Managing CMR

Managing Cardiometabolic Risk in Abdominally Obese Patients

Nutrition

Key Points


Tips on how to eat/live healthy:

  • Eat more vegetables. They are rich in nutrients and low in calories.
  • Make wholegrain breads and cereals that contain soluble fibre—such as those made with oats—part of every meal.
  • Eat more high-fibre foods (wholegrain cereals, lentils, dried beans and peas, brown rice, vegetables, and fruits).
  • Enjoy soy products (soy milk, burgers, and hot dogs), nuts (almonds and walnuts), and pulses (dried beans, peas, lentils, and peanuts) as snacks or alternatives to high-fat meats.
  • Include fish, lean meats, low-fat cheeses, eggs, or vegetarian protein choices in your meals.
  • Have a glass of low-fat milk and piece of fruit to complete your meal.
  • Limit your intake of high-fat food such as fried foods, chips, and pastries.
  • Limit sugars and sweets such as sugar, regular soft drinks, desserts, candies, jam, and honey.
  • Limit your intake of sweetened drinks (soft drinks, juice, etc.), which are sources of excess calories.
  • Drink more water if you are thirsty.
  • Make physical activity part of your lifestyle.

Managing Abdominally Obese Patients at Increased Cardiometabolic Risk: the Nutritional Perspective


Obesity is a fast-growing epidemic caused mainly by environmental influences and poor lifestyle choices. It is now accepted that obesity—abdominal obesity in particular—increases the prevalence of a cluster of metabolic abnormalities known as cardiometabolic risk factors/markers (1). Contributing to obesity’s rise is the fact that more and more people have sedentary lifestyles, eat refined diets, and consume energy-dense food of poor nutritional value. This “permissive” environment leads to a positive energy balance, weight gain, and obesity-related complications. Various therapies—including diet, physical exercise, and pharmacological treatments—can help reduce the incidence of obesity and its metabolic abnormalities. Since many patients with hypertension, diabetes, cardiovascular disease (CVD), or the metabolic syndrome are overweight/obese and have high-risk waistlines (2-4), weight loss should be the first-line therapy prescribed by health care professionals (5, 6). However, even though diet and diet/exercise combinations can help individuals lose weight, studies have consistently shown that when the diet/exercise prescription is stopped, any weight lost is regained progressively and long-term success is jeopardized if patients are not given sufficient support. 


Targeting Excess Body Weight


In overweight or obese patients, modest weight loss of roughly 5 to 10% of initial body weight can significantly decrease the severity of obesity-related risk factors (7, 8). When this initial goal is achieved and maintained for at least 6 months, further weight loss is necessary in order to improve outcomes. Weight reduction and maintenance guidelines established by the American Heart Association (AHA), the National Cholesterol Education Program-Adult Treatment Panel (NCEP-ATP III), and the North American Association for the Study of Obesity/National Institute of Health (NAASO/NIH) recommend that less than <30% of total calories should come from fat in order to induce a weight loss of 0.5 to 1 kg per week. These recommendations also use a moderate caloric deficit of 500 to 1,000 kcal/day to ensure weight loss is slow and progressive (7, 9-11). This caloric deficit is designed to produce an average loss of 10 kg after 6 months of therapy. This progressive approach to weight loss can improve insulin sensitivity and positively influence each metabolic abnormality (i.e., hypertension, diabetes, dyslipidemia, or pre-existing CVD) even if subjects rarely achieve their ideal weight. There are a host of weight-loss methods and strategies, and it is important to tailor measures to patients’ needs to help them achieve and maintain a lower body weight.

The NIH and NAASO practical guidelines for identifying, evaluating, and treating overweight and obesity in adults recommend a low-calorie diet (5, 7). In general, diets containing 1,000 to 1,200 kcal per day are suitable for most women. A diet containing 1,200 to 1,600 kcal per day is suitable for men and may be appropriate for women who weigh 75 kg or more in order to induce a moderate caloric deficit (Table 1) (7). Awareness of foods and overall eating patterns must be emphasized. Patients must also be educated to help them develop the nutritional skills they need to better cope with a “toxic” nutritional environment.


CVD and Its Nutritional Components


Dietary components known to directly influence LDL cholesterol—which is the major cholesterol-carrying lipoprotein particle in plasma—and promote atherogenesis and thrombogenesis are saturated fats, cholesterol, and trans-fatty acids. Lowering saturated fat intake is crucial in the presence of hypertension and high plasma lipids. To reduce LDL cholesterol, saturated fat intake should be limited to <7% of total energy intake, cholesterol intake to less than 300 mg/day, and <1% of total energy should come from trans-fatty acids (9). These targets can be reached by limiting intake of foods high in saturated fat, cholesterol, and/or trans-fatty acids, such as tropical oils, fatty meats, egg yolk, shellfish, high-fat dairy products, and packaged foods containing partially hydrogenated vegetable oils. Saturated fat should also be replaced with monounsaturated fat, polyunsaturated fat, and complex carbohydrates (e.g., over 10% of total calories from polyunsaturated fat, over 15% of total calories from monounsaturated fat, and 55 to 65% or more of total calories from complex carbohydrates) (5, 7).

The AHA has set out guidelines for reducing the risk of CVD through overall healthy practices (5, 9, 12). These guidelines stress the need to achieve and maintain energy balance by matching energy expenditure to energy intake, which can help patients attain a healthy body weight, a normal lipid profile, and normal blood pressure (BP) (9). Patients should also consume a variety of fruits, vegetables, whole grains and high-fibre foods, fat-free or low-fat (<1% fat) dairy products, low in saturated fat and lean meats, and fish (at least twice a week) to ensure a sufficient supply of essential nutrients (5, 9). Portion size and frequency must be monitored, and the consumption of high-calorie foods containing refined sugars and having little nutritional value should be limited (9). Your hands can be very useful in estimating portion size. Use the portion sizes shown in the Figure as a guide.

The OMNIHEART trial recently evaluated optimal macronutrient substitution for saturated fat (carbohydrates, protein, or unsaturated fat  (13). Three different diets were assessed: a high-carbohydrate diet, a high-protein diet (10% higher in protein than the other two diets), and an unsaturated fat diet (10% higher in unsaturated fat sources such as olive oil, canola, and safflower oil). The trial found that partial substitution of carbohydrates with either protein or monounsaturated fat could further lower BP, improve lipid levels, and reduce CVD risk (13). In addition, protein should be derived either from plants or lean animal protein and should provide approximately 15% of total calories. 

Long-chain omega-3 fatty acids (omega-3), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA)/fish oil and omega-3 fatty acid supplements have been shown to reduce mortality from coronary heart disease (CHD) and sudden cardiac death in both animal models and patients with and without coronary artery disease (14-18). Current guidelines recommend at least 2 servings of fatty fish per week (such as mackerel, lake trout, herring, sardines, albacore tuna, and salmon) and the inclusion of vegetable oils and food sources high in alpha-linolenic acids (canola, soybean oils, flaxseed, walnuts) for most individuals (5, 17). Evidence suggests that EPA and DHA supplementation from 0.5 to 1.8 g per day from fatty fish or supplements can significantly reduce subsequent cardiac and all-cause mortality (17). In patients with documented CVD, EPA and DHA supplements can be of benefit, as can consuming 1 g daily of EPA+DHA from a variety of fatty fishes. In patients with high levels of triglycerides, 2 to 4 g of EPA+DHA daily is recommended, ideally from supplements under medical supervision (17).

There are a number of hypotheses about how omega-3 fatty acids work to reduce CVD risk: 1) they reduce susceptibility to ventricular arrhythmias, 2) they have antithrombogenic properties, 3) they enable nitric oxide-induced endothelial relaxation, 4) they retard atherosclerotic plaque growth, 5) they have hypotriglyceridemic properties, and 6) they have hypotensive effects (19). The Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto miocardico (GISSI)-Prevenzione trial reported a 20% reduction in overall mortality and a 45% reduction in sudden death after 3.5 years with 850 mg of EPA and DHA omega-3 fatty acid supplementation (either with and without vitamin E) in subjects with preexisting CHD (14, 16). The Diet and Angina Randomized Trial (DART) trial reported a 29% reduction in all-cause mortality over a 2 year period after individuals with previous myocardial infarction increased their fatty fish intake to 200 to 400 g per week (18). Omega-3 fatty acids decrease triglyceride levels by 25% to 30% while also raising HDL cholesterol 1% to 3% and LDL cholesterol 5% to 10% (20). Though omega-3 fatty acids provide many health benefits, patients may not be aware of them. Dietitian involvement is crucial in order to educate patients and encourage them to increase their omega-3 fatty acid intake.


Reducing Blood Pressure


There is wealth of evidence tying salt (sodium chloride) intake to high BP. Accordingly, lowering salt intake can prevent hypertension in non-hypertensive individuals, lower blood pressure in conjunction with antihypertensive medication, and facilitate hypertension control (9, 21-23). Reducing sodium intake by 1.8 g per day (roughly 2/3 teaspoon of table salt) or limiting average daily consumption to 2.3 g (1 teaspoon of table salt) can significantly reduce systolic and diastolic BP (21-23).
Several scientific dietary reports and guidelines currently advocate the Dietary Approaches to Stop Hypertension (DASH) diet for preventing and treating BP in individuals with and without hypertension (5, 7, 21, 23-26). The DASH trial showed that a diet that emphasizes vegetables, fruits, low-fat dairy products, whole grains, poultry, fish, and nuts, and limits the amount of red meat, sweets, sugar-containing beverages, total fat, saturated fat, and cholesterol can substantially lower mean systolic BP by 7.1 mm Hg in people without hypertension and by 11.5 mm Hg in people with hypertension (21, 22). The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) recommends weight reduction, which may reduce systolic BP by 5 mm Hg to 20 mm Hg per 10 kg weight loss. It also recommends adopting the DASH diet and limiting daily dietary sodium intake to no more than 100 mmol or 2.4 g sodium or 6 g sodium chloride (one teaspoon of sodium chloride = 2.4 g of sodium) (27)

The Canadian Hypertension Education Program has proposed lifestyle and dietary modifications in order to prevent and/or treat hypertension. These recommendations are as follows: 30 to 60 minutes of aerobic exercise per day, achieving and maintaining an ideal body weight and waist circumference, limiting alcohol intake, reducing total fat and cholesterol intake, and limiting salt consumption (28)


Moderate Alcohol Consumption


Moderate alcohol consumption has been shown to reduce cardiovascular events in population studies (29). However, alcohol consumption cannot be recommended to reduce CVD risk because of the risk of addiction and its serious health consequences. If alcohol is consumed, intake should be limited to no more than 2 drinks per day for most men and no more than one drink per day for women and lightweight individuals (1 drink is equivalent to a 341 ml beer, 150 ml glass of wine, and 45 ml of spirits) (27, 30). Failure to heed intake guidelines can increase the risk of hypertriglyceridemia, hypertension, liver damage, and breast cancer (29). Moderate alcohol consumption is an integral part of many official guidelines, such as AHA recommendations, the DASH diet, and the NCEP-ATP III.


The Mediterranean Diet


A Mediterranean diet can reduce the recurrence of myocardial infarction and cardiac death by 70%. Such a diet gets <35% of its energy from fat (from rapeseed oil), <10% of its energy from saturated fat, 0.6% of its energy from omega-3 fatty acids (34). The Lyon Diet Heart Study tested a Mediterranean-type diet characterized by a low intake of total and saturated fats and a high intake of omega-3 fatty acids, fruits, vegetables, wholegrain cereals, and vegetable protein—in short, a diet high in antioxidants, vitamins, and minerals (34). After 46 months of follow-up, the group on the Mediterranean diet had a 72% reduction in cardiac death and non-fatal myocardial infarction compared to the group on the traditional diet. The risk of recurrent heart disease also dropped 56% (34). The Mediterranean diet has also been shown to benefit total cholesterol, apolipoprotein B concentration, and LDL particle size (35-37). Table 2 provides some nutritional tips on how to achieve cardiometabolic health.

The traditional Mediterranean diet has received a great deal of attention because of initial results from the Seven Countries Study, which demonstrated that this diet was associated with a decreased CHD mortality rate, mainly due to its low saturated fat content (31). This diet is characterized by abundant intake of fresh fruits and vegetables, whole grain products, monounsaturated fat from olive oil, and low-fat dairy products (mainly cheese and yogurt). The traditional Mediterranean diet has the following features: 1) a high monounsaturated-to-saturated fat ratio, 2) moderate alcohol consumption, and 3) limited consumption of meat and meat products. Some studies have taken a different view of daily meat consumption, suggesting the diet stresses greater consumption of fish and poultry and a restricted-to-moderate consumption of eggs (zero to 4 eggs per week) (32, 33). In terms of macronutrients, 25 to 30% of total energy intake comes from fat, with limited consumption of saturated fat (<7% to 8% of total energy intake). Monounsaturated fats as well as foods rich in antioxidants (e.g., cranberries, blueberries, and blackberries), fibre, and selenium (e.g., Brazil nuts, seafood, and poultry) also figure prominently (33).


Other Dietary Measures to Lower CVD Risk and Cholesterol Levels


Oxidative stress significantly increases the atherogenicity of cholesterol-enriched LDL particles through LDL oxidation, which initiates a series of reactions resulting in atherosclerosis (38, 39). Dietary antioxidants may contribute to cardiovascular protection and CVD risk reduction by inhibiting LDL oxidation and preserving endothelial function (5, 38, 40). Carotenoids are lipid-soluble antioxidants found in high concentrations in many yellow and green fruits and vegetables. Lycopene is a carotenoid found mainly in tomato-based foods, which account for approximately 80% of the lycopene intake in the American diet. Lycopene is heat resistant and may play a beneficial role in the early stages of atherogenesis and CVD (40-42). For the time being, there is insufficient evidence to recommend antioxidant supplementation. Some trials have documented an increased risk of heart failure and total mortality from high doses of vitamin E (43, 44). However, consuming antioxidants from a variety of plant-derived foods (vegetables, fruits, whole grains, and vegetable oils) is recommended (9).

Soy protein consumption—in the form of whole foods such as tofu and soymilk, or as soy protein added to foods—has been shown to be associated with a significant decrease in CHD risk. Soy protein has been linked to a 5 to 6% reduction in LDL cholesterol levels when substituted for animal protein (45). This reduction in total and LDL cholesterol may be explained by the fact that soy products are naturally low in saturated fat and cholesterol, unlike animal products. Eating a diet high in vegetable protein instead of one high in animal protein can lower total cholesterol, LDL cholesterol, and triglycerides by 4 to 7% without affecting HDL cholesterol (46). The isoflavone fraction present in soy products also has other lipid-independent benefits, such as lowering BP and increasing LDL oxidation resistance (45, 47). In addition, phytoestrogen isoflavones have been shown to lower cholesterol (48)

Soluble fibres such as oat bran, pectin, and guar gum as well as viscous non-fermentable fibres such as psyllium help lower LDL cholesterol and glucose levels (49-52). Current guidelines recommend increasing fibre intake to 25 to 30 g per day (current daily fibre intake in North America is approximately 10 to 15 g), with an emphasis on vegetables, cereals, and fruits (5, 7, 10). Soluble fibres lower cholesterol levels by binding bile acids in the intestinal lumen, lessening the absorption and increasing fecal excretion of cholesterol (51). Besides their effect on serum lipid concentrations, soluble fibres such as psyllium also improve glycemic control (a 1.6% decrease of HbA1c after 8 weeks of treatment with 5.1 g b.i.d. of psyllium husk fibre) (50).

Plant sterol and plant stanol esters have proven effective in reducing total and LDL cholesterol (53, 54). Plant sterols are found in small quantities in many fruits, vegetables, nuts, seeds, cereals, legumes, and other plant sources or may be added to food products. Consuming 2 to 3 g of plant sterols per day has been shown to decrease total and LDL cholesterol levels by 9 to 20% respectively, without altering HDL cholesterol (55-58). The NCEP-ATP III and AHA recommend adding 2 g of plant sterols/stanols to the daily diet of patients at risk of CVD (9, 10, 59). In examining the potential of functional ingredients (viscous fibres and plant sterols, soy protein, and nuts), Jenkins et al. (60) compared their effectiveness on the plasma lipid profile to that of traditional first-generation statin treatments (lovastatin). Jenkins’ “portfolio” diet has been shown to reduce LDL cholesterol (30%) and induce clinically significant reductions in estimated CHD risk. As mentioned above, these dietary, functional ingredients have effects on the plasma lipid profiles similar to those of first-generation statin treatments (60).

Changing poor eating habits is an efficient and inexpensive way to improve cardiometabolic risk factors/markers. Current dietary guidelines make strong recommendations that are designed to reduce health complications in conjunction with other healthy practices such as regular physical exercise and smoking cessation. To maximize its chances of success, the ideal nutritional treatment should be personalized, intensive, and supervised by qualified health care professionals.


References


  1. Després JP and Lemieux I. Abdominal obesity and metabolic syndrome. Nature 2006; 444: 881-7.
  2. Poirier P, Lemieux I, Mauriège P, et al. Impact of waist circumference on the relationship between blood pressure and insulin: the Quebec Health Survey. Hypertension 2005; 45: 363-7.
  3. Macdonald SM, Reeder BA, Chen Y, et al. Obesity in Canada: a descriptive analysis. Canadian Heart Health Surveys Research Group. CMAJ 1997; 157 Suppl 1: S3-9.
  4. Johnson D, Prud'homme D, Després JP, et al. Relation of abdominal obesity to hyperinsulinemia and high blood pressure in men. Int J Obes Relat Metab Disord 1992; 16: 881-90.
  5. Krauss RM, Eckel RH, Howard B, et al. AHA Dietary Guidelines: revision 2000: A statement for healthcare professionals from the Nutrition Committee of the American Heart Association. Circulation 2000; 102: 2284-99.
  6. Eckel RH and Krauss RM. American Heart Association call to action: obesity as a major risk factor for coronary heart disease. AHA Nutrition Committee. Circulation 1998; 97: 2099-100.
  7. The Practical Guide: Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. 2000; 1-94.
  8. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults--The Evidence Report. National Institutes of Health. Obes Res 1998; 6 Suppl 2: 51S-209S.
  9. 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: 82-96.
  10. 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: 2486-97.
  11. Grundy SM, Cleeman JI, Daniels SR, et al. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation 2005; 112: 2735-52.
  12. Klein S, Burke LE, Bray GA, et al. Clinical implications of obesity with specific focus on cardiovascular disease: a statement for professionals from the American Heart Association Council on Nutrition, Physical Activity, and Metabolism: endorsed by the American College of Cardiology Foundation. Circulation 2004; 110: 2952-67.
  13. Appel LJ, Sacks FM, Carey VJ, et al. Effects of protein, monounsaturated fat, and carbohydrate intake on blood pressure and serum lipids: results of the OmniHeart randomized trial. JAMA 2005; 294: 2455-64.
  14. Salen P and de Lorgeril M. GISSI-Prevenzione trial. Lancet 1999; 354: 1555; author reply 6-7.
  15. Matthan NR, Jordan H, Chung M, et al. A systematic review and meta-analysis of the impact of omega-3 fatty acids on selected arrhythmia outcomes in animal models. Metabolism 2005; 54: 1557-65.
  16. Marchioli R, Barzi F, Bomba E, et al. Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico (GISSI)-Prevenzione. Circulation 2002; 105: 1897-903.
  17. Kris-Etherton PM, Harris WS and Appel LJ. Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Circulation 2002; 106: 2747-57.
  18. Burr ML, Fehily AM, Gilbert JF, et al. Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial (DART). Lancet 1989; 2: 757-61.
  19. Connor WE. Importance of n-3 fatty acids in health and disease. Am J Clin Nutr 2000; 71: 171S-5S.
  20. Harris WS. n-3 fatty acids and serum lipoproteins: human studies. Am J Clin Nutr 1997; 65: 1645S-54S.
  21. Appel LJ, Moore TJ, Obarzanek E, et al. A clinical trial of the effects of dietary patterns on blood pressure. DASH Collaborative Research Group. N Engl J Med 1997; 336: 1117-24.
  22. Vollmer WM, Sacks FM, Ard J, et al. Effects of diet and sodium intake on blood pressure: subgroup analysis of the DASH-sodium trial. Ann Intern Med 2001; 135: 1019-28.
  23. Sacks FM, Svetkey LP, Vollmer WM, et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. N Engl J Med 2001; 344: 3-10.
  24. Lauber RP and Sheard NF. The American Heart Association Dietary Guidelines for 2000: a summary report. Nutr Rev 2001; 59: 298-306.
  25. Svetkey LP, Sacks FM, Obarzanek E, et al. The DASH Diet, Sodium Intake and Blood Pressure Trial (DASH-sodium): rationale and design. DASH-Sodium Collaborative Research Group. J Am Diet Assoc 1999; 99: S96-104.
  26. Zemel MB. Dietary pattern and hypertension: the DASH study. Dietary Approaches to Stop Hypertension. Nutr Rev 1997; 55: 303-5.
  27. Chobanian AV, Bakris GL, Black HR, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA 2003; 289: 2560-72.
  28. Khan NA, McAlister FA, Lewanczuk RZ, et al. The 2005 Canadian Hypertension Education Program recommendations for the management of hypertension: part II - therapy. Can J Cardiol 2005; 21: 657-72.
  29. Flesch M, Rosenkranz S, Erdmann E, et al. Alcohol and the risk of myocardial infarction. Basic Res Cardiol 2001; 96: 128-35.
  30. Goldberg IJ, Mosca L, Piano MR, et al. AHA Science Advisory: Wine and your heart: a science advisory for healthcare professionals from the Nutrition Committee, Council on Epidemiology and Prevention, and Council on Cardiovascular Nursing of the American Heart Association. Circulation 2001; 103: 472-5.
  31. Keys A, Menotti A, Karvonen MJ, et al. The diet and 15-year death rate in the seven countries study. Am J Epidemiol 1986; 124: 903-15.
  32. Kris-Etherton P, Eckel RH, Howard BV, et al. AHA Science Advisory: Lyon Diet Heart Study. Benefits of a Mediterranean-style, National Cholesterol Education Program/American Heart Association Step I Dietary Pattern on Cardiovascular Disease. Circulation 2001; 103: 1823-5.
  33. Willett WC, Sacks F, Trichopoulou A, et al. Mediterranean diet pyramid: a cultural model for healthy eating. Am J Clin Nutr 1995; 61: 1402S-6S.
  34. de Lorgeril M, Salen P, Martin JL, et al. Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction: final report of the Lyon Diet Heart Study. Circulation 1999; 99: 779-85.
  35. Goulet J, Lamarche B, Charest A, et al. Effect of a nutritional intervention promoting the Mediterranean food pattern on electrophoretic characteristics of low-density lipoprotein particles in healthy women from the Quebec City metropolitan area. Br J Nutr 2004; 92: 285-93.
  36. Lapointe A, Goulet J, Couillard C, et al. A nutritional intervention promoting the Mediterranean food pattern is associated with a decrease in circulating oxidized LDL particles in healthy women from the Quebec City metropolitan area. J Nutr 2005; 135: 410-5.
  37. Goulet J, Lamarche B, Nadeau G, et al. Effect of a nutritional intervention promoting the Mediterranean food pattern on plasma lipids, lipoproteins and body weight in healthy French-Canadian women. Atherosclerosis 2003; 170: 115-24.
  38. Gaziano JM, Manson JE, Branch LG, et al. A prospective study of consumption of carotenoids in fruits and vegetables and decreased cardiovascular mortality in the elderly. Ann Epidemiol 1995; 5: 255-60.
  39. Manson JE, Gaziano JM, Spelsberg A, et al. A secondary prevention trial of antioxidant vitamins and cardiovascular disease in women. Rationale, design, and methods. The WACS Research Group. Ann Epidemiol 1995; 5: 261-9.
  40. Rissanen T, Voutilainen S, Nyyssonen K, et al. Lycopene, atherosclerosis, and coronary heart disease. Exp Biol Med (Maywood) 2002; 227: 900-7.
  41. Sesso HD, Buring JE, Norkus EP, et al. Plasma lycopene, other carotenoids, and retinol and the risk of cardiovascular disease in men. Am J Clin Nutr 2005; 81: 990-7.
  42. Sesso HD, Buring JE, Norkus EP, et al. Plasma lycopene, other carotenoids, and retinol and the risk of cardiovascular disease in women. Am J Clin Nutr 2004; 79: 47-53.
  43. Lonn E, Bosch J, Yusuf S, et al. Effects of long-term vitamin E supplementation on cardiovascular events and cancer: a randomized controlled trial. JAMA 2005; 293: 1338-47.
  44. Miller ER, 3rd, Pastor-Barriuso R, Dalal D, et al. Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality. Ann Intern Med 2005; 142: 37-46.
  45. Sagara M, Kanda T, M NJ, et al. Effects of dietary intake of soy protein and isoflavones on cardiovascular disease risk factors in high risk, middle-aged men in Scotland. J Am Coll Nutr 2004; 23: 85-91.
  46. Anderson JW, Johnstone BM and Cook-Newell ME. Meta-analysis of the effects of soy protein intake on serum lipids. N Engl J Med 1995; 333: 276-82.
  47. Ashton EL, Dalais FS and Ball MJ. Effect of meat replacement by tofu on CHD risk factors including copper induced LDL oxidation. J Am Coll Nutr 2000; 19: 761-7.
  48. Crouse JR, 3rd, Morgan T, Terry JG, et al. A randomized trial comparing the effect of casein with that of soy protein containing varying amounts of isoflavones on plasma concentrations of lipids and lipoproteins. Arch Intern Med 1999; 159: 2070-6.
  49. Jenkins DJ, Kendall CW, Vuksan V, et al. Soluble fiber intake at a dose approved by the US Food and Drug Administration for a claim of health benefits: serum lipid risk factors for cardiovascular disease assessed in a randomized controlled crossover trial. Am J Clin Nutr 2002; 75: 834-9.
  50. Ziai SA, Larijani B, Akhoondzadeh S, et al. Psyllium decreased serum glucose and glycosylated hemoglobin significantly in diabetic outpatients. J Ethnopharmacol 2005; 102: 202-7.
  51. Jenkins DJ, Wolever TM, Rao AV, et al. Effect on blood lipids of very high intakes of fiber in diets low in saturated fat and cholesterol. N Engl J Med 1993; 329: 21-6.
  52. Sierra M, Garcia JJ, Fernandez N, et al. Therapeutic effects of psyllium in type 2 diabetic patients. Eur J Clin Nutr 2002; 56: 830-42.
  53. Heinemann T, Kullak-Ublick GA, Pietruck B, et al. Mechanisms of action of plant sterols on inhibition of cholesterol absorption. Comparison of sitosterol and sitostanol. Eur J Clin Pharmacol 1991; 40 Suppl 1: S59-63.
  54. Plat J and Mensink RP. Plant stanol and sterol esters in the control of blood cholesterol levels: mechanism and safety aspects. Am J Cardiol 2005; 96: 15D-22D.
  55. Miettinen TA, Puska P, Gylling H, et al. Reduction of serum cholesterol with sitostanol-ester margarine in a mildly hypercholesterolemic population. N Engl J Med 1995; 333: 1308-12.
  56. Patch CS, Tapsell LC and Williams PG. Plant sterol/stanol prescription is an effective treatment strategy for managing hypercholesterolemia in outpatient clinical practice. J Am Diet Assoc 2005; 105: 46-52.
  57. Cater NB, Garcia-Garcia AB, Vega GL, et al. Responsiveness of plasma lipids and lipoproteins to plant stanol esters. Am J Cardiol 2005; 96: 23D-8D.
  58. Gylling H and Miettinen TA. Serum cholesterol and cholesterol and lipoprotein metabolism in hypercholesterolaemic NIDDM patients before and during sitostanol ester-margarine treatment. Diabetologia 1994; 37: 773-80.
  59. Grundy SM. Stanol esters as a component of maximal dietary therapy in the National Cholesterol Education Program Adult Treatment Panel III report. Am J Cardiol 2005; 96: 47D-50D.
  60. Jenkins DJ, Kendall CW, Marchie A, et al. Direct comparison of a dietary portfolio of cholesterol-lowering foods with a statin in hypercholesterolemic participants. Am J Clin Nutr 2005; 81: 380-7.

Reference
Previous Reference
Next Reference
1. Després JP and Lemieux I. Abdominal obesity and metabolic syndrome. Nature 2006; 444: 881-7.
2. Poirier P, Lemieux I, Mauriège P, et al. Impact of waist circumference on the relationship between blood pressure and insulin: the Quebec Health Survey. Hypertension 2005; 45: 363-7.
3. Macdonald SM, Reeder BA, Chen Y, et al. Obesity in Canada: a descriptive analysis. Canadian Heart Health Surveys Research Group. CMAJ 1997; 157 Suppl 1: S3-9.
4. Johnson D, Prud'homme D, Després JP, et al. Relation of abdominal obesity to hyperinsulinemia and high blood pressure in men. Int J Obes Relat Metab Disord 1992; 16: 881-90.
5. Krauss RM, Eckel RH, Howard B, et al. AHA Dietary Guidelines: revision 2000: A statement for healthcare professionals from the Nutrition Committee of the American Heart Association. Circulation 2000; 102: 2284-99.
6. Eckel RH and Krauss RM. American Heart Association call to action: obesity as a major risk factor for coronary heart disease. AHA Nutrition Committee. Circulation 1998; 97: 2099-100.
7. The Practical Guide: Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. 2000; 1-94.
8. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults--The Evidence Report. National Institutes of Health. Obes Res 1998; 6 Suppl 2: 51S-209S.
9. 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: 82-96.
10. 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: 2486-97.
11. Grundy SM, Cleeman JI, Daniels SR, et al. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation 2005; 112: 2735-52.
12. Klein S, Burke LE, Bray GA, et al. Clinical implications of obesity with specific focus on cardiovascular disease: a statement for professionals from the American Heart Association Council on Nutrition, Physical Activity, and Metabolism: endorsed by the American College of Cardiology Foundation. Circulation 2004; 110: 2952-67.
13. Appel LJ, Sacks FM, Carey VJ, et al. Effects of protein, monounsaturated fat, and carbohydrate intake on blood pressure and serum lipids: results of the OmniHeart randomized trial. JAMA 2005; 294: 2455-64.
14. Salen P and de Lorgeril M. GISSI-Prevenzione trial. Lancet 1999; 354: 1555; author reply 6-7.
15. Matthan NR, Jordan H, Chung M, et al. A systematic review and meta-analysis of the impact of omega-3 fatty acids on selected arrhythmia outcomes in animal models. Metabolism 2005; 54: 1557-65.
16. Marchioli R, Barzi F, Bomba E, et al. Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico (GISSI)-Prevenzione. Circulation 2002; 105: 1897-903.
17. Kris-Etherton PM, Harris WS and Appel LJ. Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Circulation 2002; 106: 2747-57.
18. Burr ML, Fehily AM, Gilbert JF, et al. Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial (DART). Lancet 1989; 2: 757-61.
19. Connor WE. Importance of n-3 fatty acids in health and disease. Am J Clin Nutr 2000; 71: 171S-5S.
20. Harris WS. n-3 fatty acids and serum lipoproteins: human studies. Am J Clin Nutr 1997; 65: 1645S-54S.
21. Appel LJ, Moore TJ, Obarzanek E, et al. A clinical trial of the effects of dietary patterns on blood pressure. DASH Collaborative Research Group. N Engl J Med 1997; 336: 1117-24.
22. Vollmer WM, Sacks FM, Ard J, et al. Effects of diet and sodium intake on blood pressure: subgroup analysis of the DASH-sodium trial. Ann Intern Med 2001; 135: 1019-28.
23. Sacks FM, Svetkey LP, Vollmer WM, et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. N Engl J Med 2001; 344: 3-10.
24. Lauber RP and Sheard NF. The American Heart Association Dietary Guidelines for 2000: a summary report. Nutr Rev 2001; 59: 298-306.
25. Svetkey LP, Sacks FM, Obarzanek E, et al. The DASH Diet, Sodium Intake and Blood Pressure Trial (DASH-sodium): rationale and design. DASH-Sodium Collaborative Research Group. J Am Diet Assoc 1999; 99: S96-104.
26. Zemel MB. Dietary pattern and hypertension: the DASH study. Dietary Approaches to Stop Hypertension. Nutr Rev 1997; 55: 303-5.
27. Chobanian AV, Bakris GL, Black HR, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA 2003; 289: 2560-72.
28. Khan NA, McAlister FA, Lewanczuk RZ, et al. The 2005 Canadian Hypertension Education Program recommendations for the management of hypertension: part II - therapy. Can J Cardiol 2005; 21: 657-72.
29. Flesch M, Rosenkranz S, Erdmann E, et al. Alcohol and the risk of myocardial infarction. Basic Res Cardiol 2001; 96: 128-35.
30. Goldberg IJ, Mosca L, Piano MR, et al. AHA Science Advisory: Wine and your heart: a science advisory for healthcare professionals from the Nutrition Committee, Council on Epidemiology and Prevention, and Council on Cardiovascular Nursing of the American Heart Association. Circulation 2001; 103: 472-5.
31. Keys A, Menotti A, Karvonen MJ, et al. The diet and 15-year death rate in the seven countries study. Am J Epidemiol 1986; 124: 903-15.
32. Kris-Etherton P, Eckel RH, Howard BV, et al. AHA Science Advisory: Lyon Diet Heart Study. Benefits of a Mediterranean-style, National Cholesterol Education Program/American Heart Association Step I Dietary Pattern on Cardiovascular Disease. Circulation 2001; 103: 1823-5.
33. Willett WC, Sacks F, Trichopoulou A, et al. Mediterranean diet pyramid: a cultural model for healthy eating. Am J Clin Nutr 1995; 61: 1402S-6S.
34. de Lorgeril M, Salen P, Martin JL, et al. Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction: final report of the Lyon Diet Heart Study. Circulation 1999; 99: 779-85.
35. Goulet J, Lamarche B, Charest A, et al. Effect of a nutritional intervention promoting the Mediterranean food pattern on electrophoretic characteristics of low-density lipoprotein particles in healthy women from the Quebec City metropolitan area. Br J Nutr 2004; 92: 285-93.
36. Lapointe A, Goulet J, Couillard C, et al. A nutritional intervention promoting the Mediterranean food pattern is associated with a decrease in circulating oxidized LDL particles in healthy women from the Quebec City metropolitan area. J Nutr 2005; 135: 410-5.
37. Goulet J, Lamarche B, Nadeau G, et al. Effect of a nutritional intervention promoting the Mediterranean food pattern on plasma lipids, lipoproteins and body weight in healthy French-Canadian women. Atherosclerosis 2003; 170: 115-24.
38. Gaziano JM, Manson JE, Branch LG, et al. A prospective study of consumption of carotenoids in fruits and vegetables and decreased cardiovascular mortality in the elderly. Ann Epidemiol 1995; 5: 255-60.
39. Manson JE, Gaziano JM, Spelsberg A, et al. A secondary prevention trial of antioxidant vitamins and cardiovascular disease in women. Rationale, design, and methods. The WACS Research Group. Ann Epidemiol 1995; 5: 261-9.
40. Rissanen T, Voutilainen S, Nyyssonen K, et al. Lycopene, atherosclerosis, and coronary heart disease. Exp Biol Med (Maywood) 2002; 227: 900-7.
41. Sesso HD, Buring JE, Norkus EP, et al. Plasma lycopene, other carotenoids, and retinol and the risk of cardiovascular disease in men. Am J Clin Nutr 2005; 81: 990-7.
42. Sesso HD, Buring JE, Norkus EP, et al. Plasma lycopene, other carotenoids, and retinol and the risk of cardiovascular disease in women. Am J Clin Nutr 2004; 79: 47-53.
43. Lonn E, Bosch J, Yusuf S, et al. Effects of long-term vitamin E supplementation on cardiovascular events and cancer: a randomized controlled trial. JAMA 2005; 293: 1338-47.
44. Miller ER, 3rd, Pastor-Barriuso R, Dalal D, et al. Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality. Ann Intern Med 2005; 142: 37-46.
45. Sagara M, Kanda T, M NJ, et al. Effects of dietary intake of soy protein and isoflavones on cardiovascular disease risk factors in high risk, middle-aged men in Scotland. J Am Coll Nutr 2004; 23: 85-91.
46. Anderson JW, Johnstone BM and Cook-Newell ME. Meta-analysis of the effects of soy protein intake on serum lipids. N Engl J Med 1995; 333: 276-82.
47. Ashton EL, Dalais FS and Ball MJ. Effect of meat replacement by tofu on CHD risk factors including copper induced LDL oxidation. J Am Coll Nutr 2000; 19: 761-7.
48. Crouse JR, 3rd, Morgan T, Terry JG, et al. A randomized trial comparing the effect of casein with that of soy protein containing varying amounts of isoflavones on plasma concentrations of lipids and lipoproteins. Arch Intern Med 1999; 159: 2070-6.
49. Jenkins DJ, Kendall CW, Vuksan V, et al. Soluble fiber intake at a dose approved by the US Food and Drug Administration for a claim of health benefits: serum lipid risk factors for cardiovascular disease assessed in a randomized controlled crossover trial. Am J Clin Nutr 2002; 75: 834-9.
50. Ziai SA, Larijani B, Akhoondzadeh S, et al. Psyllium decreased serum glucose and glycosylated hemoglobin significantly in diabetic outpatients. J Ethnopharmacol 2005; 102: 202-7.
51. Jenkins DJ, Wolever TM, Rao AV, et al. Effect on blood lipids of very high intakes of fiber in diets low in saturated fat and cholesterol. N Engl J Med 1993; 329: 21-6.
52. Sierra M, Garcia JJ, Fernandez N, et al. Therapeutic effects of psyllium in type 2 diabetic patients. Eur J Clin Nutr 2002; 56: 830-42.
53. Heinemann T, Kullak-Ublick GA, Pietruck B, et al. Mechanisms of action of plant sterols on inhibition of cholesterol absorption. Comparison of sitosterol and sitostanol. Eur J Clin Pharmacol 1991; 40 Suppl 1: S59-63.
54. Plat J and Mensink RP. Plant stanol and sterol esters in the control of blood cholesterol levels: mechanism and safety aspects. Am J Cardiol 2005; 96: 15D-22D.
55. Miettinen TA, Puska P, Gylling H, et al. Reduction of serum cholesterol with sitostanol-ester margarine in a mildly hypercholesterolemic population. N Engl J Med 1995; 333: 1308-12.
56. Patch CS, Tapsell LC and Williams PG. Plant sterol/stanol prescription is an effective treatment strategy for managing hypercholesterolemia in outpatient clinical practice. J Am Diet Assoc 2005; 105: 46-52.
57. Cater NB, Garcia-Garcia AB, Vega GL, et al. Responsiveness of plasma lipids and lipoproteins to plant stanol esters. Am J Cardiol 2005; 96: 23D-8D.
58. Gylling H and Miettinen TA. Serum cholesterol and cholesterol and lipoprotein metabolism in hypercholesterolaemic NIDDM patients before and during sitostanol ester-margarine treatment. Diabetologia 1994; 37: 773-80.
59. Grundy SM. Stanol esters as a component of maximal dietary therapy in the National Cholesterol Education Program Adult Treatment Panel III report. Am J Cardiol 2005; 96: 47D-50D.
60. Jenkins DJ, Kendall CW, Marchie A, et al. Direct comparison of a dietary portfolio of cholesterol-lowering foods with a statin in hypercholesterolemic participants. Am J Clin Nutr 2005; 81: 380-7.