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Debate/discussion between Gary Taubes and Stephan Guyenet
Key points of disagreement
1. What causes obesity?
2. What cause...
Figures illustrating Gary and Stephan’s models of obesity:
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Debate/discussion between Gary Taubes and Stephan Guyenet

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see also:
https://softpaleo.blog/2019/03/20/references-for-my-debate-with-gary-taubes-on-the-joe-rogan-experience/
and
https://www.youtube.com/playlist?list=PLA8MDM2EQtydZpOLLoId1TzJXHxYgJwAH

Publié dans : Alimentation
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Debate/discussion between Gary Taubes and Stephan Guyenet

  1. 1. Debate/discussion between Gary Taubes and Stephan Guyenet Key points of disagreement 1. What causes obesity? 2. What causes insulin resistance (and thus insulin resistance-related diseases, particularly diabetes)? Summary of Gary and Stephan’s models for obesity Gary: Obesity is a disorder of excess fat accumulation not energy balance (how much we eat and expend). The brain is responding to what happens in the body, it’s not causing it: i.e., we don’t get fat because we eat too much, we eat too much because we’re getting fatter. Body fatness, itself, is determined by the action of hormones and enzymes that directly influence fat accumulation in fat tissue and the use of fat for fuel in lean tissue and organs. The link between what we eat and how fat we are goes primarily through the hormone insulin, and insulin levels are determined primarily by the carbohydrate content of the diet: refined grains, starchy vegetables and sugars. Elevated insulin traps fat inside fat cells and inhibits use of fatty acids for fuel, causing “internal starvation”, hunger, and a reduction in metabolic rate. Excess calorie intake and physical inactivity are secondary to this process and not themselves determinants of body fatness. Stephan: The brain (because it generates hunger and cravings, determines what and how much we eat, how much we move, and regulates body physiology) is the primary determinant of body fatness, while fat tissue is more of a receptacle and buffer for excess energy. Obesity is caused primarily by a food environment that makes it easy to eat calorie-dense, tasty food rich in both carbohydrate and fat, and insufficient physical activity, in genetically susceptible people. This causes overeating and changes in fat-regulating brain circuits that promote obesity and “lock in” fat gain, making weight loss challenging. Carbohydrate intake, including sugar, contributes to obesity but isn't the primary factor. Insulin levels are not an important determinant of fat gain in the general population. Summary of Gary and Stephan’s models for insulin resistance Gary: Insulin resistance is caused by carbohydrate consumption, primarily sugar. Calorie intake, body fatness, dietary fat intake, and physical inactivity are not important contributors to insulin resistance. Stephan: Insulin resistance is caused primarily by “energy poisoning”, meaning the chronic exposure of lean tissues to fat and glucose in excess of what they are using. This happens when fat cells begin to “fill up” and lose their ability to buffer energy effectively and protect lean tissues from energy excess. Thus, insulin resistance is ultimately caused by excess body fatness, physical inactivity, and genetics. Carbohydrate intake contributes to insulin resistance, mostly via its contribution to calorie intake and body fatness, but it isn't the primary factor.
  2. 2. Figures illustrating Gary and Stephan’s models of obesity:

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