Sex differences in genetic and environmental risk factors for irrational fears and phobias

2002 ◽  
Vol 32 (2) ◽  
pp. 209-217 ◽  
Author(s):  
K. S. KENDLER ◽  
K. C. JACOBSON ◽  
J. MYERS ◽  
C. A. PRESCOTT
Keyword(s):  
Risk Factors ◽  
Sex Differences ◽  
Genetic Risk ◽  
Threshold Model ◽  
Twin Studies ◽  
Genetic Effects ◽  
Males And Females ◽  
The Impact ◽  
Best Fit ◽  
Twin Resemblance

Background. For irrational fears and their associated phobias, epidemiological studies suggest sex differences in prevalence and twin studies report significant genetic effects. How does sex impact on the familial transmission of liability to fears and phobias?Methods. In personal interviews with over 3000 complete pairs (of whom 1058 were opposite-sex dizygotic pairs), ascertained from a population-based registry, we assessed the lifetime prevalence of five phobias and their associated irrational fears analysed using a multiple threshold model. Twin resemblance was assessed by polychoric correlations and biometrical model-fitting incorporating sex-specific effects.Results. For agoraphobia, situational and blood/injury fear/phobia, the best fit model suggested equal heritability in males and females and genetic correlations between the sexes of less than +0·50. For animal fear/phobias by contrast, the best fit model suggested equal heritability in males and females and a genetic correlation of unity. No evidence was found for an impact of family environment on liability to these fears or phobias. For social phobias, twin resemblance in males was explained by genetic factors and in females by familial–environmental factors.Conclusion. The impact of sex on genetic risk may differ meaningfully across phobia subtypes. Sex-specific genetic risk factors may exist for agoraphobia, social, situational and blood-injury phobias but not for animal fear/phobia. These results should be interpreted in the context of the limited power of twin studies, even with large sample sizes, to resolve sex-specific genetic effects.

Sex similarities and differences in risk factors for recurrence of major depression

2017 ◽  
Vol 48 (10) ◽  
pp. 1685-1693 ◽  
Author(s):  
Hanna M. van Loo ◽  
Steven H. Aggen ◽  
Charles O. Gardner ◽  
Kenneth S. Kendler
Keyword(s):  
Risk Factors ◽  
Sex Differences ◽  
Family History ◽  
Major Depression ◽  
Prediction Models ◽  
Population Sample ◽  
Disease Onset ◽  
Risk Factors For Recurrence ◽  
Males And Females ◽  
The Impact

AbstractBackgroundMajor depression (MD) occurs about twice as often in women as in men, but it is unclear whether sex differences subsist after disease onset. This study aims to elucidate potential sex differences in rates and risk factors for MD recurrence, in order to improve prediction of course of illness and understanding of its underlying mechanisms.MethodsWe used prospective data from a general population sample (n = 653) that experienced a recent episode of MD. A diverse set of potential risk factors for recurrence of MD was analyzed using Cox models subject to elastic net regularization for males and females separately. Accuracy of the prediction models was tested in same-sex and opposite-sex test data. Additionally, interactions between sex and each of the risk factors were investigated to identify potential sex differences.ResultsRecurrence rates and the impact of most risk factors were similar for men and women. For both sexes, prediction models were highly multifactorial including risk factors such as comorbid anxiety, early traumas, and family history. Some subtle sex differences were detected: for men, prediction models included more risk factors concerning characteristics of the depressive episode and family history of MD and generalized anxiety, whereas for women, models included more risk factors concerning early and recent adverse life events and socioeconomic problems.ConclusionsNo prominent sex differences in risk factors for recurrence of MD were found, potentially indicating similar disease maintaining mechanisms for both sexes. Course of MD is a multifactorial phenomenon for both males and females.

Sex Differences in Interpreting Male-Female Dyad Interactions: Males' Predominance in Perceiving Sexual Intent

2002 ◽  
Vol 9 (3) ◽  
pp. 289-297 ◽  
Author(s):  
Aldert Vrij ◽  
Emma Kirby
Keyword(s):  
Gender Differences ◽  
Sex Differences ◽  
Social Environment ◽  
Rape Myths ◽  
Rape Myth ◽  
Sexual Intent ◽  
Female Dyad ◽  
Acceptance Scale ◽  
Males And Females ◽  
The Impact

Astudy is reported investigating gender differences in judging the behaviour of males and females during mixed-dyad conversations and the impact of the endorsement of rape myths in explaining these gender differences. A total of 51 males and 40 females watched a videotape of a male actor and female actor verbally interacting in a social environment and were asked to give their impression about this interaction. They were also requested to fill in the Rape Myths Acceptance Scale (1980). Results revealed that compared to females, males had a stronger tendency to see the interaction in sexual terms. Also, male participants endorsed rape myths more strongly. Finally, gender differences in rape myth endorsements accounted for gender differences in perceiving male-female mixed-dyad interactions to alimited extent. Implications of the findings are discussed.

Assessment of The Influence of Non-Genetic Risk Factors on The Disease Onset and Progression of Androgenetic Alopecia in Egyptian Males

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Naziha Hafez Khafagy ◽  
Marwa Yassin Soltan ◽  
Ahmed Adel Ali Ali
Keyword(s):  
Risk Factors ◽  
Hair Loss ◽  
Genetic Risk ◽  
Disease Onset ◽  
Genetic Risk Factors ◽  
Androgenetic Alopecia ◽  
Major Type ◽  
Young Males ◽  
Potential Risk Factors ◽  
The Impact

Abstract Background Androgenetic alopecia (AGA) is a patterned hair loss with multifactorial background including genetic, hormonal as well as environmental and lifestyle-related risk factors. The impact of non-genetic risk factors on the onset and disease progression of androgenetic alopecia in Egyptian males. Objective To explore the potential role of non-genetic risk factors on the disease development and progression of androgenetic alopecia in Egyptian males. Patients and Methods The study included 2000 subjects with and without AGA, during the period from February 2019 to September 2019. The study protocol was approved by faculty of medicine, Ain Sham University, Research ethics committee (FWA 000017585). An informed written consent for participation in this study was obtained from patients and controls before enrollment. One thousand male patients with AGA were recruited in the study. The diagnosis was made via clinical diagnosis, dermatological findings, trichoscopic assessment. Results Our study showed that after skin examination 416 patients had acne and 344 patients had seborrhea, with statistically significant association to AGA cases. Conclusion From our study, it can be concluded that AGA became a major type of hair loss complaint among Egyptian males especially young males. Many potential risk factors were found to be associated with the disease as smoking, stress, obesity, family history, exercise, HTN and unbalanced diet. Avoidance of such risk factors may help improve the disease.

Twin studies in multiple sclerosis: A meta-estimation of heritability and environmentality

2015 ◽  
Vol 21 (11) ◽  
pp. 1404-1413 ◽  
Author(s):  
Corrado Fagnani ◽  
Michael C Neale ◽  
Lorenza Nisticò ◽  
Maria A Stazi ◽  
Vito A Ricigliano ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Threshold Model ◽  
Meta Analysis ◽  
Group Analysis ◽  
Twin Studies ◽  
Group Model ◽  
Medline Search ◽  
Genes And Environment ◽  
Environmental Component ◽  
The Impact

Background: Most twin studies of multiple sclerosis (MS) are inconclusive regarding the impact of genes and environment on disease susceptibility. In particular, high uncertainty exists about whether shared environmental factors are aetiologically relevant. Objective: To disentangle, with a reasonable degree of confidence, the relative contributions of heritability and of shared and unique environmental components of MS susceptibility. Methods: We performed a meta-analysis of previous twin studies. After a MEDLINE search, we selected eight twin studies in France, UK, Canada, Denmark, North America, Italy, Finland and Sweden. We conducted a biometric multi-group analysis under the liability-threshold model, by taking account of the study-specific ascertainment strategies and the population-specific prevalence rates of MS. Results: The meta-analytic estimates of tetrachoric correlations were 0.71 (95% confidence interval (CI): 0.67–0.74) in monozygotic pairs and 0.46 (95% CI: 0.41–0.50) in dizygotic pairs. The biometric multi-group model provided meta-analytic estimates of 0.50 (95% CI: 0.39–0.61) for heritability, 0.21 (95% CI: 0.11–0.30) for shared environmental component and 0.29 (95% CI: 0.26–0.33) for unique environmental component. Conclusion: Our results support the continuing efforts to identify unknown genetic factors that fill the gap of ‘missing heritability’; moreover, a ‘missing environmentality’ deserves future investigations into the role of non-heritable components that act as both shared and individual-specific exposures.

scholarly journals Genetic risk of dementia modifies the impact of obesity on limbic white matter and spatial navigation behavior in cognitively healthy adults

2019 ◽  
Author(s):  
Jilu P. Mole ◽  
Fabrizio Fasano ◽  
John Evans ◽  
Rebecca Sims ◽  
Derek A. Hamilton ◽  
...  
Keyword(s):  
Risk Factors ◽  
White Matter ◽  
Genetic Risk ◽  
Magnetization Transfer ◽  
Spatial Navigation ◽  
Diffusion Imaging ◽  
Axon Density ◽  
Asymptomatic Individuals ◽  
The Right ◽  
The Impact

AbstractA family history (FH) of dementia, APOE-ε4 genotype, and obesity are major risk factors for developing Alzheimer’s disease but their combined effects on the brain and cognition remain elusive. We tested the hypothesis that these risk factors affect apparent white matter (WM) myelin and cognition including spatial navigation and processing speed in 166 asymptomatic individuals (38-71 years). Microstructure in temporal [fornix, parahippocampal cingulum, uncinate fasciculus], motor and whole-brain WM was assessed with myelin-sensitive indices from quantitative magnetization transfer [macromolecular proton fraction (MPF)] and axon density from diffusion imaging. Individuals with the highest genetic risk (FH+ and APOE-ε4) compared to those with FH+ alone showed obesity-related reductions in MPF and axon density in the right parahippocampal cingulum. No effects were present for those without FH. Furthermore, FH modulated obesity-related effects on spatial navigation behaviour. In summary, an individual’s genetic dementia risk influenced the impact of obesity on WM myelin and cognition.

scholarly journals Sex differences in incidence and mortality of bloodstream infections. Results from the population-based HUNT study in Norway

2021 ◽  
Author(s):  
Randi Marie Mohus ◽  
Lise T. Gustad ◽  
Anne Sofie Furberg ◽  
Martine Kjølberg Moen ◽  
Kristin Vardheim Liyanarachi ◽  
...  
Keyword(s):  
Risk Factors ◽  
Sex Differences ◽  
Large Population ◽  
Bloodstream Infections ◽  
Hdl Cholesterol ◽  
Health Behaviours ◽  
Population Based ◽  
Incidence And Mortality ◽  
The Impact ◽  
First Time

AbstractObjectiveTo examine the effect of sex on risk of bloodstream infections (BSI) and BSI mortality and to assess to what extent known risk factors for BSI mediate this association in the general population.ParticipantsThe prospective, population-based HUNT2 Survey (1995-97) in Norway invited 93,898 inhabitants ≥20 years in the Nord-Trøndelag region, whereof 65,237 (69.5%) participated. 46.8% of the participants were men.ExposuresSex and potential mediators between sex and BSI; health behaviours (smoking, alcohol consumption), education attainment, cardiovascular risk factors (systolic blood pressure, non-HDL cholesterol, body mass index) and previous or current comorbidities.Main outcome measuresSex differences in risk of first-time BSI, BSI mortality (death within first 30 days after a BSI), BSI caused by the most frequent bacteria, and the impact of known BSI risk factors as mediators.ResultsWe documented a first-time BSI for 1,840 (2.9%) participants (51.3% men) during a median follow-up of 14.8 years. Of these, 396 (0.6%) died (56.6% men). Men had 41% higher risk of any first-time BSI (95% confidence interval (CI), 28 to 54%) than women. An estimated 34% of the excess risk of BSI in men was mediated by known BSI risk factors. The hazard ratio (HR) with 95% CI for BSI due to S. aureus was 2.09 (1.28 to 2.54), S. pneumoniae 1.36 (1.05 to 1.76), and E. coli 0.97 (0.84 to 1.13) in men vs women. BSI related mortality was higher in men compared to women with HR 1.87 (1.53 to 2.28).ConclusionsThis large population-based study show that men have higher risk of BSI than women. One-third of this effect was mediated by known risk factors for BSI. This raises important questions regarding sex specific approaches to reduce the burden of BSI.

scholarly journals The impact of age on genetic risk for common diseases

2020 ◽  
Author(s):  
Xilin Jiang ◽  
Chris Holmes ◽  
Gil McVean
Keyword(s):  
Risk Factors ◽  
Recent Work ◽  
Genetic Risk ◽  
Genetic Risk Factors ◽  
Individual Risk ◽  
Uk Biobank ◽  
Common Diseases ◽  
The Impact ◽  
The Relationship ◽  
Over Time

AbstractInherited genetic variation contributes to individual risk for many complex diseases and is increasingly being used for predictive patient stratification. Recent work has shown that genetic factors are not equally relevant to human traits across age and other contexts, though the reasons for such variation are not clear. Here, we introduce methods to infer the form of the relationship between genetic risk for disease and age and to test whether all genetic risk factors behave similarly. We use a proportional hazards model within an interval-based censoring methodology to estimate age-varying individual variant contributions to genetic risk for 24 common diseases within the British ancestry subset of UK Biobank, applying a Bayesian clustering approach to group variants by their risk profile over age and permutation tests for age dependency and multiplicity of profiles. We find evidence for age-varying risk profiles in nine diseases, including hypertension, skin cancer, atherosclerotic heart disease, hypothyroidism and calculus of gallbladder, several of which show evidence, albeit weak, for multiple distinct profiles of genetic risk. The predominant pattern shows genetic risk factors having the greatest impact on risk of early disease, with a monotonic decrease over time, at least for the majority of variants although the magnitude and form of the decrease varies among diseases. We show that these patterns cannot be explained by a simple model involving the presence of unobserved covariates such as environmental factors. We discuss possible models that can explain our observations and the implications for genetic risk prediction.Author summaryThe genes we inherit from our parents influence our risk for almost all diseases, from cancer to severe infections. With the explosion of genomic technologies, we are now able to use an individual’s genome to make useful predictions about future disease risk. However, recent work has shown that the predictive value of genetic information varies by context, including age, sex and ethnicity. In this paper we introduce, validate and apply new statistical methods for investigating the relationship between age and genetic risk. These methods allow us to ask questions such as whether risk is constant over time, precisely how risk changes over time and whether all genetic risk factors have similar age profiles. By applying the methods to data from the UK Biobank, a prospective study of 500,000 people, we show that there is a tendency for genetic risk to decline with increasing age. We consider a series of possible explanations for the observation and conclude that there must be processes acting that we are currently unaware of, such as distinct phases of life in which genetic risk manifests itself, or interactions between genes and the environment.

scholarly journals Identifying Genetic Risk Factors for Diabetic Macular Edema and the Response to Treatment

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Rajya L. Gurung ◽  
Liesel M. FitzGerald ◽  
Bennet J. McComish ◽  
Nitin Verma ◽  
Kathryn P. Burdon
Keyword(s):  
Risk Factors ◽  
Macular Edema ◽  
Diabetic Macular Edema ◽  
Genetic Risk ◽  
Vision Loss ◽  
Genetic Risk Factors ◽  
Response To Treatment ◽  
Diabetic Eye Disease ◽  
Genetic And Environmental Factors ◽  
The Impact

Diabetic retinopathy (DR) is the most common microvascular complication of diabetes mellitus (DM). DR is complex and the term encompasses several clinical subtypes of diabetic eye disease, including diabetic macular edema (DME), the most frequent cause of central vision loss in DR patients. Both genetic and environmental factors contribute to the pathophysiology of DR and its subtypes. While numerous studies have identified several susceptibility genes for DR, few have investigated the impact of genetics on DME susceptibility. This review will focus on the current literature surrounding genetic risk factors associated with DME. We will also highlight the small number of studies investigating the genetics of response to antivascular endothelial growth factor (anti-VEGF) injection, which is used to treat DME.

scholarly journals Evidence, and replication thereof, that molecular-genetic and environmental risks for psychosis impact through an affective pathway

2020 ◽  
pp. 1-13
Author(s):  
Jim van Os ◽  
Lotta-Katrin Pries ◽  
Margreet ten Have ◽  
Ron de Graaf ◽  
Saskia van Dorsselaer ◽  
...  
Keyword(s):  
Risk Factors ◽  
Genetic Risk ◽  
Molecular Genetic ◽  
Population Sample ◽  
Genetic Risk Factors ◽  
Schizophrenia Spectrum Disorders ◽  
Affective Dysregulation ◽  
Delusional Ideation ◽  
Schizophrenia Spectrum ◽  
The Impact

Abstract Background There is evidence that environmental and genetic risk factors for schizophrenia spectrum disorders are transdiagnostic and mediated in part through a generic pathway of affective dysregulation. Methods We analysed to what degree the impact of schizophrenia polygenic risk (PRS-SZ) and childhood adversity (CA) on psychosis outcomes was contingent on co-presence of affective dysregulation, defined as significant depressive symptoms, in (i) NEMESIS-2 (n = 6646), a representative general population sample, interviewed four times over nine years and (ii) EUGEI (n = 4068) a sample of patients with schizophrenia spectrum disorder, the siblings of these patients and controls. Results The impact of PRS-SZ on psychosis showed significant dependence on co-presence of affective dysregulation in NEMESIS-2 [relative excess risk due to interaction (RERI): 1.01, p = 0.037] and in EUGEI (RERI = 3.39, p = 0.048). This was particularly evident for delusional ideation (NEMESIS-2: RERI = 1.74, p = 0.003; EUGEI: RERI = 4.16, p = 0.019) and not for hallucinatory experiences (NEMESIS-2: RERI = 0.65, p = 0.284; EUGEI: −0.37, p = 0.547). A similar and stronger pattern of results was evident for CA (RERI delusions and hallucinations: NEMESIS-2: 3.02, p < 0.001; EUGEI: 6.44, p < 0.001; RERI delusional ideation: NEMESIS-2: 3.79, p < 0.001; EUGEI: 5.43, p = 0.001; RERI hallucinatory experiences: NEMESIS-2: 2.46, p < 0.001; EUGEI: 0.54, p = 0.465). Conclusions The results, and internal replication, suggest that the effects of known genetic and non-genetic risk factors for psychosis are mediated in part through an affective pathway, from which early states of delusional meaning may arise.

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