To paraphrase Mark Twain:

Reports of the death of the Carbohydrate-Insulin Model have been exaggerated.

👉17-author review @AJCNutrition
👉Deep dive on obesity mechanisms
👉Numerous hypotheses to guide constructive debate

Free text👉 doi.org/10.1093/ajcn/n…

Thread (0/12)👇
1/12
The simplicity of the Energy Balance Model belies a tautology.

Weight gain can occur only with a positive energy balance, as fever can occur only if the body generates more heat than it dissipates.

👉These reiterations of physics provide no information on biological causes
2/12
Regarding dietary drivers of obesity, the EBM often focuses on the variety and availability of “hyper-palatable” energy-dense processed foods.

But surprisingly little evidence relates palatability directly to chronic overconsumption in animals or humans (Article refs: 9-20)
3/12
A central conundrum is to understand why body weight “set point” increased so rapidly.

👉By excluding metabolic effects of diet ("all calories are alike"), EBM offer no explanation for what environment factors dysregulated the biological systems that resist weight change.
4/12
The Carb-Insulin Model proposes a causal reversal:

👉Over the long term, a positive energy balance doesn’t cause increased storage of body fat.

👉Instead, a shift in substrate partitioning favoring fat storage drives a positive energy balance
5/12
If the CIM is correct, trying to maintain a negative energy balance through conscious control of food & physical activity is likely to fail.

👉Restricting calories on a high-glycemic load diet doesn't lessen predisposition to fat storage nor diminish hunger during dieting.
6/12
By reducing anabolic drive with a low-glycemic load diet, people may experience less hunger and improved energy level.

👉In this way, weight loss may occur more easily, analogous to how an antipyretic reduces fever without conscious control of heat balance.
7/12
>12 papers claimed to disprove the CIM, but these are based on the same weak studies.

👉Animal studies confounded by non-physiological levels of sat fat
👉Feeding trials that don’t allow for adaptation to changes in nutrients
👉Diet studies that don’t much change behavior
8/12
These criticisms also premised on strawman arguments

The CIM doesn’t claim carbs affect metabolism ONLY through insulin, ONLY immediately after eating, or ONLY at fat cells

👉Type of carbs at dinner affect glucose tolerance next day. Low carb diet reduces fasting insulin
9/12
The definitive research needed to test the CIM will be challenging.

👉But this difficulty is no justification for basing knowledge on inconclusive data.

👉Let’s not repeat the public health failure of the low-fat diet for obesity, due to over-reliance on weak evidence.
10/12
The field of obesity should embrace paradigm clash as an essential step forward. Toward this end, investigators should:

👉FIRST, refrain from hyperbolic claims for having disproven (or proven) alternative explanations of the obesity pandemic.
11/12
👉SECOND, clarify EBM, specifying contrasting causal testable hypotheses

👉THIRD, form collaborations among scientists with diverse viewpoints to test predictions in rigorous, unbiased research

👉FOURTH, depersonalize the debate, scrupulously avoiding ad hominem argument
12/12
Rigorous research with complementary designs needed to resolve the debate, clarify middle ground, or point to new models that better encompass the evidence

👉With the massive burden of obesity-related diseases, this work must assume priority.

end
doi.org/10.1093/ajcn/n…

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