Work stress, obesity and the risk of type 2 diabetes: gender-specific bidirectional effect in the Whitehall II study

Psychosocial work stress has been linked to higher risk of type 2 diabetes (T2DM), with the effect being consistently higher among women than men. Also, work stress has been linked to prospective weight gain among obese men but weight loss among lean men. Here, we aimed to examine the interaction between work stress and obesity in relation to T2DM risk in a gender‐specific manner. We studied 5,568 white middle‐aged men and women in the Whitehall II study, who were free from diabetes at analysis baseline (1993). After 1993, diabetes was ascertained at six consecutive phases by an oral glucose tolerance test supplemented by self‐reports. Cox regression analysis was used to assess the association between job strain (high job demands/low job control) and 18‐year incident T2DM stratifying by BMI (BMI <30 kg/m² vs. BMI ≥30 kg/m²). Overall, work stress was associated with incident T2DM among women (hazard ratio (HR) 1.41: 95% confidence intervals: 1.02; 1.95) but not among men (HR 0.87: 95% confidence interval 0.69; 1.11) (P_INTERACTION = 0.017). Among men, work stress was associated with a lower risk of T2DM in nonobese (HR 0.70: 0.53; 0.93) but not in obese individuals (P_INTERACTION = 0.17). Among women, work stress was associated with higher risk of T2DM in the obese (HR 2.01: 1.06; 3.92) but not in the nonobese (P_INTERACTION = 0.005). Gender and body weight status play a critical role in determining the direction of the association between psychosocial stress and T2DM. The potential effect‐modifying role of gender and obesity should not be ignored by future studies looking at stress‐disease associations.     

Serum Leptin Concentrations and Weight Gain in Postobese,Postmenopausal Women

Objective : This study was designed to determine if serum leptin concentrations (adjusted for fat mass) after weight loss on a low-calorie diet predict subsequent weight gain. Research Methods and Procedures : Body composition and serum leptin concentrations were determined on 14 moderately obese, postmenopausal, nondiabetic women with a familial predisposition to obesity. Assessments were obtained under tightly controlled metabolic ward conditions of macronutrient intake and weight maintenance both before (obese state) and after a mean weight loss of 12.0 kg to normal body weight (postobese state). Four years later, without intervention, body weight and body composition were reassessed. Results : Weight loss resulted in significant decreases in fat mass (29.7 ± 5.4 vs. 20.3 ± 4.7; kg), body mass index (27.7 ± 1.6 vs. 23.0 ± 1.5; kg/m2), percent body fat (40.7 ± 4.3 vs. 33.1 ± 5.0), and serum leptin concentrations (31.8 ± 16.0 vs. 11.5 ± 5.4; ng/mL). Serum leptin concentrations were positively correlated (p<<0.05) with fat mass in both the obese and postobese states (r = 0.67 and r = 0.56, respectively). However, residual serum leptin concentrations (adjusted for fat mass) in the obese and postobese states were not related to changes in body weight (p<= 0.61 and 0.52), fat mass (p = 0.72 and 0.42), body mass index (p = 0.59 and 0.33), or percent body fat (p = 0.84 and 0.46) over the follow-up period. Discussion : These finding do not support the hypothesis that relatively low concentrations of leptin predict weight regain after weight loss. However, because the number of subjects in this study was limited, further studies are warranted.     

Adult obesity does not predict 6-year weight gain in men: the Aerobics Center Longitudinal Study

Objective: To determine the longitudinal relation between history of adult obesity and the 6‐year trajectory of weight change in men. Research Methods and Procedures: Subjects were healthy, affluent men (n = 761) between the ages of 20 and 78 years who completed at least four comprehensive medical exams at the Cooper Clinic between 1987 and 2003. Maximum adult weight was reported, and current height was measured at baseline. Body weight and cardiorespiratory fitness were measured at all examinations. Adult obesity status was determined from self‐reported maximum weight and measured height at baseline as BMI ≥ 30 kg/m². Weight at all examinations was regressed on a history of adult obesity using linear mixed effects modeling. Results: At baseline, men reporting a history of adult obesity were significantly heavier than men reporting no such history (BMI 29.8 vs. 25.0 kg/m²; p < 0.05). However, the rate of weight gain among men with a history of obesity was slower than among men without a history of adult obesity (0.04 vs. 0.18 kg/yr; p = 0.09), although this difference was only marginally significant. Fitness modulated the relationship between history of obesity and weight change over time, and both higher levels of fitness and greater frequency of dieting were associated with attenuated weight gain. In contrast, chronic disease and depression were associated with accelerated weight gain. Discussion: Although a history of obesity was associated with higher weight, it did not seem to result in accelerated weight gain over time. Additionally, dieting and fitness were important for minimizing weight gain.     

Rapid Postnatal Weight Gain and Visceral Adiposity in Adulthood: The Fels Longitudinal Study

Rapid infant weight gain is associated with increased abdominal adiposity, but there is no published report of the relationship of early infant growth to differences in specific adipose tissue depots in the abdomen, including visceral adipose tissue (VAT). In this study, we tested the associations of birth weight, infant weight gain, and other early life traits with VAT, abdominal subcutaneous adipose tissue (ASAT), and other body composition measures using magnetic resonance imaging (MRI) and dual‐energy X‐ray absorptiometry in middle adulthood (mean age = 46.5 years). The sample included 233 appropriate for gestational age singleton white children (114 males) enrolled in the Fels Longitudinal Study. Multivariate‐adjusted general linear models were used to test the association of infant weight gain (from 0 to 2 years), maternal BMI, gestational age, parity, maternal age, and other covariates with adulthood body composition. Compared to infants with slow weight gain, rapid weight gain was associated with elevated risk of obesity (adjusted odds ratio = 4.1, 95% confidence interval = 1.4, 11.1), higher total body fat (+7 kg, P = 0.0002), percent body fat (+5%, P = 0.0006), logVAT mass (+0.43 kg, P = 0.02), logASAT mass (+0.47 kg, P = 0.001), and percent abdominal fat (+5%, P = 0.03). There was no evidence that the increased abdominal adipose tissue was due to a preferential deposition of VAT. In conclusion, rapid infant weight gain is associated with increases in both VAT and ASAT, as well as total adiposity and the risk of obesity in middle adulthood.     

The Influence of Familial Predisposition to Cardiovascular Complications upon Childhood Obesity Treatment

Introduction

The aim was to investigate whether a familial predisposition to obesity related cardiovascular complications was associated with the degree of obesity at baseline and/or changes in the degree of obesity during a multidisciplinary childhood obesity treatment program.

Methods

The study included 1421 obese children (634 boys) with a median age of 11.5 years (range 3.1–17.9 years), enrolled in treatment for 0.04 to 5.90 years (median 1.3 years) at the Children''s Obesity Clinic, Denmark. At baseline, weight and height were measured, body mass index (BMI) standard deviation score (SDS) calculated, and self-reported information on familial predisposition to obesity, hypertension, type 2 diabetes mellitus (T2DM), thromboembolic events, and dyslipidaemia were obtained. A familial predisposition included events in biological parents, siblings, grandparents, uncles, and aunts. The treatment outcomes were categorically analysed according to the prevalence of familial predispositions.

Results

The median BMI SDS at enrolment was 3.2 in boys and 2.8 in girls. One-thousand-and-forty-one children had obesity in their family, 773 had hypertension, 551 had T2DM, 568 had thromboembolic events, and 583 had dyslipidaemia. Altogether, 733 had three or more predispositions. At baseline, familial T2DM was associated with a higher mean BMI SDS (p = 0.03), but no associations were found between the other predispositions and the children''s degree of obesity. During treatment, girls with familial obesity lost more weight, compared to girls without familial obesity (p = 0.04). No other familial predispositions were associated with changes in BMI SDS during treatment.

Conclusion

Obese children with a familial predisposition to T2DM showed a significantly higher degree of obesity at baseline and girls with familial obesity responded better to treatment. Besides these findings, no other associations were found between the occurrence of familial predispositions and the degree of obesity or changes herein during multidisciplinary childhood obesity treatment.     

Diet‐Induced Changes in Stearoyl‐CoA Desaturase 1 Expression in Obesity‐Prone and ‐Resistant Mice

Objective: To investigate stearoyl‐coenzyme A desaturase (SCD) 1 expression in obesity‐prone C57BL/6 mice and in obesity‐resistant FVB mice to explore the relationship of SCD1 expression and susceptibility to diet‐induced obesity. Research Methods and Procedures: Nine‐week‐old C57BL/6 and FVB mice were fed either a high‐ or low‐fat diet for 8 weeks. Body weight and body composition were measured before and at weeks 4 and 8 of the study. Energy expenditure was measured at weeks 1 and 5 of the study. Hepatic SCD1 mRNA was measured at 72 hours and at the end of study. Plasma leptin and insulin concentrations were measured at the end of study. Results: When C57BL/6 mice were switched to a calorie‐dense high‐fat diet, animals gained significantly more body weight than those maintained on a low‐calorie density diet primarily due to increased fat mass accretion. Fat mass continued to accrue throughout 8 weeks of study. Increased calorie intake did not account for all weight gain. On the high‐fat diet, C57BL/6 mice decreased their energy expenditure when compared with mice fed a low‐fat diet. In response to 8 weeks of a high‐fat diet, SCD1 gene expression in liver increased >2‐fold. In contrast, feeding a high‐fat diet did not change body weight, energy expenditure, or SCD1 expression in FVB mice. Discussion: Our study showed that a high‐fat hypercaloric diet increased body adiposity first by producing hyperphagia and then by decreasing energy expenditure of mice susceptible to diet‐induced obesity. Consumption of a high‐fat diet in species predisposed to obesity selectively increased SCD1 gene expression in liver.     

Genetic associations with temporal shifts in obesity and severe obesity during the obesity epidemic in Norway: A longitudinal population-based cohort (the HUNT Study)

BackgroundObesity has tripled worldwide since 1975 as environments are becoming more obesogenic. Our study investigates how changes in population weight and obesity over time are associated with genetic predisposition in the context of an obesogenic environment over 6 decades and examines the robustness of the findings using sibling design.Methods and findingsA total of 67,110 individuals aged 13–80 years in the Nord-Trøndelag region of Norway participated with repeated standardized body mass index (BMI) measurements from 1966 to 2019 and were genotyped in a longitudinal population-based health study, the Trøndelag Health Study (the HUNT Study). Genotyping required survival to and participation in the HUNT Study in the 1990s or 2000s. Linear mixed models with observations nested within individuals were used to model the association between a genome-wide polygenic score (GPS) for BMI and BMI, while generalized estimating equations were used for obesity (BMI ≥ 30 kg/m²) and severe obesity (BMI ≥ 35 kg/m²).The increase in the average BMI and prevalence of obesity was steeper among the genetically predisposed. Among 35-year-old men, the prevalence of obesity for the least predisposed tenth increased from 0.9% (95% confidence interval [CI] 0.6% to 1.2%) to 6.5% (95% CI 5.0% to 8.0%), while the most predisposed tenth increased from 14.2% (95% CI 12.6% to 15.7%) to 39.6% (95% CI 36.1% to 43.0%). Equivalently for women of the same age, the prevalence of obesity for the least predisposed tenth increased from 1.1% (95% CI 0.7% to1.5%) to 7.6% (95% CI 6.0% to 9.2%), while the most predisposed tenth increased from 15.4% (95% CI 13.7% to 17.2%) to 42.0% (95% CI 38.7% to 45.4%). Thus, for 35-year-old men and women, respectively, the absolute change in the prevalence of obesity from 1966 to 2019 was 19.8 percentage points (95% CI 16.2 to 23.5, p < 0.0001) and 20.0 percentage points (95% CI 16.4 to 23.7, p < 0.0001) greater for the most predisposed tenth compared with the least predisposed tenth, defined using the GPS for BMI. The corresponding absolute changes in the prevalence of severe obesity for men and women, respectively, were 8.5 percentage points (95% CI 6.3 to 10.7, p < 0.0001) and 12.6 percentage points (95% CI 9.6 to 15.6, p < 0.0001) greater for the most predisposed tenth. The greater increase in BMI in genetically predisposed individuals over time was apparent after adjustment for family-level confounding using a sibling design. Key limitations include a slightly lower survival to date of genetic testing for the older cohorts and that we apply a contemporary genetic score to past time periods. Future research should validate our findings using a polygenic risk score constructed from historical data.ConclusionsIn the context of increasingly obesogenic changes in our environment over 6 decades, our findings reveal a growing inequality in the risk for obesity and severe obesity across GPS tenths. Our results suggest that while obesity is a partially heritable trait, it is still modifiable by environmental factors. While it may be possible to identify those most susceptible to environmental change, who thus have the most to gain from preventive measures, efforts to reverse the obesogenic environment will benefit the whole population and help resolve the obesity epidemic.

In a longitudinal population-based cohort study in Norway, Maria Brandkvist and colleagues investigate how genetic predisposition relates to changes in BMI and obesity over the past six decades.     

A Low Sympathoadrenal Activity is Associated with Body Weight Gain and Development of Central Adiposity in Pima Indian Men

TATARANNI P ANTONIO JAMES B YOUNG, CLIFTON BOGARDUS, ERIC RAVUSSIN. A low sympathoadrenal activity is associated with body weight gain and development of central adiposity in Pima Indian men. To investigate the possible role of impaired sympathetic nervous system and/or adrenal medullary function in the etiology of human obesity, we studied 64 Pima Indian men (28 ± 6 years, 101 ± 25 kg, 34 ± 9% body fat, mean ± SD) in whom sympathoadrenal function was estimated at baseline by measurements of 24-hour urinary norepinephrine (NE) and epinephrine (Epi) excretion rates under weight-maintenance conditions. Body weight, body composition (hydrodensitometry), and body fat distribution (waist-to-thigh circumference ratio, W/T) were measured at baseline and follow-up. Follow-up data were available on 44 subjects who gained on average 8.4 ± 9.5 kg over 3.3 ± 2.1 years. In these subjects, baseline NE excretion rate, adjusted for its determinants (i.e., fat free mass, fat mass, and W/T), correlated negatively with bodyweight gain (r=?0.38; p=0.009). Baseline Epi excretion rate correlated negatively with changes in W/T (r=?0.44; p=0.003). In conclusion, our data show for the first time that a low sympathetic nervous system activity is associated with body weight gain in humans. Also, a low activity of the adrenal medulla is associated with the development of central adiposity.     

Familial Risk of Overweight and Obesity in the Canadian Population using the WHO/NIH Criteria

Objective: To determine the familial risk of overweight and obesity in Canada. Research Methods and Procedures: The sample was comprised of 15,245 participants from 6377 families of the Canada Fitness Survey. The risk of overweight and obesity among spouses and first‐degree relatives of individuals classified as underweight, normal weight, pre‐obese, or obese (Class I and II) according to the WHO/NIH guidelines for body mass index (BMI) was determined using standardized risk ratios. Results: Spouses and first‐degree relatives of underweight individuals have a lower risk of overweight and obesity than the general population. On the other hand, the risk of Class I and Class II obesity (BMI 35 to 39.9 kg/m²) in relatives of Class I obese (BMI 30 to 34.9 kg/m²) individuals was 1.84 (95% CI: 1.27, 2.37) and 1.97 (95% CI: 0.67, 3.25), respectively, in spouses, and 1.44 (95% CI:1.10, 1.78) and 2.05 (95% CI: 1.37, 2.73), respectively in first‐degree relatives. Further, the risk of Class II obesity in spouses and first‐degree relatives of Class II obese individuals was 2.59 (95% CI: ?0.91, 6.09) and 7.07 (95% CI: 1.48, 12.66) times the general population risk, respectively. Discussion: There is significant familial risk of overweight and obesity in the Canadian population using the BMI as an indicator. Comparison of risks among spouses and first‐degree relatives suggests that genetic factors may play a role in obesity at more extreme levels (Class II obese) more so than in moderate obesity.     

Teasing History,Onset of Obesity,Current Eating Disorder Psychopathology,Body Dissatisfaction,and Psychological Functioning in Binge Eating Disorder

Objective: The primary goal of this study was to examine associations among teasing history, onset of obesity, current eating disorder psychopathology, body dissatisfaction, and psychological functioning in women with Binge Eating Disorder (BED). Research Methods and Procedures: Subjects were 115 female adults who met DSM‐IV criteria for BED. Measurements assessing teasing history (general appearance [GAT] and weight and size [WST] teasing), current eating disorder psychopathology (binge frequency, eating restraint, and concerns regarding eating, shape, and weight), body dissatisfaction, and psychological functioning (depression and self‐esteem) were obtained. Results: History of GAT, but not WST, was associated with current weight concerns and body dissatisfaction, whereas both GAT and WST were significantly associated with current psychological functioning. Patients with earlier onset of obesity reported more WST than patients with later onset of obesity, but the groups did not differ significantly in GAT, current eating disorder psychopathology, body dissatisfaction, or psychological functioning. Obese women reported more WST than non‐obese women, but no differences in GAT or the other outcome variables were observed. Higher frequency of GAT was associated with greater binge frequency in obese women, and with greater eating restraint in non‐obese women. Discussion: Although physical appearance teasing history is not associated with variability in most eating disorder psychopathology, it is associated with related functioning, most notably body dissatisfaction, depression, and self‐esteem. Our findings also suggest that the age of onset of obesity and current body mass index status in isolation are not associated with eating psychopathology or associated psychological functioning in adult patients with BED.     

S 23521 Decreases Food Intake and Body Weight Gain in Diet‐Induced Obese Rats

Objective: To investigate the effect of S 23521, a new glucagon‐like peptide‐1‐(7‐36) amide analogue, on food intake and body weight gain in obese rats, as well as on gene expression of several proteins involved in energy homeostasis. Research Methods and Procedures: Lean and diet‐induced obese rats were treated with either S 23521 or vehicle. S 23521 was given either intraperitoneally (10 or 100 μg/kg) or subcutaneously (100 μg/kg) for 14 and 20 days, respectively. Because the low‐dose treatment did not affect food intake and body weight, the subcutaneous treatment at high dose was selected to test the effect on selected end‐points. Results: Treated obese rats significantly decreased their cumulative energy intake in relation to vehicle‐treated counterparts (3401 ± 65 vs. 3898 ± 72 kcal/kg per 20 days; p < 0.05). Moreover, their body weight gain was reduced by 110%, adiposity was reduced by 20%, and plasma triglyceride levels were reduced by 38%. The treatment also improved glucose tolerance and insulin sensitivity of obese rats. Regarding gene expression, no changes in uncoupling protein‐1, uncoupling protein‐3, leptin, resistin, and peroxisome proliferator‐activated receptor (PPAR)‐γ were observed. Discussion: S 23521 is an effective glucagon‐like peptide‐1‐(7‐36) amide analogue, which induced a decrease in energy intake, body weight, and adiposity in a rat model of diet‐induced obesity. In addition, the treatment also improved glucose tolerance and insulin sensitivity of obese rats. These results strongly support S 23521 as a putative molecule for the treatment of obesity.     

Body Image Partially Mediates the Relationship between Obesity and Psychological Distress

Objective: Body image is considered as a potential mediator of the relationship between obesity and psychological distress. Research Methods and Procedures: One hundred ten men and women in a residential weight control facility completed the Multidimensional Body Self-Relations Questionnaire, the Beck Depression Inventory, the Rosenberg Self-Esteem Scale, and the Binge Eating Scale. Results: For both men and women, body-image satisfaction partially mediated the relationship between degree of overweight and depression/self-esteem. Discussion: Sociodemographic factors that may influence the relationships among weight, body image, and depression/self-esteem are discussed.     

Do Energy Density and Dietary Fiber Influence Subsequent 5‐Year Weight Changes in Adult Men and Women?

Objective: We examined whether associations between dietary components and, in particular, energy density (ED) predicted subsequent 5‐year weight changes. Research Methods and Procedures: The present longitudinal population study was part of the Danish World Health Organization Multinational Monitoring of Trends and Determinants in Cardiovascular Disease (MONICA) and the 1936 cohort dietary studies. Effects of components were studied in relation to subsequent 5‐year weight changes in 862 men and 900 women, 30 to 60 years old. Linear multiple regression analyses were conducted. Results: Mean 5‐year changes in body weight (BW) were 1.2 ± 3.9 and 1.3 ± 4.6 kg for men and women, respectively. In general, neither ED nor any of the dietary components was associated with subsequent change in BW. In women, ED was positively associated with weight gain among the obese (BMI > 30 kg/m²) and inversely associated with weight gain in normal‐weight women (BMI < 25 kg/m²) (p = 0.01). However, in men there was a non‐ significant inverse trend between ED and weight gain in the obese and no significant interaction. Discussion: To our knowledge, this is the first prospective study to examine the associations between ED and subsequent changes in BW, and despite a general belief that ED is a major determinant of obesity, the present study did not generally lend support for an association. However, among certain subgroups, an energy‐dense diet may be a risk factor for weight development.     

Parental obesity moderates the relationship between childhood appetitive traits and weight

Objective:

In this study, the independent and combined associations between childhood appetitive traits and parental obesity on weight gain from 0 to 24 months and body mass index (BMI) z‐score at 24 months in a diverse community‐based sample of dual parent families (n = 213) were examined.

Design and Methods:

Participants were mothers who had recently completed a randomized trial of weight loss for overweight/obese postpartum women. As measures of childhood appetitive traits, mothers completed subscales of the Children's Eating Behavior Questionnaire, including Desire to Drink (DD), Enjoyment of Food (EF), and Satiety Responsiveness (SR), and a 24‐h dietary recall for their child. Heights and weights were measured for all children and mothers and self‐reported for mothers' partners. The relationship between children's appetitive traits and parental obesity on toddler weight gain and BMI z‐score were evaluated using multivariate linear regression models, controlling for a number of potential confounders.

Results:

Having two obese parents was related to greater weight gain from birth to 24 months independent of childhood appetitive traits, and although significant associations were found between appetitive traits (DD and SR) and child BMI z‐score at 24 months, these associations were observed only among children who had two obese parents. When both parents were obese, increasing DD and decreasing SR were associated with a higher BMI z‐score.

Conclusions:

The results highlight the importance of considering familial risk factors when examining the relationship between childhood appetitive traits on childhood obesity.     

Beverage consumption patterns of children born at different risk of obesity

Background: Increased intake of sugar‐sweetened beverages and fruit juice has been associated with overweight in children. Objective: This study prospectively assessed beverage consumption patterns and their relationship with weight status in a cohort of children born at different risk for obesity. Methods and Procedures: Participants were children born at low risk (n = 27) or high risk (n = 22) for obesity based on maternal prepregnancy BMI (kg/m²). Daily beverage consumption was generated from 3‐day food records from children aged 3–6 years and coded into seven beverage categories (milk, fruit juice, fruit drinks, caloric and noncaloric soda, soft drinks including and excluding fruit juice). Child anthropometric measures were assessed yearly. Results: High‐risk children consumed a greater percentage of daily calories from beverages at age 3, more fruit juice at ages 3 and 4, more soft drinks (including fruit juice) at ages 3–5, and more soda at age 6 compared to low‐risk children. Longitudinal analyses showed that a greater 3‐year increase in soda intake was associated with an increased change in waist circumference, whereas a greater increase in milk intake was associated with a reduced change in waist circumference. There was no significant association between change in intake from any of the beverage categories and change in BMI z‐score across analyses. Discussion: Children's familial predisposition to obesity may differentially affect their beverage consumption patterns. Future research should examine the extent to which dietary factors may play a role in pediatric body fat deposition over time.     

Hormonal and metabolic effects of olanzapine and clozapine related to body weight in rodents

Objective: To characterize a model of atypical antipsychotic drug‐induced obesity and evaluate its mechanism. Research Methods and Procedures: Chronically, olanzapine or clozapine was self‐administered via cookie dough to rodents (Sprague‐Dawley or Wistar rats; C57Bl/6J or A/J mice). Chronic studies measured food intake, body weight, adiponectin, active ghrelin, leptin, insulin, tissue wet weights, glucose, clinical chemistry endpoints, and brain dopaminergic D2 receptor density. Acute studies examined food intake, ghrelin, leptin, and glucose tolerance. Results: Olanzapine (1 to 8 mg/kg), but not clozapine, increased body weight in female rats only. Weight changes were detectable within 2 to 3 days and were associated with hyperphagia starting ～24 hours after the first dose. Chronic administration (12 to 29 days) led to adiposity, hyperleptinemia, and mild insulin resistance; no lipid abnormalities or changes in D2 receptor density were observed. Topiramate, which has reversed weight gain from atypical antipsychotics in humans, attenuated weight gain in rats. Acutely, olanzapine, but not clozapine, lowered plasma glucose and leptin. Increases in glucose, insulin, and leptin following a glucose challenge were also blunted. Discussion: A model of olanzapine‐induced obesity was characterized which shares characteristics of patients with atypical antipsychotic drug‐induced obesity; these characteristics include hyperphagia, hyperleptinemia, insulin resistance, and weight gain attenuation by topiramate. This model may be a useful and inexpensive model of uncomplicated obesity amenable to rapid screening of weight loss drugs. Olanzapine‐induced weight gain may be secondary to hyperphagia associated with acute lowering of plasma glucose and leptin, as well as the inability to increase plasma glucose and leptin following a glucose challenge.     

Fat Intake Affects Adiposity,Comorbidity Factors,and Energy Metabolism of Sprague‐Dawley Rats

Objective: Childhood obesity is an emerging health problem. This study assesses the effects of three levels of dietary fat (10%, 32%, and 45% measured by kilocalories) on weight gain, body composition, energy metabolism, and comorbidity factors in rats from weaning through maturation. Research Methods and Procedures: The role of dietary fat on the susceptibility to obesity was assessed by feeding diets containing three levels of dietary fat to rats from weaning through 7 months of age. Body composition was analyzed by DXA after 6 and 12 weeks of dietary treatment. Energy metabolism was measured by indirect calorimetry. Results: Energy intake, weight gain, fat mass, and plasma glucose, cholesterol, triglyceride, free fatty acid, leptin, and insulin levels increased dose‐dependently with increased dietary fat. No difference in absolute lean mass among the three groups was observed. Therefore, the differences in weight gain are accounted for primarily by increased fat accretion. Compared with rats that were relatively resistant to obesity when on a 45% fat diet, diet‐induced obesity‐prone rats were in positive energy balance and had an elevated respiratory quotient, indicating a switch in energy substrate use from fat to carbohydrate, which promotes body‐fat accretion. Discussion: Our data support the hypothesis that administration of increasing amount of dietary fat to very young rats enhances susceptibility to diet‐induced obesity and its comorbidities.     

Dietary patterns and changes in body weight in women

Objective: Our objective was to examine the association between adherence to dietary patterns and weight change in women. Research Methods and Procedures: Women (51,670, 26 to 46 years old) in the Nurses’ Health Study II were followed from 1991 to 1999. Dietary intake and body weight were ascertained in 1991, 1995, and 1999. A Western pattern, characterized by high intakes of red and processed meats, refined grains, sweets and desserts, and potatoes, and a prudent pattern, characterized by high intakes of fruits, vegetables, whole grains, fish, poultry, and salad dressing, were identified with principal component analysis, and associations between patterns and change in body weight were estimated. Results: Women who increased their Western pattern score had greater weight gain (multivariate adjusted means, 4.55 kg for 1991 to 1995 and 2.86 kg for 1995 to 1999) than women who decreased their Western pattern score (2.70 and 1.37 kg for the two time periods), adjusting for baseline lifestyle and dietary confounders and changes in confounders over time (p < 0.001 for both time periods). Furthermore, among women who increased their prudent pattern score, weight gain was smaller (multivariate‐adjusted means, 1.93 kg for 1991 to 1995 and 0.66 kg for 1995 to 1999) than among women who decreased their prudent pattern score (4.83 and 3.35 kg for the two time periods) (p < 0.001). The largest weight gain between 1991 and 1995 and between 1995 and 1999 was observed among women who decreased their prudent pattern score while increasing their Western pattern score (multivariate adjusted means, 6.80 and 4.99 kg), whereas it was smallest for the opposite change in patterns (0.87 and ?0.64 kg) (p < 0.001). Discussion: Adoption of a Western dietary pattern is associated with larger weight gain in women, whereas a prudent dietary pattern may facilitate weight maintenance.     

First nationwide survey of prevalence of overweight, underweight, and abdominal obesity in Iranian adults

Objective: The goal was to estimate the prevalence of overweight, obesity, underweight, and abdominal obesity among the adult population of Iran. Research Methods and Procedures: A nationwide cross‐sectional survey was conducted from December 2004 to February 2005. The selection was conducted by stratified probability cluster sampling through household family members in Iran. Weight, height, and waist circumference (WC) of 89,404 men and women 15 to 65 years of age (mean, 39.2 years) were measured. The criteria for underweight, normal‐weight, overweight, and Class I, II, and III obesity were BMI <18.5, 18.5 to 24.9, 25 to 29.9, 30 to 34.9, 35 to 39.9, and ≥40 (kg/m²), respectively. Abdominal obesity was defined as WC ≥102 cm in men and ≥88 cm in women. Results: The age‐adjusted means for BMI and WC were 24.6 kg/m² in men and 26.5 kg/m² in women and 86.6 cm in men and 89.6 cm in women, respectively. The age‐adjusted prevalence of overweight or obesity (BMI ≥25) was 42.8% in men and 57.0% in women; 11.1% of men and 25.2% of women were obese (BMI ≥30), while 6.3% of men and 5.2% of women were underweight. Age, low physical activity, low educational attainment, marriage, and residence in urban areas were strongly associated with obesity. Abdominal obesity was more common among women than men (54.5% vs. 12.9%) and greater with older age. Discussion: Excess body weight appears to be common in Iran. More women than men present with overweight and abdominal obesity. Prevention and treatment strategies are urgently needed to address the health burden of obesity.     

High allelic burden of four obesity SNPs is associated with poorer weight loss outcomes following gastric bypass surgery

Genome‐wide association and linkage studies have identified multiple susceptibility loci for obesity. We hypothesized that such loci may affect weight loss outcomes following dietary or surgical weight loss interventions. A total of 1,001 white individuals with extreme obesity (BMI >35 kg/m²) who underwent a preoperative diet/behavioral weight loss intervention and Roux‐en‐Y gastric bypass surgery were genotyped for single‐nucleotide polymorphisms (SNPs) in or near the fat mass and obesity‐associated (FTO), insulin induced gene 2 (INSIG2), melanocortin 4 receptor (MC4R), and proprotein convertase subtilisin/kexin type 1 (PCSK1) obesity genes. Association analysis was performed using recessive and additive models with pre‐ and postoperative weight loss data. An increasing number of obesity SNP alleles or homozygous SNP genotypes was associated with increased BMI (P < 0.0006) and excess body weight (P < 0.0004). No association between the amounts of weight lost from a short‐term dietary intervention and any individual obesity SNP or cumulative number of obesity SNP alleles or homozygous SNP genotypes was observed. Linear mixed regression analysis revealed significant differences in postoperative weight loss trajectories across groups with low, intermediate, and high numbers of obesity SNP alleles or numbers of homozygous SNP genotypes (P < 0.0001). Initial BMI interacted with genotype to influence weight loss with initial BMI <50 kg/m², with evidence of a dosage effect, which was not present in individuals with initial BMI ≥50 kg/m². Differences in metabolic rate, binge eating behavior, and other clinical parameters were not associated with genotype. These data suggest that response to a surgical weight loss intervention is influenced by genetic susceptibility and BMI.