Our results show that the HPUFA diet, which incorporated corn and tortilla chips fried in corn oil, resulted in the best overall CVD risk profile, although it was higher in total fat. All 3 diets lowered total and LDL cholesterol, but only the HPUFA diet tended also to reduce triacylglycerol concentrations. In addition, changes in total and LDL cholesterol were significantly greater with the HPUFA diet than with the HF diet; the change in triacylglycerol also was significantly greater with the HPUFA diet than with the LF diet. In addition to these traditional CVD risk factors, the pattern of LDL particle size was significantly more favorable with the HPUFA diet than with the LF diet. Taken together, these results indicate that substituting snack chips high in polyunsaturated fats for other high-saturated and trans fat or low-fat snacks leads to a significantly less atherogenic lipid profile.
The HPUFA diet caused significantly greater reductions in total and LDL cholesterol than did the HF diet and significantly greater reductions in triacylglycerol than did the LF diet. These changes are in accordance with a report estimating predicted change in coronary disease incidence on the basis of changes in the lipoprotein profile (3
). The change in coronary disease incidence was predicted to decrease by 19% in men and 16% in women when 25 g or 10% of daily calories as saturated fat was replaced with unsaturated fat from vegetable and nut oils. Controlled substitution of oils to alter dietary fatty acid profile has also shown that replacing saturated fats with polyunsaturated and monounsaturated fats leads to significant reductions in total and LDL cholesterol (17
). A novel finding of the present study is that whole-food substitutions, in the form of high-fat savory snacks, can result in improvements in dietary fat intake that lead to beneficial health effects.
Our LF diet reduced total and LDL cholesterol to a significantly greater extent than did the HF diet. This finding is in agreement with data from Ginsberg et al (18
). However, unlike that group, we found no significant difference in HDL cholesterol or triacylglycerol between these 2 diets. This may be due to the shorter duration of our feeding periods—25 d, instead of the 8 wk used by Ginsberg et al (18
). However, previous studies found significant effects of diet on HDL cholesterol and triacylglycerol within a 3-wk period (4
). Although changes in total and LDL cholesterol were significantly greater with the LF and HPUFA diets than with the HF diet in the present study, it should be noted that the HF diet also resulted in significant reductions in total and LDL cholesterol. The HF diet was designed to resemble the average American diet, as described previously (20
), however, it was likely an improvement over our subjects’ habitual diet.
LDL particle size is linked to the risk of CVD: small, dense particles (pattern B) are associated with greater risk. Diet has been shown to modify LDL particle size, with near-maximal reductions being observed within 2 wk (21
). A shift toward a Mediterranean diet leads to less-dense LDL particles in women who have a high proportion of small, dense LDL particles at baseline (22
) and in persons with a particular apolipoprotein E genotype (23
). Mixed results have been observed, however, and another study reported that effects on particle size were the same with the high-fat, high-polyunsaturated fat, and high-saturated fat diets (24
). In those studies, dietary intake often was not strictly controlled, and the exact dietary fat profile was unknown or not reported. In controlled feeding studies, LDL particle size reduction with olive oil–, sunflower oil–, and rapeseed oil–rich diets did not differ significantly from that with a saturated fat-rich diet (25
), but LDL particle density decreased with the increasing degree of hydrogenation—and hence the trans
fatty acid content—of the diet (26
). This latter study suggests that shifting dietary fat intakes from trans
fatty acids to unsaturated fatty acids may have beneficial effects on LDL particle size. A recent study showed that dietary carbohydrate intake may also have an effect on LDL particle size (27
), with the peak LDL particle diameter increasing to a greater extent with diets containing lower proportions of carbohydrates (39% and 26% of energy) than with a control diet providing 54% of energy from carbohydrates. The macronutrient distribution of the control diet in that study was similar to that of our LF diet. Our HPUFA diet had ≈49% of energy from carbohydrates, which suggests that even modest reductions in dietary carbohydrate can have beneficial effects on the LDL pattern. Furthermore, Krauss et al (27
) have observed that, in persons who start out with LDL pattern A, a low-fat, high-carbohydrate diet results in a conversion to LDL pattern B. Although the overall diet effect was not significant (P
= 0.08) in modeling the odds of LDL pattern B, our data suggested that the odds that a person would have LDL pattern B when following an LF diet are ≈ 3.5 times the odds for a person following a HPUFA diet. This finding supports the notion that shifting dietary patterns toward a pattern with greater PUFAs, rather than carbohydrates, leads to a better LDL pattern. More research is necessary to fully understand the effect of macronutrient and fatty acid profiles on LDL density patterns.
Lp(a) is a new CVD risk factor that has been shown, in a meta-analysis of prospective studies, to have independent predictive power for coronary heart disease (28
). Moreover, concomitant increases in LDL cholesterol and Lp(a) have been reported to have synergistic effects on CVD risk in hypercholesterolemic subjects (29
) by enhancing arterial cholesterol deposition (30
). However, this marker seems to be relatively resistant to therapies: statins are ineffective at reducing Lp(a) concentrations, and nicotinic acid produces only modest benefits (31
). Our data show no effect of diet on Lp(a). This finding agrees with Brown et al (32
), who also found no effect of dietary fatty acid type, whether low or high in polyunsaturated fats and low or high in cholesterol, on Lp(a). One study found significant reductions in Lp(a) when restricting carbohydrate intake (33
); however, this study was of longer duration (12 wk) than the present study, and it did not have a high-carbohydrate comparison group but a carbohydrate-restricted group supplemented with 3 g dietary fiber. Furthermore, changes in Lp(a) in the present study were correlated with changes in fat mass, and, therefore, the change in body composition may have been at least partly responsible for the change in Lp(a). It is interesting that one group found that Lp(a) was increased after 5 wk of consumption of low-fat diets similar to our LF diet (34
). Perhaps a longer study duration is needed to effect changes in Lp(a).
hs-CRP is an acute-phase immune reactant that has been associated with increased risk for CVD. Its concentrations have been correlated with adipose tissue, and it follows that weight loss leads to reductions in hs-CRP (35
). However, studies to determine the effect of diet on hs-CRP are conflicting. A study comparing the effects of consuming a Mediterranean-style diet and of consuming an American Heart Association Step 1 diet for 2 y found that hs-CRP was lower in the Mediterranean-diet group than in the control group (36
). The Mediterranean-style diet provided a greater percentage of energy from complex carbohydrates, PUFA, and monounsaturated fat; a lower percentage of energy from saturated fat; and less overall energy than did the Step I diet. Similarly, a diet containing a combination of cholesterol-lowering foods and ingredients (eg, almonds, soy protein, viscous fiber, and phytosterols) led to reductions in CRP of 28.2%, whereas no reduction in CRP was seen with consumption of a diet very low in saturated fat (37
). In contrast, others have not observed a diet effect on CRP. Desroches et al (38
) found that consumption of a low-fat diet (25.8% of energy from fat), a high-fat diet (40% of energy from fat), and a high-monounsaturated fat diet (22.5% of energy from monounsaturated fat) did not affect CRP concentrations differently. Increasing the trans
fat content of a diet also has not been found to affect CRP concentrations (39
). It has been suggested that diet plays a role in modulating CRP concentrations only if a subject’s body weight also changes (40
). Our data did not show any effect of diet on hs-CRP after a 25-d period, but we found a correlation between change in CRP and change in waist circumference. Perhaps a longer study duration or greater changes in body composition are necessary for observable changes in this biomarker. The present study did not produce any changes in body composition.
The present study had several limitations. First, subjects were mildly hyperlipidemic and normoglycemic. It is not known whether similar results would have been obtained in persons with lower or higher lipid concentrations or with type 2 diabetes. Second, the sample size was modest (ie, 33), which limited our power to examine sex and ethnicity effects. Another limitation of the present study was the length of the feeding periods. Although we found significant diet effects on some of our main endpoints, it is not implausible to postulate that 25 d may not have been enough time to initiate a change in some of our secondary end-points, such as Lp(a) and hs-CRP. On the other hand, it is very difficult to obtain compliance with a controlled feeding protocol when the feeding period is extended beyond a few weeks. Free-living studies in which subjects are counseled to consume diets of a particular macronutrient profile may be necessary to circumvent this issue and would be a logical next step for this study. Finally, we cannot exclude the possibility that subjects were not entirely compliant with the diet requirements. However, the relatively short feeding periods and the lack of weight change are good indicators that the subjects consumed the study foods. In any case, deviations from protocol would most likely have weakened the present study and prevented our observation of changes in the variables measured.
The findings of the present study are in agreement with Dietary Guidelines for Americans 2005
) and the American Heart Association Diet and Lifestyle Recommendations (27
), which have acknowledged that fat type is more influential than total fat in reducing CVD risk and which no longer recommend “low-fat” diets (ie, < 30% of energy from fat). Weight-maintaining diets containing up to ≈ 40% of calories from fat may favorably affect CVD risk factors (42
). It is important to note that our study does not promote the consumption of snacks above and beyond weight-maintaining energy requirements but does promote their inclusion in and contribution to a healthy diet. The role of snacks in body weight regulation is still controversial. Some studies have found that snacking frequency is associated with increased BMI (43
), whereas others have not found that (44
), and others have even not found snacking to prevent weight loss when incorporated in a weight-loss diet (46
Because snacks are an integral part of most people’s dietary habits, it is important to understand their nutritional contribution. The present study shows that snack foods can be incorporated into a healthy diet at a practical level and can affect metabolic risk profiles. Moreover, the study design was unique in that the only dietary manipulation was the type of snack offered—a whole-food substitution. This is a simple concept that could be very useful in educating persons about making healthy food choices. Finally, the present study shows that common beliefs about the nutritional value of foods may be quite erroneous. What constitutes a healthy snack is debatable; however, the present study shows that snack chips fried in corn oil is an effective and simple means of delivering healthy unsaturated fats into the diet while maintaining a low-saturated fat and low-trans fat diet. Therefore, if chosen wisely, even snack foods that are often considered to be “junk food” can contribute to a heart-healthy diet.