HLA associations with obesity

A subgroup of 351 subjects with human leukocyte antigen (HLA) typing were available from the Framingham Heart Study for analyses to identify associations with obesity. The subjects consisted of 143 males and 208 females aged 58-88 years at the 15th biennial examination in 1978. The obese classification was based on maximum body mass index (BMI) over the 16 available biennial examinations of the Framingham Heart Study. The subjects were classified as obese if they exceeded the 95th percentile of BMI for 20- to 29-year-old subjects as described in the NHANES II study; males were obese if BMI greater than 31.1 and females were obese if BMI greater than 32.3. There were 27 obese males (18.9%) and 44 obese females (21.2%) in the sample. Gene frequencies were compared between the nonobese and obese groups for the pooled sample as well as by sex. Among alleles previously shown to be related to obesity, HLA Bw35 appeared to be more frequent in obese females but these data did not confirm a difference for the B18 or Cw4 alleles. More importantly, HLA Aw30 was found to be significantly higher among the obese subjects in both males and females. Further analyses adjusting for potential confounding variables reduced the estimated relative risk for obesity for subjects with the Bw35 allele to approximately 1.30 and no longer significant for this sample size. In contrast, the relative risk for Aw30, while reduced, remained significant after adjustment for confounding variables. Based on these data, individuals with the Aw30 allele have a relative risk of 2.61 for obesity.(ABSTRACT TRUNCATED AT 250 WORDS)     

Youth BMI Trajectories: Evidence From the NLSY97

We examined heterogeneity in BMI trajectory classes among youth and variables that may be associated with trajectory class membership. We used data from seven rounds (1997–2003) of the 1997 National Longitudinal Survey of Youth (NLSY97), a nationally representative, longitudinal survey of people born between 1980 and 1984 who were living in the United States in 1997. The analyses were based on an accelerated longitudinal design. General growth mixture modeling implemented in Mplus (version 4.1) was used to identify subtypes of youth BMI growth trajectories over time. Four distinct youth BMI trajectories were identified. Class 1 includes youth at high risk for becoming obese by young adulthood (at age 12 and 23, ～67 and 90%, respectively, are classified as obese, and almost 72% will have had a BMI ≥ 40 at some time during this developmental period). Class 2 includes youth at moderate‐to‐high risk (at age 12 and 23, ～55 and 68%, respectively, are classified as obese). Class 3 includes youth at low‐to‐moderate risk (i.e., at age 12 and 23, ～8 and 27%, respectively, are classified as obese). Class 4 includes youth at low risk (few of these youth are obese at any age during this developmental period). These results highlight the importance of considering heterogeneity in BMI growth among youth and early interventions among those most at risk of the adverse health consequences of excess weight.     

Intensity and duration of obesity-related counseling: association with 5-Year BMI trends among obese primary care patients

We examined 5-year trends in BMI among obese primary care patients to determine whether obesity-related education such as nutrition counseling or a weight management program was associated with declines in BMI. Veterans with BMI ≥30 kg/m(2) and ≥1 primary care visits in fiscal year 2002 were identified from the Veterans Health Administration's (VHA) national databases. Outpatient visits from fiscal year 2002-2006 for nutrition counseling, exercise, or weight management were grouped into five categories varying in intensity and duration: (i) intense-and-sustained, (ii) intense-only, (iii) irregular, (iv) limited, and (v) no counseling. Generalized estimating equation assessed associations between obesity-related counseling and BMI trend (annual rate of BMI change fiscal year 2002-2006) among cohort members with complete race/ethnic data (N = 179,881). Multinomial logistic regression compared intensity and duration of counseling among patients whose net BMI increased or decreased by ≥10% vs. remained stable. Compared with patients receiving "intense-and-sustained" counseling, the BMI trend of those receiving "intense-only" or "irregular" counseling was not significantly different, but patients receiving "no counseling" or "limited counseling" had significantly higher rates of decreasing BMI (-0.12 and -0.08 BMI per year; P < 0.01, respectively). This was especially true for veterans in their 50-60s, compared with the oldest veterans who were most likely to lose weight. In contrast, younger veterans (18-35 years) were least likely to lose weight; their BMI tended to increase regardless of counseling intensity and duration. Enhanced efforts are needed to detect and combat increasing weight trajectories among veterans who are already obese, especially among those aged 18-35 who are at greatest risk.     

The effect of obesity on overall,circulatory disease- and diabetes-specific mortality

This paper explores the relationship between body mass and risk of death among US adults. The National Health Interview Survey-Multiple Cause of Death linked data set is used for the years 1987-1997, and Cox proportional hazard models are employed to estimate the association between obesity, as measured by the body mass index (BMI), and overall, circulatory disease-specific and diabetes-specific mortality. A U-shaped relationship is found between BMI and overall mortality. Compared with normal weight individuals, mortality during the follow-up period is 34% higher among obese class II individuals and 77% higher among obese class III individuals, controlling for age and sex. A J-shaped relationship exists between circulatory disease mortality and obesity, with a slightly higher risk of death for all categories of BMI. The relationship between BMI and diabetes mortality is striking. Compared with normal weight individuals, obese class I individuals are 2.8 times as likely to die, obese class II individuals are 4.7 times as likely to die, and obese class III individuals are 9.0 times as likely to die of diabetes during the follow-up period, controlling for age and sex. These results demonstrate that obesity heightens the risk of overall and circulatory disease mortality, and even more substantially increases the risk of diabetes mortality. These mortality findings, together with the substantial recent increases in obesity, lend urgency to public health programmes aimed at reducing the prevalence and consequences of obesity.     

Regional body volumes, BMI, waist circumference, and percentage fat in severely obese adults

Objective: This study presents total body volume (TBV) and regional body volume, and their relationships with widely used body composition indices [BMI, waist circumference (WC), and percentage body fat (% fat)] in severely obese adults (BMI ≥35 kg/m²). Research Methods and Procedures: We measured TBV, trunk volume (TV), arm volume (AV), leg volume (LV), and WC and estimated % fat in 32 severely obese persons with BMI 36 to 62 kg/m² (23 women; age, 19 to 65 years; weight, 91 to 182 kg) and in 58 persons with BMI <35 kg/m² (28 women; age, 18 to 83 years; weight, 48 to 102 kg) using a newly validated 3‐day photonic image scanner (3DPS, Model C9036–02, Hamamatsu Co., Japan) and calculated TV/TBV, AV/TBV, and LV/TBV. Results: Men had significantly larger TBV and higher TV/TBV and AV/TBV, but significantly lower LV/TBV than women, independently of BMI. TV/TBV increased while AV/TBV and LV/TBV decreased with increasing BMI, WC, and % fat, and the rate of increase in TV/TBV per % fat was significantly greater in severely obese individuals than in individuals with BMI <35 kg/m². The relationships for TBV with % fat were much lower than with BMI or WC. Conclusion: Body volume gains were mainly in the trunk region in adults, irrespective of sex or BMI. For a given BMI, WC, or % fat, men had a significantly larger TV than women. The implication is that men could have higher health risks due to having higher trunk body weight as a proportion of total body weight compared with severely obese or less severely obese women.     

The fatty acid amide hydrolase (FAAH) Pro129Thr polymorphism is not associated with severe obesity in Greek subjects

Fatty amid acid hydrolase (FAAH) has been implicated at both protein and gene level with obesity. An association between Pro129Thr variant of the FAAH gene and obesity has been described, but various studies have yielded conflicting results. Our aim was to determine whether this polymorphism is related to severe obesity and whether it confers a risk for variability of quantitative metabolic traits in a cohort of Greek obese subjects. Two groups of severely obese subjects (BMI > 40 kg/m (2)) were studied: a group of 158 metabolically healthy and a group of 145 obese subjects with metabolic syndrome, which were compared to a control group consisting of 121 lean individuals. We did not find any association between the Pro129Thr polymorphism with severe obesity in both subgroups of obese subjects, between these two subgroups (p= 0.11) or on basic anthropometric characteristics in the three groups. Statistically significant differences were found for glucose and HDL in metabolically healthy subjects and HDL in the control group. The borderline significant p-values were not significant after correction for multiple testing. We were unable to find robust evidence of an association of the Pro129Thr variant with severe obesity, and any related quantitative traits among the obese Greek subjects examined.     

Polysomnographic sleep, growth hormone insulin-like growth factor-I axis, leptin, and weight loss

Short sleep appears to be strongly associated with obesity and altered metabolic function, and sleep and growth hormone (GH) secretion seems interlinked. In obesity, both the GH-insulin-like-growth-factor-I (GH-IGF-I) axis and sleep have been reported to be abnormal, however, no studies have investigated sleep in relation to the GH-IGF-I axis and weight loss in obese subjects. In this study polygraphic sleep recordings, 24-h GH release, 24-h leptin levels, free-IGF-I, total-IGF-I, IGF-binding protein-3 (IGFBP-3), acid-labile subunit (ALS), cortisol and insulin sensitivity were determined in six severely obese subjects (BMI: 41+/-1 kg/m(2), 32+/-2 years of age), cross-sectional at baseline, and longitudinal after a dramatically diet-induced weight loss (36+/-7 kg). Ten age- and gender-matched nonobese subjects served as controls. Sleep duration (360+/-17 vs. 448+/-15 min/night; P<0.01), 24-h GH (55+/-9 vs. 344+/-55 mU/l.24 h; P<0.01), free-IGF-I (2.3+/-0.42 vs. 5.7+/-1.2 microg/l; P<0.01), and total-IGF-I (186+/-21 vs. 301+/-18 microg/l; P<0.01) were significantly decreased and 24-h leptin levels were increased (35+/-5 vs. 12+/-3 microg/l; P<0.01) in obese subjects at pre-weight loss compared with nonobese subjects After diet-induced weight loss the differences in GH, free IGF-I, and leptin were no longer present between previously obese and nonobese subjects, whereas a significant difference in sleep duration and total IGF-I levels persisted. Rapid eye movement (REM) sleep, non-REM sleep, IGFBP-3, ALS, and cortisol levels were similar in obese and nonobese subjects. Sleep duration, 24-h GH, and IGF-I levels were decreased and 24-h leptin levels were increased in obese subjects. We conclude that hyposomatotropism and hyperleptinemia in obesity are transient phenomena reversible with weight loss, whereas short sleep seems to persist after weight has been reduced dramatically.     

Analysis of 825C/T polymorphism of G proteinbeta3 subunit in obese/diabetic Japanese

The GNB3 825C/T polymorphism, which is common worldwide, is associated with enhanced G-protein activation. The frequency of 825-T allele was increased with body mass index (BMI) and finally had a high frequency in relatively mild obese (BMI >27 kg/m(2)) subjects in some populations. In the present study, we investigated 208 severely obese [BMI >or=30 kg/m(2) (97th percentile)] Japanese subjects including 146 probands with diabetes. No increase in the 825-T allele frequency was observed in the 208 severely obese and even in a subgroup of the 55 most obese [BMI >or=35 kg/m(2) (99.7th percentile)] subjects compared with that in 150 controls (BMI <25 kg/m(2)) (0.48 and 0.48 vs 0.51, respectively). Also, the frequency was not increased in the 146 obese subjects with diabetes (0.48). We concluded that the 825-T allele is not associated with obesity or diabetes associated with obesity at least in the Japanese population.     

Traditional Anthropometric Parameters Still Predict Metabolic Disorders in Women With Severe Obesity

It is well established that fat distribution rather than the total quantity of fat is the major determinant of cardiovascular risk in overweight subjects. However, it is not known whether the concept of fat distribution still makes sense in severely obese subjects. Particularly, the role of visceral fat accumulation and/or of adipocyte hypertrophy in insulin resistance (IR) has not been studied in this population. Therefore, the aim of this study was to clarify the determinants of metabolic disorders in severely obese women. We performed a cross‐sectional study in 237 severely obese women (BMI >35 kg/m²). We assessed total body fat mass and fat distribution by anthropometric measurements (BMI and waist‐to‐hip ratio (WHR)) and by dual‐energy X‐ray absorptiometry (DXA). In 22 women, we measured subcutaneous and visceral adipocyte size on surgical biopsies. Mean BMI was 44 ± 7 kg/m² (range 35–77), mean age 37 ± 11 years (range 18–61). Lipid parameters (triglycerides, high‐density lipoprotein cholesterol) and IR markers (fasting insulin and homeostasis model assessment (HOMA) index) correlated with fat distribution, whereas inflammatory parameters (C‐reactive protein, fibrinogen) correlated only with total fat mass. An association was observed between android fat distribution and adipocyte hypertrophy. Visceral adipocyte hypertrophy was associated with both IR and hypertension, whereas subcutaneous fat‐cell size was linked only to hypertension. Our results obtained in a large cohort of women showed that fat distribution still predicts metabolic abnormalities in severe obesity. Furthermore, we found a cluster of associations among fat distribution, metabolic syndrome (MS), and adipocyte hypertrophy.     

Individual igf-I responsiveness to a fixed regimen of low-dose growth hormone replacement is increased with less variability in obese compared to non-obese adults with severe growth hormone deficiency

BACKGROUND/AIMS: Decreased GH and IGF-I levels and increased GH responsiveness are frequently reported in obesity. As GH-deficient adults are commonly obese, the role of obesity in affecting hepatic responsiveness of IGF-I generation to GH stimulation is unclear in severe GH-deficient states. To address this question, we challenged a cohort of severely GH-deficient non-obese and obese adults with a fixed low GH dose (0.2 mg/day), and examined the relationship of body mass index (BMI) with IGF-I response. METHODS: 12 non-obese (6 males, median BMI 24.7 kg/m2) and 14 obese (7 males, median BMI 45.2 kg/m2) adults with severe GH deficiency were studied for 8 weeks. Blood samples were collected at baseline, and weeks 4 and 8. RESULTS: There was a larger increment and reduced variability of IGF-I levels in obese compared to non-obese GH-deficient adults at week 8, but not at week 4. A similar but smaller increment and less variability was observed with IGFBP-3. Increment IGF-I positively correlated with baseline BMI at weeks 4 (r=0.49, p<0.02) and 8 (r=0.47, p<0.02). No gender differences were observed with the IGF-I and IGFBP-3 response. CONCLUSIONS: This study demonstrates that there is a larger increment and deceased individual variability of IGF-I to the low GH replacement dose in obese compared to non-obese adults with severe GH deficiency, regardless of gender. The positive association of IGF-I increment with BMI implies a greater impact of obesity rather than GH deficiency in enhancing hepatic sensitivity to GH. These findings, thus, question the reliability of interpreting single serum IGF-I levels in non-obese adults with severe GH deficiency treated with low GH replacement doses.     

Forecasting the obesity epidemic in the aging U.S. population

Objective: The objective was to forecast BMI distribution in the U.S. population along with demographic changes based on past race‐, sex‐, and birth cohort‐specific secular trends. Research Methods and Procedures: We compiled data from 44,184 subjects from 4 National Health and Nutrition Examination Surveys (NHANES; 1971 to 2004). By race and sex, we fit regression models to create smoothed mean BMI curves by age for 1970 to 2010. Linking corresponding birth cohorts across age‐ and year‐specific mean BMI projections, we estimated the trajectory of relative BMI throughout each cohort's lifetime. These projections were validated using actual cohorts in the Nurses’ Health Study and Health Professionals Follow‐up Study. Combined with U.S. census, we predicted BMI distributions in 2010 and examined the joint impact of the obesity epidemic and population aging. Results: BMI secular trends in the past 3 decades differ significantly by birth cohort, sex, and race. If these trends continue, the prevalence of obesity is expected to reach 35%, 36%, 33%, and 55% in 2010 among white men, white women, black men, and black women, respectively, far from the Healthy People 2010 goal of 15%. Such forecasts translate into 9.3 million more obese adults 20 to 74 years of age than in 2000, 8.3 million of whom would be 50 years of age or older, and 8.5 million of whom would be white. The mean age among obese men and women is also expected to rise from 47 to 49 years among whites and from 43 to 44 years among blacks. Discussion: As the baby boom generation approaches retirement age, the continuing obesity epidemic signals a likely expansion in the population with obesity‐related comorbidities. A framework to combine BMI and demographic trends is essential in evaluating the burden and disparity associated with the epidemic in the aging U.S. population.     

The Changing Body Mass–Mortality Association in the United States: Evidence of Sex-Specific Cohort Trends from Three National Health and Nutrition Examination Surveys

The association between body mass index (BMI) categories and mortality remains uncertain. Using three National Health and Nutrition Examination Surveys covering the 1971–2006 period for cohorts born between 1896 and 1968, this study estimates separately for men and women models for year-of-birth (cohort) and year-of-observation (period) trends in how age-specific mortality rates differ across BMI categories. Among women, relative to the normal weight (BMI 18.5–24.9 kg/m²), there are increasing trends in mortality rates for the overweight (BMI 25–29.9) or obese (BMI ≥ 30). Among men, mortality rates relative to the normal weight decrease for the overweight, do not change for the moderately obese (BMI 30–34.9), and increase for the severely obese (BMI ≥ 35). Period and cohort trends are similar, but the cohort trends are more consistent. In the latest cohorts, compared with the normal weight, mortality rates are 50 percent lower for overweight men, not different for moderately obese men, and 100–200 percent higher for severely obese men and for overweight or obese women. For U.S. cohorts born after the 1920s, a lower overweight than normal weight mortality is confined to men. I speculate on possible reasons why the mortality association with overweight and obesity varies by sex and cohort.     

Myotubes from Severely Obese Type 2 Diabetic Subjects Accumulate Less Lipids and Show Higher Lipolytic Rate than Myotubes from Severely Obese Non-Diabetic Subjects

About 80% of patients with type 2 diabetes are classified as overweight. However, only about 1/3 of severely obese subjects have type 2 diabetes. This indicates that several severely obese individuals may possess certain characteristics that protect them against type 2 diabetes. We therefore hypothesized that this apparent paradox could be related to fundamental differences in skeletal muscle lipid handling. Energy metabolism and metabolic flexibility were examined in human myotubes derived from severely obese subjects without (BMI 44±7 kg/m²) and with type 2 diabetes (BMI 43±6 kg/m²). Lower insulin sensitivity was observed in myotubes from severely obese subjects with type 2 diabetes. Lipolysis rate was higher, and oleic acid accumulation, triacylglycerol content, and fatty acid adaptability were lower in myotubes from severely obese subjects with type 2 diabetes compared to severely obese non-diabetic subjects. There were no differences in lipid distribution and mRNA and protein expression of the lipases HSL and ATGL, the lipase cofactor CGI-58, or the lipid droplet proteins PLIN2 and PLIN3. Glucose and oleic acid oxidation were also similar in cells from the two groups. In conclusion, myotubes established from severely obese donors with established type 2 diabetes had lower ability for lipid accumulation and higher lipolysis rate than myotubes from severely obese donors without diabetes. This indicates that a difference in intramyocellular lipid turnover might be fundamental in evolving type 2 diabetes.     

Study of insulin-like growth factor I in human obesity.

In obesity there is a decrease in basal and stimulated GH secretion. IGF-I, which has negative feedback effects on GH secretion, could be the initial mediator of such alterations. We studied IGF-I levels in obese subjects and their relationship to the obesity level and GH secretion. We determined plasma IGF-I, basal and stimulated GH in 30 normal and 30 obese women and related these variables to obesity indices (body mass index, BMI, and % overweight). Baseline plasma GH values were 1.2 +/- 0.3 and 2.3 +/- 0.6 micrograms/l in obese subjects and controls, respectively (NS). Mean peak GH secretion after stimuli were 11.2 +/- 1.4 and 34.4 +/- 5.6 micrograms/l in obese subjects and controls, respectively (p less than 0.001). Plasma IGF-I were 1.0 +/- 0.1 U/ml and 0.7 +/- 0.1 U/l in obese subjects and controls, respectively (NS). There was a significant negative correlation between plasma IGF-I and age (r = -0.55, p less than 0.001) and a significant negative correlation between mean peak GH secretion and weight (r = -0.60, p less than 0.001), BMI (r = -0.64, p less than 0.001) and percentage of ideal body weight (r = -0.67, p less than 0.001). We did not find any correlation between IGF-I and indices of overweight. These data suggest that the reduced GH secretion found in obesity is not related to a negative feedback inhibition by elevated levels of IGF-I and that adiposity is not associated with a decline in IGF-I levels. We confirm the existence of a negative correlation between GH secretion and obesity indices.     

Lack of association of glutamate decarboxylase 2 gene polymorphisms with severe obesity in utah

Three polymorphisms of the glutamate decarboxylase 2 gene, which encodes the glutamic acid decarboxylase enzyme, have been associated with severe obesity in a large French cohort. One of these polymorphisms was shown to have functional consequences on promoter expression. Another polymorphism was associated with insulin levels and secretion. These associations were examined in 855 severely obese Utah subjects (mean BMI = 48 kg/m(2)) and a normal-weight and normoglycemic subset (N = 130, mean BMI = 22 kg/m(2)) of a random sample of the Utah population (N = 462). Comparisons of the normal-weight random group with the severely obese group did not result in significant genotype or allele frequency differences for any of the three polymorphisms, C61450A, T83897A, or A-243G (all p > or = 0.18). Haplotypes were also not related to severe obesity (p = 0.10). None of the polymorphisms was significantly related to fasting glucose, insulin levels, or homeostasis model assessment insulin resistance or secretion indices. This study of normal-weight and severely obese subjects from Utah does not provide evidence for involvement of the three genotyped polymorphisms in the glutamate decarboxylase 2 gene with obesity or with insulin- and glucose-related measures associated with obesity.     

Body Mass Index Development from Birth to Early Adolescence; Effect of Perinatal Characteristics and Maternal Migration Background in a Swedish Cohort

Background

Well documented diversity in risk of developing overweight and obesity between children of immigrant and of native mothers, might be explained by different body mass index (BMI) development trajectories in relation to maternal and perinatal characteristics of offspring.

Objectives

To assess BMI development trajectories among children born to immigrant and to Swedish mothers from birth to adolescence in relation to perinatal characteristics.

Methods

A cohort of 2517 children born in Stockholm during 1994 to 1996 was followed with repeated measurement of height and weight at eleven time points until age 12 years. We estimated changes over time for BMI in relation to maternal and perinatal characteristics of offspring using mixed linear model analysis for repeated measure data.

Results

We observed a significant BMI change over time in children and time interaction with maternal migration status (P<0.0001). Estimated BMI over time adjusted for maternal and perinatal characteristics of offspring, showed slower BMI growth before age of 5, followed by an earlier plateau and steeper BMI growth after 5 years among children of immigrant mothers compared with children of Swedish mothers. These differences in BMI growth were more prominent among children with mothers from outside Europe.

Conclusion

Beside reinforcing early childhood as a crucial period in development of overweight, the observed slower BMI development at early childhood among children of immigrants followed by a steeper increase in BMI compared with children of Swedish mothers is important for further studies and for planning of preventive public health programs.     

Substantial changes in epicardial fat thickness after weight loss in severely obese subjects

We sought to evaluate the effect of weight loss on echocardiographic epicardial fat thickness, as index of visceral adiposity, and whether epicardial fat change after the weight loss can be proportionally different from overall body weight changes and related to cardiac parameters changes in severely obese subjects. This was an interventional study in 20 severely obese subjects (12 women, 8 men, BMI 45+/-5 kg/m(2), 35+/-10 years) who underwent 6-month very low calorie diet weight loss program. Baseline and after 6-month weight loss anthropometrics, echocardiographic epicardial fat thickness, left ventricular mass (LVM), and diastolic function parameters were assessed. Subjects lost 20% of original body weight, BMI reduced by 19% of original BMI, waist circumference decreased by 23% of initial waist circumference. Epicardial fat thickness decreased from 12.3+/-1.8 to 8.3+/-1 mm P<0.001 after the 6-month very low calorie diet, as -32% of baseline epicardial fat thickness. LVM and diastolic function changes were better correlated with epicardial fat changes. We showed that significant weight loss can be associated with significant reduction in the epicardial fat thickness, marker of visceral adiposity in severely obese subjects. Epicardial fat decrease, therefore visceral fat decrease, can be proportionally higher than overall adiposity decrease. Epicardial fat changes are significantly associated with obesity-related cardiac morphological and functional changes during weight loss. Measurement of echocardiographic epicardial fat thickness may provide an additional tool in understanding the metabolic risk associated with variation in fat distribution.     

Fiber Intake of Normal Weight,Moderately Obese and Severely Obese Subjects

ALFEERI, MARGARET AH, JOCELINE POMERLEAU, D MICHAEL GRACE AND LORRAINE ANDERSON. Fiber intake of normal weight, moderately obese and severely obese subjects. Obes Res. The lack of dietary fiber may be a contributing factor in obesity. This study examined the fiber intake of three weight groups: normal (20.0≤BMI≤27.0), moderately obese (27.1≤BMI≤39.9) and severely obese (BMI≥40.0). Each group contained 50 subjects. Detailed 3-day food records were used to gather the nutritional data. Fiber intake in the normal weight group was 18.8 ± 9.3 grams, the moderately obese consumed 13.3 ± 5.8 grams of fiber and the severely obese 13.7 ± 5.7 grams. Total fiber intake in grams was found to be significantly higher in the lean group (p<0.05) and was positively associated with sex and education level with men and more highly educated individuals consuming more fiber. Using regression analysis total fiber in grams and fiber in g/1000 kcalories was inversely associated with BMI after adjusting for sex, age, education level and income (p<0.01). A high fiber diet may help to promote a negative energy balance by causing early satiety secondary to gastric distention. Dietitians and physicians need to emphasize the importance of a high fiber diet to their obese patients.     

Adapted Changes in Left Ventricular Structure and Function in Severe Uncomplicated Obesity

Objective: A massive amount of fat tissue, as that observed in obese subjects with BMI over 50 kg/m², could affect cardiac morphology and performance, but few data on this issue are available. We sought to evaluate cardiac structure and function in uncomplicated severely obese subjects. Research Methods and Procedures: We studied 55 uncomplicated severely obese patients, 40 women, 15 men, mean age 35.5 ± 10.2 years, BMI 51.2 ± 8.8 kg/m², range 43 to 81 kg/m², with a history of fat excess of at least 10 years, and 55 age‐matched normal‐weight subjects (40 women, 15 men, mean BMI 23.8 ± 1.2 kg/m²) as a control group. Each subject underwent an echocardiogram to evaluate left ventricular (LV) mass and geometry and systolic and diastolic function. Results: Severely obese subjects showed greater LV mass and indexed LV mass than normal‐weight subjects (p < 0.01 for all parameters). Nevertheless, LV mass was appropriate for sex, height^2.7, and stroke work in most (77%) uncomplicated severely obese subjects. In addition, no significant difference in LV mass indices and LV mass appropriateness between obese subjects with BMI ≥ 50 kg/m² and those with BMI ≤ 50 kg/m² was found. Obese subjects also showed higher ejection fraction and midwall shortening than normal‐weight subjects (p = 0.05 and p < 0.01, respectively), suggesting a hyperdynamic systolic function. No significant difference in systolic performance between obese subjects with BMI ≥ 50 kg/m² and those with BMI ≤ 50 kg/m² was seen. Discussion: Our data show that uncomplicated severe obesity, despite the massive fat tissue amount, is associated largely with adapted and appropriate changes in cardiac structure and function.     

Age Dimorphism in the Association between Growth‐Hormone Status and the Respiratory Quotient

Objective: To investigate the impact of age on the association between the respiratory quotient (RQ) and growth‐hormone (GH) secretion and to investigate the acute lipolytic response to an exogenous GH bolus. Research Methods and Procedures: A cross‐sectional study of 36 non‐obese healthy subjects (18 women and 18 men) from two age groups was used: “younger” (mean age, 29.5 years; range, 27 to 34 years) and “older” (mean age, 50.8 years; range, 47 to 59 years). Endogenous GH secretion by means of deconvolution analysis of 24‐hour serum GH concentrations was measured every 20 minutes. Resting RQ was measured after a 12‐hour overnight fast. The lipolytic response to an intravenous exogenous GH bolus (200 μg) was assessed by measuring serum levels of free fatty acids as well as changes in RQ. Additional measurements included body composition (regional computed tomography scan and DXA) and physical fitness (Vo ₂max). Results: Resting RQ did not differ between the two age groups: 0.81 ± 0.01 (young) vs. 0.82 ± 0.01 (older; not significant). Several estimates of GH release correlated positively with RQ in the younger group, whereas a negative correlation was detected in the older subjects [GH production rate (μg/liter × kg) vs. RQ: r = 0.62, p < 0.01 (younger); r = ?0.53; p = 0.02 (older)]. By regression analysis, 52% to 58% of the variation in RQ could be explained by GH status. After an exogenous GH bolus, the incremental response in nonesterified fatty acid was slightly higher in younger individuals (p = 0.09). Discussion: Resting RQ is significantly correlated with GH status. This association is positive in younger individuals and negative in older individuals. The lipolytic response to exogenous GH is moderately higher in younger compared with older individuals. GH status should be taken into account when investigating the residual variation in RQ.