2017 Evolutionary Medicine meeting

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Mark your calendars. This August 18th-21st will be the third annual meeting of the International Society for Evolution Medicine and Public Health. The first two meetings were amazing and fun. This summer’s event promises to be that and more.

For more information click here

Important: November 15th is the deadline for abstract submissions. If you have not yet, please submit right away!

See you in Groningen, Netherlands, this summer!

 

Darwinian Medicine Interview

Screen Shot 2017-02-13 at 1.06.24 PM.pngI recently did a brief Q & A with Eirik Garnas who writes at the blog Darwinian-Medicine.com

Here is the interview:

  1. Who are you? What’s your profession and educational background?

I am an emergency physician and professor of emergency medicine at the University of New Mexico Health Sciences Center, and I am an adjunct professor in the UNM Biology Department, where I teach a course on evolutionary medicine. I have a background in evolutionary ecology, with a master’s degree in neurobiology and behavior from Cornell University. I received my MD from UCLA in 1997 and did my residency in emergency medicine at UNM.

  1. How did you get interested in Darwinian/evolutionary medicine and the human microbiome?

My original plan was to become an evolutionary biologist. I changed gears during graduate school after I heard a talk by Paul Ewald, the author of the book “The Evolution of Infectious Disease.” He explained why microbes like Vibrio cholerae (the one that causes cholera) have evolved to be deadly pathogens, untamed despite a long coevolutionary history with humans. I found his argument very convincing and I was excited to study evolutionary questions that apply to human health and disease. Soon after, I decided to go to medical school hoping to contribute to the emerging scientific field known as evolutionary medicine, or Darwinian medicine.

  1. What’s the main focus of your research?

My research uses evolutionary principles to understand cooperation and conflict in the human gut microbiome, specifically in relation to diet, stress and sleep. One of the things I am interested in is the effect of workplace stress on gut bacteria, and how that affects on-the-job eating, especially during night shifts.  It is known that overnight shift work causes weight gain, obesity, and mood disturbances. My current research is exploring whether there is a link between those outcomes and the microbiota. 

  1. 2014, you published an excellent review paper entitled Is eating behavior manipulated by the gastrointestinal microbiota? Evolutionary pressures and potential mechanisms in the journal Can you briefly summarize what that article is about?

We proposed in that paper that unhealthy food preferences, cravings and aversions may serve the evolutionary interests of our gut microbes. One possibility is that microbes hijack our nervous systems with neurotransmitters and appetite peptides that mimic our own. If so, our food choices may be less an issue of willpower, and more the result of our gut bacteria. Many examples exist of microbes manipulating the behavior of host organisms, and we hypothesized that microbes influence eating behavior, in part by rewarding us for eating the foods upon which they depend, and by making us feel bad if we do not provide a constant supply of growth-limiting nutrients. In other words, the problems of overeating, obesity and diabetes may lie less in our genes or our brains, and more in the composition of our guts.

Continue reading

Final Presentations

Start on Tuesday!

Here’s what to expect:

Be sure to click on the link that describes the grading rubric and has a template that you can (or not) use.

Do’s and Don’ts

Here is what I will be looking for: While I am listening to your presentation, I am waiting for the evolutionary hypothesis and evidence that you understand how to consider diseases in terms of evolution and natural selection. So make sure that evolution appears early in your presentation

Make eye contact with the audience.

Practice your presentation, it will be better.

Time your presentation at home. Aim for 12 – 15 minutes.

Things to avoid:

Some previous students have started their presentations with a lot of detail about proximate causes and leave their discussion of an evolutionary hypothesis until the last slide or two. That is not good.

Avoid too much text on your slides.

Make sure you don’t have too many slides!

Good luck!

 

 

Developmental origins of disease

screen-shot-2016-11-18-at-8-24-16-pmDevelopmental 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 shape the risk of later adult diseases is known as the Developmental Origins of Disease.

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. These developmental adjustments would be “thrifty” because muscle has much greater metabolic fuel demands than does fat. In addition, these small babies are also known to differ in the composition of their adipose tissues: they store fat primarily as visceral fat.  Visceral fat is the “unhealthy” abdominal fat which predisposes to diabetes and atherosclerosis. However, visceral fat has the advantage of being readily mobilized in the setting of stress or infection. The combination of metabolic thriftiness, reduced outlays devoted to costly muscle tissue, and increased ability to mobilize energy during times of stress is posited to promote survival. In terms of human development, the thrifty phenotype also preserves priority energy access for key organs, such as the brain.  For an expanded treatment of these concepts, see Kuzawa et al: Developmental Origins of Adult Function and Health: Evolutionary Hypotheses (below).

As a corollary to these arguments, it has been suggested that fetal nutrient provisioning provides a signal to the developing organism about the future state of the environment it will be born into. If conditions are good, reflected by increased maternal transfer of resources to the developing fetus, the baby will be born large. If these cues are an accurate signal of plentiful nutrition in childhood and later life, babies born large may develop as more muscular, larger, and with less stored fat, even though this strategy may be riskier in times of famine or epidemic disease.  By contrast, small babies, reflecting poor maternal nutrient provisioning in utero, may portend a resource-scarce environment during childhood and early adulthood. These infants might have an advantage if they develop a thrify phenotype that promotes a robust response to environmental stress.   The key is whether in utero conditions can predict a future state. If so, these fetal physiological adjustments, favoring a thrifty phenotype, will be adaptive in later life.

Recently, the Predictive Adaptive Response (PAR), which provides the underpinnings of the adaptive nature of the thrifty phenotype, has come under criticism. The main argument against the PAR is that fetal nutrient scarcity is a poor predictor of later scarcity. Even if a mother is pregnant in a time of famine, it does not mean that 20 years later, their adult offspring will be more likely to experience famine than a baby born to a mother who did not experience food shortage. As a result the thrifty phenotype is as likely to be maladaptive in adulthood than adaptive.

However, the fetus does have access to other cues which might be better predictors of a future state.

These are microbial cues, because infants inherit their microbiota from their mothers. Because microbiota transfer is a key determinant of the composition of the gut microbiota, with durable effects, it follows that microbiota transfer constitutes an intergenerational transfer of signals that can affect development.

Readings:

1) Kuzawa et al: Developmental Origins of Adult Function and Health: Evolutionary Hypotheses Annu Rev Anthropol 2009 

2) Gluckman Effect of in Utero and Early Life Conditions on Adult Health and Disease

3) Saben Maternal metabolic syndrome programs mitochondrial dysfunction via germline changes across three generations Cell Reports 2016

Extra 1): Muller birth mode and the neonatal intestinal microbiome

Extra 2) Of the bugs that shape us: maternal obesity, the gut microbiome, and long-term disease risk

The Evolution of Virulence

Why do some infections kill us, while others are hardly noticed? Rapper Baba Brinkman may have the answer:

“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.”

Baba Brinkman’s “Parasite Wars”:

Read:

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

Virulence in malaria: an evolutionary viewpoint MacKinnon and Read AF 2004 Proc Royal Soc B

Beyond mortality: sterility as a neglected component of parasite virulence Abbate et al. 2015 Plos Pathogens

The adaptive evolution of virulence: a review of theoretical predictions and empirical tests Cressler et al. 2015 Parasitology

Writing: If bednet deployment is successful and permanently widely adopted in countries plagued by Falciparum malaria, how would you expect the parasite to evolve over time.

Also enjoy Baba Brinkman’s “So Infectious”:

 

Baba’s full lyrics below. Continue reading

Evolution of cancer

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Multi-cellular organisms have solved a special problem that single celled organisms don’t have: how to make cells cooperate together and restrain themselves from reproduction. In single cell organisms, there is no (little) cost to replication. Every division and  replication = higher fitness. Not so for multi cell organisms. Multi-cell organisms benefit because cells can differentiate and perform different jobs. This division of labor allows increased flexibility and potential for adaptation. But, flexibility comes with a cost: specialized cells must cease or slow their own cell division. This reduction in cell division is altruistic but potentially evolutionarily unstable. How?  Rogue cells that prioritize replication are favored by short term selection. These traits benefit the cell, but not the organism as a whole. This conflict is inherent in multicellularity.  When cooperation breaks down, cancer happens.

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 cancer. However, cancer lineages are usually dead ends, so that adaptations that allow cancer 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-cancerous 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. 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.

Figure 1 from Aktipis and Nesse 2012

  1. Aktipis and Nesse Evolutionary foundations for cancer biology
  2. A second transmissible cancer in Tasmanian Devils
  3. Cancer across the tree of life.

Writing project (pick one)

  1. If cancer is an inevitable part of life, and starts with a single cell, it makes sense that early detection should allow doctors to start treatment early, and save lives. However, aggressive widespread early screening and treatment of many cancers can be counterproductive: Screening for breast cancer in young women and widespread melanoma screening have each failed to reduce death rates. If screening really does not save lives, why do you suppose this is so?
  2. Doctors often biopsy tumors to figure out how dangerous a cancer is. High genetic diversity of the tumor predicts a bad outcome, carrying an increased rate of death. From an evolutionary perspective, why is high genetic diversity in cancers bad for mortality?

Malaria in Uganda – Roland Cooper November 1st

Roland Cooper PhD of Dominican University has spent the last several summers in Kampala Uganda studying resistance patterns to the malaria parasite Plasmodium falciparum. He will be visiting UNM on November 1st to discuss his work on Artemisinin Resistance in Plasmodium falciparum.

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Read his recent article  Lack of Artemisinin resistance in Plasmodium falciparum in Uganda

For review:

  1. Malaria Infection Increases Attractiveness of Humans to Mosquitoes. Lacroix R, Mukabana WR, Gouagna LC, Koella JC (2005) PloS Biol 3(9):e298.
  2. NPR Mosquitoes are more likely to seek out human blood after infection with Plasmodium. Another example of hijacking of host neural machinery?
  3. Malaria Chapter
  4. Read Curious Orthodoxy Antibiotic Prescribing

Writing Assignment: Artemisinin is modern drug derived from wormwood, an ancient remedy for malaria. Artemisinin in combination with other drugs is the last effective treatment for Falciparum malaria in many places in Asia, and especially in Africa. If you were in charge of the World Health Organization, what are two things you would recommend to ensure that we can still use artemisinin for malaria in Africa 20 years from now.

Make up extra credit (only do this if you have missed a writing assignment, or missed a class because of illness, or previously turned in an assignment late). Some research supports the idea that malaria parasites manipulate their hosts. How and why might the malaria parasites affect  mosquitoes and their human hosts?

Tuesday, November 1st 2016, 5:30PM; 107 Castetter Hall, guest lecture for the Evolutionary Medicine Class:

Campus map – (Castetter is #21):screen-shot-2016-10-25-at-11-09-29-am