Elevated LDL Cholesterol with a Carbohydrate-Restricted Diet: Evidence for a "Lean Mass Hyper-Responder" Phenotype.
HDL cholesterol
LDL cholesterol
atherosclerosis
lean mass hyper-responder
low-carbohydrate diet
precision nutrition
triglycerides
Journal
Current developments in nutrition
ISSN: 2475-2991
Titre abrégé: Curr Dev Nutr
Pays: United States
ID NLM: 101717957
Informations de publication
Date de publication:
Jan 2022
Jan 2022
Historique:
received:
11
10
2021
revised:
05
11
2021
accepted:
22
11
2021
entrez:
2
2
2022
pubmed:
3
2
2022
medline:
3
2
2022
Statut:
epublish
Résumé
People commencing a carbohydrate-restricted diet (CRD) experience markedly heterogenous responses in LDL cholesterol, ranging from extreme elevations to reductions. The aim was to elucidate possible sources of heterogeneity in LDL cholesterol response to a CRD and thereby identify individuals who may be at risk for LDL cholesterol elevation. Hypothesis-naive analyses were conducted on web survey data from 548 adults consuming a CRD. Univariate and multivariate regression models and regression trees were built to evaluate the interaction between body mass index (BMI) and baseline lipid markers. Data were also collected from a case series of five clinical patients with extremely high LDL cholesterol consuming a CRD. BMI was inversely associated with LDL cholesterol change. Low triglyceride (TG) to HDL cholesterol ratio, a marker of good metabolic health, predicted larger LDL cholesterol increases. A subgroup of respondents with LDL cholesterol ≥200 mg/dL, HDL cholesterol ≥80 mg/dL, and TG ≤70 mg/dL were characterized as "lean mass hyper-responders." Respondents with this phenotype ( These data suggest that, in contrast to the typical pattern of dyslipidemia, greater LDL cholesterol elevation on a CRD tends to occur in the context of otherwise low cardiometabolic risk.
Sections du résumé
BACKGROUND
BACKGROUND
People commencing a carbohydrate-restricted diet (CRD) experience markedly heterogenous responses in LDL cholesterol, ranging from extreme elevations to reductions.
OBJECTIVES
OBJECTIVE
The aim was to elucidate possible sources of heterogeneity in LDL cholesterol response to a CRD and thereby identify individuals who may be at risk for LDL cholesterol elevation.
METHODS
METHODS
Hypothesis-naive analyses were conducted on web survey data from 548 adults consuming a CRD. Univariate and multivariate regression models and regression trees were built to evaluate the interaction between body mass index (BMI) and baseline lipid markers. Data were also collected from a case series of five clinical patients with extremely high LDL cholesterol consuming a CRD.
RESULTS
RESULTS
BMI was inversely associated with LDL cholesterol change. Low triglyceride (TG) to HDL cholesterol ratio, a marker of good metabolic health, predicted larger LDL cholesterol increases. A subgroup of respondents with LDL cholesterol ≥200 mg/dL, HDL cholesterol ≥80 mg/dL, and TG ≤70 mg/dL were characterized as "lean mass hyper-responders." Respondents with this phenotype (
CONCLUSIONS
CONCLUSIONS
These data suggest that, in contrast to the typical pattern of dyslipidemia, greater LDL cholesterol elevation on a CRD tends to occur in the context of otherwise low cardiometabolic risk.
Identifiants
pubmed: 35106434
doi: 10.1093/cdn/nzab144
pii: nzab144
pmc: PMC8796252
doi:
Types de publication
Journal Article
Langues
eng
Pagination
nzab144Commentaires et corrections
Type : CommentIn
Type : CommentIn
Informations de copyright
© The Author(s) 2021. Published by Oxford University Press on behalf of the American Society for Nutrition.
Références
Nutrients. 2021 Mar 02;13(3):
pubmed: 33801247
Atherosclerosis. 2021 Jul;328:108-113
pubmed: 33863548
Atherosclerosis. 2018 Dec;279:52-61
pubmed: 30408717
Intern Med. 2020 Nov 1;59(21):2661-2669
pubmed: 32669498
Arch Intern Med. 2001 Feb 12;161(3):361-6
pubmed: 11176761
Front Endocrinol (Lausanne). 2019 Jun 05;10:348
pubmed: 31231311
Nature. 2021 Apr;592(7855):524-533
pubmed: 33883728
Front Physiol. 2019 Dec 19;10:1499
pubmed: 31920704
BMJ Open Sport Exerc Med. 2018 Oct 4;4(1):e000429
pubmed: 30305928
Am J Clin Nutr. 2022 Jan 11;115(1):154-162
pubmed: 34582545
Mayo Clin Proc. 2003 Nov;78(11):1331-6
pubmed: 14601690
N Engl J Med. 2003 May 22;348(21):2074-81
pubmed: 12761364
Circulation. 2001 Dec 18;104(25):3046-51
pubmed: 11748098
Nutr Diabetes. 2018 Apr 25;8(1):21
pubmed: 29695708
PLoS One. 2020 Jan 14;15(1):e0225348
pubmed: 31935216
Nat Commun. 2017 Apr 19;8:15010
pubmed: 28422089
Arterioscler Thromb Vasc Biol. 2005 Mar;25(3):553-9
pubmed: 15618542
Front Med (Lausanne). 2020 Apr 15;7:97
pubmed: 32351962
Mol Cell Biochem. 2006 Jun;286(1-2):1-9
pubmed: 16652223
Am J Med. 2004 Sep 15;117(6):398-405
pubmed: 15380496
Am J Clin Nutr. 2021 Oct 4;114(4):1455-1466
pubmed: 34159352
Trends Mol Med. 2020 Dec;26(12):1086-1100
pubmed: 32861590
JCI Insight. 2019 Jun 20;4(12):
pubmed: 31217353
BMC Endocr Disord. 2021 Mar 22;21(1):54
pubmed: 33752643
PLoS One. 2018 Sep 5;13(9):e0200817
pubmed: 30183740
Arterioscler Thromb Vasc Biol. 2018 Sep;38(9):2207-2216
pubmed: 30354257
Diabetes Care. 2000 Nov;23(11):1679-85
pubmed: 11092292
Curr Pharm Des. 2013;19(21):3858-68
pubmed: 23286436
J Nutr. 2004 Apr;134(4):880-5
pubmed: 15051841
JAMA Cardiol. 2021 Apr 1;6(4):437-447
pubmed: 33471027