Sympathetic overactivity has been found to be associated with blood pressure and lipid abnormalities (1,2,3). In this respect a recent study has demonstrated that sympathetic overactivity may favour the development of sustained hypertension and hypercholesterolemia early in life, and lead to increased susceptibility of vascular complications. (4).
In fact accumulating data collected in animals and humans suggest that metabolic syndrome is associated with markers of adrenergic overdrive. Several markers of adrenergic drive, such as plasma norepinephrine, norepinephrine spillover from adrenergic nerve terminals, heart rate and others, have all show an increase in the different conditions clustering in metabolic syndrome like obesity, hypertension and insulin resistance state (5,6). Evidence also has shown that the sympathetic activation participates in the development of hypertension-related target organ damage, such as left ventricular diastolic dysfunction (7).
It is well established that the sympathetic nervous system (SNS) activity is also influenced by food ingestion, and that diet composition plays an important role. What is interesting to note is that, among dietary types, carbohydrates (starch and sugars) ingestion significantly increases SNS activity, especially in high-glycemic load, with deleterious effects to human health (8). On the other side protein or fat ingestion have no significant sympathoexcitatory effect (9,10,11).
The evidences above mentioned strengthen our views regarding to the acidity theory of atherosclerosis where continuous stress is placed as the most important risk factor (12). However, this do not undermine the value of other key factors as expressed in our monography:
“The acidity theory of atherosclerosis does not underestimate the importance of other key factors for atherosclerosis like ageing, improper diet, environmental pollution, lifestyle, physical inactivity, tobacco smoking and genetic predisposition. However, most of these risk factors might result in altered autonomic nervous system, sympathetic bias, increased lactic acid and acidic environment thus propitiating atherogenesis. Our proposal may extend to any respiratory or metabolic disturbances resulting in acidosis.“
Carlos Monteiro
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2. Nakao M, Nomura K, Karita K, Nishikitani M, Yano E. Relationship between brachial-ankle pulse wave velocity and heart rate variability in young Japanese men. Hypertens Res 2004; 27:925–931.
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5. Mancia G, Bousquet P et al. The sympathetic nervous system and the metabolic syndrome. Journal of Hypertension 2007, 25 (5):909-920
6.Grassi G, Quarti-Trevano F et al. Cariovascular risk and adrenergic overdrive in metabolic syndrome. Nutr Metab Cardiovasc Dis 2007, 17(6): 473-81
7. Grassi G, Seravalle G et al. Sympathetic and baroreflex cardiovascular control in hypertension-related left ventricular dysfunction. Hypertension 2009;53:205-209. Full free paper at http://hyper.ahajournals.org/cgi/content/full/53/2/205
8. Koop W. Chronically increased activity of the sympathetic nervous system: our diet-related “evolutionary” inheritance. The Journal of Nutrition, Health & Aging Volume 13, Number 1, 2009
9. 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
10. Welle SL, Lilavivathana U,Campell RG. Increased plasma nor epinephrine concentrations and metabolic rates following glucose ingestion in man. Metabolism 1980; 29: 806-09
11. 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
12. Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008 at http://www.infarctcombat.org/AcidityTheory.pdf
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