Caroline Louise Vandeleur

Background: Attention-deficit hyperactivity disorder (ADHD) is one of the most frequent neurodevelopmental disorders in youth, and persists into adulthood in the majority of cases. Our objective was to examine which factors are associated with ADHD in women across different disorder levels (subthreshold, full, persistent). Methods: Analyses were carried out using data from the CoLaus|PsyCoLaus study (N = 2741, age range 35–88 years). The factors of interest comprised familial aggregation, age of ADHD onset, somatic comorbidity, adverse childhood experiences and trauma, parental bonding, as well as immunological and cardio-metabolic markers. Association analyses were combined with a person-centered analysis approach (latent class/ latent profile analysis (LCA/ LPA)). Results: Subthreshold and full ADHD both comprised higher levels of adverse childhood experiences and lower scores of parental bonding. Familial aggregation and earlier age of onset were prominent features in full ADHD, but less relevant regarding persistence. There, increased levels of immunological and cardiometabolic markers played the major role (monocytes, neutrophils, hsCRP, insulin and leptin). In a subgroup perspective, adverse childhood experiences were the most prominent feature of the “burdened” opposed to the “idiopathic” LCA/LPA subgroup. The “burdened” subgroup showed higher persistence rates than the “idiopathic” subgroup in subthreshold and full ADHD. Conclusions: The full picture of subthreshold, full and persistent ADHD in women was characterized by surprisingly heterogeneous association patterns. The heterogeneity does not only rely on severity levels but is primarily associated with additional factors, including familial aggregation in full ADHD or proinflammatory immune and cardiovascular system dysregulation in persistent ADHD.

Objectives: Adverse parenting styles during childhood have been shown to contribute to influencing later pain characteristics in clinical populations with chronic pain (CP). However, few studies have addressed this question in the general population. We assessed the associations of perceived parenting styles with incident, persistent, and remitted CP during a 5-year follow-up in middle-aged community-dwellers as well as the potentially moderating effect of sex on these associations. Methods: Data stemmed from the 2 first follow-up (FU1, FU2) evaluations of CoLaus|PsyCoLaus, a prospective cohort study conducted in the general population of Lausanne, Switzerland. Parental bonding was assessed using the Parental Bonding Instrument (PBI). The 1,739 participants of this analysis were divided into 4 groups according to their CP status at follow-up: (1) incident CP, (2) persistent CP, (3) remitted CP, and (4) CP free (reference group). The associations between PBI categories (high vs low) and subsequent CP status were assessed using multinomial logistic regressions, controlling for confounding factors including lifetime major depressive disorder, neuroticism, and psychotropic drug use. Results: Sex and PBI categories did not interact regarding CP status during follow-up. The only significant main effect was between high levels of denial of autonomy by the father and a higher risk of reporting persistent CP at follow-up (odds ratio: 1.42 [1.05; 1.91] P = 0.02). Conclusion: Our results suggest that earlier perceived high psychological denial of autonomy by the father is associated with the subsequent risk of CP in mid-life. Prospective studies following adolescents into adulthood should determine the direction of this association.

The mechanisms underlying the association between major depressive disorders (MDD) and obesity are still only partially understood. We aimed to explore these mechanisms using two approaches: 1) studying the parent-offspring transmission patterns of MDD and its subtypes and of the adiposity markers BMI and waist circumference, and 2) assessing the associations of parental polygenic risk scores (PRS) for MDD and BMI with MDD and adiposity markers in parents and offspring. Data on parents (N = 467) and their 18 to 35-year-old offspring (N = 592; mean age: 26.5 (s.d. 4.4) years) were derived from a community study conducted in an urban area. Psychiatric DSM-IV disorders including MDD and its atypical and melancholic subtypes were assessed using semi-structured diagnostic interviews. Phenotypic analyses provided evidence for a strong parent-child transmission of BMI (β = 0.33 kg/m2, 95% Confidence Intervals (CI): 0.24;0.42) and waist circumference (β = 0.28 cm, 0.19;0.38), but not for MDD or its subtypes or a cross-transmission of MDD and adiposity markers. Parental PRS for MDD were not only associated with MDD and its subtypes in parents, but also with BMI and waist circumference levels in parents (β = 0.49 kg/m2, 0.11;0.86; β = 2.00 cm, 1.05;3.00, respectively) and offspring (β = 0.54 kg/m2, 0.16;0.91; β = 1.27 cm, 1.17;2.37, respectively), whereas parental PRS for BMI were only associated with adiposity marker levels in parents and offspring. In conclusion, our findings relying on PRS suggest that the associations between atypical MDD and elevated adiposity marker levels may at least be partially attributable to common genetic liability. In contrast, the absence of parent-child transmission of MDD or its subtypes as well as the cross-transmission of MDD and adiposity markers according to our phenotypic analyses could be attributable to the young age of our offspring cohort.

Previous research has unveiled an intriguing positive association between the AB blood group and mental disorders in general. In this study, we compared ABO blood groups with five major groups of mental disorders to attain a higher level of specificity. The analyses were conducted using data from the CoLaus|PsyCoLaus study (N=5111). They revealed that the AB blood group exhibited a positive association with both neurodevelopmental disorders (RR 2.29, CI 1.38– 3.82) and substance use disorders (RR 2.25, CI 1.38– 3.65) after adjusting for sex and childhood adversities. These associations could be replicated with respect to the familial aggregation of neurodevelopmental and substance use disorders. Large databases are needed to achieve more detailed results related to specific disorders. Plain Language Summary: Prior research has shown an interesting link between the AB blood group and mental disorders. In our study, we used data from a large Swiss population-based epidemiological cohort study to learn more about this connection. We examined the relationship between ABO blood groups and five major groups of mental disorders: neurodevelopmental, early onset anxiety, later onset anxiety, mood, and substance use disorders. Our analyses revealed associations between the AB blood group and neurodevelopmental and substance use disorders. The findings point to an unknown immunological mechanism that may play a role in the development of neurodevelopmental and substance use disorders.

Research on antidepressant-related weight changes over more than 12 months is scarce and adjustment for the effects of depressive episodes has rarely been applied. Accordingly, our aim was to assess the associations of the use of any antidepressants, subclasses of antidepressant and specific compounds prior to baseline and during a 5.5-year follow-up with changes in adiposity markers, and the effect of sex on these associations, with adjustment for multiple confounders including the effects of depressive episodes and their severity. Data stemmed from a prospective cohort study including 2479 randomly selected 35–66 year-old residents of an urban area (mean age 49.9 years, 53.3% women) who underwent physical and psychiatric evaluations at baseline and follow-up. Weight, height, waist circumference, and body fat were measured by trained nurses and information on diagnosis and antidepressant use prior to baseline and during follow-up was collected through standardized interviews. In the fully adjusted models, the number of antidepressants, mainly SSRIs and TCAs, used prior to baseline, was associated with a lower increase of body-mass index (BMI, β (95%CI) = −0.12 (−0.19, −0.05)) and waist circumference (β = −0.28 (−0.56, −0.01)), whereas participants treated with antidepressants during the follow-up had a steeper increase in BMI (β = 0.32 (0.13, 0.50)) and waist circumference (β = 1.23 (0.44, 2.01)). Within the class of SSRIs, the use of fluoxetine, sertraline or escitalopram during follow-up was associated with a steeper increase in adiposity markers. The associations of SSRIs with BMI and waist circumference were only observed when the SSRIs were used during the second period of the follow-up. Sex did not moderate these associations. Our findings suggest an increase of adiposity markers during sustained treatment with TCAs and SSRIs, which however return to normal levels after cessation of treatment. Hence, the benefit of long-term administration of these antidepressants should be carefully weighed against the potential risk of weight gain.

Purpose: Previous population-based studies have partially provided inconsistent results regarding the co-variates of chronic depression, which were likely to be attributable to methodological limitations. The present paper that compared people with chronic major depressive disorder (MDD), non-chronic MDD and no mood disorder in the community focused on specific atypical and melancholic depression symptoms and subtypes of MDD, family history (FH) of mood disorders, measured physical cardio-vascular risk factors (CVRF), personality traits, coping style and adverse life-events. Methods: Data stemmed from a population-based cohort including 3618 participants (female 53%, n=1918; mean age 50.9 years, s.d. 8.8 years). Among them 563 had a lifetime history of chronic MDD, 1060 of non-chronic MDD and 1995 of no mood disorder. Diagnostic and FH information were elicited through semi-structured interviews, CVRF were assessed through physical investigations. Results: The major findings were that chronic MDD was associated with increase in appetite/weight and suicidal ideation/attempts during the most severe episode, higher exposure to life-events in adulthood, higher levels of neuroticism, lower levels of extraversion and lower levels of informal help-seeking behavior but less frequent FH of MDD compared to non-chronic MDD. Conclusion: Chronic MDD is associated with a series of potential modifiable risk factors which are accessible via psychotherapeutic approaches that may improve the course of chronic MDD.

Background: The factors involved in the transmission of mood disorders are only partially elucidated. Aside from genes, the family environment might play a crucial role in parent–child transmission. Our goals were to (1) assess the associations of parental bipolar disorder (BPD) and Major Depressive Disorder (MDD) with individual or shared family environmental factors, including traumatic events in offspring, parental separation, family cohesion and parental attitudes; and 2) test whether these factors were mediators of the association between exposure to parental mood disorders and the onset of these disorders in offspring. Methods: The sample stems from an ongoing family high-risk study of mood disorders conducted in the French-speaking part of Switzerland. Given the strong impact of the age of onset of parental disorders on their transmission to children, parental disorders were dichotomized according to the onset (cut-off 21 years). Probands with early-onset (n = 30) and later-onset BPD (n = 51), early-onset (n = 21) and later-onset MDD (n = 47) and controls (n = 65), along with their spouses (n = 193) and offspring (n = 388; < 18 years on study inclusion), were assessed over a mean follow-up duration of 14 years (s.d: 4.6). The environmental measures were based on reports by offspring collected before the onset of their first mood episode. Results: Offspring of probands with later-onset BPD and offspring of probands with both early-onset and later-onset MDD reported traumatic events more frequently than comparison offspring, whereas exposure to parental separation was more frequent in all groups of high-risk offspring. Moreover, several familial environment scores including parenting attitudes differed between offspring of probands with BPD and comparison offspring. However, none of these factors were mediators of the parent–child transmission of BPD. Among the environmental factors, traumatic events were shown to be modest mediators of the transmission of early-onset MDD. Conclusions: Our data do not support the implication of the assessed environmental factors in the parent–child transmission of BPD. In contrast to BPD, traumatic events partially mediate the parent–child transmission of early-onset MDD, which has important implications for intervention and prevention. Early therapeutic efforts in offspring exposed to these events are likely to reduce their deleterious impact on the risk of subsequent MDD.