Mercury Detox using the Selenium Method

Mercury Detox Using the Selenium Method 

Written by Dennis N Crouse.PhD author of  5 books 'Prevent Alzheimer's Autism and Stroke with 7 Supplements, 7 Lifestyle Changes and a Dissolved Mineral' and 'Silica Water the Secret to Healthy Blue Zone Longevity' 'Discovering Magic in Water that makes life possible'

Dennis' Books   

Mercury can be inhaled as mercury vapor, absorbed in the gut from ingested food and water, or injected in the body by vaccinations with Thimerosal. Mercury’s toxicity primarily stems from its ability to tightly bind with the essential element selenium and thereby lower available selenium levels in the body creating a selenium deficiency¹.  

Selenium is used in some enzymes to protect us from oxidative effects of toxic metals commonly found in the body such as aluminum, manganese, nickel, lead, and mercury. Selenoenzymes are involved in reducing the oxidative effects of these metals by reducing the amount of reactive oxygen species (ROS) induced by these metals in the body.  ROS causes damage to our bodies by weakening and killing mitochondria and the cells powered by these mitochondria. 

Mercury is particularly toxic because it induces ROS that kills mitochondria and prevents selenoenzymes from providing protection from ROS by both creating selenium deficiency and inhibiting selenoenzymes. Selenium supplementation provides four levels of protection from mercury: 
1.Prevents mercury induced selenium deficiency in the brain^2,3 
2. Prevents mercury induced mitochondrial death and neurotoxicity in the brain due to ROS^2,3,4 
3.Facilitates detoxification of mercury by elimination of mercury in the urine⁵) 
4. Facilitates detoxification of mercury by formation of insoluble mercury selenide (HgSe)¹

It has been demonstrated that humans taking 100mcg of selenomethionine daily for twelve weeks had significantly enhanced urinary excretion of mercury⁵. In those with mercury induced selenium deficiency it may take on average 2 - 4 weeks to first restore the body’s selenium reserves before enhanced mercury excretion is observed (See Figure 1)⁵.

Figure 1. Mercury concentrations in urine samples on different days, where the supplementation group took 100mcg/day Se-enriched yeast (SelenoPrecise, Pharma Nord, Denmark) and the placebo group did not take a selenium supplement.  The supplementation group was 53 volunteers (27 men and 26 women) and the placebo group was 50 volunteers (25 men and 25 women). The results were statistical significance, as indicated with ++ p < 0.01 and +++ p < 0.001, compared with the placebo group⁵. 
 

The selenium method of mercury detox requires taking orally a selenomethonine supplement, daily for at least 12 weeks:

·         Children 0 to 3 years of age: 25mcg/day

·         Children 4 to 8 years of age: 50mcg/day

·         Children 9 to 13 years of age: 100mcg/day

·         Adolescents 14 to 18 years of age and adults: 200mcg/day

Most selenomethionine is made from selenium enhanced yeast (e.g. Saccharomyces cerevisiae), such as Bio-SelenoPrecise tablets manufactured in Denmark by Pharma Nord under patent no. 1 478 732 B1. This type of selenium is approximately 90% absorbed⁶, however only about 34% may actually be converted to free selenomethionine after absorption⁷.  

Other sources of selenomethionine from selenium enhanced yeast include Puritan Pride (200mcg absorbable tabs made from “baker’s yeast”) and Doctor’s Best (200mcg selenium and 200mg CoQ10 in capsules with selenomethionine made from Saccharomyces cerevisiae yeast). California Gold Nutrition, Neurobiologix, Thorne Research, Now Foods, and Bluebonnet Nutrition make a yeast-free 200mcg selenomethionine capsule.  Source Naturals, makes a yeast-free 200mcg selenomethionine tablet.

The Food and Nutrition Board (FNB) of the U.S. Institute of Medicine has set the tolerable upper intake levels (UL) for selenium based upon age, including both selenium obtained from food and selenium obtained from supplements, as indicated in Table 1⁶.

Table 1. Tolerable Upper Intake Level (UL) for Selenium6
Age  Group	UL (mcg/day)
Infants 0 - 6 months	45
Infants 6 - 12 months	60
Children 1 – 3 years	90
Children 4 – 8 years	150
Children 9 – 13 years	280
Adolescents 14-18 years	400
Adults 19 years and older	400

Symptoms of Chronic Mercury Toxicity and Selenium Deficiency

The risk of hypothyroidism is increased with exposure to mercury and/or selenium deficiency because a selenoenzyme (e.g. iodothyronine deiodinase) is required to make the thyroid bioactive hormone T3 from prohormone T4⁸.  Mercury both inhibits this enzyme and slows its production by creating a selenium deficiency⁹.  Symptoms of hypothyroidism, mercury toxicity and selenium deficiency all include:

·         Memory Loss

·         Fatigue

·         Brain Fog

·         Muscle Weakness

Mercury and/or selenium deficiency also causes a number of additional symptoms not seen in hypothyroidism:

·         Physical Tremors¹⁰

·         Seizures¹¹

·         Impaired Language Skills^12-15

·         Impaired Psychomotor Functions^12-15

·         IQ Loss in Children^16,17

·         Mild Cognitive Impairment in Adults^17,18

Outcomes associated with prenatal mercury exposure include the loss of IQ points, and decreased performance on tests, including memory, attention, language skills, visuospatial cognition and psychomotor fuctions^12,13. Outcomes associated with prenatal selenium deficiency also include both impaired language skills and psychomotor function^14,15.

Acute Mercury Toxicity

When exposed to a large dose of mercury during a relatively short time period you should seek immediate medical assistance.  There are some chelating agents for mercury that work faster than selenomethionine.  For instance, severe elemental mercury poisoning has been managed by a combination of selenium and N-acetylcysteine (NAC) ¹⁹. 

  

FACEBOOK GROUP: If you would like to learn more my wife Laurie Adamson has set up a facebook group 'Mercury Detox using the Selenium Method'   https://www.facebook.com/groups/341263176792506/

References

1)      Spiller, H.A.; Rethinking mercury: the role of selenium in the pathophysiology of mercury toxicity; Clin. Toxicology; DOI: 10.1080/15563650.2017 . 1400555 (2017) http://dx.doi.org/10.1080/15563650.2017.1400555

2)      Ralston, N.C.V., et al.; Dietary and tissue selenium in relation to methylmercury toxicity; Neurotoxicology; 29:802-11 (2008)

3)      Ralston, N.C.V., et al.; Importance of molar ratios in selenium dependent protection against methylmercury toxicity; Biol. Trace Elem. Res.; 119:225-268 (2007)

4)      Glaser, V., et al.; Diphenyl diselenide administration enhances cortical mitochondrial number and activity by increasing hemeoxygenase type 1 content in a methylmercury-induced neurotoxicity mouse model; Mol. Cell Biochem.; 390:1-9 (2014) 

5)      Li, Y-F, et al.; Organic selenium supplementation increases mercury excretion and decreases oxidative damage in long-term mercury exposed residents from Wanshan, China; Environ. Sci. Technol.; 46:11313-18 (2012)

6)      Food and Nutrition Board, Institute of Medicine, Selenium. Dietary reference intakes for vitamin C, vitamin E, selenium, and carotenoids. Washington, D.C.: National Academy Press; 284-324 (2000)

7)      Reyes, L.H., et al.; Selenium bioaccessibility assessment in selenized yeast after “in vitro” gastrointestinal digestion using two-dimensional chromatography and mass spectrometry; J. Chromatogr. A.; 1110(1-2):108-116 (2006)   

8)      Peeters, R.P. and Visser, T.J.; Metabolism of thyroid hormone; NCBI Bookshelf (2017) https://www.ncbi.nlm.nih.gov/books/NBK285545/

9)      Pantaleao, T.U., et al.; Effect of thimerosal on thyroid hormones metabolism in rats; Endocr. Connect; Nov.; 6(8):741-7 (2017)

10)  Lucchini, R.G. and Hashim, D.; Tremor secondary to neurotoxic exposure: mercury, lead, solvents, pesticides; Handb. Clin. Neurol.; 131:241-9 (2015)

11)  Wirth, E.K., et al.; Neuronal selenoprotein expression is required for interneuron development and prevents seizures and neurodegeneration; The FASEB J.; Nov.; 844-52 (2009)

12)  Bose-O’Reilly, et al.; Mercury exposure and children’s health; Curr. Probl. Rediatr. Adolesc. Health Care; Sept.; 40(8):186-215 (2010)

13)  Grandjean, P., et al.; Cognitive defict in 7-year-old children with prenatal exposure to methylmercury; Neurotoxicology and Teratology; 19(6):417-28 (1997)

14)  Polanska, K., et al.; Selenium status during pregnancy and child psychomotor development – Polish mother and child cohort study; Pediatric Res.; 79(6):863-69 (2016)

15)  Skroder, H.M., et al.; Selenium status in pregnancy influences children’s cognitive function at 1.5 years of age; Clin. Nutr.; Oct.; 34(5):923-30 (2015) 

16)  Ralston, N.V. and Raymond, L.J.; Dietary selenium’s protective effects against methylmercury toxicity; Toxicology;  Nov.; 278(1):112-23 (2010)

17)  Cardoso, B.R., et al.; Effects of Brazil nut consumption on selenium status and cognitive performance in older adults with mild cognitive impairment: a randomized controlled trial; European J. Nutr,; Feb.; 55(1):107-16 (2016)

18)   Weil, M., et al.; Blood mercury levels and neurobehavioral function; JAMA; Apr.; 293(15):1875-82 (2005)

19)   Spiller, H.A., et al.; Severe elemental mercury poisoning managed with selenium and N-acetylcysteine administration; Tox. Comm.; 1(1):24-28 (2017)

Seizures and Aluminum

Excerpt from the book by Dennis N Crouse, PhD titled 'Silica Water, the Secret of  Healthy Blue Zone Longevity in the Aluminum Age'   This book is available on Amazon. 

Seizures

Epilepsy is a condition in which seizures occur on a repeated basis. Seizures occur in the brain when too many nerve cells “fire” too quickly creating what has been referred to as an “electrical storm”.  There are over 40 different types of seizures.  Symptoms can either include convulsions, such as in tonic-clonic (a.k.a. grand mal) seizures, or no convulsions, such as in absence (a.k.a. petit mal) seizures. Other symptoms of seizures include: confusion, fainting, blackouts, blank staring, sudden and unexplained falls, episodes of blinking and chewing at inappropriate times.

The highest incidence rates of epilepsy have been reported in children particularly in the first few years of life³⁷¹. Currently the worldwide annual incidence rate of epilepsy is 68 per 100,000 people and in the U.S. the annual incidence rate is 35.5-38.6 per 100,000 people³⁷².  The Epilepsy Foundation estimates there are 326,000 children in the U.S. who have been diagnosed with epilepsy making it the 4^th most prevalent neurological disease. Epilepsy not only lowers the quality of life of those who suffer its symptoms but also has a negative impact on their longevity. Two recent studies in Nova Scotia and the Netherlands have found that children with epilepsy are 5 to 9 times more likely to die than healthy children^373-374.             

It is well known that aluminum causes seizures in monkeys and humans:   In 1954 it was reported that three months after aluminum hydroxide is injected in the brains of rhesus (macaca mulatta) monkeys, chronic epileptic seizures are observed in the monkeys that by EEG correlate with those in humans³⁷¹.  In 1978 chronic temporal lobe seizures were induced in 11 monkeys with bilateral implantation of aluminum hydroxide in their hippocampi³⁷². The hippocampus is a known hotspot for aluminum accumulation²⁶⁶.  In 1982 chronic absence seizures (a.k.a. petit mal epilepsy) were induced in juvenile rhesus monkeys with bilateral implantation of aluminum hydroxide in their thalami³⁷³.  Aluminum induced chronic epileptic seizures in monkeys have been shown to spontaneously continue for at least 7 years³⁷⁴.

Aluminum encephalopathy is a neurological condition usually occurring in humans undergoing regular dialysis treatment due to aluminum accumulation in the brain³⁷⁵. Epileptic seizures are observed in 57% of those diagnosed with aluminum encephalopathy³⁷⁶.  Dialysis-associated seizures were seen in 7.2% of 180 children and adolescents on regular dialysis treatment³⁷⁷.   Seizures have also been observed after 6 months of occupational exposure to aluminum and 36 to 42 days after the use of aluminum containing bone cement during brain surgery^378,379.  Serum aluminum concentration is normally less than 1mcg/L but in the case of the occupational aluminum exposure, serum concentration was 22mcg/L and in the cases of exposure to aluminum containing bone cement it was 4.4 to 4.3mcg/L^378,379.  

371.        Kopeloff, L.M., et al.; Chronic experimental epilepsy in Macaca mulatta; Neuology, 4:218-227 (1954)

372.        Soper, V., et al.; Chronic alumina temporal lobe seizures in monkeys; Exp. Neurology; Oct.; 62(1):99-121 (1978)

373.        David, J., et al.; Behavioral and electrical correlates of absence seizures induced by thalamic stimulation in juvenile rhesus monkeys with frontal aluminum hydroxide implants: A pharmacologic evaluation; J. Pharmacological Methods; May; 7(3):219-229 (1982)

374.        Ward, A.A.; Topical convulsant metals. In: Experimental models of epilepsy. A manual for the laboratory worker, eds. D.P. Purpura, et al.; pp.13-35 New York: Raven Press (1972)  

375.        Alfey, A.C.; Aluminum toxicity in patients with chronic renal failure; Ther. Drug Monit.; 15:593-97 (1993) 

376.        Elger, C.E., et al.; Therapeutic problems in patients suffering from aluminum encephalopathy; Neuroimmunologie spinale krankenheiten neuropsychologie metalische enzephalopathien neurologische notfalle interventionelle neuroradiologie verhandlungen der deutschen gesellschaft fur neurologie; 4; K. Poeck, et al. editors; Springer (1987)

377.        Glenn, C.M., et al.; Dialysis-associated seizures in children and adolescents; Pediatr. Nephrol.; 6(2):182 (1992)

378.        Freiman, S.B., et al.; Seizure and elevated blood aluminum in a remelt furnace operator: connection of coincidence?; Am. J. Emergency Med.; May; 23(3):419-20 (2005)

379.        Hantson, P.H., et al.; Encephalopathy with seizures after use of aluminum-containing bone cement; The Lancet; Dec.; 344:1647 (1994)

as 4.4 to 4.3mcg/L^378,379.