As the demographics of the American public
shifts towards an older population, the incidence of age-related
macular degeneration is on the rise. However, lutein and zeaxanthin
accumulation in the macular region of the retina has been shown
to protect against this debilitating eye disorder among elderly.
These 2 carotenoids are readily found in dark-green leafy vegetables,
corn, and eggs. But chloroplasts or chromoplasts and other plant
structural materials make plant sources of zeaxanthin and lutein
less bioavailable. Eggs on the other hand are better source since "the
carotenoids in egg yolk are in a digestible lipid matrix consisting
of cholesterol, phospholipids, and triacyglycerols."
In this study, the investigators examined the
effects of added egg yolk intake on plasma concentrations of lutein
and zeaxanthin in 11 hypercholesterolemic older adults. The plasma
samples analyzed in this study were originally collected for a
study investigating the effects of egg yolk on plasma cholesterol
levels with either a PUFA
or saturated fat enriched diet. The 2 baseline diets contained
20% of energy as either corn oil or beef tallow, while the 2 test
diets contained an additional 1.3 egg yolk/d. All meals were prepared
in a metabolic kitchen. Each diet was consumed for 4.5 weeks with
at least 2 weeks of washout period. Handelman et al. used frozen
blood samples from each test diet to analyze for plasma carotenoid
levels. Blood levels of lutein and zeaxanthin increased during
both egg yolk supplemented diets compared to baseline corn oil
or beef tallow diet. For example, lutein levels increased 50%,
from 0.269 µmol/l to 0.403 µmol/l, when egg yolk was added to the
corn oil diet. Zeaxanthin levels increased by 114%, (0.049 to 0.105 µmol/l).
With intake of the tallow diet plus egg, plasma lutein concentrations
increased by 28% (0.333 to 0.427 µmol/l) and zeaxanthin by 142%
(0.048 to 0.116 µmol/l) compared to the baseline diet. The increases
in lycopene and beta carotene levels were not statistically significant.
Blood cholesterol levels following added egg yolk were 5% higher
than the baseline diets.
The 6 samples of eggs analyzed for lutein and
zeaxanthin content indicated that average lutein and zeaxanthin
levels in egg yolk were 292±117 µg and 213±85 µg, respectively,
or 1.19±0.32 µg/mg cholesterol of lutein and 0.87±0.23 µg/mg cholesterol
of zeaxanthin. Eggs contain 38% more lutein than zeaxanthin and
this difference is reflected in the observed changes in plasma
carotenoid levels. The average change in plasma lutein (0.114 µmol/l)
with added egg yolk was greater than in plasma zeaxanthin levels
(0.062 µmol/l). Lycopene and ß carotene levels were very low in
eggs.
These findings demonstrate that eggs are an excellent
source of lutein and zeaxanthin with high bioavailability, much
more than spinach and corn, 2 foods commonly recommended for their
high lutein and zeaxanthin content. When Hammond et al. fed 60
gm cooked spinach or 150 gm cooked corn, which increased dietary
zeaxanthin by 300 µg/d each, plasma zeaxanthin levels did not change
whereas in this study it increased by 0.062 µmol/l following intake
of 1.3 egg yolks (280 µg zeaxanthin). The researchers attributed
this enhanced absorption of zeaxanthin to the lipid matrix found
in the egg yolk. Also, in light of these dramatic increases in
plasma zeaxanthin and lutein levels, which have been shown to protect
against age-related macular degeneration, small increases in plasma
total and LDL cholesterol levels in these hypercholesterolemic
subjects is less a concern.
Hammond BR, Johnson EJ, Russell RM, et al. Dietary
modification of human macular pigment density. Invest Ophthalmol
Vis Sci. 1997;38-1795-1801
Handelman G, Nightingdale ZD, Lichtenstein AH,
et al. Lutein and zeaxanthin concentrations in plasma after dietary
supplementation with egg yolk. Am J Clin Nutr. 1999;70:247-251.
Inconsistent lipid responses following controlled
hypothesis that energy reduction in the self-selected diet is and
self-selected low-fat diet has led Flynn et al. to test the hypothesis
that energy reduction in the self-selected diet is responsible
for greater decline in plasma lipids following this diet. According
to the investigators, a modest energy reduction in a NCEP II diet
results in a better plasma lipoprotein profile compared to the
NCEP diet without energy reduction. In this feeding study, 20 hypercholesterolemic
volunteers were provided with 3 test diets for 4 weeks each. The
high fat, high saturated fat (HFSF) diet contained 40% of energy
from fat and 18% from saturated fat. The two NCEP II diets contributed
25% of energy from fat and 7% saturated fat. The 2 baseline diets,
HFSF and isocaloric NCEP 2 diet, were isocaloric, while the energy
level in the hypocaloric NCEP 2 diet was reduced by 15%. Supplemental
muffins were used to increase caloric levels in the baseline diets.
Exercise was discouraged beyond three 30 minute sessions per week.
Compared to the HFSF diet, plasma total, LDL,
and HDL cholesterol levels during the isocaloric NCEP 2 diet decreased
by 4%, 4%, and 13%, respectively. However, plasma VLDL, TAG, and
TC:HDL ratio increased by 29%, 27%, and 11%, respectively. The
lipid profile changes following initiation of the hypocaloric NCEP
2 diet were much more favorable with additional decreases in total
cholesterol, LDL cholesterol, and apolipoprotein B levels, without
any further decrease in HDL cholesterol levels. Also, the increases
in TAG and TC:HDL ratio were lower compared to the isocaloric NCEP
II diet. Body weights decreased an average of 1.9 kg. The results
from this study show that combined energy and fat restrictions
in a hypocaloric NCEP II diet result in a better plasma lipid response
compared to only a low-fat diet. These observations suggest that
reducing calories is as important, if not more important, in managing
lipids than simply replacing fat calories with CHO. Yet the observed
lipid responses following both NCEP II diets were much less than
the 17% to 24% estimated by NCEP or predicted by either the Keys
or Hegsted equations. Also, neither diet lowered LDL cholesterol
to less than 160 mg/dl. Perhaps more of a concern was the observation
that the 7% decrease in HDL levels compared to 4% decrease in total
cholesterol resulted in the increase in the of TC:HDL cholesterol
ratio from 4.9 to 5.5, a change associated with a more negative
lipid profile.
In conclusion, a hypocaloric NCEP II diet which
mimicks self-selected low-fat diets in other studies was more effective
than an isocaloric NCEP II diet in reducing plasma apo B, TAG,
and cholesterol levels without changes in HDL levels. Clearly restrictions
of both saturated fat and total calories should be emphasized in
the more rigorous lipid lowering diets.
Flynn MM, Zmuda JM, Milosavljevic D, et al.
Lipoprotein response to a National Cholesterol Education Program
Step II diet with and without energy restriction. Metabolism. 1999;48:822-826.
Table of Contents
As everyone knows, cigarette smoking is considered
the number one risk factor for CHD but, accassive smoking is also
associated with increased CHD risk. Based on 18 epidemiological
studcording to a recent meta-analysis, passive smoking is also
associated with increased CHD risk. Based on 18 epidemiological
studies, the relative risk (RR) of CHD was 1.25 in nonsmokers regularly
exposed to tobacco smoke compared to nonsmokers not exposed to
smoke.
Using Medline, Dissertation Abstracts Online
data bases, and reviewed citations searches, the researchers selected
10 cohort and 8 case-control studies which met the defined criteria
for analysis. The cohort sizes ranged from 513 to 478,680 in the
selected studies. Follow-up periods were between 6-20 years. The
number of subjects in the case-control studies ranged from 34-343
cases and 68-825 controls. All studies adjusted for sex and age,
but the confounding effects of serum cholesterol levels, blood
pressure values, and BMI were not included in 8 of the 18 case-control
studies.
The RR of environmental exposure to tobacco
smoke for CHD in the cohort and the case-control studies were 1.21
and 1.51, respectively; the combined RR was 1.25. The amount and
duration of tobacco exposure was also a factor in CHD risk. For
example, the RR for CHD in people exposed to 1-19 cigarette/d was
1.23 compared to 1.31 in the ³20 cigarettes/d group. And 1-9 years
of passive tobacco exposure was associated with an 18% higher risk
compared to 31% in the 10-19 years group. These relationships were
not different based on gender, however, secondhand smoke exposure
at home had slightly higher CHD risk than in the workplace exposure.
But only 8 out of 18 studies included data on workplace cigarette
exposure.
Even though passive smoking increases CHD
risk by 25%, much less than direct smoking with a 70% increase,
due to the shear number of smoker in America, the researchers conclude
that there is a pressing public health need to eliminate smoking
from public places, workplaces, and even homes. This should reduce
one environmental CHD risk factor.
He J, Vupputuri S, Allen K. et al. Passive smoking
and the risk of coronary heart disease- a meta-analysis of epidemiologic
studies. N Engl J Med. 1999;340:920-926.
Table of Contents
Since the 70s there has been mounting evidence
linking elevated plasma homocysteine levels to increased CVD risk.
Now the latest studies by Bostom et al. and Ridker et al. suggest
that elevated non-fasting plasma total homocysteine levels (tHcy)
are an independent risk factor for CVD.
The baseline clinical characteristics of subjects
showed that gender, age, total cholesterol, blood pressure, and
creatinine levels were directly associated with plasma tHcy levels,
but smoking and diabetes were not related. Based on their plasma
tHcy levels, 1,933 elderly from the Framingham Heart Study were
divided into quartiles: 4.13-9.25 µmol/l, 9.26-11.43 µmol/l, 11.44-14.25 µmol/l,
and 14.26-219.84 µmol/l. Of the 655 total deaths and 244 CVD deaths
reported during the 10-year follow-up period, a higher number occurred
among the uppermost quartile group. Bostom et al. found that the
RR of total and CVD mortality was 2.2 in people with tHcy of >14.26 µmol/l
compared to subjects with <14.25 µmol/l. When other risk factors
for CVD (age, sex, diabetes, smoking, systolic blood pressure,
total and HDL cholesterol, and creatinine) were included in the
analysis, the relationship was slightly attenuated. The adjusted
RR was 1.5 for both total and CVD mortality.
In a similar study, Ridker et al. tested the
relationship between plasma tHcy levels and CVD outcomes. In this
prospective study, baseline tHcy levels of 28,263 post menopausal
women in the Women's Health Study were compared relative to nonfatal
MI, percutaneous transluminal coronary angioplasty, coronary artery
bypass graft, and CVD death cases. One hundred twenty-two study
outcomes were reported during the 3-year follow-up.
The tHcy levels in cases averaged 14.1µmol/l
compared to 12.4 µmol/l among study controls. And the adjusted
RR for CVD events in the highest tHcy quartile level (>13.26 µmol/l)
was 2.3, significantly greater than in subjects with lower tHcy
levels. The RR values were 1.0, 1.1, and 1.2, respectively for
the first 3 quartile groups. Also, each 5 µmol/l increase in tHcy
was associated with a 24% increase in risk. The subgroup of women
taking multivitamin supplements had lower tHcy levels relative
to women not taking vitamins. However, even among the vitamin users,
the ones with the highest tHcy levels were more likely to suffer
a CVD event compared to those with lower tHcy levels.
Using data from the Framingham Offspring Study
cohorts, Jacques et al. was able to determine the effects of the
1996 Food and Drug Administration's folic acid fortification policy
on plasma folic acid levels. The blood folate samples of subjects
seen in the first half of the sixth examination (January 1995 to
September 1996), before the regulation, was lower than the plasma
folate levels following the second half of the sixth examination
(September 1997 to March 1998). According to Jacques et al. the
folic acid fortified grain products were effective in increasing
plasma folate concentrations from 11 to 23 nmol/l in non-vitamin
users and from 11.7 to 18.9 nmol/l in vitamin users. The fasting
tHcy level decreased from 10.1 to 9.4 µmol/l in the same time period,
thus reducing the prevalence of high tHcy concentrations (>13 µmol/l)
from 18.7 to 9.8%.
A possible mechanisms behind the association
of elevated tHcy concentrations with CVD is its role in damaging
endothelial function related to oxidative processes. When 20 healthy
adults were subjected to a methionine load test, their plasma tHcy
increased from 10.5 µmol/l to 27.1 µmol/l. The associated response
resulted in an increased coagulation and circulation adhesion molecule
levels following methionine ingestion. However, when antioxidants
vitamin E (800 IU) and ascorbic acid (1,000 mg) were ingested along
with methionine, these effects of elevated tHcy were not observed.
Nappo et al. concluded that "mild to moderate elevations of plasma
tHcy levels in healthy subjects activated coagulation, modify the
adhesive properties of endothelium, and impair the vascular responses
to L-arginine."
In conclusion, studies by Bostom et al. and
Ridker et al. clearly show that an elevated tHcy concentration
is associated with increased CVD risk in the elderly and in women.
And the best way to minimize this risk is by decreasing tHcy levels
by increasing plasma folate concentrations by taking B6 vitamins
in the form of fortified grain products or multivitamins. Also,
antioxidants in the diet have been shown to reverse the endothelial
injury due to hyperhomocysteinemia.
Bostom AG, Silbershatz H, Rosenburg IH, et
al. Nonfasting plasma total homocysteine levels and all-cause and
cardiovascular disease mortality in elderly Framingham men and
women. Arch Intern Med. 1999;159:1077-1080.
Jacques PF, Selhub J, Bostom AG, et al. The
effect of folic acid fortification on plasma folate and total homocysteine
concentrations. N Engl J Med. 1999;340:1449-1454.
Nappo F, De Rosa N, Marfella R et al. Impairment
of endothelial functions by acute hyperhomocysteinemia and reversal
by antioxidant vitamins. JAMA. 1999;281:2113-2118.
Ridker PM, Manson JE, Buring JE, et al. Homocysteine
and risk of cardiovascular disease among postmenopausal women. JAMA. 1999;281:1817-1821.
Table of Contents
With the release in 1996 of the Surgeon General's
report on the protective effects of physical activity against CHD,
the American public was advised to exercise not just for aesthetics
but also for health benefits. However, a majority of people are
still not exercising 30 minutes per day as recommended. Yet, according
to the latest Honolulu Heart Program and Nurses' Health Study,
walking is an excellent, moderate-intensity exercise that can protect
against future heart disease.
In the Honolulu Heart Program, the investigators
classified 2,678 men between the ages of 71-93 years into 3 groups
based on distance walked per day; <0.25 mi/d (n=805), 0.25 to
1.5 mi/d (n=1067), and >1.5 mi/d (806) and followed these groups
for 2-4 years. As expected, the group of men who walked more than
1.5 mi/d suffered the lowest number of CHD deaths. The age adjusted
incidence rate was 2.6% (20/806) in the >1.5 mi/d group compared
to 5.0% (40/805) and 4.4% (48/1067) in <0.25 and 0.25 to 1.5
mi/d groups, respectively. The RR for CHD was 2.3 between the least
active group vs. the most active group, and 2.1 between those walking
0.25 to 1.5 mi/d vs. >1.5 mi/d. However, there was no significant
RR difference between the 2 least active groups. When the distance
walked was analyzed as a continuum, an additional 0.5 miles of
walking per day was associated with an additional 15% reduction
in RR of CHD.
These data show that elderly men can reap significant
health benefits by regularly walking for at least 1.5 mi/d. This
is good news since walking is a very inexpensive and readily available
exercise that anyone can easily add to their busy schedule.
Using data from the Nurses' Health Study,
Manson et al. tested the efficacy of vigorous activity and walking
in preventing CHD in women. These investigators found that moderate-intensity
exercise such as walking, at the same energy expenditure level,
was as effective as vigorous exercise in reducing CHD risk. Regardless
of the type of activity, women in the highest quintile group for
total physical-activity score, express as MET-hours/week, were
less likely to experience CHD events compared to women in the first
quintile group.
In this prospective study, 72,488 women between
the 40-65 years in 1986 were followed for 8 years. During this
time 475 cases of nonfatal MI and 170 CHD deaths were documented.
The highest number of CHD events was reported in the least physically
active group, while the most physically active group had the lowest
number of CHD events. For example, women who exercised between
4-6.9 hours/week had 31% lower CHD risk compared to women who exercised
less than 1 hour/week. Exercising more than 7 hrs/week was associated
with a CHD risk reduction of 37%. Also, when other CHD risk factors
were included in the analysis, physical activity continued to show
an inverse relationship with CHD risk in all strata for smoking,
body weight, and familiar history of premature MI. The adjusted
RR of CHD was 0.88, 0.81, 0.74, and 0.66 for 2nd, 3rd, 4th, and
5th quintile groups for total physical activity score, respectively.
Also, sedentary women who began exercising during the study reaped
health benefits compared to women who continued to be sedentary.
When the walkers were separated from the total
population, it was evident that walking was associated with protection
against future CHD events. Walking 1-2.9 hrs/week decreased CHD
risk by 30% and volunteers who walked >3 hrs/week further
reduced their CHD risk by an additional 5%. In addition to exercise
duration, walking pace was determined to be an independent predictor
of CHD. Walking speed of >3 mph was related to the most
CHD benefit.
Based on their findings, Manson et al. concluded
that moderate-activity of brisk walking was as effective as vigorous
physical activity in reducing CHD risk. Women can reduce their
CHD risk by 30-40% simply by either walking 3 hrs/week or vigorously
exercising for 1.5 hrs/week. These findings support current exercise
guidelines, which recommend that everyone exercise for 30 min/d
everyday, instead of 20 min of vigorous exercise 3 or more
time per week recommended previously. This new guideline is feasible
for many sedentary people and could lead to enormous health benefit.
Hakim AA, Curb JD, Petrovitch H., et al. Effects
of walking on coronary heart disease in elderly men. The Honolulu
Heart Program. Circulation. 1999;100:9-13.
Manson JE, Hu FB, Rich-Edwars JW, et al. A
prospective study of walking as compared with vigorous exercise
in the prevention of coronary heart disease in women. N Engl
J Med. 1999;341:650-658.
Table of Contents
Thanks to Lichtenstein and colleagues, the confusion
over which is better, butter versus margarine, in a heart healthy
diet is clearer. The results of this study showed that fat products
high in trans-fatty acids and saturated fats are associated
with negative blood lipid parameters compared to vegetable oils
and minimally hydrogenated fats.
In this study the investigators tested the
effects of different levels of trans-fatty acids on serum
lipoprotein levels by feeding 6 different diets to 36 adults with
elevated LDL cholesterol levels. The test diets were identical
in all nutrient components except the source of fat. Test fats
were selected based on different degrees of trans-fatty
acid content: soybean oil (<0.5% trans-fatty acid), semi-liquid
margarine (<0.5%), soft margarine (7.4%), shortening (9.9%),
and stick margarine (20.1%). Except for a semi-liquid margarine
which was made from corn oil, all other fat were derived from soy
bean oil. Each diet was fed for 35 days.
The change in plasma total and LDL cholesterol
levels were directly associated with the trans-fatty acid
content of the fat. Following the butter diet, the stick margarine
diet was associated with the highest plasma total and LDL cholesterol
levels. The soybean oil diet resulted in the lowest levels. Unlike
the response seen for total and LDL cholesterol, the saturated
fat diet resulted in a more favorable pattern of plasma HDL, TAG,
and VLDL than a high trans-fatty acid diet. Compare to the
butter diet with the highest HDL and lowest TAG and VLDL levels,
the stick margarine diet with high trans-fatty acid content
resulted in the lowest HDL and highest TAG and VLDL levels. The
plasma total cholesterol to HDL cholesterol ratio was the most
favorable following the soy bean oil diet and least favorable with
the stick margarine diet. The total cholesterol to HDL cholesterol
ratio during the butter diet was 4% less than during the stick
margarine diet due to higher HDL cholesterol levels. Plasma lipid
and lipoprotein responses following the different trans-fat diets,
compared to values during the butter diet, showed that the soybean
oil diet lowered total cholesterol by 10%, LDL cholesterol by 12%,
and HDL cholesterol by 3% compared to 3%, 5%, and 6%, respectively
after the stick margarine diet.
These data indicate that oil in its natural
state, or with minimal hydrogenation, are the best choice for protecting
against heart disease since this results in the greatest lowering
effect on an important indicator of heart disease risk, the total
cholesterol: HDL cholesterol ratio. The stick margarine with high trans-fatty
acid levels resulted in an elevated TAG and lowered HDL cholesterol
which appears to negate the advantage it has over butter. Fortunately,
advances in food technology have substantially reduced the production
of trans-fatty acids in margarine production.
Lichtenstein AH, Ausman LM, Jalbert SM, et
al. Effects of different forms of dietary hydrogenated fats on
serum lipoprotein cholesterol levels. N Engl J Med. 1999;340:1933-1940.
Table of Contents
Scientific evidence supporting the beneficial
effects of dietary fiber in lowering CHD risk in men Wolk et al.
found a similar relationship in female subjects. Women in the high
are widely available. This prospective study by Wolk et al. found
a similar relationship in female subjects. Women in the highest
category of fiber intake (22.9 gm/d) had a 43% lower risk of nonfatal
MI and a 59% lower risk of CHD death compared to the lowest category
(11.5 gm/d).
In this 10 year follow-up study, researchers
examined the long-term fiber intake and CHD incidence in 68,782
women in the Nurses' Health Study. In 1984, all subjects were healthy
and free of chronic illness. Dietary patterns were determined in
1984,1986, and 1990 using a semiquantitative food frequency questionnaire.
Based on their fiber intake, subjects were divided into quartiles
of fiber intake. The mean fiber intake in each quintile was 11.5
gm/d, 14.3 gm/d, 16.4 gm/d, 18.8 gm/d, and 22.9 gm/d, respectively.
Of the 591 CHD cases reported during the study, 148 incidences
occurred in quintile 1 compared to 95 incidences in quintile 5.
The age adjusted RR for total CHD was 0.53, however, when other
risk factors were included in the analysis, the RR was 0.77 in
the highest fiber group. When fiber intake was analyzed as a continuous
variable, each 10 gm increase in fiber intake was associated with
a RR of 0.81. Higher levels of dietary folate, beta carotene, magnesium,
and vitamins B6, C, and E in the high fiber intake group did not
affect this relationship.
When the efficacy of fiber intake was further
analyzed against CHD based on type of fiber, cereal fiber was most
effective. For example, the multivariate RR for cereal fiber was
0.66 compared to RR of 0.94 and 1.13 for fruit fiber and vegetable
fiber, respectively. The findings from this study show that higher
fiber intakes also reduce CHD risk in women as previously seen
in men.
Wolk A, Manson JE, Stampfer MJ, et al. Long-term
intake of dietary fiber and decreased risk of coronary heart disease
among women. JAMA. 1999; 281:1998-2004.
Table of Contents
Similar Lipid Profile Following Lean Red Meat Intake Vs. Lean
White Meat Intake
Like eggs, for many years, lean red meats
(LRM) have received a bad rap for its presumed role in elevating
blood cholesterol and CHD risk. However, according to Davidson
et al., LRM such as beef, veal, and pork produced similar lipid
profiles as lean white meats (LWM), poultry and fish. When 191
volunteers with plasma total cholesterol levels near 240 mg/dl
followed an NCEP Step I diet with either 6 oz of LRM (n=89) or
6 oz of LWM (n=102) for 9 months, their mean total cholesterol
levels decreased to 236 mg/dl and 235 mg/dl, respectively. The
LDL, HDL, TAG, and total cholesterol:HDL cholesterol ratio levels
did not differ between the 2 test diets. But, the decreases in
total cholesterol and LDL cholesterol from baseline were 0.8% and
1.2% more, respectively, following the LWM diet than the LRM diet.
The 2% increase in HDL cholesterol level during the treatment period
was the same within test groups. In light of their finding, the
investigators concluded that LRM, which contains less saturated
fat and cholesterol, should not be restricted among hypercholesterolemics,
especially since LRM is now readily available at the market
Davidson MH, Hunninghake D, Maki KC, et al.
Comparison of the effects of lean red meat vs lean white meat on
serum lipid levels among free-living persons with hypercholesterolemia. Arch
Intern Med. 1999;159:1331-1338.
CVD Rate on the Decline
Even though CVD remains the leading cause
of death in the United States, a report from the Centers for Disease
Control and Prevention (CDC) indicates that there is much to celebrate
in the progresses made reducing the incidence of this disease.
For example, in the past 50 years, the CVD mortality rate has dropped
by 60%. In 1996, the death rate from heart disease was 134.6 per
100,000 people compared to 307.4 in 1950. The stroke death rate
also decreased to 26.5 per 100,000 people from 88.8 per 100,000
during the same time period. This translates into 621,000 lives
saved in 1996 alone. This trend began in 1900 for stroke, while
heart disease mortality rates peaked in 1963 before steadily declining.
The CDC attributes the decline in CVD
mortality to decreases in cigarette smoking, blood pressure
and blood cholesterol levels, and better treatment options
following heart attack and stroke. But, they estimate that
the mortality rate can be further reduced by getting CVD
risk factors under even tighter control. This shift in the
CVD mortality rate has resulted in a higher mortality rate
from cancer. According to the National Vital Statistics Report,
the death rate from cancer has jumped from 179.6 deaths per
100,000 in 1979 to 201.6 in 1997.
Anonymous. Decline in deaths from heart
disease and stroke-United States, 1900-1999. Morbidity
and Mortality Weekly Report. 1999;48:649-656.
Table of Contents
While clinical studies and meta-analyses
indicate that dietary cholesterol does have a small effect
on blood cholesterol, epidemiological studies report no relationship
between dietary cholesterol (independent of saturated fat)
and heart disease incidence. The question is, how can dietary
cholesterol raise blood cholesterol and not increase heart
disease risk?
Historically, cholesterol feeding studies
measured the effects on plasma total cholesterol levels,
and epidemiological data indicated that high plasma cholesterol
increased CHD risk. But then studies began showing that dietary
cholesterol and saturated fat were collinear variables in
most study populations, and that with multiple regression
analyses, dietary cholesterol was not a significant factor
in CHD. This contradiction could be due to the fact that
measuring total cholesterol doesn't tell the whole story.
The meta-analysis published by Clarke et
al. [BMI. 1997;314:112-117] reported that dietary
cholesterol significantly raised plasma total cholesterol
levels by increasing both atherogenic LDL cholesterol and
anti-atherogenic HDL cholesterol. Since the LDL:HDL ratio
is an important determinant of CHD risk, a dietary factor
which increased both could conceivably raise plasma total
cholesterol without raising risk of CHD.
Clarke et al. estimate that a 1 mg/day
increase in dietary cholesterol plasma would increase plasma
total cholesterol by 0.025 mg/dl, LDL by 0.019 mg/dl, and
HDL by 0.004 mg/dl. With these predictions, one can calculate
the effects of dietary cholesterol on lipoprotein cholesterol
levels, as well as the LDL:HDL ratio. (see table below)
A dietary cholesterol increase in total
cholesterol has limited impact on the LDL:HDL cholesterol
ratio and would be predicted to have little effect on CHD
risk. The contradictory findings from clinical studies
versus epidemiological surveys could be accounted for by
the fact that dietary cholesterol affects levels of both
the good and the bad plasma cholesterols. Clearly, emphasizing
dietary effects on total cholesterol levels doesn't tell
the whole CHD risk story.
| Cholesterol
(mg/dl) |
Change
in Dietary Cholesterol (mg/day) |
| 0 |
100 |
250 |
| Total |
250 |
253 |
256 |
| LDL |
175 |
177 |
180 |
| HDL |
50.0 |
50.4 |
51.0 |
| LDL:HDL ratio |
3.50 |
3.51 |
3.53 |
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
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