Let's say you and I are identical twins. We eat the exact same things, do the exact same amount of work, etc every single day.
Let's say I am getting sick and go to my doctor, who prescribes a round of Cipro to kill a bug I've picked up.
We continue to eat the same and workout the same. Will be both gather the same nutrients from that equal amount of food?
Or similar situation but one twin has a thryroid that isn't functioning properly. Same question.
Calories in and out is the main equation, but there are variables that can impact it dramatically.
Primal since August 2012. CW: 317.
1/8/13: 303.5 | 2/12/13: 298.5 | 2/26/13 295 | 3/07/2013 291.5
I'm asking why you think a low carbohydrate diet increases insulin sensitivity; what the mechanism is.
Less dietary carbohydrate --> less stimulus for the beta cells of the pancreas to secrete insulin --> less serum insulin --> less insulin tolerance in the body tissues
I'm not claiming to be a molecular biologist. That makes sense to me. If it's inherently a wrong thought process, please explain why.
I still don't understand how you think the study you linked to proves that calorie restriction and calorie restriction alone is responsible for the changes in the subjects. As I mentioned, any 600kCal/day diet is a low carbohydrate diet by definition.
Calorie restriction in general leads to a loss of fat, which in that study was the cause of the increased insulin sensitivity, because free fatty acids are lipotoxic. Reduce the fat, reduce the lipotoxicity, restore function to the organs. Nothing to do with carbohydrates.
Absence of rapid insulin secretion in response to a rise in plasma glucose is the hallmark of type 2 diabetes [3, 21], and the decline in beta cell function determines the progression towards a need for insulin therapy . However, conventional therapy, even with sulfonylurea, fails to produce more than a small increase in the first-phase insulin response. As a consequence, the rapidity and extent of return of beta cell function in response to dietary energy restriction in the present study is striking. It supports the accumulating information on the inhibitory effect of fatty acids on insulin secretion in vitro and in vivo [22–24] and is the first direct evidence in humans that the beta cell defect of type 2 diabetes is reversible by sustained negative energy balance. Prolonged elevation of plasma fatty acids in humans decreases insulin secretion [25, 26], and it has previously been shown that there is an association between pancreatic fat content and type 2 diabetes [27–29]. Prior to the onset of spontaneous diabetes in rodents, both total pancreatic fat and islet triacylglycerol content increase sharply [30, 31]. In vitro, chronic saturated fatty acid exposure of beta cells inhibits the acute insulin response to glucose, and removal of fatty acids allows recovery of this response .
The present data provide clear evidence that decreasing total pancreatic fat is associated with a return of beta cell function. However, it is probable that the negative effect on beta cell function is exerted by toxic intermediaries such as diacylglycerol and ceramides, which change rapidly in response to acute metabolic changes , rather than by stored triacylglycerol per se, which acts as an index of fatty acid intermediary concentration.