scholarly journals The effects of puberty on genetic risk for disordered eating: evidence for a sex difference

2011 ◽  
Vol 42 (3) ◽  
pp. 627-637 ◽  
Author(s):  
K. L. Klump ◽  
K. M. Culbert ◽  
J. D. Slane ◽  
S. A. Burt ◽  
C. L. Sisk ◽  
...  
Keyword(s):  
Disordered Eating ◽  
Genetic Risk ◽  
Pubertal Development ◽  
Indirect Evidence ◽  
Ovarian Hormones ◽  
Genetic Effects ◽  
Developmental Differences ◽  
Genetic Influences ◽  
Specific Effects ◽  
Female Specific

BackgroundDifferences in genetic influences on disordered eating are present across puberty in girls. Heritability is 0% before puberty, but over 50% during and after puberty. Emerging data suggest that these developmental differences may be due to pubertal increases in ovarian hormones. However, a critical piece of evidence is lacking, namely, knowledge of genetic influences on disordered eating across puberty in boys. Boys do not experience increases in ovarian hormones during puberty. Thus, if pubertal increases in genetic effects are present in boys, then factors in addition to ovarian hormones may drive increases in heritability in girls. The current study was the first to examine this possibility in a sample of 1006 male and female twins from the Michigan State University Twin Registry.MethodDisordered eating was assessed with the Minnesota Eating Behavior Survey. Pubertal development was assessed with the Pubertal Development Scale.ResultsNo significant differences in genetic influences on disordered eating were observed in males across any developmental stage. Heritability was 51% in boys during pre-puberty, puberty and young adulthood. By contrast, in girls, genetic factors accounted for 0% of the variance in pre-puberty, but 51% of the variance during puberty and beyond. Sex differences in genetic effects were only significant during pre-puberty, as the best-fitting models constrained heritability to be equal across all males, pubertal females and young adult females.ConclusionsThe results highlight sex-specific effects of puberty on genetic risk for disordered eating and provide indirect evidence of a role for ovarian hormones and/or other female-specific factors.

scholarly journals Preliminary evidence that estradiol moderates genetic influences on disordered eating attitudes and behaviors during puberty

2010 ◽  
Vol 40 (10) ◽  
pp. 1745-1753 ◽  
Author(s):  
K. L. Klump ◽  
P. K. Keel ◽  
C. Sisk ◽  
S. A. Burt
Keyword(s):  
Disordered Eating ◽  
Eating Attitudes ◽  
Genetic Effects ◽  
Genetic Influence ◽  
Genetic Influences ◽  
Attitudes And Behaviors ◽  
And Behaviors ◽  
Estradiol Levels ◽  
Disordered Eating Attitudes ◽  
Twin Correlation

BackgroundPuberty moderates genetic influences on disordered eating attitudes and behaviors, with little genetic influence before puberty but large (⩾50%) genetic effects during and after puberty. To date, however, nothing is known about the mechanisms that underlie these effects. Estradiol is a particularly promising candidate, as estrogens become elevated at puberty and regulate gene transcription within neurotransmitter systems important for eating-related phenotypes. The aim of this pilot study was to examine whether estradiol levels moderate genetic influences on disordered eating during puberty.MethodParticipants included 198 female twins (ages 10–15 years) from the Michigan State University Twin Registry. Disordered eating attitudes and behaviors were assessed with the total score, weight preoccupation, body dissatisfaction and binge eating/compensatory behavior subscales of the Minnesota Eating Behavior Survey (MEBS). Afternoon saliva samples were assayed for estradiol levels. Moderation of genetic effects was examined by comparing twin correlations in low versus high estradiol groups.ResultsIn the low estradiol group, monozygotic (MZ) and dizygotic (DZ) twin correlations for all MEBS scales were similar, suggesting little genetic influence. In the high estradiol group, the MZ twin correlation was more than double the DZ twin correlation, indicating the presence of genetic effects. Findings could not be accounted for by age, body mass index or the physical changes of puberty.ConclusionsEstradiol may be one important moderator of genetic effects on disordered eating during puberty. Larger twin studies are needed to replicate this pilot work and quantify the extent of genetic moderation.

scholarly journals Predicting alcohol consumption in adolescence from alcohol-specific and general externalizing genetic risk factors, key environmental exposures and their interaction

2010 ◽  
Vol 41 (7) ◽  
pp. 1507-1516 ◽  
Author(s):  
K. S. Kendler ◽  
C. Gardner ◽  
D. M. Dick
Keyword(s):  
Risk Factors ◽  
Alcohol Consumption ◽  
Alcohol Use ◽  
Genetic Risk ◽  
Genetic Risk Factors ◽  
Genetic Effects ◽  
Prosocial Behaviors ◽  
Genetic Influences ◽  
Alcohol Availability ◽  
Peer Deviance

BackgroundAlcohol consumption is influenced by specific genetic risk factors for alcohol use disorders (AUDs), non-specific genetic risk factors for externalizing behaviors and various environmental experiences. We have limited knowledge of how these risk factors inter-relate through development.MethodRetrospective assessments in 1796 adult male twins using a life history calendar of key environmental exposures and alcohol consumption from early adolescence to mid-adulthood. Analysis by linear mixed models.ResultsThe importance of non-specific genetic risk factors on maximal alcohol consumption rose rapidly in early to mid-adolescence, peaked at ages 15–17 years and then declined slowly. Alcohol-specific genetic risk factors increased slowly in influence through mid-adulthood. We detected robust evidence for environmental moderation of genetic effects on alcohol consumption that was more pronounced in early and mid-adolescence than in later periods. Alcohol availability, peer deviance and low prosocial behaviors showing the strongest moderation effects. More interactions with environmental risk factors were seen for the non-specific externalizing disorder risk than for specific genetic risk for AUDs.ConclusionsThe impact of specific and non-specific genetic influences on alcohol consumption have different development trajectories. Genetic effects on alcohol use are more pronounced when social constraints are minimized (e.g. low prosocial behaviors or parental monitoring) or when the environment permits easy access to alcohol and/or encourages its use (e.g. high alcohol availability or peer deviance). Gene–environment interactions influencing alcohol intake may be more robust at younger ages, indicating greater plasticity of genetic influences early in the development of drinking patterns.

Polygenic Risk Score for Smoking is associated with Externalizing Psychopathology and Disinhibited Personality Traits but not Internalizing Psychopathology in Adolescence

2020 ◽  
Author(s):  
Brian M. Hicks ◽  
D. Angus Clark ◽  
Joseph D. Deak ◽  
Mengzhen Liu ◽  
C. Emily Durbin ◽  
...  
Keyword(s):  
Personality Traits ◽  
Genetic Risk ◽  
Behavioral Control ◽  
Cumulative Exposure ◽  
Genetic Influences ◽  
Behavioral Disinhibition ◽  
Polygenic Risk ◽  
Externalizing Psychopathology ◽  
Internalizing Psychopathology ◽  
Random Intercept

Importance: Large consortia of genome wide association studies have yielded more accurate polygenic risk scores (PRS) that aggregate the small effects of many genetic variants to characterize the genetic architecture of disorders and provide a personalized measure of genetic risk. Objective: We examined whether a PRS for smoking measured genetic risk for general behavioral disinhibition by estimating its associations with externalizing and internalizing psychopathology and related personality traits. We examined these associations at multiple time points in adolescence using more refined phenotypes defined by stable characteristics across time and at young ages, which reduced potential confounds associated with cumulative exposure to substances and reverse causality. Methods: Random intercept panel models were fit to symptoms of conduct disorder, oppositional defiant disorder, major depressive disorder (MDD), and teacher ratings of externalizing and internalizing problems and personality traits at ages 11, 14, and 17 years-old in the Minnesota Twin Family Study (N = 3225). Results: The smoking PRS had strong associations with the random intercept factors for all the externalizing measures (mean standardized ꞵ = .27), agreeableness (ꞵ=-.22, 95% CI: -.28, -.16), and conscientiousness (ꞵ=-.19, 95% CI: -.24, -.13), but was not significantly associated with the internalizing measures (mean ꞵ = .06) or extraversion (ꞵ=.01, 95% CI: -.05, .07). After controlling for smoking at age 17, the associations with the externalizing measures (mean ꞵ = .13) and personality traits related to behavioral control (mean ꞵ = -.10) remained statistically significant. Conclusions and Relevance: The smoking PRS measures genetic influences that contribute to a spectrum of phenotypes related to behavioral disinhibition including externalizing psychopathology and normal-range personality traits related to behavioral control, but not internalizing psychopathology. Continuing to identify the correlates and delineate the mechanisms of the genetic influences associated with disinhibition could have substantial impact in mitigating a variety of public health problems (e.g., mental health, academic achievement, criminality).

Genetic Influences on Eating and the Eating Disorders

2010 ◽  
pp. 102-122
Author(s):  
Tracey D. Wade
Keyword(s):  
Eating Disorders ◽  
Disordered Eating ◽  
Association Studies ◽  
Twin Studies ◽  
Genetic Influences ◽  
Shared Environment ◽  
Complex Nature ◽  
Current State ◽  
Increase Risk ◽  
Eating Practices

The current chapter reviews our progress in understanding how genes influence eating and eating disorders (EDs) by addressing the following areas: (1) how recognition of genetic influences on eating and EDs emerged; (2) the complex nature of genetic action; (3) what twin studies can tell us about genetic influences; and (4) the current state of linkage and association studies. It is concluded that genes are an important part of the explanatory framework for the etiology of EDs, with an important contribution of the shared environment to the development of cognition and attitudes that may initiate disordered eating practices, and a critical contribution of the environment in providing a context within which genetic risk is more likely to be expressed. We currently have a limited understanding of the specific genes that are implicated, and the ways in which genes and the environment work together to increase risk for disordered eating.

Region-specific effects of ovarian hormones on estrogen receptor immunoreactivity

Neuroreport ◽  
1995 ◽  
Vol 6 (15) ◽  
pp. 2054-2058 ◽  
Author(s):  
Lydia L. DonCarlos ◽  
Karl Malik ◽  
Joan I. Morrell
Keyword(s):  
Estrogen Receptor ◽  
Ovarian Hormones ◽  
Specific Effects

scholarly journals Common Genetic Risk of Major Depression and Nicotine Dependence: The Contribution of Antisocial Traits in a United States Veteran Male Twin Cohort

2007 ◽  
Vol 10 (3) ◽  
pp. 470-478 ◽  
Author(s):  
Qiang Fu ◽  
Andrew C. Heath ◽  
Kathleen K. Bucholz ◽  
Michael J. Lyons ◽  
Ming T. Tsuang ◽  
...  
Keyword(s):  
Risk Factors ◽  
Major Depression ◽  
Predominantly White ◽  
Nicotine Dependence ◽  
Genetic Risk ◽  
Genetic Risk Factors ◽  
Diagnostic Interview ◽  
Genetic Influences ◽  
Vietnam Era ◽  
Shared Genetic

AbstractMany studies that found associations between depression and nicotine dependence have ignored possible shared genetic influences associated with antisocial traits. The present study examined the contribution of genetic and environmental effects associated with conduct disorder (CD) and antisocial personality disorder (ASPD) to the comorbidity of major depression (MD) and nicotine dependence (ND). A telephone diagnostic interview, the Diagnostic Interview Schedule-III-R, was administered to eligible twins from the Vietnam Era Twin (VET) Registry in 1992. Multivariate genetic models were fitted to 3360 middle-aged and predominantly white twin pairs (1868 monozygotic, 1492 dizygotic pairs) of which both members completed the pertinent diagnostic interview sections. Genetic influences on CD accounted for 100%, 68%, and 50% of the total genetic variance in risk for ASPD, MD and ND, respectively. After controlling for genetic influences on CD, the partial genetic correlation between MD and ND was no longer statistically significant. Nonshared environmental contributions to the comorbidity among these disorders were not significant. This study not only demonstrates that the comorbidity between ND and MD is influenced by common genetic risk factors, but also further suggests that the common genetic risk factors overlapped with those for antisocial traits such as CD and ASPD in men.

Ovarian hormones, age and pubertal development and their association with days of headache onset in girls with migraine: An observational cohort study

Cephalalgia ◽  
2017 ◽  
Vol 38 (4) ◽  
pp. 707-717 ◽  
Author(s):  
Vincent T Martin ◽  
Janelle R Allen ◽  
Timothy T Houle ◽  
Scott W Powers ◽  
Marielle A Kabbouche ◽  
...  
Keyword(s):  
Pubertal Development ◽  
Urinary Metabolites ◽  
Ovarian Hormones ◽  
Urine Samples ◽  
Standard Deviation Increase ◽  
Separate Model ◽  
Headache Severity ◽  
Headache Onset ◽  
Daily Urine ◽  
Observational Cohort

Background Fifty-three percent of adolescent girls report headaches at the onset of menses, suggesting fluctuations of ovarian hormones trigger migraine during puberty. Aims To determine if urinary metabolites of estrogen and progesterone are associated with days of headache onset (HO) or severity in girls with migraine. Methods This was a pilot study and included 34 girls with migraine balanced across three age strata (pre-pubertal (8–11), pubertal (12–15), and post-pubertal (16–17) years of age). They collected daily urine samples and recorded the occurrence and severity of headache in a daily diary. Urine samples were assayed for estrone glucuronide (E1G) and pregnandiol glucuronide (PdG) and the daily change was calculated (ΔE1G, ΔPdG). Pubertal development was assessed by age, pubertal development score (PDS), and menstrual cycle variance. The primary outcome measures were HO days and headache severity. Generalized linear mixed models were used, and included the hormonal variables and three different representations of pubertal development as covariates. Results Models of HO days demonstrate a significant age*PdG interaction (OR 0.85 [95% CI 0.75, 0.97]) for a 1 standard deviation increase in PdG and three-year increase in age. A separate model showed a significant PDS*PdG interaction (OR −0.85 [95% CI; 0.76, 0.95]). ΔPDG was associated with headache severity in unadjusted models ( p < 0.017). Conclusion Age and pubertal development could moderate the effect of ovarian hormones on days of headache onset in girls with migraine.

Puberty moderates genetic influences on disordered eating

2007 ◽  
Vol 37 (05) ◽  
pp. 627 ◽  
Author(s):  
KELLY L. KLUMP ◽  
PATRICK S. PERKINS ◽  
S. ALEXANDRA BURT ◽  
MATT McGUE ◽  
WILLIAM G. IACONO
Keyword(s):  
Disordered Eating ◽  
Genetic Influences
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