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

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. Figures illustrating Gary and Stephan’s models of obesity: