| Volume 15 – Number 1 | Spring 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
Hyperlipidemia and Response to Dietary Cholesterol
A criticism of previous studies of the effects of adding eggs to the diet on plasma cholesterol levels has been that the studies were carried out in young, normocholesterolemic subjects. While this has not been a justifiable criticism, since many studies were carried out in middle-aged and older men and women, there has not been a study specifically investigating the effects of added eggs on the plasma cholesterol levels of middle-aged men and women with different types of hyperlipidemic.
In the past, egg feeding studies conducted in healthy populations with normal plasma lipid levels showed that dietary cholesterol had a minimal effect on blood cholesterol levels in these individuals. Now, a study by Knopp et al. has investigated the effects of egg feeding in 161 free-living adults with either hypercholesterolemia (HC, n=79) or combined hyperlipidemia (CHL, n=52 ). All subjects had LDL cholesterol levels between 130-190 mg/dl, but ones with TAG greater than the 75th percentile for age and sex were classified as CHL. The subjects selected for this study were free of diabetes, uncontrolled hypothyroidism or heart disease. All women in this study were post-menopausal and averaged 60 years of age and the average age of men was 52 years.
Prior to initiating the experimental phase of this double-blind study, all subjects were instructed on NCEP Step1 Diet by a registered dietitian. They followed this diet for 6 weeks. Then 60% of subjects were randomly assigned to the egg diet and 40% were assigned to an egg-substitute placebo diet. The total duration of the experimental phase was 12 weeks. Each egg supplement contained either 100 grams of homogenized whole egg, the equivalent of 2 eggs, or 100 grams of a cholesterol-free egg substitute. Subjects were instructed to keep a food record to assess dietary compliance. On week 4, 8, 11, and 12, subjects returned to the clinic to receive egg products and check weights and obtain fasting blood measurements.
Following the study, researchers found that 131 subjects complied with study protocol of maintaining their baseline weight and eating egg supplements more than 80% of the time. At week 12, subjects in the egg group consumed 29.6% of energy from fat, an increase of 2.7% from baseline, while total fat intake in the placebo group remained relatively stable at 25.8% of energy. In addition to the increase in total fat, saturated fat and dietary cholesterol increased in the egg-fed group, 8.2% to 9.1% of calories and 187 mg/d to 601 mg/d, respectively, in contrast, saturated fat and dietary cholesterol in the placebo group decreased slightly from 7.8% to 7.3% of calories and 185 mg/d to 155 mg/d dietary cholesterol.
Researchers found the following changes in plasma lipoprotein concentrations. The plasma LDL cholesterol increased in both the HC and CHL egg-fed groups, 3 mg/dl and 12 mg/dl (P<0.001), respectively, but no significant change was noted in either placebo groups. Only the increase in LDL cholesterol in CHL subjects were significant. Plasma HDL cholesterol levels also increased in the egg-fed group but no changes occurred in the placebo groups. HC subjects on the egg diet increased their HDL cholesterol by 4 mg/dl and CHL group s HDL cholesterol increased by 3 mg/dl. The total cholesterol level increased in both egg fed and placebo CHL subjects but it did not change in HC groups. TAG levels did not change in any of the 4 groups following the diet change. Apo A and apo B concentrations did change in certain groups. Apo A in egg fed HC subjects increased by 11 mg/dl and apo B increased by 4 mg/dl in egg fed CHL and 8 mg/dl in placebo CHL. Plasma glucose and immunoreactive insulin concentrations were not altered by the intervention diet. Egg feeding did not have an effect on LDL subclass phenotype expression or on the composition of postprandial lipoprotein. Knopp and colleagues concluded that adding 2 eggs to a NCEP Step 1 Diet did not result in significant increase in LDL cholesterol in HC subjects, however, it did raise LDL cholesterol in CHL subjects.
KEY Messages
- Adding 2 eggs per day did not increase LDL cholesterol in middle-aged hypercholesterolemic men and women.
- Adding 2 eggs per day did increase LDL cholesterol in middle-aged combined hyperlipidemic men and women.
- 2 eggs per day increased HDL cholesterol by 4 mg/dl in combined hyperlipidemic subjects and 3 mg/dl in hypercholesterolemics.
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Editor’s Comment: |
Knopp, R.H., Retzlaff, B.M., Walden, C.E., et al. A double-blind, randomized, controlled trial of the effect so two eggs per day in moderately hypercholesterolemic and combined hyperlipidemic subjects taught the NCEP Step 1 Diet. J Am Coll Nutr 1997; 16:551-561.
Effects of Aggressive and Moderate Fat-Restriction on Plasma Lipids of Hyperlipidemic Men
In spite of the conflicting findings from studies of the effects of very low-fat diet on plasma lipids, thereare still many proponents for this restrictive diet. To answer questions regarding the effects of a moderate fat-restriction diet versus an aggressive fat-restriction diet in free-living hyper-lipidemics, Knopp and colleagues conducted a randomized, parallel, comparison trial in men from the Seattle-Puget Sound region. The study addressed two questions: one, does greater fat restrictions result in greater LDL reductions, and two, does the plasma lipoprotein response differ between patients with various hyperlipidemias. Of the 444 men who completed this year long study, all subjects had LDL cholesterol levels greater than the 75th age-specific percentile (160 mg/dl). Those with plasma levels of TAG at or above the 75th age-specific percentile were classified as combined hyperlipidemic (CHL) and those with TAG less than 75th age-specific percentile were defined as hypercholesterolemic (HC).
Baseline clinical characteristics were measured and HC subjects were randomly assigned to study diets 1, 2, 3, and 4 and CHL were assigned to study diets 1, 2, and 3. Study diet 4 was eliminated from the CHL group due to the smaller number of CHL subjects (174) compared to HC subjects (270). Study diet 1, 2, 3, and 4 provided 30%, 26%, 22%, and 18% calories from fat and 300 mg, 200 mg, 100 mg, and 100 mg/d of cholesterol, respectively. The target protein intake of the 4 diets were between 16% and 18% of energy. However, the 4 day food records indicated that the majority of subjects did not achieve their target fat intake. For example, subjects in the HC groups consumed 27%, 26%, 25%, and 22% of energy from fat for the four test diets and subjects in the CHL groups consumed 28%, 26%, and 25% fat. Target cholesterol intakes were also not achieved. The subjects in diet groups 1 and 2 consumed less than their goals of 300 mg and 200 mg/d, while subjects in groups 3 and 4 consumed greater than 100 mg/d. The table below presents the results of different fat restriction diet on plasma lipids and lipoprotein levels in HC and CHL subjects. Study diets 2 and 4 resulted in lower total cholesterol, LDL, and apo B levels in HC. More restrictive fat diets did not yield further benefits on body weight, glucose, insulin, or blood pressure. On the contrary, the very low-fat diet actually resulted in an unwanted lipoprotein profile by increasing TAG and VLDL levels and decreasing HDL cholesterol in HC subjects and decreasing apo B in HC and CHL groups.
The authors concluded that implementation of NCEP Step 1 and Step 2 diets in HC and CHL individuals can be effective in lowering plasma levels of atherogenic lipoproteins. However, aggressive fat restrictions did not show evidence of further benefit. In fact, the observed decrease in HDL levels in HC subjects on the 25% and 22% fat diets suggest potentially adverse effects. The results of this study suggest that more aggressive dietary fat lowering recommendations are probably not appropriated for free-living population at this time.
Percent changes in plasma lipids, lipoproteins and apo B from baseline
| % Change | Hypercholesterolemic | Combined Hyperlipidemic | |||||
| Diet 1 (78) |
Diet 2 (62) |
Diet 3 (71) |
Diet 4 (59) |
Diet 1 (57) |
Diet 2 (55) |
Diet 3 (62) |
|
| Total-C | -3.86 | -10.40 | -7.17 | -9.01 | -5.52 | -4.49 | -5.83 |
| LDL-C | -6.34 | -14.10 | -9.63 | -13.89 | -7.68 | -3.71 | -5.79 |
| Apo B | -12.70 | -14.73 | -8.60 | -11.02 | -17.10 | -14.18 | -12.59 |
| HDL-C | 0.78 | 0.79 | -3.15 | -4.40 | -1.75 | -1.84 | -2.70 |
| TAG | 2.70 | -2.52 | -11.97 | -28.44 | 14.29 | -6.80 | -1.84 |
Knopp, R. H., Walden, C.E., Retzlaff, B.M., et al. Long-term cholesterol-lowering effects of 4 fat-restricted diets in hypercholesterolemic and combined hyperlipidemic men. The dietary alternative study. JAMA 1997;278:1509-1515.
BMI Associated with Mortality in Younger People
Using data from the Cancer Prevention Study I, Stevens et al. investigated the effect of age on the association between BMI and mortality. From the original study cohort, 62,116 men and 263,019 women were selected for this study. These subjects were Caucasian in heritage, free of chronic disease, and nonsmokers. The follow-up period lasted from 1960 to 1972. For the purpose of this study, subjects were separated into the following BMI and age categories: BMI of <19.0, 19.0-21.9, 22.0-24.9, 25.0-26.9, 27.0-28.9, 29.0-31.9, and >32.0, and 30-44 year, 45-54 year, 55-64 year, 65-74 year, 75-84 year, and >85 year old, respectively.
As expected, the incidence of death from all causes and death from CVD were higher in the older population. The mean BMI was relatively constant in males of all age groups except the oldest group. The mean BMI in women increased from 23.8 to 25.2 from the 30-44 year old group to 55-64 year old group, then steadily declined in the older age category. Results indicated a higher incidences of CVD mortality among heavier people than thin people within the same age category. For example, CVD mortality was 22 deaths per 100,000 person-year in 30-44 year old with BMI of 19.0-21.9 compared to 51 deaths per 100,000 person-year in the same age group of women with BMI of 29.0-31.9. However, the incidence of CVD mortality was much higher in older women. Women in the 65-74 year old group with BMI of 19.0-21.9 had CVD mortality incidence of 1854 per 100,000 person-year and ones with BMI 29.0-31.9 was 1854 per 100,000 person-year. This trend was not observed in people over 75 years old. CVD mortality was relatively constant in this older group; 5259 per 100,000 person-year and 5227 per 100,000 person-year in the 19.0 to 21.9 BMI and 29.0 to 31.9 BMI group, respectively. A higher BMI was associated with a higher relative risk for all causes of death and CVD death in younger subjects than older people.
The authors concluded that excess body weight increases the risk of death from both CVD and all causes in adults between the ages of 30 and 74 years. The data are consistent with the hypothesis that the relative risk of death associated with excess adiposity is lower for older than for younger adults. Overall, the results support the healthy weight ranges in the 1995 Dietary Guidelines for Americans which omitted the age-specific weight recommendations of earlier version of the Guidelines.
Stevens, J., Cai, J., Pamuk, E.R., et al. The effect of age on the association between body-mass index and mortality. N Engl J Med 1998;338:1-7.
Effects of Diet Intervention on CVD Risk Factors
A meta-analysis of dietary intervention trial by Brunner and colleagues evaluated the effectiveness of dietary recommendations on CVD risk factors. Based on study criteria, 17 published studies were selected for the meta-analysis dietary recommendations on CVD risk factors. Based on study criteria, 17 published studies were selected for the meta-analysis. All 6893 subjects in the studies were free-living adults randomly assigned to either a dietary intervention or control group for greater than 3 month. The outcomes Brunner et al. compared were percent calories from fat, serum total cholesterol, urinary sodium, and diastolic blood pressure levels divided into either 3-6 months or 9-18 months duration.
Subjects in the intervention groups consumed an average 6% less dietary fat than controls, except for women in a breast cancer prevention study. Subjects in this study were highly motivated and reduced their fat intake by 40%. The median serum total cholesterol level in intervention groups decrease by 10.8 mg/dl at 3 to 6 months and 8.5 mg/dl at 9 to 18 months. However, researchers noted a significant heterogeneity in total cholesterol levels among different studies. An increase in frequency of interaction between subjects and researchers resulted in a greater decline in serum cholesterol level. The mean urinary sodium excretion was 32 mmol/24 hr less in the intervention group. This level equals 19 grams of sodium chloride or a 20% reduction in salt intake. Lastly, except in 2 studies, dietary intervention also resulted in a decline in diastolic blood pressure. At 3 to 6 months and 9 to 18 months, diastolic blood pressure of intervention groups was 0.7 mm Hg and 1.2 mm Hg less, respectively, than control subjects.
In spite of the differences in the study design, data collection, and possible bias due to missing follow-up data, Brunner and associates were able to observe an improvement in subjects CVD risk as a result of dietary intervention. Using data from a primary prevention trial and cohort studies which estimated that a 10% reduction (23 mg/dl) in serum cholesterol reduces CHD by 25%, and a 5 mm Hg reduction in diastolic blood pressure results in a 21% reduction in CHD and a 34% reduction in stroke, researchers concluded that dietary intervention could reduce incidence of CHD and stroke by 14% and 8%, respectively, decline in CHD risk due to a decrease in serum cholesterol was 9%. Brunner et al. also noticed following trends; subjects were more likely to change and adhere to a low fat diet if they thought it would reduce future disease, programs with greater intervention were associated with greater net effect, and dietary compliance was low beyond 18 months. Researchers concluded that individual dietary interventions can achieve moderate reduction in CVD risk.
Brunner, E., White, I., Thorogood, M., et al. Can dietary interventions change diet and cardiovascular risk factors? A meta-analysis of randomized controlled trials. Am J Public Health 1997;87:1415-1422.
Efficacy of Diet and Weight Loss on CHD Risk of Obese, Post-menopausal Women
There are limited data on the effects of a Step 1 Diet on plasma lipids and lipoproteins of obese, postmenopausal women. It is also unclear what effects the Step 1 Diet plus weight loss will have on plasma lipoprotein profiles in this population. In this study, Nicklas and colleagues investigated the changes in lipoprotein lipids of obese postmenopausal women as a result of consuming a Step1 Diet alone and then with weight loss. The baseline mean age and BMI for the 48 study subjects were 61 years and 32.7 kg/m2, respectively. Following baseline measurements of height, weight, dietary intake, and plasma lipoprotein lipid concentrations, all subjects underwent a 2 month eucaloric Step 1 Diet followed by 6 months of dietary intervention with weight loss. During both dietary interventions, volunteers were enrolled in a weekly nutrition class taught by a registered dietitian. The attendance rate was 90% during the Step1 Diet phase and 79% during the diet-weight loss phase. The weight loss diet was designed to provide a gradual weight loss of 0.25-0.5 kg/week by decreasing energy by 1.0-1.5 mJ/d. Physical activity level was constant throughout the study period. Lipoprotein lipid concentrations were measured following each intervention period.
Baseline data showed that the diet consisted of 33% calories from fat, 10% saturated fat, 6% polyunsaturated fat, 215 mg/d dietary cholesterol, and 2842 mg Na per day. Following initiation of the Step 1 Diet, subjects consumed less total fat calories (23%), saturated fat (6.7%), cholesterol (170 mg/d), and sodium (2,456 mg/d) and more calories from carbohydrate (59%). While on this diet, subjects lost a small, but significant amount of weight (2.0+0.3 kg) and during the weight loss phase of the study, the average weight loss was 5.6 +0.7 kg. Also, following the dietary intervention, all lipoprotein lipid concentrations, except HDL cholesterol, improved. For example, after the Step 1 Diet, total cholesterol, LDL cholesterol, and HDL cholesterol levels decreased by 7%, 6%, and 14%, respectively. Volunteers with undesirable TAG levels decreased from 10% to 2%, LDL cholesterol from 54% to 44%, and total cholesterol from 67% to 50%. However, the number of subjects with undesirable HDL (<35 mg/dl) increased from 8% to 13% of the study population. Following the weight loss phase, HDL cholesterol and HDL2 cholesterol increased by 8% and 11%, respectively, thus reducing the number of women with undesirable HDL cholesterol levels from 40% to 21%. While weight loss resulted in a 9% decrease in plasma TAG levels, but total and LDL cholesterol concentrations did not change with weight loss. Lastly, the data indicated that hypercholesterolemic subjects responded better to the Step 1 Diet and the Step1 with weight loss than normocholesterolemic and mildly hypercholesterolemic individuals. For example, following both diet interventions, TAG, total cholesterol, and LDL cholesterol concentrations decreased by 19%, 13%, and 14%, respectively, in hypercholesterolemic women but there were no significant plasma lipid changes in the other 2 groups.
In conclusion, even though the Step 1 Diet plus weight loss did improve the plasma lipoprotein lipid profile, and in theory the risk for CVD, in obese, postmenopausal women with hypercholesterolemia, it had minimal benefit for obese, postmenopausal women with normal or mildly elevated plasma cholesterol. In that the Step 1 Diet decreased HDL levels when no weight loss was achieved raises serious question about the efficacy of a low-fat diet in improving the overall plasma lipoprotein profile.
Nicklas, B.J., Katzel, L.I., Bunyard, L.B., et al. Effects of an American Heart Association diet and weight loss on lipoprotein lipids in obese, postmenopausal women. Am J Clin Nutr 1997;66:853-859.
High HDL Cholesterol Levels in Japanese Children
A recently published study reported on differences in HDL cholesterol concentrations in Japanese, American, and Australian children. The data show that concentrations of HDL cholesterol were higher in Japanese than U.S. or Australian children. More importantly, the plasma total cholesterol:HDL ratio remained stable between ages 8 to 10 years and 12 to 15 years in Japanese boys and girls whereas it increased in U.S. and Australian boys. Comparisons of Japanese and Australian children showed that BMI values were similar but the Japanese children were considerably more physically active. Japanese children consumed less fat (27% ene) than the Australian children (37% ene) yet they consumed more total calories. Japanese children consumed more soy bean products, fish, and eggs than Australian children. For tofu and related products, there was virtually no consumption by Australian children while 61% of Japanese children included this food items in their 24-hour dietary recall. Sixty-eight percent of Japanese children consumed eggs compared to only 18% of Australian children. [Editor’s Note: Japan has the highest per capita egg consumption in the world.] These observed differences in HDL levels and in the age-related changes in plasma total:HDL cholesterol ratio may help to explain why CHD mortality rates in Japan are low compared to other developed countries.
Dwyer, T., Iwane, H., Dean, K., et al. Differences in HDL Cholesterol Concentrations in Japanese, American, and Australian Children. Circulation 1997;96:2830-2836.
Effects of Diet and Sexual Maturation on LDL Cholesterol in Children
The multicenter, randomized, controlled Dietary Intervention Study in Children (DISC) investigated the safety and efficacy of dietary fat and cholesterol reductions on plasma LDL cholesterol in 663 pubescent children stigated the safety and efficacy of dietary fat and cholesterol reductions on plasma LDL cholesterol in 663 pubescent children wi th elevated baseline LDL cholesterol. Investigators also examined the association between baseline BMI and sexual maturation on LDL cholesterol concentrations.
Children were divided into intervention and usual care study groups. Subjects in the intervention group were provided with individual eating plans as well as continuous nutritional education classes throughout the follow-up period. Parents of the usual care children were told that their children had elevated blood cholesterol and provided with general publications on heart-health at the onset of the study. Following the 3 year intervention period, children in the intervention group consumed less total fat (28.6% vs 33%), saturated fat (10.2% vs 12.3%), and cholesterol (95.0 vs 112.9 mg/ 4.2 MJ) than the usual care group. During the study period, subjects weight, height, and lipoprotein concentrations were measured at baseline, and first and third year of follow-up. Subjects sexual maturation were assessed annually using Tanner Stage method.
Sexual maturation and BMI were two biological factors which had strong influences on LDL levels. A 1 unit increase in BMI was associated with a 0.6 mg/dl increase in LDL cholesterol in boys and 1.1 mg/dl in girls. Sexual maturation was inversely associated with plasma LDL cholesterol concentrations. The LDL cholesterol levels in boys in Tanner stage 4+ were 23.3 mg/dl lower than boys in stage 1 and girls in Tanner stage 4 were 10.6 mg/dl lower than girls in Tanner stage 1.
Dietary factors also had significant effects on LDL cholesterol concentrations. The children in the intervention group had lower LDL cholesterol than children in the usual group. The LDL cholesterol level was 5.0 2.1 mg/dl lower in intervention girls and 2.7 2.4 mg/dl in intervention boys. The difference in LDL cholesterol was significant in girls only. However, dietary cholesterol was directly associated with LDL cholesterol level in boys. For each 10 mg/1000 kcal decrease in dietary cholesterol, plasma LDL cholesterol decreased by 0.7 mg/dl. [2.8 mg/dl per 100 mg/d cholesterol]
In boys, higher dietary cholesterol and BMI were associated with higher plasma LDL cholesterol. However, in girls, only high BMI was associated with higher LDL cholesterol. There was no relationship between dietary fat intake and LDL cholesterol in girls. But “Tanner stage 4+ was significantly related to lower LDL cholesterol in both boys and girls.”
Kwiterovich, P.O., Barton, B.A., McMahon, R.P., et al. Effects of diet and sexual maturation on low-density lipoprotein cholesterol during puberty. The dietary intervention study in children (DISC) Circulation 1997;96:2526-2533.
Roles of Childhood and Parental Obesity in Adult Obesity
In our weight conscious society, many people, both scientists and lay persons, have arguedabout the role genetics plays in body weight. Using medical records of 854 subjects, Whitaker et al. analyzed the effects of childhood and parental obesity on a child s risk of becoming obese in their 20s. All the cohorts in this retrospective study were members of a Group Health Cooperative and their longterm weight and height records were available for analysis. Parents weight and height were also available for the majority of subjects. Researchers classified children with BMI at or above the 85th percentile for age and sex as obese and BMI at or above 95th of age and sex as very obese. In adults, men with BMI of >27.8 were considered obese as were women with BMI >27.3.
The data indicated a direct relationship between the age of initial obesity and adult obesity. For example, the odds ratio for obese child developing adult obesity was 1.3 between ages 1-2 years, 4.1 between 3-5 years, 10.3 between 6-9 years, 28.3 between 10-14 years, and 20.3 between 15-17 years. Also, very obese children at all ages were always more likely to become an obese young adult. At every age, children with obese parents had a higher risk of adult obesity, and this was especially significant in children under 10 years of age. Parents obesity status was a primary predictor of adult obesity in children younger than 3 years old, while a child s obesity status was more important in predicting adult obesity in children over 10 years old. Lastly, children with two obese parents had a higher risk of obesity than children with only one obese parent.
Childhood and parental obesity were good predictors of adult obesity. Knowing this, researchers concluded that infant and toddlers with obese parent and obese children should benefit from treatments to prevent excessive weight gain.
Whitaker, R.C., Wright, J.A., Pepe, M.S., et al. Predicting obesity in young adulthood from childhood and parental obesity. N Engl J Med 1997;337:869-73.
Alcohol Consumption and Coronary Heart Disease
Recently, many studies suggest that moderate alcohol intake has a protective effect against CHD. However, with all the known side effects of heavy alcohol intake, one must be cautious when promoting alcohol s beneficial effects in reducing CHD risk. This is especially true since data on the upper limit of alcohol s benefit for CHD risk reduction is unclear. Using data from the National Health and Nutrition Examination Survey I (NHANES I) Epidemiologic Follow-up Study (NHEFS), Rehm et al. analyzed the association between alcohol consumption and CHD incidence and mortality rates. Researchers selected 6,788 subjects (3,828 females, 2,960 males) for the follow-up study. All subjects were European-Americans, 40-75 years old, and free of CHD. With the aid of a 4-question questionnaire, a subject s baseline alcohol consumption between 1971 to 1975 was determined. Follow-up was conducted from 1982 to 1984, in 1986, and again in 1987.
Subjects in the 2-7 drinks/week category had the lowest risk of CHD. For women in this category, the RR for CHD incidence and mortality was 0.51 and 0.55, respectively, and in men it was 0.62 and 0.73, respectively. However, as alcohol consumption increased, RR for CHD also increased. The women with the highest alcohol consumption, greater than 29 drinks per week, had a RR of 2.6 and 4.6 for CHD incidence and mortality, respectively. Surprisingly, high alcohol consumption did not affect CHD risk in males to the degree it affected women. In men, RR for CHD incidence was 0.62 for greater than 42 drinks per week and RR for CHD mortality was 0.89 for greater than 29 drinks per week. There were other sex-related differences noted in this analysis. The female light drinkers, less than 2 drinks per week, had less benefit from alcohol consumption than men in the same drinking category. Also, the RR for CHD incidence was higher for female current abstainers (1.21) than males (0.87). The data suggest that in women, the benefit of alcohol consumption is associated with a specific level of intake. Too much or too little alcohol was actually related to increased CHD risk in women. This was not the case in males. Females exhibited a U-shaped relationship between alcohol consumption and CHD whereas males had a L-shaped relationship.
In conclusion, this study showed that alcohol intake resulted in decreased CHD risk compared to abstainers. Also, there is a definite gender difference in the relationship between alcohol use and CHD risk reduction. Females obtained maximum benefit on less than 1 drink per week and the least benefit with levels greater than 4 drinks per day. In contrast, heavy drinking, greater than 4 drinks per day, did not increase CHD risk in men.
Rehm, J.T., Bondy, S.J., Sempos, C.T., et al. Alcohol consumption and coronary heart disease morbidity and mortality. Am J Epidemiol 1997;146:495-501.
Editorial:
“Industry-funded Research”: They’re Not Dirty Words
Once upon a time the credibility of a research publication was based on four criteria: reputations of the investigators; quality of the journal; a reader s evaluation of the methods, data analysis and interpretation; and ability of other investigators to reproduce the results. In a more cynical era it seems the determinant of the validity of a study is who funded it. In nutritional sciences, industry-funded studies [especially from those members of the “bad-food group”] are automatically suspect, despite satisfying the classic criteria for scientific veracity. Critics have no problem asking credible scientists, published in the most prestigious journals, “That’s all very well and good, but who funded it?” If a group is unwilling, or unable, to attack the science, then the diversionary tactic is to attack the funding and, by inference, the credibility of the researchers.
As a research scientist who received government, foundation, association and industry funding over many years, and now administers an industry research grant-in-aid program, I am bothered by the “who funded it” assessment process. Is it really so easily imagined that scientists with international reputations, various sources of funding, and involvements with government agencies and nonprofit organizations, would jeopardize their careers for the meager funds available from the food industry, and falsify research published in the best scientific journals? I would hope that we would give our colleagues credit for professionalism and integrity, while also recognizing the expertises of journal reviewers, editors and readers.
A recent newspaper article stated that if industry uses research it funds for promotion, they have blurred “the line that separates science from marketing” (The Sunday Record, 4 January 1998, Hackensack NJ). What line? With TV ads encouraging an overdose of cereal to lower cholesterol levels, to taking a statin drug to lower the risk of a first heart attack, it is clear that many blurs this unlikely line. The same article stated that “Critics, though, accuse food producers of seeking out scientists whose views closely match their own, and manipulating the scientific agenda by influencing what research gets funded.” It seems improbable that the American Egg Board, with its level of research funding, could “manipulate the scientific agenda.” And the argument that industry only funds “scientists whose views closely match their own” is equally untenable when industry-funded scientists continue to advocate the nutritional conventional wisdom even when their studies suggest otherwise.
Two examples of this criticism are worth evaluating. The American Egg Board/Egg Nutrition Center partially supported a study by Howell et al. (Nutrition Close-Up 14(2), 1997) which has received industry-funded criticism even though the results were reproduced in a study by Clarke et al. ((Nutrition Close-Up 14(1), 1997) which was not funded by industry. [Interestingly, scientific advisors of some advocacy groups themselves receive industry funding for research. It must be that they get it from ‘good-food groups’!] Industry-funded studies also run the risk of unintended consequences as shown by the study of Knopp et al. reported in this issue of Nutrition Close-Up. Knopp et al. found that, while adding eggs to the diets of mildly hypercholesterolemic individuals had little effect on blood cholesterol levels, those with combined hyperlipidemia were sensitive to the plasma cholesterol raising effects of dietary cholesterol. The fact is, for any industry-funded research it is a case of pay your money, take your chances.
The stigma of “industry-funded research” is strong enough that we often are unable to get investigators to research specific questions. We have tried to have the relationship between egg consumption and heart disease incidence analyzed using data from epidemiological trials. Clearly the population studies are there, the data collected, and the CHD incidence high enough for statistical analysis. We know because we read results from these studies almost monthly. Nevertheless, we get turned down when offering to fund a grant, a fellowship, or any other funding venue. Why? Because the investigators fear that if the data do not show a positive relationship then the findings will be interpreted as industry-funded research. For many investigators the level of funds available are not worth the accusations and credibility challenges.
So let’s look at the position of the egg industry. Dietary cholesterol is accused of being a contributor to high blood cholesterol. The USDA Dietary Guidelines established that dietary cholesterol intake should be no more than 300 mg per day. And the American Heart Association advises that individuals limit their egg intake to “no more than 3 to 4 per week.” There are scientists in this country, and those on the nutrition advisory committees of most countries of the world, who believe that eggs are not a contributor to CHD risk. How do we test the hypothesis if we cannot fund studies of the question? And when we do have applications from highly qualified investigators with protocols reviewed by a Scientific Advisory Panel with impeccable credentials, then the study gets published in a prestigious peer-reviewed journal, the only response from the nay sayers of nutritional politics is “invalid, flawed, unsound industry-funded study.” I guess in today s approach to science it’s just a case of “damned if you do, out of business if you don’t.”
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.
