Evidence map›Paper›PMID 38706496›Full record

ArticleObesity pillars2024

Obesity, dyslipidemia, and cardiovascular disease: A joint expert review from the Obesity Medicine Association and the National Lipid Association 2024.

Harold Edward Bays, Carol Kirkpatrick, Kevin C Maki, Peter P Toth, Ryan T Morgan, Justin Tondt, Sandra Michelle Christensen, Dave Dixon, Terry A Jacobson

Abstract read
In one paragraph

Article in Obesity pillars, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

49 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Potential lipid-lowering effects ofFrontiers in nutrition · 2026
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  6. Review
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  18. Genetic Influence ofInternational journal of molecular sciences · 2026
    Article
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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

9 authors.

Harold Edward BaysLouisville Metabolic and Atherosclerosis Research Center, Louisville, KY, 40213, USA.
Carol KirkpatrickMidwest Biomedical Research, Addison, IL, USA.
Kevin C MakiMidwest Biomedical Research, Addison, IL, USA.
Peter P TothCGH Medical Center, Sterling, IL, USA.
Ryan T MorganVitalis Metabolic Health, USA.
Justin TondtDepartment of Family and Community Medicine Penn State College of Medicine Penn State Milton S. Hershey Medical Center, Hershey, PA, USA.
Sandra Michelle ChristensenIntegrative Medical Weight Management, 2611 NE 125th St, Suite 100B, Seattle, WA, 98125, USA.
Dave DixonDeptartment of Pharmacotherapy & Outcomes Science, 410 N 12th Street, Box 980533, Richmond, VA, 23298-0533, USA.
Terry A JacobsonLipid Clinic and Cardiovascular Risk Reduction Program, Emory University Department of Medicine, Atlanta, GA, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: This joint expert review by the Obesity Medicine Association (OMA) and National Lipid Association (NLA) provides clinicians an overview of the pathophysiologic and clinical considerations regarding obesity, dyslipidemia, and cardiovascular disease (CVD) risk. Methods: This joint expert review is based upon scientific evidence, clinical perspectives of the authors, and peer review by the OMA and NLA leadership. Results: Among individuals with obesity, adipose tissue may store over 50% of the total body free cholesterol. Triglycerides may represent up to 99% of lipid species in adipose tissue. The potential for adipose tissue expansion accounts for the greatest weight variance among most individuals, with percent body fat ranging from less than 5% to over 60%. While population studies suggest a modest increase in blood low-density lipoprotein cholesterol (LDL-C) levels with excess adiposity, the adiposopathic dyslipidemia pattern most often described with an increase in adiposity includes elevated triglycerides, reduced high density lipoprotein cholesterol (HDL-C), increased non-HDL-C, elevated apolipoprotein B, increased LDL particle concentration, and increased small, dense LDL particles. Conclusions: Obesity increases CVD risk, at least partially due to promotion of an adiposopathic, atherogenic lipid profile. Obesity also worsens other cardiometabolic risk factors. Among patients with obesity, interventions that reduce body weight and improve CVD outcomes are generally associated with improved lipid levels. Given the modest improvement in blood LDL-C with weight reduction in patients with overweight or obesity, early interventions to treat both excess adiposity and elevated atherogenic cholesterol (LDL-C and/or non-HDL-C) levels represent priorities in reducing the risk of CVD.

Indexed as

Adiposopathic dyslipidemiaAdiposopathyCholesterolObesityTriglycerides

Identifiers

PMID38706496
PMCPMC11066689

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.