The other day, Stephan Guyenet shared some of his own thoughts on David Despain's can't-say-enough-nice-things-about-it interview with Dr. John Sievenpiper. In case you missed it, Stephan discusses his post looking at the links or lack thereof between sugar consumption per se and obesity. See: Is Sugar Fattening? At the end of the current post is the following footnote:
** If fructose is fattening due to its ability to become fat, then dietary fat should be even more fattening because it doesn't have to undergo an inefficient conversion process-- it's already fat.
Excellent point! I might add that if saturated fat is such a healthy fat for your body, fat produced by de novo lipogenesis -- mostly palmitic acid in the liver -- would be an even better source of that fat as it would give you a "metabolic advantage"! It takes almost no calories to digest and store dietary fat in body fat. It is highly energy intensive to convert fructose to fat, so you get some free calories!
The comments on Stephan's post demonstrate that those who have learned their biochemistry/metabolism from the likes of Taubes and Eades and Lustig, are woefully misguided in same. And this is the reason I will keep on keeping on doing what I do here to try to undo some of that "knowledge" learned from the damaging education they are getting. The vast majority of fatty acids that are "rebundled" by the liver are NEFA -- free fatty acids released by adipose tissue that were in excess of needs and are sent back to the fat tissue. See: Where do triglycerides come from? Part I , Part II , Part III. Another main conclusion of the radioactive tracer studies discussed in that series is that the increase in fasting VLDL-triglycerides on higher carb diets is attributable to reduced clearance, not increased production.
So what of the fate of VLDL. Well, when all is said and done, these lipoproteins carry the triglyceride load. They can "dock" and release that load to peripheral tissues or sent to fat tissue for storage. This is actually part of a "Fat Accumulation" series post I have on the back burner, but:
- There can be no doubt that ASP plays an integral role in fatty acid uptake and esterification by adipose tissue. This is likely the dominant player on the uptake side in the postprandial state.
- Women seem to have higher fasting ASP levels vs. men
- ASP seems to be a more adipogenic, "fattening", hormone in women than men
- ASP is responsive to chylomicron stimulus moreso than VLDL for fatty acid uptake
- NEFA release in the triglyceride/fatty acid cycle is more from upper body fat
- VLDL uptake seems to be greater in gluteofemoral (butt & thighs) fat than upper body fat.*
- Endogenous lipid production is a highly unlikely route to fat accumulation (aka obesity) in humans
What to make of all of this? Still putting some thoughts together, but ...
- Dietary fat is more likely to be incorporated into body fat than "triglycerides" transported from the liver -- VLDL -- including small amounts of fatty acids generated from carbs in general or fructose more specifically.
- Not all adipose tissue is created equally ... lots to sort out there, but the keys to female protection against CVD vs. men probably lie in fat bottomed girls ;-)
Hit it Freddy!