Saturday, June 23, 2012

High carbohydrate diets significantly activate SNS, while proteins and fats don't

Many studies are suggesting that high-carbohydrate diets, particularly in the form of high-glycemic index load, may activate the sympathetic nervous system with deleterious effects to human health (1). On the other side protein or fat ingestion have no significant sympathoexcitatory effect (2,3,4).

Also, the sympathetic activation have been linked in several studies to obesity, hypertension, insulin resistance, diabetes, and even atherosclerosis (5, 6, 7)

If the above studies are right, continuing to give support to high carbohydrate diets is both a wrong choice as well a bad advice.

Carlos Monteiro

1) Koop W. Chronically increased activity of the sympathetic nervous system: our diet-relatedevolutionary inheritance. The Journal of Nutrition, Health & Aging Volume 13, Number 1, 2009
2) Welle S, Ulavivat U, Campell G. Thermic effect of feeding in men: Increased plasma norepinephrine levels following glucose but not protein or fat consumption. Metabolism 1981; 30: 953-958
3) Welle SL, Lilavivathana U,Campell RG. Increased plasma nor epinephrine concentrations and metabolic rates following glucose ingestion in man. Metabolism 1980; 29: 806-09
4) Tentolouris N, Tsigos D, Perea E et al. Differential effect of high-fat and high carbohydrate isoenergetic meals on cardiac autonomic nervous system activity in lean and obese women. Metabolism 2003; 52: 1426-32
5)Troisi RJ, Weiss ST, Parker DR, Sparrow D, Young JB and Landsberg L. Relation of obesity and diet to sympathetic nervous system activity.  Hypertension. 1991;17:669-677 at
6) Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008 at  
7) Book "Acidity Theory of Atherosclerosis: New Evidences", 2012,

Wednesday, May 23, 2012

Why alcoholics have a lower risk for coronary heart disease

The Spanish EPIC cohort study (European Prospective Investigation into Cancer), published in 2010, including 15630 men and 25808 women, has concluded that alcohol intake (moderate, high and very high consumption) in men aged 29–69 years was associated with a more than 30% lower CHD incidence (1).

Reading an old article by Leary (2) from 1935, I see that his interest in arteriosclerosis arose out of information that a class persons suffering from alcoholism appeared to show a lesser degree of atherosclerosis than their ages would justify. So, I have searched for recent papers that could confirm this relationship and found a study from 1997 comparing a
cohort of alcoholics who underwent a medico-legal autopsy during a five-year period with non-alcoholic controls who did not differ from the alcoholics in selection criteria. This study has show in the examinations, that alcoholic men and old women had a significantly lower degree of atherosclerosis in the coronary arteries (3)

A paper published in 2002 may have the answer to why alcoholics have a significantly lower degree of atherosclerosis in the coronary arteries and risk for coronary heart disease (4). Regarding this paper, a release from EurekAlert (5), with an interview by William Lovallo, one of the authors, told that:

“Before testing alcoholics for their responses to a public-speaking task, researchers first needed to establish if their sympathetic nervous system was able to respond at all. "This would tell us if their blunting was specific to psychological stressors like public speaking," said Lovallo, "or due to a generalized autonomic deficit."

He and his colleagues examined 20 alcohol-dependent subjects, abstinent for 21 to 28 days, and 10 age-matched nonalcoholics. All subjects were males between the ages of 22 and 55 years. The researchers used impedance cardiography and dinamap blood pressure monitoring to assess the participants' heart rate, stroke volume, cardiac output, total peripheral resistance, mean arterial pressure, systolic blood pressure, and diastolic blood pressure during orthostasis and public speaking. Self-reported mood was also assessed during these two tasks.

Cardiovascular responses to orthostasis were similar for the two groups. However, the alcoholics had blunted heart-rate responses to public speaking even though they reported similar anxiety responses to the nonalcoholics. This suggests a disconnection between perception of threat and resulting physiological responses among the alcoholics.

"The similar cardiovascular responses to orthostasis among the alcohol-dependent patients indicate that their autonomic nervous systems were working normally," said Lovallo. "Yet when we asked them to prepare and memorize a short speech and then deliver the speech to a video camera, the patients reacted with little or no change in heart rate, and of course, they failed to have a cortisol response. The patients reacted as if the social challenge of public speaking had no special meaning for them. So, the sympathetic nervous system in the patients looked normal, but their response to a psychological stressor was almost absent. When faced with a socially meaningful stressor, neither part of their fight-flight mechanism was working."

These results support the concept of the acidity theory where sympathetic predominance is the primary factor leading to atherosclerosis (6)

Carlos Monteiro

1. L Arriola, P Martinez-Cambor, N Larranaga, M Basterretxea. Alcohol intake and the risk of coronary heart disease in the Spanish EPIC cohort study. Heart 2010;96:124-130 doi:10.1136/hrt.2009.173419
2. Leary T. Atherosclerosis, the important form of arteriosclerosis, a metabolic disease. Vol 104, N7. JAMA, 1935
3. Thomsen JL. Atherosclerosis in alcoholics. Forensic Sci Int. 1995 Oct 30;75(2-3):121-31 and in Ugeskr Laeger. 1997 Feb 3;159(6):757-.60
4. Tera L. Panknin, Stacey L. Dickensheets, Sara J. Nixon, William R. Lovallo. Attenuated Heart Rate Responses to Public Speaking in Individuals With Alcohol Dependence. Alcohol Clin. Exp. Res. 2002 Jun; 26 (6): 841
5. Alcoholics have 'blunted' responses to psychological stressors such as public speaking. Public release date: 17-Jun-2002 at
6. Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis, 2008 at

Thursday, March 8, 2012

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

Think that fat causes heart disease? Think again!

By Zoe V. Harcombe* Review at Amazon

This must be the academic equivalent of the "Collection of short stories" format so popular in the fiction world. It's a collection of articles, all different, but related by a common theme - heart disease.

I really enjoyed the format - it gives a taste of each topic without going into massive detail on each. The comprehensive references point the way if you want to know more about any particular factor in coronary artery disease. I never knew that the condition of having Down syndrome seems to have some protective properties when it comes to heart disease. What about the role of bacteria, or lactic acid? Is erectile dysfunction trying to tell us something? More familiar topics, such as smoking and stress, are covered but in a really new and often surprising way. I lost count of the number of times I learned something new or saw a well known topic covered in an innovative way.

I like the way the author thinks and challenges everything and makes connections between seemingly unrelated things. I also liked the inputs from colleagues - for example David Diamond's contribution to the article "Is LDL unquestionably and unequivocally a causal risk factor for heart attack?" The role of glucose (not fat) in the working of the body was fascinating and should be far more widely known.

You cannot fail to learn something if you read this book. If you are interested in our number one killer of humans - men especially - this is well worth your time.

*Zoe Harcombe, Author of The Obesity Epidemic: What caused it? How can we stop it? at

Tuesday, February 14, 2012

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

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:

*Dr. Seneff essay on sulfur and heart disease and other chronic diseases:

*Dr. Stephanie Seneff interviewed by Dr. Mercola:

Monday, February 13, 2012

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

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

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
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 

Monday, January 16, 2012

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).
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
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  
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
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
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
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
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; 2:2932.
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