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> Fructose is low GI, and most of it is converted to glucose in the gut, anyway. The first half of this sentence (fructose is low GI) is factually correct. The

> Fructose is low GI, and most of it is converted to glucose in the gut, anyway. The first half of this sentence (fructose is low GI) is factually correct. The second half (most fructose is converted to glucose in the gut) is factually incorrect. The entire sentence and comment oversimplify sugar metabolism. tl;dr: control your fructose intake. First, nitpicky corrections: about half of ingested fructose is converted to glucose, not most of it, and this occurs in the liver, not the gut (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3649104/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3649104/). Second, and more importantly: GI is a woefully inadequate measure of the healthfulness of a food. the glycemic index (GI) of a food is indexed to a standard amount of carbohydrate mass (usually 50 g) from that food. GI captures the impact on blood glucose per gram of carbohydrate, but it certainly misses crucial aspects of sugar metabolism. For example, carrots have a high GI (above 70), but that's not a reason to stop eating carrots. You'd need to eat a huge amount of carrots to spike your blood sugar. Glycemic load is a more useful metric (https://www.diabetesselfmanagement.com/blog/glycemic-index-and-glycemic-load/ https://www.diabetesselfmanagement.com/blog/glycemic-index-a...), but even that is beside the point when it comes to fructose and its deleterious health effects. Fructose, being fructose and not glucose, of course has a low glycemic index, since GI is defined based on blood glucose. Dr. Robert Lustig (UCSF pediatric endocrinologist) has devoted years of effort to communicating the disproportionate damage that fructose causes to human metabolism. In brief, fructose is processed along different metabolic paths than glucose, and is better than glucose at making people fat, diabetic, and metabolically unhealthy (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4592517/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4592517/) A top-level summary from 2013: https://www.theguardian.com/commentisfree/2013/oct/21/fructose-poison-sugar-industry-pseudoscience https://www.theguardian.com/commentisfree/2013/oct/21/fructo... A very detailed lecture (video and transcript): https://robertlustig.com/fructose2/ https://robertlustig.com/fructose2/

ZeroFries 7y ago
It takes high doses of sugar for frutose to not get converted in the small intestine. https://www.cell.com/cell-metabolism/comments/S1550-4131(17)30729-5 https://www.cell.com/cell-metabolism/comments/S1550-4131(17)... Lustig is a highly biased source. I would be interested in summaries of controlled studies which aren't cherry-picked comparing iso-caloric diets of sugar vs fat.
- EForEndeavour 7y ago
  > Lustig is a highly biased source. I would be interested in summaries of controlled studies which aren't cherry-picked comparing iso-caloric diets of sugar vs fat. The very paper you cite asserts "strong ties between fructose and disease," points out that "high fructose consumption is appreciated as a culprit in metabolic disease," and presents a supremely well-researched case against fructose. Regardless of the precise metabolic fate of low-dose fructose (whatever "low dose" ends up meaning for humans), the practical takeaway of your paper (and mountains of research) agrees with Lustig's: avoid fructose. Also, that paper is a mouse study. Even if metabolic pathways are exactly identical between mice and humans, how much fructose constitutes a "high" dose that they show overflows from the small intestine to the liver? They address this, emphasis mine: > The extent of passage of unmetabolized fructose through the small intestine to the liver depended on dose. Conversion of doses between mice and humans is not straightforward. Across mammals, total metabolic activity more closely mirrors body surface area than mass. For a typical adult mouse, daily intake is ~12 kcal, versus ~2,400 kcal for an adult human. One sensible way of converting doses of macronutrients is based on caloric intake: a dose of 0.5 g/kg fructose in mouse is ~0.5% of daily calorie intake, or the same as 3 g of fructose in a person (one orange or about 2 ounces of soda). Thus, the doses that we study here are in the range of typical human fructose consumption (Marriott et al., 2009; Macdonald, 2016). That mouse dose they convert, 0.5 g/kg, is halfway to the 1 g/kg threshold they define as "high dose fructose." So if you drink more than 4 ounces of soda per day, your liver is doing the bulk of fructose metabolism. What makes you call Lustig "highly biased"? While he is admittedly argumentative and even a bit sensationalist in his presentation, he bases all of his claims on extensively sourced physiology and epidemiology research, and his credentials and career are highly relevant, for what it's worth. Again, the conclusion from decades of research is abundantly clear at this point: avoid fructose.

ZeroFries 7y ago

It takes high doses of sugar for frutose to not get converted in the small intestine. https://www.cell.com/cell-metabolism/comments/S1550-4131(17)30729-5 https://www.cell.com/cell-metabolism/comments/S1550-4131(17)... Lustig is a highly biased source. I would be interested in summaries of controlled studies which aren't cherry-picked comparing iso-caloric diets of sugar vs fat.

EForEndeavour 7y ago
> Lustig is a highly biased source. I would be interested in summaries of controlled studies which aren't cherry-picked comparing iso-caloric diets of sugar vs fat. The very paper you cite asserts "strong ties between fructose and disease," points out that "high fructose consumption is appreciated as a culprit in metabolic disease," and presents a supremely well-researched case against fructose. Regardless of the precise metabolic fate of low-dose fructose (whatever "low dose" ends up meaning for humans), the practical takeaway of your paper (and mountains of research) agrees with Lustig's: avoid fructose. Also, that paper is a mouse study. Even if metabolic pathways are exactly identical between mice and humans, how much fructose constitutes a "high" dose that they show overflows from the small intestine to the liver? They address this, emphasis mine: > The extent of passage of unmetabolized fructose through the small intestine to the liver depended on dose. Conversion of doses between mice and humans is not straightforward. Across mammals, total metabolic activity more closely mirrors body surface area than mass. For a typical adult mouse, daily intake is ~12 kcal, versus ~2,400 kcal for an adult human. One sensible way of converting doses of macronutrients is based on caloric intake: a dose of 0.5 g/kg fructose in mouse is ~0.5% of daily calorie intake, or the same as 3 g of fructose in a person (one orange or about 2 ounces of soda). Thus, the doses that we study here are in the range of typical human fructose consumption (Marriott et al., 2009; Macdonald, 2016). That mouse dose they convert, 0.5 g/kg, is halfway to the 1 g/kg threshold they define as "high dose fructose." So if you drink more than 4 ounces of soda per day, your liver is doing the bulk of fructose metabolism. What makes you call Lustig "highly biased"? While he is admittedly argumentative and even a bit sensationalist in his presentation, he bases all of his claims on extensively sourced physiology and epidemiology research, and his credentials and career are highly relevant, for what it's worth. Again, the conclusion from decades of research is abundantly clear at this point: avoid fructose.