Nature's Sunshine Products NSP Forum Index Nature's Sunshine Products NSP
For customer and distributor discussions of Nature's Sunshine Products. Not an official site of NSP.
 
 FAQFAQ   SearchSearch   MemberlistMemberlist   UsergroupsUsergroups   RegisterRegister 
 ProfileProfile   Log in to check your private messagesLog in to check your private messages   Log inLog in 

Heart - Cardiovascular Micro-nutrients

 
This forum is locked: you cannot post, reply to, or edit topics.   This topic is locked: you cannot edit posts or make replies.    Nature's Sunshine Products NSP Forum Index -> Forum Archive
View previous topic :: View next topic  
Author Message
CombinedNSP
Site Admin


Joined: 13 Dec 2006
Posts: 1406
Location: Cleveland, OH

PostPosted: Dec Fri 15, 2006 6:32 pm    Post subject: Heart - Cardiovascular Micro-nutrients Reply with quote

Heart - Cardiovascular Micro-nutrients

This is a rather long article but since it is from a medical website and some members of the forum can't access internet, I thought it worthwhile to reprint the entire article.

Cardiovascular Disease and Micronutrient Therapies
Judith Anderson, ARNP, PhD, Cathy R. Kessenich, ARNP, DSN [Mdscape Nursing 1(2), 2001. 2001 Medscape, Inc.]

Cardiovascular disease is a problem of epidemic proportions. Its prevalence, morbidity, and mortality have encouraged millions of Americans to seek prevention and treatment by ingesting micronutrients and antioxidants. Patients actively seek information about these complementary therapies in health food stores, via mail order catalogs, and through the Internet. Healthcare providers must acquire knowledge about these substances so they can impart reliable information to their patients. This article reviews the current scientific evidence on the use of garlic, coenzyme Q-10, fish oils, vitamins (B6, B12, C, and E), and folic acid in the treatment and prevention of coronary artery disease.

INTRODUCTION
A great deal of recent biomedical and nursing research has focused on the modification of known cardiovascular risk factors. Despite this attention, coronary artery disease (CAD) continues to be a chief cause of death in the United States. It has been estimated that more than half of the deaths due to cardiovascular disease are related to atherosclerotic pathology.[1] In the last several decades, great strides have been made in the diagnosis and treatment of CAD. New categories of pharmacologic agents have been developed, and intervention strategies to mitigate the progression of CAD have evolved. While these advances are promising, they have not substantially reduced the morbidity and mortality associated with CAD. Improved prevention and treatment strategies for CAD are public health issues of critical importance to all.

Patients and providers are actively seeking alternative methods, such as the use of micronutrients and antioxidants, to prevent and treat CAD. Micronutrients are defined as essential nutrients that are needed for survival, but only in small amounts. The most common micronutrients are vitamins, which are vital organic dietary substances essential in very small amounts for particular metabolic functions or for prevention of disease due to deficiency. In treating CAD, the most important vitamins are C, E, B6, B12, and Folic Acid (the vitamin supplement for folate). Antioxidants are substances that interfere with the oxidation of low-density lipoprotein (LDL) and thus prevent formation of foam cells, which are pathogenic in atherosclerosis development. The antioxidant vitamins are C and E. Other alternative therapies for lowering cholesterol levels include Garlic, Fish Oils, and CoEnzyme Q-10.

The role of many micronutrients and antioxidants is undetermined. Even so, many CAD patients use these substances in large quantities. A study by Eisenberg and colleagues[2] published in 1998 estimated that Americans made 629 million visits annually to practitioners of alternative medicine a number that exceeds the total number of visits to primary care providers. Primary care providers must be knowledgeable about the scientific evidence that supports or refutes the use of complementary therapies. The purpose of this paper is to review the current evidence on the use of Garlic, Vitamin C, Vitamin E, Coenzyme Q-10, Fish Oils, Vitamin B6, Vitamin B12, and Folate in the treatment/prevention of CAD.

GARLIC (Allium sativum) has been used since medieval times as a food, a magical substance to cast off evil spirits, and a miracle cure for disease. It may be taken in the form of fresh bulbs, bulk powder, granules, or oils. The proposed action of garlic is to lower blood pressure and lower LDL and triglycerides by several percentage points. Additionally, some reports indicate that garlic contains antiplatelet properties.[3] Many of the proposed beneficial effects of garlic are unsubstantiated. However, there are several meta-analyses that have supported the efficacy of garlic in lowering lipids in the blood[4] and reducing blood pressure.[5] The effect on blood pressure has mixed reviews, with a number of studies demonstrating no effect. Several small studies have found garlic to be effective in reducing atherosclerotic plaques[6] and inhibiting platelet aggregation.[7]

Research shows that garlic might have some effect on the prevention and treatment of CAD. No harmful effects have been discovered, although it is noted that several types of garlic preparations cause malodorous breath and body odor. Therefore, patients who use garlic therapy are probably choosing a safe therapy that complements other lifestyle modifications. The proper use of garlic may deter even the most ardent supporter, however. According to Roberts,[3] the best way to attain the positive effects of garlic is to eat 5-20 raw cloves per day. This therapy may cause gastrointestinal difficulty, including flatulence and esophageal and abdominal pain. To avoid these side effects, manufacturers have developed extracts, powders, and tablets. Unfortunately, many of these preparations contain little or no active garlic ingredient and are no better than placebo for the prevention and treatment of CAD. [Editorial Note: This is the reason NSP does NOT remove anything. The odor is avoided with High Potency Garlic by making it not release until it reaches the intestines and being coated by Chlorophyll]

VITAMIN C (ascorbic acid) is an essential micronutrient that is required for normal metabolic functioning. Vitamin C must be obtained through the diet [or supplements], because humans are unable to reproduce it via biosynthesis. The vitamin is plentiful in most diets, particularly those with adequate citrus fruits and vegetables. The role of vitamin C as an antioxidant for the prevention of cardiovascular morbidity and mortality has been demonstrated in several large clinical and epidemiologic trials. Data recently published from The Third National Health and Nutrition Examination Survey (NHANES III) study showed that the risk of angina was decreased with higher intakes of vitamin C, particularly among men and women who drank alcohol.[9] Gokce and colleagues[10] recently demonstrated that long-term therapy with vitamin C provided a sustained beneficial effect on endothelial function and ultimately protected patients with CAD. Earlier observational studies have demonstrated a relationship between vitamin C and CAD[11-13] and have suggested that the use of vitamin C may decrease the risk of stroke and death from CAD. The majority of research conducted with vitamin C has investigated daily doses that are much higher than the current recommended levels. These amounts should be safe and effective for most individuals. Historically, there has been some concern about the occurrence of kidney stones in individuals ingesting high doses of vitamin C. According to Goodwin and Tangum,[15] this commonly held perception is based on speculation and is not supported by scientific evidence.

VITAMIN E (alpha-tocopherol) exists as at least 8 naturally occurring compounds. Alpha-tocopherol is the most active compound. Vegetables, seed oils, eggs, and liver are substantial sources of this nutrient.[16] However, it is postulated that the amount of vitamin E needed for maximal reduction of cardiovascular risk (at least 100 IU per day) cannot be obtained through food intake alone.[14]

The beneficial effects of vitamin E supplementation have been demonstrated in the Nurses' Health Study.[17] This large, prospective study (with up to 8 years' follow-up) demonstrated that women given vitamin E supplements (median dose of 208 IU per day) had a lower risk of CAD. This same observation has been demonstrated in male cohorts.[18] Large, double-blind, placebo-controlled trials such as the Cambridge Heart Antioxidant Study (CHAOS)[19] have also shown that vitamin E supplementation is a safe and economical mechanism for reducing the risk of CAD.

Vitamin E supplements (200 IU per day, 400 IU per day for smokers) appear to be a safe and effective complementary therapy.[14] There has been some concern about the potential of vitamin E supplementation to promote hemorrhage, particularly in patients on warfarin or aspirin therapy. While these issues should be considered in the overall plan of care, the overwhelming majority of patients should benefit from the addition of vitamin E to their preventive regimen.[22]

COENZYME Q-10 -- (ubiquinone) is a nutrient that every cell in the body must have in order to produce energy. It is the coenzyme for at least 3 mitochondrial enzymes of the oxidative phosphorylation pathway which are essential for the production of adenosine triphosphate (ATP). Coenzyme Q-10 also has antioxidant and membrane-stabilizing properties.[23] Because the nutrient is essential to the optimal function of all cell types, it can be beneficial in a wide variety of diseases. Since it was first isolated in 1957, coenzyme Q-10 has demonstrated beneficial uses in the treatment of heart conditions, hypertension, periodontal disease, immune disorders, cancer, and other diseases.[23] As a natural substance, the US Food and Drug Administration does not regulate Coenzyme Q- 10, and it is still not widely prescribed in the United States. Therefore, much of the research has been completed outside the United States. Early studies involving patients with New York Heart Association class III or IV heart failure demonstrated that treatment with coenzyme Q-10 reduced hospitalizations and serious complications such as pulmonary edema and ventricular arrhythmia,[24] improved clinical signs and symptoms,[25] and improved quality of life and exercise capacity.[26]

More recent studies in patients with congestive heart failure have produced mixed results. In one study, treatment for 3 months with coenzyme Q-10 failed to improve resting left ventricular function or quality of life.[27] Conversely, in a smaller study, patients who received coenzyme Q-10 daily for 5 years had an 87% increase in mean ejection fraction after only 6 months.[28] This improvement in left ventricular function was supported in several other studies.[29] Aside from its use in heart failure, coenzyme Q-10 has been used after myocardial infarction and has been found to provide rapid protective effects from arrhythmia and left ventricular dysfunction if administered within 3 days of the onset of symptoms.[30] Additionally, coenzyme Q-10 has been found to decrease lipoprotein (a) in patients with acute coronary disease[31] and to decrease blood pressure in patients with known hypertension, possibly by decreasing oxidative stress.

Epidemiologic evidence suggests that coenzyme Q-10 may make vitamin E an even more efficient antioxidant for LDL.[28] There is evidence that several current therapies for CAD, including lipid-lowering agents such as lovastatin and beta-blockers, lower coenzyme Q-10 levels in tissues, thus increasing the risk for heart disease. It is possible that patients taking lovastatin and beta-blockers should be supplemented with coenzyme Q-10.[23] The dosage reported in experiments ranged from 50-200 mg daily, with no significant adverse effects reported after 6 years of therapy at 100 mg daily.[31] Positive clinical and hemodynamic effects of oral coenzyme Q-10 have been observed in numerous clinical trials, especially in patients with chronic heart failure. Despite its usefulness in the symptomatic treatment of heart failure, it has not been shown to reduce mortality. These clinical findings need further investigation before use of coenzyme Q-10 can be recommended. There have been no studies examining coenzyme Q-10 supplementation for general health, and the effects of prophylactic use are not known.

FISH OILS Diets high in saturated fat are linked to high blood cholesterol levels, a risk factor for cardiovascular disease. It has been postulated that lowering saturated fat intake by just 3% would prevent about 100,000 new cases of CAD by the year 2005.[32] When dietary saturated fats are decreased, they can be partially replaced with the marine n-3 fatty acids. It is known that native fishing populations have low rates of CAD, possibly associated with their high intake of fatty acids from fish. The fatty acids important in fish oil are eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids. The n-3 fatty acids improve endothelial function by promoting the synthesis of nitric oxide.[32] EPA has several antithrombotic actions, particularly in inhibiting the synthesis of thromboxane A2, the prostaglandin that causes platelet aggregation and vasoconstriction. In addition, fish oil retards the growth of atherosclerotic plaque by inhibiting both cellular growth factors and the migration of monocytes.[32] Fish oil may decrease cardiac afterload by an antivasopressor action and by reducing blood viscosity.[33]

Several researchers have examined the effect of fish oil on cholesterol levels. Fish oil supplementation has been shown to significantly decrease triglyceride concentration[34] and very-low-density lipoprotein (VLDL) levels.[35] However, fish oil supplementation alone has had no effect on total plasma cholesterol, and, in fact, has been shown to increase LDL concentrations. [NSP has this in Omega 3 EPA]
Studies have examined the use of fish oil supplementation alone, in combination with a fish diet, and in combination with garlic. Adding garlic to a fish oil regimen reversed the moderate increase in LDL caused by fish oil, and the garlic-fish oil combination significantly decreased both total cholesterol and LDL.[34] Coadministration of garlic with fish oil seems to be well tolerated and appears to have a beneficial effect on lipid and lipoprotein concentration by providing a combined lowering of total cholesterol, LDL, and triglycerides. At the present time, there is not enough evidence to recommend the routine use of fish oil supplementation. However, for the hypercholesterolemic patient, the combination of garlic and fish oil may be of benefit.

FOLATE is a crucial cofactor in DNA synthesis, contributing a carbon unit to oxidation at various levels of purine synthesis. During purine synthesis the amino acid methionine is produced from homocysteine. Lack of folate leads to impaired DNA synthesis and results in decreased production of methionine and accumulation of homocysteine. Elevated levels of homocysteine may induce endothelial injury, inhibit prostacyclin production, and promote thrombogenesis by increasing production of thromboxane A2. Thromboxane A2 produces platelet aggregation and vasoconstriction, whereas prostacyclin promotes vasodilation. This combination may be a major cause of damage to the endothelium.[36] A common mutation in the gene encoding for the enzyme methylenetetrahydrofolate reductase has been identified as a genetic risk for high levels of homocysteine. Mild hyperhomocystinemia due to gene mutation is estimated to occur in 5% to 10% of the general population.[37]

Homocysteine is an amino acid formed during the metabolism of methionine. Elevated levels may induce endothelial injury, inhibit prostacyclin production, and promote thrombogenesis by increasing production of thromboxane A2. Thromboxane A2 produces platelet aggregation and vasoconstriction, whereas prostacyclin promotes vasodilation. This combination may be a major cause of damage to the endothelium.[36] A common mutation in the gene encoding for the enzyme methylenetetrahydrofolate reductase has been identified as a genetic risk for high levels of homocysteine. Mild hyperhomocystinemia due to gene mutation is estimated to occur in 5% to 10% of the general population.[37]

A plasma homocysteine concentration of more than 15 mcmol/L is referred to as hyperhomocystinemia. Such elevated levels induce pathologic changes in the arterial wall, and the prothrombic environment created in the endothelium accounts for the association between increased plasma homocysteine levels and cardiovascular disease. Elevated levels have been observed among smokers, men, and postmenopausal women.[38] Many cross-sectional and prospective studies have demonstrated the relationship between high levels of total homocysteine and coronary, cerebral, and peripheral artery disease.[38-40] A recent meta-analysis has conclusively established the relationship between hyperhomocystinemia and cardiovascular disease.[37]

Homocysteine levels are inversely related to blood concentrations of folate, and folic acid supplementation, which is the vitamin supplement for folate, can lower homocysteine levels. Studies have demonstrated that daily doses of folic acid at 5-10 mg resulted in higher serum folate levels, lower total plasma homocysteine levels, and improved endothelial function.[37,41,42] Since 1998, folate fortification of foods has been mandated. Even with fortification, however, 76% of the population is below the minimum requirement of folate.[43] Much of the fortification is in whole grains. The Nurses' Health Study demonstrated that whole-grain intake reduces the risk of coronary heart disease in women.[44] Increased consumption of vegetables and citrus fruit, both good sources of folate, has also been associated with the reduction of coronary heart disease.[45] Folate lowers elevated homocysteine levels, but evidence for routine supplemental use does not yet exist.[46] However, it is recommended that all patients suffering from atherosclerosis and elevations of serum homocysteine receive supplementation of folic acid.[47]

Vitamin B6 (pyridoxine) and Vitamin B12 (cobalamin) are water-soluble vitamins that are absorbed in the small intestine, converted to an acid form, and excreted, with very little stored in the body. Both vitamins B6 and B12 are important in the function of protein metabolism reactions, particularly in the conversion of homocysteine. Increased plasma homocysteine concentration is an independent risk factor for premature atherosclerosis. Deficiency of vitamin B6 and vitamin B12, as well as folic acid, leads to mild-to-moderate elevation in homocysteine level. Studies of the association between dietary intake and blood levels of folate, vitamin B6, and vitamin B12 show positive and dose-dependent associations with the risk of cardiovascular disease.[38] Therapy to decrease homocysteine levels includes folic acid taken alone or in combination with vitamins B6 and B12.

Lobo and associates[48] studied a combination of daily low-dose folic acid supplements combined with vitamins B12 and B6 to reduce homocysteine levels in patients with CAD. Patients received 1-5 mg of folic acid, 12.5 mg of vitamin B6, and 500 micrograms of B12. They concluded that a daily does of 4 mg of folic acid combined with vitamins B6 and B12 normalized homocysteine levels in patients with CAD. In addition to deficiencies in folic acid and vitamins B6 and B12, long-term diuretic therapy has been implicated as a cause of elevated homocysteine levels. It has been demonstrated that hypertensive patients receiving long-term diuretic therapy have elevated homocysteine levels. In one study, patients receiving long-term diuretic therapy had significant increases in serum homocysteine concentrations and significant decreases in folate concentration with no change in vitamins B6 and B12.[49]

CONCLUSION AND RECOMMENDATION The micronutrients described in this article are widely used for the treatment and prevention of cardiac disease. On the whole, these substances do not appear to be harmful, and clinical evidence suggests that they may provide some beneficial effects. Micronutrient therapy may be a useful adjunct to traditional cardiovascular therapies. However, each patient must be considered individually, and a thorough history, physical examination, and laboratory work-up should be conducted prior to the initiation of micronutrient therapy. It is hoped that future research will continue to build a positive case for these economical and generally well-tolerated substances.

If a variety of healthy foods are eaten, the necessary vitamins can possibly be obtained from diet alone. However, supplementation may be required for some patients, particularly those with deficiencies. For supplementation, vitamins should have 50% to 150% of the RDA, and daily treatment should not provide more than 2-10 times the RDA for a specific vitamin.[50] Healthcare providers can safely advise patients that childbearing women need 4 mg of folic acid daily. In addition, vitamins C, E, B6, and B12 may be helpful for the prevention of CAD.

REFERENCES
US Department of Health and Human Services. Centers for Disease Control and Prevention, National Center for Health Statistics. Births, marriages, divorces, and deaths. Monthly Vital Statistics Report. Vol. 46, No. 9; May 8, 1998.
Eisenberg DM, Davis RB, Ettner SL, et al. Trends in alternative medicine use in the United States, 1990-1997. Results of a follow-up national survey. N Engl J Med. 1998;280:1569-1575.
Roberts S. Garlic likely to help health. Diabetes Forecast. 2000;53:38-40.
Silagy C, Neil A. Garlic as a lipid lowering agent: A meta-analysis. J R Coll Physicians Lond. 1994;28:39-45.
Silagy CA, Neil HA. A meta-analysis of the effect of garlic on blood pressure. J Hypertens. 1994;12:463-468.
Koscielny J, Klussendorf D, Latza R. The antiatherosclerotic effect of allium sativum. Atherosclerosis. 1999;144:237-249.
Das I, Khan NS, Sooranna SR. Potent activation of nitric oxide syntheses by garlic: A basis for its therapeutic applications. Curr Med Res Opin. 1995;13:257-263.
National Research Council. Recommended dietary allowances. 11th ed. Washington, DC: National Academy Press; 2001.
Simon JA, Hudes ES. Serum ascorbic acid and cardiovascular disease prevalence in U.S. adults: The Third National Health and Nutrition Examination Survey. Ann Epidemiol. 1999;9:358-365.
Gokce N, Keaney JF Jr, Frei B, et al. Long term ascorbic acid administration reverses endothelial vasomotor dysfunction in patients with coronary artery disease. Circulation. 1999; 29:3234-3240.
Gale CR, Martyn CN, Winter PD, Cooper C. Vitamin C and risk from stroke and coronary heart disease in cohort of elderly people. BMJ. 1995;310:1563-1566.
Knekt P, Reunanen A, Jarvinen R, Seppanen R, Heliovaara M, Aromaa A. Antioxidant vitamin intake and coronary mortality in a longitudinal population study. Am J Epidemiol. 1994;139:1180-1190.
Kushi LH, Folsom AR, Prineas RJ, Mink PJ, Wu Y, Bostick RM. Dietary antioxidant vitamins and death from coronary heart disease in postmenopausal women. N Engl J Med. 1996; 334:1156-1162.
Kendler BS. Recent nutritional approaches to the prevention and therapy of cardiovascular disease. Prog Cardiovasc Nurs. 1997;12:3-23.
Goodwin JS, Tangum MR. Battling quackery: Attitudes about micronutrient supplements in American academic medicine. Arch Intern Med. 1998;158:2187-2191.
Spencer AP, Carson DS, Crouch MA. Vitamin E and coronary artery disease. Arch Intern Med. 1999;159:1313-1320.
Stampfer MJ, Hennekens CH, Manson JE, Colditz GA, Rosner B, Willett WC. Vitamin E consumption and the risk of coronary disease in women. N Engl J Med. 1993;328:1444-1449.
Rimm EB, Stampfer MJ, Aschiero A, Giovanucci E, Colditz GA, Willett WC. Vitamin E consumption and the risk of coronary disease in men. N Engl J Med. 1993;328:1450-1456.
Stephens NG, Parsons A, Schofield P, Cheeseman K, Mitchinson MJ. Randomised controlled trial of vitamin E in patients with coronary artery disease: Cambridge Heart Antioxidant Study (CHAOS). Lancet. 1996;347:781-786.
Yusuf S, Dagenais G, Pogue J, Bosch J, Sleight P. Vitamin E supplementation and cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med. 2000;342:154-160.
Brown M. Do vitamin E and fish oil protect against ischaemic heart disease? Lancet. 1999;354:441-442.
Steiner M. Vitamin E, a modifier of platelet function: rationale and use in cardiovascular and cerebrovascular disease. Nutr Rev. 1999;57:306-309.
Schachter M. Coenzyme Q10. Health World Online; Integrative Medicine. 1996. Available at: http://www.healthy.net/asp/templates/Article.asp?PageType=Article&Id=534
Morisco C, Trimarco B, Condorelli M. Effect of coenzyme Q10 therapy in patients with congestive heart failure: A long-term multicenter randomized study. Clin Investig. 1993;71:S134-S136.
Baggio E, Gandini R, Plancher AC, Passeri M, Carmosino G. Italian multicenter study of safety and efficacy of coenzyme Q 10 adjunctive therapy in heart failure (interim analysis). The CoQ10 Drug Surveillance Investigators. Clin Investig. 1993;71:S145-S149.
Hofman-Bang C, Rehnqvist N, Swedberg K, Wiklund I, Astrom H. Coenzyme Q10 as an adjunctive in the treatment of chronic congestive heart failure. The Q10 Study Group. J Card Fail. 1995;1:101-107.
Watson PS, Scalia GM, Galbraith A, Burstow DJ, Bett N, Aroney CN. Lack of effect of coenzyme Q on left ventricular function in patients with congestive heart failure. J Am Coll Cardiol. 1999;33:1549-1552.
Sinatra ST. CoEnzyme Q10: A vital therapeutic nutrient for the heart with special application in congestive heart failure. Conn Med. 1997;61:707-711.
Munkholm K, Hansen H, Rasmussen K. Coenzyme Q10 treatment in serious heart failure. Biofactors. 1999;9:285-289.
Singh RB, Wander GS, Rastogi A, et al. Randomized, double-blind placebo-controlled trial of coenzyme Q10 in patients with acute myocardial infarction. Cardiovasc Drugs Ther. 1998; 12:347-353.
Singh RB, Niaz MA, Rastogi SS, Shukla PK, Thakur AS. Effect of hydrosoluble coenzyme Q10 on blood pressures and insulin resistance in hypertensive patients with coronary artery disease. J Hum Hypertens. 1999;13:203-208.
Overvad K, Diamant B, Holm L, Holmer G, Mortensen SA, Stender S. Coenzyme Q10 in health and disease. Eur J Clin Nutr. 1999; 53:764-770.
Connor SL, Connor WE. Are fish oils beneficial in the prevention and treatment of coronary artery disease? Am J Clin Nutr. 1997;66:1020S-1031S.
McCarty MF. Fish oil and other nutritional adjuvants for treatment of congestive heart failure. Med Hypotheses. 1996;46:400-406.
Adler AJ, Holub BJ. Effect of garlic and fish-oil supplementation on serum lipid and lipoprotein concentrations in hypercholesterolemic men. Am J Clin Nutr. 1997;65:445-450.
Brown AJ, Roberts DC, Pritchard JE, Truswell AS. A mixed Australian fish diet and fish-oil supplementation: impact on the plasma lipid profile of healthy men. Am J Clin Nutr. 1990;52:823-833.
Puddu P. Homocysteine and risk for atherothrombotic events. Cardiologia. 1999;44:627-631.
Andreotti F, Burzotta F, Mazza A, Manzoli A, Robinson K, Maseri A. Homocysteine and arterial occlusive disease: a concise review. Cardiologia. 1999;44:341-345.
Eikelboom J, Lonn E,Genest J, Hankey G, Yusuf S. Homocysteine and cardiovascular disease: a critical review of the epidemiologic evidence. Ann Intern Med. 1999;131:363-375.
Whincup PH, Refsum H, Perry IJ, et al. Serum total homocysteine and coronary heart disease: Prospective study in middle aged men. Heart. 1999;82:448-454.
Bellamy MF, McDowell IF, Ramsey MW, Brownlee M, Newcombe RG, Lewis MJ. Oral folate enhances endothelial function in hyperhomocysteinaemic subjects. Eur J Clin Invest. 1999;29:659-662.
Woo KS, Chook P, Lolin YI, Sanderson JE, Metreweli C, Celermajer DS. Folic acid improves arterial endothelial function in adults with hyperhomocystinemia. J Am Coll Cardiol. 1999;34:2002-2006.
Stampfer MJ, Rimm EB. Folate and cardiovascular disease. Why we need a trial now. JAMA. 1996;26:1893-1896.
Liu S, Stampfer MJ, Hu FB, et al. Whole-grain consumption and risk of coronary heart disease: Results from the Nurses' Health Study. Am J Clin Nutr. 1999;70:412-419.
Brouwer I, Van Dusseldorp M, West D, et al. Dietary folate from vegetables and citrus fruit decreases plasma homocysteine concentrations in humans in a dietary controlled trial. J Nutr. 1999;129:1135-1139.
Adams AK, Wermuth EO, McBride PE. Antioxidant vitamins and the prevention of coronary heart disease. Am Fam Physician. 1999;60:895-904.
Newman PE. Can reduced folic acid and vitamin B12 levels cause deficient DNA methylation producing mutations which could initiate atherosclerosis? Med Hypotheses. 1999;53:421-424.
Lobo A, Naso A, Arheart K, et al. Reduction of homocysteine levels in coronary artery disease by low-dose folic acid combined with vitamins B 6 and B12. Am J Cardiol. 1999;83:821-825.
Morrow LE, Grimsley EW. Long-term diuretic therapy in hypertensive patients: effects on serum homocysteine, vitamin B6, vitamin B12, and red blood cell folate concentrations. South Med J. 1999;92:866-870.
Carr AC, Frei B. Toward a new recommended dietary allowance for vitamin C based on anti-oxidant and health effects in humans. Am J Clin Nutr. 1999;69:1086-1107.
Judith Anderson, ARNP, PhD, has no significant interests to disclose. Cathy Kessenich, DSN, has no significant interests to disclose.
-Glenda Hadley
Back to top
View user's profile Send private message
Display posts from previous:   
This forum is locked: you cannot post, reply to, or edit topics.   This topic is locked: you cannot edit posts or make replies.    Nature's Sunshine Products NSP Forum Index -> Forum Archive All times are GMT - 6 Hours
Page 1 of 1

 
Jump to:  
You cannot post new topics in this forum
You cannot reply to topics in this forum
You cannot edit your posts in this forum
You cannot delete your posts in this forum
You cannot vote in polls in this forum


Powered by phpBB © 2001, 2005 phpBB Group