ImmuNova

Mineral Supplements and Viral Infections and Conditions

How minerals and mineral supplements can help with Chronic Fatigue Syndrome, HIV/AIDS & Hepatitis C
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Viral Conditions and Minerals

THREE SERIOUS VIRAL INFECTIONS THAT THE IMMUNOVA PRODUCTS MAY HELP ALLEVIATE:

1. CHRONIC FATIGUE SYNDROME
2. HIV/AIDS
3. HEPATITIS C

1. CHRONIC FATIGUE SYNDROME

Chronic fatigue syndrome (CFS) is a newly defined syndrome that describes varying combinations of symptoms, including recurrent fatigue, sore throat, low-grade fever, and lymph node swelling, headache, muscle and joint pain, intestinal discomfort, emotional distress and/or depression, and/or loss of concentration.

Although newly defined and currently receiving a great deal of attention, CFS has in fact been mentioned in references in the medical literature all the way back to the 1860s. In the past CFS has been known by a variety of names, including: the Epstein-Barr virus (EBV) syndrome, yuppie flu, post and viral fatigue syndrome, chronic fatigue, immune dysfunction syndrome and ME.

CFS was formally defined in *1988 by a consensus panel convened by the Centres for Disease Control (CDC). Their definition was an attempt to establish a guide for evaluating patients with chronic fatigue of unknown cause by clinical physicians and researchers. (*G.P. Holmes et al, "Chronic fatigue Syndrome: A Working Case Definition," Ann Intern Med 108 (1988): 387-9.)

A VIRAL CAUSE

The prime (though still controversial) candidate as a cause of chronic fatigue syndrome is the Epstein-Barr virus, a member of the Herpes group of viruses, which include Herpes simplex types one and two. Current knowledge about EBV infection can be summarised as follows:

EBV and the Herpes-group of viruses produce latent lifelong infections.
The host's immune system normally holds this latent infection in check.
Any compromise in the immune system can lead to the reactivation of the virus and recurrent infection.
The infection itself can compromise and/or disrupt immunity, thereby leading to other diseases.
Elevated EBV antibody levels are observed in a significant number of diseases characterised by disorders in immune function.
Elevated EBV antibody levels of the herpes-group viruses, measles, and the other viruses have also been observed in patients suspected of having chronic fatigue and who also display elevated EBV antibodies.

IMMUNE RESPONSE

Most mainstream medical investigations into a possible cause of chronic fatigue syndrome have centred on the search for a viral invader like EBV, rather than reducing susceptibility and supporting the individual's immune system to deal with the organism effectively.

There is little doubt that a disturbed immune system plays a central role in chronic fatigue syndrome. A variety of immune system abnormalities have been reported in CFS patients. The most consistent abnormality is a decreased number or activity of natural killer (NK) cells.

Other consistent findings include a reduced ability of lymphocytes (a type of white blood cell that is critical in the battle against viruses) to respond to stimuli. One of the reasons for this lack of response may be a reduced activity or a decreased production of interferon, a key compound produced by the body to fight viruses. (Low levels of interferon have been commonly observed in patients with CFS.) When interferon levels are low, reactivation of latent viral infection is likely.

There are a number of underlying factors that must be addressed in the effective treatment of CFS. Most notably: depression, stress, impaired detoxification, excessive gut permeability, impaired immune function, chronic candidiasis, food allergies, hypothyroidism, hypoglycaemia, and low adrenal function.

MAGNESIUM AND CFS

Nutritional supplementation is essential in the treatment of chronic fatigue. A deficiency of virtually any nutrient can produce the symptoms of fatigue and render the body more susceptible to infection. Individuals with chronic fatigue require at the bare minimum: a high potency multiple vitamin and mineral formula, along with extra vitamin C and magnesium (500 to 1,200 mg in divided doses).

Magnesium deficiency, even if very mild, can result in chronic fatigue and exhibit symptoms similar to CFS. In addition, low red blood cell magnesium levels, a more accurate measure of magnesium status than routine blood analysis, have been found in many patients with chronic fatigue and CFS. Several studies have shown good results with magnesium supplementation.

For example, in one double-blind placebo controlled trial conducted at Southampton University's Complementary Medicine Clinic, thirty-two CFS patients received either an intra-muscular injection of a magnesium sulphate (1 gram in 2 ml of injectable water) or a placebo (2ml of injectable water) for two weeks. At the end of the study, twelve of the fifteen patients receiving the magnesium reported, based on strict criteria, significantly improve energy levels, better emotional states, and much less pain. In contrast, only three of seventeen placebo patients reported that they felt better, and only one reported an improved energy level. (I.M.Cox, M.J.Campbell and D. Dowson, 'Red Blood Cell Magnesium and Chronic Fatigue Syndrome' Lancet 337 (1991): 757-60.)

This study seems to confirm some impressive results obtained in clinical trials during the 1960s on patients suffering from chronic fatigue. These studies utilised oral magnesium and potassium aspartate (1 gram each) rather than injectable magnesium. Between 75% and 91% of the nearly 3,000 patients studied experienced relief of fatigue during the treatment with magnesium and potassium aspartate. In contrast, the number of patients responding to a placebo was between in 9% and 26%. The beneficial effect was usually noted after only four to five days, but sometimes ten days were required. Patients usually continued the treatment for four to six weeks; afterward fatigue frequently did not return. (H.Ahlborg et al, "Effect of Potassium-Magnesium Aspartate on the Capacity for Prolonged Exercise in Man," Acta Physiologica Scandinavia 74 (1968): 238-45.)

2. HIV/AIDS:

Acquired immune deficiency syndrome (AIDS) is characterised by a profound defect in cell-mediated immunity. The primary cause of AIDS is infection with the human immuno deficiency virus (HIV). The spectrum of HIV infection ranges from a person with a positive test for HIV without any signs of immune deficiency to a person with the full-blown disease, characterised by all of the now well-known components of the disease. AIDS is now viewed as a late stage of HIV infection. HIV itself does not kill; what it does do is cripple the immune system to such an extent that a person dies from severe infection or cancer.

Diagnosis of HIV is made by a positive blood test for HIV antigen and antibodies.

Diagnosis of AIDS depends on meeting certain criteria, such as:
Presence of one of the 23 opportunistic infections (an infection that is caused by a normally non infectious organism) and accounts as linked to the AIDS, or;
A positive HIV test plus a total helper lymphocyte (an important white blood cell) count (CD4 count) of less than 200 cells per micro litre, or;
A percentage of helper cells to total lymphocytes (CD8 count) of less than fourteen per cent.

HIV

HIV (human immuno deficiency virus) infection plays a major role in the progression to AIDS (acquired immuno-deficiency syndrome), but other factors, particularly nutritional status, lifestyle, and mental/emotional state, also play significant roles.

In general, since the immune system is dependant on many nutrients and minerals, deficiencies (or malnutrition) are very common in immune compromised patients, it is vitally important to supply optimum levels of all nutrients to patients, especially those with HIV/AIDS.

Electron Microscope picture of infected cell
How HIV infects and attaches to CD4 receptors on human cells (Graphic - courtesy of The Body)

ANTIOXIDANTS AND HIV

Numerous studies have shown that individuals infected with HIV have a compromised antioxidant defence system. Of all the antioxidants that show promise in slowing the progression of HIV to AIDS, vitamin C and E, selenium, magnesium and zinc have showed the greatest and most consistent effects. Several studies have shown selenium status is a major determinant of how fast HIV will progress to AIDS.

Numerous studies have shown that individuals infected with HIV have a compromised antioxidant defence system. Blood levels of antioxidants are decreased and peroxidation products of lipids (fats) and proteins are increased in these patients. This blood profile may contribute to the progression of AIDS, because antioxidants such as Glutathione (GSH) prevent viral replication, while reactive oxidants tend to stimulate the virus. Consequently, it has been suggested that HIV infected patients may benefit from an antioxidant supplementation therapy. Antioxidant therapy, especially with vitamin E and selenium does appear to slow down the progression from HIV to AIDS. (In fact, Professor Dr. E Will Taylor of the University of Georgia, Athens, Computational Centre for Molecular Structure and Design, College of Pharmacy, predicted in 1994, whilst studying the genome of HIV that: " Se (selenium) levels should be a factor in disease progression in AIDS."

He continued, in a later article: "We have now identified the same gene in Hepatitis C virus (HCV). In both HIV and HCV the GPx gene is in the -1 reading frame overlapping a known gene (NS4a gene in the cause of HCV) contains an in-frame "stop" codon " (Journal of Orthomolecular Medicine - Fourth quarter-1997.)

(Left:The five stages of HIV infection)



How RemiSel Selenium may help prevent
HIV replication in human cells

SELENIUM AND HIV/AIDS

Selenium supplementation is an absolute necessity in the treatment of HIV positive and AIDS patients. Levels of selenium dependant glutathione peroxidase (GSH-PX), an important antioxidant enzyme, are usually found to be quite low in HIV patients, and even lower in AIDS patients. Selenium supplementation significantly increases GSH-PX activity in HIV positive subjects. Given the fact that low levels of glutathione and other sulphur-containing compounds are extremely important contributing factors in the progression of AIDS, it is obvious just how essential selenium supplementation is to the HIV-infected individual. In addition, several studies have shown selenium status is a major determinant of how fast HIV will progress to AIDS.

Professor E Will Taylor quoted above, discovered so-called "Selenoproteins". Taylor suggests selenium deficiency may be important in pathogenesis; he derives the ideas from comparisons of genetic requirements of viruses (see J Med Chem 1994, 37:2637 2654). Suppose it's possible that if HIV needs selenium, this may in fact be "feeding the virus" but Taylor thinks this keeps the virus happy so it doesn't feel the need to go elsewhere in search of selenium, replicating along the way. Therefore, ipso facto selenium deficiency may result in more lethal viral variants.

References:

E W Taylor et al, "A basis for new approaches to the chemotherapy of AIDS: novel genes in the HIV-1 potentially encode selenoproteins expressed by ribosomal frameshifting and termination suppression". J Med Chem, 37, (1994): 2637-2654.

F.J.Staal et al, "Glutathione Deficiency and HIV," Lancet 339 (1992): 909-12

M.C.Delmus-Beauvieux et al, "The Enzymic Antioxidant System in Blood and Glutathione Status in HIV-Infected Patients: Effects of Supplementation with Selenium and Beta-Carotene," Am J Cln Nutr 64 (1998): 101-7

C.Allevena et al, "Are zinc and selenium markers of worsening in HIV infected subjects?" Press Med 20 (1991): 1737.

Dr M.K.Baum et al, " High risk of mortality in HIV infection is associated we had selenium deficiency," J AIDS Human Retroviral 15 (1997): 370-374

Dr M. P. Rayman, " Dietary Selenium: Time to Act," (editorial); British Medical Journal 314 (1997): 387

ZINC AND HIV/AIDS

Zinc is perhaps the most important trace element for immune function. It is also one of the more common nutrient deficiencies in cases of AIDS, presumably due to the decreased intake, impaired absorption, and an increased need for zinc.

Zinc supplementation has been shown to reduce the incidence of opportunistic infections in *AZT-treated AIDS patients. Zinc supplementation also showed an ability to increase and stabilise their weight, increase the number of CD4 cells and increase the blood level of an important immune system and regulating hormone known as thymulin. (E. Mocchegiani et al, "Benefits of Oral Zinc Supplementation as an Adjunct to AZT Therapy against Opportunistic Infections in AIDS," International Journal of Immunopharmacology 17 (1995): 719-27).

3. HEPATITIS C:

Hepatitis refers to inflammation of the liver. Hepatitis C is the most serious of the five hepatitis conditions: ABCD and G. All forms of hepatitis are very contagious and hepatitis C is the most dangerously contagious of all. There are, according to the National Institute of Health in the USA, more than 180,000,000 estimated cases of hepatitis C in the world! This astonishing figure includes over 4,000,000 cases in the United States alone: representing over two per cent of the entire American population. Current estimates are set to rise by 50% within ten years and therefore far outweighs in number (so far) even the terrible infection rates of HIV/AIDS.

The mortality rate for hepatitis C (one to twelve percent) is much higher than for the other forms of hepatitis. Viruses suspected of causing hepatitis symptoms include: Herpes simplex virus, cytomegalovirus and Epstein-Barr virus.

Acute viral hepatitis can be extremely debilitating, requiring total bed rest. It can take anywhere between two to sixteen weeks to recover. Some 10 to 40% of hepatitis C cases develop into chronic viral hepatitis forms. The symptoms of chronic hepatitis vary and they can be virtually nonexistent, or they can lead to chronic fatigue, liver damage, and even death due to cirrhosis of the liver or liver cancer.

ZINC AND SELENIUM AND HEPATITIS C

Many nutrients function as important cofactors in the manufacture, secretion, and function of thymic hormones. Deficiencies of any one of these nutrients may result in decreased thymic action and impaired immune function. Zinc, vitamin B6 and vitamin C are perhaps the most critical. Supplementation with these nutrients has been shown to increase thymic hormone function and cell mediated immunity. Zinc is perhaps the critical mineral involved in thymus gland function and thymus hormone action. Zinc is involved in virtually every aspect of immunity. When zinc levels are low, the number of T cells is reduced; thymic hormone levels are lower, and many white blood functions critical to the immune response are severely lacking. All of these effects are reversible with zinc supplementation.

Zinc is absolutely necessary for the metabolism of selenium (and vitamin B6). Both minerals are commonly reduced in the majority of hepatitis C patients.

References:

L.Kiremidjan-Schumacher, " Selenium and Immune Responses," Environmental Res 42 (1987): 277-303.

Same author: "Supplementation with Selenium and Human Immune Cell Functions II: Effect on Cyto toxic
Lymphocytes and Natural Killer Cells," Biol Trace Elem Res 41 (1994): 115-27.

J.D.Bogden et al, "Zinc and immunocompetence in the Elderly: Baseline Data on Zinc Nutriture and Immunity in Unsupplemented Subjects," Am J Cln Nutr 46 (1987: 101-9.

M.Dardenne et al, "Contribution of Zinc and Other Metals to the Biological Activity of the Serum Thymic Factor," Proc Natl Acad Sci 79 (1982): 5370-3

J.W.Hadden, "The Treatment of Zinc Deficiency Is an Immunotherapy," Int J Pharmacology 17 (1995): 697-701



Does Zinc Supplementation Help Interferon Alfa for Chronic Hepatitis C?

In a randomised Japanese trial, "polaprezinc" supplements increased sustained virologic response from 10% to 32% in those with low baseline viral loads

Previously, patients with chronic liver disease have been found to have low levels of "trace elements" including zinc and selenium. Trace elements are necessary for normal cellular metabolism. Therapy with interferon can lead to even lower levels of zinc in blood serum (no cells) and urine. Since the response to interferon alfa * monotherapy among patients with chronic hepatitis C is less than 20%, Japanese researchers attempted to determine the potential benefits of zinc supplementation on the response rate to interferon alfa. (Note that the standard therapy today for chronic hepatitis C is combination interferon alfa plus ribavirin and not monotherapy with interferon alfa.) The lead author was Hitoshi Tagaki, MD from Gunma University in Maebashi, Japan.

Criteria for entry into the study included having HCV (hepatitis C virus) genotype 1b and an HCV RNA viral load that was at least 100,000 (5 log) copies per milliliter. There was no mention as to whether patients had had previous treatment for chronic hepatitis C; however, there is an assumption that all were treatment-nave (no previous treatment).

A complete response in this study was defined as an undetectable HCV RNA viral load six months after the 6-month treatment duration and normal liver enzyme tests at the same time.

For both arms, the dose of natural interferon alfa was 10 million units injected daily for four weeks, followed by every other day for 20 weeks. (Note that this form of interferon alfa is not the same as any of the three marketed versions of interferon alfa in the US.) For the arm that took supplemental zinc, the oral dose was 150 mg of "polaprezinc" for 24 weeks.

A total of 68 patients (34% women) were randomized to participate in the study. An insignificantly lower proportion of women (28%) were randomized to the interferon arm (IFN) than the arm that was randomized to alfa interferon plus zinc (IFN+Z, 41%). All had HCV (hepatitis C virus) genotype 1b. (Genotype 1 is the most difficult to treat.) The mean baseline HCV RNA level was not presented. However, the number of patients in each of three levels of viral load was presented. Twelve (18%) had a baseline viral load between 100,000-199,000 copies per milliliter, 25 (37%) had a baseline level between 200,000-499,000 copies per milliliter and the remaining 31 (45%) had a baseline level that was 500,000 copies per milliliter or greater.

Even with randomization, however, there were disproportionate percentages in each of the three categories of viral load, when comparing the two arms. This is one limitation of the study that is discussed below. For example, 64% of the IFN arm had a baseline viral load that was greater than 500,000 copies per milliliter, while only 25% of the IFN+Z arm had baseline levels that high. Conversely, only 5% of the IFN arm had a baseline viral load between 100,000-199,000 copies per milliliter, while 31% of the IFN+Z arm fell into that level at baseline.

There was no significant difference between the two study arms when comparing mean baseline liver enzymes and liver biopsy abnormalities. The mean baseline ALT (alanine aminotransferase, liver enzyme) was 79 international units per milliliter (IU/mL) in the IFN arm and 66 IU/mL in the IFN+Z arm. The mean baseline AST (aspartate aminotransferase, liver enzyme) was 77 and 66 IU/mL in the IFN and IFN+Z arms, respectively. Liver biopsy abnormalities were not significantly different when comparing the two arms: chronic active hepatitis grade 2A was present in 69% of the IFN arm and 81% if the IFN+Z arm. Chronic active hepatitis grade 2B was present in the remaining 31% of the IFN arm and 16% of the IFN+Z arm. (One patient in the IFN+Z arm did not have a biopsy due to the risk of bleeding with hemophilia.) The mean baseline serum zinc levels were not significantly different in the two arms: 75 micrograms per deciliter in the IFN arm and 84 micrograms per deciliter in the IFN+Z arm (both are low).

The results were as follows. Using a strict "intent-to-treat" analysis (all patients included in the results), the IFN arm had a 10% complete response (defined in third paragraph), while the IFN+Z arm had a 32% complete response. Using an "as treated" analysis (dropouts excluded), the IFN arm had an 11% complete response, while the IFN+Z arm had a 38% complete response.

All other reported results were "as treated," with patient dropouts excluded. Unfortunately, due to the manner of presentation, this reviewer could not recalculate these remaining results as "intent-to-treat." When complete response rates were evaluated by baseline viral loads, the IFN+Z performed better, but only for those with baseline levels that were between 100,000 and 199,000 copies per milliliter. For the highest baseline level (greater than 500,000 copies per milliliter), 9% of the IFN arm and 13% of the IFN+Z arm achieved a complete response. (Note that this baseline level was present in 64% or 23 patients in the IFN arm and only 25% or eight patients in the IFN+Z arm.) However, for those with a baseline level between 200,000-499,000 copies per milliliter, the IFN+Z arm had a complete response rate that was twice (36%) that of the IFN arm (18%). Notwithstanding a lower percentage of patients in the IFN arm that were in this baseline viral load grouping (31%) than in the IFN+Z arm (44%), those results did not reach statistical significance. Yet, for those in the lowest baseline viral load level between 100,000-199,000 copies per milliliter, a significantly greater proportion of those randomized to IFN+Z (60% or 6 of 10) had a complete response than those randomized to IFN alone (zero of two patients).

The researchers also found that some patients who did not have a sustained virologic response did have normal liver enzymes six months after treatment was stopped. If those patients are included in a treatment response analysis, then those in the intermediate grouping of baseline viral loads randomized to IFN+Z also achieved a significantly greater complete response rate, when compared to IFN monotherapy.

In a separate analysis, the authors showed that the IFN+Z group achieved a significantly higher blood serum level of zinc after four and eight weeks, while the IFN arm had no significant change. The IFN+Z arm achieved a near normal level of zinc.

Adverse events in the two arms were similar: "flu"-like symptoms, low white cells and low platelets (blood cells for normal clotting). There are known to occur as a result of interferon alfa. Adverse events in patients who discontinued are described below.

The researchers then performed a statistical analysis ("logistic multiple regression model") that examined complete response for five baseline factors. Those were gender (sex), age, baseline liver enzymes, baseline liver biopsies and type of therapy. The only factor that was highly significantly associated with a complete response was type of therapy: IFN or IFN+Z ("odds ratio" of 5.9). (Note this analysis excluded baseline viral load.)

Discontinuations were as follows. Six patients (14%) originally randomized to the IFN arm discontinued therapy due to severe allergic reaction ("erythema multiforme"), severe fatigue, "serious" liver enzyme increases, depression, mouth inflammation ("stomatitis") or loss of consciousness. Five patients (14%) originally randomized to the IFN+Z arm prematurely discontinued therapy. Reasons included insomnia (inability to fall asleep), low thyroid hormone, headache or pneumonia. The authors reported that all dropouts' adverse events resolved after stopping therapy.

The authors concluded that "zinc supplementation to interferon for the patients with chronic hepatitis C having both genotype 1b and high virus load significantly enhanced the effect of interferon to eradicate HCV." Unless there was a typographical error on the poster, this reviewer would conclude that the virologic benefits were only observed among those with a low baseline viral load, between 100,000-199,000 copies per milliliter.

This study has several limitations. First, it has a small number of patients. Second, the mean baseline and post-levels of HCV RNA were not presented. This is very important, since it appears that the baseline HCV RNA was higher in the IFN arm. Third, with the exception of the overall complete response rate, all other results were presented as an "as treated" analysis. Fourth, the baseline viral loads of those who discontinued were not presented. It would have been helpful to know whether those who discontinued had low or high viral loads. Fifth, in spite of randomization, the percentage in each hierarchy of viral loads was not equal. Sixth, these results would not be relevant for patients starting treatment today, since the standard of care is dual therapy with interferon alfa plus ribavirin and not monotherapy with interferon alfa. Whether similar or better results might occur if ribavirin were added to interferon alfa and polaprezinc is unknown.

Seventh, natural interferon alfa is not the same formulation as any of the three interferon alfa formulations available in the US. Eighth, after personal communication with the lead author, he did not know whether the polaprezinc formulation is the same as the over-the-counter formulations of zinc lozenges in the US. Dr. Takagi said that in Japan, polaprezinc is available only by prescription. Ninth, the change in liver biopsy results was not presented. This is the true gold standard of treatment end-points in viral hepatitis. Tenth, baseline viral load was not incorporated into the "multiple regression analysis." This is important since a greater percentage of those randomized to the IFN arm (64%) had a baseline viral load greater than 500,000 copies per milliliter than the IFN+Z arm (25%). And lastly, it would have been helpful for the authors to determine whether there were other locations or compartments within the body that had changes in zinc levels in the IFN+Z arm. One example would be in liver cells (hepatocytes). A concern would be possible zinc toxicity in locations other than blood serum. Could toxicity from excess zinc develop?

Notwithstanding these limitations, the findings are interesting and provocative. Any factor that might increase the sustained virologic response rate in treatment for chronic hepatitis C would be helpful.

Note that all four generic versions use the spelling 'alfa' and not 'alpha' interferon
5/30/00

Reference:

Takagi H and others. Additive effect of zinc on interferon therapy for chronic hepatitis C. Abstract and poster presentation 229 at Digestive Disease Week 2000; May 21-24, 2000; San Diego, California.

Zinc supplementation and amino acid-nitrogen metabolism in patients with advanced cirrhosis

Author(s): Marchesini G, Fabbri A, Bianchi G, Brizi M, Zoli M
Source: Hepatology 1996; 23:1084-92

Description: Zinc is a necessary trace element in liver cell activity. Zinc deficiencies are common in patients who have advanced cirrhosis. When there is liver damage, the nitrogen from proteins, or the amino acids that form proteins, cannot be metabolised and disposed of as efficiently as they are normally. One of the nitrogen waste products that builds up to abnormal levels in the blood is ammonia, while in healthy people, the nitrogen takes the form of urea. Since alanine is a commonly found amino acid in proteins, it was used in this experiment. Sixteen patients with advanced cirrhosis were given alanine. Half (eight) of the patients had been treated with zinc supplements for three months before the alanine was administered. The patients who had been given zinc before the alanine were able to dispose of the nitrogen from the alanine in a normal way, but the other patients could not. Urea levels were higher in the patients with zinc treatments than with the control patients, but ammonia levels were higher in the untreated controls. Those patients who had taken zinc supplements also had improved mental function.

Explanation of what all that said:

Glucagon: A protein hormone that is produced from the pancreas in response to low blood sugar levels.

The experimental patients were given 200 mg of zinc sulphate three times a day for three months. There were no signs of side effects from these zinc supplements.

To monitor how each patient metabolised nitrogen-containing compounds, each of the 16 patients was given intravenous alanine for 4.5 hours. Urine and blood samples were collected.

The results showed that both groups of patients had reduced zinc levels to begin with. However, those who got supplements showed 60% increases of zinc in their blood by the end of the three months. After alanine was given, the patients who had received zinc had half the glucagon levels of the controls and 30% more insulin in their blood. The ammonia levels in the zinc-treated group were 30% lower than in the control group. Other liver function tests were significantly improved. Mental function tests based on several parameters also improved greatly in the patients with zinc supplement treatment.

Two patients who had received zinc supplements were tested again six months later to measure zinc levels in the blood. At this time, their zinc levels had dropped back down to where they had been before supplements had started.

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