Multiple chemical sensitivity is a response to chemicals acting as toxicants via excessive NMDA activity
Abstract
Letters to the Editor Multiple chemical sensitivity is a response to chemicals acting as toxicants via excessive NMDA activity Dear Editor: Meulders et al. [1] claim to have presented evidence for symptom learning in multiple chemical sensitivity (MCS). They make this claim even though they studied only normal people and they studied the responses of such normals to chemicals not implicated in MCS. They present not one iota of evidence that can be clearly linked to MCS. They do this while completely ignoring a vast array of evidencethatiscompletelyincompatiblewiththeir interpretation. There are seven classes of chemicals implicated in MCS [2–5]. Members of these classes of chemicals are known to produce increases in NMDA activity and it is also known that the toxic responses in the body produced by members of all seven classes are greatly lowered by using NMDA antagonists [2,3]. These studies show, therefore, that these classes of chemicals not only produce increases in NMDA activity but that their toxic responses in the body are largely produced by such NMDA stimulation, so we know that these classes of chemicals can act as toxicants producing a common toxic response in the body. Excessive NMDA activity is also implicated in MCS through a series of additional studies. For example, chemical responses in MCS patients have been reported to be greatly lowered by an NMDA antagonist [3,5,6]. In a genetic polymorphism study of susceptibility to MCS, the allele of the CCK-B receptor gene associated with increased susceptibility is known to produce increased NMDA activity [3,5]. Thus, we have compelling evidence that MCS is a response to chemicals acting as toxicants, with these chemicals acting to produce a common response that is otherwise implicated in MCS. What do Meulders et al. [1] have to say about this extensive evidence that chemicals in MCS act as toxicants in the body? Nothing; they pretend that none of this literature exists. This role of chemicals acting as tox
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