Biology subjects

Petersen, L.

Publications and source records attributed to Petersen, L..

3 recordsLinked to original sources

bioRxiv2018

Statin treatment and the risk of depression

The effect of statin treatment on the risk of developing depression remains unclear. Therefore, we aimed to assess the association between statin treatment and depression in a nationwide register-based cohort study with up to 20 years of follow up. We identified all statin users among all individuals born in Denmark between 1920 and 1983. One non-user was matched to each statin user based on age, sex and a propensity score taking several potential confounders into account. Using Cox regression we investigated the association between statin use and: I) redemption of prescriptions for antidepressants, II) redemption of prescriptions for any other drug, III) depression diagnosed at psychiatric hospitals, IV) cardiovascular mortality and V) all-cause mortality. A total of 193,977 statin users and 193,977 non-users were followed for 2,621,282 person-years. Statin use was associated with I) increased risk of antidepressant use (hazard rate ratio (HRR)=1.33; 95% confidence interval (95%-CI)=1.31-1.36), II) increased risk of any other prescription drug use (HRR=1.33; 95%-CI=1.31-1.35), III) increased risk of receiving a depression diagnosis (HRR=1.22, 95%-CI=1.12-1.32) - but not after adjusting for antidepressant use (HRR=1.07, 95%-CI=0.99- 1.15), IV) reduced cardiovascular mortality (HRR=0.92, 95%-CI=0.87-0.97) and V) reduced all-cause mortality (HRR=0.90, 95%-CI=0.88-0.92). These results suggest that the association between statin treatment and antidepressant use was unspecific (equivalent association between statins and other drugs) and that the association between statin use and depression diagnoses was mediated by antidepressant use. Thus, statin users and non-users appear to be equally likely to develop depression, but the depression is more often detected/treated among statin users.

epidemiology↗

bioRxiv2017

The Anorexia Nervosa Genetics Initiative: Overview and Methods

BackgroundGenetic factors contribute to anorexia nervosa (AN); and the first genome-wide significant locus has been identified. We describe methods and procedures for the Anorexia Nervosa Genetics Initiative (ANGI), an international collaboration designed to rapidly recruit 13000 individuals with AN as well as ancestrally matched controls. We present sample characteristics and the utility of an online eating disorder diagnostic questionnaire suitable for large-scale genetic and population research.\n\nMethodsANGI recruited from the United States (US), Australia/New Zealand (ANZ), Sweden (SE), and Denmark (DK). Recruitment was via national registers (SE, DK); treatment centers (US, ANZ, SE, DK); and social and traditional media (US, ANZ, SE). All cases had a lifetime AN diagnosis based on DSM-IV or ICD-10 criteria (excluding amenorrhea). Recruited controls had no lifetime history of disordered eating behaviors. To assess the positive and negative predictive validity of the online eating disorder questionnaire (ED100K-v1), 109 women also completed the Structured Clinical Interview for DSM-IV (SCID), Module H.\n\nResultsBlood samples and clinical information were collected from 13,364 individuals with lifetime AN and from controls. Online diagnostic phenotyping was effective and efficient; the validity of the questionnaire was acceptable.\n\nConclusionsOur multipronged recruitment approach was highly effective for rapid recruitment and can be used as a model for efforts by other groups. High online presence of individuals with AN rendered the Internet/social media a remarkably effective recruitment tool in some countries. ANGI has substantially augmented Psychiatric Genomics Consortium AN sample collection. ANGI is a registered clinical trial: clinicaltrials.gov NCT01916538; https://clinicaltrials.gov/ct2/show/NCT01916538?cond=Anorexia+Nervosa&draw=1&rank=3.

genetics↗

bioRxiv2017

Paternal-age-related de novo mutations and risk for five disorders

BackgroundThere are well-established epidemiologic associations between advanced paternal age and increased offspring risk for several psychiatric and developmental disorders. These associations are commonly attributed to age-related de novo mutations. However, the actual magnitude of risk conferred by age-related de novo mutations in the male germline is unknown. Quantifying this risk would clarify the clinical and public health significance of delayed paternity.\n\nMethodsUsing results from large, parent-child trio whole-exome-sequencing studies, we estimated the relationship between paternal-age-related de novo single nucleotide variants (dnSNVs) and offspring risk for five disorders: autism spectrum disorders (ASD), congenital heart disease (CHD), neurodevelopmental disorders with epilepsy (EPI), intellectual disability (ID), and schizophrenia (SCZ). Using Danish national registry data, we then investigated the degree to which the epidemiologic association between each disorder and advanced paternal age was consistent with the estimated role of de novo mutations.\n\nResultsIncidence rate ratios comparing dnSNV-based risk to offspring of 45 versus 25-year-old fathers ranged from 1.05 (95% confidence interval 1.01-1.13) for SCZ to 1.29 (95% CI 1.13-1.68) for ID. Epidemiologic estimates of paternal age risk for CHD, ID and EPI were consistent with the dnSNV effect. However, epidemiologic effects for ASDs and SCZ significantly exceeded the risk that could be explained by dnSNVs alone (p<2e-4 for both comparisons).\n\nConclusionIncreasing dnSNVs due to advanced paternal age confer a small amount of offspring risk for psychiatric and developmental disorders. For ASD and SCZ, epidemiologic associations with delayed paternity largely reflect factors that cannot be assumed to increase with age.

genetics↗