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 dramatcially lowered rates of miscarriage and congential 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 »
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.
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).
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?
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 »
John W. Pepper, Barbara K. Dunn, Richard M. Fagerstrom, John K. Gohagan, and Nadarajen A. Vydelingum, “Using Systems Biology to Understand Cancer as an Evolutionary Process,” Journal of Evolutionary Medicine, vol. 2, Article ID 235678, 8 pages, 2014. doi:10.4303/jem/235678 (Open Access)
Abstract: Unsatisfactory progress in cancer medicine and prevention calls for new research approaches. Research can broaden its view of cancer to include not only specific molecular elements, but also the process that explains their origin and dynamics. This process is Darwinian evolution of somatic cells. Applicable modeling techniques are available from process-oriented systems biology. We review relevant concepts and techniques, and their application to four key open questions in cancer prevention research. Helpful concepts are transferable from classical evolutionary biology and ecology, while useful techniques include computational agent-based modeling. The research questions we review include (1) why do benign neoplasms often progress to malignancy? (2) what is the chronological sequence of molecular events in cancer progression? (3) how can we find reliable molecular biomarkers for cancer? and (4) will evolved drug resistance stymie efforts at a long-term cancer chemoprevention? We conclude that molecular analysis can be usefully augmented with process-oriented systems biology to guide empirical research into the most productive directio
The first author, Ann Demogines, will receive the $5000 Prize. She is a Research Associate in the Center for Systems and Synthetic Biology, College of Natural Sciences, University of Texas, Austin, where she works in the laboratory of Sara Sawyer. The Foundation is grateful to Gilbert Omenn for making this prize possible.
The Committee cited four other papers for Honorable Mention:
A prion is a protein that can adopt a conformation other than the ‘standard’ functional conformation and this alternative conformation favors self-association. The aggregation-associated conformation can then be imposed on additional copies of the protein in the original conformation. This self-templating mechanism for propagation is known primarily for causing neurodegenerative conditions in humans and in animals, such as kuru or Creutzfeldt-Jakob disease in humans or bovine spongiform encephalopathy (i.e., mad cow disease) in cattle. Since this process of converting protein conformations can be transmitted from one animal to another or one person to another by some routes, such as cannibalism in the case of kuru, the name prion was created to indicate an infectious protein particle. This concept of an infectious agent that involved no nucleic acid was the basis for the Nobel Prize in Physiology or Medicine awarded to Stanley Prusiner in 1997 (http://www.nobelprize.org/nobel_prizes/medicine/laureates/1997/press.html). Continue Reading »
Troubled sleep: Night waking, breastfeeding and parent–offspring conflict
A target article in Evolution, Medicine, and Public Health by David Haig on why infants cry at night, has accompanying responses from Jim McKenna, Katie Hinde, Bernie Crespi, Patrick McNamara, and Jon Wilkins. Open access
Abstract: Disrupted sleep is probably the most common complaint of parents with a new baby. Night waking increases in the second half of the first year of infant life and is more pronounced for breastfed infants. Sleep-related phenotypes of infants with Prader-Willi and Angelman syndromes suggest that imprinted genes of paternal origin promote greater wakefulness whereas imprinted genes of maternal origin favor more consolidated sleep. All these observations are consistent with a hypothesis that waking at night to suckle is an adaptation of infants to extend their mothers’ lactational amenorrhea, thus delaying the birth of a younger sib and enhancing infant survival.
This past December, science writer David Dobbs published an essay (2013) in the online magazine Aeon (aeon.co/magazine/) that purports to explain why the ‘selfish gene’ concept is outmoded and should be retired. It elicited a good deal of commentary, and in early March, Aeon published responses (Sapolsky et al., 2014) to the original article from four individuals (two scientists, a genetic counselor, and a philosopher) as well as additional comments by Dobbs. For those who are interested in this controversy, responses to the original Dobbs article were also posted elsewhere by Richard Dawkins (2013) and Jerry Coyne (2013a, b). Below, I provide a sense of the arguments of Dobbs, the tenor of the criticisms of Dobbs’s piece, and selected other critiques of the gene-centric approach to evolution. Continue Reading »