Genetic explanations for behavior gained ground in part through
great leaps in our understanding of mood disorders. In the early 1990s,
research at the federal labs of Stephen Suomi and Dee Higley found that
monkeys with low levels of serotonin—now known to be a major player in
human anxiety and depression—were prone to alcoholism, anxiety and
aggression. Around the same time, Klaus-Peter Lesch at the University of
Wuertzburg in Germany identified the serotonin transporter gene, which
produces a protein that ferries serotonin between brain cells. Prozac and
other drugs work by boosting levels of serotonin in the brain, so this
gene seemed like an obvious target in the search for the genetic roots of
depression.
Lesch, who was working on the connection between this gene and
psychiatric disorders, later found that people who had at least one copy
of the short version of this gene were much more likely to have an
anxiety disorder. Short and long versions of genes function much like
synonymous words: Different lengths, or "spellings," generate subtle but
critical differences in biology.
Despite these groundbreaking insights, it quickly became clear that
complex human behaviors couldn't be reduced to pure genetics. Apart from
a few exceptions, scientists couldn't find a gene that directly caused
depression or schizophrenia or any other major mental or mood disorder.
The new research also failed to answer a lot of common-sense questions:
If identical twins are genetically indistinguishable, how could just one
end up schizophrenic or homosexual? And it couldn't address subtler
questions about character and behavior. Why do some people bounce back
from terrible trauma that shatters others? Why are some people ruthlessly
ambitious and others laid-back?
Thanks to misfit monkeys like George, a rhesus macaque living in a
lab in Maryland, researchers have clues to the missing element. In most
ways, George is a typical male monkey. He's covered in sandy fur and has
a rubbery, almost maniacal grin. But a couple of things set George apart.
After he was born, Higley and Suomi's team separated George from his
mother, raising him instead in a nursery with other macaque infants his
own age. George has another strike against him: a short version of the
serotonin transporter gene (monkeys, like people, can have either a short
form or a long form of the gene).
But the most notable thing about George is that he is an alcoholic.
Each day, George and his simian chums have happy hour, with alcohol
freely available in their cage for one hour. Unlike his buddies, George
drinks like the resident barroom lush—he sways and wobbles and can't
walk a straight line.
And his problems go beyond the bottle. He's reluctant to explore
new objects, and he is shy around strangers. He always seems to be on
edge and tends to get aggressive and impulsive quickly. In short, he's a
completely different animal from his cousin Jim, who also has the short
version of the transporter gene but was raised by his biological mom.
Jim's "normal" upbringing seems to have protected him from the gene: This
monkey is laid-back and prefers sugar water to booze.
After studying 36 family-raised monkeys and 79 nursery-raised
animals, the team found that the long version of the gene seems to help
the animals shrug off stress. The short form of the gene, by contrast,
doesn't directly cause alcoholism: Monkeys with the short gene and a
normal family upbringing have few personality problems. But the short
version of the gene definitely puts the animals at a disadvantage when
life gets tough. Raised without the care and support of their mothers,
their predisposition toward anxiety and alcoholism comes to the
fore.
"Maternal nurturing and discipline seem to buffer the effect of the
serotonin gene," says Suomi. "If they don't have good mothers, then the
[troubled] behavior comes out loud and clear."
The implications of this research are tantalizing, since people
also carry long and short versions of the transporter gene. These
variants, unlike those that have been identified as making people
susceptible to diseases like breast cancer or Alzheimer's, are very
common: Among Caucasians, about one-fifth of the population has two
copies of the short gene (everyone gets one copy from Mom and the other
from Dad), and another third have two copies of the long gene. The rest
have one of each. (The gene has not yet been studied in other
populations.) The evidence indicated that this gene was related to
resilience and depression in humans. Why, then, had researchers thus far
failed to find a convincing correlation between the gene and the risk of
depression?
Terrie Moffitt and Avshalom Caspi, a husband-and-wife team of
psychologists at King's College in London, had the insight that
environmental influences might be the missing part of the puzzle. Moffitt
and Caspi turned to a long-term study of almost 900 New Zealanders,
identified these subjects' transporter genes and interviewed the subjects
about traumatic experiences in early adulthood—like a major breakup,
death in the family or serious injury—to see if the difficulties brought
out an underlying genetic tendency toward depression.
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