Research article summary (published 30 Aug 2009):

Reversing bacteria-induced vitamin D receptor dysfunction is key to autoimmune disease.

Full Abstract

Vitamin D research is discussed in light of the hypothesis that the lower average levels of vitamin D frequently observed in autoimmune disease are not a sign of deficiency. Instead, it is proposed that the lower levels result from chronic infection with intracellular bacteria that dysregulate vitamin D metabolism by causing vitamin D receptor (VDR) dysfunction within phagocytes. The VDR dysfunction causes a decline in innate immune function that causes susceptibility to additional infections that contribute to disease progression. Evidence has been accumulating that indicates that a number of autoimmune diseases can be reversed by gradually restoring VDR function with the VDR agonist olmesartan and subinhibitory dosages of certain bacteriostatic antibiotics. Diseases showing favorable responses to treatment so far include systemic lupus erythematosis, rheumatoid arthritis, scleroderma, sarcoidosis, Sjogren's syndrome, autoimmune thyroid disease, psoriasis, ankylosing spondylitis, Reiter's syndrome, type I and II diabetes mellitus, and uveitis. Disease reversal using this approach requires limitation of vitamin D in order to avoid contributing to dysfunction of nuclear receptors and subsequent negative consequences for immune and endocrine function. Immunopathological reactions accompanying bacterial cell death require a gradual elimination of pathogens over several years. Practical and theoretical implications are discussed, along with the compatibility of this model with current research.

Author information

Author/s: Waterhouse, Joyce C (JC); Perez, Thomas H (TH); Albert, Paul J (PJ);

Affiliation: Autoimmunity Research Foundation, Thousand Oaks, California 91360, USA. jcw(-atsign-)autoimmunityresearch.org

Journal and publication information

Publication Type: Journal Article

Journal: Annals of the New York Academy of Sciences (Ann N Y Acad Sci), published in United States. (Language: eng)

Reference: 2009-Sep; vol 1173 (issue ) : pp 757-65

Dates: Created 2009/09/17; Completed 2009/10/29;

PMID: 19758226, status: MEDLINE (last retrieval date: 10/29/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Animals Anti-Bacterial Agents - therapeutic use Arthritis, Reactive - drug therapy; metabolism; physiopathology Arthritis, Rheumatoid - drug therapy; metabolism; physiopathology Autoimmune Diseases - drug therapy; metabolism; physiopathology Bacterial Infections - drug therapy; physiopathology Calcifediol - metabolism Calcitriol - metabolism Diabetes Mellitus, Type 1 - drug therapy; metabolism; physiopathology Diabetes Mellitus, Type 2 - drug therapy; metabolism; physiopathology Humans

Imidazoles - therapeutic use Minocycline - therapeutic use Psoriasis - drug therapy; metabolism; physiopathology Receptors, Calcitriol - agonists; physiology Sarcoidosis - drug therapy; metabolism; physiopathology Scleroderma, Systemic - drug therapy; metabolism; physiopathology Sjogren's Syndrome - drug therapy; metabolism; physiopathology Spondylitis, Ankylosing - drug therapy; metabolism; physiopathology Tetrazoles - therapeutic use Thyroid Diseases - drug therapy; metabolism; physiopathology Uveitis - drug therapy; metabolism; physiopathology

Associated Chemicals: Anti-Bacterial Agents (0) ; Imidazoles (0) ; Receptors, Calcitriol (0) ; Tetrazoles (0) ; olmesartan (0) ; Minocycline (10118-90-8) ; Calcifediol (19356-17-3) ; Calcitriol (32222-06-3)

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