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Newsletters & Publications
Volume
18 - Number 2 |
Summer 2001 |
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COMMON ABBREVIATIONS
BMI: body mass index (kg/m2)
CAD: coronary artery disease
CHD: coronary heart disease
CHO: carbohydrate
CI: confidence interval
CVD: cardiovascular disease
ene: energy
HDL: high density lipoprotein
LDL: low density lipoprotein
Lp(a): lipoprotein (a)
MI: myocardial infarction
MUFA: monounsaturated fatty acids
NCEP: National Cholesterol Education Program
P:S: dietary polyunsaturated:saturated fat ratio
PUFA: polyunsaturated fatty acids
RR: relative risk
SFA: saturated fatty acids
TAG: triacylglycerol
VLDL: very low density lipoprotein
Numerous studies have documented a large degree
of individual heterogeneity of plasma lipid responses to changes
in dietary fat and cholesterol. Unfortunately, there is no clear
explanation for this variability in response to dietary cholesterol.
However, earlier results from Knopp et al. indicated that subjects
with combined hyperlipidemia were more sensitive to dietary cholesterol
than were hypercholesterolemics. Therefore, based on this observation
and the knowledge that combined hyperlipidemics tend to also be
more insulin-resistant, Reaven et al. tested the hypothesis that
insulin-resistance is linked to dietary cholesterol sensitivity.
Using steady-state plasma glucose and insulin
measurements (SSPG), Reaven et al. determined each volunteer's
insulin resistance status. Thirty-one women were insulin resistant
with an average SSPG of 206 mg/dl and 34 women were insulin-sensitive
with SSPG values of 75 mg/dl. Women in both groups were similar
in age (56 y) and had similar total (172.5 mg/dl) and LDL (107.5
mg/dl) cholesterol levels. But as seen with other studies, insulin-resistant
women were heavier and had more negative TAG, VLDL, HDL, apo B,
apo A, and Lp(a) concentrations than their insulin-sensitive counterparts.
Following 4 weeks of a baseline diet with
113 mg/day dietary cholesterol and a 4 week washout period, women
were randomly divided into one of 3 dietary cholesterol groups
with cholesterol intakes of either 319 mg/day, 523 mg/day, or 941
mg/day. The experimental diet period also lasted 4 weeks. Plasma
total and LDL levels following the increase in dietary cholesterol
showed no set trend (see table). For example, compared to women
with the highest increase in dietary cholesterol, women in the
319 mg/day group saw the largest increase in their plasma total
cholesterol levels. Also, contrary to the study hypothesis, insulin
sensitivity was unrelated to the changes in lipoprotein concentrations
with incremental increases in dietary cholesterol. The change in
concentrations of plasma HDL2, IDL cholesterol, apo A and apo B
levels following increased cholesterol intakes were modest. For
example, plasma HDL2 levels changed from 13.3�1.3 to 15.5�1.7 mg/dl
when the cholesterol intake was increased from 113 to 941 mg/day.
Dietary Cholesterol
(added mg/day) |
Change
in Plasma Total and LDL Cholesterol (mg/dl) |
Total
Group |
Insulin
Sensitive |
Insulin
Resistant |
Total |
LDL |
Total |
LDL |
Total |
LDL |
319 |
11 |
7 |
4 |
4 |
17 |
12 |
523 |
6 |
4 |
6 |
5 |
5 |
3 |
941 |
8 |
6 |
9 |
7 |
8 |
6 |
In conclusion, results from Reaven et al.'s
study identified 2 very important points regarding the dietary
and plasma cholesterol relationship. First of all, it confirmed
earlier findings that even an increase of 828 mg/day of dietary
cholesterol had a minimal effect on blood cholesterol levels. Secondly,
compared to those with normal insulin sensitivity, these results
disprove that insulin-resistant individuals are more sensitive
to dietary cholesterol. In spite of the 3-fold difference in insulin-mediated
glucose disposal between the 2 study groups, changes in plasma
lipid and lipoprotein levels following the incremental increase
in dietary cholesterol were similar. Clearly more studies are needed
to identify those physiological and genetic factors that attribute
to some individuals being more sensitive to dietary cholesterol
than the general population.
Knopp RH, Retzlaff BM, Walden CW et al. A
double-blind, randomized controlled trial of the effects of two
eggs per day in moderately hypercholesterolemic and combined hyperlipidemic
subjects thought the NCEP step 1 diet. J Am Coll Nutr. 1997;16:551-561.
Reaven GM, Abbasi F, Bernhart S et al. Insulin
resistance, dietary cholesterol, and cholesterol concentration
in postmenopausal women. Metabolism. 2001;50:594-597.
Key Messages
- Plasma total and LDL levels following an increase in dietary
cholesterol showed no set trend.
- 828 mg/day increase in dietary cholesterol did not negatively
affect blood lipid and lipoprotein profiles.
- Insulin resistant individuals were not more sensitive to dietary
cholesterol than insulin sensitive individuals.
Table of Contents
After 30 years of being maligned for its supposed
role in raising blood cholesterol levels, eggs are making a comeback
thanks to mounting scientific evidence refuting this myth. Last
year, the American Heart Association increased their egg recommendation
from 3-4 egg yolks to 7 egg yolks per week. However, there are
some who still discourage egg consumption. Weggemans et al., found
little change in plasma total, LDL, and HDL cholesterol levels
following higher dietary cholesterol intake, yet advised people
to "limit cholesterol intake by reducing consumption of eggs
and other cholesterol rich foods." Compared to the meta-analysis
by Howell et al. and Clarke et al, Weggemans et al.'s study analyzed
few studies (n=17) with less subjects (n= 556) and included both
metabolic ward and free-living studies. The analysis included studies
that only differ in the amount of dietary cholesterol with similar
dietary fat.
Based on their analysis, total cholesterol,
LDL, HDL cholesterol levels increased by 2.2 mg/dl, 1.9 mg/dl,
and 0.3 mg/dl, respectively, for each 100 mg/d of dietary cholesterol.
Total:HDL cholesterol ratio increased an average of 0.020�0.005
units while HDL:LDL cholesterol ratio decreased 0.006�0.001 units.
Change in plasma LDL cholesterol level was greater among those
with higher saturated fat intake; each additional 100 mg of dietary
cholesterol increased serum LDL cholesterol by 1.39 mg/dl with
a P:S ratio of < 0.7, while it increased by 2.36 mg/dl with
P:S ratio of >0.7. HDL was not affected by the P:S ratio. These
changes in lipoprotein levels with dietary cholesterol were in
line with findings by Howell et al. and Clarke et al.
Since one egg yolk has 200 mg of cholesterol,
the authors estimated that this would raise total: HDL ratios by
0.04 units which might
raise MI risk by 2.1%. Despite numerous studies showing no relationship
between dietary cholesterol or eggs intake and CHD risk, the researchers
recommended that egg intake be limited. [See editorial for comments.]
Clarke R, Frost C, Collins R, et al. Dietary
lipids and blood cholesterol: quantitative meta-analysis of metabolic
ward studies. BMJ. 1997;314:112-117.
Howell WH, McNamara DJ, Tosca MA, et al. Plasma
lipid and lipoprotein responses to dietary cholesterol fat and
cholesterol: a meta-analysis. Am
J Clin Nutr. 1997;65:1747-1764.
Weggemans R, Zock PL, Katan MB. Dietary cholesterol
from eggs increases the ratio of total cholesterol to high-density
lipoprotein cholesterol in humans: a meta-analysis. Am J Clin
Nutr. 2001;73:885-891.
Table of Contents
Benefits of moderate alcohol intake in lowering
CHD risk have clearly been shown. Hines
et al. and Corella et al. have gone further to identify those individuals
who receive the greatest CHD benefit from moderate alcohol consumption
based on their genes. Using genetic variations in alcohol dehydrogenase
levels of men in the Physicians' Health Study and women in the
Nurses' Health Study, Hines et al. found that individuals who are
homozygous for the slow-oxidizing alcohol dehydrogenase type 3
(ADH3) allele (g2g2) had the lowest MI risk (RR=0.14) compared
to individuals who were homozygous for the fast-oxidizing ADH3
allele (g1g1) or heterozygous (g1g2). And according to a study
by Corella et al., moderate alcohol intake lowered LDL cholesterol
levels most dramatically in men with the apo E2 allele compared
to those with apo E3.
Hines et al.'s study with 1166 male subjects
(396 MI patients and 770 controls) and 325 post-menopausal women,
observed that 1 drink per day lowered MI risk by 38%. The reduction
in MI risk was directly associated with the number of g2 alleles.
The multivariate RR for MI risk was 0.83 in heterozygous men and
0.65 in g2 homozygous men. When both ADH3 genotypes and alcohol
consumption were included in the analysis, the relationship between
ADH3 genotypes and MI risk became even stronger. The multivariate
RR for MI was 0.62, 0.68, and 0.14 for ADH3 genotypes g1g1, g1g2,
and g2g2, respectively, for cohorts who drank at least one drink
per day. Alcohol consumption of less than one drink per day was
not associated with significant reduction in MI risk.
This study also looked at the relationship
between plasma HDL levels, alcohol intake, and ADH3 genotype. It
showed that regular intake of greater than 1 drink per day was
associated with a 3.5 mg/dl increase in HDL cholesterol levels
in men. But the actual HDL cholesterol level was highest among
those with the g2g2 allele, followed by g1g2 and then the g1g1.
No such trend was noted in subjects who drank less than one drink/day.
The relationship between ADH3 genotype, alcohol intake, and plasma
HDL was much greater in female subjects; women who consumed at
least 1/2 drink/day had a 7.8 mg/dl increase in their HDL levels.
This study clearly shows that individuals
with the g2g2 genotype for ADH3, who metabolizes alcohol more slowly,
have a greater CHD benefit from alcohol intake. Clearing alcohol
more slowly appears to raise HDL cholesterol levels as well as
to lower MI risk.
According to a study conducted by Corella
et al., men who drink alcohol in moderation exhibit serum LDL cholesterol
concentrations which are affected by their apolipoprotein E (APOE)
gene locus. Based on data from the Framingham Offspring Study with
2,147 subjects, the distribution of E3, E4, and E2 alleles were
82%, 11%, and 7%, respectively. E2 subjects had significantly lower
plasma total and LDL cholesterol than E3 and E4 cohorts, despite
similar dietary fat, saturated fat, and alcohol intakes among the
3 apo E allele types.
Food frequency questionnaires showed that
a higher percentage of men drank compared to women and were more
likely to drink more alcohol than women. Compared to nondrinkers,
LDL cholesterol levels of male drinkers were 5.0 mg/dl higher,
while female drinkers
had a 4.3 mg/dl reduction in their plasma LDL. Analysis of mean
LDL cholesterol concentrations across apo E allele types showed
that male drinkers with the apo E2 allele had lower LDL cholesterol
levels, while apo E4 allele subjects had the highest concentrations.
LDL cholesterol levels of male drinkers with E2, E3, and E4 alleles
were 110 mg/dl, 131, and 137 respectively, compared to 127, 127,
and 120, respectively in nondrinkers. In women, LDL cholesterol
levels were the lowest in apo E2 subjects and highest in apo E4,
regardless of alcohol consumption pattern.
Including other CHD risk factors into the
apo E allele and LDL cholesterol relationship further strengthen
the effect of alcohol intake on LDL cholesterol in men, but minimized
it in women. The average effect of the E2 allele on the LDL cholesterol
concentration was -12.9 mg/dl, the E3 allele was 1.3 mg/dl, and
the E4 allele was 3.8 mg/dl. This relationship was stronger among
male drinkers and weaker among male nondrinkers. Further stratification
of alcohol intake into none, moderate, and high intakes showed
that for the benefits of alcohol consumption, more was not necessarily
better.
Results from the study by Corella et al. indicate
that the LDL cholesterol concentration is affected by the APOE
allele in both genders, but in men, moderate alcohol consumption
dramatically enhances the gene effect. While the mechanism is unknown,
the researchers hypothesized that the APOE allele influences LDL-receptor
binding affinity. Of the 3 phenotypes, E2 allele has a lowest affinity
for binding to LDL receptor therefore individuals with E2 allele
had the lowest LDL cholesterol levels. While "in subjects
with E4 allele, VLDL are apo E enriched and these particles may
be taken up more readily by the liver, thus decreasing the expression
of LDL receptor and increasing plasma LDL-cholesterol concentration." Moderate
alcohol intake could enhance both of these genotypic expressions.
Corella D, Tucker K, Lohoz C et al. Alcohol
drinking determines the effect of the APOE locus on LDL-cholesterol
concentrations in men: the Framingham Offspring Study. Am J
Clin Nutr. 2001;73:736-745
Hines LM, Stampfer MJ, Ma J, et al. Genetic
variation in alcohol dehydrogenase and the beneficial effect of
moderate alcohol consumption on myocardial infarction. N Engl
J Med. 2001;344:549-555.
Table
of Contents
Ever since consumers learned of the cardioprotective
benefits associated wistudies by Pedersen et al. suggest that rapeseth
olive oil, consumption of this oil has dramatically increased.
But the latest studies by Pedersen et al. suggest that rapeseed
oil may be even more beneficial than olive oil in lowering an atherogenic
plasma lipid profile. For example, compared to diets containing
rapeseed and sunflower oil, plasma total cholesterol, TAG, apo
B, VLDL, LDL concentrations were 10-20% higher following an olive
oil containing diet.
In this double-blind, randomized, crossover
feeding study, 18 young men consumed 3 test diets. Aside from 19%
of calories coming from olive oil, rapeseed oil, or sunflower oil,
the three test diets contained 35% of calories from fat and were
identical for all nutrients. Each test diet was consumed for 3
weeks followed by a washout period of 5-12 weeks. Men in the study
were healthy with a mean plasma total cholesterol level of 183
mg/dl (4.74 mM), HDL of 42.5 mg/dl (1.10 mM), and TAG of 106 mg/dl
(1.2 mM).
The results from this feeding study indicate
that rapeseed oil (RO) and sunflower oil (SO) had a more favorable
effect on blood lipid and lipoprotein levels than olive oil (OO).
For example, following the OO diet, fasting plasma total cholesterol
concentrations were 12% higher than with the RO or SO diets. Also,
plasma TAG and apo B concentrations were 20% higher with the OO
diet. No differences in total cholesterol, TAG, and apo B were
noted between the RO and SO diets. On the other hand, the average
plasma apo A-I level was higher after the OO and RO than SO diet.
Analysis of number, size and composition of
LDL and HDL subclasses following each test diet showed that the
sizes of IDL, VLDL, and LDL subfractions were similar between test
diets, but following the OO diet there was an increase in large
and medium sized LDL particles. There were no differences in concentrations
of small, dense LDL subfractions following the test diets. Even
though an increase in small, dense LDL has been related to increased
CVD risk, currently there is not enough evidence to show a relationship
between large and medium size LDL particles and CVD risk. The researchers
also observed that the LDL:HDL ratio and total cholesterol:LDL
ratio were higher with the OO and SO diet than with the RO diet,
suggesting that the OO and SO diets resulted in a more atherogenic
plasma lipoprotein profile than the RO diet.
Results from this study indicate that different
types of fatty acids have different effects on plasma lipids and
lipoprotein levels. For example, the RO diet was the least atherogenic
compared to the OO and SO diets, with the most favorable plasma
total cholesterol, VLDL, IDL, LDL, HDL, TAG, nonesterified fatty
acids, and plasma insulin levels. The differences in plasma lipids
and lipoproteins following intakes of RO and OO, 2 highly MUFA,
were initially thought to be a result of the higher omega-3 content
in RO, but these data did not support this hypothesis. Pedersen
et al. speculated that the differences in plasma lipid and lipoprotein
concentrations were possibly due to a higher squalene content,
an intermediate in the biosynthesis of cholesterol, in the OO diet,
which would result in higher plasma squalene:cholesterol and desmosterol:cholesterol
ratios with the OO diet. In conclusion, these data suggest that
healthy men could reap the most cardiovascular benefit from including
rapeseed oil in their diet, more so than the widely touted olive
oil.
Pedersen A, Baumstark MW, Marckmann P, et
al. An olive oil-rich diet results in higher concentrations of
LDL cholesterol and a higher number of LDL subfraction particles
than rapeseed oil and sunflower oil diets. J Lipid Res. 2000.
41:1901-1911.
Table of Contents
Ever since homocysteinemia emerged as a risk
factor for CHD, folate, B12, and B6 vitamins have also received
more attention since these B vitamins play an important role in
regulating plasma homocysteine levels. However, unlike folic acid,
the evidence supporting beneficial effects in treating hyperhomocysteinemia
with B6 supplements is mixed. According to data from McKinley et
al., low dose B6 vitamin (1.6 mg/d) is effective in lowering plasma
total homocysteine levels. In their 12-week, randomized double-blind,
placebo-controlled trial, B6 supplements were evaluated in 22 healthy
elderly between 63-80 years.
Prior to supplementing vitamin B6, subjects
received 6 weeks of 400 mg/d of folic acid and 18 weeks of 1.6
mg/d of riboflavin to replete their plasma folic and riboflavin
levels. This resulted in improved serum folate and plasma total
homocysteine levels. Fasting plasma total homocysteine levels decreased
from 12.65�6.19 to 10.17�3.86 mmol/l. However, to minimize the
effect folate plays in lowering total homocysteine levels, the
B6 supplement was introduced after the plasma total homocysteine
level reached a plateau. Folate and riboflavin supplements were
continued throughout the study.
Based on plasma pyridoxal-P and the erythrocyte
asparate aminotransferase activation coefficient, two measures
of plasma B6 levels used in the study, the B6 supplement group
had better vitamin B6 status, as well as lower plasma total homocysteine
levels (7.5%) than the placebo group. Dietary intakes of folate,
B6, B12, and riboflavin were above the lower reference nutrient
intake in all subjects.
In conclusion, results from this study indicate
that folate supplementation is more effective than vitamin B6 in
lowering fasting plasma homocysteine levels. However, even in elderly
with adequate folate and riboflavin levels, it is possible to further
reduce their homocysteine levels with intake of low doses of B6
supplement along with continued intake of adequate dietary sources
of B vitamins.
McKinley MC, McNulty H, McPartlin J, et al.
Low-dose vitamin B-6 effectively lowers fasting plasma homocysteine
in healthy elderly persons who are folate and riboflavin replete. Am
J Clin Nutr. 2001;73:759-764.
Table of Contents
Diets high in fruits, vegetables and whole
grains have long been touted for their beneficial role in preventing
many chronic illnesses but recent epidemiological outcomes have
begun to question the benefits of these foods in the prevention
of certain cancers. The Nurses' Health Study (NHS) and Health Professionals
Follow-up Study, both showed that fruit, vegetable, and fiber intakes
did not reduce colon cancer risk, and now, according to a meta-analysis
by Smith-Warner et al., fruit and vegetable consumption has little
effect on breast cancer risk.
Based on this study, which looked at dietary
habits of 351,825 women in 8 prospective, cohort studies (Adventist
Health Study, Canadian National Breast Screening Study, Iowa Women's
Health Study, Netherlands Cohort Study, New York State Cohort,
New York university Women's Health Study, Sweden Mammography Cohort,
and NHS), fruit and vegetable consumption was not associated with
reducing breast cancer risk. For example, the RR for the highest
quartile for fruit intake was 0.93 (95% CI 0.86-1.00), highest
vegetable intake was 0.96 (95% CI 0.89-1.04) and highest total
fruit and vegetable intake was 0.93 (95% CI 0.86-1.00). Separate
analysis of fruits and vegetables based on 8 botanical groups or
17 specific fruit and vegetable items showed no significant differences
in the relationship between breast cancer and overall fruit and
vegetable intake. Also, menopausal status of the cohort or other
cancer risk factors had little effect on the relationship. Similar
results were found in 2 other cohort studies; however, other case-control
studies showed an inverse association between fruit and vegetable
intake and breast cancer risk. Seven thousand three hundred and
seventy-seven cases of invasive breast cancer were reported among
the study cohort.
In conclusion, even though the study finding was
unexpected by showing that high fruit and vegetable intake only
lowered breast cancer risk by 4%, it in no way recommends consumers
decrease intake of these foods. As other studies have clearly shown,
high fruit and vegetable intakes can protect against other types
of cancers as well as other chronic diseases.
Smith-Warner SA, Spiegelman D, Yaun SS, et
al. Intake of fruits and vegetables and risk of breast cancer.
A pooled analysis of cohort studies. JAMA. 2001;28:769-776.
Table of Contents
We all know that CHD is a multifaceted illness,
and hypercholesterolemia has long been considered a major risk
factor for CHD. However, results from the Pathobiological Determinants
of Atherosclerosis in Youth (PDAY) Study indicate that non-lipid
risk factors for CHD - smoking, hypertension, obesity, and impaired
glucose tolerance, play important roles in atherosclerosis progression,
irrespective of lipoprotein profile.
All 856 subjects in the study died of external
causes such as accidents, homicides, or suicides, and had plasma
lipoprotein profiles within desirable levels. Examination of autopsy
samples of abdominal aorta and right coronary arteries (RCA) of
15-34 year olds showed that nonlipid CHD risk factors had dramatic
effects on the extent and severity of coronary and aortic atherosclerosis.
Smoking was associated with early development of fatty streaks
in the abdominal aorta, and raised lesion developed approximately
a decade later. On the other hand, smoking did not negatively affect
RCA at any age. Hypertension was associated with raised lesions
in both vessels, but it did not increase fatty streaks. Also, compared
to Caucasians, African-Americans had a higher incidence of raised
lesions due to the higher incidence of hypertension. Obesity was
only associated with fatty streaks of the RCA in the 15-24 year
old group. On the other hand, obesity was not related to fatty
streaks or raised lesions in women. Elevated glycohemoglobin was
associated with fatty streaks in the RCA of 15-24 year old group
only. Gender also played a specific role in atherosclerosis progression.
For example, compared to women, men had less extensive fatty streaks
in the abdominal aorta, but more fatty streaks in the RCA. The
extent of raised lesions in both vessels was similar between men
and women.
The odds ratio of nonlipid risk factors; male
sex, smoking, hypertension, obesity, and elevated glycohomoglobin
in the subjects with advanced lesions as defined by AHA, compared
to the subjects with normal or isolated foam cells were 4.09, 1.22,
3.72, 0.31, and 1.78, respectively. Compared to individuals with
no CHD risk, individuals with all 4 non-lipid risk factors had
dramatically higher extent of raised lesion in the RCAs across
all age groups. For example, 30-34 year old males with all 4 risk
factors had 5 times more raised lesions than found in the RCA of
15-19 year old boys with no CHD risk factors.
These data clearly show that even in people
with favorable lipoprotein profiles, non-lipid risk factors play
important roles in atherosclerosis progression and must be addressed
to prevent CHD. And in light of the fact that 47% of the study
subjects had 1 nonlipid risk factor, 13% with 2 risk factors, 0.7%
with 3 risk factors, and 0.1% with 4 risk factors, early intervention
should be initiated to delay further development of atherosclerosis
in young adults.
McGill HC, McMahan A, Zieske AW, et al. Effects
of nonlipid risk factors on atherosclerosis in youth with a favorable
lipoprotein profile. Circulation. 2001;103:1546-1550.
Table of Contents
During the early '70s, it was thought that
in order for exercise to be beneficial, it had to be vigorous,
however, recent findings indicate that even a light-to-moderate
activity level can lower CHD risk. In a study by Lee et al., walking
one hour per week resulted in a 50% reduction in CHD risk among
middle-aged women. These data support current physical activity
recommendations of 30 minutes of moderate intensity physical activity
most days of the week.
The 39,372 women in this study were originally
part of the Women's Health Study. During the 5-year follow-up period,
244 cases of CHD incidents were reported. An initial analysis of
the cohort indicated that the overall lifestyle pattern of the
active women in the study was healthier than that of the inactive
group. Examination of the association between physical activity
and CHD risk showed an inverse relationship. For example, compared
to women who expended less than 200 kcal/week, women who expended
between 200-599 calories per week and 600-1499 calories per week
lowered their CHD risk by 24% and 51%, respectively. Energy expenditure
beyond 1500 calories per week did not result in further reduction
in CHD risk. Participation in vigorous recreational activities
of at least 6 metabolic equivalent rate also lowered CHD risk,
but less dramatically than the low-intensity level.
Since walking is the exercise of choice among
many women, the researchers compared the role of walking on CHD
risk in a 22,865 subgroup and found that women who walked at least
1 hour/week or whose usual walking pace was at least 3 miles per
hour had their CHD risk lowered by 50% compared to women who didn't
walk regularly. But of the 2 walking parameters, duration of the
walk had a greater effect on lowering CHD risk compared to the
intensity. Lastly, of the 4 major CHD risk factors; smoking status,
body weight, blood pressure, and blood cholesterol levels, the
researchers noted that exercise was especially important in lowering
CHD risk among current and past smokers and non-hypertensive individuals.
Based on this study, it would appear that
the "no pain, no gain" approach to exercise is pass�.
Middle-age women can dramatically lower their CHD risk by simply
getting out and walking for at least 1 hour per week, regardless
of pace.
Lee IM, Rexrode KM, Cook NR, et al. Physical
activity and coronary heart disease in women. Is "no pain,
no gain" pass�? JAMA. 2001;285:1447-1454.
Table of Contents
You really do have to love their tenacity,
their conviction, their unwavering commitment to their belief no
matter the evidence. Members of the Flat Earth Society? No! Members
of the "Dietary Cholesterol Will Kill You No Matter What the
Science Shows Society." The true believers really do validate
that old concept that hypotheses only die when their proponents
do. The dietary cholesterol - blood cholesterol - heart disease
debate has followed the classic sequence involved in changing concepts.
First, disbelief. Four years ago two meta-analysis of the effects
of dietary lipids on plasma lipids and lipoproteins were summarily
rejected because they didn't fit with the prevailing conventional
wisdom of the time. Surely dietary cholesterol increased blood
cholesterol levels more than 2.2 mg/dl per 100 mg/day, everyone
knew it was more than that, closer to 10 mg/dl per 100 mg/day.
Stage two, okay that's right but it still increases blood cholesterol
a little and any increase in blood cholesterol increases heart
disease risk and therefore is bad. And then come the reports showing
that dietary cholesterol increases both the "bad" LDL
cholesterol and the "good" HDL cholesterol with little
change in the LDL:HDL ratio, an important marker of heart disease
risk. Stage three, wait a minute, just a minute, hold on now, let's
really look at the data, maybe there's still something there, we
couldn't have been wrong for the last thirty years! And the latest
salvo in the war of the words shows that dietary cholesterol raises
LDL cholesterol more than HDL cholesterol and "an egg a day" would
raise the LDL:HDL ratio by 0.04 and increase heart disease risk
by, drum role please, 2%. Two percent!
What is even worse, the calculation of this
huge, monstrous, gigantic 2% increase in heart disease risk with
consumption of those dastardly eggs is WRONG! Changes in ratios
are dependent upon the values of the variables, not a fixed value.
Consider the following: 2 patients with 2 different LDL and HDL
levels (low versus high risk) add an egg a day to a diet with 30%
of calories as fat and a P:S ratio of 1.0 will result in 2.8 mg/dl
and 0.8 mg/dl increase in LDL and HDL levels, respectively, according
to Weggemans et al. [See table below for calculated changes in
plasma lipoprotein cholesterol levels and LDL:HDL ratio.]
Cholesterol (mg/dl) |
Mr.
Smith |
Mr.
Jones |
Baseline |
+ 1 egg/day |
Baseline |
+ 1 egg/day |
LDL |
120 |
122.8 |
160 |
162.8 |
HDL |
60 |
60.8 |
40 |
40.8 |
LDL:HDL |
2.00 |
2.02 |
4.00 |
3.99 |
CHD Risk |
|
+ 1.0% |
|
- 0.5% |
So Mr. Smith increases a very low risk by
1.0% while Mr. Jones actually lowers a high risk by 0.5%. Seems
Mr. Jones comes out ahead on this deal since lowering a high risk
by 0.5% would have more benefit than the risk of increasing a low
risk by 1.0%. And while statistically all these numbers may be
significant, from a biological perspective they are meaningless.
Statistical significance is not the same as biological importance.
Which brings me to my last tirade: Who came
up with the TLC (Total Lifestyle Change) diet concept? For the
National Cholesterol Education Program to make it a national policy
to have high risk individuals lower their dietary cholesterol intake
to less than 200 mg/day as part of an intensive plasma cholesterol
lowering program certainly does put the wrong emphasis in the wrong
direction. Changing your cholesterol intake from 300 mg/day to
200 mg/day in a low saturated fat diet will have the magnificent
effect of lowering your plasma LDL cholesterol level by 1.4 mg/dl.
What a big deal about nothing, public health attack on the scourge
of heart disease! But the dietary cholesterol-blood cholesterol-heart
disease Truth Sayers will not be deterred by anything as mundane
as a decade of research showing that DIETARY CHOLESTEROL IS NOT
THE PROBLEM.
All I need to do now is wait for the next phase
of the long, slow process involved in changing scientific opinion,
the phase where everyone says yes, you're right, we knew it all
along. I should live so long with my 1.0% change in heart disease
risk!
Donald J. McNamara, Ph.D.
Executive Editor, Nutrition Close-Up
Table of Contents
Executive
Editor: Donald J. McNamara, Ph.D.
Writer/Editor: Linda Min, M.S., R.D.
Nutrition Close-Up is published quarterly
by the Egg Nutrition Center. Nutrition Close-Up presents
up-to-date reviews, summaries and commentaries on the latest research
investigating the role of nutrition in health promotion and disease
prevention, and the contributions of eggs to a nutritious and healthful
diet. Nutrition and health care professionals can receive a FREE
subscription for the newsletter by contacting the ENC.
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