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PubMed2003

Psychosocial functioning in the obese before and after weight reduction: construct validity and responsiveness of the Obesity-related Problems scale.

OBJECTIVE: The Obesity-related Problems scale (OP) is a self-assessment module developed to measure the impacts of obesity on psychosocial functioning. Our principal aim was to evaluate the construct validity and responsiveness of the OP scale. Our specific aims were to test: (1). the psychometric performance of OP; (2). if OP scores differed by gender and weight category; (3). if OP scores are inversely related to mental well-being; (4). if weight reduction in the obese is accompanied by improvements in psychosocial functioning (OP). SUBJECTS: Four samples were used: 6863 subjects in the SOS cross-sectional study; 2128 in the SOS intervention study; 1017 nonobese in the SOS reference study; and 3305 obese subjects in the XENDOS study. MEASUREMENTS: Psychosocial functioning was measured by OP. Overall mood was measured by MACL. Anxiety and depression symptoms were measured by HAD. RESULTS: Psychometric testing provided strong support for the construct validity of OP. Factor analysis confirmed the homogeneity of the construct and multitrait/multi-item scaling analysis demonstrated strong item-convergent/discriminant validity. Reliability coefficients were high and floor and ceiling effects were small. Psychometric results were cross-validated and replicated in subgroups by gender, age and body mass index (BMI). As expected, large differences in OP were observed between obese and nonobese (P<0.0001). Obese women reported more weight-related psychosocial problems than obese men (P<0.0001). Psychosocial disturbances (OP) among the obese were significantly related to poor mood (MACL; P<0.0001) and anxiety and depression symptoms (HAD; P<0.0001). Change in OP over time was strongly correlated with weight loss (P<0.0001). A distinct dose-response effect between weight reduction and improvements in OP was demonstrated. Scores on psychosocial functioning (OP) and mental well-being (MACL, HAD) in nonobese (BMI<30) surgical patients at 4-y follow-up were equal to scores observed in nonobese reference subjects (NS). CONCLUSION: OP is a psychometrically valid obesity-specific measure suitable for evaluating HRQL effects of obesity interventions. The negative impact of obesity on psychosocial functioning is considerable and disturbances are connected with poor mental well-being. Weight reduction in the obese is followed by improvements in both psychosocial functioning and mental well-being.

Affect↗
PubMed2004

Physical activity in relation to development and maintenance of obesity in men with and without juvenile onset obesity.

OBJECTIVE: To examine long-term effects of leisure time physical activity (ltpa) and occupational physical activity (opa) on later obesity, and to examine the effect of body weight on later physical inactivity in men with and without juvenile onset obesity. DESIGN: Population-based longitudinal study of obese and nonobese men, who were identified as draftees of median age of 19 y in 1943-77 and later examined at general health surveys in 1982-84, and in 1991-93. SETTING: Copenhagen and adjacent regions, Denmark. PARTICIPANTS: In all, 1143 juvenile obese men with a BMI > or =31 kg/m2 (corresponding to 35% overweight by an originally used national standard) at draft board examination, and, as a nonobese control group, 1278 men selected as a 0.5% random sample of the approximately 255,600 men examined at the draft board and thus representing the study population. MAIN OUTCOME MEASURES: Obesity, defined as BMI > or =30 kg/m2, and physical inactivity at the last survey. RESULTS: In the cross-sectional analyses, there were strong concurrent inverse associations between ltpa and prevalence of obesity in both groups, whereas there was no relation to opa. In logistic regression analyses of obesity at the last survey, including both ltpa and opa as well as age, BMI at draft board examination, BMI at first follow-up, length of education, smoking and drinking habits, there were no significant effects of ltpa and opa on the risk of development of obesity in the nonobese group or maintenance of obesity in the obese group. Similar analyses of physical inactivity at the last follow-up as outcome showed a significant direct effect of BMI at first follow-up, with a significant trend in the nonobese group, but not in the obese group and no effects on opa. CONCLUSION: There is no long-term influence of physical activity on development and maintenance of obesity in men, whereas greater body weight increases risk of later physical inactivity during leisure time.

Adult↗
PubMed2006

Is China facing an obesity epidemic and the consequences? The trends in obesity and chronic disease in China.

BACKGROUND: Over the past two decades, China has enjoyed impressive economic development, and her citizens have experienced many remarked changes in their lifestyle. These changes are often associated with an increase in obesity and chronic disease. METHODS: In this meta-analysis, based on nationally representative data, we studied the current prevalence of obesity and the trends in obesity, mortality and morbidity in China. RESULTS: Between 1992 and 2002, the prevalence of overweight and obesity increased in all gender and age groups and in all geographic areas. Using the World Health Organization body mass index cut points, the combined prevalence of overweight and obesity increased from 14.6 to 21.8%. The Chinese obesity standard shows an increase from 20.0 to 29.9%. The annual increase rate was highest in men aged 18-44 years and women aged 45-59 years (approximately 1.6 and 1.0% points, respectively). In general, male subjects, urban residents, and high-income groups had a greater increase. With the increase in overweight and obesity, obesity-, and diet-related chronic diseases (e.g., hypertension, cardiovascular disease (CVD), and type 2 diabetes) also increased over the past decade and became a more important preventable cause of death. Hypertension increased from 14.4% in 1991 to 18.8% in 2002 in adults; in older adults aged 35-74 years, it increased from 19.7 to 28.6%. Between 1993 and 2003, the prevalence of CVD increased from 31.4 to 50.0%; diabetes increased from 1.9 to 5.6%. During 1990-2003, although total mortality rate (per 100 000) decreased, overall the mortality rate and contribution (as percentages) to total death of obesity-related chronic disease increased, in particular, in rural areas. Mortality rate (per 100 000) of CVD increased from 128 to 145 and its contribution to total death, 27 to 32%, in rural areas; the figures decreased slightly in urban areas. The mortality rate of 'nutrition, endocrinology and metabolism-related disease' (NEMD) increased in both rural and urban areas between 1990 and 2000, 8.0 to 10.6 and 4.9 to 5.3, respectively. The current prevalence of hypertension, dyslipidaemia, metabolic syndrome, and diabetes among Chinese adults is approximately 20, 20, 15, and 3%, respectively. CONCLUSION: The prevalence of overweight and obesity and obesity-related chronic diseases have increased in China in the past decade. Our findings provide useful information for the projection of future trends and the formulation of national strategies and programmes that can address the challenges of the growing obesity and chronic disease epidemic.

Adolescent↗
PubMed2002

Insulin secretion and sensitivity in non-obese and obese Japanese patients with coronary artery disease.

In a cross-sectional study of 240 patients with angiographically documented coronary artery disease (CAD), we investigated whether obese and non-obese subjects differed as to the influence of insulin deficiency and insulin resistance on glucose intolerance and cardiovascular risk. Patients were classified according to a 75-g oral glucose tolerance test as having normal glucose tolerance (NGT), impaired glucose tolerance (IGT), or diabetes mellitus (DM). We defined obesity as a body mass index (BMI) exceeding 25 kg/m(2). Early phase insulin secretion (insulinogenic index) declined with worsening glucose intolerance in non-obese (tau = -.216, P <.001; Kendall's correlation coefficient) and obese subjects (tau = -.392, P <.001). Total insulin secretion was higher in obese subjects with NGT or IGT than in controls and decreased in association with worsening glucose intolerance in obese subjects (tau = -.239, P <.001). Insulin sensitivity was calculated by 3 proposed indices. The first of these decreased in association with worsening in glucose tolerance in non-obese subjects (tau = -.137, P <.01). The second showed such a pattern in both groups (non-obese, tau = -.407, P <.001; obese, tau = -.311, P <.001), as did the third (non-obese, tau = -.512, P <.001; obese, tau = -.488, P < 0.001). Because even prediabetic Japanese subjects with CAD showed a latent insulin secretion defect in response to a glucose load, as well as impaired insulin sensitivity, compensatory hyperinsulinemia is not a sensitive indicator of coronary risk.

Aged↗
PubMed2000

Obstructive sleep apnoea: multiple comparisons of cephalometric variables of obese and non-obese patients.

BACKGROUND: Pathogenesis of obstructive sleep apnoea (OSA) is complex and not yet fully understood. Several factors contribute to OSA severity. Obesity is believed to play an important role. Nevertheless, not all OSA patients are obese. Therefore, the different features that cause nocturnal upper airway obstruction in obese and non-obese OSA patients could be expected. PURPOSE: To investigate the different components of cervico-craniofacial skeletal and upper airway soft tissue morphology among obese OSA, non-obese OSA patients and the controls. PATIENTS: One hundred male OSA patients were classified into two groups on the basis of body mass index (BMI) as obese (BMI > or = 30 kg/m2) and non-obese (BMI < 30 kg/m2). Consequently, 57 obese and 43 non-obese OSA patients were examined and compared with a control group of 36 healthy males. STUDY DESIGN: A comprehensive cephalometric analysis of cervico-craniofacial skeletal and upper airway soft tissue morphology was performed. Sixty-eight cephalometric variables were compared among the three groups by one way analysis of variance with Bonferroni's test. RESULTS: Both OSA groups had aberrations of cervico-craniofacial skeletal as well as upper airway soft tissue morphology when compared with the controls. These anatomic deviations were confined to cervico-craniofacial skeletal structures in the non-obese OSA patients, whereas the obese OSA patients had more abnormalities in the upper airway soft tissue morphology, head posture and position of the hyoid bone. CONCLUSION: The findings imply that there should be different treatment regimens for the two subgroups of OSA patients. Cephalometric analysis together with various considerations of BMI is highly recommended as one of the most important tools in diagnosis and treatment planning for OSA patients.

Adult↗
PubMed1990

Metabolic profiles and lipoprotein lipid concentrations in non-obese and obese patients with polycystic ovarian disease.

Clinical parameters, androgen status and lipoprotein lipid profiles were assessed in 10 non-obese and 10 obese patients with polycystic ovarian disease (PCOD) and reference subjects matched for age, height and weight. Both obese and non-obese women with PCOD had significantly higher androgen levels when compared to the reference groups. When comparison of lipoprotein lipid profiles were made between groups, non-obese women with PCOD had significantly higher total cholesterol, triglycerides and LDL-cholesterol levels than non-obese reference subjects. Obese PCOD women manifested significantly higher total cholesterol, LDL-cholesterol, cholesterol/HDL, and LDL/HDL values than did obese reference subjects. Correlations between serum androgens and lipoprotein lipid concentrations in PCOD and normal women were unhelpful. Both non-obese and obese patients with PCOD had significantly higher systolic and diastolic blood pressures (BPs) than the reference groups. Thus, both non-obese and obese women with PCOD manifest hyperandrogenaemia which may result in a male pattern of lipoprotein lipid concentrations.

Adolescent↗
PubMed1976

Personality characteristics in obesity: relation of MMPI profile and age of onset of obesity to success in weight reduction.

A group of 142 obese subjects was seen in an obesity clinic over a 2-year period. Of these, 116 had assessment of personality factors by the Minnesota Multiphasic Personality Inventory (MMPI), and 71 were followed for periods of 4 to 28 months in order to determine success at weight reduction by means of a conventional dietary regimen. The MMPI profiles of the obese subjects were compared to those of a general medical population of 50,000 patients seen in the Department of Internal Medicine at the Mayo Clinic. Obese male subjects had significantly higher scores on the F and MA scales. Obese female subjects had significantly higher scores on the F, PD, PA, SC, and MA scales, and a significantly lower score on the Q scale than the reference population. Even though these findings show that certain personality traits as measured by the MMPI may occur more frequently in obese persons, the individual MMPI profile codes point out the presence of diverse behavior patterns among obese persons rather than a single personality pattern characteristic of obesity. There were no apparent differences in the success in achieving a loss of 10% or more of initial weight among the male and female obese subjects having normal or abnormal MMPI profiles. Obese subjects having onset of obesity before age 12 years were slightly more successful in weight reduction than those whose obesity began later than this, but the differences were not statistically significant for either the male or female subjects.

Adolescent↗
PubMed1999

Contrasting blood pressure effects of obesity in leptin-deficient ob/ob mice and agouti yellow obese mice.

OBJECTIVE: Recent advances in understanding the neuroendocrine pathways regulating appetite, metabolism and body weight afford an opportunity to explore further the mechanisms by which obesity influences arterial pressure. ob/ob(Lep(ob)/Lep(ob)) mice have a mutation in the ob gene and are leptin-deficient. Leptin possesses pressor actions and has been shown to increase arterial pressure when infused chronically or over-expressed transgenically. In contrast, agouti yellow obese(Ay) mice have overexpression of an agouti peptide that blocks melanocortin receptors. Stimulation of melanocortin receptors by alpha-melanocyte-stimulating hormone decreases arterial pressure. DESIGN AND METHODS: This study measured arterial pressure in leptin-deficient ob/ob mice, agouti yellow obese mice and their lean controls to test the hypothesis that the effects of obesity on arterial pressure are importantly influenced by the genetic and neuroendocrine mechanisms causing the obesity. We measured arterial pressure directly in conscious ob/ob mice (n = 14), agouti yellow obese mice (n = 6) and the same number of lean littermates. RESULTS: Body weight was nearly twice as high in ob/ob mice as in their lean controls, but mean arterial pressure was significantly lower in ob/ob mice (92+/-3 mmHg) compared with their lean controls (106+/-2 mmHg; P = 0.00017). In contrast, mean arterial pressure was significantly higher in agouti yellow obese mice (124+/-3 mmHg) than in their lean controls (99+/-1 mmHg; P = 0.000002) despite the fact that the agouti mice had milder obesity. CONCLUSIONS: This study prompts three conclusions: (1) leptin-deficient ob/ob mice and agouti yellow obese mice have contrasting blood pressure responses to obesity, (2) obesity does not invariably increase arterial pressure in mice, and (3) the arterial pressure response to obesity may depend critically on the underlying genetic and neuroendocrine mechanisms.

Animals↗
PubMed2004

Beta-cell function and islet morphology in normal, obese, and obese beta-cell mass-reduced Göttingen minipigs.

Herein, we bridge beta-cell function and morphology in minipigs. We hypothesized that different aspects of beta-cell dysfunction are present in obesity and obesity with reduced beta-cell mass by using pulsatile insulin secretion as an early marker. Measures for beta-cell function (glucose and arginine stimulation plus baseline and glucose-entrained pulsatile insulin secretion) and islet morphology were studied in long-term (19-20 mo) obese (n = 5) and obese beta-cell-reduced [nicotinamide + streptozotocin (STZ), n = 5] minipigs and normal controls, representing different stages in the development toward type 2 diabetes. Acute insulin response (AIR) to glucose and arginine were, surprisingly, normal in obese (0.3 g/kg glucose: AIR = 246 +/- 119 vs. 255 +/- 61 pM in control; 67 mg/kg arginine: AIR = 230 +/- 124 vs. 214 +/- 85 pM in control) but reduced in obese-STZ animals (0.3 g/kg glucose: AIR = 22 +/- 36, P < 0.01; arginine: AIR = 87 +/- 92 pM, P < 0.05 vs. control). Baseline pulsatile insulin secretion was reduced in obese (59 +/- 16 vs. 76 +/- 16% in control, P < 0.05) and more so in obese-STZ animals (43 +/- 13%, P < 0.01), whereas regularity during entrainment was increased in obese animals (approximate entropy: 0.85 +/- 0.14 vs. 1.13 +/- 0.13 in control, P < 0.01). Beta-cell mass (mg/kg body wt) was normal in obese and reduced in obese-STZ animals, with pancreatic fat infiltration in both groups. In conclusion, obesity and insulin resistance are not linked with a general reduction of beta-cell function, but dynamics of insulin secretion are perturbed. The data suggest a sequence in the development of beta-cell dysfunction, with the three groups representing stages in the progression from normal physiology to diabetes, and assessment of pulsatility as the single most sensitive marker of beta-cell dysfunction.

Animals↗
PubMed1998

Plasma growth hormone secretion is impaired in obesity-prone rats before onset of diet-induced obesity.

Sprague-Dawley rats, which become obese (obesity prone) when fed a moderately high-fat (MHF; 32.5% of kcal as fat) diet, have decreased growth hormone (GH) concentrations compared with obesity-resistant rats fed the same diet. To determine whether plasma GH concentrations are different in obesity-prone rats compared with obesity-resistant rats before diet-induced obesity occurs, total integrated GH concentrations were determined in male Sprague-Dawley rats before exposure to the MHF diet. After initial blood sampling, rats were fed an MHF diet for 15 wk, over which time the animals were separated into two discrete populations based on body weight gain. Analysis of GH in episodic blood samples showed that the obesity-prone group had a GH secretion deficit before the onset of obesity (115.2 +/- 12.9 ng . ml-1 . 200 min-1) compared with obesity-resistant rats (237.2 +/- 47.1 ng . ml-1 . 200 min-1). The GH concentration difference was due to a decrease in mean GH peak height in rats that later became obese (34.8 ng/ml) compared with rats that remained lean (74.2 ng/ml). The results suggest that GH secretion impairment exists before dietary challenge or onset of obesity and may contribute to the susceptibility to obesity observed in these animals.

Animals↗
PubMed2006

Obesity, abdominal obesity and Alzheimer disease.

BACKGROUND/AIMS: Obesity has a strong association with vascular and metabolic diseases, which have been linked with Alzheimer disease (AD). While recent studies have reported an association between mid-life obesity and dementia, the role of later-life obesity is less clear. This study investigated the relation between AD, obesity and abdominal obesity at later-life in a case-control study. METHODS: Participants were 50 consecutive patients with probable AD from memory disorders clinics in Launceston, Australia, and Bristol, England, and 75 cognitively normal controls. Height and weight [from which body mass index (BMI) was calculated] and hip and waist circumferences (from which waist-hip ratio was calculated) were measured. Participants were classified according to their BMI as: underweight (BMI <20.0 kg/m2); normal weight (BMI 20.0-24.9 kg/m2); overweight (BMI 25-29.9 kg/m2), or obese (BMI > or = 30 kg/m2). They were classified as abdominally obese if their waist-hip ratio was >0.9 (men) or >0.8 (women). RESULTS: AD was associated with obesity [OR 9.5, 95% CI 2.4-37.3, p = 0.001], underweight (OR 5.4, CI 0.9-33.7, p = 0.07) and abdominal obesity (OR 2.5, CI 1.1-5.7, p = 0.027) using logistic regression analyses adjusted for age, sex and location. The inclusion of metabolic risk factors in the model increased the ORs for obesity (OR 12.6, CI 2.8-56.5, p = 0.001) and underweight (OR 7.9, CI 1.0-66.3, p = 0.056). CONCLUSION: AD may be associated with obesity, underweight and abdominal obesity at later life. Larger prospective studies are required to investigate this further.

Abdominal Fat↗
PubMed2005

Mid-term Body Mass Index increase among obese and non-obese individuals in middle life and deprivation status: a cohort study.

BACKGROUND: In the UK, obesity is associated with a clear socioeconomic gradient, with individuals of lower socioeconomic status being more likely to be obese. Several previous studies, using individual measures of soecioeconomic status, have shown a more rapid increase in Body Mass Index (BMI) over time among adults of lower socioeconomic status. We conducted a study to further examine whether ecologically defined deprivation status influences within-individual BMI change during middle life, as the answer to this question can help determine optimal preventive strategies both for obesity per se, and its' associated socioeconomic disparities. METHODS: Anonymised records of participants to the Stockport population-based cardiovascular disease risk factor screening programme were analysed. Individuals aged 35-55 who had a first screening episode between 1989 and 1993, and a subsequent screening episode were included in the study. Deprivation status was defined using quintiles of the Townsend score. Mean annual BMI change by deprivation group was calculated using linear regression. Subsequently, deprivation group was included in the model as an ordinal variable, to test for trend. The modelling was repeated separately for individuals who were obese (BMI < 30) and non-obese at the time of first screening. In supplementary analysis, regression models were also adjusted for baseline BMI. RESULTS: Of 21,976 women and 19,158 men initially screened, final analysis included just over half of all individuals [11,158 (50.8%) women and 9,831 (51.3%) men], due to the combined effect of loss to follow-up and incomplete BMI ascertainment. In both sexes BMI increased by 0.19 kg/m2 annually (95% Confidence Intervals 0.15-0.24 for women and 0.16-0.23 for men). All deprivation groups had similar mean annual change, and there was no evidence of a significant deprivation trend (p = 0.801, women and 0.892, men). Restricting the analysis to individuals who were non-obese at baseline did not alter the results in relation to the lack of a deprivation effect. When restricting the analysis to individuals who were obese at baseline however, the findings were suggestive of an association of BMI increase with higher deprivation group, which was further supported by a significant association when adjusting for baseline BMI. CONCLUSION: In the study setting, the BMI of non-obese individuals aged 35-55 was increasing over time independently of deprivation status; among obese individuals a positive association with higher deprivation was found. The findings support that socioeconomic differences in mean BMI and obesity status are principally attained prior to 35 years of age. Efforts to tackle inequalities in mean BMI and obesity status should principally concentrate in earlier life periods, although there may still be scope for focusing inequality reduction efforts on obese individuals even in middle life.

Adult↗
PubMed2006

The outcome of total hip replacement in obese and non-obese patients at 10- to 18-years.

We studied a consecutive series of 285 uncemented total hip replacements in 260 patients using the Taperloc femoral component and the T-Tap acetabular component. The outcome of every hip was determined in both living and deceased patients. A complete clinical and radiological follow-up was obtained for 209 hips in 188 living patients, followed for a mean of 14.5 years (10 to 18.9). They were divided into two groups, obese and non-obese, as determined by their body mass index. There were 100 total hip replacements in 89 patients in the obese cohort (body mass index > or = 30 kg/m(2)), and 109 in 99 non-obese (body mass index < 30 kg/m(2)) patients. A subgroup analysis of 31 patients of normal weight (body mass index 20 kg/m(2) to 25 kg/m(2)) (33 hips) and 26 morbidly obese patients (body mass index > or = 35 kg/m(2)) (30 hips) was also carried out. In the obese group five femoral components (5%) were revised and one (1%) was loose by radiological criteria. Femoral cortical osteolysis was seen in eight hips (8%). The acetabular component was revised in 57 hips (57%) and a further 17 (17%) were loose. The mean Harris hip score improved from 52 (30 to 66) pre-operatively to 89 (49 to 100) at final follow-up. Peri-operative complications occurred in seven patients (7%). In the non-obese group six (6%) femoral components were revised and one (1%) was loose. Femoral cortical osteolysis occurred in six hips (6%). The acetabular component was revised in 72 hips (66%) and a further 18 (17%) were loose. The mean Harris hip score increased from 53 (25 to 73) prior to surgery to 89 (53 to 100) at the time of each patient's final follow-up radiograph. No statistically significant difference was identified between the obese and non-obese patients with regards to clinical and radiological outcome or complications. The subgroup analysis of patients of normal weight and those who were morbidly obese showed no statistically significant difference in the rate of revision of either component. Our findings suggest there is no evidence to support withholding total hip replacement from obese patients with arthritic hips on the grounds that their outcome will be less satisfactory than those who are not obese.

Acetabulum↗
PubMed2004

Correlates of adiponectin and the leptin/adiponectin ratio in obese and non-obese children.

Adiponectin is an adipocyte secreted protein that has been reported to increase fatty acid oxidation and improve insulin sensitivity. Our aim was to study the relationship between adiponectin and leptin, body fat, insulin and lipoproteins in obese compared to non-obese children matched for age and gender. Adiponectin serum concentrations were significantly lower in the obese compared to the non-obese children (9.1+/-3.7 vs 17.1+/-12.3 microg/ml, p <0.05), in contrast to serum leptin concentrations which were greater in the obese compared to the non-obese subjects (31.8+/-11.1 vs 8.2+/-5.7 ng/ml, p <0.001). When considered as a single group to assess adiponectin concentrations over a spectrum of body size, adiponectin values correlated inversely with body weight (r = -0.33, p <0.05) and BMI (r = -0.35, p <0.05). Adiponectin values correlated directly with HDL-C (r = 0.47, p <0.005), but not with total cholesterol, IGF-I, or leptin binding activity. Since leptin and adiponectin change inversely in relation to BMI, the leptin/adiponectin (L/A) ratio was determined as a potential index relating adiposity to the development of complications of obesity. The L/A ratio was eight-fold greater in the obese compared to the non-obese children, and correlated more strongly with BMI (r = 0.779, p <0.0001) and with HDL-C (r = -0.53, p <0.001), than did adiponectin alone. The L/A ratio also correlated significantly with triceps skinfold thickness (TSF) (r = 0.77, p <0.001) and percent body fat (r = 0.79, p <0.0001) in non-obese children. These data suggest that adiponectin concentrations are already differentially regulated in childhood obesity. The index of increased leptin concentration corrected by reduced adiponectin values (L/A ratio) merits investigation as a marker for morbidities associated with childhood obesity.

Adiponectin↗
PubMedDate not supplied

[Familial obesity as a predictor of child obesity].

INTRODUCTION: Studies carried out in various parts of the world indicate that family obesity significantly affects the incidence of obesity in children. This is especially a characteristic of children whose both parents are obese. MATERIAL AND METHODS: The study was conducted using a polling method. Questionnaires were filled out by parents and brothers and sisters, including their body height and weight. The collected data served as the basis for assessing the family nutritional status. RESULTS: Statistical analysis of the results showed that obese children frequently have obese parents, brothers and sisters in regard to normal-weight children. Differences are statistically significant in relation to fathers (p=0.043), i.e. statistically obese schoolchildren have more frequently obese fathers than those of normal nutritional status. Other differences could not be considered significant (p > 0.05). DISCUSSION: Obese children have more often obese parents, brothers and sisters than normal-weight children. It was found that the nutritional status of moderately and extremely obese children was quite different from that of normal-weight children and that there was a statistically significant dependence between the nutritional status of children and their fathers. CONCLUSION: This research showed that family obesity is a potential contributing factor to obesity of schoolchildren.

Child↗
PubMed1997

Leptin levels and insulin sensitivity in obese and non-obese patients with polycystic ovary syndrome.

The study was conducted to assess leptin levels and insulin sensitivity in obese and non-obese patients with polycystic ovary syndrome (PCOS). Twenty-two women with PCOS and 19 control healthy women were included in the study, divided into obese and non-obese groups. Leptin was determined using Linco Research radio-immunoassay while insulin sensitivity was calculated from intravenous glucose tolerance tests with frequent blood sampling using MINMOD analysis. Significantly higher basal leptin levels were found in obese compared to non-obese PCOS (31.76 +/- 3.06 vs. 10.42 +/- 2.31 ng/ml; p < 0.05) as well as in obese in comparison to non-obese controls (29.16 +/- 5.06 vs 8.51 +/- 0.88 ng/ml; p < 0.05). A negative correlation was found between insulin sensitivity and leptin levels in both obese (r = -0.2480; p > 0.05) and non-obese PCOS groups (r = -0.4620; p > 0.05). In conclusion, high serum leptin, insulin and testosterone levels together with reduced insulin sensitivity were found in obese PCOS women, suggesting that high leptin levels could be a characteristic of the obese PCOS phenotype.

Adult↗
PubMed2001

[Evaluation of obesity and diagnostic criteria of obesity as a disease for Japanese].

Obesity causes many undesirable health disorders such as diabetes mellitus, hyperlipidemia, hypertension and so on. Recently, those life style-affecting diseases is increasing, especially the increment of diabetes mellitus is prominent. In 2000, Japan obesity society issued the new standard of the evaluation of obesity and new diagnostic criteria of obesity as a disease for Japanese. According to this issue, obesity was evaluated by body mass index(BMI). And, 18.5 < BMI < 25 is normal, 25 < BMI < 30 is obese 1, 30 < BMI < 35 is obese 2, 35 < BMI < 40 is obese 3, and 40 < is obese 4. Obesity as a disease is defined by two cases. The first category is composed of two items; one is BMI > 25, and the other is having one disease worsen by obesity, such as diabetes mellitus, hyperlipidemia, hypertension, hyperuricemia, coronary heart disease, cerebral infarction, sleep apnea syndrome, fatty liver, deformative arthritis. The second category is the visceral type of obesity with BMI > 25, which was diagnosed by west size, over 85 cm for men, and over 90 cm for women, and by visceral fat area over 100 cm2 in abdominal CT.

Asian People↗
PubMed2002

[Alveolar hypoventilation in the obese: the obesity-hypoventilation syndrome].

The obesity-hypoventilation syndrome (or alveolar hypoventilation in the obese) is a new name for an old syndrome, Pickwickian syndrome. It is defined as chronic alveolar hypoventilation (PaO(2)<70 mmHg, PaCO(2) > 45 mmHg) in obese patient with a body mass index > 30 kg/m(2) who have no other respiratory disease explaining the gas anomalies. The large majority of obese subjects are not hypercapnic, even in case of severe obesity. There are three principal causes explaining alveolar hypoventilation in obese subjects: high cost of the work of respiration, dysfunction of the respiratory centers, repeated episodes of nocturnal obstructive apnea. The obesity-hypoventilation syndrome is generally found in males aged over 50 years. Exercise-induced breathlessness is a constant finding. Diagnosis is often made after an episode of severe respiratory failure. Associated diseases favored by obesity are frequent: diabetes, high blood pressure, heart disease. By definition, there is a hypoxemia-hypercapnia syndrome persisting after an acute episode. Spirography usually demonstrates moderate volume restriction. Pulmonary hypertension is frequent but not constant. Obesity-hypoventilation syndrome must be distinguished from obstructive sleep apnea, although the two conditions are often associated. Obstructive sleep apnea may be absent in certain patients with obesity-hypoventilation syndrome (we have had several cases) and inversely, obesity is not observed in certain patients with obstructive apnea. It should be recalled that the term Pickwickian syndrome designates obesity-hypoventilation syndrome (with or without obstructive apnea) and not obstructive sleep apnea syndrome.

Hemodynamics↗