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Departments of Nutrition and * Exercise Wellness, Arizona State University, Mesa AZ 85212
3To whom correspondence should be addressed. E-mail: carol.johnston{at}asu.edu.
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ABSTRACT |
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 TOP ABSTRACT SUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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KEY WORDS: • high-protein diets • satiety • weight loss • cholesterol • insulin response • renal function
The scientific evidence that fueled the initial development of the nutritional health policy by the U.S. government 25 years ago [first presented in 1977 as the publication: Dietary Goals for the United States by the Senate Selection Committee on Nutrition and Human Needs (1)] was mainly the direct association between dietary fat (particularly saturated fat), sugar, and salt consumption and risk for heart disease, cancer, and stroke (2,3). Accordingly, 5 of the 6 original dietary goals recommended reductions in total fat consumption (from 
40% of energy intake to <30% of energy intake) and reductions in saturated fat, cholesterol, sugar, and salt consumption. The remaining dietary goal, to increase carbohydrate consumption to 55–60% of energy intake, was not specifically supported by scientific evidence. Yet to achieve the recommended reductions in fat and sugar, the recommendation to increase cereal grain, fruit, and vegetable consumption was considered appropriate. The promotion of high-protein foods, specifically meat products high in saturated fat and cholesterol, contradicted the basic premise of the new nutrition policy (4).
Today, diets rich in carbohydrates (grains, fruits, and vegetables) and moderate in low-fat dairy and meats continue to be promoted for health and weight management by the U.S. government and leading medical societies (5–7). However, the low-carbohydrate, high-protein, high-fat diet promoted by Atkins (8,9) is perhaps the most popular diet in America for weight loss. In a survey of >32,000 U.S. dieters, nearly 34% of respondents stated that the Atkins diet helped them to lose weight and keep it off (10). Moreover, in a recent government funded, randomized clinical trial, the Atkins diet produced a greater weight loss at 3 and 6 mo than did a low-fat, high-carbohydrate diet based on the U.S. dietary guidelines (11). However, because diet records were not kept by subjects, and because 40% of the subjects randomly assigned to the Atkins diet group did not test positive for urinary ketones at study wk 2, 4, or 6, documentation that these subjects actually adhered to the Atkins diet is lacking. The authors speculated that the difference in weight loss between groups was related to a greater energy deficit in the Atkins group, a consequence of alterations in factors affecting appetite and diet adherence (11).
Dietary protein is the macronutrient generally associated with increased satiety, and voluntary reductions in energy consumption have been noted in subjects consuming high-protein meals compared with high-carbohydrate meals ad libitum (12–14). Furthermore, in short-term trials, energy consumption at subsequent meals was significantly less in subjects consuming high-protein vs. high-carbohydrate preloads (14–16). Thus, the Atkins plan may be well tolerated by dieters because of the satiety value related to its high protein content (>30% energy). However, healthcare professionals do not recommend long-term adherence to an Atkins-like, high-protein diet because the fat content of the diet (60% energy), particularly the saturated fat (25% energy), is not healthful and would eventually lead to elevations in total and LDL cholesterol (17). In controlled trials, elevations in total and LDL cholesterol were noted in subjects adhering to the Atkins diet (18), whereas significant reductions in these indices were noted in individuals following the conventional low-fat, high-carbohydrate diet (11,19).
Although diet plans high in protein (30% energy) but low in fat (<30% energy) and moderate in carbohydrate (40% energy) are as effective at promoting weight loss as Atkins-type diets, and reduce total cholesterol and LDL cholesterol as well as triglycerides (19–21), these diets have not received the same attention as the Atkins diet. High-protein diets that are low in fat may represent an appealing diet plan for healthful weight loss and deserve further investigation. We conducted a randomized 6-wk feeding trial to evaluate the effect of a high-protein, low-fat diet vs. a high-carbohydrate, low-fat diet on weight loss and biomarkers for health and disease, including blood lipids, insulin sensitivity, creatinine clearance, calciuria, uricosuria, and nitrogen balance. The 24-h intakes were strictly controlled, and only common foods and food combinations were used; diet plans were designed to promote weight loss and provided 70–75% of the energy required for weight maintenance.
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SUBJECTS AND METHODS |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Experimental protocol. Subjects were stratified by age, gender, and BMI and randomly assigned to one of two experimental groups designated as high-protein, low-fat (HPLF)4 (4) or high-carbohydrate, low-fat (HCLF). Two weeks before the initiation of the 6-wk feeding trial, subjects consumed an energy-adequate, control diet based on the U.S. Dietary Guidelines (5) for 2 d. Meals were prepared in the Nutrition Department’s metabolic kitchen at Arizona State University East and distributed to subjects for consumption at home. On d 2, complete 24-h urine samples were collected, defined as all urine excreted after the first morning void through the initial next morning void. The following morning, subjects reported to the test site in a rested, fasted state (no light to heavy activity for 24 h and no food or beverage with the exception of water for 12 h), and resting energy expenditure (REE) was measured.
Metabolic measurements were recorded using a respiratory mask and 2-way, nonrebreathing valve (Hans-Rudolph) interfaced with a MAX-1 metabolic cart (Physiodyne Instrument). Upon arrival at the laboratory, subjects were positioned in a reclining chair and habituated to the open circuit spirometry metabolic analysis apparatus for 30 min in a temperature controlled (25–27°C), darkened, quiet room. The respiratory mask was placed over the subject’s face and carefully checked and sealed to prevent air leakage. Subjects were instructed to remain awake and not to move, fidget, or talk once the mask was in place. Following the 30-min habituation period, REE was estimated from a mean of 20 min of continuous gas sampling via indirect calorimetry using the Weir formula (23). The CV for this procedure was 3.08%, and the between- and within-day correlations were 0.70 and 0.90, respectively. Gas analyzers were calibrated before and after each test by nitrogen and two primary standard gases accurate to 0.01%. The pneumotachometer was calibrated using a 3-L syringe to deliver fixed volumes at variable flow rates. Immediately after REE testing, a baseline blood sample was collected.
Two weeks after the initial metabolic testing, subjects began the 6-wk feeding trial. Both experimental diets were low-fat (<30% total energy), low in refined sugar (<10% total energy), and high-fiber (>20 g/d); the HCLF diet plan, based on the U.S. Dietary Guidelines (5), was high-carbohydrate (66% total energy) and moderate protein (15% total energy), and the HPLF diet plan was high-protein (32% total energy) and moderate carbohydrate (41% total energy) (Table 1). Diets were devised using the Food Processor for Windows Nutrition Analysis Software (Version 7.71, Esha Research), and only common foods and food combinations were used (see sample menu, Table 2). Because animal protein sources (low-fat dairy and meats) were utilized in the HPLF diets, total fat was 33% higher for this diet plan compared with the HCLF diet plan (28 and 21% total energy, respectively), as was the saturated fat content of the diets (8 and 6% total energy, respectively). A 14-d rotating menu was devised for each diet plan. Test meals and the experimental diets were prepared using scales and liquid measures in the metabolic kitchen. Lunches were prepared hot and served to the subjects Monday through Friday in an eating area adjacent to the metabolic kitchen. Breakfast and dinner meals, and weekend meals, were prepared and packaged for subjects to take home. The energy content of the diets was determined for individual subjects using the Harris-Benedict equation to estimate basal metabolic rate (BMR); hence, daily energy consumption during the 6-wk trial was 70–75% of that needed for weight maintenance. BMR was closely related to REE for most subjects. Within diet groups, subjects consumed similar meal plans, and energy was adjusted using unit foods (such as graham crackers and soy nuts).
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Analytical measurements. Blood was collected in EDTA-treated vacutainer tubes, and plasma was processed immediately and frozen (-45°C) until analysis. A separate sample of blood was clotted and serum analyzed for total cholesterol, LDL cholesterol, and triacylglycerols by photometric assays (Sonora Quest Laboratories). HDL cholesterol was determined using a homogenous enzyme immunoassay (Sonora Quest Laboratories). Plasma glucose was determined colorimetrically using glucose oxidase methodology (Sigma Aldrich; kit #510), and plasma insulin was determined by competitive RIA utilizing anti-insulin antibodies (ICN Diagnostics). Insulin sensitivity was assessed using the quantitative insulin-sensitivity check index: 1/[(log fasting plasma insulin, mIU/L) + (log fasting plasma glucose, mg/dL)] (24). Total 24-h urine volumes were recorded, and an aliquot frozen (-45°C) until analysis. Plasma and urine urea nitrogen were measured using an enzymatic (urease), colorimetric (phenol nitroprusside reagent) method (Sigma Aldrich; kit #640). Creatinine was measured colorimetrically using the picric acid reagent, and uric acid was determined using a modified Trinder peroxide assay with the 2,4,6-tribromo-3-hydroxy benzoic acid reagent (Sigma Aldrich; kits #555, and 683–20). For nitrogen balance calculations, urine urea nitrogen was extrapolated to total urine nitrogen (x1.25), and a correction of 1.8 g N/d was made for obligatory and fecal losses. Urinary pH was determined using a pH meter (Corning), and urinary calcium was measured photometrically (Sonora Quest Laboratories).
Statistical analysis. Data are reported for those subjects completing the feeding trial in its entirety (n = 9 and n = 7 for the HPLF and HCLF diets, respectively). All 9 HPLF subjects and 5 of 7 HCLF subjects returned for follow-up measurements 4 wk after the feeding trial was completed, and the follow-up data comparisons are reported for these subjects only. Data are reported as means ± SEM, and statistical analysis was performed using SPSS for WINDOWS (version 11.5; SPSS). A multivariate general linear model for repeated measures was used to determine significant time and time x diet interactions. Paired t tests with Bonferroni correction were used to make post-hoc comparisons within groups if a time effect was demonstrated by the multivariate test. Differences were considered significant at P < 0.05.
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RESULTS |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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6 and 10%, respectively, in both diet groups, and the pattern of weight loss over time did not differ between the groups (Fig. 2). BMI fell significantly in both groups (-5 to -6%), but fat-free mass also fell in both groups of subjects, accounting for 35% of total weight loss. Total cholesterol fell significantly in both groups, but LDL cholesterol and the total cholesterol:HDL ratios were not significantly affected by either diet treatment. The fluctuations in serum triacylglycerols did not differ between the treatment groups (-19% in HPLF subjects vs. +12% in HCLF subjects).
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24% in both experimental groups after the diet interventions, but fasting plasma glucose concentrations were unaffected by dietary treatments. Accordingly, insulin sensitivity improved 5% with both diet plans (P = 0.083 and P = 0.052 for the HPLF and HCLF groups, respectively) (Table 3). REE (kJ/kg) was not affected by either diet intervention (Table 3).
HCLF subjects were in nitrogen balance after the 6-wk diet intervention (0.7 ± 1.7 g N/d), whereas HPLF subjects displayed a marked positive nitrogen balance at the end of the 6-wk diet intervention (3.9 ± 1.4 g N/d) (P < 0.05). Plasma urea nitrogen differed significantly between diet treatments with the high-protein diet raising and the high-carbohydrate diet reducing this marker (Table 3). Glomerular filtration rates (as indicated by creatinine clearance) were not altered by diet treatments. Both diets significantly reduced plasma uric acid from baseline values, but urine uric acid was reduced from baseline values only in the high-carbohydrate diet group. Urinary pH was unaffected by diet treatments, whereas 24-h urine calcium concentrations did vary significantly by diet treatment, rising 42% in subjects consuming the HPLF diet and falling 23% with the HCLF diet, which is equivalent to 170 and 92 mg total calcium excreted daily for the HPLF and HCLF diets, respectively (Table 3).
At 4 wk after the end of the feeding trial (wk 10), both HPLF and HCLF subjects had maintained their mean weight loss (Fig. 3). Total serum cholesterol concentrations at follow-up were similar to preintervention concentrations in both HPLF (5.11 ± 0.53 and 5.30 ± 0.40 mmol/L, respectively) and HCLF subjects (4.75 ± 0.26 and 5.07 ± 0.25 mmol/L, respectively) (Fig. 3).
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DISCUSSION |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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6% (4.7–5.1 kg) after the 6-wk diet intervention; furthermore, the pattern of body weight loss during the 6-wk trial did not differ for the two experimental diets. Other investigators reported comparable results (19–21,25), and it may be concluded from these trials that weight loss is related to energy restriction and not to the macronutrient distribution of the diet. Although both HPLF and HCLF energy-reduced diets are successful at reducing body weight and fat mass, HPLF diets may be better tolerated by dieters at-large. In the present study, subjects consuming the HPLF experimental diet reported feeling more satiated during the trial, particularly in study weeks 3 and 4, compared with subjects consuming the HCLF experimental diet. Moreover, two subjects in the latter diet group quit the feeding trial at week 3 due to unendurable hunger. These subjects had difficulty complying with the study protocol and reported eating food items in addition to those foods provided by the study diet. In short-term trials, subjects consuming high-protein meals consumed 12–40% less energy [70–200 fewer kcal (293–837 fewer kJ)] in the subsequent 2–3 h when food was freely available (14–16). Accordingly, cognitive feelings of less hunger and greater satiety were noted in subjects ingesting high-protein foods vs. high-carbohydrate or high-fat foods (15,16,26). In long-term trials, the greater magnitude of weight loss in the subjects consuming high protein diets compared with subjects consuming high-carbohydrate diets, has been attributed to voluntary reductions in energy intake in these subjects (11,13).
Based on our data and that of others, both HPLF and HCLF diets are effective at reducing total cholesterol concentrations by 7–20% after 4–8 wk of dietary intervention (13,19–21). However, these diets also caused reductions in HDL cholesterol, and the total cholesterol/HDL cholesterol ratio did not change significantly. Moreover, plasma triacylglycerols were not affected by either diet regimen. Because diets high in monounsaturated fat have been demonstrated to reduce triacylglycerols, total cholesterol, and LDL cholesterol and to maintain or raise HDL cholesterol (27,28), the inclusion of monounsaturated fats in high-protein diets should be explored for their favorable effect on blood lipids. Insulin concentrations in fasting subjects fell significantly (-24%) in both diet groups after the 6-wk intervention, and insulin sensitivity was improved by 5% in both groups of dieters. These data demonstrate the effectiveness of mild energy restriction [500 kcal/d (2092 kJ/d)] for improving insulin sensitivity regardless of the macronutrient profile of the diet.
Consumption of high-protein diets has been linked with potentially adverse effects, notably uricemia, uricosuria, and calciuria (18,29–32), factors associated with increased risk for gout and urinary stone formation. In the present study, plasma uric acid concentrations fell significantly in both diet groups; however, urinary uric acid as well as urinary calcium concentrations increased 14 and 42%, respectively, in subjects consuming the high-protein diet and fell 40 and 23%, respectively, in subjects consuming the high-carbohydrate diet. Although these urinary markers remained in normal ranges in subjects consuming the high-protein diet, dietary protein restriction is a rational strategy for patients with a history of nephrolithiasis or idiopathic hypercalciuria (33,34).
The calciuretic effect of dietary protein has been related to increased glomerular filtration rates and to decreased tubular calcium reabsorption, a consequence of increased acid production during the oxidation of the sulfur amino acids (35). Although absolute calcium excretion was significantly affected by diet treatment, calcium intake was 50% higher for subjects following the HPLF diet plan. When expressed as a percentage of intake, calcium excretion rates did not differ between the diet groups, 9 and 7% for the HPLF and HCLF diets, respectively, which is equivalent to 170 and 92 mg calcium. Thus, calcium balance did not appear to be adversely affected by the high-protein diet treatment. Glomerular filtration rates, as estimated by creatinine clearance, were not elevated in subjects ingesting the HPLF diet for 6 wk, perhaps a reflection of the lack of change in urinary creatinine excretion in these subjects. High-protein diets based on meat provide an exogenous source of creatinine, which in turn increases creatinine excretion and the apparent glomerular filtration rate (36). In the present trial, nonmeat items (e.g., low-fat dairy, egg beaters, tofu) were generally utilized as a protein source for the HPLF diets. Furthermore, Roughead et al. (36) recently reported that the initially higher renal acid excretion in subjects consuming high-meat diets (20% energy) abated between 3 and 8 wk, reversing the initial hypercalciuria by wk 5.
The apparent nitrogen balance differed significantly by group after the 6-wk diet intervention, 0.7 ± 1.7 and 3.9 ± 1.4 g N/d in HCLF and HPLF subjects, respectively (P < 0.05). These data closely match the values reported by Pannemans et al. (37) for subjects ingesting levels of nitrogen similar to those in the present study (11 and 20 g/d). Others also documented positive nitrogen balance in subjects consuming high-protein diets, but an explanation for this apparent retention of protein is lacking, particularly because lean body mass is not measurably increased in healthy individuals consuming high-protein supplements (38,39). In the present trial, fat-free mass actually decreased 4% in both diet groups. However, several articles have related rates of protein synthesis to dietary protein level supporting the theory of a labile protein pool that is expanded with high-protein diets (37,40). These visceral proteins are believed to be located in various tissues such as the gut and liver.
The 24-h REE (kJ/kg) was not affected by diet treatment [+7.5%, about +1.5 kcal/kg (6.26 kJ/kg), and –0.3%, about -0.3 kcal/kg (1.26 kJ/kg), for HPLF and HCLF dieters, respectively]. Although Hwalla Baba et al. (20) reported that REE (kcal/d) decreased in subjects consuming either high-protein or high-carbohydrate energy restricted diets for 4 wk, when adjusted for body weight, this decrease was significant only in subjects consuming the high-carbohydrate diet. REE and nitrogen balance have been related to protein synthesis (41,42), and in the present study, nitrogen balance (g N/d · kg) and REE (kJ/kg) were weakly associated (r = 0.30, P = 0.091).
At the completion of the 6-wk trial, the subjects were invited to return for a follow-up visit that included body composition measurements and blood lipid analyses. Nine HPLF subjects (100%) and five HCLF subjects (71%) were tested at follow-up. Subjects from both diet groups had maintained their weight loss after 4 wk of unrestricted food intake; however, total cholesterol concentrations at follow-up were not significantly different from baseline concentrations. The cause for this reversal in blood lipids cannot be addressed because diet records were not kept during this 4-wk period. These data imply that food components (e.g., saturated fatty acids, trans-fatty acids, soluble fibers) are important for controlling blood cholesterol levels, not weight loss per se.
In conclusion, under tightly controlled experimental conditions, energy-restricted, low-fat diets of varying protein content (15 or 30% energy) were equally effective at promoting steady weight loss over a 6-wk period. However, subjects adhering to the high-protein diet reported less hunger and a greater degree of diet satisfaction than their counterparts consuming the lower-protein diet. Biomarkers of health and disease, including blood lipid profile, insulin sensitivity, uricosuria, hypercalciuria, and glomerular filtration rates, were not adversely affected by the high-protein, low-fat diet. In addition, only the high-protein diet regimen resulted in a marked positive nitrogen balance, signaling perhaps an advantage of high-protein intakes. It is important, however, to differentiate high-protein, low-fat diet plans from high-protein, high-fat, low-carbohydrate, Atkins-like diet plans because adherence to these latter diets has been associated with elevations in total and LDL cholesterol and plasma uric acid (18).
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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2 Supported by a Faculty-Grant-in-Aid, Arizona State University East Office of Research and Sponsored Projects and by the Lloyd S. Hubbard Nutrition Research Fund of the Arizona State University Foundation.
4 Abbreviations used: BMR, basal metabolic rate; HCLF, high-carbohydrate, low-fat; HPLF, high-protein, low-fat; REE, resting energy expenditure.
Manuscript received 30 July 2003. Initial review completed 28 September 2003. Revision accepted 18 December 2003.
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LITERATURE CITED |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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1. Select Committee on Nutrition and Human Needs (1977) Dietary Goals for the United States 1977 U.S. Government Printing Office Washington, DC.
2. USDA/DHHS (U.S. Department of Agriculture/Department of Health and Human Services) (1979) Food. Home & Garden Bulletin no. 228. 1979 U.S. Department of Agriculture and Department of Health and Human Services Washington, DC .
3. Department of Health and Human Services (1979) Healthy People: The Surgeon General’s Report on Health Promotion and Disease Prevention. DHEW (PHS) Publication no. 79–55071A 1979:177-179 U.S. Government Printing Office Washington DC .
4. Hegsted, D. M. (1978) Dietary goals—a progressive view. Am. J. Clin. Nutr. 31:1504-1509.
5. USDA/DHHS (U.S. Department of Agriculture/Department of Health and Human Services) (2000) Nutrition and Your Health: Dietary Guidelines for Americans. Home & Garden Bulletin no. 232. 5th ed. 2000 U.S. Department of Agriculture and Department of Health and Human Services Washington, DC .
6. Expert Panel on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults (2000) NHLBI Obesity Education Initiative. 2000 USDHHS, PHS, NIH, National Heart, Lung, and Blood Institute. Bethesda, MD. NIH Publication no. 00–4084,.
7. Cummings, S., Parham, E. S. & Strain, G. W. (2002) Position of the American Dietetic Association: weight management. J. Am. Diet. Assoc. 102:1145-1155.[Medline]
8. Atkins, R. (1992) Dr. Atkins’ New Diet Revolution 1992 HarperCollins Publishers New York, NY.
9. Atkins, R. (2003) Atkins for Life 2003 St. Martin’s Press New York, NY.
10. Anonymous, (2002) The truth about diet. Consum. Rep. 67:26-32.[Medline]
11. Foster, G. D., Wyatt, H. R., Hill, J. O., McGuckin, B. G., Brill, C., Mohammed, B. S., Szapary, P. O., Rader, D. J., Edman, J. S. & Klein, S. (2003) A randomized trial of a low-carbohydrate diet for obesity. N. Engl. J. Med. 348:2082-2090.
12. Eisenstein, J., Roberts, S. B., Dallal, G. & Saltzman, E. (2002) High-protein weight-loss diets: are they safe and do they work?A review of the experimental and epidemiologic data. Nutr. Rev. 60:189-200.[Medline]
13. Skov, A. R., Toubro, S., Ronn, B., Holm, L. & Astrup, A. (1999) Randomized trial on protein versus carbohydrate in ad libitum fat reduced diet for the treatment of obesity. Int. J. Obes. 23:528-536.[Medline]
14. Araya, H., Hills, J., Alvina, M. & Vera, G. (2000) Short-term satiety in preschool children: a comparison between high protein meal and a high complex carbohydrate meal. Int. J. Food Sci. Nutr. 51:119-124.[Medline]
15. Popitt, S. D., McCormack, D. & Buffenstein, R. (1998) Short-term effects of macronutrient preloads on appetite and energy intake in lean women. Physiol. Behav. 64:279-285.[Medline]
16. Ludwig, D. S., Majzoub, J. A., Al-Zahrani, A., Dallal, G. E., Blanco, I. & Roberts, S. B. (1999) High glycemic index foods, overeating, and obesity [electronic article]. Pediatrics 103:E26.
17. Anderson, J. W., Konz, E. C. & Jenkins, D.J.A. (2000) Health advantages and disadvantages of weight-reducing diets: a computer analysis and critical review. J. Am. Coll. Nutr. 19:578-590.
18. Larosa, J. C., Fry, A. G., Muesing, R. & Rosing, D. R. (1980) Effects of high-protein, low-carbohydrate dieting on plasma lipoproteins and body weight. J. Am. Diet. Assoc. 77:264-270.[Medline]
19. Parker, B., Noakes, M., Luscombe, N. & Clifton, P. (2002) Effect of a high-protein, high-monounsaturated fat weight loss diet on glycemic control and lipid levels in type 2 diabetes. Diabetes Care 25:425-430.
20. Hwalla Baba, N., Sawaya, S., Torbay, N., Habbal, Z., Azar, S. & Hashim, S. A. (1999) High protein versus high carbohydrate hypoenergetic diet for the treatment of obese hyperinsulinemic subjects. Int. J. Obes. 23:1202-1206.
21. Piatti, P. M., Monti, L. D., Magni, F., Ferma, I., Baruffaidi, L., Nasser, R., Santambrogio, G., Librenti, M. C., Galli-Kienle, M., Pontiroll, A. E. & Pozza, G. (1994) Hypocaloric high-protein diet improves glucose oxidation and spares lean body mass: comparison to hypocaloric high-carbohydrate diet. Metabolism 43:1481-1487.[Medline]
22. Lee, R. D. & Neiman, D. C. (2003) Nutritional Assessment 2003 McGraw-Hill New York, NY.
23. Weir, J. B. (1949) New methods for calculating metabolic rate with special reference to protein. J. Physiol. 109:1-49.
24. Katz, A., Nambi, S. S., Mather, K., Baron, A. D., Follmann, D. A., Sullivan, G. & Quon, M. J. (2000) Quantitative insulin sensitivity check index: a simple, accurate method for assessing insulin sensitivity in humans. J. Clin. Endocrinol. Metab. 85:2402-2410.
25. Farnsworth, E., Luscombe, N. D., Noakes, M., Wittert, G., Argyiou, E. & Clifton, P. M. (2003) Effect of a high-protein, energy-restricted diet on body composition, glycemic control, and lipid concentrations in overweight and obese hyperinsulinemic men and women. Am. J. Clin. Nutr. 78:31-39.
26. Latner, J. D. & Schwartz, M. (1999) The effects of a high-carbohydrate, high-protein or balanced lunch upon later food intake and hunger ratings. Appetite 33:119-128.[Medline]
27. Jansen, S., Lopez-Miranda, J., Castro, P., Lopez-Segura, F., Marin, C., Ordovas, J. M., Paz, E., Jimenez-Pereperez, J., Fuentes, F. & Perez-Jimenez, F. (2000) Low-fat and high-monounsaturated fatty acid diets decrease plasma cholesterol ester transfer protein concentrations in young, healthy, normolipemic men. Am. J. Clin. Nutr. 72:36-41.
28. Kris-Etherton, P. M., Pearson, T. A., Wan, Y., Hargrove, R. L., Moriarty, K., Fishell, V. & Etherton, T. D. (1999) High-monounsaturated fatty acid diets lower both plasma cholesterol and triacylglycerol concentrations. Am. J. Clin. Nutr. 70:1009-1015.
29. Nguyen, Q. V., Kalin, A., Drouve, U., Casez, J. P. & Jaeger, P. (2001) Sensitivity to meat protein intake and hyperoxaluria in idiopathic calcium stone formers. Kidney Int 59:2273-2281.[Medline]
30. Skov, A. R., Topubro, S., Bulow, J., Krabbe, K., Parving, H. H. & Astrup, A. (1999) Changes in renal function during weight loss induced by high versus low-protein low-fat diets in overweight subjects. Int. J. Obes. Relat. Metab. Disord. 23:1170-1177.[Medline]
31. Kerstetter, J. E., O’Brien, K. O. & Insogna, K. L. (1998) Dietary protein affects intestinal calcium absorption. Am. J. Clin. Nutr. 68:859-865.[Abstract]
32. Reddy, S. T., Wang, C. Y., Sakhaee, K., Brinkley, L. & Pak, C. Y. (2002) Effect of low-carbohydrate high-protein diets on acid-base balance, stone-formation propensity, and calcium metabolism. Am. J. Kidney Dis. 40:265-274.[Medline]
33. Giannini, S., Nobile, M., Sartori, L., Dalle Carbonare, L., Ciuffreda, M., Corro, P., D’Angelo, A., Calo, L. & Crepaldi, G. (1999) Acute effects of moderate dietary protein restriction in patients with idiopathic hypercalciuria and calcium nephrolithiasis. Am. J. Clin. Nutr. 69:267-271.
34. Borghi, L., Schianchi, T., Meschi, T., Guerra, A., Allegri, F., Maggiore, U. & Novarini, A. (2002) Comparison of two diets for the prevention of recurrent stones in idiopathic hypercalciuria. N. Engl. J. Med. 346:77-84.
35. Schuette, S. A., Zemel, M. B. & Linkswiler, H. M. (1980) Studies on the mechanism of protein induced hypercalciuria in older men and women. J. Nutr. 110:305-315.
36. Roughead, Z. K., Johnson, L. K., Lykken, G. I. & Hunt, J. R. (2003) Controlled high meat diets do not affect calcium retention or indices of bone status in healthy postmenopausal women. J. Nutr. 133:1020-1026.
37. Pannemans, D.L.E., Halliday, D., Westerterp, K. R. & Kester, A.D.M. (1995) Effect of variable protein intake on whole-body protein turnover in young men and women. Am. J. Clin. Nutr. 61:69-74.
38. Garlick, P. J., McNurlan, M. A. & Patlak, C. S. (1999) Adaptation of protein metabolism in relation to limits to high dietary protein intake. Eur. J. Clin. Nut. 53(suppl. 1):S34-S43.
39. Rozenek, R., Ward, P., Long, S. & Garhammer, J. (2002) Effects of high-calorie supplements on body composition and muscular strength following resistance training. J. Sports Med. Phys. Fitness 42:340-347.[Medline]
40. Pannemans, D.L.E., Wagenmakers, A.J.M., Westerterp, K. R., Schaafsma, G. & Halliday, D. (1998) Effect of protein source and quantity on protein metabolism in elderly women. Am. J. Clin. Nutr. 68:1228-1235.[Abstract]
41. Gougeon, R., Pencharz, P. B. & Marliss, E. B. (1995) Whole-body protein turnover in obese subjects during two very low energy diets of differing amino acid composition. Int. J. Obes. Relat. Metab. Disord. 19:739-748.[Medline]
42. Liu, Z., Jahn, L. A., Wei, L., Lonng, W. & Barrett, E. J. (2002) Amino acids stimulate translation initiation and protein synthesis through an Akt-independent pathway in human skeletal muscle. J. Clin. Endocrinol. Metab. 87:5553-5558.
43. USDA Food Guide Pyramid () http://www.nal.usda.gov:8001/py/pmap.htm (now http://schoolmeals.nal.usda.gov/py/pmap.htm) [accessed June 30, 2003].
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