Suchergebnisse

SummaryGarenne (2009) presented data on the sex ratio of a present birth by the numbers of previous brothers and sisters. In unisexual sibships, the probability of a further girl increases with the number of previous girls; and the probability of a further boy increases with the number of previous boys. Garenne noted that there is an asymmetry in that the effect is stronger with regard to girls than boys. He was uncertain of the cause of this. Here I suggest a potential solution to this problem. Garenne also seems to imply that parental reproductive stopping rules cause heterogeneity of sex ratios. I suggest that they may reveal it – but do not cause it. Moreover, I suggest that the effects of such stopping rules may be counter-intuitive.

SummaryIn a recent paper in this Journal, I offered hypotheses on the offspring sex ratios of women infected with the parasite Toxoplasma gondii, and on the offspring sex ratios of people who are carriers of hepatitis B virus (HBV) (James, 2008). Subsequent research suggests that these hypotheses need amending. A detailed account of the amendments is given elsewhere in a specialized journal (James, 2010a). Here they are summarized.

SummaryThis note categorizes the evidence for the hypothesis that mammalian offspring sex ratios (proportions male) are causally related to the hormone levels of both parents around the time of conception. Most of the evidence may be acknowledged to be correlational and observational. As such it might be suspected of having been selected; or of having been subject to other forms of bias or confounding; or, at any rate, of being inadequate as a firm basis for causal inference. However, there are other types of evidence that are not vulnerable to these types of criticism. These are from the following sources: (1) previously neglected data from Nazi Germany and Soviet Russia; (2) fulfilled predictions; (3) genetics; and (4) a network of logically (mathematically) related propositions, for some of which there is overwhelming empirical evidence. It is suggested that this variety of evidence confers greater overall credibility on the hypothesis than would be the case if all the evidence were of the same observational/correlational status. This observational/correlational evidence is tabulated to illustrate its consistency.

AbstractFellman and Eriksson (2010) cited my suggestion that the sex ratio (proportion male) of monozygotic (MZ) twins is lower than that of dizygotic (DZ) twins (James 1975). Here I offer elaborations on and potential explanations for this.

SummaryThe human sex ratio SR (proportion male) at birth has been reported to vary with many variables. The explanation of this variation is not established, but I have hypothesized that it is partially caused by the hormonal concentrations of both parents around the time of conception. The present note suggests how this hypothesis might accommodate recent sex ratio findings relating to 'psychosexual restriction', female genital cutting, sexes of prior sibs, finger length ratios, the autism spectrum disorder, parental occupation and maternal eating disorders. Tests of such suggestions are offered, and it is hypothesized that: (a) in women, Manning'sR(the ratio of the lengths of the 2nd and 4th digits) is positively correlated with offspring sex ratio (proportion male); (b) women who have undergone female genital cutting (FGC) have high androgen levels; (c) offspring sex ratio correlates positively with 'masculinity' of parental occupation, the correlation being mediated by testosterone levels. It is noted that the lines of evidence for three hypotheses (James', Manning's and Baron-Cohen's) are mutually supportive.

SummaryDuring the past year, data have been published on the offspring sex ratios of people diagnosed with toxoplasmosis, hepatitis B, and pre- and post-menopausal breast cancer. It is shown here how these offspring sex ratios constitute further support for the hypothesis that mammalian (including human) parental hormone concentrations around the time of conception partially control the sexes of the resulting infants. If this interpretation were correct, then hormonal treatments might be considered for some or all of these conditions. It is intended that anyone who has read the present note and my two previous papers (James, 1996, 2004) should be aware of all the data relating to the hypothesis.

AbstractFellman and Eriksson (2008) wondered whether there is variation in the probability that a human birth will be male. Accordingly, they examined the sexes of sibs of index MM, MF, and FF twin pairs. For this purpose they used 19th century German data published by Geissler and Lommatsch. In these data, the sex ratio (proportion male at birth) of sibs of MM pairs was significantly high; while that of MF pairs was normal and that of FF pairs was significantly low (as contrasted with contemporaneous live birth sex ratios). Accordingly Fellman and Eriksson concluded that there is, indeed, variation across couples in the probability of producing a son. Here it will be noted that though there are external grounds supporting this conclusion, there is nevertheless some reason to suspect a form of systematic error in the data cited by these authors. (In Geissler's data, there is very substantial unexplained variation of sex ratio of the sibs preceding index twins by the sex and birth order of the twins). Both these points will be addressed here. In addition, evidence is adduced that (1) the sex ratio of MZ twins is low, and (2) the sex ratios of DZ twins and of their sibs are high. Lastly, appeals are made for (a) data that would test the reliability of the data of Geissler and Lommatsch on the point questioned above, and (b) data on the sex ratios of offspring of twins by the sex and zygosity of the twin parents.

AbstractEvidence continues to accumulate that Weinberg's Differential Rule is a useful approximation. This is in spite of the fact that one of the premises he used in its derivation is almost certainly, to some extent, false. An explanation is offered here.

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.

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-à-vis their exclusively homosexual and heterosexual peers. methods of testing some of these ideas are presented.

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.