Eye Problems Related to Mercury

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Studies document that mercury and similar toxic metals accumulate in endothelial cells, such as those in the eye retina, cornea, and macula, depleting glutathione and lipoate by binding to thiols. These are needed to counteract free radicals caused by toxic metals that damage the endothelial layers of the retina, cornea and macula, as major factors in such conditions. Such generated free radicals have been found to cause cataracts, and such conditions can be prevented, slowed, and even reversed to some degree by detox and antioxidant eye drops. Mercurialentis (brown discoloration—caused by mercury—of anterior capsule of eye lens) is documented in medical texts as the first sign of mercury toxicity; it is an indicator and early sign of further eye damage.

Cataracts, retinitis pigmentosa, iritis, color vision problems, and other eye conditions are documented to commonly be caused by mercury/metals toxicity. It is commonly caused by systemic poisoning from absorption of mercury vapor through the respiratory tract or through the gastrointestinal tract.

From my experience, I know of five eye problems related to mercury. There are probably more. One eye problem mercury causes is chronic iritis; I don’t know much about that, but it’s documented in the medical literature and someone I know had it. Another problem is color vision, which is also documented in the medical literature and several people’s color vision has improved after having their amalgams removed, including me.

I have Fuch’s disease (clouding of cornea caused by deterioration/ glumping of endothelial cells in the cornea), also known as an aggressive form of cataracts. Animal studies and in vitro studies have shown mercury causes similar damage to endothelial cells in various body parts due to deterioration and free radical effects. Since having my amalgams removed over the last two years, my ophthalmologist says that the deterioration of the endothelial layer of my corneas has slowed considerably compared to two years ago. My vision has also improved so much that I cannot see at all through my glasses that I got four years ago. My optometrist who did the glasses and reexamined me was really surprised and said my vision had improved almost 50%. I no longer wear glasses.

Another eye problem related to mercury is dry eyes. Several clinics have had success with improvements after amalgam replacement. The other eye problem known to sometimes be related to mercury is macular degeneration. The buildup of mercury in the eye is similar to the buildup in Fuch’s and causes clouding and degeneration. Someone I know told me that a relative got better after amalgam replacement.

Strabismus is where one eye moves freely of the other, either inwardly or outwardly to focus independently. This condition, which was present at an early age in my now five-year-old, was quickly corrected by supplementing the RDA of vitamin A in cis-trans form and cutting out all other vitamin A sources (Megson protocol). Pupil dilation was always a factor in my son too. Interestingly, his pupils reacted normally within the first two doses of DMSA he received, but the dilation returned post-round. After 5 months of chelation, I saw very normal eye function, with normal pupil reactivity for the most part. I believe the dilation is a symptom of mercury toxicity.

Dilation, poor accommodative function (focusing) and convergence insufficiency, which if severe is strabismus, are characteristic of mercury poisoning. They are all due to a mild, symmetrical impairment of the third cranial nerve. Since this nerve connects to the brain right next to the hypothalamus, where mercury is known to concentrate, degeneration many occur in the macula lutea of the eye. This is often caused by free radical or oxidation damage.

The first symptom I had of mercury toxicity was double vision, then drooping eyelids. I also had floaters for years and bright lights blinded me. When I was 42, my keen eyesight started to go, and I had to wear glasses to sew or read. By the time 1998 rolled around, I was wearing 250 magnifying glasses. Within a short period of time after amalgam removal I no longer needed reading glasses, and today I do not wear glasses and am able to read any size print. However, I still have very slight double vision to the extreme right and left; I no longer have floaters but still have some sensitivity to bright lights. Mercury has been found to be a factor in retinitis pigmentosa and retina degeneration.

Inorganic mercury (Hg(2+)) is a prevalent environmental contaminant to which exposure to can damage rod photoreceptor cells and compromise scotopic vision. The retinal pigment epithelium (RPE) likely plays a role in the ocular toxicity associated with Hg(2+) exposure in that it mediates transport of substances to the photoreceptor cells. In order for Hg(2+) to access photoreceptor cells, it must first be taken up by the RPE, possibly by mechanisms involving transporters of essential nutrients. In other epithelia, Hg (2+), when conjugated to cysteine(Cys) or homocysteine (Hcy), gains access to the intracellular compartment of the target cells via amino acid and organic anion transporters. Accordingly, the purpose of the current study was to test the hypothesis that Cys and Hcy S-conjugates of Hg(2+) utilize amino acid transporters to gain access into RPE cells. Time- and temperature-dependence, saturation kinetics, and substrate-specificity of the transport of Hg(2+) was assessed in ARPE-19 cells exposed to the following S-conjugates of Hg(2+): Cys(Cys-S-Hg-S-Cys), Hcy (Hcy-S-Hg-S-Hcy), N-acetylcysteine (NAC-S-Hg-S-NAC) or glutathione (GSH-S-Hg-S-GSH). We discovered that only Cys-S-Hg-S-Cys and Hcy-S-Hg-S-Hcy were taken up by these cells. This transport was Na(+)-dependent and was inhibited by neutral and cationic amino acids. RT-PCR analyses identified systems B(0,+) and ASC in ARPE-19 cells. Overall, our data suggest that Cys-S-Hg-S-Cys and Hcy-S-Hg-S-Hcy are taken up into ARPE-19 cells by Na-dependent amino acid transporters, possibly systems B(0,+), and ASC. These amino acid transporters may play a role in the retinal toxicity observed following exposure to mercury.

Proximal tubular epithelial cells are major sites of homocysteine (Hcy) metabolism and are the primary sites for the accumulation and intoxication of inorganic mercury (Hg(2+)). Previous in vivo data from our laboratory have demonstrated that mercuric conjugates of Hcy are transported into these cells by unknown mechanisms. Recently, we established that the mercuric conjugate of cysteine [2-amino-3-(2-amino-2-carboxy-ethylsulfanylmercuricsulfanyl) propionic acid; Cys-S-Hg-S-Cys] is transported by the luminal, amino acid transporter, system b(0,+). As Cys-S-Hg-S-Cys and the mercuric conjugate of Hcy (2-amino-4-(3-amino-3-carboxy-propylsulfanylmercuricsulfanyl) butyricacid; Hcy-S-Hg-S-Hcy) are similar structurally, we hypothesized that Hcy-S-Hg-S-Hcy is a substrate for system b (0,+). To test this hypothesis, we analyzed the saturation kinetics, time dependence, temperature dependence, and substrate specificity of Hcy-S-Hg-S-Hcy transport in Madin-Darby canine kidney (MDCK) cells stably transfected with system b (0,+). MDCK cells are good models in which to study this transport because they do not express system b (0,+). Uptake of Hg(2+) was twofold greater in the transfectants than in wild-type cells. Moreover, the transfectants were more susceptible to the toxic effects of Hcy-S-Hg-S-Hcy than wild-type cells. Accordingly, our data indicate that Hcy-S-Hg-S-Hcy is transported by system b(0,+) and that this transporter likely plays a role in the nephropathy induced after exposure to Hg(2+). These data are the first to implicate a specific, luminal membrane transporter in the uptake and toxicity of mercuric conjugates of Hcy in any epithelial cell.

Mercury accumulates in cornea endothelial cells and causes oxidative damage resulting in cataracts, etc. Methylmercury in seafood may cause lens clouding, contributing to cataract development. Optometrist Ben Lane noted that his cataract patients liked seafood, while those who didn’t like fish were clear-eyed. A study of 17 patients revealed that the cataract patients had eaten salt water fish or shellfish at least once a week on the average, but those cataract-free reported using these foods an average of once every five weeks. The cataract patients showed far higher concentrations of mercury in their hair. Dr. Lane’s study showed that the presence of 2.3 ppm or more of mercury in hair samples was related to a 23-fold increase in the risk of cataracts. Dr. Lane encourages his patients to eat such foods as garlic and pectin-rich foods, such as apples, to help remove the mercury and to receive adequate, while avoiding excessive, amounts of vitamins A, C, and E.

I would like look into the possibility of mercury poisoning being capable of causing both cataracts and light sensitivity, but so are other things. I have seen many babies born with mercury poisoning (further exacerbated by the mercury in vaccinations) from their mother’s dental amalgams.

Mobilization and excretion are required for mercury detoxification. Consuming foods high in sulfur such as garlic, onions, beans, and eggs or supplemental sulfur in the form of MSM can help move mercury around but it is only bound loosely and caution is advised. There have been reported cases of reversible cataract development from individuals mobilizing mercury without excreting it. Consult a qualified doctor for a detoxification protocol appropriate for you. Antioxidant eye drops (n-acetylcarnosine) have been documented to prevent and sometimes reverse cataracts (such as Can C drops).

The following is a list of conditions successfully treated by chelation that has been assembled by physicians who did much of the early research work. Many of these problems are common and are generally considered incurable:

  • scleroderma;
  • digitalis intoxication;
  • heavy-metal poisoning (especially acute plumbism);
  • calcinosis (pipestem calcinosis of the vessels, prostatic calcinosis);
  • vascular atheromatous disorders including atherosclerosis, atheromatous deposits, arteriosclerosis obliterans, peripheral vascular insufficiency with intermittent claudication, and acute brain syndrome secondary to cerebral ischemia secondary to calcific atherosclerosis; myocardial or coronary insufficiency;
  • collagenosis;
  • arteriosclerosis, including cerebrovascular arteriosclerosis;
  • arthritis including hypertrophic and rheumatoid;
  • calcific tendinosis;
  • calculi;
  • diabetic retinopathy;
  • multiple sclerosis;
  • macular degeneration of the retina;
  • cataracts;
  • Parkinsonism;
  • emphysema;
  • poisonous snake and insect bites;
  • calcified necrotic ulcers;
  • heart valve calcification;
  • hemochromatosis;
  • calcific bursitis; and
  • calcified granulomas and hypertension.

Mercury accumulates in the uvea and retina of the eye. The problem with mercury is that it affects our nervous system. Mercury accumulates in what we call end organs, like kidneys, brain, thyroid, and eyes, and this is why it is detected on hair analysis. It may contribute to cataracts, headaches, numbness and tingling, irritability, joint pain and autism in kids, as well as chronic fatigue syndrome and general allergies.

Vitamin C also helps to pull out the toxic mercury resulting from the consumption of large fish, such as tuna, swordfish and shark. Dr. Lane said that his 1982 study found that mercury, which would accumulate in the crystalline lens, resulted in the depression of enzymes such as superoxide dismutase and glutathione peroxidase. The latter is the primary enzyme that helps prevent mercury cataracts from forming. “Organic mercury is the worst offender because it’s able to penetrate membranes and get into organic tissues,” he said.

I do not know of any direct science references tying mercury with macular degeneration. However, from indirect information there appears to be a connection. Johnathon Wright and Alan Gaby have developed a nutritional protocol that is quite effective. It is interesting to note that the nutrients are all those that mercury reduces in the body, ie. taurine, vitamin E, selenium, and zinc.

Mercury is still used in eye makeup as a preservative. The use of mercury compounds as cosmetic ingredients is limited to eye area cosmetics at concentrations not exceeding 65 parts per million(0.0065%) of mercury calculated as the metal (about 100 ppm or 0.01% phenylmercuric acetate or nitrate) and provided no other effective and preservative is available for use.

Mercury compounds are readily absorbed through the skin on topical application and have the tendency to accumulate in the body. They may cause allergic reactions, skin irritation, or neurotoxic manifestations.

References

  1. Olynyk F, Sharpe DH. Mercury poisoning in paper pica. NEJM. 1982; 306(17): 1056-57.
  2. Uchino M, Tanaka Y, Ando M, et al. Neurologic features of chronic minamata disease (organic mercury poisoning). J Environ Sci Health B. 1995; 30(5): 699-715.
  3. Ulshafer RJ. Distributions of elements in the human retinal pigment epithelium. Arch Ophthalmol. 1990; 108(1): 113-117.
  4. Bridges CC, Battle JR, Zalups RK. Transport of thiol-conjugates of inorganic mercury in human retinal pigment epithelial cells. Toxicol Appl Pharmacol. 2007; 221(2): 251-60.
  5. Lane B. Methylmercury in seafood contributes to cataract development. Medical World News. 1982.
  6. Rudolph CJ, Samuels RT, McDanagh EW, Cheraskin E. Visual field evidence of macular degeneration reversal using a combination of EDTA chelation and multiple vitamin and trace mineral therapy. In: Cranton EM. A Textbook on EDTA Chelation Therapy. 2nd ed. Charlottesville, VA: Hampton Roads Publishing Company; 2001.
  7. Khayat A, Dencker L. Whole body and liver distribution of inhaled mercury vapor in the mouse: Influence of ethanol and aminotriazole retreatment. J Appl Toxicol. 1983; 3(2): 66-74.
  8. Hachet E. Inorganic mercury has been found to be associated with cataract formation. Cataracts, Bull Soc Ophtalmol Fr. 1985; 87-107.
  9. Healthy Living in Asia. Available at: http://www.healthinasia.com/mercury.html. Accessed December 30, 2014.
  10. Cavalleri A, Belotti L, Gobba FM, Luzzana G, Rosa P, Seghizzi P. Color vision loss in workers exposed to elemental mercury vapour. Toxicology Letters. 1995; 77(1-3): 351-356.
  11. Urban P, Gobba F, Nerudova J, Lukas E, Cabelkova Z, Cikrt M. Discrimination impairment in workers exposed to mercury vapor. Neurotoxicology. 2003; 24(4-5): 711-716.
  12. Olynyk F, Sharpe DH. Mercury poisoning in paper pica (retinitis pigmentosa). NEJM. 1982; 306(17): 1056-1057.
  13. Uchino M, Tanaka Y, Ando Y, et al. Neurologic features of chronic minamata disease (organic mercury poisoning) and incidence of complications with aging. J Environ Sci Health B. 1995; 30(5): 699-715.
  14. Tessier-Lavigne M, Mobbs P, Attwell D. Lead and mercury toxicity and the rod light response. Invest Ophthalmol Vis Sci. 1985; 26(8): 1117-1123.
  15. Van Horn DL, Edelhauser HF, Prodanovich G, Eiferman R, Pederson HF. Effect of the ophthalmic preservative thimerosal on human and rabbit corneal endothelium. Invest Opthalmol. Visual Sci. 1977; 16(4): 273-280.
  16. Garron LK, Wood IS, Spencer WH, Hayes TL. A clinical pathologic study of mercurlalentis medicamentosus. Trans Am Ophthalmol Soc. 1977; 74: 295-320.
  17. Klein, CL, Kohler, H, Kirkpatrick CJ. Increased adhesion and activation of polymorphonuclear neutrophil granulocytes to endothelial cells under heavy metal exposure in vitro. Pathobiology. 1994; 62(2): 90-98.
  18. Sillman AJ, Weidner WJ. Low levels of inorganic mercury damage the corneal endothelium. Experimental Eye Research. 1993; 57(5): 549-555.
  19. Toimela TA, Tahti H. Effects of mercuric chloride exposure on the glutamate uptake by cultured retinal pigment epithelial cells. Toxicol In Vitro. 2001; 15(1): 7-12.
  20. Michiels J. Cataracts (Mercury). Bull Soc Ophtalmol. 1985: 87-107.
  21. Hachet E. Oftalmol Zh. Eye manifestations of chronic mercury poisoning. 1974; 29(7): 501-503.
  22. Fomicheva IV. Inhibition of corneal epithelial cell migration by cadmium and mercury. Bull Environ Contam Toxicol. 1991; 46(2): 230-236.
  23. Klein CL, Kohler H, Kirkpatrick CJ. Increased adhesion and activation of polymorphonuclear neutrophil granulocytes to endothelial cells under heavy metal exposure in vitro. Pathobiology. 1994; 62(2): 90-98.
  24. Warfvinge K, Bruun A. Mercury accumulation in the squirrel monkey eye after mercury vapour exposure. Toxicology. 1996; 107(3): 189-200.
  25. Gitter S, Pardo A, Kariv N, Yinon U. Enhanced electroretinogram in cats induced by exposure to mercury acetate. Toxicology. 1988; 51(1): 67-76.
  26. Kleinschuster SJ, Yoneyama M, Sharma RP. A cell aggregation model for the protective effect of selenium and vitamin E on toxicity. Toxicology. 1983; 26(1): 1-9.
  27. Sillman AJ. Heavy metals affect rod, but not cone, photoreceptors. Science. 1979; 206(4414): 78-80.
  28. Warfvinge K, et al. Mercury accumulation in the monkey eye after mercury vapour exposure. Toxicology. 1996; 107: 189-200.
  29. Saari J. Methylmercury injury of cultured human vascular endothelial. Journal of Trace Elements in Experimental Medicine. 1993; 6(4): 155-162.
  30. Cavalleri A, Gobba F. Reversible color vision loss in occupational exposure to metallic mercury. Environ Res. 1998; 77(2): 173-7.
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