ArticleRoyal Society open science2022
Testing the protein-leverage hypothesis using population surveillance data.
Article in Royal Society open science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Consuming an unprocessed diet reduces energy intake: a post-hoc analysis of a randomized controlled trial reveals a role for human nutritional intelligence.The American journal of clinical nutrition · 2026Trial
- Protein Decoys, Alcohol, and Energy Intake: Testing a Mechanistic-Ecological Model.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026Review
- Dietary Macronutrient Composition and Protein Concentration for Weight Loss Maintenance.Obesity (Silver Spring, Md.) · 2025Article
- Dietary macronutrient content and energy intake in the mouse: hedonic or homeostatic override?Obesity (Silver Spring, Md.) · 2025Article
- Protein appetite as an integrator in the obesity system: the protein leverage hypothesis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is hypothesized that humans exhibit 'protein leverage' (PL), whereby regulation of absolute protein intake results in the over-consumption of non-protein food on low percentage protein diets. Testing for PL using dietary surveillance data involves seeking evidence for a negative association between total energy intake and percentage energy from protein. However, it is unclear whether such an association might emerge without PL due to the structure of intake data (protein and non-protein intakes have different means and variances and covary). We derive a set of models that describe the association between the expected estimate of PL and the distributions of protein and non-protein intake. Models were validated via simulation. Patterns consistent with PL will not emerge simply because protein intake has a lower mean and/or variance than non-protein. Rather, evidence of PL is observed where protein has a lower index of dispersion (variance/mean) than non-protein intake. Reciprocally, the stronger PL is the lower the index of dispersion for protein intake becomes. Disentangling causality is ultimately beyond the power of observational data alone. However, we show that one can correct for confounders (e.g. age) in generating signals of PL, and describe independent measures that can anchor inferences around the role of PL.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.