Dietary Lipid Approaches to the Prevention and Management of CVD

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Level of Dietary Fat

Dietary fat serves as a major energy source for humans. One gram of fat contributes 9 cal, a little more than twice that contributed by protein or carbohydrate (4calg—1) and somewhat more than that contributed by alcohol (7calg—1). When considering the importance of the level of dietary fat with respect to CVD prevention and management there are two major factors to consider; the impact on plasma lipoprotein profiles and body weight. The potential relationship with body weight is important because of secondary effects on plasma lipids, blood pressure, dyslipidemia, and type 2 diabetes, all potential risk factors for CVD.

With respect to the effect of the level of dietary fat on plasma lipoprotein profiles, the focus is usually on triglyceride and HDL cholesterol levels or total cholesterol to HDL cholesterol ratios. Evidence indicates that when body weight is maintained at a constant level, decreasing the total fat content of the diet, expressed as a per cent of total energy, and replacing it with carbohydrate results in an increase in triglyceride levels, decrease in HDL cholesterol levels, and a less favorable (higher) total cholesterol/HDL cholesterol ratio. Low HDL cholesterol levels are an independent risk factor for CVD. Low fat diets are of particular concern in diabetic or overweight individuals who tend to have low HDL cholesterol levels.

With respect to the effect of the level of dietary fat on body weight two reviews of the long-term data published on the relationship between per cent of energy from fat and body weight have concluded that even a relatively large downward shift in dietary fat intake (approximately 10% of energy) resulted in only modest weight loss of 1.0 kg over a 12-month period in normal weight subjects and 3 kg in overweight or obese subjects. Some evidence suggests that dietary fiber content may be a mitigating factor. That is, substituting fruits, vegetables, and whole grains for fat instead of fat-free cookies, cakes, and snack foods may be more efficacious in promoting weight loss within the context of low-fat diets. The area of dietary fat and obesity is clearly complex. However, it is important to note that in those long-term studies where patients achieved a drastic reduction in dietary fat intake, in no case was weight gain reported.

Type of Fat

Studies done in the mid-1960s demonstrated that changes in the dietary fatty acid profiles altered plasma total cholesterol levels in most individuals.

Table 1 Dietary fatty acids

Code Common name

Saturated

Monounsaturated

16:1n-7 cis 18:1n-9 cis 18:1n-9 trans

Polyunsaturated 18:2n-6,9 all cis 18:3n-3,6,9 all cis 18:3n-6,9,12 all cis 20:4n-6,9,12,15 all cis

20:5n-3,6,9,12,15 all cis 22:6n-3,6,9,12,15,18 all cis

As analytical techniques became more sophisticated, data on lipid, lipoprotein, and apolipoprotein levels routinely became available. Although many studies have confirmed these early observations, inconsistencies among the more recent results are not rare. These inconsistencies, when they do occur, are attributable to differences among the experimental diets, such as the magnitude or type of dietary perturbation, length of study period, habituation to nutrient intakes prior to the start of the study period, and the background diet on which the dietary variable was superimposed, as well as differences among experimental subjects, such as in age, sex, genetics, efficiency of cholesterol absorption, and initial blood lipid concentrations.

Saturated Fatty Acids

Early evidence demonstrated that the consumption of foods relatively high in saturated fatty acids (SFAs) increased plasma total cholesterol levels and that not all SFAs had identical effects. Subsequent work confirmed the hypercholesterolemic effect of SFAs, demonstrated that SFA intake results in an increase in both LDL and HDL cholesterol levels, and reaffirmed that not all SFAs have the same effect. Short-chain fatty acids (6:0 to 10:0) and stearic acid (18:0) produce little or no change in blood cholesterol levels, whereas SFAs with intermediate chain lengths (lauric (12:0) to palmitic (16:0) acids) appear to be the most potent in increasing blood cholesterol levels (Table 1). It has been postulated that stearic acid (18:0) is not absorbed or is rapidly converted to oleic acid (18:1), and for this reason has a relatively neutral effect on blood cholesterol levels. The underlying mechanism by which fatty

Formula ch3(ch2)iocooh CH3(CH2)i2COOH CH3(CH2)i4COOH CH3(CH2)ieCOOH

CH3(CH2)5CH=(c)CH(CH2)/COOH CH3(CH2)yCH=(c)CH(CH2)yCOOH CH3(CH2)/CH=(t)CH(CH2)7COOH

CH3(CH2)4CH=(c)CHCH2CH=(c)CH(CH2)yCOOH CH3CH2CH=(c)CHCH2CH=(c)CHCH2CH=(c)CH(CH2)7COOH CH3(CH2)4CH=(c)CHCH2CH=(c)CHCH2CH=(c)CH(CH2)4COOH CH3(CH2)4CH=(c)CHCH2CH=(c)CHCH2CH=(c)CHCH2CH

=(c)CH(CH2)3COOH CH3(CH2CH=(c)CH)5(CH2)3COOH CH3(CH2CH=(c)CH)e(CH2)2COOH

Lauric acid Myristic acid Palmitic acid Stearic acid

Palmitoleic acid Oleic acid Elaidic acid

Linoleic acid a-Linolenic acid 7-Linolenic acid Arachidonic acid

Eicosapentenoic acid Docosahexenoic acid acids with 10 or fewer carbon atoms have different effects from those with 12-16 carbons is unknown.

When SFAs displace carbohydrate in the diet, total cholesterol levels increase (Figure 1). SFAs tend to be solid at room temperature. Notable exceptions are the tropical oils (palm, palm kernel, and coconut), which are liquid at room temperature because they have high levels of short-chain SFAs. Efforts to reduce dietary SFA intakes should include use of lean meat, the trimming of excess fat and skin from poultry, limiting portion size, and the substituting of non-fat and low-fat dairy products for their full-fat counterparts. The judicious use of ingredient listings and nutrient labels on processed foods will also help achieve the goal of reducing the SFA intakes.

Unsaturated Fatty Acids

Unsaturated fatty acids are fatty acids that contain one or more double bonds in the acyl chain. As the name implies, monounsaturated fatty acids (MUFAs) have one double bond and polyunsaturated fatty acids (PUFAs) have two or more double bonds. The majority of double bonds in fatty acids occurring in food are in the cis configuration, that is, the hydrogen atoms attached to the carbons forming the double bond are on the same side of the acyl chain. Alternatively, some double bonds occur in the trans configuration, that is, the hydrogen atoms attached to the carbons forming the double bond are on the opposite side of the acyl chain. This part of the discussion of unsaturated fatty acids will be restricted to those containing cis double bonds.

Relative to SFAs, MUFAs and PUFAs lower both LDL and HDL cholesterol levels. The absolute magnitude of the change is greater for LDL cholesterol than HDL cholesterol. Most of the data suggest that MUFAs have a slightly smaller effect than PUFAs in lowering both LDL and HDL cholesterol levels so that the change in the total cholesterol/HDL

Saturated fat:

Crossover design Parallel design Latin square design Sequential design

Multivariate regression coefficient (SE)

0.048 (0.007) 0.060 (0.010) 0.033 (0.007) 0.054 (0.004)

Multivariate regression coefficient (99% confidence interval)

All solid food

Liquid formula

Polyunsaturated fat:

Crossover design -0.022 (0.009)

Sequential design -0.033 (0.005)

Liquid formula -0.021 (0.021)

Monounsaturated fat: Crossover design Parallel design Latin square design Sequential design

-0.012 (0.006) -0.018 (0.011) 0.015 (0.008) 0.016 (0.005)

All solid food

Liquid formula

-0.1 0.0 0.1 Decrease Increase

Change in total blood cholesterol (mmol l-1 per 1% increase in total calories)

Figure 1 Change in total cholesterol when each fatty acid class displaces carbohydrate from the diet. (Reproduced from Clarke R, Frost C, Collins R, Appleby P, and Peto R (1997) Dietary lipids and blood cholesterol: quantitative meta-analysis of metabolic ward studies. British Medical Journal 314: 112-117.)

cholesterol ratio (decrease) is similar. Because of the changes in plasma lipids and lipoproteins caused when unsaturated fat displaces SFAs from the diet, such a shift should be encouraged in the prevention and management of CVD.

MUFAs The major MUFA in the diet is oleic acid (18:1) (Table 1). Vegetable oils high in MUFAs include canola (rapeseed) and olive oils. Fat from meats are also relatively high in MUFAs but unlike vegetable oils, they also contain relatively high levels of SFA, hence would not be recommended as good sources of MUFAs. When MUFAs displace carbohydrate in the diet, there is little effect on total cholesterol levels (Figure 1). When MUFAs displace SFA in the diet, total cholesterol levels tend to decrease.

PUFAs There is a wider range of PUFAs than MUFAs in the diet. Dietary PUFAs vary on the basis of chain length, degree of saturation (number of double bonds), and position of the double bond(s) (positional isomers). Two positional isomers of interest with respect to diet and CVD risk are n-6 and n-3 (Table 1). The distinction is made on the basis of the location of the first double bond counting from the methyl end of the fatty acyl chain (as opposed to the carboxyl end). If the first double bond is six carbons from the methyl end, the fatty acid is classified as an n-6 fatty acid. If the first double bond is three carbons from the methyl end the fatty acid is classified as an n-3 fatty acid. When PUFAs displace carbohydrate in the diet, total cholesterol levels decrease (Figure 1). Vegetable oils high in PUFA include soy bean, corn, sunflower, and safflower oils. The major n-6 PUFA in the diet is linoleic acid (18:2n-6); other n-6 PUFAs, such as 7-linolenic acid (18:3 n-6) and arachidonic acid (20:4n-6), occur in smaller amounts but are important biologically.

n-3 fatty acids Quantitatively, the major n-3 PUFA in the diet is a-linolenic acid (18:3n-3). Major dietary sources include soy bean and canola oils. Two other n-3 PUFAs are eicosapentenoic acid (EPA, 20:5n-3) and docosahexenoic acid (DHA, 22:6n-3) and are sometimes referred to as very long-chain n-3 fatty acids (Table 1). The major source of these fatty acids is marine oils found in fish. Dietary intakes of very long-chain n-3 fatty acids are associated with decreased risk of heart disease and stroke (Figure 2). Interventions studies have substantiated these findings. The beneficial effects of EPA and DHA are attributed to decreased ventricular fibrillation resulting in decreased sudden death, and decreased triglyceride levels, platelet aggregation, and blood pressure.

Kromhout, 1985 Dolecek, 1991 Ascherio, 1995 Kromhout, 1995 Salonen, 1995 Rodriguez, 1996 Daviglus, 1997 Pietinen, 1997 Albert, 1998 Oomen, 2000 Yuan, 2001 Hu, 2002 Osler, 2003 Pooled estimate

Figure 2 Mean relative risk of coronary heart disease for those consuming any amount of fish versus those reporting none. (Reproduced from Whelton SP, He J, Whelton PK, and Muntner P (2004) Meta-analysis of observational studies on fish intake and coronary heart disease. American Journal of Cardiology 93: 1119-1123.)

Trans-Fatty Acids

Trans-fatty acids, by definition, contain at least one double bond in the trans configuration (Figure 3). Dietary trans-fatty acids occur naturally in meat and dairy products as a result of anaerobic bacterial fermentation in ruminant animals. Trans-fatty acids are also introduced into the diet as a result of the consumption of hydrogenated vegetable or fish oils. Hydrogenation results in a number of changes in the fatty acyl chain: the conversion of cis to trans double bonds, the saturation of double bonds, and the migration of double bonds along the acyl chain, resulting in multiple positional isomers. Oils are primarily hydrogenated to increase viscosity (change a liquid oil into a semiliquid or solid) and extend shelf life (decrease susceptibility to oxidation). The major source of dietary trans-fatty acids worldwide is from hydrogenated fat, primarily in products made from this, such as commercially fried foods and baked goods.

Since the early 1990s attention has been focused on the effects of trans-fatty acids on specific lipo-protein fractions. The findings of this work have suggested that, similar to saturated fatty acids,

Figure 2 Mean relative risk of coronary heart disease for those consuming any amount of fish versus those reporting none. (Reproduced from Whelton SP, He J, Whelton PK, and Muntner P (2004) Meta-analysis of observational studies on fish intake and coronary heart disease. American Journal of Cardiology 93: 1119-1123.)

Trans form /

Cis form

Elaidic acid

Figure 3 Geometric isomers of 18:1n-9 (oleic and elaidic acids).

Oleic acid

Elaidic acid

Figure 3 Geometric isomers of 18:1n-9 (oleic and elaidic acids).

trans-fatty acids result in increased LDL cholesterol levels. In contrast to saturated fatty acids, they do not raise HDL cholesterol levels. The changes result in a less favorable LDL cholesterol:HDL cholesterol ratio, with respect to CVD risk (Figure 4). A trend towards increased triglyceride levels is frequently reported. Some research has also suggested that trans-fatty acids may increase Lp(a) levels. Levels of Lp(a) tend to be positively correlated with risk of developing CVD. However, at this time it appears that the magnitude of increase in Lp(a) levels

Mensink and Katan Zock and Katan Nestel et al. Judd et al. Judd et al. Lichtenstein et al. Aro et al. Sundram et al. Lichtenstein et al.

2 3 4 5 6 7 8 Percentage of energy from fat

Figure 4 Change in LDL:HDL cholesterol ratio in response to trans-fatty acids (solid line) and saturated fatty acids (dashed line). (Reproduced from Ascherio A, Katan MB, Zock PL, Stampfer MJ, and Willett WC (1999) Trans fatty acids and coronary heart disease. New England Journal of Medicine 340: 1994-1998.)

2 3 4 5 6 7 8 Percentage of energy from fat

Figure 4 Change in LDL:HDL cholesterol ratio in response to trans-fatty acids (solid line) and saturated fatty acids (dashed line). (Reproduced from Ascherio A, Katan MB, Zock PL, Stampfer MJ, and Willett WC (1999) Trans fatty acids and coronary heart disease. New England Journal of Medicine 340: 1994-1998.)

reported is not within the physiological range that would be predicted to increase CVD risk.

Recent estimates from 14 Western European countries report trans-fatty acid intakes ranging from 0.8% (Greece) to 1.9% (Iceland) of energy in women and 0.5% (Greece and Italy) to 2.1% (Iceland) of energy in men. Data collected in the US and Canada suggest average trans-fatty acid intakes ranging from 1% to 2.5% of energy. By way of contrast, estimates of saturated fat intake range from 10% to 19% per cent of energy.

Dietary Cholesterol

The observation that dietary cholesterol increased blood cholesterol levels and was associated with the development of arteriosclerosis was originally made early in the 20th century in rabbits. In humans, a positive correlation has been repeatedly observed between dietary cholesterol and both blood cholesterol levels and CVD risk, although relative to SFA, the effect is modest. Whether the increase in plasma cholesterol levels induced by dietary cholesterol is linear or curvilinear, or whether there is a break point or threshold/ceiling relationship beyond which individuals are no longer responsive, remains to be determined. With few exceptions, dietary cholesterol is present in foods of animal origin. Therefore, restricting saturated fat intake is likely to result in a decrease in dietary cholesterol.

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