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Have we found the fingerprints of ongoing human evolution?

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From Shawna Williams at The Scientist:

Genetic variants linked to a predisposition for Alzheimer’s disease and heavy smoking are less common in older people than in younger people, researchers report today (September 5) in PLOS Biology. Their study analyzed genetic alleles in two large genomic databases to find those associated with longevity, which they used as a proxy for evolutionary fitness.

“Nobody’s really had the data to measure single-generation shifts in allele frequencies in humans before,” says geneticist Jonathan Pritchard of Stanford University who was not involved in the study. “It’s an important part of understanding how evolution works to go down to the smallest scale of evolutionary change, namely, what’s happening in one generation.” More.

But how would variants that play into diseases that manifest late in life, such as Alzheimer’s, be affected by natural selection? Pickrell says that for men, at least, it might be through fertility. “A genetic variant like the one we see at APOE4 that influences probability of death after, say, 65 or 70—even if a tiny proportion of men still have kids after that age, that is plausibly still affected by natural selection.”

Biophysicist Kirk Durston writes to say,

Unless I’m missing something, this looks like someone is ignoring a more obvious conclusion in favour of a very questionable inference, for the purpose of supporting ongoing human evolution vs genetic entropy.

They found that two harmful alleles were slightly less frequent in senior citizens than in younger members of the population. They suggest that even though 65 to 70 year-old men do not produce many offspring, it could still “plausibly” affect natural selection. Maybe so, but if we are accumulating an average of 90 – 100 mutations/generation, could not genetic entropy be a better explanation as to why younger people have a higher incidence of those two alleles?

Oh, probably, but don’t expect them to bring that up.

Laurent Duret, a geneticist at the Laboratory of Biometrics and Evolutionary Biology in Lyon, France, raises a second possible connection between late-manifesting variants and natural selection: after people have stopped reproducing, they can continue to care for their children and grandchildren, increasing their odds of making it to reproductive age and therefore passing on their grandparents’ alleles.

In any event, what does it mean to say that even though 65- to 70-year-old men do not produce many offspring, it could still “plausibly” affect natural selection?  Are there figures? How were they derived?

Similar item in Nature.

I (O’Leary for News) come from a family where people routinely live ridiculously long lives and can say for sure that seniors tend to be more of a burden to mid-life adults than a help, mainly because they tend to have more and more difficult chronic illnesses as they age, competing with children/grandchildren for attention. They get the easy home jobs because that is what they can still do. It probably wasn’t any different in the Pleistocene era except that the lack of modern medicine meant that the untreatable serious ravages kicked in much earlier. The trouble is, we’d need tens of thousands of skeletons to be sure…

If it’s evolution, maybe we should check the direction…

See also: Devolution: Getting back to the simple life


The Science Fictions series at your fingertips: Human evolution

Dean_from_Ohio at 1, the only way the grandmother hypothesis would make any sense as science, as opposed to grantsman-style speculation: Say we found 50k human skeletons from an approx 1 ky time period (a millennium) and it became apparent that the burial sites of those groups that had more skeletons of older folks also had significantly more skeletons of their apparent descendants. And that those sites with few skeletons of old folks had lots more child skeletons. Now that would be a strong *science* case. Otherwise, it's just face-saving for Darwinism. News

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