Yesterday, I attended a talk by the son of Jonas Salk about the history of the Pittsburgh area in the research and the creation of the polio vaccine. This reagent bottle was displayed on the artifacts table along with other memorabilia from the Shalom Research Farm where many animal trials and experiments for the vaccine were being done. There was one word on the label of the bottle, which gave me pause: MERTHIOLATE.
As a chemist, the word was instantly recognizable an acronym for thimerisol, a mercury containing compound. If you have been around the autism community for a bit, you know that thimerisol and mercury containing compounds are a hot topic, but in reality it should be of concern for others, I believe. Including those in the mitochondrial community and beyond. It appears to be MITOXIC and here is some supporting evidence of why…
Before I provide some of the references that I have come across, I believe it is important to define 3 types of mercury: Elemental, Inorganic and Organic Mercury.
- Elemental Mercury is known best as quicksilver and exists as liquid metallic mercury at room temperature, it is poorly absorbed through skin and GI contact (except perhaps for those with ileus).
- Inorganic Mercury simply means the mercury atom has combined with another element which is non- carbon containing. Examples of inorganic mercury include: mercuric chloride, mercuric acetate, mercuric sulfide.
- Organic Mercury or Organomercury simply means that the mercury molecule is bound to a carbon (and other functional carbon containing groups). For example, Ethyl Mercury and Methyl Mercury are both organomercury compounds, as is Thimerisol which is bound to an ethyl group as well as a thiol group.
This paper provides a convincing argument for why Mitochondrial disease patients (and really all of us) may want to be aware of our exposure to mercury, particularly in this instance thimerisol, and organomercury compound: (one definition Astrocytes=most abundant cell of the HUMAN BRAIN)
Thimerosal-Derived Ethylmercury Is a Mitochondrial Toxin in Human Astrocytes: Possible Role of Fenton Chemistry in the Oxidation and Breakage of mtDNA.
AuthorsSharpe MA, et al.
J Toxicol. 2012;2012:373678. doi: 10.1155/2012/373678. Epub 2012 Jun 28.
Affiliation: Department of Neurosurgery, The Methodist Hospital, 6565 Fannin Street, Houston, TX 77030, USA.
Additionally, this paper is annotated on the ICHNFM site.
Some Quotes from the PAPER:
Thimerosal generates ethylmercury in aqueous solution and is widely used as preservative. We have investigated the toxicology of Thimerosal in normal human astrocytes, paying particular attention to mitochondrial function and the generation of specific oxidants. We find that ethylmercury not only inhibits mitochondrial respiration leading to a drop in the steady state membrane potential, but also concurrent with these phenomena increases the formation of superoxide, hydrogen peroxide, and Fenton/Haber-Weiss generated hydroxyl radical. These oxidants increase the levels of cellular aldehyde/ketones. Additionally, we find a five-fold increase in the levels of oxidant damaged mitochondrial DNA bases and increases in the levels of mtDNA nicks and blunt-ended breaks. Highly damaged mitochondria are characterized by having very low membrane potentials, increased superoxide/hydrogen peroxide production, and extensively damaged mtDNA and proteins. These mitochondria appear to have undergone a permeability transition, an observation supported by the five-fold increase in Caspase-3 activity observed after Thimerosal treatment.
“Thimerosal is a preservative that is widely used in medical products, including as a preservative in vaccines, immunoglobulin preparations, skin test antigens, antivenins, ophthalmic and nasal products, and tattoo inks, and is composed of 49.6 percent ethylmercury by weight . The widespread use of Thimerosal exposes many to its potential toxic effects, especially 𝑖 𝑛 𝑢 𝑡 𝑒 𝑟 𝑜 and in neonates. ”
“We postulate that this compound is preferentially taken up into the mitochondria of NHA causing damage to the respiratory chain and subsequent ROS production. The damage of a cell’s mitochondria leads to the activation of the apoptotic cascade and subsequent cell death [3, 4, 24, 26–31]. This may be clinically relevant in the setting of a patient who harbors a known or unknown mitochondrial disorder. In the setting of a mitochondrial disorder, a specific mitochondrial toxin could be life altering or life threatening.”
“The results of this study suggest that ethylmercury is a mitochondrial toxin in human astrocytes. We believe that this finding is important, particularly since the number of diseases in which mitochondrial dysfunction has been implicated are rapidly increasing.”
Another Journal Article regarding Mito and Mercury:
“Toxic metals, especially mercury, generate many of their deleterious effects through the formation of free radicals, resulting in DNA damage, lipid peroxidation, depletion of protein sulfhydryls (eg, glutathione) and other effects (Valko et al., 2005 ). These reactive radicals include a wide-range of chemical species, including oxygen-, carbon-, and sulfurradicals originating from the superoxide radial, hydrogen peroxide, lipid peroxides, and also from chelates of amino acids, peptides, and proteins complexed with the toxic metals (Valko et al., 2005 ). One major mechanism for metals toxicity appears to be direct and indirect damage to mitochondria via depletion of glutathione, an endogenous thiol-containing (SH-) antioxidant, which results in excessive free radical generation and mitochondrial damage (Sanfeliu et al., 2001 ). Anecdotally, Dr. Neustadt, in his clinic, frequently observes an elevation of pyroglutamate, a urinary organic acid that is a specific marker for glutathione depletion (Bralley and Lord, 2001 ), in patients with confirmed mercury toxicity. Not surprisingly, these patients also complain of fatigue, a hallmark symptom of mitochondrial damage.”
And another journal article talking about the hypersensitivity to Mercury in Autism and siblings:
B-Lymphocytes from a Population of Children with Autism Spectrum Disorder and Their Unaffected Siblings Exhibit Hypersensitivity to Thimerosal
The role of thimerosal containing vaccines in the development of autism spectrum disorder (ASD) has been an area of intense debate, as has the presence of mercury dental amalgams and fish ingestion by pregnant mothers. We studied the effects of thimerosal on cell proliferation and mitochondrial function from B-lymphocytes taken from individuals with autism, their nonautistic twins, and their nontwin siblings. Eleven families were examined and compared to matched controls. B-cells were grown with increasing levels of thimerosal, and various assays (LDH, XTT, DCFH, etc.) were performed to examine the effects on cellular proliferation and mitochondrial function. A subpopulation of eight individuals (4 ASD, 2 twins, and 2 siblings) from four of the families showed thimerosal hypersensitivity, whereas none of the control individuals displayed this response. The thimerosal concentration required to inhibit cell proliferation in these individuals was only 40% of controls. Cells hypersensitive to thimerosal also had higher levels of oxidative stress markers, protein carbonyls, and oxidant generation. This suggests certain individuals with a mild mitochondrial defect may be highly susceptible to mitochondrial specific toxins like the vaccine preservative thimerosal.
A few More articles confirming a risk of thimerisol to mitochondria:
Thimerosal induces neuronal cell apoptosis by causing cytochrome c and apoptosis-inducing factor release from mitochondria.
“However, even when this precautionary measure is taken, local reactions can be expected in such a high percentage of merthiolate-sensitive persons that merthiolate in vaccines should be replaced by another antibacterial agent.”
A video showing how Mercury impacts Brain Neurons:
Interestingly these journal articles are all focusing on Ethylmercury and thimerisol (merthiolate) toxicity to one’s mitochondria. According to the American Academy of Pediatrics position statement from 2001:
“Mercury in all of its forms is toxic to the fetus and children, and efforts should be made to reduce exposure to the extent possible to pregnant women and children as well as the general population. Pediatricians can contribute to the effort of decreasing the amount of mercury in the waste stream by phasing out mercury-containing devices, such as thermometers and sphygmomanometers, from their offices and other medical facilities and encouraging parents to remove mercurythermometers from their homes.”
And the CDC has this to say about Thimerisol:
Scrolling down the page sourced above you can find this explanation on the CDC’s website:
This seems to imply that methylmercury and elemental mercury are MORE TOXIC to a human body than thimerisol/merthiolate which it says breaks down to ethyl mercury and thioSALICYLATE which are “easily eliminated”. Hmmmmm not a word about mitochondrial disease or mitochondrial dysfunction or mitochondrial toxicity. Thiosalicylate… hmmmm wonder if you have problems breaking down salicylates if thiosalicylate could be toxic to the human body in that case… or is it a case of chicken and the egg~ did too much mercury exposure cause hypersensitivity to salicylates??
So if METHYLMERCURY is more toxic…what does it do to your mitochondria??
“Methylmercury (MeHg) mediated cytotoxicity is associated with loss of intracellular calcium (Ca2+) homeostasis. The imbalance in Ca2+ physiology is believed to be associated with dysregulation of Ca2+intracellular stores and/or increased permeability of the biomembranes to this ion. In this paper we summarize the contribution of glutamate dyshomeostasis in intracellular Ca2+ overload and highlight the mitochondrial dysfunctions induced by MeHg via Ca2+ overload. Mitochondrial disturbances elicited by Ca2+ may involve several molecular events (i.e., alterations in the activity of the mitochondrial electron transport chain complexes, mitochondrial proton gradient dissipation, mitochondrial permeability transition pore (MPTP) opening, thiol depletion, failure of energy metabolism, reactive oxygen species overproduction) that could culminate in cell death.”
Methylmercury inhibits electron transport chain activity and induces cytochrome c release in cerebellummitochondria.
Methylmercury neurotoxicity is associated with inhibition of the antioxidant enzyme glutathione peroxidase.
Modulation of methylmercury uptake by methionine: prevention of mitochondrial dysfunction in rat liver slices by a mimicry mechanism.
Hmmm…. Methylmercury doesn’t look much better for any of our mitochondria! Soooo where does that leave us? All forms of mercury look pretty toxic to one’s mitochondria, so say if you are born with a mitochondrial disorder or mitochondria that just aren’t working at 100%, or perhaps you have faulty methylation, perhaps an MTHFR mutation, or impaired glutathione synthesis. Say you are a baby and you receive quite a few vaccines in the first year, most of them containing aluminum because the mercury has been removed, but you also get a flu shot that still contains mercury. Could this exposure to organomercury trigger a metabolic crisis or cause more damage to your mitochondria than you were already born with? Possibly? Probably? With the links between mitochondrial disease and autism, is it possible mercury can be linked to autism?. Thimerisol doesn’t cause autism as the CDC and that thimerisol does not cause harm as other groups conclude… but there is a body of evidence that shows that thimerisol (and other mercury compounds) does harm and damage mitochondria, and impaired mitochondrial function (OXPHOS) has been implicated as a cause of autism… so if A=B and B=C does A=C?? The controversy will continue to rage on for years, with new books coming on the market as we speak, more will contest that it is all just a coincidence. Maybe it is? Maybe it isn’t? It is up to each of us as parents to do our own research and make an educated decision for our family.
Video about Mercury and Autism
(from Dr. Haley, retired professor of Chemistry, University of Kentucky)
What is Pink’s Disease?
“Pink Disease was and still is a very nasty disease. The severity and duration of the disease vary. In the English speaking western world, the age of onset is usually between 6-14 months.
The most common KNOWN cause of Pink Disease was mercury containing teething powders. In the English speaking Western World, the use of mercury in teething powders was banned in the 1950’s. There were, and still are, numerous other household, industrial, natural, agricultural and medical sources of mercury in the environment.” (source)
Ancestry of Pink Disease (Infantile Acrodynia) Identified as a Risk Factor for Autism Spectrum Disorders
Video: From Acrodynia to Autism: Mercury Across Generations, More Evidence of Harm
Dr. Mark Hyman shares his personal story of mercury toxicity and mitochondria.
Editor’s Note- After many comments about mercury being removed from all vaccines…I felt it important to write this post- https://babyfoodsteps.wordpress.com/2014/08/16/where-is-the-mitoxic-mercury/