, AHEI,
aMED, and DASH scores were consistently associated with around a 20%
reduction in CVD mortality (50). Sotos-Prieto et al. reported that improvement in
these scores was also associated with lower risk of total and CVD mortality in two
large cohorts (51,52). Similar findings have been observed among MI survivors. Li
et al, found that a greater increase in the AHEI score from pre- to post-MI was
significantly associated with lower all-cause and cardiovascular mortality (53) and
Lopez-Garcia et al. found that adherence to a Mediterranean-style dietary pattern
was associated with lower all-cause mortality among individuals with CVD (54).
Principal component and factor analyses have generally identified two dietary
patterns that explain most of the variation in population-level eating habits: prudent
and Western. Prudent diets are rich in fruits, vegetables, legumes, whole grains,
fish, and poultry, whereas Western diets include high amounts of processed meat,
French fries, desserts, sugar sweetened beverages, red meat, and high-fat dairy
(55). A meta-analysis of 22 cohort studies found that those in the highest category
of adherence to a prudent diet had a 31% lower risk of CVD compared to those
with the lowest adherence (56), whereas a Western dietary pattern was associated
with a 14% increase in risk (56). The consistency of findings from cohort studies
across many countries for various dietary factors and indices and similar findings
from intervention trials support the causal role of a high quality diet in CVD
prevention (57,58).
Carbohydrates
Added sugars such as sucrose and high fructose corn syrup derived from industrial
processes have been associated with a significant increase in CVD risk (61), with
the greatest source and majority of evidence originating from SSBs (includes soda,
flavored fruit juices, sports drinks, and energy drinks), which accounts for 6.9% of
daily calories in the US (62). Higher consumption of added sugars appears to
increase risk of CVD independent of body weight or other dietary components
(63), likely through lowered HDL-c (64), increased plasma triglyceride
concentration (65), and higher blood pressure (66).
Dietary fiber has been consistently demonstrated to lower risk of CVD and
improve cardiovascular risk factors in both observational (67) and dietary
intervention studies (68,69). In a meta-analysis of 22 cohorts, a 7g/d increase in
fiber intake was associated with a 9% decrease in CHD incidence (67). Intake of
fiber, particularly cereal fiber has also been shown to reduce all-cause mortality
among MI survivors, with a 27% (HR 0.73, 95% CI: 0.58, 0.91) reduction in risk
of death in the highest compared to lowest quintile of cereal fiber intake (70). It is
thought that the cardioprotective action of fiber operates through decreased LDL-c,
decreased serum triglycerides, blunted postprandial glucose response (71), and
changes in bile acid metabolism (72).
Dietary Fat
Of the three primary types of dietary fat—trans fatty acids, saturated fatty acids,
and unsaturated (includes mono- and polyunsaturated fats) fatty acids—trans fatty
acids have been most strongly associated with adverse cardiovascular outcomes
(73), and its ban in the U.S. is one of the greatest success stories in public health,
the details of which are discussed later in the review. Among the other types of fat,
saturated fatty acids have received the most controversy. Higher intake of saturated
fat has been found to be either harmful or neutral for CVD risk in most meta-
analyses (74). One explanation for the inconsistent findings is that studies that
most observational studies did not specify comparison or replacement
macronutrient for saturated fat, , leaving carbohydrates (primarily from refined
grains and added sugar) as the default comparison macronutrient.
Lack of nutrition knowledge has been suggested as a contributor to poor diet (85),
particularly among low income or minority populations (86,87), and in low income
countries (88,89), where access to education is limited. However, most individuals
in high income countries appear to possess a reasonable level of nutritional
knowledge, with elements such as fruits and vegetables being widely recognized as
healthy and highly processed grain products, added sugar, and salt as unhealthy
(90). In a large European study of 14,331 participants, lack of knowledge was not
cited as a common barrier to healthy eating (91).
On the other hand, lack of availability of healthful foods has been identified as a
potential driver of unhealthy eating. ‘Food deserts’ refer to areas with long
distances to supermarkets and low access to fresh foods, while food swamps refer
to areas with an abundance of unhealthy processed and fast foods (92,93). This
simultaneous availability of cheap low-quality food and expensive or lack of
availability of high-quality food can drive individuals to choose unhealthy eating
options (94,95). These elements together create an obesogenic environment that
can lead to excess adiposity and subsequent cardiometabolic disease (96).
Branding and marketing are also major factors that influence both taste and choice.
Advertising has long been known to affect taste, possibly by linking positive
sensory thoughts with the target product (108). Regulations on food branding and
restriction of advertising to children have also been proposed as ways to improve
diet quality and reduce obesity (109,110).
Social determinants of food choice include influences of culture, friends/family,
and community. Social norms have powerful influences on eating patterns, and that
healthy food norms can result in healthier food choices (111). Sacks et al. reported
that the number of support sessions attended was the strongest predictor of weight
loss at 2 years (0.2 kg for every session attended) regardless of macronutrient
composition (82). Recent analyses indicate that food choices tend to be shared
among family members (112), and that alcohol drinking and snacking were the
most “transmissible” eating patterns (113).
Given the magnitude of the CVD burden in the US and globally and complexity of
dietary risk factor modification, simultaneous prevention strategies and policies
across multiple societal levels are needed to make a measurable impact on
reducing prevalence rates. In contrast to clinical decision-making where the
evidence base is dominated by randomized clinical trials and large cohort studies,
there is a paucity of data evaluating preventive actions to improve diet. Thus, to
gauge the effectiveness of prevention strategies we also consider different types of
evidence such as natural experiments and simulation models and discuss actions
that have great potential for benefit and scalability that represent important
knowledge gaps.
Nutrition and agricultural policies are powerful instruments for reducing CVD risk
if they align with evidence-based dietary goals to improve diet quality. One
example is nutrition labeling of industrially produced trans fats and legislation for
removal of trans fats from the food supply, which was recently enacted in the US
with the removal of trans fats from the FDA’s generally regarded as safe category.
This action which will be implemented in 2018 is expected to reduce as many as
20,000 coronary events and 7,000 deaths from coronary causes each year in the
United States (114).
Some governments are considering taxing select foods and beverages, particularly
SSB’s, as a means to improve consumer choice and generate revenue. Whether
these programs will have the desired effect is yet to be determined. Some studies
have suggested that for such interventions to have an appreciable impact, tax
increases of at least 10% are needed (115). In Mexico, a peso-per-liter (roughly
$0.80 per liter) tax on sugar-sweetened beverages enacted in 2014 has resulted in
an average reduction in sales of 7.6 % of taxed beverages two years after
implementation. Households at the lowest socioeconomic level had the largest
decreases in purchases of taxed beverages over this time and purchases of untaxed
beverage increased 2.1% (116). To date, at least eight cities in the US have enacted
an SSB tax along with a number of countries including Mexico, Chile, France,
Norway, Finland, the United Kingdom and Hungary. Careful evaluation will be
key in determining the effectiveness of these strategies on reducing intake of these
beverages and subsequently on reducing prevalence of obesity and cardiometabolic
disease.
Government regulation of school lunch programs has the potential to improve diet
quality of children on a large scale. In 2012 the nutrition standards of federally
assisted meal programs were updated for the first time in 15 years, to reduce
sodium, saturated fat and trans fats and increase fruits, vegetables and whole
grains largely based on recommendations by the Institute of Medicine of the
National Academies, as part of efforts to curb childhood obesity (120). Some of
these nutrition standards including the sodium and whole grain requirements have
been recently relaxed by the USDA due to concerns of perceived palatability and
food wastage (121).
Food marketing and advertising are able to create major shifts in food demand
because marketing leads people to increase their consumption of advertised
products (123). A growing body of evidence indicates that food marketing can
influence the food preferences and consumption habits of children (124). However,
evidence from systematic reviews is lacking, and few studies have evaluated the
impact of advertising on energy intake or body weight. A systematic review of
seven randomized trials aiming to assess the effect of television advertising on
food intake of children from 4 to 12 years of age concluded that there is a positive
association between television and energy intake, but this association is based on a
limited number of trials lacking a solid ground of first-level evidence (125). In
2010, the WHO released a set of recommendations on the marketing of foods and
nonalcoholic beverages high in fat, sugar, and salt to children in an effort to
encourage healthy dietary choices and promote the maintenance of healthy weight
(126). In France, marketing of foods high in fat, sugar, and salt is banned unless
they are taxed and labeled with a health warning. At the same time, governments
can institute zoning laws, if available, that limit the number of fast food restaurants
in a given area.
Education/Comm unity
Physicians and other health-care providers should monitor the body weight of
patients and be trained on how to measure waist circumference, which may be
more informative than weight as a marker for cardiometabolic risk. Clinicians
should provide suitable evidence-based advice about weight management (115)
and refer individuals identified as high-risk for screening of metabolic risk factors.
Evaluation of such actions is needed to address this evidence gap. Medical
associations and nongovernmental organizations also have central roles in
advocacy and can influence policy on issues related to health and the environment.
For example, the American Heart Association released a scientific statement,
calling for a reduction in intake of added sugar to improve health (131), which has
become an integral part of the dialogue regarding regulation of sugar-sweetened
beverages. Nutrition education in medical schools and continuing medical
education programs can improve nutrition literacy and nutrition communication
skills among health-care providers.
Individuals
Footnotes
Disclosures: None to report.
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References
1. Pearson TA, Blair SN, Daniels SR et al. AHA Guidelines for Primary
Prevention of Cardiovascular Disease and Stroke: 2002 Update. Consensus Panel
Guide to Comprehensive Risk Reduction for Adult Patients Without Coronary or
Other Atherosclerotic Vascular Diseases. Circulation 2002;106:388–391.
[PubMed] [Google Scholar]
13. Fortmann SP, Burda BU, Senger CA, Lin JS, Whitlock EP. Vitamin and
mineral supplements in the primary prevention of cardiovascular disease and
cancer: An updated systematic evidence review for the u.s. preventive services task
force. Ann Internal Med. 2013;159:824–834. [PubMed] [Google Scholar]
14. Aune D, Giovannucci E, Boffetta P et al. Fruit and vegetable intake and the
risk of cardiovascular disease, total cancer and all-cause mortality-a systematic
review and dose-response meta-analysis of prospective studies. International J
epidemiology 2017. [PMC free article] [PubMed] [Google Scholar]
15. Bazzano LA, Serdula MK, Liu S. Dietary intake of fruits and vegetables and
risk of cardiovascular disease. Current Atherosclerosis Reports 2003;5:492–499.
[PubMed] [Google Scholar]
16. Muraki I, Rimm EB, Willett WC, Manson JE, Hu FB, Sun Q. Potato
Consumption and Risk of Type 2 Diabetes: Results From Three Prospective
Cohort Studies. Diabetes care 2016;39:376–84. [PMC free
article] [PubMed] [Google Scholar]
17. Borgi L, Rimm EB, Willett WC, Forman JP. Potato intake and incidence of
hypertension: results from three prospective US cohort
studies. BMJ 2016;353. [PMC free article] [PubMed] [Google Scholar]
25. Del Gobbo LC, Falk MC, Feldman R, Lewis K, Mozaffarian D. Effects of tree
nuts on blood lipids, apolipoproteins, and blood pressure: systematic review, meta-
analysis, and dose-response of 61 controlled intervention trials. Am J Clinical Nutr.
2015;102:1347–1356. [PMC free article] [PubMed] [Google Scholar]
31. Bernstein AM, Sun Q, Hu FB, Stampfer MJ, Manson JE, Willett WC. Major
dietary protein sources and risk of coronary heart disease in
women. Circulation 2010;122:876–83. [PMC free article] [PubMed] [Google
Scholar]
32. Li S, Flint A, Pai JK et al. Low carbohydrate diet from plant or animal sources
and mortality among myocardial infarction survivors. J Am Heart
Assoc 2014;3:e001169. [PMC free article] [PubMed] [Google Scholar]
35. Ronksley PE, Brien SE, Turner BJ, Mukamal KJ, Ghali WA. Association of
alcohol consumption with selected cardiovascular disease outcomes: a systematic
review and meta-analysis. BMJ 2011;342. [PMC free article] [PubMed] [Google
Scholar]
38. Brien SE, Ronksley PE, Turner BJ, Mukamal KJ, Ghali WA. Effect of alcohol
consumption on biological markers associated with risk of coronary heart disease:
systematic review and meta-analysis of interventional
studies. BMJ 2011;342. [PMC free article] [PubMed] [Google Scholar]
42. Malik VS, Popkin BM, Bray GA, Despres J-P, Hu FB. Sugar Sweetened
Beverages, Obesity, Type 2 Diabetes and Cardiovascular Disease
risk. Circulation 2010;121: 1356–1364. [PMC free article] [PubMed] [Google
Scholar]
44. Butt MS, Sultan MT. Coffee and its Consumption: Benefits and Risks. Critical
Reviews in Food Science and Nutrition 2011;51:363–373. [PubMed] [Google
Scholar]
45. Wang Z-M, Zhou B, Wang Y-S et al. Black and green tea consumption and the
risk of coronary artery disease: a meta-analysis. Am J Clinical
Nutrition 2011;93:506–515. [PubMed] [Google Scholar]
46. Wang X, Ouyang YY, Liu J, Zhao G. Flavonoid intake and risk of CVD: a
systematic review and meta-analysis of prospective cohort studies. British J
nutrition 2014;111:1–11. [PubMed] [Google Scholar]
53. Li S, Chiuve SE, Flint A et al. Better diet quality and decreased mortality
among myocardial infarction survivors. JAMA Intern Med 2013;173:1808–
18. [PMC free article] [PubMed] [Google Scholar]
60. Fung TT, van Dam RM, Hankinson SE, Stampfer M, Willett WC, Hu
FB. Low-carbohydrate diets and all-cause and cause-specific mortality: Two
cohort Studies. Ann intern med. 2010;153:289–298. [PMC free
article] [PubMed] [Google Scholar]
61. Johnson RK, Appel LJ, Brands M et al. Dietary Sugars Intake and
Cardiovascular Health. A Scientific Statement From the American Heart
Association 2009;120:1011–1020. [PubMed] [Google Scholar]
64. Nutrient intake and its association with high-density lipoprotein and low-
density lipoprotein cholesterol in selected US and USSR subpopulations. The US-
USSR Steering Committee for Problem Area I: The pathogenesis of
atherosclerosis. Am J Clin Nutr 1984;39:942–52. [PubMed] [Google Scholar]
67. Threapleton DE, Greenwood DC, Evans CEL et al. Dietary fibre intake and
risk of cardiovascular disease: systematic review and meta-analysis. BMJ.
2013;347. [PMC free article] [PubMed] [Google Scholar]
68. Streppel MT, Arends LR, van ‘t Veer P, Grobbee DE, Geleijnse JM. Dietary
fiber and blood pressure: a meta-analysis of randomized placebo-controlled
trials. Archives of internal medicine 2005;165:150–6. [PubMed] [Google Scholar]
70. Li S, Flint A, Pai JK et al. Dietary fiber intake and mortality among survivors
of myocardial infarction: prospective cohort study. BMJ 2014;348:g2659. [PMC
free article] [PubMed] [Google Scholar]
79. Kinsella JE, Lokesh B, Stone RA. Dietary n-3 polyunsaturated fatty acids and
amelioration of cardiovascular disease: possible mechanisms. The American
Journal of Clinical Nutrition 1990;52:1–28. [PubMed] [Google Scholar]
86. Cluss PA, Ewing L, King WC, Reis EC, Dodd JL, Penner B. Nutrition
Knowledge of Low Income Parents of Obese Children. Translational behavioral
medicine 2013;3:218–225. [PMC free article] [PubMed] [Google Scholar]
95. Walker RE, Keane CR, Burke JG. Disparities and access to healthy food in the
United States: A review of food deserts literature. Health & Place 2010;16:876–
884. [PubMed] [Google Scholar]
103. Lustig RH, Schmidt LA, Brindis CD. Public health: the toxic truth about
sugar. Nature 2012;482:27–29. [PubMed] [Google Scholar]
109. Veerman JL, Van Beeck EF, Barendregt JJ, Mackenbach JP. By how much
would limiting TV food advertising reduce childhood obesity? The European
Journal of Public Health 2009;19:365–369. [PMC free article] [PubMed] [Google
Scholar]
117. Zenk SN, Schulz AJ, Israel BA, James SA, Bao S, Wilson ML. Fruit and
vegetable access differs by community racial composition and socioeconomic
position in Detroit, Michigan. Ethn Dis 2006;16:275–80. [PubMed] [Google
Scholar]
123. Popkin BM, Adair LS, Ng SW. Global nutrition transition and the pandemic
of obesity in developing countries. Nutr Rev 2012;70:3–21. [PMC free
article] [PubMed] [Google Scholar]
136. Leung CW, Epel ES, Ritchie LD, Crawford PB, Laraia BA. Food insecurity is
inversely associated with diet quality of lower-income adults. Journal of the
Academy of Nutrition and Dietetics 2014;114:1943–1953. e2. [PubMed] [Google
Scholar]
138. Katan MB. Regulation of trans fats: The gap, the Polder, and McDonald’s
French fries. Atherosclerosis Supplements 2006;7:63–66. [PubMed] [Google
Scholar]
140. Nestle M Food politics: How the food industry influences nutrition and
health: Univ of California Press, 2013. [Google Scholar]