twin registry
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2021 ◽  
Vol 12 ◽  
Author(s):  
Alice J. Kim ◽  
Alaina I. Gold ◽  
Laura Fenton ◽  
Matthew J. D. Pilgrim ◽  
Morgan Lynch ◽  
...  

Although several studies have shown small longitudinal associations between baseline loneliness and subsequent dementia risk, studies rarely test whether change in loneliness predicts dementia risk. Furthermore, as both increase with advancing age, genetic and environmental selection processes may confound the putative causal association between loneliness and dementia risk. We used a sample of 2,476 individual twins from three longitudinal twin studies of aging in the Swedish Twin Registry to test the hypothesis that greater positive change in loneliness predicts greater dementia risk. We then used a sample of 1,632 pairs of twins to evaluate the hypothesis that effects of change in loneliness on dementia risk would remain after adjusting for effects of genetic and environmental variance. Phenotypic model results suggest that mild levels of baseline loneliness predict greater dementia risk. Contrary to our hypothesis, change in loneliness did not correlate with dementia risk, regardless of whether genetic and environmental selection confounds were taken into account. Worsening loneliness with age may not confer greater dementia risk.


Author(s):  
Hannah Gordon ◽  
William Blad ◽  
Frederik Trier Møller ◽  
Timothy Orchard ◽  
Alan Steel ◽  
...  

Epigenomics ◽  
2021 ◽  
Author(s):  
Meng Lu ◽  
Qin Xueying ◽  
Peng Hexiang ◽  
Gao Wenjing ◽  
Sara Hägg ◽  
...  

Aim: Alcohol intake alters DNA methylation profiles and methylation might mediate the association between alcohol and disease, but limited number of positive CpG sites repeatedly replicated. Materials & methods: In total, 57 monozygotic (MZ) twin pairs discordant for alcohol drinking from the Chinese National Twin Registry and 158 MZ and dizygotic twin pairs in the Swedish Adoption/Twin Study of Aging were evaluated. DNA methylation was detected using the Infinium HumanMethylation450 BeadChip. Results: Among candidate CpG sites, cg07326074 was significantly correlated with drinking after adjusting for covariates in MZ twins in both datasets but not in the entire sample or dizygotic twins. Conclusion: The hypermethylation of cg07326074, located in the tumor-promoting gene C16orf59, was associated with alcohol consumption.


2021 ◽  
pp. 095679762096853
Author(s):  
S. Alexandra Burt ◽  
D. Angus Clark ◽  
Elizabeth T. Gershoff ◽  
Kelly L. Klump ◽  
Luke W. Hyde

In the current study, we leveraged differences within twin pairs to examine whether harsh parenting is associated with children’s antisocial behavior via environmental (vs. genetic) transmission. We examined two independent samples from the Michigan State University Twin Registry. Our primary sample contained 1,030 families (2,060 twin children; 49% female; 6–10 years old) oversampled for exposure to disadvantage. Our replication sample included 240 families (480 twin children; 50% female; 6–15 years old). Co-twin control analyses were conducted using a specification-curve framework, an exhaustive modeling approach in which all reasonable analytic specifications of the data are interrogated. Results revealed that, regardless of zygosity, the twin experiencing harsher parenting exhibited more antisocial behavior. These effects were robust across multiple operationalizations and informant reports of both harsh parenting and antisocial behavior with only a few exceptions. Results indicate that the association between harsh parenting and children’s antisocial behavior is, to a large degree, environmental in origin.


2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Bojing Liu ◽  
Arvid Sjölander ◽  
Nancy L. Pedersen ◽  
Jonas F. Ludvigsson ◽  
Honglei Chen ◽  
...  

AbstractTo examine whether irritable bowel syndrome (IBS) was related to the future risk of Parkinson’s disease (PD), we conducted a nested case-control study in the Swedish total population including 56,564 PD cases identified from the Swedish Patient Register and 30 controls per case individually matched by sex and year of birth. Odds ratios (ORs) with 95% confidence intervals (CIs) for having a prior diagnosis of IBS were estimated using conditional logistic regression. We furthermore conducted a cohort study using the Swedish Twin Registry following 3046 IBS patients identified by self-reported abdominal symptoms and 41,179 non-IBS individuals. Through Cox proportional hazard models, we estimated hazard ratios (HRs) and 95% CIs for PD risk. In the nested case-control study, 253 (0.4%) PD cases and 5204 (0.3%) controls had a previous IBS diagnosis. IBS diagnosis was associated with a 44% higher risk of PD (OR = 1.44, 95% CI 1.27–1.63). Temporal relationship analyses showed 53% and 38% increased risk of PD more than 5 and 10 years after IBS diagnosis, respectively. In the cohort analysis based on the Swedish Twin Registry, there was no statistically significantly increased risk of PD related to IBS (HR = 1.25, 95% CI = 0.87–1.81). Our results suggest a higher risk of PD diagnosis after IBS. These results provide additional evidence supporting the importance of the gut–brain axis in PD.


2020 ◽  
Vol 23 (6) ◽  
pp. 338-344
Author(s):  
Moritz Herle ◽  
Juan J. Madrid-Valero ◽  
José J. Morosoli ◽  
Lucía Colodro-Conde ◽  
Juan Ordoñana

AbstractResearch has emphasized the genetic basis of individual differences in body mass index (BMI); however, genetic factors cannot explain the rapid rise of obesity. Eating behaviors have been stipulated to be the behavioral expression of genetic risk in an obesogenic environment. In this study, we decompose variation and covariation between three key eating behaviors and BMI in a sample of 698 participants, consisting of 167 monozygotic, 150 dizygotic complete same-sex female twins and 64 incomplete pairs from a population-based twin registry in the southeast of Spain, The Murcia Twin Registry. Phenotypes were emotional eating, uncontrolled eating and cognitive restraint, measured by the Three Factor Eating Questionnaire and objectively measured BMI. Variation in eating behaviors was driven by nonshared environmental factors (range: 56%−65%), whereas shared environmental and genetic factors were secondary. All three eating behaviors were correlated with BMI (r = .19–.25). Nonshared environmental factors explained the covariations (Emotional eating–Uncontrolled eating: rE = .54, 95% CI [.43, .64]; BMI–Cognitive restraint: rE = .15, 95% CI [.01, .28]). In contrast to BMI, individual differences in eating behaviors are mostly explained by nonshared environmental factors, which also accounted for the phenotypic correlation between eating behaviors and BMI. Due to the sample size, analyses were underpowered to detect contributions of additive genetic or shared environmental factors to variation and covariation of the phenotypes. Although more research is granted, these results support that eating behaviors could be viable intervention targets to help individuals maintain a healthy weight.


Hypertension ◽  
2020 ◽  
Vol 76 (5) ◽  
pp. 1428-1434
Author(s):  
Bin Wang ◽  
Ting Wu ◽  
Michael C. Neale ◽  
Renske Verweij ◽  
Gaifen Liu ◽  
...  

Blood pressure (BP) and obesity phenotypes may covary due to shared genetic or environmental factors or both. Furthermore, it is possible that the heritability of BP differs according to obesity status—a form of G×E interaction. This hypothesis has never been tested in White twins. The present study included 15 924 White male twin pairs aged between 15 and 33 years from the National Academy of Sciences–National Research Council World War II Veteran Twin Registry. Systolic and diastolic BPs, as well as height and weight, were measured at the induction physical examination. Body mass index (BMI) was used as the index of general obesity. Quantitative genetic modeling was performed using Mx software. Univariate analysis showed that narrow sense heritabilities (95% CI) for systolic BP, diastolic BP, height, and BMI were 0.401 (0.381–0.420), 0.297 (0.280–0.320), 0.866 (0.836–0.897), and 0.639 (0.614–0.664), respectively. Positive phenotypic correlations of BMI with systolic BP (r=0.13) and diastolic BP (r=0.08) were largely due to genetic factors (70% and 86%, respectively). The gene-BMI interaction analysis did not show any support for a modifying effect of BMI on genetic and environmental influences of systolic BP and diastolic BP. Our results suggest that correlations between BP and BMI are mainly explained by common genes influencing both. Higher BMI levels have no influence on the penetrance of genetic vulnerability to elevated BP. These conclusions may prove valuable for gene-finding studies.


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