We now move onto the next Myth/Fact Combo:
Myth: Insulin makes you hungry
Fact: Insulin suppresses appetite
Which leads to:
Myth: Carbohydrate is singularly responsible for driving insulin
Fact: Protein is a potent stimulator of insulin too
This is just more poor research and unsubstantiated claims. It is well-known that hyperinsulinemia precedes dietary-induced obesity and it is also well documented that increased levels of insulin produce appetite and hunger, increase food intake, and cause obesity.
Again, there are variations all along the bodyweight-body fat continuum that dictate responses from the ingestion of foodstuffs.
Overweight individuals consume more carbohydrates and have higher basal levels of insulin and also have chronically high levels of insulin throughout the day, another actual Fact in conflict with Mr. Kreiger’s assertions.
Grey & Kipnis in their 1971 publication showed that obese patients whose ad lib diets were high in carbohydrates maintained high levels of basal insulin. When these patients were placed on a low-carbohydrate, high-fat diet (either equal calorie or lower calorie to their ad lib diets), they showed a significant decrease in basal insulin levels; and, when given a diet equal in calories to their ad lib diet with high-carbohydrate, low-fat content, these individuals showed an increase in insulin levels.
Additional research during these years in which subjects were provided with a low- or high-carbohydrate diet both prior to and after inducing experimental obesity, showed that there were significant changes in insulin levels. In the obese as well as the lean condition, subjects showed increased plasma insulin levels when given the high-carbohydrate diet.
These experiments collectively suggest that the high-carbohydrate intake characteristic of the obese may act to perpetuate the obese condition by maintaining hyperinsulinemia and the consequent hypoglycemia and hyperphagia. Hyperphagia is defined as ravenous overeating.
The conclusion of this review article by appetite expert Donald Novin from the University of California in Los Angeles was that:
1) appetite and hunger may be direct functions of dietary carbohydrate. Therefore, low-carbohydrate diets are probably effective by reducing appetite and hunger motivation and thereby affecting weight loss indirectly,
2) we have attributed the appetite- and hunger effects of carbohydrates to insulin-induced hypoglycemia,
3) post-absorptive insulin-induced hypoglycemia can stimulate hunger after a high-carbohydrate meal,
4) rather than increasing appetite and hunger in general, insulin-induced hypoglycemia may specifically increase appetite and hunger for carbohydrates, then one can easily envision that a vicious cycle might ensue and ultimately may lead to exhaustion of the pancreatic beta cells,
5) all carbohydrates are probably not equally important in the prevention and treatment of obesity, and
6) in addition to causing obesity by increasing appetite and hunger, high-carbohydrate diets may also
perpetuate the obese condition by maintaining hyperinsulinemia and the consequent hypoglycemia and hyperphagia.
Importantly, the Metabolic Control of Food Intake argues that it is primarily a deficiency in ATP production because of fuel partitioning that drives appetite and hunger. Clearly, we are beginning to see that carbohydrates and insulin deserve a very bad reputation and that Mr. Kreiger’s analysis cannot hold up under scrutiny.
One of his weakest arguments is the one in which he suggests that protein stimulates a significant release of insulin. I’ve already shown that many studies of people eating real food that is high in protein actually led to a reduction in insulin secretion.
In addition, the paragraphs above describing Donald Novin’s work, confirm that high-carbohydrate diets strongly drive insulin release while low-carbohydrate, high-protein diets promote a decrease in blood levels of insulin.
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