Newsletters & Publications

Volume 16 – Number 1 Spring 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

Hyper-Response to Dierary Fat and Cholesterol in Apolipoprotein E 4/4 Subjects

Wide variations in plasma cholesterol concentrations of individuals following an identical diet strongly suggest genetic components regulating dietary effects on lipid metabolism. This heterogeneity in individual responses to dietary factors has been shown to be in part attributed to the apolipoprotein E phenotype. Previous studies have suggested that individuals with apo E 4/4 alleles were the most sensitive to diet mediated changes in plasma lipid levels.

In a prospective study, Sarkkinen et al. investigated the effects of apolipoprotein E genotype on serum lipid responses to a modified NCEP diet and a NCEP diet high in cholesterol. Forty-five volunteers with known apo E genotypes were included in the study. One-third had an apo E phenotype of E 4/4 and the remaining 2/3 were equally divided between phenotypes E 3/4 and E 3/3. All subjects were matched for age, gender, BMI, and menopausal status. Other study criteria were that subjects be between 30-65 years, hypercholesterolemic with cholesterol levels between 193-328 mg/dl, and free of serious illnesses associated with abnormal lipid levels.

Study cohorts followed 3 prescribed isocaloric Finnish diets in a designated order. During the first 4 weeks, subjects ate a baseline diet that consisted of 43% CHO, 16% protein, 38% total fat, 18% SFA, 13% MUFA, 5% PUFA, and 300 mg of cholesterol/d, followed by 8 weeks of a modified NCEP diet which provided 48% CHO, 17% protein, 34% total fat, 9% SFA, 14% MUFA, 8% PUFA, and 265 mg cholesterol/d, and the last 4 weeks subjects consumed a high cholesterol NCEP diet with dietary cholesterol of 566 mg/d. Dietary cholesterol was increased by either adding egg yolks or cholesterol-enriched cookies. The purpose of the baseline diet was to minimize the carry over effects from the subjects’ normal diets. Compliance on each diet was closely monitored with regular collection of food records and analysis of fatty acid composition of serum cholesterol levels. These analyses indicated that subjects were adhering to the prescribed diets.

Blood samples were collected and assayed on weeks 2, 4, 6, 8, 12, and 16. Plasma lipids responded differently to dietary modification depending on apo E phenotype. The subjects with apo E 4/4 were the most sensitive to dietary changes. During the NCEP diet, the apo E 4/4 group decreased their plasma total cholesterol by 39 mg/dl compared with 24 mg/dl for apo E 3/4 group and 12 mg/dl for apo E 3/3 group. These values represent decreases in plasma cholesterol of 14%, 9%, and 4% for apo E 4/4, apo E 3/4, and apo E 3/3 groups, respectively. The LDL cholesterol levels also decreased by 28 mg/dl, 18 mg/dl, and 8 mg/dl in apo E 4/4, apo E 3/4, and E 3/3 group, respectively. The plasma total and LDL cholesterol levels steadily decreased in apo E 4/4 subjects throughout the NCEP diet, however, in apo E 3/4 subjects, after an initial drop, it leveled off. Surprisingly, it increased in apo E 3/3 subjects in the last 6 weeks. The plasma HDL cholesterol decreased in apo E 4/4 and apo E 3/4 subjects by 3.8 mg/dl and 4.3 mg/dl, respectively. The change in HDL cholesterol levels in apo E 3/3 subjects was not significant.

During the high cholesterol (+300 mg/dl) diet phase, plasma total cholesterol levels increased by 22 mg/dl and LDL cholesterol increased by 15 mg/dl in the apo E 4/4 group, twice as much as the apo E 3/4 and apo E 3/3 subjects. The percent change in total cholesterol was also 2 fold in this group. The HDL cholesterol increases of 4.6% and 4.5% in apo E groups 4/4 and 3/4 were not significant. The HDL cholesterol level was stable in the apo E 3/3 group during the high cholesterol diet phase.There was no significant difference among the genotype groups with TAG and blood pressure levels. However, even though plasma total cholesterol, LDL cholesterol, HDL cholesterol, and TAG levels increased the most in subjects with apo E 4/4, these plasma lipoprotein levels were still less than the baseline values.

The results from this study clearly show a relationship between apo E polymorphism and lipid response to fat and cholesterol modified diets in moderately hypercholesterolemic, middle-aged subjects. Compared to subjects with the apo E 3/3 genotype, subjects with apo E 4/4 alleles were more sensitive to an increase in dietary fat and cholesterol. Apo E 3/4 was associated with moderate lipid responses to an increase in dietary fat and cholesterol. The mechanisms by which apo E polymorphism regulates lipid metabolism which makes apo E 4/4 subjects hyper-respond to increased fat and cholesterol is unclear, but researchers speculate “that LDL receptor regulation could explain the differences in LDL-cholesterol concentrations among the apo E genotypes.” For example, apo E 4/4 subjects might be more efficient in absorbing dietary cholesterol or delivering chylomicron and nonchylomicron fraction to the liver thus down-regulating LDL receptors and increasing plasma LDL cholesterol levels.

Sarrkinen and colleagues concluded that dietary modification be implemented as a treatment in reducing CHD risk in all people, not just people with apo E 4/4 allele who are very sensitive to fat and cholesterol in the diet. It is estimated that 30% of Finnish and 15-25% of Western populations have apo E 4/4 genotype, which places them at a higher risk for CHD.

Changes in plasma total cholesterol with added cholesterol

Phenotype Plasma Cholesterol Change
(mg/dl per 100 mg/day cholesterol)
apo E 3/3 1.7
apo E 3/4 2.3
apo E 4/4 7.3

Key Messages

  • Apolipoprotein E genotype modified the lipid response to dietary fat and cholesterol.
  • Subjects with apo E 4/4 genotype were the most sensitive to dietary changes.
  • Apo E 3/4 genotype increase total cholesterol and LDL cholesterol more than apo E3/3.

Sarkkinen E, Korhonen M, Erkkila A, et al. Effect of apolipoprotein E polymorphism on serum lipid response to the separate modification of dietary fat and dietary cholesterol. Am J Clin Nutr. 1998;68:1215-1222.

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Moderate Physical Activity as Effective as Structured Exercise Program

The benefits of physical activity on protecting one from major diseases such as hypertension, diabetes, heart disease, and cancer are common knowledge among people; however, only a fifth of the population is regularly exercising. This percentage remains unchanged in the past 14 years. The excuses people frequently site for not exercising are lack of time, lack of access to a gym, and lack of energy. But according to Dunn et al. moderate increases in regular physical activity level throughout the day can be as effective as a structured exercise program in improving long-term cardiorespiratory fitness and physical activity in sedentary adults.

In this study, 235 adults were randomly enrolled in a structured exercise program (n=114) and a lifestyle change program (n=121) for 2 years with a dropout rate of 18% and 20%, respectively. During the 6-month intervention period, the structured exercise group was prescribed an exercise regiment that required them to workout in a state of the art fitness center for 5 days a week. The duration of exercise was between 20-60 minutes at a target heart rate of 50-85%. Based on an individual’s motivational readiness, each participant in the lifestyle group was taught an individual physical activity that they could incorporate into their daily life for 30 minutes. Researchers used the Social Cognitive Theory model to evaluate each individual’s motivational readiness. In addition, regular small group meetings provided extra support to encourage compliance, and both groups were provided with monthly activity calendars and quarterly newsletters for ongoing support.

Subjects in the 2 different intervention groups were similar in age, gender, physical and health attributes. Following the intervention period, both groups gained similar improvements in physical activity, blood pressure, % body fat, and the total cholesterol to HDL cholesterol ratio. However, participants in the structured exercise group had better cardiorespiratory fitness levels than the lifestyle group. For example, the VO2 peak increased by 3.64 ml/kg-min compared to 1.58 ml/kg-min in the lifestyle group. But during the 1-1/2 year maintenance phase, participants in the structured group and lifestyle group decreased their VO2 peak by 2.4 ml/kg-min and 0.7 ml/kg-min, respectively, resulting in a comparable end VO2 peak levels.

The comparison of physical activity levels between baseline and end of study revealed that although participants in the structured exercise group were 3 times more likely to vigorously exercise than the lifestyle group, they expended less total energy (0.69 kcal/kg-day), lost less body fat (1.85%), and gained 1.5 pounds compared to the lifestyle group with energy expenditure of 0.84 kcal/kg-day, weight and body fat losses of 0.11 pounds and 2.39%, respectively. One possible explanation for this outcome is that three times as many participants in the lifestyle group were involved in a moderate activity than in the structured exercise group during the maintenance phase. Regardless of study group, subjects who continued to exercise regularly during the maintenance period expended the most energy, 1.29 kcal/kg-day and lost 3 pounds of body weight. Men in the study improved their physical fitness and activity levels more than women.

Lipid and lipoprotein parameters were relatively stable in the lifestyle group throughout the study, but it improved significantly in the structured exercise participants during the active intervention phase. However, no overall improvement was noted during follow-up, but rather the total cholesterol to HDL cholesterol ratio increased more in the structured exercise group (0.20) than in the lifestyle group (0.06) during the study. The changes in lipid and lipoprotein parameters between the study groups during the 2 year study were not significant. Blood pressure levels, especially diastolic levels, improved in both groups during the maintenance period. Diastolic blood pressure decreased by 3.16 mm Hg and 2.66 mm Hg in life-style and structured exercise groups, respectively.

These findings reiterate the outcome noted in the fable about a race between a rabbit and a turtle. As in the story, those who exercised diligently regardless of the intensity were able to achieve the long term health benefits. Dunn et al. were able to show that moderate lifestyle changes can be effective in controlling one’s weight, percent body fat, blood pressure, and expending more energy than a structured exercise program if the changes are followed continuously. Fitness does not have to cost a lot of money to achieve great results, but rather cost-free activities such as walking, gardening, climbing stairs are as effective as state of the art facilities in promoting fitness. Lastly, this study also demonstrated that it is possible to teach sedentary people to increase their physical activity and cardiorespiratory fitness on a long-term basis.

Dunn AL, Marcus BH, Kampert JB, et al. Comparison of lifestyle and structured interventions to increase physical activity and cardiorespiratory fitness, a random trial. JAMA. 1999;281:327-334.

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Transfer of Human Apo A-I gene in Mice Increses Apo A-I and HDL Cholesterol Levels

Studies indicate that a 1% increase in plasma HDL cholesterol can result in a 3-4% decrease in CHD risk. Studies also indicate that a major factor in premature CHD is a low HDL cholesterol level. But how can HDL levels be increased? In this study by Benoit et al. the effects of adenovirus apo A-I gene therapy on plasma HDL levels and atherosclerosis progression in mice were tested. The study protocol involved administering the human apo A-I gene into 3 different types of mice; normal mice, human apo-A-I transgenic mice, and apo E deficient mice expressing human apo A-I, using a recombinant adenovirus (AV) to determine effects on HDL cholesterol levels and atherosclerosis progression. The purpose of using human apo A-I transgenic mice was to eliminate effects of immune reaction against the human protein. The apo E deficient transgenic mice were to test the effects of gene therapy on mice prone to develop atherosclerosis.

The adenovirus-mediated human apo A-I gene transfer in normal mice resulted in a significant increase in plasma levels of human apo A-I and HDL cholesterol. The peak of human apo A-I (130 mg/dl) and HDL cholesterol (95 mg/dl) occurred on the 11th day and represented a 40% increase in HDL cholesterol levels. In the human apo A-I transgenic mice, the plasma levels of human apo A-I and HDL cholesterol increased to a greater degree following AV apo A-I administration than in the normal mice. This difference indicates that immune reaction does play a role in apo A-I expression in normal mice following apo A-I injection compared to those who express the gene during development. For example, human apo A-I increased by 300% (143 mg/dl to 425 mg/dl) and HDL cholesterol level by 36% (97 to 346 mg/dl) on the 7th day after injection. Human apo A-I and HDL cholesterol levels remained high for more than 6 weeks in AV apo A-I treated transgenic mice but the levels in control mice remained unchanged throughout the study. Also, the plasma TAG levels did not change following adenovirus infection in transgenic mice.

In adenovirus mediated human apo A-I mice with apo E deficiency, injection with AV apo A-I resulted in a dramatic increase in plasma levels of human apo A-I from a baseline of 112 mg/dl to 237 mg/dl on the 14th day and a decrease to 140 mg/dl on the 42nd day. The HDL cholesterol level increased by 190%. However, there was little change in HDL cholesterol levels and human apo A-I concentrations in control mice and in the apo E-knock out/human apo A-I gene mice. Conversely, in the apo E-knock out/human apo A-I gene mice, the mean lesion areas were much higher than AV apo a-I treated mice. The percent of lesion in AV apo A-I mice was 56.4% of control.

Results from this study showed an increase in HDL cholesterol levels following the AV apo A-I transfer in all 3 types of mice. This ultimately resulted in a reduction of atherosclerosis development in apo E deficient transgenic mice. The authors noted that “overexpression of apo A-I to higher-than-normal concentrations can be considered as potential therapy to increase HDL concentration and induce inhibition or regression of atherosclerotic lesions in a large population.”

Benoit P, Emmanuel F, Caillaud JM, et al. Somatic gene transfer of human apo A-I inhibits atherosclerosis progression in mouse models. Circulation. 1999;99:105-110.

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Heterogeneity in Lipoprotein Response to Diet

Health providers sometimes label their CVD patients “noncompliant” when their blood cholesterol levels do not change following prescription of a low-cholesterol diet, but according to Sehayek and colleagues, this might be an incorrect assessment. They found a wide inter-individual variation in dietary cholesterol absorption which could in part explain the seemingly erratic changes in the blood cholesterol levels after a dietary modification.

In this randomized crossover trial, 18 healthy subjects between the ages of 19 to 60 yrs (mean 30.3 yrs) were fed 3 isocaloric, metabolic ward diets. The low-fat low-cholesterol (LFLC) diet consisted of 60% CHO, 15% protein, 25% fat, and 80 mg cholesterol per 1000 kcal. The high-fat low-cholesterol (HFLC) diet consisted of 42% CHO, 15% protein, 43% fat and 80 mg cholesterol per 1000 kcal. And the last diet, a high-fat high-cholesterol (HFHC) diet had the same nutrient composition as HFLC with an increase in cholesterol to 200 mg per 1000 kcal. Each test diet was consumed for 3 weeks without a washout period. Subjects’ plasma lipids, lipoproteins, apolipoprotein E genotype, and cholesterol absorption were measured during the last week of each diet.

The percent cholesterol absorption was similar with the 3 test diets. The mean cholesterol absorption rate with LFLC, HFLC, and HFHC were 60%, 58%, and 56%, respectively. However, the individual absorption rates within each diet varied widely. For example, during the LFLC diet, one test subject absorbed 36% while another person absorbed 74%, with the others in between. Similar outcomes were noted during HFLC and HFHC diets. The increase in dietary cholesterol intake resulted in decreased absorption rates in some, while it increased or remained the same in others. The individual LDL cholesterol levels responded in similar fashion on the high cholesterol diet. But as a collective group, their total cholesterol levels increased by 11.7%, LDL cholesterol by 11.6% and HDL by 1.2% on a high cholesterol diet. The total cholesterol, LDL cholesterol, and HDL cholesterol levels increased by 12.9%, 6.8%, and 5.2% on the high fat diet.

Analysis of dietary cholesterol-induced changes in % cholesterol absorption and % change in LDL cholesterol yielded a U-shaped parabolic relationship. For example, as the % cholesterol absorption deviated in either direction from a normal absorption rate, the % LDL cholesterol increased. A similar relationship was noted between HDL cholesterol and % dietary cholesterol absorption, but not as much as LDL.

Dietary cholesterol and fat also affected the mass absorption of dietary cholesterol. The average cholesterol absorbed with the HFLC and HFHC diets were 1.7 mg/kg-day and 4.6 mg/kg-day, respectively. The increase in absorbed dietary cholesterol switching from the HFLC to HFHC diet resulted in an extra 1 to 4.7 mg of dietary cholesterol absorbed per kg body weight per day. On the high fat diet, only 3 of the 18 subjects increased the mass absorption of dietary cholesterol and the remaining 15 decreased, suggesting an unknown independent effect.

Large variability in individual levels of LDL cholesterol, % cholesterol absorption, and dietary cholesterol mass absorption among the study subjects following a metabolic diet suggest that genetics plays an important role in an individual’s responsiveness to a high cholesterol or a high fat diet. Also, according to this study, dietary fat and dietary cholesterol independently affect dietary cholesterol mass absorption.

Sehayek E, Nath C, Heinemann T, et al. U-shape relationship between change in dietary cholesterol absorption and plasma lipoprotein responsiveness and evidence for extreme interindividual variation in dietary cholesterol absorption in humans. J Lipid Res. 1998;39:2415-2422.

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Iron Status and CHD Risk

Due to its pro-oxidative effects, excessive iron in the body has been postulated to increase CHD risk. However, epidemiological evidence does not conclusively support such a hypothesis. According to a meta-analysis by Danesh and Appleby, there is no evidence supporting an association between iron status and CHD. Based on 12 prospective studies with 7,800 cases, the investigators found that those subjects with baseline serum ferritin levels of > 200 mg/l had similar risk of CHD as people with baseline serum ferritin levels of < 200 mg/l. Other markers of iron status; transferrin saturation, total iron-binding capacity, serum iron concentration, and total dietary iron intake, showed similar results. The risk ratio for CHD in subjects in the top third of transferrin saturation, total iron-binding capacity, serum iron concentration, and total dietary iron intake levels were 0.92, 0.98, 0.83, and 0.84 compared to people in the bottom third of each markers.

This analysis found “no good evidence for the existence of strong epidemiological associations between iron status and CHD,” but does encourage future investigators to measure iron status periodically rather than only at baseline as it can fluctuate with changes in medical condition or lifestyle.

Danesh J, Appleby P. Coronary heart disease and iron status meta-analyses of prospective studies. Circulation. 1999;99:852-854.

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Intensive Lifestyle Change Decreases CHD Risk

According to the Lifestyle Heart Trial, intensive lifestyle changes can reduce CHD risk. In this randomized case-control study, 35 subjects (20 cases,15 controls) completed a 5-yr study of the effects of comprehensive lifestyle changes on coronary athero-sclerosis progress. Initially, this was a 1 year trial extended 4 more years following a positive outcome and excellent compliance rate. However, compliance rates decreased during the last 4 yrs.

An intervention group was prescribed an intensive lifestyle changing program that included a 10% fat, vegetarian diet, aerobic exercise, stress management, smoking cessation and group psychosocial support components. The control group followed an NCEP Step 2 diet with moderate exercise. The experimental diets were of 8.5% fat, 15% protein, 76.5% CHO, 19 mg of cholesterol per day in the intervention group and in controls 25% fat, 18% protein, 52% CHO, and 139 mg/day cholesterol.

Based on angiograms, the experimental group exhibited a regression in coronary atherosclerosis, while the control group coronary lesions continued to progress. For example, the average percent diameter stenosis decreased by 1.75% in the 1st yr and 3.1% in the 5th yr in case subjects, but increased by 2.3% and 11.8% in the 1st and 5th yr in the control group. The relationship between stenosis and lifestyle change in controls was not directly observable due to introduction of lipid lowering medication in 9 subjects. This confounder explains the 19% decrease in plasma LDL levels in controls. During the 5-yr follow-up, 3 control subjects underwent revascularization thus significantly reducing the frequency of reported angina in controls. The frequency of angina was reduced by 91% and 72% in case subjects between the 1st and 5th yr. Also, plasma HDL levels decreased and TAG levels increased on the intervention diet, but the LDL:HDL ratio improved.

The rate of cardiac events was higher in the control group than the intervention group, 45 vs. 25. Cardiac events data were based on 20 control and 28 case subjects and included subjects who dropped out.

Ornish et al. were able to demonstrate that highly motivated subjects, following a strict lifestyle change, were able to decrease their plasma levels of LDL cholesterol, cardiac events, frequency of angina, and stenosis of coronary arteries. The improvements in CHD symptoms were dose-dependent on adherence to the intervention treatment.

There were several limitations to the current study. The subjects were a highly motivated self-selected group and do not represent the general population. The restricted intervention of an 8% fat, vegetarian diet is not easily achievable or maintainable by the general population. The change in coronary stenosis was statistically significant, yet the changes were very small. Lastly, throughout the study, data were analyzed based on 20 case subjects and 15 controls, however, the cardiac events were based on 28 case subjects and 20 controls, thus favoring cardiac events on behalf of the controls.

Ornish D, Scherwitz LW, Billings JH, et al. Intensive lifestyle changes for reversal of coronary heart disease. JAMA. 1998;280:2001-2007.

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Alcohol Reduces Ischemic Stroke

The beneficial effect of moderate alcohol consumption on heart disease has been well established, but its relationship with stroke is disputed. One explanation for the mixed results is that older studies did not distinguish between hemorrhagic and ischemic strokes. A prospective, case-control study by Sacco et al. suggests that 2 alcoholic drinks per day can reduce ischemic stroke risk in the elderly.

Study groups consisted of 677 cases with fatal or nonfatal ischemic stroke and 1139 age, sex, and race/ethnicity matched controls. The average age was 70 years old. Sixty-seven percent of cases and 53% of controls reported no alcohol consumption in the past year while 24% and 41% of cases and controls, respectively, drank less than 2 drinks per week. The case subjects had higher rates of hypertension, cardiac disease, and diabetes, but were less obese than the control group.

The odds ratio for ischemic stokes for moderate alcohol consumption (>0 in past year to <2/d) was 0.42, and for intermediate (>2/d to <5/d) and heavy (>5/d) alcohol consumption were 0.58 and 1.38, respectively. Seven drinks per day were associate with an odds ratio of 2.96. The relationships between alcohol intake and ischemic strokes fit a J shaped curve with the lowest risk at 2 drinks per day.

The types of alcoholic beverages made no difference in the relationship between alcohol and stroke. Also, this study found no difference in the relationship between moderate alcohol intake and stroke in male vs. female subjects, people less than 65 vs. greater than 65 years of age, or people of different ethnic origin. Researchers noted that the protective effects of moderate alcohol consumption were independent of plasma HDL levels.

Results from this study add to the evidence supporting a protective effect of moderate alcohol intake on ischemic strokes. Up to 2 alcoholic drinks per day were associated with decreasing the risk of strokes, and heavy drinking was shown to increase risk. However, ex-heavy drinkers were able to reduce their risk by reducing their alcohol intake to 2 drinks per day.

Sacco RL, Elkind M, Boden-Albala B, et al. The protective effect of moderate alcohol consumption on ischemic stroke. JAMA. 1999;281:53-60.

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Abdominal Fat Distribution Associated with Increased CHD Risk Factors in Women and Children

An apple-shaped physique in males has been linked to increased diabetes, hypertension, and elevated plasma TAG levels. Now, according to the results from Nurses’ Health Study and a report by Daniels et al., abdominal adiposity is an independent contributor to CHD risk in middle-aged women and associated with risk factors in children. During the 8-year nurses prospective study (1986 to 1994), 251 nonfatal MI and 69 confirmed CHD deaths were reported in this cohort of 44,702 women. The analysis of biennial questionnaires revealed a direct relationship between waist to hip ratio (WHR) and CHD incidence and waist circumference and CHD, independent of subjects’ BMI. The incidence of CHD was twice as high in the highest WHR and waist circumference tertile compared to the lowest WHR and waist circumference tertile. Also, regardless of whether WHR or waist circumference was analyzed in quintiles or stratified levels, the relative risk for CHD was significantly higher in women with abdominal obesity. For example, after adjustment for age and other CHD risks, the relative risk for women with WHR of 0.88 was 3.25 compared to women with WHR of < 0.72. The relative risk for waist circumference of >96.5 cm was 3.06 compared to women with waist circumference of > 71.1 cm. The multivariate analysis for relative risk for women in the highest quintile of WHR (0.83 – <1.90) and waist circumference (86.3 – <139.7) were 2.58 and 2.44, respectively. When subjects’ BMI were eliminated from the analysis, the relationship between abdominal obesity and CHD increased.

The WHR and waist circumference were better indicators of CHD in women younger than 60 years old compared to women over 60. Also, the WHR was strongly associated with increased CHD in women at all weight levels. However, “waist circumference was strongly associated with high CHD among women with a BMI of less than 25 kg/m2 but not significantly predictive for women with a BMI of 25 kg/m2 or higher.” The relationship between CHD and abdominal obesity measures were only significant in women who never received estrogen replacement therapy, but the number of past and current users in the study were too small for a definitive answer.

The results from the Nurses’ Health Study showed that abdominal obesity is associated with increased CHD risk in middle-aged women. Women with a waistline greater than 38 inches were 3 times more likely to suffer CHD during the follow-up period than women with a waistline of less than 28 inches. Women with WHR of greater than 0.88 were also at 3 times the risk of CHD of women with WHR of less than 0.72. These findings confirmed previous data that showed a strong relationship between regional fat distribution and CHD. Rexrode et al. recommend WHR and waist circumference measurements as two easy methods for determining CHD risk.

Daniel et al. investigated the association between body fat distribution and CVD risk factors in 127 children between the ages of 9 to 17. In this cross sectional study, researchers used Dual Energy X-ray Absorptiometry (DEXA) to directly measure total and regional fat mass instead of waist to hip circumference or skin-fold thickness measurements.

According to the univariate correlation coefficients, plasma TAG and HDL cholesterol levels were related to fat distribution. The HDL cholesterol was inversely associated with central fat distribution and total percent body fat. Total cholesterol and LDL cholesterol were not significantly associated with any of the measures of body fat. While systolic blood pressure was correlated with fat distribution, diastolic blood pressure was related to total body fat. The multiple regression analysis also showed similar relationships between fat distribution and CVD risk. High abdominal fat was associated with higher plasma TAG and lower HDL cholesterol levels and higher systolic blood pressure and left ventricular mass. Also, fat distribution was more strongly correlated with CVD than percent body fat which represent overall body fat.

These two studies indicate that high body fat, especially its distribution around the abdominal area, is related to increased CHD risk. Daniel et al. showed negative plasma lipid and lipoprotein parameters with higher body fat in young children which can potentially lead to CHD events later in life if the excess adiposity persists, while the data from Rexrode et al. actually showed increased CHD events in women with larger waist circumference and WHR. The evidence from both studies strongly support weight control in children and weight loss in obese adults to reduce CHD risk.

Daniels SR, Morrision JA, Sprecher DL, et al. Association of body fat distribution and cardiovascular risk factors in children and adolescents. Circulation. 1999;99:541-545.

Rexrode K M, Carey VJ, Hennekens CH, et al. Abdominal adiposity and coronary heart disease in women. JAMA. 1998;280:1843-1848.

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Editorial: Non-Functional Foods

I envision a future when the break at a conference will be a soft drink (fat-free, cholesterol-free, caffeine-free, sodium-free, calorie-free) and cookies made with psyllium fiber, fake fat, artificial sweetener and only a single calorie. Some will gloat over their good fortune to live in this nutritionally correct (NC) world. While others wonder what horrible deeds we committed to exist in this tasteless NC world filled with cookbooks for coffee tables; kitchen utensils and appliances, which few use; and wonderfully varied cuisines which no one dares enjoy without sugar, fat, cholesterol, and flavor extraction.

It seems today as in 1678 that “To safeguard one’s health at the cost of too strict a diet is a tiresome illness indeed.” [François, Duc de La Rochefoucauld, Sentences et Maximes Morales] We seem headed in two directions at once: food as medicine and food selection based not on taste or enjoyment but rather on what we’ve been told is good for us; and on the other side we are phobic about what we’ve been told we must avoid and only buy products appropriately cleansed.

And as these messages barrage the public, consumer confusion and cynicism grows while our effectiveness for real dietary improvements shrivels. The public hears that if you eat our cereal your blood cholesterol will fall down and down. But who’s going to eat three servings every day? And the messages keep on coming: lower the fat, eggs out of the diet, and lower calories from fat to loss weight. Is this perhaps what George Bernard Shaw meant by “Science becomes dangerous only when it imagines that it has reached its goal.” [The Doctor’s Dilemma 1911].

Today’s hot marketing trends are to sell products as either completely devoid of all those bad things or as a sure fire way to lower the risk of heart disease, cancer, obesity or diabetes. Functional food is the new buzzword and soon everything will be nutritionally improved with “good things” and sanitized of “bad things.”

And so our overweight, sedentary society is convinced that food either causes or cures illnesses with less of that non-NC thinking that food can actually be eaten and enjoyed. There will be no joy at the dinner table then, just eat your medicine and get on with it. And since you’re being so good, for desert you can have some special cookies!

[In fact, eggs are actually nature’s original “functional food” (and for the sake of this argument, the egg came first). What could be a more functional food than one whose purpose is to provide all the structural components and nutritional requirements needed for the development of an embryo. Now that’s functionality! I guess we’ve all been eating functional foods for centuries, and enjoying it.]

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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