Evolutionary medicine goes (more) mainstream

[Oolon Colluphid]

Science Vol. 324. no. 5924, pp. 162 - 163 10 April 2009

News of the Week
EVOLUTIONARY MEDICINE: Darwin Applies to Medical School

Elizabeth Pennisi

When George Williams and Randolph Nesse made their first pitches for Darwinian medicine in the early 1990s, they turned some heads, but not the right ones. Reviving and building on European traditions that melded medicine and evolutionary biology, the duo argued that diseases could be best understood from an evolutionary perspective. Their first meeting on the subject in 1996 attracted 60 enthusiasts but few practicing clinicians, probably because physicians couldn't envision practical applications. "The folks who were excited about it weren't in a position to do anything about it," recalls anthropologist Peter Ellison of Harvard University. Although a better understanding of the evolution of drug resistance has helped shape the use of antibiotics, when it comes to evolution, "medical schools are mostly oblivious," says Nesse, a psychiatrist at the University of Michigan, Ann Arbor.

But times may be changing. Last week, a similar meeting* in Washington, D.C., attracted dozens of physicians, including the dean of Harvard Medical School and the president of the Institute of Medicine (IOM).

[...]

During her talk, Barnes presented several examples that suggest that how humans evolved to cope with past parasitic diseases has predisposed some of us to contemporary health problems. The malaria parasite Plasmodium vivax, for instance, depends on a surface protein called Duffy to gain entry into human red blood cells. In certain malaria-endemic areas, a mutation in the gene for Duffy, called DARC, leads to the loss of this surface protein, and malaria can't gain a foothold. But Duffy also acts as a sponge to keep immune system messengers in check; otherwise excess immunoglobulin E (IgE), which underlies allergic asthma and other allergic reactions, may be produced. Barnes and her colleagues have found that asthma is associated with the defective Duffy gene in populations in Brazil, Columbia, and the Caribbean whose recent African ancestors lived where malaria was endemic.

Similarly, others have found asthma associated with high IgE in areas such as Egypt where schistosomiasis is common. Today, cockroach and dust mite allergens are well-established triggers for asthma, and those proteins are quite similar to the schistosomiasis worm protein tropomyosin, which sets off the IgE response. People with high IgE are most able to curb parasite infection, but there can be a downside. "Individuals who are most resistant in these [worm-ridden] environments are the ones who produce the most IgE, and they are primed to respond to the common household allergens," says Barnes. She has traced this sensitivity to some variants of the gene for the immune system messenger interleukin 13.

[...]

Knowing these evolutionary connections could help physicians recognize who might be at increased risk for asthma and who should take precautions to limit exposure to allergens, says Barnes.

Nesse and Williams's excellent book on evolutionary medicine is Why We Get Sick: The New Science of Darwinian Medicine (http://www.amazon.co.uk/Why-We-Get-Sick-Neese/dp/0679746749) (AKA Evolution and Healing in the UK).

All this seems perfectly common sense to me... but I suppose it would :D

And we can add it to the list of the uses of evolutionary thinking.

[Oolon Colluphid]

Oooh, there's more:

Science Vol. 324. no. 5924, pp. 162 - 163 (10 April 2009)

News of the Week
EVOLUTIONARY MEDICINE: Two Sides of the Same Coin?

Constance Holden
Scientists have long puzzled over the persistence of schizophrenia--a deleterious condition that by rights should have been pretty much bred out of the human gene pool.

At the Sackler Colloquium on Evolution in Health and Medicine held last week at the National Academy of Sciences (NAS) in Washington, D.C., evolutionary geneticist Bernard Crespi of Simon Fraser University in Burnaby, Canada, threw some evolutionary firepower at the question. He proposes that both schizophrenia and autism are disorders of the "social brain"--but at opposite ends of the same spectrum. Psychiatrist Ezra Susser of Columbia University calls it an "imaginative proposal, … although I don't think it's supported yet by the data."

Last year Crespi, with Christopher Badcock of the London School of Economics, presented the hypothesis in a lengthy article in Behavioral and Brain Sciences. At the NAS meeting, Crespi claimed that recent research on copy number variations (CNV), segments of DNA containing duplications or deletions, further bolster his case. These new studies suggest that schizophrenia may be the result of multiple rare mutations that occur spontaneously. A number of studies have shown some overlap in genomic "hot spots" for CNVs in schizophrenia and autism, with, in some cases, deletions in one condition just where there are duplications for the other. Some scientists suspect some overlap between the two conditions. Crespi and Badcock think, rather, that they are diametric opposites, occupying the same continuum and thus affecting the same pathways.

That would fit with their theory that psychotic disorders--including not only schizophrenia but also bipolar disorder and some major depression--result from "overdevelopment" of the social brain, and autism spectrum disorders reflect underdevelopment of that brain. Many scientists believe socialization is the main force behind the rapid expansion of human brains, said Crespi, pointing out that in primates the size of the cortex increases with size of social groups. The components of the social brain, according to Crespi, include language, self-awareness, "social emotions" such as pride and guilt, logical thinking, pursuit of goals, and awareness of the mental states of others.

In autism, he pointed out, these functions are deficient. In schizophrenia, on the other hand, they are out of control--the language function leads to auditory hallucinations; awareness of others' mental states becomes paranoia; and logic is distorted by uninhibited associations.

Although the data are admittedly preliminary, Crespi maintains they support the notion that autism and schizophrenia are "cognitive, neurodevelopmental, and genomic opposites." He pointed out that some existing theories about the disorders complement this view--for example, some have proposed that glutamate, the brain's main neurotransmitter, is deficient in schizophrenia and overactive in autism.

To evolutionary biologist Randolph Nesse of the University of Michigan, Ann Arbor, who organized the talks on evolution and mental health, the hypothesis shows "the heuristic value of an evolutionary approach in medicine." If correct, "it will fundamentally change our understanding of schizophrenia and autism, … [and] even if it is not, the research is deepening our understanding."