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Volume 16 - Number 3 Fall 1999



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


Egg Yolk Intake Increases Plasma Lutein and Zeaxanthin Levels

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 �mol/l to 0.403 �mol/l, when egg yolk was added to the corn oil diet. Zeaxanthin levels increased by 114%, (0.049 to 0.105 �mol/l). With intake of the tallow diet plus egg, plasma lutein concentrations increased by 28% (0.333 to 0.427 �mol/l) and zeaxanthin by 142% (0.048 to 0.116 �mol/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 �g and 213�85 �g, respectively, or 1.19�0.32 �g/mg cholesterol of lutein and 0.87�0.23 �g/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 �mol/l) with added egg yolk was greater than in plasma zeaxanthin levels (0.062 �mol/l). Lycopene and � 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 �g/d each, plasma zeaxanthin levels did not change whereas in this study it increased by 0.062 �mol/l following intake of 1.3 egg yolks (280 �g 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.

Key Messages

  • Egg yolk contains 292 �g lutein and 213 �g of zeaxanthin
  • Intake of 1.3 egg yolk per day increased plasma lutein by 39% and zeaxanthin by 128%.
  • Dietary lutein and zeaxanthin in eggs are readily absorbed due to the lipid matrix of egg yolk.

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Energy Reduction Linked to Improved Lipid and Lipoprotein Levels

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.

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Secondhand Smoke Increases CHD Risk

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 �20 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.

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Elevated Homocysteine Levels Increase CVD Risk

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 �mol/l, 9.26-11.43 �mol/l, 11.44-14.25 �mol/l, and 14.26-219.84 �mol/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 �mol/l compared to subjects with <14.25 �mol/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 14.1�mol/l compared to 12.4 �mol/l among study controls. And the adjusted RR for CVD events in the highest tHcy quartile level (>13.26 �mol/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 �mol/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 �mol/l in the same time period, thus reducing the prevalence of high tHcy concentrations (>13 �mol/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 �mol/l to 27.1 �mol/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

Walking Associated with Reduced CHD Risk

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.  

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Comparison of Lipid Response Following Trans-fat Diets Versus Saturated Fat Diet

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.

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Dietary Fiber Intake Reduces CHD Risk in Females

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.

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News and Noteworthy

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.

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Editorial: A Curious Contradiction

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 professionals can receive a FREE subscription for the newsletter by contacting the ENC.

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