The Evolution and Medicine Review

…bridging the gap.

Author: The Editors (Page 1 of 20)

ISEMPH Meeting Program Posted–Registration fees increase May 1

The June 22-25th meeting of the International Society for Evolution, Medicine & Public Health program is now available.

Registration fees increase on May 1st. 

To register for the meeting click here.
Visit the conference website
To print a version of this poster, click here



Progress on reconstituting the depleted biome to prevent immune disorders

A review and update of an important topic

By William Parker and Rajendra A. Morey
Departments of Surgery (WP) and Psychiatry (RAM)
Duke University Medical Center, Durham, NC 27707

Historical Developments

The story of resolving immune dysfunction in Western society is one of uncovering a profound evolutionary mismatch. The story began 39 years ago when a parasitologist, John Turton, intentionally colonized himself with the human hookworm and eliminated his own hayfever [1].  Sadly, the story is littered with long pauses, and Turton’s observations went unappreciated for decades. The story took a new turn in the late 1980s when David Strachan pointed an accusing finger at some aspects of modern sanitation as being responsible for the plague of chronic immune disease affecting Western society [2].

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Grants available for evolutionary medicine research in Zurich

The Centre for Evolutionary Medicine (ZEM), University of Zurich, is calling for grant applications.  The applicants are free to submit any research project within the wider field of Evolutionary Medicine,  preferably, but not exclusively, on the study of the evolution of human musculo-skeletal disease.  Primary current ZEM research topics (which show the area of research projects covered by this  scheme) can be found at

Evolution and Cancer Conference at UCSF June 12-16

From Unicellularity to Multicellularity and Back Again
2nd International Biannual Evolution and Cancer Conference at UCSF

Registration now open

Keynote talks by Mel Greaves and Anna Barker


  1. cancer suppression in the evolution of multicellularity and
  2. applying insights from the evolution of single cellular organisms to the study of cancer

Sessions include:

  • Insights  from Experimental Evolution
  • Cancer  and the Evolution of Multicellularity
  • Dynamics of Somatic Evolution
  • Peto’s  Paradox, Comparative Oncology and the Evolution of Tumor Suppression
  • Somatic  Mutation and Levels of Selection
  • Applying  the Tools of Evolutionary Biology to Cancer
  • Life  History Theory in Cancer
  • The Evolutionary Medicine of Cancer

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Paleofantasy: New book by Marlene Zuk

Paleofantasy: What Evolution Really Tells Us about Sex, Diet, and How We Live

By Marlene Zuk  (Norton, 2013)

Free sample from NCSE     Review in Salon   Review in the WSJ  Review in Nature

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Weight loss from gastric bypass via changed microbiota?

Conserved Shifts in the Gut Microbiota Due to Gastric Bypass Reduce Host Weight and Adiposity
Liou, Alice P., Paziuk, Melissa, Luevano, Jesus-Mario, Machineni, Sriram, Turnbaugh, Peter J., & Kaplan, Lee M. (2013).
Science Translational Medicine, 5(178), 178ra141. doi: 10.1126/scitranslmed.3005687  (Not open access)

Roux-en-Y gastric bypass (RYGB) results in rapid weight loss, reduced adiposity, and improved glucose metabolism. These effects are not simply attributable to decreased caloric intake or absorption, but the mechanisms linking rearrangement of the gastrointestinal tract to these metabolic outcomes are largely unknown. Studies in humans and rats have shown that RYGB restructures the gut microbiota, prompting the hypothesis that some of the effects of RYGB are caused by altered host-microbial interactions. To test this hypothesis, we used a mouse model

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Positive selection for alleles that increase inflammation

Common Risk Alleles for Inflammatory Diseases Are Targets of Recent Positive Selection
Towfique Raj, Manik Kuchroo, Joseph M. Replogle, Soumya Raychaudhuri, Barbara E. Stranger, Philip L. De Jager
The American Journal of Human Genetics – 21 March 2013       Not Open Access

Genome-wide association studies (GWASs) have identified hundreds of loci harboring genetic variation influencing inflammatory-disease susceptibility in humans. It has been hypothesized that present day inflammatory diseases may have arisen, in part, due to pleiotropic effects of host resistance to pathogens over the course of human history, with significant selective pressures acting to increase host resistance to pathogens.

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Antibiotic exposure increases risk of inflammatory bowel disease

Antibiotic Exposure and IBD Development Among Children: A Population-Based Cohort Study

By Matthew P. Kronman, Theoklis E. Zaoutis, Kevin Haynes, Rui Feng,and Susan E. Coffin

Pediatrics 2012; 130:4 e794-e803  Open Access

OBJECTIVE: To determine whether childhood antianaerobic antibiotic exposure is associated with the development of inflammatory bowel disease (IBD).

METHODS: This retrospective cohort study employed data from 464 UK ambulatory practices participating in The Health Improvement Network. All children with ≥2 years of follow-up from 1994 to 2009 were followed between practice enrollment and IBD development, practice deregistration, 19 years of age, or deat
; those with previous IBD were excluded. All antibiotic prescriptions were captured. Antianaerobic antibiotic agents were defined as penicillin, amoxicillin, ampicillin, penicillin/β-lactamase inhibitor combinations, tetracyclines, clindamycin, 

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Cancer stem cells as ‘units of selection’

By Mel Greaves, in Evol Appl. 2013 Jan;6(1):102-8. doi: 10.1111/eva.12017. Open access

Cancer development is widely recognized to be a somatic cell evolutionary process with complex dynamics and highly variable time frames. Variant cells and descendent subclones gain competitive advantage via their fitness in relation to micro-environmental selective pressures. In this context, the ‘unit’ of selection is the cell, but not any cell. The so-called ‘cancer stem cells’ have the essential properties required to function as the key units of selection, particularly with respect to their proliferative potential and longevity. These cells drive evolutionary progression of disease and provide reservoirs for relapse or recurrence and drug resistance. They represent the prime, but elusive and moving, targets for therapeutic control.

Have TB strains co-evolved with human subpopulations?

HIV Infection Disrupts the Sympatric Host–Pathogen Relationship in Human Tuberculosis    By  Fenner L, Egger M, Bodmer T, Furrer H, Ballif M, et al. (2013) . PLoS Genet 9(3): e1003318. doi:10.1371/journal.pgen.1003318   Open Access

Author Summary  Human tuberculosis (TB) caused by Mycobacterium tuberculosis kills 1.5 million people each year. M. tuberculosis has been affecting humans for millennia, suggesting that different strain lineages may be adapted to specific human populations. The combination of a particular strain lineage and its corresponding patient population can be classified as

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