Why The Child Is Not Always Father (Parent) To The Man (Person)
There is a global crisis in mental health that existed long before the ravages of Covid-19. So where are we with respect to prevention and intervention? As a benchmark, the last 50 years clinical medicine achieved a 75% decrease in the rate of premature death from heart disease. This remarkable achievement occurred as a function of 1) the discovery of risk factors to identify the most vulnerable, 2) definition of the processes that link risk to disease, 3) interventions that target these processes to reduce risk, and 4) personalizing the intervention to the specific needs of the individual. I fear that with respect to the most common forms of mental disorders we are still in the starting blocks, unable to effectively identify high risk individuals. This is frustrating because mental disorders are preventable. So why? One reason is that unlike heart disease, we haven’t much time. Common forms of mental illness show a peak age on onset over the peripubertal period and some, such as ADHD and anxiety, even earlier. Effective prevention requires assessment of risk in childhood and the identification of operative targets for intervention. My impression is that we continue to embrace perspectives that suggest that brain circuitry and function are crystalized in early childhood. And children do vary in social, emotional and cognitive function early in life. But in the case of the most common mental disorders, including depression, anxiety and ADHD, these overt measures of brain function do not predict outcomes at the level of the individual? There are certainly statistical associations between measures such as ‘temperament’ in early childhood and later mental health outcomes. But the associations are generally weak and apparent only at the level of group analyses. Prediction at the level of the individual is poor. Likewise genome-wide association studies report significant associations, but account for only a small fraction of the variation in mental health status. The same can be said even for measures of environmental adversity. Poverty, harsh parenting and abuse in childhood all predict an increased risk for mental disorders, but with remarkable variability. Here as well there is poor prediction at the level of the individual. In this lecture I will suggest that the very nature of the highly plastic and adaptive brain, especially in youth, complicates our ability to identify predictive markers of common mental disorders. The transitions from family to school life and peer groups, puberty to emerging adulthood all drive experience-dependent plasticity with the potential for considerable discontinuity from one stage to another. The normal transitional challenges of development drive the dynamic, plastic brain and will frustrate our search for predictive ‘markers’ of risk for certain mental disorders at the level of the individual. But there is an alternative perspective. Our studies of child development employ the methods of epidemiology, which statistically associates measures of exposures or conditions with health status in populations. Epidemiology is the science of public health, not individual developmental trajectories. I suggest we can capture the existing knowledge for the sake of interventions at the level of the group rather than the individual. I will cite examples of ‘psychosocial’ interventions targeting emotional (or self) regulation in classes of pre-school children as an approach that is consistent with developmental science and effective. If common forms of mental disorders are a population health issue, perhaps we should consider a population health solution.
The lecture is free to attend and will be held virtually via Zoom. To ensure that you will receive access to the event, register now. We will send out a link to the event on April 12th.