Nicolas Foray's team (INSERM Lyon) published the DEMETER study results in May 2025: a measurable cell repair defect in all 26 electrosensitive participants tested. A closer look at a finding that redefines the debate.

Real symptoms, no diagnosis

Francis is twenty. For three years he has suffered from dizziness, fainting spells in the street, insomnia, tremors, deep fatigue and heart palpitations. His friends think he is making it up. Salomé, seventeen, grew up in a top-floor flat. Persistent tiredness, nervousness, memory lapses, headaches creeping in over time. Her GP finds nothing wrong. When her family moves to the countryside, almost all of her symptoms vanish within weeks. Her mother then discovers, through the Cartoradio app, that the old flat faced a mobile phone mast.

These stories are not unusual. People who describe themselves as electrosensitive report a consistent cluster of symptoms: headaches, sleep disturbance, cognitive fatigue, tinnitus, irritability, a burning or pressure sensation in the skull. For some, the discomfort is manageable. For others, it leads to sick leave, social isolation, sometimes relocation to areas with no network coverage.

What these accounts share is a long period of confusion. Several years, on average, between the first symptoms and the moment the person works out what is happening. And often, a single sentence from the doctor that sums the whole problem up: "it's all in your head."

Twenty years of studies that found nothing

This scepticism has a scientific explanation. Over the past two decades, dozens of so-called "provocation" studies have been conducted on electrosensitivity. The protocol is straightforward: place EHS individuals in a room, switch an electromagnetic field source on or off without telling them, and ask whether they feel anything.

The outcome is consistent: under blind conditions, EHS individuals detect the active source no better than chance. More strikingly, some report symptoms when told the source is on, even though it is not. This phenomenon, known as the nocebo effect, led a substantial part of the scientific community to regard EHS as a psychological condition.

The World Health Organisation does not recognise EHS as a medical disorder. A systematic review published in 2025 in Frontiers in Public Health still concludes that there is "no robust empirical evidence that electromagnetic fields are the causal agent."

That is where matters stood when Nicolas Foray and his team decided to take a different approach.

The DEMETER approach: looking at the cells

Nicolas Foray is a research director at INSERM in Lyon, specialising in radiobiology. His unit (UA8, "Radiations: defence, health, environment") has spent years studying DNA repair mechanisms and individual radiosensitivity. DEMETER grew out of that work: not to prove or disprove the existence of EHS, but to look for an objective marker in the cells of those affected, independent of what they feel or report.

Twenty-six volunteers who described themselves as electrosensitive agreed to take part. Each completed a detailed questionnaire covering their symptoms and reactions to various sources (Wi-Fi, masts, mobile phones, but also chemicals, light and noise). In parallel, a skin biopsy was used to establish fibroblast cell lines, skin cells cultured in the laboratory.

The critical point of the method: the two strands were kept strictly separate. As Foray himself put it, the team built "un mur de Berlin" (a Berlin Wall) between the questionnaire responses and the biological studies. The researchers analysing the cells did not know what the patients had reported. And vice versa.

A delay in cell repair

To understand what DEMETER found, we need to revisit a fundamental mechanism of cell biology.

Our cells are constantly subjected to damage that harms their DNA: natural radiation, oxidative stress, toxins. Each time a break occurs, a protein called ATM (Ataxia Telangiectasia Mutated, named after the genetic disease through which it was discovered) migrates rapidly to the cell nucleus to coordinate the repair. This migration mechanism is known as RIANS (Radiation-Induced ATM Nucleoshuttling).

In a person whose cells function normally, this migration is rapid and efficient. Breaks are detected, repaired, and the cell resumes its activity.

In all 26 DEMETER participants, this migration was systematically delayed. The ATM protein remained trapped in the cytoplasm, partly sequestered by other proteins. The consequence: DNA breaks were less effectively detected, and repair was incomplete. After X-ray irradiation, participants' cells showed on average half as many repair foci as control cells, and retained residual breaks 24 hours after exposure.

This finding is all the more significant because it applied to every single participant. One hundred per cent. As Foray noted of the cells: "elles ne mentent jamais" (they never lie).

A sensitivity that goes beyond radio waves

This cell repair defect is not specific to electromagnetic fields. It affects the cell's overall capacity to handle stress, regardless of its source. That explains a clinical observation familiar to EHS sufferers: the sensitivity is not limited to radio waves. Many also report intolerance to chemicals, certain types of light, noise, or disproportionate fatigue in the face of everyday stress.

The DEMETER questionnaire confirms this. The sections on non-electromagnetic sources (household products, textiles, medical procedures) show high reactivity profiles, consistent with the cellular data.

So it is not so much that radio waves "cause" additional damage; rather, the cell's capacity to absorb stress is reduced. And in a modern environment, radio waves represent an omnipresent and largely unavoidable source of stress.

Oxidative stress: a reversible pathway

Among the DEMETER results, one received relatively little attention in the media coverage, yet it may be the most important for patients.

The researchers exposed six representative cell lines to hydrogen peroxide (H₂O₂), a molecule that generates oxidative stress. They then measured the proportion of cells showing severe damage. In cells from the HBLR subgroup (associated with accelerated ageing), that proportion was significantly higher than in controls, and appeared earlier (60 minutes instead of 240).

The next step is the one that shifts the outlook. The researchers pre-treated the same cells with anethole trithione (AOL), an antioxidant compound, for 24 hours before exposing them to oxidative stress. The result: the proportion of damaged cells dropped significantly.

This experiment does not prove that an antioxidant "cures" EHS. But it does show that the chronic oxidative stress observed in these cells is, at least in part, reversible. That is a concrete lead, and the first time it has rested on cellular data from EHS patients.

Two distinct biological profiles

Cross-referencing the questionnaire with the biological data revealed two distinct subgroups among the 26 participants.

The first, called LBHR (Low Background, Highly Responsive), comprises roughly 54% of participants. Their cells show little spontaneous damage but react strongly to stress. The molecular profile of this subgroup resembles that described in radiobiology as predisposing to cancer.

The second, called HBLR (High Background, Lowly Responsive), accounts for 46% of participants. Their cells show a high baseline level of damage and respond weakly to insults. This profile is associated in the literature with accelerated cellular ageing and a risk of neurodegenerative diseases.

The most striking finding is the match. The subgroups identified by the questionnaire alone (based on reported symptoms) overlap with those identified by the cellular data with 65% agreement. According to the authors, this is a "very significant result for a concept as vaguely defined as electrosensitivity still is." It is precisely this finding that led Foray to state that, in terms of recognition, it represents a major step for electrosensitive individuals, because it places them within an already defined and well-documented molecular pathology group in radiobiology.

The limitations of the study

The scientific honesty of the DEMETER study is also one of its strengths. The authors explicitly acknowledge several limitations.

The cohort is small: 26 people. Foray explains this constraint by the difficulty EHS individuals face in travelling to and staying in a medical environment, which is by definition saturated with electronic equipment. It is a genuine paradox: the most severely affected patients are also the hardest to recruit.

Participants were self-declared electrosensitive. There is, to date, no recognised diagnostic criterion for independently confirming or ruling out EHS. The study does not resolve this problem; it sidesteps it by focusing on the cells.

Most importantly: the DEMETER cells have not yet been exposed to electromagnetic fields. The irradiation used was X-ray, a standard radiobiology tool. The results demonstrate a cell repair defect, but they do not yet demonstrate that this defect is specifically triggered by everyday radio waves. Foray is clear on this point: "la prochaine étape logique, c'est d'exposer les cellules à des ondes électromagnétiques" (the next logical step is to expose the cells to electromagnetic waves).

What DEMETER proves is that people who describe themselves as electrosensitive show an objective, measurable dysfunction in their cells. What it does not yet prove is a direct causal link between that dysfunction and exposure to radio waves.

Towards appropriate care

Pending the results of the next phase of research, the existing data already open therapeutic avenues.

The anethole trithione experiment suggests that oxidative stress can be reduced through targeted antioxidant support. On this basis, nutritional protocols are beginning to be proposed, combining compounds such as resveratrol, N-acetylcysteine, magnesium, zinc and curcumin, each targeting a specific step in the cell repair chain.

Photobiomodulation (low-level laser light therapy) is another avenue. Used for decades in physical medicine, it stimulates mitochondrial activity and DNA repair pathways, including those involving the ATM protein. In Switzerland, it is covered by basic health insurance (LAMal) as part of physiotherapy.

These approaches do not claim to cure electrosensitivity. The ATM protein migration defect appears to be a constitutional characteristic, much like other forms of radiosensitivity known in medicine. The goal is to optimise compensatory mechanisms and reduce the impact of symptoms on daily life.

As Foray sums it up: "Aujourd'hui, on peut faire disparaître certains symptômes d'une personne radiosensible. On doit pouvoir trouver pour l'électrosensibilité." (Today, we can make certain symptoms of a radiosensitive person disappear. We should be able to find the same for electrosensitivity.)

References

  • Sonzogni L, Al-Choboq J, Combemale P, et al. Skin Fibroblasts from Individuals Self-Diagnosed as Electrosensitive Reveal Two Distinct Subsets with Delayed Nucleoshuttling of the ATM Protein in Common. Int J Mol Sci. 2025;26(10):4792. DOI: 10.3390/ijms26104792
  • Calabrese EJ, Kozumbo WJ. The hormetic dose-response mechanism: Nrf2 activation. Pharmacol Res. 2021;167:105526. DOI: 10.1016/j.phrs.2021.105526
  • Belpomme D, Irigaray P. Electrohypersensitivity as a Newly Identified and Characterized Neurologic Pathological Disorder: How to Diagnose, Treat, and Prevent It. Int J Mol Sci. 2020;21(6):1915. DOI: 10.3390/ijms21061915