There's widespread misunderstanding of the energy balance model (EBM) of obesity. The EBM does NOT postulate that food intake is primarily under conscious control or that obesity is a failure of willpower and can be effectively treated by calorie counting or advice to “eat less”.
The EBM postulates that the food environment & the foods we eat affect feedback control of appetite & body weight regulation mediated by a variety of hormones & other signals acting on brain regions involved in sensory processing, reward, incentive salience, habit & homeostasis.
The EBM does NOT imply that all calories are equal. Different foods and nutrients can differentially affect the neural systems responsible for controlling food intake as well as affect metabolic health independent of body weight.
Alas, the EBM is far from complete because we are only beginning to understand the neural systems responsible for appetite control & the mechanisms underlying the influence of internal signals and their interaction with nutrients and the food environment.
Just submitted a Rapid Response to @BMJNutrition entitled "Erroneous assumptions invalidate the calculated effects of reducing ultra-processed food consumption on child and adolescent obesity". I hope the full text is posted soon. Basically, there are two problems:
The first involves calculating energy intake changes resulting from eliminating ultra-processed food. The authors rely on our metabolic ward study in 20 adults and make several unjustified assumptions to extrapolate to free-living children and adolescents pubmed.ncbi.nlm.nih.gov/31105044/
The second involves simulating weight losses in response to (likely erroneous) energy intake changes. The authors cite our math model childhood growth and obesity, but instead of implementing the model they misinterpret a rule of thumb about excess weight pubmed.ncbi.nlm.nih.gov/24349967/
The idea that the carbohydrate-insulin model (CIM) has always stated that it takes >2 weeks for changes to hunger and metabolism to occur is a major goal-post shift. Let's discuss...
The mechanisms proposed by the CIM involve known *rapid* actions of insulin, within hours after meals containing carbs insulin acts to suppress lipolysis and stimulate fat uptake and storage in adipose tissue. Insulin thereby traps fat in the "One-way Calorie Turnstile"
The CIM goes on to suggest that these established rapid actions of insulin on adipose to sequester and accumulate calories is the cause of increased hunger, overeating and slowing metabolism because anabolic adipose starves non-adipose tissues of fuel.
I hadn't expected @davidludwigmd to criticize the recent perspective in @ScienceMagazine with @JohnSpeakman4 on the basis that it presents a "straw man" version of the carbohydrate-insulin model (CIM) of obesity. We tried to faithfully represent his version of the CIM. Thread.
Dr. Ludwig's description: “a high-carbohydrate diet … produces postprandial hyperinsulinemia, promotes deposition of calories in fat cells instead of oxidation in lean tissues, and thereby predisposes to weight gain through increased hunger, slowing metabolic rate, or both.”
This was also described as "the fat cell theory of obesity" in Always Hungry by where @davidludwigmd describes insulin as the "fat cell fertilizer" that acts as "The One-Way Calorie Turnstile" trapping fat in adipose tissue and leading to increased hunger & slowing metabolism.
Just submitted our latest manuscript entitled "A plant-based, low-fat diet decreases ad libitum energy intake compared to an animal-based, ketogenic diet: An inpatient randomized controlled trial". I'm looking forward to all constructive comments! osf.io/preprints/nutr…
20 adults without diabetes were admitted as inpatients to the NIH Clinical Center and randomized to consume ad libitum either a plant-based, low-fat (PBLF) diet or an animal-based, ketogenic, low-carbohydrate (ABLC) diet for 2 weeks followed immediately by the alternate diet .
The PBLF diet was 75.2% carbohydrate, 10.3% fat, 14.5% protein and had a non-beverage energy density of 1.1 kcal/g. The ABLC diet was 75.8% fat,10.0% carbohydrate, 14.2% protein and had a non-beverage energy density of 2.2 kcal/g. Subjects consumed as much or as little as desired
The video cites our 2015 @Cell_Metabolism paper that didn’t investigate a keto diet. We even refused to call the diet “low carb” because the calorie restriction achieved by selectively cutting carbs resulted in a diet ~30% of total calories from carbs. ncbi.nlm.nih.gov/pubmed/26278052
Our study was NOT an efficacy study as portrayed in the @nutrition_facts video. Rather, it was designed to investigate the physiology of selective restriction of carbs vs fat &the effects on insulin secretion and body fat. The body fat differences were clinically meaningless!
Our latest RCT paper was just submitted for peer review and now available as a @NutriXiv preprint: "Ultra-processed diets cause excess calorie intake and weight gain: A one-month inpatient randomized controlled trial of ad libitum food intake". osf.io/preprints/nutr… 1/7
We investigated whether ultra-processed foods affect energy intake in 20 weight-stable adults who were admitted to the NIH Clinical Center and randomized to receive either ultra-processed or unprocessed diets for 2 weeks immediately followed by the alternate diet for 2 weeks. 2/7
Meals were designed to be matched for presented calories, energy density, macronutrients, sugar, sodium, and fiber. Subjects were instructed to consume as much or as little as desired. 3/7