Dominique Belpomme’s research while affiliated with Paris-Est Sup and other places

Background: A fundamental property of cancer cells is their metabolic reprogramming, allowing them to increase glucose uptake and glycolysis. Using a rat colon adenocarcinoma model, we previously showed that blood levels of free methylglyoxal (MG), a side-product of glycolysis, remained normal in animals grafted with a non-growing tumor cell clone, while MG levels were significantly increased and positively correlated with tumor growth in animals grafted with a tumorigenic cell clone issued from the same tumor. Methods: We measured free MG in the blood of cancerous non-diabetic patients and compared the results to healthy subjects and non-cancerous diabetic patients. We also measured free MG in tumors and in the corresponding non-cancer tissues, and the peripheral blood. Results: We show that free MG levels in the peripheral blood of cancer patients are significantly increased in comparison with free MG levels in the peripheral blood of healthy controls (p < 0.0001), and similar to those in the peripheral blood of hyperglycemic diabetic patients (p = 0.965). In addition, we show that repeated free MG level measurement could be used for the therapeutic monitoring of cancer patients. Moreover, we confirmed that free MG is produced by tumor cells at significantly higher levels than cells from their corresponding tissues (p < 0.0001), and is subsequently released in the peripheral blood. Conclusions: Free MG measured in the blood could be a new metabolic biomarker useful for the diagnostic, prognostic and follow-up of non-diabetic patients with cancers, such as bronchus carcinoma, pancreatic carcinoma and glioblastoma, for which there are presently no available useful biomarkers.

Electrohypersensitivty (EHS) and multiple chemical sensitivity (MCS) are new worldwide emerging neurologic disorders in the framework of sensitivity-related environmental pathology. We have recently extended and confirmed our previous observation showing that EHS and MCS share clinically identical symptoms and may co-exist as a unique, common, sensitivity-related neurologic syndrome in 25% of the cases. There is presently no published biological study of these disorders, except the one we have previously published as preliminary. In the present study, we show that EHS and MCS and the combined syndrome share identical biochemical changes. More precisely, by measuring levels of peripheral blood and urine molecular biomarkers in a cohort of 2,018 consecutive cases, we show that both disorders and the combined syndrome can be objectively characterized, in about 90% of the cases, by a decrease in the production of 6-hydroxymelatonin sulfate in urine, while in 30-50% they are characterized by increased levels of histamine and of heat shock proteins (HSP) 27 and/or 70, and of protein S100B and nitrotyrosine in the peripheral blood. Increased levels of histamine and HSP are indicators of low grade inflammation while increased levels of protein S100B and nitrotyrosine are indicators of blood-brain barrier disruption/opening. In addition, we show that in about 15% of the cases anti-myelin autoantibodies can be detected in the peripheral blood, accounting for the occurrence of an autoimmune response. Sensitivity, specificity and reproducibility of the biochemical tests are discussed, as well as the role of these indicators used as biomarkers for the diagnosis and follow-up of patients. We also discuss cases with undetectable biological change for which they can be nevertheless diagnosed by cerebral neurotransmitters analysis in urine and brain imaging. On the basis of these biological data it is suggested that EHS and/or MCS are new brain disorders, generated via a common etiopathogenic mechanism.

From a cohort of 2018 evaluable consecutive cases issued from the European Clinical Trial Database, we describe the complete clinical symptomatic presentation of electrohypersensitivity (EHS) and multiple chemical sensitivity (MCS) and their association in the framework of a unique, sensitivity-related environmental neurologic syndrome. Eligibility criteria are those of the Atlanta consensus meeting for MCS, and those of WHO for EHS. There were 1428 EHS, 85 MCS and 505 EHS/MCS evaluable cases, so EHS was associated with MCS in 25%. Women appeared to be much more susceptible to EHS and/or to MCS than men, with no statistical significance between the EHS and MCS groups (p = 0.07), but the combined group revealed a more significant female sex ratio of 80.4% (p < 0.0001). All symptoms except emotional behavior were significantly more frequent in EHS patients than in healthy controls (p < 0.0001). We found no pathognomonic symptoms to establish the diagnosis of both disorders or to distinguish EHS from MCS. The three groups of patients were found to share identical symptoms, while several symptoms were found to be more significantly frequent in EHS/MCS than in EHS (p < 0.0001). From these data, we suggest that EHS and MCS are new brain disorders, generated via a common etiopathogenic mechanism.

Much of the controversy over the cause of electrohypersensitivity (EHS) lies in the absence of recognized clinical and biological criteria for a widely accepted diagnosis. However, there are presently sufficient data for EHS to be acknowledged as a distinctly well-defined and objectively characterized neurologic pathological disorder. Because we have shown that 1) EHS is frequently associated with multiple chemical sensitivity (MCS) in EHS patients, and 2) that both individualized disorders share a common pathophysiological mechanism for symptom occurrence; it appears that EHS and MCS can be identified as a unique neurologic syndrome, regardless its causal origin. In this overview we distinguish the etiology of EHS itself from the environmental causes that trigger pathophysiological changes and clinical symptoms after EHS has occurred. Contrary to present scientifically unfounded claims, we indubitably refute the hypothesis of a nocebo effect to explain the genesis of EHS and its presentation. We as well refute the erroneous concept that EHS could be reduced to a vague and unproven “functional impairment”. To the contrary, we show here there are objective pathophysiological changes and health effects induced by electromagnetic field (EMF) exposure in EHS patients and most of all in healthy subjects, meaning that excessive non-thermal anthropogenic EMFs are strongly noxious for health. In this overview and medical assessment we focus on the effects of extremely low frequencies, wireless communications radiofrequencies and microwaves EMF. We discuss how to better define and characterize EHS. Taken into consideration the WHO proposed causality criteria, we show that EHS is in fact causally associated with increased exposure to man-made EMF, and in some cases to marketed environmental chemicals. We therefore appeal to all governments and international health institutions, particularly the WHO, to urgently consider the growing EHS-associated pandemic plague, and to acknowledge EHS as a new real EMF causally-related pathology.

Clinical research aiming at objectively identifying and characterizing diseases via clinical observations and biological and radiological findings is a critical initial research step when establishing objective diagnostic criteria and treatments. Failure to first define such diagnostic criteria may lead research on pathogenesis and etiology to serious confounding biases and erroneous medical interpretations. This is particularly the case for electrohypersensitivity (EHS) and more particularly for the so-called “provocation tests”, which do not investigate the causal origin of EHS but rather the EHS-associated particular environmental intolerance state with hypersensitivity to man-made electromagnetic fields (EMF). However, because those tests depend on multiple EMF-associated physical and biological parameters and have been conducted in patients without having first defined EHS objectively and/or endpoints adequately, they cannot presently be considered to be valid pathogenesis research methodologies. Consequently, the negative results obtained by these tests do not preclude a role of EMF exposure as a symptomatic trigger in EHS patients. Moreover, there is no proof that EHS symptoms or EHS itself are caused by psychosomatic or nocebo effects. This international consensus report pleads for the acknowledgement of EHS as a distinct neuropathological disorder and for its inclusion in the WHO International Classification of Diseases.