Wednesday, May 5, 2010

Cigarette smoking in the development and progression of atherosclerosis: Is sympathetic overactivity the key factor to explain this association?

Sympathetic overactivity seems, in our point of view (1), to be the key factor in cigarette smoking as responsible for the development and progression of atherosclerosis.
Cigarette smoking increases efferent sympathetic nerve traffic acutely, as well norepinephrine and epinephrine release. The adverse effects of cigarette smoking are related to the mixture of chemicals, including nicotine that has been largely accused for many of the adverse effects of smoking on the cardiovascular system, including autonomic imbalance, endothelial dysfunction and coronary blood flow dysregulation. The acute sympathoexcitatory effects of smoking on the cardiovascular system are partially mediated by catecholamine release, muscle sympathetic nerve excitation and peripheral chemoreceptor sensitivity increase, consecutive to nicotinic receptor stimulation in the autonomic nervous system (2).
Both active smoking and exposure to enviromental tobacco smoke are associated with the progression of atherosclerosis as indexed by intimal-medial thickness of the carotid artery assessed by ultrasound (8)
It is interesting to notice about the results from a study published in 2006 revealing that sublingual administration of a 4-mg tablet of Nicotine Replacement Therapy exerts acute deleterious cardiovascular effects and sympathetic activation (3).
Also interesting is the high sugar content (up to 20% - including high fructose corn syrup) of the popular brands of cigarettes (4,5). Sugars and other high-carbohydrate diets, particularly in the form of high-glycemic index carbohydrate, may also contribute for keeping the sympathetic nervous system overactive as discussed recently in this blog (6,7).
Carlos Monteiro
1. Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008 at http://www.infarctcombat.org/AcidityTheory.pdf
2. Adamopoulus D, van de Borne P and Argacha JF, New insights into the sympathetic, endothelial and coronary effects of nicotine. Clin Exp Pharmacol Physiol 2008; 35(4): 458-63
3. Najem B et al. Acute cardiovascular and sympathetic effects of nicotine replacement therapy. Hypertension 2006; 47:1162-67 Full free text at http://hyper.ahajournals.org/cgi/content/full/47/6/1162
4. Elson LA, Betts TE, Passey RD, The sugar content and the pH of the smoke of cigarette, cigar, and pipe tobbacos in relation to lung cancer. International Journal of Cancer, V 9, I 3; 666-675, 1972
5. Stavanja et al. Safety assessment of high fructose corn syrup (HFCS) as an ingredient added to cigarette tobacco. Exp Toxicol Pathol, 57(4): 267-81, 2006
6. Koop W. Chronically increased activity of the sympathetic nervous system: our diet-related “evolutionary” inheritance. The Journal of Nutrition, Health & Aging Volume 13, Number 1, 2009
7. Carlos Monteiro, Fermentable carbohydrates: A link between periodontal disease and cardiovascular disease? Thursday, April 15, 2010 at http://aciditytheory.blogspot.com/2010/04/fermentable-carbohydrates-link-between.html
8. Howard G et al, Cigarette smoking and progression of atherosclerosis: The Atherosclerosis Risk in Communities (ARIC) Study. JAMA, 1998 Jan 14;279(2):119-24. Full free text at http://jama.ama-assn.org/cgi/reprint/279/2/119.pdf

1 comment:

  1. Carlos, I've been looking at the release of FFAs from adipose tissue (under sympathetic stimulation by nicotine) a major driver of CVD. The inappropriate release of FFAs when glucose and insulin are present in generous amounts gives the palmitic acid physiological insulin resistance at a time when this is completely inappropriate. Hyperglycaemia follows...

    The nicotine patches usually release nicotine at dose rates which do not stimulate FFA release. Do you think they will be safe from a vascular sympathetic nervous system stimulation effect?

    Peter

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