Abstract Purpose This study examined associations of gender identity and sexual orientation with self-reported eating disorder (SR-ED) diagnosis and compensatory behaviors in transgender and ...cisgender college students. Methods Data came from 289,024 students from 223 U.S. universities participating in the American College Health Association–National College Health Assessment II (median age, 20 years). Rates of past-year SR-ED diagnosis and past-month use of diet pills and vomiting or laxatives were compared among transgender students (n = 479) and cisgender sexual minority (SM) male (n = 5,977) and female (n = 9,445), unsure male (n = 1,662) and female (n = 3,395), and heterosexual male (n = 91,599) and female (n = 176,467) students using chi-square tests. Logistic regression models were used to estimate the odds of eating-related pathology outcomes after adjusting for covariates. Results Rates of past-year SR-ED diagnosis and past-month use of diet pills and vomiting or laxatives were highest among transgender students and lowest among cisgender heterosexual men. Compared to cisgender heterosexual women, transgender students had greater odds of past-year SR-ED diagnosis (odds ratio OR, 4.62; 95% confidence interval CI, 3.41–6.26) and past-month use of diet pills (OR, 2.05; 95% CI, 1.48–2.83) and vomiting or laxatives (OR, 2.46; 95% CI, 1.83–3.30). Although cisgender SM men and unsure men and women also had elevated rates of SR-ED diagnosis than heterosexual women, the magnitudes of these associations were lower than those for transgender individuals (ORs; 1.40–1.54). Conclusions Transgender and cisgender SM young adults have elevated rates of compensatory behavior and SR-ED diagnosis. Appropriate interventions for these populations are urgently needed.
Objective
Research indicates a link between ovarian hormones and eating pathology, suggesting that some women with an eating disorder may be ovarian hormone sensitive. Using premenstrual symptoms ...(PMS) as an indirect measure of ovarian hormone sensitivity, we investigated the association between 11 PMS domains and four core eating disorder symptoms: body dissatisfaction, binge eating, purging, and restriction.
Method
Participants were young adult women (N = 455) who completed an online survey. PMS were assessed using the Daily Record of Severity of Problems and eating pathology with the Eating Pathology Symptoms Inventory. Pearson correlations were calculated between PMS domains and eating disorder symptoms followed by a stepwise regression to create a more refined model for each eating disorder symptom, including relevant covariates.
Results
Significant correlations between a majority of eating disorder symptoms and PMS emerged (r's = .13–.37; p < .01). Backward regression revealed significant PMS domain predictors for each symptom. The final models captured a small‐to‐moderate amount of variance for each eating disorder symptom (R2 = 0.06–0.25).
Discussion
Women who experience physical and psychological PMS may be at risk for eating disorder symptoms; PMS could be a marker of ovarian hormone sensitivity in women at risk for an eating disorder. Future studies should address mechanisms underlying this association.
Background: Twin studies have demonstrated shared genetic and environmental effects between eating disorders and alcohol involvement in adults and middle adolescents. However, fewer studies have ...focused on late adolescents or investigated a wide range of eating disorder dimensions and alcohol involvement subscales in both sexes. We examined genetic and environmental correlations among three eating disorder dimensions and two alcohol involvement subscale scores in late adolescent twins using bivariate twin models.Methods: Participants were 3568 female and 2526 male same-sex twins aged 18 years old from the Child and Adolescent Twin Study in Sweden. The Eating Disorder Inventory-2 (EDI) assessed the drive for thinness, bulimia, and body dissatisfaction. Alcohol involvement was assessed with the Alcohol Use Disorder Identification Test consumption (AUDIT-C) and problem (AUDIT-P) subscales.Results: Only phenotypic and twin correlations in female twins met our threshold for twin modeling. The proportion of total variance for each trait accounted for by additive genetic factors ranged from 0.50 to 0.64 in female twins, with the rest explained by nonshared environmental factors and measurement error. Shared environmental factors played a minimal role in the variance of each trait. The strongest genetic correlation (r(a)) emerged between EDI bulimia and AUDIT-P (r(a) = 0.46, 95% confidence interval: 0.37, 0.55), indicating that the proportion of genetic variance of one trait that was shared with the other trait was 0.21. Nonshared environmental correlations between eating disorder dimensions and alcohol involvement ranged from 0.03 to 0.13.Conclusions: We observed distinct patterns of genetic and environmental effects for co-occurring eating disorder dimensions and alcohol involvement in female vs. male twins, supporting sex-specific treatment strategies for late adolescents with comorbid eating disorders and alcohol use disorder. Our findings emphasize the importance of assessing family history of multiple eating disorder dimensions while treating late adolescents with problematic alcohol use, and vice versa, to improve detection and treatment.
Cyclic AMP (cAMP)-dependent signaling is highly implicated in the pathophysiology of alcohol use disorder (AUD), with evidence supporting the efficacy of inhibiting the cAMP hydrolyzing enzyme ...phosphodiesterase 4 (PDE4) as a therapeutic strategy for drinking reduction. Off-target emetic effects associated with non-selective PDE4 inhibitors has prompted the development of selective PDE4 isozyme inhibitors for treating neuropsychiatric conditions. Herein, we examined the effect of a selective PDE4B inhibitor A33 (0–1.0 mg/kg) on alcohol drinking in both female and male mice from two genetically distinct C57BL/6 substrains. Under two different binge-drinking procedures, A33 pretreatment reduced alcohol intake in male and female mice of both substrains. In both drinking studies, there was no evidence for carry-over effects the next day; however, we did observe some sign of tolerance to A33’s effect on alcohol intake upon repeated, intermittent, treatment (5 injections of 1.0 mg/kg, every other day). Pretreatment with 1.0 mg/kg of A33 augmented sucrose intake by C57BL/6NJ, but not C57BL/6J, mice. In mice with a prior history of A33 pretreatment during alcohol-drinking, A33 (1.0 mg/kg) did not alter spontaneous locomotor activity or basal motor coordination, nor did it alter alcohol’s effects on motor activity, coordination or sedation. In a distinct cohort of alcohol-naïve mice, acute pretreatment with 1.0 mg/kg of A33 did not alter motor performance on a rotarod and reduced sensitivity to the acute intoxicating effects of alcohol. These data provide the first evidence that selective PDE4B inhibition is an effective strategy for reducing excessive alcohol intake in murine models of binge drinking, with minimal off-target effects. Despite reducing sensitivity to acute alcohol intoxication, PDE4B inhibition reduces binge alcohol drinking, without influencing behavioral sensitivity to alcohol in alcohol-experienced mice. Furthermore, A33 is equally effective in males and females and exerts a quantitatively similar reduction in alcohol intake in mice with a genetic predisposition for high versus moderate alcohol preference. Such findings further support the safety and potential clinical utility of targeting PDE4 for treating AUD.
The prevalence of psychiatric disorders, such as major depression and anxiety, is higher in sexual minority individuals (eg, those who identify as gay, lesbian, or bisexual or are unsure of their ...orientation) than heterosexual individuals.
Eating disorders and alcohol use also are more common in sexual minority groups, yet the extent to which they co-occur in these individuals is limited. The co-occurrence of eating and alcohol use disorders results in increased morbidity than either disorder alone
and increased mortality for eating disorders.
Extant studies have primarily included young women (for whom sexual identity is not assessed), suggesting that binge eating and inappropriate compensatory behaviors (eg, self-induced vomiting, diet pill misuse, and fasting) are key symptoms contributing to the co-occurrence, regardless of the primary eating disorder diagnosis. Despite its severity, treatment settings frequently overlook eating disorder and alcohol use co-occurrence and no empirically supported treatments exist to treat the disorders when they occur simultaneously. This is problematic because decreasing symptoms for one behavior might increase the presence or frequency of symptoms for the other disorder. One way to provide useful information for the treatment of eating disorder and alcohol use co-occurrence is to examine these associations within more homogeneous groups, ultimately identifying group-specific risk factors.
Background
Alcohol involvement has familial associations with bulimic symptoms (i.e., binge eating, inappropriate compensatory behaviors), with several studies indicating a genetic overlap between ...the two. It is unclear whether overlapping familial risk with alcohol involvement extends to other eating disorder symptoms. Understanding the genetic overlap between alcohol involvement and other eating disorder symptoms may aid in more targeted interventions for comorbid alcohol use‐eating disorder symptoms. Thus, we investigated associations between alcohol involvement and 2 core eating disorder symptoms: drive for thinness and body dissatisfaction in adolescent female and male twins.
Methods
We assessed 3 levels of alcohol involvement: alcohol use in the last month, having ever been intoxicated, and alcohol intoxication frequency via self‐report. The Eating Disorder Inventory‐II assessed drive for thinness and body dissatisfaction. Sex‐specific biometrical twin modeling examined the genetic overlap between alcohol involvement and eating disorder symptoms.
Results
Phenotypic associations between alcohol involvement, drive for thinness, and body dissatisfaction were significantly greater in girls compared with boys. A majority of the associations between alcohol involvement, drive for thinness, and body dissatisfaction in girls, but not boys, met our threshold for twin modeling (phenotypic r > 0.20). Moderate genetic correlations were observed between the 3 aspects of alcohol involvement and drive for thinness. Moderate genetic correlations were observed between alcohol use and intoxication frequency and body dissatisfaction.
Conclusions
Together with the literature on alcohol involvement and bulimic symptoms, these findings suggest a generalized association between alcohol involvement and eating disorder symptoms in girls, whereas this association may be symptom specific in boys. Genetic correlations indicate that the amount and direction of this genetic overlap differs across specific symptoms. When intervening on comorbid alcohol involvement and eating disorder symptoms, it may be important to target‐specific eating disorder symptoms.
It is unclear whether alcohol involvement (AI) has familial associations with eating disorder symptoms beyond symptoms of bulimia nervosa. We investigated associations between alcohol involvement and drive for thinness (DT) and body dissatisfaction (BD) in adolescent twins using sex‐specific biometrical twin modeling. Moderate genetic correlations were observed between AI and DT. Findings suggest the amount and direction of the genetic overlap between AI and eating disorder symptoms differs across specific symptoms.
Objective
Cardiovascular complications occur in up to 80% of patients with anorexia nervosa (AN), yet the underlying mechanisms warrant further investigation. We assessed the genetic correlation (rg) ...between AN and cardiovascular disease (CVD) events to inform whether elevated cardiovascular risk among individuals with AN is due to shared genetic effects.
Method
We used genome‐wide association study summary statistics for AN (N = 72,517), AN with binge eating (N = 12,630), AN without binge eating (N = 12,516), and six CVD events (N = 390,142 to 977,323). We calculated the rgs via linkage disequilibrium score regression and corrected for multiple testing using false discovery rate.
Results
Significant rgs emerged between AN with heart failure (rg = –0.11, SE = 0.05, q = .04) and myocardial infarction (rg = –0.10, SE = 0.03, q = .01). AN with binge eating had a significant rg with myocardial infarction (rg = –0.15, SE = 0.06, q = .02). No significant rg emerged between AN without binge eating and any CVD event.
Discussion
Some loci affect the liability to AN and CVD in opposite directions and the shared genetic effects may not be consistent across all CVD events. Our results provide further evidence suggesting that the elevated cardiovascular risk in AN may not be due to shared genetic underpinnings, but more likely a downstream consequence of the disease.
We calculated the genetic correlation between three anorexia nervosa (AN) phenotypes and six cardiovascular disease (CVD) events. We observed significant (q<.05) genetic correlations between AN with heart failure and myocardial infarction, and between AN with binge eating and myocardial infarction. No significant genetic correlation emerged between AN without binge eating and any CVD event.
Genetics of Anorexia Nervosa Baker, Jessica H.; Schaumberg, Katherine; Munn-Chernoff, Melissa A.
Current psychiatry reports,
11/2017, Volume:
19, Issue:
11
Journal Article
Peer reviewed
Open access
Purpose of Review
Genetic factors contribute to the etiology of anorexia nervosa (AN). This review synthesizes the current state of knowledge about the genetic etiology of AN, provides directions for ...future research, and discusses clinical implications for this research.
Recent Findings
Candidate gene meta-analyses indicate serotonin genes may be involved in the genetic etiology of AN. Three genome-wide association studies have been conducted and one genome-wide significant locus was identified. Cross-disorder analyses suggest shared genetic risk between AN and several psychiatric, educational, and medical phenotypes.
Summary
Much has been learned about the genetic etiology of AN over the past 3 decades. However, to fully understand the genetic architecture, we must consider all aspects including common variation, cross-disorder analysis, rare variation, copy number variation, and gene-environment interplay. Findings have important implications for the development of treatment and prevention approaches and for how AN, and psychiatric and medical diseases in general, are conceptualized.
The extent to which genetic and environmental factors influenced anorexia nervosa (AN), major depressive disorder (MDD), and suicide attempts (SA) were evaluated. Participants were 6,899 women from ...the Swedish Twin Study of Adults: Genes and Environment. A Cholesky decomposition assessed independent and overlapping genetic and environmental contributions to AN, MDD, and SA. Genetic factors accounted for a substantial amount of liability to all three traits; unique environmental factors accounted for most of the remaining liability. Shared genetic factors may underlie the coexpression of these traits. Results underscore the importance of assessing for signs of suicide among individuals with AN.
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