New Explanation For The Cause Of Atherosclerosis: The Acidity Theory

Main Category: Cardiovascular / Cardiology
Article Date: 10 Aug 2006 - 0:00 PDT

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Recent findings were reported by a team of scientists at the University of California, San Diego, linking mechanical forces with structural and biochemical changes in blood vessel cells that could explain why atherosclerotic lesions form preferentially at branches of coronary arteries. The study from Roland Kaunas and colleagues was published online in Cellular Signalling on February 28, 2006 and will appear in the journal's October 2006 issue.

Carlos Monteiro, an independent researcher and president of Infarct Combat Project, wondering about the precursor (s) of the mechanical forces over the coronary flow, generating atherosclerostic lesions, researched through medical literature and came to the following findings:

-- Lowered pH increase perfusion pressure and enhance contractility of coronary arteries (von Ardenne M and Reitnauer PG, 1989; Horai Y et al, 2005).

-- Lactate, lowered pH and lactic acid induce endocardial damage (Carter G and Gavin JB, 1989)

-- Blood does not flow symmetrically, as scientists originally believed. Instead, it flows in two opposing corkscrews surrounded by a third corkscrew-like flow. This combination creates an asymmetrical, spiraling flow that is encouraged by the natural curves and bends of human arteries
(Spiraling Through the Arteries, Karniadakis G, 1998)

-- Changes in flow patterns can produce potentially deleterious effects on vascular biology. Lowered shear stress and oscillatory shear stress are essential conditions in atherosclerotic lesion size and vulnerability
(Cunningham KS and Gotlieb AI, 2005; Cheng et al, 2006)

Acidity Theory of Atherosclerosis

Based in the findings above-mentioned, and taking into account that pH sympathetic dominance migrates towards acidity, Carlos Monteiro formulated a new hypothesis to explain the cause of atherosclerosis in a revolutionary, straightforward and simple idea. The sequence of events in Acidity Theory of Atherosclerosis:

I. Sympathetic dominance by continuous stress plus

II. Deficiency in production of endogenous digitalis-like compounds with alterations in Na(+), K(+)-ATPase activity results in

III. Lowered pH (acidity) that leads to the generation of mechanical forces in blood flow which may cause atherosclerosis.

Many cardiovascular disease processes, including myocardial ischemia, congestive heart failure, unstable angina pectoris, acute myocardial infarction, heart broken syndrome and arrhythmias, are precipitated or worsened by perturbations in the autonomic nervous system, with sympathetic activation and release of acidic pH - stress hormones.

Carlos Monteiro intends to publish an article about the Acidity Theory of Atherosclerosis, in a scientific journal in the near future.

Conflicts of interest:
-- Infarct Combat Project supports the "Myogenic Theory of Myocardial Infarction"
-- Carlos Monteiro is an unofficial member of The International Network of Cholesterol Skeptics (THINCS - www.thincs.org)

Infarct Combat Project is an international non-profit organization that provides information, research and education to fight heart disease. ICP website is http://www.infarctcombat.org

References:

1. Beyond Lipids: Understanding the Mechanics of Atherosclerosis. UCSD News, July 12, 2006, at http://tinyurl.com/llmdx
2. Regulation of stretch-induced JNK activation by stress fiber orientation, Kaunas R et al, Cellular Signalling, 2006 (Epub ahead the print) at http://tinyurl.com/na6pt
3. Increase of perfusion pressure at constant perfusion rate caused by low pH values, von Ardenne M, Reitnauer PG, Biomed Biochim Acta, 1989;48(4):317-23 at http://tinyurl.com/jfomd
4. Changes in pH increase perfusion pressure of coronary arteries in the rat, Yasushi Horai et al, J Pharmacol Sci 97; 400: 407, 2005 (Full paper) at http://www.jstage.jst.go.jp/article/jphs/97/3/400/_pdf
5. George Karniadakis, "Spiraling Through the Arteries", NCSA News, 1998 at http://tinyurl.com/h26aq
6. Atherosclerotic lesion size and vulnerability are determined by patterns of fluid shear stress. Cheng C et al, Circulation 2006, 113:2744-2753 at http://circ.ahajournals.org/cgi/content/abstract/113/23/2744
7. The role of shear stress in the pathogenesis of atherosclerosis (Mini review), Cunningham KS and Gotlieb AI, Laboratory Investigation (2005) 85, 9-23, http://www.nature.com/labinvest/journal/v85/n1/full/3700215a.html
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