Newsletters & Publications

Volume 18 – Number 2 Summer 2001



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


Insulin Resistance Not a Factor in the Dietary Cholesterol Effect on Blood Cholesterol

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.

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Dietary Cholesterol Raises MI Risk by 2.1 Percent

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.

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Genetic Influence on the Benefits of Moderate Alcohol Intake

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.

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Rapeseed Oil Improves Plasma Lipid and Lipoprotein Levels Better than Olive Oil

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.

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Vitamin B6 Improves Fasting Homocysteine Levels in Elderly

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.

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Fruit and Vegetable Intake Has No Beneficial Effect on Breast Cancer Risk

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.

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Nonlipid CHD Risk Factors Promote Atherosclerosis Progression in Young Adults

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.

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Walking and Other Low-Intensity Activities Lower CHD Risk

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 passé. 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” passé? JAMA. 2001;285:1447-1454.

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Editorial: Perpetuating the Myth

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

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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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