Final projects

I hope everybody enjoys Thanksgiving!  For myself, I have a lot to be grateful for, including the privilege of teaching this class.

Here is what I will be looking for in your presentations: Try to spend at least 50%, preferably more, of your time talking about ultimate causation, evolutionary considerations, or natural selection. Do not leave the evolutionary parts to the end of your presentation. Be sure to review the grading rubric.

I would like you to correctly identify an evolutionary concept (or evolutionary hypothesis category). These include (in no particular order):

  • evolution of virulence
  • host-pathogen arms race
  • red queen hypothesis
  • evolutionary trade-offs
  • life history theory
  • balancing selection
  • gene-environment mismatch
  • paleolithic diet hypothesis (and criticism)
  • inclusive fitness (kin selection)
  • adaptation
  • natural selection
  • genetic drift
  • antagonistic pleiotropy
  • declining power of selection with age (mutation accumulation)
  • evolution of resistance (to antibiotics, pesticides, chemotherapy)
  • disposable soma
  • host defenses (like fever, cough)
  • reaction norms
  • developmental plasticity, developmental programming
  • predictive adaptive response
  • thrifty genes, thrifty phenotype
  • hygiene hypothesis, old friends hypothesis
  • genetic conflicts, parasite manipulation
  • adaptive sickness behavior
  • cancer as somatic evolution, cancer as infectious process
  • conflict and cooperation in the microbiome

This is not an exhaustive list. If there is another concept you want to discuss, email me and I will add it. If you are confused, I want you to get it right, so email me or email John prior to your presentation.

It is good to also include at least one alternative hypothesis. In that case the alternative, or null hypothesis, might be a non-evolutionary hypothesis.

Please practice your presentation, preferably with a timer. I want you to aim for 12 – 15 minutes per presentation.

Finally, remember Dec 1 will be potluck, as discussed in class. See you then!



Pathogen virulence

Next Tuesday November 24th, we will cover the evolution of virulence.

From Baba Brinkman’s Parasite Wars:

“For the pathogens, that’s why some are deadly serious
And others are mild: it’s the evolution of virulence…We got the pattern figured out. Some can only spread if they keep you walkin’ around
Others spread better if you’re stuck in bed in agony.”

There will be no writing assignment. Two students will be giving final presentations on Tuesday starting at 7:00pm.

Why do some infections kill us, while others are hardly noticed?


Evolution of virulence. Ewald PW. 2004. Infect Dis Clin N Am (18)

Watch and Read Baba Brinkman’s “Parasite Wars” and “So Infectious”

For discussion:

Why do “hospital-acquired” infections get different antibiotics than “community acquired” infections? Which are generally worse and why?


Suppose the New Mexico Legislature is taking up the following bill for consideration. It promotes the use of hand sanitizer before every handshake; it would be illegal for somebody to not use hand sanitizer before shaking hands with another person. The bill would be accompanied by a massive public information campaign and incentive program, for instance free hand sanitizer. Explore the effects of this initiative on the evolution of Rhinovirus, the virus that causes the common cold. Assume that after enactment,this bill results in a change in behavior of New Mexico citizens.  Would you expect a change in virulence, the duration of infectivity, transmission rates, and mortality of Rhinovirus in New Mexico?

Update: Enjoy Baba Brinkman’s “So Infectious” and “Parasite Wars”

Be prepared to discuss these tracks, full lyrics below.

Continue reading

Special Guest Katie Hinde PhD 11/17/15

Katie Hinde PhD

Katie Hinde

Title: Milk in Evolutionary and Clinical Perspectives

Castetter 258. Time 5:30pm
Why Mammals Suck: Mother’s Milk and Infant Development

The maternal environment, physiological during fetal life and behavioral during infancy, has well-established influences on infant development. However among mammals physiological investment in the form of mother’s milk continues postnatally but remains poorly understood. Although mother’s milk fundamentally frames the infant’s nutritional ecology and socioendocrinology, until recently very little research effort has been allocated to understanding the behavioral biology of mother’s milk and infant outcomes from an evolutionary perspective. Here I will present emerging research from the Comparative Lactation Lab that addresses the magnitude, sources, and consequences of inter-individual variation of milk bioactives in humans, monkeys, and other mammals. Of particular note, my long-term, inter-generational research at the California National Primate Research Center has produced >1000 milk samples from hundreds of rhesus macaque mothers (Macaca mulatta). Just as individuals vary in their “mothering style,” the fats, proteins, sugars, minerals, hormones, bacteria, and other constituents in mother’s milk vary substantially. That inter-individual variation is associated with differences in infant behavior, growth, health, and development, and through those effects has consequences for transitions to adulthood and reproductive debut. For example, milk not only builds the infant’s body, but fuels the infant’s behavioral activity. Moreover, the biological “recipe” of milk can differ for sons and daughters and the critical windows for maternal effects differ between sons and daughters, likely reflecting sex-differentiated developmental priorities and sensitivities. A better understanding of variation in milk composition enhances an evolutionary biological perspective of parent-offspring dynamics. Moreover, biological and social scientific research on breastfeeding and breast milk can directly translate to more personalized clinical recommendations and health optimization for mothers and their infants.  Further, a better understanding of the composition and function of milk informs the composition of a more representative infant formula for those mothers facing obstacles or contraindications to breastfeeding. Transdisciplinary approaches to mother’s milk, along with public engagement, facilitate discoveries at the bench and their translation to applications at the bedside.

In preparation for Tuesday, read this Carl Zimmer piece in the New York Times about cortisol in mother’s milk having lasting effect on their offspring’s behavior:

Screen Shot 2014-11-07 at 9.52.16 PM

Click on the image for the Zimmer article. Photo by Kathy West from NYT

Reading for Tuesday’s talk:

  1. Babies get buddies
  2. Maternal Cortisol 2014-Hinde
  3. Infant Gut Microbiota: Developmental Influences and Health Outcomes by Melanie Martin and David Sela

Writing assignment:  Would you support a law making breast milk mandatory for babies, as long as it had a provision to supply donated milk for mothers unable to breastfeed? Is there a downside to formula, or to donated milk?

Extra link, just for discussion: Breast milk ice cream

Developmental programming and the predictive adaptive response for Tuesday 11/10

Developmental programming is thought to be a source of many adult diseases, including obesity, diabetes, and cardiovascular disease. The notion that early life experiences, including nutrient transfer from the mother in utero, can anticipate future environments and also shape the risk of later adult diseases has been termed the predictive adaptive response, or PAR.

This relationship first came to light when Barker documented a curious association between birth weight and adult cardiac events in British men. Babies born small had a higher risk of chronic inflammatory diseases as adults. These small babies have been described as adopting a “thrifty phenotype.” That is, nutrient deprivation as a fetus is thought to have shaped the developmental trajectory in these individuals. This shift results in reduced expenditure on muscle and increased energy storage as fat.


1) Kuzawa Evolution developmental plasticity, and metabolic disease

2) Birth Weight and Coronary Heart Disease

3) Birth Weight and Insulin Resistance

4) PNAS-2013-Hayward PAR

5) Horta Metaanalysis of breastfeeding and obesity


5) Developmental Origins of Obesity

6) Predictive Adaptive Response

In keeping with the last two weeks, there will be no writing project. Instead, find examples from  the internet how early life experiences change the body’s development in ways that cause disease? Could these changes also be adaptive, or not? (Try using the search terms “Predictive Adaptive Response” and or “Developmental Origin of Health and Disease” or DOHAD)

Watch You Tube Video on Epigenetics and Fetal Programming:

  Paul Franks: Genetic and epigenetic catalysts in early-life programming of adult cardiometabolic disorders.

Evolutionary biology of cancer

Asian elephants

I. Whales and elephants have many more cells than humans. You might think that they would get more cancer since each cell has an opportunity to accumulate somatic mutations that could lead to cancer. In fact whales and elephants, despite their larger size have lower cancer rates compared to humans. This phenomenon is called Peto’s paradox, the lack of association between larger body size and cancer incidence.

Why do elephants have little cancer? My friends Carlo Maley and Josh Schiffman set out to figure out why. Their answer that has to do with DNA repair mechanisms and apoptosis, the process whereby damaged cells kill themselves. They published their results in JAMA this month:

Abegglen Maley Schiffman Potential Mechanisms

(Students scroll to the bottom for assignments for 11/3/15)

II. Clam cancer

Metzger et al. 2105

In cancer, clonal cells evolve ways to escape restraints on growth and motility. These evolved traits favor the fitness of the clones (in the short term anyway) usually to the detriment of the organism that gave rise to the neoplasm. However, cancer lineages are usually dead ends, so that adaptations that allow neoplasia are not passed on from generation to generation. New cancers have to start from scratch, evolving de novo mechanisms to evade controls on growth and reproduction in each lineage. At the same time, anti-cancer adaptations have evolved in multicellular organisms that control and remove proto-neoplastic cells. Multi-generational selection thus permits ongoing evolution of adaptations against outlaw cells, keeping cancer at bay, at least most of the time.

What happens when cancer lineages don’t die with their host? Those cancers would not require de novo mutations to escape control. One might suppose that a cancer that can jump from host to host would evolve to be a formidable parasite with efficient means of evading host control. Recently a transmissible leukemia found in clams seems to support this view. Transmissible cancer in clams joins only two other contagious cancers, the facial tumors of Tasmanian devils and a venereal cancer of dogs.  In these unfortunate cases, the cancers is apparently passed from generation to generation. These cancers do not have the handicap of starting from scratch in carcinogenic evolution. They behave more like pathogens, in a never ending evolutionary arms race with the host organism.

In soft shell clams found in the Northeastern US and Canada, a leukemic cancer is genetically identical and widespread, suggesting it has evolved a parasite-like capacity for infection and transmission.

Skim Metzger et al’s article: Horizontal Transmission of Clonal Cancer Cells Causes Leukemia in Soft-Shell Clams

For an in depth article on Tasmanian Devil facial cancer, read David Quamman’s 2008 article

III. Why does cancer evolve in the first place?

Figure 1 from Aktipis and Nesse 2012

Read: Aktipis and Nesse Evolutionary foundations for cancer biology

IV. Maternal fetal conflicts and the evolution of cancer.

Screen Shot 2015-10-29 at 9.34.30 PM

Read: Maternal-fetal conflict, genomic imprinting and mammalian vulnerabilities to cancer

Assignment for Tuesday 11/3/15: There will be no writing assignment due. Instead come prepared to talk about these readings. Read all of them, but specific assignments will depend on your birthday month: If your birthday is January, February or March, you will discuss elephants and Peto’s paradox. If your birthday is April, May or June you will discuss cancer in clams and Tasmanisn devils. If your birthday is July, August or September, Evolutionary foundations of cancer. If your birthday is October, November, or December you will discuss Maternal-fetal conflict imprinting and cancer.

Good luck!