Mood Disorders and Suicide 225
are experiencing a manic episode than it is in a control group of people who are not
manic (Altshuler et al., 2005). The more reactive the amygdala, the more readily it
triggers strong emotional reactions—and hence the fact that it is especially active
during a manic episode makes sense.
Neural Communication
As we’ve discussed earlier in this chapter and in Chapter 2, imbalances in the levels
of certain chemicals in the brain can contribute to psychological disorders. There’s
reason to believe that serotonin (Goodwin & Jamison, 1990) and norepinephrine
play a role in bipolar disorders. For example, treatment with lithium (discussed
shortly) not only lowers norepinephrine levels, but also reduces the symptoms of
a bipolar disorder (Rosenbaum et al., 2005). As noted in Chapter 2, serotonin is
an inhibitory neurotransmitter, and low levels of it are associated with depression
(Mundo et al., 2000). However, we’ve also emphasized that glitches in neural com-
munication contribute to psychological disorders in complex ways; the problem
rarely (if ever) is limited to an imbalance of a single substance, but rather typically
involves complex interactions among substances. In fact, researchers have also re-
ported that the left frontal lobes of patients with mania produce too much of the
excitatory neurotransmitter glutamate (Michael et al., 2003), so at least three
neurotransmitters—serotonin, norepinephrine, and glutamate—are involved in
bipolar disorders. Thus, changing the level of any one of these substances above is
not likely to be suffi cient.
Genetics
One day, Jamison and another scientist who does research on mood disorders
sat down together, and Jamison drew her family tree: circles represented women,
squares represented men, and darkened shapes noted family members who had a
mood disorder. Here is what Jamison remembers about this:
I was amazed at how many of my squares and circles were darkened, or darkened with
a question mark placed underneath (I knew, for instance, that my great-uncle had spent
virtually all of his adult life in an asylum, but I didn’t know what his diagnosis had
been). Manic-depressive illness occurred repeatedly, throughout the three generations
I had knowledge of, on my father’s side of the family; asterisks, representing suicide at-
tempts, showed up like a starfi eld. My mother’s side of the family, in comparison, was
squeaky clean.
(p. 189 )Jamison’s discovery of her paternal relatives’ mood disorders mirrors the results
of research on the frequency of mood disorders in families: Twin and adoption
studies suggest that genes infl uence who will develop bipolar disorders. If one
monozygotic twin has a bipolar disorder, the co-twin has a 40–70% chance of
developing the disorder; if one dizygotic twin has the disorder, the co-twin has
only about a 5% chance of developing the disorder, which is still over twice the
prevalence in the population in general (Fridman et al., 2003; Kieseppä et al.,
2004; McGuffi n et al., 2003). In general, if you have a fi rst-degree relative who
has bipolar disorder, you have a 4–24% risk of developing the disorder (American
Psychiatric Association, 2000).
Depressive disorders and bipolar disorders—even though they now are con-sidered distinct disorders—may be different manifestations of the same genetic
vulnerability (Akiskal, 1996; Angst, 1998). When a dizygotic twin has a bipolar
disorder, the other twin has an 80% chance of developing any mood disorder
(MDD, dysthymia, a bipolar disorder, or cyclothymia; Karkowski & Kendler,
1997; McGuffi n et al., 2003; Vehmanen, Kaprio, & Loennqvist, 1995). Even so,
researchers do not know how specifi c genes contribute to an inherited vulner-
ability for mood disorders. But they do know that genes alone cannot account for
the development of such disorders—and thus, we next will examine the role that
psychological factors play in bipolar disorders.