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

High-Monounsaturated Fatty Acid Diet Protects Against CVD

Recent outcomes following a high-MUFA diet have lead scientists to question the efficacy of low-fat, high-CHO diet as the primary dietary method in preventing and treating CVD. According to Kris-Etherton et al., a high MUFA diet is as effective as the NCEP Step II diet in lowering both plasma total and LDL cholesterol levels without negatively altering the plasma HDL cholesterol and TAG concentrations as seen with the NCEP's Step II diet.

In this 5-period cross-over study, 22 subjects consumed an Average American Diet (AAD), NCEP Step II diet, olive oil diet (OO), peanut oil diet (PO), and peanut and peanut butter diet (PPB) for 24 days each. The AAD consisted of 50% of calories as CHO, 16% protein, 34% fat, 16% SFA, 11% MUFA, 7% PUFA, and 400 mg/d cholesterol and served as the reference diet to compare the changes in lipid and lipoprotein levels with the 4 cholesterol-lowering diets. The NCEP step II diet provided 7% of energy as SFA, 25% from fat, 59% CHO, and 200 mg/d cholesterol. The 3 high MUFA diets maintained the same amount of SFA as the NCEP diet, however some CHO energy was replaced with MUFAs. The percent of MUFA in OO, PO, and PPB diets were 21%, 17%, and 18%, respectively. The total fat in the diet was similar to the AAD diet at 35% of calories.

Compared to lipid and lipoprotein levels following the AAD phase, the plasma cholesterol level improved after all 4 test diets. For example, plasma total cholesterol levels decreased by 9% on the Step II diet, 11% on the OO diet, 9% on the PO diet, and 11% on the PPB diet from an average total cholesterol level of 209 mg/dl on the AAD. The average LDL cholesterol levels decreased by approximately 14% following the 4 cholesterol lowering diets compared to the AAD. However, the 11% increase in TAG and 4% decrease in HDL levels following the Step II diets differed from the 13% decrease in TAG levels and no net change in HDL cholesterol following the 3 high-MUFA diets. Also, plasma Lp(a) was highest with the Step II diet. The degree of change in plasma lipids was directly associated with the baseline LDL cholesterol concentration.

Finally, by using the following estimate, "a 1% decrease in LDL cholesterol decrease CVD risk by 1.5%, a 1 mg/dl (0.026 mmol/l) decrease in HDL cholesterol increase CVD risk by 2-3%, and a 89 mg/dl (1 mmol/l) increase in triacylglycerol increases CVD risk by 25%," from earlier studies, the researchers were able to determine improvement in CVD risks associated with different test diets. For example, based on these estimates, the researchers predicted that the OO diet would result in the largest reduction in CVD risk of 25%, compared to 16% and 21% with the PO and PPB diets. On the other hand, as a result of an increase in TAG and decrease in HDL cholesterol, the net decrease in CVD risk on the Step II diet was only 12%. These data suggest that high-MUFA diets are more effective in lowering CVD risk than the more commonly recommended Step II diet.

Current evidence strongly suggests that diets high in MUFA are superior to a low-fat, high-CHO diet in reducing CVD risk. Even though the NCEP Step II diet is often recommended for preventing and treating CVD, because of its negative impact on plasma TAG and HDL levels associated with replacing fat with CHO calories, its suitability and efficacy needs to be re-evaluated. The data from this study indicate that olive oil is more beneficial than either peanut oil or peanut and peanut butter, however, these products can offer alternative foods as a means to increase the level of MUFA in the diet.

Lipid and lipoprotein changes (%) compared to Average American Diet

Kris-Etherton PM, Pearson TA, Wan Y et al. High-monounsaturated fatty acid diets lower both plasma cholesterol and triacylglycerol concentrations. Am J Clin Nutr. 1999;70:1009-1015.

Key Messages

Smoking Increases CVD Risk in Individuals with Desirable Cholesterol Levels

The prevalence of cigarette smoking is at an all time high in Asian populations. It is estimated that 72% of Korean men, 50% of Chinese men, and 58% of Japanese men are current smokers. This is a frightening statistic in light of the fact that smoking is considered the number one risk factor for CVD. Even though Asians typically have lower plasma cholesterol levels than Westerners, according to Jee et al., a lower cholesterol level does not seem to protect against smoke related CVD. For example, based on data from 106,745 middle-aged Korean men enrolled in the Korean Medical Insurance Corporation (KMIC) between 1990 and 1992, smoking was a major independent risk factor for ischemic heart disease (IHD), stroke, and atherosclerotic cardiovascular disease (ASCVD). The majority (93%) of the subjects had blood cholesterol levels below 239 mg/dl.

During the 6-year follow-up period, 3,086 cases of fatal and non-fatal ASCVD events were noted. It broke down into 1,006 cases of nonfatal IHD events, 1,364 cases of nonfatal stroke, 716 cases of nonfatal ASCVD, 131 cases of fatal IHD, 270 cases of fatal stroke, and 168 cases of fatal ASCVD. The multivariate RR for IHD, stroke, and ASCVD were 2.2, 1.6, and 1.6 for smokers compared to nonsmokers. The ex-smokers fared slightly better than current smokers with RR values of 2.2, 1.1, and 1.3 for IHD, stroke, and ASCVD, respectively. Also, as expected, people who smoked a greater number of cigarettes per day and for a greater number of years had higher risk of both IHD and stroke. However, no such noticeable trend occurred with different levels of baseline plasma total cholesterol concentrations. For example, the RR for IHD was 3.3 in the group with the lowest plasma total cholesterol compared to 2 in those with the highest plasma total cholesterol.

In conclusion, despite mixed earlier findings, current data indicate that smoking does increase both stroke and CVD risk among middle aged, normocholesterolemic Korean men. And in light of this result, it would be prudent to recommend that everyone, including those with normal plasma cholesterol levels, to either abstain from smoking or at the very least reduce the number of cigarettes smoked per day.

Jee SH, Suh I, Kim IS, et al. Smoking and atherosclerotic cardiovascular disease in men with low levels of serum. The Korea Medical Insurance Corporation Study. JAMA. 1999;282:2149-2155.

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Excess Body Weight Associated with Negative Health Related Quality of Life

We know that excess body weight is associated with many chronic health problems. But now, thanks to a study by Must et al., we have a much clearer perspective of the health impact of overweight and obesity on the US population. By using results from the third National Health and Nutrition Examination Survey (NHANES III), the researchers analyzed the relationship between BMI and morbidities associated with CHD, blood pressure, blood cholesterol levels, type 2 diabetes, gall bladder disease, and osteoarthritis in people over 25 years old.

According to this survey, which included 16,884 subjects, 63% of males and 55% of females in the US are either overweight or obese. This problem was equally common among all ethnic and racial groups. And as expected, body weight was directly associated with prevalence of type 2 diabetes, gallbladder disease, osteoarthritis, and hypertension. As for blood cholesterol levels, values were higher in the overweight and obese groups than the normal weight group, however, it did not seem to increase proportionately with further weight.

Regardless of weight categories, the prevalence ratio for all study outcomes was much greater in the younger group than in people 55 years or older. For example, the prevalence ratio for type 2 diabetes in overweight men under 55 years was 3.27 compared to 1.77 in the older group. The prevalence ratios for diabetes were 18.08 and 3.44, respectively, in the younger and older men with the highest body weights. For gallbladder disease, prevalence was twice as high in normal weight females than males in the same weight group; however, the change in prevalence ratio was much higher in men than women with increased body weight. Age did not effect CHD risk, but obesity was associated with CHD in all subgroups. Also, the researchers observed that hypertension was the most common health problem associated with both overweight and obesity. Finally, the incidence of people having 2 or more comorbidities increased directly across different weight classes.

The results reported by Must and colleagues strongly suggest that Americans are losing the battle of the bulge, and are affected by the various consequences associated with obesity-related health conditions such as type 2 diabetes, hypertension, gallbladder disease, hypercholesterolemia, osteoarthritis, and CHD. The most disconcerting aspect of their findings is that these numerous health problems were not limited to only the grossly obese subjects, but were prevalent among those who were slightly overweight. These data support the need for a national program to prevent and treat excess body weight in adults.

In a comparable study, Fine et al. observed that weight gain was associated with impaired physical function, decreased vitality, and associated bodily pain. During the 4 year follow-up period, 39% (n=15,602) of women in the Nurses' Health Study maintained their weight within 5 pounds of their original weight compared to 38% (n=15,160) who gained between 5-20 pounds and 17% (n=6,667) who lost between 5-20 pounds. Based on the self-administered questionnaire that measured health related quality of life, regardless of baseline weight, subjects associated weight gain with lower physical function and vitality and increased pain. Weight loss, on the other hand, was positively viewed by everyone, except for the group of women with the lowest BMI values. Fine and colleagues suspected that the large amount of weight loss observed in this small group of women was probably a result of underlying illness rather than an intentional weight loss, since they had the lowest physical activity level. Weight change was more strongly related with physical health than mental health. In the young, lean women, a weight gain of 20 pounds or more was associated with a greater decline in physical function than cigarette smoking. The impact of weight change on quality of life was similar between women over 65 years and women younger than 65 years.

Both studies support the current recommendation, which emphasize the need to maintain a normal BMI, or in the case of people with excess weight, to reduce weight for optimal physical function. However, in light of the growing prevalence of obesity among the American population, comprehensive programs aimed at preventing obesity is needed along with treating chronic illnesses associated with this growing disease.

Fine JT, Colditz GA, Coakley EH, et al. A prospective study of weight change and health-related quality of life in women. JAMA. 1999,282:2136-2142.

Must A, Spadano J, Coakely EH, et al. The disease burden associated with overweight and obesity. JAMA. 1999;282:1523-1529.

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Antioxidant Supplement Reduces LDL Oxidation in Diabetics

In the fight against heart diseases, a-tocopherol has emerged as a new magic bullet for protecting against atherosclerotic CVD. It has been shown that this antioxidant, which is transported in the LDL particle, reduces the susceptibility of LDL to oxidation and protects against the atherogenic effects associated with oxidized LDL particles.

Anderson and colleagues conducted a 2 pronged study to determine if LDL from diabetics is more susceptible to oxidation than LDL from non-diabetics, and to determine the effects of antioxidant supplementation on the oxidation kinetics of LDL in the same populations. In the study, 20 male type 2 diabetic subjects not taking insulin were matched with 20 control subjects. All subjects followed an isocaloric America Diabetes Association's diet during all 3 phases of the 28 weeks study. The first and last 8 weeks of the study were pre-treatment and post-treatment phases, during which time both case and control groups consumed placebo capsules. During the treatment phase, weeks 9-20, the diabetic group received a daily supplement of 24 mg b-carotene, 1000 mg ascorbate, and 800 IU of a-tocopherol and the control group continued the placebo regimen. The plasma antioxidant levels and LDL oxidation status were measured following each test period.

The researchers used 4 different techniques to determine LDL oxidation rates; 30oC Cu oxidation, 37oC Cu oxidation, AAPH [2,2'-azobis (2-amidinopropane) dihydrochloride] oxidation, and hypochlorite oxidation methods. All 4 assay systems were used since each has distinct advantages. For example, the 30oC Cu oxidation assay is better at continuously and visually monitoring the lag and propagation phases of conjugated dienes (CD) formation. The 37oC oxidation analysis is better at detecting the differences between control and diabetic subjects. "The AAPH technique was used as a distinctly different oxidation probe since this compound generates free radicals in solution, rather than facilitating oxidation as with copper" and hypochlorite is a selective protein oxidant that spares lipids.

Results with copper oxidation at 30oC showed that both groups had similar initial LDL oxidation status reflected by similar lag phases (a measure of resistance to oxidation), maximum conjugated diene (a product of early lipid oxidation) formation, production of thiobarbituric reactive substances (TBARS are a product of late lipid oxidation), and trinitrobenzene sulfonic acid (TNBS measures loss of free amine groups associated with protein damage) levels. However, following the antioxidant supplementation, the lag phase increased from 56 minutes to 129 minutes, the maximum CD formation decreased from 1.23 to 0.62 OD units, the formation of TBARS decreased from 78 to 33 nmol/mg of protein, and the loss of free amine groups (TNBS) decreased from 41% to 12%, indicating that antioxidant supplements were effective in reducing the susceptibility of LDL to oxidation. Improvement in LDL oxidation parameters was also observed following antioxidant supplement when tested using the copper oxidation at 37oC method. But, unlike copper oxidation at 30oC, copper oxidation at 37oC indicated that LDL from diabetic subjects was more susceptible to oxidation with a 10% shorter lag time and higher baseline TBARS and TNBS levels. Anderson et al. were also able to show that untreated LDL from the diabetic group was taken up more readily by macrophages compared to LDL from the control group, and that following antioxidant supplement, LDL uptake was reduced. Finally, antioxidant supplements were not associated with any appreciable changes in glycemic control or plasma glycohemoglobin and lipid values.

In conclusion, the data indicate that LDL from diabetic subjects is more susceptible to oxidation than LDL from non-diabetics. Daily antioxidant supplementation could be of benefit in this population, especially since they are prone to CVD due to the increased prevalence of dyslipidemia, hypertension and obesity.

Anderson JW, Gowri MS, Turner J. et al. Antioxidant supplementation effects on low-density lipoprotein oxidation for individuals with type 2 diabetes mellitus. J Am Coll Nutr. 1999;18:451-461.

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Vitamin E Supplement Yields Minimal CVD Benefit

In an effort to protect their high CVD risk patients, it has become a common practice for clinicians to recommend 400 IU of vitamin E supplement along with daily use of aspirin and B vitamin supplements. However, according to the latest finding from the Heart Outcome Prevention Evaluation Study (HOPE), with 9,541 subjects (2,545 women and 6,996 male), no CVD benefit was found following 4.5 years of vitamin E supplementation. This study, along with several smaller studies, contradicts previous observational and experimental studies which found an association between vitamin E and lower CHD risk.

The incidence of primary CVD events, death from cardiovascular causes, MI, and stroke were similar between the 4,761 vitamin E group and 4,780 placebo group. For example, the relative risk for death from cardiovascular causes was 1.05 (95% CI 0.95-1.16) with 342 cases in the vitamin E group compared to 328 cases in the placebo group. In the cases of MI and stroke, 532 vs. 524 and 209 vs.180 events were reported in experimental group vs. placebo group, respectively. The relative risk for MI and stroke were 1.02 and 1.17, respectively. There were also no significant difference in the number of secondary outcomes; angina, claudication, heart failure, complications of DM, and vascularization or limb amputation, between study groups. Further analysis of subgroups based on age, sex, previous CVD episodes, and smoking and diabetes status revealed similar rates of primary CVD outcomes. Even though this study found no cardio-protective effect of vitamin E supplements on CVD risk, supplementation was not associated with any adverse events.

The researchers speculated that the lack of benefits associated with vitamin E supplements and CVD events in the current study was possibly due to the short study duration. Unlike medications that lower blood pressure and plasma cholesterol levels immediately, antioxidants such as vitamin E are thought to take more than 5 years to affect any detectable clinical outcomes associated with a decrease in new lesions, especially in high CVD risk groups like these study subjects. Also, unlike epidemiological studies that found a relationship between high vitamin E intake and lower rate of CHD, the current study did not include other antioxidants.

Results from this study indicate that the commonly accepted beneficial effects of 400 IU/day of vitamin E supplementation against MI, stroke, and CVD deaths are far from established. Even though earlier observational and experimental studies showed that vitamin E protected against CVD, the null findings found in this high-risk patient population of the HOPE study suggest that a larger and longer study is needed to fully evaluate the effect of vitamin E on CVD risk.

The Heart Outcomes Prevention Evaluation Study Investigators. Vitamin E supplementation and cardiovascular events in high-risk patients. N Engl J Med. 2000;342:154-160.

Moderately High-Protein Diet Improves Plasma Lipid Profile

A study by Wolfe and Piche suggests that replacing some sources of CHO in the diet with low-fat, high-protein foods can result in an improved plasma lipid profile in healthy adults. In this randomized, cross-over study, researchers fed 10 healthy, normolipidemic volunteers either a isocaloric low-protein or high-protein diet and determined the effect on plasma lipid and lipoprotein levels. Both test diets contained 35% of energy as fat, 230 mg/day cholesterol, and 24 gm/day fiber, however, the percentage of protein in the high-protein diet was 22% compared to 12% in the low-protein diet. The duration of each diet phase was 4 weeks.

Like similar high-protein feeding studies conducted in hyperlipidemic subjects, this study found that the mean plasma cholesterol concentration was lower following the high-protein diet. For example, plasma total cholesterol, LDL cholesterol, VLDL cholesterol, TAG, and total cholesterol to HDL cholesterol ratio levels were 7%, 8%, 23%, 27%, and 11% lower, respectively, than during the low-protein diet. HDL cholesterol was slightly higher (4%) following the high-protein diet, however, the increase was not statistically significant. The subjects reported slightly higher levels of satiety following the high-protein diet.

With this study, the researchers were able to show that when CHO is replaced with a higher amount of protein in the diet, with no change in the percent of fat calories, it leads to an improved plasma lipid and lipoprotein profile in normocholesterolemic adults as was previously shown in hypercholesterolemic and postmenopausal women. Even though the actual changes in lipid levels were relatively small, this study supports earlier studies which suggest that all things, even CHO, should be eaten in moderation.

Wolfe BM and Piche LA. Replacement of carbohydrate by protein in a conventional-fat diet reduces cholesterol and triglyceride concentrations in healthy normolipidemic subjects. Clin Invest Med. 1999;22:140-148.

Fortified B Vitamin in Prepared Meal Plan Lowers Plasma Homocysteine Levels in Healthy Adults

A good healthy diet, complete with recommended nutrients, continues to be a key factor in managing one's health. In a multicentered study, Chait and colleagues were able to reduce plasma homocysteine levels, a risk factor for CHD, by feeding a prepared meal plan (PMP) fortified with 23 micronutrients to adults with histories of type 2 diabetes, hypertension, dyslipidemia, or any combination of these conditions. In this study, the investigators randomly divided 491 participants into 2 test groups. Depending on the group assigned, study subjects followed the PMP diet (n=244) or a self-selected diet (SSD, n=247) for 10 weeks. Both diets were similar in macronutrient composition, 20% of energy as fat, 55-60% as CHO, and 15-20% as protein, however, the micronutrient content of the PMP diet was much higher compared with the SSD diet. In the PMP diet, 22 micronutrients were fortified with >100% of the RDA for adults and folate was increased to 400 µg/day. The group in the SSD diet ate regular foods they prepared at home. The SSD group was taught to eat a fixed number of servings from the exchange list.

As expected, the dietary intakes of folate, vitamin B₆, and vitamin B₁₂ increased significantly in the PMP diet group compared to the SSD group. For example, dietary folate, vitamin B₁₂, and vitamin B₆ increased by 399 µg/day, 7.4 µg/day, and 2.1µg/day, respectively, with the PMP diet, while it only changed by 68 µg/day for folate, 0.3 µg/day for vitamin B₆, and -0.4 µg/day for vitamin B₁₂ following the SSD diet. The plasma homocysteine levels in the PMP group fell by 1.5 µmol/l (13.8%) compared to a 0.1µmol/l increase in the SSD group. Also, the changes in serum and RBC folate concentrations and serum vitamin B₁₂levels were greater in the PMP group. The serum folate level increased by 81% (14.1 nmol/l) and decreased by 9.5% following the PMP and the SSD diets, respectively. RBC folate and serum vitamin B₁₂ increased by 65% (367 nmol/l) and 27% (98 pmol/l), respectively, in the PMP group. The RBC folate increased by 12% (66 nmol/l) and serum vitamin B₁₂ decreased by 6% (22 pmol/l) in the SSD group. In spite of the dietary vitamin B₆ increase, serum and RBC vitamin B₆ levels did not significantly change in either group.

The inverse relationship between serum homocysteine and dietary, serum and RCB folate were noted in both study groups. The relationship between serum homocysteine and serum vitamin B₆ and B₁₂ or RBC vitamin B₆ were weak; however, including these in the folate analysis further strengthened the folate relationship. This would indicate that vitamin B₆ and B₁₂ have a small effect on homocysteine levels. Finally, the effects of these nutrients on lowering plasma homocysteine levels were especially strong in subjects with the highest baseline homocysteine concentrations. For example, the subjects with baseline homocysteine levels of >12.15 units lowered their homocysteine level by 5.7 µmol/l (PMP) and 2.3 µmol/l (SSD) compared to a small increase in homocystein levels in people with the lowest baseline homocysteine levels.

In conclusion, this study shows that increasing dietary intakes of folate, vitamin B₆ and vitamin B₁₂, which are cofactors in numerous metabolic pathways, can effectively lower plasma homocystein concentrations in persons with increased CHD risk. Chait et al. conclude that prepackage meals such as the one used in this study are convenient ways to help people with concomitant risk factors for CVD meet their nutritional needs. However, a more disturbing finding from this study is that the SSD group was unable to achieve optimal plasma levels of serum and RBC folate and serum vitamin B₁₂ by eating regular foods off the grocery shelf.

Chait A, Malinow MR, Morris CD et al. Increased dietary micronutrients decrease serum homocysteine concentrations in patients at high risk of cardiovascular disease. Am J Clin Nutr 1999; 70:881-887.

Stearic Acid Associated with CHD Risk

Contrary to earlier scientific evidence, stearic acid (18:0), like other long chain saturated fatty acids [lauric (12:0), myristic (14:0), palmitic acid (16:0)], is also associated with CHD risk, according to data from the Nurses' Health Study. On the other hand, intake of short and medium chain fatty acids (4:0 - 10:0) was not associated with increased CHD risk. However, since the sources of these saturated fats are typically from the same foods, the researchers concluded that it was not as critical to distinguish specific type of saturated fats when advising clients.

Based on 1980 to 1994 food frequency questionnaires of 80,082 nurses, saturated fat intake was steadily on the decline. For example, beef and whole milk, two primary sources of saturated fat, decreased from 1.8 to 0.8 oz/day and 0.26 to 0.07 glasses/day, respectively. However, according to the findings, saturated fat intakes were associated with higher prevalence of smoking and cholesterol intake and lower activity levels and fiber intake.

During the 14-year follow-up, 939 cases of major CHD events occurred. The multivariate RRs of CHD, which included both dietary and non-dietary covariants were 0.97, 1.12, 1.07, and 1.19 for each 1% increase in intake of 4:0-10:0, lauric and myristic acid, palmitic acids, and stearic acid, respectively. However, when all saturated fats where combined, a 5% increase in these fats resulted in a RR value of 1.29. These results also showed an inverse relationship between CHD and an increase in polyunsaturated fat intake. The multivariate RR was 0.79 for each 0.2 unit increase in the dietary fat P:S ratio. The researchers estimated that by replacing 5% of long chain saturated fatty acids with 5% of CHO in an isocaloric meal would result in a 22% reduction of CHD risk compared to 42% and 50% reduction following replacement with MUFA and PUFA, respectively.

Even though the average red meat and high-fat dairy product consumption was on the decline, based on the multivariate analysis, women in the highest quintile of intakes for these foods had higher CHD risk. On the other hand, fish, poultry, and lean dairy products in the diet were associated with lowering CHD risk.

In conclusion, results reported by Hu et al. indicate that all high saturated fat foods, even those with high stearic acid content, increase CHD risk . Therefore, people should replace some high saturated fat foods with lower saturated foods as these foods lower blood cholesterol levels. Finally, since foods high in saturated fatty acids contain a mix of different types of fatty acids, there does not appear to be a need to distinguish the CHD effects from individual fatty acids.

Hu FB, Stampfer MJ, Manson JE, et al. Dietary saturated fats and their food sources in relation to the risk of coronary heart disease in women. Am J Clin Nutr. 1999;70:1001-1008.

Editorial: Frankenfoods and Science Forsaken

Analogies are always such dangerous critters because for certain someone will say "it's not the same thing." But why not! Ascribing health risk has taken on a life of its own these days and everything seems to be a risk for something. The risk de jour is GMOs, genetically modified organisms, which, without documented damage, have become the buzz word for the hazards science foists upon an unsuspecting public for its own devious and, as often accused, profitable motives. Clearly, the role of science is to change the world as we know it; to some that is the natural order of progress while to others it is a clear sign of our eminent demise. And as such, anything that is a step forward must defend itself against accusations that it harms the environment, kills the public, and destroys the world. GMO's have now become the embodiment of anti-techs versus techs, and frankenfoods versus science.

In a world of fixed land mass, decreasing agricultural lands, expanding populations, and more people demanding more food for less money, it is difficult to comprehend why advances which increase food production, decrease loss, reduce use of fertilizers and pesticides, and produces foods with higher nutritional value are treated as if they were an attempt to destroy the earth. Isn't this a case of trying to feed the hungry, enhance nutrition for the malnourished, reduce environmental pollution, increase production? Aren't these good things? I remember years ago environmentalist complaining that agriculture, specifically animal agriculture, was causing the destruction of the rain forests. Why then is grain produced from less land with less environmental pollution not a step in the right direction? [Maybe it was eating the animal products all along that was in fact the unacceptable part.] Can we really afford to discard advances which can make food more available, affordable and nutritious, with specific efficacies for nutrient deficiencies [children in southeast Asia would seem better off with a GMO vitamin A and iron enriched rice]. Sometimes we seem to forget just how many children in the world are malnourished, and how many die from the simple lack of food. So I'll get on a jet and go to my demonstration against those frankenfoods and get the government to keep it out of my country, and then I'll go home and enjoy a fine feast of non-GMO (vegetarian) cuisine and non-GMO (alcohol-free) wine, and know that I have stopped a maybe disaster before it maybe happened. Who cares if there's no real evidence of a disaster in the making, I know, just as I know so many other pseudo-facts, that it is wrong. I know what I know, do not confuse me with facts. And please don't tell me about the millions who would benefit from this technology. I have a loftier goal. See you at the next demonstration. And GMOs become faced with the "Reverse Onus" conundrum: it is not the responsibility of those making risk claims to prove the validity of the claim; rather, it is up to those who deny the claims to prove they could not be true. The complication is, how do you prove a negative. [First corrective step, change the terminology. Let's call them "genetically enhanced organisms."]

And the analogy? Thirty years ago it was decided that since blood cholesterol was related to heart disease risk, dietary cholesterol must also be a risk, and today restrictions and limits and good food, bad food mentalities permeated the US dietary pattern. My analogy is that once we start saying GMOs are bad, because we think, just maybe, they might be, they will be bad no matter what the next few decades of research and science show. Eventually the concept of precaution becomes the verbiage of fact and the next generation never knows just what little scientific reality the conventional wisdom is based on. A few voices will argue the issue but will be looked upon as anti-establishment noise makers because we really do not like those who challenge our preconceived view points. And it has taken many years to even begin to address the "reverse onus" quandary faced by eggs and other high cholesterol foods. We need to be very cautious of these first steps on the path of risk pronouncements; too often we find it to be a long one-way street with many roadblocks against any u-turns.

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

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

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