| Volume 18 – Number 1 | Spring 2001 |
TABLE OF CONTENTS
- Cholesterol-Lowering Diet is Safe in Young Children
- Linolenic Fatty Acids Increase Age Related Macular Degeneration Risk
- Fish and Omega-3 Fatty Acids Lower Total Stroke Risk in Women
- High-Fat, Low-Carbohydrate Diet Improves Glucose Metabolism
- Genetic Regulation of Cholesterol Absorption
- Familial Traits Play an Important Role in Individual Variance to Low-Fat Diets
- CVD Risk and Dietary Changes in a Spanish Population
- Designer Eggs Improves Plasma Vitamin E, Lutein, and Omega-3 Fatty Acid Levels
- Editorial: Science and “the truth is no there” Spin-Masters
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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
Cholesterol-Lowering Diet is Safe in Young Children
Cholesterol lowering diets have long been recommended for adults, but fears of possible growth retardation and nutritional inadequacy have prevented wide use of this diet in young children. To answer this question, the National Heart, Lung, and Blood Institute conducted a multi-center Dietary Intervention Study in Children (DISC) trial with 662, 8-10 year olds with LDL cholesterol levels between 111 and 164 mg/dl. The subjects were randomly assigned to an intervention or a usual care group.
The intervention group was told to follow the National Cholesterol Education Program’s Step 2 diet, with 28% of energy from fat, <8% from saturated fat, >9% of PUFA, and <75 mg/1000 kcal of cholesterol per day. In order to increase compliance, the subjects were given extensive nutrition and behavioral counseling. For example, during the first 6 months, they received 6 weekly and then 5 biweekly group sessions plus 2 individual sessions; then during the second 6 months, 4 group and 2 individual sessions; in the second and third year, 4 to 6 group meetings plus monthly telephone calls; and finally after the 4th year, 2 group and 2 individual sessions. All the sessions were lead by nutritionists and behaviorists. The children in the usual care group were simply told of their elevated blood cholesterol levels and given education materials on heart healthy eating. The primary safety and efficacy outcomes measured were serum LDL cholesterol, serum ferritin levels and height. The secondary efficacy and safety outcomes measured were serum total cholesterol, HDL, LDL/HDL ratio, TAG, and red blood cell folate, serum retinol and zinc, and sexual maturation.
The baseline height, weight, BMI, age, and serum lipid levels were similar in both groups. Compared to the usual care group, a higher percentage of the intervention kids were from families with household incomes of less than $20,000 (15.1% vs. 5.9%). The average length of follow-up period was 7.4 years for the DISC trial. The attendance to the intervention sessions noticeably diminished over time. For example, the average attendance rate was 96% during the first 6 months, 89% during year 3, and 72% during year 5. Attendance rates during the last 3 years of the study were a dismal 55%, 42%, and 37%, respectively.
Like the attendance rate for the nutrition education sessions, the dietary compliance rate was initially high, as reflected by significantly decreased dietary total fat, saturated fat, and cholesterol intakes in the intervention group, but over time the subjects backslid. On the other hand, the usual care subjects steadily lowered their fat and cholesterol intakes, to levels rivaling the intervention group. The results from the primary efficacy and safety outcomes showed that there were no differences in height and serum ferritin levels between the 2 study groups. Reducing dietary fat did not adversely alter the nutritional status or physical growth of the intervention group. The plasma lipid levels slightly improved during the follow-up period. For example, the baseline LDL cholesterol decreased from 130.6 mg/dl to 109.8 mg/dl in the intervention group and 112.2mg/dl in the usual care group at 5 years. But it increased to 114.1 mg/dl and 115.9 mg/dl for the intervention and usual groups, respectively, at the last visit. The difference in LDL cholesterol levels in the intervention group over the usual group was significant only at the first 3 years of follow-up. Similar trends were noted with secondary efficacy and safety outcomes of total serum cholesterol. Throughout the study, the HDL cholesterol, LDL/HDL ratio, TAG, weight and sexual maturation were similar between the 2 study groups. Analysis of a subgroup of the intervention group who maintained a high overall compliance rate showed that their plasma lipid and lipoprotein levels were better than the usual care group during the entire follow-up period.
According to the researchers, data from the DISC study indicate that reducing dietary total fat and saturated fat from the diets of young children does not lead to negative outcomes. Also, as long as the subjects were following the prescribed diet, it was effective in improving total and LDL cholesterol level. The researchers’ explanation for the limited benefits noted during the last few years of the study were due to a combination of both diminished interest in the low-fat diet by the intervention group and increased interest in a low-fat diet, in spite of a lack of formal nutrition counseling for the usual care group. The researchers also suggested that the lack of difference in plasma LDL were due to a higher percentage of poor children in the intervention group and their lack of adherence to the test diet.
Obarzank E, Kimm SY, Barton BA, et al. Long-term safety and efficacy of a cholesterol-lowering diet in children with elevated low-density lipoprotein cholesterol: Seven-year results of dietary intervention study in children (DISC). Pediatrics. 2001;107-256-264.
| Lipids (mg/dl) | Intervention Group | Usual Care Group | ||||
| Baseline | Year 3 | Final Year | Baseline | Year 3 | Final Year | |
| Cholesterol | 200 | 183 | 180 | 200 | 186 | 180 |
| LDL | 131 | 110 | 114 | 131 | 112 | 116 |
| HDL | 57 | 53 | 50 | 57 | 53 | 49 |
| TAG | 80 | 100 | 101 | 81 | 99 | 97 |
| LDL:HDL | 2.3 | 2.1 | 2.3 | 2.3 | 2.1 | 2.4 |
[See Editorial for comments].
Key Messages
- National Cholesterol Education Program’s Step 2 diet did not negatively affect serum ferritin levels or stunt physical development in young children.
- Plasma HDL, LDL/HDL ratio, TAG, weight, and sexual maturation rate were similar between 2 study groups.
- Decrease in serum LDL levels in the treatment group was significant only for the first 3 years of the study.
- Over time, compliance rate declined in the intervention group as noted by higher total fat, saturated fat, and cholesterol intake.
- Children in the usual care group improved their eating pattern to rival the intervention group.
Linolenic Fatty Acids Increase Age Related Macular Degeneration Risk
Currently 13 million Americans are afflicted with age-related macular degeneration (ARMD), a leading cause of blindness in the elderly. And according to scientists, this problem is bound to grow as the number of older members of the population increases. But what makes this problem even more dyer is that at present, there is no cure for ARMD. The mechanism behind ARMD is unclear, but since this is a vascular problem that damages the retina, Cho et al. tested for a relationship between ARMD and fat intake in subjects enrolled in the Nurses’ Health Study (NHS) and Health Professionals Follow-up Study (HPFS). It was hypothesized that high saturated fat intakes which promote atherosclerosis of the blood vessel, might be associated with increased risk of ARMD. This study included 71,486 women and 41,474 men who were over the age of 50 years at the time of their enrollment. During the 12-years of follow-up in women and 10-years of follow-up in men, 567 cases (351 women and 216 men) of ARMD with a visual loss of 20/30 or worse were reported. Based on the returned biennial food frequency questionnaires, high fat intakes were associated with cigarette smoking, higher BMI, and total calories and inversely related to alcohol, zinc, vitamin E, lutein, and zeaxanthin intakes.
The prevalence of ARMD was 54% higher in the highest quintile of total fat intake. This relationship was even stronger in the female cohort. The multivariate RR for ARMD in the highest quintile was 1.61 in women and 1.42 in men. Regardless of fat sources, animal or vegetable fat, high fat consumption increased ARMD risk. On the other hand, dietary cholesterol was not related to ARMD risk. When the dietary fat-ARMD relationship was separately analyzed based on the type of fatty acid, saturated fat, MUFA, and trans-fatty acids were significantly associated with higher ARMD incidence whereas PUFA had a non-significant positive association with ARMD.
Detailed analysis of PUFA’s role in ARMD risk showed that only linolenic acids were associated with ARMD risk with a multivariated RR for ARMD of 1.41 in the 5th quintile. The group with highest intakes of linolenic acid from beef, pork, or lamb and margarine raised their ARMD risk by 35% compared to the group that ate less than 3 serving/month of these products. Other PUFA, arachidonic, eicosapentaenoic, and docosahexaenoic acids were inversely related with ARMD risk. Also, as expected, high fish intakes, which are high in docosahexaenoic acids, lowered the RR for ARMD by 35%.
Reanalysis of the positive association of total fat and ARMD based on each fat component showed that linolenic acid and trans-fatty acids had the greatest effect on ARMD risk. For example, adjustment for linolenic acid reduced RR for total fat from 1.54 to 1.30 and including trans-fatty acids further attenuated the RR for total fat to 1.16. Separate analysis for subgroups of ARMD, early or advanced stages of ARMD, showed similar fat-ARMD relationship.
Data from this large prospective study indicate that ARMD risk, like other vascular diseases, can be modified by changing dietary fat intakes. High intakes of linolenic acids and trans-fatty acids significantly raised ARMD risk. On the other hand, high intakes of long chain omega-3 fatty acids and fish were inversely associated with ARMD. Cho et al. suspected that high intakes of omega-3 fatty acids may have a special role in the retina by repleating omega-3 fatty acid supply in the photoreceptor outer segment, which constantly undergo renewing. And by supplying omega-3 fatty acids, it prevents ARMD and other retinal degenerative disease from developing. The positive association noted between total fat and ARMD risk was a result of intakes of these individual fatty acids rather than total fat per se.
Cho E, Hung S, Willet W, et al. Prospective study of dietary fat and the risk of age-related macular degeneration. Am J Clin Nutr. 2001;73:209-218.
Fish and Omega-3 Fatty Acids Lower Total Stroke Risk in Women
Compared to other nationalities, Americans consume very little fish. This is unfortunate since a growing number of studies indicate that fish consumption is inversely related to CVD risk. Earlier studies suggest that by lowering blood viscosity, platelet aggregation, and leukotriene formation, fish intake lowers one’s risk; however, these same mechanisms have been shown to increase the incidence of hemorrhagic strokes. But the latest fish and omega-3 fatty acids study shows that both fish and omega-3 fatty acid intake protects against thrombic stroke without increasing hemorrhagic stroke.
In this prospective study with 79,839 women, 574 cases of strokes occurred during 14-year follow-up period. These strokes included 119 subarachnoid hemorrhages, 62 intraparenchymal hemorrhages, 303 ischemic strokes, and 90 strokes of undetermined types. The semiquantitative food frequency questionnaire’s results were used to determine categories of fish intake and quintiles of omega-3 fatty acid intakes. Women were divided into 5 groups of fish consumption; <1 per month, 1-3 per month, 1 per week, 2-4 per week, and ³5 per week. Compared to women who ate fish less than once per month, women who ate fish 2 or more times per week tended to eat more nutritiously, with higher fruit, vegetable, and egg intakes and lower saturated fat and trans-fat intakes. Also, fish eaters were more likely to regularly use multivitamins and aspirin supplements, and exercise, but they tended to be heavier and had higher blood pressure than women who seldom ate fish.
Based on the age and smoking adjusted analysis, high fish intake was significantly inversely associated with total stroke. For example, the RR values were 0.84 for fish consumption of 1 to 3 times per month, 0.66 for once per week, 0.60 for 2 to 4 times per week, and 0.42 for 5 or more times per week. Further adjustment for other CVD risk slightly weakens this relationship, however, similar inverse trends were observed. The multivariate analysis of stroke subtypes showed that only thrombotic and lacunar infarctions were significantly reduced with increased fish intakes. Also, even though this study showed no decrease in hemorrhagic stroke events, with increased fish intake, it did not increase the risk.
As with fish intake, high omega-3 fatty acid intake also reduced risks of total stroke and lacunar infarction. The multivariate RR was 0.72 and 0.37, respectively. The inverse relationships between omega-3 fatty acids and ischemic, thrombotic, and subarachnoid hemorrhagic strokes were not significant. Benefits of fish and omega-3 fatty acid intake in protecting against thrombotic stroke were stronger in non-aspirin users compared to women who regularly took aspirin. “Among women who did not use aspirin, the multivariate RRs of thrombotic infarction were 0.77 for the second category, 0.56 for the third category, and 0.34 for the fourth category with no cases in the highest category. The respective RRs among regular aspirin users were 0.98, 0.77, 0.96, and 0.75.” According to Iso et al., one reason for the suppressed benefits of fish and omega-3 fatty acid intake on reducing stroke incidence of regular aspirin users is that aspirin is more potent than these 2 dietary methods of reducing platelet aggregation.
Results from this large epidemiological study indicate that fish and omega-3 fatty acids may be beneficial for preventing thrombotic strokes without increasing hemorrhagic strokes among middle age women. Compared to women who ate less than 1 fish per month, women with higher fish and omega-3 fatty acid intakes reduced their total stroke risk by 52% ad 28%, respectively. This trend was especially strong among non-aspirin users.
Iso H, Rexrode KM, Stampfer MJ, et al. Intake of fish and omega-3 fatty acids and risk of stroke in women. JAMA. 2001;285:304-312.
High-Fat, Low-Carbohydrate Diet Improves Glucose Metabolism
Earlier studies suggest that high dietary fat intake might be associated with the pathogenesis of insulin resistance, however results from Bisschop et al. suggest that a high fat diet could benefit people with glucose metabolism problems. For example, compared to the low-fat, high-CHO diet (LFHC), which provided 0% calories from fat and 85% of calories from CHO, and the intermediate-fat, intermediate-CHO diet (IFIC) with 41% fat and 44% CHO, the high-fat, low-CHO diet (HFLC) with 83% fat and 2% CHO, resulted in lowered basal endogenous glucose production and improved insulin-stimulated non-oxidative glucose disposal. On the other hand, the oxidative glucose disposal rate was lowered following the HFLC diet. These mechanisms were thought to favor storage of glucose. This study was conducted with 6 healthy men following these eucaloric test diets for 11 days each.
Bisschop PH, Metz J, Ackermans MT, et al. Dietary fat content alters insulin-mediated glucose metabolism in healthy men. Am J Clin Nutr. 2001;73:554-559.
Genetic Regulation of Cholesterol Absorption
Dietary cholesterol absorption rates exhibit a wide inter-individual variability. In this study, Weinberg et al. examined the impact of genetic polymorphisms on cholesterol absorption in 52 healthy subjects. Due to logistical difficulties in identifying subjects with defined genotypes, apolipoprotein A-IV alleles (1/1) and (1/2), the study was performed in 3 stages and not all 52 subjects participated in every test diet phase. The fatty acid composition of 3 test diets varied as follows: HISAT (high saturated fat) diet was 33% of energy as fat, 18% SFA, 3% PUFA, 12% MUFA, 45% CHO, and 20% protein; HIPOLY (high PUFA) diet was 32% of energy as fat, 7% SFA, 13% PUFA, and 12% MUFA, 46% CHO, and 20% protein; LOFAT (low fat) diet was 22% energy from fat, 7% SFA, 7% PUFA, and 8% MUFA, 55% CHO, and 20% protein. All 3 diets contained 800 mg/day cholesterol and were fed for 3 weeks each. Baseline dietary habits and plasma lipids were similar between the apo A-IV 1/1 and 1/2 groups. But after the experimental diets, the factional cholesterol absorption rate differed between the 2 apo A-IV genotype groups. For example, the 1/1 group absorbed 56.7±1.9% of cholesterol and 1/2 group absorbed 47.5±2.1% during the HIPOLY diet. During HISAT and LOFAT diet, 1/1 group absorbed 52.3±1.6 and 48.9±2.7% while 1/2 group absorbed 50.6±2.1 and 46.9±2.0% of cholesterol, respectively. The analysis of variance (ANOVA) showed that apo A-IV genotype had an independent effect on cholesterol absorption following the HIPOLY diet. For example, this dietary modification resulted in decreased levels of plasma total cholesterol, LDL and HDL cholesterol. The TAG levels increased with the HIPOLY diet while plasma lipids were unchanged in LOFAT diets, regardless of genotype. The results from this study show that genetic variances interact with dietary fatty acids to determine cholesterol fractional absorption rates.
Weinberg RB, Geissinger BW, Kasala K. et al. Effect of apolioprotein A-IV genotype and dietary fat on cholesterol absorption in humans. J. Lipid Res. 2000.41:2035-2041.
Familial Traits Play an Important Role in Individual Variance to Low-Fat Diets
Earlier studies have shown that there is a high degree of individual variance in response to dietary modifications. Currently, it is thought that between 15 to 20% of population do not respond to cholesterol lowering diets. Unfortunately, there is no simple way to identify these individuals. However, Denke et al. hypothesized that familial differences may explain some individual differences in response to cholesterol lowering diets. Using 46 intact families with 2 biological parents and at least 2 children aged 5 years or older, the researchers evaluated this relationship.
During this two 5 week, out-patient, crossover trial, families followed isocaloric diets that were supplemented with either margarine or butter-based test products. Test products consisted of specifically formulated baked products (cookies, brownies, breads) and spreadable fats made with butter or margarine. Intake of the two test diets was separated by at least a month of ad libitum diet. Compliance to the test diets was above 80%.
Compared to the margarine-based diet, dietary cholesterol and saturated fat intake were higher during intake of the butter-based diet. Plasma lipid and lipoprotein levels following each test diet showed that the butter-based diet caused a more atherogenic plasma lipid profile than the margarine-based diet. For example, total cholesterol (+17.6 mg/dl), LDL cholesterol (+15.7 mg/dl) and TAG (+10.8 mg/dl) levels were significantly higher following the butter-based diet in adults. Plasma HDL (46 mg/dl) cholesterol was the same during both diets. In children, only plasma total cholesterol and LDL cholesterol were higher with the butter-based diet. Test results were confirmed when 2 families repeated the study.
These data showed that 40% and 19% of the variability in percent change in LDL-cholesterol levels in children and both children and adults, respectively, were explained by family membership. Also, of the 2 genes Denke et al. measured, only apo E genotype had an effect on dietary response in adults, while 7alpha-hydroxylase genotype had no effect. BMI, ad libitum LDL-cholesterol, and cholesterol ester 18:2/18:1 ratio were associated with dietary responsiveness. Similar to earlier findings, Denke and colleagues showed that cholesterol-lowering diets were less effective in heavy individuals than their leaner counter parts.
In conclusion, results from this study suggest that either through shared genetic make-up or environment, part of individual responsiveness to diet can be explained by familial traits. Also, Denke et al.’s findings clearly show that intake of a low-trans margarine results in a less atherogenic plasma lipoprotein profile than with intake of butter.
Denke MA, Adams-Huet B, Nguyen AT. Individual cholesterol variation in response to a margarine- or butter-based diet. A study in families. JAMA. 2000;284:2740-2747.
CVD Risk and Dietary Changes in a Spanish Population
Like the US, CVD is a leading cause of death in Spain. And as a result, in the Diet and Cardiovascular Events Risk in Spain (DRECE) Study, the Spanish researchers investigated the role of diet on CVD risk in the Spanish population. This cross-sectional study was performed in 1991 (DRECE I) and again in 1996 (DRECE II). The original cohort size was 1200 participants with CVD and 600 non-CVD patients. The second half of the study included 848 of the original subjects. Beyond informing patients of their CVD status, there was no other intervention component to this study. Ballesteros-Pomar et al. gathered and analyzed food frequency questionnaires from DRECE I and DRECE II. Results from this study showed that subjects with CVD risk modified their diets by cutting down on legumes, eggs, meat, and meat products, and increased fruits, vegetables, and fish intake in 1996. Fatty fish intake increased from 19.4 to 23.2 gm/day. On the other hand, the control group did not change their dietary habits in a “more healthy” way. Their egg intake remained unchanged from 31.0 to 29.2 gm/day, while dairy products increased from 431.8 to 462.7 gm/day. Fruit intake was slightly higher (269.7 to 291.7 gm/day) while vegetable intake was significantly higher (300.6 to 374.8 gm/day) in 1996 than 1991. As a result of these changes in dietary habits, the percent of macronutrient intake also changed. For example, % of energy from protein increased from 15.3% to 16.5% in the risk group and 15.7% to 16.5% in the control group. Carbohydrate increased by 0.7% and 1.1% in the risk group and the control group, respectively. Percent of calories from fat remained at 42.9% in both groups. Compared to the first food frequency questionnaires, the second questionnaires of the risk group showed a greater decrease in SFA and an increase in PUFA compared to the control. As a result, the P/S ratio increased from 0.60 in 1991 to 0.72 in 1996. In the control group it increased by 0.07 from 0.60. Omega-3 to omega-6 ratio for both group was 0.14. Even though the risk group had much higher omega-3 fatty acid intake, since they also had higher linoleic intakes, the omega-3 to omega-6 ratio was same as the control group. Dietary cholesterol intake increased from 474 mg to 504 mg in the control group while it decreased by only 4 mg (473 to 469 mg/day) in the risk group. In light of dietary compositions, it is easy to see why CVD is a leading cause of mortality among the Spanish population. The diets reportedly consumed by the cohorts in the DRECE I and DRECE II were far from the cardio-protective Mediterranean diet recommended by health groups. For example, the energy from fat and saturated fats were well above the recommended 30-35% and 7-10%, respectively, and low in carbohydrate. Two interesting outcomes from this study are that the knowledge of ones CVD risk prompted the members of the risk group to make healthier dietary changes without further intervention by the researchers. Secondly, as with earlier studies, this study indicates that there is no association between dietary cholesterol or egg intake and CVD risk. For example, even with higher dietary cholesterol and egg intake, the control group did not develop CVD.
Ballesteros-Pomar MD, Rubio-Herrera MA, Gutierrez-Fuentes JA, et al. Dietary habits and cardiovascular risk in the Spanish population: The DRECE Study (I). Ann Nutr Metab. 2000;44:108-114.
Designer Eggs Improves Plasma Vitamin E, Lutein, and Omega-3 Fatty Acid Levels
Micronutrient composition of eggs can easily be manipulated by altering the feed of laying hens. Using this method, commercial egg producers are increasing vitamin E, omega-3 fatty acids, or carotenoid levels in some eggs. These designer eggs currently make up only 3% of the total commercial shell egg production in the US, but demand for these enriched eggs has dramatically increased as more consumers become aware of health benefits associated with these nutrients. The designer eggs are a simple alternative method of increasing these nutrients for people who prefer dietary sources over supplement capsules. Results from a designer egg feeding study conducted in the United Kingdom show that these enriched eggs do indeed increase plasma levels of these nutrients.
The enriched eggs consumed by 40 subjects during this 8 week study were enriched with vitamin E, lutein, selenium, and docosahexaenoic acid (DHA). Compared to regular eggs, the enriched eggs were 7.7 (50% RDA), 26.8 (130% RDA), 15.9, and 6.4 (100% RDA) fold higher in selenium, vitamin E, lutein, and DHA, respectively. There is no RDA for lutein. Following the enriched egg feeding phase, plasma vitamin E, lutein, and DHA were higher than baseline. For example, the mean plasma vitamin E concentration increased from 25.6±0.9 to 30.5±1.1 mmol/l and plasma lutein increased from 0.24±0.94 to 0.45±0.03 mmol/l after designer egg intake. The plasma levels of vitamin E and lutein did not change with the regular egg diet. The DHA compositions of plasma phospholipids, TAG, cholesteryl esters, and total fatty acid were significantly higher with the designer eggs, but not with regular eggs. The plasma selenium concentration was unchanged with either treatment group. Also, as with other study findings, this study showed that eating one egg per day did not negatively affect the plasma lipid and lipoprotein profile. In contrast, including 1 designer egg per day resulted in improved systolic blood pressure and plasma HDL levels.
In light of these findings, Surai and colleagues concluded that including designer eggs in the diet is an easy and effective way to raise dietary and plasma vitamin E, lutein, and DHA levels. And by combining 2 antioxidants, vitamin E and lutein, with DHA, the designer eggs increased lipid stability against peroxidation. These enriched eggs can be used to increase plasma levels of these important nutrients without adversely affecting plasma lipid and lipoprotein concentrations.
Surai PF, MacPherson A, Speaks BK, et al. Designer egg evaluation in a controlled trial. Eur J Clin Nutr. 2000;54: 298-305.
Editorial: Science and “the truth is no there” Spin-Masters
When does a risk factor become a disease? And when does an intervention become the end-point? When the spin-masters say so,reading the comments of the “dietary fat true-believers” about theand when the media buys it, that’s when. It would seem from reading the comments of the “dietary fat true-believers” about the recently reported results from DISC that complying with the intervention is the end-point, whether it actually has benefit or not.
The Dietary Intervention Study in Children (DISC) was designed to test the efficacy and safety of a Step 2, low-fat, low-cholesterol diet in young hypercholesterolemic children. The intervention group received intensive counseling on how to adhere to a diet low in fat, saturated fat, and cholesterol. After three years the intervention group had a “significantly lower plasma cholesterol level” compared to the usual care group; however, the significant difference was 3.3 mg/dl which, all things considered, is probably of little biological significance. After 5 years there were no differences between the intervention group and the usual care group and this finding led the investigators, and those funding the study (NIH/NHLBI), to claim success in showing that a low-fat, low-saturated fat, low-cholesterol diet was safe for children with elevated plasma cholesterol levels.
Safe maybe, but what value is safety without efficacy? And this is where the spin-masters who know deep down that the low-fat diet is the true answer, begin to weave their tales of excuses, explanations and fact burying. My favorite was the suggestion that even though the intervention kids, and their parents, attended a minimum of 33 group and individual sessions with “nutritionists and behaviorists” as well as monthly phone calls, the changing dietary pattern in society was so effective that the usual care group made the correct dietary changes on their own. [A Step 2 diet? Without 33 training sessions for kids and parents? One wonders if these are the same children the experts talk about when referring to poor nutrition, too much fat, excess body weight, etc.] This suggestion no doubt came as a great surprise to all the nutrition educators out there who are frustrated trying to decipher the behavioral aspects of dietary changes and the fact that most people are simply non-compliant. But then maybe our national push has been more effective then we think and in fact the public is falling in line with the low-fat diet craze and actually doing what they are told to do. [If you buy that I have a bridge you might be interested in.]
Is a low-fat diet the end-point or is lowering plasma cholesterol levels the end-point or, just maybe, should it be that lowering heart disease risk is the end-point. And if we go so far as to assume this attitude, then the results of DISC are indeed very disappointing. Just consider the relative changes in plasma LDL cholesterol and HDL cholesterol concentrations with the low-fat, low-cholesterol dietary intervention. Plasma LDL cholesterol levels decreased 16 mg/dl (12%); however, plasma HDL cholesterol levels decreased 7 mg/dl. According to recent estimates, a 1% fall in LDL cholesterol lowers CHD risk by 1.5% which means the risk in the DISC children was lowered 18%. However, a 1 mg/dl change in HDL cholesterol is estimated to change risk by 2-3% which means the 7 mg/dl change in HDL levels in DISC increased risk 14-21%. All in all it would appear that the intervention was a wash in terms of changing the relative CHD risk.
We have seen this game played before and always fail to recognize that it is very much in the favor of the true believers. A little study called DELTA (Dietary Effects on Lipids and Thrombotic Activity) found exactly the same thing: a low-fat diet lowers plasma total, LDL, and HDL cholesterol levels with little effect on the LDL:HDL ratio. And how was DELTA interpreted (only for a short time though since it very quickly disappeared from the nutrition radar screens)? Lots of talk about lower LDL cholesterol levels and almost nothing about the decrease in HDL or the increase in Lp(a) levels.
So where are we? Well, the low-fat diet appears safe for children and may in fact have many nutritional benefits (as long as the substitutions are whole grains, fruits and vegetables and not fat-free, sugar-rich replacements). But do we really want parents putting their children on the Step 2 diet because we mislead them stating that the diet is effective in lowering heart disease risk based on the unproven hypothesis that it really does lower plasma cholesterol levels (even if we cannot document it)? What a lie to mislead the public into making changes we cannot show are effective! Lies, damn lies and statistics followed closely by those who care less about facts and more about never, ever admitting that just maybe they do not have all the answers. Such hubris will be the ruin of our professional credibility with the public. Indeed, as we watch the very, very, very-low fat diet aspirant battle the very, very-low carbohydrate want-to-be, it is clear that a rationale message is lost in the hype and that without some semblance of honesty we are in fact no better than the purveyor of the hottest diet book of the day. Nutrition is a science dependent upon the scientific method, not an agenda based on who gets the best media attention by being the best spinner.
My chagrin at the DISC spin is based in large part on the media quotes (and least we forget, the public reads the media quotes, not the research article). The National Heart, Lung and Blood Institute (who funded the study) commented that the study “confirms that dietary changes in children with high levels of LDL cholesterol may thwart the development of atherosclerosis without adverse effects.” How does one ‘confirm’ that an intervention ‘may’ do something? A representative from the American Heart Association noted that the fact that the benefits found in the intervention group weren’t significantly greater than the control group by the study’s end “should not take away from the primary finding, which was that there were no adverse effects.” I’ll agree with the safety comments, but I question the value of safety without efficacy unless, of course, the goal is the treatment irrespective of whether it does any good or not.
Donald J. McNamara, Ph.D.
Executive Editor, Nutrition Close-Up
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.
