A longitudinal study of serum insulin and insulin resistance as predictors of weight and body fat gain in African American and Caucasian children.

BACKGROUND: The influence of insulin and insulin resistance (IR) on children's weight and fat gain is unclear. OBJECTIVE: To evaluate insulin and IR as predictors of weight and body fat gain in children at high risk for adult obesity. We hypothesized that baseline IR would be positively associated with follow-up body mass index (BMI) and fat mass. SUBJECTS/METHODS: Two hundred and forty-nine healthy African American and Caucasian children aged 6-12 years at high risk for adult obesity because of early-onset childhood overweight and/or parental overweight were followed for up to 15 years with repeated BMI and fat mass measurements. We examined baseline serum insulin and homeostasis model of assessment-IR (HOMA-IR) as predictors of follow-up BMI Z-score and fat mass by dual-energy X-ray absorptiometry in mixed model longitudinal analyses accounting for baseline body composition, pubertal stage, sociodemographic factors and follow-up interval. RESULTS: At baseline, 39% were obese (BMI⩾95th percentile for age/sex). Data from 1335 annual visits were examined. Children were followed for an average of 7.2±4.3 years, with a maximum follow-up of 15 years. After accounting for covariates, neither baseline insulin nor HOMA-IR was significantly associated with follow-up BMI (Ps>0.26), BMIz score (Ps>0.22), fat mass (Ps>0.78) or fat mass percentage (Ps>0.71). In all models, baseline BMI (P<0.0001), body fat mass (P<0.0001) and percentage of fat (P<0.001) were strong positive predictors for change in BMI and fat mass. In models restricted to children without obesity at baseline, some but not all models had significant interaction terms between body adiposity and insulinemia/HOMA-IR that suggested less gain in mass among those with greater insulin or IR. The opposite was found in some models restricted to children with obesity at baseline. CONCLUSIONS: In middle childhood, BMI and fat mass, but not insulin or IR, are strong predictors of children's gains in BMI and fat mass during adolescence.

Serum leptin and loss of control eating in children and adolescents.

BACKGROUND: Both insufficiency and resistance to the actions of the adipocyte-derived hormone leptin promote hunger, increased food intake and greater body weight. Some studies suggest that adults reporting binge eating have increased serum leptin compared with those without binge eating, even after adjusting for the greater adiposity that characterizes binge eaters. Pediatric binge or loss of control (LOC) eating are prospective risk factors for excessive weight gain and may predict development of metabolic abnormalities, but whether LOC eating is associated with higher leptin among children is unknown. We therefore examined leptin and LOC eating in a pediatric cohort. METHODS: A convenience sample of 506 lean and obese youth (7-18 years) was recruited from Washington, DC and its suburbs. Serum leptin was collected after an overnight fast. Adiposity was measured by dual-energy X-ray absorptiometry or air displacement plethysmography. LOC eating was assessed by interview methodology. RESULTS: Leptin was strongly associated with fat mass (r=0.79, P<0.001). However, even after adjusting for adiposity and other relevant covariates, youth with LOC eating had higher serum leptin compared with those without LOC episodes (15.42±1.05 vs 12.36±1.04 ng ml(-1), P<0.001). Neither reported amount of food consumed during a recent LOC episode nor number of LOC episodes in the previous month accounted for differences in leptin (P>0.05). The relationship between LOC eating and leptin appeared to be significant for females only (P=0.002). CONCLUSIONS: Reports of LOC eating were associated with higher fasting leptin in youth, beyond the contributions of body weight. Prospective studies are required to elucidate whether LOC eating promotes greater leptin or whether greater leptin resistance may promote LOC eating.

Pharmacotherapy for childhood obesity: present and future prospects.

Pediatric obesity is a serious medical condition associated with significant comorbidities during childhood and adulthood. Lifestyle modifications are essential for treating children with obesity, yet many have insufficient response to improve health with behavioral approaches alone. This review summarizes the relatively sparse data on pharmacotherapy for pediatric obesity and presents information on obesity medications in development. Most previously studied medications demonstrated, at best, modest effects on body weight and obesity-related conditions. It is to be hoped that the future will bring new drugs targeting specific obesity phenotypes that will allow clinicians to use etiology-specific, and therefore more effective, anti-obesity therapies.

Construct validity of the emotional eating scale adapted for children and adolescents.

BACKGROUND: Emotional eating, defined as eating in response to a range of negative emotions, is common in youths. Yet, there are few easily administered and well-validated methods to assess emotional eating in pediatric populations. OBJECTIVE: The current study tested the construct validity of the Emotional Eating Scale (EES) Adapted for Children and Adolescents (EES-C) by examining its relationship to observed emotional eating at laboratory test meals. METHOD: A total of 151 youths (8-18 years) participated in two multi-item lunch buffet meals on separate days. They ate ad libitum after being instructed to 'eat as much as you would at a normal meal' or to 'let yourself go and eat as much as you want'. State negative affect was assessed immediately before each meal. The EES-C was completed 3 months, on average, before the first test meal. RESULTS: Among youths with high EES-C total scores, but not low EES-C scores, higher pre-meal state negative affect was related to greater total energy intake at both meals, with and without the inclusion of age, race, sex and body mass index (BMI) standard deviation as covariates (ps<0.03). DISCUSSION: The EES-C demonstrates good construct validity for children and adolescents' observed energy intake across laboratory test meals designed to capture both normal and disinhibited eating. Future research is required to evaluate the construct validity of the EES-C in the natural environment and the predictive validity of the EES-C longitudinally.

Children's binge eating and development of metabolic syndrome.

BACKGROUND: Binge eating predisposes children to excessive weight gain. However, it is unknown if pediatric binge eating predicts other obesity-associated adverse health outcomes. OBJECTIVE: The objective of this study was to investigate the relationship between binge eating and metabolic syndrome (MetS) in children. METHOD: Children aged 5-12 years at high risk for adult obesity, either because they were overweight/obese when first examined or because their parents were overweight/obese, were recruited from Washington, DC and its suburbs. Children completed a questionnaire assessment of binge eating at baseline and underwent measurements of MetS components at baseline and at a follow-up visit approximately 5 years later. Magnetic resonance imaging was used to measure the visceral adipose tissue (VAT) in a subset. RESULTS: In all, 180 children were studied between July 1996 and August 2010. Baseline self-reported binge eating presence was associated with a 5.33 greater odds of having MetS at follow-up (95% confidence interval (CI): 1.47, 19.27, P=0.01). The association between binge eating and body mass index (BMI) only partially explained changes in MetS components: baseline binge eating predicted higher follow-up triglycerides, even after accounting for baseline triglycerides, baseline BMI, BMI change, sex, race, baseline age and time in study (P = 0.05). Also, adjusting for baseline VAT and demographics, baseline binge eating predicted greater follow-up L(2-3) VAT (P = 0.01). DISCUSSION: Children's reports of binge eating predicted development of MetS, worsening triglycerides and increased VAT. The excessive weight gain associated with children's binge eating partly explained its adverse metabolic health outcomes. Reported binge eating may represent an early behavioral marker upon which to focus interventions for obesity and MetS.

Evaluating the contribution of differences in lean mass compartments for resting energy expenditure in African American and Caucasian American children.

BACKGROUND: Resting energy expenditure (REE), adjusted for total lean mass (LM), is lower in African American (AA) than Caucasian American (CA) children. Some adult studies suggest that AA-CA differences in lean mass compartments explain this REE difference. Similar data are limited in children. OBJECTIVE: To evaluate differences in compartment-specific lean mass between AA and CA children and examine the individual contributions of high-metabolic rate-at-rest trunk lean mass (TrLM) and low-metabolic-rate-at-rest appendicular lean mass (AppLM) for AA-CA differences in REE. METHODS: We studied a convenience sample of 594 AA (n = 281) and CA (n = 313) children. REE was measured by using indirect calorimetry; dual-energy X-ray absorptiometry was used to assess body composition. ANCOVAs were performed to examine AA-CA differences in TrLM, AppLM and REE. After accounting for age, sex, height, pubertal development, bone mass and adiposity, REE was evaluated adjusting for total LM (model A) and separately adjusting for TrLM and AppLM (model B). RESULTS: African American children had greater adjusted AppLM (17.8 ± 0.2 [SE] vs. 16.0 ± 0.2 kg, p < 0.001) and lower TrLM (17.2 ± 0.2 vs. 17.7 ± 0.2 kg, p = 0.022) than CA children. REE adjusted for total LM was 77 ± 16 kcal/d lower in AA than CA (p < 0.001). However, after accounting separately for AppLM and TrLM, the discrepancy in REE between the groups declined to 28 ± 19 kcal/d (p = 0.14). In the adjusted model, both TrLM (p < 0.001) and AppLM (p < 0.027) were independently associated with REE. CONCLUSION: In children, AA-CA differences in REE appear mostly attributable to differences in body composition. Lower REE in AA children is likely due to lower TrLM and greater AppLM.

Relationship of pressure to be thin with gains in body weight and fat mass in adolescents.

BACKGROUND: Sociocultural pressure to be thin is commonly reported by adolescents; yet, to what extent such pressure is associated with weight gain has not been evaluated longitudinally. OBJECTIVE: Examine whether pressure to be thin was positively associated with weight and fat gain in adolescents. METHODS: Participants were 196 healthy adolescent (age 15 ± 1 years old) girls (65%) and boys of varying weights (BMI 25 ± 7 kg/m2 ) studied at baseline and 1-year follow-up. At baseline, adolescents and their mothers reported pressure to be thin by questionnaire. At baseline and follow-up, BMI was calculated, and fat mass was assessed with air displacement plethysmography. Multiple regression was used to examine associations between baseline pressure to be thin and 1-year changes in BMI and fat mass. RESULTS: Accounting for multiple covariates, including baseline BMI or fat, adolescent-reported pressure from parents and peers and mother-reported pressure toward their teen were associated with greater gains in either adolescent BMI or fat (ps < .05). Adolescent weight status was a moderator of multiple effects (ps < .05). CONCLUSIONS: Parental and peer pressure to be thin were associated with increases in BMI and fat mass during adolescence, particularly in heavier adolescents. Further research is necessary to clarify how this association operates reciprocally and to identify underlying explanatory mechanisms.

Pyroglutamyl peptidase-II ("thyroliberinase") activity in human serum: influence of weight and thyroid status.

The tripeptide hormone, TRH, is metabolized by three enzymes, the most specific of which is pyroglutamyl peptide hydrolase-II (also termed thyroliberinase), a metalloenzyme present in serum and brain. Because pyroglutamyl peptidase-II activity in rat serum is regulated by thyroid hormone levels, we tested the hypothesis that this activity is similarly altered in humans. We studied serum pyroglutamyl peptidase-II activity in 6 patients with hyperthyroidism, 18 patients with hypothyroidism, and 31 euthyroid, normal weight volunteers. Because TRH [or its metabolite cyclo(His-Pro)] is believed to be an important hormone regulating appetite and metabolism, we also evaluated pyroglutamyl peptidase-II activity in 27 euthyroid patients with obesity. Serum pyroglutamyl peptidase-II activity was elevated in patients with hypothyroidism (mean +/- SEM, 33.9 +/- 3.7 nmol/mL.h) compared to that in euthyroid, normal weight volunteers (24.5 +/- 2.8 nmol/mL.h; P < 0.05), but not that in patients with hyperthyroidism (28.3 +/- 4.1 nmol/mL.h; P = NS). Euthyroid obese patients had the highest pyroglutamyl peptidase-II activity (43.6 +/- 2.8 nmol/mL.h; P < 0.0001 vs. normal weight volunteers). Pyroglutamyl peptidase-II activity was positively correlated with body mass index (r2 = 0.30; P < 0.0001). After correction for body mass index, there were no difference in pyroglutamyl peptidase-II activity in hypothyroid, hyperthyroid, and euthyroid individuals. We conclude that serum pyroglutamyl peptidase-II activity is regulated by, or regulates, body weight.

Differences in the hypothalamic-pituitary-adrenal axis of black and white women.

Alterations in the activity of the hypothalamic-pituitary-adrenal (HPA) axis have been associated with obesity in humans and animals. To explore possible mechanisms responsible for the higher prevalence of obesity and its associated comorbid conditions in the black population, we studied the HPA axis of 18 black and 30 white weight- and age-matched nonobese and obese women. Waist to hip ratio, 24-h urinary free cortisol excretion, plasma cortisol responses to dexamethasone, and plasma ACTH and cortisol responses to 1 micrograms/kg ovine CRH were determined. There were no racial differences in waist to hip ratio, 24-h urinary free cortisol excretion, dexamethasone suppressibility of plasma cortisol, baseline plasma cortisol and ACTH concentrations, or plasma cortisol response to CRH. However, CRH-stimulated plasma ACTH concentrations, measured in an extraction polyclonal RIA, were significantly greater in blacks than in whites at all time points, beginning 5 min after the administration of CRH [area under the curve (AUC), 2463 +/- 288 pmol/L.min in blacks vs. 1185 +/- 78 in whites; P < 0.001]. These differences persisted when ACTH was measured by a 2-site direct immunoradiometric assay measuring the intact ACTH-(1-39) molecule (AUC, 1292 +/- 177 pmol/L.min in blacks vs. 504 +/- 95 in whites; P < 0.002). There was no significant correlation between body mass index and either cortisol or ACTH AUCs for either race, with blacks showing persistently elevated AUC for ACTH compared to whites, regardless of weight. We conclude that there are differences in the HPA axis of black and white women. How these differences may relate to the increased prevalence of obesity in the black population remains to be determined.

Differences in corticotropin-releasing hormone-stimulated adrenocorticotropin and cortisol before and after weight loss.

Little is known about the effects of intentional weight loss on the function of the hypothalamic-pituitary-adrenal (HPA) axis of obese individuals. We studied the HPA axis of 34 healthy obese women (body mass index, 40.2 +/- 7.9 kg/m2) before and after a 21.0 +/- 7.9-kg weight loss induced by a 26-week weight loss program that included 12 weeks of a 3350 kJ/day (800 Cal/day) liquid formula diet, 6 weeks of gradual refeeding, and 6 weeks of caloric stabilization at 5020-6280 kJ/day (1200-1500 Cal/day). Obese subjects were evaluated twice: before caloric restriction and during the last 3 weeks of caloric stabilization with a 3-h evening 1 microg/kg ovine CRH (oCRH) stimulation test. CRH-stimulated ACTH and cortisol values were compared to those of a control group of 12 normal weight women. Before caloric restriction, both ACTH and cortisol responses to oCRH were similar in obese women and normal weight controls. Weight loss did not significantly alter the ACTH response to oCRH; however, the total plasma cortisol response to oCRH decreased significantly with weight loss (area under the curve, 96,320 +/- 21,040 nmol/L x min before weight loss; 82,450 +/- 22,460 nmol/L x min after weight loss; P < 0.001). Cortisol-binding globulin also decreased significantly after weight loss (2,270 +/- 1,050 nmol/L) compared either to values obtained before weight loss (3,590 +/- 1,360 nmol/L; P < 0.001) or to those of normal weight controls (3,910 +/- 1,400 nmol/L; P < 0.001). Assay for plasma free cortisol, either before or 180 min after oCRH treatment, showed no significant changes in cortisol responses resulting from weight loss. As plasma free cortisol was not altered by weight reduction, the decrease in the total cortisol response to oCRH after weight loss appears to be secondary to significant decreases in cortisol-binding globulin. We conclude that when obese women lose large amounts of weight with a 3350 kJ/day, very low energy diet, such weight reduction does not significantly affect the HPA axis.

Hypothalamic-pituitary-adrenal axis activity during exercise in African American and Caucasian women.

African American women have a greater prevalence of obesity than Caucasian women, but the reasons for this difference are not known. We have investigated whether activity of the hypothalamic-pituitary adrenal axis plays a role in this phenomenon. Previous studies have shown that plasma ACTH immunoreactivity (ACTH-IR) of African American women, measured after ovine CRH (oCRH) stimulation, is significantly greater than ACTH-IR of Caucasian women, but is not accompanied by greater plasma cortisol concentrations. Analysis by high pressure liquid chromatography has demonstrated that after oCRH stimulation, the plasma ACTH-IR of African American women contains many nonintact ACTH fragments not found in Caucasians. To determine whether these racial differences in ACTH-IR secretion are an artifact of exogenous oCRH administration or are also found after a physiological stimulus for ACTH secretion, we measured hormones of the hypothalamic-pituitary adrenal axis before and after a standardized, maximal exercise treadmill test in 16 African American and 19 Caucasian healthy women matched for age, socioeconomic status, and body mass index. The intensity of exercise performed was similar in the two groups, as determined by duration of exercise, perceived intensity of exertion, plasma lactate, maximal heart rate, and maximum oxygen uptake. Basal ACTH-IR measured by RIA or immunoradiometric assay and cortisol were similar in African Americans and Caucasians. Plasma ACTH-IR, measured 10 min after completion of exercise, was significantly greater in African Americans than in Caucasians [by RIA: mean +/- SD ACTH-IR, 47.1 +/- 30.9 vs. 25.4 +/- 16.7 pmol/L (P < 0.01); by immunoradiometric assay: ACTH-IR, 45.9 +/- 43.2 vs. 21.1 +/- 14.6 pmol/L (P < 0.05)]. However, plasma cortisol after exercise was not different (450.2 +/- 157.7 vs. 483.6 +/- 180.4 nmol/L; P = 0.57). We conclude that ACTH-IR is significantly greater in African American than in Caucasian women after intense exercise. The ACTH-IR of African Americans and Caucasians does not appear to be equipotent at adrenal melanocortin-2 receptors, because the greater ACTH-IR of African Americans does not lead to greater cortisol secretion. Whether some components of the ACTH-IR detected in African Americans affect signal transduction of the hypothalamic melanocortin-4 receptors implicated in body weight regulation and thus predispose African American women to weight gain without altering plasma cortisol remains to be determined.

Normal dexamethasone suppression in obese binge and nonbinge eaters with rapid weight loss.

Natural or experimental starvation is frequently associated with hypercortisolism, reflected as incomplete suppression of serum cortisol after dexamethasone. To determine whether rapid weight loss per se or some other aspect of starvation induces disruption of the hypothalamic-pituitary-adrenal (HPA) axis, we evaluated 2 categories of obese women (body mass index > 30 kg/m2) undergoing rapid weight loss: binge eaters (n = 12) and nonbinge eaters (n = 8). We performed psychometric evaluation and 1 mg overnight dexamethasone suppression tests in the obese subjects, as well as in 12 race- and age-matched normal-weight women. The obese women were tested before and after 12 weeks of a 3349 kJ/day (800 kcal/day) liquid formula diet, and lost an average of 19.3 kg, which represented 17.3% of their total body weight. Binge eaters, who were initially more depressed than either nonbinge eaters or normal-weight controls, had a significant amelioration of their symptoms with weight loss. Neither group had evidence of disruption of the HPA axis before or after weight loss. Thus, the rate of failure to suppress cortisol after dexamethasone was approximately 10% in each of the obese and control groups, and did not differ between the pre- and postweight loss condition or between binge eaters and nonbinge eaters. Serum free T4 was unchanged, whereas T3 fell significantly with weight loss. We conclude that weight loss may improve affect in the obese without altering HPA axis activity, and postulate that one of the concomitants of restricted energy intake, perhaps in combination with a threshold body weight, may be of greater importance in causing abnormalities of dexamethasone suppression testing than rapid weight loss per se.

Etiology of the differences in corticotropin-releasing hormone-induced adrenocorticotropin secretion of black and white women.

After i.v. oCRH, plasma immunoreactive ACTH (ACTH-IR) is significantly greater in blacks than in whites; however, there is no corresponding increase in cortisol secretion. To test the hypothesis that there are black-white differences in adrenal responsiveness to ACTH that underlie this phenomenon, weight-, age-, and education-matched black (n = 10) and white (n = 10) women were i.v. infused with 5 differing doses of ACTH1-24 (0, 0.003, 0.01, 0.1, and 1 microgram/kg) with measured plasma cortisol and DHEA. To test the alternative hypothesis that greater post-CRH plasma ACTH-IR in blacks is caused by qualitative differences in circulating ACTH-immunoreactive peptides, we collected pre- and post-CRH plasma from 5 black and 5 white women and measured ACTH-IR after sample fractionation, using high-pressure liquid chromatography. There were no racial differences in adrenal responsiveness to differing doses of ACTH1-24 and no differences in the distribution of the forms of ACTH-IR before CRH. After CRH, whites had predominant ACTH-IR peaks at the retention times of ACTH1-39 and ACTH1-39-sulfoxide, whereas blacks had prominent peaks at several additional retention times. The post-CRH ratio of intact to total ACTH was significantly lower in blacks than in whites (0.27 +/- 0.17 vs. 0.71 +/- 0.17, P < 0.003). We conclude that there are qualitative differences in post-CRH circulating ACTH-IR in blacks and whites, leading to a greater immunoreactive to bioactive ACTH ratio in blacks. Such differences in the circulating forms of ACTH can account for greater CRH-stimulated ACTH-IR in blacks.

Obesity: what mental health professionals need to know.

OBJECTIVE: Obesity is a highly prevalent condition with significant health implications. This report summarizes recent clinically relevant findings concerning the pathogenesis and treatment of obesity and considers their implications for psychiatric diagnosis and management. METHOD: The authors conducted selective reviews of the literature from the last 10 years. Topics included the biological and behavioral factors that contribute to the onset and maintenance of obesity, the relationship between obesity and psychiatric illness and treatment, and the questions of whether and how obesity should be treated. RESULTS: Genetic effects, some mediated by eating behavior, contribute importantly to the potential for obesity, the expression of which is promoted by environmental factors that increase the availability of calorically dense foods and discourage activity. There appear to be behaviorally distinct subsets of obese persons who display particular patterns of disordered eating and elevated rates of psychopathology. Treatment with psychotropic medications may contribute to obesity in ways that are only partly understood. Although successful obesity treatment is associated with clear health benefits and available treatments offer benefit to some, relapse remains the rule. CONCLUSIONS: Although the presence or development of obesity is a daunting problem, it should not be ignored by mental health professionals. Treatment should address not only obesity per se, but also its effects on self-esteem in a hostile cultural climate. Ongoing developments in basic and clinical research are likely to increase the range, efficacy, and acceptability of treatment options in the years ahead.

Association of binge eating disorder and psychiatric comorbidity in obese subjects.

OBJECTIVE: The authors determined the prevalence of binge eating disorder in a self-referred study group of moderately and severely obese subjects and investigated whether binge eating disorder was associated with psychiatric disorders, a history of psychotherapy, a family history of psychiatric illness, or a history of sexual abuse. METHOD: They interviewed 89 obese women and 39 obese men (body mass index > 30 kg/m2) who were not currently in weight loss treatment, using the Binge Eating Disorder Clinical Interview, the Structured Clinical Interview for DSM-III-R, and the Structured Clinical Interview for DSM-III-R Personality Disorders. RESULTS: Forty-three (34%) of the subjects met criteria for binge eating disorder--33 women and 10 men. Black and white subjects had similar rates of binge eating disorder. Subjects with binge eating disorder were significantly more likely than those without the disorder to have a lifetime prevalence of a DSM-III-R axis I or axis II diagnosis and to have undergone psychotherapy or counseling. The lifetime rates of major depression, panic disorder, bulimia nervosa, borderline personality disorder, and avoidant personality disorder were all significantly higher in subjects with binge eating disorder. The rate of reported sexual abuse was not higher among subjects with binge eating disorder; however, they were significantly more likely to have a family history of substance abuse. The relative risks for psychiatric disorders were higher in both moderately and severely obese subjects with binge eating disorder than in those without the disorder. CONCLUSIONS: Among both moderately and severely obese subjects, binge eating disorder is associated with higher rates of axis I and axis II psychiatric disorders.

Report of a National Institutes of Health--Centers for Disease Control and Prevention workshop on the feasibility of conducting a randomized clinical trial to estimate the long-term health effects of intentional weight loss in obese persons.

A workshop was convened in 1997 by the National Institutes of Health and the Centers for Disease Control and Prevention to consider the need for and feasibility of conducting a randomized clinical trial to estimate the long-term health effects of intentional weight loss in obese persons. Although the benefits of weight loss in obese individuals may seem obvious, little information is available showing that intentional weight loss improves long-term health outcomes. Observational studies may be unable to provide convincing answers about the magnitude and direction of the health effects of intentional weight loss. Workshop participants agreed that a well-designed randomized clinical trial could answer several questions necessary for developing a rational clinical and public health policy for treating obesity. Such information will ultimately provide needed guidance on the risks and benefits of weight loss to health care providers and payers, as well as to millions of obese Americans.

Visceral adipose tissue differences in black and white women.

Fat distribution and metabolic variables were studied in 8 black and 10 white age- and weight-matched obese women undergoing a 6-mo weight-reducing regimen. Fat patterning was determined by using anthropometry and computed tomography to quantitate total, subcutaneous, and visceral adipose tissue (VAT) areas at the L2-L3 and L4-L5 levels of the lumbar spine, before, during, and after a modified fast. Black women had smaller depots of VAT than white women at both the L2-L3 (P = 0.004) and L4-L5 (P = 0.054) sites. Differences persisted after an average 17.2-kg weight loss. Although waist-hip ratio was similar in both groups, black women had 23% less VAT than white women (P = 0.007). Black women had significantly lower plasma glucose (P = 0.031) and triglycerides (P = 0.006) with significantly higher plasma high-density-lipoprotein concentrations (P < 0.001). Data from this study suggest that racial differences exist in VAT and metabolic risk factors for obesity-related illness.

Food selection and intake of obese women with binge-eating disorder.

We studied food selection and intake of 19 women [body mass index (in kg/m2) > 30] [corrected], 10 of whom met proposed DSM-IV criteria for binge-eating disorder (BED). All subjects ate two multicourse meals in the laboratory, and were given tape-recorded instructions at each meal either to binge or eat in a normal fashion. Subjects with BED consumed significantly more energy than did subjects without BED at both the binge [12,400 vs 8440 kJ (2963 vs 2017 kcal), P < 0.005] and normal [9810 vs 6870 kJ (2343 vs 1640 kcal), P < 0.02] meals. During the binge meal subjects with BED consumed a greater percentage of energy as fat (38.9% vs 33.5%, P < 0.002) and a lesser percentage as protein (11.4% vs 15.4%, P < 0.01) than did subjects without BED. There were no differences in macronutrient composition of food choices between groups in the normal meal. Obese women who meet criteria for BED show differences in both intake and macronutrient composition of food choices from obese women who do not meet these criteria when asked to eat in a laboratory setting, supporting the validity of this new diagnosis.

Differences in body composition of black and white girls.

Adults have racial differences in body composition that may modulate risks resulting from obesity. Although black and white children have been shown previously to have differences in bone mineral density and subcutaneous body fat, differences in visceral adipose tissue have not been evaluated. We studied 20 black and 20 white normal-weight girls aged 7-10 y, who were matched for weight, body mass index (BMI), bone age, chronological age, Tanner breast stage, and socioeconomic status. Each underwent anthropometric measurements, bioelectrical impedance analysis, dual-energy X-ray absorptiometry (DXA), and abdominal magnetic resonance imaging (MRI) for determination of total (TAT), visceral (VAT), and subcutaneous (SAT) adipose tissue. Serum lipids and fasting and 2-h oral-glucose-tolerance test (OGTT) glucose and insulin concentrations were also measured. There were no differences between groups in absolute waist circumference or waist-to-hip ratio, but waist-to-thigh ratio was smaller in black than in white girls. Black girls had greater bone mineral density and less TAT, VAT, and SAT than whites. VAT was not significantly correlated with any measure of insulin, or with serum lipids. However, both basal and 2-h OGTT serum insulin were significantly correlated with SAT as assessed by MRI in black girls (r2 = 0.46 for basal insulin, P = 0.001: r2 = 0.31 for 2-h insulin, P = 0.01) but not in white girls (r2 < 0.05, for basal and 2-h insulin, NS). We conclude that there are significant racial differences in body composition and differences in the strength of association between abdominal adipose tissue depots and insulin sensitivity in black and white girls.

Telephone triage by primary care physicians.

To determine if experienced primary care physicians are more likely to reach correct decisions on the telephone than their less experienced colleagues, we asked 31 first-year and 29 third-year residents, 21 faculty, and 36 private practitioners in pediatrics and family practice to evaluate three pediatric patients via a telephone interview with a simulated mother and to decide whether each patient needed to be seen that evening. Compared with first-year residents, the third-year residents, faculty and private practitioners decided less frequently to see children who were not severely ill (P less than .05) or injured (P less than .01); however, less than half obtained histories considered adequate to rule out potential serious illnesses. Faculty did better than either residents or private practitioners in managing a severely dehydrated child; 100% of the faculty, but less than 60% of the residents or private practitioners, chose to see the patient promptly (P less than .001). More than one third of all residents and private practitioners reached inappropriate management decisions despite obtaining information that should have altered their decisions. In these simulations, experience in private practice was not associated with improved telephone management of very sick children. Faculty physicians appeared to be better able to identify severely ill children without inappropriately evaluating those who were less ill. In all three simulations, attainment of the correct decision appeared to be determined not by the number or type of questions asked, but rather by the physician's interpretation of the information collected.