Twin studies provide more convincing evidence. Price looked at seven twin studies and found much higher concordance rates for manic-depressives in MZ twins than DZ ones. The most revealing factor was that the concordance rate for MZ twins raised together and raised the apart was almost the same.
Adoption studies have also provided genetic evidence. In a study by Cadoret 126 adopted children, 8 of which had a manic-depressive biological parent, but health adopted parents were observed. Three out of the eight later developed a major affective disorder, compared to only eight of the remaining 118 children.
Whilst genetic evidence for manic-depression is strong no study has shown a 100% concordance level, indicating that it might be a predisposing factor, and there might be other precipitating causes.
One of these causes could be the neurological process of the brain. There is evidence that depression has been linked to a disturbance of amine metabolism. Three specific neurotransmitters have been linked: noradrenaline, serotonin and dopamine.
Post-mortems of depressed patients have however not revealed an abnormality of noradrenaline concentration. It has not been ascertained whether depression causes fluctuation of serotonin or vica versa. And the replica drug L-dopa has no specific anti-depressant effect on people with low levels of dopamine.
High levels of hormone cortisol in depressive patients have been found and techniques known to suppress cortisol secretion have been successful. However this may be due t the stress of being ill, because increased cortisol secretion is a function of the stress response.
However, one of the problems with trying to ascertain hormonal links with depression is that there are invariably social changes occurring at the same time. A possible explanation is that hormonal changes interact with a genetic predisposition to depression, together with excessive tiredness and a domestic stressful situation.