Bioactive Food as Dietary Interventions for Cardiovascular Disease: Bioactive Foods in Chronic Disease States

By Ronald Ross Watson and Victor R Preedy

One major example of the synergy of bioactive foods and extracts is their role as an antioxidant and the related remediation of cardiovascular disease. There is compelling evidence to suggest that oxidative stress is implicated in the physiology of several major cardiovascular diseases including heart failure and increased free radical formation and reduced antioxidant defences. Studies indicate bioactive foods reduce the incidence of these conditions, suggestive of a potential cardioprotective role of antioxidant nutrients.

Bioactive Food as Dietary Interventions for Cardiovascular Disease investigates the role of foods, herbs and novel extracts in moderating the pathology leading to cardiovascular disease. It reviews existing literature, and presents new hypotheses and conclusions on the effects of different bioactive components of the diet.

• Addresses the most positive results from dietary interventions using bioactive foods to impact cardiovascular disease
• Documents foods that can affect metabolic syndrome and other related conditions
• Convenient, efficient and effective source that allows readers to identify potential uses of compounds – or indicate those compounds whose use may be of little or no health benefit
• Associated information can be used to understand other diseases that share common etiological pathways

• Language: English
• Publisher: Academic Press
• Release date: Oct 22, 2012
• ISBN: 9780123965400

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USA

Chapter 1

Omega-3 Fatty Acids in Prevention of Cardiovascular Disease in Humans

Intervention Trials, Healthy Heart Concept, Future Developments

R. Sharma*,†,‡, R.J. Moffatt§, R.B. Singh¶ and J. Katz†, ‡

*Amity University Uttar Pradesh, Noida, India

†Dr Katz’s Cardiology Center, New York, NY, USA

‡Columbia University, New York, NY, USA

§Florida State University, Tallahassee, FL, USA

¶Halberg Research Center, Moradabad, India

1 Introduction

In the twentieth century, dietary intake and lifestyles have changed significantly to cause increased intake of saturated fatty acids (SFAs), linoleic acid, and a decrease in omega-3 fatty acids, from grain-fed cattle, farm houses, and inbreeding in animals. Such changes marked a reduction in the consumption of omega-3 fatty acids, vitamins, minerals, and proteins, and a significant increase in the intake of refined carbohydrates and fat (saturated, trans fat, and linoleic acid). As a result, less availability of omega-3 fatty acids in the diet or improper fatty acid omega-6/omega-3 ratio modulates or enhances blood pressure, obesity, diabetes, dyslipidemia, and coronary risk in patients with high risk of cardiovascular disease (CVD). It is believed that the proper omega-6/omega-3 ratio in the diet and a lifestyle with plenty of physical exercise may be protective because of the antioxidant, anti-inflammatory, and anti-arrhythmic action of omega fatty acids. This chapter describes the role of omega fatty acids in CVD and as functional foods, omega fatty acid supplementation, its safety, global guidelines of fatty acid intake, its lipid lowering mechanisms, ancient or tribal practices, and future developments, in the following sections.

2 Role of Omega-3 Fatty Acids in CVD

Evidence shows that reducing the incidence of coronary heart disease (CHD) with omega-3 fatty acid therapy is possible (Calder, 2004). National Cholesterol Education Program Adult Treatment Panel III (ATP III) suggested dietary changes (saturated fat <7%; polyunsaturated fat <10%; monounsaturated fat <20%; total fat 25%; carbohydrates 50%; fiber 30 g day−1; protein 15% of total calories; cholesterol <200 mg day−1) to reduce the risk factors of coronary atherosclerosis with physical activity for 30–60 min (NCEP ATP III, 2001).

2.1 Role of Omega Fatty Acids in Dietary Fat and Vascular Health

Intake of dietary SFAs, trans fatty acids (TFAs), and cholesterol has been shown to increase serum total cholesterol and low-density lipoprotein-cholesterol (LDL-C) levels in a dose-dependent manner. Recommendations specify reduced dietary saturated fat, trans fats, and cholesterol, and fat limited to 13% of energy (Van Horn et al., 2008). National Cholesterol Education Program Adult Treatment Panel III (ATP III) suggested dietary changes (saturated fat <7%; polyunsaturated fat <10%; monounsaturated fat <20%; total fat 25%; carbohydrates 50%; fiber 30 g day−1; protein 15% of total calories; cholesterol <200 mg day−1) to reduce the risk factors of coronary atherosclerosis with physical activity for 30–60 min. TFAs have the strongest effect on raising the ratio of serum total cholesterol to high-density lipoprotein (HDL) (Mensink et al., 2003)-cholesterol (HDL-C) of CHD risk. Trans fats account for 2.6% or 5.3 g day−1 of total energy intake in US populations. The American Heart Association’s (AHA’s) diet and lifestyle recommendations include limiting trans fats to ≤1 g day−1, a decrease from past consumption levels (Lichtenstein et al., 2006).

2.2 Role of Omega-3 Fatty Acids in CVD Prevention

Giugliano et al. (2006) recommended omega-3 dietary strategies to prevent CHD by increasing consumption of omega-3 fatty acids from fish or plant sources. In another study, increased omega-3 fats reduced generation of a proinflammatory milieu or anti-inflammatory activity (Connor, 2000).

Two major studies on omega-3 fatty acids in CVD prevention are GISSI and Japan EPA Lipid Intervention Study (JELIS) as described in section 1. Other small studies also support the role of omega fatty acids in CVD prevention (Daviglus et al., 1997; Galan et al., 2003; Heidarsdottir et al., 2010; Kowey et al., 2010; Marchioli et al., 2009). There is limited research evaluating the relationship between ALA and risk of CHD, but lower doses may enhance the risk of cardiac fibrillation (Aarsetøy et al., 2008). Investigations are needed to determine optimal dietary intake of omega-3 fatty acids (EPA, DHA, and ALA) and the ratio of omega-6 to omega-3 fatty acids. Current omega-3 fatty acid therapy is ambiguous or fishy protection for the heart (Albert et al., 2010).

2.3 Therapeutic Lifestyle Changes Diet: A Multifaceted Lifestyle Approach to Reduce Risk of CHD

Epidemiological, experimental, and clinical trials have pointed to a positive correlation between lifestyle and dietary factors, especially omega-3/omega-6 fatty acids, as they relate to blood lipid levels, blood pressure, and CHD. Western dietary patterns, which are high in red and processed meat, sweets and desserts, potatoes and French fries, and refined grains, have been found to warm up inflammation, whereas prudent dietary practices, which are high in fruits, vegetables, legumes, whole grains, poultry, and fish, have been found to cool it down. Dietary patterns high in refined starches, sugar, and SFAs and TFAs and poor in natural antioxidants and fiber from fruits, vegetables, and whole grains have been found to predispose susceptible people to increased incidence of CHD (Giugliano et al., 2006). The following section highlights the role of key nutrients and lifestyle factors in preventing CVD and identifies practical applications for clinicians.

2.4 Omega-Fatty-Acid-Rich Functional Foods and CVD Risk

Over the past decade, a ‘heart-healthy food strategy’ has been the cornerstone of the AHA’s dietary recommendations for combating CVD and related diseases. It is challenging to include heart-healthy foods into the diet without increasing energy intake beyond that required for a healthy body weight (Kris-Etherton et al., 2002). In relation to food, the AHA’s four goals for people are to achieve a healthy overall diet, achieve a healthy body weight, promote desirable blood lipid levels, and achieve desirable blood pressure levels. To meet these goals, omega-fatty-acid-rich nuts have been added to the list of heart-healthy foods. Monounsaturated fats, such as olive oil or canola oil, and polyunsaturated fats are found in nuts and seeds.

Consumption of 0.75–1 oz of unsalted nuts daily (almonds or walnuts) is thought to confer cardiovascular benefits. In more than 86 000 women in the Nurses Health Study, the consumption of 5 oz of nuts per week resulted in significantly lower CHD risk than those who rarely ate nuts in favor of primary cardioprotective action (Kris-Etherton et al., 2002). In a randomized, crossover trial of 28 men and women, the mean (SD) levels of total cholesterol and LDL-C were 6.0 (1.1) mmol l−1 and 4.1 (1.0) mmol l−1, respectively, with a mean body mass index (BMI) of 26.9 (3.2) kg m−2. Participants were fed a low-saturated-fat ‘nut diet’ of 30 g day−1 of nuts or a cereal diet containing canola oil for two periods of 6 weeks, separated by a 4-week gap (Chisholm et al., 2005). Investigators showed that a 30 g day−1 serving of nuts had the same effect that canola-based cereal has because the same omega-3 fatty acid profile in both diets may produce decreases in lipoprotein-mediated cardiovascular risk. A serving of almonds or walnuts gives 140 kcal and discretionary calories can add up quickly and cause weight gain, obesity, a risk factor for CVD. The authors recommend the intake of fruits and vegetables (9–11 servings per day) and dietary fiber (25 g day−1) with omega-3 fatty acids from cold-water fish at least two times per week, and plant sterol/stanols (2 g day−1) and nuts (1 oz day−1) while maintaining the energy balance, weight status, BMI, and waist circumference will keep cardiovascular health and wellness.

2.5 Cardioprotective Effects of Omega-3 Fatty Acids

Polyunsaturated fatty acids (P-OM3) are approved for use in postmyocardial infarction (MI) patients to prevent CHD events. The AHA advises ~1 g day−1 of EPA plus DHA for cardiovascular protection in patients with documented CHD, and in those without documented CHD, consumption of a variety of fatty fish at least twice per week. The AHA recommends that treatment of elevated TGs with omega-3 fatty acids at higher doses (2–4 g day−1) can be taken under a physician’s supervision (Kris-Etherton et al., 2002). Recent clinical data strongly support the cardioprotective effect of omega-3 fatty acids (Aarsetøy et al., 2008; Bays et al., 2008; Calo et al., 2005; Cleland et al., 2004; de Roos et al., 2009; Geelen et al., 2005; Geppert et al., 2005; Grundt et al., 2003, 2004; Hamaad et al., 2006; Harrison and Abhyankar, 2005; Lindman et al., 2004; London et al., 2007; Madsen et al., 2007; Metcalf et al., 2008; O’Keefe et al., 2006; Raitt et al., 2005; Rajaram et al., 2009; Sanders et al., 2006; von Schacky et al., 2001; Walser and Stebbins, 2008). Main findings are summarized in favor of fatty acids in cardioprevention as following.

• Meta-analyses of primary and secondary CHD prevention trials have shown that omega-3 fatty acids can significantly decrease the risk of all-cause mortality, CHD death, and sudden death (Ramsden et al., 2010).

• GISSI study showed efficacy of omega-3 fatty acid for secondary prevention of CHD in Prevenzione Study (GISSI, 1999). Patients who had survived a heart attack (n = 11 324) were randomized to 300 mg of vitamin E, 850 mg of omega-3 fatty acid ethyl esters, both, or usual care alone. After 3.5 years, the group given the omega-3 fatty acid alone experienced a 20% reduction in all-cause mortality (p = 0.01) and a 45% reduction in sudden death (p < 0.05) compared to the usual care group. Vitamin E provided no additional benefit. This trial, although very large and carried out in a relatively ‘real-life’ setting, did not include a placebo arm and drop-out rates were high (>25%) in both the omega-3 and vitamin E groups. Thus, there remains a need for further research to determine the efficacy, the optimal dose, and the mechanism of action of omega-3 fatty acids in the prevention of CHD death.

• A secondary prevention, JELIS, was conducted on a high-fish-consuming population in Japan included 18 645 patients (14 981 patients with no history of coronary artery disease and 3664 patients with a history), all on statin treatment, who were randomized to 1.8 g day−1 EPA (no DHA) or to usual care and followed for 4.6 years for major coronary events (Yokoyama et al., 2007). Compared with the statin-only group, the EPA-plus-statin group demonstrated a 19% reduction in major coronary events (p = 0.011). The effect was virtually the same in both the primary and secondary subgroups, but reached statistical significance only in the secondary group (p = 0.048). The beneficial effect of EPA on CHD events was not associated with changes in the levels of total cholesterol, TG, HDL-C, or LDL-C, indicating that nonlipid factors played a major role in the cardioprotective effect of EPA (Calder, 2004). Cardioprotective effects of omega-3 fatty acids were antiarrhythmic effects, decreased platelet aggregation, stabilization of atherosclerotic plaques, and lowering of blood pressure (Kris-Etherton et al., 2002).

• The Chicago Western Electric Study cohort of 1822 free-living men aged 40–55 years reported that men consuming >35 g fish per day had a significantly decreased relative risk of death from CHD. In studies examining how blood levels of DHA and EPA affect cardiovascular health, the Cardiovascular Health Study, which examined free-living adults >65 years old, found that a higher concentration of combined plasma DHA and EPA was associated with a lower risk of fatal ischemic heart disease (Daviglus et al., 1997).

• ALA and risk of CHD is less known and needs information about the efficacy of marine and plant-derived omega-3 fatty acids in women and in high-risk populations with a detailed optimal dietary intake of omega-3 fatty acids (EPA, DHA, and ALA) and the ratio of omega-6 to omega-3 fatty acids (Van Horn et al., 2008).

• An FDA-approved health claim needs recommendation of 3 g day−1 of maximum omega-3 fatty acids to reduce the risk of CHD because no conclusive research shows that consumption of EPA and DHA omega-3 fatty acids may reduce the risk of CHD (Albert et al., 2010). The AHA recommends ≥2 servings (~4 oz per serving) of oily fish per week and inclusion of foods and oils rich in ALA, such as walnuts and soy or other vegetable oils (US FDA, 2004).

• The ‘Tsim Tsoum concept’ proposes the need for exercise, lifestyle change, behavioral counseling, and dietary intervention when medication fails and the concept integrates with modern nutrition and lifestyle in mind–body diseases. The focus is on dietary fatty acid balance in which ‘mother nature’ recommends the ingestion of fatty acids in a balanced ratio (polyunsaturated (P):saturated (S) = ω-6:ω-3 = 1:1) as part of a dietary lipid pattern where monounsaturated fatty acids (MUFA) are the major fatty acids (P:M:S = 1:6:1) in the background of other dietary factors: antioxidants, vitamins, minerals, and fibers, cereal grains (refined), and vegetable oils that are rich in omega-6 fatty acids, as well as physical activity and low mental stress. Excess of alphalinolenic acid, TFAs, saturated and total fat, as well as refined starches and sugar is proinflammatory. Low dietary MUFA and n-3 fatty acids and other long-chain polyunsaturated fatty acids are important in the pathogenesis of metabolic syndrome. Approximately 30–50% of the omega-3 fatty acids in the brain are low-carbon chain-PUFA in membrane phospholipids, and it is possible that their supplementation may be protective for stroke. The ‘Tsim Tsoum concept’ explains blood lipid composition as a marker of holistic health, important in the pathogenesis of CVDs. Blood lipid composition does reflect one’s health status: (1) circulating serum lipoproteins and their ratio provide information on their atherogenicity to blood vessels and (2) circulating plasma fatty acids, such as the omega-6/omega-3 fatty acid ratio, give an indication about the proinflammatory status of blood vessels, cardiomyocytes, liver cells, and neurons (Singh et al., 2010). Cholesterol and saturated fats constitute primary risk factors, whereas omega-6 fatty acids are the secondary risk factors.

2.6 Who Needs Initial Treatment with Omega-3 Fatty Acid Supplementation?

• Initially if TC, LDL-C, non-HDL-C, or TG are elevated or HDL-C is low followed by repeat lipid profile 3 weeks later to confirm the first lipid profile as shown in Table 1.1.

Table 1.1 Acceptable, Borderline, and High Plasma Lipid, Lipoprotein, and Apolipoprotein Concentrations for Children and Adolescents

Sources: National Cholesterol Education Program (NCEP) Expert Panel on Cholesterol. Values for plasma apoB and apoA-I are from the National Health and Nutrition Examination Survey III (NHANES III); US Food and Drug Administration, 2004. FDA Announces Qualified Health Claims for Omega-3 Fatty Acids 2004. http://www.fda.gov/bbs/topics/news/2004/new01115.html.

aThe cutoff points for a high or low value represent approximately the 95th and 5th percentiles, respectively.

• If one or more of the lipid or lipoprotein values remain above the elevated cutoff point or HDL-C is low, secondary causes of dyslipidemia – need of omega-3/omega-6 in diet in all ages.

• If repeated lipoprotein profile in 6–8 weeks shows dyslipidemia, it needs <3 g day−1 maximum in all ages (US FDA, 2004).

2.7 Safety and Efficacy of Omega Fatty Acid Therapy in Infants, Children, and Adolescents

Human milk remains the gold standard for infant feeding. A low-fat, omega-3 fatty acid-supplemented diet with micronutrients, such as calcium, zinc, vitamin E, and phosphorus, is safe from the age of 7 months to 11 years as advocated by the Special Turku Coronary Risk Factor Intervention Project (Simell et al., 2009) and from the ages of 8–10 years throughout adolescence by the Dietary Intervention Study in Children (Schwartz et al., 2009). However, the efficacy and safety of a low-fat diet is based on epidemiological reports and insulin resistance; endothelial functions in adolescents are factors to interfere with lipid lowering.

3 Modern View of Omega Fatty Acid Therapy in CVD

In the modern world, fatty fish, fish oil, walnuts, oatmeal, and oat bran, and foods fortified with plant sterols or stanols are advocated to help control cholesterol. Several studies have shown that omega-3-fatty-acid-rich fish (salmon, tuna, and sardine) bring down triglycerides and total cholesterol (Brouwer et al., 2003, 2006; Christensen et al., 1999; Harris and Isley, 2001; Harris and Von Schacky, 2004; Harris et al., 2004; Jones and Lau, 2002; Kris-Etherton et al., 2002, 2003; Leaf et al., 2003a,b; Marchioli et al., 2001, 2002, 2005, 2007, 2009, 2010; McLennan and Abeywardena, 2005; Mozaffarian, 2008; Rauch et al., 2006; Verboom et al., 2006; Zhao et al., 2009).

The authors believe that claims of lipid-lowering effects are based on the mixed reports of verbal testimonies or epidemiological surveys and as such are insufficient to validate lipid lowering by omega fatty acids. However, scientific evidence supporting these effects do exist (Kris-Etherton et al., 2002, 2004). Supplementation of a low-fat diet with an omega-3 fatty acid (docosahexaenoic acid 1.2 g day−1) increased the large-sized LDL by 91% and reduced the small-sized LDL by 48%. However, the standard prescription of omega-3 fatty acids is not yet approved by the FDA. Fish oils (1–2 g day−1) lower TG by decreasing TG biosynthesis.

3.1 National Guidelines

Guidelines indicate that patients with elevated LDL cholesterol should consume <7% calories from saturated fat and <200 mg cholesterol means limited TFAs and supplementation of monounsaturated omega-3 fatty acids and stanol-rich margarine, soy products, and cereals with vegetables as shown in Tables 1.2 and 1.3 (Fonarow, 2008; Kris-Etherton et al., 2004). The major goal is lowering LDL-C, raising HDL-C, and limiting serum triglycerides (representative of very low-density lipoprotein (VLDL)) to control dyslipidemia and avoid atherogenesis and diabetes with the aim of cutting down dietary fat, as shown in Table 1.4.

Table 1.2 Food Supplements in Dyslipidemia Management and Control

Sources: Third Adult Treatment Panel of National Cholesterol Education Program. 2001; Kris-Etherton, P.M., Harris, W.S., Appel, L.J., et al., 2002. Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Circulation 106, 2747–2757; Kris-Etherton, P.M., Lichtenstein, A.H., Howard, B.V., Steinberg, D., Witztum, J.L., Nutrition Committee of the American Heart Association Council on Nutrition, Physical Activity, and Metabolism, 2004. Antioxidant vitamin supplements and cardiovascular disease. Circulation 110 (5), 637–641.

Table 1.3 Web Sites Helpful for Patient Education and Information

AHA, American Heart Association; ATP III, Third Adult Treatment Panel of the National Cholesterol Education Program.

Table 1.4 Approximate LDL-C Reduction Achievable by Dietary Modification

LDL, low-density lipoprotein.

Source: National Cholesterol Education Program, Third Adult Treatment Panel; http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3_rpt.htm.

3.2 Mechanisms

At the molecular level, omega-3 fatty acids can prevent free cholesterol from being absorbed into the bloodstream. Instead of clogging up arteries, the ‘bad’ cholesterol just goes out with the other wastes. The metabolic mechanistic basis of clearance can be described at various end points including LDL receptor activity (Goldstein et al., 2011), inability of ApoB-100 to bind with LDL-R (Rader et al., 2003), autosomal recessive hypercholesterolemia (Arca et al., 2002), and mutations in proprotein convertase subtilisin-like kexin type 9 (Horton et al., 2007). Briefly, abnormal omega fatty acid (PUFA) metabolism in FCHL and other small, dense LDL syndromes may reflect the primary defect in these patients or impaired insulin-mediated suppression of hormone-sensitive lipase in adipocytes leads to an elevation in fatty acids (Kwiterovich, 2002). Elevated PUFA may drive hepatic overproduction of TG and ApoB, leading to a two- to threefold increased production of VLDL and the dyslipidemic triad. Insulin resistance also interferes with normal upregulation of lipoprotein lipase (LPL) by insulin, leading to decreased lipolysis of TG in VLDL, as well as in intestinally derived TG-rich lipoproteins. This paradigm may also result from a defect in the normal effect of acylation stimulatory protein, which is to stimulate the normal incorporation of FFA into TG in the adipocyte (Maslowska et al., 2005).

3.3 Clinical Trials to Modify Residual Cardiovascular Risk by LDL Cholesterol Lowering

A diet limited in the LDL-raising nutrients, such as SFAs, cholesterol, and trans-unsaturated fatty acids, was suggested by NCEP’s ATP III and the ADA’s nutrition principles for the benefit of low dietary saturated fat to maintain a serum LDL-C below 100 mg dl−1 (NCEP ATP III, 2001). The following advice is described for each diet supplement in the following sections based on NCEP and ADA recommendations.

3.3.1 Saturated fatty acids

Dietary SFAs decrease synthesis and activity of LDL receptors, providing elevated serum LDL-C conducive to atherogenesis (Grundy et al., 2004b). Every 1% increase in calories from saturated fat (butter, cream) increases serum LDL-C by ~2%. ATP III guidelines limit this saturated fat to <7% of calories. A meta-analysis concluded that the previous NCEP Step 1 diet (30% calories from total fat, <10% calories from saturated fat, and 300 mg of cholesterol) lowered LDL by 12%, but the further limitations of the Step 2 diet (7% calories from saturated fat, 200 mg of cholesterol) lowered LDL to an average of 16% (Yu-Poth et al., 2005). Diet advice: keep low saturated fat to <7% of calories; select animal products low in fat, such as skim or 1% fat milk and other low-fat dairy products; keep to a daily meat intake of lean beef, poultry, or fish <6 oz; take less of saturated vegetable fats (palm and coconut oils; see Table 1.4).

3.3.2 Trans fatty acids

In the American diet, 2.6% of the calories comes from TFAs and 11% comes from saturated fat (NCEP ATP III, 2001). Trans-unsaturated fatty acids are formed from polyunsaturated fats, such as corn and soybean oil, upon hydrogenation to produce stick margarine and fats with greater shelf life. These elevate LDL-C and HDL-C. However, an omega-3 fatty acid (docosahexaenoic acid 1.2 g day−1)-supplemented low-fat diet did not lower LDL-C but significantly increased the largest LDL subclass by 91% and decreased the smallest LDL subclass by 48% (Engler et al., 2005). Metabolic diets containing various fat sources (e.g., butter, soybean oil, semiliquid margarine, shortening, or stick margarine) elevate LDL-C levels and reduce LDL by 5% on stick margarine, 9% on tub margarine, 12% on soybean oil, and 11% on margarine (Denke et al., 2000). Diet advice: less saturated fat and TFAs-polyunsaturated and monounsaturated fat intake (7% in tub margarine, and <1% in semiliquid margarine); cookies, crackers, and doughnuts, French fries or chicken (FDA HHS, 2002).

3.3.3 Dietary cholesterol

Cholesterol in the diet increases total serum cholesterol (10 mg dl−1 for every 100 mg per dietary cholesterol per 1000 calories; Grundy et al., 2004a,b). The best example is limited egg yolk intake (AHA recommends one yolk per day and NECP ATP III recommends two per week) to keep dietary cholesterol to <200 mg day−1.

3.3.4 Monounsaturated fatty acids

Monounsaturated cis fatty acids in olive oil, canola oil, avocado oil, pecan oil, and peanut oil lower LDL and triglyceride. Diet advice: olive or canola oil and salad dressing with avocado on sandwiches, snack on pecans, or pack a peanut butter sandwich for lunch.

3.3.5 Wild foods

Wild foods are mainly wild plants, wild vegetables, wild fruits, and wild mushrooms. Mushrooms, flowers, fruits, and wine berries were reported to be beneficial in cardioprotection (He et al., 2007; Heidemann et al., 2008), INTERHEART study (Iqbal et al., 2008). Other epidemiological studies reported other factors such as BMI, waist circumference, alcohol consumption, low physical activity, hypertension, diabetes, C-reactive protein, fetuin-A, and insulin resistance as risks not protected by wild foods. For a full description of the value of Mediterranean soup (mixture of tomato, grapes, raisins, carrot, spinach, walnuts, almonds, lin/chia seeds, olive oil) in acute coronary syndrome patients with pro-inflammatory effects and challenges, readers are referred to the web document written by the first author (http://www.scribd.com/doc/22527813/Wild-Foods-in-Cardioprotection) highlighting the ‘Columbus concept’ originally advocated by De Meester (2009).

3.3.6 Supplementation of omega-3 fatty acids in combinatorial therapy

NECP ATP III (Grundy et al., 2004b) estimated that the combination of major dietary principles could lower LDL-C by 20–30%. The scientific basis is that omega-3 fatty acids may reduce the synthesis of TG and VLDL and increase APO-B degradation (transcription of ATP binding protein transporter) to increase HDL-C. So, omega-3 fatty acids facilitate HDL-C mediated cholesterol efflux away from peripheral hepatic cells. A more global approach of combined fatty acid treatment strategies suggested that a low-fat diet, exercise, and vitamin supplementation with statin medication and quarterly visits by a team of physicians, nurses, and dietitians will result in better lipid profiles, better glycemic control, and good cardiovascular protection. As discussed before, it is crucial to modify all the atherogenic risk factors for better outcomes in patients during dyslipidemia or later with atherosclerotic vascular disease. To accomplish it, the options of omega fatty acid alone or in combinatorial therapy are described in the following section. The 2007 National Lipid Association’s safety task force concluded that omega therapy is a safe therapeutic option for lowering TG (Bays, 2007). Observational studies have shown several cardiovascular benefits of omega fatty acids such as decrease in cardiac dysrhythmias, sudden cardiac death, and decrease in blood pressure (see in section 1). The mechanism of omega-3 fatty acid action in the reduction of TG is unclear (Bays et al., 2008). Omega-3 fatty acids increase TG clearance from circulating VLDL particles by increasing LPL activity. In the JELIS study, a combination of omega-3 fatty acids and statin was compared with statin monotherapy. There was a 19% reduction in major coronary events by the combination therapy as compared with statin alone. Study showed an increase of HDL-C with high doses of omega-3 fatty acids (Yokoyama et al., 2007). Another trial, COMBOS (COMBination of prescription Omega-3 plus Simvastatin), also showed that a combination of omega-3 fatty acids and simvastatin reduced non-HDL-C, TG, and raised HDL as compared to statin monotherapy (Davidson et al., 2007). The AFFORD trial (atorvastatin factorial with omega-3 fatty acids risk reduction in diabetes) did not show any benefit of residual cardiovascular risk reduction (Holman et al., 2009). However, dietary supplementation with omega-3 fatty acids is not subject to FDA regulation, and thus, higher doses of fish oil supplement may be required to be equivalent to the prescription form of omega-3 fatty acids (Fonarow, 2008). Statin and lipid lowering medications became more controversial in the last 2 years than ever before for their safety as found by the Air Force/Texas Coronary Atherosclerosis Prevention (TCAP) study (Kendrick et al., 2010); SEAS: first clinical endpoint trial (Hamilton-Craig et al., 2009); PROactive trial (Dormandy et al., 2009); and OCTOPUS trial (Iseki et al., 2009). Omega-3 therapy has issues of side effects and safety (Shah and Mudaliar, 2010). Polypharmacy is still a challenge (Volpe et al., 2010).

4 Healthy Heart Concept: Less-Known Facts on Omega Fatty Acids

Omega fatty acids in the diet have drawn attention based on dietary surveys in tribal areas in India, Australia, and Greenland, as described in the following sections. Eaton et al. (1998) reported a paleolithic diet. Konner and Eaton (2010) estimated that paleolithic diet eaters had lower levels of carbohydrates and sodium, higher levels of proteins and fibers, unsaturated fat with higher physical activity, and high energy throughput quite comparable with the modern-day hunter-gatherer’s dietary intake (see Tables 1.5 and 1.6). Our ‘healthy heart concept’ aims to keep lipids and the risk of CHD/CVD low by the combined approach of ‘exercise, low fat calorie intake, higher omega-3 fatty acids >5% energy, or omega-6/omega-3 ratio <1, nonsmoking, nonalcoholic habits, a healthy, positive attitude, and a spiritual lifestyle’ under the supervision of a nutritionist and regular lipid profile checks. In support, the following less known facts about some communities at very low risk of CHD/CVD are described (Table 1.5).

Table 1.5 Estimated Fatty Acid Consumption in the Late Paleolithic Period

Source: Eaton, S.B., Eaton, S.B., III, Sinclair, A.J., Cordain, L., Mann, N.J., 1998. Dietary intake of long-chain polyunsaturated fatty acids during the Paleolithic. World Review of Nutrition and Dietetics 83, 12–23.

Table 1.6 Ethnic Differences in Fatty Acid Levels in Thrombocytes, Phospholipids, and Percentage of All Deaths from Cardiovascular Disease

Source: Singh, R.B., et al., in press. Ancient nutrition practices in India: a nutrition survey of Kuchirias. The Open Nutraceutical Journal.

4.1 Ancient Tribals: Indian Kurichiyas

The recent description of Indian Kurichiyas was published in the first time report on Kurichiyas (Singh et al., in press). He emphasized lifestyle, dietary habits (fatty acid intake), and physical activity as the main factors that keep Kurichiya tribals healthy, as shown in Table 1.6. Kurichias walk for 10–20 miles every day, which is characteristic of hunter-gatherers. Obesity and overweight, cancer, heart attack, hypertension, obesity, and diabetes mellitus are uncommon among Kurichiya hunter-gatherers.

Recently, the dietary practices in the paleolithic age were highlighted in the form of the Mediterranean diet, the Indo-Mediterranean diet, the Japanese diet, and the DASH diet documented in several studies (Aratti et al., 2004; Fung et al., 2008; Singh et al., 2002; Trichopoulou et al., 2009).

4.2 Australian Tribals

Kimberley aboriginals were reported for their diet and eating patterns of 1200 kcal per person per day, two-third quantity of meat; total fat intake (13% energy from balanced saturated, unsaturated, and P-OM3); 54% energy from proteins; and 33% energy from carbohydrates (O’Dea, 1988). The ‘hunter-gatherer lifestyle’ was associated with increased physical activity and a low-fat, high-fiber diet of low energy density and high nutrient density derived from very lean wild meat, and uncultivated vegetable foods. It was shown that low carbohydrates and high proteins in the diet with extensive physical activity kept fat in the body under the control of the ‘thrifty gene,’ driving hepatic gluconeogenesis to convert dietary protein into glucose and available fat energy precursors without therisk of diabetes (O’Dea, 1991).

4.3 Greenlandic Eskimos

Eskimos live in Greenland and have extremely low incidence of heart disease. Their dietary fat intake (18% fat energy) and intake of omega-3 PUFAs from seal and fish was about sixfold higher than that found in western diets without coronary thrombosis (Côté et al., 2004; Kristensen et al., 2001). Recently, enzyme modulatory mechanisms of omega-3-fatty-acid-induced cardiac prevention were described (Siddiqui et al., 2008).

• In addition to the high fat, the seal meat also provided high amounts of omega-3 fatty acids and low amount of omega-6 fatty acids.

• All lipoproteins, except HDL, were significantly lower in the Greenland Eskimos who ate lots of fat and had lower LDL-C and higher good cholesterol (HDL).

• Ekismos’ blood had higher EPA and DHA, two of the three types of omega-3 fatty acids.

• Electrical activity in the heart muscle is stabilized by omega-3 PUFAs as PUFAs are ‘antiarrhythmic.’ Heart rhythm remains stable and the chances of ‘sudden death’ are greatly diminished.

• Omega-3 PUFAs also prevent blood from clotting or occluding a hardened coronary artery with a blood clot is greatly reduced by omega-3 PUFAs.

• Inuit Eskimo diet has six times more omega-3s than the typical western diet. Omega-3 PUFAs maintain low total cholesterol and ‘bad’ LDL-C levels.

• L-type calcium channels, role of the Na+–Ca²+ exchanger to mobilize calcium out, activation of phospholipases, synthesis of eicosanoids, and regulation of receptor-associated enzymes and protein kinases play roles in mediating n-3 PUFA effects on cardiovascular health.

4.4 Dietary Fat Intake and Fatty Acid Ratio

Recently, the ‘fatty acid ratio’ was highlighted based on unsaturated and saturated fats in the diet and overall distribution to explain good health or risk of atherogenesis after oxidative stress in various continents as the Indian paradox, French paradox, and Israeli paradox (de Lorgeril et al., 2002; Dubnov and Berry, 2003; Pella et al., 2003). The fatty acid ratio is described in this section and oxidative stress in the next section.

4.4.1 Columbus concept

De Meester et al. (2009) developed and marketed the Columbus concept (www.columbus-concept.com) at BNL food, a concept that stands for the return of the evolutionary lipid pattern (omega-6:omega-3 = 1:1) in the human diet. The fatty acid ratio in the ‘Columbus concept’ of diet means that humans evolved on a diet that was low in saturated fat and the amount of omega-3 and omega-6 fatty acids was quite equal. In the lines of the ‘Columbus concept’ Nature recommends the ingestion of fatty acids in a balanced ratio (polyunsaturated:saturated = ω-6:ω-3 = 1:1) as part of a dietary lipid pattern in which monounsaturated fatty acid (M) is the major fat (P:M:S = 1:6:1). These ratios represent the overall distribution of fats in a natural untamed environment. (www.columbus-concept.com) (Dubnov and Berry, 2003)

According to the ‘Columbus concept,’ ancient foods included egg, milk, meat, oil, and whole grain foods, all rich in omega-3 fatty acids, similar to wild foods consumed about 150 years ago from now. Furthermore, blood lipid composition reflects one’s health status predicted by: (1) circulating serum lipoproteins, and their (LDL + VLDL)/total cholesterol ratio provides information on their atherogenicity to blood vessels; and (2) circulating plasma fatty acids, such as the omega-6/omega-3 fatty acid ratio, indicates the proinflammatory status of blood vessels. Both factors (1) and (2) are phenotype related and depend on several genetic, environmental, and developmental factors. Hence, they appear as universal markers reflecting physical, mental, social, and spiritual health. The author has described in detail other contributory factors that influence mind–body interactions and lifestyle against environmental factors (http://www.scribd.com/doc/19575964/Traditional-Therapies-Lessons).

4.4.2 Oxidative stress and fatty acid ratio

Long-term intervention with high doses of omega-3 fatty acids (PUFA) following an acute MI was reported to increase lipid peroxidation (Grundt et al., 2003). Another group’s study showed reduced oxidative stress by omega fatty acid intake (Mori et al., 2000). The author with Pella et al. (2003) reported the ‘Indian Paradox,’ the shift from an affluent fat-rich diet (vegetable ghee, butter, cream, refined oils, and refined bread) to a less fat-rich diet (mustard oil, whole grains, walnuts, and vegetables rich in ALA) in both urban and rural populations. It enhanced the ALA content in diet and reduced omega-6/omega-3 ratio, now believed to be protective against CVD (Dubnov and Berry, 2003; Pella et al., 2003). Moreover, supplementation of omega-3 fatty acids was also reported to influence the ‘arachidonic acid and eicosapentanoic acid ratio’ resulting in more safety and less oxidative stress in stable CHD patients (Burns et al., 2007).

5 Guidelines on Omega Fatty Acid in CVD to Physicians, Nurses: Healthy Heart Concept

Available omega-3 PUFA food supplements contain EPA and DHA derived from marine oils in varying proportions, and contain 180 mg EPA and 120 mg DHA per capsule. Typical cod liver oil supplements contain 173 mg EPA and 120 mg DHA. For vegetarians, there is an alternative in the form of DHA oils derived from algae, 100 mg DHA per capsule (Kris-Etherton et al., 2000). This section is a guide to medical and health-care workers who are actively involved in cardiovascular care and cardioprevention. The awareness of both dietary fat intake along with side effects of statins and their safe use is important while practicing them to perform lipid lowering in prospective patient population. The lipid dysfunction includes mainly hypercholesterolemia, hypertriglyceridemia, low HDL-cholesterol, and apolipoprotein changes. The target lipid levels (LDL-C <2.5 mmol l−1, <3.5 mmol l−1, <4.5 mmol l−1, and total cholesterol/HDL-C ratio <6.0, <5.0, <4.0) indicate the high risk, moderate risk, and low risk of dyslipidemia, respectively. The triglycerides >1.7 mmol l−1 with HDL-C <1.0–1.3 mmol l−1 indicate metabolic syndrome. Dietary PUFA fat intake (2.5–12%) to improve serum lipid profile includes mainly the intake of unsaturated omega-3 (0.5–2 energy % or 8 g day−1) and omega-6 fatty acids (2–10 energy % or 6 g day−1) with antioxidants,

L

-arginine, and folic acid. Table 1.7 shows that omega-6/omega-3 PUFA ratio varies between 2:1 and 10:1, depending on whether adequate or upper level values are selected. There is no consensus about the optimal omega-6/omega-3 PUFA ratio in the diet (Table 1.7).

Table 1.7 Fatty Acids Ratio in the Daily Diet Intake

Source: Singh, R.B., et al., in press. Ancient nutrition practices in India: a nutrition survey of Kuchirias. The Open Nutraceutical Journal.

The best fish sources of omega-3 PUFAs are mackerel, herring, halibut, and salmon. Plant sources of omega-3 PUFAs are some of the legumes (especially pinto beans and soy beans) and nuts or seeds (especially walnuts and flaxseed). Leeks and leafy purslane are also excellent sources. Canola, flaxseed, and soybean oils in salad dressings are also good sources. Cod liver oil is a good supplemental source, but it is also very high in vitamin D and vitamin A. For those who do not like fish or vegetable sources of omega-3 PUFAs, omega-3 PUFAs may be taken in capsular form (750–1000 mg total EPA) as dietary supplements. The authors recommend vegetable sources in capsular form (750–1000 mg total EPA) as dietary supplements or Res-Q 1250 rich in omega-3 marine oil. Olive oil in the ‘Mediterranean diet’ is rich in P-OM3 (omega-3 fatty acids and omega-6 fatty acids). MUFA derived from olive oil keeps the heart healthy. Of specific mention, whole foods, such as garlic, spirulina, fenugreek, ginkgo, soy, and genistein, have been on nonprescription counters as cardioprotective food supplements popular for reducing low and moderate risks.

The high-risk category (LDL-C <2.5 mmol l−1 and TC/HDL-C ratio <4.0) needs immediate attention for lipid lowering medication, preferably statins. Other choices may be BSA, fibrates (benzo-, phenol-), gemfibrozil (400–1200 mg day−1), and niacin (1–3 g). Moreover, health workers need to be aware of the prescribed limits for beneficial effects of these omega PUFA supplements and persistent risk of antioxidants and cancer promoters (Kearney, 1987; Pearce and Dayton, 1971). MUFA are more effective than PUFA (Wolk et al., 1998). It is important to keep low the risks of ventricular tachycardia and ventricular fibrillation in patients with implanted defibrillators if they are being treated with fish oil supplementation (Raitt et al., 2005). On the other hand, statins have gained popularity in acute hyperlipidemia and acute CVDs to combat them within time, but our advice is ‘keep statins low as much as possible with ‘spiritual acceptance’¹ of active fat-smoking-alcohol-free lifestyle and a positive attitude (healthy heart concept).’ Statin therapy is not free from side effects and it needs the right prescription² and safe use under supervision. The Canadian Cardiovascular Society 2009 recommendations advocated new hs-CRP, ApoB/ApoI, TC/HDL-C, carotid intima-media thickness biomarkers of risk with heavy emphasis on a restricted diet (low sodium and simple sugars, with substitution of unsaturated fatty acids for saturated and trans fats, as well as increased consumption of fruits and vegetables), smoke/alcohol cessation, calorie restriction, and least psychological stress. For full description, readers are referred to read guidelines (Genest et al., 2009; Goldstein et al., 2011).

5.1 Omega Fatty Acids in CHD: Treating Beyond LDL-C

The most common adverse affects include gastrointestinal discomfort and nausea in patients receiving high EPA doses. The gastrointestinal events are most likely in response to the ingestion of such a large volume of an oily substance or actual omega-3 PUFA. Very high doses (>20 g day−1) of omega-3 PUFA might be associated with increased bleeding times. However, moderate consumption (ranging up to 7.5 g day−1) does not appear to cause delayed bleeding time (Hathcock et al., 2006). However, PUFA amounts in commonly used supplements are safe (Dall and Bays, 2009). More progress in support of the ‘healthy heart concept’ is highlighted for an understanding of the influence of the diet-induced blood/tissue omega-6 status on premetabolic disorders (VVDs and SPDs) in different age groups in representative sample populations in different continents; to determine the lifespan of omega fatty acid intake influence, psychological, and chronological factors in maintaining good homeostasis & biorhythms; to understand the interactive relationship between the cardiac clock and diet and lifestyle, human behavior, development with lifespan, new insights into human/environment mutual interactions, biological rhythms; and to determine the complex relationships of human biological, psychosocial functions versus age/time structures (Okuyama et al., 2000).

6 Implications and Futuristic Prospective

In brief, CVD is a major health hazard and ancient concepts of nutrition appear based on eating natural foods; fruits, vegetables, roots, and tubers, sprouted whole grains, nuts, cow milk, and curd and honey to combat adverse effects of dietary fats and fat-rich foods seem to be sound. However, less is known about the secret of high cardiac protection among tribals and Eskimos. The biochemical mechanisms of fatty acid transport regulation, LDL-transport, and their relation with cardiac arrhythmia and electrical activity are less understood. There is no clear advice in modern concepts for fresh animal foods; eggs, fresh fish, and meat from running animals commonly consumed by tribals and hunter-gatherers.

Nowadays, clinical trials suggest the success of a low-fat dietary lifestyle. Supervised dietary intervention to reduce low risk of both coronary and carotid artery disease and cardiac prevention are anticipated more rigorously. Large trials such as JELIS, GISSI, and AFFORD have suggested the importance of omega-3 fatty acids, fish oil efficacy, and the need for more investigations on reducing cardiac injury in prevention of CVD. Ongoing trials are needed to demonstrate the incremental CVD benefits and the safety of combination dietary regimens. In future, more omega-3 fatty acid variants and combinatorial products will be available in CVD therapy for more extensive prophylactic prescription in normolipidemic patients with new definitions advocated by government or research agencies if patients have other conventional risk factors such as hypertension, diabetes mellitus, or other new factors identified under medical supervision. To identify new risk factors related with hyperlipidemia or cardiovascular risks, is a kind of a race to pick up the thread early and advise interventions such as omega-3 fatty acids capsules, exercise, or lifestyle changes. It remains to be established whether prolonged lipid-lowering omega-3 fatty acid treatment is risk free from any lipid lowering omega-3-fatty-acid-induced immunosuppression, or cancer in the body after long duration especially in infants, children, adolescents, and elderly of different ethnicities. It will be clear if a monounsaturated or polyunsaturated fatty-acid-rich-diet in childhood can prevent CVD in adulthood or obesity due to insulin resistance and whether it can enhance endothelial function in teenaged boys and girls, with clear information as to how much TC or LDL-C or HDL-C is the culprit.

This chapter suggested the following broader implications: (1) low fat, low sodium with a high PUFA-rich diet or capsules may cause significant cholesterol and triglyceride lowering in serum but small change; (2) omega-3 and omega-6 fatty acid intervention or fish oil supplementation in combination therapy causes lipid lowering and improves serum lipid profile more than dietary intervention alone; (3) dietary low-fat energy intake or omega-6/omega-3 fatty acid supplementation may cause significant change in HDL cholesterol; and (4) combination of low fat, low salt with omega fatty acids may show limited benefit but combination with statin therapy may contribute more to the effect of therapeutic intervention on other factors such as mortality from CVD and ischemic heart disease. However, two issues remain unclear: (1) whether prolonged low fat and higher omega fatty acids given to low socio-economic populations may further the risk of malnutrition or immunity loss or immunosupression because of less available energy or resistance to clearance of nutrients as added risk; (2) whether omega fatty acid-rich fish oils recommended for prolonged periods may contribute to any less known adverse effect. No perfect means of lipid lowering or clear lipid regulatory mechanism exists today to explain complete cure without adverse effects. No clear information is available on consumption of omega fatty acids in correct ratio due to wide variation of omega-6 and omega-3 fatty acid ratio in daily intake among different populations in different continents (see Table 1.7). The authors propose a novel approach – ‘keep the daily dietary fat intake to the minimum, low salt, combined omega-3 fatty acids with optimal cardiovascular drugs,’ which may keep dyslipidemia and CVD in control within normal limits of blood pressure, BMI, and serum lipids (Sharma et al., 2010a). Our idea is to highlight the implication of ‘low fat optimal omega-drug combination therapy’ approach to manage dyslipidemia and reduce the mortality from hypertension, coronary, or ischemic heart disease and cardiovascular disorders as shown in Figure 1.1.

Figure 1.1 The figure represents the role of omega-3 fatty acids and the importance of the omega-3/omega-6 ratio (1:1) prescribed in limit for heart disease. Notice the effect of omega fatty acids in neuroprotection and inflammation and cancer.

This chapter is focused on two main purposes: first, to introduce the mechanism of omega-fatty-acid-induced changes in plasma lipids and cardioprotection; clinical evidence of combinatorial drug + omega-3 fatty acid therapy to observe the subtle benefits or limited cardiac protection in different social populations at risk; the ‘Columbus concept’ and ‘Tsi-Tom concept’ as new concepts of balanced fatty acids in the diet. This chapter advocates the importance of omega fatty acids in reducing CVD and preventing heart disease with wider implications including rapid beta oxidation and active fatty acid transport, scavenging LDL-C transport, stabilizing electrical activity in cardiac nodes and smoothening muscle activity, reducing platelet aggregation and triglycerides, and increasing HDL-C. Still, less is known for mechanisms and long-term regulation of fatty acid and lipid transport across cardiovascular systems. Role of fatty acids and effects of low dietary fat energy intake are less known in the light of modern views and clinical trials in favor of lifestyle change and importance of social behavior. Moreover, definition of cardiovascular risks and lipid profile interpretation has own limitations in different age groups and ethnicities. Western multiracial population or mixed racial population further warrants establishing relationship between diet modification and omega fatty acid therapy in dyslipidemic population with CVD risk in terms of serum lipid changes in different ethnicities. Our recent preliminary survey showed clear differences in plasma lipid and lipoprotein levels (Sharma et al., 2010b). Another important issue is the rapidly changing lifestyle among intracountry or international migratory white collar employees. Supervised dietary or omega fatty acid intervention as primary management is anticipated in such populations or individuals to reduce the risk of high omega-3 intake in both coronary or carotid artery disease and cardiac prevention.

To accomplish these goals, attention needs to be paid to the following issues in future. First, more accurate body lipid diagnostic methods or in vivo biomarkers for early detection of cardiovascular risk or dyslipidemia must be established and standardized to assess the need of omega fatty acid alone or in combinatorial nutrition + statin option. Similarly, in advanced dyslipidemic population at high cardiovascular risk, accurate body lipid imaging and sensitive cardiac tissue diagnostic methods are must to establish sequential ‘cardiovascular incapability’ before any omega fatty acid intervention to assess the effectiveness of different dosage of omega fatty acids or need of combinatorial therapies or immediate surgical intervention in time. It is believed that the degree of association between ‘dyslipidemia switch to hypertension or CVD or atherosclerosis or diabetes’ and ‘abnormal serum lipids and size of LDL lipoproteins’ will serve as a criteria and surrogate endpoint(s) to evaluate the pleiotropic effects of omega fatty acids and/or statins in different stages to improve both dyslipidemia and cardiovascular incapability in time. Next, it is believed that one must reevaluate normal and vulnerable limits of serum lipid profiles and cardiac physiological functions carefully in populations under study with details of lifestyle, social factors, and nutrition factors at a specific place and environment (independent from specific study report or specific Government guidelines) before intervention of omega fatty acids or drugs and/or dietary fat restriction in different ethnicities, cultures, and age groups along with careful consideration of dyslipidemia resistance in populations, if any, in order to reduce the side effects of existing or new drugs. In future, possibly rigorous lipid lowering drug therapy and optimized cardioprotective dietary or omega fatty acid supplementation will be extensively applied even in normolipidemic patients to keep good health with suggestions of dietary low fat intake if they have any conventional risk factors such as hypertension, diabetes mellitus, or others under medical supervision. Furthermore, other alternate cardioprotective medication will be rationalized such as more effective omega fatty acid derivatives, antidiabetic regimens, antihypertensive therapy to intervene in early stage dyslipidemia risks such as postprandial hyperlipidemia or hyperglycemia, insulin resistant state, masked hypertension, or metabolic syndrome to further reduce mortality or morbidity of both coronary artery disease and cardiac heart disease. More facts of dyslipidemia at risk of CVD and CHD in infants, children, and adulthood will be revealed with clear recognition and definitions of blood lipids with cut-off values in different ethnicities. New foods and omega-fatty-acid-rich dietary regimens have more scope in controlling dyslipidemia to keep away hypertension and CVD, as indicated in a recent study on the prospects of the NORDIET trial (Adamsson et al., 2011).

7 Conclusions

This chapter presents the current view of the role of omega fatty acid in reducing CVD or heart disease in the light of new experiences and clinical trials in different parts of the world and ethnicities in different age groups. Present state of the art on dyslipidemia control and cardiovascular prevention by omega fatty acids still remains controversial because of lack of comparisons of omega fatty acid usage in different populations and no common agreement on dyslipidemia management risk reduction of CVD. As a result, primary management of dyslipidemia and consequences remain inconclusive bottlenecks in prevention of CVD with lot of new side effects of newly introduced omega fatty acids or new pharmaceutical drugs. Omega-6/omega-3 ratio seems a key in cardiac prevention. The growing and advanced techniques of lipid science have opened up new vistas in the characterization of different lipid molecule sizes, visualization, fatty acid and lipoprotein metabolism, metabolic regulation, and molecular basis of lipoprotein disease during sequential progress of CVD, either atherosclerosis, heart disease, or diabetes with renal complications, but medical treatment approaches remain frustrating on reversing disease or complete cure of CVD. A new ‘healthy heart concept’ is proposed with guidelines on low fat or omega fatty acid dietary therapies to show some promise because of less or no side effects due to them if used as exclusive nutrition therapy or combinatorial regimens with change in lifestyle, positive behavior. For a better understanding of omega fatty acids and the healthy heart concept, this chapter surveys the views and needs of ancient lifestyles that provided better life expectancy and good health. Evidence of Australian, Asian Indian, and Greenland Eskimo tribal practices of traditional diets and their life expectancy without any significant cardiac diseases is examined. Awareness of new practices among tribals is an exciting and explorable frontline area in both nutrition and social research. New dietary fatty acid intake information and typical lifestyles of tribals pose a challenge to both nutritionists and doctors if personal and spiritual acceptance can give some benefits.

Acknowledgments

The authors acknowledge the support of Indian Council of Medical Research for the postgraduate studies program in Applied Nutrition, and for the training and the opportunity for patient data collection given to the first author at the National Institute of Nutrition, Hyderabad. The authors acknowledge the manuscript preparation at Department of Exercise, Food, and Nutrition, Florida State University, Tallahassee, and the discussions included in this chapter.

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