Related Experiment Video
Updated: Jun 16, 2026

11:46
Shotgun Lipidomics of Rodent Tissues
Published on: November 18, 2022
Smoking intensity and lipoprotein abnormalities in active smokers
Linda K Gossett1, Heather M Johnson, Megan E Piper
1University of Wisconsin School of Medicine and Public Health; Madison, WI.
Journal of Clinical Lipidology
|February 18, 2010
Summary
Smoking increases total cholesterol, LDL-C, and triglycerides. Higher recent smoke exposure, indicated by carbon monoxide levels, lowers HDL-C and HDL particles in smokers.
Area of Science:
- Cardiovascular Health
- Metabolic Syndrome
- Tobacco Cessation Research
Background:
- Smoking is a known risk factor for cardiovascular disease.
- It negatively impacts lipid profiles, decreasing high-density lipoprotein cholesterol (HDL-C) and increasing triglycerides.
Purpose of the Study:
- To investigate the association between five smoking intensity markers and lipoprotein profiles in current smokers.
- To determine how smoking burden affects lipid concentrations and particle sizes.
Main Methods:
- Analysis of lipoprotein profiles using nuclear magnetic resonance spectroscopy in 1,504 current smokers.
- Multivariate linear regression models assessed predictors of lipoprotein fractions, including smoking intensity markers (cigarettes/day, pack-years, FTND score, CO levels).
Main Results:
- Increased daily cigarette consumption was linked to higher total cholesterol, LDL-C, and triglycerides.
- Higher carbon monoxide (CO) levels correlated with lower HDL-C and fewer HDL particles.
- The impact of smoking intensity markers on individual lipoproteins was generally small.
Conclusions:
- Higher smoking burden is associated with modest increases in total cholesterol, LDL-C, and triglycerides.
- Increased recent smoke exposure, measured by CO, is linked to reduced HDL-C and HDL particles in smokers.
Related Concept Videos
Atherosclerosis III: Management
Management of atherosclerosis involves an integrated strategy encompassing pharmacological treatment, surgical interventions, lifestyle changes, and nutrition therapy to address the multifactorial nature of the disease.Pharmacological TherapyA cornerstone of atherosclerosis management is the use of pharmacological agents. Statins, such as atorvastatin, are pivotal in inhibiting HMG-CoA reductase, an enzyme that catalyzes an initial step in cholesterol synthesis in the liver. This reduction in...
Atherosclerosis I: Introduction
Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
Chronic Obstructive Pulmonary Disease-II: Pathophysiology
Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
Chronic Inflammation
Chronic Obstructive Pulmonary Disease II: Emphysema
Emphysema, a major phenotype of chronic obstructive pulmonary disease (COPD), is characterized by irreversible destruction of alveolar walls and permanent enlargement of distal airspaces. Unlike chronic bronchitis, which primarily affects the airways, emphysema predominantly involves the lung parenchyma, where structural damage leads to airflow limitation.PathophysiologyIt most commonly results from prolonged exposure to cigarette smoke and other toxic gases, particularly cigarette smoke.
Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features
Chronic bronchitis is a key phenotype of chronic obstructive pulmonary disease (COPD), characterized by airway-centered inflammation and mucus overproduction. It develops from long-term exposure to harmful particles or gases, most commonly cigarette smoke, which triggers a persistent inflammatory response.Cellular and Structural ChangesInflammation initially affects the large bronchi and later the smaller airways, with infiltration by immune cells, including neutrophils, macrophages, and...
Inflammation
Overview

