Search

Background Obesity susceptibility genes are highly expressed in the brain suggesting that they might exert their influence on body weight through eating-related behaviors. Objectives To examine whether the genetic susceptibility to obesity is mediated by eating behavior patterns. Methods Participants were 3977 twins (33% monozygotic, 56% females), aged 31–37 y, from wave 5 of the FinnTwin16 study. They self-reported their height and weight, eating behaviors (15 items), diet quality, and self-measured their waist circumference (WC). For 1055 twins with genome-wide data, we constructed a polygenic risk score for BMI (PRSBMI) using almost 1 million single nucleotide polymorphisms. We used principal component analyses to identify eating behavior patterns, twin modeling to decompose correlations into genetic and environmental components, and structural equation modeling to test mediation models between the PRSBMI, eating behavior patterns, and obesity measures. Results We identified 4 moderately heritable (h 2 = 36–48%) eating behavior patterns labeled "snacking," "infrequent and unhealthy eating," "avoidant eating," and "emotional and external eating." The highest phenotypic correlation with obesity measures was found for the snacking behavior pattern (r  = 0.35 for BMI and r  = 0.32 for WC; P  < 0.001 for both), largely due to genetic factors in common (bivariate h 2 > 70%). The snacking behavior pattern partially mediated the association between the PRSBMI and obesity measures (β indirect = 0.06; 95% CI: 0.02, 0.09; P  = 0.002 for BMI; and β indirect = 0.05; 95% CI: 0.02, 0.08; P  = 0.003 for WC). Conclusions Eating behavior patterns share a common genetic liability with obesity measures and are moderately heritable. Genetic susceptibility to obesity can be partly mediated by an eating pattern characterized by frequent snacking. Obesity prevention efforts might therefore benefit from focusing on eating behavior change, particularly in genetically susceptible individuals. [ABSTRACT FROM AUTHOR]

Objective: Binge eating disorder (BED) is a clinical eating disorder that is strongly and bidirectionally related to overweight and obesity. Little is known about how subclinical features of BED relate to weight development in adolescence and young adulthood.Method: Women (n = 2825) and men (n = 2423) from the community-based longitudinal FinnTwin16 cohort participated. Seven eating-related cognitions and behaviors similar to the defining features of BED were extracted from the Eating Disorder Inventory-2 and were assessed at a mean age of 24. We used linear mixed models to assess the association of features of BED with BMI trajectories across four waves of data collection (mean ages 16, 17, 18, and 24).Results: The number of features of BED at wave 4 (age 24) was significantly associated with BMI from age 16 years onwards. Those reporting more features of BED had gained more weight throughout adolescence and into their twenties.Conclusions: Features of BED in young adulthood were preceded by steeper BMI trajectories in adolescence. A higher number of features were consistently associated with higher BMI and more weight gain. [ABSTRACT FROM AUTHOR]

Objectives: To assess factors associated with successful weight maintenance over ten years in a prospective general population sample of young adults.Material and Methods: Our study comprised 2452 women and 2227 men born in 1975-1979 (mean age at baseline 24 years, attrition 27.1%). Weight maintenance was defined as weight maintained within ±5% of baseline body mass index (BMI). We examined the role of various sociodemographic and lifestyle factors in successful weight maintenance.Results: Relatively few young adults were able to maintain their weight over ten years (28.6% of women vs. 23.0% of men); net weight loss was uncommon (7.5% and 3.8%). Most participants gained weight (mean annual weight gain was 0.9 kg in women and 1.0 kg in men). Among women, exercise was associated with successful weight maintenance, but having two or more children, frequent use of sweet drinks, irregular eating, history of dieting (intentional weight loss) and low life satisfaction were associated with weight gain. Among men, higher baseline BMI and higher education were associated with successful weight maintenance, whereas irregular eating, history of dieting and smoking were associated with weight gain.Conclusions: Only about a quarter of young adults were able to resist weight gain. Regular eating and having no history of dieting were associated with successful weight maintenance in young women and men. [ABSTRACT FROM AUTHOR]

Obesity and ageing are associated with lower serum testosterone levels in men. How fat distribution or adipose tissue metabolism, independent of genetic factors and age, are related to sex steroid metabolism is less clear. We studied the associations between adiposity and serum sex hormone concentrations, and mRNA expression of genes regulating sex hormone metabolism in adipose tissue in young adult male monozygotic (MZ) twin pairs. The subjects [n = 18 pairs; mean age, 32 years; individual body mass indexes (BMIs) 22–36 kg/m 2 ] included 9 male MZ twin pairs discordant for BMI [intra-pair difference (Δ) in BMI ≥3 kg/m 2 ]. Sex steroid concentrations were determined by liquid chromatography–tandem mass spectrometry, body composition by dual-energy X-ray absorptiometry and magnetic resonance imaging, and mRNA expressions from subcutaneous adipose tissue by Affymetrix. In BMI-discordant pairs (mean ΔBMI = 5.9 kg/m 2 ), serum dihydrotestosterone (DHT) was lower [mean 1.9 (SD 0.7) vs . 2.4 (1.0) nmol/l, P = 0.040] and mRNA expressions of DHT-inactivating AKR1C2 ( P = 0.021) and cortisol-producing HSD11B1 ( P = 0.008) higher in the heavier compared to the leaner co-twins. Serum free 17 β -estradiol (E2) was higher [2.3 (0.5) vs . 1.9 (0.5) pmol/l, P = 0.028], and in all twin pairs, serum E2 and estrone concentrations were higher in the heavier than in the leaner co-twins [107 (28) vs . 90 (22) pmol/l, P = 0.006; and 123 (43) vs . 105 (27) pmol/l, P = 0.025]. Within all twin pairs, i.e. independent of genetic effects and age, 1) the amount of subcutaneous fat inversely correlated with serum total and free testosterone, DHT, and sex hormone-binding globulin (SHBG) concentrations ( P < 0.01 for all), 2) intra-abdominal fat with total testosterone and SHBG ( P < 0.05), and 3) liver fat with SHBG ( P = 0.006). Also, 4) general and intra-abdominal adiposity correlated positively with mRNA expressions of AKR1C2 , HSD11B1 , and aromatase in adipose tissue ( P < 0.05). In conclusion, acquired adiposity was associated with decreased serum DHT and increased estrogen concentrations, independent of genetic factors and age. The reduction of DHT could be linked to its increased degradation (by AKR1C2 and HSD11B1) and increased estrogen levels to increased adiposity-related expression of aromatase in adipose tissue. [ABSTRACT FROM AUTHOR]

The definition of anorexia nervosa was revised for the Fifth Edition of the Diagnostic and Statistical Manual (DSM-5). We examined the impact of these changes on the prevalence and prognosis of anorexia nervosa. In a nationwide longitudinal study of Finnish twins born 1975–1979, the women (N = 2825) underwent a 2-stage screening for eating disorders at mean age 24. Fifty-five women fulfilled DSM-IV criteria for lifetime anorexia nervosa. When we recoded the interviews using DSM-5 criteria, we detected 37 new cases. We contrasted new DSM-5 vs. DSM-IV cases to assess their clinical characteristics and prognosis. We also estimated lifetime prevalences and incidences and tested the association of minimum BMI with prognosis. We observed a 60% increase in the lifetime prevalence of anorexia nervosa using the new diagnostic boundaries, from 2.2% to 3.6%. The new cases had a later age of onset (18.8 y vs. 16.5, p = 0.002), higher minimum BMI (16.9 vs. 15.5 kg/m 2 , p = 0.0004), a shorter duration of illness (one year vs. three years, p = 0.002), and a higher 5-year probability or recovery (81% vs. 67%, p = 0.002). Minimum BMI was not associated with prognosis. It therefore appears that the substantial increase in prevalence of anorexia nervosa is offset by a more benign course of illness in new cases. Increased diagnostic heterogeneity underscores the need for reliable indicators of disease severity. Our findings indicate that BMI may not be an ideal severity marker, but should be complemented by prognostically informative criteria. Future studies should focus on identifying such factors in prospective settings. [ABSTRACT FROM AUTHOR]

Objective: Some studies indicate an association between napping and increased risk of type 2 diabetes. We studied this prospectively in a sample representative of general population.Methods: A questionnaire was administered to the Finnish Twin Cohort in 1990 (response rate 77%, age 33-60 years). The study population included 12,244 subjects who replied to the question "Do you sleep during the daytime (take naps)?" with five response alternatives ranging from "no need" to "every or almost every day." Information on incident cases of diabetes was obtained by linkage to nationwide registers. Logistic regression models were used to obtain odds ratios (ORs) (95% confidence intervals) for incident type 2 diabetes risk in 1991-2004 by napping category. Adjustments were made for 11 socio-demographic and lifestyle covariates. For subjects aged 33-45 years at baseline, a questionnaire in 2011 provided information on prevalent diabetes.Results: Thirty-four per cent had no need for napping, and 15% did so on ≥3 days weekly. There were 356 incident type 2 diabetes cases during the follow-up. Using the 'no need' category as the reference, the risk of type 2 diabetes was significantly increased only among those napping most frequently [OR 1.86 (1.29-2.67), age- and sex-adjusted]. After adjusting for other covariates, the results were essentially the same, but when adjusted for body mass index, the association decreased (to about 1.3) and was statistically non-significant. Analysis of 2011 self-reported type 2 diabetes was in line with the register data.Conclusions: Frequent napping is associated with future risk of type 2 diabetes. This association is largely explained by obesity. [ABSTRACT FROM AUTHOR]