~Hypertention, Part 5 - Nutritional Therapy
Hypertension can be controlled through use of natural supplements. Mainstream practitioners believe that only prescription medications are proven to reduce hypertension. Yet, supplements are scientifically proven to help normalize blood pressure (Espeland et al. 1999).
- Coenzyme Q10
- Vitamin C
- Essential Fatty Acids
- Vitamin E
- Calcium, Magnesium, and Potassium
There are nutrients that may reduce or eliminate the need for antihypertensive medications. However, nutrients may not work immediately to lower blood pressure the way drugs do, so it is important to continue nutritional-based blood pressure-lowering therapy over a period of 4 to 12 weeks. Physician cooperation is always crucial if you are to reduce your intake of antihypertensive drugs safely. Routine blood pressure monitoring is mandatory to determine if nutritional or integrated medical regimens are controlling or reducing your blood pressure. The following sections detail many nutrients important in preventing the development of hypertension, and may ultimately delay the occurrence or onset of hypertensive vascular disease and its subsequent and related cardiovascular diseases.
CoQ10 significantly improved diastolic and systolic pressure in essential hypertension. More than half of patients receiving 225 mg/day were able to terminate use of from one and three antihypertensive medications (Langsjoen et al. 1994 b ). A number of studies confirm that CoQ10 is an important supplement for both hypertension and Parkinson's disease (Digiesi et al. 1990, 1992; Langsjoen et al. 1994 a,b ; Singh, 1998, 1999).
It is effective in combating isolated systolic hypertension (Burke et al. 2001). Patients given 60 mg/day for 12 weeks reduced their systolic blood pressure by 18 mmHg, indicating "CoQ10 may be safely offered to hypertensive patients as an alternative treatment option." CoQ10 reduces blood pressure, possibly by mitigating the underlying disease causing hypertension. Studies on patients with hypertension and coronary artery disease receiving 60 mg of CoQ10 twice per day revealed "…that coenzyme Q10 decreased blood pressure possibly by decreasing oxidative stress and insulin-response in patients receiving antihypertensive drugs… Patients treated with an average of 200 mg/day of CoQ10 showed improvement in symptoms of fatigue and dyspnea with no side effects noted" (Singh et al. 1999).
Improved diastolic function and left ventricular wall thickness after coenzyme Q10 was noted in hypertensive heart disease (Langsjoen et al. 1997). CoQ10 was tested in 109 cardiology patients presenting with hypertension for at least 1 year. After 225 mg/day orally of CoQ10 was administered with antihypertensive medication, blood levels greater than 2.0 mcg/mL (3.02 mcg/mL) were obtained. Dosage was adjusted according to clinical response and CoQ10 levels. "A definite and gradual improvement in functional status was observed with the concomitant need to gradually decrease antihypertensive drug therapy within the first one to six months."
Over half the patients were removed from 1-3 of their regular antihypertensive medications 4.4 months after starting CoQ10. Improvement was seen in left ventricular wall thickness and diastolic function. Patients with essential arterial hypertension (n = 26) received CoQ10 (50 mg twice-daily) for 10 weeks. Systolic blood pressure decreased from 164 to 147 mmHg, diastolic blood pressure decreased from 98 to 86 mmHg, plasma CoQ10 levels increased from 0.64 ± 0.10 mcg/mL to 1.6 ± 0.3 mcg/mL, serum cholesterol decreased from 223 mg/dL to 213 mg/dL (p < 0.005), and HDL cholesterol increased from 41.1 ± 1.5 mg/dL to 43.1 ± 1.5 mg/dL (p < 0.01) (Langsjoen et al. 1997).
Ascorbic acid (Vitamin C) is useful in treating age-related hypertension. There is a significant link between vitamin C and hypertension (Taddei et al. 1998). People with low levels of vitamin C had higher levels of hypertension (Salonen et al. 1988; Enstrom et al. 1992). Vitamin C at doses of 500 mg per day has caused significant drops in blood pressure in men and women with hypertension (Duffy et al. 1999). Vitamin C may control hypertension through antioxidant actions or modulate the activity of nitric oxide, an important vasodilating substance formed from arginine.
Essential Fatty Acids (Fish Oils: GLA, DHA and EPA)
Fish oil supplements are nutraceuticals endorsed by the American Heart Association (AHA). In 2002, the AHA formally declared that people with heart disease should consume approximately 1 gram of the active ingredients in fish oil (i.e., the omega-3 fatty acids, EPA and DHA). People that do not consume fresh fish every day need fish oil supplements. Besides preventing heart disease, fish oil effectively fights hypertension. Fish oil supplements decrease triglycerides, LDL-cholesterol, and decrease blood pressure (Toft et al. 1995). For greater discussion of this topic see the section on Vascular Endothelial and Smooth Muscle Cell Function.
Conjugated linoleic acid (CLA) promoted fat loss, and reduced levels of cholesterol, triglycerides, and arachidonic acid (a precursor to pro-inflammatory leukotrienes) (Liu 1998). At dietary levels as low as 0.1% CLA inhibited atherogenesis; at dietary levels of 1%, CLA caused (30%) regression of established atherosclerosis. This is the first report of substantial regression of atherosclerosis caused by diet alone (Kritchevsky et al. 2000). Essential fatty acids have antispasmodic activity; are hypotensive; reduce fibrinogen, C-reactive protein (CRP), cholesterol, and homocysteine; and improve insulin sensitivity.
Low fat diets contribute to deficiencies and imbalances of the essential fatty acids (linoleic acid and alpha-linolenic acid). Americans have an omega-6/omega-3 ratio of about 20-30/1. A healthier ratio is 2/1 (Simopoulos, 1999). Diabetes, hypercholesterolemia, nutritional deficiencies (zinc, vitamin B6, and magnesium), obesity, infection, stress, aging, alcohol, smoking, and trans -fatty acid intake are factors inhibiting delta-6-desaturase activity (Pizzorno, 2001), causing further imbalances. Individuals with poor delta-6-desaturase (10-20% of the population) should supplement their diet with fatty acids made by this enzyme, thus bypassing any deficiencies caused by low enzyme activity. Omega-3 fatty acids reduced the incidence of fatal heart attacks, even in patients with established coronary heart disease (Bucher et al. 2002; Hu et al. 2002; Iso et al. 2001). Fish oil lowered homocysteine levels and decreased fibrinogen (a major risk factor in pathological thrombosis) without adverse effects (Saynor et al. 1992).
CRP levels can be minimized by fish oils. High CRP correlated with low levels of DHA. DHA has anti-inflammatory effects that result in lower CRP levels, and fish consumption may decrease the risk of coronary artery disease (Madsen et al. 2001). With a fatty acid imbalance, the inflammatory response to stress appears to be amplified (Maes et al. 2000). Studies have shown that GLA, an omega-6 fatty acid, lowered blood pressure in animal studies. "GLA is a very potent blood-pressure-reducing nutrient" (Engler et al. 1998). Hydrogenated fats (trans -fatty acids) reduced activity in the omega-6 and omega-3 biosynthetic cascades by inhibiting the enzymes delta-6-desaturase and delta-5-desaturase (Mensink et al. 1990, 1992; Zock et al. 1996). Omega-3 fatty acids help maintain flexible cell membranes (Igal et al. 1997).
Note: If your gastrointestinal tract can tolerate high daily doses of fish oil, then you may lower your blood pressure and gain other benefits. If not, consider starting with half the normal dosage and then slowly increase it to the dose recommended.
Vitamin E supplements can fight hypertension through actions as antioxidants that decrease free radicals. These highly reactive compounds are linked to a variety of disease states, including hypertension. People with hypertension often have low levels of vitamin E (Kumar and Das 1993). Animal studies have shown that vitamin E (gamma-tocotrienol) protects animals against age-related hypertension (New e a z et al., 1999).
Garlic acts as a hypotensive and vasodilator. Researchers have isolated antihypertensive factors in garlic. An analysis of published and unpublished randomized, controlled trials (415 patients) showed that 600-900 mg a day of dried garlic powder may be of clinical value in subjects with mild hypertension (Silagy et al. 1994). Other researchers have noted a 5.5% decrease in systolic blood pressure and a modest reduction in diastolic blood pressure in response to aged garlic extract (Steiner 1996). Supplementation with aged garlic significantly reduced epinephrine, a vasoconstricting hormone released from the adrenal medulla (Steiner et al. 1998).
Garlic moderately inhibited (both in vivo and in vitro ) the activity of ACE, an enzyme that increases blood pressure by catalyzing the conversion of renin and angiotensin I to angiotensin II. Angiotensin II constricts blood vessels, conserves water and sodium, and results in hypertension (Rietz et al. 1993). Garlic increases the activity of nitric oxide synthase, an enzyme essential for nitric oxide synthesis (Morihara et al. 2002). Nitric oxide is a primary physiological vasodilator that reduces blood pressure and antispasmodic activity.
L-Arginine dilates blood vessels, reduces blood pressure, mimics the activity of nitroglycerine, and produces nitric oxide (NO). L-Arginine contributes to normal blood vessel function. Congestive heart failure often reveals blood vessels that fail to dilate in response to certain drugs, a sign that the inner blood vessel wall, or endothelium, is compromised. L-Arginine produced a fourfold increase in blood vessel dilation (Hambrecht et al. 2000). Doses of 5.6-12.6 grams of arginine increased blood flow to the extremities by 29% (Rector et al. 1996). The effectiveness of L-arginine relates to its ability to directly create NO, a vasodilator produced in endothelial cells by the enzyme nitric oxide synthase (Brunini et al. 2002). Nitric oxide counteracts the vasoconstrictive effects of adrenaline and maintains vascular elasticity. L-Arginine increases nitric oxide, but hypertension, hyperhomocysteinemia, diabetes, and smoking decrease it.
Arginine is frequently used as a treatment for hypertension. A defect in nitric oxide production is a possible mechanism of hypertensive vascular disease (Campese et al. 1997). Some cardiologists recommend L-arginine over nitroglycerine, since the two substances appear to replicate a similar vascular function, that is, the ability to relax smooth muscles and dilate blood vessels.
Aspirin reduced C-reactive protein (CRP), platelet aggregation, and cardiac inflammation. Aspirin therapy prevents a third of myocardial infarctions occurring in apparently healthy individuals (Hebert et al. 2000) and reduces all-cause mortality (Gum et al. 2001). Aspirin exerts some of its cardiovascular protection by inhibiting the enzyme cyclooxygenase, a trigger in the inflammatory process (Newmark et al. 2000). One molecule of aspirin will inactivate cyclooxygenase for 4-6 hours. After this, the body synthesizes more, active enzyme. Aspirin is more important in patients with compromised coagulation systems or in cases where the endothelial cells have been damaged by chronic hypertension. This predisposes the cell to dysfunctional regulatory responses of thromboxanes and prostaglandins.
Calcium, Magnesium, and Potassium
The DASH study (Dietary Approaches to Stop Hypertension) clearly indicates a strong dietary role for adequate potassium, calcium, and magnesium, as derived from natural diets, as beneficial to cardiovascular diseases (Appel et al. 1997). Oral potassium supplements lower blood pressure (Whelton et al. 1997). The mechanism of action of potassium may include natriuresis, reduced renin release, antagonism of the pressor effects of angiotensin II, direct vasodilation, enhanced endothelial-dependent vasodilation, decreased vasoconstrictive thromboxanes, and increased vasodilatory kallidin (Morris and Sebastian 1995).
The ability of magnesium to lower blood pressure might be greater in hypertensives which, perhaps due to diuretic use, often have low plasma levels of magnesium (Kotchen and Kotchen 1999). Magnesium stimulates human endothelial cells to produce prostaglandin I2, a vasodilator (Nadler and Rude 1995). Magnesium deficiency is associated with resistance to insulin-stimulated glucose uptake and enhanced contractility of the vasculature (Kotchen and Kotchen 1999).
Studies have shown that lower calcium intake is associated with higher blood pressures (Brown and Hu 2001; Williams 2001). It is well-known that calcium is critically important in all muscle contractions, including the smooth muscle of the vasculature. Inadequate mineral intake appears to have a correlation with hypertension. Supplemental dietary calcium lowers blood pressure, whereas restricted-calcium diets tend to elevate blood pressure.
A unifying theory showing how calcium reduces blood pressure is not available. A membrane stabilizing effect, natriuresis (the excretion of sodium), and the ability of calcium to control regulatory processes are hypothetical mechanisms (Luft et al. 1990). Epidemiologic findings suggest that the protective effects of calcium are evident when daily intake is above 700-800 mg per day. Lesser amounts increase the risk of hypertension. Other variants, such as an increased metabolic need for calcium, altered absorption rates, and genetics may modify this requirement for calcium (McCarron et al. 1991). Calcium is not a universally accepted treatment for hypertension (Meese et al. 1987). Calcium has a natriuretic effect. Yet salt-loading increases calcium excretion, parathyroid hormone, and 1,25-hydroxyvitamin D (Kotchen and Kotchen 1999).
Continued . . .
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