Mercury, Dental infections, Selenium, Magnesium, Potassium, Root canals, Adrenal fatigue, Chronic illness

USE BIO AND PHOTO from April 2019 (re: email)

“Adrenal Fatigue”: Does It Exist?

By Alfred V. Zamm, MD

“Despite the fact that the patient was seen by the best medical minds in Europe—he survived.” Voltaire (1694-1778)

This is a single case report, a description of how dental mercury interfered with a patient’s defense mechanism against an infection (primary atypical pneumonia) and permitted the infecting organism to persist as a lifelong intracellular denizen resulting in symptoms that would not be readily connected to the original infection, symptoms that included those of hypoadrenalism, yet without measurable adrenal failure. This report describes the measures taken to diagnose and mitigate this illness.

K had been lied to: He had been made ill as a result of egregious medical deceptions. The following is an account of K’s medical odyssey, an adventure that involved a series of scientific medical reports, clinical observations, anamnesis, anecdotes, and conjectures describing how he was rescued from medical misinformation—and survived.

When K was 13, the first deception occurred: he received an “amalgam” dental filling (dental amalgam contains 50% mercury, a poison). As a result of K’s constant exposure to the mercury emanating from this and later fillings and its bodily accumulation, he was sick for the rest of his life (allergies, asthma, migraine headaches, fatigue…). It took 30 years, more amalgam fillings, a variety of physicians, and his determination before the diagnosis of mercury poisoning was finally made.^1-7

Not only is mercury poisonous directly to the metabolic process, it also combines with the essential trace element selenium, thus depriving the body of selenium and its function in the defense enzyme glutathione peroxidase (a defense against tissue hydrogen peroxide).

It defies credibility that licensed dental professionals, the dental and medical professional organizations, and the Food and Drug Administration (both dental and medical divisions) allow the prescribing of mercury, a known poison. This is a gross abrogation of responsibility by all of these professional organizations acting in unison as a cabal of professional miscreants foisting a toxic substance on a trusting public—a public that doesn’t have the technical knowledge to defend itself—and telling them a poison is not a poison.

Root Canals

The next deception consisted of more professionally prescribed poison: the insertion of two “root canals” that further degraded K’s health.

Root canals have at least three health problems: (1) they are very frequently (always?) infected, and hence a source of microbiologically derived cytotoxic and immune dysregulating substances; (2) they are endodontically executed using xenobiotic and cytotoxic substances that are potentially immune dysregulating; and (3) I question whether there has been adequate scientific proof (double blind crossover studies) of the safety of the materials used in the “root canal” (endodontic) procedure.^8-22

Trying to Help

Dental help: I advised K to have the mercury-containing fillings removed and replaced with biologically inert materials, first with gold, which resulted in some improvement. The gold was then replaced with non-metallic, non-electrically conductive zirconium, when dental zirconium became available; zirconium provided further improvement. I additionally advised K to have his two “root canalled” teeth extracted and replaced with zirconium dental bridges. More improvement ensued but still not a restoration of his original health.

Chemical help: I advised K to take inorganic selenium in the form of sodium selenite solution (Allergy Research Group). Only the inorganic form of selenium and not the organic form has the chemical ability to substantially bind and inactivate mercury; this provided K with further benefit. Note: Regarding the ambient, unavoidable environmental pollution by cadmium, arsenic, and some other toxic heavy metals, selenium is also protective against these toxic metals.

Selenium also happens to be a nutritionally essential trace element whose only known enzyme function in the human body is its role in the detoxification process of glutathione peroxidase (vide supra).

Why Don’t Tuna Get Sick? A reader of the Journal of the American Medical Association asked: Since tuna, being predatory fish at the top of their food chain, and as a result have a high level of mercury in their tissues, why don’t they get sick? The expert replied: In addition to accumulating mercury, tuna accumulate selenium in a molecular ratio of 1:1 with mercury, and this is an amount sufficient to negate mercury’s ability to be toxic to the tuna.²³ (Nature figured out that selenium is safe and effective in protecting life against mercury poisoning.)

This inorganic form of selenium is innocuous and salubrious at a daily dose of 60 mcg. (micrograms) (1 ½ ml.) per day when taken on an empty stomach (vide infra) and is irreplaceable in its ability to benefit patients who have been poisoned by mercury. There is no equivalent substitute for it.^24-27 The sidebar contains an instructional form that I have provided to patients in conjunction with my prescribing selenium. Readers are welcome to employ it.

Infection as a Pernicious Force in K’s Health. K had contracted primary atypical (non-streptococcal) pneumonia in his mid-20s. Primary atypical pneumonia is commonly caused by intracellular organisms (e.g., viruses or Chlamydia) or extracellular organisms (e.g., Mycoplasma).

K’s immune system had been weakened by mercury (mercury lowers the T-cell count).²⁸ Rather than completely vanquishing the invading microorganism, as might have happened with a healthy defense mechanism, K’s impaired mercury-poisoned immune system could not prevent the infecting microorganism from establishing itself as a persistent subclinical intracellular lifelong troublemaking denizen.

K had objective evidence of a chronic subclinical infection: he had developed chronically swollen lymph nodes (lymphadenopathy) after his encounter with primary atypical pneumonia.

More clues supporting a diagnosis of a chronic lifelong infection: Throughout his life, K had taken various antibiotics for miscellaneous infections, each episode of consumption an antibiotic was followed by a temporary minimal improvement of his symptoms. Once, he received a smallpox vaccination, which was also followed by temporary minimal improvement of his symptoms. These therapies had two temporary benefits: (1) The antibiotics temporarily lowered the load on K’s already microbiologically burdened immune system; and (2) The smallpox vaccination temporarily raised the activity of his immune system. Clinically, it appeared that a persistent subclinical residual infection was an operative force in K’s lifelong illness and his symptoms of hypoadrenalism among other symptoms.

Intracellular microorganisms can hide behind a cell membrane and become invisible to the immune surveillance system, persist for the life of the victim, induce a pernicious inefficiency into cellular metabolism, and result in an elusive variety of protean clinical manifestations often not connected to the instigating surreptitious occult culprit. Some examples of this dynamic are the following:

1. Cardiovascular disease and microorganisms (viruses or bacteria)^29,30

2. Diabetes II and Hepatitis C virus³¹

3. Hypothyroidism and Hepatitis C virus ^2,33,34

4. Cancer of the cervix and Human Papillomavirus³⁵

5. Cancer of the oral cavity and Human Papillomavirus³⁵

6. Crohn’s disease and Herpes simplex virus I and II³⁶

7. Food allergies³⁸

The following essential digression is taken to share with the reader a remarkable revelation in regard to reference 36 in number 6, listed above, (U. Rüther et al) and intracellular organisms that have surprising clinical outcomes: the authors of this article recount how their patient was rescued from imminent perilous surgery for Crohn’s disease and the induction of sustained subsequent benefit by prescribing a simple generic, inexpensive, readily available, anti-viral medication, acyclovir—a disease for which this medication is not a designated use. This article supplies an explanation for the mechanism by which acyclovir resulted in this remarkable and first recorded benefit for a Crohn’s disease sufferer. I suspect that acyclovir may also be effective in ulcerative colitis and other diseases, associations yet to be revealed. (A trial of acyclovir with K was inconclusive, as K did not tolerate acyclovir and it had to be discontinued.)

Parenthetically (another digression), the essential amino acid L-lysine (not mentioned in the article) might have additionally benefited this patient with Crohn’s disease, as it competitively inhibits arginine, an essential nutrient for the replication of herpes virus I and II.³⁷ (A trial of L-lysine with K was inconclusive.)

Infections from microorganisms can also play a role in food allergies.³⁸ It is conjectured that chronic infection reduces the magnitude of the electrical charge (voltage) on the secretory IgA molecule, which sits on the surface of the gastrointestinal membrane; this reduction in voltage will permit food allergens to gain entry into the body and induce the development of allergies.

Nutrition: K was prescribed a nutritional improvement program (foods, vitamins, minerals); some improvement ensued, yet his problems persisted.

K’s Environment: His household environment was improved.³⁹ More benefit ensued, but recovery did not occur.

Prophylactic Anti-inflammatory Therapy: Aspirin (one-quarter of the standard 325 mg. tablet [approximately equal to 81 mg.]) was prescribed on a daily basis to mitigate inflammation from the conjectured chronic infection; the aspirin was substantially beneficial on a long-term basis. The frequency of this dose of aspirin, 81 mg., was raised to a daily dose from the less frequent dose mentioned in the referenced article, and the suggested addition of calcium carbonate for alkalization to mitigate the acidic effect of aspirin was found to be counterproductive and was eliminated because the aspirin was taken with a meal (the calcium carbonate’s lowering of the stomach acid is deleterious to the digestive process).⁴⁰

Other Opinions: In consideration of K’s recalcitrant and unresolved affliction, I advised him to obtain more opinions by conferring with board-certified internists of professorial rank. These professors did fine investigations and all the findings were reported as being “within acceptable statistical range;” and there were no recommendations for treatment. The examinations and tests were “healthy”; the patient was not.

A Big Clue

K reported that he craved and was clinically benefited by ingesting green leafy vegetables (even though he employed a program of sufficient and salubrious foods, vitamins, and minerals). This craving wasn’t just a minor craving; he bought pounds of all sorts of green leafy vegetables, used a kitchen blender to grind them into a slurry, which he then boiled down to a concentrate. This green super food worked: he felt remarkably improved—but why did it work?

An Epiphany

One day, while I was mulling over K’s idiosyncratic green-leaf craving, a graphic picture of the chemical structure of chlorophyll vividly appeared in my mind: a complex molecule assembled from four pentagons, and each pentagon was composed of carbon and nitrogen—all four of these structures were symmetrically arranged around a single central atom of magnesium, similar to the four sails of a windmill around a central point.

What if K was not craving chlorophyll per se but was craving the centerpiece of the chlorophyll molecule, the magnesium? Yes, he had had tests of his serum magnesium and his red blood cell magnesium (both of these are tests of extracellular magnesium); both results were “within a statistically acceptable range,” but what did these results really mean? Was this another medical deception–more healthy test results about an unhealthy person—or did K really have an intracellular hypomagnesium state, a condition inside the cells that these tests could not measure? Were these extracellular blood tests accurate only about the outside of the cell but were misleading about the inside of the cell?

Interesting fact: Only 1% of the body’s magnesium is outside of the cells—the rest (99%!) is inside the cells where it cannot be measured by tests available to the practitioner. Over 300 metabolic reactions depend on magnesium (magnesium is not only important, it is critical). To say “everything runs on magnesium” would be close to the truth.

Based on the magnitude of K’s idiosyncratic green leaf cravings and despite his “healthy” tests for extracellular magnesium, I suspected that K really did have low intracellular magnesium, and I owed it to K to make a diagnosis one way or the other. Since we have established that I couldn’t measure the magnesium level inside of K’s cells, how was I to determine the truth of K’s situation?

I prescribed a test of K’s actual in vivo magnesium status, the so-called “therapeutic trial.” This involved K taking magnesium in a controlled stepwise living test and observing what clinically occurred. K’s health dramatically improved when he took magnesium; his green-leaf craving ceased, he stopped being a “chlorophyll chef,” and another deception was revealed (the false assumption about his intracellular magnesium status based on conventional magnesium testing).

Note: The symptoms K had that are conventionally associated with hypoadrenalism (vide infra) became mitigated or disappeared when he continued taking magnesium—yes, magnesium is involved with everything (almost).

I suspected that the organism of K’s conjectured intracellular infection, acquired via his primary atypical pneumonia episode, was the metabolic burden that was impeding his internal chemistry and inducing symptoms similar to those of hypoadrenalism (among other symptoms); the therapeutic addition of magnesium compensated for this microbial burden, thereby mitigating K’s symptoms.

How Magnesium Titration Was Done

K was initially prescribed magnesium as magnesium gluconate starting with a daily dose of 50 mg of elemental magnesium b.i.d., p.c. Then the magnesium dose was incrementally raised every day by 50 mg. of elemental magnesium b.i.d., p.c. It wasn’t until he received the daily dose of 400 mg. of elemental magnesium (200 mg. b.i.d., p.c.) that his health subjectively started to improve.

The magnesium titration is very safe when one follows this titration protocol; the end point is the dose that produces sufficient clinical benefit or the first appearance of slight diarrhea. At this point the practitioner should stop raising the daily dose, reduce the daily dose, and future dosage should be guided by ongoing clinical observations. Magnesium is connected to the absorption and metabolism of potassium (another element found in higher concentration inside the cell than outside the cell). K was prescribed 80 mg. of elemental potassium as potassium gluconate b.i.d., p.c. Magnesium is also connected to the absorption and metabolism of other minerals. (This connection between magnesium and other minerals is a story that I will have to leave for another article.)

A Medical Detective Story

I decided to move the investigation forward by collecting a list of clues, i.e., signs and symptoms, and to write them down in a manner of a detective collecting notes at a crime scene. Here are my crime scene notes.

Clue #1, K’s tan: K’s face had an unexplained “tan;” even in the winter, he would often be complimented on his healthy-appearing “winter tan” and would be asked if he had recently returned from a vacation in Florida or the Caribbean.

Clue #2, Salt craving: K reported that once, while eating a porkchop he, being distracted, had “breaded” the pork chop with a layer of salt so generous that the pork chop had acquired a saline carapace, a pork chop that he nevertheless enjoyed eating in its hypersalinated state. K enjoyed eating heavily salted foods; he was a salt craver.

Clue #3, Low blood pressure: K had low blood pressure. He would become more tired after he had laid down to rest (a drop in blood pressure) than he was before he had “rested”—counterintuitive. “Dizziness and unsteadiness” would occur if he arose rapidly from a supine position (orthostatic hypotension). His blood pressure measurements were always at the lower end of acceptability.

Clue #4, Fatigue: Easy fatiguability on exercise and chronic moderate fatigue

Clue #5, Faulty glucose metabolism: Episodes of hypoglycemia.

Clue #6, Hypocholesterolemia: Hypocholesterolemia can be found in true hypoadrenalism; K’s cholesterol level was at the low margin of statistical acceptability.

Any third-year medical student would have said, “Mr. K, you have hypoadrenalism.” The student would have been right (the symptoms) but wrong (the disease)—vide infra.

On the basis of these assembled clues, I referred K to a Harvard Medical School professor of endocrinology who specialized in and wrote definitive articles about adrenal disease. The professor did a fine comprehensive investigation, including the requisite standard test to measure how well his adrenal glands functioned: the provocative test of the adrenal glands using an ACTH-like substance, Cortrosyn (Organone Pharmaceuticals). Cortrosyn is the synthetic active portion of the adrenocorticotropic hormone (ACTH molecule) that is composed of 24 amino acids rather than the actual whole ACTH molecule, which is composed of 39 amino acids (this smaller molecule acts faster and is less allergenic). K’s bete noire reappeared: the test result was reported as within the statistically acceptable range, the summation of the professor’s evaluation was that K’s overall health was without objective evidence of pathology, and once more K was not sick and sick at the same time.

Despite this excellent professorial investigation certifying K’s objective good health, still K did have symptoms similar to those found in hypoadrenalism, and his illness had not been explained by this revered professor. My next step: Get another opinion about the first opinion. I sent him to another full professor of endocrinology at another prestigious medical school where K had another fine and erudite medical investigation, and he received another authoritative report confirming that the tests of his adrenal glands and all other tests were within the statistically acceptable range; he was once more without objective evidence of medical pathology.

All of these fine physicians, their comprehensive tests, and their venerable academic analyses did not advance my knowledge of K’s illness, but at least these investigations did rule out actual hypoadrenalism.

A Microbial Hypothesis

The etiology of K’s symptoms of hypoadrenalism, “adrenal fatigue,” appeared to have nothing to do with “adrenal,” but rather appeared to be due to a metabolic defect induced by a chronic microbial intracellular denizen that resulted in some of the symptoms of hypoadrenalism but without actual hypoadrenalism. In this regard, one or more of the following three etiological possibilities help me to think about the etiology of K’s condition:

1. An infection-induced defect in the cell’s glucocorticoid receptor so that when cortisol alights upon it, an impaired signal is generated by the receptor that in turn distorts the targeted metabolic process.

2. An infection-induced epigenetic defect (a genetic lesion) that results in an impairment of the genetic control mechanism of cellular metabolism.

3. An infection-induced direct interference in metabolism.

Summary of the Ameliorative Therapies That K Received

The removal of poisons (mercury-containing amalgam dental fillings, root canals), the neutralizing of some of the residual mercury with selenium and selenium-aided repletion of glutathione peroxidase, a raising of K’s intracellular magnesium and intracellular potassium to compensate for the infection-induced burden on K’s metabolism, a nutritional program, an improvement of K’s environment, and the use of prophylactic aspirin—altogether allowed K to at least deal with his apparent microbially induced metabolic inefficiency and permitted him to function substantially more efficiently.

The author reports that he does not have any conflicting interests.

Thanks to Ms. Judith Kistler for her help with the preparation and editorialization of this manuscript.

References

1. Eggleston DW. Effect of dental amalgam and nickel alloys on T-lymphocytes: Preliminary report. J. Prosthetic Dentistry. 1984; 51-617-23.

2. Pleva J. Mercury poisoning from dental amalgam. J. Orthomol Psychiat. 1983; 12:184-93.

3. Koller, LD: Immunosuppression produced by lead, cadmium, and mercury. Am. J. Vet. Res. 1973; 34:1457-58.

4. Lawrence DA. Heavy metal modulation of lymphocyte activities. In vitro effects of heavy metals on primary humoral immune response. Toxicol. Appl. Pharmacol. 1981; 57:349-451.

5. Gilman AG, et al (eds). Goodman and Gilman’s The Pharmacological Basis of Therapeutics, 8^th ed. New York, NY: Pergamon Press, 1990; 1598-1602.

6. Hahn LJ, et al. Dental “silver” tooth fillings: a source of mercury exposure revealed by whole-body image scan and tissue analysis. The FASEB Journal. 1989; 3:2641-2646.

7. Hahn LJ, et al. Dental “silver” tooth fillings: a source of mercury exposure revealed by whole-body image scan and tissue analysis. The FASEB Journal. 1989; 3:2641-2646.

8. Nagaoka S., et al. Bacterial invasion into dentinal tubules of human vital and nonvital teeth. J Endod. 1995; Feb;21(2):70-3, PMID: 7714440.

9. Uchin RA, Parris L. Antibacterial activity of endodontic medications after varying time intervals within the root canal. Oral Surg. 1963; 16:608-1

10. Tronstad L, et al. Controlled release of medicaments in endodontic therapy. Endod Dent Traumatol. 1985; 1:130-4.

11. Engstrom B, Spangbert L. Studies on root canal medicaments. 1. Cytotoxic effect of root canal antiseptics. Acid Odontol Scand. 1967; 25:77-84.

12. Spangbert L, Engstrom B. Studies on root canal medicaments. 11. Antimicrobial effect of root canal medicaments. Odontol Revy 1968; 2:187-95.

13. Moller AJR. Microbial examination of root canals and peripical tissues of human teeth. Thesis. Odontol Tidskr (Special Issue) 1966; 74:1-380.

14. Bystrom A, Claesson R, Sundqvist G. The antibacterial effect of camphorated paramonochlorphenol, camphorated phenol and calcium hydroxide in the treatment of infected root canals. Endod Dent Traumatol. 1985; 1:170.

15. Tronstad, L, et al. pH changes in dental tissues following root canal filing with calcium hydroxide. An experimental study in monkeys. J Endod .1981, 7:17-21.

16. Baumgartner JC, Heggers JP, Harrison JW. The incidence of bacteremias related to endodontic procedures. 1. Non surgical endodontics. J. Endodon 1976; 2:135-40.

17. Debelian GJ, Olsen I, Tronstad L. Bacteremia in conjunction with endodontic therapy. Endodontics & Dental Traumatology. 1995; June; 11: 3: 142-149.

18. Debelian GJ, Olsen I, Tronstad L. Electrophoresis of whole-cell soluble proteins of microorganisms isolated from bacteremias in endodontic therapy. European Journal of Oral Sciences 1996; October-December;104: 540-546

19. Debelian GJ, Olsen I, Tronstad L. Anaerobic bacteremia and fungemia in patients undergoing endodontic therapy: an overview. Annals of Periodontology. 1998; 3:281-287.

20. Chaudhry R, et al. Anaerobic flora in endodontic infections The Indian Journal of Medical Research. 1997; 105: 262-265.

21. Baumgartner JC, Falkler WA Jr. Bacteria in the apical 5 mm of infected root canals. Journal of Endodontics. 1991: 17:380-383.

22. Oguntebi BR. Dentine tubule infection and endodontic therapy implications. International Endodontic Journal. 1994; 27: 218-222.

23. Jukes TH. When Friends or Patients Ask About… Mercury in Fish. JAMA. 1975;233:1001-1002.

24. Parizek J, Ostadalova I. The protective effective effects of small amounts of selenite in sublimate intoxication. Experientia .1967; 23:142-3.

25. Ganther HE, et al: Selenium: Relation to decreased toxicity of methyl-mercury added to diets containing tuna. Science. 1972; 175:1122-1124.

26. Koeman JH, et al: Mercury-selenium correlations in marine mammals. Nature. 1973; 245:385-386.

27. Kosta L, Byrne AR, Zelenko V. Correlation between selenium and mercury in man following exposure to inorganic mercury. Nature. 1975; 4:238-239.

28. Eggleston, ibid

29. Hemmat N, Ebadi A, Badaizadeh R, et al: Viral infection and atherosclerosis. Eur J Clin Microbiol Infect Dis. 2018; 37:225-2233. DOI: 10.1007/s10096-018-3370-z.

30. Campbell LA, Rosenfeld ME. Infection and atherosclerosis development. Arch Med Res. 2015 Jul;46:339-50. DOI: 10.1016

31. Ba-Essa EM, Mobarak EL Abd Elrahman S: Frequency and factors associated with hepatitis C virus infection among patients with diabetes, Dammam, KSQ. J Egypt Public Health Assoc. 2016 91:53-8. DOI: 10.1097/01.

32. Ferri C, et al. Thyroid involvement in hepatitis C virus-infected patients with/without mixed cryoglobulinemia. Front Endocrinol (Lausanne). 2017; 8:159. DOI: 10.3389/fendo.2017.00159.

33. Antonelli A, et al. Endocrine manifestations of hepatitis C virus infection. Nat Clin Pract Endocrinol Metab. 2009; 5:26-34. DOI: 10.1038/ncpendmet 1027.

34. Colaci M, et al. Endocrine disorders associated with hepatitis C virus chronic infection. Rev Endocr Metab Disord; 2018; 19:397-403. DOI: 10.1007/s11154-108-9475-y.

35. Haedicke J, Iftner T. Human papillomaviruses and cancer. Radiother Oncol, 2013; 108:397-402. DOI: 10.1016/j.radonc.2013.06.004.

36. Rüther U, et al. Herpes simplex-associated exacerbation of Crohn’s disease. Successful treatment with acyclovir. Dtsch Med Wochenschr. 1992; 10:46-50. DOI: 10.1055/s-2008-1062278. PMID 1309692.

37. Griffith RS, DeLong DC, Nelson JD. Relation of argenine-lysine antagonism to herpes simplex growth in tissue culture. Chemotherapy, 1981;27 (3):209-13. DOI: 10.1159/000237979. PMID 6262023.

38. Zamm A. A clinical case-based hypothesis: Secretory IgA operates as an electronic transistor controlling the selection or rejection of molecules in the absorption process in the lumen of gastrointestinal tract. Clin Exp Gastroenterol. 2013; 6:177-184. DOI: 10.2147/CEG.S47772. PMID 24068871.

39. Zamm A. Why Your House May Endanger Your Health. New York, NY: Simon & Schuster,1980.

40. Zamm A. Successful treatment of universal reactors with prophylactic aspirin, a preliminary report. J Ortho Med Vol 3 No 2, 2^nd quarter 1988, 44-46.

SIDEBAR

How and Why to Use Selenium

Some chemically sensitive and mercury-poisoned patients improve with the use of selenium. The response to the use of selenium can be divided into three clinical groups.

GROUP 1: They experience immediate benefit within the first few days. These patients feel better, stronger, and are more tolerant of xenobiotic chemicals.

GROUP 2: They improve slowly. These patients may not be aware of their slow progress until they realize that they can tolerate tobacco smoke and other xenobiotic exposures without deleterious results. Their symptoms decrease gradually in duration and magnitude.

GROUP 3: They initially react in an apparently unfavorable way. These patients are generally the most sensitive, the most debilitated, and those most in need of selenium; but they are initially unable to deal with it. It takes longer for these patients to receive benefit. It often can take these ultrasensitive patients up to six months of being free of their mercury fillings before they start to tolerate and benefit from selenium. At that point they find that they can begin to increase the amount of selenium they are taking. This may be because selenium combines with heavy metals, forming compounds that these sensitive patients may not tolerate.

Selenium is not a medicine. It is not a prescription item. It is an essential nutrient and is sold over the-counter. It is found in many over-the-counter vitamin preparations. The difference between taking selenium in a chemically pure liquid form and merely taking a selenium tablet or selenium mixed with other vitamins and minerals is that by taking selenium in solution, considerably more selenium is absorbed.

Selenium is needed in very small amounts. This means that other minerals, which are found in relatively huge quantities when compared with the amount of selenium present, “overwhelm” the absorption of the small amount of selenium, and the patient who takes selenium in a tablet form or in a vitamin-mineral mixture or with food is able to obtain very little of the selenium he swallowed.

Selenium must be taken on an empty stomach. Other substances found in foods bind to selenium and prevent its absorption.

Selenium is essential for everyone, but it is especially important to patients who have difficulty dealing with environmental xenobiotics and are mercury-poisoned from dental fillings.

l. Selenium binds with and neutralizes poisonous heavy metals found in the environment such as mercury, arsenic, and cadmium; this is especially helpful in regard to the mercury that leaches out of dental fillings.

2. Selenium is an essential part of the xenobiotic (harmful chemical) detoxification system:

1. Selenium is part of glutathione peroxidase, an important. enzyme that the body uses to detoxify harmful chemicals.

2. Mercury leaching out from dental fillings produces another problem in addition to supplying mercury as a poison. Mercury binds with selenium, thus depriving the patient of available selenium. The patient becomes “selenium starved” and can no longer manufacture adequate amounts of glutathione peroxidase. Supplying selenium overcomes this problem.

How to Take Selenium Solution

Remember: Always take selenium solution on an empty stomach!

Transfer some selenium solution from the stock bottle you purchased at the pharmacy into the glass dropper bottle using a plastic funnel. Do not use a metal funnel, as it may react with the selenium.

For GROUPS 1 and 2: When you get up in the morning:

1. Dissolve the drop(s) (see below) in 2 oz. water

2. Drink the selenium solution before you swallow any food or take any vitamins or medication

3. By the time you are ready to have your breakfast (after 5-10 minutes later) you will have absorbed a good deal of the selenium, without the interference or neutralization by any stomach contents.

Suggested schedule for Groups I and 2 to take selenium

(A total of 1 1/2 droppers. Using 3 half droppersful is more practical than trying to fill a dropper completely, as the air trapped in the glass tube in the dropper may prevent complete filling.)

On Day 12 and each morning thereafter: Continue at this dose–.you will have reached the daily maintenance dose.

For GROUP 3: The patients in Group 3 (the most sensitive patients), should increase the dose very slowly; it may take weeks to months to substantially increase the daily dose, and they may never achieve a full dose.

Addendum

Even on small doses of selenium, some patients with arthritis become symptom-free. (Veterinarians have used selenium to treat arthritis in dogs for years.)

Selenium is protective against cancer.

Some references:

Willett WC et al. Prediagnostic serum selenium and risk of cancer. Lancet Il. July 16, 1983; 130-4.

Shamberger RJ and Willis CE. Selenium Distribution and Human Cancer Mortality. Critical Reviews in Laboratory Sciences. June 1971; 2:211-21.

Shamberger, R. Relationship of Selenium to Cancer: Inhibiting Effect of Selenium on Carcinogenesis. Journal of the National Cancer Institute. April 1970; 44:931-36.

©Alfred V. Zamm, MD, 2000