Hypertension Linked to Cognitive Decline at All Ages
Oct. 4, 2004 — High blood pressure is likely to cause cognitive decline in young people as well as old, according to the results of a longitudinal study published in the Oct. 4 Online First issue of Hypertension.
“Systolic and diastolic blood pressures have been inversely related to cognitive performance in prospective and cross-sectional studies,” write Penelope K. Elias, PhD, from the University of Maine in Orono.
New-Onset Diabetes. Hypertension Drugs can cause Diabetes.
Not only is hypertension closely related to diabetes, but it has been recognized for some time that certain drugs used to treat hypertension may accelerate the appearance of new-onset diabetes. In particular, both β blockers and diuretics have been implicated in this effect. Even in comparisons with calcium channel blockers, which are metabolically neutral—the diuretics and blockers appear somewhat more likely to produce diabetes.
Prevalence of Hypertension in U.S. Hits All-Time High
NEW YORK (Reuters Health) Aug 24 – The prevalence of high blood pressure in the U.S. increased 30% over the last decade, according to a study in the October issue of Hypertension. Results of the National Health and Nutrition Examination Survey (NHANES) IV indicate that at least 65 million adults had hypertension in 1999 to 2000, compared with an estimated 50 million adults for 1988 to1994.
“The higher estimated hypertension values for 1999 to 2000 compared with 1988 to 1994 reflect an increase in the actual proportion and number of obese and older persons in the U.S. population,” lead author Dr. Larry E. Fields and his colleagues write.
Chronic Inflammation can cause Hypertension
Elevated Plasma homocysteine concentration ([Hcy]) is considered a risk factor for cardiovascular disease (CVD) and may also be associated with hypertension. Although links have been established between hyperhomocysteinemia and elevated risk for CVD, the precise role of plasma homocysteine (Hcy) in cardiovascular events is unclear. Plasma homocysteine (Hcy) is affected by health-related behaviors, including diet, smoking, and sedentary lifestyle. Genetic factors also contribute to plasma [Hcy]. This review will discuss the clinical data and reports that have examined the contribution of Hcy to hypertension and CVD.
Question:What are Natural Alternatives for Addressing Hypertension?
Author: Dr. Joseph Pizzorno, ND
Dr. Joseph Pizzorno, ND Chair, Scientific Advisory Board Bioclinic Naturals Dr. Joe Pizzorno is the Founder and President of SaluGenecists Inc., Founding President of Bastyr University, and Editor-in-Chief of Integrative Medicine, A Clinician’s Journal. He is the co-author of seven books including the internationally acclaimed Textbook of Natural Medicine and the Encyclopedia of Natural Medicine, which has sold over a million copies and been translated into six languages.
Co-authored by Joseph Katzinger, ND
Dr. Joe Katzinger consults as medical researcher and health writer with SaluGenencists, Inc. He earned his ND degree from Bastyr University, and graduated summa cum laude with a bachelors of science in honor’s biochemistry from Michigan State University.
Answer: High blood pressure (hypertension) affects nearly 30 percent of adults, and despite its frequent lack of symptoms, it poses a significant risk for strokes, heart attacks, congestive heart failure, erectile dysfunction and much more.(1) Defined as a systolic pressure of at least 140mm Hg and/or a diastolic BP of at least 90mmHg, hypertension is often accompanied by a number of other risk factors, such as dyslipidemia, insulin resistance, elevation of inflammatory markers and obesity, and often occurs as part of the metabolic syndrome. Additionally, the risk associated with elevated blood pressure occurs along a spectrum. An estimated 37 percent of U.S. adults have a blood pressure of 120 to 139/80 to 89mmHg, classified as prehypertension, which is associated not only with a greater likelihood of developing hypertension and cardiovascular disease, but also diabetes and cognitive impairment.(2) In this month’s issue, we’d like to examine some of the contributors to abnormal blood pressure, and outline therapeutic strategies to normalize it.
Most cases of hypertension are classified as primary or essential, indicating that they are not due to a secondary cause such as kidney disease or an endocrine disorder. Although the precise etiology of primary hypertension is not definitively established, many of the contributing factors have been determined, and current research suggests an important role for the interaction between environmental and genetic factors, with the influence of multiple genes accounting for an estimated 30-50 percent of the variation in blood pressure between individuals, while environmental factors account for an additional 20 percent.(3)
For example, one common pathway by which multiple factors increase blood pressure is by inhibiting nitric oxide levels. Formerly known as endothelium derived growth factor, a reduction in nitric oxide availability leads to endothelial dysfunction (an impairment in the normal metabolism of cells which line blood vessels), increased sodium retention and blood vessel constriction. Not surprisingly, polymorphisms in the gene for nitric oxide synthase (NOS3) which cause lower nitric oxide production have been associated with higher blood pressure in both adults and children, as well as treatment resistant hypertension.(4,5) However, a recent study of prehypertensive individuals found that aerobic exercise was able to increase nitric oxide bioavailability and induce the activity of nitric oxide synthase, modulating the relationship between genetic susceptibility and hypertension, effectively compensating for the deleterious effect of the NOS3 polymorphism.(6) Exercise has also been shown to modulate the effect of NOS3 polymorphisms in postmenopausal women.(7)
Nitric oxide modulation may also explain the influence of other factors on blood pressure, such as diet and environmental toxins. For example, the toxic metal lead increases reactive oxygen species and inhibits nitric oxide availability, and is considered causal for high blood pressure.(8) Cumulative exposure to lead, determined by bone lead levels, has been directly linked to hypertension, while acute exposure (blood lead levels) have not. Bone lead has been associated with over a five-fold and eight-fold risk for cardiovascular and ischemic heart disease mortality, respectively, in a prospective study of men with normal blood lead levels.(9) Cadmium and arsenic, both components of cigarette smoke, are thought to act through similar mechanisms.(10)
Similarly, some of the dietary influences on blood pressure may also involve nitric oxide regulation. In a recent international study with nearly 2,700 participants, intake of sugarsweetened beverages (glucose and fructose) was directly associated with blood pressure. Additionally, the adverse effects of sugar were also found to be amplified in those individuals consuming a high sodium diet.(11) This is thought to occur at least in part by the fructose induced increase in the production of uric acid by the liver, which is known to reduce blood levels of nitric oxide.(12) A low fructose diet was recently shown to reduce both blood pressure and inflammation in those with chronic kidney disease, and should be considered as an option for anyone with elevated blood pressure.(13)
Two other contributing factors of importance are vitamin D levels, and the intake of sodium and potassium, (although a number of other dietary factors have been associated with blood pressure, including a high intake of cholesterol, animal protein and red meat, and a low intake of calcium, magnesium, phosphorus, iron and vegetable protein).(11,14) Low vitamin D levels, which are widespread, have been associated with an increased risk for hypertension,(15) and a high ratio of sodium to potassium is known to increase blood pressure in at least some individuals. Both sodium and potassium act via multiple mechanisms, including altering endothelial and immune function as well as inflammation, and play a causative role in promoting hypertension.(16,17) While at least 50 percent of those with high blood pressure are thought to be “salt-sensitive,” a recent review concluded that “a diet containing appropriate amounts of sodium chloride and potassium might have therapeutic benefits that equal or exceed those provided by medications.”(16) Interestingly, an article published in the New England Journal of Medicine stated that a sodium intake exceeding 1,150-2,300mg per day is necessary but not sufficient for the development of primary hypertension. In populations that consume a ratio of potassium to sodium >3, hypertension is rarely found. In the U.S., the ratio is less than 0.4.(18)
As mentioned above, both diet and physical activity should play an important and primary role in normalizing blood pressure. The most studied dietary intervention, the DASH diet (high in fruits, vegetables, and low-fat dairy products and reduced in fat), has been shown to successfully reduce blood pressure, especially when combined with exercise, as well as weight loss in those who are overweight.(19) Weight loss may be particularly important for both lowering blood pressure, and also for reducing arterial stiffness and improving insulin sensitivity.(20) The DASH diet has also been shown to reduce inflammation, improve coagulation abnormalities and lower liver enzymes.(21)
Increased fiber intake alone can lower both systolic and diastolic blood pressure, though it may take months before an effect is seen, according to a recent metaanalysis.(22) For those whose blood pressure does not improve with diet or exercise changes, significant benefit has been shown for several nutritional supplements, including CoQ10, garlic, antioxidants such as vitamins C, E and pycnogenol.(23-26) CoQ10, for example, was found to lower systolic blood pressure by up to 17mmHg, and diastolic blood pressure by up to 10mmHg in a recent metaanalysis of 12 clinical trials.(27) Finally, the nutrients N-acetylcyteine and l-arginine, when taken together, have been shown to restore nitric oxide levels and reduce reactive oxygen species.(28)
1. Egan BM, et al. US trends in prevalence, awareness, treatment, and control of hypertension, 1988-2008. JAMA. 2010 May 26;303(20):2043-50.
2. Egan BM, et al. Prehypertension: an opportunity for a new public health paradigm. Cardiol Clin. 2010 Nov;28(4):561-9.
3. Singh M, et al. Pathogenesis and clinical physiology of hypertension. Cardiol Clin. 2010 Nov;28(4):545-59.
4. Cruz-González I, et al. Association between -T786C NOS3 polymorphism and resistant hypertension: a prospective cohort study. BMC Cardiovasc Disord. 2009 Aug 4;9:35.
5. Souza-Costa DC, et al. eNOS haplotype associated with hypertension in obese children and adolescents. Int J Obes (Lond). 2011 Mar;35(3):387-92.
6. Zago AS, et al. Effects of aerobic exercise on the blood pressure, oxidative stress and eNOS gene polymorphism in pre-hypertensive older people. Eur J Appl Physiol. 2010 Nov;110(4):825-32
7. Sponton CH, et al. Women with TT genotype for eNOS gene are more responsive in lowering blood pressure in response to exercise. Eur J Cardiovasc Prev Rehabil. 2010 Dec;17(6):676-81.
8. Navas-Acien A, et al. Lead exposure and cardiovascular disease—a systematic review. Environ Health Perspect. 2007 Mar;115(3):472-82.
9. Weisskopf MG, et al. A prospective study of bone lead concentration and death from all causes, cardiovascular diseases, and cancer in the Department of Veterans Affairs Normative Aging Study. Circulation. 2009 Sep 22;120(12):1056-64.
10. Zhang WZ, Venardos K, Chin-Dusting J, et al. Adverse effects of cigarette smoke on NO bioavailability: role of arginine metabolism and oxidative stress. Hypertension. 2006 Aug;48(2):278-85.
11. Brown IJ, et al. Sugar-sweetened beverage, sugar intake of individuals, and their blood pressure: international study of macro/micronutrients and blood pressure. Hypertension. 2011 Apr;57(4):695-701
12. Nakagawa T, et al. A causal role for uric acid in fructose-induced metabolic syndrome. Am J Physiol Renal. 2006;290:F625–F631
13. Brymora A, et al. Low-fructose diet lowers blood pressure and inflammation in patients with chronic kidney disease. Nephrol Dial Transplant. 2011 May 25. [Epub ahead of print]
14. Kesteloot Dagger H, et al. Relation of urinary calcium and magnesium excretion to blood pressure: the international study of macro- and micro-nutrients and blood pressure and the international cooperative study on salt, other factors, and blood pressure. Am J Epidemiol. 2011 Jul 1;174(1):44-51.
15. Martins D, et al. Prevalence of cardiovascular risk factors and the serum levels of 25-hydroxyvitamin D in the United States: data from the Third National Health and Nutrition Examination Survey. Arch Intern Med. 2007 Jun 11;167(11):1159-65.
16. Kanbay M, et al. Mechanisms and consequences of salt sensitivity and dietary salt intake. Curr Opin Nephrol Hypertens. 2011 Jan;20(1):37-43.
17. Harrison DG, et al. Inflammation, immunity, and hypertension. Hypertension. 2011 Feb;57(2):132-40.
18. Adrogué HJ, Madias NE. Sodium and potassium in the pathogenesis of hypertension. N Eng J Med. 2007 May 10;356(19):1966-78.
19. Blumenthal JA, et al. Effects of the DASH diet alone and in combination with exercise and weight loss on blood pressure and cardiovascular biomarkers in men and women with high blood pressure: the ENCORE study. Arch Intern Med. 2010 Jan 25;170(2):126-35.
20. Dengo AL, Dennis EA, Orr JS, et al. Arterial destiffening with weight loss in overweight and obese middle-aged and older adults. Hypertension. 2010 Apr;55(4):855-61. Epub 2010 Mar 8.
21. Azadbakht L, et al. The Dietary Approaches to Stop Hypertension Eating Plan Affects CReactive Protein, Coagulation Abnormalities, and Hepatic Function Tests among Type 2 Diabetic Patients. J Nutr. 2011 Jun;141(6):1083-8.
22. Whelton SP, Hyre AD, Pedersen B et al. Effect of dietary fiber intake on blood pressure: a meta-analysis of randomized, controlled clinical trials. J Hypertens. 2005 Mar;23(3):475-81.
23. Reinhart KM, Coleman CI, Teevan C, et al. Effects of garlic on blood pressure in patients with and without systolic hypertension: a meta-analysis. Ann Pharmacother. 2008 Dec;42(12):1766-71.
24. Rodrigo R, Prat H, Passalacqua W, et al. Decrease in oxidative stress through supplementation of vitamins C and E is associated with a reduction in blood pressure in patients with essential hypertension. Clin Sci (Lond). 2008 May;114(10):625-34.
25. Belcaro G, Cesarone MR, Ricci A, et al. Control of edema in hypertensive subjects treated with calcium antagonist (nifedipine) or angiotensin-converting enzyme inhibitors with Pycnogenol. Clin Appl Thromb Hemost. 2006 Oct;12(4):440-4.
26. Cesarone MR, Belcaro G, Rohdewald P, et al. Improvement of diabetic microangiopathy with pycnogenol: A prospective, controlled study. Angiology. 2006 Aug-Sep;57(4):431-6.
27. Rosenfeldt FL, Haas SJ, Krum H, etal. Coenzyme Q10 in the treatment of hypertension: a meta-analysis of the clinical trials. J Hum Hypertens. 2007 Apr;21(4):297-306.
28. Martina V, Masha A, Gigliardi VR, et al. Long-term N-acetylcysteine and Larginine administration reduces endothelial activation and systolic blood pressure in hypertensive patients with type 2 diabetes. Diabetes Care. 2008 May;31(5):940-4.