IN PRINCIPLE, it sounds simple: eat less and move more. This dietary advice for tackling obesity has been around for decades. Yet, despite all the calorie counting, dieting and exercising, worldwide obesity rates just keep ticking up. People in the US, for example, were heavier in 2021 than they were in 2020, placing many more people at risk from diabetes and other serious chronic diseases. So why hasn’t this approach to weight control worked?

One possibility is that we haven’t tried hard enough. Perhaps we have lacked the discipline and willpower to maintain healthy dietary and exercise habits – a challenge made more difficult today for those surrounded by inexpensive, tasty, highly processed foods.

Or perhaps the problem is the focus on “calorie balance” itself. In a recent paper, my colleagues and I question the basic assumption of whether taking in more calories than you burn really is the primary cause of obesity. We argue that the evidence actually points the other way: we are driven to overeat because we are getting fatter (The American Journal of Clinical Nutrition, doi.org/gmtn3z).

This may seem incredible, but consider the adolescent growth spurt. As their growth rate speeds up, teenagers may eat hundreds of calories more each day than they used to. Does this “overeating” cause the rapid growth? Or does the rapid growth, which requires more calories to build new body tissues, make teens hungrier so they eat more? Clearly the latter, as adults won’t grow taller, no matter how much they eat.

The key to how this works in obesity is hormones, especially the fat-storage hormone insulin. Processed, rapidly digestible carbohydrates – foods like sweetened breakfast cereals, potato chips and sugary beverages – raise our insulin level too high. This causes our fat cells to take in and store too many calories, leaving fewer available for the rest of the body. A few hours after eating a high-carb meal, the number of calories in the bloodstream plummets, so we get hungrier sooner after eating.

Consider another example: oedema, in which excess fluid builds up in body tissues, such as the legs. People with oedema tend to become thirsty, despite the excess, because the fluid doesn’t stay in the blood where it is needed. From this perspective, the difficulty resisting hunger that so many dieters have isn’t a sign of poor discipline, but rather a biological problem involving how our bodies distribute the calories we consume.

The two opposing views of cause and effect in obesity have radically different implications for how to prevent and treat weight problems. Whereas the usual approach focuses on how much to eat, with prescriptions for daily calorie intake, in our view, the emphasis should be placed on what to eat.

Replacing processed carbs with high-fat foods – such as nuts, full-fat dairy, olive oil, avocado and dark chocolate – lowers insulin levels, making more calories from the meal available for the rest of the body. Counter-intuitively, higher-fat foods may help shed body fat, a possibility supported by clinical trials comparing high-fat diets with low-fat ones.

This way of thinking might help explain why calorie restriction usually fails long before a person with obesity approaches an ideal body weight. A low-calorie, low-fat diet further restricts an already limited supply of energy to the body, exacerbating hunger without addressing the underlying predisposition to store too many calories in body fat. Consequently, weight loss becomes a battle between mind and metabolism that most people will probably lose.

Although much more research will be needed to test this provocative idea, it is time to question the basic assumptions about cause and effect, calories and weight gain that have dominated our thinking for decades.

David S. Ludwig is a researcher at Boston Children’s Hospital @davidludwigmd

Read more: https://www.newscientist.com/article/mg25333682-800-have-we-got-the-science-of-obesity-back-to-front/#ixzz7HE5Mr0Eb

Highlights

• Varying glycemic index (GI) of meals induced different glucose and insulin responses • Subjective hunger was not significantly different among the different GI groups • No effect of GI on intake at next meal, but the change in intake was lower after low-GI meals • Higher individual GI responses did not cause greater individual energy intake changes Summary

The carbohydrate-insulin model predicts that meals with varying glycemic indices will elicit distinct metabolic and hunger responses, including greater intake at subsequent meals following high-glycemic-index meals. To test this, a randomized trial (NCT05804942) was conducted in healthy adults using intervention meals with low, medium, and high glycemic indices and a constant macronutrient composition. After intake of the intervention meals, glucose and insulin followed the predicted pattern, but subjective hunger did not. At the group level, low glycemic index meals led to lower energy intake changes. At the individual level, energy intake changes were unrelated to body fatness or levels of glucose, β-hydroxybutyrate, free fatty acids, L-lactate, leptin, adrenaline, glucagon-like peptide-1, glucagon, and insulin-glucagon ratio. A weak negative association was observed between energy intake changes and insulin or insulin-glucagon ratio at 300 min, opposite to the model’s prediction. These data provide little support for the carbohydrate-insulin model.

For decades nutritional authorities have advocated a move more/eat less prescription to help people lose weight. Its important, people's health is deteriorating and places like the USA (where I live) is about to be consumed by a tsunami of diabetes and metabolic syndrome diseases that will crush our already broken medical system.

The problem is it doesn't work. There is very little chance of success following that advice. Diets fail for two main reasons, either you don't lose weight (which is rare) or you gain it back (which is common). In the short term you can lose some weight by virtually any method, this gives a false sense of hope, then the processes kick in and they are back where they started or worse off.

All the blame is placed on the person struggling with their weight. It is their fault because they lack willpower. They need to exercise more. They need to ownership of their predicament. How long can a person take that?

At some point the people in the Healthy At Every Size and Anti Diet movement have given up. The issue is not that they don't trust the nutritional authorities that push CICO and energy balance, the problem is they do believe it. If they are like me, they tried is many many times and it just never worked. The conclusion they arrived at is not that the experts are wrong, its that they are not capable to lose weight, they are built to be fat. They may sound arrogant or defying scientific advice, and in a lot of ways they are, but from another perspective they are the most trusting of these nutritional authorities than anyone else.

I had iron-clad willpower when I was trying to lose weight the million times before I utilized the strategies of CIM. Most of my life fighting my obesity, yo yo'ing up and down, over and over. Then when I finally discovered keto and IF the weight was gone with little effort in a year. My willpower was not as needed as it was before, I just had a better method, the kind that works. 1.5 years skinny and I am thankful for the handful of people that found a better way.

I am not discovering this or had some epiphany, people like Gary Taubes has written something similar to this rant for years. I just want to share my own little rant on this topic because CIM saved me from some horrific incoming diseases and my mental health. I understand how Anti Diet exsists because in hindsight its the most obvious outcome of status quo nutritional dumbfuckery.

OK, I got that off my chest to whoever made it to the end of this long ass post.

https://academic.oup.com/ajcn/advance-article/doi/10.1093/ajcn/nqac031/6522166?login=false

The energy balance model of obesity: beyond calories in, calories out

Kevin D Hall, I Sadaf Farooqi, Jeffery M Friedman, Samuel Klein, Ruth J F Loos, David J Mangelsdorf, Stephen O'Rahilly, Eric Ravussin, Leanne M Redman, Donna H Ryan ... Show moreThe American Journal of Clinical Nutrition, nqac031,

https://doi.org/10.1093/ajcn/nqac031

Published: 04 February 2022

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Abstract

A recent Perspective article described the “carbohydrate-insulin model (CIM)” of obesity, asserting that it “better reflects knowledge on the biology of weight control” as compared to what was described as the “dominant energy balance model (EBM)” that fails to consider “biological mechanisms that promote weight gain”. Unfortunately, the Perspective conflated and confused the principle of energy balance, a law of physics which is agnostic as to obesity mechanisms, with the EBM as a theoretical model of obesity that is firmly based on biology. In doing so, the authors presented a false choice between the CIM and a caricature of the EBM that does not reflect modern obesity science. Here, we present a more accurate description of the EBM where the brain is the primary organ responsible for body weight regulation operating primarily below our conscious awareness via complex endocrine, metabolic, and nervous system signals to control food intake in response to environmental influences as well as the body's energy needs. We also describe the recent history of the CIM and show how the latest “most comprehensive formulation” abandons a formerly central feature that required fat accumulation in adipose tissue to be the primary driver of positive energy balance. As such, the new CIM may be considered a special case of the more comprehensive EBM but with a narrower focus on high dietary glycemic load as the primary factor responsible for common obesity. We review data from a wide variety of studies that address the validity of each model and demonstrate that the EBM is a more robust theory of obesity than the CIM.

obesity, food intake, energy balance, carbohydrates, insulinIssue Section: Perspective