If Gary Taubes's carbohydrate/insulin hypothesis of obesity is correct, everyone would lose more weight on low-carbohydrate diets than on high-carbohydrate diets. This isn't the case, therefore Gary Taubes's 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 Body 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. See Control of overshoot for more information.
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 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. ∴ Body stores increase. There are also accusations of gluttony & sloth!
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. ∴ Body 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
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.
Inter-personal variations in postprandial hyperinsulinaemia, postprandial sleepiness & energy out explain the inter-personal variations in weight gain seen under hypercaloric conditions. See Bray et al shows that a calorie *is* a calorie (where weight change is concerned).
Insulin Resistance can be fixed. See Insulin Resistance: Solutions to problems.
Type 2 Diabetes can also be fixed. See Reversing type 2 diabetes, the lecture explaining T2D progression, and how to treat it.
Aim to fix the problem. If it's impossible to fix the problem, a low-carbohydrate diet as an adjunct to medication is fine.
2 comments:
"People with Insulin Resistance & Type 2 Diabetes have no 1st phase insulin response to a sudden rise in blood glucose level."
This was my understanding of the point of our 1st phase insulin response: upon detection of new incoming dietary glucose, to release that burst of stored insulin in order to rapidly suppress hepatic glucose output--otherwise the body will have to endure the double-whammy of 2 sources of glucose simultaneously entering the blood--exogenous + endogenous.
Folks who lack a decent 1st phase response probably can't fail to experience abnormal post-carb BG elevations. Peter D uses the term "physiological insulin resistance", and we would expect that his particular VLC diet would result in a rather pronounced inability to tolerate dietary carbs. Apparently, however, one can suffer the loss of 1st phase response on diets having considerably more carbs than ketogenic ones:
"In the past, it was recommended that the patient should consume
a diet containing 250g of carbohydrate or more, and calories for
maintenance of body weight, for at least 3 days before the [GTT]
test to obtain the best reproducibility of the test and to minimize
falsely abnormal results. Ingestion of smaller amounts of
carbohydrate (150 to 200g) is probably sufficient to prevent plateau
or diabetic-type curves in healthy subjects. Presently, no formal
dietary preparation is recommended UNLESS IT IS ESTIMATED
THAT LESS THAN 150g OF CARBOHYDRATE PER DAY HAS BEEN
CONSUMED. A low carbohydrate intake for several days preceding
the glucose tolerance test OBLITERATES the first-phase immediate
insulin response to administered glucose that is most important in
determining normal glucose tolerance. In subjects who have been
on a...decreased carbohydrate intake..., a diet containing 200g of
carbohydrate or more should be taken for a period of one week to
ensure maximal glucose use during the glucose tolerance test."
[Stefan S. Fajans, MD. Classification and Diagnosis of Diabetes
(Chap. 20) in: Ellenberg &Rifkin's Diabetes Mellitus. 5th ed. p.367]
Does this seem correct to you?
It looks as though there is a "sweet spot" of carbohydrate intake.
Too little carbohydrate kills the 1st phase insulin response (mechanism unknown).
Too much carbohydrate for one's activity level overfills the liver, causing chronic hyperglycaemia & hyperinsulinaemia, depleting the insulin store used for 1st phase insulin response (I think).
Post a Comment