Newsletters & Publications

Volume 17 – Number 3 Fall 2000



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

Positive Dietary and Lifestyle Pattern Lowers CVD Risk in Middle-Aged Women

Pharmacologicaltreatments of hypertension and dyslipidemia have been instrumental in lowering CHD rates. But the results from the Nurses’ Health Study strongly support a healthy lifestyle as a fundamental regimen in lowering CHD risk in middle-aged females, without the exorbitant cost and side effects associated with some drugs. Also, unlike earlier studies that investigated individual risk factors, Stampfer et al. looked at the combined effects of 5 different dietary and lifestyle patterns on CVD risks. 

Using data from 84,129 women followed for 14 years, the researchers were able to determine the role of exercise, BMI, alcohol, diet, and smoking on CVD rates. Women in the study were categorized into a low-risk group if they were nonsmokers, had a BMI of less than 25, drank at least 5 gm/day of alcohol, and exercised for 30 minutes/day (3 or more MET/hour) and had a diet that was in the top 40% for cereal fiber, marine omega-3 fatty acids, and folate, with a high ratio of PUFA to SFA, and low in trans-fat and glycemic load. Only 3.1% of the study cohort met the definition of low-risk.

Analysis of individual risk factors shows that for all 5 risk factors, smoking had the highest impact on raising CHD risk. Compared to nonsmokers, women who currently smoked more than 15 cigarettes per day had a RR of 5.48 (4.67-6.42). Other risk factors exhibited smaller RR values, ranging from 1.41(exercise) to 1.90 (diet). However, when all 5 low-risk factors were combined and analyzed, they had a synergistic effect on lowering CHD events. For example, among the low-risk group, their risk of CHD was only 17%. Their population attributable risk was 82%, meaning 82% of all coronary events would have been prevented if all cohorts were in the low-risk group. With each increase in number of healthy risk factors, the RR decreased. For example, the RR decreased from 0.43 to 0.34 in women with 3 low-risk factors versus 4 low-risk factors. Also, when smokers were excluded from the analysis, the effects of the other 4 risk factors on RR for CHD increased. The RR for CVD, both coronary events and stroke, was 0.25 in the low-risk group. 

Due to the small number of women in the low-risk group (3.1%) and limited cases of CHD (5 cases), the researchers reanalyzed the relationships using a more liberalized criteria (i.e. women who exercised for at least 15 minutes/day, drank 2 gm/day alcohol, BMI 28) to include 10% of subjects. In this group the RR was 0.36 with a population attributable risk of 62%. This increase in CHD incidence with relaxing of study criteria suggests a graded effect of these risk factors and the need for tighter control of risk factors to maximize CVD risk reduction. Adjustment for socioeconomic status, as determined by cohort’s spouse and parent’s education level, had a small (0.17 to 0.19) effect on the RR for CHD in the low-risk group. 

Results from Stampfer et al. show that adherence to the heart healthy lifestyle recommended by the public health community can reduce CHD and CVD by as much as 75% among women. And given that these lifestyle changes may offer considerable health benefits beyond CVD risk reduction, it is important to continue to spread the message about healthy lifestyles. Especially since the number of nurses in this study, as well as in the general population, following lifestyle guidelines involving diet, exercise, and abstinence from smoking is small. These factors pose a great opportunity to significantly lower future CVD events through healthful lifestyle. The researchers also hypothesized that the benefits associated with positive dietary and lifestyle patterns in their study might be low as a result of not including other positive dietary (nut, vitamin B6 and vitamin E intake) and pharmacological (aspirin, statin) factors in the overall analysis. 

Stampfer MJ, Hu FB, Manson JE, et al. Primary prevention of coronary heart disease in women through diet and lifestyle. N Engl J Med. 2000;343:16-22.

Key Messages

  • Only 3.1% (n=2,608) of study cohort were nonsmokers, had BMI <25, exercised regularly, and had a diet that was in the top 40% for fiber, omega-3 fatty acids, and folate and were classified into low-risk group.
  • Risk of CHD was 17% in the women in the low-risk group.
  • 82% of all coronary events would have been prevented if all the cohort were in the low-risk group.
  • Tight control over CHD risk factors maximized CVD risk reduction.

Table of Contents

Dietary Fiber Intake Lowers CHD and All-Cause Mortality Rates

Using data from the Scottish Heart Health Study, Todd et al. investigated the relationship between antioxidant and fiber intakes and 2 study outcomes, CHD events and all-causes mortality. A semi-quantitative food frequency questionnaire was used to determine individual dietary patterns. It was validated with subjects’ plasma antioxidant levels.

During the mean follow-up period of 7.7 years, 637 CHD events (454 men and 183 women) and 385 non-CHD deaths (224 men and 161 women) were reported in the 11,627 study cohorts. Based on the reported dietary habits, the female cohort, regardless of outcome groups, had higher energy-adjusted intakes of vitamin C, vitamin E, beta carotene, and fiber with 27.3 mg/1000 kcal, 3.23 mg/1000 kcal, 1,793 mg/1000, and 10.6 gm/1000 kcal, respectively, than men. The fully adjusted hazard ratios (HR); which adjusted for age, serum lipid levels, systolic blood pressure, BMI, activity levels, and chronic medical conditions, showed an inverse relationship between the 4 dietary factors and both CHD and all-cause mortality among male subjects. The HRs were 0.57, 0.95, 0.68, and 0.64 in the highest quartile for vitamin C, vitamin E, beta carotene, and fiber intake for CHD risk among men. Similar trends were noted with all-cause mortality risk in men. However, in spite of higher antioxidant vitamin intakes in women, only dietary fiber intake was inversely associated with the 2 study outcomes with HR value of 0.56 and 0.65 for CHD and all-cause mortalities in the highest quartile for dietary fiber. Antioxidants were not associated with reducing CHD and all-cause mortalities in women. Closer look at the data showed that maximum benefit associated with vitamin E intake was noted in the 2nd quartile rather than 3rd and 4th quartile. As a matter of fact, the group with the highest vitamin E intake saw no benefits associated with CHD.

The results from the Scottish Heart Healthy Study suggest that dietary fiber is more effective than antioxidants, vitamins C and E, and beta carotene in improving survival rates and lowering CHD cases. According to the researchers, the weak association between antioxidant intakes and the 2 study outcome measures might have been the result of suboptimal intakes of antioxidants in this population. Finally, if consumers follow the dietary recommendation of eating more fruits and vegetables, these data suggest that it can have a positive effective on lowering CHD and all-cause mortality due to dietary fibers and vitamins found in these foods.

Todd S, Woodward M, Tunstall-Pedoe H et al. Dietary antioxidant vitamins and fiber in the etiology of cardiovascular disease and all-cause mortality: Results from the Scottish Heart Health Study. Am J Epidemiol. 1999;150:1073-1080.

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Elevated C-Reactive Protein Levels in Insulin Resistant Population

Recently C-reactive protein (CRP), a marker for inflammation, has received attention for its role in predicting risk of CHD. CRP activates the complement system in vivo, accumulates in early atherosclerotic lesions, binds to lipoprotein, such as LDL and VLDL, as well as a potent procoagulant produced by macrophages. Visser et al. and Festa et al. show that overweight and obese persons and insulin resistant individuals are especially vulnerable to elevated plasma CRP levels.

Based on the hypothesis that the proinflammatory cytokine interlukin (IL-6) found in adipose tissue induces low-grade systemic inflammation, Visset and colleagues tested the relationship between excess body weight and CRP levels in a 16,616 cohort in HANES III study. Blood assays showed that 22% of men and 33% of women had elevated CRP levels (³0.22 mg/dl) and 4.4% of men and 8.9% of women had CRP levels greater than 1.0 mg/dl. Compared to normal weight individuals (BMI <25), overweight (BMI 25-29.9) and obese (BMI ³30) men were 1.41 and 2.13 times more likely to have elevated CRP levels. Each standard deviation (SD) increase in BMI was associated with 1.38 and 2.04 times more likely to have elevated CRP levels in men and women, respectively. Each SD increase in waist to hip ratio was related to 1.41 and 1.28 times more likely to have elevated CRP in men and women, respectively.

Visser and colleagues’ results confirmed earlier findings in which overweight and obese subjects tend to have higher rates of low-grade systemic inflammation as reflected by higher CRP levels than normal body weight individuals. Within the same BMI categories, a higher percentage of females had elevated CRP levels compared to men. This is not surprising since generally, women have a higher percent body fat, as well as more women than men are severely obese with a BMI of >35. An independent relationship between waist to hip ratio with CRP is also in line with previous data indicating that people with an apple shape physique, with abdominal visceral fat, are at a higher risk for CHD than pear shaped individuals.          

In a different study, Festa et al. were able to test the relationship between chronic subclinical inflammation and insulin resistance syndrome (IRS) by comparing CRP, fibrinogen, and white cell count measurements, 3 inflammatory markers, with intravenous glucose tolerance tests in 1008 subjects with no history of CAD. Strong associations were found between CRP and BMI, waist circumference, fasting insulin, dyslipidemia, and insulin resistance. For example, the mean log of CRP levels were 0.075±0.06, 0.511±0.06, 0.845±0.07, 1.43±0.10, 1.39± 0.17 in people with no risk factors for IRS versus those with 1, 2, 3, and 4 risk factors, respectively. The data from the multiple linear regression model showed that CRP levels were independently associated with BMI, systolic blood pressure, and insulin resistance.

Festa et al. concluded that elevated CRP levels in a non-diabetic populationwith an insulin sensitivity problem might be another risk factor for IRS and that early anti-inflammatory treatment, such as, aspirin could be beneficial. They also suggested that both pharmacological and non-pharmacological treatments used to improve insulin resistance might be effective in lowering plasma CRP levels.

In light of the fact that 54% of US adults over 17 years old are overweight and obese, these data clearly indicate why CVD is the leading cause of death in the US. The chronically elevated CRP levels among people with excess body fat and insulin resistant population, along with other CHD risks, commonly present in this group make them prime candidates for suffering future CHD events. 

Festa A, D’Agostino R, Howard G, et al. Chronic subclinical inflammation as part of the insulin resistance syndrome. The insulin resistance atherosclerosis study (IRAS). Circulation. 2000; 102:42-47.

Visser M, Bouter LM, McQuillan GM, et al. Elevated C-reactive protein levels in overweight and obese adults. JAMA. 1999;282:2131-2135.

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Racial Difference Noted with Dietary Fat and Plasma Cholesterol in Premenopausal Women

Studies show that the incidence of CHD is significantly lower in premenopausal women compared to middle-aged men, but recent data indicated that there is ence of CHD is significantly lower in premenopausal women compared to middle-aged men, but recent data indicated that there is a significant racial difference in CHD rates among younger females. The incidence of CHD among African-American women is reported to be 2-3 times higher than the rate for white females, a level closer to that of males. This difference has been ascribed to differences in CHD risk factors since obesity and high blood pressure are more prevalent among black women than white women. In addition, black females have higher plasma lipoprotein (a) and homocysteine concentrations, 2 emerging risk factors for CHD.

Studies on the role of dietary fat in CHD risk in premenopausal women are limited and as a result, Gerhard et al. investigated this relationship by conducting a randomized crossover trial in 13 premenopausal black women and 9 premenopausal white women. All study participants were healthy and free of chronic illnesses. Both study groups followed a low-fat, high-fiber diet and a high-fat, low-fiber diet for 4 weeks each with a washout period in between the 2 diet periods. The composition of the low-fat, high-fiber diet consisted of 20% fat, 6% saturated fat, 65% CHO, 15% protein, 29 mg cholesterol/1000 kcal, 15 gm fiber/1000 kcal, and a P:S ratio of 1 whereas the high-fat, low-fiber diet consisted of 40% fat, 20% saturated fat, 15% protein, 45% CHO, 330 mg cholesterol/1000 kcal, 9 gm fiber/1000 kcal, and a P:S ratio of 0.3. The diets were eucaloric to maintain body weights. The 2 study cohorts were matched for baseline plasma lipid and lipoprotein levels, age, body weight, and educational attainment. The women in the study were obese as reflected by their mean BMI scores of 32.1 and 36.1 in the African American and Caucasian cohorts, respectively.

The plasma lipid and lipoprotein levels measured following each test diet showed that intake of the high-fat, low-fiber diet resulted in increased plasma total, LDL, and HDL cholesterol concentrations and decreased TAG levels in both study groups. The plasma total cholesterol levels increased by 16.8% and 16.3% in white and black women, respectively. But the actual change in lipoprotein levels in the black cohort was less atherogenic than in the white women with a 23.9% increase in HDL cholesterol and only a 17.6% increase in LDL cholesterol, while the HDL and LDL cholesterol concentrations changed by 18.4% and 24%, respectively, in the Caucasian women. As a result of a greater increase in HDL cholesterol levels, the LDL:HDL ratio following the low-fat diet (2.71) was more atherogenic in African American women than with the high-fat diet (2.58). The baseline TAG levels among Caucasian women were much higher than African American women, but following the high-fat, low-fiber diet lowered plasma TAG levels in both groups.

Post-prandial TAG responses following a 24 hour fat tolerance test with the high-fat test meals containing 0.7 gm total fat/kg body weight of mixed foods showed no statistical difference in maximal TAG concentrations or percent increases between the 2 test diets or within the 2 test groups. However, the 24-hour areas under the plasma TAG curve were greater following intake of the high-fat, low-fiber diet compared to the low-fat diet indicating that catabolism of dietary fats was slower with the high-fat diet.

This study was unable to show a racial difference in plasma lipid and lipoprotein levels as a result of the 2 test diets, but the researchers proposed that there was a limitation to the study due to the small study size. Gerhard et al. also concluded from their data that the low-fat, high-fiber diet used in their feeding study was less atherogenic than the high-fat, low-fiber diet resulting in lower plasma total and LDL cholesterol levels, as well as less post-prandial lipemia in both African American and white females. However, in light of the fact that test diets not only differed in calories from saturated fat, but also in cholesterol and P:S ratio, it is not possible to strictly attribute the observed changes in plasma lipid and lipoprotein levels solely to the fat content of in the diets. [See editor’s comments.]  

Gerhard GT, Conner SL, Wander RC et al. Plasma lipid and lipoprotein responsiveness to dietary fat and cholesterol in premenopausal African American and white women. Am J Clin Nutr. 2000;72:56-63.

The study by Gerhard et al. states that it was designed to test effects of dietary fat and cholesterol on plasma lipids and lipoproteins in white and African American premenopausal women. What it in fact tests are changes in a number of dietary factors and the data cannot be simply interpreted as effects of dietary fat. To lower fat intake from 40% of calories to 20% of calories is one thing, to have that change also include changes in dietary fiber, dietary cholesterol, and monounsaturated fat calories is certainly something different. It cannot be concluded that “The 24-h area under the plasma triacylglycerol curve after the test meal was lower after the low-fat diet than after the high-fat diet.” since the effects could have been due to either the lower fat calories (40 to 20% ene), the lower intake of saturated fat calories (20 to 6% ene), the higher fiber intake (2.2 to 3.6 g/MJ), the higher P:S ratio (0.3 to 1.0) or the lower monounsaturated fat calories (14 to 8% ene); or conceivably to all the factors combined. There are many options in interpretation of this study beyond the conventional wisdom, and all options need to receive appropriate consideration in the interpretation of the results.

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Elevated Serum Cholesterol Increases CHD Risk in Young Adults

The relationship between an elevated serum cholesterol and increased CHD risk is firmly established in middle-aged populations. But until now, data on their relationship in young men have been limited. The results from Stamler et al. and McGill et al. suggest that atherogenic lipoprotein profiles and other CHD risk factors play important roles in atherosclerosis progression in young people.

Using data from the Chicago Heart Association Detection Project in Industry (CHA) study, Peoples Gas Company Study (PG), and the Multiple Risk Factor Intervention Trial (MRFIT), 3 long-term prospective epidemiological study data, Stamler et al. were able to show a positive association between high baseline serum cholesterol levels and mortality rates from CHD, MI, CVD, and other causes. The 11,017 males in the CHA study were between 18-39 years at the start of the study and were followed for 25 years. The PG study included 1,266 men between 25-39 years with a 34 year follow-up period. The 69,205 subjects from the MRFIT study were 35 to 39 years old at baseline. The mean follow-up was 16 years. All 3 cohort groups were free of diabetes and history of MI prior to the study.

In all 3 studies, the RR for all causes of death increased with higher serum cholesterol levels. The RR of CHD death was 3.46 in CHA study, 2.15 in PG study, and 3.63 in MRFIT study for people with serum cholesterol level >240 mg/dl. The RR of fatal MI and CVD were 3.99 and 2.18 in the CHA group, 3.22 and 2.10 in the PG group, and 3.47 and 2.87 in the MRFIT group. Also, in the case of subjects with the highest baseline cholesterol level (>280 mg/dl), the RR for CHD was much higher (11.93, 8.06, and 8.09 for CHA, PG, and MRFIT cohorts, respectively) compared to lowest cholesterol group (<160 mg/dl). These data show that younger men with negative lipid profile were more at risk for CHD mortality compared to middle-aged men with elevated plasma cholesterol. Comparison of a 40 mg/dl increase in serum cholesterol between young and middle aged cohorts (40-59 yo) showed higher RR among the younger group, indicating that higher serum cholesterol levels are more harmful against CHD risk in the young men.

Break down of serum cholesterol-CHD death relationships into early and late follow-up periods resulted in no difference in the relationship. In subjects with normal serum cholesterol, the life expectancy was higher by 6.1, 8.7, and 3.8 years (CHA, PG, and MRFIT cohorts, respectively) compared to hypercholesterolemics. And finally, unlike CHD related mortalities, cancer and other non-CVD deaths were not related to baseline cholesterol level in all 3 studies.

In McGill et al.’s study, the researcher determined the relationship between CHD risk factors and atherosclerotic lesion in the left anterior descending coronary artery of 760 decreased young people (ages 15-34 years old). Cause of deaths ranged from homicides, suicides, accidents, and other external causes. Complete postmortem measurement of CHD risk factors; dyslipoproteinemia, smoking, hypertension, obesity, and impaired glucose tolerance levels were available on all subjects. The lesions were classified using AHA lesion classification system, grade 0 representing a normal artery and grade 6 representing a complicated lesion with hematoma, hemorrhage, or thrombosis.

Age and gender were 2 factors that were directly related to the frequency of advanced lesion. For example, only 2.5% of 15-19 year olds had grade 4-5 lesions compared to 20.3% of 30-34 year olds. And in females, the prevalence of grade 4-5 lesions were much less with 7.8% in 30-34 age group and none in 15-19 age group. Racial factors did not alter this trend. The prevalence of atherosclerotic stenosis of >40% was also greatest among older, male cohorts. “Women had no stenosis (>40%) before age 25, and had <50% the prevalence of men in the 30-34 year age group.” The odds ratio of grade 2-3 lesions (1.83, 95% CI of 1.20-2.80), grade 4-5 lesions (2.47, 95% CI of 1.00-6.10), and stenosis (2.80, 95% CI of 1.11-7.03) were much greater in males. Also, the prevalence of advanced lesions (grade 4-5) was 60% higher in men than women. High non-HDL cholesterol concentration was associated with greater odds ratio and prevalence in all categories of atherosclerosis measurements. Smoking and low HDL levels were only associated with greater odds of grade 2-3 lesions. Hypertension and obesity were 2 risk factors associated with greater odds and prevalence of grade 4-5 lesions. 

Results from McGill and colleagues clearly show that dyslipoproteinemia along with smoking, obesity, and hypertension is indeed responsible for early development of lesion in young people. Therefore, initiating preventative measures earlier is warranted rather than having to treat advanced cases of CHD in middle-age people.

Stamler J, Daviglus ML, Garside DB, et al. Relationship of baseline serum cholesterol levels in 3 large cohorts of younger men to long-term coronary, cardiovascular, and all-cause mortality and to longevity. JAMA. 2000;284:311-318.

McGill HC, McMahan CA, Zieske AW, et al. Association of coronary heart disease risk factors with microscopic qualities of coronary atherosclerosis in youth. Circulation. 2000;102-34-379.

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Psyllium Supplement Lowers Lipid and Lipoprotein Concentration

Building on a short-term psyllium study, Anderson et al. tested  psyllium supplement on lipid and lipoprotein levels of 248 healthy adults for a 6-month period. The sthe beneficial effects of psyllium supplement on lipid and lipoprotein levels of 248 healthy adults for a 6-month period. The subjects followed AHA’s Step I diet for 8 wks before randomly being divided into either a placebo or psyllium group. During the 26-wk treatment phase, subjects incorporated 10.2 gm/d of psyllium or microcrystalline cellulose into the Step I diet.

In both study groups plasma total and LDL cholesterol concentrations were decreased by 3.9% and 4.4%, respectively, on the AHA diet. However, compared to the placebo diet, overall improvement in total and LDL cholesterol with psyllium supplement was 4.7% and 6.7%, respectively. Assuming that a 1% reduction in serum total cholesterol is associated with a 2-3% decrease in CHD risk, Anderson et al. concluded that adding 10.2 gm/day of psyllium to the Step I diet could potentially lower CHD risk by 10-15%. The mechanism behind psyllium’s role in lowering serum lipids and lipoproteins is unclear, but the researchers hypothesized that its role in increasing bile acid synthesis and delaying cholesterol absorption may be responsible for reducing serum cholesterol. 

Anderson JW, Davidson MH, Blonde L, et al. Long-term cholesterol-lowering effects of psyllium as an adjunct to diet therapy in the treatment of hypercholesterolemia. Am J Clin Nutr.  2000;71:1433-1438.

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Soy Intake Improves Lipid Profile

Using 13 healthy, premenopausal, normocholesterolemic females, Merz-Demlow et al. examined the effects of soy isoflavone on plasma lipid and lipoprotein levels. They also tested the variance due to the menstrual cycle: early follicular (EF), midfollicular (MF), periovulatory (PO), and midluteal (ML), on plasma lipid concentrations. Not surprisingly, plasma total, HDL, and LDL cholesterol levels varied significantly within the menstrual cycle. During the PO phase, plasma HDL cholesterol levels increased while total cholesterol and LDL cholesterol concentrations declined, most likely due to the estrogen surge. In addition to the hormonal effects on lipid concentrations, consumption of the high-isoflavone diet improved LDL cholesterol levels during the MF and PO phases; the LDL cholesterol was 7.6% and 10% lower in the MF and PO phases, respectively. The changes in HDL and total cholesterol levels with the high-isoflavone intake were less dramatic, but were associated with an improved lipid profile. Plasma TAG levels did not change with either the isoflavone diet or menstrual cycle. Results from this study indicate that soy isoflavones lower plasma LDL cholesterol levels in normocholesterol females.

Merz-Demlow B, Duncan AM, Wangen KE, et al. Soy isoflavones improve plasma lipids in normocholesterolemic, premenopausal women. Am J Clin Nutr. 2000;71:1462-1469.

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Editorial: Breakfast in 2020

I dreamt that in year 2020, I stopped for a quick breakfast of egg and sausage on an English muffin, hash brown potatoes, and glass of milk. The food was fine, but, Ior a quick breakfast of egg and sausage on an English muffin, hash brown potatoes, and glass of milk. The food was fine, but, I was charged $72.54 for breakfast. What an outrage! What happened to America’s low-cost, fast food? Frustrated and irritated, I went looking for answers. Somebody was going to explain why I was paying $72.54 for breakfast. Didn’t they know I was retired, living on a fixed income. After I yelled and screamed, and ranted and raved, some corporate type sat me down and told me the story.

It seems that over the years our national goal of an abundant, affordable food supply had been diverted from the consumer in favor of those with the loudest voices and most coercive tactics. For example, the wheat used to make the English muffin was 20 times the cost at the turn of the century due to the low yield of pest sensitive strains of wheat. Since genetically engineered wheat was banned in the U.S., and couldn’t be imported, grain production on the ever decreasing U.S. agricultural land mass was steadily going down, and getting of poorer and poorer quality. So my little English muffin cost $11.28.

My glass of milk cost $12.88 since there was little milk production in the U.S. and, thanks to the animal rights bunch, all cows were now free to roam the few farms left for dairy production, and by law had to be hand milked. And for sure no one was allowed that artificial hormone to stimulate milk production. Added on top of that was the fat tax, imposed by righteous consumer advocates who wanted to make sure those who sinned paid their dues. And then the cancer tax that another self-important advocate group had used fabricated science to con the government, and many consumers, into believing was true.

The potatoes in my hash browns were all imported due to the demise of the U.S. potato industry following a severe potato blight which wiped out the blight sensitive (no genetically modified resistant strains allowed) strains allowed for U.S. production. The potatoes were now imported from South America but the cost of inspection at the border and the detailed and exhaustive testing for every known human pathogen (required by laws pushed by the food safety advocates) resulted in massive spoilage and refusal of the majority of imports. Oh, and since my hash browns were fried I had to pay the fat tax. Final cost, $14.36.

And the price of eggs had increased a bit too. Thanks to the demands and threats of animal rights groups like PETA, chickens were first given more space (cost increase 20-30%), then the following demand was that only free-range eggs be available in the market place (another 70% increase), and once that was accomplished the animal activists demanded and were awarded with an animal protein tax which, on top of the cholesterol tax, really did help them achieve their goal of imposing a vegetarian life style on everyone. And, since it now required more land, not less, to produce eggs and, since the available land mass for agriculture was disappearing with urban sprawl, egg prices went through the roof. Instead of paying $0.89 a dozen, it was more like $8.90 an egg. And while the consumer kept blaming those dirty rotten egg producers for gouging the market and short supplying the demand, the chickens were said to be happy, and the animal rights gang was euphoric. So to buy it, crack it and cook it, I was charged $12.69.

And finally, the sausage! $21.33! Fat tax, animal protein tax, cancer tax, banned factory farming, banned hog pens, banned breeding pens, banned overfeeding, banned genetic manipulation for disease resistance, limited production land, high cost of imported feed grains, and layer upon layer of oversight and inspection for animal welfare and testing upon testing for food safety. Actually, more people saw that hog, tested that hog and pampered that hog than the number of people who ate that hog.

And then I woke up. What a nightmare! Seemed like every crazy cabal with an agenda had gotten their way making their life-style my life-style. How many more kids would have been hungry if this became true? How many elderly would have food insufficiency if this happened? Surely people wouldn’t sit back and let a bunch of loud, pushy, overbearing, self-appointed, self-righteous anointed few dictate and rule their lives.

And then I read the paper. Distribution of “Unhappy Meals” and gross-out ads in newspapers had finally convinced one large food chain to “require” that their suppliers meet certain guidelines for animal welfare, guidelines which PETA referred to as a “good first step” towards what they consider real change. Another gang has been able to convince the government that spending the last five years and mucho dollars on a food safety plan specific for eggs will have a major impact on health. How about some context on the issues! PETA claims 700,000 members, world-wide, who, along with FARM, and Physicians Committee for Responsible Medicine, and other assorted gangs, have a single goal: stop animal agriculture. Whether it’s food safety, heart disease or cancer risk, obesity, or some other stated risk, the most outrageous claims are fair game to achieve the moralistic end. Of course in a country with 260 million people it means that even if every PETA member lived in the U.S., 259,300,000 individuals are not members of PETA, and many seem very comfortable eating meat and eggs and other nutritious animal products.

Last year there were 74 million cases of food borne illnesses in the U.S., and 300,000 due to Salmonella enteriditis (SE) with some 80% possibly related to eggs. Two facts are noteworthy. The egg industry has, on its own, made major advances to lower risk and the effort has resulted in a 48% reduction in the number of SE cases over the last four years. And while risk assessments and public meetings and federal announcements and drafted legislation and public comment periods have all been going on for five years, one wonders what will be involved in addressing those other 73,700,000 cases of food borne illness.  

Taxpayer money well spent or a small group of “consumer advocates,” animal rights groups and anti-technology fanatics simply getting an undue amount of attention because they make the most noise? One thing is for sure, by the time these folks get done making all of us live their image of life, our grocery bills will certainly be a bigger chunk of our budget and we will all have a very different dietary pattern. And if you don’t do anything else, I hope you enjoy breakfast while you still can.

Donald J. McNamara, Ph.D.
Executive Editor, Nutrition Close-Up

If you think these comments are just satirical, guess where all this is going:

PETA Statement: October 1999.

“More than 300 demonstrations are planned at McDonald’s restaurants around the world beginning October 16, as PETA launches a new, massive, international campaign against the company. Graphic in-your-face billboards and newspaper advertisements that read, “Do you want fries with that? McCruelty to go,” above a picture of a slaughtered cow’s head will be run to inform consumers about McDonald’s failure to implement basic reforms in the way that animals are raised and killed for its restaurants.”

June 27, 2000 letter to Jack Greenberg, Chief Executive Officer, McDonald’s Corporation.

“At this time, PETA is planning a McDonald’s blitz for the fall. We are developing new advertisements and billboards, and we will be distributing the “Unhappy Meal” in the U.S., in the U.K, and on other continents at schools and McDonald’s restaurants. We also plan to issue an international call to “sponsor a restaurant,” which will involve activists from around the world committing to regular demonstrations at McDonald’s restaurants in their cities, with PETA supplying all materials free of charge. We now have our McDonald’s leaflet produced in six languages. The focus will be on the treatment of animals in the U.S.

As a sign of our good faith, we would be happy to abandon our campaign altogether if you would agree to expeditiously bring McDonald’s egg and pig suppliers up to the U.K. animal welfare standards regarding treatment of laying hens and breeding pigs.”

AP and Reuters Press Releases: 8 September 2000

“PETA faxed a letter to Jack Greenberg, CEO of McDonald’s, commending the corporation’s recent actions. The letter said the group had suspended its campaign “to afford McDonald’s a decent amount of time to make other important changes in line with its public pledge to keep moving forward with animal welfare improvements.”

The letter also included a request for measures that PETA says would relieve chronic leg pain in fowl, as well as a bid for an increase in the number of unannounced audits in slaughter houses. PETA said it would contact fast-food chains Burger King, Wendy’s International and Kentucky Fried Chicken, as well as grocery stores such as Kroger Co, Albertson’s Inc and Safeway Inc, to identify possible new targets for its campaign.”

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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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