If Gary Taubes' carbohydrate/insulin hypothesis of obesity was correct, everyone would get more weight loss on low-carbohydrate diets. This isn't the case, therefore Gary Taubes' hypothesis is not correct.
Although insulin is involved, it has nothing to do with "Hormonal clogs" or "Insulin fairies"!
The Aragon Insulin Fairy |
The Energy Balance Equation
Change in Bodily Stores = Energy in - Energy out, where...
Energy in = Energy entering mouth - Energy exiting anus, and...
Energy out = BMR/RMR + TEF + TEA + SPA/NEAT
See The Energy Balance Equation to find out what the above terms mean.
People with Insulin Resistance (IR), Impaired Glucose Tolerance (IGT) & Type 2 Diabetes (T2DM) have excessive insulin secretion in response to meals (postprandial hyperinsulinaemia). See Hyperinsulinaemia and Insulin Resistance - An Engineer's Perspective.
People with Insulin Resistance (IR), Impaired Glucose Tolerance (IGT) & Type 2 Diabetes (T2DM) also have impaired/no 1st phase insulin response to a sudden rise in blood glucose level. This introduces a time-lag into the negative feed-back (NFB) loop that regulates blood glucose level. If the input rise-time is less than the time-lag in a NFB loop, the output of the NFB loop overshoots. This is standard NFB loop behaviour. Trust me, I'm a retired Electronic Engineer. I've observed this (too) many times!
1. On a high-refined-carbohydrate or high-GL diet, blood glucose level rises rapidly, with a rise-time that's less than the time-lag in the blood glucose regulation NFB loop. Insulin secretion from the pancreas overshoots in a positive direction. The resulting massive postprandial hyperinsulinaemia results in down-regulation of insulin receptors in the brain, which reduces insulin action in the brain. When the insulin level eventually falls to normal a few hours later, the brain interprets a normal insulin level as hypoinsulinaemia. Hypoinsulinaemia results in ravenous hunger, as insulin is a short-term satiety/satiation hormone in the brain (leptin is a long-term satiety/satiation hormone in the brain). Ravenous hunger results in over-eating. Energy in increases. Postprandial hyperinsulinaemia also results in postprandial sleepiness. Energy out decreases. ∴ Bodily stores increase. There are also accusations of sloth & gluttony!
2. On a low-carbohydrate or low-GL diet, there are small fluctuations in blood glucose & insulin levels. There is no ravenous hunger. There is much less/no over-eating. Energy in decreases. There is no massive postprandial hyperinsulinaemia. There is much less/no postprandial sleepiness. Energy out increases. ∴ Bodily stores decrease.
In addition, there is a loss of water weight due to a loss of liver & muscle glycogen. This can be ~2kg in one day (it varies from person to person). Kidneys can increase their output of urine for hormonal reasons. This can increase water weight loss to ~5kg. See Why counting Calories and weighing yourself regularly can be a waste of time.
There are also other hormones involved. For a Facebook discussion with James Krieger that led to the updating of this post, see https://www.facebook.com/james.krieger1/posts/10153228943648587
P.S. In Metabolic Ward studies, food intake is tightly controlled, so postprandial hunger doesn't result in over-eating. Energy expenditure is also controlled, so postprandial sleepiness doesn't significantly affect energy expenditure. This is why varying Fat:Carb ratios (with Protein held constant) makes no significant difference to weight in a Metabolic Ward. See Energy intake required to maintain body weight is not affected by wide variation in diet composition.
P.P.S. Inter-personal variations in postprandial hyperinsulinaemia, postprandial sleepiness & energy out explain the inter-personal variations in weight gain seen under hypercaloric conditions.
P.P.P.S. Insulin Resistance can be fixed in the long-term. See Insulin Resistance: Solutions to problems.
Type 2 Diabetes can be fixed in the long-term. See Reversing type 2 diabetes, the lecture explaining T2D progression, and how to treat it.
Aim to fix the problem in the long-term. If a long-term fix isn't possible (due to excessive destruction of pancreatic beta cells), use a low-carbohydrate diet as an adjunct to medication.
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