I am an obesity researcher and I think that in some sense the idea that we are programmed to eat and to store fat for lean days is correct, and that our current environment of abundance combines with this innate tendency to increase the prevalence of obesity. But this general statement hides many unknowns. For example, why are some people more prone to weight gain than others (in the same environment)? Why is obesity heritable (20-80% heritable depending on how you calculate it and the population you use)? Taubes is absolutely correct in stating that the “low-fat diet” mantra was promoted without any evidence to back it up and the evidence we do have seems to favor low-carb diets, at least in the short run. Fructose (and its not just high fructose corn syrup...sucrose is 50% fructose, HFCS is 55% fructose) does indeed seem to be deleterious above and beyond just adding calories, but its not the whole story either. Toxins and endocrine disruptors may play a role, but we really dont know too much about that yet.
Bottom line: the notion that we know NOTHING about nutrition is false. But the notion that we know all we need to know about diets and obesity is also false. The notion that higher carb intake is responsible for most of our increased weight gain is plausible (supported by data about total carb intake in the population..its the only macronutrient that has actually increased in per capita consumption. Fat intake has declined in the last 30 years, yet weight gain has accelerated) but not the whole story either.
Its also worth keeping in mind that there is no one-to-one correlation between obesity and particular disease outcomes (diabetes, heart disease). On a public health level, there is an increased risk, but there are a very large number of “healthy obese” people; there is good evidence that modestly obese adults trying to lose weight have higher mortality than those whose weight remains static or slightly increases; there is very good evidence that most diets and other prescriptions dont work and lead to yo-yo weight change that may itself be unhealthier than the baseline moderate obesity; there is good evidence that lack of fitness is a far more significant risk factor for morbidity and mortality than BMI (in adults), and so on....the “moral panic” about obesity is not always grounded in sound science.
“Prevention of obesity” by focusing on weight gain in children may bypass some of these concerns, but we have to be careful to see if we are responding to a fashionable moral panic or focusing on truly evidence-based fears AND interventions (even if the fears are real, all responses are not automatically justified; some responses to the disease may be worse than the original disease, others may be ineffective and hence a waste of time and money)?
Fructose (and its not just high fructose corn syrup...sucrose is 50% fructose, HFCS is 55% fructose) does indeed seem to be deleterious above and beyond just adding calories
I’ve heard this claim often, and I appreciate your pointing out that sucrose is hardly better than HCFS.
What evidence is there for human health being improved by avoiding fructose (on the margin, not absolutely)? Isn’t it pretty weak? There are plenty of high-dose rat studies, but I don’t typically adjust my lifestyle every time a rat study shows something.
I think you may want to look at the fact that glucose can enter the blood stream and be used as glucose by muscle/brain/other tissues. Fructose does not leave the liver as glucose does but is trapped there. It is used by the liver to make glycogen and when glycogen is not needed it is used to make triglyeride fats in LDL cholesterol packets. Much, much more of the fructose goes into storage molecules then into immediate energy use by tissues compared to glucose.
Fructose also creates problems in the gut.
Sucrose is less soluble and so less can be used for sweeting drinks etc. More fructose can be used with HFCS.
That sounds reasonable. I’ve heard that glycogen is stored in proximity to muscle for fuel, and if you do a lot of work (e.g. a long walk) any available glycogen is used to replenish those stores. That is, the only time it’s reasonable to gorge on carbs (which in practice always means some fructose) is when you’ve somewhat depleted your muscle glycogen.
There are human studies as well on fructose showing that it causes problems, one of which is obesity (but other problems like liver scarring are more serious). I am not going to include citations but if you go to ScienceDaily news and search on fructose you will find the latest research.
I am an obesity researcher and I think that in some sense the idea that we are programmed to eat and to store fat for lean days is correct, and that our current environment of abundance combines with this innate tendency to increase the prevalence of obesity. But this general statement hides many unknowns. For example, why are some people more prone to weight gain than others (in the same environment)? Why is obesity heritable (20-80% heritable depending on how you calculate it and the population you use)? Taubes is absolutely correct in stating that the “low-fat diet” mantra was promoted without any evidence to back it up and the evidence we do have seems to favor low-carb diets, at least in the short run. Fructose (and its not just high fructose corn syrup...sucrose is 50% fructose, HFCS is 55% fructose) does indeed seem to be deleterious above and beyond just adding calories, but its not the whole story either. Toxins and endocrine disruptors may play a role, but we really dont know too much about that yet. Bottom line: the notion that we know NOTHING about nutrition is false. But the notion that we know all we need to know about diets and obesity is also false. The notion that higher carb intake is responsible for most of our increased weight gain is plausible (supported by data about total carb intake in the population..its the only macronutrient that has actually increased in per capita consumption. Fat intake has declined in the last 30 years, yet weight gain has accelerated) but not the whole story either. Its also worth keeping in mind that there is no one-to-one correlation between obesity and particular disease outcomes (diabetes, heart disease). On a public health level, there is an increased risk, but there are a very large number of “healthy obese” people; there is good evidence that modestly obese adults trying to lose weight have higher mortality than those whose weight remains static or slightly increases; there is very good evidence that most diets and other prescriptions dont work and lead to yo-yo weight change that may itself be unhealthier than the baseline moderate obesity; there is good evidence that lack of fitness is a far more significant risk factor for morbidity and mortality than BMI (in adults), and so on....the “moral panic” about obesity is not always grounded in sound science. “Prevention of obesity” by focusing on weight gain in children may bypass some of these concerns, but we have to be careful to see if we are responding to a fashionable moral panic or focusing on truly evidence-based fears AND interventions (even if the fears are real, all responses are not automatically justified; some responses to the disease may be worse than the original disease, others may be ineffective and hence a waste of time and money)?
Awesome comment, I really do wish you would use more paragraphs :)
You make a lot of interesting points, but how do you apply them to the question at hand: what should you have for dinner, and why?
I’ve heard this claim often, and I appreciate your pointing out that sucrose is hardly better than HCFS.
What evidence is there for human health being improved by avoiding fructose (on the margin, not absolutely)? Isn’t it pretty weak? There are plenty of high-dose rat studies, but I don’t typically adjust my lifestyle every time a rat study shows something.
I think you may want to look at the fact that glucose can enter the blood stream and be used as glucose by muscle/brain/other tissues. Fructose does not leave the liver as glucose does but is trapped there. It is used by the liver to make glycogen and when glycogen is not needed it is used to make triglyeride fats in LDL cholesterol packets. Much, much more of the fructose goes into storage molecules then into immediate energy use by tissues compared to glucose.
Fructose also creates problems in the gut.
Sucrose is less soluble and so less can be used for sweeting drinks etc. More fructose can be used with HFCS.
That sounds reasonable. I’ve heard that glycogen is stored in proximity to muscle for fuel, and if you do a lot of work (e.g. a long walk) any available glycogen is used to replenish those stores. That is, the only time it’s reasonable to gorge on carbs (which in practice always means some fructose) is when you’ve somewhat depleted your muscle glycogen.
There are human studies as well on fructose showing that it causes problems, one of which is obesity (but other problems like liver scarring are more serious). I am not going to include citations but if you go to ScienceDaily news and search on fructose you will find the latest research.
I’ve never heard this before, can you provide some links/references for more info please?