462436347
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(Replying to PARENT post)
HFCS consumption (along with added sugar consumption in general) peaked in 2000 and declined steadily until 2020: https://news.ycombinator.com/item?id=38094768
(Replying to PARENT post)
Look up Pontzer's Constrained Total Energy Expenditure Model. His doubly-labeled water experiments show that Hadza and other hunter-gathers have--contrary to his (and your) initial expectations--roughly comparable TDEEs to sedentary western counterparts (controlling for lean body mass) due to metabolic compensation (i.e., the more they exercise, the more their bodies compensate by expending less energy elsewhere, on things like inflammation and thyroid/sex hormones): : https://pmc.ncbi.nlm.nih.gov/articles/PMC4803033/
Regardless, they're in energy balance, meaning they aren't gaining or losing weight, and despite their high-sugar diets, they aren't presenting any of the metabolic maladies that Lustig ascribes to sugar specifically, and not to weight gain--maladies that saturated fat seems to cause with no weight gain.
> This is akin to asking why do long-distance cyclists who spend 10-16hrs a day on bike on long cross country rides can drink liters of cola every day and be skinny like a fig.
Sugar has 4 calories per gram. Fat has 9. Are you arguing that sugar calories are more fattening than fat calories?
> I'm getting second hand embarrassment from just reading the question.
It's remarkable that I've had less derogatory and flippant comments than yours downvoted and even flagged in this thread: https://news.ycombinator.com/user?id=462436347
(Replying to PARENT post)
(Replying to PARENT post)
I cited RCTs in other comments pertaining to macronutrient intake and metabolic health. Lustig instead relies on mouse models and mechanistic speculation to make his case, because the RCTs in humans haven't shown sugar to cause all the ills he claims, without associated weight gain. Meanwhile saturated fat (given the available literature) ironically seems to be able to do much of what Lustig claims (impair insulin sensitivity, increase visceral fat), even without weight gain.
(Replying to PARENT post)
HFCS consumption is still higher than it was in 1970, but it has declined since 2000, and its decline has driven the overall decline in sugar consumption, yet obesity and diabetes incidence have only increased.
> some cases T2D can be reversed by minimizing sugars/carbs and increasing fats so your mitochondria is primarily using ketones rather than glucose.
"Reversed" means you can eat carbohydrates normally again. If anything, high-fat, low-carb diets seem to worsen actual insulin sensitivity, which carbohydrate restriction just masks (even then, not always, as many on keto find when they check their BG): https://pmc.ncbi.nlm.nih.gov/articles/PMC5291812/
Severely restricting carbohydrate enough to get an artificially low HbA1c or fasting BG and claiming you "reversed" diabetes is like claiming you "reversed" your lactose intolerance by never drinking milk. But actual weight-loss (however you achieve it) does improve real insulin sensitivity, but low-carb isn't magic when it comes to that either.
(Replying to PARENT post)
> different approach to nutrition
The "different approach" HNers gravitate towards is eating bacon and butter (i.e., keto/low-carb) and denying all of the evidence linking these foods to CVD, probably because fat and sodium are so addictive, much more so than sugar: https://news.ycombinator.com/item?id=42028432
(Replying to PARENT post)
The best study done to date on hyperpalatable foods found that fat and sodium were the most common drivers of hyperpalatability:
https://onlinelibrary.wiley.com/doi/10.1002/oby.22639
> The HPF criteria identified 62% (4,795/7,757) of foods in the FNDDS that met criteria for at least one cluster. Most HPF items (70%; 3,351/4,795) met criteria for the FSOD cluster. Twenty-five percent of items (1,176/4,795) met criteria for the FS cluster, and 16% (747/4,795) met criteria for the CSOD cluster. The clusters were largely distinct from each other, and < 10% of all HPF items met criteria for more than one cluster.
(CSOD, carbohydrates and sodium; FS, fat and simple sugars; FSOD, fat and sodium; HPF, hyper-palatable foods.)
> Check out books by Robert Lustig on the subject
Lustig is a crackpot who relies on animal studies and mechanistic speculation, because the highest-quality RCTs (like the ones I cited) don't support his theory.
(Replying to PARENT post)
(Replying to PARENT post)
And if sugar is so metabolically harmful, where are the RCTs showing this? All I've seen is that outside of a caloric surplus, it isn't especially metabolically harmful, and ironically, even outside of a surplus, saturated fat is much worse:
https://diabetesjournals.org/care/article/41/8/1732/36380/Sa...
https://link.springer.com/article/10.1007/s00394-015-1108-6
Meanwhile tribes of hunter-gatherers in Africa get 15-80% of their daily calories from honey during certain seasons; why aren't they obese and diabetic? https://www.sciencedirect.com/science/article/abs/pii/S00472...
(Replying to PARENT post)