- Email: [email protected]
Can posttraumatic insulin resistance be attenuated by prior glucose loading?
354
Editorial Opinions
Nutrition Volume 17, Number 4, 2001
circumference), might be more feasible and rewarding, regardless of the individual’s ethnicity.
Fary M. Cachelin, PhD California State University Los Angeles, California, USA REFERENCES 1. Kuczmarski RJ, Flegal KM, Campbell SM, Johnson CL. Increasing prevalence of overweight among U.S. adults. JAMA 1994;272:205 2. Crago M, Shisslak CM, Estes LS. Eating disturbances among American minority groups: a review. Int J Eat Disord 1996;19:239 3. Rosen EF, Brown A, Braden J, et al. African-American males prefer a larger female body silhouette than do whites. Bull Psychonomic Soc 1993;31:599 4. Thompson SH, Sargent RG, Kemper KA. Black and white adolescent males’ perceptions of ideal body size. Sex Roles 1996;34:391 5. Rucker CE, Cash TF. Body images, body-size perceptions, and eating behaviors among African-American and white college women. Int J Eat Disord 1992;12: 291 6. Powell AD, Kahn AS. Racial differences in women’s desires to be thin. Int J Eat Disord 1995;17:191 7. Altabe M. Ethnicity and body image: quantitative and qualitative analysis. Int J Eat Disord 1998;23:153 8. Cachelin FM, Striegel-Moore RH, Elder KA. Realistic weight perception and body size assessment in a racially diverse community sample of dieters. Obes Res 1998;6:62 9. Allison DB, Hoy MK, Fournier A, Heymsfield SB. Can ethnic differences in men’s preferences for women’s body shapes contribute to ethnic differences in female adiposity? Obes Res 1993;1:425 10. Stunkard AJ, Sorenson T, Schlusinger F. Use of the Danish adoption register for the study of obesity and thinness. In: Kety SS, Rowland LP, Sidman RL, Matthysse SW, eds. The genetics of neurological and psychological disorders. New York: Raven Press, 1983:115 11. Williamson DA, Davis CJ, Bennet SM, Goreczny AJ, Gleaves DH. Development of a simple procedure for assessing body image disturbances. Behav Assess 1989;11:433 12. Bell C, Kirkpatrick SW, Binn R. Body image of anorexic, obese and normal females. J Clin Psychol 1986;42:431 13. Kemper KA, Sargent RG, Drane JW, Valois RF, Hussey JR. Black and white females’ perceptions of ideal body size and social norms. Obes Res 1994;2:117 14. Foster GD, Wadden TA, Vogt RA, Brewer G. What is a reasonable weight loss? Patients’ expectations and evaluations of obesity treatment outcome. J Consult Clin Psychol 1997;65:79
PII S0899-9007(00)00590-6
Can Posttraumatic Insulin Resistance Be Attenuated by Prior Glucose Loading? The presence of a “diabetes-like state” after injury has been recognized for almost 150 y1 and has been attributed since the 1950s to acute resistance to the anabolic effects of insulin.2 Like many features of the metabolic response to trauma and infection, insulin resistance appears to be highly conserved from the evolutionary point of view and presumably occurs to spare glucose for obligatory non-insulin– dependent glucose– utilizing tissues such as the brain, immune system, and the healing wound. Insulin resistance is perhaps best characterized in skeletal muscle,3 which is the principal site of insulin-mediated glucose uptake in vivo.4 An acute reduction in skeletal-muscle insulin sensitivity results in defective glucose storage,5 although oxidation is preserved. These changes are associated with marked catabolism, muscle wasting,
Correspondence to: Clare R. Byrne, PhD, MRC Trauma Group,University of Manchester, Hope Hospital, Salford M6 8HD, UK. E-mail: mdsnscrb@ fs1scg.man.ac.uk
and a negative nitrogen balance.6 Furthermore, the severity of insulin resistance was directly correlated with length of hospital stay.3 Although there might have been intrinsic physiologic value in promoting an insulin-resistant state in the setting of the prehistoric injured, starving, and immobile human, the teleologic value of insulin resistance in the context of modern medical treatment and nutritional support is unclear. While nutritional support might be ineffective in the critically ill, insulin-resistant patient, supplementary insulin therapy has been shown to stimulate protein synthesis in severely burned patients,7 inhibit the increase in muscle catabolism seen after injury,8 preserve protein stores after major elective surgery,9 and even improve wound healing.10 Unfortunately, administration of insulin in the doses required can expose patients to risk of fatal hypoglycemia with the attendant requirement for regular and close monitoring of blood glucose levels, making insulin supplementation unlikely to be of clinical value. Recent interest has therefore focused on alternative therapies that might attenuate posttraumatic insulin resistance. Many studies, clinical and animal, aiming to prevent or control this type of insulin resistance have concentrated in particular on carbohydrate loading before trauma. Elective surgery, which results in a marked, transient reduction in insulin sensitivity,9,11,12 is routinely performed after 12 to 18 h of fasting. However, it has been suggested13 that this might not be the optimal “metabolic setting” in which to undertake surgery because preoperative glucose infusion seems to markedly attenuate postoperative insulin resistance. This effect also can be reproduced by administering a preoperative carbohydrate drink14,15 that, when given the evening before and 2 h before surgery, was sufficient to stimulate insulin release, convert the patient to a postabsorptive state, and reduce postoperative insulin resistance by 50%. Interestingly, this treatment did not correct the defect in glucose storage14 but increased glucose oxidation. Given this finding and the fact that glucose oxidation does not seem to be impaired in acute insulin resistance, it is unclear whether the use of carbohydrate loading (which does not improve glucose storage) would improve nitrogen retention in muscle and hence reduce muscle wasting. In this issue of Nutrition, data from an ex vivo animal study (Stro¨mmer et al.16) also cast some doubt as to how clinically useful carbohydrate loading might really be. In their study, insulin-stimulated glucose uptake was measured ex vivo in isolated strips of rat soleus muscle taken from animals that had undergone laparotomy (or control animals), with or without an oral glucose load 1 h before surgery. These studies indicated that oral glucose loading failed to attenuate the very considerable (⬎50%) reduction in insulin-mediated glucose uptake in soleus muscle after surgery. In addition, a preoperative fast of 16 h was not associated with a greater degree of insulin resistance after surgery than that observed in animals that had been allowed to feed freely until surgery. The apparent contradiction between the results of Stro¨mmer et al.16 and previous clinical studies very clearly indicates the difficulties inherent in extrapolating between small-animal and human clinical studies. The human studies used markedly different regimens for carbohydrate loading, with two doses of a complex mixture of carbohydrates rather than an oral glucose load. In addition, it is unclear whether the improved whole-body glucose disposal resulting from carbohydrate loading in humans would improve skeletal-muscle glucose uptake because non-oxidative glucose disposal does not seem to be the mechanism by which glucose loading achieves its protective effect. It might be argued that the degree of insulin resistance that resulted from this trauma model was so large that it was maximal even in fed animals and could not have been made more conspicuous even by preoperative starvation for 16 h. Clearly the quest for ways to modulate postoperative insulin resistance continues, despite the negative findings by Strommer et al. Ongoing industry-funded clinical trials have been evaluating the outcome of preoperative glucose loading in patients undergoing major abdominal surgery and those evaluations are eagerly awaited. Whatever the result, it remains to be shown that posttrau-
Nutrition Volume 17, Number 4, 2001 matic insulin resistance is more than yet another epiphenomenon. This will require proof that preventing insulin resistance can produce clinically useful improvements in outcome and that insulin resistance is causally related to (as opposed to simply associated with) catabolism and muscle wasting.
C. R. Byrne, PhD G. L. Carlson, BSc, MD, FRCS MRC Trauma Group and Department of Surgery University of Manchester Hope Hospital, Salford, UK REFERENCES 1. Fischer P. Du diabete consecutif aux traumatismes. Arch Gen Med 1862;20:413 2. Howard JM. Studies of the absorption and metabolism of glucose following injury. Ann Surg 1955;141:321 3. Thorell A, Nygren J, Ljungqvist O. Insulin resistance: a marker of surgical stress. Curr Opin Nutr Metab Care 1999;2:69 4. DeFronzo RA, Gunnarsson R, Bjorkman O, et al. Effects of insulin on peripheral and splanchnic glucose metabolism in noninsulin-dependent (type II) diabetes mellitus. J Clin Invest 1985;76:149 5. Saeed M, Carlson GL, Little RA, Irving MH. Selective impairment of glucose storage in human sepsis. Br J Surg 1999;86:813 6. Michie HR. Metabolism of sepsis and multiple organ failure. World J Surg 1996;20:460 7. Sakurai Y, Aarsland A, Herndon DN, et al. Stimulation of muscle protein synthesis by long-term insulin infusion in severely burned patients. Ann Surg 1995;222:283 8. Woolfson AMJ, Heatley RV, Allison SP. Insulin to inhibit protein catabolism after injury. N Engl J Med 1979;300:14 9. Brandi LS, Frediani M, Oleggini M, et al. Insulin resistance after surgery: normalisation by insulin treatment. Clin Sci 1990;79:443 10. Pierre EJ, Barrow RE, Hawkins HK, et al. Effects of insulin on wound healing. J Trauma 1998;44:342 11. Thorell A, Efendic S, Gutniak M, Haggmark T, Ljungqvist O. Insulin resistance after abdominal surgery. Br J Surg 1994;81:59 12. Uchida I, Asoh T, Shirasaka C, Tsuji H. Effect of epidural analgesia on postoperative insulin resistance as evaluated by insulin clamp technique. Br J Surg 1988;75:557 13. Ljungqvist O, Thorell A, Gutniak M, Haggmark T, Efendic S. Glucose infusion instead of preoperative fasting reduces postoperative insulin resistance. J Am Coll Surg 1994;178:329 14. Nygren J, Soop M, Thorell A, et al. Preoperative oral carbohydrate administration reduces postoperative insulin resistance. Clin Nutr 1998;17:65 15. Nygren J, Soop M, Thorell A, Sree-Nair K, Ljungqvist O. Preoperative oral carbohydrates and postoperative insulin resistance. Clin Nutr 1999;18:117 16. Stro¨mmer L, Isaksson B, Wickbom B, et al. Effect of carbohydrate feeding on insulin action in skeletal muscle after surgical trauma in the rat. Nutrition 2001;17:331
PII S0899-9007(00)00591-8
Frequent Dieting and the Development of Obesity Among Children and Adolescents Obesity is a growing and serious public health problem among both children and adults in the United States. During the past two
Drs. Field and Colditz were partially supported by the Boston Obesity Nutrition Research Center (DK 46200). Additional funding was provided by a research grant (DK-46834) from the National Institutes of Health and the Kellogg Company. Correspondence to: Alison E. Field, ScD, Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, 181 Longwood Avenue, Boston, MA 02115, USA. E-mail: [email protected]
Editorial Opinions
355
decades, the prevalence of overweight has increased by 100% among adolescents in the United States.1 Preadolescents and adolescents who are overweight are likely to become overweight adults,2 thus the prevalence of overweight in adulthood and its consequences can be expected to increase markedly during the next several decades unless active measures are taken to combat excessive pediatric weight gain. Although the prevalence of overweight and obesity are increasing, the desire to be thin or to have well-defined or toned muscles is still very widespread. Dieting to lose weight is common among preadolescent and adolescent girls,3–5 as well as adult women.6 Although dieting is less common among males,7,8 recent data suggest that weight concerns may be becoming more prevalent.9 In cross-sectional studies researchers have observed a strong association between dieting and being overweight or obese.10 In addition, in cross-sectional samples of adults there is a relatively high prevalence of binge eating disorder (BED) among the overweight11,12; however, there are relatively few studies investigating the temporal relationship between dieting and weight status. There are at least three mechanisms through which dieting could lead to the development of overweight. Dieting may result in an increase in metabolic efficiency, thus, dieters over time may require fewer calories to maintain weight. Moreover, an increase in metabolic efficiency would result in dieters gaining weight when they consumed a diet that previously had been effective for maintaining their weight. Alternatively, the weight gain associated with dieting may be due to the fact that restrictive diets are rarely maintained for an extended period of time.13,14 It has been postulated that dieting may lead to a cycle of restrictive dieting, followed by bouts of overeating or binge eating. In that scenario it would be the repeated cycles of overeating between the restrictive diets that would be responsible for weight gain. Another possible explanation is that the composition of the diet is responsible for the weight gain. Low-fat, high-carbohydrate diets frequently are high-glycemic index diets (i.e., they are rich in foods that increase blood glucose levels). Although there are no long-term studies, short-term studies observed that people consumed more calories after being fed high-glycemic index meals than low-glycemic meals.15,16 It is also possible that the cross-sectional association between dieting and weight status is due to overweight individuals being more likely than their normal weight peers to go on diets to lose weight. Since most dieting efforts are not successful, or at least not successfully maintained, overweight individuals may remain overweight despite, not because of, their dieting attempts. Only prospective analyses can help to determine whether dieting increases the risk of becoming overweight, is simply an ineffective strategy to lose and maintain weight, or is only effective in conjunction with increasing physical activity (the weight loss recommendation contained in the United States Dietary Guidelines).17 Unfortunately, prospective investigations of this topic in children and adolescents are few. Stice et al.18 followed 692 adolescent girls for 4 y. At baseline 16% of the girls were on a diet and 15% of the girls were overweight. Over 4 y, 63 (10.7%) girls became overweight. Girls who labeled themselves as dieters at baseline were approximately 3 times (odds ratio [OR] ⫽ 3.2) more likely than non-dieters to become overweight. However, since the authors adjusted for only sexual maturity and baseline body mass index (BMI), it is unclear how much of the association is due to dieting per se in that two other factors, the score on the restraint scale and exercising to lose weight, were also associated with the development of overweight. Because dieting to control weight is associated with both dietary restraint and exercising to lose weight, it is unclear which of the factors were independently predictive of becoming overweight. Moreover, there was no measure of dietary intake so it was unclear whether the association was due to or independent of actual dietary intake. To assess the relationship between dieting and weight change in greater detail we conducted a prospective analysis using data
Editorial Opinions
Nutrition Volume 17, Number 4, 2001
circumference), might be more feasible and rewarding, regardless of the individual’s ethnicity.
Fary M. Cachelin, PhD California State University Los Angeles, California, USA REFERENCES 1. Kuczmarski RJ, Flegal KM, Campbell SM, Johnson CL. Increasing prevalence of overweight among U.S. adults. JAMA 1994;272:205 2. Crago M, Shisslak CM, Estes LS. Eating disturbances among American minority groups: a review. Int J Eat Disord 1996;19:239 3. Rosen EF, Brown A, Braden J, et al. African-American males prefer a larger female body silhouette than do whites. Bull Psychonomic Soc 1993;31:599 4. Thompson SH, Sargent RG, Kemper KA. Black and white adolescent males’ perceptions of ideal body size. Sex Roles 1996;34:391 5. Rucker CE, Cash TF. Body images, body-size perceptions, and eating behaviors among African-American and white college women. Int J Eat Disord 1992;12: 291 6. Powell AD, Kahn AS. Racial differences in women’s desires to be thin. Int J Eat Disord 1995;17:191 7. Altabe M. Ethnicity and body image: quantitative and qualitative analysis. Int J Eat Disord 1998;23:153 8. Cachelin FM, Striegel-Moore RH, Elder KA. Realistic weight perception and body size assessment in a racially diverse community sample of dieters. Obes Res 1998;6:62 9. Allison DB, Hoy MK, Fournier A, Heymsfield SB. Can ethnic differences in men’s preferences for women’s body shapes contribute to ethnic differences in female adiposity? Obes Res 1993;1:425 10. Stunkard AJ, Sorenson T, Schlusinger F. Use of the Danish adoption register for the study of obesity and thinness. In: Kety SS, Rowland LP, Sidman RL, Matthysse SW, eds. The genetics of neurological and psychological disorders. New York: Raven Press, 1983:115 11. Williamson DA, Davis CJ, Bennet SM, Goreczny AJ, Gleaves DH. Development of a simple procedure for assessing body image disturbances. Behav Assess 1989;11:433 12. Bell C, Kirkpatrick SW, Binn R. Body image of anorexic, obese and normal females. J Clin Psychol 1986;42:431 13. Kemper KA, Sargent RG, Drane JW, Valois RF, Hussey JR. Black and white females’ perceptions of ideal body size and social norms. Obes Res 1994;2:117 14. Foster GD, Wadden TA, Vogt RA, Brewer G. What is a reasonable weight loss? Patients’ expectations and evaluations of obesity treatment outcome. J Consult Clin Psychol 1997;65:79
PII S0899-9007(00)00590-6
Can Posttraumatic Insulin Resistance Be Attenuated by Prior Glucose Loading? The presence of a “diabetes-like state” after injury has been recognized for almost 150 y1 and has been attributed since the 1950s to acute resistance to the anabolic effects of insulin.2 Like many features of the metabolic response to trauma and infection, insulin resistance appears to be highly conserved from the evolutionary point of view and presumably occurs to spare glucose for obligatory non-insulin– dependent glucose– utilizing tissues such as the brain, immune system, and the healing wound. Insulin resistance is perhaps best characterized in skeletal muscle,3 which is the principal site of insulin-mediated glucose uptake in vivo.4 An acute reduction in skeletal-muscle insulin sensitivity results in defective glucose storage,5 although oxidation is preserved. These changes are associated with marked catabolism, muscle wasting,
Correspondence to: Clare R. Byrne, PhD, MRC Trauma Group,University of Manchester, Hope Hospital, Salford M6 8HD, UK. E-mail: mdsnscrb@ fs1scg.man.ac.uk
and a negative nitrogen balance.6 Furthermore, the severity of insulin resistance was directly correlated with length of hospital stay.3 Although there might have been intrinsic physiologic value in promoting an insulin-resistant state in the setting of the prehistoric injured, starving, and immobile human, the teleologic value of insulin resistance in the context of modern medical treatment and nutritional support is unclear. While nutritional support might be ineffective in the critically ill, insulin-resistant patient, supplementary insulin therapy has been shown to stimulate protein synthesis in severely burned patients,7 inhibit the increase in muscle catabolism seen after injury,8 preserve protein stores after major elective surgery,9 and even improve wound healing.10 Unfortunately, administration of insulin in the doses required can expose patients to risk of fatal hypoglycemia with the attendant requirement for regular and close monitoring of blood glucose levels, making insulin supplementation unlikely to be of clinical value. Recent interest has therefore focused on alternative therapies that might attenuate posttraumatic insulin resistance. Many studies, clinical and animal, aiming to prevent or control this type of insulin resistance have concentrated in particular on carbohydrate loading before trauma. Elective surgery, which results in a marked, transient reduction in insulin sensitivity,9,11,12 is routinely performed after 12 to 18 h of fasting. However, it has been suggested13 that this might not be the optimal “metabolic setting” in which to undertake surgery because preoperative glucose infusion seems to markedly attenuate postoperative insulin resistance. This effect also can be reproduced by administering a preoperative carbohydrate drink14,15 that, when given the evening before and 2 h before surgery, was sufficient to stimulate insulin release, convert the patient to a postabsorptive state, and reduce postoperative insulin resistance by 50%. Interestingly, this treatment did not correct the defect in glucose storage14 but increased glucose oxidation. Given this finding and the fact that glucose oxidation does not seem to be impaired in acute insulin resistance, it is unclear whether the use of carbohydrate loading (which does not improve glucose storage) would improve nitrogen retention in muscle and hence reduce muscle wasting. In this issue of Nutrition, data from an ex vivo animal study (Stro¨mmer et al.16) also cast some doubt as to how clinically useful carbohydrate loading might really be. In their study, insulin-stimulated glucose uptake was measured ex vivo in isolated strips of rat soleus muscle taken from animals that had undergone laparotomy (or control animals), with or without an oral glucose load 1 h before surgery. These studies indicated that oral glucose loading failed to attenuate the very considerable (⬎50%) reduction in insulin-mediated glucose uptake in soleus muscle after surgery. In addition, a preoperative fast of 16 h was not associated with a greater degree of insulin resistance after surgery than that observed in animals that had been allowed to feed freely until surgery. The apparent contradiction between the results of Stro¨mmer et al.16 and previous clinical studies very clearly indicates the difficulties inherent in extrapolating between small-animal and human clinical studies. The human studies used markedly different regimens for carbohydrate loading, with two doses of a complex mixture of carbohydrates rather than an oral glucose load. In addition, it is unclear whether the improved whole-body glucose disposal resulting from carbohydrate loading in humans would improve skeletal-muscle glucose uptake because non-oxidative glucose disposal does not seem to be the mechanism by which glucose loading achieves its protective effect. It might be argued that the degree of insulin resistance that resulted from this trauma model was so large that it was maximal even in fed animals and could not have been made more conspicuous even by preoperative starvation for 16 h. Clearly the quest for ways to modulate postoperative insulin resistance continues, despite the negative findings by Strommer et al. Ongoing industry-funded clinical trials have been evaluating the outcome of preoperative glucose loading in patients undergoing major abdominal surgery and those evaluations are eagerly awaited. Whatever the result, it remains to be shown that posttrau-
Nutrition Volume 17, Number 4, 2001 matic insulin resistance is more than yet another epiphenomenon. This will require proof that preventing insulin resistance can produce clinically useful improvements in outcome and that insulin resistance is causally related to (as opposed to simply associated with) catabolism and muscle wasting.
C. R. Byrne, PhD G. L. Carlson, BSc, MD, FRCS MRC Trauma Group and Department of Surgery University of Manchester Hope Hospital, Salford, UK REFERENCES 1. Fischer P. Du diabete consecutif aux traumatismes. Arch Gen Med 1862;20:413 2. Howard JM. Studies of the absorption and metabolism of glucose following injury. Ann Surg 1955;141:321 3. Thorell A, Nygren J, Ljungqvist O. Insulin resistance: a marker of surgical stress. Curr Opin Nutr Metab Care 1999;2:69 4. DeFronzo RA, Gunnarsson R, Bjorkman O, et al. Effects of insulin on peripheral and splanchnic glucose metabolism in noninsulin-dependent (type II) diabetes mellitus. J Clin Invest 1985;76:149 5. Saeed M, Carlson GL, Little RA, Irving MH. Selective impairment of glucose storage in human sepsis. Br J Surg 1999;86:813 6. Michie HR. Metabolism of sepsis and multiple organ failure. World J Surg 1996;20:460 7. Sakurai Y, Aarsland A, Herndon DN, et al. Stimulation of muscle protein synthesis by long-term insulin infusion in severely burned patients. Ann Surg 1995;222:283 8. Woolfson AMJ, Heatley RV, Allison SP. Insulin to inhibit protein catabolism after injury. N Engl J Med 1979;300:14 9. Brandi LS, Frediani M, Oleggini M, et al. Insulin resistance after surgery: normalisation by insulin treatment. Clin Sci 1990;79:443 10. Pierre EJ, Barrow RE, Hawkins HK, et al. Effects of insulin on wound healing. J Trauma 1998;44:342 11. Thorell A, Efendic S, Gutniak M, Haggmark T, Ljungqvist O. Insulin resistance after abdominal surgery. Br J Surg 1994;81:59 12. Uchida I, Asoh T, Shirasaka C, Tsuji H. Effect of epidural analgesia on postoperative insulin resistance as evaluated by insulin clamp technique. Br J Surg 1988;75:557 13. Ljungqvist O, Thorell A, Gutniak M, Haggmark T, Efendic S. Glucose infusion instead of preoperative fasting reduces postoperative insulin resistance. J Am Coll Surg 1994;178:329 14. Nygren J, Soop M, Thorell A, et al. Preoperative oral carbohydrate administration reduces postoperative insulin resistance. Clin Nutr 1998;17:65 15. Nygren J, Soop M, Thorell A, Sree-Nair K, Ljungqvist O. Preoperative oral carbohydrates and postoperative insulin resistance. Clin Nutr 1999;18:117 16. Stro¨mmer L, Isaksson B, Wickbom B, et al. Effect of carbohydrate feeding on insulin action in skeletal muscle after surgical trauma in the rat. Nutrition 2001;17:331
PII S0899-9007(00)00591-8
Frequent Dieting and the Development of Obesity Among Children and Adolescents Obesity is a growing and serious public health problem among both children and adults in the United States. During the past two
Drs. Field and Colditz were partially supported by the Boston Obesity Nutrition Research Center (DK 46200). Additional funding was provided by a research grant (DK-46834) from the National Institutes of Health and the Kellogg Company. Correspondence to: Alison E. Field, ScD, Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, 181 Longwood Avenue, Boston, MA 02115, USA. E-mail: [email protected]
Editorial Opinions
355
decades, the prevalence of overweight has increased by 100% among adolescents in the United States.1 Preadolescents and adolescents who are overweight are likely to become overweight adults,2 thus the prevalence of overweight in adulthood and its consequences can be expected to increase markedly during the next several decades unless active measures are taken to combat excessive pediatric weight gain. Although the prevalence of overweight and obesity are increasing, the desire to be thin or to have well-defined or toned muscles is still very widespread. Dieting to lose weight is common among preadolescent and adolescent girls,3–5 as well as adult women.6 Although dieting is less common among males,7,8 recent data suggest that weight concerns may be becoming more prevalent.9 In cross-sectional studies researchers have observed a strong association between dieting and being overweight or obese.10 In addition, in cross-sectional samples of adults there is a relatively high prevalence of binge eating disorder (BED) among the overweight11,12; however, there are relatively few studies investigating the temporal relationship between dieting and weight status. There are at least three mechanisms through which dieting could lead to the development of overweight. Dieting may result in an increase in metabolic efficiency, thus, dieters over time may require fewer calories to maintain weight. Moreover, an increase in metabolic efficiency would result in dieters gaining weight when they consumed a diet that previously had been effective for maintaining their weight. Alternatively, the weight gain associated with dieting may be due to the fact that restrictive diets are rarely maintained for an extended period of time.13,14 It has been postulated that dieting may lead to a cycle of restrictive dieting, followed by bouts of overeating or binge eating. In that scenario it would be the repeated cycles of overeating between the restrictive diets that would be responsible for weight gain. Another possible explanation is that the composition of the diet is responsible for the weight gain. Low-fat, high-carbohydrate diets frequently are high-glycemic index diets (i.e., they are rich in foods that increase blood glucose levels). Although there are no long-term studies, short-term studies observed that people consumed more calories after being fed high-glycemic index meals than low-glycemic meals.15,16 It is also possible that the cross-sectional association between dieting and weight status is due to overweight individuals being more likely than their normal weight peers to go on diets to lose weight. Since most dieting efforts are not successful, or at least not successfully maintained, overweight individuals may remain overweight despite, not because of, their dieting attempts. Only prospective analyses can help to determine whether dieting increases the risk of becoming overweight, is simply an ineffective strategy to lose and maintain weight, or is only effective in conjunction with increasing physical activity (the weight loss recommendation contained in the United States Dietary Guidelines).17 Unfortunately, prospective investigations of this topic in children and adolescents are few. Stice et al.18 followed 692 adolescent girls for 4 y. At baseline 16% of the girls were on a diet and 15% of the girls were overweight. Over 4 y, 63 (10.7%) girls became overweight. Girls who labeled themselves as dieters at baseline were approximately 3 times (odds ratio [OR] ⫽ 3.2) more likely than non-dieters to become overweight. However, since the authors adjusted for only sexual maturity and baseline body mass index (BMI), it is unclear how much of the association is due to dieting per se in that two other factors, the score on the restraint scale and exercising to lose weight, were also associated with the development of overweight. Because dieting to control weight is associated with both dietary restraint and exercising to lose weight, it is unclear which of the factors were independently predictive of becoming overweight. Moreover, there was no measure of dietary intake so it was unclear whether the association was due to or independent of actual dietary intake. To assess the relationship between dieting and weight change in greater detail we conducted a prospective analysis using data