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Newsletters & Publications
| Volume
17 - Number 3 |
Fall 2000 |
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
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
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.
Table of Contents
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.
Table of Contents
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.
EDITOR'S COMMENTS
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. |
Table of Contents
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.
Table of Contents
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.
Table of Contents
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.
Table of Contents
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." |
Table of Contents
 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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