RF Safe argues that non-native RF-EMF affects biology primarily through voltage-gated ion channels (VGICs), proposing an “Ion Forced Oscillation” model in which pulsed RF signal components influence the S4 voltage sensor and downstream cellular signaling. The post frames electromagnetic hypersensitivity (EHS) as a continuum of individual sensitivity thresholds to a proposed VGIC → mitochondrial ROS → immune activation cascade, rather than a distinct condition. It cites multiple external studies and reviews (including a WHO-commissioned animal review) to support a mechanistic narrative linking RF exposure to oxidative stress, inflammation, and certain tumor findings in rodents, but the article itself is a mechanistic/interpretive argument rather than original research.

RF Safe publishes a mechanistic white-paper-style post arguing that pulsed/low-frequency components of RF exposure could introduce “phase noise” into voltage-gated ion channel (VGIC) voltage sensors (S4), degrading the timing of membrane potentials and calcium (Ca²⁺) oscillations that immune cells use for activation and tolerance decisions. The post claims such timing disruption could mis-set immune thresholds, promote inflammation, and trigger mitochondrial ROS and mtDNA release that sustains a feed-forward inflammatory loop. It frames reported tumor patterns in animal bioassays (e.g., cardiac schwannomas, gliomas) as consistent with this proposed “timing-fidelity” mechanism, while acknowledging competing views on whether RF at current limits can couple to VGICs.

This in vitro study compared proteomic profiles of PBMCs from three human donors after 24-hour exposure to a 50 Hz, 1 mT extremely low-frequency magnetic field versus unexposed cells. The abstract reports broad protein expression changes, including upregulation of proteins associated with metabolic processes and downregulation of proteins linked to T cell costimulation/activation and immune processes. No effects were observed on cell proliferation, viability, or cell cycle progression. The authors interpret the proteomic shifts as metabolic reprogramming with potential implications for immune regulation.