Melanoma,Growth Factors,and Cutaneous Paraneoplastic Syndromes

Paraneoplastic syndromes are systemic reactions in patients with cancers that are unrelated to tumor size or location. Cutaneous paraneoplastic syndromes include proliferative, metabolic, and inflammatory skin disorders. Both systemic and cutaneous paraneoplastic reactions may occur in patients with malignant melanoma. Cancers, including melanoma, may produce growth factors, which may be responsible for proliferative cutaneous paraneoplastic syndromes. A patient with malignant melanoma we previously reported, who had the sudden onset of acanthosis nigricans, skin tags (acrochordons), and seborrheic keratoses provides a model for proliferative cutaneous paraneoplastic syndromes. High levels of α-TGF were found in the patient's urine prior to melanoma removal. The increased level of α-TGF declined after the melanoma was removed, and a corresponding clinical improvement in his acanthosis nigricans, skin tags, and seborrheic keratoses occurred. In the skin lesions, EGF receptors were abnormally present throughout all epidermal layers prior to melanoma removal, and returned to their normal distribution in the basal layers after surgery. Ectopic growth factor production by malignant melanomas and other epithelial neoplasms may cause rare, but distinctive cutaneous paraneoplastic lesions. The model of melanoma, cutaneous paraneoplastic syndromes, and growth factors may provide understanding of both cutaneous lesions associated with neoplasia, and benign cutaneous lesions.     

Hyperinsulinemia Associated With Acanthosis Nigricans,Finger Pebbles,Acrochordons, And The Sign Of Leser-Trélat

ObjectiveTo review common skin manifestations associated with type 2 diabetes mellitus (DM), and to discuss a potential underlying mechanism for these manifestations.MethodsA PubMed literature search was conducted for articles describing the skin manifestations associated with hyperinsulinemia and type 2 DM. A case presentation describes a morbidly obese patient with type 2 DM treated with metformin who developed acanthosis nigricans, finger pebbles, scores of skin tags (acrochordons), and the sign of LeserTrelat (sudden onset shower of seborrheic keratoses) in the absence of internal malignancy.ResultsAcanthosis nigricans, acrochordons, and finger pebbles have been associated with type 2 DM and obesity. While the LeserTrelat sign is classically associated with internal malignancy, it can also be idiopathic. To our knowledge, this the first report of the occurrence of the LeserTrelat sign in a patient with DM absent internal malignancy.ConclusionSeveral skin manifestations can be seen in this patient with DM because of underlying insulin resistance and subsequent stimulation of insulinlike growth factor receptors. Management strategies could include weight loss, diet, and insulinsensitizing pharmacologic therapy. (Endocr Pract. 2013;19:522525)     

Role of obesity and hyperinsulinemia in the insulin resistance of obese subjects with the clinical triad of polycystic ovaries, hirsutism and acanthosis nigricans

The insulin resistance of 4 nonobese and 8 obese patients with polycystic ovaries, hirsutism and benign acanthosis nigricans, and of 6 'obese normal' apart from obesity and 10 normal female subjects was evaluated by means of an intravenous insulin tolerance test and by measuring basal and insulin responses to an oral glucose load. The patients with polycystic ovaries, hirsutism and acanthosis had a decreased hypoglycemic response to exogenous insulin. The subjects with polycystic ovaries presented a significantly greater mean glucose response area for the same or greater mean insulin response area than the obese or nonobese normal subjects. The insulin resistance in the patient with polycystic ovaries, hirsutism and acanthosis nigricans could not be exclusively ascribed to a reduced receptor number, but also appeared to be due to a simultaneous postbinding defect probably related to the high insulin levels in patients with polycystic ovaries be they obese or not. The elevated plasma androgens and the presence of acanthosis found in these patients are likely also related to the hyperinsulinemia. To evaluate the influence of obesity, obese and nonobese patients with acanthosis nigricans and polycystic ovaries were compared. Higher insulin levels were found in the thin subjects, which could explain their greater insulin resistance and more severe hyperandrogenism. The comparison between obese patients with and those without acanthosis nigricans and polycystic ovaries suggested that, despite similar insulin levels, the greater known duration of obesity (probably also of the hyperinsulinemia) of the former was a possible explanation for their more intense insulin resistance and higher testosterone levels.     

The autosomal dominant trait of obesity, acanthosis nigricans, hypertension, ischemic heart disease and diabetes type 2.

OBJECTIVE: Among obese subjects, acanthosis nigricans in both males and females is not as uncommon as previously thought. Whereas this finding was extensively evaluated in females, mostly in the context of polycystic ovaries syndrome, little attention has been paid to obese males with acanthosis nigricans. As acanthosis seems to be a marker for insulin resistance, the present study was designed to evaluate the hypothesis that the clinical syndrome of obesity and acanthosis would take a different clinical course than that of simple obesity. METHODS: To characterize the course of acanthosis nigricans and obesity in males, we examined 22 children and adolescents with this complex, together with their parents and grandparents and found them to follow a detrimental sequence of the metabolic syndrome. We compared the findings to 13 age-matched males with obesity but no clinical apparent acanthosis nigricans. We analyzed the clinical course, fat distribution, glucose, insulin and C-peptide and lipoproteins. RESULTS: Onset of obesity in the metabolic syndrome group was at a mean age of 6.4 years, as compared to 2.3 years in the controls. The metabolic syndrome patients had a truncal (android) distribution of fat and their fasting blood glucose was significantly higher. HDL/total cholesterol was lower. Examination of the pedigrees suggested autosomal dominant inheritance of the obesity and acanthosis nigricans complex, extending to hypertension and ischemic heart disease in the parents' generation, and further extending to include diabetes type 2 in the grandparents' generation. CONCLUSIONS: This metabolic syndrome is inherited as an autosomal dominant trait, with onset of truncal obesity at age 6-7 years, acanthosis nigricans during childhood or adolescence, extending to hypertension and ischemic heart disease during young adulthood, and further extending to include diabetes type 2 in late adulthood. It is recommended that such children should be followed up as an 'at-risk' group, and would probably benefit from intensive weight reduction, which may prevent the later manifestations of the syndrome.     

The Impact of Obesity on Primary Care Visits

Objective: To investigate the influence of patient obesity on primary care physician practice style. Research Methods and Procedures: This was a randomized, prospective study of 509 patients assigned for care by 105 primary care resident physicians. Patient data collected included sociodemographic information, self‐reported health status (Medical Outcomes Study Short Form‐36), evaluation for depression (Beck Depression Index), and satisfaction. Height and weight were measured to calculate the BMI. Videotapes of the visits were analyzed using the Davis Observation Code (DOC). Results: Regression equations were estimated relating obesity to visit length, each of the 20 individual DOC codes, and the six DOC Physician Practice Behavior Clusters, controlling for patient health status and sociodemographics. Obesity was not significantly associated with the length of the visit, but influenced what happened during the visit. Physicians spent less time educating obese patients about their health (p = 0.0062) and more time discussing exercise (p = 0.0075). Obesity was not related to discussions regarding nutrition. Physicians spent a greater portion of the visit on technical tasks when the patient was obese (p = 0.0528). Mean pre‐visit general satisfaction for obese patients was significantly lower than for non‐obese patients (p = 0.0069); however, there was no difference in post‐visit patient satisfaction. Discussion: Patient obesity impacts the medical visit. Further research can promote a greater understanding of the relationships between obese patients and their physicians.     

Production Rates of Cortisol in Obesity

Objective: To determine the metabolic clearance rates (MCRs) and endogenous production rates (PRs) of cortisol (F) in grades 2 and 3 obese men (n = 9) and women (n = 6). Research Methods and Procedures: The MCRs and the endogenous PRs of cortisol (F) were determined in grades 2 and 3 obese men (n = 9) and women (n = 6) using the stable isotope dilution technique and mass spectrometry. Results: In obese women, endogenous PRs of F (0.6 ± 0.4 mg/h) were similar to those of nonobese women, but MCRs of F were higher in obese women (9 ± 4 L/h) compared with nonobese women (5 + 2 L/h; p < 0.05). The MCR of F was correlated with the ratio of excreted cortisone to F metabolites. Furthermore, obese women were characterized by an increased ratio of androsterone to etiocholanolone (p < 0.01). In obese men, the MCRs (11 ± 6 L/h) and the endogenous PRs of F (0.6 ± 0.3 mg/h) were both similar to those of nonobese men, but the MCR of F was directly correlated with the ratio of excreted cortisone to F metabolites (r = 0.7833, p = 0.012). Discussion: These data demonstrate sex‐specific differences in F metabolism in obesity. The rise in MCRs of F is more pronounced in obese women than in men. However, the increase in the MCR of F is moderate in both genders and exceeds the normal range only in a subgroup of obese individuals.     

Resistin,Adiponectin, Ghrelin,Leptin, and Proinflammatory Cytokines: Relationships in Obesity

Objective: To evaluate interactions among leptin, adiponectin, resistin, ghrelin, and proinflammatory cytokines [tumor necrosis factor receptors (TNFRs), interleukin‐6 (IL‐6)] in nonmorbid and morbid obesity. Research Methods and Procedures: We measured these hormones by immunoenzyme or radiometric assays in 117 nonmorbid and 57 morbidly obese patients, and in a subgroup of 34 morbidly obese patients before and 6 months after gastric bypass surgery. Insulin resistance by homeostasis model assessment, lipid profile, and anthropometrical measurements were also performed in all patients. Results: Average plasma lipids in morbidly obese patients were elevated. IL‐6, leptin, adiponectin, and resistin were increased and ghrelin was decreased in morbidly obese compared with nonmorbidly obese subjects. After adjusting for age, gender, and BMI in nonmorbidly obese, adiponectin was positively associated with HDLc and gender and negatively with weight (β = ?0.38, p < 0.001). Leptin and resistin correlated positively with soluble tumor necrosis factor receptor (sTNFR) 1 (β = 0.24, p = 0.01 and β = 0.28, p = 0.007). In the morbidly obese patients, resistin and ghrelin were positively associated with sTNFR2 (β = 0.39, p = 0.008 and β = 0.39, p = 0.01). In the surgically treated morbidly obese group, body weight decreased significantly and was best predicted by resistin concentrations before surgery (β = 0.45, p = 0.024). Plasma lipids, insulin resistance, leptin, sTNFR1, and IL‐6 decreased and adiponectin and ghrelin increased significantly. Insulin resistance improved after weight loss and correlated with high adiponectin levels. Discussion: TNFα receptors were involved in the regulatory endocrine system of body adiposity independently of leptin and resistin axis in nonmorbidly obese patients. Our results suggest coordinated roles of adiponectin, resistin, and ghrelin in the modulation of the obesity proinflammatory environment and that resistin levels before surgery treatment are predictive of the extent of weight loss after bypass surgery.     

Getting Worse: The Stigmatization of Obese Children

Objective: The prevalence of childhood obesity more than doubled in the period from 1961 to 2001. We replicated a 1961 study of stigma in childhood obesity to see what effect this increased prevalence has had on this stigma. Research Methods and Procedures: Participants included 458 5th‐ and 6th‐grade children attending upper‐middle and lower‐middle income U.S. public schools. Children ranked six drawings of same‐sex children with obesity, various disabilities, or no disability (“healthy”), in order of how well they liked each child. Results: Children in both the present and the 1961 study liked the drawing of the obese child least. The obese child was liked significantly less in the present study than in 1961 [Kruskal‐Wallis H (1) = 130.53, p < 0.001]. Girls liked the obese child less than boys did [H (1) = 5.23, p < 0.02]. Children ranked the healthy child highest and significantly higher than in 1961 [H (1) = 245.40, p < 0.001]. The difference in liking between the healthy and obese child was currently 40.8% greater than in 1961. Discussion: Stigmatization of obesity by children appears to have increased over the last 40 years.     

The Feet of Overweight and Obese Young Children: Are They Flat or Fat?

Objective: The purpose of this study was to determine whether the flat feet displayed by young obese and overweight children are attributable to the presence of a thicker midfoot plantar fat pad or a lowering of the longitudinal arch relative to that in non‐overweight children. Research Methods and Procedures: Foot anthropometry, an arch index derived from plantar footprints, and midfoot plantar fat pad thickness measured by ultrasound were obtained for 19 overweight/obese preschool children (mean age, 4.3 ± 0.9 years; mean height, 1.07 ± 0.1 m; mean BMI, 18.6 ± 1.2 kg/m²) and 19 non‐overweight children matched for age, height, and sex (mean age, 4.3 ± 0.7 years; mean height, 1.05 ± 0.1 m; mean BMI, 15.7 ± 0.7 kg/m²). Results: Independent t tests revealed no significant between‐subject group differences (p = 0.39) in the thickness of the midfoot plantar fat pad. However, the overweight/obese children had a significantly lower plantar arch height (0.9 ± 0.3 cm) than their non‐overweight counterparts (1.1 ± 0.2 cm; p = 0.04). Discussion: The lower plantar arch height found in the overweight/obese children suggests that the flatter feet characteristic of overweight/obese preschool children may be caused by structural changes in their foot anatomy. It is postulated that these structural changes, which may adversely affect the functional capacity of the medial longitudinal arch, might be exacerbated if excess weight bearing continues throughout childhood and into adulthood.     

Stigmatized Students: Age,Sex, and Ethnicity Effects in the Stigmatization of Obesity

Objective: To assess the stigmatization of obesity relative to the stigmatization of various disabilities among young men and women. Attitudes across ethnic groups were compared. In addition, these findings were compared with data showing severe stigmatization of obesity among children. Research Methods and Procedures: Participants included 356 university students (56% women; mean age, 20.6 years; mean BMI, 23.3 kg/m²; range, 14.4 to 45.0 kg/m²) who ranked six drawings of same‐sex peers in order of how well they liked each person. The drawings showed adults with obesity, various disabilities, or no disability. These rankings were compared with those obtained through a similar procedure with 458 fifth‐ and sixth‐grade children. Results: Obesity was highly stigmatized relative to physical disabilities. African‐American women liked obese peers more than did African‐American men, white men, or white women [F (1, 216) = 4.02, p < 0.05]. Overweight and obese participants were no less stigmatizing of obesity than normal weight participants. Adults were more accepting than children of their obese peers [t (761) = 9.16, p < 0.001]. Discussion: Although the stigmatization of obesity was high among participants overall, African‐American women seemed to have more positive attitudes toward obesity than did white women, white men, or African‐American men. Participants’ weight did not affect their stigmatization of obesity: obese and overweight adults were as highly stigmatizing of obesity as non‐overweight adults. Such internalized stigmatization could help to explain the low self‐esteem and poor body image among obese young adults. However, adults seemed to have more positive attitudes about obesity than children. An understanding of the factors that limit the stigma of obesity among African‐American women could help efforts to reduce stigma.     

Comparison of body fat composition and serum adiponectin levels in diabetic obesity and non-diabetic obesity

Objective: Clinical aspects of diabetes and obesity are somewhat different, even at similar levels of insulin resistance. The purpose of this study was to determine differences in body fat distribution and serum adiponectin concentrations in diabetic and non‐diabetic obese participants. We were also interested in identifying the characteristics of insulin resistance in these two groups, particularly from the standpoint of adiponectin. Research Methods and Procedures: Adiponectin concentrations of 112 type 2 diabetic obese participants and 124 non‐diabetic obese participants were determined. Abdominal adipose tissue areas and midthigh skeletal muscle areas were measured by computed tomography. A homeostasis model assessment of the insulin resistance score was calculated to assess insulin sensitivity. The relationships among serum adiponectin, body fat distribution, and clinical characteristics were also analyzed. Results: Both abdominal subcutaneous and visceral fat areas were higher in the non‐diabetic obese group, whereas midthigh low‐density muscle area was higher in the diabetic obese group. The homeostasis model assessment of the insulin resistance score was similar between groups, whereas serum adiponectin was lower in the diabetic obese group. Abdominal visceral fat (β = ?0.381, p = 0.012) was a more important predictor of adiponectin concentration than low‐density muscle (β = ?0.218, p = 0.026) in cases of non‐diabetic obesity, whereas low‐density muscle (β = ?0.413, p = 0.013) was a better predictor of adiponectin level than abdominal visceral fat (β = ? 0.228, p = 0.044) in diabetic obese patients. Discussion: Therefore, factors involved in pathophysiology, including different serum adiponectin levels and body fat distributions, are believed to be responsible for differences in clinical characteristics, even at similar levels of insulin resistance in both diseases.     

Autonomic Nervous System Activity and the State and Development of Obesity in Japanese School Children

Objective: The autonomic nervous system (ANS) plays an important role in regulating energy expenditure and body fat content; however, the extent to which the ANS contributes to pediatric obesity remains inconclusive. The aim of this study was to evaluate whether sympathetic and/or the parasympathetic nerve activities were altered in an obese pediatric population. We further examined a physiological association between the duration of obesity and the sympatho‐vagal activities to scrutinize the nature of ANS alteration as a possible etiologic factor of childhood obesity. Research Methods and Procedures: Forty‐two obese and 42 non‐obese healthy sedentary school children were carefully selected from 1080 participants initially recruited to this study. The two groups were matched in age, gender, and height. The clinical records of physical characteristics and development of the obese children were retrospectively reviewed to investigate the onset and progression of obesity. The ANS activities were assessed during a resting condition by means of heart rate variability power spectral analysis, which enables us to identify separate frequency components, i.e., total power (TP), low‐frequency (LF) power, and high‐frequency (HF) power. The spectral powers were then logarithmically transformed for statistical testing. Results: The obese children demonstrated a significantly lower TP (6.77 ± 0.12 vs. 7.11 ± 0.04 ln ms², p < 0.05), LF power (6.16 ± 0.12 vs. 6.42 ± 0.05 ln ms², p < 0.05), and HF power (5.84 ± 0.15 vs. 6.34 ± 0.07 ln ms², p < 0.01) compared with the non‐obese children. A partial correlation analysis revealed that the LF and HF powers among 42 obese children were negatively associated with the duration of obesity independent of age (LF: partial r = ?0.55, p < 0.001; HF: partial r = ?0.40, p < 0.01). The obese children were further subdivided into two groups based on the length of their obesity. All three spectral powers were significantly reduced in the obese group with obesity of >3 years (n = 18) compared to the group with obesity of <3 years. Discussion: Our data indicate that obese children possess reduced sympathetic as well as parasympathetic nerve activities. Such autonomic depression, which is associated with the duration of obesity, could be a physiological factor promoting the state and development of obesity. These findings further imply that preventing and treating obesity beginning in the childhood years could be an urgent and crucial pediatric public health issue.     

Calcium and Magnesium ATPase Activities in Women with Varying BMIs

Objective: Intracellular calcium (Ca) is increased in obese humans, and magnesium (Mg)‐ATPase activity is increased in monosodium glutamate‐induced obese rats. The aims of this study were to test the hypotheses that Ca‐ATPase activity is negatively correlated with BMI, and that Mg‐ATPase activity is positively correlated with BMI and Ca‐ATPase activity in obese women. Research Methods and Procedures: Thirty healthy adult women, with BMIs of 20 to 40, donated a single sample of whole blood and were interviewed as to medical history and family history of obesity. Erythrocyte membranes were isolated and assayed for Ca‐ATPase and Mg‐ATPase. Weight and height were self‐reported. Regression analysis was used to determine relationship between BMI and enzyme activity. Family history of obesity served as a covariant. Results: Ca‐ATPase was negatively correlated with increasing BMI (r = ? 0.38, p = 0.02). The relationship between BMI and Ca‐ATPase remained valid after controlling for family history of obesity (r = ?0.36, p = 0.03). There was a positive correlation between Mg‐ATPase activity and Ca‐ATPase (r = 0.42, p = 0.024), and this relationship remained valid after controlling for BMI and family history of obesity (r = 0.41, p = 0.03). Discussion: Ca‐ATPase activity decreases as BMI increases. Decreased ATPase activity may contribute to increased intracellular calcium, previously reported in obese persons. Further studies are needed to determine whether a drop in Ca‐ATPase activity can serve as a marker for the development of obesity.     

Weight Loss Reduces Tissue Factor in Morbidly Obese Patients

Objective: To investigate the tissue factor (TF) pathway in clinical obesity and associated metabolic syndrome. Research Methods and Procedures: Thirty‐seven morbidly obese patients (4 men; BMI, 48 ± 7 kg/m²; range, 42 to 53 kg/m²), undergoing elective gastroplasty for the induction of weight loss, were examined for hemostatic, metabolic, and inflammatory parameters at baseline and 14 ± 5 months postoperatively. Results: Weight loss significantly reduced circulating plasma TF (314 ± 181 vs. 235 ± 113 pg/mL, p = 0.04), coagulation factor VII (130 ± 22% vs. 113 ± 19%, p = 0.023), and prothrombin fragment F1.2 (2.4 ± 3.4 vs. 1.14 ± 1.1 nM, p = 0.04) and normalized glucose metabolism in 50% of obese patients preoperatively classified as diabetic or of impaired glucose tolerance. The postoperative decrease in plasma TF correlated with the decrease of F1.2 (r = 0.56; p = 0.005), a marker of in vivo thrombin formation. In subgroup analysis stratified by preoperative glucose tolerance, baseline circulating TF (402.6 ± 141.6 vs. 176.2 ± 58.2, p < 0.001) and TF decrease after gastroplasty (ΔTF: 164.7 ± 51.4 vs. ?81 ± 31 pg/mL, p = 0.02) were significantly higher in obese patients with impaired glucose tolerance than in patients with normal glucose tolerance. Discussion: Procoagulant TF is significantly reduced with weight loss and may contribute to a reduction in cardiovascular risk associated with obesity.     

Lipoprotein Oxidation and Plasma Vitamin E in Nondiabetic Normotensive Obese Patients

Objective: To correlate the susceptibility of low‐(LDL) and very‐low‐density lipoprotein to oxidation in vitro and the concentrations of serum antibodies against malondialdehyde‐modified LDL and plasma vitamin E with the anthropometric and laboratory characteristics of obesity. Research Methods and Procedures: A total of 75 nondiabetic, normotensive obese patients were assigned to one of four groups according to their body mass index (BMI): moderately obese (30 ≤ BMI ≤ 34.9 kg/m², n = 11), severely obese (35 ≤ BMI ≤ 39.9 kg/m², n = 20), morbidly obese (40 ≤ BMI ≤ 50 kg/m², n = 29), and very severely obese (BMI > 50 kg/m², n = 15). Results: The oxidation lag time for LDL from patients with a BMI ≥35 kg/m² was shorter than that for LDL from non‐obese controls (n = 13), whereas very‐low‐density lipoprotein oxidation lag times were not significantly different. The serum antibodies against modified LDL were similar in all groups, whereas the plasma vitamin E concentrations of obese patients were decreased (p ≤ 0.01). There was a negative correlation between LDL oxidation lag time and BMI (r = ?0.35, p = 0.0008), and between plasma vitamin E and BMI (r = ?0.53, p < 0.0001) and waist‐to‐hip ratio (r = ?0.40, p = 0.0003). Discussion: The LDL of nondiabetic, normotensive obese patients is more readily oxidized, and plasma vitamin E concentrations are low. These are both risk factors for coronary heart disease.     

Association of Obesity,but not Diabetes or Hypertension,with Glucocorticoid Receptor N363S Variant

Objective: To determine whether the N363S variant in the glucocorticoid receptor (encoded by nuclear receptor subfamily 3, group C, member 1: NR3C1) is associated with obesity, type 2 diabetes, or hypertension. Research Methods and Procedures: This was a cross‐sectional case‐control study involving 951 Anglo‐Celtic/Northern European subjects from Sydney. This study consisted of the following: 1) an obesity clinic group, most of whom had “morbid obesity” (mean BMI for group = 43 ± 8 kg/m²; n = 152); 2) a type 2 diabetes clinic group (n = 356); 3) patients with essential hypertension who had a strong family history (n = 141); and 4) normal healthy controls (n = 302). N363S genotype, BMI, and a range of other parameters relevant to each group were measured. Results: Compared with the frequency of 0.04 in nonobese healthy subjects, the S363 allele was significantly higher in obesity clinic patients (0.17; p = 5.6 × 10^?8), subjects with diabetes who were also obese (0.09; p = 0.0045), subjects with hypertension who were also overweight (0.08; p = 0.0016), and overweight healthy subjects (0.12; p = 0.0004). Discussion: The NR3C1 N363S variant is associated with obesity and overweight in a range of patient settings but is not associated with hypertension or type 2 diabetes.     

Central obesity as a risk factor for prostatic hyperplasia

Objective: Obesity‐related metabolic diseases may influence prostatic hyperplasia. This study examined the impact of obesity on prostate volume in men without overt obesity‐related metabolic diseases. Research Methods and Procedures: We recruited 146 men over the age of 40 years who did not have overt obesity‐related diseases, such as diabetes, impaired fasting glucose, hypertension, or dyslipidemia. Transrectal ultrasonography was performed on all subjects. The subjects were divided into three groups according to their BMI: normal (18.5 to 22.9 kg/m²), overweight (23 to 24.9 kg/m²), and obese (≥25 kg/m²), and two groups according to their waist circumference: normal waist (≤90 cm) and central obesity (>90 cm). The classification of the subgroups was based on the Asia‐Pacific criteria of obesity. We compared the prostate volume among subgroups and assessed factors related to prostatic hyperplasia. Results: Mean prostate volume was 18.8 ± 5.0, 21.8 ± 7.2, and 21.8 ± 5.6 mL in the normal, overweight, and obese groups, respectively, and was 20.0 ± 5.9 and 23.7 ± 5.3 mL in the normal waist and central obesity group, respectively. Prostate volume was significantly greater in the obese group than in the normal group (P = 0.03) and in the central obesity group compared with the normal waist group (P = 0.002). Prostate volume was positively correlated with BMI and waist circumference after adjustment for age. After adjusting for confounding factors, central obesity was an independent factor affecting prostatic hyperplasia, which was defined as a prostate volume >20 mL (odds ratio = 3.37, p = 0.037). Relative to men with both low BMI (18.5 to 22.9 kg/m²) and normal waist circumference, those with high BMI (≥25 kg/m²) and central obesity were at significantly increased risk of prostatic hyperplasia (odds ratio = 4.88, p = 0.008). However, those with high BMI (≥25 kg/m²) and normal waist circumference were not at significantly increased risk. Discussion: Prostate volume was greater in the obese and central obesity groups than in the normal group after patients with overt obesity‐related metabolic diseases were excluded. Although both BMI and waist circumference were positively correlated with prostate volume, central obesity was the only independent factor affecting prostate hyperplasia. We suggest that central obesity is an important risk factor for prostatic hyperplasia.     

Dietary Intake in Relation to Restrained Eating,Disinhibition, and Hunger in Obese and Nonobese Swedish Women

The aims of this study were to: describe dietary intakes of obese and nonobese middle-aged women using a validated food frequency questionnaire; to assess dietary restraint, disinhibition, and hunger by the three factor eating questionnaire (TFEQ) in obese and nonobese samples and determine which of the factors are independently associated with obesity; and to examine correlations between selected nutritional variables and the TFEQ factors. Subjects studied included 179 obese Swedish women (BMI>32) and 147 nonobese population-based controls (BMI<28). Age-adjusted mean energy intake was significantly higher in obese women (2730 ± 78 vs. 2025 ± 85 kcal, p<0.0001). In absolute and relative terms, fat intake was higher and alcohol intake was lower in the obese subjects. Disinhibition was the strongest TFEQ factor independently differentiating the obese and nonobese states, i.e., after adjustment for restraint and hunger. Within the obese sample, strong associations were seen between energy intake and disinhibition (p=0.0005) and hunger (p=0.0004). The association between energy intake and restrained eating was negative and weaker (p=0.04). No such associations were seen in nonobese women. Thus, using a dietary instrument that is valid and unbiased with respect to obesity, strong psychological correlates, possibly causal, of variability in energy intake were detected in middle-aged women with obesity. Disinhibition is associated with both obesity and high-energy intakes and is therefore an important factor to consider in the treatment of women with obesity.