A review from the book "Acidity Theory of Atherosclerosis: New Evidences", 2012 (Kindle Edition)

A Must Read for Anyone Taking Statin Drugs

By Dr. Stephanie Seneff, Senior Research Scientist, MIT*. Review at Amazon.com

This is a fabulous book, highly recommended for anyone who has the slightest doubt about the lipid theory for cardiovascular disease. The book is jam packed with fascinating observations at every page turn. The writing is not dumbed down for the masses (not an "easy" read), but on the other hand the author does not get caught up in biological jargon that might cause the non-expert to get lost.

The basic premise of the book is that cardiovascular disease is caused by the build-up of acid in the blood, which, in turn, is caused by excitation of the sympathetic nervous system (fight-or-flight response). Each chapter is short and compelling, building on the theory with support from a different slant. While details are left out, a long list of references at the end of every chapter allows the interested read to delve further if they so desire.

The book effortlessly explains many observed associations with heart disease. For example, cigarette smoke is a risk factor because nicotine excites the sympathetic nervous system. Meditation reduces risk because deep breathing promotes the expulsion of carbon dioxide, an acid promoter. A newly learned fact that I relished is that the adrenal glands produce a natural cardiac glycoside similar to digoxin, which is used therapeutically to treat heart failure. Cholesterol is the substrate, and statin drugs interfere with its synthesis, which may help explain the observed association between statin therapy and heart failure.

By the time you arrive at the final chapter, you have seen clearly how all the risk factors for cardiovascular disease can be explained by the acid theory, and this is where he lays it out "plain and simple" and ties it all together. After having read this book, you will never again believe that lowering LDL levels has any merit in the treatment of cardiovascular disease.

*Homepage of Dr. Stephanie Seneff at MIT:
http://people.csail.mit.edu/seneff

*Dr. Seneff essay on sulfur and heart disease and other chronic diseases:
http://people.csail.mit.edu/seneff/sulfur_obesity_alzheimers_muscle_wasting.html

*Dr. Stephanie Seneff interviewed by Dr. Mercola:
http://articles.mercola.com/sites/articles/archive/2011/09/17/stephanie-seneff-on-sulfur.aspx

A review from the book "Acidity Theory of Atherosclerosis: New Evidences", 2012 (Paperback)

By Livin' La Vida Low-Carb Man "Jimmy Moore"*. Review at Amazon.com

Rethinking What Really Contributes To Heart Disease

For the past few decades we have been led to believe that the reason why people develop heart disease is because they are consuming too much saturated fat and cholesterol in their diet that it has led to "clogged arteries" that give us a heart attack and puts us one foot in the grave. The weeping and gnashing of teeth that takes place over this has people scared half to death to consume any fat or cholesterol anymore. But what if that theory of atherosclerosis was just plain wrong? This is what author Carlos Monteiro explores in his book ACIDITY THEORY IN ATHEROSCLEROSIS: NEW EVIDENCES (VOLUME 1).

Monteiro does a brilliant job at examining other aspects of vascular health that people may not even realize exists. Try some of these on for size and see if you knew they had any relation to the health of your heart:

- People with Down's syndrome tend to have very little heart disease
- Diabetics are more likely to develop heart disease
- If you a man with ED, then you are very likely at risk for heart disease
- Wanna make your heart healthier? Marry a comedian
- LDL cholesterol plays a lot less role in a cardiovascular event than people realize
- Salt intake is pretty much irrelevant in whether you develop heart disease or not
- If you have rheumatoid arthritis, then you are at greater risk for atherosclerosis
- The health of your teeth can play a factor in developing heart disease

For some, the information contained in this book will rock your world and make you rethink most of what you thought was true about the development of arterial plaque. Monteiro's alternative theory that this is really all about acidity in the body and that this leads to a chain reaction of events the increases LDL oxidation which makes atherosclerosis become a reality is absolutely plausible if not probable. And lest you think this book is just full of a bunch of opinions by a wayward voice, think again. Monteiro does an outstanding job of providing literally hundreds of excellent scientific references for you to do further research on each of his points.

This book should be required reading for every first-year medical school student so they can have a much broader focus on some of the true causes of atherosclerotic development that can lead to myocardial infarction. And here's the headline-making secret that you don't hear many people talking about--it's not necessarily about what your LDL or total cholesterol is! That's why statin medications are pretty much useless in preventing heart attacks from happening and why you need to read the ACIDITY THEORY OF ATHEROSCLEROSIS for an alternative viewpoint that just might be spot on. It's time we start rethinking what REALLY contributes to heart disease.

* Jimmy Moore Blog & Podcast

http://www.livinlavidalowcarb.com/blog
http://www.thelivinlowcarbshow.com/shownotes
livinlowcarbman@charter.net
Author of "21 Life Lessons From Livin' La Vida Low-Carb: How The Healthy Low-Carb Lifestyle Changed Everything I Thought I Knew" (BookSurge 2009) Order Jimmy's book at Amazon.com 

Both restriction and high salt intake may result in cardiovascular disease

For centuries, salt has been regarded as essential to human health. Recently there has been an intense discussion on the benefits and potential harm of reducing salt (sodium chloride) intake in the general population. A long-term advocate of salt reduction is Dr. Graham MacGregor from Queen Mary University of London, UK. In the opposite side there is a growing number of Doctors who disagree about a generalized sodium restriction. One of these is Dr. Michael Alderman from the Albert Einstein College of Medicine, New York, USA, that says the available data provides no support for any universal recommendation of a particular level of dietary sodium (1, 2).
Anyway, it is important to emphasize that a general reduction in dietary salt intake can only be achieved by reducing the sodium chloride content of processed foods, as these account for 75% to 80% of the sodium chloride consumed daily (3). Even the existent table salt is industrially processed with the essential and trace minerals removed almost completely.
Recently an European study questioned the need to reduce the salt intake in the general population and refuted the computer-generated estimates of the lives and healthcare costs that would be saved by lowering sodium consumption. The authors have stressed that previous studies on which recommendations to lower sodium intake are based are all short term, controlled intervention trials, in which there are reductions in blood pressure in hypertensive patients and a small decrease in blood pressure in normotensive volunteers with sodium reduction, and these studies have been extrapolated to the population as a whole. The authors also note that the assumption that lower salt intake would in the long run lower blood pressure, has not confirmed in longitudinal population-based studies. The most controversial finding from this prospective population study involving 3681 participants, without cardiovascular disease, was that the lower sodium intake - as measured by 24-hour sodium excretion - was associated with higher cardiovascular mortality. In their study the authors say that the underlying mechanisms explaining the inverse association between cardiovascular mortality and 24-hour urinary sodium excretion might be that a salt intake low enough to decrease blood pressure also increases sympathetic nerve activity, decreases insulin sensitivity, activates the renin-angiotensin system and stimulates aldosterone secretion (4).
This European study is not the first to find that a low-sodium diet is detrimental for health. The NHANES study published in 2006, constituting a sample with 7154 participants, found that the low sodium diet was associated with the stimulation of the sympathetic nervous system, with an increase in mortality outcomes in cardiovascular disease and by all causes (5). In other short term trials was also observed activation of the renin-angiotensin-aldosterone system and in the sympathetic nervous system, a decrease in insulin sensitivity and increases in LDL cholesterol concentrations, triglycerides and uric acid (6).
Graham MacGregor, invited for commenting the study by Heartwire (7) have demonstrated irritation regarding the remarks on the possible underlying mechanisms cited in the European study (4), saying “We have shown in our meta-analysis that reducing salt by the amounts we are recommending does not increase sympathetic tone, there is a trivial increase in renin, and no evidence of any adverse effects, no physiologic meaning whatsoever” Dr. MacGregor also have reacted in 2003 (8), in a correspondence to Circulation on the findings by Grassi and colleagues that found effects of modest salt reduction on sympathetic activity (9).
On the other side, because plasma norepinephrine levels during high salt intake remain unaltered in salt-sensitive hypertensive patients but are reduced in normal subjects and non-salt-sensitive hypertensive patients, abnormal relationships between salt intake and sympathetic activity have been suggested (10). It is interesting to note about the discovery that a high sodium diet may depress arterial baroreceptor reflex in normotensive people, with sympathetic activation (11).
A recent review article by researchers at Boston University School of Medicine (BUSM) debunks the widely-believed concept that hypertension, or high blood pressure, is the result of excess salt causing an increased blood volume, exerting extra pressure on the arteries. Published online in the Journal of Hypertension (13), the study demonstrates that excess salt stimulates the sympathetic nervous system to produce adrenalin, causing artery constriction and hypertension. This study cites that several investigators throughout the 1960s and 1970s had reported elevated plasma catecholamine levels in up to 40% of patients with essential hypertension (14-17), as well as an association of increase in catecholamines with high sodium intake in experimental animals and humans (18-21).
Taking in view that both restriction and high intake of dietary sodium may be deleterious to human health, I do not share the opinion that indiscriminate restriction in dietary sodium intake at population level and as a universal recommendation is the a good solution to help in the prevention of cardiovascular disease. In my idea salt balance should be thought according individual requirements.
Moreover because we believe that sympathetic predominance is the primary factor in the cascade of events leading to cardiovascular disease, according our acidity theory of atherosclerosis (12).
Note:
A new study (22) has shown that people consuming too much salt and too little potassium in their diet have had a significantly raised risk of death from cardiovascular disease compared with those who had the lowest ratio of sodium to potassium. The study, with an average of 14.8 years of follow-up, collecting data on 12,267 people, isn't the first study to find an association between high blood pressure and high levels of salt consumption and low levels of potassium intake.
However, Dr. Elena Kuklina, co-author of this study, told to Heartwire (23) that this was the first large, nationwide study looking at sodium and potassium at the same time. She also told that "The major implications of their findings are that a diet balance in both nutrients is important. People should try to reduce sodium in particular by consuming less processed food, but also they should increase potassium intake".
Dr. Kublina have also stressed join Heartwire that people must understand the massive impact that processing has on foods. She cites, for example, that 100 g of unprocessed pork contains 61 of sodium and 340 mg of potassium, but turning this into ham alters that ratio significantly, to yield a whopping 921 mg of sodium and, to boot, reduces the potassium content to 240 mg.
Talking about the results of this study, Dr. David Brownstein, a colleague from THINCs, has made an interesting observation inside of our internal forum, on the high intake of salt depending of his kind if refined or unrefined salt. Dr. David told that "Refined salt lacks potassium. Refined salt use leads to sodium/potassium imbalances. This can be rectified by using unrefined salt which contains both sodium (lower amounts as compared to refined salt) and potassium. This article should have been titled "The problems with Refined Salt: Potassium Deficiency."
I agree with Dr. David Brownstein, on his opinion. Mainly taking the importance of alterations in sodium/potassium activity expressed in the acidity theory of atherosclerosis paper (12).
Carlos Monteiro
1. He FJ and MacGregor GA, . How far should salt intake be reduced? Hypertension 2003; 42:1093-1099. Full free text at http://hyper.ahajournals.org/cgi/reprint/42/6/1093
2. Michael H. Alderman, Evidence Relating Dietary Sodium to Cardiovascular Disease. Journal of the American College of Nutrition, Vol. 25, No. 3, 256S–261S (2006). Full free text at http://www.jacn.org/content/25/suppl_3/256S.full  
3. Klaus D et al. Salt restriction for the prevention of cardiovascular disease. Dtsch Arztebl Int 2010; 107(26):457-62. Full free text at http://www.aerzteblatt.de/int/article.asp?id=77388
4. Stolarz-Skrypek K, et al. Fatal and nonfatal outcomes, incidence of hypertension, and blood pressure changes in relation to urinary sodium excretion. JAMA 2011; 305:1777-1785
5. Cohen HW, et al. Sodium Intake and Mortality in the NHANES II Follow-up Study. The American Journal of Medicine (2006) 119, 275.e7-275.e149.
6. Jurgens G, Graudal NA. Effects of low sodium data versus high sodium diet on blood pressure, renin aldosterone, catecholamines cholesterols, and triglyceride. Cochrane Database Syst Rev. 2004; Issue 1. Art. No.: CD004022
7. New Salt paper causes controversy. Heartwire, May 3, 2011
8. He FJ and MacGregor GA. Salt intake and sympathetic activity. Circulation 2003 Apr 29; 107 ((16): 108 author reply. Full free text at http://circ.ahajournals.org/ggi/reprint/107/16/e108
9. Guido Grassi, et al. Short- and Long-Term Neuroadrenergic Effects of Moderate Dietary Sodium restriction in Essential Hypertension. Circulation. 2002;106: 1957-1961. Full free text at http://circ.ahajournals.org/cgi/reprint/106/15/1957
10. Campese VM, et al. Abnormal relationship between sodium intake and sympathetic nervous system activity in salt-sensitive patients with essential hypertension. Kidney Int., 1982; 21: 371-378
11. MA Creager, et al. Sodium depresses arterial baroreceptor reflex function in normotensive humans. Hypertension 1991;17;989-996
12. 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
13. Volume-expanded' hypertension: the effect of fluid overload and the role of the sympathetic nervous system in salt-dependent hypertension, Journal of Hypertension, V30; N1: January 2012 doi: 10.1097/HJH.0b013e32834f6de1
14. de Champlain J, Farley L, Cousineau D, van Ameringen MR. Circulating catecholamine levels in human and experimental hypertension. CircRes 1976; 38:109–114.
15. Louis WJ, Doyle AE, Anavekar S. Plasma norepinephrine levels in essential hypertension. N Engl J Med 1973; 288:599–601.
16. Sever PS, Osikowska B, Birch M, Tunbridge RD. Plasma noradrenaline in essential hypertension. Lancet 1977; 1:1078–1081.
17. Lake CR, Kopin IJ, Ziegler MG, Coleman MD. Plasma catecholaminesand neurogenic hypertension. N Engl J Med 1977; 297:53–54.
18. de Champlain J, Krakoff L, Axelrod J. Interrelationships of sodium intake, hypertension, and norepinephrine storage in the rat. Circ Res 1969; 24 (Suppl):75–92.
19. Reid JL, Zivin JA, Kopin IJ. Central and peripheral adrenergic mechanisms in the development of deoxycorticosterone-saline hypertension in rats. Circ Res 1975; 37:569–579.
20. Murray RH, Luft FC, Bloch R, Weyman AE. Blood pressure responses to extremes of sodium intake in normal man. Proc Soc Exp Biol Med 1978; 159:432–436.
21. Nicholls MG, Kiowski W, Zweifler AJ, Julius s, Schork MA, Greenhouse J. Plasma norepinephrine variations with dietary sodium intake. Hypertension 1980; 2:29–32.
22. Yang Q, Liu T, Kuklina EV et al. Sodium and potassium intake and mortality among US adults. Prospective data from the Third National Health and Examination Survey. Arch Intern Med 2011, 171 (13):1183-91
23. Sodium/potassium ratio important for health. Heartwire, July 11, 2011

Why atherosclerosis is milder or non-existent in individuals with Down syndrome?

Different necropsy studies have shown that the occurrence of atherosclerosis is milder or non-existent in subjects with Down syndrome (1, 2, 3, 4). Indeed, a study have suggested that women with Down syndrome (DS) may be less likely to express the insulin resistance syndrome*, and men and women with Down syndrome may possess fewer atherosclerotic risk factors than the comparison groups (5)
Confirming the results that DS individuals possess low levels of atherosclerosis a recent study have examined the relation between cardiovascular disease risk factors and intima-media thickness (IMT), a measure for atherosclerosis, in 52 adults with DS. The adults with DS possessed lower IMT, systolic blood pressure and diastolic blood pressure, than controls. The study’s conclusion was that the adults with DS may be protected against atherosclerosis despite elevated body fat and elevated cardiovascular risk factors (6).
It is interesting to note about the results from some studies demonstrating that at lower degrees of IMT, the thickening appears to reflect an equilibrium state in which the effects of pressure and flow on the arteries are in balance, given a characteristic relation between shear stress and local transmural pressure (7, 8).
A reasonable explanation for the reduced incidence of atherosclerosis is the altered autonomic regulation in individuals with DS, with effects of smaller changes in baroreflex sensitivity and in sympatho-excitation response (9, 10, 11). The reduced sympathetic response to stress in DS is supported by the low circulating catecholamines levels in response to incremental cycle ergometer exercise in individuals with DS (12).
In the acidity theory of atherosclerosis the sympathetic predominance is the primary step and shear stress is the last step in the cascade of events leading to the atherogenic process (13, 14)
Carlos Monteiro
*Note:
Insulin resistance may contribute to enhanced SNS activity (15) and SNS activity may similarly increase insulin resistance (16)

1. Ylä-Herttuala S, Luoma J, Nikkari T, Kivimäki T. Down's syndrome and atherosclerosis. Atherosclerosis. 1989 Apr;76(2-3):269-72.
2. Murdoch JC, Rodger JC, Rao SS, Fletcher CD, Dunnigan MG. Down's syndrome: an atheroma-free model? Br Med J. 1977 Jul 23;2(6081):226-8.
3. Moss TJ, Austin GE. Pre-atherosclerotic lesions in Down syndrome. J Ment Defic Res. 1980 Jun;24(2):137-41.
4. Chaney RH. Neurogenic atherosclerosis in mentally retarded persons. J Ment Defic Res. 1987 Sep;31 ( Pt 3):235-40
5. Draheim CC, McCubbin JA, Williams DP. Differences in cardiovascular disease risk between nondiabetic adults with mental retardation with and without Down syndrome. Am J Ment Retard. 2002 May;107(3):201-11
6. Draheim CC, Geijer JR, Dengel DR. Comparison of intima-media thickness of the carotid artery and cardiovascular disease risk factors in adults with versus without the Down syndrome. Am J Cardiol. 2010 Nov 15;106(10):1512-6
7. Gnasso A, et al. Association Between Intima-Media Thickness and Wall Shear Stress in Common Carotid Arteries in Healthy Male Subjects. Circulation. 1996;94:3257-3262
8. Bots M. L, et al. Increased Common Carotid Intima-Media Thickness. Adaptive Response or a Reflection of Atherosclerosis? Findings From the Rotterdam Study. Stroke. 1997;282442 .
9. Agiovlasitis S, Collier SR, et al. Autonomic response to upright tilt in people with and without Down syndrome. Res Dev Disabil. 2010 May-Jun;31(3):857-63.
10. Iellamo F, Galante A, et al. Altered autonomic cardiac regulation in individuals with Down syndrome. Am J Physiol Heart Circ Physiol. 2005 Dec;289(6):H2387-91.
11. Bo Fernhall and Mari Otterstetter. Attenuated responses to sympathoexcitation in individuals with Down syndrome. J Appl Physiol 94: 2158–2165, 2003.
12. Eberhard Y, Etarradossi J and Terminarias A. Biochemical changes and catecholamine response in Down’s syndrome adolescents in relation to incremental maximal exercise. J Ment Defic Res 35: 140-146, 1991
13. 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
14. Sympathetic predominance: a primary factor in the cascade of events leading to the atherogenic spiraling, Carlos Monteiro, Monday, February 22, 2010 at http://aciditytheory.blogspot.com/2010/02/sympathetic-predominance-primary-factor.html
15. Pikkujamsa SM, Huikuri HV, Airaksinen KE, Rantala AO, Kauma H, Lilja M, Savolainen MJ, Kesaniemi YA. Heart rate variability and baroreflex sensitivity in hypertensive subjects with and without metabolic features of insulin resistance syndrome. Am J Hypertens 1998;11:523–31
16. Moan A, Nordby G, Rostrup M, Eide I, Kjeldsen SE. Insulin sensitivity, sympathetic activity, and cardiovascular reactivity in young men. Am J Hypertens 1995;8:268–75

Sympathetic predominance: The link between diabetes and cardiovascular disease?

It has long been recognized that cardiac autonomic neuropathy increases morbidity and mortality in diabetes and may have greater predictive power than traditional risk factors for cardiovascular events. Significant morbidity and mortality can now be attributable to autonomic imbalance between the sympathetic and parasympathetic nervous system regulation of cardiovascular function (1)
It is also interesting to notice that plasma lactate was strongly associated with type 2 diabetes in older adults as demonstrated in a recent paper (2). According to the authors plasma lactate deserves greater attention in studies of oxidative capacity and diabetes risk.
Both lines of studies come in favour of our point of view (3, 4,5) where the sympathetic predominance represents the primary factor in the cascade of events leading to a higher lactic acid production that provokes an increased perfusion pressure and effects on contractility of coronary arteries resulting in changes in hemodynamic shear stress and atherosclerosis as consequence.
Carlos Monteiro
1. Vinik AI, Zieglert D. Autonomic imbalance: prophet of doom or scope for hope? Diabet. Med. 28, 643-651 (2011) Full free text at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3123705/
2. Stephen O Crawford et al, Association of blood lactate with type 2 diabetes: the Atherosclerosis Risk in Communities Carotid MRI Study. International Journal of Epidemiology 2010;1–9. Free full text at http://ije.oxfordjournals.org/content/early/2010/08/25/ije.dyq126.full.pdf+html
3. Sympathetic predominance: a primary factor in the cascade of events leading to the atherogenic spiraling, Carlos Monteiro, Monday, February 22, 2010 at http://aciditytheory.blogspot.com/2010/02/sympathetic-predominance-primary-factor.html
4. 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
5. Association of lipid abnormalities with lactate and coronary artery disease progression. Carlos Monteiro, October 3, 2010 at http://aciditytheory.blogspot.com/2010/10/lactate-coronary-artery-disease-insulin.html

Some news.....

David M Diamond* made in public the following declaration in the THINCS Forum on June 22, 2011: “Carlos, your thesis on stress, acidic environment and CHD is brilliant. Particularly impressive is how you relate reduced pH to increased oxidation of LDL, which increases its atherogenicity”
* Ph.D, Professor, Depts of Psychology and Molecular Pharmacology and Physiology, Center for Preclinical and Clinical Research on PTSD. Director, University of South Florida, Neuroscience Collaborative)

Sympathetic Predominance: The link between erectile dysfunction, atherosclerosis and cardiovascular disease?

Erectile dysfunction affects 40% of men above 40 year old, in some degree, and two thirds of men over 70 have significant symptoms of ED.
The association between erectile dysfunction and coronary artery disease (CAD) was suggested years ago, by observational studies. More recently it was found that erectile dysfunction is an early marker of CAD, as the canary in the coal mine*.
Indeed some studies have demonstrated that coronary atherosclerosis is more severe in patients with vascular ED, with the authors considering that ED may be an additional, early warning sign of coronary atherosclerosis (1).
A recent meta-analysis of prospective cohort studies, involving 36,744 participants, have suggested that ED significantly increases the risk of cardiovascular disease, coronary heart disease, stroke, and all cause mortality, and the increase is probably independent of conventional risk factors (2)
Erection is initiated through the parasympathetic nervous system, activation of which overrides the sympathetic tone that maintains the penis in a nonerectile (flaccid) state. This state is maintained mainly through the release of norepinephrine from penile adrenergic nerves. Norepinephrine contracts the vasculature and cavernosal smooth muscle. Arousal/erection is associated with a decrease of norepinephrine release in the penis, with a release of nitric oxide, and with a reduction in penile smooth muscle tone. Thus, nitric oxide is a mediator of the parasympathetic vasodilation in erectile function (3). So, when the parasympathetic system is continuously disabled there is a reduced production of NO.
Lifestyle and nutrition have been increasingly recognized as central factors influencing vascular nitric oxide (NO) production and erectile function. ED is associated with smoking, excessive alcohol intake, abdominal obesity, diabetes, hypertension and decreased antioxidant defenses, all of which reduce NO production (4,). Recent studies have discussed about the benefits of lifestyle interventions like healthier eating habits, getting exercise and avoiding smoke for improving erectile dysfunction (5) and also targeting CAD risk factors reduction (4, 6).
It is interesting to note that ED and atherosclerosis have many risk factors in common like ageing, physical inactivity, improper diet, psychological stress, cigarette smoking, high blood pressure and diabetes. In relation to this point there are diverse studies showing that: a) increased sympathetic activity and mental stress may affect erectile function with studies suggesting that an elevated central sympathetic tone may be one of the causes of psychogenic impotence (7, 8, 9); b) a study suggested that drugs acting within the central nervous system that reduce the sympathetic antierectile flow and enhance the parasympathetic proerectile flow to the penis may restore penile erection in cases of erectile dysfunction of both psychogenic and organic origin (10); c) other study have demonstrated that patients complaining of daytime sexual dysfunction and found by sleep-related erection monitoring to suffer from organic erectile dysfunction, have altered cardiac autonomic balance during both stages of sleep (11); d) A study has shown that men with idiopathic ED have evidence of endothelial dysfunction in forearm resistance vessels, increased pulse pressure and impaired heart rate variability. According the authors this support the concept that erectile dysfunction is a predictor of cardiovascular dysfunction and a precursor of clinical cardiovascular disease (13). e) and, finally, a very recent study have shown that patients with ED exhibited different heart rate variability compared with normal controls. This suggested to the authors that the patients with ED may have some kind of imbalance in the autonomic nervous system (ANS) and it may be possible that general imbalance of the ANS is one of the causes of ED (12).
Taking in view the above studies and our postulation that sympathetic predominance is the primary factor in the cascade of events leading to the atherogenic spiraling (14, 15), we have to assume that it really is the link between ED and cardiovascular disease.
14. 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
15. Sympathetic predominance: a primary factor in the cascade of events leading to the atherogenic spiraling, Carlos Monteiro, Monday, February 22, 2010 at http://aciditytheory.blogspot.com/2010/02/sympathetic-predominance-primary-factor.html
Carlos Monteiro

*As long as the canary still singing, it is all ok. However, a dead canary is a warning of a larger problem.

References:
1. Chiurlia E et al. Subclinical coronary artery atherosclerosis in patients with erectile dysfunction. J Am Coll Cardiol, 2005; 46:1503-6
2. Dong JY et al. Erectile dysfunction and risk of cardiovascular disease. Meta-analysis of prospective cohort studies. J Am Coll Cardiol, 2011; 58:1378-1385
3. Andersson K, Stief C. Penile erection and cardiac risk: pathophysiologic and pharmacologic mechanisms. Am J Cardiol. 2000 Jul 20;86(2A):23F-26F
4. Meldrum DR et al. The link between erectile and cardiovascular health: the canary in the coal mine. Am J Cardiol. 2011 Aug 15; 108(4): 599-606
5. Horasanli K et al. Do lifestyle changes work for improving erectile dysfunction? Asian J Androl, 2008; 10(1):28-35
6. Gupta PB et al. The effect of lifestyle modification and cardiovascular risk factor reduction on erectile dysfunction: A systematic review and meta-analysis. Arch Intern Med, 2011. Published online September 12.
7. Junemann KP et al. Neurophysiological aspects of penile erection: the role of the sympathetic nervous system. Br J Urol, 1989 Jul;64(1):84-92
8. Pagani M. Hypertension, stress and erectile dysfunction: potential insights from the analysis of heart rate variability. Curr Med Res Opin, 2000; 16 Suppl1:s3-8
9. Diederichs W et al. The sympathetic role as an antagonist of erection. Urol Res. 1991;19(2):123-6
10. Allard J, Giuliano F. Central nervous system agents in the treatment of erectile dysfunction: how do they work? Curr Urol Rep 2001 Dec;2(6):488-94
11. Lavie P et al. Cardiac autonomic function during sleep in psychogenic and organic erectile dysfunction. J Sleep Res. 1999 Jun;8(2):135-42
12. Lee JY et al. Heart rate variability in men with erectile dysfunction. Int Neurourol J 2011;15:87-91. Full free text at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3138849/pdf/inj-15-87.pdf
13. Stuckey BG, Walsh JP ET al. Erectile dysfunction predicts generalised cardiovascular disease. Evidence from a case control study. Atherosclerosis 2007, 194(2):458-6414.