Type: Conference presentation
Presenter: Chris Benediktsson, Janet Raty, Trevor Marshall, PhD
Conference: 7th International Congress on Autoimmunity
Location: Ljubljana, Slovenia
Date: May 2010
Additional Content: PDF of poster
Since the mid 1800s we have known that some infectious agents can cause dramatic personality changes, for example in diseases such as syphilis, rabies, toxoplasmosis and neurologic lyme disease. Treatment was dominated for many years by psychological theorizing, much of it Freudian; biological approaches were essentially limited to genetics. Recently both persistent viruses and antibodies to pathogens have been detected in samples from patients with bipolar disease. “Autoantibodies” to brain proteins, nuclear material, and brain lipids, among others, have been detected in both schizophrenic and bipolar populations. Higher levels of interleukin (IL1, IL 2, IL 1 RA), CD 4, CD 8 and Th1 and Th2 cytokinesAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system. have been found in bipolar patients before, during and after medical treatment, strongly suggesting that bipolar disorders and autoimmune disease share a similar etiology.
We have been conducting an observational study since 2002 of a VDR agonistA substance such as olmesartan (Benicar) or 1,25-D which activates the Vitamin D Receptor and transcribes the genes necessary for a proper innate immune response. along with pulsed low dose antibiotics for treatment of chronic inflammatory diseases. Intriguingly, many of the study subjects had initially reported comorbid symptoms of cognitive impairment, including brain fogThe loss of intellectual functions such as reasoning; memory loss; and other neurological abilities that is severe enough to interfere with daily functioning. and major depression, consistent with advanced chronic disease. Four patients, who had noted prior diagnoses of bipolar disorder 1 and II, reported significant improvement in bipolar symptoms after therapy. The improvement in mental function was concurrent with improvements in the symptoms of the comorbid autoimmune disease. This is consistent with a shared etiology and strongly suggestive of the involvement of bacterial pathogens.