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Biomedical subjects

William H James

Publications and source records attributed to William H James.

At least 19 recordsLinked to original sources
PubMed2006

Are there preconceptional determinants of mammalian sex? A response to Boklage (2005).

Boklage (2005, Hum Reprod 20,583-587) wrote: 'Changes in, or mediated by, the epigenetic environment of embryogenesis provide the most plausible prospects for causes of changes in secondary sex ratio'. Without impugning this notion, I suggest here that other causes of variation in secondary sex ratio antedate fertilization or, in other words, that there are circumstances under which unequal numbers of male and female zygotes are formed. It will be documented here that this suggestion has repeatedly been made on the basis of data on many mammalian species (golden hamster, sheep, mouse, white-tailed deer, American bison, springbok, domestic cattle and Barbary macaque). It may be acknowledged that the causes of this hypothesized preconceptional variation are not established. I have suggested one (parental hormones around the time of conception). But the truth of that hypothesis is not germane to the thrust of the present argument--which is to document the strong suspicions that such preconceptional determinants do, indeed, exist. Efforts should be made to confirm or discredit these suspicions.

Animals↗
PubMed2006

Offspring sex ratios at birth as markers of paternal endocrine disruption.

There is good evidence that paternal (and maternal) hormone levels at the time of conception are associated with offspring sex ratios (proportions male) at birth. The mechanisms underlying this association (pre- or postzygotic) are not of primary relevance here. When people are exposed to endocrine-disrupting agents, these agents may have different hormonal effects on men and women. So, if endocrine disruption is to be revealed by offspring sex ratios, it is necessary to categorize the sexes of subsequent offspring by the four possible parental mating classes, viz. exposed/unexposed mothers/fathers. In general, substantially altered sex ratios may reveal endocrine disruption, but the tiny (admittedly significant) secular meanderings of national live birth sex ratios across the 20th Century (and before) are not now readily interpretable.

Animals↗
PubMed2005

Two hypotheses on the causes of male homosexuality and paedophilia.

This note considers two hypotheses on the causes of homosexuality and paedophilia in men, viz. the hypotheses of maternal immunity and of postnatal learning. According to the maternal immune hypothesis, there is progressive immunization of some mothers to male-specific antigens by each succeeding male fetus, and there are concomitantly increasing effects of anti-male antibodies on the sexual differentiation of the brain in each succeeding male fetus. An attempt is made to assess the status of this hypothesis within immunology. Knowledge of the properties of anti-male antibodies is meagre and there has been little direct experimentation on them, let alone on their effects on the developing male fetal brain. Moreover until the relevant antigens are identified, it will not be possible to test mothers of male homosexuals or paedophiles for the presence of such antibodies. Yet until this experimentation has been done, it would seem premature to regard the hypothesis as more than a very provisional explanatory tool. The evidence in relation to the postnatal learning hypothesis is quite different. There is an abundance of data suggesting that male homosexuals and paedophiles report having experienced more sexual abuse (however defined) in childhood (CSA) than do heterosexual controls. The question revolves round the interpretation of these data. Many (though not all) of these studies are correlational and thus subject to the usual qualifications concerning such data. However, there are grounds for supposing that some of the reports are veridical, and there is support from a longitudinal study reporting a small but significant increase in paedophilia in adulthood following CSA. To summarize: most boys who experience CSA do not later develop into homosexuals or paedophiles. However, the available evidence suggests that a few do so as a result of the abuse.

Birth Order↗
PubMed2005

Possible constraints on adaptive variation in sex ratio at birth in humans and other primates.

There is general agreement that adaptive variation of sex ratio at birth has not been decisively demonstrated in primates (including human beings). So some workers have questioned whether it actually exists. Others have conjectured that it exists but is subject to as yet unidentified 'constraints' (factors opposing the modifying influences of selection in the phenotype). Meanwhile though most workers have called for research to reveal the proximate causes of sex ratio variation, few (if any) have directed studies toward that end. Here it is argued that hormonal action is responsible both for much adaptive and non-adaptive sex ratio variation, and for constraints on the adaptive variation. My hypothesis proposes that levels of steroid hormones (testosterone and oestrogen) of both parents around the time of conception are positively associated with offspring sex ratio (proportion male at birth) of mammals including man. Testosterone in men and oestrogen in women are also known to be positively associated with the health, attractiveness and fertility of individual human beings. However, high levels of testosterone in women are frequently associated with adverse medical conditions. It is suggested that for these reasons (and contrary to some adaptive theory) some classes of people (particularly women) in suboptimal health ("condition") produce excesses of sons. It seems that gonadal hormones are responsible for adaptive variation; and that maternal adrenal hormones are responsible for maladaptive variation. In evolutionary terms, gonadal hormones precede adrenal hormones.

Adaptation, Physiological↗
PubMed2005

Biological and psychosocial determinants of male and female human sexual orientation.

Some propositions on male and female sexual orientation will be considered. Some of these are established; others are more speculative. The aim is to offer some notes towards a coherent, comprehensive theory of sexual orientation. 1. The distinction between butch and femme lesbians seems real rather than a social construct. 2. High levels of prenatal steroid hormones seem to be causally associated with the sexual orientation of butch lesbians. However it is not established whether the causal process operates prenatally or postnatally (or both). This is so because prenatal hormone levels are thought to correlate positively with postnatal hormone levels. And high postnatal hormone levels may facilitate homosexual behaviour as a consequence of sensation-seeking. 3. Male bisexuals also are interpreted to have been exposed to high prenatal testosterone levels. But (for reasons similar to those outlined above in regard to butch lesbians) it is unclear whether these have a direct prenatal effect on the brain or whether they are precursors of high postnatal testosterone levels, which are associated with male bisexual orientation by promoting sensation-seeking behaviour. 4. Postnatal learning processes seem to be causally involved in the sexual orientation of some femme lesbians and some exclusive male homosexuals. 5. Some homosexual men have genes that predispose to their sexual orientation. 6. The same may apply to some lesbians, but such genes have not, as far as I know, been identified. 7. People (of both sexes) who engage in same-sex sexual behaviour may be classified simultaneously in two ways, viz (1) 'active' vs 'passive' and (2) those who do and those who do not engage (or consider engaging) in sex with members of the opposite sex. Ex hypothesi, some of the 'active' ones initiate some of the 'passive' ones. The active ones are driven more by hormones and the passive ones by psychosocial factors. The active males contain a substantial proportion of self-identified bisexuals; and the active females a substantial proportion of self-identified butches. 8. These two active categories (butch lesbians and male bisexuals) share a number of endocrinological, psychological, morphological and behavioural features vis-a-vis their exclusively homosexual and heterosexual peers. Methods of testing some of these ideas are presented.

Androgens↗
PubMed2004

Hypotheses on how selection for some traits in rodents led to correlated responses in offspring sex ratios.

Selective breeding of some species of rodent has sometimes occasioned unexpected and unexplained correlated changes in sex ratio (proportion male) at birth. Experiments in selective breeding for blood pH, sexual drive, body weight, sexual dimorphism in adult body weight, and for resistance to a dietary toxin have all been reportedly accompanied by this strange phenomenon. Here attempts are made to explain this. The overall form of explanation is that selection for any one of these characters is incidentally accompanied by selection for hormone concentrations which in turn are responsible for the variation in sex ratio. For example one may suppose that selection for sexual drive ipso facto selects for offspring sex ratios because, (1) Androgen levels are partially responsible for sexual drive and (2) Androgen levels are also (weakly) genetically determined and (3) Lastly, ex hypothesi, androgen concentrations are partially responsible for offspring sex ratios. If this line of reasoning were correct, the selection for sex drive would be expected to be accompanied by correlated changes in offspring sex ratio.

Animals↗
PubMed2004

'Over-ripeness ovopathy, sex ratio increase and sex ratio reversal a challenging hypothesis for sex ratio modulation': an alternative interpretation.

It is suggested here that Jongbloet has misinterpreted data on the variation of sex ratio with maternal age, social class, placental dysfunction, twinning and season. When all these matters are considered, it is not clear whether there is any truth in his supposition that male fetuses are generally conceived in suboptimal conditions. Finally, it is suggested that there is a circularity in his presentation of his concept of sex ratio 'reversal'.

Cellular Senescence↗
PubMed2004

Evidence that intrauterine and postnatal androgens affect the development of pyloric stenosis.

BACKGROUND: It is rather well established that the causal antecedents of pyloric stenosis (PS) contain both genetic and environmental factors. However, in spite of substantial quantities of epidemiological data, no widespread environmental causal agent has yet been established. There have been recent extensions of our knowledge of the endocrine consequences of fetal growth restriction and of the endocrine determinants of sex ratio. It seemed worth reviewing the epidemiological data on PS in the light of these new developments to see whether this would provide a basis for a plausible hypothesis on these suspected environmental causes of PS. METHODS AND RESULTS: The search terms "pyloric stenosis" and ("epidemiology" or "risk factors") were combined on the Ovid Medline data base for the years 1966 onwards. The data from the resulting papers were augmented by notes occasioned by almost daily reading at the Library of the Royal Society of Medicine (London) for the past 25 years. (Electronic data retrieval systems do not access incidentally recorded data such as sib sex ratios). CONCLUSIONS: It is hypothesized that high intrauterine and early postnatal androgen levels constitute an environmental cause of PS.

Androgens↗
PubMed2004

The cause(s) of the fraternal birth order effect in male homosexuality.

It has been established that the probability that a man is homosexual is positively related to his number of older brothers, but not older sisters when the brothers are accounted for. This is known as the 'fraternal birth order' effect. In the past, efforts have been made to explain this phenomenon in terms of several alternative biological hypotheses and a psychosocial hypothesis. This note examines how well these hypotheses accommodate the fraternal birth order effect. It is concluded that: (1) the evidence for the hypothesis of maternal immunoreactivity to the male fetus is weak; (2) the evidence for the intrauterine hormone exposure hypothesis is also weak; (3) the evidence for the hypothesis of postnatal learning is stronger. Lastly, there seem likely to be causes common to male homosexuality and paedophilia. They may include sexual (or quasi-sexual) experience in childhood or adolescence.

Birth Order↗
PubMed2004

The sexual orientation of men who were brought up in gay or lesbian households.

Elsewhere the author has suggested that adolescent and adult male homosexual orientation is, in some cases, causally associated with sexual or quasi-sexual experience in childhood (James, 2004). Here it is argued that the available data on men raised by same-sex parents cannot validly be interpreted as supporting or refuting this suggestion.

Adolescent↗