| Winter 1997 |
TABLE OF CONTENTS
COMMON ABBREVIATIONS 
BMI: body mass index (kg/m2)
CHD: coronary heart disease
CHO: carbohydrate
CVD: cardiovascular disease
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 Fat and CHD Risk in Women
Over the years of studies on the role of diet in CHD risk, a major question has been whether the relationships between dietary fat and CHD risk are a function of fat amount, fat type, or both. Clearly, dietary recommendations to reduce total dietary fat to 30% of calories and saturated fat to no more than 10% of calories, are aimed at changing both fat quality and quality. However, some question the appropriateness and necessity of a low-fat, high-carbohydrate diet in CHD risk reduction since there is evidence that such a diet lowers plasma HDL and increases TAG levels. The question becomes, which is better, a low-fat, low SFA diet or a moderate fat, low SFA diet?
Hu et al. used data from the Nurses? Health Study to determine the relationships between dietary intakes of specific types of fat and CHD incidence in women. These investigators prospectively studied 80,082 nurses who were 34 to 59 years of age in 1980 with no known CHD or other major disease. The population used in this analysis has been followed for 14 years during which there were 658 nonfatal MI and 281 CHD deaths. The dietary patterns of the participants were determined at baseline by a food-frequency questionnaire and three follow-up questionnaires. The dietary patterns from the 1980 data set indicated that the women averaged 15.6% of calories from SFA, 16.0% from MUFA, 4.3% from PUFA and 2.2% from trans-fatty acids.
The authors reported that in age-adjusted analysis there was a positive association between total fat intake and CHD incidence over a range from 29.1% to 46.1% of calories. However, in multivariant analysis, the relationship between total fat and CHD disappeared. In the multivariate model the RR for a 5% increase in energy from total fat compared to carbohydrates was 1.02 (95% CI 0.97-1.07). The investigators reported that an increase of 5% of calories from SFA, compared to the same energy from carbohydrates, increased risk by 17%. The RR estimates for all dietary lipids are given in the table below.
| VARIABLE | RR | 95% CI | P Value |
| SFA (+5% energy) | 1.17 | 0.97-1.41 | 0.10 |
| MUFA (+5% energy) | 0.81 | 0.65-1.00 | 0.05 |
| PUFA (+5% energy) | 0.62 | 0.46-0.85 | 0.003 |
| Trans-FA (+2% energy) | 1.93 | 1.43-2.61 | <0.001 |
| Cholesterol (+200 mg/1000 kcal) | 1.12 | 0.91-1.40 | 0.29 |
The investigators also found that CHD risk was lowest among women with the lowest intake of trans-fatty acids coupled with the highest intake of PUFA (RR=0.31) compared to those with the highest intake of trans-fatty acids and lowest quintile of PUFA intake. Using models generated from the data, the authors determined that replacing 5% of energy from SFA with unsaturated fat would lower risk by 42%, and replacing 2% of energy from trans-fatty acids with unsaturated fat would result in a 53% lower risk. An unexpected finding from the data analysis was the observation that exchanging 5% of energy from PUFA with 5% from carbohydrates results in a 60% increase in CHD risk while a similar change from MUFA to carbohydrates increases risk by 20%.
What does all this mean for nutritionists and consumers? It should be noted that the lowest quintile of SFA intake was 10.7% of energy compared to the highest quintile at 18.8% of energy. Obviously there is a substantial range of intakes which make the potential for lowering SFA intake, and associated CHD risk, significant. In contrast, trans-fatty acid intakes ranged from the lowest quintile at 1.3% of energy to 2.9% in the highest quintile, the only quintile with a significant increase in RR. Using estimates of risk from this study it is evident that a decrease of 8% of energy from SFA (from the highest to the lowest quintile) will have a greater effect on CHD incidence relative to a 1.6% of energy decrease in trans-fatty acids in the diet. The point is, effective CHD risk reduction requires a reduction in SFA and trans-fatty acids but, since consumers have no information regarding trans-fatty acids in their diets, they should not lose perspective of what is important, reductions in SFA. With new products such as trans-fatty acid free margarines these concerns might eventually become less important in dietary interventions. Meanwhile, the evidence that fat type, rather than fat amount, is a major factor in CHD risk is a message that needs to be communicated to the fat-phobic public. The suggestion that replacing MUFA and PUFA calories in the diet with carbohydrates actually increases CHD risk raises serious questions regarding our national crusade to lower all types of fats in the diet. intake.
KEY Messages
- The kind of fats consumed, not the total amount of fat, determines a woman’s risk of heart disease.
- Replacing 5% of calories from SFA with unsaturated fat reduces risk by 42%.
- Replacing 2% of calories from trans-fatty acids with unsaturated fat reduces risk by 53%.
- Dietary cholesterol is not a significant dietary factor in CHD risk for women.
- Replacing SFA and trans-fatty acids in the diet with unsaturated fats (MUFA and PUFA) is more effective in lowering a woman’s CHD risk than lowering total fat intake.
- Intake of trans-fatty acids is positively associated with risk of coronary death.
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Editor’s Comment: The findings of Hu et al. relative to the question of dietary cholesterol effects on CHD risk in women adds additional evidence to the “no effect” hypothesis. While it appears almost impossible to prove that a dietary factor, especially dietary cholesterol, has no effect on heart disease risk, the number of recently published, large epidemiological studies which report no significant relationship between dietary cholesterol and CHD incidence provide pretty strong evidence of innocence. As we have previously reported, a number of studies in the past two years have reported that dietary cholesterol is not a significant contributor to CHD risk. Esrey et al. (Nutrition Close-Up 13 #2, 1996) reported data for 4,546 men and women in the LRC Prevalence Follow-Up Study that the RR for a 10 mg per 5000 kJ increase in dietary cholesterol was 1.00. Ascherio et al. (Nutrition Close-Up 13 #4, 1996) reported data from studies of over 43,000 male health professionals indicating that the RR for a 100 mg/1000 kcal change in dietary cholesterol was 1.03 for MI and 1.06 for fatal CHD. In the last issue of Nutrition Close-Up (14 #3) we reported on a study by Pietinen et al. of 21,930 men indicating that at the highest quintile of cholesterol intake (768 mg/day) RR for a major coronary event was 0.93 and for coronary death was 0.92. And now the paper by Hu et al. with 80,082 women reports that the RR for a 200 mg/1000 kcal increase in dietary cholesterol is 1.12. In not one of these 4 large epidemiological studies with almost 150,000 participants was dietary cholesterol significantly related to either all CHD or to either nonfatal or fatal CHD. The question remains, how many more studies are needed before dietary cholesterol is found innocent in the diet-heart disease relationship? |
Hu, F.B., Stampfer, M.J., Manson, J.E., et al. Dietary fat intake and the risk of coronary heart disease in women. N Engl J Med 1997;337:1491-1499.
Relationship Between Birth Weight and Adult CVD
A number of recently published studies suggest a significant relationship between an individual’s birth weight and their risk of CVD later in life. Most studies report an inverse relationship between birth weight and adult CVD incidence which suggest an important role of prenatal nutrition in lowering CVD risk 40-60 years later. Rich-Edwards et al. report data which add to the growing body of evidence for a “fetal origins” hypothesis for adult CVD. According to Rich-Edward et al., high birth weight women in the Nurses’ Health Study had the lowest relative risk for nonfatal CVD. The age adjusted relative risk for specific birth weight categories are 1.49 for <5 lb, 1.25 for >5 lb to 5 lb 8 oz, 1.12 for >5 lb 8oz to 7 lb 0 oz, 1.0 for >7 lb 0 oz to 8 lb 8 oz, 0.96 for >8 lb 8 oz to 10 lb 0 oz, and 0.68 for >10 lb 0 oz. This finding was based on a 1992 retrospective self report of birth weight by 70,297 women in the longitudinal Nurses’ Health Study. There was a total of 1,216 cases of nonfatal CVD. Other common risk factors for heart disease did not significantly alter the outcome. Based on these data, the researchers estimated that for every 1 lb increase in birth weight, the risks of non-fatal CHD and stroke were decreased by 5% and 11%, respectively.
However, two factors question the validity of this finding. First, accuracy of self reported birth weight compared to birth certificates was 70% for nurses between the ages 27- 44 years. Researchers suspected that it was the same for all age groups. Secondly, 13% of women with birth weights at extreme ends were the driving force behind the inverse association between birth weight and CVD. The relationship was minimal in women with birth weight between 5 lb 8 oz and 10 lb.
Despite the two confounders mentioned above, these researchers concluded that the data support an inverse relationship between birth weight and adult CVD. They estimated that in this cohort, born between 1921 and 1946, a low birth weight was associated with no more than 20% of the non-fatal CVD observed. Interestingly, 11% of this cohort had a low birth weight, whereas low birth weight in the U.S. in 1990 was only 7%.
Rich-Edwards, J.W., Stampfer, M.J., Manson, J.E. et al. Birth weight and risk of cardiovascular disease in a cohort of women followed up since 1976. BMJ 1997;315:396-400.
Plasma Homocysteine and CHD Risk
Lately, the role of plasma homocysteine in CHD risk has received considerable attention. According to an article entitled “Hidden Causes of Heart Disease” in the August 11, 1997 issue of Newsweek, an elevated plasma homocysteine was compared with smoking and high plasma cholesterol, two well-established risk factors for CHD. In spite of an accumulation of studies which claim a direct relationship between high homocysteine levels and CHD, the report by Evans et al. shows that this research question is far from settled.
In this nested case-control study from the 12,866 subjects in the Multiple Risk Factor Intervention Trial (MRFIT), researchers investigated the relationship between plasma homocysteine levels and nonfatal MI and CHD death. In this prospective study, the mean homocysteine levels for subjects with nonfatal MI (n=93) and CHD death (n=147) were 12.6 µmol/L and 12.8 µmol/L, respectively. The control subjects for the nonfatal MI and CHD death subjects had homocysteine levels of 13.1 µmol/L (n=186) and 12.7 µmol/L (n=286), respectively. In the statistical analysis, the subjects were divided into quartiles of homocysteine levels. According to the multiple logistic regression analysis, subjects in quartile 2 (9.6-11.8 µmol/L), quartile 3 (11.9-14.9 µmol/L), and quartile 4 (15.0-80.4 µmol/L) had similar risk of CHD death and nonfatal MI as subjects in the first quartile (3.7-9.5 µmol/L). One unusual finding was that 11 subjects who died within the first five years of the study had higher homocysteine levels than the remaining 136 cases of CHD death (15.7 µmol/L versus 12.4 µmol/L).
Even though the data from this study contradict the hypothesis that high serum homocysteine results in increased CHD risk, the findings of Evans et al. are consistent with other longitudinal studies investigating this association. Unlike the retrospective studies, longitudinal studies have consistently shown that serum homocysteine levels in subjects with MI and CHD are similar to the control group. Researchers speculate that the difference between longitudinal and retrospective outcomes are possibly due to various factors. One, homocysteine levels from stored serum are less than levels from a fresh sample. Two, long-term dietary variations can result in altered homocysteine levels. Three, MI or stroke is the cause behind elevated blood homocysteine levels rather than the result of high homocysteine levels. Four, the prospective studies lack enough cases to identify the risk associated with high homocysteine concentrations and CHD. Five, elevated homocysteine levels are associated with other CHD risk factors. The authors discussed each of these possibilities, rejecting most of them based on an available data. One other possible mechanism is that homocysteine may be a late-stage predictor of CHD.
In conclusion, this longitudinal study showed no association between high plasma homocysteine and increased CHD risk.
Evans, R.W., Shaten, B.J., Hempel, J.D. et al. Homocyst(e)ine and risk of cardiovascular disease in the Multiple Risk Factor Intervention Trial. Arterioscler Thromb Vasc Biol 1997;17:1947-1953
Abstracts from the 1997 American Heart Association Meeting
The following briefs cover some of the many abstracts presented at the 70th Scientific Sessions of American Heart Association (AHA) held in Orlando, Florida this past November. Abstracts are published in Circulation, AHA’s bimonthly journal.
CHOLESTEROL AND COGNITIVE PERFORMANCE
For many years there have been uncertainties regarding the relationship between plasma cholesterol levels and brain function. Some studies of plasma cholesterol lowering effects on CHD incidence suggest an increase in deaths from violent causes and suicides. Muldoon investigated the effects of cholesterol lowering with a statin drug on cognitive performance. Using a double-blind study design he provided 20 mg/day statin or placebo to 194 healthy adults for 6 months. Measures of cognitive performance were tested before and after treatment. Test for mental flexibility, working memory, and memory recall were unaffected by treatment. However, treatment reduced performance in attention and psychomotor speed measures. There was a relationship between the extent of plasma cholesterol lowering and the decrease in performance. The author noted that in all cases the changes in performance were relatively small and that the long term effects of the newer, more effective statins on attention and psychomotor speed need to be evaluated.
Muldoon, M.F. Effects of cholesterol reduction on cognitive performance. Circulation 1997;96:I-66.
GENDER DIFFERENCES IN DIET RESPONSIVENESS
Three studies of the effects of a Step 2 diet on plasma cholesterol levels in men and women indicate significant gender differences. These data raise questions of the general applicability of this dietary pattern for hypercholesterolemic women. Thirty-three subjects (19 M, 14 F) were provided two test diets containing either 14.1% or 4.0% of calories as SFA in the study by Li et al. The dietary cholesterol differed by 100mg/1000 kcal-day. Significantly greater reductions in LDL cholesterol (-16 vs -5%) and in apo B levels (-18 vs -9%) were observed in males compared to females. The LDL:HDL ratio was significantly reduced in men but not in women. Surprisingly, decreases in LDL particle size were greater in women than in men. It is unclear why males have a more favorable plasma lipid response to a Step 2 diet than females.
In a comparable study, Walden et al. studied the effects of following a Step 2 diet for one year on LDL and HDL levels in hypercholesterolemics (112 M, 73 F) and combined hyperlipidemics (106 M, 92 F). The Step 2 diet averaged 24-26% calories from fat, 7-8% saturated fat and 95 mg/1000 kcal cholesterol. At one year males and females had similar LDL decreases. However, the hypercholesterolemic females had a greater reduction in HDL cholesterol (-7.6%) and apo AI levels (-5.3%) compared to combined hyperlipidemic females and all males. The major changes occurred in the HDL2 subfraction which was decreased to a greater extent in women compared to men irrespective of lipid phenotype.
To determine how low-fat diets lower plasma HDL levels, Carrasco et al. studied 21 male and female subjects fed a baseline diet with 36% of calories as fat and then a Step 2 with 25% fat for 6 weeks each. HDL apo AI turnover kinetics were determined at the end of each diet phase. Intake of the low-fat diet resulted in reduced levels of HDL cholesterol (-15%) and apo AI (-13%). The decrease in plasma apo AI was due to a reduced apo AI secretion rate -18%) while the fractional catabolic rate remained constant. The authors conclude that the HDL lowering effect of a low-fat diet is due to a decrease in HDL apo AI production.
Li, Z., Otvos, J.D., Carrasco, W.V., Lichtenstein, A.H., et al. Effects of gender lipoprotein subspecies response to a National Cholesterol Education Program Step 2 diet. Circulation 1997;96:I-34.
Walden, C.E., Retzlaff, B.M. & Knopp, R.H. Effect of NCEP Step II diet on HDL-C differs in women and men at one year. Circulation 1997;97:I-34.
Carrasco, W.V., Lichtenstein, A.H., Welty, F.K., et al. Effects of a Step 2 diet on HDL apolipoprotein (apo) AI catabolism and secretion in postmenopausal females and older males. Circulation 1997;96:I-34.
GENETICS AND CHOLESTEROL ABSORPTION
Previous studies have shown that variant alleles of the apo A-IV gene effect the response to dietary cholesterol in humans. To determine whether these variants alter the fractional absorption of dietary cholesterol, investigators measured cholesterol absorption rates in 13 apo A-IV-1/1 homozygotes and 11 apo A-IV-1/2 heterozygotes fed a 35% fat diet containing 15% of calories as polyunsaturated fat and 750 mg of dietary cholesterol. All subjects were apo E 3/3. The investigators found a significant difference in percent cholesterol absorption between A-IV-1/1 (56.7%) and A-IV-1/2 (47.4%) subjects; however, there were no significant differences in the increase in plasma lipids with the dietary changes between the two groups. These data are different from results reported last year where the fractional absorption of cholesterol was identical, and the plasma cholesterol increase with a 15% saturated fat diet was greater in subjects with the apo A-IV-1/1 compared to the apo A-IV-1/2 group. The authors suggest that the polyunsaturated fat content of the diet negated the differential response of the variant apo A-IV alleles. It would appear that the effects of variants in the apo A-IV gene on cholesterol metabolism have multiple interactive effects with dietary factors.
Weinberg, R.B., Geissinger, B.W., Terry, J.G., et al. Effect of the apo A-IV-2 allele on cholesterol absorption and the plasma lipid responses to a high cholesterol/polyunsaturated fat diet. Circulation 1997;96:I-479.
HYDROGENATED VEGETABLE OIL AND PLASMA CHOLESTEROL
The effects of dietary trans-fatty acids on plasma lipids and lipoproteins continues to be an area of some debate, especially when the question is whether margarine or butter is more heart healthy. In this cross-over study in 11 postmenopausal women, the investigators provided diets consisting of 30% of calories as fat, with either soybean oil, hydrogenated soybean oil or butter contributing between 20% and 2/3 of the fat. Each diet was fed for 5 weeks. Plasma total and LDL cholesterol levels were highest with intake of the butter diet and lowest with the soybean oil intake. The total cholesterol-HDL ratio were unaffected by the type of dietary fat. For most of the plasma lipid, lipoprotein and apolipoprotein variables, intake of the hydrogenated vegetable oil resulted in values which fell in between those with intake of the soy bean oil compared to butter intake. The authors used the results to generate a predictive equation indicating that 1 % of calories from trans-fatty acids in the diet will increase plasma cholesterol by 1.9 mg/dl.
Lichtenstein, A.H., Ausman, L.M., Vilella-Bach, M., Schaefer, E.J. Hydrogenated vegetable oil results in higher lipoprotein levels than the naturally occurring oil and lower lipoprotein levels than butter. Circulation 1997;96:I-480.
HIGH-FAT VERSUS LOW-FAT DIETS FOR HYPERTRIGLYCERIDEMICS
The existence of true, persistent carbohydrate-induced hypertriglyceridemia, and the associated plasma HDL lowering, has been questioned for years. Two recently reported studies investigating this question continue this debate by arriving at very different conclusions.
Duell et al. tested a very-low fat diet in 11 normolipidemic and 8 hypertriglyceridemic subjects using a phased approach going from 37% to 30% to 20% to 10% of calories from fat over 6.5 weeks. The diets were kept relatively low in sugar. Total cholesterol levels fell 18% in both groups while HDL fell 21% in the controls and 7% in the hypertriglyceridemics. Only the hypertriglyceridemic subjects lowered their LDL:HDL ratio. There were no major effects on plasma triglyceride levels in either group. The authors concluded that the phased introduction of a eucaloric very-low fat diet effectively lowered plasma LDL levels with modest effects on HDL and triglycerides.
In contrast, Cater and Denke reported that they observed no changes in plasma LDL or HDL levels in 12 males with moderate hypertriglyceridemia fed a 40% fat (7% saturated fat) compared to a 20% fat diet (8% saturated fat). Plasma triglyceride levels were significantly lower during intake of the 40% fat diet and the authors concluded that intake of a high fat diet, low in saturated fat, results in a significantly better plasma lipoprotein profile in hypertriglyceridemic patients compared to a low-fat diet.
While these studies are not directly comparable, they illustrate the quandary regarding low-fat diets relative to plasma HDL and triglyceride concentrations. For the moment it would appear that moderation is the best approach and that low-fat and very-low fat diets have highly variable effects on plasma lipids.
Duell, P.B., Hatcher, L.F., Connor, W.E. Is a very-low fat diet detrimental to fasting and postprandial plasma lipid levels? Circulation 1997; 96:I-479.
Cater, N.B., Denke, M.A. Comparison of high and low fat diets for treatment of hypertriglyceridemia. Circulation 1997;96:I-480.
Salicylate Exposure and Ubiquitous Use of Heaters are Two Possible Factors for the Decrease in CHD Mortality
In the past 30 years, the incidence of CVD mortality in the U.S. has decreased dramatically. Many have attributed this trend to decreases in blood cholesterol, blood pressure, and cigarette smoking in the population. However, changes in risk factors during this period cannot be credited for all of the CVD decline. The results from two recent studies propose different hypotheses for factors contributing to the decline in CVD rates. In the first study, Ingster and Feinleib speculated that increased exposure to salicylate in the environment might have contributed to the decrease in CVD mortality. Seretakis et al. evaluated the changes in the seasonal patterns of primary deaths or related to the pattern of declining coronary mortality.
Using data from the International Trade Commission and US Census Bureau reports, Ingster and Feinleib estimated aspirin and other salicylate production from 1920 to 1980 and calculated daily aspirin and salicylate exposure per person. Based on the data, the investigators noted a steady increase in aspirin and salicylate production through the decades; however, starting in 1966, salicylate production increased dramatically. For example, in 1966 salicylate production was 13.8 pounds per 100 people, and in 1980 it was 36.8 pounds per 100 people. This translates to 259 mg of aspirin/salicylate exposure per day in 1960 and 341 mg per person per day in 1970. Ingster and Feinleib proposed that at these levels, like aspirin, salicylate could also effect CVD mortality since salicylate has similar anti-inflammatory effects seen with aspirin.
Seretarkis et al. investigated the secular tend in the intensity of the seasonal pattern on the U.S. coronary mortality. By using data from Vital Statistic of the United States and other abstracts, these researchers were able to track ischemic heart disease from 1937 to 1997. The authors estimated the seasonal patterns of coronary deaths by calculating the ratio of the peak months rate of coronary deaths to the trough for each year. According to the ratio of the seasonal pattern, the CHD mortality rate sharply decreased from 1930 to 1970 and gradually thereafter. Seretakis et al. suggested this was due to increased heater and air-conditioning use in homes, work places, and automobiles, since these appliances allowed people to control the temperature in their environment. When the data were separated based on deaths in the winter months, December, January, and February, and deaths in the summer months, June, July, and August, it showed that winter death rates decreased and summer death rates increased over the years. Also, the rates of CVD mortality decrease more significantly in people from New England states than residents from 4 southern states. If this hypothesis is accurate, it could help explain the high CHD mortality rates among low-income groups which have less control over their microclimate.
These studies are just two examples of other possible contributors to the decrease in CVD mortality rates seen over the past thirty years.
Ingster, L.M., Feinleib, M. Could salicylates in food have contributed to the decline in cardiovascular disease mortality? A new hypothesis. J Public Health 1997;87:1554-1557.
Seretakis, D., Lagious, P., Lipworth, L. et al. Changing seasonality of mortality from coronary heart disease. JAMA 1997;278:1012-1014.
Editorial:
Goals, Guidelines, and Fat-Phobia
One of the most striking observations from the recent American Dietetics Association meeting was the much heralded absence of dietary fat from virtually everything. Practically every booth in the exhibit hall touted its place in the reduced-fat or fat-free market place. From the American Heart Association booth of certified foods to the fat-free, egg-free egg replacer, there was barely a fat calorie in the hall. The public health campaign against dietary fat has obviously worked well; almost as well as the anti-cholesterol campaign which generated an avalanche of cholesterol-free food items (many of which never had any cholesterol to begin with) which were all the rage a dozen years ago. And, based on the available evidence, the next major food aversion campaign will be against those twin villains, saturated and trans-fats. Meanwhile, the public makes food choices based on numbers from the Nutrition Facts Labels using calculators to tallying up the cholesterol (less than 300 mg per day), total fat (less than 30% of calories) and saturated fat (less than 10% of calories) allocations for the day.
It is surprising that those involved in nutrition education and policy development are only now beginning to address the problems faced by the public in interpreting and implementing the dietary goals they are given. The average consumer cannot readily comply with the dietary goals, which nutrition professionals have established to quantitate changes in dietary patterns, without the help of practical, livable dietary guidelines for achieving those goals. Now you might wonder what in the world I’m talking about, we have all the dietary recommendations and guidelines one population can possibly handle. But the fact is that we have given the public a set of numerical dietary goals [the famous 30 (10:10:10), 300] which, while of use to nutrition professionals, has little practical meaning in daily life. And to the public our dietary goals place the emphasis on reductions in fat, saturated fat and cholesterol with limited notice of the need for more balance, variety and moderation in the diet. The exclusion message is more widely heard than any perception of inclusive, and the pattern of new products in the market place puts added emphasis on our collective fat aversion.
There have been two interesting repercussions from our insistence that consumers pay attention to our quantitative dietary numbers game rather than applicable dietary guidelines. It is clear that the criminalization of fat and cholesterol has been a much more widely and effectively communicated message than programs such as the 5-A-Day for increased fruits and vegetables in the diet. One wonders if this isn’t partly due to the fact that commercial concerns couldn’t generate new products and markets for those simple fruits and vegetables, or establish certification programs to promote them. So rather than changing eating patterns, we now consume reduced-fat, fat-free (and sugar rich) foods with as little nutrient density as the old versions. Ironically, we have succeeded in reducing the percent of calories from fat while our national waist line gets bigger. By emphasizing nutrients, not foods, we achieve a great awareness for counting fat grams, and amnesia about total calories.
Just in case anyone wonders, I recognize that at least one set of numerical dietary goals contains a stated recommendation: i.e., limit egg consumption to no more than 4 a week. So, since most consumers have no idea what 300 milligrams of cholesterol actually is, the approach of many has been “zero tolerance” in the hope that, since 300 mg is unknown, zero eggs will help them hit the number. And what about the efficacy of this recommendation? In 1945 per capita egg consumption was 405 eggs per year, and in 1995 the number had fallen to 235 per year. A decrease of 170 eggs per year equals 3.3 per week or 0.47 per day resulting in a decrease in dietary cholesterol of 100 mg per day (0.47 eggs x 215 mg cholesterol per egg). It can be estimated, based on meta-analysis data from cholesterol feeding studies, that this 42% decrease in egg consumption between 1945 and 1995 has lowered the mean plasma cholesterol level of the population by 2 mg/dl (100 mg cholesterol/day x 0.022 mg/dl per mg cholesterol/day). So for the single, most widely recognized dietary guideline given to the public we can only say – gee whiz!
The Dietary Guidelines Alliance provides some help to address many of these concerns in their “It’s All About You” program to encourage people to follow the recommendations in the USDA/HHS Dietary Guidelines for Americans. Using the guideline as a base, their primary message to consumers is: “Make healthy choices that fit your life-style so you can do the things you want to do.” And to work with the seven points of the Dietary Guidelines, they encourage consumers to:
- BE REALISTIC: Make small changes over time in what you eat and the level of activity you do. After all, small steps work better than giant leaps.
- BE FLEXIBLE: Go ahead and balance what you eat and the physical activity you do over several days. No need to worry about just one meal or one day.
- BE ADVENTUROUS: Expand your tastes to enjoy a variety of foods.
- BE SENSIBLE: Enjoy all foods, just don’t overdo it.
- BE ACTIVE: Walk the dog, don’t just watch the dog walk. And you don’t even need a calculator to make it work. .
And you don’t even need a calculator to make it work. We wish the Dietary Guidelines Alliance success in their efforts to bring some guidance into the guidelines, and in helping the public understand that the best dietary recommendations put the major emphasis on what a healthy diet should include to achieve maximal nutritional and health benefits
Donald J. McNamara, Ph.D.
Executive Editor, Nutrition Close-Up
Elevated Plasma TAG Increases CHD Risk
Gaziano et al. investigated “the interrelationships of the fasting TG level, other lipid parameter, and nonlipid risk factors with risk of MI.” In this case-control study, 340 subjects with recent diagnosis of MI were recruited from 6 Boston hospitals. All subjects were white, less than 76 years old, and no history of MI or angina pectoris prior diagnosis. The remaining 340 age and sex adjusted control subjects were randomly selected from case subjects neighborhoods.
All subjects were interviewed and baseline risk factors for CHD recorded. In addition to the usual CHD risk factors; age, sex, HTN, diabetes, cigarette smoking, BMI, family history of premature MI, dietary intake, and alcohol intake, and subject physical, psychological, and socioeconomical conditions were measured. Also, from the fasting venous blood sample, subject’s TAG, total cholesterol, LDL, and HDL cholesterol were measured. As expected, case subjects had more CHD risk factors than the control group. Also, people with the highest TAG levels were more likely to be males, have HTN, diabetes, higher BMI, more active, and consume more alcohol than ones with lower TAG levels. The investigators found a strong direct relationship between TAG and total cholesterol and VLDL and an inverse relationship between TAG and HDL cholesterol. The relationship between TAG and LDL was less strong. The age and sex adjusted relative risk of MI, based on quartile of TAG levels, were 1, 3.2, 4.5, and 6.8 for each increase in quartile. The relative risk did not change significantly when other CHD risk factors were included. However, the HDL level did attenuate the relative risk for CHD. The relative risk was 1.0, 2.2, 2.1, and 2.7, for respective quartiles. When the RR was measured base on quartile of TAG/HDL, subjects in the 4th quartile had 16 fold higher risk of MI than subjects in 1st quartile. Also, subjects with small dense LDL were more likely to have higher TAG and lower HDL than subjects with large buoyant LDL. Lastly, the TAG level was strongly associated with higher risk of MI in women than men. For example, for each increase in log TAG level, RR for MI increased by 2.6 fold in men and 4.5 fold in men.
In conclusion, this study by Gaziano et al. were able to show that elevated fasting TAG is a marker for CHD risk.
Gaziano, J.M., Hennekens, C.H., O’Donnell, C.J. et al. Fasting triglycerides, high-density lipoprotein, and risk of myocardial infarction. Circulation 1997;96:2520-2525.
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.
