A Mechanistic Model of Ehlers-Danlos Syndrome, Mast Cell Activation Syndrome, and Postural Orthostatic Tachycardia Syndrome
Environmental Stressors and Mitochondrial Dysfunction
This addendum expands on the role of environmental stressors as mitochondrial toxins in the mechanistic model of Ehlers-Danlos Syndrome (EDS), Mast Cell Activation Syndrome (MCAS), and Postural Orthostatic Tachycardia Syndrome (POTS).
1. Circadian Rhythm Disruption and Blue Light Toxicity
Blue light (400–500 nm) from LED screens and artificial lighting disrupts circadian rhythms, mitochondrial function, and cellular integrity, exacerbating the vicious cycle of mitochondrial dysfunction central to EDS, MCAS, and POTS. Ultraviolet (UV) and red/infrared (IR) light exposures, naturally present in sunlight, mitigate these effects by supporting physiological homeostasis.
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2. Non-Native Electromagnetic Fields
Non-native electromagnetic fields (nnEMF), including extremely low frequency (ELF) fields from power lines and radiofrequency (RF) fields from wireless technologies (e.g., Wi-Fi, 5G), impair mitochondrial function at non-thermal levels. These disruptions amplify symptoms across EDS, MCAS, and POTS by inducing cellular stress and systemic dysregulation.
3. Heavy Metals, Xeno/Phytoestrogens, and Vaccines
Heavy metals (e.g., aluminum, mercury), xenoestrogens (e.g., bisphenol A), phytoestrogens (e.g., soy isoflavones), and vaccine components (e.g., aluminum adjuvants, lipid nanoparticles [LNPs], immune sensitizers) disrupt cellular processes, intensifying symptoms in EDS, MCAS, and POTS. Aluminum’s substitution for magnesium in mitochondria and ionic mimicry are key mechanisms driving dysfunction.
4. Chronic Stress and Trauma as Environmental Stressors
Chronic stress and trauma, encompassing prolonged psychological, emotional, or physical strain, disrupt mitochondrial function and systemic processes, amplifying symptoms across EDS, MCAS, and POTS through interconnected pathways.