What if we had the ability to predict or even prevent mental illness? A study in the Australian Journal of Psychology1 suggests that we may be able to soon. We estimate that by 2030 depression will be the leading cause of disease burden worldwide2 This is forecasted despite the fact that our genetic and molecular understanding of the brain is advancing rapidly.
However, the Chinese Society of Psychiatry’s Chinese Classification of Mental Disorders-3 (CCMD-3), used by clinicians and researchers to guide them in making diagnoses regarding the mental health of patients, has not been updated to a degree compatible to those advances. The same is true of the CCMD-3 counterpart, the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders IV (DSM-IV; although they will be publishing the DSM-5 in March of 2013. The CCMD-3 has not been updated in over a decade and the DSM-IV has been around unchanged for three times as long.
As to preventive protocols and treatments for depression, psychology and psychiatry are limited by the rather subjective diagnostic criteria often used to diagnose depression. The diagnosis often pivots on how a patient answers a series of questions about their recent psychological state, such as whether or not they perceive a decreased interest in their sexual desire. In this way, a mental health practitioner is looking for what we call clinical phenotypes. A phenotype is an observable characteristic of an organism, for instance, certain genetic phenotypes have been determined to correlate with depression and have offered some answers to the familial nature of the disease.
The study points out; however, “it is not sensible to presume that…criteria for diagnosis of mental disorder will necessarily map to the human genome. It is more likely that simple clusters of symptoms, which reflect risk dispositions for complex mental disorders, will provide a better behavioural map of the genome.”
Instead, the authors suggest the use of an endophenotype. An endophenotype is a term used in psychiatric genetics to correlate high-level symptom presentation with low-level genetic variability.
Among other criteria, a biomarker can only be considered an endophenotype if it is heritable, associated with the illness and is present in an individual whether or not the illness is appreciable. There is ongoing research to identify endophenotypes for pathologies such as bipolar disorder, schizophrenia and even suicidal tendencies. With such a powerful metric, we may be able to gain insight into the genetic influence on abnormal behavior and depressive symptomatology.
Brain activity, a neurobiological endophenotype can be measured using functional magnetic resonance imaging (fMRI). This technology can for instance detect the decreased blood flow that might happen when a particular section of the brain is not being used as much. In much the same way as Nobel Prize Laureate and psychiatrist Eric R. Kandel argues for the existence of a neurological correlate of consciousness, technology can be utilized to isolate a neurological correlate of depression.
As it applies to consciousness, fMRI is able to identify an ongoing process in real time; however, with regard to depression, the authors make a solid argument for its usefulness in identification, but uselessness in the prevention of depression.
Instead, the authors offer behavioral endophenotypes as the solution to our limitations on being able to predict and prevent depression. Temperament, for example, is something that can be observed from early childhood. As well, the authors point out that it “ serves the dual purpose of avoiding diagnostic classifications as well as providing a useful (non-stigmatising) method to target preventive intervention.”
The biological basis of mood regulation while incompletely understood, has been identified down to astoundingly exact anatomical locations. As an example, the limbic system in the brain is known to influence the body’s endocrine system. It does this via signaling pathways to the hypothalamic-pituitary- adrenocortical (HPA) axis. The HPA axis is responsible for controlling cortisol, a hormone that indirectly increases glucose sugar levels in the blood when the body needs energy. Little wonder then, why many patients with reduced HPA axis activity also suffer from the toilsome lack of energy complaint of depressive patients.
The limbic system also influences the brain’s pleasure center, and reduced activity in this area could decrease a person’s ability to experience pleasure—another typical depressive complaint. Temperament is “hypothesised to have strong biological dimensions rooted in corticolimbic brain function, essential for control of emotion and behavior.”3
To prevent depressive symptoms is to understand mood. To understand mood is to understand its biological pathways and the genes that program them. The authors believe that this will enable us to appreciate how genetic variation that influences the integrity of these pathways has the potential to create variation in the set point of the stress reactivity, which in turn contributes to individual difference in emotional behavior.
How do you think the ability to predict or prevent mental illness might change your life or the life of someone you know? Join our discussion. Until next time KEEP THINKING!
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