Evidence map›Paper›PMID 35629964›Full record

ArticleMetabolites2022

The Lipid Energy Model: Reimagining Lipoprotein Function in the Context of Carbohydrate-Restricted Diets.

Nicholas G Norwitz, Adrian Soto-Mota, Bob Kaplan, David S Ludwig, Matthew Budoff, Anatol Kontush, David Feldman

Open access · goldAbstract read
In one paragraph

Article in Metabolites, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 3 pooled it
5.4field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 3 syntheses or guidelines pooled it, 34 citations in OpenAlex.

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  12. A Case Report on the Metabolic Effects of a Very-Low-Carbohydrate Ketogenic Diet in a Patient WithDiabetes spectrum : a publication of the American Diabetes Association · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 5 institutions in 3 countries.

Nicholas G NorwitzHarvard Medical School, Boston, MA 02115, USA.ORCID 0000-0002-0826-9069
Adrian Soto-MotaMetabolic Diseases Research Unit, National Institute for Medical Sciences and Nutrition Salvador Zubiran, Tlalpan, CDMX 14080, Mexico.ORCID 0000-0002-9173-7440
Bob KaplanCitizen Science Foundation, Las Vegas, NV 89139, USA.ORCID 0000-0003-1204-8346
David S LudwigHarvard Medical School, Boston, MA 02115, USA.ORCID 0000-0003-3307-8544
Matthew BudoffLundquist Institute at Harbor-UCLA Medical Center, Torrance, CA 90502, USA.
Anatol KontushNational Institute for Health and Medical Research (INSERM), UMRS 1166 ICAN, Faculty of Medicine Pitié-Salpêtrière, Sorbonne University, 75013 Paris, France.
David FeldmanCitizen Science Foundation, Las Vegas, NV 89139, USA.
Boston Children's Hospital · USHarvard University · USInserm · FRInstituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán · MXUCLA Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

When lean people adopt carbohydrate-restricted diets (CRDs), they may develop a lipid profile consisting of elevated LDL-cholesterol (LDL-C) and HDL-cholesterol (HDL-C) with low triglycerides (TGs). The magnitude of this lipid profile correlates with BMI such that those with lower BMI exhibit larger increases in both LDL-C and HDL-C. The inverse association between BMI and LDL-C and HDL-C change on CRD contributed to the discovery of a subset of individuals-termed Lean Mass Hyper-Responders (LMHR)-who, despite normal pre-diet LDL-C, as compared to non-LMHR (mean levels of 148 and 145 mg/dL, respectively), exhibited a pronounced hyperlipidemic response to a CRD, with mean LDL-C and HDL-C levels increasing to 320 and 99 mg/dL, respectively, in the context of mean TG of 47 mg/dL. In some LMHR, LDL-C levels may be in excess of 500 mg/dL, again, with relatively normal pre-diet LDL-C and absent of genetic findings indicative of familial hypercholesterolemia in those who have been tested. The Lipid Energy Model (LEM) attempts to explain this metabolic phenomenon by positing that, with carbohydrate restriction in lean persons, the increased dependence on fat as a metabolic substrate drives increased hepatic secretion and peripheral uptake of TG contained within very low-density lipoproteins (VLDL) by lipoprotein lipase, resulting in marked elevations of LDL-C and HDL-C, and low TG. Herein, we review the core features of the LEM. We review several existing lines of evidence supporting the model and suggest ways to test the model's predictions.

Indexed as

carbohydrate restrictionHDL-cholesterolLDL-cholesterollean mass hyper-responderlipoprotein lipasetriglyceride-rich lipoproteinsVLDL-cholesterol

Identifiers

PMID35629964
PMCPMC9147253
OpenAlexW4280580298

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.