Explanations and Treatments – Uni-polar depression
BIOLOGICAL
Genetic Factors – family pedigree studies and twin studies give a clear indication of heritability. Family pedigree = select people with UP disorder, examine their
relatives to see whether depression afflicts other family members – Researchers have found that as many as 20% of those relatives are depressed, compared with less
than 10% of the general pop. (Harrington et al, 1993). Twin studies – looked at 200pairs of twins, when a MZ had UP-there was a 46% concordance rate. When a DZ had
UP-there was a 20% concordance rate (McGuffin et al, 1996).
Biochemical Factors - low activity of NT’s norepinephrine and serotonin (5HT) linked to UP. Evidence – Ayd, 1956 found that certain meds for high bp often caused
depression – some of these meds lowered norepinephrine activity whilst others lowered 5HT activity; the 1 st truly effective antidepressant relieved depression by
increasing either norepinephrine or 5HT – belief depression resulted from low nor or 5HT = too simple, now believe the interaction between these NTs (or indeed with
other NTs) = UP.
Hormones – Researchers also learned the body’s endocrine system may play a role- endocrine glands throughout body release hormones- people with UP have been
PSYCHODYNAMIC
found to have abnormal levels of cortisol (1 of the hormones released by adrenal glands during stress – obvious link as depression often triggered by stress. Also melatonin
(aka the Dracula hormone)-linked to depression (SADS) –may secrete more melatonin during winter months. Prevalence of women among the depressed poss explained by
hormones (esp estrogen and progesterone). PMS, post-partum depression (within a few days of giving birth, drop in estrogen and progesterone) and menopausal depression
AO2 – research indicates strong biological link, can explain most types of depression.
- have produced much enthusiasm, but research in this area has limitations. Some of it has relied on studies that create depression-like symptoms in lab animals
– cant be sure these symptoms reflect the human disorder. Similarly, until recently, technology was limited, and biological studies of human depression had to
measure brain activity indirectly = investigators couldn’t be certain of the biological events that were occurring in the brain. Certain studies using newer
technology, such as PET and MRI scans, are helping to clear up such uncertainties about brain activity.
Freud and his student Abraham noted the similarity between depressed and grief in people who lose loved ones; constant weeping, loss of appetite, diff sleeping, loss of
pleasure in life, and general withdrawal. According to theorists, a series of unconscious processes is set in motion when a loved one dies. Unable to accept the loss,
mourners at 1st regress to the oral stage (the period of total dependency when infants can’t separate themselves from their parents. By regressing to this stage, the
mourners merge their own identity with that of the person they have lost, and so symbolically regain the lost person. They direct all their feelings for the loved one,
including sadness and anger, towards themselves. For most mourners = temporary, for some, grief worsens over time-they feel empty, continue to avoid r’ships, and their
sense of loss increases – they become depressed. Freud & Abraham believed that 2 kinds of people are particularly likely to become depressed in the face of loss: those
whose parents failed to meet their needs during the oral stage and those whose parents gratified those needs excessively. People of either kind may devote their lives to
others, desperately in search of love and approval (Bemporad, 1992). They feel a greater sense of loss when a loved one dies.
But, many people become depressed without losing a loved one – Freud proposed the concept of symbolic or imagined loss-in which persons unconsciously equate other
kinds of events with the loss of a loved one(a college student may experience the failure of a test as the loss of her parents, believing that they love her only when she
excels academically).
AO2 – many theorists have parted company with this theory of depression but it continues to influence current psychodynamic thinking E.g. object relations
theorists (who emphasise relationships) propose that depression results when peoples r’ships leave them feeling unsafe & insecure. People whose parents pushed
them toward either excessive dependence or excessive self-reliance are more likely to become depressed when they later lose important r’ships
-Studies have offered general support for the idea that losses suffered early in life may set the stage for later depression – when a depression scale was
administered to 1,250 medical patients during visits to their family physicians, the patients whose fathers had died during their childhood scored higher on
depression (Barnes & Prosen, 1985)
-Support for idea that people whose childhood needs weren’t properly met become depressed – in some studies, depressed subjects have filled out a scale called
‘the Parental Bonding Instrument’ (which indicates how much care and protection people felt they received as a child)-many identified their parents’ child-rearing
style as ‘affectionless control’, consisting of a mixture of low care and high protection (Shah & Waller, 2000)
-Although the findings of such studies indicate that losses and inadequate parenting sometimes relate to depression, they don’t establish that such factors are
typically responsible for the disorder – in fact, its estimated that less than 10% of all people who experience early losses become depressed.
-many findings are inconsistent. Though some studies find evidence of a r’ship between childhood loss and later depression, others don’t
-Some features of the psychodynamic explanation are impossible to test–because symbolic loss is said to operate at the unconscious level,its difficult to test
whether it is occurring.
COGNITIVE
Recently updated Learned helplessness theory of behaviourists – when people view events as beyond their control, they ask themselves why this is so. If they attribute
their present lack of control to some internal cause that is both global and stable (I am inadequate at everything and I always will be), they may feel helpless to prevent
future –ve outcomes and they may experience depression. If they make other attributions (specific or unstable or external), this reaction is unlikely. 100s of studies have
supported the r’ship between styles of attribution, helplessness, and depression – In one depressed persons were asked to fill out an Attributional Style Questionnaire
both before and after successful therapy. Before therapy, their depression was accompanied by the internal/global/stable pattern of attribution. At the end of therapy
and again 1yr later, their depression was improved and their attributional styles were less internal/global/stable (Seligman, 1988).
Refined again – attributions are likely to cause depression, only when they further produce a sense of hopelessness in an individual. This factor enables clinicians to
predict depression with still greater precision.
AO2 –theory has been v influential, it still has imperfections:1) much learned helplessness research relies on animal subjects – impossible to know whether
animal’s symptoms reflect clinical depression in humans.2) attributional feature of the theory raises difficult qus – what about the dogs and rats who learned
helplessness? Can animals make attributions, even implicitly?
Negative thinking – Beck believes that –ve thinking lies at the heart of depression. According to Beck, maladaptive attitudes, a cognitive triad, errors in thinking and
automatic thoughts combine to produce clinical disorder. Beck believes that some people develop maladaptive attitudes as children (‘my general worth is tied to every task
I perform etc). These result from their own experiences, their family r’ships, and the judgments of the people around them. Many failures are inevitable in a full, active
life, so such attitudes are inaccurate and set the stage for all kinds of –ve thoughts and reactions. Beck suggests that later in these people’s lives, upsetting situations
may trigger an extended round of –ve thinking. The thinking typically takes 3 forms called the cognitive triad: the individual repeatedly interpret 1) their experiences, 2)
themselves, and 3) their futures in negative ways that lead them to feel depressed. According to Beck, depressed people also make errors in their thinking. In one
common error of logic, they draw arbitrary inferences (-ve conclusions based on little evidence) Depressed people often minimise positive experiences or magnify negative
ones (eg student receives a grade A on a difficult test-concludes that the grade is due to professors generosity, rather than his own ability). Finally, depressed people
experience automatic thoughts, a steady train of unpleasant thoughts that keep suggesting to them that thy inadequate and that their situation is hopeless – these
thoughts are labelled ‘automatic’ as they seem to just happen, as if by reflex.
Evidence - Many studies have supported Beck’s explanation. Several of them confirm that depressed people hold maladaptive attitudes, and the more of these
maladaptive attitudes they hold, the more depressed they tend to be (Whisman & McGarvey, 1995). Other research has found the cognitive triad at work in depressed
people (Ridout et al, 2003). In various studies, depressed people seem to recall unpleasant experiences more readily than +ve ones, rate their performance on lab tests as
lower and select pessimistic statements in storytelling tasks. Beck’s claims about errors in logic has received support – in one study, female subjects –some depressed,
some not-were asked to read and interpret paragraphs about women in difficult situations. Depressed made more errors in logic (such as arbitrary interference-in their
interpretations (Hammen & Krantz, 1976). Finally, research has supported the idea of automatic thoughts. In several studies, nondepressed subjects who are tricked into
reading –ve automatic-thought-like-statements about themselves become increasingly depressed (Bates et al, 1975). In a related line of study, its been found that people
who generally make ruminative responses during their depressed moods (repeatedly dwell on their mood without acting to change it)experience dejection longer and are
more likely to develop clinical depression later in life (Nolen-Hoeksema, 2002; 1998; 1995).
AO2 - This body of research shows that negative thinking is indeed linked to depression, but it fails to show that such patterns of thought are the cause and
core of UP. It could be that a central mood problem leads to thinking difficulties that take a further toll on mood, behaviour and physiology.
BEHAVIOURAL
Lewinsohn suggested that the positive rewards in life dwindle for some persons, leading them to perform fewer and fewer constructive behaviours. (The rewards of
campus life, for example, disappear when a young woman graduates from college and takes a job). Although many such people manage to fill their lives with other forms of
gratification, some become particularly disheartened. The positive features of their lives decrease even more, and the decline in rewards leads them to perform still
fewer constructive behaviours. In this manner, the individuals spiral towards depression.
In a series of studies, Lewinsohn et al (1979) found that the number of rewards people receive in life is indeed related to the presence or absence of depression. Not only
did depressed subjects in his studies report fewer positive rewards than non-depressed subjects, but when their rewards began to increase, their mood improved as well.
Similarly, more recent investigations have found a strong r’ship between positive life events and feelings of life satisfaction and happiness (Lui, 1999). Lewinsohn and other
behaviourists further proposed that social rewards are particularly important in the downwards spiral of depression.
Learned helplessness – Seligman developed this theory of depression since mid 60’s. It holds that people become depressed when they think
1) That they no longer have control over the reinforcements in their lives and 2) that they themselves are responsible for this helpless state. Experiment – in lab,
strapped dogs into an apparatus called a hammock, in which they received shocks periodically no matter what they would do. The next day each dog was placed in a shuttle
box (a box divided in half by a barrier over which the do could jump to reach the other side). Seligman applied shocks to the dogs in the box, expecting that hey, like
other dogs in this situation, would soon learn to escape by jumping over the barrier. However, most of these dogs failed to learn anything in the shuttle box. After a flurry
of activity, they simply ‘lay down and quietly whined’ and accepted the shock. Seligman decided that while receiving inescapable shocks in the hammock, the dogs learned
they had no control over unpleasant events in their lives = they were helpless to change unpleasant situations = when put in the shuttle box (where they could in face
control their fate) they continued to believe that they were generally helpless. Seligman noted that the effects of learned helplessness greatly resemble the symptoms of
human depression.
Numerous human and animal studies, subjects who undergo helplessness training have displayed reactions similar to depressive symptoms. E.g. human subjects who are
exposed to uncontrollable –ve events, they later score higher than controls on a depressive mood survey (Miller & Seligman, 1975). Similarly, helpless-trained animals lose
interest in sexual and social activities (Lindner, 1968). Finally, uncontrollable –ve events results in lower norepinephrine and 5HT activity in rats (Wu et al 1999) – reflects
NT activity found in brains of people with UP.
AO2 - This claim has been supported by research showing that depressed persons experience fewer social rewards than non-depressed persons and that as their
mood improves, their social rewards increase.
– Although depressed people are sometimes the victims of circumstances, it may also be that their dark mood and flat behaviours help produce a decline in social
rewards (Joiner, 2002; Coyne, 2001)
AO2 –learned helplessness theory has been v influential, it still has imperfections:1) much learned helplessness research relies on animal subjects – impossible to
know whether animal’s symptoms reflect clinical depression in humans.2) attributional feature of the theory raises difficult qus – what about the dogs and rats
who learned helplessness? Can animals make attributions, even implicitly?