[Obesity, visceral fat obesity syndrome].
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Decreased insulin sensitivity patients, although normal-weight, are treated with a "prudent" hypocaloric diet and exercise, in order to reduce insulin resistance. Metabolic (glycolipidic) alterations can be easily diagnosed by combination of clinic and laboratory tests. A diet model aimed at controlling insulin levels and inducing a light weight loss is proposed.
BACKGROUND: The rapidly increasing prevalence of obesity among children is one of the most challenging dilemmas facing pediatricians today. While the medical community struggles to develop effective strategies for the treatment of this epidemic, timely identification of obesity by pediatric health care providers remains the crucial initial step in the management of obesity. OBJECTIVE: Direct assessment of pediatric clinicians' performance in identifying and managing obesity in clinical practice has not been conducted to date. The objective of this study was to determine rates of identification of obesity by pediatric residents, nurse practitioners, and faculty members in an academic primary care setting and to describe the actions taken by these providers in their evaluation and management of obesity. DESIGN: A retrospective medical record review of all health supervision visits for children 3 months to 16 years of age, examined between December 1, 2001, and February 28, 2002, was performed. For children <5 years of age, a weight >120% of the 50th percentile of weight-for-height was defined as obese. For children > or =5 years of age, a body mass index of >95th percentile for age and gender was defined as obese. SETTING: A large, primary care practice located in a tertiary-care, academic, pediatric hospital, which serves a predominantly urban, minority (70% African American), Medical Assistance-insured (90%) population. PARTICIPANTS: Primary care providers, including pediatric residents, nurse practitioners, and faculty physicians. RESULTS: Of the 2515 visits reviewed, a total of 244 patients met the study definition of obesity, yielding an estimated prevalence of obesity visits of 9.7% among health supervision visits for children 3 months to 16 years of age. This prevalence of obesity visits cannot be used to estimate the population prevalence of obesity, given the skewed distribution of visits toward very young children. For all children who met the study definition of obesity, providers documented obesity in their assessments in only 53% of the reviewed visits (129 visits). Although the majority of charts (69%) contained an adequate dietary history, only 15% included a description of the child's activity level or television viewing. Obesity was noted in the physical examination in 39% of cases. For children for whom obesity was identified as a problem by their clinicians (129 patients), 81% of charts contained an adequate dietary history, whereas 27% contained a description of the child's activity level or television viewing. Obesity was noted in the physical examination in 64% of cases. Most children identified as obese by their providers received some management specific to their obesity, including education, screening, and specialist referral. Dietary changes were recommended for 71%, increased activity for 33%, and limitation of television viewing for only 5%. Eighty-three percent of providers recommended close follow-up monitoring. Other recommendations included referral to a dietitian (22%), screening laboratory studies (13%), a food diary (9%), endocrine referral (5%), or preventive cardiology referral (3%). Provider identification of obesity was affected by the age of the patient and by the degree of obesity. Obesity identification was lowest among preschool children (31%) and highest among adolescent patients (76%). Providers evaluating older and heavier children were also more likely to obtain activity histories, note obesity in the physical examination, recommend changes in activity, refer the patient to a nutritionist, obtain screening laboratory studies, and recommend close follow-up monitoring. Identification of obesity and other outcome variables were not significantly influenced by the level of provider training or patient gender. CONCLUSIONS: Although the prevalence of childhood obesity has now reached epidemic proportions, it was under-recognized and under-treated by pediatric primary care providers in our study. Providers identified obesity as a problem for only one-half of the obese children examined for health supervision. The lowest rates of obesity identification occurred among children <5 years of age and those with milder degrees of obesity. Identification did not improve with additional years of pediatric training. Even for the subset of children identified as obese by their providers, evaluation and treatment often were not consistent with current recommendations. For example, more attention was given to the role of diet, compared with activity, in the evaluation of obesity. In particular, only a small number of providers (5%) recommended a decrease in television viewing to their obese patients, despite evidence linking television viewing and pediatric obesity. This finding is of concern, because obesity is known to be a multifactorial disease that responds only to significant changes in both dietary and activity behaviors. Only 13% of providers requested laboratory studies as part of their recommendations. The American Academy of Pediatrics currently recommends obtaining a lipid profile, total cholesterol level, and screening test for type 2 diabetes mellitus as part of the evaluation of obesity. The majority of clinicians who requested laboratory studies included thyroid function tests, which are not recommended by the American Academy of Pediatrics because of the very low likelihood of hypothyroidism as a cause of obesity. Although the extent of evaluation and management for children who were recognized as obese did not meet current guidelines, it was far better than that for patients who were not identified as obese by their providers. This demonstrates the importance of timely identification as the crucial initial step in the management of obesity. The results of this study are disheartening, especially as evidence mounts regarding the importance of early intervention in preventing the medical and psychosocial sequelae of obesity, as well as the persistence of obesity into adulthood. This study highlights the need for increased awareness and identification of obesity in the primary care setting, especially among younger children and those with mild obesity.
OBJECTIVE: To assess tracking for body weight from childhood to adulthood in obese Japanese children who were treated for obesity, investigate the relation between the changes in body weight status and morbidity, and identify correlates of the changes in body weight status. STUDY DESIGN: Twelve-year retrospective cohort study. SUBJECTS: A sample of 276 subjects (age 23.9+/-4.1, 176 males and 100 females) who responded to a questionnaire mailed in 1998 to 1047 children (age 10.6+/-2.2) treated for obesity at Mie National Hospital in Japan between 1976 and 1992. MEASUREMENTS: Based on height and weight from medical records during childhood, the relative weight (RW; weight expressed as a percentage of the standard body weight for age, height, and sex) was calculated. Degrees of childhood obesity were based on RW: slight obesity (120% < or = RW<130%; n=17), moderate obesity (130% < or = RW <150%; n=131), and severe obesity (RW > or = 150%; n=128). Adult body mass index (BMI), which was obtained from the mailed questionnaires, was classified as normal, overweight and obese according to the WHO/NIH criteria. Body weight tracking by degree of obesity was evaluated. Subjects with severe obesity during childhood (n=128) were examined for their weight status in adulthood, prevalence of chronic diseases in adulthood, and factors such as parental obesity, dietary and exercise habits and obesity treatment during childhood. RESULTS: Childhood obesity tracked into adulthood obesity or overweight in 54.7% of all cases. Severely obese children (36.7%) were more likely to be obese as an adult than moderately obese children (16.8%). The prevalence of adult obesity tended to be greater in boys with moderate childhood obesity than in girls (29.7% in boys vs 14.9% in girls, P=0.058). Among the severely obese children who became normal-weight adults, the prevalence of chronic diseases was about one-fifth of those who remained obese in adulthood (P=0.041). Four factors were associated with changes in body weight status: maternal BMI at entry (P=0.044), the changes in dietary and exercise habits after treatment (P=0.014, P=0.030, respectively), and satisfaction with obesity treatment in childhood (P=0.035). CONCLUSIONS: Severely obese children have a higher risk of becoming obese adults even when they received obesity treatment in childhood. The risk of adulthood obesity was twice as high in moderately obese boys than in girls. On the other hand, many cases of childhood obesity can be corrected with obesity treatment, which in turn can decrease the risk for adult chronic diseases.
The basic tenet of this investigation was that obesity is not a prerequisite in the development of polycystic ovary syndrome (PCOS), as indicated by the fact that 50% of PCOS women are not obese. Further, obesity itself is a disease entity with the common manifestation of insulin resistance/hyperinsulinemia with PCOS. Given recent evidence that insulin and GH may have gonadotropin-augmenting effects, we have determined the common and distinguishing features of neuroendocrine-metabolic dysfunctions of lean [body mass index (BMI), < 23 kg/m2] and obese (BMI, > 30 kg/m2) women with the classical form of PCOS. Insulin sensitivity, as determined by rapid i.v. glucose tolerance testing; 24-h dynamics of insulin/glucose levels, somatotropic [GH/GH-binding protein/insulin-like growth factor I (IGF-I)/IGF-binding proteins (IGFBP)], and LH axes; and their downstream effects on ovarian steroids were simultaneously assessed in eight lean PCOS and eight obese PCOS patients and an equal number of BMI-matched normal cycling controls. Our results show that insulin sensitivity was reduced 50% (P < 0.01) in lean PCOS from that in lean controls. There was a further decrease in obese controls (P < 0.01) and a 2-fold greater reduction (P < 0.001) in obese PCOS than in obese controls, suggesting that insulin resistance (IR) is a common lesion in PCOS, and that obesity contributes an additional component to IR in obese PCOS. Consistent with the degree of IR, the manifestation of compensatory hyperinsulinemia in lean PCOS was incipient, being evident only in response to meals (P < 0.05), and became overt during the 24-h fasting/feeding phases of the day in obese control (P < 0.001) with a 2- to 3-fold greater elevation (P < 0.001) in obese PCOS. An enhanced early insulin response to glucose occurs equally in obese control (P < 0.01) and obese PCOS (P < 0.05), but not in their lean counterparts. Considering the more profound IR and the associated hyperglycemia in obese PCOS, the magnitude of the early insulin release is inadequate, suggesting that beta-cell dysfunction exists in obese PCOS. Remarkable differences in the somatotropic axis were also observed; although 24-h GH pulse frequency and levels of IGF-I and IGFBP-3 were unaltered by either PCOS or obesity, the 24-h mean GH pulse amplitude was increased by 30% (P < 0.01) in lean PCOS in the presence of normal levels of high affinity GHBP and normal GH response to GHRH. In distinct contrast, the somatotropic axis in both obese control and obese PCOS was profoundly modified, with attenuation of GH pulse amplitude (P < 0.001) and GH response to GHRH (P < 0.001), resulting in a state of hyposomatotropinism with a more than 50% reduction (P < 0.001) of 24-h mean GH levels. In addition, GHBP levels were elevated 2-fold and were correlated inversely with GH (r = -0.81) and positively with insulin (r = 0.75) concentrations. IGFBP-I levels were suppressed in both obese groups, with a 4-fold greater reduction in obese PCOS than that in obese controls. Thus, the downstream effects of hyperinsulinemia on the somatotropic axis may include up-regulation of hepatic production of GHBP, suppression of IGFBP-1 (r = 0.82) and sex hormone-binding globulin (r = -0.69) levels, and a more than 3-fold increase in ratios of IGF-I/IGFBP-1 and estradiol-testosterone/sex hormone-binding globulin, thereby increasing their bioavailabilities. In contrast, LH pulsatility was unaffected by obesity alone. An accelerated LH pulse frequency was evident in both lean and obese PCOS (P < 0.001), whereas the mean 24-h LH pulse amplitude was increased in lean (P < 0.001), but not obese, PCOS patients. These events resulted in a 3-fold increase in 24-h mean LH levels in lean PCOS and a 2-fold increase in obese PCOS. Thus, increased LH pulse frequency and augmented LH response to GnRH are characteristic of PCOS, independent of obesity, and the presence of obesity in PCOS is associated with an attenuated LH pulse amplitude, not accounted f
BACKGROUND: Obesity is a relative contraindication to performing restorative proctocolectomy. The aim of this study was to assess the morbidity and functional results after restorative proctocolectomy in obese patients as compared to a matched cohort of non-obese patients. METHODS: 334 patients who had restorative proctocolectomy were reviewed; obesity was defined as a body mass index (BMI) greater than or equal to 30 kg/m2. 31 obese patients were matched to 31 non-obese patients for age, gender, steroid use, and diagnosis. Operative time, length of hospitalization, and both perioperative (< 6 weeks) and long-term morbidity (> 6 weeks), especially sepsis, were evaluated. RESULTS: The BMI was significantly higher in the obese group (33.7 vs 23.2) (p < 0.0001), and no difference was found between the obese and non-obese groups relative to the matched parameters of age, gender, steroid use and diagnosis. There was no difference in the rate of mucosectomy performed between the obese and non-obese patients (9.6% vs 3.2%, p = NS). 16% of the obese patients underwent one stage restorative proctocolectomies as compared to 10% in the non-obese group. Operative time was longer in the obese group (229 min vs 196 min; p = 0.02), but overall hospital length of stay was similar (9.7 days vs 7.7 days; p = 0.13). Perioperative morbidity was higher in obese patients (32% vs 9.6%, p = 0.058). However, there was no statistical significance in long-term morbidity (23% vs 32%, p = 0.57) at a mean follow-up of 51 months in the obese group and 53 months in the non-obese group. Obese patients had more stomal complications (10 vs 0%) and incisional hernias (13 vs 3%) (p = NS). Overall the pelvic sepsis-rate was significantly higher in the obese group (16 vs 0%; p < 0.05). 60% of the obese patients who developed pelvic sepsis had pouch-anal anastomosis performed without proximal fecal diversion. Mean bowel movements/24 hours, pad use, nocturnal evacuation, accidents/24 hours and incontinence scores were not statistically significant between the groups. CONCLUSION: Obese patients have a higher rate of pelvic sepsis and peri-operative morbidity when compared to a matched non-obese cohort of patients; however, the functional outcome of restorative proctocolectomy in obese patients is not significantly different than in non-obese patients.
OBJECTIVE: To assess the prevalence and impact of overweight and obesity in an Australian obstetric population. DESIGN, SETTING AND PARTICIPANTS: The Mater Mother's Hospital (MMH), South Brisbane, is an urban tertiary referral maternity hospital. We reviewed data for the 18 401 women who were booked for antenatal care at the MMH, delivered between January 1998 and December 2002, and had a singleton pregnancy. Of those women, 14 230 had an estimated pre-pregnancy body mass index (BMI) noted in their record; 2978 women with BMI < or = 20 kg/m2 were excluded from further study; the remaining 11 252 women were divided into four categories: "normal" (BMI 20.01-25 kg/m(2)), "overweight" (BMI 25.01-30 kg/m(2)), "obese" (BMI 30.01-40 kg/m(2)) and "morbidly obese" (BMI > 40 kg/m(2)). MAIN OUTCOME MEASURES: Prevalence of overweight and obesity in an obstetric population; maternal, peripartum and neonatal outcomes associated with raised BMI. RESULTS: Of the 14 230 women, 6443 (45%) were of normal weight, and 4809 (34%) were overweight, obese or morbidly obese. Overweight, obese and morbidly obese women were at increased risk of adverse outcomes (figures represent adjusted odds ratio [AOR] [95% CI]): hypertensive disorders of pregnancy (overweight 1.74 [1.45-2.15], obese 3.00 [2.40-3.74], morbidly obese 4.87 [3.27-7.24]); gestational diabetes (overweight 1.78 [1.25-2.52], obese 2.95 [2.05-4.25], morbidly obese 7.44 [4.42-12.54]); hospital admission longer than 5 days (overweight 1.36 [1.13-1.63], obese 1.49 [1.21-1.86], morbidly obese 3.18 [2.19-4.61]); and caesarean section (overweight 1.50 [1.36-1.66], obese 2.02 [1.79-2.29], morbidly obese 2.54 [1.94-3.32]). Neonates born to obese and morbidly obese women had an increased risk of birth defects (obese 1.58 [1.02-2.46], morbidly obese 3.41 [1.67-6.94]); and hypoglycaemia (obese 2.57 [1.39-4.78], morbidly obese 7.14 [3.04-16.74]). Neonates born to morbidly obese women were at increased risk of admission to intensive care (2.77 [1.81-4.25]); premature delivery (< 34 weeks' gestation) (2.13 [1.13-4.01]); and jaundice (1.44 [1.09-1.89]). CONCLUSIONS: Overweight and obesity are common in pregnant women. Increasing BMI is associated with maternal and neonatal outcomes that may increase the costs of obstetric care. To assist in planning health service delivery, we believe that BMI should be routinely recorded on perinatal data collection sheets.
UNLABELLED: Gene PPARgamma is one of the pivotal factors that influence adipocyte differentiation. It is transcriptional factor that plays a crucial role in the regulation of genes involved in lipid utilisation and storage as well as insulin action. The aim of this study was to evaluate whether PPARgamma Pro12Ala and Pro115Gln polymorphisms are connected with obesity and its anthropological parameters. MATERIAL AND METHODS: we investigated 93 subjects: 72 women (37 non-obese and 35 obese) and 21 men (8 non-obese and 13 obese). We performed anthropological examination: BMI, WHR and total-body densitometry in the whole group. PPARg polymorphism was studied using PCR and RFLP. RESULTS: Pro12Pro ("wild" type) variant was present in 57 subjects (32 obese and 25 non-obese): 45 women (26 obese and 19 non-obese) and 12 men (6 obese and 6 non-obese). Heterozygosity Pro12Ala was observed in 20 subjects (8 obese and 12 controls): 15 women (4 obese and 11 lean) and 5 men (4 obese). Homozygosity Ala12Ala was discovered in 16 subjects (8 obese and 8 controls): 12 women (5 obese and 7 non-obese) and 4 men (3 obese). Pro115Gln variant was not found in any of the studied subjects. CONCLUSIONS: The frequency Ala allele (pro12Ala and Ala12Ala variant) was 28% in the whole group and 25% in the obese subjects. However the Pro12Ala polymorphism is quite common, it does not seem to be directly connected with onset of obesity. But it is interesting that the Ala allele is more frequent in non-obese women comparing to obese women (33 vs 20%). Reverse tendency was seen in men. Pro12Ala and/or Ala12Ala polymorphism is twice more frequent in obese subjects comparing to non-obese ones (38 vs 19%).