Volume 14 – Number 1


Spring 1997


BMI: body mass index (kg/m2)
CHD: coronary heart disease
CVD: cardiovascular disease
HDL: high density lipoprotein
LDL: low density lipoprotein
Lp(a): lipoprotein (a)
MI: myocardial infarction
MUFA: monounsaturated fatty acids
NCEP: National Cholesterol Education Program
P:S: dietary polyunsaturated:saturated fat ratio
PUFA: polyunsaturated fatty acids
SFA: saturated fatty acids
TAG: triacylglycerol
VLDL: very low density lipoprotein

Dietary Lipids and Plasma Lipoprotein Levels: A Meta-Analysis

There have been a number of reports over the past few years which quantitate the average plasma lipoprotein response to changes in dietary lipids. A recently reported meta-analysis of metabolic ward studies provides additional data to predict changes in the average cholesterol levels of the population with changes in the type and amount of dietary fat and the amount of cholesterol in the diet. The analysis involved 80 reports of metabolic ward studies which included 72 reports using solid food diets (395 experiments in 129 groups) and 32 experiments in 8 reports using liquid formula diets. 227 studies provided data for dietary lipid effects on LDL and HDL cholesterol levels. All feeding periods were for a minimum of two weeks. In addition, data from studies detailing the major fatty acids in the test diets were used to determine effects of specific fatty acids on plasma cholesterol levels. The authors used a Multilevel regression analysis which included age, weight and dietary intakes to determine the plasma lipid and lipoprotein response factors.

Multivariant analysis of changes in plasma cholesterol per isocaloric unit change in dietary factor from the 395 solid food studies (227 studies for LDL and HDL values) generated predictive values for changes in total and lipoprotein cholesterol [see table].

The predictive values were not significantly altered by differences in experimental design, gender, age, body weight, caloric intake, baseline dietary cholesterol, or study duration. Interestingly, the response factor for saturated fatty acids was less with intake of liquid formula diets. Clearly, dietary SFA have the greatest effect on plasma total, LDL and HDL cholesterol levels, while PUFA in the diet are the next most important determinant of the plasma lipoprotein profile. MUFA intake results in a non-significant decrease in LDL levels while plasma HDL cholesterol were significantly increased. Total fat intake has positive affects on both plasma LDL and HDL levels.

Detailed analysis of specific fatty acid effects on plasma cholesterol levels indicated that lauric, myristic and palmitic acids were positively associated with plasma cholesterol, stearic acid had no effect, and trans-monounsaturated fat had an effect comparable to SFA. Based on the average British diet, the authors estimated that replacement of 60% of the SFA (16.5% of calories to 6.6%) by other fats, and avoidance of 60% of the dietary cholesterol (from 390 mg/day to 156 mg/day) would reduce plasma cholesterol levels by 31 mg/dl (25 mg/dl reduction in LDL and 6 mg/dl reduction in HDL). Given an average cholesterol of 210 mg/dl the predicted plasma cholesterol changes from this dietary restriction would be a reduction to 179 mg/dl for total cholesterol, a lowering of LDL from 130 to 105 mg/dl and a decrease in HDL levels from 50 to 44 mg/dl. And while these changes in the plasma lipid profile are substantial, the changes in the overall dietary pattern are fairly extreme. Given a more reasonable dietary shift, from the average American diet [34% fat (7% PUFA, 17% MUFA, 13% SFA), 385 mg/day cholesterol] to the NCEP Step I diet [30% fat (10% PUFA, 10% MUFA, 10% SFA), 300 mg/day cholesterol], the predicted changes would be: total cholesterol from 210 to 199 mg/dl; LDL from 130 to 121 mg/dl, and HDL from 50 to 47 mg/dl, with the LDL: HDL ratio changed only slightly from 2.60 to 2.57.

The decrease in total plasma cholesterol can be ascribed to each of the dietary lipid alterations as: -6.0 mg/dl due to the decrease in SFA, -3.0 mg/dl from the increase in PUFA, and -2.3 mg/dl from the reduction in dietary cholesterol. Clearly the shift in dietary fat type and amount accounts for the major effect with almost 80% of the diet induced 5% decrease in plasma total cholesterol levels. The report by Clarke et al. provides a better understanding of the relative effects of dietary fatty acids and cholesterol on plasma lipids and lipoproteins which can be used to generate quantitative estimates of the expected population-wide changes in plasma lipids and CVD risk with changes in dietary fats. It also provides data documenting that the effects of specific saturated and trans-fatty acids on lipids and lipoproteins are unique and quantifiable.

Dietary Factor Change in PLasma Cholesterol (mg/dl)
1% kcal SFA 2.01 1.47 1.50
1% kcal PUFA -1.01 -0.85 0.19
1% kcal MUFA 0.19 -0.19 0.23
1 mg/day cholesterol 0.027 -0.019 0.004
1% kcal fat 0.77 1.46 0.39

Key Messages

  • A 1% reduction in calories from SFA will lower plasma LDL cholesterol by 1.5 mg/dl.
  • A 1% increase in calories from PUFA will lower plasma LDL cholesterol by 0.5 mg/dl.
  • A 50 mg/day decrease in dietary cholesterol will lower plasma LDL cholesterol by 0.9 mg/dl.
  • Trans-fatty acids have a comparable effect on plasma cholesterol levels to that of SFA.

[Clarke, R., Foster, C., Colins, R., et al. Dietary lipids and blood cholesterol: qualitative meta-analysis of metabolic ward studies. BMJ 1997;314:112-117.]

Editor’s Comment
This analysis of dietary effects on plasma lipids provides valuable data on the predicted changes in plasma total and lipoprotein cholesterol levels which can be achieved from a population-wide change in dietary lipid intakes. It is also possible to use these data to predict diet-mediated changes in CHD mortality rates based on epidemiological data. Based on data from the Seven Countries Study (see Nutrition Close-Up 12(3): 2, 1995), a 20 mg/dl change in the plasma cholesterol level is associated with a 17% change in CHD risk. Using these data it can be predicted that an 11 mg/dl fall in total cholesterol levels would lower CHD risk by 9%. What is discouraging is that overall, the effects of dietary fat and cholesterol interventions on plasma cholesterol levels are quantitatively relatively small, and seem to have only a small effect on CHD relative risk in the U.S. population, a population with a high CHD absolute risk as compared to other industrialized countries. There appears to be more to CHD risk reduction than simply cutting out the fat and cholesterol in the diet

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Effects of Shrimp and Egg Consumption on Plasma Lipoproteins

Like eggs, shrimp has also received much negative publicity for its high cholesterol content. As a result of this bad image, both egg and shrimp consumption plummeted in the 1980’s. However, no studies have tested whether the source of cholesterol can have a differential effects on plasma cholesterol levels. To test this, De Oliveira e Silva et al. compared the effects of adding shrimp versus eggs to a low-fat baseline diet on plasma lipoproteins in normolipidemic volunteers. In this randomized cross-over trial, 18 healthy subjects between the ages of 19 to 33 years were fed a metabolic diet. Subjects ate breakfast and dinner at The Rockefeller Clinical Research Center and a box lunch was consumed off-site. Using the Harris-Benedict formula, volunteer caloric needs were assessed and appropriate eucaloric meals were provided to maintain a steady weight throughout the study period.

Subjects were randomly assigned to one of the three test diets; low-fat baseline diet, 300 gram shrimp diet, and 2 large egg diet. All three diets had similar macronutrient composition. The cholesterol content was the only varying factor in these diets. Based on 2,400 calories, the baseline diet contained 107 mg/day dietary cholesterol while the shrimp and egg diets contained 590 and 581 mg/day, respectively. Subjects diets were crossed over after 3 weeks on each test diet. Four fasting blood samples collected during the third week of each diet period were analyzed for lipids and lipoproteins.

Volunteers LDL cholesterol and total cholesterol levels were higher on the shrimp and the egg diet. For example, compared to the total cholesterol concentration of 156 mg/dl during the baseline period, the total cholesterol levels increased by 13 mg/dl on the shrimp diet and 16 mg/dl on the egg diet. The LDL level increased by 7 mg/dl on the shrimp diet and 9 mg/dl on the egg diet. The HDL level also increased by 6 mg/dl and 4 mg/dl for the shrimp and egg diet.

Compared to the egg diet, lipoprotein profiles with the shrimp diet were considered less atherogenic since the LDL:HDL ratio was 1.92 for baseline, 1.88 for the shrimp diet, and 2.10 for the egg diet. Base on the data, De Oliveira e Silva et al. concluded that shrimp consumption does not adversely affect the overall plasma lipoprotein profile in normolipidemic subjects.

[De Oliveira e Silva, E.R., Seidman, C.E., Tian, J.J., et al. Effects of shrimp consumption on plasma lipoproteins. Am J Clin Nutr 1996;64:712-717.]

Editor’s Comment
According to the data from De Oliveira e Silva et al. it is not possible to say that dietary cholesterol from shrimp is more or less hypercholesterolemic than cholesterol from egg since the differences in plasma total, LDL, and HDL cholesterol levels between the two diets were not significantly different. The authors conclusion regarding the atherogenic profile of the plasma lipids is based on the difference in the LDL: HDL ratio which are derived from non-significant changes in the plasma lipoprotein concentrations. Interestingly, the plasma cholesterol response to the shrimp diet (2.4 mg/dl per 100 mg/day) is almost exactly the predicted response from over 140 cholesterol feeding studies (2.5 mg/dl per 100 mg/day) whereas the observed response to the egg diet is almost 30% higher (3.5 mg/dl per 100 mg/day). In both diets, the increase in plasma cholesterol was due to an increase in both LDL and HDL levels. Also, the higher level of omega 3 fatty acids in the shrimp diet could have a greater impact on triglyceride and VLDL levels than the dietary cholesterol source. In spite of a high cholesterol content, eggs and shrimps, both of which contain low amounts of saturated fat, can be incorporated into a heart healthy diet since dietary cholesterol has substantially less impact on blood cholesterol than saturated fat.

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Benefits of a Low-Fat, Low-Cholesterol Diet in Infants

In spite of the association between dietary fat intake and CVD incidence, scientists have been reluctant to recommend low-fat diets for children less than two years old due to concerns of delaying their growth. However, using the premise that children who are introduced to a low-fat diet earlier in life will accept a low-fat diet better and thus potentially minimize the risk of atherosclerosis in later years, Finnish researchers tested the effects of a low-fat, low cholesterol eucaloric diet in infants. In this random, prospective study, seven month old infants were recruited from well-baby clinics in the city of Turku and followed for six months. The parents of the intervention group infants (n=540) were instructed to provide the infants with a diet that consisted of 30-35% fat, 55% carbohydrate, 15% protein, dietary cholesterol of less than 200 mg per day, and PUFA/MUFA/SFA (P/M/S) ratio of 1/1/1. To assure that care providers were able to follow this diet, registered dietitians provided extensive nutrition counseling on every visit (7, 8, 10, 13 months). Also, based on 3-day food records, parents were given a specific recommendation to adjust portion sizes and food compositions if necessary. Parents of the control group infants (n=522) were only provided with a basic instruction on their initial and final study visits.

Children in both groups remained on either breast milk or infant formula until the age of 1 year. After this time, milk for the intervention children was switched to skim while the control children were switched to milk with a fat content greater than 1.9%. In addition to milk, all infants were on solid foods. Throughout the study period researchers monitored food records, serum lipid profiles, and indices of physical development.

According to the nutrient analysis of selected 3-day food records, children in the intervention group were consuming fewer calories than the control group, 3427 kJ vs. 3680 kJ at 8 months of age and 4065 kJ and 4370 kJ at age 13 months, respectively [difference of 6.8% at 8 months and 7.5% at 13 months of age]. Also, the total fat intake in both groups was significantly lower than the levels researchers anticipated. For example, intervention infants consumed 29% and 26% of calories as fat while the control group consumed 28% and 28% of calories at ages 8 months and 13 months, respectively. The P/M/S ratio of the diet for the two groups was similar at 8 months, but at 13 months, P/M/S was significantly higher in the intervention group (0.7/1.2/1.0) compared to the control infants (0.3/0.7/1/0).

As expected, both groups had a similar plasma lipid profile at 8 months of age, however, at 13 months, the overall plasma lipoprotein profile of the intervention group was more positive than the control group. For example, total cholesterol and non-HDL levels increased in the control group and remained the same in the intervention group. Also, the researchers observed a decreased serum apolipoprotein A1 and slight increase in apolipoprotein B in the intervention group. Parents of children in the intervention group also exhibited an improvement in their serum total cholesterol levels compared to parents of the control group.

Interestingly, at both 7 months and 13 months, on average, infants in this study were taller and had higher mean weight-for height ratios than the national mean. Further analysis of the data from 103 children in the lowest decile for weight-for-height (i.e.>7% below the average weight-for-height for healthy Finnish children at age 13 months) revealed that these children were small even before entering the study. The incidence of low weight-for-height characteristics was similar in both groups. Lastly, total calories and fat composition of the slow-growing childrens’ diets were similar to other children in the study.

As a result of their findings, Lapinleimu et al. concluded that early introduction of a low-fat diet will help children develop heart healthy eating patterns which might reduce the risk of atherosclerosis in their middle ages.

[ Lapinleimu, H., Viikari, J., Jokinen, E., et al. Prospective randomized trial in 1062 infants of diet low in saturated fat and cholesterol. Lancet 1995;345:471-76.]

Editor’s Comment
Even though one can support benefits of providing nutrition education to the parents, the extend of the conclusions could be a concern. This short study followed the subjects for only 6 months, and one has to wonder if the outcome would be different if the length of the study was prolonged. Also, the researchers were unable to achieve two of their original dietary objectives; a dietary fat P/M/S ratio of 1/1/1 was never achieved in the intervention group. Also, both control and intervention groups were already consuming fat at the level the intervention was trying to achieve for the treatment group at age 13 months. Finally, it is far from clear that the children will continue to follow a heart healthy eating pattern just because they consumed a low-fat diet in infancy. When dietary intervention and restrictions should be initiated in children is a topic of considerable debate with opinions ranging from 7 months in this study to after two years of age to not until linear growth stops. The fact is we do not know the answer.

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Effects of Specific Saturated Fatty Acids on Serum Lipids and Lipoproteins

Many studies have shown that dietary saturated fat is a hypercholesterolemic agent. However, the extent to which different saturated fatty acids increase blood cholesterol levels remains unclear. Therefore, in an effort to explain the mixed results seen in previous studies, Temme and colleagues studied the effects of dietary lauric, palmitic, and oleic acids on serum lipid and lipoprotein levels in 32 Dutch volunteers. These healthy subjects had initial mean fasting plasma cholesterol of 198 mg/dl, HDL of 58 mg/dl, and BMI of 25 for both males (n=14) and females (n=18). In this randomized, crossover feeding study, all subjects consumed diets enriched in either lauric acid, palmitic acid, or, oleic acid for 6 weeks. During the two 2-week washout periods, participants resumed their habitual diet. Fasting blood samples were drawn once on week 5 and week 6 and analyzed for total cholesterol, HDL cholesterol, TAG, apolipoproteins AI and B, and Lp(a). LDL cholesterol was calculated using the Friedewald equation.

The 3 test diets contained 40% of energy as fat. Seventy percent of fat was in the form of experimental fats which were incorporated into the food items, while 30% of the fat intake was self-selected by the volunteers from a list of free-choice fat containing products. The fatty acid composition of the three diets were similar except for the extra 8.5% of energy derived from the respective test fatty acid. The lauric acid diet (P:S = 0.21) was a mixture of palm kernel oil (75%) and sunflower oil (25%); the palmitic acid diet (P:S = 0.24) was a mixture of dairy fat (55%), palmstearin (36%), and sunflower oil (9%); and the oleic acid diet (P:S = 0.46) was a mixture of dairy fat (37%) and sunflower oil (63%).

Dietary cholesterol level was adjusted to 1.45 mg cholesterol per gram of fat. Also, linoleic acid intake was increased in all three diets to equal 4-5% of total energy. To assure that the subjects weight remained the same, daily food energy intake was based on 3 day food records collected prior to the study.

Compared to lipid levels in the oleic diet period, during the lauric and palmitic diets, researcher observed an increase in total cholesterol of 19 mg/dl and 10 mg/dl, respectively. The difference in plasma total cholesterol concentrations between the lauric and palmitic acid diets was statistically significant. LDL levels increase by 14 mg/dl and 9 mg/dl with intake of the lauric and palmitic diets, respectively. However, the differences between the lauric and palmitic diet phases were not significant. On the lauric diet, plasma HDL levels were 5.4 mg/dl higher than on the oleic diet and 4.6 mg/dl higher than during the palmitic diet period. HDL levels did not differ for the palmitic and oleic diets.

Apo A-I concentrations during the lauric acid diet were 156 mg/L higher than on the oleic diet and 90 mg/L higher than palmitic acid. Apo B concentrations were 83 mg/L higher with the lauric acid diet and 58 mg/L higher with the palmitic acid diet compared to the oleic diet, but similar between the 2 saturated fat diets. The HDL:LDL cholesterol ratio, TAG, ratio of apo AI to B, and Lp(a) did not differ among the three diet phases. Response to the diets did not differ significantly between men and women.

Based on the data, Temme et al. concluded that the two saturated fatty acids, lauric and palmitic were hypercholesterolemic compared to oleic acid. However, lauric acid in the diet raised serum total cholesterol concentrations more than palmitic acid because HDL concentrations increased more on the lauric than on the palmitic diet. Even though the lauric acid diet contained a higher amount of myristic acid (2% energy), considered the most potent plasma cholesterol-raising saturated fatty acid, the authors concluded that lauric acid in the diet is more hypercholesterolemic than dietary palmitic acid with or without myristic acid.

“… at a total fat intake of 40% of energy, both lauric and palmitic are hypercholesterolemic compared with oleic acid. Lauric acid raises serum total cholesterol more than does palmitic acid, which is partly because of a greater increase in HDL cholesterol.”

[Temme, E.H., Mensink, R.P., Hornstra, G. Comparison of the effects of diets enriched in lauric, palmitic, or oleic acids on serum lipids and lipoproteins in healthy women and men. Am J Clin Nutr 1996;63:897-903.]

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Supplementary Antioxidant Vitamins and Atherosclerosis

There is an accumulating body of evidence that antioxidant vitamins can significantly alter the risk of CHD. Using data from the Cholesterol Lowering Atherosclerosis Study (CLAS), Azen et al. investigated the effects of vitamin E and vitamin C supplement on the development of atherosclerosis in male subjects with previous coronary artery bypass grafting. In this study, out of the original 188 subjects in the CLAS trial, 146 subjects with a complete carotid arterial wall intima-media thickness (IMT) measurements were followed by Azen et al. for 2 years. These subjects were randomly divided into drug therapy (Colestipol-niacin) and a placebo group. During this serial arterial imaging trial, researchers measured carotid IMT using a high-resolution B-mode ultrasound technique on a 6 month interval. Based on subjects supplemental vitamin intakes before and during the study, researchers were able to determine that 22 subjects had high supplemental vitamin E intakes (>100 IU/day), 124 subjects had low vitamin E intakes (<100 IU/day), 29 subjects had vitamin C intakes of >250 mg/day and 117 subjects had vitamin C intakes of <250 mg/day.

Vitamin C supplement had no significant effect on the progression of atherosclerosis in either the placebo or the drug therapy group. However, the placebo sub-set with high vitamin E supplement intakes had the lowest progression compared to the low vitamin E placebo group. The placebo group with a high on-trial vitamin E intake had a common carotid IMT change of 0.008 mm/year compared to 0.023 for low vitamin E placebo group. The value did not differ for the high vitamin E and low vitamin E drug groups. Also, the benefit of vitamin E supplementation was demonstrated (p<0.02) for mild/moderate lesions (baseline percent diameter stenosis <50%)but not for severe lesions (>50% diameter stenosis).

Researchers speculated that the minimal effect of vitamin E seen in the drug group was probably due to the overpowering effect the drug therapy had on any progression of atherosclerosis. These authors had previously reported that vitamin E intakes > 100 IU per day was associated with significantly less progression than in those with < 100 IU per day vitamin E intake (see Nutrition Close-Up 13(1):1, 1996). The results in this report extend that to include effects of vitamin E supplement on the progression of early preintrusive atherosclerosis as measured by common carotid artery IMT measurements. However, in spite of the positive effects of high vitamin E intakes on slowing atherosclerosis progression in the high vitamin E placebo group, Azen et al. note that vitamin E supplement has also been reported to be associated with an increased rate of hemorrhagic stroke and in some studies with no change in coronary mortality.

[Azen, S.P., Qian, D., Mack, W.J., et al. Effect of supplementary antioxidant vitamin intake on carotid arterial wall intima-medial thickness in a controlled clinical trial of cholesterol lowering. Circulation 1996;94:2369-2372.]

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Safety of the Nicotine Patch for Cardiac Patients

Now that nicotine patches are available over-the-counter, the demand is bound to increase. However, due to nicotines ability to increase heart rate and blood pressure, its safety in cardiac patient is a concern. Joseph and colleagues investigated the safety of transdermal nicotine patches in a randomized, double-blind test in 584 volunteers with a history of CVD. The average age was 60 years with a smoking history of 44 years. The experimental group received nicotine patches containing 3 different nicotine levels. For the first 6 weeks, each patch contained 21 mg followed by 2 weeks of 14 mg and 7 mg each. The control group received placebo patches. In addition to nicotine patches, subjects also received 2 smoking cessation pamphlets and brief behavior counseling.

Researchers monitored both primary and secondary cardiovascular events, side effects of transdermal nicotine patch, and abstinence from smoking. The primary end points of the study was death, MI, cardiac arrest, and admission to the hospital due to increase severity of angina, arrhythmia, or congestive heart failure; the secondary end point was admission to the hospital for other reasons and out patient visits necessitated by increase severity of heart disease.

Overall, the experimental group faired better than the placebo group. Sixteen subjects (5.4%) from the nicotine group suffered a primary end point compared to 23 subjects (7.9%) from the placebo group. However, more subjects in the nicotine patch group (11.9%) experienced a secondary end point than in the placebo group (9.7%). These numbers were not significantly different. A higher percentage of the nicotine patch group abstained from smoking immediately following the study than the placebo group. (21% vs. 9%) However, after 24 weeks, only 14% of nicotine patch subjects abstained while 11% abstained in the placebo group. Joseph et al. concluded that the concern about the use of nicotine-replacement therapy for smoker with CVD is not warranted.

[Joseph, A.M., Norman, S.M., Ferry, L.H., et al. The safety of transdermal nicotine as an aid to smoking cessation in patients with cardiac disease. N Engl J Med 1996;335:1792-1798.]

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Body Weight Changes and Plasma Lipids

Excess abdominal adiposity is associated with increased CVD risk due to the accompanying elevated TAG and low HDL levels. Aging is associated with an increased proportion of abdominal fat and adverse changes in the plasma lipoprotein profile. The question is, Are these factors related? Couillard et al. investigated the relationship between changes in body composition and subcutaneous fat distribution in 95 women and 93 men over a 12 year period (1980 to 1992) with changes in plasma lipoprotein levels. The mean age of the study population in 1980 was 43 years for men and 41 years for women. Initially all subjects were healthy and free from hypertension, diabetes or CHD. In 1992, the men had gained an average of 2.4 kg, BMI values increased from 25.6 to 26.7 and percent body fat went from 20.4% to 26.2%. In the women there were comparable changes with a gain of 4.5 kg, an increase in BMI from 22.7 to 24.8, and percent body fat shift from 28.5% to 36.1%.

The results indicated a strong relationship between a high body fat mass and deterioration in the plasma lipoprotein lipid profile. In men and women, an increased body fat mass was associated with an increased total cholesterol: HDL ratio. In man, there was a significant correlation between changes in subcutaneous trunk fat and plasma HDL levels while in women there was a correlation between changes in abdominal adiposity with changes in plasma total cholesterol and TAG concentrations. The authors concluded that the increased adiposity observed among aging adult men and women is a significant component of the deterioration in the plasma lipoprotein-lipid profile noted over a 12 year follow-up period.

[Couillard, C., Lemieux, S., Moorjani, S. et al. Association between 12 year changes in body fatness and lipoprotein-lipid levels in men and women of the Quebec Family Study. Internat J Obesity 1996;20:1081-1088.]

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Risk Reduction in Patients with CHD: The CARE Study

The Cholesterol and Recurrent Events (CARE) study tests the effectiveness of pravastatin for lowering LDL levels in patients with average LDL levels and prior MI. Patients were divided into placebo (n=2,078) and pravastatin (n=2,081) groups. Subjects were between 21 to 75 years of age and had suffered an acute MI between 3 and 20 months prior to the study. The baseline LDL levels were between 115 to 174 mg/dl, fasting TAG levels were less than 350 mg/dl, and fasting glucose less than 220 mg/dl. The average length of the study period was 5 years. The subjects plasma total, HDL, and TAG levels were measured at baseline, 6 and 12 weeks after randomization, at the end of each quarter during the first year, and semi-annually thereafter. If a subjects LDL level was greater than 175, the patient was given dietary counseling and cholestyramine to control LDL levels to 175 mg/dl. If this level was not reached, subjects were removed from the study and told to seek treatment from their doctor.

Mean LDL levels of the pravastatin group decreased from 139 mg/dl to 97 mg/dl, a 32% reduction. The data from the follow-up analysis showed that the pravastatin group had a 28% lower LDL cholesterol, a 20% lower total cholesterol, 5% higher HDL, and 14% lower TAG level compared to the placebo group. Patients treated with pravastatin had a 24% lower incidence of the primary end point, fatal CHD or confirmed MI, 20% decrease in death from CHD, 37% lower rate of fatal MI, 26% lower rate of coronary bypass surgery, 23% lower rate of angioplasty, 27% lower rate of either procedure, and 31% lower incidence of stroke than the placebo counter parts.

Women on pravastatin had significantly lower rates of a major coronary event than men on pravastatin; 46% vs. 20%. Also, individuals with higher pretreatment LDL levels decreased their risk of a coronary event to a greater extent than ones with lower LDL levels. Subjects with initial LDL levels greater than 150 mg/dl had a 35% reduction, while those with LDL levels between 125 to 150 mg/dl had a 26% reduction, and there was a 3% increase in risk in subjects with LDL values less than 125 mg/dl. The author suggested that an LDL cholesterol level of 125 mg/dl may be an appropriate lower boundary for a clinically important influence of the LDL cholesterol level on coronary heart disease.

In conclusion, the CARE study indicates that pravastatin is effective in reducing CVD risk in people with prior MI and total plasma cholesterol levels of less than 240 mg/dl. Based on the study’s results, it is estimated that 151 people out of 1000 could be protected from CVD events by pravastatin treatment.

[Sack, F.M., Pfeffer, M.A., Moye, L.A., et al. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. N Engl J Med 1996;335:1001-1009.]

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Editorial: Nutrition Made Simple: Just Tell Them What They Can Eat

A recent notice in a national newspaper informed me that grapefruit juice has now been certified as a component of a heart healthy diet. While not terribly surprised by this statement, I must admit to being rather perplexed as to who thought grapefruit juice wasn’t particularly heart healthy, or more simply, just plain healthy and nutritious in the first place. That started me wondering about the practice of health agencies accrediting which foods should and should not be part of a heart healthy, or cancer reducing, or weight maintaining diet. Its unsettling to think that today’s consumers are so uninformed about basic nutritional facts that they need health promotion agencies to sanction the food items they should, and by inference items they should not, include in their diet. When a leading health agency vouches for the assumed benefits of this food item, but not that food item, it isn’t surprising that many consumers believe that the absence of such endorsements equates to unhealthiness. The programing and perpetuation of this good-food, bad-food mind set no doubt makes the consumers life less complicated. Compared to interpreting a Nutrition Facts label, they can be told what to eat based on an agency seal of nutritional health authenticity. So if a food item fits the current dietary dogma (low in total and saturated fat, sodium, and cholesterol; high in complex carbohydrates and fiber) then the notice of acceptance assures the concerned consumer that they are following the nutritional high ground. And while nutrition educators struggle to get the public to think about fat, cholesterol, and sodium in terms of averages, and consumption patterns over days and weeks, endorsement of specific food items effectively obscures the concept of eating patterns behind a rather large stamp of approval.

One must naturally wonder whether such endorsement programs are in the best interest of the consumer, or of the agency marketing its reputation. Clearly commodity groups exist because of the need for research and promotion related to a specific food item. It now seems that healthy agencies have their version of a commodity: the set of nutritional guidelines for which, with a small fee, one can get the agency’s seal of approval. I understand that it will be a long time, if ever, before eggs and other items from the bad food group will ever be considered eligible for such nutrient quality recognition. But the fact is that I can readily put together a weeks worth of meals which include eggs, red meats, dairy products, fruits and vegetables, and grains which fit into whatever diet formula is currently enshrined by health promotion agencies. All one needs to do is adjust the portion sizes, balance the nutrient pattern over meals and days, and use those old time nutritional concepts of balance, variety and moderation. As clinical and epidemiological research put more emphasis on dietary diversity and variety as an essential in good health, it seems a shame that consumers limit their food choices to those sanctioned by the self-appointed police of the American diet. Our thanks to the American Heart Association Nutrition Committee for so clearly stating in their 1996 dietary recommendations that one should have flexibility in food choices, consider average eating patterns for defining goals, and recognize individual variability in the responses to dietary patterns. Recurring public messages on the importance of the nutrient value of foods, in contrast to simply fat gram counting, are essential if effective and healthful changes are to be made in the American diet. There is more to good nutrition than just telling them what they can eat.

Donald J. McNamara, Ph.D.
Executive Editor, Nutrition Close-Up

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Executive Editor: Donald J. McNamara, Ph.D.
Writer/Editor: Linda Min, M.S., R.D.

Nutrition Close-Up is published quarterly by the Egg Nutrition Center. Nutrition Close-Up presents up-to-date reviews, summaries and commentaries on the latest research investigating the role of nutrition in health promotion and disease prevention, and the contributions of eggs to a nutritious and healthful diet. Nutrition and health care professionals can receive a FREE subscription for the newsletter by contacting the ENC.

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