The "Liberalized Ketogenic Diet," Insulin Sensitivity, Resistance Exercise

The authors of this article [Pfeifer and Thiele, 2005: (http://www.direct-ms.org/pdf/NutritionNonAuto/KetogenicDietModifiedEpilepsy.pdf)(http://www.ncbi.nlm.nih.gov/pubmed/16344529)] used a liberalized ketogenic diet in people who had epilepsy, and this essentially meant that the people ate low glycemic index carbohydrates instead of no carbohydrates at all. A food with a low glycemic index is one that doesn't create a spike in plasma glucose and therefore does not cause a lot of insulin to be released. The glycemic index (GI) is the ratio of the area under the plasma glucose vs. time curve for the food in question (a bowl of a specific cereal, for example) [AUC(food)] to the AUC of pure glucose, times 100. So it's AUC(food)/AUC(glucose), and pure glucose has a GI of 100. The concept has been applied to the management of the diets of people who have diabetes, but there's research showing that it may be more important to keep the size of a meal small than to eat big meals with low GI foods. So a person who ate a giant meal of the best quality bread, with a low-GI, the amount of insulin released over the period following the meal (and hence the suppressive effect on ketone formation in the liver or in astrocytes, in theory at least) might well be larger than if a person ate a small meal of candy or something. I don't know the details on the amounts of carbohydrates used in that study, and so this is obviously something a person would want to discuss with one's doctor.

I'm mentioning this because it's relevant to other supposed applications of the "ketogenic diet," and the effect of the use of low GI foods, in combination with the use of low doses of some sort of ketogenic supplement (such as HMB or sodium butyrate, which doesn't provide a lot of calcium and phosphate, added to supposedly compensate for the phosphate-sequestering effect, in the GI tract, of a calcium salt of an organic anion), would be similar to the use of those low-doses of ketogenic substrates with resistance exercise, in my opinion. I'm just saying that resistance exercise generally has, in my opinion, a much stronger insulin-sensitizing effect than endurance exercise, and that's the idea behind this type of modified ketogenic diet. The idea is to increase insulin sensitivity, but it's also relevant that the growth hormone release and elevations of serum IGF-1 (or even IGF-1 released locally from satellite cells, in the muscles) are known to contribute to ketogenesis [so is epinephrine (adrenaline), released much more during resistance exercise than aerobic exercise] [(http://scholar.google.com/scholar?num=100&hl=en&lr=&q=ketogenesis+%22growth+hormone%22+OR+IGF); (http://scholar.google.com/scholar?num=100&hl=en&lr=&q=epinephrine+ketogenesis)]. Doing that type of exercise may or may not be practical for everyone, and a person would obviously want to talk to one's doctor before starting an exercise program. But the other implication of that article is that some factors that improve insulin sensitivity could, under some circumstances, produce "beneficial" effects by increasing ketogenesis and not just by maintaining low plasma glucose and insulin levels, etc.