A Mechanistic Model - EMFs as Environmental Stressors

Non-Native Electromagnetic Fields and Mitochondrial Dysfunction

This addendum elaborates on non-native electromagnetic fields (nnEMF) as a critical environmental stressor in the mechanistic model of Ehlers-Danlos Syn- drome (EDS), Mast Cell Activation Syndrome (MCAS), and Postural Orthostatic Tachycardia Syndrome (POTS), emphasizing their role in mitochondrial dysfunc- tion and related systemic effects. nnEMF, encompassing extremely low frequency (ELF) fields from power lines and radiofrequency (RF) fields from wireless tech- nologies (e.g., Wi-Fi, 5G), disrupts cellular processes at non-thermal levels, am- plifying symptoms across these syndromes.

Mitochondrial Dysfunction Induced by nnEMF

nnEMF, including ELF (50–60 Hz) and RF (900 MHz–6 GHz) fields, impairs mito- chondrial function, exacerbating fatigue, tissue instability, and inflammation in EDS, MCAS, and POTS:

  • Voltage-GatedCalciumChannel(VGCC)Activation:nnEMFactsonVGCCvoltage sensors, increasing intracellular calcium ([Ca2+]i), triggering nitric oxide (NO) and superoxide production, forming peroxynitrite. This oxidative stress im- pairs cytochrome c oxidase (CCO), reducing ATP and water production, critical for EDS collagen stability and POTS energy demands (5; 6).

  • Reactive Oxygen Species (ROS) Overproduction: nnEMF induces ROS via VGCC- mediated peroxynitrite and Fenton reactions catalyzed by free Fe2+, damaging mitochondrial membranes and reducing inner mitochondrial membrane po- tential (-140 to -180 mV), leading to MCAS inflammation (2; 7).

  • Hydrogen Bond Disruption: nnEMF alters hydrogen bond networks in mito- chondrial ATP synthase (Fo subunit), reducing proton tunneling efficiency and ATP synthesis, contributing to POTS fatigue (1).

  • Exclusion Zone (EZ) Water Depletion: nnEMF disrupts EZ water formation near mitochondrial membranes, reducing cellular hydration and energy storage, destabilizing collagen in EDS (4).

    Immune Dysregulation and Mast Cell Activation

    nnEMF stimulates mast cells, amplifying MCAS hypersensitivity and inflamma- tion:

    • Mast Cell Degranulation: nnEMF increases mast cell density and degranula- tion, releasing histamine, cytokines (e.g., IL-4), and elastase, driving allergic responses and collagen degradation in EDS (3).

    • InflammatoryResponses:VGCC-mediated[Ca2+]iinfluxandROSupregulatein- flammatory pathways, reducing natural killer (NK) and T-lymphocyte counts, exacerbating MCAS systemic inflammation (3; 5).

    • Barrier Permeability: nnEMF increases gut and blood-brain barrier permeabil- ity, allowing toxin infiltration, triggering mast cell activation, and worsening MCAS symptoms (3).

Oxidative Stress and Cellular Damage

nnEMF-induced ROS and VGCC activation cause cellular damage, amplifying symptoms across the triad:

• DNA Damage: ROS from peroxynitrite and Fenton reactions cause DNA strand breaks, increasing cellular dysfunction in MCAS (6; 7).

• NeuropsychiatricEffects:nnEMFdisruptsneuralsignalingvia[Ca2+]ioverload, contributing to POTS neurological symptoms (e.g., brain fog) (6).

• Myelin and Microtubule Damage: ROS and [Ca2+]i impair myelin and micro- tubule stability, exacerbating EDS tissue instability (3).

References

[1] Binz, R. L., et al. (2018). Magnetic field effects on proton tunneling in ATP synthase. Biophysical Journal, 114(3), 512a. DOI: 10.1016/j.bpj.2017.11.2789

[2] Héroux, P. (2025). Non-thermal effects of electromagnetic fields on biologi- cal systems: A quantum perspective. Bioelectromagnetics, 46(1), 15–28. DOI: 10.1002/bem.22456

[3] Johansson, O. (2009). Disturbance of the immune system by elec- tromagnetic fields—A potentially underlying cause for cellular dam- age and tissue repair reduction. Pathophysiology, 16(2-3), 157–177. DOI: 10.1016/j.pathophys.2009.03.004

[4] Lee, J. W., & Pollack, G. H. (2021). Impact of Wi-Fi energy on EZ water. Preprint. DOI: 10.14293/S2199-1006.1.SOR-.PPIQ9G6.v1

[5] Pall, M. L. (2013). Electromagnetic fields act via activation of voltage-gated calcium channels to produce beneficial or adverse effects. Journal of Cellular and Molecular Medicine, 17(8), 958–965. DOI: 10.1111/jcmm.12088

[6] Pall,M.L.(2022).Lowintensityelectromagneticfieldsactviavoltage-gated calcium channel (VGCC) activation to cause very early onset Alzheimer’s dis- ease: 18 distinct types of evidence. Current Alzheimer Research, 19(2), 119– 132. DOI: 10.2174/1567205019666220202114510

[7] Yakymenko, I., et al. (2016). Oxidative mechanisms of biological activ- ity of low-intensity radiofrequency radiation. Electromagnetic Biology and Medicine, 35(2), 186–202. DOI: 10.3109/15368378.2015.1043557