No, Ed Clint did not give a good response to Rebecca. He produced a bunch of information orthogonal to her point and called her a science denialist. Other people gave her relevant information, and she incorporated it into subsequent deliveries of her talk.

I don’t know what Rob Kurzban said to Marcotte, but given my experience reading him and your wording in presenting the information–along with the fact that you refuse to read the transcript to find out what criticisms she did make on this panel–I doubt that he said much worth reading.

There is data that indicates that high levels of nausea in early pregnancy is associated with better fetal outcomes, but that could have nothing to do with exposure to teratogens as affected by food choice. The association could be a spandrel.

http://en.wikipedia.org/wiki/Spandrel_%28biology%29

I suspect that the nausea of early pregnancy is a side effect of a high NO level (my current field of research), and that nausea is also triggered by high NO as part of what regulates sickness behaviors. During an acute infection, the NO level is made very high by iNOS and that triggers things like nausea so as to reduce digestion metabolic load on the liver.

NO has to be very high during the first trimester so as to facilitate hemoglobin production (via HIF and Epo), angiogeness for placental vascularization, and mitochondria biogenesis in the liver (to later support gluconeogenesis for lactation). I suspect that the metabolic demands during later pregnancy have increased quite fast (in evolutionary terms) so as to support a large infant brain made out of fat. The metabolic demands during the first trimester are actually quite low.

What would make the idea of first trimester nausea not a “just so” story would be actual data on teratogen content of foods eaten and avoided during pregnancy. Non-human animals should also avoid foods containing teratogens. Do they? If animals are compelled to eat foods they would otherwise reject during pregnancy do they have increased birth defects?

Many teratogens are nitric oxide synthase inhibitors (for example thalidomide).

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3447183/

As a nitric oxide synthase inhibitor, thalidomide would likely work pretty well as an anti-nausea medication. If eating something that reduces nausea actually increases birth defects, that kind of falsifies the hypothesis of nausea being something that protects against teratogens by altering food choice.

And to be clear, I’m not accusing just you of being entrenched. I’m accusing most of us, even myself. People committed to a particular perspective rarely change their minds. Max Planck famously said, “A scientific truth does not triumph by convincing its opponents and making them see the light, but rather because it’s opponents simply die off. Science progresses one funeral at a time.”

I hope you’ll understand why I’m bowing out from this discussion.

Someone above asks “why is there not a real evolutionary psychologist on the panel.” At the time of the birth of Evol Psych, I had essentially the same training and background as anyone else in the field, and for several years I regularly attended conferences, read the journals, participated in research (though it was not my main area). Today there are actually people trained as evolutionary psychology at a couple of institutions that focus heavily on this, but in the end they get their PhD in Anthropology (or something else general) just like everybody else does. There are no “board certified” evolutionary psychologists.

According to David J. Buller’s chapter in the Cambridge Companion to the Philosophy of Biology (2007), the phrase evolutionary psychology has been used to denote two different things:

– as a specific research program (i.e. the one that you are criticizing)
– as an entire field of “evolution of behavior” (including many different research programs, such as behavioral ecology, sociobiology, evolutionary psychology etc.).

How much of the criticisms against the “Laden / Zvan / PZM arguments against evo psych program” do you think stems from not understanding the difference between evolutionary psychology as a specific research program and “evolutionary psychology” as the research field regarding evolution of behavior?

i.e. could it be the case that a lot of your critics falsely assume that you are criticizing behavioral biology when you are actually criticizing the evolutionary psychology program?

Also, people certainly can pick and chose what answers that are raised can be responded to or ignored. Otherwise, individuals can determine the validity of the conversation based on whether or not their particular questions are addressed, and since there is no a priori reason to assume that any one individuals’s questions are interesting or relevant, that would be bad!

Regarding the scramble for food, it is important to contrast what most primates, including chimps, do vs. what humans do, when it comes to acquiring and distributing food. We have been doing something very different for a long(ish) time. (check out an upcoming Skeptically Speaking for my comments related to that, just recorded last night.)

how do you explain our taste preferences for sugar and fat

I recall a very simple behavioural explanation from Colin Tudge in The Food Connection (I no longer have it so I can’t check if my memory is incomplete or wrong in some other way).

The argument was that in pre-agricultural societies, very calorie dense / high nutritional value foods like fat and sugar were pretty hard to get. You either had to kill a largish animal and break open bones and skull to get at marrow and brain or you had to climb and / or fight off bees to collect honey.

The people who had the strongest drive to do such things were the ones who got the best nutrition by acquiring those foods. My feeling is that this presumes that food is only consumed by immediate family rather than more extended groups. Even then, I suppose you could argue that groups with a higher proportion of people willing to take those risks were more likely to succeed.

I suspect that the real story is more sophisticated. Maybe a social one – those who elbow their way to the fore or otherwise grab such foods before others will also succeed in some way. Or maybe rationing and distributing such foods is a strong social driver and people who supply the foods are held in high esteem / get first pick / whatever.

The real story is probably some narrative that links high nutritional value with more social value of some kind. Different groups would work this out in different ways. But all of those ways lead to a strong preference for calorie dense foods.

Also, I listened to the audio of the panel over a week ago, so I don’t remember what study Greg ran in his class. Please tell me at what point in the video this is mentioned. Also, I’m not sure which work you’re referring to being conducted at UCLA. All work related to human behavior and evolution? All evolutionary psychology? All evolutionary anthropology? Specific studies?

Finally, before I answer your questions, I would appreciate it if you answered my original questions: Without referring to evolution, how do you explain our taste preferences for sugar and fat and how do you explain women’s pregnancy sickness.

We can’t have a productive discussion if we pick and choose which questions we respond to.

Thanks.