Students delivered many thoughtful and creative presentations today. These included consideration of co-evolutionary arms races in lymphatic filariasis, antagonistic pleiotropy in Alzheimer’s, adaptive vs. maladaptive hypotheses regarding OCD symptoms, ADHD and schizophrenia-risk alleles, and polycystic ovary disease. Also the interaction of anemia and malaria in Africa was discussed, as well as microbiota transfer in kissing, and the evolution of AIDS.
Great points made by students were: the inclusion of many alternative hypotheses, both adaptive and non-adaptive; highlighting the evolutionary hypothesis and contrasting it with proximate causation. I also appreciated the participation of the audience and the very well-informed questions posed by undergrads and graduate students. Nice work, all.
Regarding HIV, I made reference to 30K years ago being the last common ancestor of immunodeficiency viruses. That date was proposed as an early date of divergence of SIV among primates (not HIV). As Michael presented, HIV and SIV have a common ancestor that diverged 100-200 years ago by some estimates. Worobey and colleagues have published one of the best dating estimates in the literature. Also here.
- gluten-free diet and celiac disease
- inter-pathogen interactions in a single host
- evolution of obsessive-compulsive disorder
- co-evolution of viruses with our bodies
- evolution of schizophrenia
- allocation of resources during pregnancy
- MHC and mate choice
- genetics of mental illness, bipolar diseases
- evolution of HIV
- cancer: acute vs. chronic and metastasis
- Alzheimer’s disease
Here are the links that Dr. Cooper mentioned today in class regarding artemisinin:
Wooly bear caterpillars seek out foods with plant toxins when they are parasitized. Is this self-medication behavior? Are we, like the caterpillars, predisposed to take medication when we don’t feel well.
Sometimes, when we get sick, we are not interested in eating at all. This loss of appetite (anorexia) is art of what has been termed “sickness behavior.” Is sickness behavior adaptive? Could anorexia, too, be adaptive?
Read: Immune Brinksmanship
On November 12th the topic will be microbial manipulation of host behavior. Can this be an important feature of human health and behavior?
For an introduction, read this Berkeley Science Review.
I am writing a hypothesis paper with Athena Aktipis and Carlo Maley entitled: “Could microbial manipulators be the culprits behind unhealthy eating” The abstract is here:
Two of the greatest unsolved mysteries of our time are (1) why obesity has reached epidemic proportions in the western world, and (2) why we crave foods that are so bad for us. Here we suggest that solving these mysteries may require a closer examination of the influence that gut microbes may have on our physiology and behavior. Unhealthy food preferences, according to conventional wisdom, have evolved because high-fat, calorie dense, and salty foods were much more limited in the environment of our distant ancestors. However, some evidence suggests an alternative explanation: our cravings and aversions may serve the evolutionary interests of our gastrointestinal microbiota. Here we investigate whether our gut microbes have the means, motives, and opportunity to control our eating behavior. Gut microbiota have direct access to the blood stream (via absorption of small molecules through our intestines) and nervous system (via enteric nerves), giving them the ability to manipulate us to consume nutrients that promote their survival and proliferation. Many examples exist of microbes manipulating the behavior of host organisms; we hypothesize that microbes influence eating behavior, in part by rewarding us for eating the foods upon which they depend, or by making us feel bad if we do not provide a constant supply of their 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. Here we consider the interplay of competing fitness interests of host and microbiota and review the evidence supporting our hunch that microbial puppetmasters may be the culprits behind unhealthy eating behavior and the obesity epidemic.
I can email students a draft of the revised document but cannot post it here (it is not a required reading). A similar argument has been published by Lyte (2013) above, which is a required reading.
Writing assignment (1 page max): Do you think it is likely that our food cravings are driven by the evolutionary interests of our gut microbiota? Why or why not? Are there other explanations for why we crave fatty, sugary, and salty foods?
Optional extra credit: (3/4 page max):
Conditional virulence expression is common among bacteria inhabiting the human gut. The system of intra- and inter-specific communication known as quorum sensing uses detection of signal molecules, including nutrients, to regulate virulence and growth. Carbon growth substrates (e.g., glucose) and critical micronutrients (e.g., iron) have key signaling roles that regulate virulence-related factors. Many pathogens are sensitive to the availability of iron, activating virulence when iron is limited. The same is true for zinc and manganese, and glucose. “Nutrient virulence” is a newly coined term to describe the pathogen strategy of harnessing or destroying host cellular machinery to exploit the nutrients held within. The concept of nutrient virulence suggests that when gut microbes are starved for nutrients needed for growth, they will attack host cells to gain access to those resources. Drawing on the Ponton article, do you think that facultative virulence by gut microbes could affect our food choices?