People 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).
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).
Carlos Monteiro
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 http://www.bmj.com/cgi/content/full/341/aug24_1/c3966
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.
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 http://www.infarctcombat.org/AcidityTheory.pdf
Wednesday, August 25, 2010
Monday, August 9, 2010
Slow breathing increases baroreflex sensitivity and reduces sympathetic activity with beneficial effects on cardiovascular disease
Control 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).
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.
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).
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.
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).
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?”
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).
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).
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).
Carlos Monteiro
Remarks:
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).
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
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 http://www.psychosomaticmedicine.org/cgi/reprint/58/1/32.pdf
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.
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
5. Grossman E, Grossman A, et al. Breathing-control lowers blood pressure, Hum Hypertens. 2001 Apr;15(4):263-9.
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.
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.
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.
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
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]
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
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
13. Bernardi L, Porta C, Slow Breathing Increases Arterial Baroreflex Sensitivity in Patients With Chronic Heart Failure, Circulation 2002;105;143-145
14. Jimmy Moore “A Reader Asks ‘Does Acidic Blood Lead To Arterial Inflammation?’ Let’s Ask The Low-Carb Experts!”, published at http://livinlavidalowcarb.com/blog/?p=7270, in February 10, 2010:
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
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
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.
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 http://www.infarctcombat.org/AcidityTheory.pdf
19. Sympathetic predominance: a primary factor in the cascade of events leading to the atherogenic spiraling, Carlos Monteiro, Monday, February 22, 2010 at http://aciditytheory.blogspot.com/2010/02/sympathetic-predominance-primary-factor.html
20. Hypertension, atherosclerosis, stress and lactic acid, Carlos Monteiro,
Friday, November 27, 2009 at http://aciditytheory.blogspot.com/2009/11/hypertension-atherosclerosis-stress-and.html
21. Cooper M, Aygen M. Transcendental Meditation in the management of hypercholesterolemia, Journal of Human Stress 1979; 5:24-27
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
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
24. Michael C. Dillbeck, David W Orme-Johnson. Physiological differences between meditation and rest. American Psychologist, Vol 42(9), Sep 1987, 879-881
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 http://www.tm.cme.edu/article.pdf
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.
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).
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.
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).
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?”
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).
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).
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).
Carlos Monteiro
Remarks:
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).
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
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 http://www.psychosomaticmedicine.org/cgi/reprint/58/1/32.pdf
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.
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
5. Grossman E, Grossman A, et al. Breathing-control lowers blood pressure, Hum Hypertens. 2001 Apr;15(4):263-9.
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.
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.
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.
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
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]
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
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
13. Bernardi L, Porta C, Slow Breathing Increases Arterial Baroreflex Sensitivity in Patients With Chronic Heart Failure, Circulation 2002;105;143-145
14. Jimmy Moore “A Reader Asks ‘Does Acidic Blood Lead To Arterial Inflammation?’ Let’s Ask The Low-Carb Experts!”, published at http://livinlavidalowcarb.com/blog/?p=7270, in February 10, 2010:
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
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
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.
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 http://www.infarctcombat.org/AcidityTheory.pdf
19. Sympathetic predominance: a primary factor in the cascade of events leading to the atherogenic spiraling, Carlos Monteiro, Monday, February 22, 2010 at http://aciditytheory.blogspot.com/2010/02/sympathetic-predominance-primary-factor.html
20. Hypertension, atherosclerosis, stress and lactic acid, Carlos Monteiro,
Friday, November 27, 2009 at http://aciditytheory.blogspot.com/2009/11/hypertension-atherosclerosis-stress-and.html
21. Cooper M, Aygen M. Transcendental Meditation in the management of hypercholesterolemia, Journal of Human Stress 1979; 5:24-27
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
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
24. Michael C. Dillbeck, David W Orme-Johnson. Physiological differences between meditation and rest. American Psychologist, Vol 42(9), Sep 1987, 879-881
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 http://www.tm.cme.edu/article.pdf
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