BIOLOGICAL EXPLANATIONS OF DEPRESSION
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
EVOLUTIONARY
EXPLANATIONS
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Social competition
hypothesis
Social navigation
hypothesis
Bipolar disorder
and increased
fitness
GENETIC EXPLANATIONS BIOCHEMICAL
EXPLANATIONS
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Research evidence
for and against
Evaluation
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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.
EVALUATION OF THE SOCIAL COMPETITION HYPOTHESIS
 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.
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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.
RESEARCH EVIDENCE FOR THE SOCIAL NAVIGATION HYPOTHESIS
 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 selfserving bias—they attribute success to their own ability but failure to bad
luck (Ackermann & DeRubeis, 1991, see A2 Level Psychology page 433).
EVALUATION OF THE SOCIAL NAVIGATION HYPOTHESIS
 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.
EVALUATION OF INCREASED FITNESS
 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.
OVERALL EVALUATION OF EVOLUTIONARY EXPLANATIONS
 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.
RESEARCH EVIDENCE FOR GENETIC FACTORS
 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
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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).
RESEARCH EVIDENCE AGAINST GENETIC FACTORS
 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).
EVALUATION OF RESEARCH INTO GENETIC FACTORS
 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.
RESEARCH EVIDENCE FOR BIOCHEMISTRY
 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.
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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.
RESEARCH EVIDENCE AGAINST BIOCHEMISTRY
 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.
RESEARCH EVIDENCE FOR HORMONAL FACTORS
 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.
RESEARCH EVIDENCE AGAINST HORMONAL FACTORS
 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).
EVALUATION OF THE RESEARCH INTO BIOCHEMICAL AND HORMONAL FACTORS
 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 nonsuppression 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)