| Introduction
The key question concerning major depression is
about difference--why do some people become depressed
while others do not? There is an increasing consensus
about etiology, with the proponents of genetic/
biological theories of causation acknowledging
the inextricable links between these influences
and social factors. Thus Plomin (1995) writes
that 'the same genetic research that has demonstrated
the important contribution of genetics also provides
the best available evidence for the importance
of environmental influence.'
Classification: Clarification Or Confusion?
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The study of the causation of major depression
requires clear and sufficiently uncontroversial
descriptions of the condition. Farmer points but
the importance of this in relation to understanding
genetics--we do have reliable definitions, but
perhaps too many from which to chose, and the
most appropriate for research purposes remain
unclear. Studies on the genetics of unipolar major
depression are only now coming to the fore--much
work to date has focused on bipolar disorder.
While the latter is easier to diagnose and classify,
there is likely to be at best only a partial genetic
overlap with the more common unipolar form. (Fombonne
1995)
Two aspects of classification are of particular
importance. First, recognition of the value of
a 'polydiagnostic' approach, and secondly, the
acknowledgement of the heterogeneity of depressive
states and in particular that much may be gained
from studying individual symptom constellations.
Brain imaging studies are helping to identify
regions which subserve individual symptom clusters
and we must be wary of over-zealous attempts at
classification in light of the refinements which
imaging studies may bring.
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There is controversy surrounding the diagnosis
of dysthymia, as distinct from other 'neurotic'
conditions, particularly if, as some contend,
cothymia or the 'general neurotic syndrome' of
mixed major depression and anxiety are in fact
more accurate descriptions (Tyrer et al., 1993;
Tyrer, 1989). Indeed, we may have to extend research
to such syndromes. The question of quantity and
quality clearly arise here--where does unhappiness
become dysthymia, and dysthymia major depression,
and where do apparently more restricted depressive
syndromes sit--those for example of seasonal affective
disorder and post-natal major depression?
Single causes or chains of events?
Genetic factors underlie major depression in a
complex manner, but the biologists agree that
we are looking at an inherited liability to develop
major depression in response to environmental
stressors rather than an entirely genetically
determined condition. The biological basis of
this vulnerability is being studied. Key possibilities
include, perhaps most simply, a mutation disrupting,
for example, some stage of amine neurotransmission--a
likely candidate based on the empirical evidence
of effective therapeutic drugs. But changes in
the central control of corficosterold hormones
in major depression also occur and may be paramount.
The work on the hypothalamic-pituitary axis, the
stress response and cortisol brings us back towards
basic mechanisms and treatments aimed at both
the hypercortisolaemia which may underlie some
depressive states and the defective negative feedback
mechanisms which may cause or exacerbate this.
Improved understanding of these systems may well
have implications for refining both pharmacological
and psychological treatments.
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More subtle links between genes and the propensity
to become depressed have also been proposed, and
we can start to conceive of a model whereby genetic
factors influence people's behavior and cognitive
style, leading in turn to a tendency to respond
to certain environmental factors by becoming depressed.
The extent to which our behavior--and thus our
experiences and life-events, and indeed our interpretation
of these, are genetically determined remains to
be discovered. Inherited attributes may contribute
to vulnerability and major depression through
influences on people's exposure to environmental
factors--'gene environment correlation', and effects
on choices--those of partners, friends and lifestyle.
A complex chain of inherited predisposition to
certain lifestyles coupled with the adverse effects
of a vulnerability to some of the events arising
as a result of these lifestyles could act together
to determine a depressive reaction. In addition,
the impact of events is mediated by their interpretation,
and the extent to which they may be assimilated
relatively painlessly.
It is also emphasized that the importance of factors
which may mediate between, for example, childhood
adversity and later major depression. Early unprocessed
trauma, such as that of sexual abuse, may lead
to chronic and recurrent major depression mediated
by factors such as self-blame and bodily shame.
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It is believed that we must ascertain whether
the course of a depressive illness is indeed critically
determined by early childhood trauma and that
trauma processing could thus have an important
place in the cognitive therapy of major depression.
The involvement of economic circumstances in major
depression is clear, and researchers must unravel
the complex ramifications of seemingly straightforward
problems such as poverty. For example, there is
evidence that single mothers who try to cope with
a spiral of poverty by finding full-time employment
miss out on the protection against major depression,
which this higher socioeconomic status should
bring. Negative life-events may become more common
and the mother's reactions to them can be detrimental--a
mother whose child becomes delinquent may well
feels guilty at the possibility that her job made
her neglect her child. Here again we see life-events
and cognitions conspiring together.
Poverty and deprivation worsen inter-personal
relationships, but it is contended that it is
essentially problems with the latter that cause
major depression. What mechanisms underlie this
at the neurochemical level? As mentioned, we have
some empirical clues from the drugs effective
at treating major depression, but our understanding
of their mode of action remains fairly sketchy.
Imaging studies, which allow identification of
sites of action of labeled compounds with known
receptor targets, compared in depressed and non-depressed
subjects and during mood manipulation can help
us to identify involved brain regions and what
the drugs may be doing to modify them.
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Major Depression Across The Lifespan And Between
The Sexes: Clues To Understanding The Etiology?
Given that the interplay of genetic and social
factors conspires to cause major depression by
determining our experiences and behavior, and
the degree of support available to us, can we
understand age and gender differences? The former
are perhaps easier to consider--penetrance of
genetic factors at different stages in the lifespan
are not uncommon in disease, and social and environmental
status clearly change with age.
As we grow older, the influence of heritable factors
in the etiology of major depression appears to
increase for a time, taking over from the apparently
predominating factor of shared environment in
children, and then decreases again in the elderly.
The twin studies which have shed such light on
the relative importance of genetic and environmental
factors become harder to conduct as people age,
confounding our unraveling of the issues.
Evidence for biochemical and structural alterations
in the brain associated with the ageing process,
and for age-related physical and social changes
has been presented. Together these may be responsible
for maintaining the prevalence of major depression,
despite the decrease in influence of heritable
factors. We need to refine our instruments for
assessing major depression in the elderly, recognize
that it is not an inevitable consequence of the
ageing process, and acknowledge that intervention
can be successful and must be made available.
Resolution of etiological subtypes of old age
major depression is an important aim and will
in turn have implications for therapeutic approaches.
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Cultural variations and societal beliefs are likely
to be important and must be further investigated.
The honor of looking after elderly relatives in
India has made it virtually impossible to develop
measures for burden of care for younger relatives
and variations in the onset of depressive disorders
may reflect culturally different views and treatment
of older people. The 'Eurodep' survey (a BIOMED2
project bringing together old-age major depression
researchers, coordinated by Professor John Copeland
in Liverpool, UK) is using GMS internationally
in a way that should shed light on this. Strong
cultural determinants of major depression may
emerge from such studies, which in turn will help
to clarify the extent to which the biological
correlates of old age--the neurochemical, neuroendocrinological
and physical changes--are important etiological
factors.
Major depression in children has its puzzles too.
Social and environmental factors will be unique
to this period of life and are clearly important,
but again we have some more apparently biological
determinants: the striking ineffectiveness of
antidepressants in children highlights the possibility
of developmental factors related to major depression
and its nature at different ages. Other examples
of age-related drug effects-perhaps the most striking
that of methylphenidate in hyperactivity--suggest
that this is not untenable. There are interesting
leads to follow up on the cognitive side too---the
efficacy of cognitive behavior therapy (CBT) in
major depression in children is marked, but curiously,
the cognitions, which this targets often, remain
apparently untouched by the therapy (Spence, 1994).
Taken together, the inefficacy of antidepressants
and efficacy of CBT suggest that we are not simply
dealing with a difference in terminology about
feelings in children. Intervention at school age--which
could help prevent the carrying through of both
predisposing behaviors and interpretations, and
major depression itself, into adult life, is clearly
important.
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What of the gender difference? Twice as many women
as men suffer from major depression during child-beating
years, and we need to determine what underlies
this and to consider it in all our attempts to
understand the etiology of major depression as
a whole. The causes of major depression must explain
the gender difference but not all the causes may
be involved, indeed a single one may be sufficient
explanation.
Perhaps counter-intuitively, social causes of
this imbalance are favored over biological ones.
Nazroo and his colleagues (1996) report that the
discrepancy pertains even in cases where male/female
couples were selected for study because they shared
a significant life experience predicted to impinge
on both of them and to cause major depression.
However, the events most obviously responsible
for the gender difference in causing major depression
were entirely those concerning reproduction, children
and housing. There was no gender difference at
all when other types of events were looked at,
and most strikingly, the difference disappeared--the
incidence of male major depression in-creased--in
a small sub-group where men took a stronger role
in more traditionally female activities.
The gender difference may be determined very strongly
by role commitments, although differences in commitments
themselves then demand explanation. It will be
interesting to see what happens as more men became
active partners, if indeed they do, and whether,
as this study suggests, the overall burden of
major depression will increase. Again though,
unraveling cause and effect will become important:
perhaps men enter this group because of difficulties,
which could themselves increase a propensity to
major depression.
Animal Models: Can We Trust Them?
The overall applicability of animal models of
major depression in clarifying both biological
and environmental etiologies is generally accepted,
and their continued use is likely. There needs
to be an awareness of the ways in which the neurochemistry
of animals and man may differ, but this may not
be such a great problem. We have seen how responses
to both psychological and chemical anti-depressant
interventions differ at different ages in humans.
By the same token, despite variation, animals
remain good general experimental models for some
purposes.
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It must be borne in mind, however, that the animal
models often seek to test out single etiological
theories in the simplest possible ways. The need
to consider the interplay between genetic and
environmental theories of etiology in parallel
exceeds the capacity of animal models.
Evolutionary Theories: Does Major Depression Help
Us?
Why is major depression so common? Affecting perhaps
as many as 10% of the population at any time,
it has the hallmarks of a beneficial trait which
has survived the processes of natural selection.
Is it possible to view major depression as an
adaptation to survival--perhaps prompting people
to adopt passive responses to distressing life
events and thereby maintaining, for example, relative
equanimity within tight social groups?
Plorain is cautious about the value of focusing
on the admittedly intriguing evolutionary perspective,
which he fears may mislead more than it helps.
Genetic selection tends to aim for a mid-point--against
extremes and towards characteristics, which will
be beneficial in the widest range of circumstances.
If this is the case, investigating theories of
adaptive advantage may not be very rewarding.
Indeed, the hugely distressing and disruptive
effects of major depression hardly support arguments
that it is advantageous to the sufferer, so we
must reconcile ourselves to the possibility that
it is either an adaptive process gone much awry,
or that any adaptive advantage it may once have
had is now lost.
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