A rat study in Bioelectromagnetics examined GSM-modulated 3.5 GHz RF-EMF exposure (2 h/day for 30 days) and reported adverse changes in male reproductive hormones, oxidative stress markers, and testicular histology. The authors also tested Coenzyme Q10 (CoQ10) and found it partially ameliorated some RF-associated alterations. The paper notes that because the exposure used a GSM-modulated waveform, findings cannot be extrapolated to FR1 5G NR signals, and calls for further research under real-world conditions.

This article summarizes expert presentations and a panel discussion on radiological protection systems for ionizing and non-ionizing radiation at an international congress. It highlights that ionizing radiation protection is mature and continually revised, while non-ionizing radiation protection lacks a comparable international framework. The authors emphasize that emerging non-ionizing technologies create complex exposure scenarios and unresolved concerns about chronic and acute exposures, calling for a more cohesive and protective framework.

This animal experiment assessed GSM-modulated 3.5 GHz RF exposure in male Wistar rats and reported hormonal, oxidative, and histological changes consistent with testicular impairment. RF exposure was associated with lower testosterone, LH, and FSH, higher oxidative stress (increased MDA and TOS), and degenerative testicular histology. Coenzyme Q10 supplementation partially mitigated several reported changes. The authors caution against generalizing these results to FR1 5G NR signals and call for further research.

This RF Safe position piece argues that long-term exposure to “non-native,” low-fidelity electromagnetic environments (including man-made RF) can degrade biological timing and coherence, contributing to downstream issues such as immune dysregulation and oxidative stress. It frames this as a systems-level claim rather than asserting RF “causes” specific diseases, and it cites proposed biophysical mechanisms (e.g., coupling into dense tissues, membrane voltage-sensing domains, mitochondrial/redox pathways). The article also references Heinrich Hertz’s historical exposure to early radio experiments and a retrospective medical analysis of his illness, while stating it is not claiming RF caused his condition.

This RF Safe commentary argues that wireless communications “took a wrong turn” by prioritizing radiofrequency/microwave transmission over light-based approaches, citing Alexander Graham Bell’s 1880 photophone as an alternative model. It suggests that widespread, continuous RF exposure in modern environments is undesirable and proposes light-based, room-scale wireless as more biologically compatible. The piece also speculates about a historical association between Heinrich Hertz’s close-range RF experiments and his later fatal illness, while acknowledging there is no controlled evidence proving causation.

RF Safe publishes a commentary describing a public feud between Dr. Jack Kruse and RF Safe founder John Coates over how to address health concerns attributed to non-native electromagnetic fields (nnEMFs), especially regarding children. The piece portrays Kruse as emphasizing personal “light/circadian” biohacks and Coates as pushing technology and policy changes such as LiFi adoption and repealing/altering telecom-related legal constraints. It includes numerous claims about EMF-related harms and references to research (e.g., NTP/Ramazzini, a Henry Lai meta-analysis) but presents them within an advocacy narrative rather than as a balanced review.

RF Safe presents the “Herzification / Bioelectric Fidelity Hypothesis,” arguing that modern RF/EMF exposure has rapidly altered the human electromagnetic environment and may degrade biological electrical signaling (“bioelectric fidelity”). The post frames this as an “evidence-anchored hypothesis” that could help explain a wide range of outcomes (e.g., cancer, infertility, ADHD-like traits, some autism phenotypes, emotional dysregulation), while acknowledging it is not definitive proof. It also cites Heinrich Hertz’s illness as a suggestive historical anecdote and references proposed non-thermal interaction mechanisms involving voltage-gated ion channels.

This animal study exposed Aedes aegypti larvae to 5G-NR RF-EMF at 3.6 GHz for 5 days under two feeding regimes. The study reports delayed development at a lower exposure level mainly in nutritionally weakened larvae, and at a higher exposure level reports developmental changes and reduced adult size attributed to dielectric heating. Mortality and wing length asymmetry were reported as unchanged, and the authors note such high exposure levels are unlikely in natural aquatic settings.

This animal study exposed mice to 2.45 GHz electromagnetic fields daily for up to 5 months and assessed liver effects using serum tests, lipidomics, histology, and single-cell/spatiotemporal transcriptomics. The authors report that hepatic cell types differed in sensitivity, with hepatocytes, endothelial cells, and monocytes showing notable transcriptomic disruptions. Reported changes involved lipid metabolism and immune regulation and were spatially enriched in peri-portal liver regions. The authors frame the findings as evidence of significant biological impacts on the liver from long-term EMF exposure.

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.

This randomized, double-blind, sham-controlled study tested whether CACNA1C rs7304986 genotype modifies sleep EEG responses to 5G RF-EMF exposure. The authors report a genotype-by-exposure interaction, with 3.6 GHz exposure in T/C carriers associated with a faster NREM sleep spindle center frequency versus sham. The abstract also notes longer sleep latency in T/C compared with T/T carriers, and concludes that genetically susceptible groups may show differential physiological responses to 5G RF-EMF.

This animal study reports that prolonged RF-EMR exposure (2.45 GHz for 8 weeks) increased oxidative stress and ferroptosis in mouse testicular tissue and was associated with reduced sperm quality. Melatonin administration reportedly mitigated oxidative injury and inhibited ferroptosis. The abstract attributes the protective effect to Nrf2 pathway activation via MT1/MT2 receptors.

This cross-sectional epidemiologic study enrolled 100 employees of an electricity company to assess whether occupational low-frequency electromagnetic field exposure is associated with cataract development. Cataract frequency was higher in exposed versus non-exposed groups, and nuclear opacity grading differed significantly between groups. Within exposed workers, nuclear and posterior subcapsular cataract grades were associated with longer work experience, suggesting occupational exposure may be a risk factor, particularly for nuclear cataracts.

This animal study examined repeated asymmetrical head exposure to a 5G-modulated 3.5 GHz signal in adult male mice for six weeks. It reports no significant changes in locomotion, anxiety, or object-based memory performance under the tested conditions. However, it found statistically significant but limited cortical gene expression changes (<1% of expressed genes), including enrichment for glutamatergic synapse-related genes and lateralized differences involving mitochondrial genome-encoded genes. The authors caution that potential health risks from these intracortical transcriptomic modifications should not be downplayed and note uncertainties about longer exposures and other populations.

This animal study exposed juvenile and young adult Wistar rats to 5G (3.5 GHz) or 2G (900 MHz) radiofrequency fields (1.5 V/m) for 1–2 weeks and measured brown adipose tissue-related gene expression by RT-qPCR. The abstract reports significant downregulation of PRDM16 and C/EBP mRNA after 5G exposure, while UCP1-dependent thermogenesis markers were not significantly changed at the transcriptional level. The authors interpret these findings as a potential partial disruption of brown adipocyte differentiation and raise EMF safety concerns, while calling for further confirmatory research.