tag:blogger.com,1999:blog-17779919975156347462024-03-13T10:06:24.624-07:00New Evidences: Acidity Theory of Atherosclerosis"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" by David M Diamond, PhD*, THINCS forum on June 22, 2011.
*Professor Depts of Psychology and Molecular Pharmacology and Physiology, University of South Florida.
Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.comBlogger39125tag:blogger.com,1999:blog-1777991997515634746.post-4184103123555007222018-06-21T06:47:00.000-07:002018-06-21T07:01:10.364-07:00“Cholesterol & Thrombosis Are Not the Cause of Stroke!!!”<div class="" data-block="true" data-editor="7hopr" data-offset-key="81dd5-0-0" style="background-color: white; color: #1d2129; font-family: Helvetica, Arial, sans-serif; font-size: 14px; white-space: pre-wrap;">
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<span style="font-family: inherit;">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.</span></div>
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<span data-offset-key="7qv6h-0-0" style="font-family: inherit;">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.’ </span></div>
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<span data-offset-key="302j1-0-0" style="font-family: inherit;">It is published in Positive Health Online, Edition 247, July 2018 at <a href="http://www.positivehealth.com/article/heart/intense-stress-leading-to-accumulation-of-lactate-in-brain-ischemia.">http://www.positivehealth.com/article/heart/intense-stress-leading-to-accumulation-of-lactate-in-brain-ischemia.</a></span><br />
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<span style="font-family: inherit;"> </span><u style="font-family: inherit;">“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] </u></div>
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<span data-offset-key="86g0h-0-0" style="font-family: inherit;">Abstract</span></div>
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<span data-offset-key="b8pob-0-0" style="font-family: inherit;">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. </span></div>
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<span data-offset-key="3204r-0-0" style="font-family: inherit;">It explains how stress (sympathetic dominance) may lead to a raised lactate production.</span></div>
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<span data-offset-key="cnecl-0-0" style="font-family: inherit;">The fundamental therapeutic for prevention and management of acute stroke, according to this proposed concept, are old drugs called cardiac glycosides (CGs).</span></div>
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<span data-offset-key="eai3v-0-0" style="font-family: inherit;">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). </span></div>
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<span data-offset-key="bvn18-0-0" style="font-family: inherit;">The use of CGs has also show a very low total mortality (including for stroke) in cardiac patients taking low doses of these drugs.</span></div>
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<span data-offset-key="ai0ks-0-0" style="font-family: inherit;">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.</span></div>
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<span data-offset-key="85npj-0-0" style="font-family: inherit;">The paper also discusses on the limitations and failures in the concept of thrombus as the cornerstone of acute ischemic stroke (AIS)</span></div>
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<span data-offset-key="6eg5r-0-0" style="font-family: inherit;">You can see links to a collection of recent published medical articles and presentations by ourselves at (https://www.facebook.com/infarctcombat.org/)</span></div>
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<span data-offset-key="44m22-0-0" style="font-family: inherit;">Carlos Monteiro</span></div>
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Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-1692618627869360402017-01-22T03:59:00.001-08:002017-01-23T09:12:14.910-08:00<h2 style="text-align: center;">
<b><span style="background-color: white; color: red; font-family: "helvetica" , "arial" , sans-serif; font-size: small;">New Book (2016) </span></b></h2>
<h2 style="text-align: center;">
<b><span style="background-color: white; color: #073763; font-family: "helvetica" , "arial" , sans-serif; font-size: large;">“Fat and Cholesterol Don’t Cause Heart Attacks </span></b></h2>
<h3 style="text-align: center;">
<b><span style="background-color: white; color: #0c343d; font-family: "helvetica" , "arial" , sans-serif; font-size: small;">And Statins Are Not The Solution”</span><span style="background-color: white; color: #1d2129; font-family: "helvetica" , "arial" , sans-serif; font-size: small;"> </span></b></h3>
<b><br /></b>
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<div class="separator" style="clear: both; text-align: center;">
<img border="0" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEic0INoafJ5q95YpS3sw1woU9OcPTJCg-vqYw6bZPb-skmuC8Mf55o55tbGKNT7yhsRJe1XXrB1LGlWWu_ShZNE_KOhxFDf9QqhE0B0TALIVLlRuNgh77Js445BmYb0BmB_2SXrT4ZyeX8/s320/41v3CfOnVeL._SX331_BO1%252C204%252C203%252C200_.jpg" width="213" /></div>
<b><br style="background-color: white; color: #1d2129; font-family: Helvetica, Arial, sans-serif; font-size: 14px;" /></b><span style="background-color: white; color: #1d2129; font-family: "helvetica" , "arial" , sans-serif; font-size: 14px;"><br /></span><br />
<span style="background-color: white; color: #1d2129; font-family: "helvetica" , "arial" , sans-serif;">Edited by Prof. Dr. Paul Rosch this book is a tribute to Dr. Uffe Ra</span><span class="text_exposed_show" style="background-color: white; color: #1d2129; display: inline; font-family: "helvetica" , "arial" , sans-serif;">vsnkov, an extraordinary and tireless researcher, founder of “The International Network of Cholesterol Skeptics (THINCS)”. Among other bookstores you can find this book at <a href="https://www.amazon.com/Cholesterol-Cause-Attacks-Statins-Solution/dp/190779753X/" rel="nofollow" style="color: #365899; cursor: pointer; text-decoration: none;" target="_blank">https://www.amazon.com/Cholesterol-Cause-Attacks-Statins…/…/</a></span><br />
<span class="text_exposed_show" style="background-color: white; color: #1d2129; display: inline; font-family: "helvetica" , "arial" , sans-serif;"><br /></span>
<span class="text_exposed_show" style="background-color: white; color: #1d2129; display: inline; font-family: "helvetica" , "arial" , sans-serif;">Uffe Ravsnkov’s monograph, “The Cholesterol Myths”, can be read free of charge, at <a href="https://www.smashwords.com/books/view/486704" rel="nofollow" style="color: #365899; cursor: pointer; text-decoration: none;" target="_blank">https://www.smashwords.com/books/view/486704</a> </span><br />
<span class="text_exposed_show" style="background-color: white; color: #1d2129; display: inline; font-family: "helvetica" , "arial" , sans-serif;"><br /></span>
<span class="text_exposed_show" style="background-color: white; color: #1d2129; display: inline; font-family: "helvetica" , "arial" , sans-serif;">The present book contains 17 chapters written by a select group of medical researchers and scientists. </span><br />
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<span class="text_exposed_show" style="background-color: white; color: #1d2129; display: inline; font-family: "helvetica" , "arial" , sans-serif;">I’m honored to participate in this tribute to Uffe Ravsnkov.</span><br />
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<span class="text_exposed_show" style="background-color: white; color: #1d2129; display: inline; font-family: "helvetica" , "arial" , sans-serif;">My chapter is entitled “Stress as Cause of Atherosclerosis – The Acidity Theory”.</span><br />
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<span class="text_exposed_show" style="background-color: white; color: #1d2129; display: inline; font-family: "helvetica" , "arial" , sans-serif;">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 (<a href="http://l.facebook.com/l.php?u=http%3A%2F%2Fgoo.gl%2FAejGAV&h=ATP2v9mlmZmfjzS1yYIZL0_DbpdMr8_z2ZvlU1YqtSi2XzM_FOYEYuP9fUxYequVOMRNaCdwO_nB1Y_ocQAibmTowt-pn2oi_uN6LOT_yRg-Ibj-rrPafrliQ-qYMG2uUT1yKVJKk_VEnjYOz1A&enc=AZOUd3qwBouYAi8CYUbRUlaGsOMaJvjIsWM3XSAehT5K-zknW3YjAQqGOx4n_8cIwnX-PD6eUnjK-EuCtvfUoWxi3b-DOGMnK0R5w1j5u800t0M9pFYYvpEzwzNQLUvAXpHz3UuVVNC_kghvuk6RjNIEh_adqT-HlZ0ZtOovX8yjmJdtpNUGMxm3Ac_TGNVm538&s=1" rel="nofollow" style="color: #365899; cursor: pointer; text-decoration: none;" target="_blank">http://goo.gl/AejGAV</a>). </span><br />
<span class="text_exposed_show" style="background-color: white; color: #1d2129; display: inline; font-family: "helvetica" , "arial" , sans-serif;"><br />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:</span><br />
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<span class="text_exposed_show" style="background-color: white; color: #1d2129; display: inline; font-family: "helvetica" , "arial" , sans-serif;"><b>Abstract</b><br />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.</span><br />
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<span class="text_exposed_show" style="background-color: white; color: #1d2129; display: inline; font-family: "helvetica" , "arial" , sans-serif;">* You can also see the studies confirming about </span><span style="background-color: white; color: #1d2129; font-family: helvetica, arial, sans-serif;">the inverse association between cancer and atherosclerosis at our article <a href="http://www.positivehealth.com/article/cancer/cancer-atherosclerosis-and-sympathetic-dominance">Cancer, Atherosclerosis and Sympathetic Dominance, Positive Health Online, issue 223, 2015 </a></span>Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-73267496006086863562016-03-15T05:59:00.000-07:002016-03-15T06:00:47.081-07:00"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<a href="http://www.positivehealth.com/article/heart/acidity-theory-of-atherosclerosis-history-pathophysiology-therapeutics-and-risk-factors-a-mini-revie"> http://www.positivehealth.com/article/heart/acidity-theory-of-atherosclerosis-history-pathophysiology-therapeutics-and-risk-factors-a-mini-revie</a><br />
Carlos MonteiroCarlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-17244250602500278812012-06-23T15:23:00.001-07:002012-06-23T15:26:12.832-07:00High carbohydrate diets significantly activate SNS, while proteins and fats don't<span style="font-family: Times New Roman;">
</span><span lang="EN-US" style="font-family: "@Arial Unicode MS","sans-serif"; font-size: 10pt; mso-ansi-language: EN-US; mso-font-kerning: 14.0pt; mso-hansi-font-family: Calibri; mso-hansi-theme-font: minor-latin;">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).</span><br />
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<span style="font-family: Times New Roman;">
</span><span lang="EN-US" style="font-family: "@Arial Unicode MS","sans-serif"; font-size: 10pt; mso-ansi-language: EN-US; mso-hansi-font-family: Calibri; mso-hansi-theme-font: minor-latin;">Also, the sympathetic activation have been
linked in several studies to obesity, hypertension, insulin resistance,
diabetes, and even atherosclerosis (5, 6, 7) </span><br />
<br />
<span style="font-family: Times New Roman;">
</span><span lang="EN-US" style="font-family: "@Arial Unicode MS","sans-serif"; font-size: 10pt; mso-ansi-language: EN-US; mso-hansi-font-family: Calibri; mso-hansi-theme-font: minor-latin;">If the above studies are right, continuing
to give support to high carbohydrate diets is both a wrong choice as well a bad
advice. </span><br />
<br />
<span lang="EN-US" style="font-family: "@Arial Unicode MS","sans-serif"; font-size: 10pt; mso-ansi-language: EN-US; mso-hansi-font-family: Calibri; mso-hansi-theme-font: minor-latin;">Carlos Monteiro</span><br />
<br />
<span style="font-family: Times New Roman;">
</span><span lang="EN-US" style="font-family: "@Arial Unicode MS","sans-serif"; font-size: 10pt; mso-ansi-language: EN-US; mso-hansi-font-family: Calibri; mso-hansi-theme-font: minor-latin;">References:<o:p></o:p></span><br />
<span style="font-family: Times New Roman;">
</span><span lang="EN-US" style="font-family: "@Arial Unicode MS","sans-serif"; font-size: 10pt; mso-ansi-language: EN-US; mso-hansi-font-family: Calibri; mso-hansi-theme-font: minor-latin;">1) Koop W. Chronically increased activity of the sympathetic nervous
system: our diet-related</span><span lang="EN-US" style="font-size: 10pt; mso-ansi-language: EN-US; mso-ascii-font-family: "@Arial Unicode MS"; mso-bidi-font-family: "@Arial Unicode MS"; mso-fareast-font-family: "@Arial Unicode MS";"><span style="font-family: Calibri;">“</span></span><span lang="EN-US" style="font-family: "@Arial Unicode MS","sans-serif"; font-size: 10pt; mso-ansi-language: EN-US; mso-hansi-font-family: Calibri; mso-hansi-theme-font: minor-latin;">evolutionary</span><span lang="EN-US" style="font-size: 10pt; mso-ansi-language: EN-US; mso-ascii-font-family: "@Arial Unicode MS"; mso-bidi-font-family: "@Arial Unicode MS"; mso-fareast-font-family: "@Arial Unicode MS";"><span style="font-family: Calibri;">”</span></span><span lang="EN-US" style="font-family: "@Arial Unicode MS","sans-serif"; font-size: 10pt; mso-ansi-language: EN-US; mso-hansi-font-family: Calibri; mso-hansi-theme-font: minor-latin;"> inheritance. The Journal of Nutrition, Health & Aging Volume 13,
Number 1, 2009<o:p></o:p></span><br />
<span style="font-family: Times New Roman;">
</span><span lang="EN-US" style="font-family: "@Arial Unicode MS","sans-serif"; font-size: 10pt; mso-ansi-language: EN-US; mso-hansi-font-family: Calibri; mso-hansi-theme-font: minor-latin;">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<o:p></o:p></span><br />
<span style="font-family: Times New Roman;">
</span><span lang="EN-US" style="font-family: "@Arial Unicode MS","sans-serif"; font-size: 10pt; mso-ansi-language: EN-US; mso-hansi-font-family: Calibri; mso-hansi-theme-font: minor-latin;">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<o:p></o:p></span><br />
<span style="font-family: Times New Roman;">
</span><span lang="EN-US" style="font-family: "@Arial Unicode MS","sans-serif"; font-size: 10pt; mso-ansi-language: EN-US; mso-hansi-font-family: Calibri; mso-hansi-theme-font: minor-latin;">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<o:p></o:p></span><br />
<span style="font-family: Times New Roman;">
</span><span lang="EN-US" style="font-family: "@Arial Unicode MS","sans-serif"; font-size: 10pt; mso-ansi-language: EN-US; mso-hansi-font-family: Calibri; mso-hansi-theme-font: minor-latin;">5)</span><span lang="EN-US" style="font-family: "Arial","sans-serif"; font-size: 10pt; mso-ansi-language: EN-US;">Troisi RJ, Weiss ST, Parker DR, Sparrow D, Young JB and Landsberg L. <span style="mso-bidi-font-weight: bold;">Relation of obesity and diet to sympathetic
nervous system activity. </span></span><span lang="EN-US" style="font-family: "Arial","sans-serif"; font-size: 10pt; mso-ansi-language: EN-US; mso-fareast-font-family: "@Arial Unicode MS";"><span style="mso-spacerun: yes;"> </span></span><span lang="EN-US" style="font-family: "Arial","sans-serif"; font-size: 10pt; mso-ansi-language: EN-US; mso-bidi-font-style: italic;">Hypertension. </span><span lang="EN-US" style="font-family: "Arial","sans-serif"; font-size: 10pt; mso-ansi-language: EN-US;">1991;17:669-677 at </span><span lang="EN-US" style="font-family: "Arial","sans-serif"; font-size: 10pt; mso-ansi-language: EN-US; mso-fareast-font-family: "@Arial Unicode MS";"><a href="http://hyper.ahajournals.org/content/17/5/669.full.pdf">http://hyper.ahajournals.org/content/17/5/669.full.pdf</a> </span><span lang="EN-US" style="font-family: "@Arial Unicode MS","sans-serif"; font-size: 10pt; mso-ansi-language: EN-US; mso-hansi-font-family: Calibri; mso-hansi-theme-font: minor-latin;"><o:p></o:p></span><br />
<span style="font-family: Times New Roman;">
</span><span lang="EN-US" style="font-family: "@Arial Unicode MS","sans-serif"; font-size: 10pt; mso-ansi-language: EN-US; mso-font-kerning: 14.0pt; mso-hansi-font-family: Calibri; mso-hansi-theme-font: minor-latin;">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 <a href="http://www.infarctcombat.org/AcidityTheory.pdf">http://www.infarctcombat.org/AcidityTheory.pdf</a> </span><span lang="EN-US" style="font-family: "@Arial Unicode MS","sans-serif"; font-size: 10pt; mso-ansi-language: EN-US; mso-hansi-font-family: Calibri; mso-hansi-theme-font: minor-latin;"><o:p></o:p></span><br />
<span style="font-family: Times New Roman;">
</span><span lang="EN-US" style="font-family: "@Arial Unicode MS","sans-serif"; font-size: 10pt; mso-ansi-language: EN-US; mso-hansi-font-family: Calibri; mso-hansi-theme-font: minor-latin;">7) Book "Acidity Theory of
Atherosclerosis: New Evidences", 2012, Amazon.com
<a href="http://tinyurl.com/7KK4a78">http://tinyurl.com/7KK4a78</a> <o:p></o:p></span><br />
<span style="font-family: Times New Roman;">
</span>Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-55296366632858629642012-05-23T13:17:00.000-07:002012-05-24T10:39:35.713-07:00Why alcoholics have a lower risk for coronary heart disease<span lang="PT-BR"><span style="font-family: Arial, Helvetica, sans-serif;">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). </span><br />
<span style="font-family: Arial, Helvetica, sans-serif;">
</span><br />
<span style="font-family: Arial, Helvetica, sans-serif;">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 </span></span><span style="font-family: Arial, Helvetica, sans-serif;"><span lang="EN">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</span><span lang="PT-BR">. 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)</span></span><br />
<span style="font-family: Arial, Helvetica, sans-serif;">
</span><br />
<span style="font-family: Arial, Helvetica, sans-serif;">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). </span><span style="font-family: Arial, Helvetica, sans-serif;">Regarding this paper, a release from EurekAlert (5), with an interview by William Lovallo, one of the authors, told that:</span><br />
<span style="font-family: Arial, Helvetica, sans-serif;">
</span><br />
<span style="font-family: Arial, Helvetica, sans-serif;">“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." </span><br />
<span style="font-family: Arial, Helvetica, sans-serif;">
</span><br />
<span style="font-family: Arial, Helvetica, sans-serif;">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. </span><br />
<span style="font-family: Arial, Helvetica, sans-serif;">
</span><br />
<span style="font-family: Arial, Helvetica, sans-serif;">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. </span><br />
<span style="font-family: Arial, Helvetica, sans-serif;">
</span><br />
<span style="font-family: Arial, Helvetica, sans-serif;">"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."</span><br />
<span style="font-family: Arial, Helvetica, sans-serif;">
</span><br />
<span style="font-family: Arial, Helvetica, sans-serif;">These results support the concept of the acidity theory where sympathetic predominance is the primary factor leading to atherosclerosis (6)</span><br />
<span style="font-family: Arial, Helvetica, sans-serif;">
</span><br />
<span style="font-family: Arial, Helvetica, sans-serif;">Carlos Monteiro</span><br />
<span style="font-family: Arial, Helvetica, sans-serif;">
</span><br />
<span style="font-family: Arial, Helvetica, sans-serif;">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 </span><br />
<span style="font-family: Arial, Helvetica, sans-serif;">
2. Leary T. Atherosclerosis, the important form of arteriosclerosis, a metabolic disease. Vol 104, N7. JAMA, 1935</span><br />
<span style="font-family: Arial, Helvetica, sans-serif;">
<span lang="EN">3. <span lang="PT-BR">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-</span></span></span><span lang="PT-BR"><span style="font-family: Arial, Helvetica, sans-serif;">.60</span></span><br />
<span lang="PT-BR"><span style="font-family: Arial, Helvetica, sans-serif;">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</span></span><br />
<span style="font-family: Arial, Helvetica, sans-serif;">5. Alcoholics have 'blunted' responses to psychological stressors such as public speaking. Public release date: 17-Jun-2002 at </span><br />
<a href="http://www.eurekalert.org/pub_releases/2002-06/ace-ah061002.php"><u><span style="color: blue;"><span style="color: blue;"><span style="color: blue; font-family: Arial, Helvetica, sans-serif;"><span lang="PT-BR">http://www.eurekalert.org/pub_releases/2002-06/ace-ah061002.php</span></span></span></span></u><span style="color: blue;"><span style="color: blue;"><span style="color: blue;"></span></span></span></a><span style="font-family: Arial, Helvetica, sans-serif;"><span lang="PT-BR"> </span></span><br />
<span style="font-family: Arial; font-size: x-small;"><span style="font-family: Arial; font-size: x-small;"><span style="font-family: Arial, Helvetica, sans-serif; font-size: small;">
</span><span lang="EN"><span style="font-family: Arial, Helvetica, sans-serif; font-size: small;">6. Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis, 2008 at <a href="http://www.infarctcombat.org/AcidityTheory.pdf">http://www.infarctcombat.org/AcidityTheory.pdf</a></span></span></span></span><br />
<span style="font-family: Arial; font-size: x-small;"><span style="font-family: Arial; font-size: x-small;"></span></span>Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-38492044032370380212012-03-08T03:42:00.001-08:002012-03-08T03:49:23.166-08:00A review from the book "Acidity Theory of Atherosclerosis: New Evidences", 2012 (Paperback)<strong><span style="font-family: Arial, Helvetica, sans-serif;">Think that fat causes heart disease? Think again!</span></strong><br />
<br />
<span style="font-family: Arial, Helvetica, sans-serif;">By Zoe V. Harcombe* Review at </span><a href="http://tinyurl.com/7KK4a78"><span style="font-family: Arial, Helvetica, sans-serif;">Amazon</span></a><br />
<span lang="EN" style="font-family: Arial, Helvetica, sans-serif;"></span><br />
<span style="font-family: Times New Roman;"><span style="font-family: Arial, Helvetica, sans-serif;">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.<br />
<br />
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.<br />
<br />
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.<br />
<br />
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. <br />
<br />
*Zoe Harcombe, Author of The Obesity Epidemic: What caused it? How can we stop it? at </span><a href="http://www.theobesityepidemic.org/"><span style="font-family: Arial, Helvetica, sans-serif;">http://www.theobesityepidemic.org/</span></a><span style="font-family: Arial, Helvetica, sans-serif;"> <br />
Website: </span><a href="http://www.zoeharcombe.com/"><span style="font-family: Arial, Helvetica, sans-serif;">http://www.zoeharcombe.com/</span></a><br />
<span style="font-family: Arial, Helvetica, sans-serif;"> Blog: </span><a href="http://www.zoeharcombe.com/blog/"><span style="font-family: Arial, Helvetica, sans-serif;">http://www.zoeharcombe.com/blog/</span></a> </span>Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-9464246413690117442012-02-14T09:25:00.003-08:002012-02-14T09:38:13.775-08:00A review from the book "Acidity Theory of Atherosclerosis: New Evidences", 2012 (Kindle Edition)<span style="font-family: Times New Roman;"> </span><b><span lang="EN-US" style="color: black; font-family: "Verdana","sans-serif"; mso-ansi-language: EN-US;"><span style="font-family: Arial, Helvetica, sans-serif;">A Must Read for Anyone Taking Statin Drugs</span></span></b><br />
<br />
<span lang="EN-US" style="color: black; font-family: "Verdana","sans-serif"; mso-ansi-language: EN-US;"><o:p><span style="font-family: Arial, Helvetica, sans-serif;"><span lang="EN-US" style="color: black; font-family: "Verdana","sans-serif"; mso-ansi-language: EN-US; mso-bidi-font-weight: bold;">By<strong> </strong></span><span lang="EN-US" style="mso-ansi-language: EN-US;">Dr. Stephanie Seneff, Senior Research Scientist, MIT*. Review at <a href="http://tinyurl.com/89ea7ln">Amazon.com</a></span></span></o:p></span><br />
<br />
<span lang="EN-US" style="color: black; font-family: "Verdana","sans-serif"; mso-ansi-language: EN-US;"><o:p><span lang="EN-US" style="mso-ansi-language: EN-US;"></span><span lang="EN-US" style="color: black; font-family: "Verdana","sans-serif"; mso-ansi-language: EN-US; mso-bidi-font-family: "Times New Roman";"><o:p><span style="font-family: Arial, Helvetica, sans-serif;"> </span><span lang="EN-US" style="color: black; font-family: "Verdana","sans-serif"; mso-ansi-language: EN-US; mso-bidi-font-family: "Times New Roman";"><span style="font-family: Arial, Helvetica, sans-serif;">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.<br />
<br />
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.<br />
<br />
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.<br />
<br />
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.</span></span></o:p></span></o:p></span><br />
<br />
<span lang="EN-US" style="color: black; mso-ansi-language: EN-US;"><o:p><span lang="EN-US" style="color: black; mso-ansi-language: EN-US; mso-bidi-font-family: "Times New Roman";"><o:p><span lang="EN-US" style="color: black; mso-ansi-language: EN-US; mso-bidi-font-family: "Times New Roman";"><span style="font-family: Arial, Helvetica, sans-serif;"><span lang="EN-US" style="line-height: 115%; mso-ansi-language: EN-US; mso-ascii-theme-font: minor-latin; mso-bidi-font-family: "Times New Roman"; mso-bidi-language: AR-SA; mso-bidi-theme-font: minor-bidi; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: PT-BR; mso-fareast-theme-font: minor-fareast; mso-hansi-theme-font: minor-latin;">*Homepage of Dr. Stephanie Seneff at MIT:<br />
</span><span style="line-height: 115%; mso-ansi-language: PT-BR; mso-ascii-theme-font: minor-latin; mso-bidi-font-family: "Times New Roman"; mso-bidi-language: AR-SA; mso-bidi-theme-font: minor-bidi; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: PT-BR; mso-fareast-theme-font: minor-fareast; mso-hansi-theme-font: minor-latin;"><a href="http://people.csail.mit.edu/seneff" target="_blank"><span lang="EN-US" style="color: #366388; mso-ansi-language: EN-US;">http://people.csail.mit.edu/seneff</span></a></span></span><span lang="EN-US" style="line-height: 115%; mso-ansi-language: EN-US; mso-ascii-theme-font: minor-latin; mso-bidi-font-family: "Times New Roman"; mso-bidi-language: AR-SA; mso-bidi-theme-font: minor-bidi; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: PT-BR; mso-fareast-theme-font: minor-fareast; mso-hansi-theme-font: minor-latin;"><br />
<span style="font-family: Arial, Helvetica, sans-serif;"> <br />
*Dr. Seneff essay on sulfur and heart disease and other chronic diseases:<br />
</span></span><span style="line-height: 115%; mso-ansi-language: PT-BR; mso-ascii-theme-font: minor-latin; mso-bidi-font-family: "Times New Roman"; mso-bidi-language: AR-SA; mso-bidi-theme-font: minor-bidi; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: PT-BR; mso-fareast-theme-font: minor-fareast; mso-hansi-theme-font: minor-latin;"><a href="http://people.csail.mit.edu/seneff/sulfur_obesity_alzheimers_muscle_wasting.html" target="_blank"><span lang="EN-US" style="color: #366388; font-family: Arial, Helvetica, sans-serif; mso-ansi-language: EN-US;">http://people.csail.mit.edu/seneff/sulfur_obesity_alzheimers_muscle_wasting.html</span></a></span><span lang="EN-US" style="line-height: 115%; mso-ansi-language: EN-US; mso-ascii-theme-font: minor-latin; mso-bidi-font-family: "Times New Roman"; mso-bidi-language: AR-SA; mso-bidi-theme-font: minor-bidi; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: PT-BR; mso-fareast-theme-font: minor-fareast; mso-hansi-theme-font: minor-latin;"><br />
<span style="font-family: Arial, Helvetica, sans-serif;"> <br />
*Dr. Stephanie Seneff interviewed by Dr. Mercola:<br />
</span></span><span style="line-height: 115%; mso-ansi-language: PT-BR; mso-ascii-theme-font: minor-latin; mso-bidi-font-family: "Times New Roman"; mso-bidi-language: AR-SA; mso-bidi-theme-font: minor-bidi; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: PT-BR; mso-fareast-theme-font: minor-fareast; mso-hansi-theme-font: minor-latin;"><a href="http://articles.mercola.com/sites/articles/archive/2011/09/17/stephanie-seneff-on-sulfur.aspx" target="_blank"><span lang="EN-US" style="color: #366388; font-family: Arial, Helvetica, sans-serif; mso-ansi-language: EN-US;">http://articles.mercola.com/sites/articles/archive/2011/09/17/stephanie-seneff-on-sulfur.aspx</span></a></span></span></o:p></span></o:p></span>Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-77848952927891578722012-02-13T09:49:00.001-08:002012-02-14T03:02:41.242-08:00A review from the book "Acidity Theory of Atherosclerosis: New Evidences", 2012 (Paperback)<span style="font-family: Times New Roman;"> </span><span lang="EN-US" style="color: black; font-family: "Verdana","sans-serif"; line-height: 115%; mso-ansi-language: EN-US;"><span style="font-family: Arial, Helvetica, sans-serif;">By </span></span><span lang="EN-US" style="color: black; font-family: "Verdana","sans-serif"; line-height: 115%; mso-ansi-language: EN-US;"><span style="font-family: Arial, Helvetica, sans-serif;"><span lang="EN-US" style="color: black; font-family: "Verdana","sans-serif"; mso-ansi-language: EN-US; mso-bidi-font-family: "Times New Roman"; mso-bidi-font-weight: bold;">Livin' La Vida Low-Carb Man "Jimmy Moore"*</span><span lang="EN-US" style="color: black; font-family: "Verdana","sans-serif"; font-size: 10pt; line-height: 115%; mso-ansi-language: EN-US;">. </span><span lang="EN-US" style="color: black; font-family: "Verdana","sans-serif"; line-height: 115%; mso-ansi-language: EN-US;"><span style="font-family: Arial, Helvetica, sans-serif;">Review at </span><a href="http://tinyurl.com/7kk4a78"><span style="font-family: Arial, Helvetica, sans-serif;">Amazon.com</span></a></span></span></span><br />
<br />
<span style="vertical-align: middle;"><b>Rethinking What Really Contributes To Heart Disease</b></span><br />
<br />
<span lang="EN-US" style="color: black; font-family: "Verdana","sans-serif"; line-height: 115%; mso-ansi-language: EN-US;"><span style="font-family: Arial, Helvetica, sans-serif;"><span lang="EN-US" style="color: black; font-family: "Verdana","sans-serif"; line-height: 115%; mso-ansi-language: EN-US;"></span></span></span><span lang="EN-US" style="color: black; font-family: "Verdana","sans-serif"; mso-ansi-language: EN-US; mso-bidi-font-family: "Times New Roman";"><span style="font-family: Arial, Helvetica, sans-serif;">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).<br />
<br />
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:<br />
<br />
- People with Down's syndrome tend to have very little heart disease <br />
- Diabetics are more likely to develop heart disease <br />
- If you a man with ED, then you are very likely at risk for heart disease <br />
- Wanna make your heart healthier? Marry a comedian <br />
- LDL cholesterol plays a lot less role in a cardiovascular event than people realize <br />
- Salt intake is pretty much irrelevant in whether you develop heart disease or not <br />
- If you have rheumatoid arthritis, then you are at greater risk for atherosclerosis <br />
- The health of your teeth can play a factor in developing heart disease<br />
<br />
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.<br />
<br />
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.<o:p></o:p></span></span><br />
<span style="font-family: Arial, Helvetica, sans-serif;"> </span><br />
<div class="MsoNormal" style="line-height: normal; margin: 0cm 0cm 0pt;"><span style="font-family: Arial, Helvetica, sans-serif;"><span lang="EN-US" style="color: black; font-family: "Verdana","sans-serif"; mso-ansi-language: EN-US; mso-bidi-font-family: "Times New Roman"; mso-fareast-font-family: "Times New Roman";"><span style="color: #366388;"><span style="color: black;">* Jimmy Moore</span> </span>Blog & Podcast</span><span lang="EN-US" style="font-family: "Times New Roman","serif"; mso-ansi-language: EN-US; mso-fareast-font-family: "Times New Roman";"><o:p></o:p></span></span></div><span style="font-family: Arial, Helvetica, sans-serif;"> <span style="color: black; font-family: "Verdana","sans-serif"; mso-bidi-font-family: "Times New Roman"; mso-fareast-font-family: "Times New Roman";"><a href="http://www.livinlavidalowcarb.com/blog" target="_blank"><span lang="EN-US" style="color: #366388; mso-ansi-language: EN-US; mso-bidi-font-size: 11.0pt;">http://www.livinlavidalowcarb.com/blog</span></a></span><span lang="EN-US" style="font-family: "Times New Roman","serif"; mso-ansi-language: EN-US; mso-fareast-font-family: "Times New Roman";"><o:p></o:p></span></span><br />
<span style="font-family: Arial, Helvetica, sans-serif;"> <span style="color: black; font-family: "Verdana","sans-serif"; mso-bidi-font-family: "Times New Roman"; mso-fareast-font-family: "Times New Roman";"><a href="http://www.thelivinlowcarbshow.com/shownotes" target="_blank"><span lang="EN-US" style="color: #366388; mso-ansi-language: EN-US; mso-bidi-font-size: 11.0pt;">http://www.thelivinlowcarbshow.com/shownotes</span></a></span><span lang="EN-US" style="font-family: "Times New Roman","serif"; mso-ansi-language: EN-US; mso-fareast-font-family: "Times New Roman";"><o:p></o:p></span></span><br />
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<span style="font-family: Times New Roman;"> </span>Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-11219732005378579412012-01-16T07:02:00.000-08:002012-01-16T07:34:15.239-08:00Both restriction and high salt intake may result in cardiovascular diseaseFor 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).<br />
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. <br />
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). <br />
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). <br />
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). <br />
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). <br />
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).<br />
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.<br />
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). <br />
Note:<br />
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.<br />
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".<br />
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. <br />
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." <br />
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).<br />
Carlos Monteiro <br />
1. He FJ and MacGregor GA, . How far should salt intake be reduced? Hypertension 2003; 42:1093-1099. Full free text at <a href="http://hyper.ahajournals.org/cgi/reprint/42/6/1093">http://hyper.ahajournals.org/cgi/reprint/42/6/1093</a> <br />
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 <a href="http://www.jacn.org/content/25/suppl_3/256S.full">http://www.jacn.org/content/25/suppl_3/256S.full</a> <br />
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<br />
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<br />
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. <br />
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<br />
7. New Salt paper causes controversy. Heartwire, May 3, 2011<br />
8. He FJ and MacGregor GA. Salt intake and sympathetic activity. Circulation 2003 Apr 29; 107 ((16): 108 author reply. Full free text at <a href="http://circ.ahajournals.org/ggi/reprint/107/16/e108">http://circ.ahajournals.org/ggi/reprint/107/16/e108</a> <br />
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 <a href="http://circ.ahajournals.org/cgi/reprint/106/15/1957">http://circ.ahajournals.org/cgi/reprint/106/15/1957</a> <br />
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 <br />
11. MA Creager, et al. Sodium depresses arterial baroreceptor reflex function in normotensive humans. Hypertension 1991;17;989-996 <br />
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 <a href="http://www.infarctcombat.org/AcidityTheory.pdf">http://www.infarctcombat.org/AcidityTheory.pdf</a> <br />
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<br />
14. de Champlain J, Farley L, Cousineau D, van Ameringen MR. Circulating catecholamine levels in human and experimental hypertension. CircRes 1976; 38:109–114.<br />
15. Louis WJ, Doyle AE, Anavekar S. Plasma norepinephrine levels in essential hypertension. N Engl J Med 1973; 288:599–601.<br />
16. Sever PS, Osikowska B, Birch M, Tunbridge RD. Plasma noradrenaline in essential hypertension. Lancet 1977; 1:1078–1081.<br />
17. Lake CR, Kopin IJ, Ziegler MG, Coleman MD. Plasma catecholaminesand neurogenic hypertension. N Engl J Med 1977; 297:53–54.<br />
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.<br />
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.<br />
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.<br />
<span lang="EN">21. Nicholls MG, Kiowski W, Zweifler AJ, Julius s, Schork MA, Greenhouse J. Plasma norepinephrine variations with dietary sodium intake. Hypertension 1980; 2:29</span><span lang="PT-BR">–</span><span lang="EN">32.</span><br />
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<br />
23. Sodium/potassium ratio important for health. Heartwire, July 11, 2011Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-27049409697901187232011-12-16T08:07:00.000-08:002011-12-16T08:07:34.375-08:00Why 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)<br />
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). <br />
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). <br />
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).<br />
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)<br />
Carlos Monteiro<br />
*Note:<br />
Insulin resistance may contribute to enhanced SNS activity (15) and SNS activity may similarly increase insulin resistance (16)<br />
<br />
1. Ylä-Herttuala S, Luoma J, Nikkari T, Kivimäki T. Down's syndrome and atherosclerosis. Atherosclerosis. 1989 Apr;76(2-3):269-72.<br />
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.<br />
3. Moss TJ, Austin GE. Pre-atherosclerotic lesions in Down syndrome. J Ment Defic Res. 1980 Jun;24(2):137-41.<br />
4. Chaney RH. Neurogenic atherosclerosis in mentally retarded persons. J Ment Defic Res. 1987 Sep;31 ( Pt 3):235-40<br />
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<br />
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<br />
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<br />
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 .<br />
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.<br />
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.<br />
11. Bo Fernhall and Mari Otterstetter. Attenuated responses to sympathoexcitation in individuals with Down syndrome. J Appl Physiol 94: 2158–2165, 2003.<br />
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<br />
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 <a href="http://www.infarctcombat.org/AcidityTheory.pdf">http://www.infarctcombat.org/AcidityTheory.pdf</a> <br />
14. Sympathetic predominance: a primary factor in the cascade of events leading to the atherogenic spiraling, Carlos Monteiro, Monday, February 22, 2010 at <a href="http://aciditytheory.blogspot.com/2010/02/sympathetic-predominance-primary-factor.html">http://aciditytheory.blogspot.com/2010/02/sympathetic-predominance-primary-factor.html</a> <br />
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<br />
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;8:268–75Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-36047171545652968762011-10-20T13:42:00.000-07:002011-10-21T06:28:38.016-07:00Sympathetic 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)<br />
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. <br />
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. <br />
Carlos Monteiro<br />
1. Vinik AI, Zieglert D. Autonomic imbalance: prophet of doom or scope for hope? Diabet. Med. 28, 643-651 (2011) Full free text at <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3123705/">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3123705/</a> <br />
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 <a href="http://ije.oxfordjournals.org/content/early/2010/08/25/ije.dyq126.full.pdf+html">http://ije.oxfordjournals.org/content/early/2010/08/25/ije.dyq126.full.pdf+html</a> <br />
3. Sympathetic predominance: a primary factor in the cascade of events leading to the atherogenic spiraling, Carlos Monteiro, Monday, February 22, 2010 at <a href="http://aciditytheory.blogspot.com/2010/02/sympathetic-predominance-primary-factor.html">http://aciditytheory.blogspot.com/2010/02/sympathetic-predominance-primary-factor.html</a> <br />
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 <a href="http://www.infarctcombat.org/AcidityTheory.pdf">http://www.infarctcombat.org/AcidityTheory.pdf</a><br />
<span lang="PT-BR">5. Association of lipid abnormalities with lactate and coronary artery disease progression. </span><span lang="EN">Carlos Monteiro, October 3, 2010 at <a href="http://aciditytheory.blogspot.com/2010/10/lactate-coronary-artery-disease-insulin.html">http://aciditytheory.blogspot.com/2010/10/lactate-coronary-artery-disease-insulin.html</a> </span>Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-18331326270008909592011-09-28T05:43:00.000-07:002012-01-15T02:47:41.612-08:00Some 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” <br />
* 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)Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-91203806364754221272011-09-23T07:54:00.000-07:002011-12-12T08:09:15.030-08:00Sympathetic 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. <br />
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*. <br />
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). <br />
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)<br />
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.<br />
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).<br />
<span lang="EN"><span lang="EN">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 <span lang="EN">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).</span></span></span><br />
<span lang="EN"><span lang="EN"><span lang="EN">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.<br />
<span lang="EN"><span lang="EN">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 <a href="http://www.infarctcombat.org/AcidityTheory.pdf">http://www.infarctcombat.org/AcidityTheory.pdf</a><br />
15. Sympathetic predominance: a primary factor in the cascade of events leading to the atherogenic spiraling, Carlos Monteiro, Monday, February 22, 2010 at <a href="http://aciditytheory.blogspot.com/2010/02/sympathetic-predominance-primary-factor.html">http://aciditytheory.blogspot.com/2010/02/sympathetic-predominance-primary-factor.html</a></span></span></span></span></span><span lang="EN"><span lang="EN"><br />
Carlos Monteiro<br />
<br />
*As long as the canary still singing, it is all ok. However, a dead canary is a warning of a larger problem.<br />
<br />
References:<br />
1. Chiurlia E et al. Subclinical coronary artery atherosclerosis in patients with erectile dysfunction. J Am Coll Cardiol, 2005; 46:1503-6<br />
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<br />
3. Andersson K, Stief C. Penile erection and cardiac risk: pathophysiologic and pharmacologic mechanisms. Am J Cardiol. 2000 Jul 20;86(2A):23F-26F<br />
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<br />
5. Horasanli K et al. Do lifestyle changes work for improving erectile dysfunction? Asian J Androl, 2008; 10(1):28-35<br />
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. <br />
7. Junemann KP et al. Neurophysiological aspects of penile erection: the role of the sympathetic nervous system. <span lang="EN-US" style="font-family: "Times New Roman", "serif"; line-height: 115%; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: PT-BR; mso-fareast-theme-font: minor-fareast;"><span lang="EN-US" style="font-family: "Times New Roman", "serif"; line-height: 115%; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: PT-BR; mso-fareast-theme-font: minor-fareast;"><span style="font-family: Arial, Helvetica, sans-serif;">Br J Urol, 1989 Jul;64(1):84-92</span></span></span><br />
<span lang="EN-US" style="font-family: "Times New Roman", "serif"; font-size: 12pt; line-height: 115%; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: PT-BR; mso-fareast-theme-font: minor-fareast;"><span lang="EN-US" style="font-family: "Times New Roman", "serif"; font-size: 12pt; line-height: 115%; mso-ansi-language: EN-US; mso-bidi-language: AR-SA; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: PT-BR; mso-fareast-theme-font: minor-fareast;"></span></span>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<br />
9. Diederichs W et al. The sympathetic role as an antagonist of erection. Urol Res. 1991;19(2):123-6<br />
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<br />
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<br />
12. Lee JY et al. Heart rate variability in men with erectile dysfunction. Int Neurourol J 2011;15:87-91. Full free text at <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3138849/pdf/inj-15-87.pdf">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3138849/pdf/inj-15-87.pdf</a><br />
<span lang="EN">13. Stuckey BG, Walsh JP ET al. Erectile dysfunction predicts generalised cardiovascular disease. Evidence from a case control study. Atherosclerosis 2007, 194(2):458-64</span>14. </span></span>Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-66573284487054044982011-09-05T12:26:00.000-07:002012-01-20T06:14:51.282-08:00The positive impact of humor and negative of stress over the vascular functionChronic stress is correlated with increases in stress hormones cortisol and cathecolamines. There is strong scientific evidence linking negative emotional states like depression, anxiety, or anger with increased risk for cardiovascular disease. However, much less is known about the association between positive emotional states, the so called eustress, like laughter and happiness. The nicest of all laughter types is associated with humor and it is specified as mirthful laughter. <br />
In this respect there are some studies made by Berk and colleagues, from the Loma Linda University, demonstrating that in comparison with chronic stress mirthful laughter reduced the levels of Cortisol by 39%; adrenaline by 70% and dopac by 38%. The conclusion in one of their papers was that humor appears to attenuate catecholamines and MI recurrence and thus could be an effective adjunct in post-MI care (1, 2, 3). <br />
On the other hand Michael Miller, from the University of Maryland, presented a study at the European Society of Cardiology in the 2011 Congress (4) highlighting the link between endothelial function and laughter. His study showed that when people laughed their major blood vessels dilated allowing for easier blood flow, that indicates a reduced risk of cardiac events. <br />
Dr. Miller’s idea to study positive emotions such as laughter came after studies that had shown that mental stress caused blood vessels to constrict. His first study about sense of humor and coronary artery disease was published in 2001 (5). In other paper, published in 2009 (6), he told about the tests made to confirm the hypothesis that mirthful laughter also favorably affect endothelial dependent flow-mediated vasodilation (FMD). In this way volunteers were randomized for two different phases in a randomized-crossover design. One phase included watching a movie or segment of popular comedies (ex: Saturday Night Live) whereas a second phase was to view a movie known to promote mental stress (ex: The opening segment of “Saving Private Ryan”). The assessment of endothelial dependent vasoreactivity was performed using high resolution ultrasound of the brachial artery, also referred as brachial artery reactivity test (BART). A total of 160 BART measurements were performed and demonstrated a divergent effect after watching a movie provoking mental stress as compared to mirthful laughter. Specifically, a 35% reduction in FMD compared to baseline followed mental stress whereas a 22% increase in FMD occurred in response to laughter (7). In 2008, Dr. Miller and colleagues, in an oral presentation entitled “Positive emotions and the endothelium: Does joyful music improve vascular health?”, made at the American Association Scientific Sessions, on 11/11/2008, conclude that the cardiovascular benefits of music are similar to those found in their previous study of mirthful laughter (8)<br />
Dr. Sugawara and colleagues in 2010 have confirmed the findings from Dr. Miller saying that their results suggest mirthful laughter elicited by comic movies induces beneficial impact on vascular function (9).<br />
Again, in the presentation made by Dr. Miller at the ESC, 2011, volunteers watched segments of a funny movie, such as the farce “There's Something About Mary” on one day and on another day watched the opening segment of the stressful movie “Saving Private Ryan”. When study volunteers watched the stressful movie, their blood lining developed a potentially unhealthy response called vasoconstriction, reducing blood flow. Overall, in this time, more than 300 measurements were made with a 30-50% difference in blood vessel diameter between the laughter and mental stress phases (4). <br />
We think the above studies give additional evidence to our acidity theory of atherosclerosis (10), that has the following sequence of events: <br />
I. Sympathetic dominance by continuous stress plus <br />
II. Deficiency in production of endogenous digitalis-like compounds (DLCs) with alterations of Na(+), K(+)-ATPase activity results in: <br />
III. Lowered pH (acidity) that increases perfusion pressure and provokes effects on contractility of coronary arteries leading to changes in hemodynamic shear stress and atherosclerosis as consequence.<br />
<span lang="PT-BR"><em><strong>Sympathetic activation, metabolic acidosis and vascular reactivity</strong></em> The studies by Berk and Miller confirm previous studies suggesting that the sympathetic activation with elevation of circulating catecholamine (adrenaline, etc..), cause coronary vasoconstriction and consequent reduction in blood flow.<br />
On the other hand it is interesting to notice that increased lactate (or decreased blood pH) may evoke vascular smooth muscle relaxation and increase of blood flow (11). <br />
These opposite forces working in sequence - with the sympathetic overdrive leading to metabolic acidosis -, in our view, may be reconciled to partially explain the occurrence of the resulting abnormal stretching/relaxing of coronary arteries, in different directions, simultaneously, producing atherosclerosis (10).</span>Carlos Monteiro<br />
<br />
1. Berk LS, Tan SA and Berk B. Cortisol and cathecolamine stress hormone drecrease is associated with the behavior of perceptual anticipation of mirthful laughter. The FASEB Journal. 2008; 22;946.11 <br />
2. Tans SA, Berk LS et al. Humor as an adjunct therapy in cardiac rehabilitation, attenuates cathecolamines and myocardial infarction recurrence. Adv Mind Body Med 2007; 22(3-4): 8-12 <br />
3. Berk LS et al. The neuroendocrine and stress hormone changes during mirthful laughter. Am J Med Sci 1989;6:390-396 <br />
4. Miller M. Laughter and vascular function, ESC 2011.<br />
5. Clark A, Seidler A, Miller M. Inverse association between sense of humor and coronary heart disease. Int J Cardiol. 2001 Aug; 80(1):87-8<br />
6. Miller M, Fry WF. The effect of mirthful laughter on the human cardiovascular system. Med. Hypothesis 2009; 73(5):636 . Full free text at <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2814549/pdf/nihms-154943.pdf">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2814549/pdf/nihms-154943.pdf</a><br />
7. Miller M, Mangano C, Park Y, et al. Impact of cinematic viewing on endothelial function. Heart 2006; 92:261-262<br />
8. Miller M, Beach V, Mangano C, Vogel RA. Positive emotions and the endothelium: Does joyful music improve vascular health? American Association Scientific Sessions, on 11/11/2008<br />
9. Sugawara et al. Effect of mirthful laughter on vascular function. Am J Cardiol 106:856-9 (2010).<br />
10. Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008 at <a href="http://www.infarctcombat.org/AcidityTheory.pdf">http://www.infarctcombat.org/AcidityTheory.pdf</a><br />
11. Celotto AC, Capellini VK et al. Effects of acid-base imbalance on vascular reactivity. Brazilian Journal of Medical and Biological Research (2008) 41:439-445 Full free text at http://www.scielo.br/pdf/bjmbr/v41n6/7099.pdfCarlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-12178889312795721572011-08-15T05:44:00.000-07:002012-01-20T06:20:36.504-08:00Is it LDL cholesterol unquestionably and unequivocally a causal risk factor for myocardial infarction?<div class="MsoNormal" style="line-height: normal; margin: 5pt 0cm; mso-layout-grid-align: none; mso-pagination: none;">It is my pleasure to share the following point of view of Dr. David Diamond, researcher, scientist and professor from the University of South Florida – and our colleague from <a href="http://www.thincs.org/">THINCs</a> – about low density lipoprotein and its relationship with the incidence of myocardial infarction: </div><div class="MsoNormal" style="line-height: normal; margin: 5pt 0cm; mso-layout-grid-align: none; mso-pagination: none;"><em><span style="font-family: Arial, Helvetica, sans-serif;">“If only it were that simple, then reducing LDL by any means would reduce and even eliminate MI from occurring, and enable people to live longer. However, serum cholesterol levels had been reduced with treatments long before statins were developed, first with corn oil, and then GI surgery and cholestyramine and then there were the statins, including Baycol and Torcetrapib, which reduced LDL and even raised HDL. Baycol and Torcetrapib were very effective as LDL reducing agents, but they were also very effective at killing people, which is why they are no longer on the market. So lowering LDL levels, alone, is not sufficient to reduce the incidence of MI and to enable someone to survive the treatment.</span></em></div><div class="MsoNormal" style="line-height: normal; margin: 5pt 0cm; mso-layout-grid-align: none; mso-pagination: none;"><em><span style="font-family: Arial, Helvetica, sans-serif;">The question should be, why are elevated levels of LDL associated with MI? The answer is that LDL is not "bad cholesterol" which is destined to harm blood vessel walls and "clog arteries" as drug company ads incorrectly state. Part of the problem is that LDL gets glycated by glucose, which distorts the lipoprotein sufficiently that it can't bind to the LDL receptor. The glycated LDL molecule then accumulates in the blood and becomes oxidized. It is the oxidized LDL that contributes to the deterioration of the blood vessel wall, not the native (normal) LDL. How do you stop sugar from glycating LDL? Keep blood sugar low through exercise and a low carb diet - 2 rather simple strategies which have never been compared head-to-head to statins in a clinical trial for reducing CHD, perhaps because the outcome would be unappealing to the drug companies that sponsor this research.</span></em></div><div class="MsoNormal" style="line-height: normal; margin: 5pt 0cm; mso-layout-grid-align: none; mso-pagination: none;"><em><span style="font-family: Arial, Helvetica, sans-serif;">The other way of looking at LDL and MI is that when LDL becomes oxidized and glycated it becomes ineffective at doing what it's supposed to do, which is to kill bacteria (yes, LDL is a part of the immune system) and to build new cells. In response to the increasing concentration of oxidized (ineffective) LDL, the liver makes more LDL, thereby raising the concentration of total serum LDL. This is actually why total LDL levels can correlate with MI incidence, but it's actually the synergy between high sugar diets and oxidized LDL (and high blood pressure) which causes to damage to artery walls. </span></em></div><div class="MsoNormal" style="line-height: normal; margin: 5pt 0cm; mso-layout-grid-align: none; mso-pagination: none;"><em><span style="font-family: Arial, Helvetica, sans-serif;">So, it's not that LDL is inherently atherogenic. The LDL molecule is an essential part of optimal health, serving to work with white blood cells to kill pathogens and to rebuild damaged tissue. It is the oxidization of LDL, which is precipitated by stress, smoking, lack of exercise and a high sugar diet, that is atherogenic. The literature on this work is vast, but I cite at the end of this little article some papers showing that ox-LDL levels are a much better indicator of CHD than native LDL (1, 2, 3). </span></em><em><br />
</em></div><em><span style="font-family: Arial, Helvetica, sans-serif;">I have reviewed only a small part of the thousands of medical papers and dozens of books I've read on this subject. Based on my reading, and the findings of experts in the field, there is good reason to be skeptical about the claims that statins have enhanced cardiac health in the absence of substantial side effects. In my recent talk** I reviewed well-documented evidence published in highly respected medical journals of more extensive adverse side effects of statins than is typically reported in the drug company sponsored research papers. For a relatively small reduction of cardiac events in the treated population, the cost of statins financially and in terms of insufficient improvement in overall health and survival is unjustified.”</span></em><br />
* David Diamond, Ph.D, is Professor from the Depts of Psychology and Molecular Pharmacology and Physiology, Center for Preclinical and Clinical Research on PTSD. Director, USF Neuroscience Collaborative, 4202 E. Fowler Ave (PCD 4118G), Tampa, FL 33620. His homepage is <a href="http://psychology.usf.edu/faculty/diamond/">http://psychology.usf.edu/faculty/diamond/</a> <br />
** The web article that summarizes his talk and includes the on-line video is at <a href="http://www.cas.usf.edu/news/s/176/">http://www.cas.usf.edu/news/s/176/</a><br />
<em>References:</em><br />
<em>1. Margareta Kristenson, Bo Ziedén, et al. Antioxidant state and mortality from coronary heart disease in Lithuanian and Swedish men: concomitant cross sectional study of men aged 50. BMJ 1997;314:629–33</em><br />
<em>2. Christa Meisinger, Jens Baumert, et al. Plasma Oxidized Low-Density Lipoprotein, a Strong Predictor for Acute Coronary Heart Disease Events in Apparently Healthy, Middle-Aged Men From the General Population. Circulation 2005;112;651-657</em><br />
<em>3. Huiling Huang, Weiyi Mai, Dan Liu, et al. The oxidation ratio of LDL: A predictor for coronary artery disease. Disease Markers 24 (2008) 341–349</em><br />
<br />
<span lang="EN"><strong>Note:</strong></span><br />
In the acidity theory of atherosclerosis we support a link between LDL oxidation and acidic pH presenting different studies showing this relationship (1). <br />
1. Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008 at <br />
<a href="http://www.infarctcombat.org/AcidityTheory.pdf"><u><span style="color: blue;"><span lang="EN">http://www.infarctcombat.org/AcidityTheory.pdf</span></span></u><span style="color: blue;"></span></a><br />
<br />
<div align="center"></div>Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-22175920011068075222011-07-20T07:34:00.000-07:002011-07-20T07:36:57.339-07:00Hemodynamic shear stress, calcification and atherosclerosisAtherosclerosis calcification occurs at sites of atherosclerotic plaques, where there is a combination of cellular necrosis, inflammation and cholesterol deposition.<br />
Ectopic vascular calcification was viewed until recently as a passive consequence of aging. Although it is recognized that ectopic vascular calcification is a consequence of a dysregulated process, the specific molecular etiology remains unclear. There are conflicting ideas regarding the mechanisms underlying cardiovascular calcification, and the pathological and prognostic importance of vascular calcification still a matter of debate (1).<br />
Osteoporosis, that is associated with calcium deficiency, has been also associated with atherosclerosis in many studies, with findings that bone mineral density declined while atherosclerotic plaque increased. We have discussed about this subject during the last year advocating acidosis as the link between these two diseases (2). <br />
Coronary artery calcification measured by computed tomography (CT scans) is considered a radiographic confirmation of atherosclerosis, predicting cardiovascular events, and has been evaluated as a surrogate measure in randomized trials. However, in a study published in 2009 the annual rate of CAC increase was measured in 10 trials having observed a rate of 17% which was seen as moderately higher for patients with chronic kidney disease and those receiving dialysis. The study observed no consistent or reproducible treatment effect of any therapy on this outcome. These data have suggested to the authors that CAC may not be a suitable surrogate target for treatment trials in patients with cardiovascular or renal disease when measured after 12 months or reported on an annualized basis (3) <br />
Nevertheless a very recently study from MESA (Multi Ethnic Study of Atherosclerosis) has shown that even healthy patients with low-density lipoprotein cholesterol (LDL-C) are associated with adverse coronary heart disease events if their CT scans demonstrate calcium buildup in their coronary arteries. Of 5,627 participants who were not receiving any baseline lipid-lowering therapies 3,714 (66%) had LDL-C 130mg/dl. Among the persons with low LDC-C, older age, male sex, hypertension, diabetes and low HDL-C were associated with adverse events (4). <br />
It is interesting to notice that increased calcium content in diets supplemented with cholesterol has been show to decrease atherosclerosis in rabbits. Also, some epidemiological studies suggested that high levels of calcium in drinking water may decrease atherosclerosis (5).<br />
<strong><em>Hemodynamic shear stress and calcification</em></strong><br />
A recent study developed in Switzerland, aimed to investigate regional plaque morphology and using intravascular ultrasound and virtual histology in coronary artery bifurcations, found that segments on the contralateral wall of the bifurcation which have previously identified as regions with low shear stress not only exhibited a higher plaque burden but also a higher degree of calcification (6). An analogous relationship was suggested by previous studies indicating that mechanical forces play a role in aortic valve calcification. Since calcium deposits occur almost exclusively on the aortic surfaces of AV leaflets it has been hypothesized that adverse pattern of fluid shear stress on the aortic surface of AV leaflets promotes calcification (7,8,9) <br />
In the acidity theory of atherosclerosis the hemodynamic shear stress is an important step in the process leading to atherogenesis (10).<br />
Carlos Monteiro<br />
1. Johnson RC, Leopold JA and Loscalzo J. Vascular calcification: Pathological mechanisms and clinical implications. Circulation Research 2006; 99: 1044 -1059. Full free text at <a href="http://circres.ahajournals.org/content/99/10/1044.full">http://circres.ahajournals.org/content/99/10/1044.full</a> <br />
2. Acidity: The link between atherosclerosis and osteoporosis, January 5, 2010 at <a href="http://aciditytheory.blogspot.com/2010/01/acidity-link-between-atherosclerosis.html">http://aciditytheory.blogspot.com/2010/01/acidity-link-between-atherosclerosis.html</a><br />
3. McCullow PA and Chinnayan KM. Annual progression of coronary calcification in trials of preventive therapies: A systematic review. Arch Intern Med 2009, 169 (22):2064-70. Full free text at <a href="http://archinte.ama-assn.org/cgi/reprint/169/22/2064">http://archinte.ama-assn.org/cgi/reprint/169/22/2064</a> <br />
4. Blankstein R, Budoff MJ, Shaw LJ et al. Predictors of coronary heart disease events among asymptomatic persons with low low-density lipoprotein cholesterol. J Am Coll Cardiol, 2011;58:364-374<br />
5. HSU HH and Culley NC. Effects of dietary calcium on atherosclerosis, aortic calcification, and icterus in rabbits fed a supplemental cholesterol diet. Lipids in Health and Disease 2006, 5.16. Full free text <a href="http://www.lipidworld.com/content/5/1/16">http://www.lipidworld.com/content/5/1/16</a> <br />
6. Toggweiler S, Urbanek N, Schoenenberger AW, Erne P. Atherosclerosis, 2010 Oct;212(2):524-7<br />
7. Hoehn D, Sun L and Sucosky P. Role of pathologic shear stress alterations in aortic valve endothelial activation. Cardiovascular Engineering and Technology 2010, V1;N2: 165-178. Full free text at <a href="http://www.springerlink.com/content/f777qk521lr48237/">http://www.springerlink.com/content/f777qk521lr48237/</a> <br />
8. Ge L, Sotiropoulos F. Direction and magnitude of blood flow shear stresses on the leaflets of aortic valves: is there a link with valve calcification? J Biomech Eng 2010 Jan;132(1): 014505<br />
9. Yap CH, Saikrishnan N, Tamilselvan G and Yoganathan AP. Experimental measurement of dynamic fluid shear stress on the aortic surface of the aortic valve of the aortic valve leaflet. Biomech Model Mechanobiol, 2011 Mar 18<br />
10. Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008 at <a href="http://www.infarctcombat.org/AcidityTheory.pdf">http://www.infarctcombat.org/AcidityTheory.pdf</a>Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-72565328117693987112011-06-06T07:39:00.000-07:002011-07-20T07:26:25.703-07:00The final evidence: Milk and dairy products prevent heart attacks!Dr. J. E. Crewe, in 1929, along with the Mayo Foundation, reported uniformly excellent results using whole milk in the treatment of tuberculosis, diseases of the nervous system, cardiovascular and renal conditions, hypertension, and in patients who are underweight, run-down, etc. Striking results were seen in diseases of the heart and kidneys and high blood pressure. The milk used was, in all cases, the only kind of milk available in those days—raw milk from pasture-fed cows, rich in butterfat. Dr. Crewe asserted that the only problem of using raw milk to treat these diseases, was that it was too simple. So, the therapeutic use of milk didn’t attracted the interest from his colleagues in their patients (1). <br />
In 1991, the New Scientist magazine reported that Dr. Peter Elwood, director of the Epidemiology Unit of Landough Hospital in Penarth, South Glamorgan, in his study of lifestyle involving 5,000 men between the ages of 45 and 59, with a duration of 10 years, found that men who drank the most full-fat milk and ate butter (rather than margarine) had a lower risk of suffering from heart attacks! (New Scientist 1991; 129(1759):17). According to Dr. David Williams article published the same year, discussing the findings of Peter Elwood, among those who drank at least a pint of milk per day, only 1% suffered heart attacks (2, 3). <br />
Dr. Peter Elwood, in a paper published in 2004, reported the data about the Caerphilly Study dietary data, including consumption of milk, were they have collected by a semiquantative food frequency questionnaire, during a period of 1979-1983. The group was followed by 20-24 years in a population sample of 2,512 men aged 45-49, with incident ischemic heart disease and stroke events identified. The study reached the conclusion that their data provide no convincing evidence that milk consumption is associated with an increased risk of vascular disease (4). At the same time and in the same issue of the European Journal of Clinical Nutrition he had published another study saying that no group studies have provided convincing evidence to date on the milk to be harmful (5). <br />
In 2007, Peter Elwood and his group published another study concluding that the consumption of milk and other dairy products is associated with a markedly reduced prevalence of metabolic syndrome, and these items, therefore, would fit well within a healthy eating pattern (6).<br />
More recently, in 2009, a survey conducted by the Universities of Reading, Cardiff and Bristol found by reviewing the evidence from 324 published studies that milk intake may reduce the chances of dying from diseases such as coronary heart disease and stroke, in 15-20% (7).<br />
Contrary to what is usually advocated by conventional medicine, that saturated fats can lead to myocardial infarction, a very recent study found that nutrients in milk and its derivatives (cheese, butter) actually neutralize the effects of cholesterol that the researchers (still) consider harmful. Their findings, taken from 3630 middle-aged men and women from Costa Rica, have shown that the intake of dairy products in those that had myocardial infarction was not different from those who had not. Assessing about the amount of dairy food that was ingested by the participants in the Epidemiologic study between 1994 and 2004, there was no link between consumption and risk of myocardial infarction, even among those who consumed as much as 593 grams per day. This research (8), confirm the results of several other studies showing the benefits of milk and dairy products in cardiovascular disease. <br />
Interestingly to note is that endogenous digitalis like compounds (DLCs), similar to the cardiotonics used to treat heart failure, were found in tissues and fluids of animals and humans with increased concentration in amniotic fluid, umbilical cord, serum and urine of pregnant women and neonates, the saliva of pregnant women, and in the milk collected from women during breastfeeding at different days after birth. According to an article published in 1992 DLCs could be secreted or concentrated in human milk providing to children with a exogenous contribution of DLCs to replace the endogenous production which tends to decrease after the first few weeks of life out of the womb. The authors have place in the article that additional studies were needed before the physiological actions in children be assigned to DLCs in human milk (9). <br />
Certainly there are other mechanisms that could explain the benefits of the whole milk in the prevention of diseases. However, we believe that the increased concentration of DLCs in milk fits perfectly with our postulation that an insufficient production of endogenous DLCs, to attend the demand in some medical conditions such as coronary artery disease, can be resolved through the use of cardiac glycosides in low doses as a supplement. This is confirmed by clinical studies using cardiac glycosides in prevention of acute coronary syndromes (10).<br />
Some other benefits of milk fat in atherosclerosis:<br />
Milk fat, included among animal ones, does not impend over sclerosis, on the contrary, it prevent diseases of cardiovascular system, because it contains various bioactive constituents (11), that: <br />
a) limit synthesis of liver cholesterol and triglycerides (short chain saturated fatty acids, Omega-3 polyunsaturated fatty acids, oleic acid); <br />
b) intensify estrification and metabolism of cholesterol (phospholipids, oleic acid, Omega-6 and Omega-3 polyunsaturated fatty acids in optimal proportions); <br />
c) prevent cholesterol oxidation (conjugated linoleic acid--CLA, alpha-tokoferol, coenzyme Q10, vitamins A and D3, phospholipids), <br />
d) reduce level of LDL-cholesterol in blood plasma (linolenic acids Omega-3, linoleic acid W-6, also oleic acid). <br />
e) Unique components of milk fat i.e. short chain saturated fatty, conjugated linoleic acid, vaccenic acid (natural trans isomer), and other milk components possess additionally anticancerogenic activity.<br />
Moreover, the fatty acid series n-3 (or omega-3), through its ability to reduce blood lactic acid production (12), and butyric acid (GABA), which has an inhibitory effect on the sympathetic nervous system (13) may possibly reduce the progression of coronary atherosclerosis, according to the concepts of the theory of acidity in atherosclerosis (10).<br />
As Peter Elwood and colleagues said recently, “An evaluation based upon a single risk factor for a disease can, however, be misleading. At the same time as affecting lipid markers of heart disease, the consumption of milk and dairy produce is associated with an increase in the level of high-density lipoprotein cholesterol and with a reduction in blood pressure and furthermore, milk and dairy food items are likely to have effects upon many other biological mechanisms and disease processes” (14)<br />
Carlos Monteiro<br />
Referências:<br />
1) Real Milk Cures Many Diseases, Dr. J. R. Crewe, Certified Milk Magazine, January 1929, em <a href="http://www.realmilk.com/milkcure.html">http://www.realmilk.com/milkcure.html</a> <br />
2) Milk Decreases Heart Attacks? Dr. David Williams, Alternatives Newsletter, 1991 em <a href="http://www.realmilk.com/heart_disease.html">http://www.realmilk.com/heart_disease.html</a> <br />
3) Fuss over fat leads to rethink on publicity, issue 1759 of News Scientist magazine, 09 March 1991, page 17. Texto integral em <a href="http://www.newscientist.com/article/mg12917592.800-fuss-over-fat-leads-to-rethink-on-publicity-.html">http://www.newscientist.com/article/mg12917592.800-fuss-over-fat-leads-to-rethink-on-publicity-.html</a> <br />
4) Milk drinking, ischaemic heart disease and ischaemic stroke I. Evidence from the Caerphilly cohort. Elwood PC, Pickering JE, Hughes J, Fehily AM, Ness AR, Eur J Clin Nutr. 2004 May;58(5):711-7. <br />
5) Milk drinking, ischaemic heart disease and ischaemic stroke II. Evidence from cohort studies. Elwood PC, Pickering JE, Hughes J, Fehily AM, Ness AR. Eur J Clin Nutr. 2004 May;58(5):718-24. <br />
6) Milk and dairy consumption, diabetes and the metabolic syndrome: the Caerphilly prospective study, Elwood PC, Pickering JE, Hughes J, Fehily AM, J Epidemiol Community Health. 2007 Aug;61(8):695-8. Texto integral gratuito em <a href="http://jech.bmj.com/cgi/reprint/61/8/695.pdf">http://jech.bmj.com/cgi/reprint/61/8/695.pdf</a> <br />
7) The survival advantage of milk and dairy consumption: an overview of evidence from cohort studies of vascular diseases, diabetes and cancer. Elwood et al . Journal of the American College of Nutrition. 2009 V27, N6, &23S-734S em <a href="http://www.jacn.org/cgi/content/abstract/27/6/723S">http://www.jacn.org/cgi/content/abstract/27/6/723S</a> <br />
8) Aslibekyan S, Campos H, Baylin A. Biomarkers of Dairy intake and the risk of heart disease. Nutr Metab Cardiovasc Dis. May 4, 2011<br />
9) Endogenous Digitalis-Like Factors in Human Milk, Aldo Clerico, Anna Pad, Maria Grazia Del Chicca, Pascal Biver,’ and Ottavio Giampietro, Clin Chem 38/4, 504-506 (1992). Texto integral gratuito em <a href="http://www.clinchem.org/cgi/reprint/38/4/504.pdf">http://www.clinchem.org/cgi/reprint/38/4/504.pdf</a> <br />
10) <span lang="PT-BR">Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008 at </span><a href="http://www.infarctcombat.org/AcidityTheory.pdf"><u><span style="color: blue;"><span lang="PT-BR">http://www.infarctcombat.org/AcidityTheory.pdf</span></span></u></a><span lang="PT-BR"> </span><br />
11) Atherogenic properties of milk fat: facts or myths?, Cichosz G. Przegl Lek 2007; 64 Suppl 4:32-4 <br />
12) Ogilve GK, Fettman MJ et al. Effect of fish oil, arginine, and doxorubicin chemotherapy on remission and survival time for dogs with lymphoma: A double-blind, randomized placebo-controlled study, Cancer; 2000, 88: 1016-28. <br />
13) Hayakawa K et al. Effect of a gamma-aminobutyric acid enriched dairy product on the blood pressure of spontaneously hypertensive and normotensive Wistar-Kyoto rats. Br. J. Nutr 2004; 92:411-417<br />
14. Peter Elwood et al. The consumption of milk and dairy foods and the incidence of vascular disease and diabetes: An overview of the evidence. Lipids. 2010 Oct;45(10):925-39. Full free paper at <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2950929/?tool=pubmed">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2950929/?tool=pubmed</a>Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com1tag:blogger.com,1999:blog-1777991997515634746.post-6311237543203145622011-05-04T15:10:00.000-07:002015-08-17T07:06:57.235-07:00Lactic acid elevation: the link between rheumatoid arthritis and atherosclerosis?Rheumatoid arthritis (RA) is considered a systemic autoimmune disease. However, what triggers the onset of rheumatoid arthritis still unknown.<br />
Patients with RA have a high prevalence of preclinical atherosclerosis independent of traditional risk factors, suggesting that chronic inflammation, and, possibly, disease severity are atherogenic in this population (1).<br />
Regarding this matter an editorial published at Circulation Journal in 1999 have discussed about the many similarities shared by RA and atherosclerosis (2). <br />
Recent investigations found that the atherosclerotic process begins very early in the course of rheumatoid arthritis with the study revealing a significant increase in intima-media thickness, an indicator of atherosclerosis, in just 18 months (3). <br />
Other investigators found a rapid increase in myocardial infarction risk following diagnosis of RA amongst patients diagnosed between 1995 and 2006 (4)<br />
Studying about the matter we have looked for studies investigating cardiovascular autonomic dysfunction in rheumatic diseases. Although there are few studies in this direction, we have noticed that the sympathetic nervous system activity may be elevated in RA compared with health patients (5, 6). According our view the sympathetic predominance is the primary factor in the cascade of events leading to increased lactic acid and acidic environment generating atherogenesis (7, 8).<br />
Also, we have discovered a study from the eighties showing high values of lactate in seropositive RA and crystal-induced arthritis, with the author suggesting that synovial lactate measurement could be a reliable indicator for differentiating inflammatory arthritides (9). In parallel, the amount of lactate released by the myocardium has been shown to be related to the severity of coronary artery disease (10, 11). <br />
Going deeper on our research I got very surprised with the following information from a paper published in 1924 (12), entitled “The alleged role of lactic acid in arthritis and rheumatoid conditions”, that says:<br />
“In 1858 Richardson published the results of extensive experiments on dogs in which the injection of large quantities of lactic acid, intraperitoneally, was followed by severe joint involvement. The condition of the joints was similar to that seen in acute arthritis, and Richardson suggested that the arthritic syndrome was due to an accumulation of lactic acid in the body. This theory found further support in 1877, when Foster reported that the administration of lactic acid by mouth to two diabetic patients resulted in painful and swollen joints. The pain and swelling persisted as long as the lactic acid administration was continued and disappeared promptly after the acid was discontinued. These early experiments were apparently never repeated or extended but they have exerted some influence in the formation of hypotheses regarding the disease”. <br />
This paper from 1924 strengthen our thoughts placed in the article “Old experiments with rabbits and dogs provide powerful evidence for the Acidity Theory of Atherosclerosis” where was shown that acid-fed rabbits and dogs may develop atherosclerotic lesions (13).<br />
Carlos Monteiro<br />
1. Roman M. J, et al. Preclinical carotid atherosclerosis in patients with rheumatoid arthritis. Ann Intern Med. 2006; 144: 249-256. Full free text at <a href="http://www.annals.org/content/144/4/249.full.pdf+html">http://www.annals.org/content/144/4/249.full.pdf+html</a> <br />
2. Vincenzo Pasceri and Edward Yeh. Editorial, “A tale of two diseases - Atherosclerosis and Rheumatoid Arthritis“, Circulation, 1999; 100:2124-2126. Full free text at <a href="http://circ.ahajournals.org/cgi/content/full/circulationaha;100/21/2124">http://circ.ahajournals.org/cgi/content/full/circulationaha;100/21/2124</a> <br />
3. Sodergren et al. Atherosclerosis in early rheumatoid arthritis: very early endothelial activation and rapid progression of intima media thickness. Arthritis Research & Therapy 2010, 12:R158. Full free text at <a href="http://arthritis-research.com/content/12/4/R158">http://arthritis-research.com/content/12/4/R158</a> <br />
4. Holmqvist M. E. et al. Rapid increase in myocardial infarction risk following diagnosis of rheumatoid arthritis amongst patients diagnosed between 1995 and 2006”, J Intern Med 2010; 268:578-585.<br />
5. Aydemir , V. Yazisiz et al. Cardiac autonomic profile in rheumatoid arthritis and systemic lupus erythematosus. Lupus (2010) 19, 255—261. <br />
6. Dekkers JC et al. Elevated sympathetic nervous system activity in patients with recently diagnosed rheumatoid arthritis with active disease. Clin Exp Rheumatol. 2004 Jan-Feb;22(1):63-70.<br />
7. Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008 at <a href="http://www.infarctcombat.org/AcidityTheory.pdf">http://www.infarctcombat.org/AcidityTheory.pdf</a> <br />
8. Sympathetic predominance: a primary factor in the cascade of events leading to the atherogenic spiraling, Carlos Monteiro, Monday, February 22, 2010 at <a href="http://aciditytheory.blogspot.com/2010/02/sympathetic-predominance-primary-factor.html">http://aciditytheory.blogspot.com/2010/02/sympathetic-predominance-primary-factor.html</a> <br />
9. Gobelet C and Gerster J. C. Synovial fluid lactate levels in septic and non-septic arthritides. Annals of the Rheumatic diseases, 1984, 43, 742-745.<br />
10. G. Jackson, Lynne Atkinson, M. Clark, B. Crook, P. Armstrong, and S. Oram, Diagnosis of coronary artery disease by estimation of coronary sinus lactate. British Heart Journal, 1978, 40, 979-983 Full free text at <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC483520/">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC483520/</a> <br />
11 Gertz EW, Wisneski JA, Neese R, Bristow JD, Searle GL, Hanlon JT: Myocardial lactate metabolism: evidence of lactate release during net chemical extraction in man. Circulation 1981, 63: 1273-1279. Full free text at <a href="http://circ.ahajournals.org/cgi/reprint/63/6/1273">http://circ.ahajournals.org/cgi/reprint/63/6/1273</a><br />
12. F . A Cajori et al. The alleged role of lactic acid in arthritis and rheumatoid conditions. Arch Intern Med. 1924;34(4):566-572. <br />
13. Old experiments with rabbits and dogs provide powerful evidence for the Acidity Theory of Atherosclerosis, Carlos Monteiro, July 13, 2010 at http://aciditytheory.blogspot.com.br/2010/07/old-experiments-with-rabbits-and-dogs.html <a href="http://aciditytheory.blogspot.com/2010/07/old-experiments-with-rabbits%C2%ADand-dogs.html"></a>Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-52204408410077816182011-03-09T06:27:00.000-08:002011-11-19T14:59:19.355-08:00The potential positive effect of improvement in baroreflex function on prevention and treatment of atherosclerosisThe baroreflex or baroreceptor reflex is one of the body’s homeostatic mechanisms for regulating blood pressure by controlling heart rate, strength of heart contractions, and diameter of blood vessels. The most important arterial baroreceptors are located in the carotid sinus and in the aortic arch. These baroreceptors respond to stretching of the arterial wall so that if arterial pressure suddenly rises, the walls of these vessels passively expand, which stimulates the activation of these receptors. If arterial blood pressure suddenly falls, decreased stretch of the arterial walls lead to a decrease in receptor activation. The loss of the stabilizing influence of vagal control raise the susceptibility to sympathetic influences. On the other hand the result of the baroreceptor improvement is the inhibition of the sympathetic nervous system and activation of the parasympathetic nervous system. <br />
It is interesting to notice the impairment or decrease of baroreflex sensitivity in front of some key factors for atherosclerosis, cardiovascular disease and stroke, like in ageing, ingestion of sugars, in special high-fructose diets and smoking.<br />
Related to atherosclerosis there are some studies showing that in bilateral carotid atherosclerosis (1) and in greater intima-media thickness (2) the baroreflex sensitivity is reduced or impaired.<br />
In this direction a study published in 2005 have indicated that arterial baroreflex dysfunction promotes the development of atherosclerosis in rats, and that inflammation may be involved in this process (3). The same authors have demonstrated in a very recent publication that low dose ketanserin, an anti-hypertensive, prevented the development of atherosclerosis in spontaneous hypertensive rats and rabbits at least in part via enhancement of arterial baroreflex function (4). Other anti-hypertensive drugs like Beta blockers may also enhance baroreflex sensitivity (5) with positive effects on atherosclerosis (6). Digitalis glycosides, another class of drugs, also augments cardiopulmonary baroreflex control of sympathetic activity (7), that probably is responsible for potential benefic effects of digitalis on atherosclerosis (6,8,9).<br />
Aside of the above mentioned drugs there are some recent studies suggesting that polyunsaturated fatty acids - PUFA (19), cacao (10), vitamins like vitamin C (11,12), vitamin E (13) and folic acid (14,15), apart of aerobic exercise (16,17) and slow breathing (18), improve baroreflex sensitivity with possible positive effects on the treatment or prevention of atherosclerosis according to the acidity theory of atherosclerosis point of view (6) where sympathetic predominance is the primary factor in the cascade of events leading to the atherogenic spiraling.<br />
Carlos Monteiro<br />
<br />
1. Nasr N et al. Baroreflex sensitivity is impaired in bilateral carotid atherosclerosis. Stroke, 2005;36:1891-1895<br />
2. Gianoros PJ et al. Greater intima-media thickness in the carotid bulb is associated with reduced baroreflex sensitivity. Am J Hypertens. 2002; 15(6): 486-491<br />
3. Cai GJ et al. Arterial baroreflex dysfunction promotes atherosclerosis in rats. Atherosclerosis, 2005 Nov; 183(1):41-7<br />
4. Yu YS et al. Effects of low-dose ketanserin on atherosclerosis in rats and rabbits. Can J Pysiol Pharmacol 2010 Nov;88(11):1054-60<br />
5. Truijen J et al. Baroreflex sensitivity is higher during acute psychological stress in healthy subjects under B-adrenergic blockade. Clin Sci (Lond), Feb 2011; 120(4):161-167<br />
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 <a href="http://www.infarctcombat.org/AcidityTheory.pdf">http://www.infarctcombat.org/AcidityTheory.pdf</a> <br />
7. Schobel HP et al. 1991.Contrasting effects of digitalis and dobutamine on baroreflex sympathetic control in normal humans, Circulation V84, 1118-1129. Full free paper at <a href="http://circ.ahajournals.org/cgi/reprint/84/3/1118">http://circ.ahajournals.org/cgi/reprint/84/3/1118</a> <br />
8. Jagielska J. et al. Digitoxin elicits anti-inflammatory and vasoprotective properties in endothelial cells: Therapeutic implications for the treatment of atherosclerosis?, doi:10.1016/j.atherosclerosis.2009.03.019<br />
9. Kolkhof P et al. Cardiac glycosides potently inhibit C-reactive protein synthesis in human hepatocytes. Biochem Biophys Res Commun. 2010 Mar 26;394(1):233-9. Epub 2010 Mar 3.<br />
10. Akita M et al., Effects of cacao liquor polyphenols on cardiovascular and autonomic nervous functions in hypercholesterolaemic rabbits. Basic Clin Pharmacol Toxicol. 2008 Dec;103(6):581-7.<br />
11. Kevin D. Monahan et al, Ascorbic acid increases cardiovagal baroreflex sensitivity in healthy older men. Am J Physiol Heart Circ Physiol 286: H2113–H2117, 2004.<br />
12. Gianfranco Piccirillo et al., Influence of Vitamin C on Baroreflex Sensitivity in<br />
Chronic Heart Failure. Hypertension. 2003; 41:1240-1245.<br />
13. Peter Studinger et al., Effect of vitamin E on carotid artery elasticity and baroreflex gain in young, health adults. Autonomic Neuroscience, V 113, I1, Pages 63-70; 2004<br />
14. Béchir M et al., Folic Acid Improves Baroreceptor Sensitivity in Hypertension. J Cardiovasc Pharmacol;45:44–48), 2005<br />
15. Xiu-juan MA et al, Clonidine, moxonidine, folic acid, and mecobalamin improve baroreflex function in stroke-prone, spontaneously hypertensive rats. Acta Pharmacol Sin 2007 Oct; 28 (10): 1550–1558<br />
16. Deley G et al., Arterial baroreflex control of cardiac vagal outflow in older individuals can be enhanced by aerobic exercise training. Hypertension, 2009;53:826-832<br />
17. Effects of long-term exercise training on cardiac baroreflex sensitivity in patients with coronary artery disease: a randomized controlled trial. Clin Rehabil. 2011 Mar;25(3):217-27<br />
18. Carlos Monteiro, Slow breathing increases baroreflex sensitivity and reduces sympathetic activity with benefic effects to cardiovascular disease, August 9, 2010 at <a href="http://www.aciditytheory.blogspot.com/">http://www.aciditytheory.blogspot.com/</a><br />
19. <span lang="PT-BR">Radaelli A, Cazzaniga M, Viola A, et al. Enhanced baroreceptor control of the cardiovascular system by polyunsaturated fatty acids in heart failure patients J Am Coll Cardiol 2006;48:1600-1606. Free full text at <span lang="EN"></span><a href="http://content.onlinejacc.org/cgi/reprint/48/8/1600.pdf"><u><span style="color: blue;"><span style="color: blue;"><span lang="EN">http://content.onlinejacc.org/cgi/reprint/48/8/1600.pdf</span></span></span></u></a> </span>Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-83451353060676297742010-11-03T12:20:00.000-07:002011-02-07T14:19:24.917-08:00Infection through bacteremia leads to sympathetic overactivity and then to the atherosclerotic processResearch long suggested infection to be a cause or to promote atherosclerosis. This idea is supported by many reports and epidemiological studies (1).<br />
However, main trials using antibiotics have failed to prove their protective effects in secondary prevention of coronary artery disease (2).<br />
Periodontal disease, one of the most common chronic bacterial infection, may represent a favorable scenario to verify the connection of infection and atherosclerosis/cardiovascular disease.<br />
The first researchers to indicate a relationship between oral infections and atherosclerosis were Mattila and colleagues. In their study published in 1989 they have identified periodontal disease as an independent predictor of elevated risk of myocardial infarction (3). <br />
Several studies are suggesting an oral source for atherosclerotic plaque - associated bacteria with demonstration about the presence of viable periodontal pathogens in atherosclerotic plaques (4, 5, 6, 7). In this regard an interesting hypothesis was proposed in 2004 that periodontal infection may lead to brief episodes of bacteremia with inoculation of atherosclerotic plaque by periodontal pathogens such as Porphyromonas gingivalis, Actinobacillus actinomycetemcomitants and Tannerela forsythensis (8).<br />
Related to the subject a recent review says that clinical procedures by dentists on the teeth and periodontal, along with the daily brush made by patients, produce a transient bacteremia, which may cause a secondary infection in a distant tissue or organ, including arteries. For the authors of this review it is evident that both endodontic surgical procedures and non-surgical instrumentation of root channels during endodontia can produce a transient bacteremia. Also, they have stressed that a tooth extraction causes bacteremia in 100% of times (9).<br />
Coincidently to the present matter a study published last month revealed data from Medicaid patients showing that the risk of adverse vascular events sharply increases in the month following invasive dental treatment and then gradually returns to normal over six months (10).<br />
However, an important information is generally left aside by investigators studying the connection between oral infection and atherosclerosis/cardiovascular disease. These investigators don’t take in consideration that the sympathetic nervous system is intensely activated during bacteremia. This was demonstrated by studies showing that the sympathetic tone rapidly increases after the experimental injection or infusion of bacteria and similarly during bacteremia in humans (11, 12, 13, 14).<br />
Moreover, in a systematic review published in 2007 about 57 per cent of studies reviewed showed a positive relationship between stress/psychological factors and periodontal disease (15). These results are reinforced by a very recent study indicating that the sympathetic nervous system is involved in the development of periodontitis and that blockade of beta-receptors in periodontal tissue by a sympatholitic (propranolol) inhibited osteoclast differentiation and prevented alveolar bone loss induced by Porphyromonas gingivalis (16)<br />
In the acidity theory of atherosclerosis point of view the sympathetic predominance is the primary factor in the cascade of events leading to the atherogenic spiraling.<br />
Therefore, we think infection through bacteremia can be added to the long list of risk factors for atherosclerosis/cardiovascular disease, as mentioned in the acidity theory paper and in other previous articles published in this blog (17).<br />
Carlos Monteiro <br />
1. Epstein SE, Zhou YF, Zhu J. Infection and atherosclerosis. Emerging mechanistic<br />
paradigms. Circulation 1999;100:20–8.<br />
2. Anderson JL. Infection, antibiotics and atherothrombosis: end of the road or new beginnings?, N Eng J Med 2005;352:1706-1709<br />
3. Mattila K, Nieminen MS, Valtonen VV, et al. Association between dental health and acute myocardial infarction. Br Med J 1989;298:779–82.<br />
4. Haraszthy VI, Zambon JJ, Trevisan M, Zeid M, Genco RJ. Identification of<br />
periodontal pathogens in atheromatous plaques. J Periodontol 71:1554–1560, 2000<br />
5. Stelzel M, et al. Detection of Porphyromonas gingivalis DNA in aortic tissue by PCR. J Periodontol 73:868–870, 2002<br />
6. Kozarov EV, Dorn BR, Shelburne CE, Dunn WA, Jr, Progulske-Fox A. Human atherosclerotic plaque contains viable invasive Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis. Arterioscler Thromb Vasc Biol 25:e17–e18, 2005<br />
7. Gaetti-Jardim E, Jr, Marcelino SL, Feitosa AC, Romito GA, Avila-Campos MJ. Quantitative detection of periodontopathic bacteria in atherosclerotic plaques from coronary arteries. J Med Microbiol 58:1568–1575, 2009<br />
8. Giacona MB, Papapanou PN, Lamster IB, Rong IL, D’Agati VD, Schmidt AM, and Lalla E. Porphyromonas gingivalis induces its uptake by human monocytes/macrophages and promotes foam cell formation in vitro. FEMS Microbiol Letter. 241, 95-101, 2004<br />
9. Cotti E, Dessi C, Piras A, Mercuro G. Can a chronic dental infection be considered a cause of cardiovascular disease? A review of the literature. International Journal of Cardiology, 2010, doi 10.1016/j.ijcard.2010.08.011<br />
10. Minassian C, D’Aiuto F, Hingoriani AD, Smeeth L. Invasive dental treatment and risk for vascular events. A self-controlled case series. Ann Intern Med 2010; 153:499-506<br />
11. Palsson J, Ricksten SE, Delle M, Lundin S. Changes in renal sympathetic nerve activity during experimental septic and endotoxin shock in conscious rats. Circ Shock 1988; 24:13341. <br />
12. Jones SB, Kovarik MF, Romano FD. Cardiac and splenic norepinephrine turnover during septic peritonitis. Am J Physiol 1986; 250:R8927. <br />
13. Leinhardt DJ, Arnold J, Shipley KA, Mughal MM, Little RA, Irving MH. Plasma NE concentrations do not accurately reflect sympathetic nervous system activity in human sepsis. Am J Physiol 1993; 265:E2848. <br />
14. Straub RH, Pongratz G, Weidler C, Linde HJ, Kirschning CJ, Glück T, Schölmerich J, Falk W. Ablation of the sympathetic nervous system decreases gram-negative and increases gram-positive bacterial dissemination: key roles for tumor necrosis factor/phagocytes and interleukin-4/lymphocytes. Infect Dis. 2005 Aug 15;192(4):560-72. <br />
15. Daiane C. Peruzzo, Bruno B. Benatti, Glaucia M.B. Ambrosano, Getúlio R. Nogueira-Filho, Enilson A. Sallum, Márcio Z. Casati, and Francisco H. Nociti Jr. A Systematic Review of Stress and Psychological Factors as Possible Risk Factors for Periodontal Disease. Journal of Periodontology, August 2007, Vol. 78, No. 8, Pages 1491-1504 <br />
16. Okada Y, Hamada N, Kim Y, Takahashi Y, Sasaguri K, Ozono S, Sato S. Blockade of sympathetic b-receptors inhibits Porphyromonas gingivalis-induced alveolar bone loss in an experimental rat periodontitis model. Arch Oral Biol. 2010 Jul;55(7):502-8. <br />
17. Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008 at <a href="http://www.infarctcombat.org/AcidityTheory.pdf">http://www.infarctcombat.org/AcidityTheory.pdf</a>Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-14436668962510723572010-10-03T19:07:00.000-07:002011-10-20T11:01:05.127-07:00Association of lipid abnormalities with lactate and coronary artery disease progression<strong>Lactate as a screening test for coronary artery disease</strong><br />
The association of increased lipid levels with abnormal lactate metabolism may provide a useful screening test for the detection of coronary artery disease (1). In fact it was demonstrated that plasma lipid abnormalities and myocardial lactate production at the time of the initial study were significantly associated with subsequent arteriographic progression (2).<br />
In our opinion the raise in plasma lipids presented in these studies might be a response to injury of the arterial endothelium due to an increased release of lactate. The response to injury concept is supported by the acidity theory of atherosclerosis (4)<br />
<strong>Lactate and severity of coronary artery disease</strong><br />
The amount of lactate released by the myocardium has been shown to be related to the severity of coronary artery disease (1,2,3). One of these studies (3) have shown heterogeneity of myocardial lactate metabolism at rest in patients with coronary-myocardial disease. Lactate was released or produced by the myocardium when there was no clinical evidence of ischemia and the chemical arterial-coronary sinus lactate difference showing net global lactate extraction (3).<br />
Carlos Monteiro<br />
1. G. Jackson, Lynne Atkinson, M. Clark, B. Crook, P. Armstrong, and S. Oram, Diagnosis of coronary artery disease by estimation of coronary sinus lactate. British Heart Journal, 1978, 40, 979-983 Full free text at <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC483520/">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC483520/</a> <br />
2. Bemis CE, Gorlin R, et al. Progression of coronary artery disease: A clinical arteriographic study. Circulation, Vol XLVII, March 1973. Full free text at <a href="http://circ.ahajournals.org/content/47/3/455.full.pdf">http://circ.ahajournals.org/content/47/3/455.full.pdf</a> <br />
3. Gertz EW, Wisneski JA, Neese R, Bristow JD, Searle GL, Hanlon JT: Myocardial lactate metabolism: evidence of lactate release during net chemical extraction in man. Circulation 1981, 63: 1273-1279. Full free text at <a href="http://circ.ahajournals.org/cgi/reprint/63/6/1273">http://circ.ahajournals.org/cgi/reprint/63/6/1273</a> <br />
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 <a href="http://www.infarctcombat.org/AcidityTheory.pdf">http://www.infarctcombat.org/AcidityTheory.pdf</a>Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-14239017004262462552010-09-05T01:55:00.000-07:002010-09-05T01:57:39.996-07:00Does serum lactic acid and lactate dehydrogenase (LDH) levels increase with age?Loiseleur and Morel were the first to report in 1931 about an increase of serum lactic acid with age (1).<br />However, in a study by Gottfried, Pelz and Clifford published in 1961 it was observed no difference in serum lactic acid levels between a group of 49 men and women over 70 years of age and a control group under 50 years of age (2).<br />Also, Davis and colleagues in a study published in 1966 have reported that serum lactic acid does not increase with age. In two groups of ambulatory patients with average age of 67 years, totaling 544 subjects who were free of overt acute diseases, the regression analysis for both serum lactic acid and LDH not revealed any significant change (3).<br />Contrasting with the reports from Gottfried (2) and Davis (3), a study by Nagamine and Shima published in 1989 indicated from the serum chemical analysis, obtained from 1822 male and 1870 women outpatients, the values for LHD were higher in female over 50 years of age than in their counterpart. When male and female were combined the normal reference ranges for LDH tended to be elevated. The values for total cholesterol and triglyceride reached a peak at a certain age (4).<br />Taking in view the conflicting results in the above mentioned papers, we think that new investigations are warranted in order to definitively clarify if serum lactic acid and LDH are increased with ageing, if there is correlation with cholesterol levels, and about the potential of causal relations, as preached by the acidity theory of atherosclerosis (5).<br />Recalling O. J. Pollak, 1952:<br /><em>“Certainly all tissues change with age. There is anatomic and chemical aging. The acidity of tissues increases with age; this favors the precipitation of cholesterol”</em><br />Carlos Monteiro<br />1. Loiséleur J and R Morel. Influence de l’age et de L’état fonctionnel du foie sur la lacticémie. C. R. Soc. Biol, Paris, 106:35-37, 1931<br />2. Gottfried S. P., K. S. Pelz and R. C. Clifford. Carbohydrate metabolism in healthy old men over 70 years of age. Amer J. med. Sci, 242: 475-480, 1961<br />3. Davis R. L., Lawton A. H. et al. Serum lactate and lactic dehydrogenase levels of aging males. J. Gerontology 1966, Oct 21(4):571-4<br />4. Nagamine Y, Shima K. Changes in normal reference ranges for serum chemical analyses with ageing. Nippon Ronen Igakkai Zasshi. 1989 Jan;26(1):31-6.<br />5. Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008 at <a href="http://www.infarctcombat.org/AcidityTheory.pdf">http://www.infarctcombat.org/AcidityTheory.pdf</a>Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-47623153818747953912010-08-25T09:25:00.000-07:002010-08-29T17:25:15.842-07:00Migraine, cardiovascular disease and higher lactic acid concentration in plasmaPeople with migraine, particularly those with aura (temporary visual or sensory disturbances before or during a migraine headache) , are at increased risk of death from coronary heart disease and stroke, according to research published this week on the the British Medical Journal. The study assessed the impact of mid-life migraine episodes in 18,725 men and women born between 1907 and 1935 who took part in the Reykjavik Study (set up in 1967 by the Icelandic Heart Association to study heart disease in Iceland). In total the research team explored over 470,000 person-years of data with a follow-up of 26 years. Their conclusion was that migraine with aura is an independent risk factor for cardiovascular and all cause mortality in men and women(1). <br />Interesting is that migraine suffers have higher lactic acid concentration in plasma (2), a decisive risk factor for cardiovascular disease, according to the acidity theory of atherosclerosis (3). <br />Carlos Monteiro<br />1.Larus S Gudmundsson, Ann I Scher, Thor Aspelund, Jon H Eliasson, Magnus Johannsson,Gudmundur Thorgeirsson, Lenore Launer and Vilmundur Gudnason. Migraine with aura and risk of cardiovascular and all cause mortality in men and women: prospective cohort study. Published 24 August 2010, doi:10.1136/bmj.c3966, BMJ 2010;341:c3966. Full free text at <a href="http://www.bmj.com/cgi/content/full/341/aug24_1/c3966">http://www.bmj.com/cgi/content/full/341/aug24_1/c3966</a><br />2.Okada H, Araga S, Takeshima T, Nakashima K. Plasma lactic acid and pyruvic acid levels in migraine and tension-type headache. Headache. 1998 Jan;38(1):39-42.<br />3.Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008 at <a href="http://www.infarctcombat.org/AcidityTheory.pdf">http://www.infarctcombat.org/AcidityTheory.pdf</a>Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-61998930851510779382010-08-09T11:34:00.000-07:002011-06-29T07:45:31.705-07:00Slow breathing increases baroreflex sensitivity and reduces sympathetic activity with beneficial effects on cardiovascular diseaseControl breathing have been used as an effective strategy to calm down during stressful situations in daily life during centuries. The usual advice to “take a deep breath” under emotion circumstances such as stress, anxiety and anger is a clear indication of this, yet we do not normally stop to consider the connection between our breathing and emotional states. There is a study realized in Japan where two hundred and forty-one male and female undergraduates completed the questionnaire concerning stressful events in the real life and relaxation strategies they used to overcome these stressful events. The result clearly showed that the most numerous relaxation strategy was deep breathing. About 60% of subjects reported that they control breathing to calm down in their stressful situation. Many subjects have answered this question telling that abdominal breathing technique (diaphragmatic) was an effective strategy to calm down (1). <br />
Relaxation through slower breaths ( fewer than 10 cycles per minute) , used in relaxation techniques like yoga and meditation, have been thought for a long time to have positive effects in the reduction of blood pressure.<br />
Basic studies which support these empirical and clinical observations and looking to clarify the relationship between relaxation and respiratory functions, were started in the 1970s. A paper published in 1996 in Psychosomatic Medicine have referenced many of these basic studies in discussing about the therapeutic usages of the slowed respiration maneuver in attenuating the cardiac autonomic responses in patients with anxiety disorder (2).<br />
However, despite the many clinical observations suggesting this direction, the medical science in general, particularly in cardiology, have overlooked about the influence of breathing and its relationship with the autonomic nervous system and the heart in weighing cardiac risk factors.<br />
Fortunately, recent studies are shedding more light and evidences to the subject giving new grounds for the scientific establishment regarding the link breathing/emotional states. Their findings show that sympathetic activation and parasympathetic withdrawal is implicated in the pathogenesis of hypertension, obstructive sleep apnea, and congestive heart failure and that respiration contributes importantly to the decrease of sympathetic hyperactivity and the improvement of baroreflex sensitivity (3 - 13).<br />
It is interesting to notice what Dr. William Davis, cardiologist and author of “The Heart Scan Blog”, said recently in an invited response to the article by Jimmy Moore “A Reader Asks ‘Does Acidic Blood Lead To Arterial Inflammation?’ Let’s Ask The Low-Carb Experts (14): “One final thought: Interestingly, the easiest and fastest way to increase the alkaline state of the blood is to breathe deeply. Deep breathing results in lower carbon dioxide in the blood, resulting in net alkalinization. Wouldn’t it be neat if we could study and quantify this response over time and its effects on atherosclerotic disease?”<br />
Also interesting is that while some studies have documented greater total muscle sympathetic nerve activity (MSNA) during hypercapnia compared with hypoxia, other studies observed a higher MSNA response to hypoxia compared with hypercapnia in participants with slow and fast spontaneous breathing rates. Whereas the authors were unable to distinguish between chemo reflex, respiratory or cardiovascular induced activation their data suggest that hypercapnia and hypoxia cause distinct patterns of activation within regions normally associated with sympathetic control (15, 16).<br />
Taking in view that continuous positive airway pressure treatment may reverse early signs of atherosclerosis (17) we think the slow breathing practice may also contribute for the prevention or regression of atherosclerosis, by reducing the sympathetic hyperactivity, be it stimulated by hypercapnia, hypoxia or other factors, according to the acidity theory concept (18, 19).<br />
Moreover, hypertension is an important risk factor for the development of atherosclerosis, with these processes sharing some common mechanisms. The endothelium is usually placed as a probable central focus for the effects in both diseases, with evidences leading to the postulation that hypertension predispose and accelerate atherosclerosis (20).<br />
Carlos Monteiro<br />
Remarks:<br />
Transcendental Meditation not only lowers colesterol (21) and blood pressure (22, 23) but also reduce atherosclerosis (18). Most interesting is that a meta-analysis of 31 studies found that TM produces a lowering of plasma lactate (24, 25). Lower plasma lactate indicates profound relaxation, since high concentrations of lactate have been associated with stress situations (for example high anxiety), and high blood pressure (20). More data about lactate, stress, hypertension and reduction of atherosclerosis on patients submitted to Ioga or TM at the acidity theory of atherosclerosis article (18).<br />
1. Yutaka Haruki, I Homma, Akio Umezawa, Y Hasaoka. Facilitation and Emotion of Breathing During Changes in Emotion, Chapter by Akio Umezawa, Book Respiration and Emotion, Springer, 2001<br />
2. Sakakibara M and Hayano J. Effect of Slowed Respiration on Cardiac Parasympathetic Response to Threat. Psychosomatic Medicine 58:32-37 (1996). Full free text at <a href="http://www.psychosomaticmedicine.org/cgi/reprint/58/1/32.pdf">http://www.psychosomaticmedicine.org/cgi/reprint/58/1/32.pdf</a> <br />
3. Clark ME, Hirschman R., Effects of paced respiration on anxiety reduction in a clinical population, Biofeedback Self Regul. 1990 Sep;15(3):273-84.<br />
4. Meles E, Giannattasio C, et al. Nonpharmacologic treatment of hypertension by respiratory exercise in the home setting, Am J Hypertens. 2004 Apr;17(4):370-4<br />
5. Grossman E, Grossman A, et al. Breathing-control lowers blood pressure, Hum Hypertens. 2001 Apr;15(4):263-9.<br />
6. Viskoper R, Shapira I et al. Nonpharmacologic treatment of resistant hypertensives by device-guided slow breathing exercises. Am J Hypertens. 2003 Jun;16(6):484-7.<br />
7. Schein MH, Gavish B, et al. Treating hypertension with a device that slows and regularises breathing: a randomised, double-blind controlled study, J Hum Hypertens. 2001 Apr;15(4):271-8.<br />
8. Elliot WJ, Izzo JL Jr, et al. Graded blood pressure reduction in hypertensive outpatients associated with use of a device to assist with slow breathing. J Clin Hypertens (Greenwich). 2004 Oct;6(10):553-9; quiz 560-1.<br />
9. Oneda B, Ortega KC et al. Sympathetic nerve activity is decreased during device-guided slow breathing, Hypertension Research 33, 708-712 (July 2010) | doi:10.1038/hr.2010.74<br />
10. Anderson DE, McNeely JD, Windham BG. Regular slow-breathing exercise effects on blood pressure and breathing patterns at rest, J Hum Hypertens. 2010 Mar 4. [Epub ahead of print]<br />
11. Joseph CN, Porta C, et al. Slow Breathing Improves Arterial Baroreflex Sensitivity and Decreases Blood Pressure in Essential Hypertension, Hypertension 2005;46;714-718; originally published online Aug 29, 2005<br />
12. Narkiewicz K et al. Sympathetic Neural Outflow and Chemoreflex Sensitivity Are Related to Spontaneous Breathing Rate in Normal Men. Hypertension 2006;47;51-55; originally published online Dec 12, 2005<br />
13. Bernardi L, Porta C, Slow Breathing Increases Arterial Baroreflex Sensitivity in Patients With Chronic Heart Failure, Circulation 2002;105;143-145<br />
14. Jimmy Moore “A Reader Asks ‘Does Acidic Blood Lead To Arterial Inflammation?’ Let’s Ask The Low-Carb Experts!”, published at <a href="http://livinlavidalowcarb.com/blog/?p=7270">http://livinlavidalowcarb.com/blog/?p=7270</a>, in February 10, 2010:<br />
15. Bernardi L, Gabutti A et al. Slow breathing reduces chemoreflex response to hypoxia and hypercapnia, and increases baroreflex sensitivity, Journal of Hypertension, V 19;I 12 - pp 2221-2229, 2001<br />
16. Steinback C. et al. Hypercapnic vs. hypoxic control of cardiovascular, cardiovagal and sympathetic function, Am J Physiol Regul Integr Comp Physiol 296: R402-R410, 2009<br />
17. Drager LF, Bortolotto LA, Figueiredo AC, Krieger EM, Lorenzi-Filho G. Effects of continuous positive airway pressure on early signs of atherosclerosis in obstructive sleep apnea. Am J Respir Crit Care Med 2007; 176: 706–712.<br />
18. Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008 at <a href="http://www.infarctcombat.org/AcidityTheory.pdf">http://www.infarctcombat.org/AcidityTheory.pdf</a> <br />
19. Sympathetic predominance: a primary factor in the cascade of events leading to the atherogenic spiraling, Carlos Monteiro, Monday, February 22, 2010 at <a href="http://aciditytheory.blogspot.com/2010/02/sympathetic-predominance-primary-factor.html">http://aciditytheory.blogspot.com/2010/02/sympathetic-predominance-primary-factor.html</a><br />
20. Hypertension, atherosclerosis, stress and lactic acid, Carlos Monteiro, <br />
Friday, November 27, 2009 at <a href="http://aciditytheory.blogspot.com/2009/11/hypertension-atherosclerosis-stress-and.html">http://aciditytheory.blogspot.com/2009/11/hypertension-atherosclerosis-stress-and.html</a><br />
21. Cooper M, Aygen M. Transcendental Meditation in the management of hypercholesterolemia, Journal of Human Stress 1979; 5:24-27<br />
22. Schneider RH, Staggers F, Alexander C, et al. A randomized controlled trial of stress reduction for hypertension in older African Americans. Hypertension 1995; 26: 820-827<br />
23. Alexander C, Schneider RH, Staggers F. A trial of stress reduction for hypertension in older African Americans (part II); sex and risk factor subgroup analysis, Hypertension 1996; 28:228-237<br />
24. Michael C. Dillbeck, David W Orme-Johnson. Physiological differences between meditation and rest. American Psychologist, Vol 42(9), Sep 1987, 879-881 <br />
25. The Effects of the Transcendental Meditation Technique on Common Risk Factors and Overall Health. Adapted from Chalmers, R. Scientific Research on Maharishi's Vedic Approach to Health: Part I Transcendental Meditation Introduction and Overview of Research, January 1998, at <a href="http://www.tm.cme.edu/article.pdf">http://www.tm.cme.edu/article.pdf</a>Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0tag:blogger.com,1999:blog-1777991997515634746.post-24824601721066088132010-07-26T07:56:00.000-07:002010-08-18T13:53:48.260-07:00Obstructive sleep apnea: Intermittent hypoxia leads to sympathetic overactivity and then to atherosclerotic processObstructive sleep apnea (OSA) syndrome is caused by upper airway collapse during inspiration, causing intermittent hypoxemia, hypercapnia, acidosis, sympathetic nervous system activation, and arousal from sleep.<br />Mounting evidence shows that OSA is a risk factor for cardiovascular disease which is supported by epidemiological association studies. Longitudinal cohort studies also provide evidence that patients with untreated severe sleep apnea have an increased rate of cardiovascular events. The prevalence of coronary artery disease (CAD) is 3 to 5 times higher in patients with OSA compared with control populations (1, 2, 3, 4, 5, 6, 7). <br />Atherosclerosis is recognized as the precursor stage of coronary-myocardial disease.<br />A very recent paper published in Circulation Journal (8), by far the largest study to date, has showed that moderate to severe obstructive sleep apnea increases the risk of coronary heart disease or death by 68% in men under the age of 70, but does not increase the risk for men over 70 or for women. A total of 1927 men and 2495 women 40 years of age and free of coronary heart disease and heart failure at the time of baseline polysomnography were followed up for a median of 8.7 years in this prospective longitudinal epidemiological study.<br />Increased carotid intima-media thickness (IMT) and plaque occurrence was reported in OSA patients without any other significant co-morbidity compared to matched controls (9, 10, 11, 12). <br />The prevalence of hypertension is very high and the incidence of hypertension increases as the number of apneic and hypopneic events per hour rises. The association of OSA and hypertension has additive effects on the development of atherosclerosis. Daytime hypertension develops secondary to the persistently elevated sympathetic state (13). In a recent study of 94 middle-aged patients, the intima-media thickness of carotid artery was positively related to systolic blood pressure and apnea-hypopnea index (14). <br /><strong>Pathophysiological mechanisms linking OSA to atherosclerosis</strong><br />OSA patients experience intermittent hypoxaemia and CO2 retention that modify the autonomic and haemodynamic responses to sleep (15). Indeed, chronic intermittent hypoxia may lead to sympathetic overactivity (16, 17). A study has shown that with mild apneic events (duration < 20 seconds), pretreatment with 100% oxygen effectively eliminated most of the increase in sympathetic nerve activity (25).<br />It is interesting to notice that continuous positive airway pressure treatment may reverse early signs of atherosclerosis (18).<br />There is increasing evidence that intermittent hypoxia is independently associated with dyslipidemia (19). In addition to clinical data, animal experiments also support a role of intermittent hypoxia in the pathogenesis of dyslipidaemia in sleep-disordered breathing (20, 21, 22).<br />The studies above mentioned confirm old experiments performed on rabbits where oxygen deficiency was attained by placing the animals daily into a chamber with decreased oxygen content (down to 12%) for 3–6 hours, for 4 months. It was shown that prolonged hypoxia brings about a high hypercholesterolemia and greatly intensifies the development of aortic and coronary atherosclerosis (26). <br />The demonstration that chronic intermittent hypoxia may lead to sympathetic overactivity and dyslipidemia adds more evidence to the acidity theory concept (23), with intermittent hypoxemia joining to other key factors for atherosclerosis, as discussed recently in this blog (24).<br />Carlos Monteiro<br />1. Levy P, Pepin JL, McNicholas WT. Should all sleep apnoea patients be treated? Yes. Sleep Med Rev 2002; 6:17–26.<br />2. Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoea–hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet 2005; 365: 1046–1053.<br />3. Pepperell JC, Ramdassingh-Dow S, Crosthwaite N, et al. Ambulatory blood pressure after therapeutic and sub therapeutic nasal continuous positive airway pressure for obstructive sleep apnoea: a randomised parallel trial. Lancet 2002; 359: 204–210.<br />4. Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet. 2005;365:1046-1053. <br />5. Unruh ML, Enright PL, Polak JF, et al. The relationship of sleep apnea to carotid wall thickness among a large cohort of older adults. Sleep. 2005;20:A112. <br />6. Peker Y, Hedner J, Kraiczi H, Loth S. Respiratory disturbance index: an independent predictor of mortality in coronary artery disease. Am J Respir Crit Care Med. 2000;162:81-86.<br />7 Mooe T, Franklin KA, Holmstrom K, Rabben T, Wiklund U. Sleep-disordered breathing and coronary artery disease: long-term prognosis. Am J Respir Crit Care Med. 2001;164:1910-1913. <br />8. Daniel J. Gottlieb et al. Prospective Study of Obstructive Sleep Apnea and Incident Coronary Heart Disease and Heart Failure. The Sleep Heart Health Study. Circulation, Published online before print July 12, 2010<br />9. Drager LF, Bortolotto LA, Lorenzi MC, Figueiredo AC, Krieger EM, Lorenzi-Filho G. Early signs of atherosclerosis in obstructive sleep apnea. Am J Respir Crit Care Med 2005; 172: 613–618.<br />10. Baguet JP, Hammer L, Levy P, et al. The severity of oxygen desaturation is predictive of carotid wall thickening and plaque occurrence. Chest 2005; 128: 3407–3412. <br />11. Minoguchi K, Yokoe T, Tazaki T, et al. Increased carotid intima–media thickness and serum inflammatory markers in obstructive sleep apnea. Am J Respir Crit Care Med 2005; 172: 625–630.<br />12. Baguet JP, Hammer L, Levy P, Pierre H, Launois S, Mallion JMv, et al. The severity of oxygen desaturation is predictive of carotid wall thickening and plaque occurrence. Chest 2005; 128: 3407-12.<br />13. Narkiewicz K, Somers VK. Sympathetic nerve activity in obstructive sleep apnoea. Acta Physiol Scand. 2003;177:385-390<br />14. Drager LF, Bortolotto LA, Krieger EM, Lorenzi-Filho G. Additive effects of obstructive sleep apnea and hypertension on early markers of carotid atherosclerosis. Hypertension 2009; 53 : 64-9.<br />15. Somers VK, Dyken ME, Mark AL, Abboud FM. Sympathetic nerve activity during sleep in normal subjects. N Engl J Med 1993; 328 : 303-7.<br />16. Johnson, T. S., J. B. Young, and L. Landsberg. Sympathoadrenal responses to acute and chronic hypoxia in the rat. J. Clin. Invest. 71: 1263-1272, 1983.<br />17. Greenberg HE, Sica A, Batson D, Scharf SM. Chronic intermittent hypoxia increases sympathetic responsiveness to hypoxia and hypercapnia. J Appl Physiol 1999; 86: 298–305. Full free text at <a href="http://jap.physiology.org/cgi/content/full/86/1/298">http://jap.physiology.org/cgi/content/full/86/1/298</a><br />18. Drager LF, Bortolotto LA, Figueiredo AC, Krieger EM, Lorenzi-Filho G. Effects of continuous positive airway pressure on early signs of atherosclerosis in obstructive sleep apnea. Am J Respir Crit Care Med 2007; 176: 706–712.<br />19. Drager, Luciano F; Jun, Jonathan; Polotsky, Vsevolod Y. Obstructive sleep apnea and dyslipidemia: implications for atherosclerosis. Curr Opin Endocrinol Diabetes Obes. 2010 Apr;17(2):161-5.<br />20. Li J, Grigoryev DN, Y e SQ, Thorne L, Schwartz AR, Smith PL, et al. Chronic intermittent hypoxia upregulates genes of lipid biosynthesis in obese mice. J Appl Physiol 2005; 99 :<br />1643-8.<br />21. Li J, Thorne LN, Punjabi NM, Sun CK, Schwartz AR, Smith PL, et al. Intermittent hypoxia induces hyperlipidemia in lean mice. Circ Res 2005; 97 : 698-706.<br />22. Li J, Savransky V, Nanayakkara A, Smith PL. O’Donnell CP, Polotsky VT. Hyperlipidemia and lipid peroxidation are dependent on the severity of chronic intermittent hypoxia. J Appl Physiol 2007; 102 : 557-63.<br />23. Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008 at <a href="http://www.infarctcombat.org/AcidityTheory.pdf">http://www.infarctcombat.org/AcidityTheory.pdf</a> <br />24. Sympathetic predominance: a primary factor in the cascade of events leading to the atherogenic spiraling, Carlos Monteiro, Monday, February 22, 2010 at <a href="http://aciditytheory.blogspot.com/2010/02/sympathetic-predominance-primary-factor.html">http://aciditytheory.blogspot.com/2010/02/sympathetic-predominance-primary-factor.html</a><br />25. Leuenberger U, Jacob E, Sweer L, Waravdekar N, Zwillich C, Sinoway L. Surges of muscle sympathetic activity during obstructive apnea are linked to hypoxemia. J Appl Physiol 1995;79:581– 8.<br />26. N. N. Kipshidze.The effect of oxygen deficiency on the development experimental atherosclerosis of the coronary arteries Bulletin of Experimental Biology and Medicine, Volume 47, Number 4, 447-453, 1958, DOI: 10.1007/BF00779624Carlos Monteirohttp://www.blogger.com/profile/12396024632643601408noreply@blogger.com0