ABSTRACT
Typically, adults give a primary role to the agent's intention to harm when performing a moral judgment of accidental harm. By contrast, children often focus on outcomes, underestimating the actor's mental states when judging someone for his action, and rely on what we suppose to be intuitive and emotional processes. The present study explored the processes involved in the development of the capacity to integrate agents' intentions into their moral judgment of accidental harm in 5 to 8-year-old children. This was done by the use of different metacognitive trainings reinforcing different abilities involved in moral judgments (mentalising abilities, executive abilities, or no reinforcement), similar to a paradigm previously used in the field of deductive logic. Children's moral judgments were gathered before and after the training with non-verbal cartoons depicting agents whose actions differed only based on their causal role or their intention to harm. We demonstrated that a metacognitive training could induce an important shift in children's moral abilities, showing that only children who were explicitly instructed to "not focus too much" on the consequences of accidental harm, preferentially weighted the agents' intentions in their moral judgments. Our findings confirm that children between the ages of 5 and 8 are sensitive to the intention of agents, however, at that age, this ability is insufficient in order to give a "mature" moral judgment. Our experiment is the first that suggests the critical role of inhibitory resources in processing accidental harm.
ABSTRACT
BACKGROUND: Antidepressant medication is a major cornerstone in treatment of mood and anxiety disorders. Numerous substances are available on the market; however, only 60% of treated patients show sufficient response to medication and side effects are common. Lengthy trials are not uncommon until the optimized drug and dose is found and unfortunately, no valid predictors to match the 'right' drug to the 'right' patient exist nowadays. Genetic factors are thought to be involved as evidenced by numerous pharmacogenetic studies. This comprehensive review summarizes the most interesting findings and discusses clinical implications of pharmacogenetic results. METHODS: We reviewed available literature on pharmacogenetics of antidepressant response and side effects until summer 2011 using the PubMed database. RESULTS: Promising findings exist for several variants in candidate genes involved in the pharmacokinetics or pharmacodynamics of antidepressants. These include association findings in the serotonin transporter gene (5-HTT), serotonin receptor genes, a gene coding an efflux pump in the blood-brain-barrier (ABCB1), and genes involved in the HPA axis. Promising candidate genes increasing risk for side effects include some of the genes associated with treatment response and cytochrome P450 genes. CONCLUSION: A high number of studies on pharmacogenetics of antidepressants have been published during the past decades. However, contradictory results still limit clinical use of these findings. Future studies should include functional analyses and consider gene-gene and gene-environment interactions. This will aid in facilitating a future use of pharmacogenetics in clinical practice, likely leading to improved patient care.
