Archive for the 'Cardiovascular' Category

Jan 20 2009

Turmeric Component Protects Against Toxic Compound Consumed in Many Meals

Curcumin, the pigment that gives turmeric its yellow color, may reduce the damaging effects of acrylamide (AA), a potential carcinogen created when starchy foods are baked, roasted, fried or toasted.

Swedish scientists first reported on acrylamide’s widespread presence in the food supply in 2002, when they found unexpectedly high levels of acrylamide in carbohydrate-rich foods. This was of concern since the toxin causes cancer in laboratory rats. Other scientists have found that acrylamide causes DNA to fragment, increases formation of damaging reactive oxygen species (ROS) and triggers the death of liver cells. It is also genotoxic, meaning that it damages a cell’s genetic material affecting the cell’s integrity. Genotoxic substances have the potential to be carcinogens and can cause genetic mutations that lead to the development of tumors.

Due to its antioxidant abilities, researchers studied curcumin’s effects on human liver cells exposed to acrylamide. They found that curcumin significantly reduced the production of reactive oxygen species that occurred in acrylamide-treated cells. Curcumin also inhibited the acrylamide-induced DNA fragments and significantly reduced the acrylamide-triggered cell death, indicating curcumin could ameliorate acrylamide’s known genotoxicity.

The researchers believe that curcumin’s effects are likely due to its antioxidant abilities. They concluded, “Consumption of curcumin may be a plausible way to prevent AA-mediated genotoxicity.”

Reference:

Cao J, Liu Y, Jia L, Jiang LP, Geng CY, Yao XF, Kong Y, Jiang BN, Zhong LF. Curcumin Attenuates Acrylamide-Induced Cytotoxicity and Genotoxicity in HepG2 Cells by ROS Scavenging. J Agric Food Chem. 2008 Nov 14. Published Online Ahead of Print.

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Jan 20 2009

Grape Seed Extract May Stop Bacteria Involved in Bad Breath and Gum Disease

A new study suggests that grape seed extract may inhibit the bacteria known to cause bad breath and gum disease.

Periodontitis is a gum disease that destroys the soft tissue and bone supporting the teeth. Thirty to 50 percent of the US population suffers from the condition, which is thought to be the second most common disease worldwide.

In an in vitro study, researchers investigated whether grape seed extract could inhibit Porphyromonas gingivalis and Fusobacterium nucleatum, bacteria responsible for both periodontitis and bad breath. The researchers tested the effects of grape seed extract (97 percent polyphenols) on these two anaerobic bacteria.

The results indicated that grape seed extract exhibited antibacterial activity against the two strains. Moreover, the grape seed extract could penetrate the biofilm that surrounded the bacteria. Biofilms serve to protect bacteria against antimicrobial agents and dental plaque’s biofilm is particularly complex.

Grape seed extract also had an antioxidant activity higher than vitamins C and E, according to measures taken with the Trolox equivalent antioxidant capacity (TEAC) test. This was important to the findings of the study because gum disease originates due to the bacteria’s presence and its biofilm protection, but the disease progresses because of an excess release of reactive oxygen species that trigger the inflammatory process. Grape seed extract’s antioxidant abilities may quench the free radicals implicated in the progression of gum disease.

The researchers concluded, “These findings indicated that GSE could be used in oral hygiene for the prevention of periodontitis.”

Reference:

Furiga A, Lonvaud-Funel A, Badet C. In vitro study of antioxidant capacity and antibacterial activity on oral anaerobes of a grape seed extract. Food Chemistry. 15 April 2009;113( 4);1037-1040. Available online prior to April publication date.

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Jan 20 2009

Low Antioxidant Levels Linked to Asymptomatic Coronary Artery Disease

Low plasma concentrations of the antioxidant vitamins A and E and the carotenoids beta carotene and lycopene are significantly associated with atherosclerosis of the carotid arteries, a new study has found.

Atherosclerosis remains clinically mute for a long time and frequently manifests itself with an acute cardiovascular event. The possibility of detecting this disease in a subclinical phase and reducing or reversing its progression is therefore an issue of relevance.

Researchers studied 220 consecutive, asymptomatic participants and examined their carotid arteries by ultrasound to determine the thickness of the arteries and whether the arteries had developed pre-atherosclerotic lesions. A medical history also was taken, a physical examination was performed and blood samples were analyzed for concentrations of antioxidant vitamins and carotenoids.

The scientists found that low concentrations of vitamin A, vitamin E, lycopene and beta carotene were significantly associated with carotid atherosclerosis as measured by increased thickness of the carotid arteries. In addition, marginally higher body mass index and low levels of high-density lipoprotein cholesterol were also associated with carotid atherosclerosis. Other factors considered in the study (total cholesterol, low-density lipoprotein cholesterol, triglycerides and C-reactive protein) were not significantly associated with carotid atherosclerosis.

According to the researchers, “Low plasma concentrations of antioxidant vitamins (vitamins A, E and beta-carotene) and lycopene were associated with early carotid atherosclerotic lesions as measured by carotid intima-media thickness (CIMT). Regular intake of foods rich in lycopene and antioxidant vitamins may slow the progression of atherosclerosis.”

Reference:

Riccioni G, Bucciarelli T, D’Orazio N, Palumbo N, di Ilio E, Corradi F, Pennelli A, Bazzano LA. Plasma Antioxidants and Asymptomatic Carotid Atherosclerotic Disease. Ann Nutr Metab. 2008 Oct 21;53(2):86-90.

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Jan 20 2009

The Latest Research on Fatigue, Heart Health, Cognitive Function and More

Omega-3s Linked to Prostate Health

Men who increase their intake of omega-3-rich fish have a greater chance of surviving prostate cancer, according to a new study.

Researchers studied 20,167 men who were participating in the Physician’s Health Study. The subjects were free of cancer in 1983, when the study began. During follow-up, 2,161 men were diagnosed with prostate cancer and 230 died of the disease.

Although intake of omega-3-rich fish was unrelated to prostate cancer incidence, it was linked to survival from the disease. Among the men diagnosed with prostate cancer, those consuming fish five or more times per week had a 48 percent lower risk of prostate cancer death than did men consuming fish less than once weekly.

In this study the scientists found no link between fish consumption and a reduced incidence of prostate cancer, but the same researchers conducted an earlier study that found higher intake of the omega-3 fatty acids DHA (docosahexaenoic acid) and EPA (eicosapentaenoic acid) may reduce the risk of developing prostate cancer by 41 percent.

Reference:

Chavarro JE, Stampfer MJ, Hall MN, Sesso HD, Ma J. A 22-y prospective study of fish intake in relation to prostate cancer incidence and mortality. Am J Clin Nutr. 2008 Nov;88(5):1297-303.

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Dec 04 2007

Homocysteine

Published by under Cardiovascular

Homocysteine

Its Destructive Role in Cardiovascular, Cognitive and Bone Health

Homocysteine is one of the most destructive compounds found in the human body. Although oxidized LDL cholesterol (the “bad” cholesterol) is commonly considered the arteries’ worst enemy, homocysteine has emerged as an equally powerful threat to heart health. In fact, research now shows that damage from homocysteine paves the way for LDL to have an even more destructive effect on the vascular system, indicating these two agents can work together to cause heart disease. Furthermore, as time goes on, more and more research is uncovering homocysteine’s role in other health conditions such as infertility, depression, cognitive decline and bone fractures.

Homocysteine is considered a primary risk factor for cardiovascular disease including stroke and deep vein thrombosis.1 Elevated blood levels of homocysteine also are considered an independent risk factor for atherosclerosis and thromboembolism (the obstruction of a blood vessel by a clot), and are correlated with a significant risk for coronary, cerebral and peripheral vascular disease, myocardial infarction (heart attacks), peripheral vascular occlusive disease, cerebral vascular occlusive disease, and retinal vascular disease.2 In fact, high homocysteine, even in the absence of other risks, such as smoking and obesity, is a serious but controllable risk factor for heart disease.

Homocysteine is an amino acid commonly found in the blood as a result of protein metabolism. It is mainly derived from another amino acid known as methionine, which is found in a number of food sources primary among them being meat. Blood levels of homocysteine can also be affected by genetic and physiologic factors.

Homocysteine is thought to cause vascular disease because of its effect on blood vessel walls. Homocysteine binds to certain proteins in the body affecting their structure and function. The binding of homocysteine to proteins will degrade and inhibit repair and maintenance of three main vascular connective tissue structures—cartilage, elastin and proteolgycans—making them more susceptible to disease processes, including vascular disease. Homocysteine can damage the cells lining the artery walls (known as the endothelium) in the vascular system. Homocysteine causes a reduction in nitric oxide activity, impairing blood vessels’ ability to dilate and leaving the endothelium more susceptible to oxidative damage.3 Damaged vascular walls will then allow more low density lipoprotein (LDL) to be absorbed, further harming the vessel. This damage then promotes the growth of new smooth muscle cells within the vessel, which then narrows it. Endothelial damage also allows for increased platelet adhesiveness and activation of the clotting cascade, increasing the risk of cardiac arrest (heart attack) or cerebrovascular accident (stroke).

HomocysteineIn the Western world, homocysteine serum levels are most commonly found at 10-12 μmol/L. A level above 12 is generally considered elevated while levels below 6 are considered minimal. An increase of homocysteine levels by 5 μmol/L has been shown to increase the risk of cerebrovascular disease in the general population by 50 percent, and will increase the risk of coronary artery disease by 80 percent in women and 60 percent in men. In general, women have 10-15 percent less homocysteine than men during their reproductive years, which is thought in part to be the reason why women have fewer heart attacks than men, and why they tend to have them 10-15 years later than the time men commonly do.4

Genetic Causes of High Homocysteine

Dietary factors, while often cited as the chief cause for elevated homocysteine, are not the only factor. A rare hereditary disease known as homocystinuria results in several systemic disorders and is charachterized by the accumulation of homocysteine in the blood and an increased rate of excretion in the urine. Nearly 25 percent of people with this disorder die from cardiovascular complications before the age of thirty.

Ten percent of the population in general have another more common yet related condition where they are unable to effectively metabolize homocysteine and will be predisposed to the negative effects of elevated homocysteine levels, including blood clots and cardiovascular disease. This disorder is known as a methylenetetrahydrofolate-reductase (MTHFR) polymorphism genetic trait. People that have this condition are unable to effectively metabolize homocysteine and will be predisposed to the negative effects of elevated homocysteine levels, including blood clots and cardiovascular disease.

Homocysteine’s Widespread Role

Elevated homocysteine, also known as hyperhomocysteinemia, may contribute to many other conditions.

Infertility

Women who have high levels of homocysteine have been shown to have a more difficult time getting pregnant and are two times as likely to have complications during pregnancy. Furthermore, women with high homocysteine levels are at risk of having miscarriages early in pregnancy.5-6 Researchers are not sure what role homocysteine has in infertility, but it has been theorized that high homocysteine contributes to subfertility, or difficulty achieving a pregnancy.

Mental Health

Elevated levels of homocysteine are also a risk factor for diseases affecting the brain. Epidemiologic studies show a dose-dependent relationship between homocysteine levels and risk for neurodegenerative diseases such as stroke, Parkinson’s disease, multiple sclerosis, and depression.7 Researchers continue to collect evidence that correlates several cardiovascular disease risk factors, homocysteine being one, with the incidence of cognitive decline and Alzheimer’s disease.8 High homocysteine by itself is considered a strong independent risk factor for dementia and Alzheimer’s disease. A study looking at data collected from the Framingham Study showed that a homocysteine level over 14 μmol/L increased the risk of developing Alzheimer’s disease by 150 percent.9

Bone Fractures

Homocysteine is considered an independent risk factor for osteoporosis fractures in the elderly.10 It is thought that homocysteine leads to fractures in the same way in which it contributes to heart disease in that homocysteine affects certain connective tissue proteins and prevents them from functioning correctly. In the case of fractures, homocysteine interferes with the cross-linking ability of collagen (a major connective tissue protein) with the tissues it supports such as the skeletal system. Because homocysteine affects the structural proteins of which bone is comprised, it does not actually affect bone density. Therefore, traditional measures used to build bones (weight bearing exercise, adequate calcium and vitamin D, etc.) will not necessarily correct the damage from homocysteine on the bones.

Controlling Elevated Homocysteine

HomocysteineCurrently, there is no standard recommendation that all people have their homocysteine levels checked. Despite this, the American Heart Association does encourage testing for homocysteine in people with a personal or family history of heart disease. In order to address all possible aspects of heart disease (and other conditions), testing homocysteine levels is a good idea.

Controlling homocysteine can be achieved by supplementing with 4 common nutrients: vitamins B6, B12, folic acid and betaine. Vitamins B6, B12, and folic acid blood levels are found to be inversely related to plasma homocysteine concentration. Combination therapy with the aforementioned vitamins provides an effective way to reduce homocysteine levels,11 and side effects of this therapy are relatively unknown.12 Another supplement that has demonstrated usefulness in lowering homocysteine levels is betaine, also known as trimethylglycine.

High dietary consumption of methionine, which can be found in meats and dairy products, can result in the overproduction of homocysteine. Once homocysteine is produced it is metabolized in the body through one of two possible pathways—remethylation or transsulfuration. Remethylation is a process that utilizes folate, vitamin B12 or betaine (trimethylglycine) to convert homocysteine back to methionine. Alternately, transsulfuration utilizes vitamin B6 (pyridoxal-5-phosphate) to break down excess homocysteine into a number of metabolites for eventual excretion from the body.13,3 B6 has been shown to be effective in reducing homocysteine levels following the ingestion of significant amounts of methionine.14

Vitamin B12 in the form of methylcobalamin is needed for the conversion (remethylation) of homocysteine back to methionine.15 This remethylation reaction also requires folic acid. B12 is thought to provide an additive effect to the lowering of homocysteine when supplied in conjunction with folic acid.16

Folic acid is needed for the metabolism of homocysteine; low levels of folate in the blood are associated with higher levels of homocysteine. Folic acid is involved in one of the two pathways (remethylation) by which homocysteine is metabolized; this pathway also requires vitamin B12. Enzymes involved in remethylation of homocysteine are dependent upon folate and vitamin B12.17-18 Supplementation with folic acid will increase the activity of the remethylation pathway and thereby reduce homocysteine levels.19

Betaine is derived from choline and occurs naturally in the body. It can also be found in foods like cereal, seafood, spinach and beets, to name a few. Betaine acts as a methyl donor and contributes in the remethylation pathway when converting homocysteine back to methionine,20 thereby reducing homocysteine levels. Betaine has been shown to lower homocysteine levels in the majority of patients unresponsive to vitamin B6 therapy. In one study, daily doses of 250 mg of vitamin B6, 5 mg of folic acid, and 6 gm of betaine by themselves or in combination normalized the majority of high homocysteine levels in patients administered high doses of methionine.21

Homocysteine-lowering strategies also include a diet low in methionine since homocysteine is an intermediate product of methionine metabolism in the body. Foods rich in methionine include cheddar cheese, eggs, chicken, and beef.


Conclusion

Homocysteine is considered a primary, independent risk factor for cardiovascular disease and is thought to contribute to a host of other conditions such as miscarriages and difficult pregnancy, bone fractures, strokes, blood clots, depression, dementia, Alzheimer’s and Parkinson’s diseases. Due to this amino acid’s role in a host of diseases, individuals at risk for high homocysteine levels should consider a supplement regimen that includes vitamins B12 and B6, folic acid, and betaine. The physicians at Griffin Medical Group can prescribe a treatment protocol to help lower homocysteine levels.

References

1. Blum A, Hijazi I, Eizenberg MM, Blum N. Homocysteine (Hcy) follow-up study. Clin Invest Med. 2007;30(1):21-5.

2. Lentz SR. Mechanisms of homocysteine-induced atherothrombosis. J Thromb Haemost. 2005 Aug;3(8):1646-54.

3. Keebler ME, De Souza C, Fonesca V. Diagnosis and treatment of hyperhomocysteinemia. Curr Atheroscler Rep. 2001;3:54-63.

4. Boushey CJ, Beresford SA, Omenn GS, Motulsky AG. A quantitative assessment of plasma homocysteine as a risk factor for vascular disease. Probable benefits of increasing folic acid intakes. JAMA. 1995;274:1049-57.

5. D’Uva M, Di Micco P, Strina I, et al. Hyperhomocysteinemia in women with unexplained sterility or recurrent early pregnancy loss from Southern Italy: a preliminary report. Thromb J. 2007 Jul 11;5:10.

6. Forges T, Monnier-Barbarino P, Alberto JM, et al. Impact of folate and homocysteine metabolism on human reproductive health. Hum Reprod Update. 2007 May-Jun;13(3):225-38. Epub 2007 Feb 16.

7. Herrmann W, Lorenzl S, Obeid R. Review of the role of hyperhomocysteinemia and B-vitamin deficiency in neurological and psychiatric disorders–current evidence and preliminary recommendations] Fortschr Neurol Psychiatr. 2007 Sep;75(9):515-27.

8. Rosendorff C, Beeri MS, Silverman JM. Cardiovascular risk factors for Alzheimer’s disease. Am J Geriatr Cardiol. 2007 May-Jun;16(3):143-9.

9. Seshadri S, Beiser A, Selhub J, et al. Plasma homocysteine as a risk factor for dementia and Alzheimer’s disease. N Engl J Med. 2002 Feb 14;346(7):476-83.

10. Perier MA, Gineyts E, Munoz F, Sornay-Rendu E, Delmas PD. Homocysteine and fracture risk in postmenopausal women: the OFELY study. Osteoporos Int. 2007 Oct;18(10):1329-36.

11. Krishnaswamy K, Lakshmi AV. Role of nutritional supplementation in reducing the levels of homocysteine. J Assoc Physicians India 2002 May;50 Suppl:36-42.

12. O’Connor JJ, Meurer LN. Should patients with coronary disease and high homocysteine take folic acid? J Fam Pract. 2003 Jan;52(1):16-8.

13. Sunder-Plassmann G, Winkelmayer WC, Fodinger M. Therapeutic potential of total homocysteine-lowering drugs on cardiovascular disease. Exp Opin Invest Drugs. 2000;9:2637-51.

14. Mayer EL, Jacobsen DW, Robinson K. Homocysteine and coronary atherosclerosis. J Am Coll Cardiol. 1996;27:517-27.

15. Selhub J, Jacques PF, Bostom AG, et al. Relationship between plasma homocysteine and vitamin status in the Framingham study population. Impact of folic acid fortification. Publ Health Rev. 2000;28:117-45.

16. Landgren F, Israelsson B, Lindgren A, et al. Plasma homocysteine in acute myocardial infarction: homocysteine-lowering effect of folic acid. J Intern Med. 1995;237:381-8.

17. Woodside JV, Yarnell JW, McMaster D, et al. Effect of B-group vitamins and antioxidant vitamins on hyperhomocysteinemia: a double-blind, randomized, factorial-design, controlled trial. Am J Clin Nutr. 1998;67:858-66.

18. Fohr IP, Prinz-Langenohl R, Bronstrup A, et al. 5,10-Methylenetetrahydrofolate reductase genotype determines the plasma homocysteine-lowering effect of supplementation with 5-methyltetrahydrofolate or folic acid in healthy young women. Am J Clin Nutr. 2002;75:275-82.

19. Vermeulen EG, Stehouwer CD, Twisk JW, et al. Effect of homocysteine-lowering treatment with folic acid plus vitamin B6 on progression of subclinical atherosclerosis: a randomised, placebo-controlled trial. Lancet. 2000;355:517-22.

20. Brouwer IA, Verhoef P, Urgert R. Betaine supplementation and plasma homocysteine in healthy volunteers (letter). Arch Intern Med. 2000;160:2546-7.

21. Boers GHJ. Hyperhomocystinemia: A Newly Recognized Risk Factor For Vascular Disease. Netherlands Journal of Medicine. 1994; 45:34-41.

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