Digging deeper into the Carb-Insulin-Hormonal-Obesity Theory. This site (INSULIN…AN UNDESERVED BAD REPUTATION) criticizes the theory:
MYTH: Carbohydrate Drives Insulin, Which Drives Fat Storage
FACT: Your Body Can Synthesize and Store Fat Even When Insulin Is Low
One of the biggest misconceptions regarding insulin is that it’s needed for fat storage. It isn’t. Your body has ways to store and retain fat even when insulin is low. For example, there is an enzyme in your fat cells called hormone-sensitive lipase (HSL). HSL helps break down fat. Insulin suppresses the activity of HSL, and thus suppresses the breakdown of fat. This has caused people to point fingers at carbohydrate for causing fat gain.
However, fat will also suppress HSL even when insulin levels are low. This means you will be unable to lose fat even when carbohydrate intake is low, if you are overeating on calories. If you ate no carbohydrate but 5,000 calories of fat, you would still be unable to lose fat even though insulin would not be elevated. This would be because the high fat intake would suppress HSL. This also means that, if you’re on a low carbohydrate diet, you still need to eat less calories than you expend to lose weight.
Ignoring the n=1 experiments where people have eaten 5,000 calories a day of fat and maintained or even lost weight is this a practical case? I think it’s probably the case that it is hard to lose weight when eating 5,000 calories of fat a day. After all, why would your body free it’s own fat while there’s plenty of dietary fat available.
But it still may be possible to lose weight on a 5,000 calories a day of fat diet. It depends upon the feeding schedule. If the food was spread all day and into the night without any time to draw from body fat it might be possible to not lose weight.
Here’s the study that was cited (Am J Physiol. 1999 Feb;276(2 Pt 1):E241-8.
Effects of an oral and intravenous fat load on adipose tissue and forearm lipid metabolism. Evans K, Clark ML, Frayn KN.).
We have studied the fate of lipoprotein lipase (LPL)-derived fatty acids by measuring arteriovenous differences across subcutaneous adipose tissue and skeletal muscle in vivo. Six subjects were fasted overnight and were then given 40 g of triacylglycerol either orally or as an intravenous infusion over 4 h. Intracellular lipolysis (hormone-sensitive lipase action; HSL) was suppressed after both oral and intravenous fat loads (P < 0.001). Insulin, a major regulator of HSL activity, showed little change after either oral or intravenous fat load, suggesting that suppression of HSL action occurred independently of insulin. The rate of action of LPL (measured as triacylglycerol extraction) increased with both oral and intravenous fat loads in adipose tissue (P = 0.002) and skeletal muscle (P = 0.001).
I’m not sure the following supports the claim (it may, I am just not sure):
There was increased escape of LPL-derived fatty acids into the circulation from adipose tissue, shown by lack of reesterification of fatty acids.
So the body fat, it seems released fatty acids in response to the meal.
There was no release into the circulation of LPL-derived fatty acids from skeletal muscle. These results suggest that insulin is not essential for HSL suppression or increased triacylglycerol clearance but is important in reesterification of fatty acids in adipose tissue but not uptake by skeletal muscle, thus affecting fatty acid partitioning between adipose tissue and the circulation, postprandial nonesterified fatty acid concentrations, and hepatic very low density lipoprotein secretion.