Tweet
You are ****ing retard, genetic defect is quite rare, but still having a chance of twice as much geting it if you marry relatives proof that cousing marriage is bad. We talk here about genetics you retard the precentage here would be ofcourse really small, its always small, still 2X higher chance a person with normal brains would not risk it.
“Thirty-one per cent of all anomalies in children of Pakistani origin could be attributed to consanguinity” or marriage between first cousins, said the study.
Fynny how you skipped this part. The other anomalies are due to bad health conditions and what not. Still this is quite a big number.
“Thirty-one per cent of all anomalies in children of Pakistani origin could be attributed to consanguinity” or marriage between first cousins, said the study.
Fynny how you skipped this part. The other anomalies are due to bad health conditions and what not. Still this is quite a big number.
But for several reasons, any overall calculation of risk is in fact quite complicated. First, even assuming that the deleterious phenotype arises solely from homozygosity at a single locus, the increased risk depends on the frequency of the allele involved; it is not an immediate consequence of the degree of relatedness between cousins. (Interestingly, despite the British biometricians' harsh criticism of Mendelism, they were the first to describe this dependency in 1911 [17,18].) If a deleterious recessive allele has a frequency q, the ratio of the recessive phenotype in the offspring of first cousins relative to a panmictic population is (1 + 15q)/16q, which means the increase in risk is greater for rarer conditions [19]. For example, if q is 0.01, the ratio is 7.2; if q is 0.001, it is 63.4. Consequently, statistics on the risks associated with cousin marriage are necessarily averages across many traits, and they are likely to be different for different populations, which will often vary in the frequency of particular deleterious alleles. In the Pakistani immigrant population, for example, the quoted high average rate of birth defects may mask a single trait (or small number of traits) at very high frequency, a situation with different medical consequences from one characterized by a larger number of less-frequent disorders.
Second, children of cousin marriages are likely to manifest an increased frequency of birth defects showing polygenic inheritance and interacting with environmental variation. But as the NSGC report notes, calculating the increased frequency of such quantitative traits is not straightforward, and properly controlled studies are lacking. Moreover, socio-economic and other environmental influences will vary among populations, which can easily confound the effects of consanguinity. Inbred populations, including British Pakistanis, are often poor. The mother may be malnourished to begin with, and families may not seek or have access to good prenatal care, which may be unavailable in their native language [20]. Hence it is difficult to separate out genetic from socio-economic and other environmental factors.
Third, as the report also notes, the degree of increased risk depends on the mean coefficient of inbreeding for the population. That is, whether first-cousin marriage is an occasional or regular occurrence in the study population matters, and it is thus inappropriate to extrapolate findings from largely outbred populations with occasional first-cousin marriages to populations with high coefficients of inbreeding and vice-versa. Standard calculations, such as the commonly cited 3% additional risk, examine a pedigree in which the ancestors (usually grandparents) are assumed to be unrelated. In North America, marriages between consanguineal kin are strongly discouraged. But such an assumption is unwarranted in the case of UK Pakistanis, who have emigrated from a country where such marriage is traditional and for whom it is estimated that roughly 55%–59% of marriages continue to be between first cousins [21–23]. Thus, the usual risk estimates are misleading: data from the English West Midlands suggest that British Pakistanis account for only ~4.1% of births, but about 33% of the autosomal recessive metabolic errors recorded at birth [24]. However, for a variety of reasons (including fear that a cousin marriage would result in their being blamed for any birth defects), UK Pakistanis are less likely to use prenatal testing and to terminate pregnancies [20,25]. Thus the population attributable risk of genetic diseases at birth due to inbreeding may be skewed by prenatal elimination of affected fetuses in non-inbred populations. Moreover, the consequences of prolonged inbreeding are not always obvious. The uniting of deleterious recessives by inbreeding may also lead to these alleles being purged from the population. The frequency of such deleterious alleles, then, may be decreased, which (as shown above) means the relative risk is greater, even as the absolute risk decreases.
Second, children of cousin marriages are likely to manifest an increased frequency of birth defects showing polygenic inheritance and interacting with environmental variation. But as the NSGC report notes, calculating the increased frequency of such quantitative traits is not straightforward, and properly controlled studies are lacking. Moreover, socio-economic and other environmental influences will vary among populations, which can easily confound the effects of consanguinity. Inbred populations, including British Pakistanis, are often poor. The mother may be malnourished to begin with, and families may not seek or have access to good prenatal care, which may be unavailable in their native language [20]. Hence it is difficult to separate out genetic from socio-economic and other environmental factors.
Third, as the report also notes, the degree of increased risk depends on the mean coefficient of inbreeding for the population. That is, whether first-cousin marriage is an occasional or regular occurrence in the study population matters, and it is thus inappropriate to extrapolate findings from largely outbred populations with occasional first-cousin marriages to populations with high coefficients of inbreeding and vice-versa. Standard calculations, such as the commonly cited 3% additional risk, examine a pedigree in which the ancestors (usually grandparents) are assumed to be unrelated. In North America, marriages between consanguineal kin are strongly discouraged. But such an assumption is unwarranted in the case of UK Pakistanis, who have emigrated from a country where such marriage is traditional and for whom it is estimated that roughly 55%–59% of marriages continue to be between first cousins [21–23]. Thus, the usual risk estimates are misleading: data from the English West Midlands suggest that British Pakistanis account for only ~4.1% of births, but about 33% of the autosomal recessive metabolic errors recorded at birth [24]. However, for a variety of reasons (including fear that a cousin marriage would result in their being blamed for any birth defects), UK Pakistanis are less likely to use prenatal testing and to terminate pregnancies [20,25]. Thus the population attributable risk of genetic diseases at birth due to inbreeding may be skewed by prenatal elimination of affected fetuses in non-inbred populations. Moreover, the consequences of prolonged inbreeding are not always obvious. The uniting of deleterious recessives by inbreeding may also lead to these alleles being purged from the population. The frequency of such deleterious alleles, then, may be decreased, which (as shown above) means the relative risk is greater, even as the absolute risk decreases.
Comment