DEPRESSION
Hopelessness theory of depression. The most re-
cent reformulation of the learned helplessness
theory, referred to as the ‘‘hopelessness theory’’ of
depression (Abramson, Seligman, and Alloy 1989)
holds that depression is a result of expectations
that highly undesired outcomes will occur and that
one is powerless to change these outcomes. The
hopelessness theory of depression is receiving a
large amount of attention as it has been found to
be particularly useful in predicting the likelihood
of suicide among depressed people.
Biological Theories of Depression. The most
compelling of the recent theories of depression
rely heavily on the biological bases of behavior.
Biological theories assume the cause of depression
lies in some physiological problem, either in the
genes themselves or in the way neurotransmitters
(the chemicals that carry signals between nerve
cells in our brains and around our bodies) are
produced, released, transported, or recognized
(see Honig and van Praag 1997 for a detailed
review of biological theories of depression). Most
of the work focuses on neurotransmitters, espe-
cially a category of chemicals in our bodies called
the monoamines, the main examples of which are
norepinephrine (also called noradrenalin), dopamine,
and serotonin. These chemicals first attracted at-
tention in the 1950s when physicians discovered
that severe depression arose in a subset of people
who were treated for hypertension with a drug
(reserpine) that depleted monoamines. Simulta-
neously, researchers found that a drug that in-
creased the monoamines, this time given to medi-
cate tuberculosis, elevated mood in users who
were depressed. Together these results suggested
that low levels of monoamines in the brain cause
depression. The most important monoamine seems
to be norepinephrine although it is now acknowl-
edged that changes in levels of this neurochemical
do not influence moods in everyone. Neverthe-
less, this biochemical theory has received much
experimental support.
Apart from the neurochemicals, there are also
other physiological differences between depressed
and nondepressed individuals. Hormones are
chemical substances that circulate in the blood
and enable communication between different sys-
tems of the body. Some hormones control the
release of other hormones which then stimulate
growth and help prepare the body to deal with,
and respond to, stress (e.g., adrenocorticotropic
hormone or ACTH). Depressed patients have re-
peatedly been demonstrated to show abnormal
functioning of these hormones (see Nemerof 1998
for a detailed review). Another difference is seen
in one of the major systems of the body that affects
how we respond to stress; the hypothalamic-pitui-
tary-adrenal (HPA) axis. From the late 1960s and
early 1970s, researchers have found increased ac-
tivity in the HPA axis in unmedicated depressed
patients as evidenced by increased levels of stress
markers in bodily fluids. Now a large volume of
studies confirm that substantial numbers of de-
pressed patients display overactivity of the HPA
axis. According to Charles Nemeroff (1998) and
his colleagues, and based on studies on animals, all
these biological factors including genetic inherit-
ance of depression, neurotransmitter and hormo-
nal levels, and HPA axis and related activity, could
relate to early childhood abuse or neglect, al-
though this theory has yet to be fully substantiated.
The antecedents and consequences notwithstand-
ing, it is well accepted that one of the major causes
of depression is based in our biology.
RISK FACTORS
Depression can have many different causes as
indicated by the different theories that have been
formulated to explain it. Accordingly, there are
different factors that indicate a risk for depres-
sion. Some of the main risk factors for long-term
depression include heredity, age, gender, and lack
of social support.
Studies of twins and of families clearly suggest
a strong genetic component to clinical depression,
which increases with genetic closeness. There is a
much greater risk of developing a major depres-
sion if one’s identical twin has had it than if one’s
parent, brother, or sister developed it. Chances
are even less if no close relatives have ever had it.
Furthermore, the younger people are when they
experience depression, the higher the chances
that one of their relatives will also get severely
depressed. Relatives of people who were over forty
when they first had a major depression have little
more than the normal risk for depression.
One of the most clear risk factors is gender.
Women are at least twice as likely to experience