Newsletters & Publications
16 - Number 2
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
For decades, eggs represented the visual icon
for dietary cholesterol for many health conscious consumers and
became a food to limit in the pursuit of heart health. But according
to 2 large prospective epidemiological surveys, the Nurses Health
Study (NHS) and the Health Professionals Follow-up Study (HPFS),
its not eggs that increase CVD risk but rather the high saturated
fat company eggs keep on the plate. Data from the NHS evaluated
the 14 year (1980-1994) eating habits of 80,082 healthy women,
while the HPFS measured the 8 year (1986-1994) eating habits of
37,851 males. Males in the HPFS were dentists, optometrist, pharmacists,
podiatrists, and veterinarians, between the ages of 40 to 75 years
at the start of the study. Nurses in the NHS were 34 to 59 years
old at baseline. All study subjects were initially free of CVD,
hypercholesterolemia, diabetes, and cancer at study onset. Biennial
questionnaires were used to screen for the occurrence of fatal
CHD, nonfatal MI and strokes, and reported cases were confirmed.
During the follow-up period, 866 cases of CHD and 258 cases of
stroke were confirmed in men and 939 cases of CHD and 563 cases
of stroke were confirmed in women.
Based on food frequency questionnaires, high
egg consumption was associated with many negative lifestyle and
dietary habits in male health professionals. They were more likely
to smoke; exercise less; consume more saturated fats in the form
of red meat, bacon, whole milk; and eat less fruits and vegetables.
The total grams of saturated fat intake increased directly with
number of egg consumed. These trends, except for bacon intake,
were less evident in nurses. During the study period, the average
per capita egg consumption decreased from 2.3 egg/week in 1986
to 1.6 egg/week in 1990 in males and 2.8 egg/week in 1980 to 1.4
egg/week in 1990 in females. Also, eggs typically replaced breakfast
cereals intake. The accuracy of food frequency questionnaires was
confirmed by validation studies.
Using data from NHS and HPFS, Hu et al. tested
the hypothesis that there is a direct relationship between egg
intake and CHD risk and stroke. The investigators found that consumption
of up to 1 egg per day had no overall impact on the risk of CVD
among healthy men and women. For example, initially, the male cohorts
with the highest egg intakes (> 1 egg/day) were only slightly
more likely to develop CHD than males who ate less than
1 egg/week. However, when smoking, dietary fiber intake, and other
risk factors for CHD were included in the analysis, this association
was null. In women, there was no relationship between CHD and egg
intake at any level. The adjustment for cohorts bacon intake
further attenuated the association between egg intake and CHD.
The adjusted relative risk for CHD was 1.0 for 1 egg/week, 1.04
for 2-4 eggs/week, 0.78 for 5-6 eggs/week, and 0.93 for 1 egg/day
in males and 0.81, 0.96, 0.91, and 0.78, respectively in females.
Based on a small number of subjects who ate more than 2 eggs per
day, the multivariate RR for CHD was 0.76 in women and 1.10 in
men. Further analysis suggested that neither short-term nor long-term
egg consumption was associated with CHD risk. As in the case of
CHD risk, egg consumption was not associated with increased total
stroke, ischemic stroke, or hemorrhagic stroke.
When subjects with other risk factors for
CHD were included in the analysis, only diabetics were found to
have increased CHD risk associated with high egg intake. The multivariate
relative risk for 1 egg/week was 1.0 and 1.0, 1 egg/week 1.0 and
0.91, 2-4 egg/week 1.16 and 1.05, 5-6 eggs/week 1.16 and 1.87,
and 1 egg/day 2.02 and 1.49 for diabetic men and women, respectively.
Results from these large epidemiological studies clearly show that
it possible to eat an egg a day without increasing CHD risk in
healthy men and women. This in part may relate to the fact that
eggs contain antioxidants, folate, and other B vitamins which have
been shown to reduce CHD risk. And by substituting for breakfast
cereals, egg consumption can both increase HDL cholesterol and
decrease TAG levels. The relationship between egg consumption and
CVD seen with diabetics might have been "related to abnormal
cholesterol transport due to decreased levels of apolipoprotein
E and increased levels of apolipoprotein C-III" and thus needs
further studies to evaluate the situation.
Hu FB, Stampfer MJ, Rimm EB, et al. A prospective
study of egg consumption and risk of cardiovascular disease in
men and women. JAMA. 1999;281-1387-1394.
- Egg consumption is not associated with CHD risk in healthy
men and women.
- Antioxidants, folate, other B vitamins, and unsaturated fats
found in eggs can potentially counterbalance small effects of
cholesterol in eggs on plasma LDL levels.
- Egg consumption is associated with improved plasma HDL and
- The total grams of saturated fat intake increased directly
with number of egg consumed.
- Higher egg consumption is associated with increased CHD risk
in people with diabetes.
It would be easy to dismiss the findings
of the Nurses Health Study and the Health Professionals
Follow-Up Study as just a single report with an unexpected
finding. The fact is the findings reported by Hu and colleagues
are not in the least unexpected or an aberrant, one-of-a-kind
report. Over the past five years there have been numerous
reports of a null relationship between cholesterol intakes,
plasma cholesterol levels and CVD incidence. Data from
MRFIT indicated that neither total dietary cholesterol
nor egg consumption were related to the plasma cholesterol
levels of 12,553 men (1). Results from the Framingham Heart
Study indicated no relationship between dietary cholesterol
and either plasma cholesterol levels or heart disease incidence
in 1,422 women (2). Data from both the Nurses Health
Study of 80,082 women (3) and the Health Professionals
Follow-Up Study of 43,757 men (4) indicated that dietary
cholesterol was not significantly related to CHD morbidity
or mortality. Analysis of data from the Lipid Research
Clinics Follow-Up Study in 4,546 men and women (5) found
no relationship between dietary cholesterol and CHD incidence.
The Alpha-Tocopherol, Beta-Carotene Cancer Prevention Trial
in 21,930 men (6) also reported that dietary cholesterol
was not significantly related to CHD incidence. The fact
is that over the last five years I know of no report from
any large epidemiological trial indicating a positive relationship
between dietary cholesterol and heart disease risk. Rather
than questioning the validity of the observations reported
by Hu et al.(7) maybe it is time that the nutritional scientists
question the validity of those thirty year old studies
which suggested that dietary cholesterol was a factor in
1. Tillotson JL, Bartsch GE, Gorder
D, Grandits GA, Stamler J. Food group and nutrient intakes
at baseline in the Multiple Risk Factor Intervention Trial. Am
J Clin Nutr 1997;65 (Suppl):228S-257S.
2. Millen BE, Franz MM, Quatromoni
PA, et al. Diet and plasma lipids in women .1. Macronutrients
and plasma total and low-density lipoprotein cholesterol
in women: The Framingham nutrition studies. J Clin
3. Hu FB, Stampfer MJ, Manson JE,
et al. Dietary fat intake and the risk of coronary heart
disease in women. N Engl J Med 1997;337:1491-1499.
4. Ascherio A, Rimm EB, Giovannucci
EL, Spiegelman D, Stampfer M, Willett WC. Dietary fat and
risk of coronary heart disease in men: Cohort follow up
study in the United States. BMJ 1996;313:84-90.
5. Esrey KL, Joseph L, Grover SA.
Relationship between dietary intake and coronary heart
disease mortality: Lipid research clinics prevalence follow-up
study. J Clin Epidemiol 1996;49:211-216.
6. Pietinen P, Ascherio A, Korhonen
P, et al. Intake of fatty acids and risk of coronary heart
disease in a cohort of Finnish men - The alpha-tocopherol,
beta-carotene cancer prevention study. Am J Epidemiol 1997;145:876-887.
7. Hu FB, Stampfer MJ, Rimm EB, et
al. A prospective study of egg consumption and risk of
cardiovascular disease in men and women. JAMA 1999;281:1387-1394.
Table of Contents
Recently, Lp(a) has received much attention
for its possible role in CHD. This new risk factor was initially
thought to be unaffected by diet, however, a recent study by Nilausen
and Meinertz shows that dietary casein can dramatically lower plasma
Lp(a) concentrations. The casein protein diet decreased Lp(a) levels
much more than a soy protein rich diet; however as predicted, the
soy diet was more effective in lowering total and LDL cholesterol
Nine healthy normolipidemic males between
21 and 64 years of age with a BMI of 21.7 to 25.1 kg/m2 consumed
3 different diets. The diets were: a self-selected baseline diet,
a liquid soy diet containing 20% of calories as soy protein, and
a liquid casein diet with 20% of calories as casein. Subjects consumed
each diet for 33-45 days with a washout period in-between. The
test diets consisted of 20% of calories from protein as calcium
caseinate or soy protein isolate, 55% CHO from cornstarch hydrolysate,
and 25% fat high oleate safflower oil. Cholesterol was added to
the soy protein diet to equal the casein diets level of 55
mg/MJ and the calcium level in the soy diet was adjusted to equal
the casein diet.
Compared with the self-selected diet, both
test diets decreased plasma lipid and lipoprotein levels. Total
cholesterol levels decreased by 42 mg/dl and 40 mg/dl with the
soy protein and casein diets, respectively. The LDL cholesterol,
HDL cholesterol, and TAG levels decreased by 34 and 23 mg/dl, 7
and 12 mg/dl, and 8 and 15 mg/dl, respectively with the soy and
casein diets. Only the plasma HDL cholesterol concentrations were
significantly different between the 2 protein diets. However, plasma
Lp(a) concentrations following initiation of the casein diet were
almost 2 times lower than during intake of the soy diet or the
self-selected diets. The average Lp(a) levels following the self-selected,
soy protein, and casein diets were 92.1, 93.5, and 44.7 mg/dl,
respectively. However, there was a wide individual variation in
Lp(a) levels and the magnitude of change was directly correlated
to baseline Lp(a) during the self selected diet phase. During the
soy diet period, subjects Lp(a) levels slightly increased
before falling to the baseline level, while the Lp(a) levels steadily
decreased during intake of the casein diet to 65% below baseline.This
study showed that a liquid casein diet was effective in lowering
plasma Lp(a) levels compared to a soy protein diet in healthy men.
But in spite of the lower Lp(a), it is too early to assume that
this diet is an antiatherogenic diet leading to reduced CHD. For
example, this diet consisted of 20% casein, which is difficult
for an average American to tolerate. Also, at this point the researchers
do not know what mechanisms are involved in the observations or
if its actually casein protein rather than whats missing
in the soy protein and self selected diet that might cause elevated
Nilausen, K, Meinertz, H. Lipoprotein (a)
and dietary proteins: casein lowers lipoprotein(a) concentrations
as compared with soy protein. Am J Clin Nutr. 1999;69:419-425.
Table of Contents
In this diverse country, people of different
ethnic origins are battling CVD risks with very different results
National Health and Nutrition Examination Survey (NHANES III, 1988-1994),
minority children h. For example, based on the third National Health
and Nutrition Examination Survey (NHANES III, 1988-1994), minority
children have a higher number of risk factors for CVD than white
children. Also, even between minority groups, there are major differences
in their risk for CHD.
Using NHANES III data, Winkleby et al. reported
that black and Mexican-American children had more CVD risk factors
than whites even after socioeconomic status was adjusted in the
analysis. Based on questionnaires and medical examination data
of 2,063 white, 2,769 black, and 2,854 Mexican-American children,
investigators found that a higher percentage of minority children
lived below the poverty level, had parents with less formal education,
and exhibited a greater number of CVD risk factors than their white
counterparts. Also, compared to white children, minority children
had more CVD risk factors and negative life style factors at an
earlier age. For example, young minority girls between 6-9 years
old had a higher BMI (17.7 kg/m2) and consumed more
calories from fat (35.1%) than white girls of the same age, 17.1
kg/m2 and 33.3%, respectively. This trend continued
in older minority girls between 18-24 years old with an average
BMI of 25.5 compared to 23.1 in white girls. Black children had
higher blood pressure and hemoglobin A1c levels than white or Mexican-American
children. However, among boys, black boys ate a higher percentage
of calories from fat than both Mexican-American and white boys
and the hemoglobin A1c levels were higher for minority boys than
white boys. On the other hand, white children of all ages smoked
more than minority children. This was especially true in white
children from lower educational homes.
This national, cross-sectional survey indicates
that minority children are at a high risk of future CVD and interventions
are warranted even in these young children to counter this negative
trend. Current data suggest that heart health programs should begin
to target children as young as 6-9 years old and to custom tailor
programs for different ethnic groups for maximum benefit. Sundquist
et al. also reported differences in CVD risk among subgroups of
Mexican-American groups. Based on the NHANES III data, among Mexican-Americans,
US born, Spanish-speaking Mexican-Americans had the highest risk
of CVD followed by US born, English-speaking Mexican-Americans
and the lowest risk in Mexico born Mexican-Americans. The age and
education level adjusted 10 year CHD mortality rates for US born,
Spanish-speaking Mexican men and women were 27.5 and 11.4, respectively,
per 1,000 persons. The 10-year mortality rates were 22.5 and 7.0
per 1,000 persons in the highly assimilated English-speaking Mexican-American
men and women, and 20.0 and 6.6 in the first generation Mexican-Americans.
Also, Spanish-speaking Mexican-Americans had the highest levels
of primary CVD risk factors while Mexico born Mexican-Americans
had the least CVD risk factors. The levels of CVD risk factors
for US born, English-speaking Mexican-Americans were very similar
to non-Hispanic whites in the general population. Compared to first
generation Mexican-Americans, all US-born Mexican-Americans smoked
more and had higher BMI levels. However, when CVD risk factors
were analyzed based on education level, English-speaking and Spanish-speaking
Mexican-American men in the highest education group had the same
risk factors for CVD.
Current findings from 2,791 Mexican-Americans,
aged 25 to 64 years, in the NHANES III confirmed the researchers
initial hypotheses that less assimilated Spanish-speaking Mexican-Americans
would have the highest CHD risk since "they may have lost
some of the advantages associated with the Mexican lifestyle without
gaining the advantages associated with acculturation into the English-speaking
culture." This heterogeneity in CVD risk factors among Mexican-Americans
indicated that certain sub-populations need more intensive intervention
programs to lower their CVD risk profile.
Sundquist, J. Winkleby, M.A. et al. Cardiovascular
risk factors in Mexican American Adults: A transcultural analysis
of NHANES III, 1988-1994. Am J Public Health. 1999;89:723-730.
Winkleby MA, Robinson TN, Sunquist J, et al.
Ethnic variation in cardiovascular disease risk factors among children
and young adults. Findings from the third national health and nutrition
examination survey, 1988-1994. JAMA. 1999;281:1006-1013.
Table of Contents
For a long time, the American public viewed
CHD as primarily a disease which afflicted males, but thanks to
better media coverage, women are starting to realize that heart
disease is also a leading cause of death in their gender. This
message is especially important since CHD risk factors increase
dramatically with age in women. A Finnish study by Jousilahti et
al. specifically addresses the effects of gender difference in
CVD risk factors in 14,786 adults between 25-64 years old. The
7,090 men and 7,696 women in the study were initially recruited
in either 1982 and 1987 and followed through 1994. During this
time, 520 CHD incidences and 231 CHD death were reported in males
compared with 209 CHD incidences and 63 CHD death in females. As
a collective group, males had higher plasma total cholesterol,
blood pressure, and BMI; lower plasma HDL cholesterol levels; and
more smoked and had diabetes relative to the female subjects. Similar
risk factors were noted in the 24-49 age group, however, women
in the 2 older groups had similar or higher plasma total cholesterol
levels, blood pressure, and BMI than their male counterparts. The
plasma HDL cholesterol was still higher in females than males but
lower than in the youngest female group. The percentage with diabetes
increased with age, but at a similar rate between the sexes. In
univariate analysis, male gender was associated with a RR of 3.38
for CHD incidence and 5.00 for mortality but decreased to 2.31
and 3.20 for incidence and mortality, respectively, based on multivariate
analysis using other major CHD risk factors. The HDL/total cholesterol
ratio and smoking were 2 leading determinants of the sex difference
in CHD risk.
This investigation found that younger women
had lower levels of CHD risk factors compared to men of the same
age, but this was not found in older females. Plasma total cholesterol,
systolic blood pressure, BMI, and HDL/total cholesterol ratio in
older females were all indicative of a more atherogenic profile
than older males exhibited, indicating that the risk of CHD increases
rapidly in females as they age. This study poses the challenging
public health task of lowering CHD risk among middle-aged men while
preventing the marked increase in CHD risk with aging in women.
Jousilahti P, Vartiainen E, Tuomilehto J.
et al. Sex, age, cardiovascular risk factors, and coronary heart
disease. A prospective follow-up of 14,786 middle-aged men and
women in Finland. Circulation. 1999;99:1165-1172.
Table of Contents
Besides the traditional dietary and pharmacological
methods to lower an elevated plasma cholesterol, for the past several
years a stanol-ester containing margarine has been available in
Finland. Now, a new study by Hallikainen and Uusitupa shows it
is also possible to significantly reduce total cholesterol and
LDL cholesterol levels using a low-fat stanol ester-containing
margarine in a low-fat, low-cholesterol diet. Consumption of the
wood stanol ester-containing margarine (WSEM) lead to a 47 mg/dl
(18.3%) decrease in plasma total cholesterol levels in 18 subjects
on the WSEM diet. Decreases of 38 mg/dl (15.7%) and 19 mg/dl (7.7%)
in total cholesterol were observed in 20 subjects consuming the
vegetable oil stanol ester-containing margarine (VOSEM) and in
17 adults on the control diet. The plasma LDL cholesterol levels
decreased by 41 mg/dl (23.6%), 31 mg/dl (18.4%), and 17 mg/dl (9.9%)
following 8 weeks of the WSEM, VOSEM, and control diets, respectively.
Although the absolute change in total and LDL cholesterol levels
were greater with the WSEM diet than with the VOSEM diet, the values
were not significantly different. The effects of dietary stanol-esters
on plasma HDL, TAG, retinol, beta-carotene, and alpha-tocopherol
were not significant.
The fifty-five subjects in this 12-week double-blind
trial were randomly assigned to one of the 3 low-fat margarine
diets following a 4-week baseline diet. The control diet consisted
of 28-30% of calories from fat, 20% protein, 50-52% CHO, 23.8 mg/MJ
cholesterol, and 25 grams low-fat margarine/d. In addition to these
nutrients, the WSEM diet contained 2.31 gm sitostanol and 0.19
gm campestanol, while the VOSEM diet contained 2.16 gm sitostanol
and 0.69 gm campestanol. Unlike sitostanols proven ability
to inhibit cholesterol absorption, the effects of campestanol in
inhibiting cholesterol absorption have not yet been firmly confirmed.
These results from this study indicate that
low-fat plant stanol ester-containing margarines are more effective
in reducing plasma cholesterol levels of hypercholesterolemic adults
than a low-fat, low-cholesterol diet alone. The levels achieved
were similar to outcomes following initiation of some cholesterol
lowering drugs. The sitostanol and campesterol in the margarine
decrease plasma total and LDL cholesterol levels without adversely
affecting HDL and TAG levels, by competing with both dietary and
biliary cholesterol absorption in the small intestine. Finally,
the compliance rate on the diets was high indicating that subjects
tolerated the experimental diets well.
Hallikainen MA, Uusitupa MI. Effects of 2
low-fat stanol ester-containing margarines on serum cholesterol
concentrations as part of a low-fat diet in hypercholesterolemic
subjects. Am J Clin Nutr. 1999;69:403-410.
Table of Contents
Contrary to a common belief, a very low-fat
diet might be associated with a negative plasma lipoprotein profile.
As reported in 1994 and 1995, the current study by Dreon et al.
found that a low-fat, high CHO diet resulted in some males with
an LDL subclass phenotype A to convert to the more atherogenic
phenotype B. Instead of having large buoyant LDL associated with
phenotype A, following a 10% fat and 76% CHO diet for 10 days resulted
in 32% of the study subjects to convert to a phenotype B profile
with small dense LDL particles.
Thirty-six participants in the study were
specifically recruited from 2 earlier studies based on the finding
that their phenotype A status did not change following initiation
of a 20-24% fat diet. This randomized, cross-over study allowed
the researchers to test the effects of a very low-fat diet, 10%,
on plasma lipid and lipoprotein concentrations. All subjects consumed
both the usual diet with 32% of calories from fat (10.8% SFA, 11.8%
MUFA, 6.9% PUFA, 52% CHO, 14% protein, and 295 mg cholesterol)
and the very low-fat diet of 10.4% calories from fat (2.7% SFA,
3.7% MUFA, 2.6% PUFA, 76% CHO, 15% protein, and 301 mg cholesterol)
for 10 days each. Following each diet, plasma lipids, lipoproteins,
and lipoprotein subclasses were analyzed. Total calories were regularly
adjusted to maintain stable weight.
As in the previous studies, the very low-fat
diet resulted in increased plasma TAG levels, VLDL subfractions
mass, smaller LDL particles (LDL III and LDL IV), and apo B concentrations.
In contrast, the masses of small IDL, LDL cholesterol, mass of
large LDL I, HDL cholesterol, mass of HDL2 and HDL3, and apo A
levels in plasma decreased. With the very low-fat diet, 12 men
converted to phenotype B. The difference in lipoprotein parameters
between stable phenotype A subjects versus new phenotype B subjects
during the usual diet was not significantly different; however,
the plasma lipoprotein profile was much more atherogenic in the
second group with intake of a 10% fat diet. The concentration of
plasma TAG and smaller LDL III and LDL IV subfractions were higher,
while LDL I and HDL cholesterol levels were lower. The LDL cholesterol
level was not significantly different in either group. The comparison
of plasma lipid and lipoprotein concentrations during the 10% fat
diet with the 20-24% fat diet showed that the lower fat diet resulted
in higher plasma concentrations of VLDL, apo B, and HDL3. Also,
rather than decreasing plasma LDL cholesterol levels compared to
the 20-24% fat diet, the very low-fat diet increased plasma LDL
by 27 mg/dl in new phenotype B men. There was no change in plasma
LDL cholesterol level between the very low-fat diet and the 20-24%
diet in the stable phenotype A group.
At this point researchers can not explain
the mechanisms involved or the dietary factors responsible, high
CHO versus very low-fat, for the changes in LDL phenotype in a
third of study cohort. However, they suspect genetics is a key
factor in this outcome. Finally, these data raise serious issues
regarding the advisability of a very low-fat diet to lower the
CHD risk as this diet can result in a negative plasma lipid profile
in some individuals.
Dreon, DM, Fernstrom, HA, Williams, PT. A
very-low-fat diet is not associated with improved lipoprotein profiles
in men with a predominance of large, low-density lipoproteins. Am
J Clin Nutr. 1999;69:411-418.
Table of Contents
Beneficial effects of exercise against CVD
have been firmly established, however, the mechanism behind this
protection is unclear. According to Smith et al., one possible
solution to this multi-factorial question lies in ones immune
system. By measuring changes in atherogenic and atheroprotective
cytokine levels following a 6-month exercise program in 43 adults
(18 men and 25 women) the investigators observed a beneficial effects
of exercise on blood mononuclear cell production of cytokines.
The average duration and frequency of supervised exercise was 70
minutes for twice a week of aerobic exercises and weight lifting.
The atherogenic cytokines, interferon gamma
(IFN-gamma), tumor necrosis factor (TNF-alpha), and interleukin
(IL) 1-a levels produced by blood mononuclear cells fell by 58.3%
and atheroprotective cytokines, IL-4, IL-10, and transforming growth
factor beta (TGF-�) levels increased 35.9% following the exercise
period. The C-reactive protein levels which represent CHD risk,
also decreased from baseline. The changes in both atherogenic and
atheroprotective cytokine levels were directly correlated with
duration of walking, running, cycling, rowing, climbing, skiing,
and an aerobic program.
IFN-gamma and TNF-alpha cytokines are found
in atherosclerotic lesions and thought to be involved in atherogenesis.
The decrease in IFN-gamma and TNF-alpha and increase in TGF-� and
IL-10 production after a long-term exercise program suggests protection
against ischemic heart disease. These data show that besides weight
loss and improved lipoprotein levels, exercise can decrease CHD
risk by improving the blood cytokine profile.
Smith JK, Dyes R, Douglas JE, et al. Long-term
exercise and atherogenic activity of blood mononuclear cells in
persons at risk of developing ischemic heart disease. JAMA.
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Results from to the Lyon Heart Study indicated
that subjects with prior MI who consumed a Mediterranean type diet
were less likely to experience secondary cardiovascular complications
during the 46 month follow-up compared with controls on a prudent
Western diet. Only 14 of 218 subjects on the Mediterranean diet
suffered nonfatal MI or cardiac death compared with 44 of 204 controls.
The incidence of both major and minor secondary cardiac events
were 81 in the experimental group and 136 in the control group.
Based on the dietary records from a subset group, the control group
consumed higher amounts of total fat, saturated fat, and cholesterol,
while experimental subjects had higher intakes of linolenic acid
and dietary fiber; alcohol intake was the same for the 2 groups.
Other cardiac risk related parameters, such as plasma lipid and
lipoprotein concentrations, blood pressure, and BMI were similar
in the control and experimental groups. However, when other CVD
risk factors were included in the analysis, the data showed that "a
low-fat Mediterranean diet does not quantitatively alter the usual
relationship between the risk factors and recurrence rate." The
conditional risk ratios for diet was 0.28 compared with age (0.99),
smoking (1.65), total cholesterol (1.28), systolic blood pressure
(1.02), leukocyte count (2.84), and aspirin (0.59) for the primary
outcomes of CVD death and nonfatal MI. These data indicate that
smoking, total cholesterol, and leukocyte counts have a stronger
impact on CHD risk than diet.
This study confirms the findings from an earlier
intermediate analysis from the same cohorts at 27 months. The Mediterranean
diet, high in fruits, vegetables, fish, and olive oil, was associated
with a lower risk of CHD recurrence. The positive outcome obtained
following the Mediterranean diet with high linolenic acid was independent
of other major CHD risk factors on the recurrence rate.
de Lorgeril, M, Salen P, Martin, J et al.
Mediterranean diet, traditional risk factors, and the rate of cardiovascular
complications after myocardial infarction. Final report of the
Lyon Heart Study. Circulation. 1999;99:779-785.
Findings from the Lyon Heart Study
clearly show that there is more to managing CHD than simply
reducing plasma cholesterol levels. Even with similar end
lipid and lipoprotein levels, the rate of cardiac death
and nonfatal infarction in the experimental group was 1.24
per hundred patients per year compared with 4.07 per hundred
patients per year in the control group. Thus suggesting
that the difference in nutrients, especially linolenic
acid, in the experimental diet might have had a protective
effect on CHD risk in the study cohorts.
Table of Contents
Editorial: I Know What I Know. Dont Confuse Me With Facts
Its usually hard for most of us to say "I
was wrong." But it seems to be almost impossible for the exin Nutrition
Close-Up over the past half dozen years there are many reperts
who propose dietary recommendations. As documented in Nutrition
Close-Up over the past half dozen years there are many reported
epidemiological studies showing a null relationship between dietary
cholesterol, plasma cholesterol, and CVD incidence. Clinical studies
and meta-analyses also demonstrate that dietary cholesterol has
little effect on plasma cholesterol levels in most individuals.
Even though the evidence shows that dietary cholesterol isnt
really related to either high plasma cholesterol or heart disease
risk, consumers are still told that getting the dietary cholesterol
out is a big step towards a heart healthy diet. And it would seem
that, based on the responses to the Harvard School of Public Health
JAMA report on eggs and heart disease, few in the dietary recommendations
arena are willing to even consider informing the public that the
changes theyre making are of little value.
This large prospective study of egg consumption
and CVD risk in men and women was tagged as "just a single
report," albeit in over 117,000 people followed for 8 to 14
years. Unfortunately, those in health promotion seem unable to
expand their perceptions to include these findings with a long
list of studies coming to the same conclusion: eggs are not the
CVD risk so many religiously believe. And some of the other comments
in response to this report were equally short-sighted.
"Egg consumption is associated with eating
foods high in saturated fat such as bacon, red meat and whole milk.""most
people eat two eggs, rather than one egg in a serving a single
meal that contains double the amount of suggested (daily) dietary
cholesterol. "most of the study participants were
health professionals who ate well anyway and tended to eat fewer
eggs.""eggs can raise cholesterol significantly in someone
who already eats a lot of other animal fats.""The American
Heart Association and other responsible public health associations
wont change their guidelines of 3-4 eggs per week."
Clearly many of the responses were not well
rationalized. Based on this logic we should ban broccoli because
of all the cheese sauce used! Do we really believe that if people
who do eat high saturated fat foods would only not eat eggs theyll
get rid of those items, or that if people who avoid high saturated
fat foods eat eggs their prudent diet will be subverted? And what
is lost in the comment about two egg servings is that the 300 mg
cholesterol per day recommendation is an average over days or a
week. Whether I choose to eat 7 eggs a week one a day or a couple
every few days really shouldnt matter [unless I want to market
those daily cholesterol calculators]. And the argument that these
were somehow unique populations fails to recognize that what the
study shows is that eggs are clearly not a problem in a healthy
diet, its the saturated fat, excess calories, obesity, lack
of physical activity, etc., etc., etc. And how does one conclude
that 18,900 people eating 5 or more whole eggs per week is a low
egg consumption when the average total egg consumption in the USA
is 4.5 eggs per week? The comment regarding "other animal
fat" shows an ignorance of the evidence that plasma cholesterol
responses to dietary cholesterol in humans is independent of dietary
fat type or amount. The combined result of all these expert opinions
was nothing more than to further confuse the issue for consumers
while not admitting that maybe a 25 year old opinion could maybe
Amazingly, some dismissed the findings of
this report on the day of its publication with the "expert
opinion" that the results had no bearing on nutritional recommendations
and policies. No evaluation, no deliberation, no discussion, no
incorporation of the data into the existing body of knowledge;
only summary dismissal of findings which disagree with opinions.
This doesnt seem to be a rationale formulation of public
nutrition policy, or evidence of scientific evaluation of new research
findings. It would seem that once nutritional policies are set
and solidified, there are no adjustments or corrections based on
science? This would seem to be a case of guilty until proven innocent,
with the complication that there never ever seems to be enough
Most countries do not bother having a dietary
cholesterol, much less egg, restriction in their dietary guidelines.
In 1972 it might have seemed like a good idea given the available
evidence but after twenty-seven years of research results to the
contrary maybe its time to reconsider this outdated and obsolete
view that eggs are a health risk for the population. Egg consumption
certainly isnt a risk in countries with low rates of heart
disease [Japan, 6.5 eggs per week; Spain, 5.1 eggs per week; and
France, 5.0 eggs per week]. But then any changes in policy would
require the ability to say "we were wrong."
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.
Nutrition Close-Up is published quarterly
by the Egg Nutrition Center. Nutrition Close-Up presents
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investigating the role of nutrition in health promotion and disease
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