A new short review by David Haig will be of interest to all who study human reproduction and pregnancy.
Haig, D. (2019). Cooperation and conflict in human pregnancy. Current Biology, 29(11), R455–R458. https://doi.org/10.1016/j.cub.2019.04.040
Abstract: For many humans living today, obstetric care begins early in pregnancy, and most babies are born in hospitals. These are precautionary measures. Medical complications during the brief nine months of pregnancy are such a common part of human experience that we rarely ask ourselves why gestation does not always proceed as smoothly and reliably as the lifelong beating of our heart or filtration of blood by our kidneys. The birth of a healthy child is central to reproductive fitness and must have been subject to strong natural selection. Why then should placentas be less reliable organs than hearts or kidneys? Why should maternal hearts and kidneys be more subject to catastrophic failures during pregnancy than at other times? A crucial contrast distinguishes obstetrics from cardiology and nephrology. The coordinated activities of heart and kidneys take place within an individual comprised of genetically largely identical cells, whereas pregnancy involves an interaction between genetically-distinct individuals whose cooperation is obviated by evolutionary conflicts of interest.
Natri, H., Garcia, A. R., Buetow, K. H., Trumble, B. C., & Wilson, M. A. (2019). The Pregnancy Pickle: Evolved Immune Compensation Due to Pregnancy Underlies Sex Differences in Human Diseases. Trends in Genetics, 35(7), 478–488. https://doi.org/10.1016/j.tig.2019.04.008
Abstract: We hypothesize that, ancestrally, sex-specific immune modulation evolved to facilitate survival of the pregnant person in the presence of an invasive placenta and an immunologically challenging pregnancy – an idea we term the ‘pregnancy compensation hypothesis’ (PCH). Further, we propose that sex differences in immune function are mediated, at least in part, by the evolution of gene content and dosage on the sex chromosomes, and are regulated by reproductive hormones. Finally, we propose that changes in reproductive ecology in industrialized environments exacerbate these evolved sex differences, resulting in the increasing risk of autoimmune disease observed in females, and a counteracting reduction in diseases such as cancer that can be combated by heightened immune surveillance. The PCH generates a series of expectations that can be tested empirically and that may help to identify the mechanisms underlying sex differences in modern human diseases.
A new article by Rozhok and DeGregori uses an evolutionary lens to propose a more sophisticated analysis of why cancer becomes more common with age, and the role of tissue ecology.
Rozhok, A., & DeGregori, J. (2019). A generalized theory of age-dependent carcinogenesis. ELife, 8. https://doi.org/10.7554/eLife.39950
Abstract: The Multi-Stage Model of Carcinogenesis (MMC), developed in the 1950 s-70s, postulated carcinogenesis as a Darwinian somatic selection process. The cellular organization of tissues was then poorly understood, with almost nothing known about cancer drivers and stem cells. The MMC paradigm was later confirmed, and cancer incidence was explained as a function of mutation occurrence. However, the MMC has never been tested for its ability to account for the discrepancies in the number of driver mutations and the organization of the stem cell compartments underlying different cancers that still demonstrate nearly universal age-dependent incidence patterns. Here we demonstrate by Monte Carlo modeling the impact of key somatic evolutionary parameters on the MMC performance, revealing that two additional major mechanisms, aging-dependent somatic selection and life history-dependent evolution of species-specific tumor suppressor mechanisms, need to be incorporated into the MMC to make it capable of generalizing cancer incidence across tissues and species.
The $5,000 Omenn Prize for the best article published in the previous calendar year in any scientific journal on a topic related to evolution in the context of medicine and public health goes to Roderich Römhild for his paper: Roemhild, R., Gokhale, C. S., Dirksen, P., Blake, C., Rosenstiel, P., Traulsen, A., … Schulenburg, H. (2018). Cellular hysteresis as a principle to maximize the efficacy of antibiotic therapy. Proceedings of the National Academy of Sciences, 115(39), 9767–9772. doi:10.1073/pnas.1810004115
The prize, provided by the generosity of Gilbert S. Omenn, is awarded to the first author of the winning article. It includes $5000 and an invitation to present a talk at the International Society for Evolution, Medicine, and Public Health annual meeting, August 13-16 in Zurich, with travel and lodging expenses covered. The prize committee including Isabel Gordo, Mel Greaves, Thom McDade, Steve Simpson, and Nina Wale was unanimous in its decision.
Dr. Römhild will present a talk based on the paper at the 5th annual meeting of the International Society for Evolution, Medicine, and Public Health in Zurich, August 13-18. Registration is open now. http://isemph.org . The full meeting schedule is posted at http://evmedconference.com
A new article by Robert Chevalier offers a broad-ranging view of how evolutionary medicine can help to understand the epidemic of chronic kidney disease. It is open access for a limited time. Chevalier, R. L. (2019). Evolution, kidney development, and chronic kidney disease. Seminars in Cell & Developmental Biology, 91, 119–131. https://doi.org/10.1016/j.semcdb.2018.05.024
Abstract: There is a global epidemic of chronic kidney disease (CKD) characterized by a progressive loss of nephrons, ascribed in large part to a rising incidence of hypertension, metabolic syndrome, and type 2 diabetes mellitus. There is a ten-fold variation in nephron number at birth in the general population, and a 50% overall decrease in nephron number in the last decades of life. The vicious cycle of nephron loss stimulating hypertrophy by remaining nephrons and resulting in glomerulosclerosis has been regarded as maladaptive, and only partially responsive to angiotensin inhibition. Advances over the past century in kidney physiology, genetics, and development have elucidated many aspects of nephron formation, structure and function. Parallel advances have been achieved in evolutionary biology, with the emergence of evolutionary medicine, a discipline that promises to provide new insight into the treatment of chronic disease.
This review provides a framework for understanding the origins of contemporary developmental nephrology, and recent progress in evolutionary biology. The establishment of evolutionary developmental biology (evo-devo), ecological developmental biology (eco-devo), and developmental origins of health and disease (DOHaD) followed the discovery of the hox gene family, the recognition of the contribution of cumulative environmental stressors to the changing phenotype over the life cycle, and mechanisms of epigenetic regulation. The maturation of evolutionary medicine has contributed to new investigative approaches to cardiovascular disease, cancer, and infectious disease, and promises the same for CKD. By incorporating these principles, developmental nephrology is ideally positioned to answer important questions regarding the fate of nephrons from embryo through senescence.