My recent discovery of Karl Smith’s “obesity” tag led me down a rabbit hole on sugar metabolism, the basic result of which was “Holy shit, fructose is pretty nasty stuff”. Also, I learned that I’ve been using the term “lipid hypothesis” embarrassingly wrongly; it’s particularly galling that I confused the “lipid” in same for dietary lipids (“eating high-fat, high-cholesterol foods will give you heart disease”) rather than serum lipids (“having high serum LDL and triglyceride levels will give you heart disease”), which is a confusion I gleefully roast others for making. Oh well, live and learn.
Anyway, have some links. First a pair of Gary Taubes articles from the New York Times Magazine:
Next, a random T-Nation article on fructose:
Then a trio of
ScienceDirect ScienceDaily blurbs on fructose metabolism:
- Fructose metabolism by the brain increases food intake and obesity, review suggests
- What makes fructose fattening? Some answers found in the brain
- Excess fructose may play role in diabetes, obesity, and other health conditions
tl;dr: Glucose can be metabolized by pretty much any cell in the body, while fructose only really gets metabolized by the liver to replenish glycogen stores. So regardless of your metabolic demands, if your liver’s topped up with glycogen and you consume fructose, it’s going to get stored as fat. Extra credit: Fructose actually seems to increase hunger, rather than satiety.
A lot of the above hammers sugar (sucrose, or glucose bound to fructose) as hard as high-fructose corn syrup (glucose and fructose in similar proportions but not bound up into a sucrose molecule). Anyone know if the molecular bond in sucrose makes a difference for how sugar is metabolized relative to HFCS? My vague understanding is that the liver needs glucose to metabolize fructose, so sucrose probably gets broken down pretty early in the process, but I’m not at all sure about that. (And if so, could the difference between the 50:50 glucose:fructose ratio in sucrose and the 45:55 split in HFCS make a significant difference?)
Finally, a hilariously biased article from the Journal of the Institute of Brewing on beer as a low-carb beverage. (Yeah, turns out most of the maltose inputs in beer get fermented by the yeast.) Mostly I just wanted to make sure I wasn’t inadvertently chugging tons of fructose with my evening beverage of choice, and it turns out I’m not — the sugars in beer are mostly maltose and maltodextrins, which are tiny little starches composed of glucose pretty much exclusively.
The article contains this sentence, which I desperately want to believe:
It is believed that ethanol induces an increase in the sensitivity of muscle to insulin with a down-regulation of the effect of insulin on adipose tissue, so fat mass decreases.
19. McCarty, M.F., The alcohol paradox. Am. J. Clin. Nutr., 1999, 70, 940–941.
Post-workout beers, anyone?