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The major scientific clue has always been the triggered onset and growth rate of autism. Additionally, the witness of people being diagnosed with severe mercury poisoning from eating high fish diets cannot be ignored. It is not too much a stretch of the imagination to ask if this can happen to an adult what it might do to a small fetus. The development of vaccine therapy and the invention of pharmaceutical drugs has been a wonderful achievement lengthening many lives. However, like many things it has to be controlled and regulated especially when toxic adjuvants are added for enhancement effects. Likewise, the fish we eat are now contaminated worldwide in the lakes and oceans and will not return to natural levels possibly for many centuries.

During counselling, the patient should be advised that, according to evidence from randomized clinical trials, dental amalgam does not result in toxic effects and that replacement of amalgam fillings with nonmercury materials is not recommended. A precautionary approach could include avoiding dental amalgam work during pregnancy unless absolutely necessary, although no clinical evidence supports this recommendation.

In this study we investigated the additive effect of mercury on the brain mitochondrial dysfunction in experimental autoimmune encephalomyelitis (EAE) model. Experimental animals (female C57BL/6 mice) are divided into four groups (n = 8); control, Hg, EAE, EAE with Hg. EAE model of MS induced by injecting myelin oligodendrocyte glycoprotein (MOG). Neurobehavioral alterations are recorded and then mice were sacrificed at day 28 and brain mitochondria were isolated and mitochondrial toxicity parameters including mitochondrial swelling, reactive oxygen species (ROS) formation, collapse of mitochondrial membrane potential (MMP) and cytochrome c release were measured. Our results showed that repeated treatment of mercury following induction of EAE in mice significantly increased the neurobehavioral scores, as well as mitochondrial toxicity through ROS formation, mitochondrial swelling, collapse of MMP and cytochrome c release. Our findings proved that repeated exposure with mercury accelerates progression of MS through mitochondrial damage related to oxidative stress and finally apoptosis.

This is the first study to explore the potentially causal relationship between levels of serum neurokinin A and blood mercury (BHg) in children with ASD. Levels of serum neurokinin A and BHg were measured in 84 children with ASD, aged between 3 and 10 years, and 84 healthy-matched children. There was a positive linear relationship between the Childhood Autism Rating Scale (CARS) and both serum neurokinin A and BHg. ASD children had significantly higher levels of serum neurokinin A than healthy controls (P < 0.001). Increased levels of serum neurokinin A and BHg were respectively found in 54.8 % and 42.9 % of the two groups. There was significant and positive linear relationship between levels of serum neurokinin A and BHg in children with moderate and severe ASD, but not in healthy control children. It was found that 78.3 % of the ASD patients with increased serum levels of neurokinin A had elevated BHg levels (P < 0.001). Neuroinflammation, with increased levels of neurokinin A, is seen in some children with ASD, and may be caused by elevated BHg levels. Further research is recommended to determine the pathogenic role of increased levels of serum neurokinin A and BHg in ASD. The therapeutic role of tachykinin receptor antagonists, a potential new class of anti-inflammatory medications, and Hg chelators, should also be studied in ASD.

With great interest, we have read the article by Shahidi et al1 entitled “Effect of magnetic resonance imaging on microleakage of amalgam restorations: an in vitro study” that is published in Dentomaxillofacial Radiology. The first report on the role of exposure to MRI or microwave radiation emitted by mobile phones in enhancing the release of mercury from dental amalgam restoration waspublished in 2008.2

Although the paper authored by Daokar et al. addresses a challenging issue, it has some shortcomings. One of the shortcomings of this study comes from this point that the authors have ignored substantial evidence which indicates the role of exposure to electromagnetic fields (e.g. mobile phones, Wi-Fi and cordless phones) on oxidative stress induction [20-23]. It should be noted that in modern life, due to rapid advances in telecommunication technology, we are all surrounded by electromagnetic fields produced by a variety of sources. Daokar et al. in their study collected saliva samples before restoration and 24 h, 7 days, and 14 days after restoration. Therefore, alterations observed in salivary oxidative stress (MDA levels) could be simply due to frequent use of mobile phones or cordless phones.