Is Mental Illness Preventable?

Of the 10 leading causes of disability in the world in 1990, five were mental disorders; specifically unipolar depression, alcohol use, manic depression, schizophrenia and obsessive-compulsive disorder (Murray and Lopez, 1996). It is clear that both the extent of mental health problems and the enormous associated personal, social and financial cost can not be addressed by treatment services alone. _Robinson et Pennebaker

Schizophrenia.com
Schizophrenia is one of the most debilitating and disabling of the mental illnesses. So if we could find a way to prevent schizophrenia -- even a substantial proportion of the disease -- we would be making impressive progress toward the goal of preventing mental illness.

Recent research findings from Duke and Johns Hopkins suggest that a proportion of schizophrenia with genetic causes could be prevented by early detection of susceptible persons in early childhood, with appropriate intervention before symptoms manifest themselves in late adolescence or early adulthood. Scientists have known for decades that brain structure in schizophrenia was not normal -- and even pointed toward an early developmental "lesion" as the cause of the structural abnormalities.

The critical network of signals which control early brain development is becoming better understood -- both in terms of general development and in terms of specific brain diseases when the signaling network goes awry. Here is more about the recent Duke et Johns Hopkins research:

Katsanis, who directs the Duke Center for Human Disease Modeling, and Akira Sawa, M.D., Ph.D., a Professor in the Department of Psychiatry at Johns Hopkins, were introduced to each other by a clinical colleague who thought that Bardet-Biedl syndrome (BBS) proteins that are involved in transport duties within cells might have a role in schizophrenia. Katsanis is an expert in using BBS genetic mutations and proteins to learn more about other diseases. BBS is a complex genetic disease with autism-like symptoms, cognitive defects and depression. Sawa is an expert on DISC1, the protein named Disrupted in Schizophrenia 1, known to be a major susceptibility factor for schizophrenia and related disorders.

Together, they discovered that these proteins are involved in a key switch for neurons that is necessary for brain development. When DISC1 gains a phosphate group at a specific site, it recruits BBS1. When BBS1 is missing in this system, the team could observe defective neuron migration, while a model with no DISC1 at all leads to defects in both cell proliferation and migration.

...Katsanis predicts that, for perhaps 10 percent of psychiatric illness, the illness is primarily driven by defects in this switch system. "So we now have ways to interpret variation in humans, in a context that is relevant to their particular cases, to their physiology -- that is where medicine will move next," Katsanis said.

...The study was published by Nature journal on April 6 in its advance online publication. _SD

The researchers were looking at brain signaling which controls early brain development -- the multiplying of brain neurons and subsequent placement in proper locations, orientiation, and connectivity to other parts of the brain. But there is another "brain growth spurt" which occurs just before adolescence, which could be just as critical to the subsequent development of schizophrenia and other types of mental illness which first manifest in adolescence or early adulthood. This neuronal growth spurt is no doubt also under the control of brain signaling proteins.

Prevention comes into the picture when scientists learn to correct abnormal signaling in early stages of development, or to compensate for abnormal brain development, later in childhood. Some genetic abnormalities can be treated now, and the opportunities to treat more genetic problems are growing rapidly.

That means that besides mental illness, many disadvantages which are widespread in the third world and in disadvantaged ethnic groups -- and which are at least partially genetically mediated (such as low intelligence and poor executive function) -- should be amenable to treatment in the not so distant future.

It is the denial of such genetically mediated disadvantages and disabilities which dooms sufferers to lifetimes of misery and underachievement. Such HBD deniers likewise doom entire societies and regions to generations of misery, poverty, widespread disease, and hopelessness.