Indiana University has organized an extensive survey on the roles of evolutionary biology and theory in modern medical education. The survey targets students, alumni and faculty members of schools of medicine, nursing, veterinary medicine and public health. The aims are to assess 1) the level of education in evolutionary biology that current health practitioners have and students are receiving, 2) opinions about the utility of evolutionary biology in health practice and research, and 3) opinions as to when and where training in evolutionary biology might be most appropriate in medical education.
The survey should take less than 15 minutes to complete, and one out of every 250 respondents will be randomly selected to receive a new Apple iPod Shuffle!
Please note that this is a re-advertisement. If you have completed this survey in the past, please do not participate again.
If you are a physician, nurse, veterinarian or public health practitioner, or a student or faculty member at a school of medicine, nursing, veterinary medicine or public health, please follow the appropriate URL above to participate in the survey. Your valuable time and critical contribution to the field of evolutionary medicine are appreciated.
If you would consider advertising this survey at the schools you are affiliated with, please contact Prof. Michael Muehlenbein of Indiana University (firstname.lastname@example.org) for advertisements.
For decades food manufacturers have marketed saccharin, along with other non-caloric artificial sweeteners (NAS), as healthy alternatives to sugar. Artificial sugar substitutes cannot be digested by humans and have been recommended for patients with diabetes and for those trying to lose weight. However, a new report in the journal Nature suggests that NAS are harmful to metabolic health. In this study, saccharin given to mice and to healthy human subjects worsened glucose control compared to sugar, and had the paradoxical effect of increasing blood glucose levels.
Saccharin increased blood glucose in mice (Suez et al. doi:10.1038/nature13793)
Lead investigator Eran Elinov and his colleagues showed that the intestinal microbiota was responsible for the adverse metabolic effects of saccharin. Saccharin increased numbers of Bacteroides bacteria in the gut and also increased the density of bacteria in the Enterobacteriaceae group while decreasing the number of certain beneficial bacteria, such as Akkermansia mucinophila. Remarkably when fecal bacteria from saccharin-fed humans were transferred to germ-free mice, the mice became glucose intolerant, similar to their human donors. Some human subjects were non-responders, maintaining normal metabolism of glucose after exposure to saccharin. Fecal samples from non-responders were inoculated into germ free mice without causing glucose intolerance. These findings indicate a causal role for the microbiota in the impairment of metabolism by artificial sweeteners.
Bernard Crespi has for several years developed evidence to support the theory, first proposed with CR Badcock, that schizophrenia and autism are flip sides of excessive or deficient maternal or paternal imprinting. A study published today in the Proceedings of the Royal Society b finds further support from data on size at birth and risks of schizophrenia and autism in 1.75 million Danes. Smaller babies are at increased risk for schizophrenia, larger babies are at increased risk for autism. A press release is here. Details below.
Opposite risk patterns for autism and schizophrenia are associated with normal variation in birth size: phenotypic support for hypothesized diametric gene-dosage effects
By Sean G. Byars, Stephen C. Stearns, and Jacobus J. Boomsma
Proc. R. Soc. B 7 November 2014 vol. 281 no. 1794 20140604 doi: 10.1098/rspb.2014.0604 (not open access)
Abstract: Opposite phenotypic and behavioural traits associated with copy number variation and disruptions to imprinted genes with parent-of-origin effects have led to the hypothesis that autism and schizophrenia share molecular risk factors and pathogenic mechanisms, but a direct phenotypic comparison of how their risks covary has not been attempted. Here, we use health registry data collected on Denmark’s roughly 5 million residents between 1978 and 2009 to detect opposing risks of autism and schizophrenia depending on normal variation (mean ± 1 s.d.) in adjusted birth size, which we use as a proxy for diametric gene-dosage variation in utero. Above-average-sized babies (weight, 3691–4090 g; length, 52.8–54.3 cm) had significantly higher risk for autism spectrum (AS) and significantly lower risk for schizophrenia spectrum (SS) disorders. By contrast, below-average-sized babies (2891–3290 g; 49.7–51.2 cm) had significantly lower risk for AS and significantly higher risk for SS disorders. This is the first study directly comparing autism and schizophrenia risks in the same population, and provides the first large-scale empirical support for the hypothesis that diametric gene-dosage effects contribute to these disorders. Only the kinship theory of genomic imprinting predicts the opposing risk patterns that we discovered, suggesting that molecular research on mental disease risk would benefit from considering evolutionary theory.
Over the past several weeks the health news has been dominated by the outbreak of infections by Ebola virus (EBOV) in several West African nations: Guinea, Sierra Leone, Liberia, and Nigeria. A study (Gire et al., 2014) published online at the end of August and now in print by a large collaborative group based in the U.S., the U.K., or West Africa applied massively parallel sequencing of the genomes of clinical isolates of the Ebola virus primarily from Sierra Leone. The results bear on the origins of the outbreak and the transmission patterns of the responsible virus lineages and may inform future investigations pertaining to diagnostic tests, the development of vaccines, and the design of therapies based on small-molecule drugs or biologics. Continue Reading »
A link here and on the right hand column of this page (“For Medical students”), takes you to a new page that is creating a network of medical and other health professional students who share an interest in evolution, medicine, and public health. If you are such a student, click the link to add your information, and/or to offer to help to organize students at your university.
Authors: Kirsten I. Bos, Kelly M. Harkins, Alexander Herbig, Mireia Coscolla, Nico Weber, Iñaki Comas, Stephen A. Forrest, Josephine M. Bryant, Simon R. Harris, Verena J. Schuenemann, Tessa J. Campbell, Kerrtu Majander, Alicia K. Wilbur, Ricardo A. Guichon, Dawnie L. Wolfe Steadman, Della Collins Cook, Stefan Niemann, Marcel A. Behr, Martin Zumarraga, Ricardo Bastida, Daniel Huson, Kay Nieselt, Douglas Young, Julian Parkhill, Jane E. Buikstra, Sebastien Gagneux, Anne C. Stone & Johannes Krause
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
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.
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
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.
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 »
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.
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.
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 »
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
Toxoplasma gondii is an intracellular protozoan parasite that infects many different vertebrate species asexually and undergoes a sexual cycle after infecting cats (http://www.cdc.gov/parasites/toxoplasmosis/, 2013). Parasite oocysts are potentially introduced into the human environment in cat feces. T. gondii is of interest in clinical medicine because humans can serve as accidental intermediate hosts when they ingest oocysts in, for example, undercooked, contaminated meat or ingest parasites in contaminated drinking water. Mother-to-child transmission can also occur. In most healthy individuals the infection does not cause illness, but in individuals with immune deficiencies and in fetuses it can cause substantial morbidity. In the case of congenital infection of a fetus, morbidity, including vision loss, cognitive deficits, and seizures tends to be more severe with earlier infection and mortality can result in either miscarriage or stillborn birth. L. David Sibley (Washington University) and colleagues (Etheridge et al., 2014) have now further clarified the molecular basis for the variation in virulence among different T. gondii lineages for mice, an important prey species for cats and therefore an important intermediate host species. Continue Reading »