“The common cold of psychological problems”

(Seligman, 1973)

Depression is a mood, or ‘affective’ disorder in which a sustained emotional state colours a person’s perceptions, thoughts and behaviour. However, with reference to the quote, depression is far more serious than a mere cold.


It is difficult to diagnose depression – it often accompanies other types of disorders that must be ruled out. Diagnosis requires five or more of the following symptoms for at least two weeks:


1. Extreme sadness, tearfulness, depressed mood.

2. Loss of interest in activities normally enjoyed, social withdrawal.

3. Disturbed sleep – loss of sleep (insomnia), or more sleep than normal.

4. Changed activity level: often agitated (or slowed down and lethargic).

5. Disturbed appetite and weight change – may be increased or decreased.

6. Loss of energy and tiredness.

7. Self-reproach, guilt, low self-esteem, anxiety.

8. Difficulty making decisions, diminished concentration-span.

9. Thoughts of death and suicide, suicide attempts.

There is a key distinction between major depression (sometimes called unipolar depression, and bipolar disorder (also known as manic-depressive disorder).

According to DSM-IV, the diagnosis of a major depressive episode requires that the following symptoms occur nearly everyday for a minimum of 2 weeks.

Emotional symptoms: sad, depressed mood; loss of pleasure in usual activities.

Motivational symptoms: changes in activity level; passivity; loss of interest and energy.

Somatic symptoms: difficulties in sleeping (insomnia) or increased sleeping (hypersomnia); weight loss or gain; tiredness.

Cognitive symptoms: negative self-concept, hopelessness, pessimism, lack of self-esteem, self-blame, and self-reproach; problems with concentration or the ability to think clearly; recurring thoughts of suicide or death.

Patients with bipolar depression experience both depression and mania (a mood state involving elation, talkativeness, and unjustified high self-esteem). About 10% of men and 20% of women become clinically depressed at some time in their lives. Over 90% of them suffer from unipolar rather than bipolar depression.

In addition to the distinction between unipolar and bipolar depression, there is also a distinction in unipolar depression between reactive and endogenous depression.

  • Reactive depression is caused by some stressful event(s), such as the death of a close friend. The event triggers an episode of depression.
  • Endogenous depression is caused from within the person, for instance it may be due to hormonal imbalances.

Neither of these categories are represented in the classification schemes DSM and ICD but the distinction is an important one for understanding the causes of depression. Endogenous depression is linked to biological factors, whereas with reactive depression an individual may have a genetic predisposition to depression but it is social psychological factors that are a primary cause.

Summary of Explanations for Depression

School of thought:

Explanation for depression:


Unconscious conflicts to do with loss and grief – leading to regression and anger turned inward on self.

Cognitive Negative thinking or distorted attribution of failure – blaming self if things go wrong.


Learned helplessness – person unable to control unpleasant experiences in the past, so new trauma is met with passivity and depression.

Medical / biological

Genetic factors, faulty functioning of neurotransmitters in the brain and hormonal changes.

Social Stressful life events and difficult or sparse interpersonal relationships lending little support in crises.

Read the following article from The Guardian.

The low country

We are wealthier and physically healthier than ever, and yet one in four of us has suffered depression. As a new report reveals a dramatic increase in students experiencing mental health problems, Sarah Boseley asks if we really are more miserable.


Sarah Boseley

Tuesday January 9, 2001

Stone Age man must have been pretty depressed. It can’t have been a lot of fun squatting in a cave with no central heating and a food source that was almost as likely to have you for dinner. It wouldn’t have been perpetually joyous in the middle Ages, either; if you weren’t murdered for your purse in a stinking alley or sent off to fight in some hellish war, you fell prey to some pretty vicious diseases. Nor were the Victorians exactly a light-hearted bunch.

Why is it then that we – blessed with health, wealth and leisure undreamed of by our benighted forebears, likely to live a lot longer than the biblical threescore years and 10 and with every type of cultural diversion available to us, even if only as a spectator in our own home through the television – seem just as miserable as any of them? Why, in fact, are we so depressed?

Millions of us are falling prey to what is now identified as a disease. Five million of us each year have some sort of depressive illness that would justify medical intervention. That’s not much less than a tenth of the population. A third of those who go to the GP have underlying depression. The young, with the world ahead of them, should have the blithest hearts. Yet 12% of male students and 15% of female students at university are depressed. Yesterday, meanwhile, it emerged that university counsellors are reporting a dramatic increase in the number of students seeking help for severe mental problems. Just over a year ago, the World Health Organisation declared that depression had reached epidemic proportions. Within 20 years, the WHO said, it would be the world’s second most debilitating illness after cardiovascular disease in terms of lost years of human productivity. Depression is paralysing human-kind, destroying our capacity to work and create, in a way that infection used to.

Or is it? Are we really more depressed than ever before, as the patient group Depression Alliance believes, or is this the same sadness that Hippocrates classified as melancholy – something that has always been with us. Some might say that what has really changed is that we can now diagnose depression, and that there is an incentive to diagnose depression because for the past few decades, the psychiatrists have been able to do something about it. Does the real rise in depression date from the advent of the antidepressants?

Patricia White of the Depression Alliance agrees that depression has always been with us even if it was not identified. In the past, she thinks, “We had too much else to do so that was not a question that was asked. We asked, ‘Do you have enough money?’ or ‘Has your husband got a job?’ “ But for her, what has happened is more than a redefinition. She believes that “we are now more predisposed to being depressed” because of the phenomenal pace of social change, a view with which the WHO concurs. “We have never come this far in such a short period of time,” she says. “I think we’re under more pressure now than we ever have been before. Technology is supposed to have made our lives so much better, but has it? There has been such rapid progress over the past 30 years – in fact probably postwar. There has been a breakdown of what we used to call the family. Students are under more pressure.” Although human beings have proved themselves incredibly adaptable over the ages, she wonders how good their coping mechanisms are in the face of such enormous and rapid change.

The alliance is firmly wedded to treatment for everyone with depression, and has been campaigning, along with the Royal College of Psychiatrists and others, for greater recognition of the illness by GPs and the public, and the removal of the stigma attached to so many who are diagnosed with mental health problems.

Not all depression is severe. Some is mild enough probably to go away by itself. But the alliance believes that everybody must be urged to get treatment, because it is the only way to catch those whose depression will become severe enough to make them try to kill themselves. “There were almost 7,000 suicides in the UK last year. Almost 75% are attributed to depression,” says White. “That is because in that 75% we know there had been a history and a diagnosis of depression. But in all truth it is highly unlikely that anyone will kill themselves if they are not depressed.”

Jo Borrill of the Mental Health Foundation says that some people can get better without treatment, which includes counselling and cognitive behaviour therapies as well as medication, but the problem is that some people have no idea what to do about their depression, if they recognise it as depression. They do not know that the GP has help and advice to give.

In the past, she says, some people must have come out of their depression without drugs or therapy. “I think some people did, but some people suffered. The most important thing is that we’re always trying to do better. We have got higher expectations and we don’t want to be satisfied with people being miserable.”

Depression is diagnosed when people have a number of classic symptoms over a number of weeks. They include feeling tired, sleeping too much or too little, increased anxiety, difficulty concentrating, a feeling that life is pointless and a loss of sex drive. A few of these over some time or all of them for a few days does not qualify as depression.

The cause, say doctors, is a chemical imbalance – a fall in the serotonin levels that are responsible for our happier feelings. But that is not an unnatural event. They must fluctuate for us to feel any emotion. What the scientists who devised medication to alter serotonin levels – the basis of the SSRIs (selective serotonin reuptake inhibitors) like Prozac – do not know is whether low serotonin levels cause depression or whether depression causes serotonin levels to fall.

Psychiatrist Jim Bolton, who lectures at St George’s hospital medical school in London, suggests that people may need both medication and therapy. “Imagine you are being thrown overboard into the sea. You need two things – a lifebelt, which is the medication, to stop you drowning, and once you have reached shallower water, swimming lessons (therapy) to prevent it happening again,” he says.

Cognitive behaviour therapy is probably the treatment most likely to help people climb permanently out of the cycle of depression. It helps people set targets for changing their life and dispelling negative thinking and beliefs.

But it is in short supply. Drugs are cheaper, quicker and easier for the NHS to hand out. They help a lot of people. They undoubtedly save lives. But their very ease and availability may be increasing the pool of people now categorised as depressed – the very many whose depression is at the mild end of the scale. We have drugs to treat depression, and so the medical profession is keen to invite more people to come forward and be treated. The pharmaceutical companies who make those drugs urge them on in the war against depression.

Edward Shorter, psychiatrist and medical historian at the University of Toronto, believes that there is a difference between unhappiness, which is part of the human condition, and depression. Giving a paper in London in October 1999, he said: “Unhappiness, as we know, responds readily if not durably to ethanol [alcohol]. It certainly responds to such street drugs as cocaine. And it responds, as a generation of users can now testify, to SSRIs.”

When discussing the worldwide burden of depression, he said, “we therefore do well to keep in mind that there is indeed an enormous worldwide burden of unhappiness, that some of this unhappiness is the result of psychiatric illness, and, finally, that some of this illness is clinical depression.”

In an earlier paper, in 1997, he wrote that he believed the definition of depression had been changed to encompass more people than ever before. “The boundaries of what constitutes depression have been expanded relentlessly outward. Depression as a major psychiatric illness involving bleakness of mood, self-loathing, and inability to experience pleasure and suicidal thoughts has been familiar for many centuries. The illness has a heavy biological component.

“Depression in the vocabulary of post 1960s American psychiatry has become tantamount to dysphoria, meaning unhappiness, in combination with loss of appetite and difficulty sleeping.” Taken to the extreme, depression in its mildest form becomes a quality of life issue. We have better health and longer life than ever before. Why should we not have relief from unhappiness, just as readily as from pain?

  • For information on depression, call the Depression Alliance on: 020-7633 0557. Visit the Depression Alliance website at:


  • Family Studies

Family studies suggest the involvement of genetic factors. Gershon (1990) presented the findings from numerous family studies in which depression was assessed in the first-degree relatives of patients with depression. For both major depression and bipolar disorder, the rates of depression were about two to three times the rates in the general population.

One particular study claimed to identify a gene that might be responsible. Egeland et al. (1987) studied the Amish, a small religious community living in Pennsylvania. The community has a relatively low incidence of major depressive illness, in comparison with the surrounding communities, but one family that was studied had an extremely high level of bipolar disorder. Eleven out of 81 members had manic depression. On examination of their genes it was found that two marker genes on chromosome II appeared to be different. Importantly, these genes were “neighbours” of those genes that are involved in the production of monoamines, a biochemical implicated in depression.

Subsequent attempts to support Egeland et al.’s findings have not been successful. For example, Hodgkinson (1987) studied extended families in Iceland and found no evidence of the different genes in relation to manic depression. It is possible that, in family groups, other factors such as patterns of interaction, may account for depressive illness.

·       Twin Studies

The clearest evidence about the role of genetic factors in the development of major depression and bipolar depression comes from studies on monozygotic and dizygotic twins. Allen (1976) reviewed the relevant studies. For major depression, the mean concordance rate was 40% for monozygotic or identical twins, whereas it was only 11% for dizygotic twins. For bipolar disorder, the mean concordance rate was 72% for monozygotic twins, compared with 14% for dizygotic twins.

Similar findings were reported in a large study by Bertelsen, Harvald, and Hauge (1977). They found a concordance rate for major depression of 59% for monozygotic twins and of 30% for dizygotic twins. For bipolar disorder, the concordance rate was 80% for identical twins and 16% for fraternal twins. In the population at large, about 5% have been diagnosed withmajor depression and I% with bipolar disorder, and all of the figures for monozygotic and dizygotic twins are much higher.

These findings suggest that genetic factors are involved in both types of depression, and that their involvement is greater for bipolar than for major depression. However, it is not known whether the monozygotic and dizygotic twin pairs experienced equally similar environments. As a result, it is possible that some of the higher concordance rate for monozygotic than for dizygotic twins reflects environmental rather than genetic influences.

·       Adoption Studies

Additional evidence supporting the notion that genetic factors are of importance comes from adoption studies. Wender et al. (1986) found that the biological relatives of adopted sufferers from major depression were about eight times more likely than adoptive relatives to have had major depression themselves. In similar fashion, it has been found with adopted children who later developed depression that their biological parents were eight times as likely as their adoptive parents to have suffered from clinical depression (Wender et al., 1986).


There has been much interest in the possibility that depressed patients might have either elevated or reduced levels of various neurotransmitters such as noradrenaline and serotonin which may play a role in the development of depression. It has also been suggested that there may be increased levels of these neurotransmitters when bipolar disorder patients are in their manic phase.

·       The permissive amine theory

Kety (1975) put forward a permissive amine theory of mood disorder. According to this theory, the level of noradrenaline is generally controlled by the level of serotonin. When the level of serotonin is low, however, noradrenaline levels are less controlled, and so they may fluctuate wildly. A third neurotransmitter, dopamine, is also involved.

Noradrenaline, serotonin, and dopamine are all neurotransmitters which act at the synapses, or junctions, between neurons in the brain. They may either facilitate or block nervous transmission. Noradrenaline is associated with physiological arousal in general, and whilst serotonin is also related to arousal and sleep, increases in serotonin generally reduce arousal. Dopamine is normally inhibited by serotonin and has been linked with schizophrenia. Under normal conditions all three neurotransmitters play a role in arousal and also are related to mood.

It is suggested that, in depression, serotonin levels are low as a consequence of individual differences that are inherited, and the abnormal serotonin level prevents adequate control of the other two neurotransmitters. Support for this hypothesis comes from studies that establish a link between mood and these monoamines, and from studies of the effects of anti-depressant drugs.

·       Mood and monoamine transmitters

Teuting, Rosen, and Hirschfeld (1981) compared the substances found in the urine of depressed patients and normals. Compounds that are produced as a by-product of the action of enzymes on noradrenaline and serotonin were present in smaller amounts in the urine of depressed patients. This finding suggests that depressed patients have lower levels of noradrenaline and serotonin. Kety (1975) found very high levels of compounds derived from noradrenaline in the urine of patients suffering from mania.


The main problem arises from the direction of causality. It is hard to know whether the high or low levels of noradrenatlne and serotonin helped to cause the depression, or whether the depression altered the levels of those neurotransmitters.

·       Anti-depressants

Anti-depressant drugs such as the monoamine oxidase inhibitors (MA0Is) increase the active levels of noradrenaline and serotonin in depressed patients, and typically reduce the symptoms of depression. Lithium carbonate, which is very effective in reducing manic symptoms in bipolar disorder, is thought to decrease the availability of noradrenaline and serotonin. These drug effects suggest the potential importance of altered levels of serotonin and noradrenaline.


The drugs rapidly affect neurotransmitter levels, but take much longer to reduce the symptoms of depression or mania. It is possible that the MAOIs reduce depression by increasing the sensitivity of receiving neurons, and it takes time for this increased sensitivity to occur .It is important to note that these drug effects do not provide direct evidence of what causes depression in the first place. MacLeod (1998) called this the treatment aetiology fallacy – the mistaken notion that the success of a given form of treatment reveals the cause of the disorder.


The endocrine system produces hormones that have an influence over a huge range of behaviours: growth, menstruation, sleep, sexual activity, and so on. There are a number of conditions that are linked to hormone changes and where depression is a major symptom. Examples include premenstrual syndrome (PMS), postpartum depression (PPD), and seasonal affective disorder (SAD).

  • Premenstrual syndrome (PMS)

The female menstrual cycle involves changes in the levels of oestrogen and progesterone over the monthly cycle. In the week or two prior to menstruation, some women develop symptoms such as irritability, bloating, breast tenderness, mood swings, decreased ability to concentrate, depression, headache, acne, and constipation. These changes are related to the hormonal fluctuations.

Abramowitz, Baker, and Fleischer (1982) studied the female admissions to one psychiatric hospital and found that 41% entered on the day before or the first day of their menstrual period. Another study, this time looking at women in the normal population, found depressive symptoms during the pre-menstrual period in about 43% of the women interviewed (Halbreich, Endicott, & Nee, 1983)

  • Postpartum depression (PPD)

About 20% of women report moderate depression in the period after giving birth and a few of these women become chronically depressed. In extreme cases severe depression has led mothers to commit infanticide. Symptoms include sadness, anxiety, tearfulness, and trouble sleeping. These symptoms usually appear within several days of delivery and go away by 10 to 12 days after the birth.

Women who have recently given birth undergo massive hormonal changes and this is one possible explanation for postpartum depression. A further possibility is that levels of the stress hormone cortisol are very low after birth and this may make it difficult for women to cope with stress in the period after birth.

Evaluation. In many cases women who suffer postpartum depression have previously had episodes of clinical depression. This suggests that PPD is a combination of hormonal imbalances and a pre-existing predisposition to depression. Lack of emotional support, low self-esteem, and unrealistic ideas about motherhood are also found in cases of PPD, suggesting that psychological factors are important.

·       Cortisol

The role of cortisol may be important in depression generally. Levels of cortisol tend to be elevated in depressed patients (Barlow & Durand, 1995). The notion that cortisol may be relevant to depression has been examined by using the dexamethasone suppression test. Dexamethasone suppresses cortisol secretion in normals, but about 50% of depressed patients show very little suppression (Carroll et al., 1980). Presumably this happens because the levels of cortisol are so high in these patients that they cannot be easily suppressed.


There are two limitations with the cortisol research. First, reduced suppression on the dexamethasone suppression test is also found in anxiety disorders and other mental disorders, and so high levels of cortisol are not specific to depression. Second, high cortisol levels may be a result of depression rather than forming part of the cause.

·       Depression and diet

Explanations of depression that are based on biological factors are generally related to endogenous depression, i.e., depression that is caused by internal factors. There is some evidence that what you eat may affect your mood and may, in extreme cases, lead to depression,

Tryptophan is a substance that is found in some foods, such as maize and other starchy foods. Delgado et al. (1990) found that acute tryptophan depletion (ATD) induces a temporary relapse in patients suffering from major depressive disorder. This is supported in a study by Smith et al. (1997) who found that women experienced depression when tryptophan was removed from their diets. In addition it has been suggested that serotonin may be involved in some cases of eating disorder, and that the reason why bulimics often eat a lot of starchy foods is in order to increase their levels of tryptophan and serotonin.


Several evolutionary explanations have been suggested for depression. In essence the evolutionary view is that depression is in part genetic and the gene for schizophrenia must offer some advantage in order to  explain why it has remained in the gene pool.

·       Depression could be an adaptive response to certain situations. Nesse and Williams (1995) suggest that in certain threatening situations it may be a better strategy to sit tight and do nothing. However, what was an adaptive response in the past may no longer be so.

  • The rank theory of depression suggests that the loser in a conflict accepts the loss as an act of damage limitation. The adaptive significance of the loss of rank is that depression prevents further loss. There is not a great deal of supporting evidence for the rank theory of depression.

  • The evolutionary theory also holds that the manic phase of bipolar depression is linked with creativity and is therefore an adaptive trait. However if this was the case it might be argued that the rates of bipolar depression might be higher


Freud argued that depression is like grief, in that it often occurs as a reaction to the loss of an important relationship. However, there is an important difference, because depressed people regard themselves as worthless. What happens is that the individual identifies with the lost person, so that repressed anger towards the lost person is directed inwards towards the self. This inner-directed anger reduces the individual’s self-esteem, and makes him or her vulnerable to experiencing depression in the future.

Losses, whether real or symbolic, can produce depression by causing the individual to re-experience childhood episodes when they experienced loss of affection from some significant person (e.g., a parent).

According to Freud, the depressive phase of bipolar disorder occurs when the individual’s superego or conscience is dominant. In contrast, the manic phase occurs when the individual’s ego or rational mind asserts itself, and he or she feels in control.

In order to avoid loss turning into depression, the individual needs to engage in a period of mourning work, during which he or she recalls memories of the lost one. This allows the individual to separate himself or herself from the lost person, and so reduce the inner-directed anger. However, individuals who are very dependent on others for their sense of self-esteem may be unable to do this, and so remain extremely depressed.

There is good evidence that depression is caused in part by loss events. For example, Finlay-Jones and Brown (1981) found that depressed patients experienced more stressful life events than normal controls in the year before onset of the depression, and most of these were loss events. However, Freud would predict that the repressed anger and hostility of depressed people would emerge at least partly in their dreams, but Beck and Ward (1961) found no evidence of this. Freud would also predict that depressed people should express anger and hostility inwards. Evidence from Weismann, Klerman & Paykel, 1971 suggest that the anger is often directed outwards at those closest to the depressive patient.

Finally, it follows from Freud’s theory that individuals who experienced some major loss early in their lives should be more vulnerable than others to developing clinical depression in adult life. The evidence is inconsistent, but often suggests that early loss does not predict adult depression (Crook & Eliot, 1980), though the opposite was found by Bifulco et al. (1992)

Separation and loss

You might also consider anaclitic depression which is a state of resigned helplessness and loss of appetite in young children who have been separated from their mothers. Bowlby’s (1969) theory of attachment proposed that there might be long-term emotional damage as a consequence of early loss. Bifulco et al. (1992) offered support for this in a study of about 250 women who had lost mothers, through separation or death, before they were 17. They found that loss of their mother through separation or death doubles the risk of depressive and anxiety disorders in adult women. The rate of depression was especially high among those whose mothers had died before the child reached the age of 6.


  • Reinforcement

Lewinsohn (1974) put forward a behavioural theory based on the notion that depression occurs as a result of a reduction in the level of reinforcement or reward. This relates to the psychodynamic view that depression is caused by the loss of an important relationship, because important relationships are a major source of positive reinforcement. There is also a reduction in reinforcement with other losses, such as being made redundant. People who become depressed because of a major loss may be reinforced in being depressed by the sympathy and understanding shown by other people.

Lewinsohn’s behavioural theory clearly presents an oversimplified view of the causes of depression. For example, many people experience major losses without becoming depressed, and the theory does not explain how this happens. The theory also omits any consideration of other causes of depression such as genetic factors.

  • Learned helplessness

Seligman’s (1975) theory and research on learned helplessness have probably been more influential than any other behavioural approach to depression. Learned helplessness refers to the passive behaviour shown when animals or humans believe that punishment is unavoidable. In his original studies, Seligman exposed dogs to electric shocks they could not avoid. After that, they were put in a box with a barrier in the middle. The dogs were given shocks after a warning signal, but they could escape by jumping over the barrier into the other part of the box. However, most of the dogs passively accepted the shocks, and did not learn to escape. Seligman described this as learned helplessness, and argued that it was very similar to the behaviour shown by depressed people.

Evaluation of learned helplessness research

Seligman used dogs to illustrate how lack of control over one’s experiences might contribute to feeling helpless. In his experiments each dog was “yoked” with another dog. The first dog learned to escape from electric shocks, whereas whether the second dog received a shock or not depended on the expertise of its partner. Later in the experiment the dogs were separated and put into a “shuttle box” where they could escape an electrified floor by jumping over a partition. The dogs that had previous learned to avoid shocks soon learned to jump the partition. However, the dogs who had been yoked behaved passively and gave up trying to escape soon after being put in the shuttle box.

From this research it appears that the most important factor in the animals behaviour was not the electric shocks, but the failure to learn avoidance. The dogs had learned that they were helpless, so they displayed inappropriate behaviour in the shuttle box and didn’t try to escape. Seligman went on to propose that depression in humans may be due to learned helplessness. For example, stressful situations may be experienced as unavoidable and not under the control of the individual.

Although symptoms of learned helplessness in Seligman’s dogs and symptoms of depression in humans do appear to be similar, there are problems with these conclusions The experiments were carried out on dogs in controlled conditions, but do the findings apply to humans in society? Later research indicated that what may be important is not so much the learned helplessness that a person feels, but the way in which the individual might perceive and react to the stressful situation.


Abramson et al. (1978) developed Seligman’s learned helplessness theory by focusing on the thoughts of people experiencing learned helplessness. People respond to failure in various ways:

  • Individuals either attribute the failure to an internal cause (themselves) or to an external cause (other people, circumstances). For example, your boyfriend finishes your relationship and you are convinced it is because of your moodiness (internal cause) or the fact that you have little money for nice clothes (external cause).

  • Individuals either attribute the failure to a stable cause (likely to continue in future) or to an unstable cause (might easily change in future). For example, the moodiness may be a permanent feature of your character (stable) or perhaps it is just because exams are looming ahead (unstable).

  • Individuals either attribute the failure to a global cause (applying to a wide range of situations) or to a specific cause (applying to only one situation). For example, you may be moody with everyone (global) or just with your boyfriend because you didn’t feel that he really loved you (specific cause).

People with learned helplessness attribute failure to internal, stable, and global causes. In other words, they feel personally responsible for failure, they think the factors causing that failure will persist, and they think that those factors will influence most situations in future. In view of these negative and pessimistic thoughts, it is no wonder that sufferers from learned helplessness are depressed.


Beck, A.T. (1967), Depression: Clinical, experimental, and theoretical aspects. developed the most widely used inventory of depressive symptoms. Each question assesses one symptom of depression, and provides a score for severity of that symptom on a scale of 0 to 3. The symptoms are divided into mood, thought, motivation and physical characteristics. The inventory is not intended to be used to diagnose depression, but just to assess the range of symptoms present and the severity.

Research has shown that a “normal” American college student would score above 3 or 4. Mildly depressed students score between 5 and 9, and a score above 10 suggests moderate to severe depression. If an individual scored more than 10 for a period of more than two weeks, he or she should seek help.


Beck and Clark (1988) also argued that cognitive factors may play an important role in the development of depression. They referred to depressive schemas, which consist of organised information stored in long-term memory. Beck and Clark’s (1988, p.26) cognitive theory is as follows:

“…The schematic organisation of the clinically depressed individual is dominated by an overwhelming negativity. A negative cognitive trait is evident in the depressed person’s view of the self, world, and future … As a result of these negative maladaptive schemas, the depressed person views himself as inadequate, deprived and worthless, the world as presenting insurmountable obstacles, and the future as utterly bleak and hopeless…”

The term cognitive triad is used to refer to the three elements: the depressed person’s negative views of himself or herself, the world, and the future.


Depressed people undoubtedly have the kinds of negative thoughts described by Abramson et al. (1978) and by Beck and Clark (1988). Do these negative thoughts help to cause depression, or do they merely occur as a result of being depressed? Lewinsohn et al. (1981, p.218) carried out a prospective study in which negative attitudes and thoughts were assessed before any of the participants became depressed. Here are their conclusions:

“…Future depressives did not subscribe to irrational beliefs, they did not have lower expectancies for positive outcomes or higher expectancies for negative outcomes and they did not attribute success experiences to external causes and failure experiences to internal causes. People who are vulnerable to depression are not characterised by stable patterns of negative cognitions…”

Most of the evidence suggests that negative thoughts and attitudes are caused by depression rather than the opposite direction of causality. However, Nolen-Hoeksma, Girgus, and Seligman (1992) found that a negative attributional style in older children predicted the development of depressive symptoms in response to stressful life events. Therefore negative thoughts may make people vulnerable to depression.

Therapies based on this cognitive view of depression have proved very successful. However, one must be careful about suggesting that the success of a treatment reveals the cause of the disorder, a problem called the treatment aetiology fallacy, described earlier.


Patients suffering from major depression typically experience an above average number of stressful life events in the period before the onset of depression. For example, Brown and Harris (1978) carried out an interview study on women in London. They found that 61% of the depressed women had experienced at least one very stressful life event in the 8 months before interview, compared with 19% of non-depressed women. However, many women manage to cope with major life events without becoming clinically depressed. Of those women who experienced a serious life event, 37% of those without an intimate friend became depressed, compared with only 10% of those who did have a very close friend. This suggests that social support, another social factor, may moderate the effects of life events on depression.

The findings of Brown and Harris (1978) have been replicated several times. Brown (1989) reviewed the various studies. On average, about 55% of depressed patients had at least one severe life event in the months before onset, compared with only about 17% of controls.


There are two main limitations of most life-event studies. First, the information is obtained retrospectively several months afterwards, and so there may be problems in remembering clearly what has happened. Second, the meaning of a life event depends on the context in which it happens. For example, losing your job is very serious if you have a large family to support, but may be much less serious if you are nearing the normal retirement age and have a large pension. This second limitation does not apply to the research of Brown and Harris (1978), because they took full account of the context in which the life events occurred.

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