Does the Carbohydrate-Insulin Model Explain Obesity? Evidence from Mechanistic and Clinical Studies: A Critical Review.
Level 5 - mechanism / opinion, no new human data
Narrative critical review synthesizing theoretical and empirical evidence without systematic review methodology
PubMed 42616211 · doi:10.1007/s13679-026-00751-2
What was done
This critical review evaluated the Carbohydrate-Insulin Model (CIM) versus the Energy Balance Model (EBM) of obesity across eleven lines of evidence: isocaloric and ad libitum dietary interventions, energy expenditure studies, population-level dietary trends, glycemic index manipulations, glucagon-like peptide-1 receptor agonist therapies, overfeeding experiments, the insulinotropic effects of protein, central effects of insulin on appetite, insulin spikes and 24-hour fat balance, temporal relationships between hyperinsulinemia and obesity, and de novo lipogenesis.
What was found
The abstract reports no numerical findings. Qualitatively, several lines of evidence conflict with central CIM predictions, notably the insulinotropic yet anti-obesogenic effects of dietary protein and the central anorexigenic role of insulin. Overall, the evaluated mechanistic, clinical, and epidemiological evidence did not consistently support hyperinsulinemia and fuel partitioning as the primary causal drivers of common obesity.
Why it matters
This review synthesizes multiple physiological domains to challenge the premise that insulin dynamics and carbohydrate quality are the primary etiology of obesity, supporting a broader framework for energy balance regulation.
Limits
As a narrative review, it lacks a formal systematic search or quantitative meta-analytic pooling. The abstract notes that many underlying studies are limited by design constraints, confounding factors, and data limitations that prevent definitive distinctions between competing models.
Cited by
- supports The carbohydrate-insulin model of obesity has largely been disbanded and lacks strong evidentiary support.