title: Biome depletion in conjunction with evolutionary mismatches could play a role in the etiology of neurofibromatosis 1.
abstract: Neurofibromatosis 1 (NF1) arises de novo in a striking 30-50% of cases, pointing toward an environmental etiology, though none has been clearly identified. The Biome Depletion Theory posits that the absence of mutualistic and commensal organisms within the human body coupled with modern lifestyle alterations may have profoundly deleterious effects, inclusive of immunologic derangement that is thought to result in allergy, atopy, and numerous autoimmune diseases. Biome depletion has been implicated as a factor in the etiology of both multiple sclerosis and autism spectrum disorders; biome reconstitution, i.e. replenishment of the biome with certain keynote species, is being used in the treatment of these and other autoimmune states. Neurofibromatosis 1 has been associated with allergy, various autoimmune states, multiple sclerosis, and autism. Recent research has posited that NF1, multiple sclerosis and autism may all arise from disturbances in the neural crest during gestation. This paper hypothesizes that there is indirect evidence that a highly inflammatory uterine state may precipitate epigenetic changes in vulnerable NF-related genes in the course of fetal development. The etiology of NF1 may lie in the absence of immunomodulation by commensal and mutualistic species once ubiquitously present in the environment, as well as through adoption of a modern lifestyle that contributes to chronic inflammation. Replenishment of helminths and other missing organisms to the human biome prior to conception as well as addressing nutritional status, psychological stress, and environmental exposures may prevent the development of NF1.
authors: Lowell General Hospital, Medical Library, 295 Varnum Avenue, Lowell, MA 01854, United States. Electronic address: Donna.Beales@lowellgeneral.org.
authors: Donna L
authors: DL
authors: Beales
mesh_terms: D005075:Biological Evolution; D005260:Female; D047109:Fetal Development / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D064307:Microbiota; D008954:Models, Biological; D009456:Neurofibromatosis 1 / Q000209:etiology* / Q000517:prevention & control; D013559:Symbiosis; D014599:Uterus / Q000503:physiopathology