An article in the April, 2009 issue of Evolution, offers provocative support for George Williams’s 1957 prediction that decreased extrinsic mortality rates will select for slower rates of aging. The article compares data from subsistence and European societies in the past 200 years, and concludes that selection may have slowed aging rates in just 10 generations, and it may account for differences in aging rates in different populations. The multiple measures of aging rates are a strength of the article, but they also add complexity that makes interpretation of the results challenging, as the authors note.
Has Actuarial Aging “Slowed” Over the Past 250 Years?
A Comparison of Small-Scale Subsistence Populations and European Cohorts
Michael Gurven and Andrew Fenelon
Evolution 63(4):1017-1035. 2009
Williams’s 1957 hypothesis famously argues that higher age-independent, or ‘extrinsic,’ mortality should select for faster rates of senescence. Long-lived species should therefore show relatively few deaths from extrinsic causes such as predation and starvation. Theoretical explorations and empirical tests of Williams’s hypothesis have flourished in the past decade but it has not yet been tested empirically among humans. We test Williams’s hypothesis using mortality data from subsistence populations and from historical cohorts from Sweden and England/Wales, and examine whether rates of actuarial aging declined over the past two centuries. We employ three aging measures: mortality rate doubling time (MRDT), Ricklefs’s ω, and the slope of mortality hazard from ages 60–70, m′50–70, and model mortality using both Weibull and Gompertz-Makeham hazard models. We find that (1) actuarial aging in subsistence societies is similar to that of early Europe, (2) actuarial senescence has slowed in later European cohorts, (3) reductions in extrinsic mortality associate with slower actuarial aging in longitudinal samples, and (4) men senesce more rapidly than women, especially in later cohorts. To interpret these results, we attempt to bridge population-based evolutionary analysis with individual-level proximate mechanisms.
JAMA published two articles to commemorate Darwin’s 200th birthday.
They illustrate the delicate state of medical knowledge about evolutionary biology. The one by Jim Evans offers a succinct and sophisticated overview of what evolution offers to medicine now. The other illustrates how far we have yet to go. (more…)
2008 American College of Epidemiology Meeting Program
The Dawn of Evolutionary Epidemiology:
Applying Evolutionary Theory in an Epidemiologic Context
September 14-16, 2008
Early Bird Rates until Sept 9th, register online!
The meeting is at The Westin LaPaloma Resort & Spa
3800 East Sunrise Drive, Tucson, AZ 85718
Full meeting info is at:
It is pretty obvious that fever is useful. Work by Kluger and others has shown that increased temperatures decrease mortality during infection. Even for lizards! (When infected they crawl to warmer places.)
The mystery has been how fever works. Can higher body temperature alone inhibit pathogen growth? It seems unlikely that changing temperature by just a degree or so would have a major effect. Pathogens are too adaptable.
In a seminar discussion this week, Karl Sperling, from the Institute of Human Genetics, Charité – Universitätsmedizin Berlin, brought up the protective role of heat shock proteins, and how highly conserved they are. This quickly suggested that their original function might have been co-opted to cope with infection.
Sure enough, a quick search revealed (more…)
Ten years ago, most of us paying attention were exhilarated about the prospects for psychiatric genetics. Heritability is high for many disorders-80% of the variation in vulnerability to bipolar disorder and schizophrenia can be attributed to genetic variations. We thought we would soon find the responsible abnormal genes, and this would quickly reveal the biochemical defects that cause these disorders, and this would quickly lead to ways to cure, or at least dramatically alleviate, these terrible scourges.
Candidate genes were examined by the best researchers using larger and larger samples and sophisticated statistics; a few were identified as prime suspects. Most results could not be replicated, but a few loci were very suspicious based on multiple studies.
Now, in an article by in this month’s American Journal of Psychiatry, Saunders et al. report on 433 SNPs associated with 14 candidate genes that were prime suspects for schizophrenia in about 1900 cases and 2000 controls of European ancestry. The results? Not one of the genes was significantly associated with schizophrenia prevalence. Even a 25% increase would have been detected with high probability.
An editorial by Steven Hamilton tries to put the best possible face on the results by noting that studies of tens of thousands of subjects were required to find genes that contribute to real but small (<25%) increases in risk for Type II diabetes. But that is not the point. Sanders, et al. deserve commendation for stating their conclusion clearly:
Our results suggest that, taken together, common DNA variants in these 14 genes are unlikely to explain a large proportion of the genetic risk for schizophrenia in populations of European ancestry. More robust findings are likely to be discovered using genome-wide association methods and, as our knowledge of the biology of mental illness continues to improve, focused studies of genes based on more precise mechanistic hypotheses. Nevertheless, although larger samples could possibly detect small genetic effects that were missed in this experiment, our findings suggest it is unlikely that true associations exist at the population level for the alleles that have formed the basis for the large candidate gene literature for these 14 postulated schizophrenia candidate genes.
Now what? (more…)