Thursday, July 10, 2014

Upcoming Talks

I have two talks planned over the next two months.  Hope to see you there!

Ancestral Health Symposium 2014: UC Berkeley, August 7-9

If you want to understand the most rigorous science available on leptin resistance-- a key mechanism of obesity and a major barrier to fat loss-- this talk is for you.  This is my primary area of professional expertise; I have years of firsthand research experience on the subject and I've published a number of related papers in peer-reviewed journals.  The talk will be accessible to nearly all levels of expertise.  AHS14 tickets are available here.  I've pasted the talk's abstract below.

What Causes Leptin Resistance?

Leptin is the primary hormonal regulator of body fatness.  Obese people exhibit a resistance to leptin’s effects in the brain, causing the brain to oppose fat loss by multiple mechanisms.  Research in animal models suggests that leptin resistance may be required for obesity to develop.  How does leptin resistance occur, and what causes it?  Research has not yet provided us with definitive answers, but several plausible possibilities have emerged.  This talk will review what is known about leptin resistance and its causes.

McDougall Advanced Study Weekend: Santa Rosa, CA, September 5-7

Dr. John McDougall invited me to speak at his yearly symposium after viewing my TEDx talk "The American Diet: a Historical Perspective".  I look forward to sharing my thoughts and interacting with a different audience than I'm used to.  The talk will be an expanded version of the one I presented at AHS13.  Tickets are available here.  I've pasted a modified version of my AHS13 abstract below.

Insulin and Obesity: Reconciling Conflicting Evidence

The pancreatic hormone insulin regulates the trafficking and metabolism of carbohydrate and fat, and its secretion is particularly stimulated by carbohydrate and protein.  Since circulating insulin is elevated in common obesity, and insulin influences fatty acid flux into and out of fat tissue, this has raised the possibility that elevated insulin causes common obesity, and that dietary carbohydrate is particularly fattening.  A large amount of evidence appears to support the hypothesis that insulin causes obesity, and a large amount of evidence appears to falsify it.  This presentation will outline a framework capable of reconciling this seemingly conflicting evidence.


Unknown said...

Looking forward to seeing you in a few weeks at AHS14!

Stephan Guyenet said...

Thanks Aaron-- Likewise!

ProfessorEd said...

How well established is the idea of beta cell "exhaustion?"

The standard diabetes type II account is insulin resistance, followed by increased level of insulin production from the beta cells. It is then claimed that eventually they become "exhausted" (plausibly due to accumulation of oxidation damage), and can no longer produce enough insulin, leaving too high blood glucose and the usual bad effects of high glucose.

If correct, it seems to me that the logical implication is to try from an young age to limit the need for high insulation secretion (less over eating, less high glycemic foods, less heavily sugared food, less carbohydrates, especially of the rapidly digested type). Hopefully, this could delay the time of diabetes until old age, (or even never).

This general account could explain why rates are high in the modern world, with high added sugar diets, easy to chew highly digestible carbohydrate foods, etc., while rates seem to be low in a wide range of traditional eating societies. When the point of "exhaustion" is reached could easily depend on the number and size of the beta cells which is probably under genetic control, with people differing widely.

Evolution would have selected for traits that kept the beta cells functioning in those societies that had historically ate diets that stressed the beta cells.

The beta cells are a very small fraction of total body weight and energy consumption, and one would have expected evolution to have given them enough spare capacity to keep functioning into old age under the diets typical in prehistory (and even early agriculture).

An immediate implication might be to resist the demands of children for lots of sweet food, cokes, ice cream,high sugar breakfast cereals, etc.

tomR said...

I have some problems with McDougals identification of ancestral diets. In his book The Starch Solution he has a chapter on what he calls a true ancestral diet, where he kind of compares poor starch-eating, and healthy people to rich, who he claims had dieseases on "richer" diets.

The problem with such approach is that it's the rich people who were to become our ancestors. Disproportionately so. A leading researcher on the influence of diets on wealth on fertility is Gregory Clark, he wrote 2 books: "A farewell to alms", and "The Son also Rises". His conclusions are staggering; eg. 90% of English at the dawn of industrial revolution are descendants of just 10% of the richest from the middle ages.
Because of such uneven distribution of survability when talking about the ancestral diet it's crucial to identify:
1) out of the entity of any past population - what is the subset that become ancestors of most of the moderns - the safe bet is on richer than average, excluding the poorest, unlikely to be ancestors to moderns
2) what is the diet specific to this subgroup of "dominant ancestors"

Just counting a typical food intake for an average member of a past population fails to include skewed distribution of survability of lines; that we already know was there. Especially would it be a good advice to emulate the traditions of those who failed to survive?

There are a lot of free videos about it, eg: