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RCCX Genetic Module Theory
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==Silent epidemic== Over time, it became clear to Meglathery that there is an epidemic involving a large number of syndromes/symptoms/diseases with overlapping symptoms affecting mainly young, vibrant, talented people (predominantly women). She found that many of these people manifesting different signs and symptoms, but not all, have joint hypermobility (double jointedness, ligament laxity). Clusters of the above chronic illness conditions are found in many families and individuals. For example, a family member, often female, who is hypermobile, very fatigued and suffers from severe [[allergy]] symptoms and [[orthostatic intolerance]] ([[Ehlers-Danlos syndrome|EDS]]-HT, [[Mast cell activation syndrome|MCAS]], [[Postural orthostatic tachycardia syndrome|POTS]], [[Chronic fatigue syndrome|CFS]]) has children who may be diagnosed with attention deficit disorder (ADD), sensory processing issues and/or autistic features. In the extended family there often is at least one of the following: [[autoimmune disease]]; cutting (self-injury) and eating disorders (anorexia, bulemia); mood disorders; gender fluidity; a highly successful and innovative genius; someone with CFS or FM; someone with severe PTSD and/or someone else with bouts of psychosis. Many family members will react strongly to stress. The degree of hypermobility correlates with the degree of musculoskeletal involvement (joint pain/dislocations/surgeries required to stabilize joints) and orthostasis/dysautonomia, but not with the other "sick" symptoms which tend to develop later in life in some, mostly women. To date, no gene has been found to explain the prevalence of EDS-hypermobility type, in the general population. Nor why these individuals become so ill with such a wide range of not easily explainable symptoms, including: psychiatric issues; white matter lesions; hormone disruptions; autoimmune diseases; and MCAS, and why some individuals with hypermobile relatives develop these same conditions without hypermobility. As discussed above, TNXB mutations are common with CYP21A2 (hormones, inflammation, psychiatric issues) and C4 (autoimmune) gene clusters. TNXB mutations are associated with most cases of calcified aortic valves and vesicoureteral reflux (urine backing up into kidneys) but not always associated with enough hypermobility to meet criteria for EDS.
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