After 32 years of psychiatric practice I, like many of my colleagues, can't help but be alarmed by the dramatic increase in acute and chronic depression in the last three decades. If anything the incidence of clinical depression and tragically suicide have undergone a dramatic upsurge with the recent economic downturn (and associated unemployment, bankruptcies, foreclosures and homelessness).
The most recent epidemiological data, which predates the October 2008 crash, is as follows:
- 5.3% of adults are depressed on any given day
- 12% of women and 7% of men will experience depression in any given year
- 20% of women will experience depression in their lifetime (the prevalence of depression in men is more difficult to estimate as they are less likely to acknowledge feeling depressed or to seek help).
Animal Models of Depression
The other argument against a strictly biochemical cause of clinical depression is the reality that other mammals including primates don't experience genetically based serotonin deficiency. In order to study the effect of new antidepressants in laboratory animals, depressive disordershave to be artificially created because they don't exist in the wild. Given the high prevalence of depression in human beings, coupled with the fact that the human and chimpanzee DNA is 99% identical, one would expect great apes to show some evidence of genetic, biochemically based depression if this were a genuine medical disorder.
Because depression occurs so rarely in lower mammals, pharmaceutical companies artificially create depressive states in lab animals to test new antidepressants on them. Traditionally researchers employ one of six approaches in making animals depressed all of which induce depression by depleting neurotransmitters (mainly serotonin and norepinephrine):
1. Causing the animal massive, unrelenting stress
2. Imposing social isolation by removing it from other animals
3. Premature separation of pups from their mother
4.Deliberate brain injury
5. Administering neurotransmitter depleting drugs, such a reserpine (an old blood pressure medication) and tetrabenazine (used to treat movement disorders)
6.Triggering amphetamine withdrawal (by first "addicting" rats to amphetamine, resulting in profound depression with its withdrawal).
Recently a strain of mice (the Flinders Sensitive Line) has been deliberately inbred and a second strain (HPA Transgenic) genetically engineered to develop depressive symptoms for use in testing new antidepressants.
However most animal testing of new antidepressants is based on the "learned helplessness" model and involves submitting mice and rats to traumatic stress levels of stress. In the most common experiment, mice are dropped into a large vat of water and the researcher times how long they keep swimming before they give up. After taking a dose of Prozac, they swim longer before giving up.