| Volume 14 – Number 3 | Fall 1997 |
TABLE OF CONTENTS
COMMON ABBREVIATIONS 
BMI: body mass index (kg/m2)
CHD: coronary heart disease
CHO: carbohydrate
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
RR: relative risk
SFA: saturated fatty acids
TAG: triacylglycerol
VLDL: very low density lipoprotein
Dietary Fat and Cholesterol and CHD in Men
The Finnish Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study is a randomized, double-blind, primary prevention trial carried out in 21,930 male smokers aged 50-69 years. In this group, diet was assessed at baseline by a self-administered 12 month dietary history. The diet questionnaire included 276 food items and mixed dishes commonly consumed in the population and a portion size picture booklet with 122 photographs of foods in different portion sizes. The validity of the dietary analysis method was determined in a pilot project comparing the dietary history values with 24 days of food records collected over 6 months. The end points of this study were major coronary events (n=1,399) and coronary deaths (n=581) during the 6.1 years of follow-up.
Cigarette smoking (per day and years), blood pressure, BMI, and serum total cholesterol were directly associated with CHD risk while HDL cholesterol, education and physical activity were inversely associated. Fiber intake was inversely related to the risk of CHD. Of all the dietary fatty acids, only trans-fatty acids were found to be directly related to risk of a major coronary event. The multivariate relative risk [RR] for the highest intake (6.2 g/day) compared to the lowest intake (1.3 g/day) was 1.14 (95% CI 0.96-1.35). Similar data were obtained for coronary death RR with the highest quintile multivariate RR 1.39 (95% CI 1.09-1.78). There were no significant relationships for CHD incidence and intakes of SFA, MUFA, PUFA or omega-3 fatty acids.
Further analysis of the data indicated that men in the lowest quintile of trans-fatty acid intakes had higher intakes of butter, and lower intakes of margarine, than men in the highest quintile. The investigators also presented data indicating that the negative effects of dietary trans-fatty acids on CHD were related to elaidic acid from vegetabletrans-fatty acids. Animal trans-fatty acids in the diet were not related to increased CHD risk. Interestingly, it was only in the highest quintile of trans-fatty acid intakes (6.2 g/day equal to 2% of total energy intake) which was related to a significant increase in CHD risk; the three intermediate quintiles of intakes were not significantly different from the lowest quintile.
The data for dietary cholesterol intake and CHD risk indicated that there was no significant relationship either for age-adjusted RR or multivariate RR of CHD [Table]. As noted by the authors, the subjects in this study had a much higher than average dietary cholesterol intake than noted in previously reported cohorts. However, even at the highest cholesterol intake (768 mg/day), there was no significant increase in age-adjusted CHD incidence or mortality or after multivariate adjustment [smoking, BMI, blood pressure, intakes of energy, alcohol, and fiber, education, and physical activity].
| Cholesterol Intake (mg/day) |
Major Coronary Event | Coronary Death |
| Multivariate RR (95% CI) | Multivariate RR (95% CI) | |
| 390 | 1.00 | 1.00 |
| 477 | 0.86 [0.72-1.02] | 0.90 [0.71-1.16] |
| 543 | 0.91 [0.77-1.08] | 0.81 [0.63-1.05] |
| 621 | 0.87 [0.73-1.03] | 0.86 [0.67-1.11] |
| 768 | 0.93 [0.79-1.10] | 0.92 [0.72-1.18] |
These data, combined with an earlier report [Pietinen et al. Circulation 1996;94:2720- 2727], demonstrate that independent of other risk factors, intake of foods rich in fiber substantially reduces the risk of coronary heart disease in middle-aged, smoking men whereas intake of trans-fatty acids significantly increases risk in this population. In this study, dietary cholesterol intakes were clearly unrelated to CHD risk consistent with other recent epidemiological reports [see Nutrition Close-Up 13 (2):1-2, and 13 (4)1-2, 1996]. These data provide additional evidence against a contributory role of dietary cholesterol to CHD risk, either indirectly through changes in plasma cholesterol levels or directly through other atherogenic mechanisms. [see related story below]
Key Messages
- Intake of trans-fatty acids is positively associated with risk of coronary death.
- Fiber intake is inversely related to the risk of coronary heart disease.
- Dietary cholesterol is not associated with coronary heart disease risk.
|
Editor’s Comment |
Pietinen, P., Ascherio, A., Korhonen, P., et al. Intake of fatty acids and risk of coronary heart disease in a cohort of Finnish men – The Aklpha-Tocopheral, Beta-Carotene Cancer Prevention Study. Am J Epidemiol 1997;145:876-887.
Effects of Low-Fat, High-Carbohydrate Diets on Plasma Lipoproteins
For a longtime low-fat, high-carbohydrate diets have been recommended as the first line of defense in treating heart disease. However, in light of new findings, researchers are beginning to question the effectiveness of this diet therapy.
Jeppesen et al. conducted a feeding study with 10 healthy postmenopausal females not on estrogen replacement therapy. Subjects were randomly assigned to one of two isocaloric diets. The first experimental diet was composed of 15% calories from protein, 45% fat, and 60% CHO and the second diet was 15% protein, 45% fat, and 40% CHO. Subjects consumed each experimental diet for 3 weeks. Following each study period, subject’s glucose, insulin, TAG, and retinyl palmitate concentration were measured. Plasma TAG, insulin, and VLDL levels increased and plasma HDL levels decreased during the 60% CHO diet. Also, the daylong post-prandial TAG and retinyl palmitate concentrations were higher on a 60% CHO diet. For insulin resistant subjects the changes in plasma glucose, insulin, postprandial TAG and retinyl palmitate concentration were much greater than the response in non-insulin resistant subjects. Therefore, even though a low-fat, high-carbohydrate diet lowers plasma LDL cholesterol, its negative effect on plasma TAG, HDL, and insulin levels raise questions of the efficacy of recommending low-fat, high-carbohydrate diet to women with high blood cholesterol levels. The researchers propose that instead of increasing CHO, MUFA and PUFA be increased.
Dreon et al. also investigated the effects of a low-fat, high-carbohydrate diet on women. Subjects in the study were pre-menopausal females (n=72) with no major health problems. After both subjects and subjects’ parents baseline lipid, lipoprotein, and apoprotein concentration were measured, females began consuming an isocaloric diet that consisted of 20% calories from fat, 65% CHO, and 15% protein. The test period lasted between 7 to 9 weeks. Following the experimental diet, plasma lipid, lipoprotein, and apoprotein were measured. Subjects and parents were classified according to LDL size (pattern A: large, buoyant LDL and pattern B: small, dense LDL).
Four women had both parents with pattern B, 25 women had one parent with pattern B, and 43 women had no parent with pattern B. Researchers found that women with 2 parents with pattern B were likely to be young, heavier and have higher baseline TAG, VLDL, and IDL levels than women with parents without pattern B. Baseline LDL cholesterol concentrations were similar among all subjects. However, following the experimental diet, plasma HDL and LDL cholesterol levels decreased and TAG and VLDL increased in association with the number of pattern B parents. Also, the number of women with LDL subclass pattern B increased from 3 to 9. Even though this study showed that a low-fat, high carbohydrate diet was effective in lowering LDL concentrations in women with 2 parents with pattern B, one must question the benefit of a low-fat, high carbohydrate diet in light of increased plasma TAG, VLDL, and IDL and decreased HDL concentration.
The beFit Study conducted by Walden and colleagues investigated the efficacy of NCEP Step 2 diet. This study was conducted in 409 free-living subjects with hypercholesterolemia or combined hyper-lipidemia. Subjects in the first intervention group were instructed to follow the NCEP Step 2 diet for 6 months. Subjects in the second group consumed a control diet for the first 6 months then switched to the NCEP Step 2 diet beginning on the seventh month. After following the NCEP diet, total fat, saturated fat, and dietary cholesterol intake decreased and CHO intake increased in both intervention groups. In addition to the changes in food composition, plasma lipoprotein levels decreased following the experimental diet in both groups. Total plasma cholesterol, LDL, and HDL decreased by 18 mg/dl, 19 mg/dl, and 2 mg/dl, respectively.
Researchers discovered that subjects with combined hyperlipidemia had high plasma cholesterol levels, lower HDL, and similar LDL levels than the hypercholesterolemic group. Women had higher HDL levels than men in both groups. Based on the changes in lipoproteins following the Step 2 diet, total and LDL cholesterol decreased significantly in all groups. Men with hypercholesterolemia experienced the greatest LDL drop followed by combined hyperlipidemic men and women, and than hypercholesterolemic women. HDL cholesterol levels decreased in both hyperlipidemic and hypercholesterolemic women but not in men. Also, following NCEP Step 2 diet, greater than 50% of each group had LDL cholesterol values in the desirable range based on NCEP goals.
Results indicate that it is possible for large numbers of free-living volunteers to follow a Step 2 diet and reduce their plasma lipoprotein levels to eliminate the need for lipid lowering medication. Unlike the two previous studies, TAG levels did not increase with the NCEP Step 2 diet. Based on the data, a low-fat, high-carbohydrate diet for subjects with high blood cholesterol has a large degree of heterogenesity of plasma lipid response.
[Dreon, D.M., Fernstrom, H.A., Williams, P.T., et al. LDL subclass patterns and lipoprotein response to a low-fat, high-carbohydrate diet in women. Arterioscler Thromb Vasc Biol. 1997:17:707-714.
Jeppesen, J., Schaaf, P., Jones, C., et al. Effects of low-fat, high carbohydrate diets on risk factors for ischemic heart disease in postmenopausal women. Am J Clin Nutr. 1997;65:1027-1033.
Walden, C. E., Retzlaff, B.M., Buck, B.L., et al. Lipoprotein lipid response to the National Cholesterol Education Program step II diet by hypercholesterolemic and combined hyperlipidemic women and men. Arteriosler Thromb Vasc Biol. 1997;17:375-382.]
Fish Consumption and the Risk of Non-sudden Myocardial Infarction
In the past 15 years, research of the effects of fish consumption on CHD risk have had mixed results. Using data from the Chicago Western Electric Study, Daviglus et al. investigated the issue in 1822 men between the age of 40 to 55 years who were followed for 30 years to determine incidences of CHD mortality. Based on a dietary questionnaire obtained during the first and second year of the study, subjects were categorized into four different fish intake groups; zero, 1-17 gm, 18-34 gm, and > 35 gm per 28 days. During the follow-up period from 1957 to 1988, 1042 subjects died. Five hundred seventy-three deaths were due to CVD, and 430 due to CHD of which 293 died of MI, 196 were sudden and 94 were non-sudden. Subjects in the highest fish consumption category had a lower CHD risk than subjects with zero fish consumption [relative risk from MI, CHD, and CVD; 0.56, 0.62, and 0.74]. The multivariate-adjusted relative risk of death at 30 years from sudden death was 0.62 and non-sudden was 0.56. However, when MI deaths were excluded, relative risk for CHD and CVD increased to 0.82 and 1.02, respectively. The investigators concluded that fish consumption has an inverse association with 30-year risk of non-sudden MI. In contrast, studies by Albert et al. and Siscovick et al. found that fish consumption had beneficial effects on sudden MI risk. Daviglus et al. stated that mixed results from different fish studies were possibly due to differences in study methods and definitions used to characterize events. What does appear clear from most of the studies is that moderate fish consumption does have a beneficial effect on CVD risk.
[Daviglus, M.L., Stamler, J., Orencia, A.J., et al. Fish consumption and the 30-year risk of fatal myocardial infarction. N Engl J Med. 1997;336:1046-53.
Albert, C.M., Manson, J.E., O’Donnell, C.J., et al. Fish consumption and the risk of sudden death in the Physician’s Health Study. Circulation. 1996;94:Suppl I:I-578. Abstract
Siscovick, D.S., Raghunathan, T.E., King, I, et al. Dietary intake and cell membrane levels of long-chain n-3 polyunsaturated fatty acids and the risk of primary cardiac arrest. JAMA. 1995;274:1363-1367. ]
Coronary Heart Disease Risk Increase with Low Job Control and Low Pay
Between 1985-1988, Bosma and colleagues recruited 10,308 British civil servants (6,895 men and 3,413 women) between the ages of 35 -55 years to test the association between psychosocial work environment and CHD incidence. Psychosocial work environments were assessed based on subjects’ personal opinion as well as personnel manager’s opinion. The incidences of angina, ischemic heart disease, and other coronary events were the main outcomes measured in the study. Job control was found to be related to CHD events. Job demand and social support were not related to any of the measured outcomes. The odds ratio of a CHD event were 0.97 and 1.11 for job demand and work support for men. In women, the values were 1.17 and 1.15, respectively. However, there was an inverse relationship between job control and CHD. For example, subjects with low job control had a 50% higher incidence of CHD than subjects with higher job control. The odds ratio was 1.93. Lastly, the data indicated that there was a cumulative effect of low job control and chance of future CHD. Men in the low control group during all three phases were more likely to suffer a CHD than men who remained in high control group during the entire duration of the study.
In a similar study, Lynch et al. measured the progression of carotid atherosclerosis based on ones job demand and income. In this longitudinal study, 2632 participants in the Kuopio Ischemic Heart Disease Risk Factor Study were followed for 4 years. Baseline and final intima-media thickness (IMT) were measured and analyzed in relation to subjects’ work environment and income stated on baseline questionnaires.
Subjects with high job demand and low economic reward had significantly greater progressions of IMT and plague heights than men with low job demand and high economic reward. The change in IMT measures for the high demand, low income group and, the low demand, high income group were 0.31 mm and 0.26 mm, and plague height were 0.33 mm and 0.27 mm, respectively.
Income had a stronger association with higher mean progression of IMT than workplace demand. Also, workplace resources, social support at work, or employment status, and other atherosclerotic risk factors did not alter the above findings. However, baseline IMT level did impact on the degree of IMT progression. For example, subjects in the high demand, low income group with greater baseline stenosis had larger plague height (0.40 mm) compared to men in the low demand, high income group (0.24). “There were no differences in progression of plague height between the demand-economic rewards groups for men who were free of IHD and no advanced atherosclerotic disease.”
In conclusion, the results from these two studies indicate that psychosocial characteristics at work do play a role in an individual’s CHD risk. Specifically, ones job control and financial compensation are inversely associated with CHD risk.
[Bosma, H., Marmot, M.G., Hemingway, H., et al. Low job control and risk of coronary heart disease in Whitehall (prospective cohort) study. BMJ 1997;314:558-565.
Lynch, J., Krause, N., Kaplan, G.A., et al. Workplace demands, economic reward, and progression of carotid atherosclerosis. Circulation. 1997;96:302-307. ]
Noteworthy Nutrition News
Populationwide Education to Reduce Serum Cholesterol Levels: Cost-Effectiveness Analysis
Even though CHD mortality rates are down, the cost of treating CHD continues to usurp a large portion of the nation’s health care dollars. Therefore, an effective method of reducing CHD continues to be important in public health planning. Using a Coronary Heart Disease Policy Model and published data on the cost-effectiveness of reducing serum cholesterol levels, Tosteson et al. estimated the cost-effectiveness of population wide programs to reduce serum cholesterol levels in Americans. Approximately 624,000 life-years and 2.1 billion dollars would be saved if the Stanford Five-City Project outcome of a 2% plasma cholesterol reduction was achieved with a population wide program that costs $4.95 per person per year. This equals $3,200 cost per year of life save on this program. The cost per year of life saved increases to $6,100 if the North Karelin Study outcome of a 3% cholesterol lowering was achieved with a per person program cost of $16.55 for the first year and $8.21 per year thereafter. However, when the program cost increases to $16.55 per person per year, the expected cost per year of life saved jumped to greater than $38,500. In conclusion, some population wide programs would be cost effective in reducing CHD in U.S.A..; however, the authors note “any populationwide benefit of cholesterol reduction would be substantially blunted if dietary changes reduced HDL cholesterol as well as LDL cholesterol.”
[Tosteson, A.N., Weinstein, M.C., Hunink, M.G., et al. Cost-effectiveness of populationwide education approaches to reduce serum cholesterol levels. Circulation.1997;95:24-30.]
Lipid and Lipoprotein Decrease is Associated with Age and Weight Change
In this cross-sectional longitudinal study, Ferrara et al. investigated the effects of age, weight loss, and life-style changes on plasma total and lipoprotein cholesterol levels. In the cross-sectional study, 2,344 subjects (1041 men and 1303 women) between the ages of 50 and 93 years were recruited from the Rancho Bernardo Heart and Chronic Disease Study. Their baseline plasma lipids and lipoproteins showed that in men, total and LDL cholesterol decreased and HDL cholesterol increased with age. However, this association was not seen in female subjects.
In longitudinal portion of the study, total, LDL, and HDL cholesterol decreased with age in both men and women at a rate of one percent per year. Also, weight loss was associated with decreases in total and LDL cholesterol and increase HDL cholesterol. Life-style changes, such as quitting smoking, starting lipid lowering drugs or estrogen replacement therapy, resulted in improved lipid values.
The authors found that age was not an independent predictor of plasma lipid changes, however, weight change was strongly associated with beneficial changes in plasma lipid and lipoprotein levels.
[Ferrara, A., Barrett-Connor, E., Shan, J. Total, LDL, and HDL Cholesterol decrease with age in older men and women The Rancho Bernardo Study 1984-1994. Circulation. 1997;96:37-43.]
Margarine Intake and CHD Incidence
A new study has provided additional evidence for a relationship between increased intake of trans-fatty acids (margarine consumption) and increased CHD in middle aged men. During a 21-year follow-up period, 267 subjects of the 832 initial group developed CHD. Baseline 24 hour dietary records indicated that men with a high margarine intake had a higher incidence of CHD. There was a stronger association between CHD risk and margarine intake during the second half of the follow-up period compared with the first 10 years. The relative risk for each teaspoon of margarine on CHD during the first and second follow-up were 0.99 and 1.12, respectively. Butter intake was not associated with CHD incidence. Gillman et al. concluded that intake of high-fat and high trans-fatty acid margarines commonly used in the 1960s were significant contributors to increased CHD risk; however, current margarines, which are lower in total fat and trans-fatty acid, is expected to be less atherogenic.
[Gillman, M.W., Cupples, A., Gagnon, D., et al. Margarine intake and subsequent coronary heart disease in men. Epidemiology. 1997;8144-149. ]
An American Paradox: Fat Calories Down and Obesity on the Rise
National surveys such as NHANES, USDA Nationwide Food Consumption Survey, Behavior Risk Factor Survey Systems, and Calorie Control Council Report have independently revealed a wealth of information regarding behavior and dietary changes in the U.S. Analyzing the data from all four surveys, Heini et al. have uncovered an American Paradox.
In spite the decrease in total calories and the percent of calories from fat between the 1970s and 1980s, both the average BMI and prevalence of obesity have increased in the adult population. Between 1977 and 1987, the average caloric intake and calories from fat decreased by 4% and 11%, respectively, yet the number of overweight people and the average BMI increased by 8% and 4%, respectively. These trends were similar for both sexes. Based on the survey data, recreational activity levels did not significantly change between 1986 (58%) and 1991 (60%). The authors concluded that the increase in weight gain, despite the decrease in energy intake, is due to a decrease in non-exercise-related physical activity. They believe Americans will increase both recreational and non-recreational activity level if physical activity is promoted in public health programs.
[Heini, A.F., Weinsier, R.L. Divergent trends in obesity and fat intake patterns: The American paradox. Am J Med. 1997;102:259-264.]
Inflammation and Coronary Heart Disease
In this nested, case-controlled the association between first MI, ischemic stroke, and venous thrombosis among sued, prospective study, Ridker et al. measured the association between first MI, ischemic stroke, and venous thrombosis among subjects in the Physician’s Health Study with baseline levels of plasma C-reactive protein. “C-reactive protein is an acute-phase reactant that is a marker for underlying systemic inflammation.” In addition to CVD incidences, these researchers also investigated the effects of aspirin usage on C-reactive protein levels and CVD risk. Of the original 1,086 subjects, 543 developed CVD during the follow-up (246 with MI, 196 with stroke, and 101 with venous thrombosis). Baseline C-reactant protein levels of cases were significantly higher than in the control group. The median plasma C-reactive protein for the control group was 1.13 mg/l while C-reactive protein levels for cases who developed MI, ischemic stroke, and venous thrombosis averaged 1.51 mg/l (p<0.001), 1.38 mg/l (p=0.02), and 1.26 mg/l (p=0.34), respectively. Also, subjects in the highest quartile of C-reactive protein (>2.11 mg/l) had 3 times the risk of a future MI, and 2 times the risk of ischemic stroke, compared to men in the lowest quartile of C-reactive protein (<0.55 mg/l). Risk of developing venous thrombosis did not change with plasma C-reactive protein concentrations. Relative risk for developing MI during the first 2 years and after more than 6 years were 2.4 and 3.2, respectively, for subjects with the highest baseline plasma C-reactive protein. Even though smokers had higher C-reactive protein than nonsmokers, 2.20 mg/l versus 1.19 mg/l, further analysis revealed that nonsmokers had a similar relative risk for MI as the total cohort. A subject’s BMI, history of diabetes, presence of hypertension, or plasma levels of lipids, t-PA antigen, fibrinogen, and homocysteine did not alter the relationship between C-reactive protein concentrations and risk of MI.
Compared with the placebo group, subjects on aspirin therapy had a lower risk of MI. The benefit was directly associated with the baseline plasma C-reactive protein concentration. For example, “the reduction in the risk of MI associated with the use of aspirin was 13.9% in first (lowest) quartile of C-reactive protein values, 33.4% in second quartile, 46.3% in third quartile, and 55.7% in fourth quartile.”
In conclusion, plasma C-reactive protein concentrations are a good indicator for identifying individuals at risk for MI and stroke. The results also indicate that aspirin and other anti-inflammatory medicines can have a significant role in preventing CVD.
[Ridker, P.M., Cushman, M., Stampfer, M.J. et al. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med. 1997;336:973-979.]
Editorial:
Opinions in Junk-Science to Maximize Media Attention
I write to vindicate the lowly egg, for it has been accused of despicable deeds as of late. Charges of murder and mayhem are being leveled against this innocent staple, and its contributions to the American diet dismissed out of hand. What has brought about these vicious, dare I say vindictive, attacks on what some consider an almost perfect food? Did we speak too loud? Was our message too clear? Was our science too sound? Did we challenge conventional wisdom?
It’s been a “good news, bad news” time for the egg industry. First good news with publication of two meta-analysis showing that dietary cholesterol has little effect on plasma cholesterol. Then bad news with attacks for telling the good news. It seems the facts have little meaning to some advocacy groups; what matters is the hype. I call such organizations OJSMMA [Opinions in Junk-Science to Maximize Media Attention]. An OJSMMA is excellent at getting its name in press by raising a ruckus about some real, or imaginary, menace to the public. Unlike those required to work with science and facts, an OJSMMA pays minimal attention to any uncertainties of an issue but rather emphasis on dogmatic statements to gain maximal media response (and might I suggest more contributions to their “non-profit” organization). Opinions are more important than evidence, sound bites more imperative than stating uncertainties.
But why are these people saying such hateful things about eggs? Animal rights groups, consumer advocate groups, cholesterol issues, food safety issues, etc. Is this an industry which mistreats animals to sell a hazardous product which kills thousands each year? That’s what I keep hearing! Unfortunately, the comments are, to say the least, alarmists exaggerations designed to foster more fear than understanding. But then an OJSMMA knows that the media likes “colorful language.”
“Eggs contaminated with Salmonella enteritidis cause hundreds – and possibly thousands -of deaths each year.” states one rather disparaging report. But according to the Centers for Disease Control and Prevention (CDC), in 1995 and 1996 there were 10 reported deaths from Salmonella enteritidis; 7 in nursing homes. And while the industry considers 10 deaths in 2 years to be 10 deaths too many, it’s a stretch to extrapolate 5 deaths a year to “possible thousands – of deaths each year.”
In another article a self-appointed guardian of national nutritional health wrote that “Two eggs also have three grams of saturated fat – that’s 15 percent of your daily limit.” [Note: limit versus recommended.] But the real question is – so what? Without knowing the rest of the diet what does this mean? The article goes on to say “Worse yet, in a typical restaurant, a ham-and-cheese omelet has 17 grams of sat.fat … awfully close to the 20-grams-a-day quota.” No wonder consumers buy pocket calculators to keep tract of their fat “quota”. And while the egg contributes 3 grams of “sat.fat” the other 14 grams is damning by “quilt by the company you keep” tactic. So not only are we bad, we cause people to make it worse. Should we blame the peas for getting buttered?
In another article, a noted epidemiologist states “The decline in egg yolk consumption is among the factors responsible for the sizable decline in heart disease deaths over the last three decades.” Quite a contrast from one in Eating Well magazine (March/April 1997) by the noted nutritional epidemiologist, Dr. Ancel Keys, that “… there’s no connection whatsoever between cholesterol in the food and cholesterol in the blood. None. And we’ve known that all along.” It’s so confusing when experts disagree, and yet so easy to get the quote for your opinions. So please explain how the Japanese have a low rate of heart disease and the highest per capita egg consumption in the world. There is no relationship between egg consumption and heart disease incidence either between or within populations.
And after getting beat up for cholesterol and salmonella, animal rightists suggest that consumers “Wash your hands of eggs, egg whites, and poultry products.” And stories about eggs containing chemicals and pesticides (combining nutritional junk-science and animal rights politics). I wonder how all those chicks get hatched without thousands of birth defects from all those chemicals concentrated in that little developmental package? It’s a triple header of cholesterol, salmonella and animal rights which is grist for the media mill. But do all the exaggerations and silly metaphors really serve to inform and educate the public. Super-hype of issues scares some, but usually just turns off most, and what nutrition educators are left with is a public wearied by the incessant crying wolf by the OJSMMA and a distrust of so called “experts”. There are real nutritional concerns out there, and the needed messages are obliterated by the shrieking sounds of some OJSMMA looking to expand its donation list. Real issues like nutrition education, excessive adiposity in the population, low intakes of fruits and vegetables, and nutrient needs of the poor, elderly, and children all need real consumer education and outreach. I urge someone to start an advocacy group based on the nutritional concept of “cut down, not out” coupled with those non-media attention-getting principles of balance, variety and moderation. No chance! Not financially viable. But please, at a minimum, let us all demand that every OJSMMA “show me the science.”
Donald J. McNamara, Ph.D.
Executive Editor, Nutrition Close-Up
OPINIONS FIXED IN STONE
“Those who do reduce their egg intake can rest assured that other foods can readily supply the nutrients found in eggs. Calorie-for-calorie, green peas supply similar amounts of total protein, calcium, phosphorous, Vitamin A, and riboflavin. Surprisingly, the peas significantly surpass eggs as a source of iron, thiamin, niacin, and vitamin C. The egg may have ‘high quality’ protein, but protein quality is unlikely to be a problem among adults eating enough calories or in children consuming dairy products, meat, poultry, and fish – as long as the diet does not contain inordinate amounts of added sugar and fats.” [Nutrition Action, December 1978]
“Eggs do contain nutrients, but they’re nothing special. Calorie for calorie, they have roughly the same vitamins, minerals, and protein as green peas … except that ‘incredible, edible’ peas are a good source of fiber and have no fat or cholesterol.
The egg industry proudly hails the ‘complete’ or ‘perfect’ protein in eggs. But complete protein only matters if you get all you’re protein from a single food and if you’re just barely getting enough protein. Neither applies to most Americans.” [Nutrition Action Newsletter, July/August 1997]
High Homocysteine Increases CHD Risk
Many studies have shown that an increased plasma homocysteine level is an independent risk factor for atherosclerosis. Reports by Malinow et al. and Graham et al. add support to this theory. The three fold higher CHD incidence and mortality rate among Northern Ireland men compared with French men can not be explained by traditional CHD risk factors. In a case-control study of 420 previous MI patients and 521 control subjects between the ages of 25 to 64 from either Belfast or Lille and Strasbourg region, the baseline plasma lipids, lipoproteins, and homocysteine were measured and analyzed based on CHD status. Dietary intake and vitamin supplement use was not measured for this study. Case subjects from both Northern Ireland and France had higher homocysteine levels than controls; however, controls from Northern Ireland had much higher homocysteine levels than controls from France.
The age adjusted relative risk (RR) for MI in Northern Ireland was 3.4 for men in the highest quartile (>17.2 µmol/l) versus lowest quartile (<9.8 µmol/l) while for the French the RR was 5.2. When other risk factors such as BMI, alcohol intake, smoking, and lipid levels were accounted for, the RR decreased to 3.3 and 1.8 in French and Irish men; for Irish men this was no longer statistically significant. The study by Graham et al. also showed that cases (n=750) had higher fasting and postload homocysteine levels than controls (n=800). The mean fasting homocysteine and postload homocysteine levels were 16% and 17% higher than controls. The relative risk for subjects with both high fasting and postload homocysteine levels was 2.5 compared with 1.6 and 1.5 for high fasting or high postload homocysteine levels, respectively.
The RR for subjects in the top 10th fasting and postload homocysteine were 3.1 and 3.7, respectively, when compared with the bottom 10th. Each incremental increase of 5 µmol/l in the fasting homocysteine level equals an increase in relative risk of 1.35 for men and 1.42 for women. Smokers and hypertensive subjects were more sensitive to the effects of high homocysteine. Folate, pyridoxal, and cyanocobalamin use were correlated with lower plasma homocysteine levels.
These studies show that high plasma homocysteine levels are associated with increased MI incidence in men and women. Higher homocysteine levels in Irish men were correlated with a greater chance of CHD than in French men. Conventional risk factors such as hypertension and smoking had synergistic effects on increasing CHD risk when high plasma homocysteine levels were present.
[Graham, I.M., Daly, L.E., Refsum, H.M., et al. Plasma homocysteine as a risk factor for vascular disease. The European concerted action project. JAMA. 1997;277:1775-1781.
Malinow, M.R., Ducimetiere, P., Luc, G., et al. Plasma homocysteine levels and graded risk for myocardial infarction: findings in two populations at contrasting risk for coronary heart disease. Atherosclerosis. 1996;126:27-34. ]
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.
