The Unusual Reality of Depression

© 2012 by Richard J. Kosciejew. All rights reserved.

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Published by AuthorHouse 09/24/2012

ISBN: 978-1-4772-7369-2 (sc)

ISBN: 978-1-4772-7370-8 (e)

Library of Congress Control Number: 2012917927

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Discussions of depression often start with a statement that has come over time to be found that it is the common cold of psychopathology, a ubiquitous affliction to which most of us are subject from time to time. Such discussions may be noted that at any one time, one fifth of the adult population will have significant depressive symptoms, and that most of this depression goes untreated (Weissman and Meyers, 1981). It may also be suggested that whoever is most likely to become depressed is largely a matter of psychological background and social conditions; depression is a ‘curse of civilization’ and its occurrence as formulating the disintegration of relationships, and depressing life circumstances. Thus, Pearlin (1975) had stated that depression is ‘intertwined’ with the values and aspirations that people acquire. That within the nature of the situation in which they are engaged of major roles, such as in occupation and family; with the location of people in broader social structures, such as age and class; and the coping devices that they use.

Even so, discussions of depression may begin with assertions that it is one of the most serious of mental-health problems. The discussion may then go on to emphasize that it is primarily a biological disturbance, an illness, the predisposition to which lies in genes and biochemistry. While people, may react to their circumstances with happiness and unhappiness, this is of questionable relevance to the clinical phenomena of depression.

Advocates of each of the positions, we can marshal impressive evidence; yet, taken together, they present a basic contradiction. They differ not only in their view of the causes of depression but it’s very definition. Beck (1967) has noted, ‘there are few psychiatric syndromes whose clinical descriptions are constant through successive eras of history.’ However, as these opposing positions demonstrate, definitional problems continue to plague the study of depression, and they are not to be readily resolved. There remains considerable disagreement as to what extent and what purpose a depressed mood of some normal persons can be seen as one end of a continuum with the mood disturbance seen in hospitalized psychiatric patients and to what extent the clinical phenomenon is distinct and discontinuous with normal sadness and unhappiness.

It should become apparent that there is a tremendous heterogeneity to what falls under the broad rubic of depression and that there is an arbitrariness of any boundaries that are drawn on these phenomena. There are striking differences among depressed persons that invite some form of subtyping. A well, however, efforts to derive such subtyping are generally controversial, and any scheme is likely to be more satisfactory for some purposes than for other. Confronted with all of this ambiguity and confusion, one must be cautious and not seek more precision than the phenomena of depression afford, and one should probably be sceptical about any decisive state about the nature of depression.

A major source of confusion is due to the fact the term ‘depression’ variously refers to a mood state, a set of symptoms, and a clinical syndrome, as a reference to mood, depression identifies a universal human experience (Luckerman and Lubin, 1965) point to subjective feelings associated with depressed mood: sad, unhappy, blue, low, discouraged, bore, hopeless, dejected, and lonely. Similarities between every day-depressed mood and the complaints of depressed patients have encouraged the view that clinical depression is simply an exaggeration of a normal depressed mood. However, patients sometimes indicate that their experiences of depression are quite distinct from normal feelings of sadness, even in extreme form.

Yet, the view that depressed mood in otherwise normal persons is quantitatively but not qualitatively different from the depression found in hospitalized patients has been termed the ‘continuity hypothesis.’ Beck (1967) has provided a useful analogy to suggest the alternative to the continuity hypothesis. He notes that every day fluctuation in body temperature can be measured on the same thermometer as the changes associated with fever. Yet the conditions giving rise to a fever are distinct from those causing fluctuations in temperatures in healthy individuals. Similarly, the condition giving rise to clinical depression may be distinct from those producing fluctuations in normal moods.

Studies have compared the subjective mood of persons who are distressed but not seeking help to those who are seeking treatment for depression (Depue and Monroe, 1978). The two groups may be similar in subjective mood, but they differ in other ways. Those persons who are not seeking treatment for depression tend to lack the anxiety and the physical complaints, including loss of appetite, sleep disturbances, and fatigue shown by the group seeking treatment. Still, it could be that there is a continuum between the two groups, with these additional features arising when a normal depressed mood becomes more prolonged or intensified. The controversy is likely to continue until either questions about the etiology of depression as resolved or unambiguous markers for depression are identified.

Advocates of biomedical approaches to depression tend to assume that there is a discontinuity between a normal depressed mood and clinical depression, and the appropriate biological markers will be found. Yet, as the article by Winokur, and suggests, even if that proves to be the case, there is likely to be many individuals suffering from extremes of depressed mood who do not have these markers.

Advocates of psychoanalytic, cognitive and behaviour, and interpersonal and social perspectives on depression have generally assumed a continuum between a normal depressed mood and clinical depression. They tend to exclude psychotic and bipolar depressed persons from issues (Gilbert, 1984). For unipolar depression, at least, they have assumed that whatever discontinuities in the biology of mild and severe moods there might be are not necessarily relevant to the psychological and social processes in which they are most interested.

All the same, sadness and dejection are not only emotional manifestations of depression, although about half of all depressed patient report these feelings as their principal complaint. Most depressed persons are also anxious and irritable. Classical descriptions of depression tend to emphasize that depressed persons’ feelings of distress, disappointment, and frustration are focussed primarily on themselves, yet a number of studies suggest that, that their negative feelings, including overt hostility, are also directed at the people around them. Depressed persons are often intensely angry persons (Kahn, Coyne and Margolin, Weissman, Klerman and Paykel, 1971).

Perhaps 10 or 15 percent of severely depressed patients deny feelings of sadness, reporting instead that all emotional experience, including sadness has been blunted or inhibited (Whybrow, Akiskal and McKinney, 1984). The identification of these persons as depressed depends upon the presence of other symptoms. The inhibition of emotional expression in severely depressed persons may extend to crying. Nevertheless, mildly and moderately depressed persons may feel that every activity is a burden, yet still derive some satisfaction from their accomplishments. Despite their low mood, they may still crack a smile at a joke. Yet, as depression intensifies, a person may report both a loss of any ability to get gratification from activities that had previously been satisfying—family, work, and social life—and a loss of any sense of humour. Life becomes stale, flat, and not at all amusing. The loss of gratification may extend to the depressed persons’ involvement in close relationships. Often, a loss of affection for the spouse and children, a feeling of not being able to care anymore, a sense of a wall being erected between the depressed person and others are the major reason for seeking treatment.

In the past decade, a number of theorists, notably Beck and Abramson, Seligman, and Teasdale have given particular attention to the cognitive manifestations of depression and have assumed that these features are causal of the other aspects of the disorder. Depressed persons characteristically view themselves, their situation, and their future possibilities in negative and pessimistic terms. They voice discouragement, hopelessness and helplessness. They see themselves as inadequate and deficient in some crucial way. They may be thought of death, wishing to be dead, and suicide attempts.

Depressed persons’ involvements in their daily lives are interpreted by them in terms of loss, defeat, and deprivation, and they expect failure when they undertake an activity. They may criticize themselves for minor shortcomings and seemingly search for evidence that confirm their negative view of themselves. (Beck, Kovacs and Beck) suggest that they will tailor the facts to fit these interpretations and hold to them in the face of contradictory evidence. Depressed persons overgeneralize from negative experiences, selectively abstract negative details out of context, ignore more positive features of their situations, and negative characterize themselves in absolutist and dichotomous term in absolute a dichotomous term. The revised learn-helplessness model emphasizes that depressed persons are particularly prone to blame themselves for their difficulties and to see their defects as stable and global attributes.

Aside from these content aspects of their thinking, depressed persons frequently complain that their thinking processes have slowed down, that they are distracted and they cannot concentrate. Decisions pose a particular problem. Depressed persons are uncertain, feel in need of more simply feel paralysed, and that the work of making a choice and a commitment is an overwhelming task to be avoided at any cost.

Perhaps one of the most frustrating aspects of depressed persons for those around them is their difficulty in mobilizing themselves to perform even the most simple task. Encouragement, expression of support, even threats and coercion seem only to increase their inertia, leading to other ss to make attributions of laziness, stubbornness, and malingering. Despite their obvious distress and discomfort, depressed persons frequently fail to take a minimal initiative to remedy their situations or to do only halfheartedly. To observe, depressed persons may seem to have a callous indifference to what happens to them.

Depressed persons often procrastinate, they are avoidant and escapists in their longing for a refuge from demands and responsibilities. In severe depression, the person may experience an abulia or paralysis of will, extending even to getting out of bed, washing, and dressing.

In more severe depression, there may be psychomotor retardation, expressed in slowed body movements, slowed and monotonous speech, or even muteness. Alternatively, psychomotor agitation may be seen in an inability to sit still, pacing, and outbursts of shouting.

Mild depression heightens sexual interest in some people, but generally depression is associate with a loss of interest in sex. In severe depression, there may be an aversion to sex. Overall, though, women who are depressed do not have sex frequently, but they initiate it less, enjoy it less, and are less responsive (Weissman and Paykel, 1974). As well, depressed persons report diffuse aches and pains. They have frequent headache, and they are more sensitive to existing sources of pain, such as dental problems.

A brief interaction with a depressed person can have a marked impact on one’s own mood. Uninformed strangers may read to a conversion with a depressed person with depression, anxiety, hostility, and may be rejecting of further contact (Coyne, 1976). Jacobson (1968) has noted that depressed persons often unwittingly succeed in making every one in their environment feel guilty and responsible and that others may react to the depressed person with hostility and even cruelty. Despite this visible impact of depression on others, there is a persistent tendency in the literature to ignore it and to concentrate instead on the symptoms and complaints of depressed persons out of their interpersonal context. Depressed persons can be difficult, but they may also be facing difficult interpersonal situations with which their distress and behaviour make more sense.

Depressed persons tend to withdraw from social activities, and their close relationships tend to be strained conflictual. Depressed women have been more intensely studied than depressed men, in part because women are approximately twice as likely to be depressed. Depressed women are dependent, acquiescent and inhibited in their communication in close relationships, and prone to interpersonal tension, friction and open conflict (Weissman and Paykel, 1974). Interestingly, the interpersonal difficulties of depressed persons are less pronounced when they are interacting with strangers than with intimates (Hinchcliffe, Hooper and Roberts, 1975).

About half of all depressed persons report marital turmoil (Rousabville, Weissman, Prusoff and Heraey-Bsron, 1975). There is considerable hostility between depressed persons and their spouses, but often there is more between depressed persons and their children. Being depressed makes it more difficult to be a warm, affectionate, consistent parent (KcLean, 1976). The children of depressed parents are more likely to have a full range of psychological and social difficulties than the children of normal or even schizophrenic parents (Emery, Weintrsub and Neale, 1982), yet one must be cautious in making causal inferences. There is evidence that the child’s problems are more related to a conflictual marital relationship and a stressful home life than depression of the parent, and so on.

Depression thus tends to be indicative of an interpersonal situation fraught with difficulties, and this need to be given more attention in both theorizing and planning treatment. Although depression is associated with interpersonal severity of depression and the extent of interpersonal problems tend to be modest. This may suggest that these problems are a matter not only how depressed persons are in their functioning, but of the response of key people around them as well (Coyne, Kahn, and Gotlib, 1985).

Depression can take shape in several other forms. In bipolar disorder we sometimes call manic-depressive illness, where a person’s moods swings back and forth between depression and mania. People with seasonal effective disorder typically suffer from depression only during autumn and winter, when fewer hours of daylight diminish. In dysthymia, people feel depressed, have low self-esteem, and concentrate poorly most of the time—often, over a period of years—but their symptoms are milder than in major depression. Some people with dysthymia experience occasional episodes of major depression.

Bipolar Disorder, is consistent of a mental illness in which a person’s mood alternates between extreme mania and depression, even so, they also call that Bipolar disorder manic-depressive illness. When manic, people with bipolar disorder feel intensely elated, self-important, energetic, and irritable. When depressed, they experience painful sadness, negative thinking, and indifference to things that used to bring them happiness.

Bipolar disorder is much less common than depression. In North America and Europe, about 1 percent of people experience bipolar disorder at some point in their lives. Rates of bipolar disorder are similar throughout the world. In comparison, at least 8 percent of people experience serious depression during their lives. Bipolar disorder affects men and women equally and is more common in higher socioeconomic classes. At least 15 percent of people with bipolar disorder commit suicide. This rate roughly equals the rate for people with major depression, the most severe form of depression.

Bipolar disorder is a mental illness that causes mood swings. In the manic phase, a person might feel ecstatically overcome with excitation, and self-importance, and full of life. Nevertheless, when the person becomes depressed, the mood shifts to extreme sadness, negative thinking, and apathy. Some studies that favor actively in the face of opposition that in the finding in support that the disease occurs at unusually high rates in creative people, such as artists, writers, and musicians. Nonetheless, other researchers contend that the methodologies of these studies were very misleading. In the October 1996 Discover magazine article, anthropologist Jo Ann C. Gutin presents the results of several studies of illness. Repression is one of the most common mental illnesses. At least 8 percent of adults in the United States experience serious depression at some point during their lives, and estimates range as high as 17 percent. The illness affects all people, regardless of sex, race, ethnicity, or socioeconomic standing. However, women are two to three times more likely than men to suffer from depression. Experts disagree on the reason for this difference. Some cite differences in hormones, and others point to the stress caused by society’s expectant expectations of women. Depression occurs in all sections of the world, although the pattern of symptoms can vary. The prevalence of depression in other countries varies widely, from 1.5 percent of people in Taiwan to 19 percent of people in Lebanon. Some researchers believe methods of gathering data on depression account for different rates.

A number of large-scale studies indicate that depression rates have increased worldwide over the past several decades. Furthermore, younger generations are experiencing depression at an earlier age than did previous generations. Social scientists have proposed many explanations, including changes in family structure, urbanization, and reduced cultural and religious persuasions. Although it may appear anytime from childhood to old age, depression usually begins during a person’s 20s or 30s. The illness may come on slowly, then deepen gradually over months or years. On the other hand, it may erupt suddenly in a few weeks or days. A person who develops severe depression may appear confusing, frightened, and unbalance that the perceiver give tongue to a ‘nervous breakdown.’ However it begins such that depression causes serious changes in a person’s feelings and outlook. A person with major depression feels sad nearly every day and may cry often. People, work, and activities that used to bring them pleasure no longer do. Symptoms of depression can also vary by culture. In some cultures, depressed people may not experience sadness or guilt but may complain of physical problems. In Mediterranean cultures, for example, depressed people may complain of headaches or nerves. In Asian cultures they may complain of weakness, fatigue, or imbalance. If left untreated, an episode of major depression typically lasts eight or nine months. About 85 percent of people who experience one bout of depression will experience future episodes. Depression usually alters a person’s appetite, sometimes increasing it, but usually reducing it. Unceasing sleep habits frequently change from time to time as well. People with depression may oversleep or, more commonly, sleep for fewer hours. A depressed person might go to sleep at midnight, sleep restlessly, then wake up at 5:00 a.m. feeling tired and foreign to his immediate environment. For many depressed people, early morning is a dreadful and terrible time of the day. Depression also changes one’s energy level. Some depressed people may be restless and agitated, engaging in fidgety movements and pacing. Others may feel sluggish and inactive, experiencing great fatigue, lack of energy, and a feeling of being worn out or carrying a heavy burden. Depressed people may also have difficulty thinking, poor concentration, and problems with memory.

People with depression often experience feelings of worthlessness, helplessness, guilt, and self-blame. They may interpret a minor failing on their part as a sign of incompetence or interpret minor criticism as condemnation. Some depressed people complain of being spiritually or morally dead. The mirror seems to reflect someone ugly and repulsive. Even a competent and decent person may feel deficient, cruel, stupid, phony, or guilty of having deceived others. People with major depression may experience such extreme emotional pain that they consider or attempt suicide. At least 15 percent of seriously depressed people commit suicide, and many more attempt it.

In some cases, people with depression may experience psychotic symptoms, such as delusions (false beliefs) and hallucinations (false sensory perceptions). Psychotic symptoms indicate an especially severe illness. Compared to other depressed people, those with psychotic symptoms have longer hospital stays, and after leaving, they are more likely to be moody and unhappy. They are also more likely to commit suicide. Some depressions seem to come from no pinpointed place, even when things are going well. Others seem to have an obvious cause: a marital conflict, financial difficulty, or some personal failure. Yet many people with these problems do not become deeply depressed. Most psychologists believe depression results from an interaction between stressful life events and a person’s biological and psychological vulnerabilities. Clinical depression is one of the most common forms of mental illness. Although depression can be treated with psychotherapy, many scientists believe there are biological causes for the disease. According to the June 1998 Scientific American article, Neurobiologist Charles B. Nemeroff discusses the connection between biochemical changes in the brain and depression. Depression runs in families, or as the descendable transmissions, such as the irregularity of studying twins. Researchers have found evidence of a strong genetic influence in depression. Genetically identical twins raised in the same environmental conditions are three times more likely to have depression in common than fraternal twins, who have only about half of their genes in common. In addition, identical twins are five times more likely to have bipolar disorder in common. These findings suggest that vulnerability to depression and bipolar disorder can be inherited. Adoption studies have provided more evidence of a genetic role in depression. These studies show that children of depressed people are vulnerable to depression even when raised by adoptive parents. Genes may influence depression by causing abnormal activity in the brain. Studies have shown that certain brain chemicals called neurotransmitters play an important role in regulating moods and emotions. Neurotransmitters involved in depression include norepinephrine, dopamine, and serotonin. Research in the 1960s suggested that depression result from lower than normal levels of these neurotransmitters, as in of the sectors cased within the brain. Support for this theory came from the effects of antidepressant drugs, which work by increasing the levels of neurotransmitters involved in depression. However, later studies have discredited this simple explanation and have suggested a more complex relationship between neurotransmitter levels and depression. An imbalance of hormones may also play a characteristic role in depression. Many depressed people have higher than normal levels of hydrocortisone (cortisol), a hormone secreted by the adrenal gland in response to stress. In addition, an underactive or overactive thyroid gland can lead to depression. A variety of medical conditions can cause depression. These include dietary deficiencies in vitamin B6, vitamin B12, and folic acid; degenerative neurological disorders, such as Alzheimer’s disease and Huntington’s disease; strokes in the frontal part of the brain; and certain viral infections, such as hepatitis and mononucleosis. Certain medications, such as steroids, may also cause depression. Psychological theories of depression focuses on the way people adaptively adjust of its hindering with the normal growth and developmental capabilities for being thought, such that the thinkable of concepts enabling by reasoning from evidence or from premises we can find an easier process from which we can think about the unthinkable. Also, behaving is not taken into account for being idle. As an essay of mind in 1917, the pioneer involving the Austrian psychoanalyst Sigmund Freud explained melancholia, or major depression, as a response to loss—either real loss, such as the death of a spouse, or symbolic loss. Such as the failure to achieve an important goal that Freud believed that a person’s unconscious anger over loss weakens the ego, resulting in self-hate and self-destructive behaviour. Cognitive theories of depression emphasize the role of irrational thought processes. American psychiatrist Aaron Beck proposed that depressed people tend toward viewing themselves, their environment, and the future in a negative light because of errors in thinking. These errors include focussing on the negative aspects of any situation, misinterpreting facts in negative ways, and blaming themselves for any misfortune. In Beck’s view, people learn these self-defeating ways of looking at the world during early childhood. This negative thinking makes situations seem much worse than they really are and increases the risk of depression, especially in stressful situations.

In support of this cognitive view, people with ‘depressive’ personality traits might be more vulnerable than others to actual depression. Examples of depressive personality traits include, gloominess, pessimism, introversion, self-criticism, excessive skepticism and criticism of others, deep feelings of inadequacy, and excessive brooding and worrying. In addition, people who regularly behave in dependent, hostile, and impulsive ways appear at greater risk for depression. American psychologist Martin Seligman proposed that depression stem from ‘learned helplessness,’ an acquired belief that one cannot control the outcome of events. In this view, prolonged exposure to uncontrollable and inescapable events leads to apathy, pessimism, and loss of motivation. An adaptation of this theory by American psychologist Lynn Abramson and her colleagues argue that depression result not only from helplessness, but also from hopelessness. The hopelessness theory attributes depression to a pattern of negative thinking. Which people blame themselves for their negative lives? Events, without variation or fluctuation occur in circumstances in that of an action has to the occasion to achieve is a matter worthy of acknowledging that in the presence of freedom. Such an effect or outcome rides totally of infinite time, as a view that causes those of the events for being unchangeable, and the overgeneralized weaknesses as applying to many areas of life. Psychologists agree that stressful experiences can trigger depression in people who are predisposed to the illness. For example, the death of a loved one may trigger depression. Psychologists usually distinguish true depression from grief, a normal process of mourning a loved one who has died. Other stressful experiences may include divorce, pregnancy, the loss of a job, and even childbirth. About 20 percent of women experience an episode of depression, known as postpartum depression, after having a baby. In addition, people with serious physical illnesses or disabilities often develop depression. Through participation or observer, people experienced child abuse and appear more vulnerable to depression than others. So, too, do people living under chronically stressful conditions, such as single mothers with many children with little or no support from friends or relatives. Depression typically cannot be shaken or willed away. An episode must therefore run its course until it weakens either on its own or with treatment. Depression can be treated effectively with antidepressant drugs, psychotherapy, or a combination of both. Despite the availability of effective treatment, most depressive disorders go untreated and undiagnosed. Studies indicate that general physicians fail to recognize depression in their patients at least half the time. In addition, many doctors and patients view depression in elderly people as a normal part of aging, though treatment for depression in older people is usually very effective. Up to 70 percent of people with depression respond to antidepressant drugs. These medications appear to work by altering the levels of serotonin, norepinephrine, and other neurotransmitters in the brain. They generally take at least two to three weeks to become effective. Doctors cannot predict which type of antidepressant drug will work best for any particular person, so depressed people may need to try several types. Antidepressant drugs are not addictive, but they may produce unwanted side effects. To avoid a relapse, people must usually continue taking the medication for several months after their symptoms improve. Commonly used antidepressant drugs fall into three major classes: Tricyclics, Monoamine oxidase inhibitors (MAO inhibitors), and Selective serotonin reuptake inhibitors (SSRIs). Tricyclics, named for their three-ring chemical structure, include amitriptyline (Elavil), imipramine (Tofanil), desipramine (Norpramin), doxepin (Sinequan), and nortriptyline (Pamelor). Side effects of tricyclics may include drowsiness, dizziness upon standing, blurred vision, nausea, insomnia, constipation, and a dry mouth. MAO inhibitors include isocarboxazid (Marplan), phenelzine (Nardil), and tranylcypromine (Parnate). People who take MAO inhibitors must follow a diet that excludes tyramine—a substance found in wine, beer, some cheeses, and many fermented foods—to avoid a dangerous rise in blood pressure. In addition, MAO inhibitors have many of the same side effects as tricyclics. Selective serotonin reuptake inhibitors include Fluoxetine (Prozac), sertraline (Zoloft), and paroxetine (Paxil). These drugs generally produce fewer and milder side effects than do other types of antidepressants, although SSRIs may cause anxiety, insomnia, drowsiness, headaches, and sexual dysfunction. Some patients have alleged that Prozac causes violent or suicidal behaviour in a small number of cases, but the US Food and Drug Administration has failed to substantiate this claim. Prozac became the most widely used antidepressant in the world soon after its introduction in the late 1980s by drug manufacturer Eli Lilly and Company. Many people find Prozac extremely effective in lifting depression. In addition, some people have reported that Prozac actually transforms their personality by increasing their self-confidence, optimism, and energy level. However, mental health professionals have expressed serious ethical concerns over Prozac’s use as a ‘personality enhancer,’ especially among people without clinical depression. Doctors often prescribed lithium carbonates, a natural mineral salt, to treat people with bipolar disorder. People often take lithium during periods of relatively normal moods to delay or even prevent subsequent mood swings. Side effects of lithium include nausea, stomach upset, vertigo, and frequent urination. Studies have shown that short-term psychotherapy can relieve mild to moderate depression as effectively as antidepressant drugs. Unlike medication, psychotherapy produces no physiological side effects. In addition, depressed people treated with psychotherapy appear less likely to experience a relapse than those treated only with antidepressant medication. However, psychotherapy usually takes longer to produce benefits. There are many kinds of psychotherapy. Cognitive-behavioural therapy assumes that depression stem from negative, often irrational thoughts about oneself and of one’s future. In this type of therapy, a person learns to understand and eventually eliminate those habits of negative thinking. In interpersonal therapy, the therapist helps a person resolve problems in relationships with others that may have caused the depression. The subsequent improvement in social relationships and support helps alleviate the depression. Psychodynamic therapy views depression as the result of internal, unconscious conflicts. Psychodynamic therapists focus on a person’s experiences and the resolution of childhood conflicts. The psychoanalysis is an example of this type of therapy. Critics of long-term Psychodynamic therapy argue that its effectiveness is scientifically unproven. Electroconvulsive therapy (ECT) can often relieve severe depression in people who fail to respond to antidepressant medication and psychotherapy. In this type of therapy, a low-voltage electrical current is passed through the brain for one to two seconds to produce a controlled seizure. Patients usually receive six to ten ECT treatments over several weeks. ECT remains controversial because it can cause disorientation and memory loss. Nevertheless, research has found it highly effective in alleviating severe depression. For milder cases of depression, regular aerobic exercise may improve moods as effectively as psychotherapy or medication. In addition, some research indicates that dietary modifications can influence one’s mood by changing the level of serotonin in the brain. An overview of the phenomena of depression and to take notice on some of the diagnostic distinctions that are currently being made, where it should become apparent that there is a tremendous heterogeneity to what falls under the broad rubic of depression and that there is an arbitrariness to any boundaries that are drawn on this phenomenon. There are striking differences among depressed persons that invite some form of subtyping.

However, efforts to derive such subtyping are generally controversial, and any scheme is likely to be more satisfactory for some purposes that for others. Confronted with all of this ambiguity and confusion, one must be cautious and not seek more precision than the phenomena of depression afford, and one should probably be sceptical about any decisive statement about the hidden and underlying nature of depression. Contemplating the phenomena of depression, one can readily detect patterns and come to a conclusion that some aspects of depression are more central than others; some are primary and causal, and others are secondary. One observer may be struck with the frequency of complaints about appetite and sleep disturbances by depressed persons and infer that some sort of biological disturbance must be the key to understanding depression. Another might find their self-derogation and pessimism irrational in away that suggests that there must be some kind of fundamental deficit in self-esteem or cognitive distortion occurring. Still another may listen to the incessant complaining of a depressed person, get annoyed and frustrated, and yet feel guilty in a way that makes it easier to encourage the depressed person to continue to talk in this way than to verbalize these negative feelings. Cognizance of this, the observer might conclude that there is some sort of interpersonal process going on that is critical to any understanding of depression. A major source of confusion is due to the fact that the term ‘depression’ variously refers to a mood state, a set of symptoms, and a clinical syndrome. As to a reference regarding moods, depression identifies as a universal human experience. Adjectives from a standard measure of a mood (The Multiple Effect Adjective Checklist; Zuckerman and Lubin, 1965) point to subjective feelings associated with a depressed mood, for being sad, unhappy, blue, low, discouraged, bored, hopeless, dejected and lonely. Similarities between every day-depressed mood and the complaints of depressed patients have encouraged the view that clinical depression is simply an exaggeration of a normal depressed mood. However, patients sometimes indicate that their experience of depression is quite distinct from normal feelings and sadness, even in its extreme form. A patient once remarked that her sadness was overwhelming when her husband died but that it did not compare with her sense of overflowing emptiness and her loss of any ability to experience pleasure at the time that she entered the hospital. The view that depressed mood in otherwise normal persons is quantitatively but not qualitatively different from the depression found in hospitalized patients has been termed the ‘continuity hypothesis’. Aaron Beck (1967) has provided a useful analogy to suggest the alternative to the continuity hypothesis. He notes that everyday fluctuations in body temperature can be measured on the same thermometer as the changes associated with a fever. Yet the conditions giving rise to a fever are distinct from those causing fluctuations in temperature in healthy individuals. Similarly, the conditions giving rise to clinical depression may be distinct from those studies producing fluctuations in a normal mood.

Studies have compared the subjective mood of persons who are distressed but not seeking help to those who are seeking treatment for depression or a review (Depur and Monroe, 1978). The two groups may be similar in subjective moods, but they differ in other ways. Those persons who are not seeking treatment for depression tend to lack the anxiety and the physical complaints, including loss of appetite, sleep disturbance, and fatigue shown by the group seeking treatment. Still, it could be argued that there is a continuum between the two groups, with these additional features arising when a normal depressed mood becomes more prolonged or intensified. The controversy is likely to continue until either questions about the etiology of depression are resolved or unambiguous markers for depression and identified. Advocates of biomedical approaches to depression tend to assume that there is a discontinuity between a normal depressed mood and clinical depression, and that appropriate biological markers will be found. Yet, as the article by Winokur suggests, even if that proves to be the case, there are likely to be many individuals suffering from extremes of a depressed mood who do not have these markers. Advocates of psychoanalytic, cognitive and behavioural, and interpersonal and social perspectives or depressions have generally assumed a continuum between a normal depressed mood and clinical depression. They tend to exclude psychotic and bipolar depressed persons from treatment, but, beyond that, they have tended to disregard classification issues (Gilbert, 1984). For unipolar depression, at least, they have assumed that whatever discontinuities the biology of mild and severe moods there might be are not necessarily relevant to the psychological and social processes in which they are most interested. Writers since antiquity have noted the core symptoms of depression, besides a sad or low mood, reduced ability to experience pleasure, pessimism, inhibition and retardation of action, and a variety of physical complaints. For the purposes of dialogue, we can distinguish among the emotional, cognitive, motivational, and vegetative symptoms of depression, although these features are not always so neatly divisible. Beyond these symptoms, there are some characteristic interpersonal aspects of depression that are not usually considered as formal symptoms. But they are frequently, distinctive, and troublesome enough to warrant attention. Sadness and dejection are not the only emotional manifestations of depression, although about half of all depressed patient reports these feelings as their principal complaint. Most depressed persons are also anxious and irritable. Classical descriptions of depression tend to emphasize that depressed persons’ feelings and distress, disappointment, and frustration are focussed primarily on themselves, yet a number of studies suggest that their negative feelings, including over hostility, are also directed at the people around them. Depressed persons are often intensely angry persons (Kahn, Coyne, Margolin, Weissman and Paykel, 1971). Perhaps 10 or 15 percent of severely depressed patients refuse to take or sustain in the signifying approval to or with subscriptions that are true of the feelings of sadness, reporting instead that all emotional experience, including sadness, has been blunted or inhibited (Whybrow, Akiskal, and Kinney, 1984). The identification of these persons as depressed depends upon the presence of other symptoms. The inhibition of emotional expression in severely depressed persons may extend to crying. Whereas, mild and moderately depressed persons may readily and frequently cry, as they become more depressed, they may continue to feel like crying, but complain that no tears come. Mildly and moderately depressed persons may feel every activity is a burden, yet they derive some satisfaction from their accomplishments. Despite their low mood, they may still crack a smile at a joke. Yet, as depression intensifies, a person may report both a loss of and ability to get gratification from activities that had previously been satisfying—family, work, and social life—and a loss of any sense of humour. Life becomes stale flat and not at all amusing. The loss of gratification may extend to the depressed persons’ involvement in close relationships, but, often, a loss of affection for the spouse and children, a feeling of not being able to care anymore; a sense of a wall being erected between the depressed person and others are the major reason for seeking treatment.

In the past decade, a number of theorists, notably Beck and Abramson, Seligman and Teasdale have given particular attention to the cognitive manifestations of depression and have assumed that these features are causal of the other aspects of the disorder. Depressed persons characteristically view themselves, their situations, and their future possibilities in negative and pessimistic terms. They voice discouragement, hopelessness and helplessness. They see themselves as inadequate and deficient in some crucial way. There may be thoughts of death, wishing to be dead, and suicide attempts. The depressed people involved in their daily lives are interpreted by them in terms of loss, defeat, and deprivation, and they experience failure when they undertake an activity. They may criticize themselves for minor shortcomings and seemingly search for evidence that confirms their negative view of them. Aaron Beck suggests, that they will make of the facts to accommodate of these interpretations and hold to them in the face of contradictory evidence. Depressed persons overgeneralise from negative experiences, selectively abstract negative details out of context, ignore more positive features of their situation, and negatively characterise themselves as absolutists and dichotomous terms. The revised learned-helplessness model emphasizes that depressed persons are particularly prone to blame themselves for their difficulties, and to see their defects as stable and global attributes.

Aside from these contentual aspects in their thinking, depressed persons frequently complain that their thinking processes have slowed down, that they are distracted, and they cannot concentrate. Decisions pose a particular problem. Depressed persons are uncertain, feel in need of more information, and are afraid of making the wrong decisions. They may simply feel paralysed, and that the work of making a choice and a commitment is an overwhelming task to be avoided at any cost.

Depressed persons’ involvements in their daily lives are interpreted by them in terms of loss, defeat, a deprivation, and they expect failure when they undertake an activity, they may criticize themselves for minor shortcomings and seemingly search for evidence that confirms their negative views of themselves. Beck and Kovacs suggest that they tailor the facts to fit these interpretations and hold on the in the face of contradictory evidence. Depressed persons over generalize from negative experience, selectively abstract negative details out of context, ignore more positive features of their situations, and negatively characterize themselves in absolutist and dichotomous terms. The revised learned-helplessness model emphasizes that their depressed persons are particularly prone to blame themselves for their difficulties and to see their defects as stable and global attributes. Aside from these content aspects of their thinking, depressed persons frequently complain that their thinking processes have slowed down, that they are distracted, and they cannot concentrate. Decisions pose a particular problem. Depressed persons are uncertain, feel in need of more information, and are afraid of making the wrong decision. They may simply feel paralysed, and that the work of making a choice and a commitment is an overwhelming task to be avoided at any cost. Bipolar disorder, is a categorical mental illness in which a person’s mood alternates between the extreme fixation of mania and the objective sadness or unhappiness is caught in the grasp of its depression. Bipolar disorder is also called manic-depressive illness. When manic, people with bipolar disorder feel intensely elated, self-important, energetic, and irritable. When depressed, they experience painful sadness, negative thinking, and indifference to things that used to bring them happiness. American psychiatrist Kay Redfield Jamison is regarded as one of the world’s leading authorities on bipolar disorder, also known as manic-depressive illness. In her book ‘An Unquiet Mind, A Memoir of Moods and Madness’ (1995), Jamison reveals her own struggle against the illness, which caused her to experience violent mood swings. She describes her initial resistance to taking medication that, while necessary to prevent debilitating depression, extinguished the exhilarating highs of mania. Bipolar disorder is less common than depression. In North America and Europe, about 1 percent of people experience bipolar disorder during their lives. Rates of bipolar disorder are similar throughout the world. In comparison, at least 8 percent of people experience serious depression during their lives. Bipolar disorder affects men and women about equally and is somewhat more common in higher socioeconomic classes. At least 15 percent of people with bipolar disorder commit suicide. This rate roughly equals the rate for people with major depression, the most severe form of depression. Bipolar disorder is a mental illness that causes mood swings. In the manic phase, a person might feel ecstatic, self-important, and energetic. But when the person becomes depressed, the mood shifts to extreme sadness, negative thinking, and apathy. Some studies indicate that the disease occurs at unusually high rates in creative people, such as artists, writers, and musicians. But some researchers contend that the methodology of these studies was flawed and their results were misleading. In the October 1996 Discover Magazine article, anthropologist Jo Ann C. Gutin presents the results of several studies that explore the link between creativity and mental illness.

Bipolar disorder usually begins in a person’s late teens or 20s. Men usually experience mania as the first mood episode, whereas women typically experience depression first. Episodes of mania and depression usually last from several weeks to several months, on average, people with untreated bipolar disorder experience four episodes of mania or depression over any ten-year period. Many people with bipolar disorder function normally between episodes. In ‘rapid-cycling’ bipolar disorder, however, which represents five to 15 percent of all cases, a person experiences four or more mood episodes within a year and may have little or no normal functioning in between episodes. In rare cases, swings between mania and depression occur over a period of days.

People of the depressive bipolar disorder feel intensely sad or profoundly indifferent to work, activities, and people that once brought them pleasure. They think slowly, concentrate poorly, feel tired, and experience changes—usually an increase—in their appetite and sleep. They often feel a sense of worthlessness or helplessness. In addition, they may feel pessimistic or hopeless about the future and may think about or attempt suicide. In some cases of severe depression, people may experience psychotic symptoms, such as delusions (false beliefs) or hallucinations (false sensory perceptions). In the manic phase of bipolar disorder, people feel intensely and inappropriately happy, self-important, and irritable. In this highly energized state they sleep less, have racing thoughts, and talk in rapid-fire speech that goes off in many directions. They have inflated self-esteem and confidence and may even have delusions of grandeur. Mania may make people impatient and abrasive, and when frustrated, physically abusive. They often behave in socially inappropriate ways, think irrationally, and show impaired judgment. For example, they may take aeroplane trips all over the country, make indecent sexual advances, and formulate grandiose plans involving indiscriminate investments of money. The self-destructive behaviour of mania includes excessive gambling, buying outrageously expensive gifts, abusing alcohol or other drugs, and provoking confrontations with obnoxious or combative behaviour. Clinical depression is one of the most common forms of mental illness. Although depression can be treated with psychotherapy, many scientists believe there are biological causes for the disease. In the June 1998 Scientific American article, Neurobiologist Charles B. Nemeroff discusses the connection between biochemical changes in the brain and depression. The genes that a person inherits seem to have a strong influence on whether the person will develop bipolar disorder. Studies of twins provide evidence for this genetic influence. Among genetically identical twins where one twin has bipolar disorder, the other twin has the disorder in more than 70 percent of cases. But among pairs of fraternal twins, who have about half their genes in common, both twins have bipolar disorder in less than 15 percent of cases in which one twin has the disorder. The degree of genetic similarity seems to account for the difference between identical and fraternal twins. Further evidence for a genetic influence comes from studies of adopted children with bipolar disorder. These studies show that biological relatives of the children have a higher incidence of bipolar disorder than do people in the general population. Thus, bipolar disorder seems to run in families for genetic reasons. Privately or work-related stress can trigger a manic episode, but this usually occurs in people with genetic vulnerability. Other factors—such as prenatal development, childhood experiences, and social conditions—seem to have relatively little influence in causing bipolar disorder. One study examined the children of identical twins in which only one member of each pair of twins had bipolar disorder. The study found that regardless of whether the parent had bipolar disorder or not, all of the children had the same high 10-percent rate of bipolar disorder. This observation clearly suggests that risk for bipolar illness comes from genetic influence, not from exposure to a parent’s bipolar illness or from family problems caused by that illness. Different therapies may shorten, delay, or even prevent the extreme moods caused by bipolar disorder. Lithium carbonates, a natural mineral salt, can help control both mania and depression in bipolar disorder. The drug generally takes two to three weeks to become effective. People with bipolar disorder may take lithium during periods of relatively normal moods to delay or prevent subsequent episodes of mania or depression. Common side-effects of lithium include nausea, increased thirst and urination, vertigo, loss of appetite, and muscle weakness. In addition, long-term use can impair functioning of the kidneys. For this reason, doctors do not prescribe lithium to bipolar patients with kidney disease. Many people find the side effects so unpleasant that they stop taking the medication, which often results in a relapse. From 20 to 40 percent of people do not respond to lithium therapy. For these people, two anticonvulsant drugs may help dampen severe manic episodes: carbamazepine (Tegretol) and valproate (Depakene). The use of traditional antidepressants to treat bipolar disorder carries risks of triggering a manic episode or a rapid-cycling pattern. Antidepressant, medication used to treat depression, a mood disorder characterized by such symptoms as sadness, decreased appetite, a difficulty in sleeping, fatigue, and a lack of enjoyment of activities previously found pleasurable. While everyone experiences episodes of sadness at some point in their lives, depression is distinguished from this sadness when symptoms are present most days for a period of at least two weeks. Antidepressants are often the first choice of treatment for depression. The severe disorders of mood or effect are among the most commons of the major psychiatric syndromes. Lifetime expectancy rates for such disorders are between 3 and 8 percent of the general population. Only a minority is treated by psychiatrists or in psychiatric hospitals and about 70 percent of prescriptions for antidepressants are written by nonpsychiatric physicians. These and other modern medical treatments of severe mood disorders have contributed to a virtual revolution in the theory and practice of modern psychiatry since the introduction of mood-altering drugs three decades ago. These agents include lithium salts (1949), the antimanic and Antipsychotic (neuroleptics) agents as the chlorpromazine (1952), the Monoamine oxidase (MAO) inhibitors (1952), and the Tricyclic or heterocyclic (imipramine-like) antidepressant agents (1957). In addition, electroconvulsive therapy (ECT) continue s to have a place in the treatment of very severe and acute mood disorders, especially life-threatening forms of depression.

The development of these modern medical therapies has had several important effects. First, these agents have provided relatively simple, specific, effective, and safe forms of treatment with a profound impact on current patterns of medical practice, for example, many depressed or hypomanic patients can be managed adequately in outpatient facilities to avoid prolonged, expensive, and disruptive hospitalization which were formally common. Second, partial understanding of the pharmacology of the new psychotropic drugs has led to imaginative hypotheses concerning the pathophysiology or etiology of severe mood disorders. These, in turn, have encouraged a revolution in experimental psychiatry in which the hypotheses have been tested in clinical research. Many of the earlier hypotheses have been found wanting or simplistic, nevertheless, they have led to increase d understanding of the diagnosis, biology, and treatment of mood disorders and to newer research that represents a third level of development, at this level. This is the focus and the promises to have practical clinical benefit now and in the near future.

Although the cause of depression is unknown, researchers have found that some depressed people have altered levels of chemicals called neurotransmitters, chemicals made and released by nerve cells, or neurons. One neuron, referred to as the presynaptic neuron, releases a neurotransmitter into the synapse, or space, between the neuron and a neighbouring cell. The neurotransmitter then attaches, or binds, to a neighbouring cell—the postsynaptic cell—to trigger a specific activity.

Antidepressants work by interacting with neurotransmitters at three different points: they can change the rate at which the neurotransmitters are either created or broken down by the body; they can block the process in which a spent neurotransmitter is recycled by a presynaptic neuron and used again, called reuptake; or they can interfere with the binding of a neurotransmitter to neighbouring cells. The first antidepressants, developed in the 1950s, are the Tricyclic antidepressants (TCA) and the Monoamine oxidase (MAO) inhibitors. TCAs block the reuptake of neurotransmitters into the presynaptic neurons, keeping the neurotransmitter in the synapse longer, and making more of the neurotransmitters available to the postsynaptic cell. TCAs include amitriptyline, doxepin, imipramine, nortriptyline, and desipramine. MAO inhibitors decrease the rate at which neurotransmitters are broken down by the body so they are more available to interact with neurons. MAO inhibitors currently available in the United States include phenelzine and tranylcypromine. Another group of antidepressants, known as selective serotonin reuptake inhibitors (SSRI), became available in 1987. SSRIs block the reuptake of the neurotransmitter serotonin into presynaptic neurons, thereby prolonging its activity. There are currently four SSRIs available in the United States: Fluoxetine, sertraline, paroxetine, and fluvoxamine. Of this group, the best known is Fluoxetine, commonly known by its brand name, Prozac. Another antidepressant is venlafaxine, which works like TCAs but does not share their chemical structure, and it also causes different side effects. The antidepressant nefazodone prevents serotonin from binding to neighbouring neurons at one specific binding site (serotonin can bind to neurons on many sites). It also weariedly blocks the reuptake of serotonin. All antidepressants decrease symptoms of depression in about 70 percent of depressed people who take them. Most antidepressants take about two to three weeks of treatment before beneficial effects occur. Because no antidepressant is more effective than the others, doctors determine which antidepressant to prescribe according to the type of side effects an individual can tolerate. For instance, a person who takes TCAs and MAO inhibitors may notice dizziness and fainting when standing up, mouth dryness, difficulty urinating, constipation, and drowsiness. If people who take MAO inhibitors eat certain foods, such as aged cheese or some aged meats, they can experience severe headaches and raised blood pressure. SSRIs can cause side effects such as restlessness, difficulty sleeping, and interference with sexual function. Clinical depression is quite different from the blues everyone feels at one time or another and even from the grief of bereavement. It is more debilitating and dangerous, and the overwhelming sadness combines with a number of other symptoms. In addition to becoming preoccupied with suicide, many people are plagued by guilt and a sense of worthlessness. They often have difficulty thinking clearly, remembering, or taking pleasure in anything. They may feel anxious and sapped of energy and have trouble eating and sleeping or may, instead, want to eat and sleep excessively. Psychologists and Neurobiologists sometimes debate whether ego-damaging experiences and self-deprecating thoughts or biological processes cause depression. The mind, however, does not exist without the brain. Considerable evidence indicates that regardless of the initial triggers, the final common pathways to depression involve biochemical changes in the brain. These changes ultimately give rise to deep sadness and the other salient characteristics of depression. The full extent of those alterations is still being explored, but in the past few decades—and especially in the past several years—efforts to identify them have progressed rapidly. At the moment, those of us teasing out the neurobiology of depression somewhat resemble blind searchers feeling different parts of a large, mysterious creature and trying to figure out how their deductions fit together. In fact, it may turn out that not all of our findings will intersect: biochemical abnormalities that are prominent in some depressives may differ from those that are more predominant than in others. Still, the extraordinary accumulation of discoveries is fuelling optimism that the major biological determinants of depression can be understood in detail and that those insights will open the way to improved methods of diagnosing, treating and preventing the condition. One subgoal is to distinguish features that vary among depressed individuals. For instance, perhaps decreased activity of a specific neurotransmitter (a molecule that carries a signal between nerve cells) is central in some people, but in others, overactivity of a hormonal system is more influential (hormones circulate in the blood and can act far from the site of their secretion). A related goal is to identify simple biological markers able to indicate which profile fits a given patient; those markers could consist of, say, elevated or reduced levels of selected molecules in the blood or changes in some easy visualizational areas of the brain. After testing a depressed patient for these markers, a psychiatrist could, in theory, prescribe a medication tailored to that individual’s specific biological anomaly, much as a general practitioner can run a quick strep test for a patient complaining of a sore throat and then prescribe an appropriate antibiotic if the test is positive. Today psychiatrists have to choose antidepressant medications by intuition and trial and error, a situation that can put suicidal patients in jeopardy for weeks or months until the right compound is selected. (Often psychotherapy is needed as well, but it usually is not sufficient by itself, especially if the depression is fairly severe.) Improving treatment is critically important. Although today’s antidepressants have fewer side effects than those of old and can be extremely helpful in many cases, depression continues to exact a huge toll in suffering, lost lives and reduced productivity. The prevalence is surprisingly great. It is estimated, for example, that 5 to 12 percent of men and 10 to 20 percent of women in the US will suffer from a major depressive episode at some time in their life. Roughly half of these individuals will become depressed more than once, and up to 10 percent (about 1.0 to 1.5 percent of Americans) will experience manic phases in addition to depressive ones, a condition known as manic-depressive illness or bipolar disorder. Mania is marked by a decreased need for sleep, rapid speech, delusions of grandeur, hyperactivity and a propensity to engage in such potentially self-destructive activities as promiscuous sex, spending sprees or reckless driving. Beyond the pain and disability depression brings, it is a potential killer. As many as 15 percent of those who suffer from depression or bipolar disorder commits suicide each year. In 1996 the Centre for Disease Control and Prevention listed suicide as the ninth leading cause of death in the US (slightly behind infection with the AIDS virus), taking the lives of 30,862 people. Most investigators, however, believe this number is a gross underestimate. Many people who kill themselves do so in a way that allows another diagnosis to be listed on the death certificate, so that families can receive insurance benefits or avoid embarrassment. Further, some fractions of automobile accidents unquestionably are concealed suicides. The financial drain is enormous as well. In 1992 the estimated costs of depression totalled $43 billion, mostly from reduced or lost worker productivity. Accumulating findings indicate that severe depression also heightens the risk of dying after a heart attack or stroke. And it often reduces the quality of life for cancer patients and might reduce survival time. Geneticists have provided some of the oldest proof of a biological component to depression in many people. Depression and manic-depression frequently run in families. Thus, close blood relatives (children, siblings and parents) of patients with severe depressive or bipolar disorders are much more likely to suffer from those or related conditions than are members of the general population. Studies of identical twins (who are genetically indistinguishable) and fraternal twins (whose genes generally are no more alike than those of other pairs of siblings) also support an inherited component. The finding of illness in both members of a pair is much higher for manic-depression in identical twins than in fraternal ones and is somewhat elevated for depression alone. In the past 20 years, genetic researchers have expended great effort trying to identify the genes at fault. So far, though, those genes have evaded discovery, perhaps because a predisposition to depression involves several genes, each of which makes only a small, hard-to-detect contribution.

In support of this cognitive view, people with ‘depressive’ personality traits appear to be more vulnerable than others to actual depression. Examples of depressive personality traits include gloominess, pessimism, introversion, self-criticism, excessive skepticism and criticism of others, deep feelings of inadequacy, and excessive brooding and worrying. In addition, people who regularly behave in dependent, hostile, and impulsive ways appear at greater risk for depression.

American psychologist Martin Seligman proposed that depression stem from ‘learned helplessness,’ an acquired belief that one cannot control the outcome of events. In this view, prolonged exposure to uncontrollable and inescapable events leads to apathy, pessimism, and loss