Newsletters & Publications

Lutein Delays Early Atherosclerosis Progression

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.

Key Messages

• 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

Ethnic Differences in Energy Expenditure and Food Intake in Women

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.

Table of Contents

Statin Therapy Lowers C-reactive Protein Levels

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. 2001;103:1933-1935.

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

Positive Lifestyle Changes Prevent Type 2 Diabetes in High Risk Group

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 chronic illnesses. 

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

Direct Relationship Noted Between Oxidized LDL and Severity of Acute Coronary Syndromes

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

HDL Cholesterol Lowers Ischemic Stroke Risk Among Minorities and Elderly

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 ³50 gm/dl lowered their stroke risk by half. The odds ratio for stroke in the highest HDL cholesterol group (³50 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 events. 

Sacco RL, Benson, RT, Kargman DE, et al. High-density lipoprotein cholesterol and ischemic stroke in the elderly. JAMA. 2001;285:2729-2735.

Table of Contents

Maternal History of MI has Stronger Impact on Their Offspring's CVD Risk

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 CVD risk.

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 life. 

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

Large Waistline and Small Hip Size Increases CVD Risk

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 baseline.

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 risk factors.

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.

Table of Contents

Editorial: But Then I Could Be Wrong

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