JCPP advances最新文献

All psychiatric phenomena are positively associated, and several different models can account for this observation. These include the correlated factors, network, general psychopathology as outcome, and hierarchical models. Advantages of hierarchical models, which consist of one general and several (general factor-residualized) specific factors, is that the general factor provides an opportunity to reliably measure global distress and impairment, while the specific factors might improve the ability to discriminate between individuals with different kinds of problems. Nevertheless, other models also have their respective advantages, and it remains challenging to empirically determine which model best accounts for the positive manifold in psychiatry. Instead, I present two non-empirical arguments in favor of hierarchical models. First, by measuring the general factor in isolation, the specific factors tend to include both favorable and unfavorable correlates, which might reduce stigma compared to psychiatric diagnoses that by and large are associated with only unfavorable outcomes. Second, the general psychopathology factor displays an unusual psychometric property in that it includes symptoms of opposite meaning if they have similar valence (e.g., self-reported symptoms such as gullible and paranoid, lazy and workaholic, and terrified and apathetic load in the same direction), which one might want to measure in isolation from variance capturing the content of symptoms. I conclude by speculating that tests designed based on hierarchical models might help clinical assessment.

Attention deficit/hyperactivity disorder (ADHD) used to be studied at age of diagnosis–the typical time that professional help is sought and children get an ADHD diagnosis was also the time that they typically enrolled in scientific studies. As a consequence, most of our knowledge is about referred children with ADHD in middle childhood in the age range of 6–12 years. One implication of this is that for a long time ADHD research was not bothered so much by studying causes of ADHD after its onset—in other words, within the total of studies aimed at understanding the causes of ADHD, prospective studies in ADHD research have been rare.

The first paper that I will highlight in this editorial is by Miller et al. (2023) who discuss the development of ADHD in the period from conception to age of onset. They stress that for understanding the causes of ADHD prospective research prior to its onset is needed and explain that any differences observed in children with ADHD (i.e., after its onset) compared to children without ADHD may be secondary to personal and environmental alterations that are evoked by the ADHD symptoms themselves. At the same time, they point out that an onset of ADHD is gradual and the distinction between pre-onset and post-onset not clear-cut: precursor behaviors of ADHD may already evoke personal and environmental alterations. Thus, for a causal understanding of ADHD, we need to know these as well. Prospective research from conception to full clinical onset allows us to chart such alterations and their temporal sequence up to a full onset of ADHD.

The value of establishing the temporal sequence of personal and environmental alterations leading to a clinical onset of a disease cannot be underestimated. It is one element (albeit by no means a sufficient element) in establishing the causality of a risk factor (the risk factor should occur prior to the onset of the disease), and a very important one in observational research. The accumulation of knowledge as to whether a risk factor is (likely) causal is necessary if we want to target the risk factor for interventions: that is, only causal risk factors can actually influence the outcome. Prospective research charting the sequences of personal and environmental alterations in risk during the gradual unfolding of ADHD over time provides opportunities to identify mediators that are useful as intervention targets in particular developmental periods. Also, prospective research may identify protective factors, by comparing children who have the same risk profile (e.g., at conception, at birth) but one group progressing to a full clinical onset of ADHD yet another not. That is, if we only study those who already have an onset of ADHD like we used to do we can never know if onset of ADHD (particularly the impairments experienced by the children) can be prevented, postponed or reduced in severity and thus if and how a developmental trajectory heading toward onset