Individuals who self-harm may have an increased risk of aggression toward others, but this association has been insufficiently investigated. More conclusive evidence may affect assessment, treatment interventions, and clinical guidelines.
To investigate the association between nonfatal self-harm and violent crime.
This population-based longitudinal cohort study, conducted from January 1, 1997, through December 31, 2013, studied all Swedish citizens born between 1982 and 1998 who were 15 years and older (N?=?1?850?252). Individuals who emigrated from Sweden before the age of 15 years (n?=?104?051) or immigrated to Sweden after the age of 13 years (ie,
Teenage motherhood is associated with poor offspring outcomes but these associations may be influenced by offspring birth year because of substantial social changes in recent decades. Existing research also has not examined whether these associations are due to the specific effect of mother's age at childbirth or factors shared by siblings in a family. We used a population-based cohort study in Sweden comprising all children born from 1960 to 1989 (N = 3,162,239), and a subsample of siblings differentially exposed to maternal teenage childbearing (N = 485,259) to address these limitations. We examined the effect of teenage childbearing on offspring violent and non-violent criminal convictions, poor academic performance, and substance-related problems. Population-wide teenage childbearing was associated with offspring criminal convictions, poor academic performance, and substance-related problems. The magnitude of these associations increased over time. Comparisons of differentially exposed siblings indicated no within-family association between teenage childbearing and offspring violent and non-violent criminal convictions or poor academic performance, although offspring born to teenage mothers were more likely to experience substance-related problems than their later-born siblings. Being born to a teenage mother in Sweden has become increasingly associated with negative outcomes across time, but the nature of this association may differ by outcome. Teenage childbearing may be associated with offspring violent and non-violent criminal convictions and poor academic performance because of shared familial risk factors, but may be causally associated with offspring substance-related problems. The findings suggest that interventions to improve offspring outcomes should delay teenage childbearing and also target risk factors influencing all offspring of teenage mothers.
The study aimed to investigate whether the association between birth weight and the risk of breast cancer can be confounded by familial factors, such as shared environment and common genes.
Eligible were all female like-sexed twins of the Swedish Twin Registry, born during the period 1926-1958 and alive in 1973. Data were obtained from birth records, and the final study population with reliable birth weight data was made up of 11,923 twins. Hazard ratios (HR) for breast cancer according to birth weight were estimated through Cox regression, using robust SE to account for the dependence within twin pairs. Paired analysis was done to account for potential confounding by familial factors.
In the cohort analysis, a birth weight >or=3,000 g was associated with an increased risk of breast cancer diagnosed at or before 50 years [adjusted HR, 1.57; 95% confidence interval (95% CI), 1.03-2.42] but not with breast cancer with a later onset (adjusted HR, 0.80; 95% CI, 0.57-1.12). From >or=2,500 g, a 500-g increase in birth weight conferred a HR of 1.62 (95% CI, 1.16-2.27) for breast cancer diagnosed at or before 50 years. This risk remained in analysis within twin pairs (HR, 1.57; 95% CI, 1.00-2.48).
In the present study, findings indicate that the association between birth weight and breast cancer risk, seen only in women diagnosed early (
Associations between low birth weight (=2,500 g) and increased risk of mortality and morbidity provided the foundation for the "developmental origins of health and disease" hypothesis. Previous between-family studies could not control for unmeasured confounders. Therefore, we compared differentially exposed siblings to estimate the extent to which the associations were due to uncontrolled factors. Our population cohort included 3,291,773 persons born in Sweden from 1973 to 2008. Analyses controlled for gestational age, among other covariates, and considered birth weight as both an ordinal and a continuous variable. Outcomes included mortality after 1 year, cardiac-related death, hypertension, ischemic heart disease, pulmonary circulation problems, stroke, and type 2 diabetes mellitus. We fitted fixed-effects models to compare siblings and conducted sensitivity analyses to test alternative explanations. Across the population, the lower the birth weight, the greater the risk of mortality (e.g., cardiac-related death (low birth weight hazard ratio = 2.69, 95% confidence interval: 2.05, 3.53)) and morbidity (e.g., type 2 diabetes mellitus (low birth weight hazard ratio = 1.79, 95% confidence interval: 1.50, 2.14)) outcomes in comparison with normal birth weight. All associations were independent of shared familial confounders and measured covariates. Results emphasize the importance of birth weight as a risk factor for subsequent mortality and morbidity.
Maternal Smoking During Pregnancy (SDP) has consistently been associated with increased risk of attention-deficit/hyperactivity disorder (ADHD) in offspring, but recent studies indicate that this association might be due to unmeasured familial confounding.
A total of 813,030 individuals born in Sweden between 1992 and 2000 were included in this nationwide population-based cohort study. Data on maternal SDP and ADHD diagnosis were obtained from national registers and patients were followed up from the age of 3 to the end of 2009. Hazard Ratios (HRs) were estimated using stratified Cox regression models. Cousin and sibling data were used to control for unmeasured familial confounding.
At the population level maternal SDP predicted ADHD in offspring (HR(ModerateSDP) = 1.89; HR(HighSDP)= 2.50). This estimate gradually attenuated toward the null when adjusting for measured confounders (HR(ModerateSDP)= 1.62; HR(HighSDP)= 2.04), unmeasured confounders shared within the extended family (i.e., cousin comparison) (HR(ModerateSDP)= 1.45; HR(HighSDP)= 1.69), and unmeasured confounders within the nuclear family (i.e., sibling comparison) (HR(ModerateSDP)= 0.88; HR(HighSDP)= 0.84).
Our results suggest that the association between maternal SDP and offspring ADHD are due to unmeasured familial confounding.
CONTEXT: The association between maternal smoking during pregnancy (SDP) and offspring disruptive behaviors has been well documented, but it is unclear whether exposure to SDP or the effects of factors correlated with SDP account for the increased risk. OBJECTIVE: To test whether the association between SDP and offspring criminal convictions was consistent with a causal connection or due to familial background factors by controlling for measured covariates and using a quasi-experimental approach. DESIGN: We used a population-based study of children born in Sweden from 1983 to 1989 (N = 609,372) to examine the association between SDP and offspring criminal convictions while controlling for measured traits of both parents. We also compared siblings differentially exposed to SDP (n = 50,339) to account for unmeasured familial factors that could account for the association. SETTING: Population-based study of all children born in Sweden from 1983 to 1989 with information on maternal SDP and offspring criminal convictions based on national registries collected by the Swedish government. PATIENTS OR OTHER PARTICIPANTS: Children born in Sweden from 1983 to 1989 (N = 609,372) and siblings differentially exposed to SDP (n = 50,339). MAIN OUTCOME MEASURES: Violent and nonviolent convictions, based on the Swedish National Crime Register, a register with detailed information on all convictions in the country. RESULTS: Moderate (hazard rate [HR], 2.47; 95% confidence interval [CI], 2.34-2.60) and high (HR, 3.43; 95% CI, 3.25-3.63) levels of maternal SDP were associated with an increased risk for offspring violent convictions, even when controlling for maternal and paternal traits. There was no association between SDP and violent convictions, however, when comparing differentially exposed siblings (HR(moderate), 1.02; 95% CI, 0.79-1.30; HR(high), 1.03; 95% CI, 0.78-1.37). Smoking during pregnancy also was associated with nonviolent convictions in the entire population (HR(moderate), 1.62; 95% CI, 1.58-1.66; HR(high), 1.87; 95% CI, 1.82-1.92) and when controlling for covariates. But, there was no association when comparing siblings who were differentially exposed (HR(moderate), 0.89; 95% CI, 0.78-1.01; HR(high), 0.89; 95% CI, 0.78-1.02). CONCLUSION: The results suggest that familial background factors account for the association between maternal SDP and criminal convictions, not the specific exposure to SDP.
Previous epidemiological, animal, and human cognitive neuroscience research suggests that maternal smoking during pregnancy (SDP) causes increased risk of substance use/problems in offspring.
To determine the extent to which the association between SDP and offspring substance use/problems depends on confounded familial background factors by using a quasi-experimental design.
We used 2 separate samples from the United States and Sweden. The analyses prospectively predicted multiple indices of substance use and problems while controlling for statistical covariates and comparing differentially exposed siblings to minimize confounding.
Offspring of a representative sample of women in the United States (sample 1) and the total Swedish population born during the period from January 1, 1983, to December 31, 1995 (sample 2).
Adolescent offspring of the women in the National Longitudinal Survey of Youth 1979 (n = 6904) and all offspring born in Sweden during the 13-year period (n = 1,187,360).
Self-reported adolescent alcohol, cigarette, and marijuana use and early onset (before 14 years of age) of each substance (sample 1) and substance-related convictions and hospitalizations for an alcohol- or other drug-related problem (sample 2).
The same pattern emerged for each index of substance use/problems across the 2 samples. At the population level, maternal SDP predicted every measure of offspring substance use/problems in both samples, ranging from adolescent alcohol use (hazard ratio [HR](moderate), 1.32 [95% CI, 1.22-1.43]; HR(high), 1.33 [1.17-1.53]) to a narcotics-related conviction (HR(moderate), 2.23 [2.14-2.31]; HR(high), 2.97 [2.86-3.09]). When comparing differentially exposed siblings to minimize genetic and environmental confounds, however, the association between SDP and each measure of substance use/problems was minimal and not statistically significant.
The association between maternal SDP and offspring substance use/problems is likely due to familial background factors, not a causal influence, because siblings have similar rates of substance use and problems regardless of their specific exposure to SDP.
The current study examined associations between labor induction and both (1) offspring attention-deficit hyperactivity disorder (ADHD) diagnosis in a Swedish birth cohort born 1992-2005 (n?=?1,085,008) and (2) indices of offspring low academic achievement in a sub-cohort born 1992-1997 (n?=?489,196). Associations were examined in the entire sample (i.e., related and unrelated individuals) with adjustment for measured covariates and, in order to account for unmeasured confounders shared within families, within differentially exposed cousins and siblings. We observed an association between labor induction and offspring ADHD diagnosis and low academic achievement in the population. However, these associations were fully attenuated after adjusting for measured covariates and unmeasured factors that cousins and siblings share. The results suggest that observed associations between labor induction and ADHD and low academic achievement may be due to genetic and/or shared environmental factors that influence both mothers' risk of labor induction and offspring neurodevelopment.
Studies have found negative associations between socioeconomic position and attention deficit/hyperactivity disorder (ADHD), but it remains unclear if this association is causal. The aim of this study was to determine the extent to which the association between family income in early childhood and subsequent ADHD depends on measured and unmeasured selection factors.
A total of 811,803 individuals born in Sweden between 1992 and 2000 were included in this nationwide population-based cohort study. Diagnosis of ADHD was assessed via the Swedish national Patient Register and the Swedish Prescribed Drug Register. Annual family income during offspring's first 5 years in life was collected prospectively from the Swedish Integrated Database for Labour Market Research and divided into quartiles by (lower) family disposable income. We predicted ADHD from family income while controlling for covariates and also comparing differently exposed cousins and siblings to control for unmeasured familial confounding.
The crude analyses suggested that children exposed to lower income levels were at increased risk for ADHD (HRQ uartile1 = 2.52; 95% CI, 2.42-2.63; HRQ uartile2 = 1.52; 95% CI, 1.45-1.58; HRQ uartile3 = 1.20; 95% CI, 1.14-1.15). This dose-dependent association decreased after adjustment for measured covariates (HRQ uartile1 = 2.09; 95% CI, 2.00-2.19; HRQ uartile2 = 1.36; 95% CI, 1.30-1.42; HRQ uartile3 = 1.13; 95% CI, 1.08-1.18). Although the association was attenuated in cousin comparisons (HRQ uartile1 = 1.61; 95% CI, 1.40-1.84; HRQ uartile2 = 1.28; 95% CI, 1.12-1.45; HRQ uartile3 = 1.14; 95% CI, 1.01-1.28) and sibling comparison models (HRQ uartile1 = 1.37; 95% CI, 1.07-1.75; HRQ uartile2 = 1.37; 95% CI, 1.12-1.68; HRQ uartile3 = 1.23; 95% CI, 1.04-1.45), it remained statistically significant across all levels of decreased disposable family income.
Our results indicated that low family income in early childhood was associated with increased likelihood of ADHD. The link remained even after controlling for unmeasured selection factors, highlighting family income in early childhood as a marker of causal factors for ADHD.
Individuals with coeliac disease have increased risk of depression and death from external causes, but conclusive studies on death from suicide are missing. We examined the risk of suicide in coeliac disease and amongst individuals where the small intestinal biopsy showed no villous atrophy.
We collected biopsy data from all 28 clinical pathology departments in Sweden for individuals diagnosed during 1969-2007 with coeliac disease (Marsh 3: villous atrophy; n=29,083 unique individuals), inflammation without villous atrophy (Marsh 1-2; n=13,263) or positive coeliac disease serology but normal mucosa (Marsh 0, n=3719). Through Cox regression we calculated Hazard ratios for suicide as recorded in the Swedish Cause of Death Register.
The risk for suicide was higher in patients with coeliac disease compared to general population controls (HR=1.55; 95%CI=1.15-2.10; based on 54 completed suicides). Whilst suicide was also more common amongst individuals with inflammation (HR=1.96; 95%CI=1.39-2.77), no such increase was seen amongst individuals with a normal mucosa but positive coeliac disease serology (HR=1.06; 95%CI=0.37-3.02).
We found a moderately increased risk of suicide amongst patients with coeliac disease. This merits increased attention amongst physicians treating these patients.