By: German Dziebel

German Dziebel — Wed, 17 Jun 2009 02:39:20 +0000

Contrary to the authors’ assertion, 15,000 YBP can’t be the time of human arrival to the Americas because this time frame can’t possibly account for the dramatic lingustic diversity in the Americas (some 140 stocks and isolates). The Ket-Na-Dene connection may well be no less than 10,000 years old, and this is just one family. Alternatively it’s quite possible that mutation rate in the American Indian lineages follows the “old”, “slow” pattern characteristic of small, isolated, Late Pleistocene populations, while the mutation rate in African lineages reflects a larger effective population size in Africa and a rapid population growth in Africa after 15,000 BC , hence the diversity of African genes. Europe and Asia experienced a slightly less dramatic acceleration of demographic evolution than Africa. This is why Asia and Europe show intermediary diversity values between America and Africa. At the same time, the number of language stocks and isolates in Africa is very low (10-15 at best), which attests to the relative recency of African populations. Africa looks old, while America looks young. The reality, I suspect, is the opposite. I hope a joint interdisciplinary effort will some day clear this confusion.

By: Tod

Tod — Sat, 06 Jun 2009 19:53:36 +0000

As I understand it purifying selection is what is relaxed when redundant adaptations, like the pigmentation of cave salamanders, can be dispensed with. There must have been tight stabilizing selection operating in northern Europe that winnowed out the rare mutants who lacked any kind of limit on their vitamin D levels, otherwise people with no defense against ever increasing serum 25(OH)D concentrations would have become the majority. The lack of ill effects in north Europeans who spend their lives at the equator proves purifying selection continued to operate against any maximizing of vitamin D levels for 30,000 years. This is despite the lack of UVB for several months in the winter. "Based on the average rate of decline observed in our subjects, it can be estimated that in individuals for whom summer sun exposure is the principal source of vitamin D, a late summer 25(OH)D level of approximately 127 nmol/liter is needed to avoid levels falling to less than 75 nmol/liter by late winter." Huge amounts of vitamin D are available in the N. European summer to store for the UVB-less months when levels are dependant on the vit' D the body has stored. If after entering northern Europe evolution's purifying selection treated Vitamin D as a substance that it was worth paying a price to limit it is reasonable to assume that higher levels have a very big down side. e.g.- Serum 25-hydroxyvitamin D3 levels are elevated in South Indian patients with ischemic heart disease. here Hypervitaminosis D and premature aging: lessons learned from Fgf23 and Klotho mutant mice "Recent in vivo genetic-manipulation studies have shown increased serum level of vitamin D and altered mineral-ion homeostasis in mice that lack either fibroblast growth factor 23 (Fgf23) or klotho (Kl) genes. These mice develop identical phenotypes consistent with premature aging. Elimination or reduction of vitamin-D activity from Fgf23 and Kl mutant mice, either by dietary restriction or genetic manipulation could rescue premature aging-like features and ectopic calcifications, resulting in prolonged survival of both mutants. Such in vivo experimental studies indicated that excessive vitamin-D activity and altered mineral-ion homeostasis could accelerate the aging process." Vitamin D and aging.

Comments on: An Improved Method On Calibrating The Human Mitochondrial Molecular Clock

By: German Dziebel

By: Tod