| Volume 15 – Number 2 | Summer 1998 |
TABLE OF CONTENTS
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COMMON ABBREVIATIONS
BMI: body mass index (kg/m2)
CHD: coronary heart disease
CHO: carbohydrate
CI: confidence interval
CVD: cardiovascular disease
ene: energy
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
RR: relative risk
SFA: saturated fatty acids
TAG: triacylglycerol
VLDL: very low density lipoprotein
Results from DELTA Study: Good News and Bad News
The majority of previous efficacy studies on CHD risk reduction with reduced fat intake have been conducted with white middle-aged men, and accordingly the plasma lipid responses to dietary fat changes for women, nonwhites, and older people are limited. The DELTA study was designed to investigate the effects of a reduced saturated fat diet on plasma lipoprotein levels in these sub-populations. In this multi-center, double-blind crossover trial, 103 healthy adults between the ages of 22-67 years old were fed three isocaloric test diets with varying total and saturated fat contents. The average American diet (AAD) consisted of 15% energy as saturated fat and 34.3% energy as total fat; the Step 1 diet consisted of 9% energy in saturated fat and 28.6% energy in total fat; and the low saturated fatty acid diet (Low-Sat) consisted of 6.1% energy from saturated fat and 25.3% energy from total fat. Subjects consumed each test diet for 8 weeks, followed by a 4-6 week washout period. Dietary cholesterol (300 mg/day), percent calories from protein (15%), and trans fatty acid content (<1.5% energy) remained constant in all three study diets. All meals, except Saturday dinner, were prepared by the research centers. Subjects ate 2 meals at the centers and a third meal and a snack were consumed offsite. Prepacked meals were consumed on weekends. Tray checks and dietary reports were used to assess compliance. The study cohort was 55% female and 45% males, of which, 35% were black females and 20% black males. Also, 32% were postmenopausal women and 35% were males over 40 years old.
Data from all 4 research sites, Columbia University, Pennington Biomedical Research Center, Pennsylvania State University, and University of Minnesota were similar. Researchers attributed this to the “virtually identical diet” eaten at each study site.
Results from this study confirmed several common theories regarding the effect of dietary fat on metabolism. For example, as percent of calories from saturated fat and total fat decreased, plasma total cholesterol, LDL, HDL, apo B, and apo A levels decreased, while plasma TAG and cholesterol:HDL ratio increased. The table below presents the percent change in plasma lipid and apolipoprotein levels as volunteers decreased their saturated fat intake from 15% to 6%. When the data were analyzed separately for subjectsÕ sex, race, age (men only), and menopausal status, the effects of the three diets on plasma lipid and lipoprotein levels were similar to results obtained as a whole. For example, the mean decrease in total cholesterol with the Step 1 diet compared to the AAD diet was 5.5% in subgroup analyses and 5.5% in the original analysis. Similar results were seen for plasma LDL cholesterol levels in both analyses. Also, even though each subgroup had different baseline plasma lipid and lipoprotein levels, the percent change was similar between groups. Plasma total cholesterol and LDL cholesterol decreased 5.2% and 6.3%, respectively in postmenopausal women on the Step 1 diet, while it decreased 5.6% and 7.4% in pre-menopausal women on the Step 1 diet. In Blacks, the plasma total cholesterol fell by 5.4% on the Step 1 diet and 4.2% on the Low-Sat diet, while in nonblacks, the total cholesterol fell by 5.5% and 3.5% with the Step 1 and the Low-Sat diet, respectively. In men, LDL cholesterol decreased by 9.3 mg/dl and 4.9 mg/dl on the Step 1 and the Low-Sat diet, respectively. In women, LDL cholesterol decreased by 9.1 mg/dl and 5.5 mg/dl on the Step 1 and the Low-Sat diet.
Researchers were surprised by the increase in plasma Lp(a) concentration on the Step 1 and Low-Sat diets since variability in plasma Lp(a) was thought to be determined by genetics rather than diet. Therefore, the increased negative lipid profile (increase in Lp(a) and TAG and decrease in HDL levels on the Step 1 and Low-Sat diet) seen in this study raises questions regarding the efficacy of these diets in lowering CHD risk. Lastly, the cholesterol lowering effects were much lower than the predicted equations of Keys et al. and Hagstead et al. Ginsberg and colleagues proposed that this might have been due to the fact that 22% of SFA was stearic acid and thus did not effect plasma lipid levels.
| Plasma Levels | % Change AAD to Step 1 | % Change Step 1 to Low-Sat |
| TC | -5.49* | -3.98* |
| LDL | -7.00* | -4.34* |
| HDL | -7.09* | -4.74* |
| TAG | +8.58* | +0.65* |
| Apo B | -2.74 | -1.76 |
| Apo A-I | -4.78* | -3.69* |
| Lp(a) | +9.68* | +7.06* |
| TC:HDL | +2.21 | +1.20 |
*P<0.01
KEY Messages
- Plasma Lp(a), TAG, and TC:HDL ratio increased on the Step 1 diet and Low-Sat diet.
- Plasma total cholesterol, LDL, apo B, HDL, and apo A decreased on the Step 1 and Low-Sat diet.
- Race, sex, age (men only), and postmenopausal status did not affect the changes in plasma lipoprotein levels.
| Editor’s Comment: The DELTA Study provides a number of interesting observations on the effectiveness of the Step 1 diet in lowering plasma lipids and lipoproteins, as well as raising a number of questions regarding the effects of this dietary pattern on CHD risk. The observed decrease in plasma cholesterol levels with initiation of the Step 1 diet in this well controlled trial was 5% (11 mg/dl) compared to the average American diet (AAD), and the percent decreases in LDL and HDL cholesterol levels were comparable. With further restrictions in saturated fat to 6% of calories, the study subjects lowered their plasma cholesterol levels an additional 4%, and again the percent decreases were virtually equal for plasma LDL and HDL cholesterol levels. The data indicate that these fat restricted diets had no effect on the plasma LDL:HDL ratio. The unanswered question from this study is whether the dietary interventions actually lower CHD risk given the studies indicating that the LDL:HDL ratio is a significant determinant of CHD relative risk. What is surprising is the observation that with decreasing saturated fat calories, plasma levels of Lp(a) increased. What this mean in terms of thrombotic risk is clearly not known, but other studies suggest that it probably is not beneficial. The observation that plasma Lp(a) concentrations are altered by diet was unanticipated, and that Lp(a) increases with decreasing fat calories is certainly a topic for further research. It should also be remembered that decreasing fat calories causes some subjects to have small, dense LDL particles and the DELTA Study had similar results in that plasma LDL cholesterol levels decreased to a greater extent than plasma apo B levels. One conclusion from the DELTA Study is that diet-mediated changes in plasma total cholesterol do not always provide an appropriate end-point for determining CHD risk reduction by the intervention. The question now becomes how to relate the benefits of LDL cholesterol lowering versus the unknown effects of plasma HDL cholesterol lowering, the increase in plasma Lp(a), and production of small, dense LDL particles? |
Ginsberg, H.N., Kris-Etherton, P., Dennis, B., et al. Effects of reducing dietary saturated fatty acids on plasma lipids and lipoproteins in healthy subjects. The Delta Study, Protocol 1. Arterioscler Thromb Vasc Biol 1998;18:441-449.
Frequency of Exercise Associated with Reduced CHD Risk
Studies by Hsieh et al. investigated the health benefits associated with physical activity in 3,331 middle-aged Japanest employees or office workers who were undergoing a routine health exam ate men. The majority of subjects were either government employees or office workers who were undergoing a routine health exam at the time of the study enrollment. Subjects were classified into sedentary, active 1 day/week, active 2 days/week, or active > 3 days/week study groups based on their response to a physical activity survey questionnaire. Also, each subject’s blood pressure, lipids, glucose levels, obesity, and smoking status were measured at the onset of the study. Upon examination of the data, researchers learned that the largest number (2,400) of study cohorts were in the sedentary group while only 204 men exercised 3 or more times per week.
The only similarity among the different study groups was their mean age of 48 years. All the other CHD risk factors were much higher in the sedentary men relative to the active groups. For example, people who exercised >1 day were more likely to have higher HDL levels and lower plasma total cholesterol, TAG, blood pressure, and fasting blood glucose levels than the sedentary group. Also, “the sum of the risk factor scores for hypertension, abnormal glucose tolerance, hypertriglyceridemia, hypercholesterolemia, and low HDL level (one point for each if present) was highest in the sedentary group (1.38, 1.19, 1.19, 0.99 for the sedentary group and the groups who exercised 1, 2, and > 3 days per week).” Men who exercised > 2 days/week had lower waist-to-height ratios, subcutaneous fat around the umbilicus, and prevalence of fatty liver. Lastly, incidence of smoking decreased with increased activity level as well as increased HDL levels in these groups. Like previous studies, this study corroborates the fact that physical activity is a positive independent factor for an increased HDL cholesterol level. Hsieh and colleagues concluded that any amount of physical activity is better than no activity, however, in order to reap the maximum health benefit, it is better to exercise for at least 30 minutes more than 3 days a week as recommended by the American College of Sports Medicine.
Hsieh, S.D., Yoshinaga, H., Muto, T., et al. Regular physical activity and coronary risk factors in Japanese men. Circulation 1998;97:661-665.
Dietary Fat and Plasma Lipoproteins in Trained Runners
High carbohydrate, low-fat diets have been recommended for endurance athletes to enhance glycogen stodiets might not be in their best interest, but rather that a high fat dirage. Now, new studies are suggesting that maybe these diets might not be in their best interest, but rather that a high fat diet could be more appropriate. In this clinical study, Leddy et al. investigated the effects of varying dietary fat intake on CHD risk factors in runners. Twenty five runners (12 men and 13 women) in Buffalo, NY were enrolled in the study. All subjects trained at least 35 miles per week and were not taking any lipid altering medication. Subjects were instructed to follow 3 test diets consisting of 16%, 30%, and 42% calories from fat for 4 week increments. However, due to their fat phobia, 13 subjects (6 men and 7 women) were noncompliant with the 42% fat diet. Therefore, the investigators used only 12 sets of data when analyzing CHD risk with the high fat diet. Physiological and blood lipid parameters were measured after each diet. Analysis of subjects’ dietary logs indicated that, on average, subjects did actually consume 16%, 30%, and 42% of calories from fat as prescribed. Also, as the percent of calories from fat increased, total calories consumed per day increased while the percent of calories from carbohydrate decreased. During the 42% fat diet, volunteers consumed 20% more calories than on the 16% fat diet. The polyunsaturated to saturated fat ratio decreased with increasing fat in the diet; 0.70 for the 16% fat diet, 0.50 with the 30% fat diet, and 0.49 on the 42% fat diet. Dietary cholesterol intake also increased as the percent of calories from fat increased indicating that subjects were consuming more animal products.
In spite of the 20% increase in total calories on the high fat diet, no negative physiological changes was observed in these athletes. Most lipoprotein parameters, except HDL cholesterol and apo A1, did not change significantly as subjects increased fat intake from 16% to 42%. However, plasma HDL cholesterol and apo A1 levels were highest on the 42% fat diet and lowest on the 16% fat diet. For example, HDL cholesterol level increased from 50 mg/dl to 69 mg/dl between 16% fat and 42% fat diet. Lastly, the TC/HDL levels were highest with the 16% fat diet and lowest with the 42% fat diet. Even though conventional wisdom holds that a high fat diet can have an adverse effect on CHD risk, these findings show that in endurance athletes, a high fat diet is more appropriate in reducing their CHD risk. Low-fat diet resulted in negating the benefit achieved by exercising by increasing plasma TAG and decreasing HDL cholesterol and apo A1 levels. In conclusion, this study shows that a diet consisting of 42% calories from fat did not increase the CHD risk factors in trained men and women.
Leddy, J., Horvath, P., Rowland, J., et al. Effect of a high or a low fat diet on cardiovascular risk factors in male and female runners. Med. Sci. Sports Exerc 1997;29:17-25.
Inverse Relationship Between Low Plasma Folate and Vitamin B6 and CHD Risk
Recently, the link between hyperhomocysteinemia and CVD has received much media attention; however, this is not a new discovery. This relationship was initially identified in 1969 by McCully in two children with an inborn metabolic disorder. But since than, many studies have shown a direct relationship between an elevated plasma homocysteine and CHD risk, and an inverse relationship between plasma folate and vitamin B6 concentrations and homocysteine levels. Results from the Nurses’ Health Study and the European Concerted Action Project have confirmed and added new information to this research area.
In the Nurses’ Health Study, researchers compared the folate and vitamin B6 intakes of 80,082 women with the incidence of nonfatal MI (n=658) and fatal CHD (n=281) during a 14 year follow-up period. Biennial semiquantitative food frequency questionnaires were used to collect the dietary data. The food frequency data showed that the major sources of folate and vitamin B6 were multivitamins followed by cold cereals, orange juice, lettuce, and eggs for folate and beef, cold cereals, and potatoes for vitamin B6. Rimm and colleagues reported that the multivariate RR for CHD was 0.69 (95% CI, 0.55-0.87) for women in the highest quintile for folate compared to the lowest quintile. The mean folate levels in each quintile were 158 µg/d, 217 µg/d, 276 µg/d, 393 µg/d, and 696 µg/d, respectively. The multivariate RR for CHD was 0.67 (96% CI, 0.53-0.85) for women in the highest vitamin B6 group. The mean dietary B6 level in each quintile was 1.1 mg/d, 1.3 mg/d, 1.7 mg/d, 2.7 mg/d, and 4.6 mg/d. The data indicated that each increase of 200 µg of folate and 2 mg of vitamin B6 was associated with a RR of 0.89 and 0.83, respectively. Unlike folate, in the case of vitamin B6, vitamin source, i.e. food or supplements, did impact the inverse relationship. Vitamin B6 supplements apparently decreased CHD risk more than dietary vitamin B6.
Smoking and vitamin E intake were 2 major confounding factors that attenuated the association between CHD and folate and vitamin B6 intake. The independent effects of folate and vitamin B6 on CHD risk were difficult to isolate in this study, since multivitamins and breakfast cereals contained both vitamins. Lastly, the RR between extreme quintiles of folate intakes were different across levels of alcohol intake, smoking status, and family history of CHD, but not with vitamin B6. Nurses in the highest folate intake group with more than 1 alcoholic drink per day had the lowest RR for CHD (0.27).
Robinson et al. conducted a multi-center, case-control study to test the interrelationship between homocysteine, B vitamins, and vascular disease. This study took place in 19 different centers in 9 European countries with 750 cases and 800 control subjects. Control groups were geographically matched with case subjects. The test subjects were recently diagnosed with vascular disease prior to being enrolled in the study. Primary measurements for this study included plasma homocysteine, red cell folate, B12, B6, and lipoprotein index. For the purpose of this study, deficiency of folate, B12, and B6 were set at concentration levels of <372 nmol/l, <125 pmol/l, and <20 nmol/l, respectively and low levels were defined as concentrations of 513 nmol/l for folate, 139.5 pmol/l for B12, and 23.3 nmol/l for B6. The incidences of vitamin B6, B12, and folate deficiency were much higher in the case group. Four percent of case subjects were deficient in folate versus 2% in the control group and 35% of cases had low B6 levels versus 20% the in control group.
As predicted, researchers observed higher fasting and post load homocysteine values in case subjects than control subjects regardless of gender. The increase in homocysteine levels with a methionine-loading test was much greater in female subjects than male subjects. The difference in folate concentrations between case and control groups was only evident in males. For example, in men red cell folate values were 819 nmol/l and 876 nmol/l in cases and controls but in women, it was 727 nmol/l and 726 nmol/l in cases and controls. Case status did not effect B12 concentrations, however, B6 levels were higher in case subjects than control subjects. The investigators reported a negative correlation between plasma homocysteine and all three vitamins, but only low levels of folate and vitamin B6 were associated with vascular disease. The RR for vascular disease was 1.50 with folate levels below 513 nmol/l and 1.84 for vitamin B6 levels below 23.3 nmol/l.
Results from the two studies corroborate previous findings regarding the relationship between low folate and B6 and CHD risk due to increased plasma homocysteine levels. But the data from the Nurses’ Health Study suggest that current RDA for vitamin B6 and folate is adequate for preventing deficiency, however, it might not be sufficient to protect people from CHD risk.
Rimm. E.B., Willett, W.C., Hu, F.B., et al. Folate and vitamin B6 from diet and supplements in relation to risk of coronary heart disease among women. JAMA 1998;279-359-364.
Robinson, K., Arheart, K., Refsum, H., et al. Low circulating folate and vitamin B6 concentration Risk factors for stroke, Peripheral vascular disease, and coronary artery disease. Circulation 1998;97:437-443.
Folic Acid Fortification Level not Adequate in Reducing Homocysteine Levels
This January 1, 1998, the Food and Drug Administration has required all cereal-grain products to be fortified with folic acid. This initiative was introduced to increase folic acid intake by women of childbearing age and thus decrease the incidence of congenital neural-tube defect in infants. One side benefit of fortification of folic acid in the food supply is the potential decrease in CHD risk resulting from lowered plasma homocysteine levels. It has even been predicted that 19,000 lives per year could be saved from vascular disease with increased folate intake.
Using 75 older volunteers (> 45 years old) with history of CHD, Malinow and colleagues conducted a double-blind, placebo-controlled, crossover trial to test this theory. The three test diets, A, B, and C, contained 127 µg, 499 µg, and 655 µg of folic acid, respectively, in 30 grams of breakfast cereal consumed each morning. The diets also provided 100% RDA for vitamins C, E, B1, B2, B3, B5, B6, B12, iron, and zinc; 25% RDA of vitamin A; and 10% RDA of vitamin D. The placebo diet contained the same amounts of all vitamins and minerals except folate, B6, and B12. Only the naturally occurring amounts of folate (10 µg), B6 (0.11 µg), and B12 (0.13 µg) were in the placebo diet. The subjects consumed either one of the test diets or a placebo diet for the first 5 weeks followed by a 5 week washout period than 5 more weeks on the crossover diet.
According to the baseline data, subjects in all 3 test groups had similar CHD risk factors, as well as similar plasma homocysteine and folic acid levels. But, following the test diets, plasma homocysteine levels in group A decreased by 3.7%, group B by 11.0%, and group C by 14%, while the plasma folic acid levels increased by 30.8%, 64.8%, and 105.7% with study diets A, B, and C, respectively. However, the changes in these levels were only significant in test groups B and C. Therefore, results from Malinow’s study, show that when it comes to reducing CHD, risk due to elevated plasma homocysteine levels, the current level of folic acid fortification (140 µg per 100 gm of cereal product) seen in group A was insufficient. Thus, in order to achieve significant CHD risk reduction benefit, folic acid fortification should be increased by 4 to 5 times current level.
Boushey, C.J., Beresford, S.A., Omenn, G.S., et al. A quantitative assessment of plasma homocysteine as a risk factor for vascular disease: probable benefits of increasing folic acid intakes. JAMA 1995;274:1049-1057.
Malinow, M.R., Duell, P.B., Hess, D.L, et al. Reduction of plasma homocyst(e)ine levels by breakfast cereal fortified with folic acid in patients with coronary heart disease. N Engl J Med 1998;338:1009-1015.
Fish Consumption Reduces Sudden Cardiac Death Rate
Using data from the Physicians’ Health Study, Albert and coworkers investigated the relationath. In this prospective cohort study, 20,551 healthy, male physicians betwship between fish consumption and risk of cardiac death. In this prospective cohort study, 20,551 healthy, male physicians between 40 to 84 years old were enrolled and followed for 11 years. Subjects’ health status and risk factors for CVD were recorded at onset of the study in 1982. Subjects’ dietary patterns were measured between 12 and 18 months of the study with a semiquantita-tive food frequency questionnaire. Also, after the first year, cardiovascular events were measured annually with a follow-up questionnaire. The reported deaths were confirmed by examining medical records and in cases of insufficient data, family members were interviewed for further information.
For the purpose of this study, types of fish consumed by volunteers were classified into 4 categories: canned tuna, dark fish, other fishes, and shellfish. The marine sources of omega-3 fatty acids consumed were calculated by multiplying the frequency of the 4 fish categories with different omega-3 fatty acid factors for these fish. The omega-3 fatty acid factors for canned tuna, dark fish, other fishes, and shellfish were 0.69 gm, 1.37 gm, 0.17 gm, and 0.46 gm, respectively. Fish intake in this study population ranged from rarely or never to 2 or more per day.
According to the returned question-naires, 80% of subjects ate fish between 1 to 4 times per week, 3.1 % rarely or never ate fish, and 10.8% ate fish more than 5 time per week. Researchers also found that people in the highest fish consumption group were physically more active, smoked less, drank more alcoholic beverages, took more vitamin supplement, and had higher plasma cholesterol levels and blood pressure than people with the lowest fish consumption. These confounding CVD risk factors were taken into account in the analysis.
During the follow-up period, 133 sudden deaths and 737 MI were reported. While the sudden cardiac deaths had an inverse relationship with fish intake, no such relationship was observed for MI cases. For example, the relative risk of sudden death for subjects with 1-3 fish intake per month and >1 fish meals per week were 0.64 ( 95% CI, 0.26-1.58) and 0.48 (95% CI, 0.24-0.96), respectively. The relative risk for MI with 1-3 fish consumption per month and >1 fish consumption per week were 0.91 ( 95% CI, 0.55-1.53) and 0.99 (95% CI, 0.64-1.54), respectively. The relative risks for the 4 quartiles of omega-3 fatty acid intake were 0.58, 0.34, 0.60, and 0.43, respectively. In the case of MI, non-sudden cardiac death, CHD death, and CVD mortality, fish intake of >1 per month did not affect risk. However, fish intake of 1 per week was associated with a significant reduction in total mortality.
This study contradicts the Western Electric Study findings, which showed no relationship between sudden cardiac death and fish intake but a significant inverse relationship in CHD death and non-sudden cardiac death. The investigators speculated that this contradicting finding was due to different definitions for sudden death. In the Physicians’ Health Study, sudden death occurred within one hour while it meant less than 12 hours in the Western Electric Study.
Albert, C.M., Hennekens, C.H., O’Donnell C.J., et al. Fish consumption and risk of sudden cardiac death. JAMA 1998;279:23-28.
Fast Food and Television: Two Culprits Behind Obesity in the U.S.
Until now, without scientific evidence, peopty of television viewing for the increased obesity in the Unile have blamed excessive consumption of fast food and the inactivity of television viewing for the increased obesity in the United States. But, thanks to a new study by Jeffery and French, we now have scientific data to support the correlation between increased fast food intake and watching television with obesity. In this cross-sectional and longitudinal study, researchers analyzed the association between fast food consumption and television viewing with change in BMI of 1,059 volunteers (198 men and 861 women) between 20-45 years of age. According to the baseline data, a high number of fast food meals consumed were positively associated with increased total calories and calories from fat in all study groups. However, this relationship was seen only in women volunteers with television viewing. Television viewing and fast food eating were also significantly associated with changes in women’s BMI but not significant in changes in men’s BMI. This relationship was strongest in low-income women. Television viewing was the most important factor in predicting weight gain in high-income women. The lack of association found between fast food intake and television viewing and BMI in men did contradict the study hypothesis, but researchers speculated that it might have been due to the fact that subjects in this study were volunteers for a weight gain prevention study. In conclusion, this study does suggest that abundance of fast food and excessive television viewing can contribute to the increase obesity in the U.S.
Jeffery, R.W., French, S.A., Epidemic obesity in the United States: Are fast foods and television viewing contributing? Am J Public Health 1998;88:277-280.
Second Hand Smoke Associated with Increased Atherosclerosis Progression Rate
Previous studies have shown that smoking increases the risk of heart disease and stroke. However, data on the relationship betwe with the progression of atherosclerosis were limien active cigarette smoking and exposure to environmental tobacco smoke (ETS) with the progression of atherosclerosis were limited. Howard et al. measured changes in carotid artery intimal-medial thickness (IMT) in 10,914 people in the Atherosclerosis Risk in Community (ARIC) Study. In this longitudinal study, baseline IMT and follow-up IMT at 3 years were measured using a B-mode real-time ultrasound. Also, physiological and lipoprotein risk factors were measured at baseline. Based on their smoking status, subjects were divided into smokers (n=2,956), past smokers without exposure to ETS (n=1,344), past smokers with exposure to ETS (n=1,849), nonsmokers without exposure to ETS (n=2,316), and nonsmokers with exposure to ETS (n=2,449). Researchers adjusted the data for demographic characteristics, CVD risk factors, and lifestyle variables to account for confounding CHD risk factors.
The adjusted data showed that nonsmokers without exposure to ETS had the lowest atherosclerosis progression rate (25.9 µm) in 3 years and smokers had the highest atherosclerosis progression rate of 43.0 µm. The mean IMT progression was 31.6 µm for nonsmokers with exposure to ETS, 32.8 µm for past smokers without exposure to ETS, and 38.8 µm for past smokers with exposure to ETS. Howard et al. concluded that continued smoking, past smoking, and exposure to ETS increased the progression of atherosclerosis by 50%, 24%, and 20%, respectively, over nonsmokers not exposed to ETS. Also, regardless of different smoke exposure, people with diabetes had higher progression rates than non-diabetics with similar smoking exposure. Hypertensives and people with CHD had slightly higher rates of atherosclerosis progression than people without these chronic conditions at the same smoking exposure. Lastly, even though atherosclerosis progression was 18% higher in current smokers than past smokers, when pack-years were included in the analysis the higher rate of progression was no longer significant. The pack-years for current smokers was 31 while for past smokers not exposed to ETS and exposed to ETS were 19 and 24, respectively.
Results from this study show that exposure to tobacco smoke through either direct smoke or second hand smoke can increase an individual’s CHD risk by increasing IMT of the carotid artery. The frequency of tobacco smoke exposure and diabetes are two strongest factors in atherosclerosis progression due to ETS.
Howard, G., Wagenknecht, L.E., Burke, G.L., et al. Cigarette smoking and progression of atherosclerosis. The atherosclerosis risk in communities (ARIC) study. JAMA 1998;279:119-124.
Editorial:
Cholesterol-phobia: An International Obession
During the past year I have been fortunate enough to give lectures on the dietary cholesterol-plasma ch Rica and Hong Kong. What I have found most startling is the enormous olesterol issue in a variety of locations including Costa Rica and Hong Kong. What I have found most startling is the enormous impact that the dietary recommendations from USA health promotion groups has world wide. This seems to be especially true when talking about the number of eggs one is allowed to eat each week. In Costa Rica the medical community is so concerned about dietary cholesterol that it recommends the public restrict their consumption to no more than three eggs per week. And while this is not all that different from some US recommendations ten years ago, what makes this restriction disturbing is that in Costa Rica 25% of the population lives in poverty. One must question the logic of telling many of those already undernourished that nutrient dense, affordable eggs should be excluded from the diet. This is clearly an exaggerated view of the relationship between dietary cholesterol and heart disease risk, as well as an unbalanced risk-benefit consideration.
In Hong Kong the dietary cholesterol restrictions are even more pronounced with physicians recommending egg yolk consumption be limited to no more than two visible eggs per week. The logic is that, since eggs are used in so many commonly eaten foods in Hong Kong, the only way to effectively limit dietary cholesterol is to restrict visible eggs in the diet. The most striking point here is that Hong Kong, as well as mainland China, is being inundated with American style fast food chains providing burgers and fries in place of steamed fish and rice noodles. And the youth of Hong Kong, like the youth of America, find the fast food chains to be just too enticing. What really makes all this so interesting is that in both countries there is very little communicated about the CHD risks associated with saturated fats in the diet. The primary emphasis of the public health approaches to reducing heart disease risk deals largely with reducing the dietary cholesterol intake of the population. Sounds a lot like the USA about a dozen years ago when “cholesterol-free” was the magic cliche for instant market acceptance by health conscience consumers. And what is the basis for these inept endeavors at public health nutrition? The egg restricting dietary recommendations from some US health promotion groups.
And the confusion about dietary cholesterol is certainly not finished in this country either. One of the most commonly heard remarks at the Egg Nutrition Center exhibit booth at the annual meeting of the American Association of Retired Persons (AARP) was, “my doctor said I couldn’t have more than two eggs a week.” It seems that the simplistic message to “cut out eggs” is still a common prescription being given to many elderly patients. This makes little sense given the number of studies showing that dietary cholesterol has little effect on plasma cholesterol levels, and that eggs are an affordable, convenient and appropriate source of high quality nutrition. For these populations, such restrictions would have little or no CHD risk lowering benefit.
So for the poor, the elderly and the fast food crowd, eggs remain a member of the “bad food group” thanks in large part to a twenty-five year old cholesterol-phobia promulgated by USA health promotion groups. Little does it matter that most countries of the world do not include dietary cholesterol restrictions in their national dietary guidelines, the fact that America does goes a long way in convincing physicians around the world that dietary cholesterol restrictions, and egg limitations, are reasonable approaches to CHD risk reduction. One wonders how long this futile path of prevention will be followed before the saturated fat and total calories message impacts on the world-wide public health establishment. Until then the only reductions that will be accomplished will be in the overall nutritional status of subsets of these populations.
Donald J. McNamara, Ph.D.
Executive Editor, Nutrition Close-Up
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.
