February, 2007

Eating Heart Smart
By Marie Spano, MS, RD
Today’s Dietitian
Vol. 9 No. 2 P. 28

Cardiovascular disease (CVD) is the No. 1 cause of morbidity and mortality in the United States, and myriad dietary factors affect one’s risk of developing this disease.1 There are several generally agreed-upon recommendations to curb this risk: avoid trans fats, minimize saturated fat intake, and eat high-fiber foods, as well as plenty of fruits and vegetables. However, the picture is not so clear when it comes to other aspects of our diet. Every person is unique, with varying risk factors, medications, and lifestyles, and their dietary recommendations should be equally unique.

In 2006, the American Heart Association (AHA) updated its dietary and lifestyle recommendations aimed at preventing CVD, mainly by recommending further reductions in saturated and trans fatty acid intake and minimizing intake of foods and beverages with added sugars (see Table 2 in “Today’s CPE”). Additional dietary factors that play a role in CVD risk follow.

Definitely Beneficial
Both epidemiologic and clinical trials have linked omega-3 fatty acid intake with a reduced CVD risk.2,3 In fact, eating fish rich in eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) one to two times per week may reduce the risk of coronary death by 36% (95% confidence interval [CI], 20% to 50%; P <0.001) and total mortality by 17% (95% CI, 0% to 32%; P = 0.046).4 There are thousands of studies examining the relationship between omega-3s and cardiovascular risk factors, and while many show positive results, a thorough review of the literature indicates that omega-3s are conclusively tied to a reduction in two main CVD risk factors: triglyceride levels and blood pressure. In fact, the relationship between omega-3s and triglyceride levels is dose dependent, with higher doses of omega-3s leading to greater decreases in triglyceride levels.5

People should obtain omega-3s from food—specifically fatty fish (salmon, mackerel, herring, halibut, lake trout, albacore tuna). Research linking omega-3 consumption to a decrease in certain CVD risk factors examined fish or fish oil supplements, which are rich in the omega-3 fatty acids EPA and DHA. Plant sources of omega-3s, such as flaxseed oil, contain the essential fatty acid alpha-linolenic acid (ALA), which can be converted to EPA and DHA. However, this process is inefficient and inhibited by several factors, such as saturated fatty acid intake, ethanol, and a diet high in linoleic acid. In healthy individuals, it is estimated that approximately 5% to 10% of ALA is converted to EPA, and approximately 2% to 5% to DHA.6,7

The AHA indicates that those without coronary heart disease (CHD) should eat at least two servings of fish per week (two 8-ounce servings correlates to approximately 3 grams of EPA and 6 grams of DHA per week).6,8 The AHA recommends patients with CHD consume 1 gram of EPA and DHA per day, preferably from fatty fish, and those who need to lower their triglycerides take 2 to 4 grams of EPA and DHA per day as capsules, under a physician’s guidance. If your client doesn’t like fish, try a fish oil supplement shown to have little to no contamination (check www.consumerlab.com). Anyone taking blood thinners such as aspirin, vitamin E, or the prescription medication warfarin (Coumadin) should consult a physician prior to taking omega-3 supplements.

Possibly Beneficial
Folic Acid, Vitamin B6, Vitamin B12, and Magnesium
Blood homocysteine levels are used as a measure of inflammation and a predictor of CVD mortality.9 The amino acid homocysteine is an intermediate product in the metabolism of methionine and its degradation is thought to damage the arteries’ main structural components. Vitamins B6, B12, and folate are vital for homocysteine metabolism.10,11 If these vitamins are in short supply, blood levels of homocysteine rise, increasing the potential for arterial plaque development and raising the risk for heart attack and stroke.11,12
While no one will argue that eating foods high in folate, B6, and B12 is beneficial, there remains much debate regarding the effect of supplementation on homocysteine and CVD risk. Although there are several cohort studies indicating that these B vitamins are associated with a lower CVD risk, randomized controlled trials (RCTs) of specific supplements haven’t effectively demonstrated a reduced risk of incidence or death from CVD.13 In addition, if these vitamins help, it is unclear what quantities should be taken to decrease homocysteine levels.

Magnesium helps muscles relax, affects the muscle tone of blood vessels, and keeps heart rhythm steady. Magnesium intake has also been associated with a decreased incidence of CHD, and low magnesium levels have been correlated with high blood pressure and angina (chest pain associated with insufficient blood supply to the heart).14

Folic acid supplementation as part of a multivitamin-mineral (MVM) supplement is fine, but additional supplementation should only be under a physician’s supervision. Magnesium can be found in MVM supplements but rarely, if ever, at 100% Daily Value (DV). Why? Magnesium takes up a fair amount of space, and therefore adding 100% of the DV would make current horse-size pills that much bigger. If supplementing, keep with 100% of the DV unless otherwise directed by a physician.

Loaded with antioxidant polyphenols, tea has been associated with a decrease in several chronic diseases related to free radical-induced damage, including heart disease. Researchers have surmised that polyphenols prevent the oxidation of low-density lipoprotein (LDL) cholesterol, thereby inhibiting the formation of atherosclerotic plaques.15

Much of the research on tea consumption and CVD is with green tea, which typically contains more polyphenols than black tea. Several animal studies have shown that green tea polyphenols may have some cardiovascular benefits. In addition, epidemiological studies have related increased tea consumption to low rates of CVD. In a study examining 40,530 Japanese adults aged 40 to 79 without a history of stroke, CHD, or cancer at baseline, participants were followed for up to 11 years (1995-2005) for all-cause mortality and up to seven years (1995-2001) for cause-specific mortality.16 Green tea consumption was inversely associated with mortality due to CVD and all-cause mortality. The inverse association with CVD mortality was stronger than with all-cause mortality. Among the types of CVD mortality, the strongest inverse association was observed for stroke mortality.

In a clinical trial, researchers examined the effect of green tea on blood lipids by supplementing 29 subjects with 1 liter of green tea per day for four weeks, followed by a washout period of 1 liter of water per day for three weeks, and, finally, another four weeks drinking 1 liter of green tea per day. Significant changes in blood lipids were noted: 90% of the subjects reduced LDL cholesterol with an average decrease of 8.9% and high-density lipoprotein (HDL) cholesterol increased in 69% of subjects (average 4%).17

Drink up, but if you are sensitive to caffeine, try decaffeinated.

Both epidemiological and clinical research have shown that those who drink alcohol in moderation, even individuals already at risk for CHD or postinfarction, have lower rates of CHD than individuals who do not drink. Alcohol can increase HDL cholesterol, lower levels of fibrinogen, C-reactive protein, LDL cholesterol, and other prothrombotic factors.

However, alcohol consumption can also increase triglyceride levels and lower antiplatelet activity.18-20

A meta-analysis of 42 experimental studies assessing the effects of moderate alcohol intake found that 30 grams per day of ethanol increased HDL cholesterol by 3.99 milligrams per deciliter (95% CI 3.25 to 4.73), apolipoprotein A1 by 8.82 milligrams per deciliter (7.79 to 9.86), and triglyceride by 5.69 milligrams per deciliter (2.49 to 8.89). The authors concluded that alcohol intake is causally related to lower risk of CHD through changes in lipids and haemostatic factors.21 The AHA does not recommend drinking wine or any other type of alcohol in an effort to prevent CVD. Individuals who already have CVD and are taking aspirin should be especially cautious about their alcohol consumption.

Potassium helps maintain cell fluid balance and plays a role in muscle contraction. Low levels of this mineral have been associated with high blood pressure, hence the DASH (Dietary Approaches to Stop Hypertension) diet recommendations to include plenty of potassium-rich fruits and vegetables in one’s daily diet.22 To ascertain whether potassium supplementation positively affects blood pressure in those with hypertension, Dickenson et al reviewed the Cochrane Library, MEDLINE, EMBASE, Science Citation Index, ISI Proceedings, ClinicalTrials.gov, Current Controlled Trials, CAB Abstracts, and reference lists of systematic reviews, meta-analyses, and RCTs. In a meta-analysis of five trials that met the inclusion criteria, potassium supplementation resulted in large but statistically nonsignificant reductions in systolic blood pressure (mean difference: -11.2, 95% CI: -25.2 to 2.7) and diastolic blood pressure (mean difference: -5.0, 95% CI: -12.5 to 2.4). The authors indicated that the evidence regarding the effect of potassium on blood pressure is inconclusive. More high-quality RCTs of longer duration are needed.23

The only way to truly increase potassium levels is by eating more potassium-rich foods. Too much potassium in the blood can be fatal and for this reason, supplements don’t have more than approximately 1% of the DV. Complicating the story further, those with CVD may already have a decline in kidney function, which can lead to high blood potassium levels.

The previously determined positive effects of soy protein on various heart disease risk factors have become questionable. Even review articles can’t seem to agree. In one particular review of 23 RCTs, soy protein intake was associated with significant decreases in serum total cholesterol, LDL cholesterol, and triglycerides and significant increases in serum HDL cholesterol. Reductions in total cholesterol and LDL cholesterol were larger in men than women.24 However, a look at six systematic reviews found that soy protein isolate containing isoflavones reduces LDL cholesterol but has no effects on triglycerides or HDL cholesterol.25 Yet another review, this one by the AHA, examined 22 randomized trials on isolated soy protein with isoflavones compared with milk or other proteins only to find very small decreases in LDL cholesterol (average effect 3%) relative to the large amount of soy—an average of 50 grams per day and no significant effects on HDL cholesterol, triglycerides, lipoprotein(a) [Lp(a)], or blood pressure.26

Potentially Harmful
The relationship between iron status, measured as serum ferritin, and CVD risk is very controversial. There is some epidemiological research linking body iron stores in men with an increased risk for an acute myocardial infarction (MI) and stroke in postmenopausal women.27-29 To determine the relationship between serum ferritin and CVD, researchers used baseline data from the National Health and Nutrition Examination Survey II and mortality follow-up data from the National Death Index. They examined data from 1,604 subjects aged 45 to 74 who were free of CHD at baseline, according to self-reported data. There were no statistically significant associations between serum ferritin and an increased risk of CVD, CHD, and MI death.30

Saturated and Trans Fats (Hydrogenated and Partially Hydrogenated Oils)
The adverse effects of saturated fats on blood lipids have been known for years, whereas recently, trans fats have stolen the spotlight. Both saturated and trans fatty acids raise LDL cholesterol levels, which increases CVD risk.31 However, saturated fatty acids also increase HDL cholesterol.32

In terms of CVD prevention, trans fat may be the worst substance you can put in your body. Even at seemingly low levels of consumption—1% to 3% of total energy intake—trans fats substantially increase one’s CHD risk. In a meta-analysis of four cohort studies involving a total of 140,000 patients, a 2% increase in energy intake from man-made trans fats was associated with a 23% increase in CHD.33 A meta-analysis of 12 RCTs of trans fatty acid consumption revealed that trans fatty acid consumption, as compared with an equal number of calories from saturated or cis unsaturated fats, raises LDL cholesterol levels and reduces HDL cholesterol, while also increasing the ratio of total cholesterol to HDL cholesterol, used as a predictor of CHD. Trans fats wreak havoc in other ways by increasing blood triglyceride levels, increasing levels of Lp(a), reducing the particle size of LDL cholesterol, and disrupting endothelial functioning.34-37 In addition, trans fatty acid intake has been associated with increased activity of tumor necrosis factor, interleukin-6, and C-reactive protein, all measures of inflammation.37,38 Inflammation is an independent risk factor for CVD.

Trans fats can be found in nature (dairy foods and meats), though most trans fats in our food supply have been produced through the chemical addition of hydrogen to saturate liquid oil, making it more solid. It is likely only the chemically processed trans fats that have such harmful effects on our bodies.33 Effective January 1, 2006, the FDA ruled that all conventional foods and supplements must list the trans fat content on their label.39

As healthcare practitioners, it is our job to stay on top of the latest research and interpret it for consumers. Per the usual with much scientific research, there are many inconclusive aspects regarding the role of various foods and nutrients and CVD risk factors. The best advice is always to recommend that our clients improve their overall diet (see Table 2 in “Today’s CPE”) while educating them on the latest research, so they, with their physician, can decide on the next steps.

— Marie Spano, MS, RD, is an exercise physiologist; vice president of the International Society of Sports Nutrition (ISSN); spokesperson for the Tea Council of the USA and the ISSN; and a freelance writer, consultant, and speaker in the nutrition, fitness, and health industries.

1. American Heart Association Nutrition Committee; Lichtenstein AH, Appel LJ, Brands M, et al. Diet and lifestyle recommendations revision 2006: A scientific statement from the American Heart Association Nutrition Committee. Circulation. 2006;114(1):82-96.

2. Kromhout D, Bosschieter EB, de Lezenne Coulander C. The inverse relation between fish consumption and 20-year mortality from coronary heart disease. N Engl J Med. 1985;312(19):1205-1209.

3. Kromhout D, Feskens EJ, Bowles CH. The protective effect of a small amount of fish on coronary heart disease mortality in an elderly population. Int J Epidemiol. 1995;24(2):340-345.

4. Mozaffarian D, Rimm EB. Fish intake, contaminants, and human health: Evaluating the risks and the benefits. JAMA. 2006;296(15):1885-1899.

5. Balk E, Chung M, Lichtenstein A, et al. Effects of Omega-3 Fatty Acids on Cardiovascular Risk Factors and Intermediate Markers of Cardiovascular Disease. Summary, Evidence Report/Technology Assessment: Number 93. AHRQ Publication Number 04-E010-1, March 2004. Agency for Healthcare Research and Quality, Rockville, Md. Available here.

6. Emken EA, Adolf RO, Gulley RM. Dietary linoleic acid influences desaturation and acylation of deuterium-labeled linoleic and linolenic acids in young adult males. Biochim Biophys Acta. 1994;1213(3):277-288.

7. Gerster H. Can adults adequately convert linolenic acid (18:3n-3) to eicosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3)? Int J Vitam Nutr Res. 1998;68(3):159-173.

8. U.S. Department of Health and Human Services and U.S. Department of Agriculture. Dietary Guidelines for Americans 2005, 6th Edition, Washington, D.C.: U.S. Government Printing Office, January 2005.

9. Montalescot G, Ankri A, Chadefaux-Vekemans B, et al. Plasma homocysteine and the extent of atherosclerosis in patients with coronary artery disease. Int J Cardiol. 1997;60:295-300.

10. Manilow MR, Bostom AG, Krauss KM. Homocyst(e)ine, diet, and cardiovascular disease: A statement for healthcare professionals from the Nutrition Committee, American Heart Association. Circulation. 1999;99(1):178-182.

11. Das UN. Folic acid says NO to vascular diseases. Nutrition. 2003;19(7-8):686-692.

12. Bazzano LA, He J, Ogden LG, et al. Dietary intake of folate and risk of stroke in US men and women: NHANES I Epidemiologic Follow-up Study. National Health and Nutrition Examination Survey. Stroke. 2002;33(5):1183-1188.

13. Morris CD, Carson S. Routine Vitamin Supplementation To Prevent Cardiovascular Disease: A Summary of the Evidence for the U.S. Preventive Services Task Force. Ann Intern Med. 2003;139(1):56-70.

14. Townsend MS, Fulgoni VL 3rd, Stern JS, et al. Low mineral intake is associated with high systolic blood pressure in the third and fourth National Health and Nutrition Examination Surveys: Could we all be right? Am J Hypertension. 2005;18(2 Pt 1):261-269.

15. St-Onge MP. Dietary fats, teas, dairy, and nuts: Potential functional foods for weight control? Am J Clin Nutr. 2005;81(1):7-15.

16. Kuriyama S, Shimazu T, Ohmori K, et al. Green tea consumption and mortality due to cardiovascular disease, cancer, and all causes in Japan: The Ohsaki study. JAMA. 2006;296(10):1255-1265.

17. Coimbra S, Santos-Silva A, Rocha-Pereira P, et al. Green tea consumption improves plasma lipid profiles in adults. Nutrition Research. 2006;26(11):604-607.

18. Sierksma A, van der Gaag MS, Kluft C, et al. Moderate alcohol consumption reduces plasma C-reactive protein and fibrinogen levels; a randomized, diet-controlled intervention study. Eur J Clin Nutr. 2002;56(11):1130-1136.

19. Baer DJ, Judd JT, Clevidence BA, et al. Moderate alcohol consumption lowers risk factors for cardiovascular disease in postmenopausal women fed a controlled diet. Am J Clin Nutr. 2002;75(3):593-599.

20. Mukamal KJ. Alcohol use and prognosis in patients with coronary heart disease. Prev Cardiol. 2003;6(2):93-98.

21. Rimm EB, Williams P, Fosher K, et al. Moderate alcohol intake and lower risk of coronary heart disease: Meta-analysis of effects on lipids and haemostatic factors. BMJ. 1999;319(7224):1523-1528.

22. Bazzano LA, He J, Ogden LG, et al. Dietary potassium intake and risk of stroke in US men and women: National Health and Nutrition Examination Survey I epidemiologic follow-up study. Stroke. 2001;32(7):1473-1480.

23. Dickinson HO, Nicolson DJ, Campbell F, et al. Potassium supplementation for the management of primary hypertension in adults. Cochrane Database Syst Rev. 2006;19(3):CD004641.

24. Zhan S, Ho SC. Meta-analysis of the effects of soy protein containing isoflavones on the lipid profile. Am J Clin Nutr. 2005;81(2):397-408.

25. Cassidy A, Hooper L. Phytoestrogens and cardiovascular disease. J Br Menopause Soc. 2006;12(2):49-56.

26. Sacks FM, Lichtenstein A, Van Horn L, et al. Soy protein, isoflavones, and cardiovascular health: An American Heart Association Science Advisory for professionals from the Nutrition Committee. Circulation. 2006;113(7):1034-1044.

27. Tuomainen TP, Punnonen K, Nyyssonen K, et al. Association between body iron stores and the risk of acute myocardial infarction in men. Circulation. 1998;97(15):1461-1466.

28. Salonen JT, Nyyssonen K, Korpela H, et al. High stored iron levels are associated with excess risk of myocardial infarction in eastern Finnish men. Circulation. 1992;86(3):803-811.

29. Van der A DL, Grobbee DE, Roest M, et al. Serum ferritin is a risk factor for stroke in postmenopausal women. Stroke. 2005;36(8):1637-1641.

30. Sempos CT, Looker AC, Gillum RF, et al. Serum ferritin and death from all causes and cardiovascular disease. The NHANES II Mortality Study. National Health and Nutrition Examination Survey. Ann Epidemiol. 2000;10(7):441-448.

31. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of HIgh Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA. 2001;285(19):2486-2497.

32. Lichtenstein AH, Ausman LM, Jalbert SM, et al. Effects of different forms of dietary hydrogenated fats on serum lipoprotein cholesterol levels. N Engl J Med. 1999;340(25):1933-1940.

33. Mozaffarian D, Katan MB, Ascherio A, et al. Trans fatty acids and cardiovascular disease. N Engl J Med. 2006;354(15):1601-1613.

34. Mensink RP, Zock PL, Kester AD, et al. Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: A meta-analysis of 60 controlled trials. Am J Clin Nutr. 2003;77(5):1146-1155.

35. Ascherio A, Katan MB, Zock PL, et al. Trans fatty acids and coronary heart disease. N Engl J Med. 1999;340(25):1994-1998.

36. Mauger JF, Lichtenstein AH, Ausman LM, et al. Effect of different forms of dietary hydrogenated fats on LDL particle size. Am J Clin Nutr. 2003;78(3):370-375.

37. Lopez-Garcia E, Schulze MB, Meigs JB, et al. Consumption of trans fatty acids is related to plasma biomarkers of inflammation and endothelial dysfunction. J Nutr. 2005;135(3):562-566.

38. Mozaffarian D, Pischon T, Hankinson SE, et al. Dietary intake of trans fatty acids and systemic inflammation in women. Am J Clin Nutr. 2004;79(4):606-612.

39. U.S. Food and Drug Administration. FDA Acts to Provide Better Information to Consumers on Trans Fats. 2005. Available here.