New Explanation for the Cause of Atherosclerosis: The Acidity Theory



A research at Infarct Combat Project resulted in a new theory that explains the development of atherosclerosis. According to the new hypothesis, acidic pH evoked by stress provokes mechanical forces in coronary flow, leading to atherosclerosis.

ICP, August 10, 2006 – 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 -

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

For more information contact:
Ary Bon, at Infarct Combat Project
Sao Paulo, Brazil
Tel: 0055.11. 6162-1431

Some references:

1. Beyond Lipids: Understanding the Mechanics of Atherosclerosis. UCSD News, July 12, 2006, at
2. Regulation of stretch-induced JNK activation by stress fiber orientation, Kaunas R et al, Cellular Signalling, 2006 (Epub ahead the print) at
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
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
5. George Karniadakis, “Spiraling Through the Arteries”, NCSA News, 1998 at
6. Atherosclerotic lesion size and vulnerability are determined by patterns of fluid shear stress. Cheng C et al, Circulation 2006, 113:2744-2753 at
7. The role of shear stress in the pathogenesis of atherosclerosis (Mini review), Cunningham KS and Gotlieb AI, Laboratory Investigation (2005) 85, 9-23,
8. Endocardial damage induced by lactate, lowered pH and lactic acid in non-ischemic beating hearts, Carter G, Gavin JB, Pathology 1989 Apr;21(2):125-30 at
9. Wilhelm Schoner - Endogenous cardiac glycosides, a new class of steroid hormones, Eur J Biochem. 268, 2440-2448, 2002 at
10. Understanding the sodium potassium pump and its relevance to disease. Rose AM and Valdes RJ, Cin. Chem. 1994; 40/9: 1674-1685
11. Acid-Evoked Currents in Cardiac Sensory Neurons – A possible mediator of myocardial ischemic sensation, Benson CJ et al, Circulation Research, 1999;84:921-928 (Full paper) at
12. Apical ballooning syndrome or takotsubo cardiomyopathy: a systematic review, Monica Gianni et al. European Heart Journal, V27,N13: 1523-1529
13. Reversible left ventricular dysfunction "takotsubo" cardiomyopathy related to catecholamine cardiotoxicity, Akashi YJ et al, J. Electrocardiol 2002; 35:351-356 at
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15. Neurohumoral features of myocardial stunning due to sudden emotional stress, Wittstein IS et al. New Engl J Med 2005 Feb 10, V352: 539-548
16. Sympathetic neural hyperactivity and its normalization following unstable angina and acute myocardial infarction, Graham LN, Smith PA et al. Clin Sci (Lond) 2004 Jun;106(6):605-11
17. Plasma catecholamine concentrations in myocardial infarction and angina pectoris, Gazes PC, Richardson JA et al. Circulation 1959;19:657-661
18. A possible role of noradrenaline in the development of myocardial infarction, Waldenstrom AP et al. Am Heart J. 1978;95:43-51
19. Plasma catecholamine in acute myocardial infarction Nadeau RA, de Champlain J, Am Heart J. 1979;98:548-554
20. Increased cardiac sympathetic nervous activity in patients with unstable coronary heart disease, McCance AJ, Thompson PA, Forfar JC. Eur Heart J 1993 Jun;14(6):751-7
21. Sympathetic neural hyperactivity and its normalization following unstable angina and acute myocardial infarction, Graham LN, Smith PA et al. Clin Sci (Lond) 2004 Jun;106(6):605-11

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