BIOLOGICAL EXPLANATIONS OF OBSESSIVE COMPULSIVE DISORDER
To read up on the biological explanations of obsessive compulsive disorder, refer to pages 521–529 of
Eysenck’s A2 Level Psychology.
Ask yourself
 How might obsessive compulsive disorder (OCD) be linked to brain
biochemicals?
 What is the genetic hypothesis?
 Could OCD have evolutionary benefits that outweigh the costs of the
disorder?
What you need to know
GENETIC EXPLANATION
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Research evidence
Evaluation
EVOLUTIONARY
EXPLANATIONS
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Research evidence
Evaluation
BIOCHEMICAL AND
ANATOMICAL
EXPLANATIONS
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Research evidence
Evaluation
Three biological explanations of obsessive compulsive disorder (OCD) consist of genetic, evolutionary,
and biochemical factors. These three factors are likely to be related. For example, evolutionary pressures
have shaped the genes that we have inherited and our biochemical systems.
Genetic explanation
Family and twin studies suggest the involvement of genetic factors. The prevalence of OCD in the random
population (about 2–3%) is the baseline against which the concordance rates can be compared.
RESEARCH EVIDENCE FOR GENETIC FACTORS
 Carey and Gottesman (1981, see A2 Level Psychology page 522) found that
identical twins showed a concordance rate of 87% for obsessive symptoms
and features compared to 47% in fraternal twins. This difference suggests
that genetic factors are moderately important. van Grootheest et al. (2005,
see A2 Level Psychology page 522) reviewed twin studies on obsessive
compulsive disorder. All of the studies reported higher concordance rates for
identical than for fraternal twins. However, the concordance rates for
identical twins were well short of 100%, indicating that environmental
factors are of major importance.
 A family study by Pauls et al. (1995, see A2 Level Psychology page 522) of
first-degree relatives (i.e. those sharing 50% of their genes with the patients)
found a 10.3% rate of OCD compared to 1.9% in relatives of healthy controls.
Nestadt et al. (2000, see A2 Level Psychology page 523) found that the
lifetime incidence of OCD was higher in the relatives of patients with
obsessive compulsive disorder (11.7%) than in the relatives of healthy
controls (2.7%).
RESEARCH EVIDENCE AGAINST GENETIC FACTORS
 The higher concordance rate found for MZ twins may be due to nurture as
MZ twins are likely to experience a more similar environment than DZ twins
since they tend to be treated the same.
 The OCD may be culturally rather than genetically transmitted as the family
members may observe and imitate each other’s behaviour, as predicted by
social learning theory. Alternatively, family members might be more
vulnerable to OCD 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.
EVALUATION OF RESEARCH INTO GENETIC FACTORS
 Strong empirical support. Twin and family studies have consistently found
evidence for genetic factors. The twin studies have good reliability because
concordances are relatively consistent across studies.
 Not 100% concordance. The concordance rates are not 100%, which
suggests that genetic factors may predispose but not cause OCD, and that
environmental factors must be involved.
 Nature vs. nurture. Do concordance rates reflect nature or are they really
due to nurture? The OCD could be culturally rather than genetically
transmitted because close family members and twins may learn the same
behaviour; one may imitate the other.
 Sample size. The samples in such studies are very small so generalisability
and population validity may be limited, which means the findings may not be
representative of other populations.
 Generalisability of twin research. Twins share a special relationship,
particularly identical twins, and so research on twins lacks generalisability to
the general population.
 Biologically deterministic. The suggestion that the genes determine OCD is
deterministic as it ignores the individual’s ability to control their own
behaviour.
 Methodological weaknesses of concordance studies. Family and twin
studies must be considered cautiously because they are retrospective, and
diagnosis may be biased by knowledge that another family member has been
diagnosed.
 Reductionism. The biological approach only focuses on one level of
explanation and therefore is too simplistic.
 Diathesis–stress model. Genes alone do not determine who will develop
OCD—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 OCD is due to an
interaction of genetic and other factors.
Evolutionary explanations
The compulsive and ritualised behaviours often involve cleaning and checking behaviours. This supports
an evolutionary basis as such cleaning is adaptive because it protects against contamination and disease,
and checking behaviours can be linked to defence of resources and territory. Thus, according to
evolutionary explanations, obsessive compulsive disorder is a distortion of adaptive grooming and
territorial behaviours.
RESEARCH EVIDENCE FOR EVOLUTIONARY EXPLANATIONS
 Abed and de Pauw (1998, see A2 Level Psychology page 523) proposed the
“Involuntary Risk Scenario Generating System”, which is a system of warning
signals about stimuli and situations that were potentially dangerous in our
evolutionary history, for example, dirt may lead to disease.
Szechtman and Woody (2004, see A2 Level Psychology page 524) suggested a
security motivation system designed to detect potential dangers and prevent
them turning into emergencies. This acts as an alarm detector, “because
repeated false alarms are much less costly than even a single failure to
prepare for upcoming danger”. They suggest that patients with OCD find it
much harder to turn off their security motivation system.
 Rachman and de Silva (1978, see A2 Level Psychology page 524) support the
universality of OCD symptoms, as they found that 80% of healthy individuals
reported obsessional thoughts and/or compulsions, with 54% reporting
both. It is also found across all cultures.
EVALUATION OF EVOLUTIONARY EXPLANATIONS
 Face validity. The evolutionary accounts have face validity; it makes sense
that the cleaning and checking obsessions have survival value. The idea that
obsessive compulsive disorder is associated with an overactive warning
system seems plausible.
 Universality of mental disorders. If evolution is correct then OCD
symptoms should be relatively universal as we have all evolved in the same
way. Rachman and de Silva (1978, see A2 Level Psychology page 524) suggest
up to 80% of healthy individuals report obsessional thoughts and so this
lends support to an evolved basis to OCD.
 Individual differences. Evolution does not explain individual differences
because it is not clear why certain individuals develop obsessive compulsive
disorder.
 Conjecture—evolutionary stories? Evolutionary explanations are post hoc
(made up after the event) and so cannot be verified or falsified, and, given
that falsification is a key criterion of science, according to Popper, then the
theory lacks scientific validity. This means they are just speculation; we
cannot be sure that compulsive cleaning or checking had an evolutionary
advantage.
 Reductionist and deterministic. Evolutionary theories are reductionist as
they focus on one factor only (the gene) when other emotional, social,
cognitive, behavioural, and developmental factors are highly relevant to the
aetiology of mental disorders. They are oversimplified accounts at best. They
are also deterministic as they suggest that the genes control behaviour,
which ignores the free will of the individual, for example, the individual may
choose to ignore their obsessions.
 Psychological explanations. The psychological models of abnormality are
counter-perspectives. Moreover, they may account for why adaptive
behaviours (the overactive warning system) have become distorted. For
example, the evolved “fight-or-flight” stress response may be genetically
predisposed and have adaptive value. But it interacts with psychological
factors, such as individual differences and self perception, which may result
in maladaptive anxiety responses.
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Social learning theory has great explanatory power. It accounts for how
children learn so much so quickly and so may provide a more valid
explanation of how children acquire OCD.
 Nature/nurture. The evolutionary explanations overemphasise the role of
nature and ignore nurture. It is not a question of nature or nurture, as
indisputably an interactionist perspective must be taken. However, as the
evolutionary explanations ignore nurture this is a key weakness.
 Maladaptive rather than adaptive. The obsessional thoughts and
compulsions severely disrupt everyday functioning so this challenges the
idea they have adaptive value.
 Alternative explanations. There are alternatives explanations to the
evolutionary claim that OCD is adaptive in some way. For example, it can be
argued that natural selection does not create perfect organisms whereby all
behaviours are adaptive in some way; instead OCD may be recessive and
therefore 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. It is possible,
therefore, that OCD is due to mutations that have persisted in our gene pool
in spite of the fact they are maladaptive.
Biochemical and anatomical explanations
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Biochemical abnormalities and brain structural abnormalities have been identified as explanations of OCD.
Biochemical explanations
According to the serotonin hypothesis, individuals with OCD have reduced levels of the neurotransmitter
serotonin or have deficient serotonin metabolism.
RESEARCH EVIDENCE FOR BIOCHEMICAL FACTORS
 Two classes of drug have proved effective in the treatment of obsessive
compulsive disorder: serotonin reuptake inhibitors (SRIs) and selective
serotonin reuptake inhibitors (SSRIs). Both classes of drug increase
serotonin levels, and so support the biochemical hypothesis.
 Drugs that mainly affect neurotransmitters other than serotonin are of little
or no value in treating obsessive compulsive disorder.
RESEARCH EVIDENCE AGAINST BIOCHEMICAL FACTORS
 Studies in which serotonin levels in obsessive disorder patients have been
assessed have typically found no differences between them and healthy
controls.
 There is no evidence that patients with relatively low levels of serotonin
respond better to drug therapy than patients whose serotonin levels are
higher.
 Antidepressant drugs do not work for all patients. Also, the drugs increase
the levels of the biochemicals immediately but can take at least 6 weeks
before they alleviate OCD, which further challenges a direct link between the
neurotransmitters and OCD.
EVALUATION OF THE RESEARCH INTO BIOCHEMICAL FACTORS
 Cause, effect, or correlate. It is difficult to establish whether the low levels
of neurotransmitters cause OCD, are an effect of having the disorder, or are
merely associated. Causation cannot be inferred as only associations have
been identified.
 Serotonin level. Contradicting the explanation that OCD is due to low
serotonin is research by Dougherty et al. (2002, see A2 Level Psychology page
525), which found that SSRIs, rather than improving symptoms, sometimes
make them worse early in treatment but are effective after about 6 weeks.
This can be explained by the fact that initially the SSRIs would increase
serotonin but by 6 weeks they actually cause serotonin to decrease. This
links OCD to high levels of serotonin, because the drugs work when they are
reducing serotonin.
 Descriptive not explanatory. The hypothesis describes the nature of
biochemical imbalance but the hypothesis doesn’t explain why and how
patients with obsessive compulsive disorder have low levels of serotonin in
the first place. Furthermore, it is unclear how low levels of serotonin would
produce obsessive and compulsive symptoms.
 Treatment aetiology fallacy. The success of antidepressant drugs as a
treatment does not necessarily mean the biochemicals are the cause of OCD
in the first place. This is known as the treatment aetiology fallacy and, using
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 oversimplified. 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 levels.
 Individual differences. The biochemistry hypothesis does not account for
individual differences because the research does not explain why one
individual develops OCD and another develops a different mental disorder,
because low serotonin levels are also found in other mental disorders. Thus,
these biochemical abnormalities are not specific to OCD, and may be true of
any form of mental distress.
Anatomical explanations
According to this explanation, certain areas of the brain do not function the same in OCD patients than they
do in healthy controls. Baxter et al. (1992, see A2 Level Psychology page 526) suggest that there is overactivity in the orbital frontal cortex and, as this area is responsible for our primitive urges concerning sex,
aggression, danger, and hygiene, explains many common obsessions of OCD.
There is also dysfunction of neural circuits, including the corpus striatum, which leads to inappropriate
repetitive behaviour. Areas such as the orbital frontal cortex and the caudate nucleus are sometimes larger
in obsessive compulsive patients than in controls, and obsessive compulsive symptoms often seem to
increase or decrease when the orbital region and/or the caudate nucleus are damaged through either illness
or accident.
A review of brain-imaging research shows elevated activity in the orbital region and the caudate nucleus
has been found consistently in OCD patients compared to healthy controls. After treatment, activity in these
brain areas reduces to a level comparable to that of controls, as found by Saxena and Rauch (2000, see A2
Level Psychology page 527).
The consistency of these findings supports reliability, and therefore validity, of an anatomical explanation.
However, findings are not completely reliable: there are studies in which no differences in brain anatomy
were found between OCD patients and controls. A key limitation is the fact that the research is
correlational so only associations are identified between elevated brain activity and OCD. As it is only an
association, we cannot be sure of the direction of effect because it’s not clear whether the brain areas cause
OCD or whether these brain abnormalities are effects of having OCD. The explanation is also reductionist
because it only focuses on biological factors, not psychological ones (such as life events), and it is unclear
how such psychological factors might influence brain activity.
So what does this mean?
There is moderately strong evidence for the role of genetics in OCD. However, these concordances could
be due to the shared environment so behavioural explanations offer a powerful alternative to the idea that
OCD is inherited. Concordance rates are not 100% so genes alone cannot explain OCD. Therefore genetic
factors do not account for individual differences in susceptibility to OCD. Any genetic vulnerability may be
general across mental disorder rather than specific to OCD.
Perhaps of more interest is why one family member may suffer with OCD while 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 OCD but this does not necessarily
result in OCD, 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.
The evolutionary explanations provide interesting insights into the possible origins of OCD; it seems
unquestionable that the fear response does ensure survival. However, whether OCD is innate is less
conclusive because, as always, evolutionary explanations are speculative and so are limited by a lack of
scientific validity.
The biochemical and anatomical explanations provide further insights but key issues are the lack of cause
and effect and unknown direction of effect in such research; biochemical and brain structural abnormalities
may be effects rather than causes of OCD.
Over to you
1. Outline and evaluate one or more biological explanation(s) of one anxiety disorder. (25 marks)