OBJECTIVES: Increased immune sensitivity to dietary gluten proteins has been reported in schizophrenia but has not been studied in bipolar disorder. In this study, we examine the levels of antibody reactivity to gliadin, deamidated gliadin, and tissue transglutaminase (tTG) in individuals with bipolar disorder and compare these levels to those in individuals who do not have any history of psychiatric disorder. METHODS: The sample of 275 individuals included 102 with bipolar disorder and 173 controls without a psychiatric disorder. Immunoglobulin G (IgG) and immunoglobulin A (IgA) antibodies to gliadin and tTG and IgG antibodies to deamidated gliadin were measured by enzyme immunoassay. Participants' levels of antibodies to deamidated gliadin and tTG were classified based on the cutoffs for positivity that are predictive of celiac disease. Quantitative levels of antibodies were compared between groups employing regression models which were controlled for demographic variables. RESULTS: Individuals with bipolar disorder had increased levels of IgG antibodies to gliadin compared with controls in multivariate analyses. We also found evidence of increased levels of antibodies to deamidated gliadin in the bipolar disorder population. The levels of IgA class antigliadin antibodies and antibodies to tTG did not differ significantly between groups. There was also not a significant difference between groups in the number of persons who were classified as having levels of antibodies to deamidated gliadin or tTG that are predictive of celiac disease. CONCLUSIONS: Individuals with bipolar disorder have increased levels of IgG antibodies to gliadin. However, such antibody increase is not accompanied by an elevation in IgA antibodies to gliadin or the celiac disease-associated antibodies against deamidated gliadin and tTG. These results warrant further detailed examination of the molecular specificity and pattern of reactivity of the antibody response to gluten antigens in bipolar disorder.
OBJECTIVES: Increased immune sensitivity to dietary gluten proteins has been reported in schizophrenia but has not been studied in bipolar disorder. In this study, we examine the levels of antibody reactivity to gliadin, deamidated gliadin, and tissue transglutaminase (tTG) in individuals with bipolar disorder and compare these levels to those in individuals who do not have any history of psychiatric disorder. METHODS: The sample of 275 individuals included 102 with bipolar disorder and 173 controls without a psychiatric disorder. Immunoglobulin G (IgG) and immunoglobulin A (IgA) antibodies to gliadin and tTG and IgG antibodies to deamidated gliadin were measured by enzyme immunoassay. Participants' levels of antibodies to deamidated gliadin and tTG were classified based on the cutoffs for positivity that are predictive of celiac disease. Quantitative levels of antibodies were compared between groups employing regression models which were controlled for demographic variables. RESULTS: Individuals with bipolar disorder had increased levels of IgG antibodies to gliadin compared with controls in multivariate analyses. We also found evidence of increased levels of antibodies to deamidated gliadin in the bipolar disorder population. The levels of IgA class antigliadin antibodies and antibodies to tTG did not differ significantly between groups. There was also not a significant difference between groups in the number of persons who were classified as having levels of antibodies to deamidated gliadin or tTG that are predictive of celiac disease. CONCLUSIONS: Individuals with bipolar disorder have increased levels of IgG antibodies to gliadin. However, such antibody increase is not accompanied by an elevation in IgA antibodies to gliadin or the celiac disease-associated antibodies against deamidated gliadin and tTG. These results warrant further detailed examination of the molecular specificity and pattern of reactivity of the antibody response to gluten antigens in bipolar disorder.
Authors: Emily G Severance; Armin Alaedini; Shuojia Yang; Meredith Halling; Kristin L Gressitt; Cassie R Stallings; Andrea E Origoni; Crystal Vaughan; Sunil Khushalani; F Markus Leweke; Faith B Dickerson; Robert H Yolken Journal: Schizophr Res Date: 2012-03-24 Impact factor: 4.939
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Authors: Emily G Severance; Kristin L Gressitt; Shuojia Yang; Cassie R Stallings; Andrea E Origoni; Crystal Vaughan; Sunil Khushalani; Armin Alaedini; Faith B Dickerson; Robert H Yolken Journal: Bipolar Disord Date: 2013-12-06 Impact factor: 6.744
Authors: Emily G Severance; Kristin L Gressitt; Cassie R Stallings; Andrea E Origoni; Sunil Khushalani; F Markus Leweke; Faith B Dickerson; Robert H Yolken Journal: Schizophr Res Date: 2013-06-06 Impact factor: 4.939
Authors: Emily G Severance; Kristin L Gressitt; Armin Alaedini; Cathrin Rohleder; Frank Enning; J Malte Bumb; Juliane K Müller; Emanuel Schwarz; Robert H Yolken; F Markus Leweke Journal: Brain Behav Immun Date: 2014-09-20 Impact factor: 7.217
Authors: Daniel S Tylee; Jiayin Sun; Jonathan L Hess; Muhammad A Tahir; Esha Sharma; Rainer Malik; Bradford B Worrall; Andrew J Levine; Jeremy J Martinson; Sergey Nejentsev; Doug Speed; Annegret Fischer; Eric Mick; Brian R Walker; Andrew Crawford; Struan F A Grant; Constantin Polychronakos; Jonathan P Bradfield; Patrick M A Sleiman; Hakon Hakonarson; Eva Ellinghaus; James T Elder; Lam C Tsoi; Richard C Trembath; Jonathan N Barker; Andre Franke; Abbas Dehghan; Stephen V Faraone; Stephen J Glatt Journal: Am J Med Genet B Neuropsychiatr Genet Date: 2018-10-16 Impact factor: 3.568