“Cholesterol & Thrombosis Are Not the Cause of Stroke!!!”

I’m delighted to inform you about our new hypothesis for the cause and therapeutic of stroke. It is backed by a large and strong number of scientific evidences.

The article is titled: ‘Intense Stress Leading to Raised Production and Accumulation of Lactate in Brain Ischemia – The Ultimate Cause of Acute Stroke: Mechanism, Risk Factors and Therapeutics.’

It is published in Positive Health Online, Edition 247, July 2018 at http://www.positivehealth.com/article/heart/intense-stress-leading-to-accumulation-of-lactate-in-brain-ischemia.

“In severe ischemia (and tissue hypoxia) oxygen delivery to brain cells is insufficient for normal energy production, and acid-base homeostasis is threatened by the accumulation of acid equivalents (metabolic acidosis)”. Stig Rehncrona, MD, PhD – Lund University, Sweden, 1985 [1]

Abstract

The present paper introduces a new hypothesis postulating that acute stress, chronic stress overload and other risk factors with intense sympathetic nervous system activity may induce a raised lactate production and accumulation in brain ischemia. This represents, in our view, the ultimate cause for the triggering of acute stroke, resulting in the cerebral infarction.

It explains how stress (sympathetic dominance) may lead to a raised lactate production.

The fundamental therapeutic for prevention and management of acute stroke, according to this proposed concept, are old drugs called cardiac glycosides (CGs).

Studies using cardiac glycosides have demonstrated neuroprotective effects in experimental brain ischemia, on the protection against vasospasm in subarachnoid hemorrhage, sympatho-inhibitory effects and a potent inhibition of glycolysis (glucose consumption and lactate).

The use of CGs has also show a very low total mortality (including for stroke) in cardiac patients taking low doses of these drugs.

Cardiac glycosides like digoxin and lanatoside C are drugs approved by the U.S. Federal Drugs Administration (FDA), and by other similar organizations around the world, with some of these having also approval for the use of digitoxin and other CGs . Therefore, these drugs can be prescribed for prevention and in the management of acute stroke, with no major obstacles, by a well informed physician.

The paper also discusses on the limitations and failures in the concept of thrombus as the cornerstone of acute ischemic stroke (AIS)

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You can see links to a collection of recent published medical articles and presentations by ourselves at (https://www.facebook.com/infarctcombat.org/)

Carlos Monteiro

New Book (2016) 

“Fat and Cholesterol Don’t Cause Heart Attacks 

And Statins Are Not The Solution” 

Edited by Prof. Dr. Paul Rosch this book is a tribute to Dr. Uffe Ravsnkov, an extraordinary and tireless researcher, founder of “The International Network of Cholesterol Skeptics (THINCS)”. Among other bookstores you can find this book at https://www.amazon.com/Cholesterol-Cause-Attacks-Statins…/…/

Uffe Ravsnkov’s monograph, “The Cholesterol Myths”, can be read free of charge, at https://www.smashwords.com/books/view/486704 

The present book contains 17 chapters written by a select group of medical researchers and scientists. 

I’m honored to participate in this tribute to Uffe Ravsnkov.

My chapter is entitled “Stress as Cause of Atherosclerosis – The Acidity Theory”.

During the last year I have presented an article about the acidity theory of atherosclerosis, developed in 2006, addressing its history, pathophysiology, therapeutics, risk factors and external markers. There I also have wrote about individuals with lower degree or absence of atherosclerosis, and on the reversion or lower progression of atherosclerosis through the use of sympatholytic drugs and by stress reduction approaches (http://goo.gl/AejGAV). 

In this book (Chapter 10) I extend the discussion about the etiology of the Acidity Theory of Atherosclerosis, aside to present new risk factors and other diseases associated to atherosclerosis, under its point of view. Also, I brought up for discussion the inverse association between cancer and atherosclerosis, confirmed by recent studies*. Follows the abstract:

Abstract
The link between stress and atherosclerosis is well-known with many studies and postulations in this regard. However, there is a general unawareness that stress can induce hyperlactatemia and lactic acidosis, because this relationship has been little discussed in medical science. The influence of adrenaline on lactic acid production was first noticed by Carl Ferdinand Cory in 1925. The heart is an organ of high metabolic activity – that cannot rest as other body muscles, being susceptible to drops in pH during ischemia and hypoxia. The chronic elevated catecholamine release, triggered by sympathetic dominance, may accelerate the myocardial glycolysis leading to significant increase in lactate production. Risk factors for atherosclerosis like hypertension, diabetes, cigarette smoking, stress conditions and high carbohydrate diets are linked to autonomic dysfunction. These risk factors present as well an increased concentration of lactate in plasma. Blood lactate is also associated with carotid atherosclerosis. Plasma lipid abnormalities and myocardial lactate production were significantly associated with subsequent arteriographic progression. The amount of lactate released by the myocardium has been shown to be related to the severity of coronary artery disease. Reduced pH increases the oxidation of low-density lipoprotein that is considered to have a significant role in atherogenesis. According to the acidity theory of atherosclerosis the acidosis evoked by sympathetic dominance or continuous stress leads to changes in shear stress, the final stage in the development of atherosclerotic lesions. The importance of mechanical forces such as those derived from changes in hemodynamic shear stress, as a decisive factor for atherosclerosis, was advocated by Meyer Texon since1957.

* You can also see the studies confirming about the inverse association between cancer and atherosclerosis at our article Cancer, Atherosclerosis and Sympathetic Dominance, Positive Health Online, issue 223, 2015 

"Acidity Theory of Atherosclerosis: History, Pathophysiology, Therapeutics and Risk Factors

My recent article "Acidity Theory of Atherosclerosis: History, Pathophysiology, Therapeutics and Risk Factors -- a Mini Review" was published at http://www.positivehealth.com/article/heart/acidity-theory-of-atherosclerosis-history-pathophysiology-therapeutics-and-risk-factors-a-mini-revie
Carlos Monteiro

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

References:
1) 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
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 http://hyper.ahajournals.org/content/17/5/669.full.pdf
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 http://www.infarctcombat.org/AcidityTheory.pdf  
7) Book "Acidity Theory of Atherosclerosis: New Evidences", 2012, Amazon.com http://tinyurl.com/7KK4a78

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
http://www.eurekalert.org/pub_releases/2002-06/ace-ah061002.php
6. Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis, 2008 at http://www.infarctcombat.org/AcidityTheory.pdf

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 http://www.theobesityepidemic.org/
Website: http://www.zoeharcombe.com/
Blog: http://www.zoeharcombe.com/blog/

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