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Original Research |
Department of Exercise and Nutrition Sciences (K.M., M.M., P.J.H., A.B.A.), School of Public Health and Health Professions and School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, New York
Department of Physiology and Biophysics (D.R.P.), School of Public Health and Health Professions and School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, New York
Department of Orthopedics (J.J.L.), School of Public Health and Health Professions and School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, New York
Address reprint requests to: David R. Pendergast, EdD, Department of Physiology and Biophysics, 124 Sherman Hall, State University of New York at Buffalo, 3435 Main Street, Buffalo, NY 14214. E-mail: dpenderg{at}buffalo.edu
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIAL AND METHODSRESULTSACKNOWLEDGMENTSREFERENCES |
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Methods: Eleven healthy subjects (5 men and 6 women) were randomized to consume diets with 19% and 50% calories from fat. Each diet lasted 3 weeks, with a one-week washout. The habitual and washout diets were determined to be 30% fat. At the beginning and the end of each diet, fasting blood was collected to determine plasma lipoproteins, and physiological factors were measured.
Results: Total caloric expenditure was similarly balanced to intake on the 30% and 50% fat diets, but intake was significantly lower on the 19% fat diet and led to a loss of 0.6 kg body weight. Consumptions of essential fatty acids, vitamin E and zinc were improved with increased fat intake, but folate intake was compromised on the 30% and 50% fat diets. Compared with the 50% fat diet, subjects consuming the 19% fat diet had significantly lower HDL cholesterol (HDL-C) (54 ± 3 vs. 63 ± 3 mg · dL-1, p < 0.05) and apolipoprotein A1 (ApoA1) (118 ± 4 vs. 127 ± 3 mg/dL, p < 0.05). Changing the levels of fat intake did not affect % body fat, heart rate, blood pressure, blood triglycerides, total cholesterol (TC), LDL cholesterol, apolipoprotein B (ApoB), TC/HDL-C and ApoA1/ApoB ratios.
Conclusion: A low fat diet (19%) may not provide sufficient calories, essential fatty acids, and some micronutrients (especially vitamin E and zinc) for healthy untrained individuals, and it also lowered ApoA1 and HDL-C. Increasing fat intake to 50% of calories improved nutritional status, and did not negatively affect certain cardiovascular risk factors.
Key words: dietary fat, nutrient intake, cardiovascular risk, lipoproteins
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIAL AND METHODSRESULTSACKNOWLEDGMENTSREFERENCES |
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A well-balanced diet that has sufficient total calories to balance energy expenditure will most likely prevent the development of nutrient deficiency. Fat is an energy dense nutrient and a good source of essential fatty acids and fat-soluble vitamins. Therefore, a very low fat diet may not provide adequate amounts of these nutrients. It is known that exercise is a stress to metabolic pathways, which require micronutrients such as vitamin B and zinc as cofactors. Individuals who are physically active may have an increased requirement for these nutrients. Adequate nutrient intake may not be met on low fat diets as they usually exclude meat products, which are high in trace elements such as iron and zinc, and are good sources of vitamin B12. In athletes zinc and calcium intakes have been found to be less than the Recommended Dietary Allowances (RDA) on low fat diets, and increasing fat intake increased intake of these micronutrients [6]. However, there is some concern that a high fat diet, low in fruits, vegetables and whole grains, could lead to a lower intake of Vitamin C, thiamin, riboflavin, niacin and folate. The US dietary Guidelines have been recently changed from "choose a diet low in fat" to "choose a diet moderate in total fat" [7].
Blood lipids and lipoproteins are affected by dietary fat intake. Several studies have indicated that low-fat, high-carbohydrate diets reduce both low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) [8–10]. However, the ratio of total or LDL cholesterol to HDL-C may not be improved by low-fat, high-carbohydrate diets [11–13]. Such diets may also raise triglycerides [9,13], which has been identified as an independent risk factor of the development of CHD [14].
The effect of dietary fat and carbohydrate on blood lipids is confounded by weight change [8,15]. When the balance between the caloric intake and expenditure is maintained, higher fat intake does not negatively affect blood lipoproteins [16,17]. In a previous study we showed that endurance runners on isocaloric diets could increase fat intake to 42% of total calories without adverse effects on their lipids, while a very low fat intake (16–17%) lowered HDL-C and ApoA1 and negatively affected lipoprotein rations [18] and immune status [19]. Endurance runners have significantly higher fitness and greater energy expenditures than sedentary individuals, so there may be different effects of low fat diets in sedentary subjects.
The optimal range of fat intake that provides the greatest benefit to untrained healthy individuals has not yet been established, and little is known about the role of total caloric balance. The present study was designed to examine the effects of decreasing fat intake to 19% and increasing it to 50% of daily calories, compared with 30% fat intake, on the nutritional status and selected CHD risk factors in healthy individuals.
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MATERIAL AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIAL AND METHODSRESULTSACKNOWLEDGMENTSREFERENCES |
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Experimental Diets
Two experimental diets were prescribed based on an initial consultation, 7-day food intake, activity records, and a list of food preferences. The diets were generated using the NutritionistPro Software (First Databank, San Bruno, CA) to be calorically balanced (intake = expenditure): a low fat diet consisting of 19% total calories from dietary fat, and a high fat diet containing 50% fat calories. Subjects were individually counseled on how to use the American Dietetic Association exchange list diet and standard serving sizes [20]. The diets were designed to provide the subjects with a number of servings from the food groups. The low fat diet included many carbohydrate-rich foods, low fat dairy products and lean and very lean meats. The high fat diet focused on high fat dairy products, added fat and high fat meats. Both diets had the same intended proportions of saturated, monounsaturated, and polyunsaturated fatty acids. The level of protein intake was set at 20% of total calories for all diets.
Experimental Procedure
The diets were randomly assigned to the subjects and blinded to the data collection and analysis teams. The subjects were given sample menus, but they selected their own food. Subjects ate their normal diets prior to the experiment (baseline 1), and each experimental diet was continued for 3 weeks with a 1-week washout period (baseline 2). The subjects recorded their food intake after each meal and turned in their diaries weekly for review. Daily activities were also recorded and turned in weekly with the diet records. The diets were analyzed with the NutritionistPro Software 1.3 (San Bruno, CA) for macronutrients, micronutrients, and fatty acids composition. Energy Expenditure was estimated from activity records according to Astrand and Rodahl [21]. At the beginning and the end of each diet, the subjects reported to the laboratory after overnight fast to complete body composition measurements and have blood drawn to determine their lipid profiles. On the following day, they performed an exercise test after breakfast, 1–3 hours, with the diets they were prescribed.
Physiological Measurement
Body weight was measured by an electronic scale (Model 8142, Toledo, Worthington, Ohio) and body fat was determined by underwater densitometry (dynamometer model TDC 4A, Schaevitz Engineering, Pennsauken, NJ). Resting heart rate (Q 750 Quinton) and blood pressure (D4000 Infasonde) were taken. Before and after each diet, subjects underwent a modified treadmill test to exhaustion to determine their peak oxygen consumption (VO2peak). Subjects walked on a treadmill at 0% grade at 2 mph and then 3 mph for 3 min each. The grade on the treadmill was then increased by 2% increments every 2 min until voluntary exhaustion. Gas exchange was measured by standard open circuit techniques in the last minute (American Standard dry-gas meter and Perkin-Elmer-1200 Multiple Gas Analyzer, Pomona, CA) of each successive work rate and VO2 was calculated. Heart rate and blood pressure were taken at the end of each stage.
Blood Lipid Analysis
Fasting blood was aseptically drawn from antecubital vein into heparinized vacutainer, and centrifuged at 2,000 rpm, 4°C for 30 mins. Plasma was collected, aliquoted, and stored at -70°C. The levels of glucose, non-esterified fatty acids (NEFA), total cholesterol, triglyceride, high-density lipoprotein cholesterol (HDL-C), apolipoprotein A1 (ApoA1) and apolipoprotein B (ApoB) were analyzed according to kit applications from Wako Diagnostics (Richmond, VA) by COBAS FARA and COBAS MIRA autoanalyzer (Roche, USA). The level of low-density lipoprotein cholesterol (LDL-C) was estimated from the standard equation according to Friedewald [22]: LDL-C = Cholesterol - HDL-C - (TG/5). The TC/HDL-C, HDL-C/LDL-C, and ApoA1/ApoB ratios were calculated.
Statistical Analysis
The descriptive values are presented as mean ± SEM. Statistical analyses of the data were carried out using SigmaStat Statistical Software (SPSS Inc). There were no gender differences and repeated measures statistics were used so the data from both genders were combined for analysis. Paired t tests were used to compare the two baseline data points and the difference between energy intake and expenditure in each diet. Individual parameters were compared by an analysis of variance for repeated measures. When there were significant differences between experimental groups, Student-Newman-Keuls Test was performed to test the significance between the groups. For data that were not normally distributed, nonparametric procedures were used. The 
< 0.05 was used for all statistical comparisons.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIAL AND METHODSRESULTSACKNOWLEDGMENTSREFERENCES |
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The composition of the diets consumed is shown in Table 2. For both genders, the mean caloric intake on the 30% fat diet was not significantly different from the 50% fat diet. However, the caloric intake was significantly lower when subjects consumed the 19% fat diet compared with the 30% and the 50% fat diets. The subjects maintained their daily activity at the same level throughout the experimental period, as estimated energy expenditure (EEE) did not change over diet. The subjects maintained energy balance (total caloric intake = EEE) when consuming the 30% and the 50% fat diets but not the 19% fat diet. The negative caloric balance (total caloric intake < EEE) on the 19% fat diet was due to reduced caloric intake.
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Micronutrients
Micronutrient intake is expressed as % Dietary Reference Intakes (DRI) of subjects on the 19%, 30%, and 50% fat diets to correct for age and gender (Table 3). With a few exceptions the subjects met or exceeded most of the daily micronutrient requirements. Vitamin A intake (%DRI) was the highest on the 19% fat diet. Vitamin E consumption was lower than recommended on the 19% and 30% fat diets, and it was significantly increased on the 50% fat diet, up to the DRI. The intakes of vitamin C, folate, and iron were greater on the 19% fat diet compared with the 50% fat diet. Zinc intakes were below the DRI for all diets; however, the level was significantly increased on the 50% fat diet compared to the lower fat diets.
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DISCUSSION |
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For decades low-fat diets have been advocated for weight reduction and to lower the risk of CHD [23]. Randomized controlled trials; however, have not confirmed that low-fat diets have accomplished this [24] or are sustainable for the long term [15,25–26]. Most of the justification for the benefit of low-fat diets comes from cross-sectional population studies [27–29], which are confounded by differences in lifestyle as these populations are also active and lean. In fact, total fat intake shows little correlation with CHD rates [30]. The amount and type of fatty acids used to substitute for carbohydrates also confound this issue [11]. This may be because the detrimental effects of some, but not all, saturated fatty acids and all trans-isomer fatty acids on serum lipoproteins [31,32] are offset by the beneficial effects of unsaturated and cis-isomer fatty acids [33,34]. Some saturated fatty acids can increase the level of HDL-C [11]. The lower prevalence of CHD in rural populations may therefore be due to their high levels of caloric expenditure and resultant low body fat [35]. Thus, the key to helping prevent some of the chronic diseases of affluent societies may be whether energy intake does not exceed energy expenditure rather than the macronutrient composition of the diets.
Macronutrient Intake
Although the benefits of low fat, high carbohydrate diets have been suggested by some studies in athletes [36,37], hyperlipidemic individuals [2,3], and obese subjects [4,5], restriction of fat intake may lead to detrimental effects on nutritional status and blood lipids. In the present study, the subjects’ total caloric intake was significantly lower on the 19% fat diets leading to a negative energy balance. This is similar to the data reported in other studies on low fat diets [38,39]. Since fat is an energy-dense macronutrient, substitution of calories from fat with carbohydrate will require higher quantity of foods to maintain the caloric intake. Protein intake was highest on the 50% fat diet, and protein intakes of the subjects for all diets were adequate based on the 2001 DRI [40]. A slight reduction in calories from protein may contribute to the reduction in total caloric intake on the 19% fat diet.
The present study showed that the 50% fat diet increased the amount of cholesterol, saturated, monounsaturated and polyunsaturated intakes. Sufficient amounts of certain fatty acids are required to promote health. Monounsaturated fat such as oleic acid (18:1) has been linked to lower risk for CHD [41,42]. Linoleic acid (18:2 n-6), and -linolenic acid (18:3 n-3) are essential fatty acids, which cannot be produced in the body, so they must be obtained from the diets. Continuing consumption of a low fat diet for 4 weeks could reduce the content of linoleic acid in serum and platelets [43]. Our results showed that intakes of oleic acid (18:1), linolenic (18:2) and linoleic acids (18:3) were significantly higher on the 50% fat diet compared with the lower fat diets.
As expected, the proportion of calories from carbohydrates decreased as the fat calories increased in the present study. High carbohydrate diets may promote high fiber intake. Soluble fiber may lower plasma total and LDL cholesterol concentration without affecting HDL-C [44]. However, the fiber intake in this study was similar in all diets, so the effect of fiber intake on blood lipid profiles was equivalent on all diets.
Micronutrient Intake
Our subjects met most dietary reference levels (DRI) for micronutrient intakes when they were on the 50% fat diet [40]. Vitamin E, an antioxidant, protects cells from free radicals, so it may reduce oxidative stress. Evidence from animal and human studies indicates that Vitamin E supplementation reduces the progression of atherosclerosis [45,46]. Although the beneficial effects of vitamin E as an antioxidant are still controversial, optimal intake of vitamin E is essential and additional vitamin E intake may be required in athletes or active individuals, who may have high production of free radicals due to intensive exercise and training. Often studies have shown that vitamin E intake is inadequate on low fat diets [47,48]. Similar results were seen in this study: vitamin E intake was below the DRI for our subjects on the 19% and 30% fat diets. The subjects increased vitamin E intake, meeting the DRI, on the 50% fat diet. The intake of vitamin A in the subjects in this study was significantly higher when they were on the 19% fat diet, compare to higher fat diet. This was most likely due to the higher intake of carotene containing fruits and vegetables. The results obtained in the present study for vitamin E and A intake were similar to what we found previously in runners [6].
Although a low fat diet has potential to increase the risk of nutrient inadequacy, the nutrient adequacy of low fat diets may highly depend on food selection [49]. A low fat diet could provide good sources of vitamins, minerals, trace elements and fiber by carefully selecting carbohydrate from grains, cereals, legumes, vegetables, and fruits, and such diets may have beneficial effects on blood lipids and lipoproteins [38]. We found that intakes of vitamin C, folate and iron increased significantly on the 19% fat diet, exceeding DRI. This may be the result of an increased intake of fruits and vegetables and/or the recommendation of the dietitian to include vitamin enriched foods on the 19% fat diet.
Zinc is an essential trace element found mainly in animal protein. It is often found that zinc intake was decreased with low amount of fat consumption [47,50,51]. We found that zinc intake in our subjects was improved, although still below the recommended level, on the 50% fat diet when compared with the two lower %fat diets. This may be the result of the meats consumed were altered by fat content (i.e., very lean and lean for the low fat diet), not the type. This finding is also consistent with the results from a previous study in runners [6].
Cardiovascular Risks
We found no adverse effects on body weight, body fat, blood pressure, resting heart rate, plasma glucose, or plasma lipoproteins in young, apparently healthy normolipidemic subjects who increased daily fat calorie intake from 19% to 30% to 50% over 3 weeks each. HDL-C was improved on the 50% fat diet when compared with the two lower fat diets and Apo A1 was improved on the two higher fat diets when compared with the 19% fat diet. These results are consistent with other controlled trials that have shown that if energy balance is maintained (i.e., body weight and adiposity remain stable), increased dietary fat in-and-of itself does not adversely affect the serum lipoprotein profile either in sedentary persons [16,17] or in endurance athletes [18,52].
Our subjects lost a small amount of weight (0.6 kg) over the three weeks of the 19% fat diet, compared with the 30% and 50% fat diets, which were not different from each other. The 30% and 50% fat diets were isocaloric; however, on the 19% fat diet the total caloric intake was reduced by 13%. The reduction in total caloric intake accounted for the weight loss of our subjects (with no change in reported energy expenditure), assuming that 0.45 kg is lost for every 3500 kcal deficit. Our study agrees with the previous study employing meta-analysis of 37 studies where a low fat diet (10% to 30% fat calories and less than 10% from saturated fat) reduced the average total caloric intake by 13%, and resulted in a similar pattern of weight loss in those subjects [53]. However, it is important to note that the energy consumption in these subjects was derived from self-reported dietary records. Inaccuracy in dietary records may occur [54]. It is clear that the 13% reduction of caloric intake on the 19% fat diet compared to the higher fat diets would have produced a theoretical body weight reduction more than 0.6 kg. Therefore, the negative energy balance observed with the 19% fat diet may be, in part, due to the underreported dietary energy intake.
In the present study, HDL-C and ApoA1 levels improved on the higher fat diets when compared with 19% fat. Serum lipoproteins has been shown to improve with changes in the macronutrient composition of the diet both with [55] and without [56] weight loss, and HDL-cholesterol levels will increase and TG levels will decline in response to increased dietary fat with concomitant reduced carbohydrate intake [32]. Our data show a non-significant trend for lower plasma TG levels on the 50% fat diet. This may be because plasma TG levels were already quite low to begin with in the subjects in this study.
It must also be acknowledged that the quality of the carbohydrates consumed on higher fat diets (with regard to fiber content, the glycemic index, the inclusion of fruits and vegetables) can independently affect serum lipoproteins and cardiovascular risk [34]. The carbohydrate diet with low glycemic index (GI) produces less glycemic load, compared with high GI. Although no significant differences in glucose levels between these diets were observed, it is likely that the glycemic load was elevated in the 19% fat diet compared with the 50% fat diet. There was an increased TG levels on the 19% fat diet; however, this increase was not significant. An inadequate statistical power due to small sample size may explain a non-significant increase in TG levels in the present study. Postprandial lipemia has been shown to injure endothelium [57] and appears to be independently associated with CHD [58]. If weight and adiposity remain stable; however, replacement of saturated fats with unsaturated oils does not increase triglycerides in sedentary humans [16,17,32,59–61], consistent with the results of the present study.
The clinical significance of the favorable changes in the HDL-C-TG axis in the setting of a high fat intake is not clear [25]. One concern had been that increased dietary fat increases sympathetic nervous system tone [62]. We found no change, however, in resting pulse or blood pressure on the higher fat diets. Low fat hypocaloric diets have been shown to reduce serum LDL-C levels [63], a beneficial effect on the risk of CHD. These diets, however, may also lower HDL-C [32] and may affect the quality of the LDL particle. The majority of the U.S. population has large, low density LDL particles (called LDL pattern A) [64]. Isocaloric substitution of dietary carbohydrates for fats may result in a qualitative shift to smaller, more atherogenic LDL particles (LDL pattern B) [64]. LDL pattern B is associated with elevated triglycerides and depressed HDL-C [65].
What accounts for the improved HDL-C levels on the 50% fat diet in our subjects? Dietary fat stimulates muscle lipoprotein lipase activity [52] and increases the transport rate and reduces the catabolic rate of ApoA1, the major transport protein for HDL particles [66]. This appears to be particularly true with saturated fatty acids [32]. It has been suggested that a high intake of saturated fat may increase HDL-C [11]. Our subjects significantly increased their saturated fat intake (both in terms of absolute grams/day and as a percentage of daily fat calories) by shifting from 19% to 30% fat diets and further from 30% to 50% fat diets (grams/day) with no adverse effect on the LDL-C:HDL-C ratio. Concurrent with this, PUFA intake was increased on the 50% fat diet compared with the 30% fat diet. Carbohydrate intake was decreased as % fat intake increased. Increased unsaturated fat [32] and reduced carbohydrate intake [32] have both been associated with increased HDL-C levels and an improved LDL-C:HDL-C ratio. One or a combination of the above mechanisms may account for the elevated HDL-C in subjects consuming the 50% fat diet.
On the other hand, the reduction of HDL-C and ApoA1 concentration by a low-fat diet has been suggested to be due to a decrease in ApoA1 transport rates [67]. Weight reduction also plays a role on blood lipid profiles. A meta-analysis study by Dattilo and Kris-Etherton [63] indicated that weight reduction was associated with significant decreases in total cholesterol, LDL-C, VLDL-C, and TG. Although weight reduction resulted in increased HDL-C, the level of HDL-C was decreased during active weight loss. Thus, another possibility that contributes to lowered plasma HDL-C and ApoA1 on the 19% fat diet may be the apparent negative energy balance in this study.
Results similar to those reported in our healthy sedentary subjects in the present study have been also demonstrated in athletes. Endurance-trained humans in energy balance who consume high-fat diets, which are high in cholesterol and saturated fatty acids, maintain low triglycerides and favorable LDL-C:HDL-C ratios [18,53,68]. This is due to rapid postprandial triglyceride removal from the circulation as a result of increased muscle lipoprotein lipase activity in athletes [69,70] in combination with training-induced increases in muscle mitochondrial volume, intramuscular TG storage, and mitochondrial fat oxidation [71]. It must be acknowledged that the long term effects of a high fat diet in sedentary humans remain to be determined and may be different than that for active humans such as athletes, who may require high energy intake for their physical activity [72].
The strengths of the current study are its randomized crossover design and the subjects’ excellent compliance with the prescribed diets. Although the subjects were trained how to complete food records and their dietary food records were reviewed weekly by the dietitians to enhance compliance, it is still possible that their reported intakes had inaccuracies [54]. The 3 week diet period is short but sufficient time for the diets to have effected measurable changes in lipoprotein levels [73,74] and the other physiological variables [18] but is of course insufficient to evaluate the longer term effects of and adherence to the high fat diet in these subjects.
In summary, our data show that a self-selected low fat diet may not offer the greatest advantage in terms of nutrient requirements or plasma lipoproteins in healthy sedentary individuals when compared with moderate and higher levels of dietary fat intake, at least over the short term. Consuming up to 50% of daily calories as dietary fat for 3 weeks improved certain nutrient intakes, HDL-C and Apo-A1 levels and had no detrimental effects on other lipoproteins, resting heart rate or blood pressure when compared with a 19% fat diet. Independent of weight loss, very low fat and high carbohydrate diets will not improve serum lipoproteins and, since long term compliance with such diets is very poor [25,75], they do not result in sustained loss of weight or body fat. Such restrictive diets may therefore not reduce the risk of CHD, particularly if the carbohydrates consumed are refined sugars and are low in fiber [34]. The intense focus on restricting total fat intake is unlikely to be beneficial for the general population if caloric intake continues to regularly exceed caloric expenditure. Newer dietary recommendations should include the concepts of "good" (i.e., low glycemic index, high fiber) carbohydrates versus "bad" (high glycemic index, low fiber) carbohydrates and "good" (i.e., unsaturated, cis-isomer) fatty acids versus "bad" (some saturated and all trans-isomer) fatty acids [34]. People are more likely to maintain a healthy body weight if they are able to choose from a variety of heart-healthy fats and carbohydrates that provide an appropriate balance of energy intake versus expenditure [18,34]. Our data suggest that a diet that severely restricts dietary fat is not beneficial to the nutritional status and plasma lipoproteins of healthy sedentary persons. Conversely, a diet consisting of a mixture of saturated and unsaturated fatty acids at or moderately greater than the current recommended level is reasonable and safe, at least over the short term. The recommendations made to improve the health of sedentary Americans should emphasize consuming a palatable blend of healthy fats and carbohydrates while achieving "negative energy balance" by increasing caloric expenditure via greater regular physical activity and reduced sedentary behaviors [76]. Further studies are needed to determine if these same principles apply to overweight, hyperlipidemic or insulin resistant individuals.
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ACKNOWLEDGMENTS |
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TOPABSTRACTINTRODUCTIONMATERIAL AND METHODSRESULTSACKNOWLEDGMENTSREFERENCES |
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This study was funded in part by the Center for Research and Education in Special Environments (CRESE) at State University of New York at Buffalo.
Received July 8, 2003. Accepted September 23, 2003.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMATERIAL AND METHODSRESULTSACKNOWLEDGMENTSREFERENCES |
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