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Psychology & Psychiatry
February 20, 2009

Schizophrenia and Bipolar Disorder Share Genetic Links

By Jennifer Gibson, PharmD | 2 Comments | Share | Print | Email | Tweet | Like | 1+

Psychiatry and Psychology CategoryThe exact causes of many psychiatric illnesses are not known, and few risk factors exist for many of them. Scientists have long been trying to decipher the genetic from environmental factors that influence the development of psychiatric illnesses. Many studies have reported that certain mental illnesses run in families, but are there common genetic causes, or are they distinct pathologies? Now, a new study in The Lancet may shed some light on the genetic link between bipolar disorder and schizophrenia.

This Swedish study evaluated more than 9 million Swedes from the population register from 1973 to 2004, and compared it to the public hospital discharge register showing all public psychiatric admissions in Sweden. The population encompassed more than 2 million nuclear families. The researchers assessed the data for the risk of schizophrenia, bipolar disorder, and their comorbidity in biological and adoptive parents and offspring, as well as siblings and half-siblings. Overall, the results indicated that individuals with a first-degree relative with one of these disorders were at an increased risk for developing either disorder.

ChromosomesFull siblings of first-degree relatives with either schizophrenia or bipolar disorder were 9 times more likely than the general population to develop schizophrenia and 8 times more likely to develop bipolar disorder during their lifetime. Half siblings also had an increased risk compared to the general population, but not as high as full siblings. Maternal half siblings were 3.6 times more likely to develop schizophrenia and 4.5 times more likely to develop bipolar disorder compared to the general population. Paternal half siblings had an even lower risk, at 2.7 times higher risk of schizophrenia and 2.4 times higher risk of bipolar disorder.

Interestingly, an increased risk of psychiatric illness exists in children – both adopted and biological – of parents with either bipolar disorder or schizophrenia. This led the researchers to conclude that, while there is a strong genetic component to these illnesses, environment also plays a factor. The portion of schizophrenia that is inherited genetically is 64%, and the portion of bipolar disorder that is inherited genetically is 59%. Approximately 63% of the causes of the cormorbidity of the two disorders is inherited genetically.

This is not the first study to show common causes and genetic links between bipolar disorder and schizophrenia. A large Danish register-based cohort study, similar to the current Swedish study, found similar results. People with first-degree relatives with schizoaffective disorder, schizophrenia, and bipolar disorder showed a significantly increased risk for developing any of the same diseases. A relative with bipolar disorder was the strongest risk factor for developing bipolar disorder, and a minor risk factor for developing schizophrenia, and a relative with schizophrenia was the strongest risk factor for developing schizophrenia, and a minor risk factor for developing bipolar disorder.

Several studies have proven that the same brain abnormalities exist in bipolar disorder and schizophrenia. Specifically, reductions in the white matter of the brain of patients with schizophrenia and bipolar disorder point towards shared mechanisms in the disease causes and pathology. Also, bipolar disorder and schizophrenia share several variations of genetic loci. Each illness also has its own unique genetic variations.

Schizophrenia affects approximately 1% of the adult population in the United States. Its symptoms include distorted thought and hallucinations, delusions, and disorganized speech and thinking, leading significant social dysfunction. Bipolar disorder affects more than 2% of the adult population in the United States and is a mood disorder that includes episodes of extreme elevated mood and depressive episodes or symptoms. Few risk factors other than family history have been identified for either disease.

The results of the current Swedish study is helping to redefine the signs, symptoms, and underlying structure of psychiatric illness. More accurate identification, diagnosis, and treatment begin with more knowledge of the causes and common disease pathways. Other researchers and authors have already challenged the diagnostic criteria in the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, as well as the World Health Organization’s International Classification of Disease. The new diagnostic criteria must account for the measurement and review of psychopathology to more effectively monitor current and future treatments.

References

J. Peter H. Burbach, Bert van der Zwaag (2009). Contact in the genetics of autism and schizophrenia Trends in Neurosciences, 32 (2), 69-72 DOI: 10.1016/j.tins.2008.11.002

T. M. Laursen (2005). Family History of Psychiatric Illness as a Risk Factor for Schizoaffective Disorder: A Danish Register-Based Cohort Study Archives of General Psychiatry, 62 (8), 841-848 DOI: 10.1001/archpsyc.62.8.841

Laursen TM, Munk-Olsen T, Nordentoft M, Bo Mortensen P. A comparison of selected risk factors for unipolar depressive disorder, bipolar affective disorder, schizoaffective disorder, and schizophrenia from a danish population-based cohort. J Clin Psychiatry. Nov 2007;68(11):1673-1681.

P LICHTENSTEIN, B YIP, C BJORK, Y PAWITAN, T CANNON, P SULLIVAN, C HULTMAN (2009). Common genetic determinants of schizophrenia and bipolar disorder in Swedish families: a population-based study The Lancet, 373 (9659), 234-239 DOI: 10.1016/S0140-6736(09)60072-6

A MCINTOSH, S MANIEGA, G LYMER, J MCKIRDY, J HALL, J SUSSMANN, M BASTIN, J CLAYDEN, E JOHNSTONE, S LAWRIE (2008). White Matter Tractography in Bipolar Disorder and Schizophrenia Biological Psychiatry, 64 (12), 1088-1092 DOI: 10.1016/j.biopsych.2008.07.026

Jessika E Sussmann, G Katherine S Lymer, James McKirdy, T William J Moorhead, Susana Muñoz Maniega, Dominic Job, Jeremy Hall, Mark E Bastin, Eve C Johnstone, Stephen M Lawrie, Andrew M McIntosh (2009). White matter abnormalities in bipolar disorder and schizophrenia detected using diffusion tensor magnetic resonance imaging Bipolar Disorders, 11 (1), 11-18 DOI: 10.1111/j.1399-5618.2008.00646.x

Jennifer Gibson, PharmD

Jennifer Gibson, PharmD, is a practicing clinical pharmacist and medical writer/editor with experience in researching and preparing scientific publications, developing public relations materials, creating educational resources and presentations, and editing technical manuscripts. She is the owner of Excalibur Scientific, LLC.

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2 Responses

  1. Greg Marlow says:
    December 8, 2009 at 5:49 am

    Have you considered that the genes responsible for the sodium level control system may be the ones responsible for bipolar disorder and schizophrenia? Both these illness have a ten fold higher frequency of hospital admissions with hyponatremia compared to hyponatremia in all other admissions. I believe that most hyponatremia in psychiatric patients is incorrectly attributed to polydipsia. Instead it should be looked at as a possible underlying cause. Patients with hyponatremia can display many mental symptoms common to bipolar disorder and schizophrenia. In addition there is a mechanism that links sodium to the circadian rhythm. In the evening the body lowers blood sodium levels in preparation for sleep. If the individual already has a low level due to some hormone problem, the evening lowering may cause levels to become hyponatremic.

    Reply
  1. I See An Encephalon Edition 65! says:
    March 1, 2009 at 6:00 pm

    [...] At Brainblogger, some great questions are posed:But, where does the acceptance end? Where is the line between “just a little bit different” and a diagnosis of a medical illness? Head over to the post at Autism – No Need For A Cure? and whilst there, you should definitely check out Schizophrenia and Bipolar Disorder Share Genetic Links. [...]

    Reply

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