This is exciting and fascinating on many levels — therapeutically and scientifically.
These women with weight-normalized anorexia nervosa showed "less dietary restraint" without weight change on the ketogenic diet. So they ate more but weight didn't change?
Is it possible that anorexia is a fat-storage disorder, not an eating disorder (just as I and others have argued about obesity)?
If so, this observation is unsurprising.
New study offers hope for anorexia nervosa.
The first-ever pilot trial of ketogenic therapy for anorexia nervosa was just published.
Here's what @GuidoFrank and his research team at @UCSDMedSchool found. 🧵
Sure, if you force people to eat more than they want, they will get fatter, and if you semi-starve them, they will get thinner. This is true of people with obesity, and it's true of people without it.
Regrettably, it says nothing about the cause of obesity, particularly as overfed people (and animals) will lose the weight as soon as the overfeeding stops.
Warning: if you study the history of obesity science--specifically, where the energy balance/overeating thinking came from--you'll learn why the best medical scientists in the world rejected it as a failed hypothesis--"the dead end of the energetic view" as it was described in 1936.
By the 1930s, European scientists had collected a world of observations about fat storage that overeating couldn't begin to explain. But their thinking got lost with the Second World War, and so we've been living with the energy balance dogma ever since.
Shouldn't Where We Get Fat (and When) Tell Us Something About Why? https://t.co/EFZHuSw36Q
What the post also shows is that no single dietary intervention has been shown, in a long term study, to improve long term human health. Not diets that substitute polyunsaturated fats for saturated fats; not diets that replace fat with carbohydrate.
Yet I doubt there is a single faculty teaching human nutrition anywhere in the world that ever makes this point.
Probably the most important study is the LookAhead study which tested dietary fat reduction in obese type 2 diabetes. After 9.5 years it was given up as a. hopeless failure. Which of course it was not. It was only a failure for those who, filled with cognitive dissonance, have and will continue to prescribe that diet in the hope that somehow their patients will respond differently.
Yet what diet does one think is prescribed by "evidence-based" doctors and dietitians, for most of the world's persons living with that condition?
On the other hand, the one diet that has yet to be properly investigated with long term trials is the low-carbohydrate high-fat diet.
Yet the reason most usually advanced by the "evidence-based" practitioners to explain why the low-carbohydrate diet should not be prescribed is "because there are no long term studies".
So instead the diets that are prescribed (because there are long-term trials - regardless of outcomes) are exactly those which long-term studies show are either harmful or without effect.
A strange situation is it not?
@garytaubes@bigfatsurprise@lowcarbGP@BenBikmanPhD@markkaplan20@AKoutnik@LoreofRunning1
Thank goodness Gary Taubes @garytaubes chose physics over medicine and then came from there to science journalism. His latest book https://t.co/ptTIjfe3Di is another masterpiece. His ability to research the history of the medical topics that interest him and to present the material with novelty, accuracy and clarity in a most engaging way, is of the highest quality.
I learned two crucial facts from his deep dive into the historical evolution of the management of diabetes of both types.
First, when insulin was discovered in 1921, it produced an instant miracle cure by saving the lives of those who were unable to produce any insulin, those with type 1 diabetes. But the honeymoon period lasted just 15-20 years after which insulin-treated diabetics began to present with premature atherosclerosis.
By which time, the prevailing opinion had become that this was caused by a diet too high in fat. For the life-saving insulin had to be innocent - Remember Semmelweis and the doctor-caused disease that he decribed.
Thus the prescribed treatment for diabetics of both types became a low-fat high-carbohydrate diet, just as was being prescribed to cardiac patients to prevent disease progression.
Second, Taubes made the telling point, overlooked by many, that one of two diets is prescribed to prevent atherosclerosis in normal persons and in those with diabetes. There are the fat substitution diet and the low-fat diet - and they act quite different especially in persons with insulin-resistance or type 2 diabetes.
In the fat substitution diet, saturated fats are replaced with polyunsaturated fats. There have been numerous long-term multi-million $ trials of this dietary intervention. They have all failed miserably to show benefit and some have caused harm https://t.co/HPWJ8OZWJE.
Thus we know that the fat substitution diet is a complete failure and may even be harmful.
In the low-fat diet, a large portion of the fat in the diet is replaced with carbohydrate. Whilst this diet may be acceptable for those who are not insulin-resistant, for those who are diabetic, it has to be the worst possible choice. Because, with time as the patient becomes progressively more insulin resistant, he/she will require ever larger doses of insulin to maintain blood glucose concentrations in a reasonable range. And didn't the problem of atherosclerosis first appear in middle-aged type 1 diabetics who had been treated with insulin for some decades?
Importantly there has never been a major multi-million $ trial of the effects of a low-fat high-carbohydrate diet on the development of atherosclerosis in otherwise health individuals. But there has been one such trial on weight loss and cardiovascular outcomes in diabetic patients - The LookAhead trial. The study was terminated after 9.5 years because it was considered "futile" to continue as there was no evidence that the diet produced any protection from coronary heart disease.
The point is that if you have diabetes, you're probably not best advised to adopt either a fat-substitution diet or a low-fat high-carbohydrate diet, since neither is likely to produce any health benefits and both could be harmful.
@BenBikmanPhD@zoeharcombe@bigfatsurprise@AKoutnik@LoreofRunning1@sweatscience@drericwestman@markkaplan20
A new FDA-tracked pill promises to extend dogs' lives by improving their insulin sensitivity and lowering their insulin levels.
But if lower insulin is the key to a longer canine life, maybe our dogs shouldn't be eating carb-rich kibble in the first place.
The history of longevity trials — in Labrador retrievers, in rhesus monkeys — suggests that what they eat matters more than how much.
So why are we waiting for a drug to solve a problem that diet might already answer?
https://t.co/4QrC6xHnzb
Yes, we now have drugs for treating obesity, but are we making progress understanding it?
Is it really a "brain disorder," as Jeff Friedman of Rockefeller has said, a dysregulation of energy intake and expenditure?
Do we do the science any favors by burdening our thinking with the idea that calories-in, calories-out tells us anything about causality?
The History of a Very Bad Idea: Understanding Obesity Before Calories In and Out. https://t.co/AUMHhCjK6I
Well, well, what do we have here? A study on carbohydrate fuelling before and during exercise is judged the 2025 research article with the best impact in the "elite" journal, the American Journal of Physiology, Cell Physiology. Now, why would the Editors choose, from amongst all the submissions to a world-leading journal publishing work on key advances in cellular biology, a publication from a usually peripheral (ie minor) discipline like sports science/sports nutrition for this prestigious award? Perhaps because we have shown, for the first time, the consequences of the existence of two separately-regulated glucose pools - the large and glucose pools - with different effects on human exercise performance.
Hopefully this recognition of the meaning of this paradigm shift for the understanding of glucose regulation in the human body, might slowly percolate into the discussion of how carbohydrates influence human exercise performance.
More science, less wrath (perhaps)
@PhilipPrins11@akoutnik@PaulBLaursen@sweatscience@theplews1@DrPhilMaffetone@TheNoakesF@Brady_H@drjamesdinic@zbitter@garytaubes@zoeharcombe@bigfatsurprise@LoreofRunning1@lowcarbGP
@garytaubes explains why he dislikes terms like "hyperpalatable" and that it is just used to complicate simple truths about nutrition.
Is it willpower or something more? Watch the full discussion. #Nutrition#Obesity
In a Swedish study, meat consumption is associated with cognitive health in individuals with a genetic risk for Alzheimer's.
Does this mean eating meat protects against Alzheimer's?
Does it mean avoiding meat increases risk--i.e., should vegetarians worry that their diets are accelerating cognitive aging?
Another trip into the nuances of nutritional epidemiology and, particularly, the implications of the anti-randomization problem.
Brain Health vs. Heart Health? Is Eating Meat Good for Cognition but Bad for Our Arteries? https://t.co/oO0Q9xSUn1
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Conventional wisdom: GLP-1RA drugs cause weight loss by inhibiting appetite.
That assumption outruns the actual evidence.
An alternative hypothesis: GLP-1RAs reverse fuel-partitioning-- ↓fat storage, ↑ fat oxidation--& that inhibits appetite.
https://t.co/weIYX4w81I