Re:Fructose reprogrammes glutamine-dependent oxidative metab...
by webmaven on Tuesday February 23, 2021 @12:07PM
(#26239745)
> Sugar derived from cane and beet and honey are exactly as bad for your health as high-fructose corn syrup.
While equivalent (calorically) amounts of other sugars certainly isn't good for you, there is a growing consensus that fructose (and thus HFCS, and probably honey, though I'm not aware of studies to the latter effect) is subtly different enough to be worse for most people over the long term, even when taking into consideration that less is needed because it is sweeter.
The ratio of fructose to glucose seems to be one important factor, another is whether the fructose and glucose are bound together into sucrose (it doesn't seem like this paper addresses the latter point).
HFCS and honey both have a higher amount of fructose than glucose, and contain these components mostly in 'free' form, sugarcane and beets produce mostly sucrose, in which the ratio of fructose to glucose is equal and the sugars are mostly bound together into sucrose.
Although the effect of these differences is subtle, other research suggests that chronic consumption of fructose in free form causes changes in insulin response that in turn are responsible for both reduced satiation and weight gain (assuming sufficient calories). Caloric restriction can counteract the weight gain, but not the other changes.
The mechnisms for this have not been entirely clear. This paper describes some changes in cellular preference for some metabolic pathways over others that among other things in turn promote inflammatory responses. As a layman it is tempting to 'connect the dots', as inflammation is (generally, and indirectly) implicated (by other research) in various conditions, but this paper by itself doesn't actually do that. Though it does seem like an important step forward to doing so.
There are a whole host of questions this opens up, like "is this inflammatory response observable in particular tissues (pancreatic, white vs. brown fat, etc.)?", "how is this inflammatory response linked to changes in insulin response (in various tissues)?", "what else does this change in preference for particular metabolic pathways affect?", "what other alternate metabolic pathways might be affected by differences in nutrient ratios, or by the presence or absence of other nutrients?", "Does this help explain the difference in effect of consuming some foods in processed form (eg. Eating fruit vs. drinking juice)?", etc.
Intriguing and suggestive questions to be sure, but as yet unanswered (particularly by this paper in isolation).
While equivalent (calorically) amounts of other sugars certainly isn't good for you, there is a growing consensus that fructose (and thus HFCS, and probably honey, though I'm not aware of studies to the latter effect) is subtly different enough to be worse for most people over the long term, even when taking into consideration that less is needed because it is sweeter.
The ratio of fructose to glucose seems to be one important factor, another is whether the fructose and glucose are bound together into sucrose (it doesn't seem like this paper addresses the latter point).
HFCS and honey both have a higher amount of fructose than glucose, and contain these components mostly in 'free' form, sugarcane and beets produce mostly sucrose, in which the ratio of fructose to glucose is equal and the sugars are mostly bound together into sucrose.
Although the effect of these differences is subtle, other research suggests that chronic consumption of fructose in free form causes changes in insulin response that in turn are responsible for both reduced satiation and weight gain (assuming sufficient calories). Caloric restriction can counteract the weight gain, but not the other changes.
The mechnisms for this have not been entirely clear. This paper describes some changes in cellular preference for some metabolic pathways over others that among other things in turn promote inflammatory responses. As a layman it is tempting to 'connect the dots', as inflammation is (generally, and indirectly) implicated (by other research) in various conditions, but this paper by itself doesn't actually do that. Though it does seem like an important step forward to doing so.
There are a whole host of questions this opens up, like "is this inflammatory response observable in particular tissues (pancreatic, white vs. brown fat, etc.)?", "how is this inflammatory response linked to changes in insulin response (in various tissues)?", "what else does this change in preference for particular metabolic pathways affect?", "what other alternate metabolic pathways might be affected by differences in nutrient ratios, or by the presence or absence of other nutrients?", "Does this help explain the difference in effect of consuming some foods in processed form (eg. Eating fruit vs. drinking juice)?", etc.
Intriguing and suggestive questions to be sure, but as yet unanswered (particularly by this paper in isolation).