scholarly journals Predicting Future Harm from Gambling over a Five-Year period in a General Population Sample: A Survival Analysis

2020 ◽  
Author(s):  
Shawn Currie ◽  
David Hodgins ◽  
Robert Williams ◽  
Kirsten Fiest

Abstract Background. There is little longitudinal evidence on the cumulative risk of harm from gambling associated with excess spending and frequency of play. The present study sought to assess the risk of gambling problems over a five-year period in adults who exceed previously derived low-risk gambling limits compared to those who remain within the limits after controlling for other modifiable risk factors. Methods. Participants were adults (N = 4212) drawn from two independent Canadian longitudinal cohort studies who reported gambling in the past year and were free of problem gambling at time 1. Multivariate Cox regression was employed to assess the impact over time of gambling above low-risk gambling thresholds (frequency ≥ 8 times per month; expenditure ≥ 75CAD per month; percent of household income spent on gambling ≥ 1.7%) on developing moderate harm and problem gambling. Covariates included presence of a DSM5 addiction or mental health disorder at time 1, irrational gambling beliefs, number of stressful life events in past 12 months, number of game types played each year, and playing electronic gaming machines or casino games. Results. In both samples, exceeding the low-risk gambling limits at time 1 significantly increased the risk of moderate harm (defined as ≥ 2 consequences on the Problem Gambling Severity Index [PGSI]) within five years after controlling for other modifiable risk factors. Other significant predictors of harm were presence of a mental disorder at time 1, cognitive distortions about gambling, stressful life events, and playing electronic gaming machines or casino games. In one sample, the five-year cumulative survival rate for moderate harm among individuals who stayed below all the low-risk limits was 95% compared to 83% among gamblers who exceeded all limits. Each additional low-risk limit exceeded increased the cumulative probability of harm by 30%. Similar results were found in models when the outcome was problem gambling.Conclusions. Level of gambling involvement represents a highly modifiable risk factor for later harm. Staying below empirically derived safe gambling thresholds reduces the risk of harm over time.

2020 ◽  
Author(s):  
Shawn Currie ◽  
David Hodgins ◽  
Robert Williams ◽  
Kirsten Fiest

Abstract Background. There is little longitudinal evidence on the cumulative risk of harm from gambling associated with excess spending and frequency of play. The present study sought to assess the risk of gambling problems over a five-year period in adults who exceed previously derived low-risk gambling limits compared to those who remain within the limits after controlling for other modifiable risk factors. Methods. Participants were adults (N = 4212) drawn from two independent Canadian longitudinal cohort studies who reported gambling in the past year and were free of problem gambling at time 1. Multivariate Cox regression was employed to assess the impact over time of gambling above low-risk gambling thresholds (frequency ≥ 8 times per month; expenditure ≥ $75CAN per month; percent of household income spent on gambling ≥ 1.7%) on developing moderate harm and problem gambling. Covariates included presence of a DSM5 addiction or mental health disorder at time 1, irrational gambling beliefs, number of stressful life events in past 12 months, number of game types played each year, and playing electronic gaming machines or casino games. Results. In both samples, exceeding the low-risk gambling limits at time 1 significantly increased the risk of moderate harm (defined as ≥ 2 consequences on the Problem Gambling Severity Index [PGSI]) within five years after controlling for other modifiable risk factors. Other significant predictors of harm were presence of a mental disorder at time 1, cognitive distortions about gambling, stressful life events, and playing electronic gaming machines or casino games. In one sample, the five-year cumulative survival rate for moderate harm among individuals who stayed below all the low-risk limits was 95% compared to 83% among gamblers who exceeded all limits. Each additional low-risk limit exceeded increased the cumulative probability of harm by 30%. Similar results were found in models when the outcome was problem gambling.Conclusions. Level of gambling involvement represents a highly modifiable risk factor for later harm. Staying below empirically derived safe gambling thresholds reduces the risk of harm over time.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Shawn R. Currie ◽  
David C. Hodgins ◽  
Robert J. Williams ◽  
Kirsten Fiest

Abstract Background There is little longitudinal evidence on the cumulative risk of harm from gambling associated with excess spending and frequency of play. The present study sought to assess the risk of gambling problems over a five-year period in adults who exceed previously derived low-risk gambling limits compared to those who remain within the limits after controlling for other modifiable risk factors. Methods Participants were adults (N = 4212) drawn from two independent Canadian longitudinal cohort studies who reported gambling in the past year and were free of problem gambling at time 1. Multivariate Cox regression was employed to assess the impact over time of gambling above low-risk gambling thresholds (frequency ≥ 8 times per month; expenditure ≥75CAD per month; percent of household income spent on gambling ≥1.7%) on developing moderate harm and problem gambling. Covariates included presence of a DSM5 addiction or mental health disorder at time 1, irrational gambling beliefs, number of stressful life events in past 12 months, number of game types played each year, and playing electronic gaming machines or casino games. Results In both samples, exceeding the low-risk gambling limits at time 1 significantly increased the risk of moderate harm (defined as ≥2 consequences on the Problem Gambling Severity Index [PGSI]) within 5 years after controlling for other modifiable risk factors. Other significant predictors of harm were presence of a mental disorder at time 1, cognitive distortions about gambling, stressful life events, and playing electronic gaming machines or casino games. In one sample, the five-year cumulative survival rate for moderate harm among individuals who stayed below all the low-risk limits was 95% compared to 83% among gamblers who exceeded all limits. Each additional low-risk limit exceeded increased the cumulative probability of harm by 30%. Similar results were found in models when the outcome was problem gambling. Conclusions Level of gambling involvement represents a highly modifiable risk factor for later harm. Staying below empirically derived safe gambling thresholds reduces the risk of harm over time.


2020 ◽  
Author(s):  
Shawn Currie ◽  
David Hodgins ◽  
Robert Williams ◽  
Kirsten Fiest

Abstract Background There is little longitudinal evidence on the cumulative risk of harm from gambling associated with excess spending and frequency of play. The present study sought to assess over a five-year period the risk of gambling problems in adults who exceed previously derived low-risk gambling limits compared to those who remain within the limits after controlling for other modifiable psychosocial risk factors. Methods Participants were adults (N = 4212) drawn from two independent Canadian longitudinal cohort studies (Quinte Longitudinal Study and Leisure, Lifestyle, and Lifecycle Project) who reported gambling in the past year and were free of problem gambling at time 1. Multivariate Cox regression was employed to assess the impact of gambling above low-risk gambling thresholds (frequency ≥ 8 times per month; expenditure ≥ $75CAN per month; percent of household income spent on gambling ≥ 1.7%) on developing gambling problems over time. Covariates included presence of a DSM 5 addiction or mental health disorder at time 1, irrational gambling beliefs, number of stressful life events in past 12 months, number of game types played each year, and playing electronic gaming machines or casino games. Results In both samples, exceeding the low-risk gambling limits at time 1 significantly increased the risk of moderate harm within five years after controlling for other modifiable risk factors. Other significant predictors of harm were presence of a mental disorder at time 1, cognitive distortions about gambling, stressful life events, and playing electronic gaming machines or casino games. In the QLS sample, the five-year cumulative survival rate among individuals who stayed below all the low-risk limits was 95% compared to 83% among gamblers who exceeded all limits. Each additional low-risk limit exceeded increased the cumulative probability of harm by 30%. Conclusions Level of gambling involvement represents a highly modifiable risk factor for later harm. Staying below empirically derived safe gambling thresholds reduces the risk of harm over time.


2019 ◽  
Vol 3 ◽  
pp. 11 ◽  
Author(s):  
Toni-Kim Clarke ◽  
Yanni Zeng ◽  
Lauren Navrady ◽  
Charley Xia ◽  
Chris Haley ◽  
...  

Background: Stressful life events (SLEs) and neuroticism are risk factors for major depressive disorder (MDD). However, SLEs and neuroticism are heritable and genetic risk for SLEs is associated with risk for MDD. We sought to investigate the genetic and environmental contributions to SLEs in a family-based sample, and quantify genetic overlap with MDD and neuroticism. Methods: A subset of Generation Scotland: the Scottish Family Health Study (GS), consisting of 9618 individuals with information on MDD, past 6 month SLEs, neuroticism and genome-wide genotype data was used in the present study. We estimated the heritability of SLEs using GCTA software. The environmental contribution to SLEs was assessed by modelling familial, couple and sibling components. Using polygenic risk scores (PRS) and LD score regression (LDSC) we analysed the genetic overlap between MDD, neuroticism and SLEs. Results: Past 6-month life events were positively associated with lifetime MDD status (β=0.21, r2=1.1%, p=2.5 x 10-25) and neuroticism (β =0.13, r2=1.9%, p=1.04 x 10-37) at the phenotypic level.  Common SNPs explained 8% of the phenotypic variance in personal life events (those directly affecting the individual) (S.E.=0.03, p= 9 x 10-4). A significant effect of couple environment was detected accounting for 13% (S.E.=0.03, p=0.016) of the phenotypic variation in SLEs. PRS analyses found that reporting more SLEs was associated with a higher polygenic risk for MDD (β =0.05, r2=0.3%, p=3 x 10-5), but not a higher polygenic risk for neuroticism. LDSC showed a significant genetic correlation between SLEs and both MDD (rG=0.33, S.E.=0.08 ) and neuroticism (rG=0.15, S.E.=0.07). Conclusions: These findings suggest that SLEs should not be regarded solely as environmental risk factors for MDD as they are partially heritable and this heritability is shared with risk for MDD and neuroticism. Further work is needed to determine the causal direction and source of these associations.


2001 ◽  
Vol 31 (7) ◽  
pp. 1193-1202 ◽  
Author(s):  
E. RUBENOWITZ ◽  
M. WAERN ◽  
K. WILHELMSON ◽  
P. ALLEBECK

Background. Stressful life events, such as family conflicts, separation, bereavement, somatic illness and financial problems are common antecedents of suicide. Studies on suicide among younger persons dominate the literature, despite the fact that a large proportion of suicides occur among elderly persons.Methods. The occurrence of stressful life events was investigated among elderly suicide cases and population controls. The study was conducted in the southwestern part of Sweden and included 85 persons (46 males and 39 females) 65 years and above who had committed suicide from January 1994 to May 1996. Population controls (84 males and 69 females) were randomly selected. Interviews were carried out with the controls and with informants for the suicide cases. Questions on sociodemographic background, mental and somatic health status, and life events (0–6, 7–12 and 13–24 months preceding suicide/interview) were included in the interviews.Results. Somatic illness, family discord and financial trouble were significant risk factors during all three time periods. Other risk factors were mental disorder, lower education, feelings of loneliness and previous suicide in the family. Factors associated with a decreased risk included active participation in organizations and having a hobby. Variables that remained in the multivariate logistic regression model were mental disorder (men, odds ratio (OR) = 62·4, 95% CI 17·9–217·5; women, OR = 55·9, 95% CI 14·1–222·3) and family discord (men, OR = 10·0, 95% CI 1·7–59·8; women, OR = 9·2, 95% CI 1·9–44·8).Conclusions. Mental disorder and family discord were the two major risk factors for suicide among elderly men and women.


2016 ◽  
Vol 46 (9) ◽  
pp. 1865-1874 ◽  
Author(s):  
K. S. Kendler ◽  
C. O. Gardner

BackgroundThe nature of the relationship between depressive vulnerability (DV) and acute adversity in the etiology of major depression (MD) remains poorly understood.MethodStressful life events (SLEs) and MD onsets in the last year were assessed at four waves in cohort 1 (females) and at two waves in cohort 2 (males and females) from the Virginia Adult Twin Study. Structural equation modeling was conducted in Mplus.ResultsIn cohort 1, DV was strongly indexed by depressive episodes over the four waves (paths from +0.72 to 0.79) and predicted by SLEs in the month of their occurrence (+0.31 to 0.36). Wave-specific DV was associated both with stable DV (+0.29 to 0.33) and by forward transmission of DV from the preceding wave (+0.33 to 0.36). SLEs were predicted by stable DV (+0.29) and from SLEs in the preceding month (+0.06). As the cohort aged, MD onsets were better indexed by DV and more poorly predicted by SLEs. Parameter estimates were similar in males and females from cohort 2. In individuals with prior depressive episodes, the association between MD onset and SLEs was weakened while the prediction of SLEs from DV was substantially strengthened. We found no evidence for ‘reverse causation’ from MD episodes to SLEs.ConclusionThe interrelationship between DV and acute adversity in the etiology of MD is complex and temporally dynamic. DV impacts on MD risk both directly and indirectly through selection into high stress environments. Over time, depressive episodes become more autonomous. Both DV and SLEs transmit forward over time and therefore form clear targets for intervention.


2018 ◽  
Vol 3 ◽  
pp. 11 ◽  
Author(s):  
Toni-Kim Clarke ◽  
Yanni Zeng ◽  
Lauren Navrady ◽  
Charley Xia ◽  
Chris Haley ◽  
...  

Background: Stressful life events (SLEs) and neuroticism are risk factors for major depressive disorder (MDD). However, SLEs and neuroticism are heritable and genetic risk for SLEs is correlated with risk for MDD. We sought to investigate the genetic and environmental contributions to SLEs in a family-based sample, and quantify genetic overlap with MDD and neuroticism. Methods: A subset of Generation Scotland: the Scottish Family Health Study (GS), consisting of 9618 individuals with information on MDD, past 6 month SLEs, neuroticism and genome-wide genotype data was used in the present study. We estimated the heritability of SLEs using GCTA software. The environmental contribution to SLEs was assessed by modelling familial, couple and sibling components. Using polygenic risk scores (PRS) and LD score regression (LDSC) we analysed the genetic overlap between MDD, neuroticism and SLEs. Results: Past 6-month life events were positively correlated with lifetime MDD status (β=0.21, r2=1.1%, p=2.5 x 10-25) and neuroticism (β =0.13, r2=1.9%, p=1.04 x 10-37) at the phenotypic level.  Common SNPs explained 8% of the phenotypic variance in personal life events (those directly affecting the individual) (S.E.=0.03, p= 9 x 10-4). A significant effect of couple environment was detected accounting for 13% (S.E.=0.03, p=0.016) of the phenotypic variation in SLEs. PRS analyses found that reporting more SLEs was associated with a higher polygenic risk for MDD (β =0.05, r2=0.3%, p=3 x 10-5), but not a higher polygenic risk for neuroticism. LDSC showed a significant genetic correlation between SLEs and both MDD (rG=0.33, S.E.=0.08 ) and neuroticism (rG=0.15, S.E.=0.07). Conclusions: These findings suggest that SLEs should not be regarded solely as environmental risk factors for MDD as they are partially heritable and this heritability is shared with risk for MDD and neuroticism. Further work is needed to determine the causal direction and source of these associations.


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