SELENIUM & HEART DISEASE
Cardiovascular disease, stroke, hypertension (high blood pressure), type-2 diabetes and “metabolic syndrome” have been virtual epidemics in the developed, Western countries for a long time, and are essentially lifestyle diseases caused largely by unsuitable diet and lack of exercise. Atherosclerosis is the underlying process in development of cardiovascular disease (also known as ischaemic heart disease). Atherosclerotic arterial disease consists of several interrelated mechanisms that combine to produce the overall effect of the disease. These include thickening of the arterial wall, abnormal arterial contraction, and tendency towards platelet aggregation and formation of thromboses (blood clots). Fibrous plaque formation is related to oxidation of unsaturated fatty acids in low density lipoprotein (LDL), caused by free radicals, and there is heavy involvement of macrophages. Plaque development begins with damage to the arterial endothelium, which is likely to involve lipid peroxidation (Reilly, 1996; Ball, 1997a).
The major risk factors for heart disease are increasing age, smoking, unemployment, obesity (especially central, “spare tyre” obesity), lack of exercise, diabetes or glucose intolerance, elevated clotting factors (factor VII and fibrinogen), male sex, hypertension, family history of heart disease, hyperlipidaemia (high LDL cholesterol, low high density lipoprotein (HDL) cholesterol), and high Lp(a) (Ball, 1997a).
Because the key antioxidant selenoenzyme glutathione peroxidase (GPx) has a major role in the prevention of oxidative stress, it may also be an important antiatherogenic enzyme. A major study in Germany (the AtheroGene Study), where Se intake is relatively low, found that low GPx1 activity in red blood cells was the strongest predictor of cardiovascular events, even stronger than the well-known risk factors of high triglycerides, LDL cholesterol, C-reactive protein, homocysteine and creatinine, and low levels of HDL cholesterol and superoxide dismutase. And glutathione peroxidase activity was lower, on average, in men and in smokers (Blankenberg et al, 2003). The higher response to Se supplementation of male smokers than any other sub-group for reduction of cancer risk is discussed elsewhere. [link to Anti Cancer page]
Elevated levels of plasma homocysteine are a well-known risk factor for heart disease, and even mild to moderate increases in total plasma homocysteine are likely to be causally involved in the development of atherosclerotic disease (Nygard et al, 1997). Further analysis of results from the AtheroGene study revealed that plasma homocysteine levels and red blood cell GPx activity are complementary in identifying individuals at high risk of cardiovascular events. Those with high homocysteine and low GPx activity are at highest risk. The authors concluded that “Joint determination of both biomarkers provides substantial information on top of classic risk factors in cardiovascular risk assessment.” (Schnabel et al, 2005). Further evidence for Se/GPx/homocysteine interaction is provided by a Spanish study that found a significant inverse association between serum and plasma homocysteine. (Gonzalez et al, 2004). Folate is generally considered to be the strongest nutritional factor for reducing homocysteine, but this study showed that serum Se had a greater effect.
Other Se deficiency – cardiomyopathy manifestations can be seen in lambs raised on deficient pastures, which may develop white muscle disease, which involves calcification of the heart. In parts of China and eastern Siberia an overt Se-deficiency condition, Keshan disease occurs. It involves impairment of cardiac function, cardiac enlargement and arrhythmia. The disease’s aetiology is likely to be complex, involving Se and vitamin E deficiencies, and the presence of the Coxsackie B virus (Reilly, 1996).
SELENIUM & DIABETES
As type-II (non-insulin-dependent) diabetes is associated with an increased risk of heart disease, a section on this condition, which is currently so prevalent in people aged over 45 years in developed countries like Australia as to constitute an epidemic, is included here.
The onset of type-II diabetes is gradual and many cases are recognised by routine or chance tests of urine or blood glucose. The prevalence is particularly high in Aboriginals and Polynesians. The early stages involve altered pancreatic secretion of insulin with a delayed response to glucose and then resistance (insensitivity) to its action in muscle tissue (Ball, 1997b).
Various laboratory and animal studies have suggested that Se has an insulin-mimetic role (i.e. it behaves like insulin in certain respects) and can reduce glucose resistance (Mueller et al, 2003). One of the main fatal consequences of type-II diabetes is cardiomyopathy. Se has been found to alleviate diabetes-related pathological changes to the heart (Ayaz et al, 2002). One of the mechanisms is by improving the activity of antioxidant enzymes in diabetic heart tissue (Ulusu & Turan, 2005), and another is inhibition of nuclear factor-kappa B (NF-kappaB), which has been linked to development of vascular disease (Faure et al, 2004).
Type-II diabetes is best controlled by weight reduction, a structured exercise program, consumption of a balanced diet containing foods with a low glycaemic index, plenty of fibre, and cooking with olive oil. Supplementation with the micronutrients chromium and selenium is also recommended.
Definitions
Cardiomyopathy: deterioration of the cardiac muscle of the heart wall.
C-reactive protein: an acute-phase protein synthesised in the liver, which is present in the blood and provides a marker for inflammation and elevated cardiovascular disease risk.
Creatinine: a breakdown product of creatine phosphate, an important muscle constituent. It is used as a marker of kidney function.
Macrophage: a large phagocytic cell occurring in the blood, lymph and connective tissue.
Lp(a): is formed from LDL and apolipoprotein(a), and high levels are associated with increased risk of heart disease. Plasma Lp(a) level is largely genetically determined.
Homocysteine: a metabolic product of methyl-group donation by the amino acid methionine. It is a risk factor for cardiovascular disease.
Glycaemic index: a classification of foods based on their blood glucose response relative to glucose (100). Low GI (<50) foods include rice bran, milk, peanuts, soybeans, apples. High GI (>70) foods include parsnips, potatoes, rice bubbles, broad beans.
References
Ayaz M, Can B, Ozdemir S, Turan B 2002. Protective effect of selenium treatment on diabetes-induced myocardial structural alterations. Biol Trace Elem Res 89(3): 215-226.
Ball M 1997a. Atherosclerotic vascular disease and hypertension. In Wahlqvist ML (ed) Food and nutrition. Sydney: Allen & Unwin, pp. 373-383.
Ball M 1997b. Diabetes. In Wahlqvist ML (ed) Food and nutrition. Sydney: Allen & Unwin, pp. 384-393.
Blankenberg S, Rupprecht HJ, Bickel C, Torzewski M, Hafner G, Tiret L, Smieja M, Cambien F, Meyer J, Lackner KJ 2003. Glutathione peroxidase 1 activity and cardiovascular events in patients with coronary artery disease. N Engl J Med 349: 1605-1613.
Faure P, Ramon O, Favier A, Halimi S 2004. Selenium supplementation decreases nuclear factor-kappa B activity in peripheral blood mononuclear cells from type 2 diabetic patients. Eur J Clin Invest 34(7): 475-481.
Gonzalez S, Huerta JM, Alvarez-Uria J, Fernandez S, Patterson AM, Lasheras C 2004. Serum selenium is associated with plasma homocysteine concentrations in elderly humans. J Nutr 134: 1736-1740.
Mueller AS, Pallauf J, Rafael J 2003. The chemical form of selenium affects insulinomimetic properties of the trace element: investigations in type II diabetic dbdb mice. J Nutr Biochem 14(11): 637-647.
Nygard O, Nordrehaug JE, Refsum H, Ueland PM, Farstad M, Vollset SE 1997. Plasma homocysteine levels and mortality in patients with coronary artery disease. N Engl J Med 337: 230-236.
Reilly C 1996. Selenium in food and health. London: Blackie.
Schnabel R, Lackner KJ, Rupprecht HJ, Espinola-Klein C, Torzewski M, Lubos E, Bickel C, Cambien F, Tiret L, Munzel T, Blankenberg S 2005. Glutathione peroxidase-1 and homocysteine for cardiovascular risk prediction. J Am Coll Cardiol 45: 1631-1637.
Ulusu NN, Turan B 2005. Beneficial effects of selenium on some enzymes of diabetic rat heart. Biol Trace Elem Res 103(3): 207-216.
Laucke Flour Mills Pty Ltd
PO Box 200 Strathalbyn SA 5255
E-mail: bread@laucke.com.au
Phone: (08) 8536 5555
Fax: (08) 8536 3636
[terms & conditions]
[privacy statement]