Lizanne Johanna Stephanie Schweren

Introduction: The number of requests for medical assistance in dying (MAID) based on psychological suffering has significantly increased in recent years. People that request MAID based on psychological suffering often have a long-term history within mental health care that has not (yet) led to recovery. The risk of death by suicide in this group is high. Relatively little is known about people who request MAID based on psychological suffering and their death wish. The lack of knowledge results in a lack of targeted counseling options and suicide prevention for people who request MAID based on psychological suffering. The current study therefore focuses on the characteristics, psychological processes and support needs of people who request MAID based on psychological suffering, and how death wishes and suicidality develop during and after a MAID request. The aim of this research is to contribute to better care and support for this vulnerable group. Methods: To answer the questions above we conduct a prospective longitudinal observational study. Participants twice complete a digital questionnaire: one shortly after registering with Expertisecentrum Euthanasie (EE) for their MAID request and one six months after completing the first questionnaire. Participants are 16 years or older and have requested MAID at EE based on psychological suffering. Ethics and dissemination: The study was approved as a study subject to the Medical Research Involving Human Subject Act (WMO) by the METC of Amsterdam UMC. Risks of participating in the study are low and explicit attention is paid to participant safety. The study results will be disseminated through scientific publication, conferences, and a webinar for mental health professionals. Based on participants support needs, a plan will be developed for support services to prevent suicide by people who requested MAID based on psychological suffering. Thus, the study will contribute to better counseling and suicide prevention for this vulnerable group.

The present study investigated whether an unhealthy diet and other lifestyle behaviors may modify the genetic susceptibility to impulsivity. A total of 33,047 participants (mean age = 42.1 years, 59.8% females) from the Dutch Lifelines cohort were included. Each diet index and other lifestyle behaviors were tested for their interactions on the effect on the attention-deficit/hyperactivity disorder (ADHD) polygenic risk score (PRS) on impulsivity using a linear regression model with adjustment for covariates. The ADHD PRS was significantly associated with impulsivity (B = 0.03 (95% CI: 0.02, 0.04); p = 2.61 × 10⁻⁹). A poorer diet, a higher intake of energy, and a higher intake of fat were all associated with higher impulsivity, and a high intake of energy amplified the effect of ADHD PRS on impulsivity (e.g., for the interaction term of ADHD PRS and highest tertile on intake of energy, B = 0.038 (95% CI: 0.014, 0.062); p = 0.002. The other lifestyle factors, namely short and long sleep duration, current and past smoking, higher alcohol intake, and more time spent on moderate-to-vigorous physical activity were associated with higher impulsivity, but no interaction effect was observed. In conclusion, we found that a high intake of energy exacerbated the genetic susceptibility to impulsivity. Our study helps to improve our understanding of the role of diet and genetic factors on impulsivity.

Purpose: Intrauterine exposures influence offspring health and development. Here we investigated maternal intake of sweetened carbonated beverages (SCB) during pregnancy and its association with ADHD symptoms in the offspring. Methods: This study was based on the Norwegian Mother, Father and Child Cohort Study (MoBa) and the Medical Birth Registry of Norway. Maternal diet mid-pregnancy was assessed using a food frequency questionnaire (FFQ). All mothers who responded to the FFQ and a questionnaire when their child was 8 years of age were included (n = 39,870). The exposure was defined as maternal intake (daily servings) of SCB, using no daily intake as reference. Outcome was offspring ADHD symptoms, evaluated as a continuous standardized ADHD score and as a binary outcome of six or more ADHD symptoms vs. five symptoms or less. Associations were analysed using log-binomial regression and linear mixed regression models with adjustment for covariates. Results: The adjusted regression coefficients for the standardized ADHD offspring symptom score were 0.31 [95% confidence intervals (0.001, 0.62)] and 0.46 (0.15, 0.77) for maternal daily intake of ≥ 1 glasses of SCB, when the models included adjustments for total energy intake or energy intake from other sources than SCBs and sweet drinks, respectively. The corresponding adjusted relative risks were 1.16 (1.004, 1.34) and 1.21. (1.05, 1.39) for drinking ≥ 1 glasses daily. Conclusion: In a large pregnancy cohort with offspring followed until 8 years of age, we found an association between maternal daily intake of SCB and offspring ADHD symptoms. These results suggest a weak positive relationship between prenatal exposure to SCB and offspring ADHD.

Behavioral disinhibition is observed to be an important characteristic of many neurodevelopmental and psychiatric disorders. Recent studies have linked dietary quality to levels of behavioral inhibition. However, it is currently unclear whether brain factors might mediate this. The current study investigates whether cortical and subcortical brain volumes mediate part of the association between dietary composition and behavioral disinhibition. A total of 15,258 subjects from the UK Biobank project were included in the current study. Dietary composition and behavioral disinhibition were based on Principle Component Analyses of self-reported dietary composition). As a further data reduction step, cortical and subcortical volume segmentations were input into an Independent Component Analysis. The resulting four components were used as mediator variables in the main mediation analyses, where behavioral disinhibition served as the outcome variable and dietary components as predictors. Our results show: (1) significant associations between all dietary components and brain volume components; (2) brain volumes are associated with behavioral disinhibition; (3) the mediation models show that part of the variance in behavioral disinhibition explained by dietary components (for healthy diet, restricted diet, and high-fat dairy diet) is mediated through the frontal-temporal/parietal brain volume component. These results are in part confirming our hypotheses and offer a first insight into the underlying mechanisms linking dietary composition, frontal-parietal brain volume, and behavioral disinhibition in the general adult population.

Disinhibition is a prominent feature of multiple psychiatric disorders, and has been associated with poor long-term somatic outcomes. Modifiable lifestyle factors including diet and moderate-to-vigorous physical activity (MVPA) may be associated with disinhibition, but their contributions have not previously been quantified among middle-aged/older adults. Here, among N = 157,354 UK Biobank participants aged 40–69, we extracted a single disinhibition principal component and four dietary components (prudent diet, elimination of wheat/dairy/eggs, meat consumption, full-cream dairy consumption). In addition, latent profile analysis assigned participants to one of five empirical dietary groups: prudent-moderate, unhealthy, restricted, meat-avoiding, low-fat dairy. Disinhibition was regressed on the four dietary components, the dietary grouping variable, and self-reported MVPA. In men and women, disinhibition was negatively associated with prudent diet, and positively associated with wheat/dairy/eggs elimination. In men, disinhibition was also associated with consumption of meat and full-cream dairy products. Comparing groups, disinhibition was lower in the prudent-moderate diet (reference) group compared to all other groups. Absolute βs ranged from 0.02–0.13, indicating very weak effects. Disinhibition was not associated with MVPA. In conclusion, disinhibition is associated with multiple features of diet among middle-aged/older adults. Our findings foster specific hypotheses (e.g., early malnutrition, elevated immune-response) to be tested in alternative study designs.

Excessive alcohol intake compromises cognitive functioning. At the same time, moderate alcohol consumption is reported to protect against Alzheimer’s disease among elderly. Little is known about dose-dependent effects of alcohol consumption on higher-order cognitive functioning among generally healthy adults. Here, we applied propensity weighted analyses to investigate associations between habitual drinking patterns and executive functioning in the general population. A community sample of N=78,832 Dutch adults (age 18-65, 40.9% male) completed the Ruff Figural Fluency Task of executive functioning (range 1-165), and self-reported their past month consumption of alcoholic beverages on a food frequency questionnaire. Participants were stratified according to drinking level (abstinent [22.0%], occasional [30 g/day, 2.3%]) and binge-drinking (yes [10.6%] vs. no [89.4%]). Groups were equivalised using multinomial propensity score weighing based on demographic, socioeconomic, health-related and psychosocial factors influencing drinking behaviour. Compared to abstinent participants, task performance was better among light drinkers (β[95% CI]=0.056[0.033-0.078] or +1.3 points, p<0.0001) and moderate drinkers (β[95% CI]=0.111[0.079-0.143] or +2.5 points, p<0.0001), but not among occasional drinkers (β[95% CI]=0.018[-0.006-0.043], p=0.1432) or heavy drinkers (β[95% CI]=0.075[-0.009-0.158], p=0.0791). No difference was found between binge-drinkers and non-binge-drinkers (β[95% CI]=0.032[-0.002-0.066], p=0.0654). In conclusion, we observed better executive functioning in light-moderate drinkers compared to abstainers, but not in occasional drinkers, heavy drinkers or binge-drinkers. This non-linear association is reminiscent of the dose-dependent effect of alcohol consumption on cardiovascular risk. Further studies may determine whether cardiovascular, inflammatory and/or other somatic factors mediate the association between moderate drinking and higher-order cognitive functions. Although analyses were adjusted for observed factors that influence drinking behaviours, we cannot exclude a contribution from unobserved residual confounding.