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By Alcock, Joe, Maley, Carlo C., & Aktipis, C. Athena. (2014). Is eating behavior manipulated by the gastrointestinal microbiota? Evolutionary pressures and potential mechanisms. Bioessays, n/a-n/a. doi: 10.1002/bies.201400071

See a nice commentary by Carl Zimmer in the NYTimes.

Abstract: Microbes in the gastrointestinal tract are under selective pressure to manipulate host eating behavior to increase their fitness, sometimes at the expense of host fitness. Microbes may do this through two potential strategies: (i) generating cravings for foods that they specialize on or foods that suppress their competitors, or (ii) inducing dysphoria until we eat foods that enhance their fitness. We review several potential mechanisms for microbial control over eating behavior including microbial influence on reward and satiety pathways, production of toxins that alter mood, changes to receptors including taste receptors, and hijacking of the vagus nerve, the neural axis between the gut and the brain. We also review the evidence for alternative explanations for cravings and unhealthy eating behavior. Because microbiota are easily manipulatable by prebiotics, probiotics, antibiotics, fecal transplants, and dietary changes, altering our microbiota offers a tractable approach to otherwise intractable problems of obesity and unhealthy eating.

By  Apari P, de Sousa JD, Müller V (2014) . in PLoS Pathog 10(8): e1004111. doi:10.1371/journal.ppat.1004111

In this Opinion piece we argue that the tendency of sexually transmitted infections (STIs) to cause infertility is likely to reflect an evolutionary adaptation of the pathogens. We use an evolutionary perspective to understand how STI pathogens may benefit from reducing fertility in the host and what clues the mechanisms of pathogenesis can offer to the evolution of this ability. While we concentrate on human infections, we will also briefly discuss the broader context of STI-induced infertility in other species. Continue reading

Adaptive variability in the duration of critical windows of plasticity:   Implications for the programming of obesity
By  Jonathan CK Wells  Evol Med Public Health published 5 August 2014, 10.1093/emph/eou019

http://emph.oxfordjournals.org/content/early/2014/08/05/emph.eou019.abstract?papetoc   (open access)

Abstract:  Developmental plasticity underlies widespread associations between early-life exposures and many components of adult phenotype, including the risk of chronic diseases. Humans take almost two decades to reach reproductive maturity, and yet the ‘critical windows’ of physiological sensitivity that confer developmental plasticity tend to close during fetal life or infancy.

Continue Reading »

Lively, C. M., Roode, J. C. d., Duffy, M. A., Graham, A. L., & Koskella, B. (2014).
Interesting Open Questions in Disease Ecology and Evolution.
The American Naturalist, 184(S1), S1-S8. doi: 10.1086/677032

Introduction:   Studies on the ecology and evolution of infectious diseases have expanded at an increasing rate over the last several decades (fig. 1). This interest seems to have originally stemmed from models suggesting that host-parasite interactions might explain previously anomalous features of the natural world, such as sexual reproduction (Hamilton 1980), female mate choice (Hamilton and Zuk 1982), the maintenance of genetic diversity (Haldane 1949), and the regulation of host populations (Anderson and May 1979; May and Anderson 1979). The interest was further increased by early theory on the evolution of parasite virulence (May and Anderson 1983) as well as by concerns regarding the emergence of infectious diseases. Here we present a short list of interesting open questions for future research. The questions are based on an American Society of Naturalists Symposium in 2013 entitled, “Disease Ecology, Evolution, and Coevolution.” Our list is not meant to be exhaustive, as many important questions remain, but we hope that it will encourage additional work in these areas.

The Questions are:

Question 1: What Is the Effect of Host Genetic Diversity on the Spread of Infectious Disease?

Question 2: How Is Host/Parasite Genetic Diversity Maintained?

Question 3: What Are the Effects of External Biotic and Abiotic Factors on Virulence and the Risk of Infection?

Question 4: Are Lessons Learned from Single Host-Parasite Pairings Generalizable to the Multihost-Multiparasite Networks That Dominate in Nature?

Question 5: What Is the Role of Host Microbiota in Shaping Disease Ecology and Evolution?

Altshuler and colleagues (Nature Genetics, 2014) recently reported a study of about 150,000 individuals representing five different ancestral groups in which they identified twelve low-frequency variants of the gene SLC30A8 through either genomic sequencing or genotyping.  These variants are all predicted to truncate the gene product (ZnT8), a protein involved in zinc transport in beta cells in the islets of Langerhans.  In beta cells, zinc is involved for insulin packaging and secretion.

Of particular interest, carriers possessing one or another of these loss-of-function mutations appeared to be at lower risk from type 2 diabetes (T2D).  Averaging over the different variants, these alleles provided an approximately 65% lower risk of T2D. Continue Reading »

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 Many have asked if there are meetings they can attend to learn more about evolutionary medicine and to get up-to-date on the latest advances.  Two just-announced major conferences will meet this need, one in Europe, one in the USA. Both will soon be inviting abstract submissions and meeting registrations.

July 30–August 1, 2015
Evolutionary Medicine Conference: Interdisciplinary Perspectives on Human Health and Disease
Institute of Evolutionary Medicine (IEM), University of Zurich, Switzerland
Details at this link.   Meeting flyer available here as a pdf. 

March 19-21, 2015
Inaugural Meeting of the Society for Evolution, Medicine, & Public Health
Co-sponsored by the Foundation for Evolution, Medicine, & Public Health and
the Arizona State University Center for Evolution & Medicine
Details available soon here at the Evolution and Medicine Review.

Koren, Gideon, Madjunkova, Svetlana, & Maltepe, Caroline. (2014). The protective effects of nausea and vomiting of pregnancy against adverse fetal outcome—A systematic review. Reproductive Toxicology, 47(0), 77-80. doi: http://dx.doi.org/10.1016/j.reprotox.2014.05.012

The article considered 2367 articles and selected 16 for inclusion in a meta-analysis. They found dramatically lowered rates of miscarriage and congenital defects in women who had nausea and vomiting during pregnancy (NVP), with odds ratios often at one half that of women who did not have NVP.  The study says little about the potential confounding effects in such studies, and nothing about previous work by Profet, Flaxman & Sherman and others proposing that NVP is an adaptation shaped by natural selection. Flaxman, S. M., & Sherman, P. W. (2000). Morning sickness: a mechanism for protecting mother and embryo. Quarterly Review of Biology, 113-148.

Missing Microbes

Martin Blaser has written a terrific book, Missing Microbes,  about the dire effects of killing off the useful bacteria we evolved with.   Book excerpt here. 

Jane Brody commentary here

NYTimes review here and excerpted below.

Genes make you … you. But where do they come from? Antibiotics save lives, but their overuse is evolving supergerms and could be changing our bodies. Who pays what rent for which room? Just use this handy calculator and never fight at the end of the month again.
Subscribe to the Podcast » David Corcoran and Jeffery DelViscio

First and foremost, the war has escalated. Imprudent antibiotic use has resulted in widespread resistance among microbes; infectious disease doctors (I am one, as well as a casual acquaintance of Dr. Blaser’s) now operate in a state of permanent near panic as common infections demand increasingly powerful drugs for control.

Second, as always, it is the hapless bystanders who have suffered the most — not human beings, mind you, but the gazillions of benevolent, hardworking bacteria colonizing our skin and the inner linings of our gastrointestinal tracts. We need these good little creatures to survive, but even a short course of antibiotics can destroy their universe, with incalculable casualties and a devastated landscape. Sometimes neither the citizenry nor the habitat ever recovers.

And finally, there is the accumulation of disheartening evidence that the war against the old plagues is simply leading to worse wars against a whole series of new ones.

 

Wick, G., Jakic, B., Buszko, M., Wick, M. C., & Grundtman, C. (2014). The role of heat shock proteins in atherosclerosis. [Review]. Nat Rev Cardiol,  doi: 10.1038/nrcardio.2014.91 (not open access)

Vulnerability to atherosclerosis is looking more and more like a result of the trade-off between protection against infection vs. vascular preservation.  Or, is the immune response to HSP 60 better interpreted as an epiphenomenon?  The answer is important as therapies are created to take advantage of this new knowledge.

Abstract: Atherosclerosis is a chronic, multifactorial disease that starts in youth, manifests clinically later in life, and can lead to myocardial infarction, stroke, claudication, and death. Although inflammatory processes have long been known to be involved in atherogenesis, interest in this subject has grown in the past 30–40 years. Animal experiments and human analyses of early atherosclerotic lesions have shown that the first pathogenic event in atherogenesis is the intimal infiltration of T cells at arterial branching points. These T cells recognize heat shock protein (HSP)60, which is expressed together with adhesion molecules by endothelial cells in response to classic risk factors for atherosclerosis. Although these HSP60-reactive T cells initiate atherosclerosis, antibodies to HSP60 accelerate and perpetuate the disease. All healthy humans develop cellular and humoral immunity against microbial HSP60 by infection or vaccination. Given that prokaryotic (bacterial) and eukaryotic (for instance, human) HSP60 display substantial sequence homology, atherosclerosis might be the price we pay for this protective immunity, if risk factors stress the vascular endothelial cells beyond physiological conditions.

Epistasis refers to the influence of one genomic mutation or variant on the phenotypic effects of another mutation or variant.  Based on available evidence and theory, this phenomenon has a major influence on evolutionary trajectories for organisms of all sorts.  The role of epistasis has been studied primarily in the context of adaptive evolutionary change.  In a recent paper (2014), Gong and Bloom attempt to determine the relative frequencies of epistatic interactions in adaptive versus stochastic evolution, i.e. evolution driven by selection as opposed to evolution resulting from random processes without a significant selective ‘pressure.’  Gong and Bloom perform this comparison by analyzing homologous nucleoprotein (NP) genes in human and swine influenza A viruses.  The authors argue that the human viruses are subject to substantially more intense selection than the swine viruses since domestic swine are much shorter lived and their viruses are not as likely to be subjected to immune memory responses. Continue Reading »

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The evolutionary paradox and the missing heritability of schizophrenia
by van Dongen, J., & Boomsma, D. I. (2013).
American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, 162(2), 122-136.
doi: 10.1002/ajmg.b.32135

Schizophrenia is one of the most detrimental common psychiatric disorders, occurring at a prevalence of approximately 1%, and characterized by increased mortality and reduced reproduction, especially in men. The heritability has been estimated around 70% and the genome-wide association meta-analyses conducted by the Psychiatric Genomics Consortium have been successful at identifying an increasing number of risk loci. Various theories have been proposed to explain why genetic variants that predispose to schizophrenia persist in the population, despite the fitness reduction in affected individuals, a question known as the evolutionary paradox. In this review, we consider evolutionary perspectives of schizophrenia and of the empirical evidence that may support these perspectives. Continue Reading »

An iTunes version of the course by Steve Stearns is now available free online, with vast supplementary material that is not available in the YouTube version.    To subscribe, launch the course on iTunes, or go to this site

 

Course Description Continue Reading »

After almost two years as an unofficial medical student interest group the Evolutionary Medicine Group at the Louisiana State University  School of Medicine in New Orleans  has gained official recognition by the institution.  If you know of other groups of medical students who are meeting to talk about evolutionary medicine, please add information as a comment below so we can establish a network of such groups.

The LSU group was started by first year medical students last year, with minimal faculty support, and continued to meet and recruit underclassmen throughout the current academic year. Participants will now receive credit hours towards the school’s “professional development” elective. The group follows a journal club style, with the presenting student choosing journal articles and leading discussion relevant to the month’s topic. Topics have included: Cancer Evolution in Human Microenvironments, Foundations of Evolution in Relation to Medicine, Evolution and Embryological Development, Infectious Disease Evolution, Current Environmental Mismatch with Evolved Human Traits, Evolutionary Basis of Aging, Epigenetics in Human Evolution, Evolution and Psychology, Using Evolution to Predict Outcomes of Medical Intervention, and The Human Microbiome. It is the hope that this group will increase the understanding of scientific literature, encourage peer-to-peer teaching, and lead to the development of evolutionary thinking in a new generation of physicians.

Any questions/comments can be directed to: Michelle Blyth (mblyth@lsuhsc.edu), Rebecca Kreston (rkrest@lsuhsc.edu) (student leaders) or Jason Mussell (jmusse@lsuhsc.edu), Hamilton Farris (hfarri@lsuhsc.edu) (faculty advisors)

45 lectures from the Yale Evolutionary Medicine course taught by Stephen Stearns are now available online, open access on a special You Tube channel.

This is a complete course, with high production values,  by a world leader in the field.

The lecture segments are 6 to 26 minutes in length, well suited to insertion into lectures or to assigning as a part of a course.

The placenta was long thought to be sterile, but a new study finds nucleic acid signatures of multiple species in a pattern similar to that in the oral cavity.

PlacentalMicrobiome
PlacentalMicrobiome

K. Aagaard, J. Ma, K. M. Antony, R. Ganu, J. Petrosino, J. Versalovic, The Placenta Harbors a Unique Microbiome. Sci. Transl. Med. 6, 237ra65 (2014).

A report in Nature by Katia Moskvitch is open access. 

The research report in Sci Trans Med is not open access, but the abstract is below.

Humans and their microbiomes have coevolved as a physiologic community composed of distinct body site niches with metabolic and antigenic diversity. The placental microbiome has not been robustly interrogated, despite recent demonstrations of intracellular bacteria with diverse metabolic and immune regulatory functions. A population-based cohort of placental specimens collected under sterile conditions from 320 subjects with extensive clinical data was established for comparative 16Sribosomal DNA–based and whole-genome shotgun (WGS) metagenomic studies. Identified taxa and their gene carriage patterns were compared to other human body site niches, including the oral, skin, airway (nasal), vaginal, and gut microbiomes from nonpregnant controls. We characterized a unique placental microbiome niche, composed of nonpathogenic commensal microbiota from the Firmicutes, Tenericutes, Proteobacteria, Bacteroidetes, and Fusobacteria phyla. In aggregate, the placental microbiome profiles were most akin (Bray-Curtis dissimilarity <0.3) to the human oral microbiome. 16S-based operational taxonomic unit analyses revealed associations of the placental microbiome with a remote history of antenatal infection (permutational multivariate analysis of variance, P = 0.006), such as urinary tract infection in the first trimester, as well as with preterm birth <37 weeks (P = 0.001).

An innovative format, Clinical Briefs cover crucial topics in just a page. They are available as html, or pdf format. All are open access.  See below and here for the first few published.

  1. Editorial

    • Gillian Bentley

    Editorial

    • Elspeth V. Best and
    • Mark D. Schwartz

    Fever Continue Reading »

The mathematician versus the malignancy

An engaging story about using mathematical models to improve chemotherapy.

 By Elie Dolgin

Nature Medicine 20, 460–463 (2014) doi:10.1038/nm0514-460 (open access)

The way in which people receive cancer therapy is pretty much the same as it’s been for decades: researchers determine the highest dose of a drug or treatment that does not cause unacceptable side effects; oncologists then administer that dose to patients on a standard timetable—usually daily tablets for oral chemotherapeutics and other pill-based regimens, infusions on a weekly schedule for injectable drugs and Monday-through-Friday treatments for radiation therapy.

Almost all current cancer therapies are given this way. And although the approach has undoubtedly extended countless patients’ lives, given that more than $80 billion is spent on cancer care in the US alone, it’s worth asking: are these schedules really yielding the best results for patients? And could alternative timetables produce better outcomes?

Franziska Michor hopes to answer these questions. Read more here

A report from the American Academy of Microbiology that is clear, short and engaging, and open access.

Executive Summary

Do you think the oncologists at a cutting-edge research hospital ever sit down with local farmers? Do you think the pharmaceutical researchers developing the next generation of anti-HIV drugs spend any time with the plant scientists working on the next generation of Roundup Ready soybeans?

If your answer to both questions is no, you would be mostly right. Even though all of these people are dealing with exactly the same evolutionary phenomena, they do not recognize themselves as a single scientific community and rarely get a chance to learn from each other. What they all have in common is that they are trying to eliminate an unwanted living entity – a cancer cell, a weed, a virus, an insect pest – but the treatments they develop eventually lose effectiveness because the target evolves resistance.

The emergence of resistance is a phenomenon with ancient evolutionary roots, Continue Reading »

Spermatogonial stem cells replicate and produce sperm throughout adult life, while oocyte precursors complete all of their mitotic cell divisions during fetal development and primary oocytes are arrested in meiosis at birth. Because many more rounds of cell division occur in spermatogenesis than in oogenesis, the incidence of germline mutations, and particularly of single base substitutions, is higher in sperm than in ova (Crow, 2000). Most single base substitutions occur roughly four or five times more frequently in sperm than in eggs, and the incidence of these mutations increases modestly with paternal age. Against this background, a handful of diseases, known as paternal age effect (PAE) diseases, stand out. PAE diseases, of which achondroplasia is the most common and best known, have several unusual features. Almost all (more than 95%) of the new mutations that cause these diseases occur in sperm; the incidence of these diseases increases significantly with paternal age, such that the fathers of affected patients are on average several years older than the fathers of unaffected babies in the same populations; and the genes underlying these diseases have unusually high apparent mutation rates. The mutations that cause PAE diseases are dominant, gain of function mutations in genes related to the RAS signal transduction pathway. Achondroplasia is due to mutations in fibroblast growth factor receptor 3 gene (FGFR3), while Costello syndrome, another PAE disease, is caused by mutations in the HRAS proto-oncogene. Continue Reading »

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