Earlier studies have shown that dietary carotenoids
such as lutein and zeaxanthin found in dark green leafy vegetables
and egg yolks may protect older adults from age-related macular
degeneration. And now, according to the results from the Los Angles
Atherorsclerosis Study, lutein may also be beneficial against early
atherosclerosis progression. In this prospective epidemiological
study, Dwyer et al. examined the relationship between changes in
intima-media thickness (IMT) of the common carotid arteries and
plasma lutein levels of 462 employees of a utility company. Dwyer
et al. also investigated the effects of lutein on early atherosclerosis
progression using in-vitro and in-vivo mouse models.
Compared to the baseline carotid IMT values,
carotid IMT levels after 18 months were inversely related to plasma
lutein concentrations. For example, the change in IMT progression
in the highest quintile of lutein was minimal (0.004�0.005 mm)
compared to 0.021�0.005 mm in the lowest lutein quintile. Including
other carotenoids and antioxidants did not attenuate this inverse
association. In addition to the prospective study, Dwyer et al.
also tested the impact of lutein on oxidative modification in an
in-vitro setting using human aorta. The investigators used a cocultured
cell model of the artery wall from endothelial and smooth muscle
cells. Based on the coculture cell model of LDL oxidation using
2 types of chemotaxis assays, lutein was shown to reduce the LDL-mediated
monocyte migration. In other words, "lutein inhibited the inflammatory
response of monocytes to LDL trapped in the artery wall." The results
clearly showed that a lutein concentration of 100 nmol/l was as
effective as human HDL cholesterol in inhibiting monocyte migration.
In the in-vivo mouse component of the study,
the researchers noted that mice feed a lutein supplemented (0.2%
by weight) chow had liver lutein levels that were nearly twice
as much as the mice without lutein supplement (0.0035 � 0.0022
mmol/g vs. 0.0018 � 0.0011 mmmol/g). Also, after 8 weeks of study,
the atherosclerotic lesion size in the aorta arch of lutein supplemented
mice was 86% less (0.6 � 0.7 x 106 vs. 4.2 � 1.8 x 106 mm2)
than the control mice. The apo E-null mice used in the study were
selected since they lack apo E and develop severe atherosclerotic
lesions similar to human arterial lesions.
By combining epidemiological studies with
in-vitro and mouse model studies, Dwyer et al. were able to show
that high lutein levels, regardless of whether in the blood or
in a petri dish, is critical in reducing atherosclerosis progression
in humans and animals. As in the case with lutein's role in protecting
against macular degeneration by preventing oxidative damage to
the retina, it was thought that high lutein levels may protect
against heart attacks and strokes by neutralize oxidative stressors
from narrowing arteries. Also, the results from this study showed
that increased intake of lutein resulted in elevated liver lutein
levels in mice.
Dwyer JH, Navab M, Dwyer KM, et al. Oxygenated
caroteinoid lutein and progression of early atherosclerosis. The
Los Angeles Atherosclerosis Study. Circulation. 2001;103:2922-2927.
According to Handelman et al. and
Sommerburg et al., egg yolks are good sources of lutein
and zeaxanthin. Also, compared to green leafy vegetables,
other sources of lutein, lutein in egg yolks have higher
bioavailablity due to natural fats found in egg yolks.
Handelman GJ, Nightingale ZD,
Lichtenstein AH, et al. Lutein and zeaxanthin concentrations
in plasma after dietary supplementation with egg yolk. Am
J Clin Nutr. 1999;70:247-251. Sommerburg,
Keunen, Bird, et al. Fruits and vegetables that are
sources for lutein and zeaxanthin: the macular pigment
in human eyes. Br J Ophthalmol. 1998;82:907-910.
- After 18 months of study, the carotid arteries of subjects
with highest baseline plasma lutein levels were unchanged while
the subjects with lowest plasma lutein levels showed thickening
of their carotid arteries.
- Compared to the control mice, mice that were fed lutein supplemented
feed doubled their liver lutein concentration.
- In mice engineered to develop artery disease, those given lutein-supplemented
diets showed significantly smaller artery-clogging plaques.
- Treating artery-wall cells with lutein reduced the oxidation
of LDL cholesterol.
Table of Contents
Obesity is a growing health problem here in
the US. But the prevalence of obesity is especially high among
African American (AA) women. Based on this knowledge, Lovejoy et
al. recruited 97 pre-menopausal AA women and 52 pre-menopausal
white women from Baton Rough, Louisiana area to test ethnic differences
in dietary intakes, physical activity, and energy expenditure.
Four day food records were used to collect food intake. The subject's
physical activity levels were measured using a triaxial motion
sensor and a validated physical-activities-recall questionnaire.
And energy expenditure was determined by whole-room calorimeter
in 56 women (12 African American and 44 whites).
Compared to the Caucasian women, the AA women
were taller and heavier than white women. Also, the BMI, fat mass,
lean mass, and percent body fat were significantly higher in blacks.
However, dietary records showed that AA women consumed slightly
fewer calories compared to their white counter part (1,611 kcal
vs. 1,689 kcal). The only significant differences in intake of
macro and micronutrients between the 2 study groups were protein,
fiber, calcium, magnesium, and PUFA. The white women consumed more
protein, fiber, calcium, and magnesium and the black women consumed
more PUFA (linoleic, arachidonic, eicosapentanoic, and gadoleic
acids). Of these nutrients, fiber, calcium, magnesium, eicosapentanoic,
and docosahexanoic acid were inversely correlated with body fat
and BMI. And total fat, saturated fat, MUFA, cholesterol were positively
correlated with 2 measures of obesity. No difference in this correlation
was noted between the study groups. The researchers concluded that
dietary fiber intake was the strongest independent predictor of
percent body fat with RR of 0.12, followed by exercise (RR=0.09)
and saturated fat (RR=0.07).
Results of measured physical activity and
energy expenditures showed that the AA women reported that they
climbed fewer flights of stairs, stood less, and participated in
fewer leisure activities than did white women. But according to
triaxial accelerometer, both groups expended similar calories (white=2,060
kcal/d and black=2,030 kcal/d). The whole-room calorimeter showed
that except for lower basal metabolism in AA women, both groups
expended similar total calories in 24-hour period.
From this study, Lovejoy et al. found that
there are several ethnic differences that may account for the higher
prevalence of obesity among AA women. For example, the AA women
ate less protein and fiber, nutrients shown to increase thermogenesis
and satiety, and ate more of certain types of fat. Also, compared
to the white cohort, the AA women had lower basal metabolism and
they tended to report that they were less active even though triaxial
accelerometer showed that they were as physically active as their
white counter parts.
Lovejoy JC, Champagne CM, Smith SR, et al.
Ethnic differences in dietary intakes, physical activity, and energy
expenditure in middle-aged, premenopausal women: the Healthy Transitions
Study. Am J Clin Nutr. 2001;74:90-95.
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Ever since the 1980s, doctors have been using
statin drugs to reduce plasma LDL cholesterol in hypercholesterolemic
individuals. But now, according to Ridker et al. and Jialal et
al., statin therapy may also be effective in lowering C-reactive
protein levels. Ridker et al. showed that lovastatin lowered C-reactive
protein levels in people who do not have overt hyperlipidemia.
And since 50% of all coronary events occur in individuals with
normal plasma cholesterol levels, this additional benefit of statin
therapy may further reduce CHD events by lowering C-reactive protein,
an emerging CHD risk factor. The 5,742 participants enrolled in
this study were part of the Air Force/ Texas Coronary Atherosclerosis
Prevention Study, which looked at the effects of lovastatin (n=2,885)
in preventing primary acute coronary events. The subjects in the
lovastatin group with LDL cholesterol levels of <110
mg/dl took 20 mg/day of lovastatin, while individuals with LDL
cholesterol >110 mg/dl took 40 mg/day of lovastatin.
Based on C-reactive protein measurements from
baseline and 1 year follow-up, the researchers determined that
statin use significantly lowered C-reactive protein levels compared
to the placebo group. For example, the median C-reactive protein
levels in the statin group were 14.8% lower at 1-year follow-up
compared to baseline. No change was noted in the placebo group.
Also, as expected, regardless of therapy regimen, the subjects
with higher C-reactive protein levels were more likely to experience
CHD events. The odds ratios were 1.0, 1.2, 1.3, and 1.7 across
the quartiles for C-reactive protein.
This study found that baseline C-reactive
protein and plasma lipid levels were not related and the beneficial
effects of lovastatin on C-reactive protein and lipid levels were
through different mechanism. Unlike the hydroxymethylglutaryl coenzyme
A reductase inhibition involved in lowering LDL levels, it was
thought that statin's anti-inflammatory properties were involved
in lowering C-reactive protein levels. However, when the researchers
separately analyzed the relationship between lovastatin, C-reactive
protein, and LDL cholesterol, they found that lovastatin was clinically
effective in lowering acute coronary events in individuals with
LDL levels higher than the median, regardless of C-reactive protein
levels (RR=0.53), and in individuals with elevated C-reactive protein
(RR=0.58). But among the subjects with both low LDL cholesterol
and C-reactive protein levels, lovastatin therapy did not lower
CHD events (RR=1.08). Also, it was shown that lovastain use was
not beneficial in the subjects with both total to HDL cholesterol
ratios and C-reactive protein levels lower than the median, but
it was beneficial in the subjects with low total to HDL cholesterol
ratio and high C-reactive protein.
By showing that lovastatin therapy can lower
C-reactive protein levels by 14.8%, independent of its beneficial
effect on lipids, Ridker et al. were able to suggest that using "statin
therapy may be clinically effective in persons without hyperlipidemia
and suggest that evaluation of the C-reactive protein level may
provide a method for the appropriate targeting of statin therapy
for primary prevention."
In a randomized, double-blind, crossover study,
Jialal et al. showed that taking 3 statins, simvastatin (20 mg/d),
pravastatin (40 mg/d), and atorvastatin (10 mg/d) for 6 weeks each,
lowered C-reactive protein levels of 22 combined hyperlipidemic
individuals. Compared to baseline C-reactive protein levels of
2.6 mg/l, the median C-reactive protein levels after simvastatin
were 1.7 mg/l, after pravastatin 1.9 mg/l, and after atorvastatin
1.7 mg/l. In addition to lowering C-reactive protein levels, the
3 statins were equally effective in reducing total and LDL cholesterol
levels. On the other hand, reductions in plasma TAG were only significant
with simvastatin and atorvastatin. The plasma HDL cholesterol level
was relatively unaffected by statin use. During the 3-week washout
period between statins, C-reactive levels did not increase but
lipid levels did increase.
The researchers also measured plasma interleukin-6
and interleukin-6 soluble receptor levels. But contrary to their
study theory, statin use did not lower either plasma interleukin-6
or interleukin-6 soluble receptor levels from baseline. These data
suggest that statins may be lowering C-reactive protein levels
through interleukin-6 independent mechanism or that the current
study size is not large enough to detect differences and more study
is needed. Regardless of the mechanism by which statins lower C-reactive
protein levels, these studies clearly indicate that statins are
effective in lowering CHD risk by lowering both LDL cholesterol
and C-reactive protein levels.
Jialal I, Stein D, Balis D, et al. Effect
of hydroxymethylglutaryl coenzyme A reductase inhibitor therapy
on high sensitive C-reactive protein levels. Circulation.
Ridker PM, Rifai N, Clearfield M, et al. Measurement
of C-reactive protein for the targeting of statin therapy in the
primary prevention of acute coronary events. N Engl J Med. 2001;344:1959-1965.
Table of Contents
According to researchers worldwide, incidence
of diabetes mellitus has reached an epidemic level. Here in the
US, it is estimated that approximately 16 million people have diabetes.
Sedentary lifestyle and obesity are 2 major factors commonly blamed
for this problem. In this Finnish Diabetes Prevention Study, Tuomilehto
et al. tested the effects of positive lifestyle changes on diabetes
prevention in 522 middle-aged subjects (172 men and 350 women).
All enrolled subjects had abnormal glucose metabolism as noted
by elevated plasma glucose concentrations of 140-200 mg/dl 2 hour
after an oral glucose tolerance test. The subjects were randomly
divided into either an intervention or a control group. Compared
to the control group, who received minimal training on a healthy
diet and exercise program, the intervention group received detailed
advice on how to achieve 5 goals of the study: lower total dietary
fat to less than 30% of calories, saturated fat to less than 10%
of calories, increase fiber intake to 15 gm/1,000 kcal, exercise
for a minimal 30 minutes/day, and lose weight by 5% or more. These
behavior changes were taught by nutritionist and fitness professionals
during regular intervention sessions during the follow-up period.
After 1 year of follow-up, the subjects in
the intervention group lost 9.2 pounds (4.7�5.4%) while the control
group only lost 1.8 pounds (0.9�4.2%). All other study parameters,
such as waist circumference, blood glucose and insulin levels,
were improved in the intervention group. After the 2nd year, on
average, the intervention group lost 7.7 pounds, fasting plasma
glucose concentrations decreased by 2�12 mg/dl, and plasma glucose
levels following a 2 hour oral glucose challenge decreased by 14�37
mg/dl compared to a weight loss of 1.8 pounds and increase in fasting
plasma glucose (3�14 mg/dl) and plasma glucose concentration following
oral glucose challenge (0�0.44 mg/dl) in the control group.
During the mean follow-up of 3.2 years, 86
individuals developed diabetes, 27 in the intervention group and
59 in the control group. The researchers also determined that,
compared to the control group, the subjects in the intervention
group were 58% less likely to develop diabetes. There was a slight
gender difference in this relationship. The incidence of diabetes
was 63% lower among men in the intervention group and 54% lower
among women in the intervention group. Separate analysis of the
number of goals achieved by study cohort found an inverse relationship
between behavior change and the incidence of diabetes. Regardless
of the study group, the subjects who achieved either four or five
of the study goals did not develop diabetes, while 38% of subjects
in the intervention group and 31% of subjects in the control group
who achieved none of the goals developed diabetes.
In conclusion, results from this study clearly
show that positive lifestyles are important factor in preventing
type 2 diabetes mellitus in high-risk population. And based on
this outcome, the current Dietary Guideline recommendations of
limiting total and saturated fat, and maintaining desirable body
weight as well as including daily moderate physical activity are
appropriate public health messages in protecting Americans from
Tuomilehto J, Lindstrom J, Eriksson JG, et
al. Prevention of type 2 diabetes mellitus by changes in lifestyle
among subjects with impaired glucose tolerance. N Engl J Med. 2001;344:1343-1350.
Table of Contents
Based on the theory that oxidized low density
lipoprotein (ox-LDL) is involved in the genesis of the inflammatory
process in atherosclerotic lesions, Ehara et al. tested the relationship
between ox-LDL levels and severity of acute coronary syndromes.
Ox-LDL levels were measured using a sandwich ELISA method, which
used an "anti-ox-LDL monoclonal antibody and an apo B polyclonal
antibody to measure ox-LDL in calculating LDL fractions of blood
plasma." The data indicate that ox-LDL is directly related to the
severity of coronary syndrome.
The first part of the study involved measuring
ox-LDL levels of 4 patient groups; acute myocardial infarction
(AMI, n=45), unstable angina pectoris (UAP, n=45), stable angina
pectoris (SAP, n=45), and controls (n=46). The results showed that
ox-LDL levels in patients with AMI were significantly higher than
in the other 3 groups. Ox-LDL levels were 1.95�1.42 ng/5 mg of
LDL protein in the AMI group compared to 1.19�0.74, 0.89�0.48,
and 0.58�0.23 in the UAP, SAP, and controls, respectively. All
other CVD risk factors, except hypertension, were similar among
the test groups. Surprisingly, the AMI group was the least hypertensive.
In the second phase of the study, coronary
atherectomy samples from 33 different patients (10 SAP and 23 UAP)
were studied for ox-LDL levels. The ox-LDL-positive macrophage
score was significantly higher in patients with UAP than in patients
with SAP. Immuno-histochemical quantification of the lesions in
the UAP patients showed abundant ox-LDL deposits in macrophage
derived foam cells.
In conclusion, using a sensitive sandwich
ELISA method, Ehara et al. showed that elevated ox-LDL levels is
associated with acute coronary syndrome since it represents "plaque
instability in human coronary."
Ehara S, Ueda M, Naruko T, et al. Elevated
levels of oxidized low density lipoprotein show a positive relationship
with the severity of acute coronary syndromes. Circulation. 2001;103:1955-1960.
Table of Contents
Unlike CHD, the association between stroke
risk and blood cholesterol levels is less firmly established. Using
volunteers from the Northern Manhattan area in New York, Sacco
et al. examined the association of specific lipoprotein classes
and ischemic stroke. The researchers selected this setting due
to the high concentration of Hispanic and African-Americans, 2
ethnic groups with high incidences of stroke. Of the 539 case subjects,
53% were Hispanic, 28% Black, and 19% Caucasian. Nine hundred and
five stroke-free subjects, matched by age and sex, were from the
same neighborhood. The study cohort included a large number of
elderly (67% were 65 yo) who are more prone to stroke.
Analysis of plasma lipoprotein concentrations
of both cases and controls indicated that, except for HDL cholesterol
and TAG, the median total and LDL cholesterol levels were significantly
lower in the cases than the controls. For example, the median total,
and LDL cholesterol concentrations were 191 mg/dl and 121 mg/dl,
respectively, in the cases, while the control group's levels were
201 mg/dl, and 126 mg/dl, respectively. Closer look at the difference
in HDL cholesterol in the 2 study groups showed that the control
group was two times more likely to have HDL cholesterol levels
greater than 50 mg/dl. And compared to the subjects with HDL cholesterol
levels of 35-49 mg/dl, the subjects with HDL cholesterol of �50
gm/dl lowered their stroke risk by half. The odds ratio for stroke
in the highest HDL cholesterol group (�50 mg/dl) was 0.29 compared
to 0.65 in the group with HDL cholesterol levels of 35-49 mg/dl.
Including LDL and other CHD risk factors in the analysis did not
dramatically change the odds ratio. Every 5 mg/dl increase in HDL
cholesterol was shown to lower stroke risk by 19%.
Regardless of race, ethnicity, or sex, a high
HDL cholesterol concentration was associated with fewer cases of
stroke, but it was especially beneficial among people over the
age of 65. This study also found that the protective effect of
HDL cholesterol was more pronounced for the atherosclerotic stroke
subtypes which stemmed from extracranial or intracranial atherosclerosis
than the nonatherosclerotic subtypes (cardioembolism).
According to Sacco et al.'s findings, high
HDL cholesterol levels are effective in protecting minorities and
elderly, high-risk populations, against atherosclerotic strokes.
Possible mechanisms behind HDL cholesterol's role in preventing
stoke are through increased reverse transport of cholesterol from
peripheral tissues to the liver or transport of antioxidants to
LDL and therefore less oxidation of LDL. Lastly, many studies have
shown that exercise, moderate alcohol consumption, weight loss,
and smoking cessation can raise blood HDL cholesterol levels, therefore,
these behavior modifications can potentially lead to lowering stroke
Sacco RL, Benson, RT, Kargman DE, et al. High-density
lipoprotein cholesterol and ischemic stroke in the elderly. JAMA.
Table of Contents
Due to shared genetic and environmental factors,
a family history of premature MI has long been considered an important
CVD risk factor. But actual data on the association between parental
history of MI and their child's potential CVD risk is limited in
women. Also, earlier epidemiological studies tended to lump both
parents together rather than analyzing the impact of paternal and
maternal history of MI separately, to their offspring's CVD risk.
Therefore, using 2 large prospective studies, the Physicians' Health
Study (PHS) and Women's Health Study (WHS), Sesso et al. investigated
the effects of maternal and paternal history of MI on their offspring's
Men from the PHS (n=20,515) and 37,985 women
from the WHS were followed for a median of 13 years and 6 years,
respectively, during which time 2,654 cases of CVD were reported
in men and 563 in women. Based on self-reported data, 65.5% of
men had no parental history of MI and 65.9% of women had no parental
history of MI. For those with parental histories of MI 5.6%, 25.3%,
and 3.5% of men had only a maternal history, only a paternal history,
and a history of both parents, respectively. Similar percentages
of women had only a maternal history of MI (7.9%), only a paternal
history of MI (21.8%), and both parents with MI (4.4%).
According to the data, compared to the group
with only a paternal history of MI, the groups with only a maternal
history of MI and both parents with MI experienced total CVD, MI,
and stroke more often. However, these groups were older and more
hypertensive than the group with only a paternal history of MI.
The RR for CVD was 1.71, 1.40, and 1.85 in men with only maternal,
only paternal, and both maternal and paternal history of MI, respectively;
among women, it was 1.46, 1.15, and 2.05, respectively. Maternal
history of MI was a better predictor of CVD risk in men than women
and it predicted MI risk better than stroke.
When the researchers included the age at which
parents suffered MI, it was shown that maternal history of MI had
a stronger association with their offspring's CVD risk than paternal
history of MI. In men, the RR for CVD was 1.0, 1.88, 1.88, 1.67,
and 1.17 for maternal age at MI of <50, 50-59, 60-69, 70-79,
and >80 years, respectively. In women, the RR for CVD
was 2.57, 1.33, and 1.52 for maternal age at MI of <50,
50-59, and >60 years. On the other hand, except for the
case of paternal age at MI of <50 years, maternal history of
MI at any age had stronger association with CVD risk than paternal
history of MI. For example, the RR for CVD in men with paternal
MI at 50-59, 60-69, 70-79, and >80 year old was 1.64,
1.42, 1.16, and 0.92, respectively, and in women, it was 1.33 and
1.13 at 50-59 and >60 years old.
In conclusion, results from this study suggest
that in men and women with mothers who suffered MI at any age or
either parent who suffered MI before the age of 60 were much more
likely to develop CVD than their counter parts with healthy parents. Sesso
et al. postulated that in addition to passing on genetic traits,
mothers also has a greater influence on their child's dietary and
behavioral pattern which will impact their risk of CVD later in
Sesso HD, Lee I, Gaziano M, et al. Maternal
and paternal history of myocardial infarction and risk of cardiovascular
disease in men and women. Circulation. 2001;104:393-398.
Table of Contents
Researchers have long considered high waist-to-hip
ratio (WHR) a good indicator of abdominal obesity and therefore
a predictor of CVD risk. But since "waist and hip circumferences
measure different aspects of body composition and fat distribution
and have independent and often opposite effects on CVD risk factors," WHR
may not accurately reflect CVD risk. Using anthropometric, abdominal
fat distribution, and percent body fat measurements of 313 men
and 382 women in the Quebec Family Study, Seidell et al. tested
the association between waist and hip circumferences and CVD risk.
BMI and WHR were calculated as well as data for blood pressure,
glucose and insulin concentrations, and fasting blood lipids at
Compared to the WHR, waist circumference and
BMI had stronger correlations with fat mass and fat-free mass.
WHR showed stronger positive correlations with plasma total cholesterol,
LDL cholesterol, and TAG concentrations. A negative correlation
was noted between HDL cholesterol and WHR. In men, WHR was better
than waist circumference in determining CVD risk. In women, WHR
and waist circumference were similar in predicting CVD risk.
Separate analysis of these 2 girth measurements
showed that waist circumference was independently related to plasma
HDL cholesterol and glucose concentrations, and hip circumference
was negatively associated with TAG and insulin concentrations,
in men and women. In women, waist circumference was also associated
with LDL cholesterol and blood pressure. The hip circumference
was negatively associated with HDL cholesterol and glucose concentrations.
Researchers noted that increased waist and
hip circumference was associated with higher total body fat and
fat-free mass. Hip circumference was associated with decreased
visceral fat and increased subcutaneous abdominal fat in men. Finally,
the association of fat mass and fat-free mass with CVD risk factors
showed that increased fat mass was associated with unfavorable
Results from this study show that a larger
waistline and small hip size increases CVD risk by lowering HDL
cholesterol while raising TAG, insulin levels, and visceral fat
mass. And this independent and opposite effect of waist and hip
circumferences on CVD risk shows that WHR does not measure visceral
fat accumulation as once thought and therefore using WHR in determining
CVD risk has limitations.
Seidell JC, Perusse L, Despres J, et al. Waist
and hip circumferences have independent and opposite effects on
cardiovascular disease risk factors: the Quebec Family Study. Am
J Clin Nutr. 2001; 74:315-321.
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The rantings of a science and policy critic
sometimes cover too wide a range of topics; from big issues wghts
of chronic irritants. To wit, some ramblings about diets, health,
activists, and otheith big questions to just random thoughts of
chronic irritants. To wit, some ramblings about diets, health,
activists, and other misdirections of life.
In a fit of "I know what I know, don't confuse
me with facts" insight, the government has decided that a Step
II diet (now called the "Therapeutic Lifestyle Change" diet, TLC
!) is the way for 50-60 million people to lower heart disease risk.
So, using the best available data from meta-analyses, let's just
see what the actual cholesterol-lowering benefits will be. Changing
the diet from <10% calories fromsaturated fat to <7%, and
changing dietary cholesterol from <300 to <200 mg/day will,
on average, lower plasma cholesterol levels by a whopping, stunning,
spectacular, incredible ****8-10 mg/dl**** [6 mg/dl from the saturated
fat reduction, 2 mg/dl from the dietary cholesterol reduction].
Of course the promised decrease is 11-15%. Oh, and they want you
to add stanol ester containing margarines to your diet to help
it along in its quest to lower that LDL level.
Speaking of dietary recommendations, why is
it that if you get your research funding from a grain/fruit/vegetable
company or stanol margarine company or a statin drug company, you
are credible and honest; yet if funded from an animal commodity
it is automatic that you have no integrity and publish phony data.
When sugar-coated whole-grain whatever cereal is touted as the
greatest cholesterol lowering agent next to a hepatectomy, no one
is concerned that the study was funded by the sugar-coated whole-grain
whatever cereal company. Publish a study saying that eating meat
will not cause instantaneous and horrific death and you'll hear
every advocacy ["food police"] group in the country screaming "INDUSTRY
FUNDED RESEARCH, INDUSTRY FUNDED RESEARCH," even if the study was
funded by the petroleum industry.
And speaking of cereals, why is it that we
promote fortified cereals while at the same time telling consumers
to get their vitamins and minerals from real foods, not supplements.
If it comes sprayed on sugar-coated whole-grain whatever cereal
is that better than if it comes in a gelatin capsule? Don't eat
meat as a source of heme-iron but eat iron supplemented sugar-coated
whole-grain whatever cereal and there's no need for supplements!
I obviously need someone to explain this to me since I sure am
confused on the concept.
And in my quest to get nutrients from real
food, I'm quickly running out of fast food chains I can patronize.
First McDonalds buckled and now Burger King and Wendy's have succumbed
to the PETA campaigns. How can 700,000 members of PETA dictate
what 279,300,000 people are going to be paying for their burger
and fries? And when PETA is done with this round of "Do it my way
or I'll scare away your customers" it will return for round two
demanding even more changes with associated cost inflation until
their ultimate goal is reached: you simply cannot afford to eat
animal products because the rules and regulations and demands have
priced them out of reach. Success at last, a vegetarian country,
not by our personal choice but by fiat of a small and vocal group.
It seems that our lives are dictated by the "Precautionary
Principle" [elimination of any substances or technology which cannot
be proven to be absolutely safe]. No GM foods, no irradiation,
no science, no technology. I guess we should all be thankful that
this approach to technological advancements is a modern millstone.
Think of applying the "Precautionary Principal" to electricity,
automobiles, airplanes, vaccinations, surgery, chemotherapy, etc.,
etc, etc. Think what would have happened if the "Precautionary
Principal" had been applied by the first person who thought about
eating a lobster! The anti-science/anti-technology forces use the "it
might be hazardous" slogan to block almost everything, and then,
if I cannot make it or test it or evaluate it, how can I prove
its safe, and then clearly it must have been dangerous or else
I would be selling it. Circular reasoning leading to walking in
circles. More success for the intimidators.
And one last suggestion for those of you tired
of advocacy groups determining your life style, and what is and
is not acceptable, and how you will or will not be allowed to live
your life, while at the same time always asking for your financial
support. You know those postage paid envelopes enclosed to make
it easier to send in your support dollars for their agendas, mail
them back empty! Let'em pay the postage, make a dent in the schema.
Giant strides through small steps, especially if you're tired of
letting the noisy few dictate with corporate intimidation and constant
hounding of government agencies the way you live, or, as seems
more evident daily, the way they'll allow you to live.
[For those interested in the anti-nanny state
I recommend Say No to the Nanny Culture.Com (www.guestchoice.com)
for daily updates on just how out of control the system is getting.]
Donald J. McNamara, Ph.D.
Executive Editor, Nutrition Close-Up
Table of Contents