This paper will consist of two parts. In the first, further support is given to the proposal that offspring sex ratios (proportions male) may usefully be regarded as indicators of public health. In the second, it is shown that sex ratios may help in the identification of the causes and effects of several pathologies that seriously impinge on public health viz. autism, testicular cancer, hepatitis B and toxoplasmosis.
Humans infected with the parasite Toxoplasma gondii display a wide variety of abnormal behaviours, from suicide and depression to stuttering. These behaviours have been seen as so serious as to constitute a public health problem. It is not clear to what extent the parasite is a cause of, or merely a marker for, these behaviours, but there is evidence for both. Some of these behaviours are associated with changes in steroid hormones, that is, estrogen in women and testosterone in men. It is suggested here that these endocrine-related states of infected people may be better understood by studying their offspring sex ratios.
I have hypothesized that mammalian offspring sex ratios (proportions male at birth) are partially controlled by the hormone levels of both parents around the time of conception. Recently data have been published (privately) which impugn suggestions of mine (based on that hypothesis) relating to the offspring sex ratios of people who are carriers of hepatitis B virus; and (publicly) to hormone profiles of women who are infected with the protozoan parasite Toxoplasma gondii. Here these data are reviewed in the light of data on offspring sex ratios of people infected with hepatitis C, and cytomegalovirus and T gondii; and of mice with T gondii and the trichostrongyline nematode Heligmosomoides polygyrus. Three proposals are made viz: I. Women infected with T gondii may have high oestrogen levels. This would potentially explain reports of their high offspring sex ratios, long gestations and (perhaps) behavioural traits. 2. Some of these infective organisms may 'prefer' a particular endocrine environment in their host (in the sense that it facilitates replication or transmission or both). 3. Some of these organisms apparently cause changes in that endocrine environment as a consequence of their presence. If both the latter two proposals were correct, it could explain recent puzzling data on the offspring sex ratios of hepatitis B carriers. And if this solution turns out to be correct, it would suggest new endocrine means of combating hepatitis B infection.