28 Ocak 2016 Perşembe

Evidence mounts that our current approach to "ADHD" is way off base

An NIH funded study published last week in the Lancet revealed that five major mental health disorders- ADHD, autism, bipolar disorder, depression and schizophrenia- share genetic roots. The authors state that their findings blur diagnostic categories. They write:
These results provide evidence relevant to the goal of moving beyond descriptive syndromes in psychiatry, and towards a nosology informed by disease cause.
Epigenetics, or the environmental influence on gene expression, must immediately be brought in to any discussion of these important findings. "Cause" is related to a complex interplay between genetic risk and environmental effects.

Another study on ADHD published this week points to the problems inherent using this oversimplified diagnostic category. The study, published in Pediatrics, showed that not only do symptoms of ADHD persist into adulthood in 30% of cases, but there is also a significant amount of "co-morbidity," including these alarming statistics:
The study also found the risk for suicide was nearly five times higher among those diagnosed with ADHD than in the comparison group, and nearly 3% of study participants were in jail when recruited for the adult portion of the study.
A review of the study published in USA today includes this telling line:
Symptoms[of ADHD] can be controlled by a combination of behavioral therapy and medication. 
Maybe the reason that so many people have such poor outcomes is that we are neglecting to understand the underlying cause of the problem and instead simply labeling and "managing" symptoms. These dismal long-term results, along with the similarly dismal results reported in the preschool ADHD study showing that 90 percent of children had signficant symptoms at 6 year follow up, state loud and clear that the way we approach what we are now calling "ADHD"  is not working. We need to do something dramatically different from the current standard of care.

What we are calling "ADHD" is a constellation of symptoms that represent problems with regulation of attention, behavior, and emotion. The term itself gives the illusion that we know the specific biological mechanism in the way that we know how lack of insulin causes diabetes. This is however, far from true.

As the first study I refer to indicates, we are just beginning to learn about the underlying biology of mental illness, and those findings suggest that "ADHD" may be an artificial construct.

My clinical experience tells me that these genes they have described may be functionally related to sensory processing.  Problems with sensory processing seem to be common to many diagnostic categories for mental illness that we currently use. However, children develop the capacity for self-regulation in the context of relationships. Identifying the problematic gene is only part of the answer. Understanding and addressing the environmental risk is the other.

If we consider the interplay of genetics and environment, then a third study published last week, this one also in Pediatrics, will point us in the direction of meaningful preventive intervention. This study identified the problem of postpartum anxiety, concluding that:
Postpartum state anxiety is a common, acute phenomenon during the maternity hospitalization that is associated with increased maternal health care utilization after discharge and reduced breastfeeding duration. 
Given what we already know about the risk of psychiatric disorders in children of parents struggling with depression,  these findings only increase the urgency of focusing our resources on supporting parent-infant pairs. We need to help set development in a healthy direction from the start.  Genetic vulnerabilities are present at birth, and if we devote maximum resources to supporting the environment, then we may significantly decrease the risk of those vulnerabilities manifesting as psychiatric illness.

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