Alison Feder wins 2017 Omenn Prize

Alison Feder wins 2017 Omenn Prize

Alison Feder

 

The International Society for Evolution, Medicine & Public Health has just announced the winner of the 2017 Omenn Prize. It is Alison Feder, and her colleagues, of Stanford University, for their paper in eLife titled “More effective drugs lead to harder selective sweeps in the evolution of drug resistance in HIV-1“. The Prize Committee included Jim Bull, Antonium Rokas and Grazyna Jasienska and was overseen by Andrew Reed. The winner receives a prize of $5000, courtesy of the generosity of Gilbert Omenn, and an invitation to present their paper at the annual meeting of the Society in Groningen in August. Congratulations to Alison!

Lectureship in Evolution and Medicine at the University of Cambridge

Lectureship in Evolution and Medicine at the University of Cambridge

Some of our readers may be interested in considering this advertisement for a lectureship at the University of Cambridge at the intersection of evolutionary biology with medicine. It is an Unestablished Lectureship in Evolution and Medicine based in the Department of Zoology and Sidney College and runs, initially, for 3 years. Details are available at the following link: http://www.jobs.cam.ac.uk/job/13493/

 

An evolutionary approach to kidney function and disease

An evolutionary approach to kidney function and disease

Robert L. Chevalier
Division of Pediatric Nephrology
University of Virginia

Evmedreview is very pleased to feature a paper on evolutionary nephrology by Robert L. Chevalier. Robert joined the University of Virginia in 1978 where he established the now internationally recognized Division of Pediatric Nephrology. Since 2010 he has devoted himself full-time to studying chronic kidney disease progression from birth to senescence. Finding his study limited by a conventional training in medicine and physiology he turned to evolutionary medicine for explanations based on ultimate causes. We believe this paper is the first comprehensive application of evolutionary medicine to understanding progressive chronic kidney disease. Chevalier traces his evolutionary perspective back to Homer W. Smith who did pioneering work on kidney evolution in the late 1930s. In his book From Fish to Philosopher, Chevalier says, Smith argued that the complex structure of the kidney can be explained by a series of evolutionary adaptations in our vertebrate ancestors, who transitioned from marine to fresh water environments and ultimately to survival on land. Written by the leading American renal physiologist of the mid- 20th century, says Chevalier, that book revealed how an evolutionary perspective explains the dependence of renal excretory function on filtration of 180 liters of plasma per day and reclamation of 99% of the filtrate. Many of the early advances in renal physiology were based on animal studies that required an understanding of evolution to apply the results to human beings.

Why is evolutionary medicine important? According to Chevalier, the primary challenge to the adoption of an evolutionary approach to disease rests on the practice of medicine itself: physicians are charged with the responsibility for diagnosing and treating a particular disorder in an individual patient, a process that appears far removed from evolutionary concerns. However, the history (present illness, past history, and family history) is the key component in diagnosis. Seeking concordance with established medical sciences (genetics, anatomy, physiology, biochemistry), evolutionary medicine relies on evolutionary biology to create a “deep” history of human populations. The rationale for the evolutionary perspective is that rather than causing disease, our evolutionary history determines our risk of disease in a given environment, a context that overlaps with public health, global health, and health care disparities.

The featured image illustrates Homer Smith’s account of the more important steps in the evolution of the vertebrate kidney in relation to saltwater (darkly shaded) and freshwater (lightly shaded) environment. The evolutionary tree is followed through primitive fish, amphibians, reptiles, birds and mammals showing the adaptation to a terrestrial environment.

Chevalier’s paper is published in Kidney International Reports and simply titled Evolutionary Nephrology. To whet your appetites here is the abstract:

“Progressive kidney disease follows nephron loss, hyperfiltration, and incomplete repair, a process described as “maladaptive.” In the past 20 years, a new discipline has emerged that expands research horizons: evolutionary medicine. In contrast to physiologic (homeostatic) adaptation, evolutionary adaptation is the result of reproductive success that reflects natural selection. Evolutionary explanations for physiologically maladaptive responses can emerge from mismatch of the phenotype with environment or from evolutionary tradeoffs. Evolutionary adaptation to a terrestrial environment resulted in a vulnerable energy-consuming renal tubule and a hypoxic, hyperosmolar microenvironment. Natural selection favors successful energy investment strategy: energy is allocated to maintenance of nephron integrity through reproductive years, but this declines with increasing senescence after ~40 years of age. Risk factors for chronic kidney disease include restricted fetal growth or preterm birth (life history tradeoff resulting in fewer nephrons), evolutionary selection for APOL1 mutations (which provide resistance to trypanosome infection, a tradeoff), and modern life experience (Western diet mismatch leading to diabetes and hypertension). Current advances in genomics, epigenetics, and developmental biology have revealed proximate causes of kidney disease, but attempts to slow kidney disease remain elusive. Evolutionary medicine provides a complementary approach by addressing ultimate causes of kidney disease. Marked variation in nephron number at birth, nephron heterogeneity, and changing susceptibility to kidney injury throughout the life history are the result of evolutionary processes. Combined application of molecular genetics, evolutionary developmental biology (evo-devo), developmental programming, and life history theory may yield new strategies for prevention and treatment of chronic kidney disease.”

Why resistance develops to antibiotics but not vaccines

Why resistance develops to antibiotics but not vaccines

David Kennedy and Andrew Read have kindly supplied the following teaser for their latest paper in Proceedings Of The Royal Society B. As they point out, this “armchair speculation” has elicited a gamut of reactions ranging from awe to scorn and so we are sure they would welcome commentary on this paper from the readers of Evmedreview!

Andrew Read

Dave Kennedy and Andrew Read

Center for Infectious Disease Dynamics, Departments of Biology and Entomolology, Penn State

David Kennedy

Evolution is perhaps the world’s greatest problem solver. It has found innumerable solutions to blistering environmental insults. Nowhere is this clearer than for drug resistance. Pathogen evolution has undermined virtually every known chemotherapeutic drug. Yet rubbing a cowpox pustule into a person’s open wound somehow confounded evolution. Most modern vaccines have done so too: they work as well as they did when they were first introduced. Why can evolution rescue pathogens from drugs but not from vaccines?

When we first discussed this question, we were surprised not to agree on an answer. It seemed that any of a laundry list of features might help explain why vaccines are more evolution-proof than drugs. We were also surprised to find barely any discussion of the problem in the literature. A few people had asked why resistance to measles or smallpox vaccines failed to evolve, but the answers were specific to those viruses. What was the general answer?

We disagreed for months before one of us (DK) persuaded the other (AR) that, ironically, the most plausible answer lay in processes well known in agricultural resistance management. This solution—which we just published after a grueling time with reviewers—is essentially armchair speculation. We cannot yet know whether it is correct. Reactions from colleagues have ranged from ‘that is obvious’ to ‘that is wrong’ and have involved adjectives like ‘superficial’ and ‘stimulating’, as well as the opinion that our article reads like an undergraduate essay. We hope that the simplicity of our argument breeds the kind of skepticism that leads to new data and new theories. The problem seems important. Will next-generation vaccines fail? Can drugs be made as evolution-proof as vaccines? Which cancer therapies have the greatest potential to work?

Is atherosclerosis a modern disease after all?

Is atherosclerosis a modern disease after all?

What factors should we blame most for the continuing pandemic of heart and artery disease throughout the Western world? The argument has endured more twists and turns than California Route 1. For years, the diet cholesterol hypothesis has held sway, with added blame attached to smoking and a couch potato lifestyle. Before the ascendency of the cholesterol hypothesis, cardiology favored inflammation as the main driving force for atherosclerosis, and interest in inflammation has returned thanks to studies suggesting C-reactive protein is a much better indicator of heart problems lying in wait for asymptomatic individuals than cholesterol levels or high blood pressure; a meta-analysis showing that dietary change has no impact on the risk of a heart attack; studies showing that atherogenic processes in arterial walls are driven by the immune system; and paleocardiology studies showing that pre-industrial and prehistoric societies had high levels of arterial plaque despite high exercise levels and a frugal diet low in saturated fat. i.e. that susceptibility to heart disease is not a modern phenomenon. Now, a study published last Friday in The Lancet, based on measurements taken from members of the Tsimane – a forager-horticulturalist population living in the Bolivian Amazon basin – dramatically switches the argument back again. The Tsimane have extraordinarily low rates of coronary artery disease, low blood pressure, low blood glucose, and low “bad” cholesterol (LDL), despite enduring chronic high levels of systemic inflammation due to the high pathogenic load they carry. It is infection that carries them off – not heart disease.

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