The figure above popped up on Twitter to show that even within a socialized medical system, in this case in the United Kingdom and its NHS, ethnic differences in infant mortality remain. But what jumped out at me immediately was the high rate for infants whose mothers were born in Pakistan, as opposed to India and Bangladesh. While the Indians are a relatively middle class community (and a diverse one with that, with a large Punjabi Sikh minority and a secondary migrant populations of East African Indian origin), the Bangladeshis are even poorer than the Pakistanis, in part because they are a predominantly immigrant population (the majority of the Pakistanis in Britain today are not immigrants). In light of other data I’ve seen my immediate thought is that the elevated infant mortality rates among the Pakistani Briton children had to be due to inbreeding because of the more common practice of cousin marriage in this community.
A little searching resulted in finding the original source of figure, Towards an understanding of variations in infant mortality rates between different ethnic groups in England and Wales. In it there is another figure, and it is clear that the elevated infant mortality among Pakistanis is be attributed to congenital defects, which are almost certainly generally of the recessive variety which get exposed due to cousin marriage. Interestingly, and unfortunately, the Pakistani infant mortality rate is also about double the Bangladeshi rate (though the base rate is much higher as these are developing nations). I assume many would superficially attribute this to greater penetration of NGOs and efficacy of development aid in Bangladesh, but it may just be a function of the difference in inbreeding (India’s rate is somewhat higher than Bangladesh’s, but much lower than Pakistan’s).
Of course because in the Pakistani culture cousin marriage has become normative, and somehow related to Islam, it can be difficult for British public health officials to broach the issue. Here’s an article from 2011, ‘Bradford is very inbred’: Muslim outrage as professor warns first-cousin marriages increase risk of birth defects:
Concern about the risks to children from first-cousin marriage has been described as the last great taboo.
Former environment minister Phil Woolas was rebuked by Downing Street in 2008 for saying British Pakistanis are fuelling rates of birth defects by marrying their cousins, with the spokesman for then prime minister Gordon Brown saying the issue was not one for ministers to comment on.
Mohammed Saleem Khan, chief executive of the Bradford Council for Mosques, said: ‘It is important to discuss these issues, but I just do not know of any firm evidence backing up Professor Jones’s claims. I think we need more conclusive studies so we can know for certain if there is any genuine risk.
‘Marriages between cousins is certainly common within south Asia, but it is becoming less so in Britain and also in Bradford. Islam allows you to marry anyone you want, so in many ways Islam promotes diversity.’
I suspect that Mohammed Saleem Khan is ignorant, but saying that there’s no evidence that inbreeding leads to elevated disease risk is classic “denialism.” There’s a whole section on inbreeding in Principles of Population Genetics, the canonical textbook in that field (actually, any text on population genetics has to tackle inbreeding since it is a deviation away from HWE random mating). There’s even a classical equation which predicts the proportion of a recessive disease that is likely to accounted for by the number of offspring of first cousin marriage within the population (the rarer the condition, the more likely inbreeding is the culprit, since rare alleles are more likely to be brought together by marriage between relations than non-relations). So we actually know the outcomes of inbreeding scientifically to a first approximation. Whether we choose to do anything in terms of public health or not (there is a ~5 IQ decrease from expectation for the products of first cousin marriage, or about 1/3 of a standard deviation).
At heart the issue is ultimately of collective social responsibility on a national level vs. individual choice & subcultural norms. Even with aggressive screening for deleterious alleles it seems unlikely that all of the fitness drag can viably be accounted for without massive preimplantation genetic diagnosis projects. A small number of first cousin marriages is something that society can easily handle in the developed world, but when inbreeding is ubiquitous, in can become the focus of public health, as it has in the Gulf countries, which combine high rates of consanginuity with extensive free health care. In other words, subcultural norms rather than individual choice are really the major dynamic to be worried about, since all things equal the preference for marrying your cousin is not that strong for individuals (to my knowledge Tindr does not have a “match cousins” option).
Of course it is easy to point fingers when something is not your cultural norm. In the developed West it is normative for educated middle class individuals to delay childbearing, often into one’s 30s (as I did). But, delaying childbearing does have some negative consequences, as we all know anecdotally and statistically. Submitted for your approval, Older fathers’ children have lower evolutionary fitness across four centuries and in four populations:
Higher paternal age at offspring conception increases de novo genetic mutations (Kong et al., 2012). Based on evolutionary genetic theory we predicted that the offspring of older fathers would be less likely to survive and reproduce, i.e. have lower fitness. In a sibling control study, we find clear support for negative paternal age effects on offspring survival, mating and reproductive success across four large populations with an aggregate N > 1.3 million in main analyses. Compared to a sibling born when the father was 10 years younger, individuals had 4-13% fewer surviving children in the four populations. Three populations were pre-industrial (1670-1850) Western populations and showed a pattern of paternal age effects across the offspring’s lifespan. In 20th-century Sweden, we found no negative paternal age effects on child survival or marriage odds. Effects survived tests for competing explanations, including maternal age and parental loss. To the extent that we succeeded in isolating a mutation-driven effect of paternal age, our results can be understood to show that de novo mutations reduce offspring fitness across populations and time. We can use this understanding to predict the effect of increasingly delayed reproduction on offspring genetic load, mortality and fertility.
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