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Hypothesis

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

1
Harvard Medical School, Boston, MA 02115, USA
2
Metabolic Diseases Research Unit, National Institute for Medical Sciences and Nutrition Salvador Zubiran, Tlalpan, CDMX 14080, Mexico
3
Citizen Science Foundation, Las Vegas, NV 89139, USA
4
New Balance Foundation Obesity Prevention Center, Boston Children’s Hospital, Boston, MA 02115, USA
5
Lundquist Institute at Harbor-UCLA Medical Center, Torrance, CA 90502, USA
6
National Institute for Health and Medical Research (INSERM), UMRS 1166 ICAN, Faculty of Medicine Pitié-Salpêtrière, Sorbonne University, 75013 Paris, France
*
Authors to whom correspondence should be addressed.
These authors contributed equally to this work.
Academic Editor: Phil Whitfield
Metabolites 2022, 12(5), 460; https://doi.org/10.3390/metabo12050460
Received: 19 April 2022 / Revised: 2 May 2022 / Accepted: 4 May 2022 / Published: 20 May 2022
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. View Full-Text
Keywords: carbohydrate restriction; lean mass hyper-responder; LDL-cholesterol; lipoprotein lipase; HDL-cholesterol; triglyceride-rich lipoproteins; VLDL-cholesterol carbohydrate restriction; lean mass hyper-responder; LDL-cholesterol; lipoprotein lipase; HDL-cholesterol; triglyceride-rich lipoproteins; VLDL-cholesterol
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MDPI and ACS Style

Norwitz, N.G.; Soto-Mota, A.; Kaplan, B.; Ludwig, D.S.; Budoff, M.; Kontush, A.; Feldman, D. The Lipid Energy Model: Reimagining Lipoprotein Function in the Context of Carbohydrate-Restricted Diets. Metabolites 2022, 12, 460. https://doi.org/10.3390/metabo12050460

AMA Style

Norwitz NG, Soto-Mota A, Kaplan B, Ludwig DS, Budoff M, Kontush A, Feldman D. The Lipid Energy Model: Reimagining Lipoprotein Function in the Context of Carbohydrate-Restricted Diets. Metabolites. 2022; 12(5):460. https://doi.org/10.3390/metabo12050460

Chicago/Turabian Style

Norwitz, Nicholas G., Adrian Soto-Mota, Bob Kaplan, David S. Ludwig, Matthew Budoff, Anatol Kontush, and David Feldman. 2022. "The Lipid Energy Model: Reimagining Lipoprotein Function in the Context of Carbohydrate-Restricted Diets" Metabolites 12, no. 5: 460. https://doi.org/10.3390/metabo12050460

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