2017/02/04

Lactase persistence genotype data is currently insufficient to explain lactase persistence phenotype

Lactase persistence genotype data is currently insufficient to explain lactase persistence phenotype


Excerpt: "
Results

We used surface interpolation of Old World lactase persistence genotype and phenotype frequency estimates obtained from all available literature and perform a comparison between predicted and observed trait frequencies in continuous space. By accommodating additional data on sample numbers and known false negative and false positive rates for the various lactase persistence phenotype tests (blood glucose and breath hydrogen), we also apply a Monte Carlo method to estimate the probability that known lactase persistence-associated allele frequencies can explain observed trait frequencies in different regions.

Conclusion

Lactase persistence genotype data is currently insufficient to explain lactase persistence phenotype frequency in much of western and southern Africa, southeastern Europe, the Middle East and parts of central and southern Asia. We suggest that further studies of genetic variation in these regions should reveal additional nucleotide variants that are associated with lactase persistence."
My comment: There are too many gene alleles that have erroneously been associated with the lactase persistence. Here's a few of them:

Evolutionists are not able to decide which one of those genetic changes determine lactase persistence. Or they seem to think that the LP trait has evolved independently, by convergent evolution. This is false science. Modern scientists understand that genes associated with the lactase persistence, especially MCM6 gene, have a clear CpG region:

CpG islands, genomic regions having a lot of cytosine-guanine pairs, are designed to experience methylation. This means that so called methyl groups attach to cytosine bases and by this mechanism the immune system, for example, is able to control gene's activity. If several cytosine bases close to each other are methylated, some cytosines may turn into thymine. And for correct pairing, a guanine base then turns to adenine. This is a designed mechanism, because glycosylase, the repair enzyme bypasses this genetic alteration.

http://www.atdbio.com/content/56/Epigenetics

So, the methylation level of the MCM6 gene is the crucial factor affecting the LP trait. It is not a random mutation. Lactase persistence has not evolved by convergent evolution. Population geneticists are not able to explain why infants are able to digest lactose independently from their genetic variation. This is because microRNAs regulate the lactase production. Gut bacteria also have a significant role within lactase persistence.
Gene sequences don't determine traits. The evolutionary theory and population genetics are the most dangerous heresies in the world. Don't get lost.
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