There are a number of theories as to what mediates the genetic risk. Suggestions include:
• other biological changes (such as genetic polymorphisms)
• the response to stress
Mood Disorders: A Handbook ofScience and Practice. Edited by M. Power. © 2004 John Wiley & Sons, Ltd. ISBN 0-470-84390-X.
• the tendency to have life events
• other factors and/or behaviours within the syndrome.
Several attempts have been made to look for polymorphic variation in gene alleles that might be linked to depression (Cravchik & Goldman, 2000). Thus, affective disorder has been associated with polymorphisms of serotonin (5-HT) receptor subtypes, of tryptophan hydroxylase (the enzyme controlling 5-HT synthesis), and of the 5-HT transporter. Some allele pairs have a functional significance, such as a differential rate of reuptake of serotonin. They could therefore provide a link between the genetics of depression and the 5-HT hypothesis of depression (see below).
There is little evidence to suggest that a higher personal genetic loading leaves an individual needing less environmental stress to become depressed. Instead, it is the tendency to become depressed in response to life events that is inherited (Hirschfield & Weissman, 2002). Moreover, recent family and twin studies show a clear genetic component of life events themselves (Kendler & Karkowski Shuman, 1997). Thus, both the tendency to suffer adversity and to respond to it by becoming depressed have genetic components.
One interesting question relates to the observation that depression tends to be recurrent, and that there is a tendency for each recurrence to be less dependent on precipitating stress, a process likened to kindling (see below). Kendler and colleagues investigated the genetic contribution to this phenomenon in their large twin-pair sample; they found that genetic risk tended to place people in a 'pre-kindled' state rather than speeding up the process of kindling (Kendler et al., 2001).
Future genetic research may also integrate elements of post-transcriptional changes and modifications, the so-called proteomics—much of the expression of genetic risk appears to be dependent on what happens during this post-transcriptional period.
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