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Newsletters & Publications

Masthead
Volume 17 - Number 4 Winter 2000

TABLE OF CONTENTS


ENC

COMMON ABBREVIATIONS
BMI: body mass index (kg/m2)
CAD: coronary artery disease
CHD: coronary heart disease
CHO: carbohydrate
CI: confidence interval
CVD: cardiovascular disease
ene: energy
HDL: high density lipoprotein
LDL: low density lipoprotein
Lp(a): lipoprotein (a)
MI: myocardial infarction
MUFA: monounsaturated fatty acids
NCEP: National Cholesterol Education Program
P:S: dietary polyunsaturated:saturated fat ratio
PUFA: polyunsaturated fatty acids
RR: relative risk
SFA: saturated fatty acids
TAG: triacylglycerol
VLDL: very low density lipoprotein


Dietary Guidelines Lowers CVD Risk

We all know that a healthful diet plays an important role in protecting us against major chronic diseases. And in an effort to assist Americans to eat more healthfully, the USDA and Health and Human Services developed the Dietary Guidelines for Americans, which is a compilation of healthy eating patterns. This tool, which was first developed in 1980 has undergone regular evaluation to insure that the recommendation is inline with current research data. However, the efficacy of this guideline has been untested until recently. Hu et al. tested the relationship between adherence to the Dietary Guidelines for Americans and risk of major chronic disease in men, than using the Nurses' Health Study (NHS) data, McCullogh and colleagues assessed the same relationship in women. However, these 2 studies arrived at 2 very different results regarding the efficacy of adherence to the Dietary Guidelines for Americans in protecting against major chronic diseases.

Using the food frequency questionnaires 67, 272 healthy women enrolled in the NHS, the researchers calculated the Healthy Eating Index (HEI) scores ranging from 0 (worst) to 100 (best). The criteria for the HEI score was based on the frequency of eating from all 5 food groups and restricting negative nutrients such as fats and sodium. The mean HEI score was 64.4 in the study cohort. This was the same HEI scores as in the CSFII subpopulation, who were matched for age and degree of education with the NHS cohorts. However, compared to the subjects in the NHS, the CSFII cohort ate less vegetables, fruits, and meats. High HEI scores were associated with overall healthier lifestyle behaviors in both cohorts. During the 12-year follow-up, 365 cases of CVD, 5216 cases of cancer, and 496 cases of traumatic deaths were reported. The researchers divided individuals into quintiles based on their HEI scores. The median HEI scores were 48, 50, 65, 75, and 80 for quintiles 1 through 5, respectively. Intakes of milk, fruits, vegetables, grains were directly associated with higher HEI scores, while fat and sodium were inversely related.

In relation to HEI scores, age-adjusted RR for the highest quintile to the lowest quintile for major chronic diseases was 0.81, 0.59 for CVD, and 0.92 for cancers. However, when other CVD risk factors were included in the analysis, it diminished the net beneficial effects of a higher HEI score. The multivariate adjusted RR for major chronic diseases, CVD, and cancer were 0.97, 0.86, and 1.02, respectively, in the highest HEI score group. The data suggest that following a healthy diet as prescribed by the Dietary Guidelines for Americans lowered CVD risk by 14% but made no difference in either cancer or mortality rates from major chronic diseases. 

The researchers postulated that the weak association between following the Dietary Guidelines for Americans and less than resounding protection against cancer, and other major chronic diseases might have been the result of several limitations in the design of the study. For example, HEI scores were developed to assess nutritional quality of a 24-hour food recall rather than for long-term dietary habits as in the case with food frequency questionnaires used in the NHS. Also, since HEI scores were based on the frequency of all 5 food groups, rather than specific foods, HEI scores would be high for people eating high qualities of red meats and refined bread products as well as someone eating lots of whole grains, fruits and vegetables. Even though this is not a perfect study, as a result of this study, it is possible to conclude that the HEI score does not necessarily measure the optimal diet to prevent major chronic diseases. And in order to help Americans eat more healthily, HEI, the Dietary Guidelines for Americans, and Food Guide Pyramid, "should be continue to be evaluated for their efficacy in reducing the incidence of disease of major public health concern."

Contrary to the NHS findings, the data from the Health Professionals Follow-Up Study (n=44,875 males) suggested that following a healthy dietary pattern does lower CHD risk, independent of other CHD risk factors. For example, of the 1089 cases of both fatal and nonfatal CHD reported during the 8 year follow-up period, it occurred more in the subjects who followed the Western pattern diet, which is higher in fat content and highly processed foods, versus the prudent pattern which is high in fruits, vegetables, fish, and poultry.

The subjects were stratified into the prudent pattern and Western pattern based on the 131-item food frequency questionnaires. And based on the analysis, the multivariate adjusted RR across increasing quintiles of prudent pattern score were 1.0, 0.87, .079, 0.75, and 0.70 (95%CI: 0.56, 0.86; p for trend=0.0009). On the other hand, the RR across increasing quintiles of the Western pattern were 1.0, 1.21, 1.36, 1.40, and 1.64 (95% CI: 1.24, 2.17, p for trend <0.00013). Separate analysis of the direct relationship between Western pattern and fatal and nonfatal CHD showed that it was much stronger for fatal CHD events.

Based on this result, Hu et al. concluded that the 2 dietary patterns shown by the food frequency questionnaire is a good predictor of CHD risk. And by replacing diets high in fat and processed foods with more fruits, vegetables, fish, and poultry, consumers should be able to lower their risk of CHD.

McCullough ML, Feskanich D, Stampfer MJ, et al. Adherence to the Dietary Guidelines for Americans and risk of major chronic disease in women. Am J Clin Nutr. 2000;72:1214-1222.

Hu FB, Rimm EB, Stampfer MJ et al. Prospective study of major dietary patterns and risk of coronary heart disease in men. Am. J. Clin Nutr. 2000;72:912-921.

Key Messages

  • According to the NHS, adhering to the Dietary Guidelines for Americans lowered CVD risk by 14% in women. It did not reduce their risk of cancer or other chronic diseases.
  • Multivariate RR for CVD, cancer, and nontraumatic deaths were 0.86, 1.02, and 0.97 for women in the highest HEI group
  • HEI need to be refined to better determine optimal diet.
  • Healthy eating pattern was associated with low CHD risk in Health Professionals Follow-up Study. 
  • The prudent pattern, diets high in fruits, vegetables, fish, and poultry was inversely associated with CHD risk, while the Western pattern, diets high in fat, red meats, processed meats, refined grains, and French-fries were directly associated with CHD risk.

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Plasma and Tissue Lutein and Zeaxanthin Increases with High Carotenoid Intake

Lutein and zeaxanthin, 2 carotenoids commonly found in egg yolks, corn age-related macular degeneration by preventing , spinach, and other green leafy vegetables, have been shown to protect against age-related macular degeneration by preventing light-initiated oxidative damage from occurring in the retina. Earlier studies showed that diets high in lutein and zeaxanthin increase the concentration of these 2 carotenoids in the macular region of the retina. But the results from Johnson et al. indicated that diets high in these carotenoids could also increase concentrations of these nutrients in other parts of the body.

In this 2-pronged study, the researchers first evaluated the changes in lutein and zeaxanthin concentrations at various tissues following a diet supplemented with 60 grams of spinach and 150 grams of corn per day. Lutein and zeaxanthin concentrations in serum, adipose tissue, and buccal mucosa cells (BMC) were measured at baseline and weeks 4, 8, 12, and 15 of supplements, as well as 2 months post study. The macular pigment density and dietary carotenoid intakes were also measured throughout the study period. Seven healthy middle-aged adults (4 women and 3 men) participated in this section of the study.

After 4 weeks of corn and spinach intake, serum lutein concentrations nearly doubled from baseline and continued to remain elevated during the feeding period. However, eating corn and spinach had a less dramatic effect on serum zeaxanthin levels. For example, zeaxanthin levels increased from 58�12 nmol/l at baseline to 74�14 nmol/l at week 4. On the other hand, 2 months after the cohort stopped adding corn and spinach to their diets, both serum lutein and zeaxanthin concentration returned to baseline level. Besides raising serum carotenoid levels, corn and spinach intake also raised lutein concentration in BMC. In contrast, BMC zeaxanthin levels were unchanged throughout the study. The mean beta-carotenoid levels did not change in any tissue.

Unlike the concentrations of lutein and zeaxanthin in serum, BMC, and adipose tissue, the lutein and zeaxanthin concentrations in retina as indicated by macular pigment (MP) density continued to be elevated even after subjects discontinued eating corn and spinach daily. Also, the researchers observed an inverse pattern for zeaxanthin and lutein levels between MP density and adipose tissue. For examples, lutein and zeaxanthin concentrations in adipose tissue initially decreased at week 4, but rebounded after 8 weeks on the diet. MP density increased at week 4 and began leveling off thereafter. This observation lead the researchers to suggest that these 2 sites might compete for carotenoids from serum. The mean beta-carotenoid levels did not change in any tissue.

In the second part of this study, using 21 study subjects (13 women and 8 men), the researchers evaluated the cross-sectional relations among anthropometric measurements, MP density, serum, adipose tissue, and dietary lutein to further test possible interactions among tissues. The data clearly showed that there was a competition for lutein among different tissues. For example, percent body fat was inversely related to lutein concentrations in BMC, meaning that in people with higher % body fat, less lutein would be available for other uses. Data also indicated that there is a difference in carotenoid metabolism between the sexes. Even with significantly lower carotenoid intakes, women had similar serum carotenoid levels as men, and a higher lutein concentration in adipose tissue.

From these results, Johnson et al. concluded that "lutein and zeaxanthin are dynamic components of tissues and that the metabolism of lutein maybe different between women and men." However, due to the small cohort size and menopausal status of the females in the study, 9 out of 13 women were postmenopausal and not on HRT, it is difficult to determine if the observations are due to a gender difference or hormonal status. 

Johnson EJ, Hammond BR, Yeum KJ, et al. Relation among serum and tissue concentrations of lutein and zeaxanthin and macular pigment density. Am J Clin Nutr. 2000;71:1555-1562.

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Whole Grain Lowers Both Ischemic Stroke and Type 2 Diabetes

Previous studies have reported an inverse relationship between whole grain consumption and CVD. And now 2 studies by Liu et al. show a similar association between whole grain intake and risk of ischemic stroke and type 2 diabetes in women. Data for both studies were based on the 12 year Nurses' Health Study in a cohort of 75,521 women.

Mortality from stroke is more common in women than men. In light of the limited data on this topic, the findings by Liu et al. are especially valuable to lower stroke risk. The median whole grain intake ranged from 0.13 serving/day in the lowest quintile to 2.70 serving/day in the highest quintile. Women with a higher whole grain intake ate healthier (diet low in fat and alcohol and higher in folate, fruits and vegetables, and carbohydrates) and practiced healthier lifestyles (exercised regularly, took supplements, hormone replacements).

There were 352 confirmed cases of ischemic stroke during follow-up and was less common among the groups with higher whole grain intakes. The age adjusted RRs of ischemic stroke were 0.68 (second quintile), 0.69 (third quintile), 0.49 (fourth quintile), and 0.57 (fifth quintile). The RRs were attenuated when other CVD risk factors were included in the analysis. The multivariate RR was 0.69 in the fifth quartile for whole grain. However, refine grains and total grains (refined plus whole grains) had no significant effect on ischemic stroke. The multivariate RRs were 0.97 and 0.79 in the highest refine and total grain intake groups, respectively. Of all the CVD risk factors, smoking was the strongest compared to dietary factors such as saturated fat or trans-fatty acids, and fruit and vegetable intake. Earlier studies have shown that different compounds found in whole grains, such as folate, vitamin E, and fiber, may explain some of the protective effects of whole grain, however, since the primary objective of this study was to evaluate the overall impact of whole grain intake on ischemic stoke, the researchers did not adjust for these in the analysis.

Results from the Nurses' Health Study also suggest that whole grain intake is inversely associated with type 2 diabetes while refined grains raise the risk of diabetes mellitus. Based on this food-based analysis, the data showed that compared to women in the lowest quintile for whole grain intake, women in the highest quintile had a 38% lower risk of developing diabetes. This relationship was slightly attenuated when BMI, cigarette smoking, alcohol intake, family history of diabetes, and use of multivitamins and supplements were included in the analysis. The age and energy adjusted RR for the highest quintile of refined grain intake was 1.31. On the other hand, total grain intake was not significantly associated with diabetes risk.

When the researchers compared the relationship between the ratio of refined to whole grain to diabetes risk, they found that women in the highest refined grain intake and lowest whole grain intake had a 57% greater risk of type 2 diabetes. In  multivariate analysis, the RR was reduced to 1.26. Surprisingly, including saturated fat and trans-fat in the analysis did not alter the RR. Also, of the 1879 reported cases of type 2 diabetes during the 10-year follow-up, 1475 cases occurred in women with BMI values greater than 25. Separate analysis of grain intake and diabetes risk in this subgroup showed similar outcomes. The multivariate-adjusted RR across ascending quintiles were 1.00, 1.07, 1.14, 1.25, and 1.33 compared to 1.00, 1.09, 1.17, 1.27, and 1.25 in the full cohort, thus indicating that high whole grain and low refined grain is beneficial regardless of weight.

The results of these studies suggest that not all grain products are alike. Whole grain products, which tend to be absorbed more slowly as well as eliciting smaller post prandial glucose responses, lower type 2 diabetes risk, while refined grain intake increases risk. Clearly, it is important to distinguish these grains when counseling patients. In light of the fact that on average consumers eat less than one serving of whole grain products in an average 2000 kcal diet, there is a clear need to educate consumers to replace refined grain products with whole grain foods to lower the risk of diabetes and other chronic diseases.

Results from these studies show that high consumption of whole grain foods lowers the risk of ischemic stroke and type 2 diabetes in healthy middle-aged women, independent of other traditional CVD risk factors. And since the current average intake of whole grain is less than the recommended 3 serving per day, there is considerable room for promotional and educational efforts to encourage consumers to increase their whole grain intake. 

Liu S, Manson JE, Stampfer MJ, et al. A prospective study of whole-grain intake and risk of type 2 diabetes mellitus in US women. Am J Public Health. 2000;90:1409-1415.

Liu S, Manson JE, Stampfer MJ, et al. Whole grain consumption and risk of ischemic stroke in women. JAMA. 2000;284:1534-1540.

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CHD Associated to Lipoprotein-Associated Phospholipase A2 Enzyme

To the ever-growing list of emerging CHD risk factors, we might be able to add lipoprotein-associated phospholipase A2, "a family of enzymes that can hydrolyze phospholipids at the sn2 position to generated lysophospholipids and fatty acids." Lipoprotein-associated phospholipase A2 is also known as platelet-activating factor acetylhydrolase. And according to Packard et al., elevated levels of lipoprotein-associated phospholipase A2, which is regulated by mediators of inflammation, appear to be a strong risk factor for CHD. Packard et al. also showed that C-reactive protein, white-cell count, and fibrinogen are good predictors of CHD risk. 

Using baseline measures of C-reactive protein, white-cell count, fibrinogen, and lipoprotein-associated phospholipase A2 in a subgroup of men in the West Scotland Coronary Prevention Study, Packard and colleagues tested the relationship between chronic inflammation and CHD events. A total of 580 men with reported cases of study outcomes; nonfatal myocardial infarction, death from CHD, or a revascularization procedure, and 1160 healthy men were enrolled in this study. The control group was matched for age and smoking pattern.

To no surprise, analysis of the data showed that the subjects who suffered a coronary event had many more CHD risk factors than the control group. Also, the plasma levels of 4 inflammation markers were higher in the case group. Univariate analysis showed that plasma fibrinogen concentrations, white-cell count, C-reactive protein levels, and lipoprotein-associated phospholipase A2 were associated with 19%, 22%, 27%, and 20% increases in study outcome. However, compared to the C-reactive protein, which is highly interdependent with white-cell count, fibrinogen, and other CHD risk factors, the lipoprotein-associated phospholipase A2 showed weak or no relationship with fibrinogen and white-cell count, respectively. And only the plasma LDL-cholesterol level was associated with lipoprotein-associated phospholipase A2. Smoking was associated with increased C-reactive protein, fibrinogen, and white-cell counts, but there was no association with the lipoprotein-associated phospholipase A2.

Data from this study also confirmed an earlier meta-analysis finding that compared to subjects in the lowest quintile for C-reactive protein, white-cell count, and fibrinogen, those in the highest quintile had RR of 2.0 for CHD. However, when other inflammation markers and CHD risk factors were included in the analysis, the risk ratio dropped to 1.49 in the highest quintile for C-reactive protein. But in the case of lipoprotein-associated phospholipase A2, other inflammation markers and CHD risk factors had little effect on lowering the RR.

In conclusion, results from the study by Packard et al. confirm earlier findings showing that chronic inflammation does increase CHD risk in hypercholesterolemic men. But, it goes one step further to suggest that lipoprotein-associated phospholipase A2 is a better predictor of CHD risk than C-reactive protein, white-cell count, and fibrinogen, since unlike these 3 other inflammation markers, it's effects are independent of other inflammatory marker or other CHD risk factors.

Packard CJ, O'Reilly DS, Caslake MJ, et al. Lipoprotein-associated phospholipase A2 as an independent predictor of coronary heart disease. N Engl J Med. 2000;343:1148-1155.

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Impaired Fat Oxidation Leads to Increased Obesity in Undernourished Children

As you all know, the prevalence of obesity is increasing worldwide. And the  a major culprit behind this problem. However, shealth community has blamed widespread acceptance of a high-fat Western diet as a major culprit behind this problem. However, since the incidence of obesity is high among undernourished populations in China, Brazil, and South Africa, the current theory of excess food calories and lack of physical activity causing obesity does not apply to all. Therefore, using Hubel and Wiesel's theory of a critical period in which early-life stimuli may permanently affect metabolic development, Hoffman et al. tested the hypothesis that nutritional stunting is associated with impaired fat oxidation in poor Brazilian children.

By comparing fasting and post-prandial energy expenditure, respiratory quotients (RQ), and substrate oxidation in 28 stunted children and 30 normal height children, the researchers were able to show that the fasting RQ was significantly higher in the stunted group (0.92�0.009) vs. the control group (0.89�0.007). Also, the rate of fasting fat oxidation was lower in the stunted group (25�2% vs. 34%�2%). The lean body mass adjusted resting energy expenditures and post-prandial thermogenesis values were not significantly different between the 2 study groups. This metabolic feeding study lasted 3 days. Parents of both study groups had similar BMI and stature.

As with other at risk populations for impaired fat oxidations such as Pima Indians, stunted children were more likely to have problems oxidizing fat and, as a result, store more fat in their adipose tissues. Due to the nature of the study design, the study was unable to identify whether deficiencies of certain nutrients or malnutrition in general were responsible for the impaired fat oxidation in the stunted group. The mechanisms behind this relation are unclear, but the researchers speculated that long-term undernutrition might have damaged enzymes and hormones responsible for optimal lipid oxidation. Finally, Hoffman et al. concluded that even though this study was conducted in a different country, undernutrition occurs in our backyard and needs to be monitored in order to prevent unnecessary weight problems in children and eventually in adults.

Hoffman DJ, Sawaya AL, Verreschi I, et al. Why are nutritionally stunted children at increased risk of obesity? Studies of metabolic rate and fat oxidation in shantytown children from San Paulo, Brazil. Am J Clin Nutr. 2000;72:702-707.

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Low-saturated Fat and Cholesterol Diets are Safe and Effective for Preschool Kids

Health promoting programs have long supported a prudent diet, low in fat and cholesterol and high in fruits, vegetables, and grain products for adults and children over 2 years old, to reduce their CHD risk and atherosclerosis development. However, the same group of health professionals stress caution when it comes to the diets of infants and toddlers less than 2 years old. But according to the result from the Special Turku Coronary Risk Factor Intervention Project (STRIP) in Finland, an early intervention diet, low in SFA and cholesterol, was effective in keeping serum total cholesterol and LDL cholesterol levels lower in young boys. However, there was no significant difference noted with girls.

Compared to the control group (n=522), which received routine health education during the well-baby check-up, parents of children in the intervention group were given specific diet instructions to offer daily cholesterol of <200 mg/day and 30-35% of total energy as fat with a PUFA, MUFA, SFA ratio of 1:1:1. Diet records and serum cholesterol levels were collected regularly to assess compliance.

Throughout the intervention period, 7 months to 60 months, the intervention boys had 6 to 10% lower mean serum cholesterol levels than the control boys. The serum non-HDL and apo B concentrations were 6-11% and 4-7%, respectively, lower than the control group. The male control group, on the other hand, had slightly higher HDL cholesterol levels and apo A-I concentrations than the male intervention group, however, the overall total cholesterol:HDL ratios were not significantly different. And from the only fasting blood sample at age 5, the mean LDL cholesterol was 9% lower in the intervention boys. Differences in serum cholesterol, non-HDL, apo B, LDL, TAG, and total cholesterol:HDL ratio were not significant between 2 female groups.

Growth analysis between control and intervention kids showed no differences in height, weight, and BMI indicating that following a low-SFA and cholesterol diet was not detrimental to their physical development.

In conclusion, these data indicate that diets which contribute 30-35% of calories as fat with equal parts MUFA, PUFA, and SFA are effective in controlling blood lipids and lipoprotein levels in young boys without negatively affecting their physical development. But the benefits of such a diet were not shown in young girls. 

Rask-Nissila L, Jokinen E, Ronnemaa T, et al. Prospective, randomized, infancy-onset trial of the effects of a low-saturated-fat, low-cholesterol diet on serum lipid and lipoproteins before school age. The special Turku coronary risk factor intervention project (STRIP). Circulation. 2000; 102:1477-1483.

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Orange Juice Improves Plasma HDL Cholesterol Levels

Thanks to many important vitamins and phytochemicals found in orange juice (OJ), it has long been considered one of the healthiest beverages. And now a report from Kurowski et al. shows that drinking 3 cups of OJ can protect the heart by raising HDL cholesterol levels. It is thought that hesperetin, a citrus flavonoid found in the orange, is responsible for improving plasma lipoprotein levels.

In this 12-week feeding study, 25 healthy adults (16 men and 9 postmenopausal women) with total blood cholesterol levels of 170 mg/dl to 325 mg/dl included 1, 2, and 3 cups of OJ in their AHA step 1 diet. Each test period lasted 4 weeks, followed by 5 weeks of an orange free diet. Plasma lipid and lipoprotein levels were measured throughout the study. As expected, the dietary records indicated that vitamin C and folate intakes were significantly higher during the highest OJ consumption period.  Also, total energy and grams of CHO intake increased incrementally with each cup of OJ.

Analysis of overall changes in lipid and lipoprotein profiles showed that plasma HDL and TAG levels increased by 21% and 30%, respectively, following the 3 cups of OJ period. The LDL-HDL ratio decreased by 16% since LDL cholesterol levels were unchanged. In addition to altering blood lipids, drinking OJ was associated with raising plasma vitamin C and folate levels by 3.8 folds and 18%, respectively, with 3 cups/day of OJ consumption. However, in spite of the significant increase in folate levels during all 3 diet periods, plasma homocysteine levels were unchanged throughout different dietary periods.

Compared to baseline levels, plasma HDL cholesterol, vitamin C, and folate levels remained elevated even after the subjects stopped drinking OJ. But only the HDL cholesterol level was higher during the washout period than the highest OJ period. The changes in HDL cholesterol concentrations with OJ consumption were inversely related to the baseline HDL indicating that people with low baseline HDL cholesterol saw higher increases in their HDL cholesterol levels than people with higher baseline HDL levels.

In conclusion, the study by Kurowska et al. suggests that drinking OJ is an easy way for adults to improve their plasma HDL cholesterol and folate levels. This cardioprotective benefit continued even after 5 weeks of not drinking OJ. But the researchers encouraged everyone to obtain a variety of nutrients by eating at least 5 serving of fruits and vegetables daily rather than simply loading up on OJ.

Kurowska EM, Spence JD, Jordan J, et al. HDL-cholesterol-raising effect of orange juice in subjects with hypercholesterolemia. Am J Clin Nutr. 2000;72:1095-1100.

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Editorial: A New Approach for a New Millennium

The American Heart Association Dietary Guidelines 2000 represent a giant step forward in transforming nutritional recommendations from a consumer-confusing quantitative game of percentages to a much friendlier qualitatively concept which individuals can actually apply in heart disease prevention. Finally, after years of fat, salt and cholesterol phobia, there is less emphasis on the numbers and more emphasis on dietary patterns; less obsession on whether one hits the targets daily (for some it was each meal, for others each item) replaced with patterns over days or weeks; and, most importantly, a softening of the "one diet fits all" approach in favor of the recognition that human beings are not physiologically an inbred genetic strain. The AHA Nutrition Committee has demonstrated both rationale thought and practical considerations into these guidelines and, unlike many diet gurus with their fixated dogmas, recognizes and admits that there are uncertainties and vagaries within the recommendations. They have left room for the fact that nutrition is a dynamic science which will change over time and will necessitate flexibility in a dynamic population with changing environments and lifestyles.

In the 70s when dietary recommendations were being debated at congressional hearings, a number of nutritionists and public health advocates were concerned about the negative messages in the guidelines, that the food industry and public might misinterpret the objectives and move in the wrong direction, and that the recommended changes might be excessive given the paucity of hard evidence. Through the next thirty years we had the "bad cholesterol" phase, the "bad fats" phase and now the "bad saturated fats" phase. And after a quarter century of avoidance, substitution and replacement, we now move from the old paradigm emphasis on removing the negative ingredients (e.g. cholesterol, fat and salt) to a new paradigm emphasis on values and benefits of positive ingredients (e.g. antioxidants, vitamins, minerals, fiber and phytochemicals). Rather than the message "don't eat fatty meats, whole dairy products and eggs" the public now hears "include fish in the diet, 5 servings of fruits and vegetables, 6 or more servings of whole grains and legumes, low-fat dairy products, lean meats and poultry." The AHA guidelines emphasize foods and an overall healthy eating pattern, and the need to achieve and maintain a healthy body weight through avoidance of excess total energy intake and a regular pattern of exercise. The concept that "most people will be able to focus on the positive message of selecting healthy foods, rather than trying to follow a diet based on percentages" should return daily meals to an enjoyable experience rather than a 'life and death' decision.

Dietary restrictions focus on "the major components that raise LDL cholesterol . saturated fats, trans-fat, and to a lesser extent, dietary cholesterol." The guidelines state "Although there is no precise basis for selecting a target level for dietary cholesterol intake for all individuals, the AHA recommends <300 mg/d on average. By limiting cholesterol intake from foods with a high content of animal fats, individuals can also meet the dietary guidelines for saturated fat intake. This target can be readily achieved, even with periodic consumption of eggs and shellfish." Finally there is a recognized disassociation of saturated fat from cholesterol, and foods low in saturated fat, like eggs and shellfish, are not tarred with the same "saturated fat and cholesterol" brush. AHA noted that a major change from the old "recommended that individuals eat no more than 3 egg yolks per week" was replaced with "The recommended intake of dietary cholesterol remains the same - however, individuals may choose to eat one egg yolk daily, if the amount of foods high in dietary cholesterol in the rest of their diet is very limited." An egg a day really is okay!

But now the real task begins. How do we educate a population which for the most part has only heard the "don't eat this, don't eat that" nutrition messages? How do we turn around the fat and cholesterol phobias into broad based acceptance of eating patterns, weekly averages, and those old fashioned concepts of balance, variety and moderation? We moved the national diet from high-fat, calorie-rich, nutrient-poor to one of low-fat, high-carbohydrate, calorie-richer, nutrient-poor and now must again shift the pattern even more dramatically to one of moderate-fat, calorie-moderate, nutrient-dense, with a healthy dose of physical activity. And you thought the last quarter century of changes and education were hard work!

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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