Webster, R.

December 8, 2011

Psychiatric Persecution: The Pitfalls Associated with a Schizophrenia Diagnosis

By Robin Webster Disclaimer: I am not a medical professional. Schizophrenia Prevalence Researchers have come a long way in recent years uncovering how prevalent schizophrenia is, its causes, and how the disease progresses. Contrary to official estimates of schizophrenia prevalence in the United States (National Institutes of Mental Health, 1993) and Canada (Health Canada, 2002), which suggest a prevalence of about 1%, recent best estimates suggest the actual median prevalence rate globally is 0.453% (Saha et al., 2005). The chance that an average person will develop schizophrenia is estimated to be 1 in 250 or 0.4%. Using current estimates of the U.S. population, which was just under 313 million on December 7, 2011 (U.S. Census Bureau, 2011), this translates into 1.25 million Americans who can expect to develop schizophrenia during their lifetime. Schizophrenia Causes/Etiology A number of environmental factors can increase the risk of schizophrenia, including living in a city, migrating to a new home, and participating in a western economy. For example, the risk of schizophrenia would be higher for an American citizen who has moved away from home to find a job in an urban environment. In England, the risk of schizophrenia increases from 0.4% to 1.0% by virtue of living in London (Kirkbride, 2006). A similar rural-urban risk gradient would also be expected to exist in the United States. Scientist attempting to discover whether schizophrenia runs in families have found that close to 80% of all cases can be explained by hereditary factors (Kvajo, McKellar, and Gogos, 2011). This represents 1 million of the 1.25 million Americans who are predicted to develop this disease in their lifetime. The remaining 250,000 Americans, or 0.08% of the current population, will develop schizophrenia despite the absence of a family history. Identical twin studies have shown that a family history of schizophrenia is not an absolute determinant of whether a person will develop schizophrenia. If one twin develops schizophrenia then the identical sibling has a 50% average chance of being schizophrenic (Kvajo, McKellar, and Gogos, 2011). The average risk of developing schizophrenia for anyone with a family history of this disease is therefore going to be below 50%. So, why do the remaining 250,000 Americans develop schizophrenia? A percentage will have experienced a sporadic genetic mutation affecting fetal and/or childhood brain development. Others may have been exposed to bacterial or viral pathogens during fetal development, which can cause brain inflammation and therefore negatively affect fetal brain development (Meyer, 2011). These diverse causes appear to result in the same outcome: dysregulation of early childhood brain development and function. A substantial body of genetic evidence using animal 1

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December 8, 2011

models and human genetic association studies has found that the dopamine, glutamate, and amino butyric acid (GABA) neurotransmitter pathways do not function appropriately in persons with schizophrenia. In particular, the interneurons in the prefrontal cortex, which are critical to memory and higher executive functions, are incapable of properly suppressing cortical neuron activity, which is essential for normal adult cognitive performance (ODonnell, 2011). This may explain why a full manifestation of symptoms typically does not appear until late adolescence. There is also a characteristic age of onset for schizophrenia. First diagnosis incidence peaks around 15 years of age for both males and females, and declines gradually to almost zero by late middle age (Abel, Drake, and Goldstein, 2010). This does not preclude the possibility of schizophrenia emerging late in life, but the chances are reduced by one third after the age of 55 (Narrow, Rae, Robins, and Regier, 2002). Growing older is therefore a protective factor against schizophrenia. Late onset disease due to hereditary factors is also protective, since members of these families have a lower risk of developing symptoms (Svensson et al, 2011). In addition, if symptoms do manifest late in life they are typically less severe. Mechanism of Schizophrenia A large number of research studies over the past two decades have shown that brain development in children who eventually develop schizophrenia is altered early in life (ODonnell, 2011). Imaging studies have revealed delayed anatomical maturation and cortical thinning consistent with below average intellectual abilities. Psychiatric symptoms consistent with a diagnosis of schizophrenia, such severe attention deficit disorder, hallucinations, and suicidal or homicidal tendencies, can appear as early as 6 years of age (Freedman, 2003, p. 1747). These findings are all consistent with schizophrenia being caused by altered brain development early in life, whether due to genetic or inflammatory causes. Discussion The main risk factors for schizophrenia is a family history, a spontaneous genetic mutation during early fetal development or earlier, or exposure to an infectious agent during gestation. About 80% of all schizophrenia cases can be explained by a family history of the disease. The remaining 20% are due to spontaneous genetic mutations, infection-induced inflammation, and other unknown causes. Current estimates suggest approximately 1.25 million Americans can expect to develop schizophrenia in their lifetime. Of these, 1 million will have a family history of the disease. The remaining 0.25 million represents 0.08% of the U.S. population, therefore the lifetime risk of schizophrenia in the absence of a disease family history is 1 in 1250. These risks are reduced by a number of factors, including a family history of late onset schizophrenia, growing older, an absence of psychiatric symptoms during childhood, living in a rural setting, staying close to the persons place of birth, or living in a developing or third world economy. The advances that have been made over the past two decades in our understanding of schizophrenia make the use of a schizophrenia diagnosis during state-run persecution campaigns problematic, especially in countries where its citizenry have access to high quality medical care. 2

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December 8, 2011

A diagnosis of schizophrenia in the absence of a family history, or severe childhood psychiatric conditions, should be considered suspect and trigger an independent assessment. A late onset diagnosis in the absence of a family history of late onset disease, is so rare that it should automatically be validated an independent party (or two). Schizophrenia is also not a disease associated with aging and in fact growing old protects everyone from the disease, regardless of whether they have a family history or not. Stated another way, the older a person gets the less likely they will develop schizophrenia. A diagnosis of schizophrenia for an older adult should therefore also be suspect, especially if the symptoms are described as severe. Late onset schizophrenia, when it does occur, tends to be less severe and limited in scope.

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December 8, 2011

References Abel, Kathryn M., Drake, Richard, and Goldstein, Jill M. (2010). Sex differences in schizophrenia. International Review of Psychiatry, 22, 417-428. Freedman, Robert. (2003). Schizophrenia. In A. J. J. Wood (Ed.) Drug Therapy (series). New England Journal of Medicine, 349, 1738-1749. Health Canada. (2002). Chapter 3: Schizophrenia. In P. Stewart et al. (Eds.) A Report on Mental Illness. Ottawa: Health Canada. Retrieved 5 Dec. 2011 from http://www.phacaspc.gc.ca/publicat/miic-mmac/ Kirkbride, James B., Fearon, Paul, Morgan, Craig, Dazzan, Paola, Morgan, Kevin, Tarrant, Jane et al. (2006). Heterogeneity in incidence rates of schizophrenia and other psychotic syndromes. Archives of General Psychiatry, 63, 250-258. Kvajo, M., McKellar, H., and Gogos, J. A. (2011). Avoiding mouse traps in schizophrenia genetics: lessons and promises from current and emerging mouse models. Neuroscience. In Press. Retrieved 5 Dec. 2011 from http://www.sciencedirect.com.ezproxy1.lib.asu.edu/science/article/pii/S03064522110087 61 Meyer, Urs. (2011). Developmental neuroinflammation and schizophrenia. Progress in NeuroPsychopharmacology & Biological Psychiatry. Published online ahead of print, 15 Nov. 2011. Retrieved 7 Dec. 2011 from http://www.sciencedirect.com.ezproxy1.lib.asu.edu/science/article/pii/S02785846110031 86 Narrow, William, E., Rae, Donald, S., Robins, Lee N., and Regier, Darrel A. (2002). Revised prevalence estimates of mental disorders in the United States. Archives of General Psychiatry, 59, 115-123. National Institute of Mental Health. (1993). Schizophrenia. NIMH.nih.gov. Retrieved 5 Dec. 2011 from http://www.nimh.nih.gov/statistics/1SCHIZ.shtml ODonnell, Patricio. (2011). Adolescent onset of cortical disinhibition in schizophrenia: Insights from animal models. Schizophrenia Bulletin, 37, 484-492. Saha, Sukanta, Chant, David, Welham, Joy, and McGrath, John. (2005). A systematic review of the prevalence of schizophrenia. PLoS Medicine, 2, 413-433. Retrieved 5 Dec. 2011 from http://www-ncbi-nlm-nihgov.ezproxy1.lib.asu.edu/pmc/articles/PMC1140952/?tool=pubmed Svensson, Anna C., Lichtenstein, Paul, Sandin, Sven, Oberg, Sara, Sullivan, Patrick F., Hultman, Christina M. (2011). Familial aggregation of schizophrenia: The moderating effect of age at onset, parental immigration, paternal age and season of birth. Scandinavian Journal of Public Health, 0, 1-8. U.S. Census Bureau. (2011). U.S. & World Population Clocks. Census.gov. Retrieved 5 Dec. 2011 from http://www.census.gov/main/www/popclock.html