ENC - Egg Nutrition Center

COMMON ABBREVIATIONS
BMI: body mass index (kg/m²)
CAD: coronary artery disease
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

Low-Fat Diets and Plasma HDL Cholesterol Levels

For a longtime, people with elevated blood cholesterol were recommended to follow a low-fat diet, but the decrease in plasma HDL cholesterol and the increase in TAG levels associated with this diet have some researchers questioning the universal use of this diet therapy. But now data by Asztalos and colleagues indicate that the degree of plasma HDL cholesterol change following initiation of a low-fat diet varies widely among individuals. For example, normocholesterolemic subjects with low baseline HDL cholesterol levels (<35 mg/dl) decreased their plasma HDL cholesterol levels by 1.3 mg/dl compared to a 5.2 mg/dl drop in HDL cholesterol levels in normal HDL cholesterol (>35 mg/dl) subjects, 6 weeks after changing to an isocaloric, Step 2 diet.

In this study, the researchers investigated the effects of 3 test diets on the plasma lipid and lipoprotein profiles in 76 normocholesterolemic males between 22 and 65 years of age. The main difference in the 3 test diets was total fat calories; the All American Diet (AAD) diet contained 36.8% fat (14.1% SFA) compared to 28.1% (8.7% SFA) and 23.7% (6.2% SFA) in the NCEP Step 1 and Step 2 diets, respectively. Daily caloric levels were regularly adjusted to maintain the subject's body weight.

Analysis of fasting blood samples following each diet phase showed that plasma total cholesterol, HDL, LDL, apo A-I, apo B, LDL:HDL cholesterol ratio, and HDL:apo A levels were all lower following the Step 1 and Step 2 diets compared to the AAD. Plasma TAG levels increased with the 2 low-fat diets. The percentage of subjects with low HDL cholesterol levels (<35 mg/dl) increased from 33% during the AAD to 55% with the Step 2 diet. However, when the plasma lipid and lipoprotein responses to the 2 low-fat diets were separately analyzed based on baseline AAD plasma HDL levels, it showed that the HDL cholesterol and apo A decreased by 1.3 mg/dl and 4.8 mg/dl, respectively, in individuals with low HDL cholesterol levels while in the normal HDL cholesterol individuals, the HDL cholesterol and apo A decreased by 5.2 mg/dl and 8.7 mg/dl. The change in total cholesterol, LDL, TAG, and apo B were similar in the two HDL cholesterol subgroups. The baseline atherosclerotic index, expressed as the LDL: HDL ratio, was higher in those with low HDL cholesterol levels on the AAD compared to those with normal HDL levels (3.92 vs 2.87). However, with intake of the low-fat diets, the LDL:HDL cholesterol ratio decreased by 11% (3.92 to 3.49) in those with low HDL as a result of the decrease in plasma LDL cholesterol with little change in HDL cholesterol levels. In contrast, those with normal HDL cholesterol levels lowered both the LDL and HDL cholesterol levels with intake of the low fat diets resulting in no change in the LDL:HDL ratio. In response to a low-fat diet, there was also a difference in distribution of HDL subpopulations between these 2 groups. For example, apo A-I decreased more in the normal HDL cholesterol subjects than in the low HDL cholesterol group. The major change in plasma HDL occurred in the alpha-1 fraction which is a large apo A-I only subpopulation corresponding to HDL₃. "The distribution of a1 concentration peaked between 14-15 mg/dl on the Step 2 diet compared to a peak at 22-25 mg/dl on the AAD." Of all the changes in lipid and lipoprotein levels following the low-fat diets, only the HDL cholesterol and alpha-1 was different between the 2 HDL groups.

Based on an earlier study which found that nomolipidemic low HDL cholesterol subjects have a significantly different distribution of apo A-I containing HDL subpopulations than individuals with normal HDL cholesterol, the researchers tested the theory that feeding a low-fat diet would decrease plasma HDL cholesterol more in normal HDL cholesterol individuals than those with low HDL cholesterol. Even though the current study supports this hypothesis showing that plasma HDL and apo A decreased more in the normolipidemics with normal HDL levels than low HDL levels, it is a paradigm shift to think that initiation of a low-fat diet in those having a lower HDL level is more advantages to the heart than intake of a low-fat diet in those with higher HDL levels. The question yet to be answered is whether a low-fat diet is beneficial in those with normal HDL cholesterol levels.

Asztalos B, Lefevre M, Wong L, et al. Differential response to low-fat diet between low and normal HDL-cholesterol subjects. J. Lipid Res. 2000. 41:321-328.

Key Messages

Lycopene Protects Against Aortic Atherosclerosis Progression

Klipstein-Grobusch et al. tested the association between serum carotenoid levels and atherosclerosis in the abdominal aorta of the Rotterdam Study participants. According to the findings from this case-control study with 217 subjects (108 cases and 109 controls), of the 6 carotenoids investigated, only serum lycopene levels exhibited a modest inverse association with the presence of atherosclerosis.

Using previously frozen sera samples from middle-aged adults in the Netherlands, the researchers determined the link between plasma carotenoid levels and atherosclerosis. The presence of atherosclerosis lesions was diagnosed by detecting calcified plaques in the abdominal aorta using a laternal radiographic film. Health status and life style factors associated with CVD were measured and included in the multivariate analysis. As expected, the incidences of hypertension, diabetes, high BMI and high systolic blood pressure were higher in the cases compared to the control group. Another difference between the 2 study groups was that the case group had lower plasma levels of alpha-carotene, ß-carotene, and ß-cryptoxanthin.

The age and sex adjusted log regression showed that serum lycopene was inversely associated with atherosclerotic risk. The odds ratio for the highest quartile of serum lycopene was 0.55 compared to the lowest quartile. The serum levels of alpha-carotene, ß-carotene, lutein, and zeaxanthin did not correlate with atheosclerosis progress. Lycopene levels were especially benifical against atherosclerosis in a subset of current and former smokers.

In conclusion, the modest inverse relationship between serum lycopene and aortic atherosclerosis found by Klipstein-Grobusch et al. suggests that lycopene, which has the strongest antioxidant properties, has a modest effect on atherosclerosis risk and that lycopene levels are especially important in neutralizing free radicals in current and former smokers.

Klipstein-Grobusch K, Launer LJ, Geleijnse JM, et al. Serum carotenoids and atherosclerosis. The Rotterdam Study. Atherosclerosis. 148: 2000; 49-56.

Anger Associated with CHD Risk in Normotensive Adults

According to a large prospective study conducted by William et al., angry people has one more reason to be angry. It seems they are 3 times more likely to suffer a heart attack than their less anger prone counterparts. When the researchers compared the degree of anger with CHD incidences in 12,986 participants in the Atherosclerosis Risk In Communities (ARIC) Study, it showed a direct relationship.

Using the responses from the 10-item Spillberger Trail Anger Scale (4 point scale), William and coworkers were able to categorized subjects into a low anger group (37.1%), a moderate anger group (55.2%), and a high anger group (7.7%). The low anger group had a trait anger score of 10-14, the moderate group had a score of 15-21, and the high group had a score of 22-40. The people in the highest anger group tended to be younger, heavy-set men, who drank and smoked, with a lower education level than the participants in the moderate and low anger groups. Plasma LDL and HDL levels were similar in all 3 groups.

During the 6-year follow-up period, 416 cases of CHD events were noted, which equals 7.4 events per 1,000 person-years. As a group, the multivariate adjusted hazard ratio (HR) for CHD was 1.54 (95% CI 1.10 to 2.16) and 1.10 (95% CI 0.88 to 1.36) for the high versus the low trait anger group and the moderate versus the low trait anger group, respectively, and 1.63 (95% CI 1.07 to 2.48) and 1.08 (95% CI 0.82 to 1.43) for "hard events" such as MI and CHD deaths. However, when the data were subdivided into hypertensives and normotensives, an anger-CHD relationship was only evident in the normotensive population. For example, the age adjusted HR for CHD events in normotensives were 2.61 in the highest anger group compared to 1.14 in the hypertensive group. The HR for hard CHD events were 2.97 and 1.05 for the normotensive and hypertensive groups, respectively. The difference in HR between the moderate anger group and the low group was substantially less than the difference between the highest to lowest group. Compared to a 3-fold difference, it was only 40% higher in the moderate anger group compared to the lowest anger group. Even though the differences in multivariate adjusted HR for CHD events in the 3 anger trait groups were 1.00, 0.95, and 1.08, respectively, the actual CHD event-free survival probability was dramatically lower than in the normotensive groups than hypertensive groups. Thus indicating that in spite of similar HR across different degree of anger trait, they are more likely to suffer a CHD event than the normotensive groups, regardless of anger traits. And in the normal blood pressure groups, the highest anger score group had a dramatically lower CHD-free survival probabilities. The CHD-free survival probabilities for the lowest and moderate anger groups with normal blood pressure were relatively similar.

The researchers initially thought that anti-hypertensive medications used by the hypertensive men and women in the study protected them against CHD by preventing vasoconstriction, thrombus formation, cardiac arrhythmias, and plaque disruption; however, subset analysis of hypertensives not taking medications for blood pressure showed no CHD-anger relationship. Results from these bi-ethnic subjects showed that the CHD-anger relationship was similar between blacks and whites, and males and females.

Results from this study suggest that anger is a major CVD risk factor in normotensive middle-aged adults independent of biological risk factors. The findings suggest that by lowering the degree of anger from high to moderate, an individual could significantly cut their risk from 300% to 40%. In contrast, hypertensive adults did not show an anger-CHD relationship, which may be related to their higher CHD risk status compared to normotensive individuals.

Williams JE, Paton CC, Siegler IC, et al. Anger proneness predicts coronary heart disease risk. Prospective analysis from the atherosclerosis risk in communities (ARIC) study. Circulation. 200;101:2034-2039.

Effects of Omega-3 Enriched and Regular Egg Consumption on Plasma Lipids in Hypercholesterolemic Adults

The popularity of functional foods has dramatically increased in the pass decade and omega-3 enriched eggs are among a growing number of functional food items available in the marketplace. High omega-3 fatty acid eggs are produced from chickens fed high flax or algae diets and not from genetically modified birds, as some consumers mistakenly believe. These omega-3 eggs are suitable alternatives for people who want to increase their omega-3 fatty acid intake but dislike fish. In light of earlier findings that showed a cardioprotective role of omega-3 fatty acids, Lewis et al. tested the effects of omega-3 enriched eggs on serum lipids in hyperlipidemic adults.

The 25 healthy volunteers (13 men and 12 women) in the study ate 3 test diets; a low-fat, self-selected diet with 12 omega-3 enriched eggs per week, a low-fat, self-selected diet with 12 control eggs per week, and a low-fat, self-selected diet without eggs. Each test diet was consumed for 6 weeks followed by a 6 week washout period. The omega-3 fatty acid levels in the high omega-3 eggs and control eggs were 412 mg/egg and 65 mg/egg, respectively. The majority of the increase in omega-3 fatty acids came from linolenic acid (260 mg/egg) compared to docohexaenoic acid (79 mg/egg). Analysis of dietary records indicated that the subjects were compliant with low-fat diet of 22% of calories from total fat and 7% SFA throughout the study. The dietary cholesterol during the 2 diets with eggs were 333 mg/day higher compared to the no egg diet.

Serum lipid levels after the test diets showed that 2 people in the study were sensitive (hyper-responders) to dietary cholesterol. In these people, the total serum cholesterol levels increased beyond 2 standard deviations following the 2 test diets with eggs compared to the other 23 subjects. And as a result, the researchers analyzed the data separately with and without the hyper-responders, which resulted in dramatic differences in study outcomes. For example, when these individuals were excluded from the analysis, including either omega-3 eggs or control eggs did not adversely alter plasma total cholesterol, LDL cholesterol, and HDL cholesterol levels. On the other hand, including the hyper-responders in the analysis resulted in a significantly higher plasma LDL cholesterol level with egg intake. The LDL cholesterol increased by 7% and 5%, respectively, with the omega-3 eggs and the control eggs. The 15% and 9% decrease in TAG levels following the omega-3 egg diet and the control egg diet compared to the no egg diet was relatively constant with or without the hyper-responders. Including eggs, regardless of type of eggs, was associated with an increase in calories from total fat and MUFA as well as increased cholesterol intake.

As other studies have shown, data from the study by Lewis et al. clearly show that a small population of individuals is sensitive to dietary cholesterol. However, it also shows that for a majority of people, including 12 eggs/week, regardless of the omega-3 fatty acid content, to a low-fat diet does not significantly alter plasma total cholesterol, LDL cholesterol, and HDL cholesterol levels. And as a matter of fact, in the case of TAG level, including eggs in the test diets had a beneficial effect by lowering TAG levels. In conclusion, this study shows that omega-3 enriched eggs are an easy way to provide a convenient source of omega-3 fatty acids in the diet without negatively altering lipid profile in majority of people.

Lewis NM, Schalch K, Scheideler SE. Serum lipid response to n-3 fatty acid enriched eggs in persons with hypercholesterolemia. JADA. 2000;100:365-367.

Relationship Between CHD Deaths and Blood Pressure Varies Among Different Ethnic Group

Along with other studies, the Seven Countries Study has established that certain ethnic groups benefit from having lower blood cholesterol levels, and as a result their rate of CHD is much lower. Now, according to a study by Van Den Hoogen et al., these ethnic groups also have lower blood pressure levels. In this 25-year follow-up study, cohorts from Japan, Serbia, and Mediterranean southern Europe were found to have lower systolic and diastolic blood pressures than the cohorts from the United States, northern Europe, and inland southern Europe. The average systolic and diastolic blood pressure of the Serbians were 132.5 mm Hg and 83.3 mm Hg, respectively, compared to 143.7 mm Hg and 86.6 mm Hg in northern Europeans. And, as expected, the percentage of hypertension in the cohorts, corresponded with mean blood pressure levels.

Of the 12,031 middle-aged men recruited between 1958 and 1964, 1,291 cases of CHD deaths were reported during the study period. The Japanese cohort had the lowest number of CHD deaths (30 cases) followed by Serbians (77 cases), Mediterraneans (116 cases), inland southern Europeans (253 cases), Americans (354 cases), and northern Europeans (461 cases). The actual rates of CHD were approximately 20 per 10,000 person-years in Japan and Mediterranean southern Europe compared to 70 per 10,000 person-year in the United States and northern Europe at a systolic blood pressure of 140 mm Hg. Even though the absolute CHD rate varied significantly among different cohorts, the relative risk for CHD was similar. For example, an increase of 10 mm Hg in systolic or 5 mm Hg in diastolic blood pressures increased the relative risk for CHD deaths by 28% in all 6 study cohorts. To minimize the effects of fluctuating blood pressure within individuals, when the data was re-analyzed using mean blood pressure from first 5 year instead of single base-line values, the adjusted RR for was 2.13 compared 1.77, indicating that high blood pressure is a strong risk factor for CHD death.

Also, similar to blood pressure levels, the absolute risk of CHD deaths associated with hypertension varied among the 6 study cohorts. For example, the age-standardized 25-year mortality rate differed by almost 4 fold. The Japanese and Mediterranean hypertensives had 44 deaths per 10,000 person-year compared to 153 per 10,000 person-year in northern Europeans.

Even with the same blood pressure level, results from this study indicate that Americans and northern Europeans are much more likely to die from CHD than people from Japan and Mediterranean countries. However, current findings show that everyone, regardless of country of origin, should control their blood pressure since any increase in systolic and diastolic blood pressure is associated with an increase in CHD events in all populations. The data are similar to a previous report from the Seven Countries Study by Veschuren et al. showing that across cohorts a 20 mg/dl change in plasma cholesterol changed CHD relative risk by 17%; however, absolute risk of CHD differed by 5 fold at the same plasma cholesterol level. These studies show clearly that CHD risk is determined by factors beyond the 3 major risk factors - smoking, hypertension, and hypercholesterolemic.

Van Den Hoogen PC, Feskens EJ, Nagelkerke NJ, et al. The relation between blood pressure and mortality due to coronary heart disease among men in different parts of the world. N Engl J Med. 2000;342:1-8.

Ethnic Difference in CVD and Diabetes Risk Observed in Children

The incidence of CVD and type 2 diabetes are much higher in the African-American and Hispanic communities compared to Caucasians. In our diverse culture, this disparity among different ethnic groups is a major public health problem yet the etiology behind this multifactorial problem is unclear. In a study of 95 healthy children (54 whites and 41 blacks), Linquist and colleagues tested the theory that differences in dietary patterns among cultures explained difference in blood lipid and insulin profiles between the study cohorts.

Both groups of children in the study were similar in age (mean 10 years), body composition, and stage of pubertal development (stage 1 or 2); however the African-American children had lower social class background as determined by parent's education level and occupational status. The mean 24-hour dietary recall revealed that the African-American children ate more fruits and vegetables and less dairy products. Contrary to earlier findings which found unfavorable lipid profiles in blacks, this study found more favorable lipid profiles among blacks. The plasma TAG were lower among black children and total cholesterol levels were similar to white kids. The 2 insulin sensitivity measurements indicated that black children were 40% less sensitive to insulin and had twice as high acute insulin levels than whites. In this study, only the insulin profiles indicated that the African-American children had potential risk factors for future CVD and diabetes compared to the white group. Multivariate analyses showed that macronutrients and food group intakes could not account for ethnic differences in lipid profiles observed in earlier studies.

Results from this study indicate that when social class, body composition, macronutrient and food group consumption were accounted for, ethnic differences in early disease risk profiles were not significantly altered by dietary patterns as the researchers hypothesized. As a matter of fact, except for slightly higher fruit (0.6 serving) and vegetable (0.7 serving) intake and lower dairy (0.6 serving) intake, diets of study cohorts were very similar regardless of race. However, the diets consumed by both groups were far from ideal. For example, 40% of the total calories in these diets came from the tip of the Food Guide Pyramid. Regardless of the dietary pattern, lower insulin sensitivity and higher insulin levels strongly suggest that the African-American children are more susceptible to metabolic disorder such as type 2 diabetes and heart disease compared to Caucasian children.

Linquist CH, Gower BA, Goran MI. Role of dietary factors in ethnic differences in early risk of cardiovascular disease and type 2 diabetes. Am J Clin Nutr. 2000;71:725-732.

MCT Diet Increases Total and LDL Cholesterol Levels

For a long time, patients with lipid metabolism disorders such as pancreatic lipase deficiency have successfully been treated with medium-chain triacylglycerol (MCT) therapy. However, the data on lipid and lipoprotein profiles following MCT therapy are mixed. According to a new study by Asakura et al., in hyper-triglyceridemic subjects, MCT has a potentially atherogenic effect by increasing both plasma total and LDL cholesterol levels.

In this study with 10 hypertriglyceridemic adults without histories of diabetes, renal, and hepatic disease, subjects followed 5 test diets with varying degrees of added corn oil and MCT. The sequence of the diet feeding was as follows; low-fat diet (2 weeks), 100% corn oil (4 weeks), and 3 subsequent periods with corn oil and MCT ratios of 3:1, 1:1, and 0:1 (2 weeks each). The two types of oils only increased the net fat content by 16 g/d to 24 g/d from the low-fat diet. The 16% and 19% increases in fasting total cholesterol and LDL cholesterol following the 100% MCT diet were the only significant changes noted between MCT and the 100% corn oil diet. The TAG level increased by 8% with the 100% corn oil diet compared to the 100% MCT diet. Analysis of postprandial plasma TAG and total cholesterol showed that the MCT diet sustained a higher total cholesterol level throughout the fat absorption phase (8 hours post meal) relative to the liquid corn oil diet. But, compared to the stable post-prandial TAG levels following the MCT diet, the liquid corn oil diet resulted in a steady increase in post-prandial TAG levels.

In conclusion, even though MCT are an effective way to provide fats for individuals with fat malabsorption, MCT use is not warranted for people with heart disease, as it seems to increase plasma total cholesterol and LDL cholesterol levels. Asakura et al. speculated that the 100% MCT diet raised these levels due to the higher saturated fat content of this diet. According to the researchers' findings, diets high in MCT were associated with an increase in both fasting and postprandial total cholesterol levels compared to the 100% corn oil diet.

Asskura L, Lottenberg AM, Neves MQ, et al. Dietary medium-chain triacylglycerol prevents the postprandial rise of plasma triacylglycerols but induces hypercholesterolemia in primary hypertriglyceridemic subjects. Am J Clin Nutr. 2000;71:701-705.

Dietary Pattern Mortality Risk

Most studies in nutrition have focused on individual nutrients or foods and their impact on prevention or promotion of certain diseases. Kant et al. examined the health effects of dietary patterns, which included a complex mixture of foods. By measuring the overall diet quality, instead of single nutrients, the data are more representative of a free-living diet. The finding of this study is that mortality risk was inversely related to eating patterns recommended by current dietary guidelines.

The 42,254 females in the study were originally part of a larger prospective study, and were enrolled in this case-control study after completing a 62-item food frequency questionnaire. Subjects were followed for 5.6 years during which time 2,065 deaths were reported. The researchers measured the overall quality of the dietary pattern in terms of the Recommended Foods Score (RFS). The RFS was determined from the number of fruits, vegetables, whole grains, low-fat dairy products, and lean meats each subjects reported consuming. The range of RFS varied from 0 to 23 and the mean was 11.4. Due to the difficult nature of accurately recalling portion sizes, the RFS was measured independent of portion amounts. The group with highest RFS, compared to rest of the study cohorts, were more educated, slightly older, more active, took supplements and hormones, and smoked less.

There was an inverse relationship between RFS and all cause mortality. The multivariate-adjusted RR was 0.82 in quartile 2, 0.71 in quartile 3, and 0.69 in quartile 4. Even though the women with the highest intakes of fruits, vegetables, whole grains, low-fat dairy products, and lean meats had a 30% lower risk of prematurely dying, the major benefit was obtained between RFS of 1-11. After a RFS value of 11, benefit associated with following the current dietary guidelines was less dramatic. This trend continued even after the data for women with medical conditions at baseline were excluded, thus indicating that the dietary pattern was not different in healthy women or women with illnesses. Finally, women in the highest intake level of recommended foods had significantly lower mortality from all types of cancers, CHD, strokes, and all other causes.

Due to the observational nature of the study, Kant et al. were unable to declare a causal relationship between low RFS and mortality, especially in light of other unhealthy lifestyle choices. However, this study strongly suggest that current food-based dietary guidelines are more applicable than single nutrients in improving overall health outcomes.

Kant AK, Scharzkin A, Graubard BI, et al. A prospective study of diet quality and mortality in women. JAMA. 2000;283:2109-2115.

Editorial: Science, Agendas and False Accusations

Each day it gets more and more difficult to distinguish fact from fiction, and to keep the agenda based pseudo-science from baffling the public, and burying those who value honest and open discourse of controversies. And with today's excitement over anything smelling of deceit and collusion, print and electronic media just seem to love giving credibility to those who yell the loudest, or at least the most outrageously. It has been said that if you tell a lie often enough and for a long enough, it will eventually be believed. Add on top of that a public mistrust of science and corporate enterprises and you have the perfect scapegoat for wide dissemination of agenda based misinformation, and public acceptance of false "facts." Watching organizations dedicated to an agenda propagate misinformation about individuals and organizations is nothing new, but, when they continue to do so publicly even after they have been provided with documentation of their error, it is clear that they put agenda above facts at a substantial cost to the credibility of those falsely accused.

In a law suit filed to block the report of the Dietary Guidelines Advisory Committee, the Physicians Committee for Responsible Medicine (PCRM) claimed that 6 of the 11 committee members were unsuitable for their position because they had "industry connections" and had taken money, or had grants, or spoken for and received honorariums from, the animal protein industries. The bad guys were meat, dairy and eggs, and those obviously disreputable scientists who ever had anything to do with these dastardly organizations were without a doubt not qualified to speak for the nutrition community. I guess that anyone who has ever been "bought and paid for" by the animal food industries is considered to no longer be capable of evaluating the science and making rationale judgments. And how dare these terrible industries support research by and pay honorariums to these national nutrition experts to do research on or speak about nutrition? It really does seem like an obvious conspiracy to me! How could anyone really trust a report on nutrition from such a clearly biased Advisory Committee?

What was most surprising was that PCRM accused Dr. Scott Grundy of being biased because he had served on the American Egg Board Grant Review Committee from 1972 to present. Since there was no basis for this statement, PCRM was informed that: [a] the American Egg Board was started in 1976, 4 years after Dr. Grundy was supposedly reviewing grants for it; [b] as a member of the American Egg Board Scientific Advisory Panel since 1984, and Executive Director of the Egg Nutrition Center since 1995, I could certainly verify that Dr. Grundy had not served as a grant reviewer during that past 16 years; and [c] If Dr. Grundy was biased towards the egg industry then the industry was doing something terribly wrong given that he is an outspoken and influential supporter of the "dietary cholesterol raises blood cholesterol" hypothesis and a strong supporter of dietary cholesterol restrictions. If he is the "bought and paid for" egg industry representative on the Dietary Guidelines Advisory Committee then the egg industry was certainly not getting its moneys worth.

And while these facts were communicated to PCRM in January 2000, as of May you could still find this misinformation on their web site and included in their press releases. Indeed it remains part of their attempt to get a restraining order against the guidelines. Maybe before the press and TV media give credibility to this organization and their unsubstantiated harangues, they should ask PCRM what they consider their "responsibility" to the facts, and what is their "concern" for the reputation of highly respected physician-scientists who have made nationally recognized contributions to our understanding of the diet-health relationships. PCRM certainly seems to have failed at living up to its high principled name. But even more important is the question of why the media accepts this garbage without doing its homework. After awhile it makes you wonder about the validity of just about everything you see, hear and read.

Editor's Comment: USDA/HHS Dietary Guidelines for Americans 2000

The USDA/HHS Dietary Guidelines for Americans 2000 have now been released and the fat guideline has been changed. The 1995 guideline read "Choose a diet low in total fat, saturated fat and cholesterol." The new guideline reads "Choose a diet low in saturated fat and cholesterol and moderate in total fat." What is confusing is, given the last five years of research showing no relationship between dietary cholesterol and heart disease risk, the fat guideline actually puts an enhanced emphasis on restricting dietary cholesterol. Given the lack of evidence for a reduction in heart disease with a reduction in dietary cholesterol, it is too bad that the committee did not recommend "Choose a diet low in saturated fat and moderate in total fat and cholesterol." Somehow we seem unable to separate "saturated fat and cholesterol" from our nutrition phrase book. A note for those who haven't noticed, not all cholesterol containing foods are high in saturated fat.

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.

Newsletters & Publications

TABLE OF CONTENTS