Thursday, June 30, 2011

'All hat, no cattle': Orac and I chat again about Darwinian medicine. (#2)

The continuation of my chat with Orac about Darwinian medicine:


In his second response to Coyne, Dr. Egnor next decides to try to use and abuse the concept of proximate versus evolutionary explanations of biology...

I do have concerns.


atherosclerosis appears to arise from a chronic inflammatory response in the endothelium brought about, most likely, by oxidized LDL. Nesse describes the evolutionary tradeoffs thusly:

One way of thinking about atherosclerosisis to view it as the result of an evolved adaptive response that protects against infection but that results in endothelial injury in modern environments.

Perhaps atherosclerosis is an evolved adaptive response. Perhaps not. The evidence we will need to establish that is the proximate evidence-- the actual scientific understanding of the process of atherosclerosis. The inference as to evolutionary cause will necessarily be only as strong as the proximate scientific evidence on which it is based. The understanding of arteriosclerosis needed to treat and prevent the disease will be derived entirely from the proximate science. The 'evolutionary cause' will always be speculation-- stories of variable credibility as to how the disease came to be in history. The value to medical science will be in the proximate science. If evolutionary biologists wish to build careers on untestable speculations about evolutionary history (as they do now), they are free to do so. But they have no claim on medical school resources, which are devoted to actual proximate science, not historical speculation.

Because the consequences of the injury occur late in life, natural selection preserves those systems promoting atherosclerosisin preferenceto those suppressingthem, a clas- sic case of antagonistic pleiotropy.

'Antagonistic pleiotropy' is the recognition that genes can be a mixed bag, and may both help and hurt reproductive fitness. It's not a particularly profound concept, and of course the inference that arteriosclerosis is an example of antagonistic pleiotrophy is not the least bit verified. When (if) it is verified, it will be verified by a mass of proximate scientific evidence, which will constitute the only part of the science valuable to medicine.

Speculation about historical origin of arteriosclerosis belongs in a department of evolutionary biology, where scientists are experienced with speculation, and not in medical schools, where scientists must of necessity understand the pathophysiology of the disease and develop prevention and treatment. As I suggested earlier, if evolutionary biologists have an insight from their speculations that might be of value in actual medical management, there's always e-mail.

I should point out that to my knowledge there has not been a single evolutionary speculation offered for any disease that has provided medical scientists with information valuable for management of the disease that was not already available from the proximate evidence.

Because the costs were probably minimal until the past century, and because they caused no harm until modern times, the genetic variations that increasevulnerability to atherosclerosis are not really "defects," but are instead excellent examples of "genetic quirks" that give rise to untoward effects only when they interact with factors encountered in modern environments.

Despite Orac's affecting enthusiasm, he has not provided any example of the genuine novel contribution of any evolutionary explanation to medical treatment or prevention.

As they say in Texas, all hat, no cattle.

These speculations about the adaptive roots of atherosclerosisgive rise to a specific prediction that individuals who have a genetic predisposition to atheroscle- rosis may be less vulnerable to infection and more susceptible to other inflammatory diseases.

It has long been known that inflammation is related to infection. Inflammation and infection have a very complex relationship. That insight has nothing to do with evolutionary biology. The relationship between inflammation, arteriosclerosis, and resistance to infection can be explored without any inference to evolution. There is an enormous literature on inflammation and infection that doesn't have a damn thing to do with evolution speculations, and it is from that literature that genuine insights into arteriosclerosis and infection will be drawn.

Evolutionary speculation is a narrative gloss, added to the real science post-hoc.

Dr. Egnor, as you might imagine, has a huge problem with this sort of application of evolutionary theory to medicine.

I reiterate: so far, Orac has provided not one clear example of substantial new insight in medicine offered by evolutionary speculation. In medicine, unlike (apparently) evolutionary biology, speculation without application is of no real value and wastes valuable resources. It also annoys people who respect and practice genuine science.

Darwinian Medicine is all hat, no cattle. Stop with the hat. Show us the cattle.

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