Genetic risk for schizophrenia is connected to reduced IQ
The relationship between the heritable risk for schizophrenia and low intelligence (IQ) has not been clear. Schizophrenia is commonly associated with cognitive impairments that may cause functional disability. There are clues that reduced IQ may be linked to the risk for developing schizophrenia. For example, reduced cognitive ability may precede the onset of schizophrenia symptoms. Also, these deficits may be present in healthy relatives of people diagnosed with schizophrenia.
In a remarkable new study published in Biological Psychiatry, Dr. Andrew McIntosh and his colleagues at the University of Edinburgh provide new evidence that the genetic risk for schizophrenia is associated with lower IQ among people who do not develop this disorder.
The authors analyzed data from 937 individuals in Scotland who first completed IQ testing in 1947, at age 11. Around age 70, they were retested and their DNA was analyzed to estimate their genetic risk for schizophrenia.
The researchers found that individuals with a higher genetic risk for schizophrenia had a lower IQ at age 70 but not at age 11. Having more schizophrenia risk-related gene variants was also associated with a greater decline in lifelong cognitive ability.
“If nature has loaded a person’s genes towards schizophrenia, then there is a slight but detectable worsening in cognitive function between childhood and old age. With further research into how these genes affect the brain, it could become possible to understand how genes linked to schizophrenia affect people’s cognitive function,” said McIntosh.
These findings suggest that common genetic variants may underlie both cognitive aging and risk of schizophrenia.
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“While this study does not show that these common gene variants produce schizophrenia per se, it elegantly suggests that these variants may contribute to declines in intelligence, a clinical feature associated with schizophrenia,” commented Dr. John Krystal, Editor of Biological Psychiatry. “However, we have yet to understand the development of cognitive impairments that produce disability in young adulthood, the period when schizophrenia develops for many affected people.”
Although the precise cause of schizophrenia isn’t known, certain factors seem to increase the risk of developing or triggering schizophrenia, including:
Having a family history of schizophrenia
Exposure to viruses, toxins or malnutrition while in the womb, particularly in the first and second trimesters
Stressful life circumstances
Older paternal age
Taking psychoactive drugs during adolescence and young adulthood
Clearly, more research is necessary, but this new study adds to the growing and substantial effort to understand how the gene variants that contribute to the development of schizophrenia give rise to the cognitive disability commonly associated with it.
A risk factor is something that increases your likelihood of getting a disease or condition.
It is possible to develop schizophrenia with or without the risk factors listed below. However, the more risk factors you have, the greater your likelihood is of developing schizophrenia. If you have a number of risk factors, ask your doctor what you can do to reduce your risk.
Family History
Schizophrenia has a genetic component. People who have a close relative with schizophrenia are more likely to develop the disorder than people without relatives with the illness. A monozygotic (identical) twin of a person with schizophrenia has the highest risk (40%-50%) of developing the illness. A child whose parent has schizophrenia has about a 10% chance. The risk of schizophrenia in the general population is only about 1%.
Brain Abnormalities
Many studies of people with schizophrenia have found abnormalities in:
Brain structure:
Enlargement of the fluid-filled cavities, called the ventricles, in the interior of the brain
Decreased size of certain brain regions
Brain function:
Decreased meta2bolic activity in certain brain regions
These abnormalities are quite subtle and are not characteristic of all people with schizophrenia. They do not occur only in people with this illness. Microscopic studies of brain tissue after death have also shown small changes in certain brain cells in people with schizophrenia. It appears that many (but probably not all) of these changes are present before a person becomes ill. Schizophrenia may be, in part, a disorder in brain development.
Environmental Factors
Schizophrenia is more common among people living in the city, those who live in the northern hemisphere, and those born during winter months.
Complications During Pregnancy or Birth
Complications during pregnancy or birth may increase an individual’s chances of developing schizophrenia later in life, although none of the following factors has been proven conclusively. Such complications include:
Oxygen deprivation during pregnancy
Bleeding during pregnancy
Maternal malnutrition
Infections during pregnancy
Long labor
Prematurity
Low birth weight
Loss of Parent During Childhood
Early parental loss, either from death or separation, may increase the risk for schizophrenia (as well as other psychiatric disorders).
Socioeconomic and Cultural Factors
Schizophrenia is much more prevalent in lower socioeconomic classes, possibly as a result of increased stress and poor nutrition. An alternative explanation is that people suffering from schizophrenia move downward to a lower social class.
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The article is “Polygenic Risk for Schizophrenia Is Associated with Cognitive Change Between Childhood and Old Age” by Andrew M. McIntosh, Alan Gow, Michelle Luciano, Gail Davies, David C. Liewald, Sarah E. Harris, Janie Corley, Jeremy Hall, John M. Starr, David J. Porteous, Albert Tenesa, Peter M. Visscher, and Ian J. Deary (doi: 10.1016/j.biopsych.2013.01.011). The article appears in Biological Psychiatry, Volume 73, Issue 10 (May 15, 2013), published by Elsevier.
Notes for Editors
Full text of the article is available to credentialed journalists upon request; contact Rhiannon Bugno at +1 214 648 0880 or .(JavaScript must be enabled to view this email address). Journalists wishing to interview the authors may contact Andrew M. McIntosh at +44 (131) 537 6274 or .(JavaScript must be enabled to view this email address).
The authors’ affiliations, and disclosures of financial and conflicts of interests are available in the article.
John H. Krystal, M.D., is Chairman of the Department of Psychiatry at the Yale University School of Medicine and a research psychiatrist at the VA Connecticut Healthcare System. His disclosures of financial and conflicts of interests are available here.
About Biological Psychiatry
Biological Psychiatry is the official journal of the Society of Biological Psychiatry, whose purpose is to promote excellence in scientific research and education in fields that investigate the nature, causes, mechanisms and treatments of disorders of thought, emotion, or behavior. In accord with this mission, this peer-reviewed, rapid-publication, international journal publishes both basic and clinical contributions from all disciplines and research areas relevant to the pathophysiology and treatment of major psychiatric disorders.
The journal publishes novel results of original research which represent an important new lead or significant impact on the field, particularly those addressing genetic and environmental risk factors, neural circuitry and neurochemistry, and important new therapeutic approaches. Reviews and commentaries that focus on topics of current research and interest are also encouraged.
Biological Psychiatry is one of the most selective and highly cited journals in the field of psychiatric neuroscience. It is ranked 5th out of 129 Psychiatry titles and 16th out of 243 Neurosciences titles in the Journal Citations Reports® published by Thomson Reuters. The 2011 Impact Factor score for Biological Psychiatry is 8.283.
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Rhiannon Bugno
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214-648-0880
Elsevier