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2023 UNM Evolutionary Medicine Syllabus

Evolutionary Medicine Overview and Expectations.

Elective starts on Jan 9, 2022.   We will schedule our first meeting on Monday Jan 9thth at noon.   

Location: Virtual (mostly).

Overview – what I expect you to take away from this elective:

Priority 1. We will discuss “tree thinking” and consider our place in the tree of life. You will learn what the evolutionary principle of common descent means, and how much we have in common with other organisms on the planet. Our shared evolutionary legacy is the basis for the One Health movement that seeks to bridge the gap between human and veterinary medicine and conservation ecology. Some commonalities of disease found in many different organisms – like fever – are the result of common descent and long term selection. Understanding how evolution shapes what have in common can guide decision to start a medical treatment, or tell us when it is better to not treat at all.

Priority 2. We will learn how cooperation and conflict affect health and disease. We have genomic conflicts that are the cause of infectious disease, are important in cancers, and happen during pregnancy. These conflicts go a long way towards understanding why we have disease. Cooperation between the body’s cells is made easier by genetic relatedness, but relatedness is not the only way that cooperation between genomes can happen. Our bodies also invest in cooperative relationships with unrelated organisms in the microbiome. The best example of this is the mutualism that happens between babies and breast fed microbes. These cooperative relationships can keep us healthy.

Priority 3. We will learn about tradeoffs in human biology, and how these affect our health. Tradeoffs are super important in life history traits like the course of human childhood, reproductive maturity, menopause, and longevity. Our bodies can’t do everything well at he same time! We prioritize one goal, often at the expense of other goals. Tradeoffs also affect how our bodies respond to injuries, infections and other challenges. We have evolved mechanisms that help our bodies negotiate those tradeoffs, often with unexpected results.

Expectations for students are as follows:

The grade of outstanding will be assigned for: a) completion of all writing assignments, b) demonstration of mastery of essential evolutionary concepts as presented, c) ability to synthesize classroom information and key evolutionary medicine concepts from readings.

We will learn how human and pathogen evolution has shaped human health and disease, with special emphasis on human adaptation and the microbiome. We will review key concepts: natural selection, phylogeny, distinction between proximate and ultimate causation, resistance evolution, and evolution and evidence-based medicine.

Readings (Read prior to the first meeting).

1. Alcock and Schwartz. A clinical perspective in Evolutionary Medicine: What we wish we had learned in medical school.  Evolution: Education and Outreach, 2011.

2. Stearns. Evolutionary Medicine: Its Scope, Interest, and Potential. Proceedings of the Royal Society B, 2013.

Also read this EvolutionMedicine blog post first: Live free and die

and second: The evolution of cooperation in the microbiome

And finally, read: Fever and COVID-19

Week 1 Topic) The evolution of fever. The evolution of cooperation.

Week 1 Second Session Friday January 13th at 12:00pm. Virtual (Zoom).

Writing assignment due at the second class (email Dr. Alcock before noon on the 13th..

You have been invited to participate in a community meeting organized by a local biotech company. This company is trying to find a cure for an epidemic disease, a green chile allergic syndrome that makes its victims experience a burning sensation in the mouth and have facial skin reddening after eating green chile. Red-green syndrome is said to involve a dangerous activation of the immune system. A local company has a new drug in the development pipeline, called ruboroblockamab, trade name Burnacaide. It is a monoclonal antibody that prevents the immune system from recognizing capsaicin, a molecule in green chile that is responsible for the findings in red-green syndrome patients. Burnacaid irreversibly binds to and blocks the capsaicin receptor, TRPV-1, that is found in many tissues of the body, including the mouth and skin. The drug company wants drug approval and public funding to distribute Burnacaid widely in the community. They are especially interested in treating children because Burnacaid completely prevents red-green syndrome, and it permanently makes green chile easier for them to eat in large doses. You have been invited to give public comment about the use of this new blockbuster drug. Will you speak in favor or against the drug? Why?

Readings for second session:

  1. Microbiome Read this article about the hygiene hypothesis / old friends hypothesis.
  2. Cancer and Peto’s paradox. a) How elephants avoid cancer. b) JAMA article on elephant cancer

Optional fever podcast:

Update: Weekend writing assignment: Why does menopause exist?

Writing project: Why do women cease to reproduce in middle age? How did menopause evolve in humans?

Some suggest that menopause evolved because grandmothers are more successful at passing on their genes by investing in grandchildren than in more babies of their own. Others argue that menopause is a consequence of modern medicine that artificially prolongs the lifespan of women compared to our ancient ancestors. So in the past reproductive aging would have been in sync with aging of the rest of the body. In this view menopause reflects the early mortality in pre-history and is a gene-environment mismatch.

The artificial lifespan prolongation hypothesis espoused by Steven Austad is described here by Paul Sherman:

[Menopause] may simply be a cultural artefact. According to this ‘blessings of modern life’ theory’, menopause occurs because women live longer now than in the past. Most animals reproduce as long as they live, but zoo specimens and pets (whose lifespans have been artificially lengthened) often stop reproducing before they die. Menopause may similarly result from medically increasing the lifespan of a primate that is born with a fixed total number of gametes.

Send to Dr. Alcock on Monday. (Please note that there is a writing assignment due Tuesday also, below)

These links might help with the assignment:

1. Age-old-question Flatt T and Promislow EL. 2007. Science (318) 1255-1256.

Optional 2. Why do we age? Kirkwood Austad Nature 2000

Week 2) Life history theory – the evolution of aging.

Week 2 Session 1 Tuesday January 17th at noon. Virtual (Zoom).

Writing assignment. Email to Dr. Alcock before Jan 17th.

Imagine that a self-supporting colony is established on Mars this century, and because of a calamity on Earth, there is no exchange of people or genetic material between Earth and Mars. Because of careful screening, the Martian colony is essentially free of infectious disease. 1) Based on lower mortality from infection, how might lifespan be expected to evolve over hundreds of years in the Martian colony. 

However, radiation exposure on Mars is 40 to 50 times what it is on earth, which causes an increase in cancer, first noticeable at about age 30 and increasing with each decade. After many generations, how might this environmental source of cancer affect the age at first reproduction (menarche or adrenarche)?

We review life history theory, its application to human health, and energetic and resource allocation tradeoffs that affect lifespan

– key evolutionary concepts: antagonistic pleiotropy, declining power of selection, selection shadow, inclusive fitness, balancing selection

Senescence – why we get old

Declining power of selection – does natural selection keep post-reproductive people alive?

Life history theory – what is it?

Antagonistic pleiotropy – do genes that promote youthful health also cause disease in the elderly?

Disposable soma hypothesis.

The role of infection in diseases of senescence. Why does COVID-19 disproportionately affect the elderly.

Read: Endogenous retroviruses and aging

Week 2 Session 2. Thursday January 19th noon at Dr. Alcock’s house.

Discussion of “why” questions and final project topics.

OPTIONAL extra: Drug use, why is it so pervasive? Ed Hagen has done important work in this area, click the link to read more. See this recent video where I interview Dr Hagen:

Readings (emailed) include The antibiotic course has had its day

The curious orthodoxy of aggressive chemotherapy

At least it won’t hurt: the personal risks of antibiotic exposure

Your job is to find a randomized controlled trial on antibiotic duration (longer or shorter) or dose (higher or lower) for any condition that we can discuss in class on Thursday. se PubMed or Google Scholar or the search engine of your choice.

No writing assignment, but start thinking about what topic you’d like to explore for the final week of the elective.

Week 3)

Insulin resistance, diabetes, and evolution

Why are so many of us vulnerable to insulin resistance, prediabetes, and type 2 diabetes

Can risky microbiomes can explain why some diets are harmful, and why we get diabetes, obesity, and lifestyle inflammation.


Second Session: Jan 27th Friday at noon at Dr.Alcock’s house

Reading: Haig D. Cooperation and conflict in human pregnancy

Week 4)

January 30th. (noon) Topic Microchimerism and health

Feb 3rd (noon). Presentations.

See the final project template here.

Microchimerism in pregnancy and beyond

Listen: Reproductive conflicts – Evolution Medicine podcast


And read this review:

Do genes derived from maternal or parental sources have different effects on offspring? Do fetal genes have an influence on the mother?


1. Boddy, Amy M., et al. “Fetal microchimerism and maternal health: A review and evolutionary analysis of cooperation and conflict beyond the womb.” Bioessays 37.10 (2015): 1106-1118.

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