Newsletters & Publications
17 - Number 1
BMI: body mass index (kg/m2)
CAD: coronary artery disease
CHD: coronary heart disease
CI: confidence interval
CVD: cardiovascular disease
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
VLDL: very low density lipoprotein
Recent outcomes following a high-MUFA diet
have lead scientists to question the efficacy of low-fat, high-CHO
diet as the primary dietary method in preventing and treating CVD.
According to Kris-Etherton et al., a high MUFA diet is as effective
as the NCEP Step II diet in lowering both plasma total and LDL
cholesterol levels without negatively altering the plasma HDL cholesterol
and TAG concentrations as seen with the NCEP's Step II diet.
In this 5-period cross-over study, 22 subjects
consumed an Average American Diet (AAD), NCEP Step II diet, olive
oil diet (OO), peanut oil diet (PO), and peanut and peanut butter
diet (PPB) for 24 days each. The AAD consisted of 50% of calories
as CHO, 16% protein, 34% fat, 16% SFA, 11% MUFA, 7% PUFA, and 400
mg/d cholesterol and served as the reference diet to compare the
changes in lipid and lipoprotein levels with the 4 cholesterol-lowering
diets. The NCEP step II diet provided 7% of energy as SFA, 25%
from fat, 59% CHO, and 200 mg/d cholesterol. The 3 high MUFA diets
maintained the same amount of SFA as the NCEP diet, however some
CHO energy was replaced with MUFAs. The percent of MUFA in OO,
PO, and PPB diets were 21%, 17%, and 18%, respectively. The total
fat in the diet was similar to the AAD diet at 35% of calories.
to lipid and lipoprotein levels following the AAD phase, the
plasma cholesterol level improved after all 4 test diets. For
example, plasma total cholesterol levels decreased by 9% on the
Step II diet, 11% on the OO diet, 9% on the PO diet, and 11%
on the PPB diet from an average total cholesterol level of 209
mg/dl on the AAD. The average LDL cholesterol levels decreased
by approximately 14% following the 4 cholesterol lowering
diets compared to the AAD. However, the 11% increase in TAG and
4% decrease in HDL levels following the Step II diets differed
from the 13% decrease in TAG levels and no net change in HDL
cholesterol following the 3 high-MUFA diets. Also, plasma Lp(a)
was highest with the Step II diet. The degree of change in plasma
lipids was directly associated with the baseline LDL cholesterol
Finally, by using the following estimate, "a
1% decrease in LDL cholesterol decrease CVD risk by 1.5%, a 1 mg/dl
(0.026 mmol/l) decrease in HDL cholesterol increase CVD risk by
2-3%, and a 89 mg/dl (1 mmol/l) increase in triacylglycerol increases
CVD risk by 25%," from earlier studies, the researchers were able
to determine improvement in CVD risks associated with different
test diets. For example, based on these estimates, the researchers
predicted that the OO diet would result in the largest reduction
in CVD risk of 25%, compared to 16% and 21% with the PO and PPB
diets. On the other hand, as a result of an increase in TAG and
decrease in HDL cholesterol, the net decrease in CVD risk on the
Step II diet was only 12%. These data suggest that high-MUFA diets
are more effective in lowering CVD risk than the more commonly
recommended Step II diet.
Current evidence strongly suggests that diets high in MUFA are superior
to a low-fat, high-CHO diet in reducing CVD risk. Even though the NCEP
Step II diet is often recommended for preventing and treating CVD, because
of its negative impact on plasma TAG and HDL levels associated with replacing
fat with CHO calories, its suitability and efficacy needs to be re-evaluated.
The data from this study indicate that olive oil is more beneficial than
either peanut oil or peanut and peanut butter, however, these products
can offer alternative foods as a means to increase the level of MUFA
in the diet.
Lipid and lipoprotein changes (%) compared to Average American Diet
|Total Cholesterol (mg/dl)
Kris-Etherton PM, Pearson TA, Wan Y et al.
High-monounsaturated fatty acid diets lower both plasma cholesterol
and triacylglycerol concentrations. Am J Clin Nutr. 1999;70:1009-1015.
- Plasma total cholesterol decreased by 9% on the Step II diet,
11% on the olive oil diet, 9% on the peanut oil diet, and 11%
on the peanut and peanut butter diet.
- TAG increased by 11% and HDL cholesterol decreased by 4% following
the Step II diet compared to 13% decrease in TAG and no change
in HDL cholesterol with 3 high- MUFA diets.
- The OO diet, PO diet, and PPB diet lowered CVD risk by 25%,
16%, and 21%, respectively, compared to 12% reduction with the
Step II diet.
Table of Contents
The prevalence of cigarette smoking is at
an all time high in Asian populations. It is estimated that 72%
of Korean men, 50% of Chinese men, and 58% of Japanese men are
current smokers. This is a frightening statistic in light of the
fact that smoking is considered the number one risk factor for
CVD. Even though Asians typically have lower plasma cholesterol
levels than Westerners, according to Jee et al., a lower cholesterol
level does not seem to protect against smoke related CVD. For example,
based on data from 106,745 middle-aged Korean men enrolled in the
Korean Medical Insurance Corporation (KMIC) between 1990 and 1992,
smoking was a major independent risk factor for ischemic heart
disease (IHD), stroke, and atherosclerotic cardiovascular disease
(ASCVD). The majority (93%) of the subjects had blood cholesterol
levels below 239 mg/dl.
During the 6-year follow-up period, 3,086
cases of fatal and non-fatal ASCVD events were noted. It broke
down into 1,006 cases of nonfatal IHD events, 1,364 cases of nonfatal
stroke, 716 cases of nonfatal ASCVD, 131 cases of fatal IHD, 270
cases of fatal stroke, and 168 cases of fatal ASCVD. The multivariate
RR for IHD, stroke, and ASCVD were 2.2, 1.6, and 1.6 for smokers
compared to nonsmokers. The ex-smokers fared slightly better than
current smokers with RR values of 2.2, 1.1, and 1.3 for IHD, stroke,
and ASCVD, respectively. Also, as expected, people who smoked a
greater number of cigarettes per day and for a greater number of
years had higher risk of both IHD and stroke. However, no such
noticeable trend occurred with different levels of baseline plasma
total cholesterol concentrations. For example, the RR for IHD was
3.3 in the group with the lowest plasma total cholesterol compared
to 2 in those with the highest plasma total cholesterol.
In conclusion, despite mixed earlier findings,
current data indicate that smoking does increase both stroke and
CVD risk among middle aged, normocholesterolemic Korean men. And
in light of this result, it would be prudent to recommend that
everyone, including those with normal plasma cholesterol levels,
to either abstain from smoking or at the very least reduce the
number of cigarettes smoked per day.
Jee SH, Suh I, Kim IS, et al. Smoking and
atherosclerotic cardiovascular disease in men with low levels of
serum. The Korea Medical Insurance Corporation Study. JAMA.
Table of Contents
We know that excess body weight is associated
with many chronic health problems. But now, thanks to a study by
Must et al., we have a much clearer perspective of the health impact
of overweight and obesity on the US population. By using results
from the third National Health and Nutrition Examination Survey
(NHANES III), the researchers analyzed the relationship between
BMI and morbidities associated with CHD, blood pressure, blood
cholesterol levels, type 2 diabetes, gall bladder disease, and
osteoarthritis in people over 25 years old.
According to this survey, which included 16,884
subjects, 63% of males and 55% of females in the US are either
overweight or obese. This problem was equally common among all
ethnic and racial groups. And as expected, body weight was directly
associated with prevalence of type 2 diabetes, gallbladder disease,
osteoarthritis, and hypertension. As for blood cholesterol levels,
values were higher in the overweight and obese groups than the
normal weight group, however, it did not seem to increase proportionately
with further weight.
Regardless of weight categories, the prevalence
ratio for all study outcomes was much greater in the younger group
than in people 55 years or older. For example, the prevalence ratio
for type 2 diabetes in overweight men under 55 years was 3.27 compared
to 1.77 in the older group. The prevalence ratios for diabetes
were 18.08 and 3.44, respectively, in the younger and older men
with the highest body weights. For gallbladder disease, prevalence
was twice as high in normal weight females than males in the same
weight group; however, the change in prevalence ratio was much
higher in men than women with increased body weight. Age did not
effect CHD risk, but obesity was associated with CHD in all subgroups.
Also, the researchers observed that hypertension was the most common
health problem associated with both overweight and obesity. Finally,
the incidence of people having 2 or more comorbidities increased
directly across different weight classes.
The results reported by Must and colleagues
strongly suggest that Americans are losing the battle of the bulge,
and are affected by the various consequences associated with obesity-related
health conditions such as type 2 diabetes, hypertension, gallbladder
disease, hypercholesterolemia, osteoarthritis, and CHD. The most
disconcerting aspect of their findings is that these numerous health
problems were not limited to only the grossly obese subjects, but
were prevalent among those who were slightly overweight. These
data support the need for a national program to prevent and treat
excess body weight in adults.
In a comparable study, Fine et al. observed
that weight gain was associated with impaired physical function,
decreased vitality, and associated bodily pain. During the 4 year
follow-up period, 39% (n=15,602) of women in the Nurses' Health
Study maintained their weight within 5 pounds of their original
weight compared to 38% (n=15,160) who gained between 5-20 pounds
and 17% (n=6,667) who lost between 5-20 pounds. Based on the self-administered
questionnaire that measured health related quality of life, regardless
of baseline weight, subjects associated weight gain with lower
physical function and vitality and increased pain. Weight loss,
on the other hand, was positively viewed by everyone, except for
the group of women with the lowest BMI values. Fine and colleagues
suspected that the large amount of weight loss observed in this
small group of women was probably a result of underlying illness
rather than an intentional weight loss, since they had the lowest
physical activity level. Weight change was more strongly related
with physical health than mental health. In the young, lean women,
a weight gain of 20 pounds or more was associated with a greater
decline in physical function than cigarette smoking. The impact
of weight change on quality of life was similar between women over
65 years and women younger than 65 years.
Both studies support the current recommendation,
which emphasize the need to maintain a normal BMI, or in the case
of people with excess weight, to reduce weight for optimal physical
function. However, in light of the growing prevalence of obesity
among the American population, comprehensive programs aimed at
preventing obesity is needed along with treating chronic illnesses
associated with this growing disease.
Fine JT, Colditz GA, Coakley EH, et al. A
prospective study of weight change and health-related quality of
life in women. JAMA. 1999,282:2136-2142.
Must A, Spadano J, Coakely EH, et al. The disease burden associated with
overweight and obesity. JAMA. 1999;282:1523-1529.
Table of Contents
In the fight against heart diseases, a-tocopherol
has emerged as a new magic bullet for protecting against atherosclerotic
CVD. It has been shown that this antioxidant, which is transported
in the LDL particle, reduces the susceptibility of LDL to oxidation
and protects against the atherogenic effects associated with oxidized
Anderson and colleagues conducted a 2 pronged
study to determine if LDL from diabetics is more susceptible to
oxidation than LDL from non-diabetics, and to determine the effects
of antioxidant supplementation on the oxidation kinetics of LDL
in the same populations. In the study, 20 male type 2 diabetic
subjects not taking insulin were matched with 20 control subjects.
All subjects followed an isocaloric America Diabetes Association's
diet during all 3 phases of the 28 weeks study. The first and last
8 weeks of the study were pre-treatment and post-treatment phases,
during which time both case and control groups consumed placebo
capsules. During the treatment phase, weeks 9-20, the diabetic
group received a daily supplement of 24 mg b-carotene, 1000 mg
ascorbate, and 800 IU of a-tocopherol and the control group continued
the placebo regimen. The plasma antioxidant levels and LDL oxidation
status were measured following each test period.
The researchers used 4 different techniques
to determine LDL oxidation rates; 30oC Cu oxidation, 37oC Cu oxidation,
AAPH [2,2'-azobis (2-amidinopropane) dihydrochloride] oxidation,
and hypochlorite oxidation methods. All 4 assay systems were used
since each has distinct advantages. For example, the 30oC Cu oxidation
assay is better at continuously and visually monitoring the lag
and propagation phases of conjugated dienes (CD) formation. The
37oC oxidation analysis is better at detecting the differences
between control and diabetic subjects. "The AAPH technique was
used as a distinctly different oxidation probe since this compound
generates free radicals in solution, rather than facilitating oxidation
as with copper" and hypochlorite is a selective protein oxidant
that spares lipids.
Results with copper oxidation at 30oC showed
that both groups had similar initial LDL oxidation status reflected
by similar lag phases (a measure of resistance to oxidation), maximum
conjugated diene (a product of early lipid oxidation) formation,
production of thiobarbituric reactive substances (TBARS are a product
of late lipid oxidation), and trinitrobenzene sulfonic acid (TNBS
measures loss of free amine groups associated with protein damage)
levels. However, following the antioxidant supplementation, the
lag phase increased from 56 minutes to 129 minutes, the maximum
CD formation decreased from 1.23 to 0.62 OD units, the formation
of TBARS decreased from 78 to 33 nmol/mg of protein, and the loss
of free amine groups (TNBS) decreased from 41% to 12%, indicating
that antioxidant supplements were effective in reducing the susceptibility
of LDL to oxidation. Improvement in LDL oxidation parameters was
also observed following antioxidant supplement when tested using
the copper oxidation at 37oC method. But, unlike copper oxidation
at 30oC, copper oxidation at 37oC indicated that LDL from diabetic
subjects was more susceptible to oxidation with a 10% shorter lag
time and higher baseline TBARS and TNBS levels. Anderson et al.
were also able to show that untreated LDL from the diabetic group
was taken up more readily by macrophages compared to LDL from the
control group, and that following antioxidant supplement, LDL uptake
was reduced. Finally, antioxidant supplements were not associated
with any appreciable changes in glycemic control or plasma glycohemoglobin
and lipid values.
In conclusion, the data indicate that LDL
from diabetic subjects is more susceptible to oxidation than LDL
from non-diabetics. Daily antioxidant supplementation could be
of benefit in this population, especially since they are prone
to CVD due to the increased prevalence of dyslipidemia, hypertension
Anderson JW, Gowri MS, Turner J. et al. Antioxidant
supplementation effects on low-density lipoprotein oxidation for
individuals with type 2 diabetes mellitus. J Am Coll Nutr. 1999;18:451-461.
Table of Contents
In an effort to protect their high CVD risk
patients, it has become a common practice for clinicians to recommend
400 IU of vitamin E supplement along with daily use of aspirin
and B vitamin supplements. However, according to the latest finding
from the Heart Outcome Prevention Evaluation Study (HOPE), with
9,541 subjects (2,545 women and 6,996 male), no CVD benefit was
found following 4.5 years of vitamin E supplementation. This study,
along with several smaller studies, contradicts previous observational
and experimental studies which found an association between vitamin
E and lower CHD risk.
The incidence of primary CVD events, death from cardiovascular causes,
MI, and stroke were similar between the 4,761 vitamin E group and 4,780
placebo group. For example, the relative risk for death from cardiovascular
causes was 1.05 (95% CI 0.95-1.16) with 342 cases in the vitamin E group
compared to 328 cases in the placebo group. In the cases of MI and stroke,
532 vs. 524 and 209 vs.180 events were reported in experimental group
vs. placebo group, respectively. The relative risk for MI and stroke
were 1.02 and 1.17, respectively. There were also no significant difference
in the number of secondary outcomes; angina, claudication, heart failure,
complications of DM, and vascularization or limb amputation, between
study groups. Further analysis of subgroups based on age, sex, previous
CVD episodes, and smoking and diabetes status revealed similar rates
of primary CVD outcomes. Even though this study found no cardio-protective
effect of vitamin E supplements on CVD risk, supplementation was not
associated with any adverse events.
The researchers speculated that the lack of benefits associated with
vitamin E supplements and CVD events in the current study was possibly
due to the short study duration. Unlike medications that lower blood
pressure and plasma cholesterol levels immediately, antioxidants such
as vitamin E are thought to take more than 5 years to affect any detectable
clinical outcomes associated with a decrease in new lesions, especially
in high CVD risk groups like these study subjects. Also, unlike epidemiological
studies that found a relationship between high vitamin E intake and lower
rate of CHD, the current study did not include other antioxidants.
Results from this study indicate that the commonly accepted beneficial
effects of 400 IU/day of vitamin E supplementation against MI, stroke,
and CVD deaths are far from established. Even though earlier observational
and experimental studies showed that vitamin E protected against CVD,
the null findings found in this high-risk patient population of the HOPE
study suggest that a larger and longer study is needed to fully evaluate
the effect of vitamin E on CVD risk.
The Heart Outcomes Prevention Evaluation Study
Investigators. Vitamin E supplementation and cardiovascular events
in high-risk patients. N Engl J Med. 2000;342:154-160.
Table of Contents
A study by Wolfe and Piche suggests that replacing
some sources of CHO in the diet with low-fat, high-protein foods
can result in an improved plasma lipid profile in healthy adults.
In this randomized, cross-over study, researchers fed 10 healthy,
normolipidemic volunteers either a isocaloric low-protein or high-protein
diet and determined the effect on plasma lipid and lipoprotein
levels. Both test diets contained 35% of energy as fat, 230 mg/day
cholesterol, and 24 gm/day fiber, however, the percentage of protein
in the high-protein diet was 22% compared to 12% in the low-protein
diet. The duration of each diet phase was 4 weeks.
Like similar high-protein feeding studies conducted in hyperlipidemic
subjects, this study found that the mean plasma cholesterol concentration
was lower following the high-protein diet. For example, plasma total
cholesterol, LDL cholesterol, VLDL cholesterol, TAG, and total cholesterol
to HDL cholesterol ratio levels were 7%, 8%, 23%, 27%, and 11% lower,
respectively, than during the low-protein diet. HDL cholesterol was slightly
higher (4%) following the high-protein diet, however, the increase was
not statistically significant. The subjects reported slightly higher
levels of satiety following the high-protein diet.
With this study, the researchers were able to show that when CHO is replaced
with a higher amount of protein in the diet, with no change in the percent
of fat calories, it leads to an improved plasma lipid and lipoprotein
profile in normocholesterolemic adults as was previously shown in hypercholesterolemic
and postmenopausal women. Even though the actual changes in lipid levels
were relatively small, this study supports earlier studies which suggest
that all things, even CHO, should be eaten in moderation.
Wolfe BM and Piche LA. Replacement of carbohydrate
by protein in a conventional-fat diet reduces cholesterol and triglyceride
concentrations in healthy normolipidemic subjects. Clin Invest
Table of Contents
A good healthy diet, complete with recommended
nutrients, continues to be a key factor in managing one's health.
In a multicentered study, Chait and colleagues were able to reduce
plasma homocysteine levels, a risk factor for CHD, by feeding a
prepared meal plan (PMP) fortified with 23 micronutrients to adults
with histories of type 2 diabetes, hypertension, dyslipidemia,
or any combination of these conditions. In this study, the investigators
randomly divided 491 participants into 2 test groups. Depending
on the group assigned, study subjects followed the PMP diet (n=244)
or a self-selected diet (SSD, n=247) for 10 weeks. Both diets were
similar in macronutrient composition, 20% of energy as fat, 55-60%
as CHO, and 15-20% as protein, however, the micronutrient content
of the PMP diet was much higher compared with the SSD diet. In
the PMP diet, 22 micronutrients were fortified with >100%
of the RDA for adults and folate was increased to 400 �g/day. The
group in the SSD diet ate regular foods they prepared at home.
The SSD group was taught to eat a fixed number of servings from
the exchange list.
As expected, the dietary intakes of folate,
vitamin B6, and vitamin B12 increased significantly
in the PMP diet group compared to the SSD group. For example, dietary
folate, vitamin B12, and vitamin B6 increased
by 399 �g/day, 7.4 �g/day, and 2.1�g/day, respectively, with the
PMP diet, while it only changed by 68 �g/day for folate, 0.3 �g/day
for vitamin B6, and -0.4 �g/day for vitamin B12 following
the SSD diet. The plasma homocysteine levels in the PMP group fell
by 1.5 �mol/l (13.8%) compared to a 0.1�mol/l increase in the SSD
group. Also, the changes in serum and RBC folate concentrations
and serum vitamin B12 levels were greater in the PMP
group. The serum folate level increased by 81% (14.1 nmol/l) and
decreased by 9.5% following the PMP and the SSD diets, respectively.
RBC folate and serum vitamin B12 increased by 65% (367
nmol/l) and 27% (98 pmol/l), respectively, in the PMP group. The
RBC folate increased by 12% (66 nmol/l) and serum vitamin B12 decreased
by 6% (22 pmol/l) in the SSD group. In spite of the dietary vitamin
B6 increase, serum and RBC vitamin B6 levels
did not significantly change in either group.
The inverse relationship between serum homocysteine
and dietary, serum and RCB folate were noted in both study groups.
The relationship between serum homocysteine and serum vitamin B6 and
B12 or RBC vitamin B6 were weak; however,
including these in the folate analysis further strengthened the
folate relationship. This would indicate that vitamin B6 and
B12 have a small effect on homocysteine levels. Finally,
the effects of these nutrients on lowering plasma homocysteine
levels were especially strong in subjects with the highest baseline
homocysteine concentrations. For example, the subjects with baseline
homocysteine levels of >12.15 units lowered their homocysteine
level by 5.7 �mol/l (PMP) and 2.3 �mol/l (SSD) compared to a small
increase in homocystein levels in people with the lowest baseline
In conclusion, this study shows that increasing
dietary intakes of folate, vitamin B6 and vitamin B12,
which are cofactors in numerous metabolic pathways, can effectively
lower plasma homocystein concentrations in persons with increased
CHD risk. Chait et al. conclude that prepackage meals such as the
one used in this study are convenient ways to help people with
concomitant risk factors for CVD meet their nutritional needs.
However, a more disturbing finding from this study is that the
SSD group was unable to achieve optimal plasma levels of serum
and RBC folate and serum vitamin B12 by eating regular
foods off the grocery shelf.
Chait A, Malinow MR, Morris CD et al. Increased
dietary micronutrients decrease serum homocysteine concentrations
in patients at high risk of cardiovascular disease. Am J Clin
Nutr 1999; 70:881-887.
Table of Contents
Contrary to earlier scientific evidence, stearic
acid (18:0), like other long chain saturated fatty acids [lauric
(12:0), myristic (14:0), palmitic acid (16:0)], is also associated
with CHD risk, according to data from the Nurses' Health Study.
On the other hand, intake of short and medium chain fatty acids
(4:0 - 10:0) was not associated with increased CHD risk. However,
since the sources of these saturated fats are typically from the
same foods, the researchers concluded that it was not as critical
to distinguish specific type of saturated fats when advising clients.
Based on 1980 to 1994 food frequency questionnaires
of 80,082 nurses, saturated fat intake was steadily on the decline.
For example, beef and whole milk, two primary sources of saturated
fat, decreased from 1.8 to 0.8 oz/day and 0.26 to 0.07 glasses/day,
respectively. However, according to the findings, saturated fat
intakes were associated with higher prevalence of smoking and cholesterol
intake and lower activity levels and fiber intake.
During the 14-year follow-up, 939 cases of
major CHD events occurred. The multivariate RRs of CHD, which included
both dietary and non-dietary covariants were 0.97, 1.12, 1.07,
and 1.19 for each 1% increase in intake of 4:0-10:0, lauric and
myristic acid, palmitic acids, and stearic acid, respectively.
However, when all saturated fats where combined, a 5% increase
in these fats resulted in a RR value of 1.29. These results also
showed an inverse relationship between CHD and an increase in polyunsaturated
fat intake. The multivariate RR was 0.79 for each 0.2 unit increase
in the dietary fat P:S ratio. The researchers estimated that by
replacing 5% of long chain saturated fatty acids with 5% of CHO
in an isocaloric meal would result in a 22% reduction of CHD risk
compared to 42% and 50% reduction following replacement with MUFA
and PUFA, respectively.
Even though the average red meat and high-fat dairy product consumption
was on the decline, based on the multivariate analysis, women in the
highest quintile of intakes for these foods had higher CHD risk. On the
other hand, fish, poultry, and lean dairy products in the diet were associated
with lowering CHD risk.
In conclusion, results reported by Hu et al.
indicate that all high saturated fat foods, even those with high
stearic acid content, increase CHD risk . Therefore, people should
replace some high saturated fat foods with lower saturated foods
as these foods lower blood cholesterol levels. Finally, since foods
high in saturated fatty acids contain a mix of different types
of fatty acids, there does not appear to be a need to distinguish
the CHD effects from individual fatty acids.
Hu FB, Stampfer MJ, Manson JE, et al. Dietary
saturated fats and their food sources in relation to the risk of
coronary heart disease in women. Am J Clin Nutr. 1999;70:1001-1008.
Table of Contents
Analogies are always such dangerous critters
because for certain someone will say "it's not the same thing." But
why not! Ascribing health risk has taken on a life of its own these
days and everything seems to be a risk for something. The risk
de jour is GMOs, genetically modified organisms, which, without
documented damage, have become the buzz word for the hazards science
foists upon an unsuspecting public for its own devious and, as
often accused, profitable motives. Clearly, the role of science
is to change the world as we know it; to some that is the natural
order of progress while to others it is a clear sign of our eminent
demise. And as such, anything that is a step forward must defend
itself against accusations that it harms the environment, kills
the public, and destroys the world. GMO's have now become the embodiment
of anti-techs versus techs, and frankenfoods versus science.
In a world of fixed land mass, decreasing
agricultural lands, expanding populations, and more people demanding
more food for less money, it is difficult to comprehend why advances
which increase food production, decrease loss, reduce use of fertilizers
and pesticides, and produces foods with higher nutritional value
are treated as if they were an attempt to destroy the earth. Isn't
this a case of trying to feed the hungry, enhance nutrition for
the malnourished, reduce environmental pollution, increase production?
Aren't these good things? I remember years ago environmentalist
complaining that agriculture, specifically animal agriculture,
was causing the destruction of the rain forests. Why then is grain
produced from less land with less environmental pollution not a
step in the right direction? [Maybe it was eating the animal products
all along that was in fact the unacceptable part.] Can we really
afford to discard advances which can make food more available,
affordable and nutritious, with specific efficacies for nutrient
deficiencies [children in southeast Asia would seem better off
with a GMO vitamin A and iron enriched rice]. Sometimes we seem
to forget just how many children in the world are malnourished,
and how many die from the simple lack of food. So I'll get on a
jet and go to my demonstration against those frankenfoods and get
the government to keep it out of my country, and then I'll go home
and enjoy a fine feast of non-GMO (vegetarian) cuisine and non-GMO
(alcohol-free) wine, and know that I have stopped a maybe disaster
before it maybe happened. Who cares if there's no real evidence
of a disaster in the making, I know, just as I know so many other
pseudo-facts, that it is wrong. I know what I know, do not confuse
me with facts. And please don't tell me about the millions who
would benefit from this technology. I have a loftier goal. See
you at the next demonstration. And GMOs become faced with the "Reverse
Onus" conundrum: it is not the responsibility of those making risk
claims to prove the validity of the claim; rather, it is up to
those who deny the claims to prove they could not be true. The
complication is, how do you prove a negative. [First corrective
step, change the terminology. Let's call them "genetically enhanced
And the analogy? Thirty years ago it was
decided that since blood cholesterol was related to heart disease
risk, dietary cholesterol must also be a risk, and today restrictions
and limits and good food, bad food mentalities permeated the US
dietary pattern. My analogy is that once we start saying GMOs are
bad, because we think, just maybe, they might be, they will be
bad no matter what the next few decades of research and science
show. Eventually the concept of precaution becomes the verbiage
of fact and the next generation never knows just what little scientific
reality the conventional wisdom is based on. A few voices will
argue the issue but will be looked upon as anti-establishment noise
makers because we really do not like those who challenge our preconceived
view points. And it has taken many years to even begin to address
the "reverse onus" quandary faced by eggs and other high cholesterol
foods. We need to be very cautious of these first steps on the
path of risk pronouncements; too often we find it to be a long
one-way street with many roadblocks against any u-turns.
Donald J. McNamara, Ph.D.
Executive Editor, Nutrition Close-Up
Table of Contents
Editor: Donald J. McNamara, Ph.D.
Writer/Editor: Linda Min, M.S., R.D.
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