scholarly journals Gene–Environment Interactions Between Depressive Symptoms and Smoking Quantity

2016 ◽  
Vol 19 (4) ◽  
pp. 322-329 ◽  
Author(s):  
Kaisu Keskitalo-Vuokko ◽  
Tellervo Korhonen ◽  
Jaakko Kaprio

We investigated genetic and environmental correlations and gene by environment interactions (GxE) between depressive symptoms measured by the Beck Depression Inventory (BDI) and quantity smoked measured by number of cigarettes smoked per day (CPD) using quantitative genetic modeling. The population-based sample consisted of 12,063 twin individuals from the Finnish Twin Cohort Study. Bivariate Cholesky decomposition revealed that the phenotypic correlation (r = 0.09) between BDI and CPD was explained by shared genetic (rg = 0.18) and environmental (re = 0.08) factors. GxE models incorporating moderator effects were built by using CPD as trait and BDI as moderator and vice versa. The importance of the genetic variance component increased with increasing moderator value in both models. Thus, the influence of genetic effects on variance of smoking quantity was enhanced in individuals with elevated depression score and vice versa; the genetic effects on depression variance were potentiated among heavy smokers. In conclusion, shared genetic and environmental factors as well as GxE underlie the association of smoking with depression.

2008 ◽  
Vol 17 (1) ◽  
pp. 75-96 ◽  
Author(s):  
Håkon K. Gjessing ◽  
Rolv Terje Lie

The field of traditional biometrical genetics uses mixed-effects models to quantify the influence of genetic and environmental factors on a biological trait, based essentially on estimating within-family trait correlations. Such analyses provide a useful preview of what may be discovered with the emerging full-scale genotyping strategies. However, biometrical analyses require unrealistically large sample sizes to obtain a reasonable precision, particularly for dichotomous traits. In addition, it may be very difficult to separate genetic and environmental effects because environmental correlations are poorly understood. We illustrate these and other difficulties using population-based cousins and nuclear family data for birth weight, collected from the Medical Birth Registry of Norway.


2018 ◽  
Author(s):  
Bart Baselmans ◽  
Yayouk Willems ◽  
Toos van Beijsterveldt ◽  
Lannie Ligthart ◽  
Gonneke WIllemsen ◽  
...  

Whether well-being and depressive symptoms can be considered as two sides of the same coin is widely debated. The aim of this study was to gain insight into the etiology of the association between well-being and depressive symptoms across the lifespan. In a cohort-sequential design, including data from 43,427 twins between age 7 and 99, we estimated the association between well-being and depressive symptoms throughout the lifespan and assessed genetic and environmental contributions to the observed overlap. For both well-being (range 31% –45%) and depressive symptoms (range 50%-61%), genetic factors explained a substantial part of the phenotypic variance across the lifespan. Correlations between well-being and depressive symptoms across ages ranged from -.34 in childhood to -.49 in adulthood. In children and adults (aged >27), environmental effects explained 51% to 59% of the phenotypic correlation, while for adolescents and young adults strong genetic influences (60%-77%) on the association were observed. Moderate to high genetic correlations (ranging from 0.60 to 0.70) were observed in adolescence and adulthood, while in childhood environmental correlations were substantial but genetic correlations small. These results suggest that environmental factors are important in explaining the relationship between well-being and depressive symptoms in childhood, while from adolescence onwards a genetic predisposition for higher well-being is indicative for a genetic predisposition for lower depressive symptoms, and vice versa. These results provided more insights into the etiological underpinnings of well-being and depressive symptoms, possibly allowing to articulate better strategies for health promotion and resource allocation in the future.


2020 ◽  
Vol 66 (8) ◽  
pp. 799-809
Author(s):  
Miriam Engel ◽  
Karl-Heinz Jöckel ◽  
Nico Dragano ◽  
Miriam Engels ◽  
Susanne Moebus

Background: Depressive symptoms are volatile over time but empirical studies of intra-individual variations of depressive symptoms over longer periods are sparse. Aims: We aim to examine fluctuation patterns of depressive symptoms and to investigate the possible influence of age, sex and socioeconomic factors on fluctuation in a population-based sample over a period of 13 years. Methods: We used data of 4,251 participants (45–75 years; 51.0% women at baseline) of the Heinz Nixdorf Recall Study with at least two of nine possible measurements obtained in the period between 2000 and 2017. Depressive symptoms were assessed via the Center for Epidemiologic Studies Depression Scale (CES-D) short form. Based on the individual mean values and standard deviation from all measurements, we categorized participants as G1 ‘stable low’, G2 ‘stable high’, G3 ‘stable around cutoff’ and G4 ‘large fluctuations’. Results: Most participants (82.3%) showed stable low depressive symptoms (G1), whereas 2.3% performed stable high values (G2), 6.9% stable around the cutoff (G3) and 8.6% large fluctuations (G4). Conclusion: Our longitudinal results reveal that almost 18% (G2, G3 and G4) of the participants have an increased depression score or strong fluctuations at times. According to our classification, a higher proportion of the participants show anomalies with regard to depression compared to a simple classification into depressed and nondepressed, especially if this is based on a single measurement. Thus, longitudinal measurements of depression can prevent misclassification and provide valuable information about the course of depressive symptoms for a better understanding of the changes of depression.


2018 ◽  
Vol 6 (4) ◽  
pp. 543-560 ◽  
Author(s):  
Naomi P. Friedman ◽  
Alta du Pont ◽  
Robin P. Corley ◽  
John K. Hewitt

Depression is associated with deficits in executive functions (EFs)—cognitive control abilities that regulate goal-directed thoughts and actions—but the etiology of these associations is unclear. We examined the relations between depressive symptoms and multiple EF latent variables in a population-based sample of 439 twin pairs assessed at mean ages 12, 17, and 23 years. Greater depressive symptoms negatively related to a Common EF factor capturing shared variance across response inhibition, working memory updating, and mental set shifting tasks, and also negatively related to an Updating-Specific factor, but not a Shifting-Specific factor. Cross-lagged panel models suggested that the Common EF correlations reflected within-wave associations rather than prospective effects, whereas the Updating-Specific correlations reflected associations of earlier depression levels with later Updating-Specific ability. Twin models were consistent with a model in which Common EF and Updating-Specific abilities relate to depression through correlated genetic risk, with no significant environmental correlations.


2011 ◽  
Vol 41 (11) ◽  
pp. 2423-2433 ◽  
Author(s):  
S. Lundström ◽  
Z. Chang ◽  
N. Kerekes ◽  
C. H. Gumpert ◽  
M. Råstam ◽  
...  

BackgroundAutistic-like traits (ALTs), that is restrictions in intuitive social interaction, communication and flexibility of interests and behaviors, were studied in two population-based Swedish twin studies, one in children and one in adults: (1) to examine whether the variability in ALTs is a meaningful risk factor for concomitant attention deficit hyperactivity disorder (ADHD), anxiety, conduct problems, depression and substance abuse, and (2) to assess whether common genetic and environmental susceptibilities can help to explain co-existence of ALTs and traits associated with such concomitant problems.MethodTwo nationwide twin cohorts from Sweden (consisting of 11 222 children and 18 349 adults) were assessed by DSM-based symptom algorithms for autism. The twins were divided into six groups based on their degree of ALTs and the risk for concomitant mental health problems was calculated for each group. Genetic and environmental susceptibilities common to ALTs and the other problem types were examined using bivariate twin modeling.ResultsIn both cohorts, even the lowest degree of ALTs increased the risk for all other types of mental health problems, and these risk estimates increased monotonically with the number of ALTs. For all conditions, common genetic and environmental factors could be discerned. Overall, the phenotypic correlation between ALTs and the traits examined were less pronounced in adulthood than in childhood and less affected by genetic compared with environmental factors.ConclusionsEven low-grade ALTs are relevant to clinical psychiatry as they increase the risk for several heterotypical mental health problems. The association is influenced partly by common genetic and environmental susceptibilities. Attention to co-existing ALTs is warranted in research on a wide range of mental disorders.


2009 ◽  
Vol 12 (8) ◽  
pp. 1052-1060 ◽  
Author(s):  
Audrey C Choh ◽  
Ellen W Demerath ◽  
Miryoung Lee ◽  
Kimberly D Williams ◽  
Bradford Towne ◽  
...  

AbstractObjectivePhysical inactivity poses a major risk for obesity and chronic disease, and is influenced by both genetic and environmental factors. However, the genetic association between physical activity (PA) level and obesity is not well characterized. Our aims were to: (i) estimate the extent of additive genetic influences on physical activity while adjusting for household effects; and (ii) determine whether physical activity and adiposity measures share common genetic effects.SubjectsThe sample included 521 (42 % male) adult relatives, 18–86 years of age, from five large families in the Southwest Ohio Family Study.DesignSport, leisure and work PA were self-reported (Baecke Questionnaire of Habitual Physical Activity). Total body and trunk adiposity, including percentage body fat (%BF), were measured using dual-energy X-ray absorptiometry. Abdominal visceral and subcutaneous adipose tissue mass were measured using MRI.ResultsHeritabilities for adiposity and PA traits, and the genetic, household and environmental correlations among them, were estimated using maximum likelihood variance components methods. Significant genetic effects (P < 0·05) were found for sport (h2 = 0·26) and leisure PA (h2 = 0·17). Significant (P < 0·05) household effects existed for leisure PA (c2 = 0·25). Sport PA had a negative genetic correlation with central adiposity measurements adjusted for height (ρG > |−0·40|). Sport and leisure PA had negative genetic correlations with %BF (ρG > |−0·46|).ConclusionsThe results suggest that the association of sport and leisure PA with lower adiposity is due, in part, to a common genetic inheritance of both reduced adiposity and the predisposition to engage in more physical activity.


2018 ◽  
Author(s):  
Patrizia Pezzoli ◽  
Jan Antfolk ◽  
Alexander Samir Hatoum ◽  
pekka santtila

Although there are multiple forms of experiences of childhood maltreatment (CM), previous research has mainly focused on its different aspects separately. Possible genetic influences on these purportedly environmental causes of later psychopathology have also been largely overlooked. In a large population-based Finnish twin-sample, we investigated the co-occurrence of 55 different adverse experiences and the covariance of the identified latent types of CM. We also estimated the genetic and environmental influences on both the individual adverse experiences and latent types of CM. We found evidence that the reported CM are influenced by genetic factors. Importantly, specific genetic and environmental factors still influenced traits that modulate the risk of sexual abuse after accounting for shared genetic influences on all types of CM and on their covariance. Genes and shared environments differently influenced the occurrence of CM within and outside the family. Finally, we found evidence that heritable traits might bias retrospective self-reports of experiences more susceptible to interpretation.


2008 ◽  
Vol 39 (2) ◽  
pp. 211-218 ◽  
Author(s):  
R. Bogdan ◽  
D. A. Pizzagalli

BackgroundAnhedonia and stress sensitivity have been identified as promising depressive phenotypes. Research suggests that stress-induced anhedonia is a possible mechanism underlying the association between stress and depression. The present proof-of-concept study assessed whether hedonic capacity and stress perception are heritable and whether their genetic and environmental contributions are shared.MethodTwenty monozygotic (MZ) and 15 dizygotic (DZ) twin pairs completed a probabilistic reward task that provides an objective behavioral measure of hedonic capacity (reward responsiveness) and completed several questionnaires including the Perceived Stress Scale (PSS). Bivariate Cholesky models were used to investigate whether covariation between (1) depressive symptoms and hedonic capacity, (2) depressive symptoms and perceived stress, and (3) perceived stress and hedonic capacity resulted from shared or residual genetic and environmental factors.ResultsAdditive genetic (A) and individual-specific environment (E) factors contributed to 46% and 54% of the variance in hedonic capacity, respectively. For perceived stress, 44% and 56% of the variance was accounted for by A and E factors, respectively. The genetic correlation between depression and hedonic capacity was moderate (ra=0.29), whereas the correlation between depression and stress perception was large (ra=0.67). Genetic and environmental correlations between hedonic capacity and stress perception were large (ra=0.72 and re=−0.43).ConclusionsThe present study provides initial feasibility for using a twin approach to investigate genetic contributions of a laboratory-based anhedonic phenotype. Although these preliminary findings indicate that hedonic capacity and perceived stress are heritable, with substantial shared additive genetic contributions, replications in larger samples will be needed.


2014 ◽  
Vol 18 (1) ◽  
pp. 52-60 ◽  
Author(s):  
Nuno R. Zilhão ◽  
Dirk J. A. Smit ◽  
Anouk den Braber ◽  
Conor V. Dolan ◽  
Gonneke Willemsen ◽  
...  

This study investigates the relative contribution of genetic and environmental factors to the stability of obsessive-compulsive (OC) symptoms in an adult population-based sample. We collected data from twin pairs and their siblings, using the Padua Inventory Revised Abbreviated, from the population-based Netherlands Twin Register (NTR) in 2002 (n = 10.134) and 2008 (n = 15.720). Multivariate twin analyses were used to estimate the stability of OC symptoms as a function of genetic and environmental components. OC symptoms were found to be highly stable, with a longitudinal phenotypic correlation of 0.63. Longitudinal broad sense heritability was found to be 56.0%. Longitudinal correlations for genetic (r = 0.58 for additive, r = 1 for non-additive genetic factors) and non-shared environment (r = 0.46) reflected stable effects, indicating that both genes and environment are influencing the stability of OC symptoms in adults. For the first time, evidence is reported for non-additive genetic effects on the stability of OC symptoms. In conclusion, this study showed that OC symptoms are highly stable across time in adults, and that genetic effects contribute mostly to this stability, both in an additive and non-additive way, besides non-shared environmental factors. These data are informative with respect to adult sample selection for future genetic studies, and suggest that gene–gene interaction studies are needed to further understand the dominance effect found in this study.


2017 ◽  
Vol 20 (4) ◽  
pp. 330-337
Author(s):  
Björn Nordlund ◽  
Cecilia Lundholm ◽  
Vilhelmina Ullemar ◽  
Marianne van Hage ◽  
Anne K. Örtqvist ◽  
...  

Background: The link between asthma and exhaled nitric oxide (FENO) is not completely understood. The aim of this study was to estimate the association between FENO and asthma, taking genetics, sensitization, and inhaled corticosteroids (ICS) into account. Methods: A total of 681 twins (53% monozygotic [MZ] and 47% dizygotic [DZ]) from the population-based STOPPA study (mean age 12.6 years) were recruited and information on FENO (parts per billion), parental report of current asthma, sensitization to airborne allergens (Phadiatop; IgE ≥0.35 kUA/l), and ICS-treatment was collected. We estimated the association between FENO and asthma, sensitization, and ICS in all twins and within pairs (DZ and MZ) to address shared genetic and environmental factors. Linear regression of log-transformed FENO was used and results presented as exponentiated regression coefficients (exp[β]), with 95% confidence interval (CI). Results: We found an association between asthma and FENO in all twins, exp(β) 1.31 [1.11, 1.54]. In within-pairs analysis, the association was stronger within DZ pairs discordant for FENO, exp(β) 1.50 [1.19, 1.89], compared to MZ pairs, exp(β) 1.07 [0.84, 1.37], p = .049. There was no difference in FENO in non-sensitized children with asthma, compared to children with neither asthma nor sensitization, exp(β) 0.89 [0.77, 1.03]. However, increased FENO was associated with sensitization, exp(β) 1.48 [1.30, 1.69], and with sensitization together with asthma, exp(β) 1.98 [1.57, 2.51], in all twins and within DZ pairs discordant for FENO, but not in MZ pairs. The FENO asthma association remained in DZ pairs without regular ICS-treatment. Conclusions: The association between FENO and asthma is explained by genetics and sensitization.


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