Smoking and HDL: Bad News for the Good Lipid

Yes, smoking hurts you; let me count the ways.

This mortal message has not yet been completely embraced: Smoking is hazardous to your health! From lung problems-including COPD, bronchitis, and lung cancer-through a host of cardiovascular diseases-coronary and peripheral vascular disease-the reasons are manifold and should be compelling to all.

For me, it has been easier to understand why smoking is bad for the lungs compared with the pathology it can visit on the heart and peripheral blood vessels. A recent review¹ adds to our understanding of cardiovascular pathology as a consequence of smoking: Atherosclerosis is the issue and one of the good lipids is damaged.

Endothelial dysfunction, platelet activation, oxidative stress, inflammation, and lipid alterations have all been suggested as risk factors for heart disease in smokers. Work recently has implicated lipids more specifically, and down to molecular and endothelial levels. Smoking can increase cholesterol, triglyceride, and LDL levels while decreasing HDL levels. The authors of this paper note that the effect of smoking on HDL levels is dose-dependent. In fact, the reference cited is a meta-analysis of 24 studies that demonstrated that a rise in mean HDL level as a result of smoking cessation might reduce coronary disease complications by 7.4% to 9.0% in men and as much as 12.5% in women.²

I read this cautionary observation at the same time I was reading Rick Atkinson’s book on World War II in Europe (The Guns at Last Light: The War in Western Europe, 1944-1945). General Eisenhower smoked 4 packs of unfiltered Camels a day. He would later become President Eisenhower and suffer multiple heart attacks and intractable heart failure as a result. It appears smoking has negative impacts on HDL metabolism (unclear as to the exact mechanism[s]), HDL biosynthesis and maturation (by decreasing apoA-I and lecithin cholesterol acyltransferase activity), intravascular remodeling of HDL (by increasing cholesterol transfer protein, thus lowering HDL levels), and enlarges HDL molecules and increases their density. This last effect can occur in vessels and in the circulation.

And, there is more (as I said, let me count the ways). Cigarette smoking impairs HDL’s atheroprotective properties through oxidative modifications of the molecule. Some of this is a result of aldehydes present in cigarette smoke (remember embalming fluid?). This “damaged” HDL particle subpopulation can accumulate in intimal lesions and make them larger and eventually prone to rupture.

I realize I am preaching to the choir (or at least I hope that I am).

Target organs for smoking damage continue to increase in number. Understanding of why these organs are harmed is also expanding. Some of the simplest things we do in primary care have the greatest impact-like treating blood pressure, for example. (By the way, Atkinson’s book also reported that Eisenhower routinely ran systolic and diastolic pressures in the 170s and 110s mm/Hg, respectively). Smoking cessation measures should be presented to our smokers ad nauseam. If they get tired of hearing the nonsmoking sermon, so be it. If pulmonary pathology doesn’t get smokers, there are a host of cardiac problems waiting in the wings.
   

References

1. He BM, Zhao SP, Peng ZY. Effects of cigarette smoking on HDL quantity and function: implications for atherosclerosis. J Cell Biochem. 2013 Jul 15; [Epub. ahead of print]. doi:10.1002/jcb.24581. (Abstract)

2. Maeda K, Noguchi Y, Fukui T. The effects of cessation from cigarette smoking on the lipid and lipoprotein profiles: a meta-analysis. Prev Med. 2003;37:283-290. (Abstract)