Biological explanations of depression

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To read up on biological explanations of depression, refer to pages 432–440 of Eysenck’s A2 Level Psychology.

Ask yourself

  • What is the genetic hypothesis?

  • How might depression be linked to brain biochemicals?

  • Could depression have evolutionary benefits that outweigh the costs of the disorder?

What you need to know




  • Research evidence for and against

  • Evaluation

  • Research evidence for and against

  • Hormonal factors

Three biological explanations of depression are evolutionary factors, genetic factors, and biochemical imbalance. These three factors are likely to be related. For example, evolutionary pressures have shaped the genes that we have inherited and our biochemical systems.

Evolutionary explanations

Social competition hypothesis

According to the social competition hypothesis (e.g. Price et al., 1994, see A2 Level Psychology page 432), human social groups are hierarchical and so conflicts arise over position and authority. Depression is adaptive when the individual has lost in a social competition because accepting loss and the consequent withdrawal ends the conflict. The loser retreats and so is protected from further injury, which represents “damage limitation”. The individual suffers in the short term but this is better than risking further losses and so is adaptive in the long term.

  • Doesn’t account for prolonged depression. The theory doesn’t account for depression that lasts for a few years as surely adjusting to a new position in the hierarchy would not take this long.

  • Reductionism. The theory only accounts for one factor, evolutionary value, when there are many possible causative factors and so the theory is too simplistic.

  • Maladaptive rather than adaptive. The main basis of the theory is that depression in the short term is adaptive. This is not consistent with what can be a very distressing and so maladaptive illness.

Social navigation hypothesis

According to the social navigation hypothesis (Watson & Andrews, 2002, see A2 Level Psychology page 433), depression provides a social rumination function because it involves the individual thinking at length about their problems and what to do about them. Also, the distress of the depressed person may elicit help from others, the social motivation function.

  • In support of the social motivation function, strong social support does facilitate recovery (Brugha et al., 1997, see A2 Level Psychology page 433).

  • In support of the social rumination function, there is some evidence that depressed individuals are more realistic than non-depressed ones in their thinking (depressive realism) because non-depressed individuals have a self-serving bias—they attribute success to their own ability but failure to bad luck (Ackermann & DeRubeis, 1991, see A2 Level Psychology page 433).


  • How effective is social rumination? Depression is not an ideal state for complex social problem solving! A lack of decision making is a key symptom, which doesn’t fit with the social rumination function.

  • Too optimistic. Depressed people who make their partner’s life a misery often find themselves losing their partner rather than receiving the help they seek.

  • More maladaptive than adaptive. There is too much focus on the idea that depression is adaptive, which is inconsistent with the fact that 5% of clinically depressed individuals commit suicide (Bostwick & Pankratz, 2000, see A2 Level Psychology page 433).

  • Social explanations may be stronger. Nesse and Williams (1995, see A2 Level Psychology page 433) suggest that developed societies are highly competitive and so create greater stress and opportunities for loss. We are exposed to images of ideal lives and material possessions that can result in feelings of inferiority, dissatisfaction, and consequently depression.

Bipolar disorder and increased fitness

The manic phase of bipolar depression (where the individual alternates between depressive and manic, i.e. euphoric, states) has been related to creativity, lack of inhibition, and charismatic leadership, and so the disorder increases the fitness of those who carry it, which is why it remains in the gene pool.

Winston Churchill, Abraham Lincoln, Vincent Van Gogh, and Ludwig van Beethoven are only a few of the many great leaders and artists who are said to have suffered with bipolar disorder, which offers support for this explanation.

Another adaptive explanation is linked to seasonal affective disorder (SAD). Nearly all individuals with SAD suffer from severe depression during the winter months. Patients with bipolar disorder are more likely to have manic phases in the warmer months (Carroll, 1991, see A2 Level Psychology page 433) and so there may be adaptive value in being most active during the lighter time of the year.

  • Adaptive or maladaptive? Do the severe disadvantages of such a debilitating disorder outweigh any possible adaptive value it might have? It is difficult to see how the extreme highs and lows have any increased fitness.


  • Post hoc. Evolutionary explanations lack evidence given that the theory is post hoc (made up after the event), which means we cannot be really sure when depression evolved as the only evidence we have is fossils and they do not provide us with answers. This means the evolutionary explanations cannot be verified or falsified, and given that falsification is a key criterion of science according to Popper then the theory lacks scientific validity.

  • Speculation rather than fact. Inter-linked with the above criticisms— because the explanations lack evidence then they are purely speculation rather than fact.

  • Adaptive or maladaptive? The evolutionary explanations try to provide adaptive explanations for how depression ended up in the gene pool, however these seem inconsistent with the very maladaptive nature of the disorder and so the explanations lack conviction.

  • Alternative explanations. There are alternative explanations to the evolutionary claim that depression is adaptive in some way. For example, it can be argued that natural selection does not create perfect organisms in which all behaviours are adaptive in some way, instead depression may be recessive and so is difficult to weed out. Or, alternatively, one theory is that there were “bottle-necks” in human evolution, which meant that the human population was too small for genetic mutations to be weeded out and so depression is a mutation than has persisted in our gene pool in spite of the fact it is maladaptive.

Genetic explanations

Family, twin, and adoption studies suggest the involvement of genetic factors. The prevalence of depression in the random population (about 7% for major depressive disorder and 1% for bipolar disorder) is the baseline against which the concordance rates can be compared.

  • Allen (1976, see A2 Level Psychology pages 434–435) reported a mean concordance rate of 40% for MZ twins compared to 11% for DZ twins. The high ratio supports the role of genetic factors. McGuffin et al. (1996, see A2 Level Psychology page 435) found a concordance rate of 46% for identical twins compared to 20% for fraternal twins.

  • Craddock and Jones (1999, see A2 Level Psychology page 435) found with bipolar disorder that the concordance rate was 40% for identical twins compared to between 5% and 10% for fraternal twins, siblings, and other close relatives.

  • Berrettini (2000, see A2 Level Psychology page 435) linked bipolar disorder to genes on chromosomes 4, 6, 11, 12, 13, 15, 18, and 22.

  • Gershon (1990, see A2 Level Psychology page 435) reviewed the findings from a number of family studies and found that depression runs in families, as the rate of depression was two to three times higher in first degree relatives of depressives compared to the general population.

  • Egeland et al. (1987, see A2 Level Psychology page 435) studied the Amish community in Pennsylvania who had a relatively low incidence of major depressive disorder compared to the surrounding communities. However, one family had an extremely high level of bipolar disorder, with 11 out of 81 members being affected. On examination of their genes, two marker genes on chromosome 11 appeared to be different. Importantly, these genes were “neighbours” of the genes involved in the production of monoamines, a biochemical implicated in depression.

  • Adoption studies have shown that the biological parents of adopted children who develop depression were eight times more likely than the adopted parents to have suffered with depression, which suggests the role of nature over nurture (Wender et al., 1986, see A2 Level Psychology page 435).


  • The higher concordance rate found for MZ twins may be due to nurture as they are likely to experience a more similar environment than DZ twins since they tend to be treated the same.

  • Hodgkinson (1987, see A2 Level Psychology page 435), who studied extended families in Iceland, couldn’t find any evidence of the different genes in relation to bipolar disorder identified in Egeland et al.’s (1987) research.

  • The depression may be culturally rather than genetically transmitted as the family members may observe and imitate depressive behaviour, as predicted by social learning theory. Or family members might be more vulnerable to depression because of the stressful environment rather than because of genetic factors.

  • The research evidence for psychological factors can be used as evidence against genetics (see later).

  • Sullivan, Neale, and Kendler (2000, see A2 Level Psychology page 435) discussed two other adoption studies on major depressive disorder, neither of which produced strong evidence for a genetic influence on major depression. This means the research findings on adoption and depression are inconsistent (unreliable).


  • Stronger evidence for bipolar disorder. The concordance figures are more convincing for bipolar disorder than for major depressive disorder, suggesting that genetic influences are stronger for bipolar disorder.

  • Nature vs. nurture. It is difficult to separate out the influence of nature and nurture. Whilst the twin studies provide strong evidence for the role of genetic factors and the adoption studies point to the role of nature over nurture, this is not conclusive.

  • Not 100% concordance. The concordance rates are not 100%, which suggests that genetic factors may predispose but not cause depression.

  • Sample size. The samples in such studies are very small and so generalisability and population validity is constrained.

  • Reliability. The twin studies have good reliability because concordances are relatively consistent across studies. However, adoption studies are not very reliable as findings have been inconsistent.

  • Diathesis–stress model. Genes alone do not determine who will develop depression—they only create vulnerability. Thus, they are not a direct cause as other factors must trigger the disorder. Evidence for this is that the concordance rates are not 100%, which shows that depression is due to an interaction of genetic and other factors.

Biochemical explanations

The monoamine hypothesis suggests that depression is due to abnormal levels of neurotransmitters in the monoamine group (noradrenaline, serotonin, and dopamine). Neurotransmitters act at the synapses or junctions between neurons in the brain. They facilitate or block nervous transmission. Noradrenaline and serotonin are related to arousal and sleep—high levels of noradrenaline are linked to high levels of arousal, and increases in serotonin generally reduce arousal. This was expanded upon with the permissive amine theory (Kety, 1975, see A2 Level Psychology pages 436–437), which proposes that the level of noradrenaline and dopamine are controlled by serotonin, and that low levels of serotonin are inherited. When serotonin is low the levels of noradrenaline fluctuate wildly; low levels are associated with depression and high levels with mania. The biochemical system depends in part on genetic factors and so the genetics and biochemical explanations are inter-linked.

  • The three neurotransmitters—serotonin, dopamine, and noradrenaline—are part of the monoamine group and play a role in normal arousal and mood.

  • By-product compounds of the enzymes that act upon noradrenaline and serotonin were lower than normal in the urine of depressives (Teuting, Rosen, & Hirschfeld, 1981, see A2 Level Psychology page 437).

  • Antidepressant drugs such as the monoamine oxidase inhibitors (MAOIs) increase the levels of noradrenaline and serotonin and alleviate the symptoms of depression, which supports the influence of the biochemicals on mood. Similarly, SSRIs inhibit the re-uptake of serotonin and the resulting increase in the level of serotonin is linked to improved mood.

  • Post-mortem studies of patients who committed suicide show reduced levels of serotonin and an increased number of serotonin receptor sites.

  • Rampello, Nicoletti, and Nicoletti (2000, see A2 Level Psychology page 437) found that patients with major depressive disorder had an imbalance in several neurotransmitters, including noradrenaline, serotonin, dopamine, and acetylcholine. This supports the theory but also shows that the neurochemicals involved may be more complex than originally hypothesised.


  • Thase et al. (2002, see A2 Level Psychology page 437) found that depressed patients (especially those with severe depression) had increased levels of noradrenaline. This is the opposite of what the theory predicts.

  • Abnormalities in serotonin function continue after recovery from depression, which suggests that there is not a clear-cut link between this and depression.

  • Antidepressant drugs do not work for all patients. Also, the drugs increase the levels of the biochemicals immediately but can take weeks before they alleviate the depression, which further challenges a direct link between the neurotransmitters and depression.

  • The research evidence on psychological factors can be used as evidence against.

Hormonal factors

Various conditions that are linked to hormone changes can also result in depression, for example, premenstrual syndrome (PMS), postpartum depression (PPD, after a woman has had a child), and seasonal affective disorder. The female menstrual cycle involves changes in the levels of oestrogen and progesterone. Even greater hormonal changes occur during pregnancy and post-birth and these hormonal fluctuations are linked to depression. Cortisol produced during the body’s response to stress has been linked to depression, as levels of cortisol tend to be elevated in depressed patients.

  • Abramowitz, Baker, and Fleischer (1982, see A2 Level Psychology page 438) studied the female admissions to a psychiatric hospital. They found that 41% entered on the day before (or the first day of) their menstrual period.

  • The link between premenstrual syndrome and depression could explain in part why more women than men suffer from depression.

  • About 20% of women report moderate depression shortly after giving birth, and a few of these women become chronically depressed.

  • Elevated blood plasma levels of cortisol have been found in 30% of depressed outpatients and 70% of depressed hospitalised patients (Thase et al., 2002, see A2 Level Psychology page 438).

  • The dexamethasone suppression test is used to assess the role of cortisol in depression. Dexamethasone is synthetic cortisol and it suppresses cortisol secretion in healthy individuals. However, about 50% of depressed patients show very little suppression (Howland & Thase, 1991, see A2 Level Psychology page 438). These findings suggest that the levels of cortisol are so high in depressed patients that they can’t easily be suppressed.


  • More women than men have suffered from child abuse, and such abuse predicts adult depression (Butcher, Mineka, & Hooley, 2004, see A2 Level Psychology page 438). Thus, social factors may account for the greater incidence of depression in women than men rather than hormonal factors.

  • Women who become depressed after childbirth have often had previous emotional problems. This suggests that their depression may be due to other factors such as a pre-existing predisposition to depression. The adjustment required when a child is born can exacerbate any marital difficulties and factors such as lack of emotional support, low self-esteem, and unrealistic ideas about motherhood play a part in postpartum depression, and so this is due to psychological not than just hormonal factors (Gotlib et al., 1991, see A2 Level Psychology page 438).


  • Cause, effect, or correlate. It is difficult to establish whether the low levels of neurotransmitters cause depression, are an effect of having the disorder, or are merely associated. Causation cannot be inferred as associations only have been identified. This is the same for the hormonal imbalances that have been linked to depression.

  • Treatment aetiology fallacy. The success of antidepressant drugs as a treatment does not necessarily mean the biochemicals are the cause of the depression in the first place. MacLeod (1998, see A2 Level Psychology page 439) described this as the treatment aetiology fallacy and used headaches as an example. Aspirin works well as a treatment but this doesn’t mean the headache was due to an absence of aspirin.

  • Reductionist and deterministic. Biological explanations are reductionist as they focus on only one factor and at present our understanding of biochemistry is limited. This means other biological factors, such as genetics and psychological factors, are ignored. The biological explanations are also deterministic because they ignore the individual’s ability to control their own behaviour, which in turn may affect their biochemistry and hormone levels.

  • Explanatory power. There is a lack of explanatory power, because the research does not explain why one individual develops depression and another develops a different mental disorder, as high cortisol levels and non-suppression are also found in other mental disorders. Thus, these hormonal abnormalities are not specific to depression, and may be true of any form of mental distress.

So what does this mean?

There are a number of biological explanations, which in reality may well be all linked, as genetics may be responsible for biochemical imbalances and evolution will have shaped the gene pool in the first place.

There is reasonably strong evidence for the role of genetics in depression, however concordances are not as high as they are for schizophrenia. Furthermore, these concordances could be due to the shared environment, which may be stressful if a family member has depression, and so psychosocial factors, as opposed to just genetic factors, may explain why depression is common within families. Perhaps of more interest is why one family member may suffer with the disorder and others do not, particularly in the case of identical twins who have 100% genetic similarity.

The diathesis–stress model provides a more comprehensive understanding of how nature and nurture may interact and so can better explain such individual differences. Individuals may be predisposed (the diathesis) to depression but this does not necessarily result in depression, as this depends on the interaction of the diathesis with environmental factors. This accounts for the lack of consistency in the findings on genetics and the fact that the abnormality differs across MZ twins who share the same genes.

Research provides convincing evidence that depression is in some way related to biochemical and hormonal abnormalities. However, we cannot be sure that these cause depression because we cannot establish cause and effect and nor can we be sure of the direction of effect. The evolutionary explanations provide interesting insights into the possible origins of depression but are limited by a lack of scientific validity.

Over to you

1. Outline and evaluate one or more biological explanation(s) of depression. (25 marks)

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