Conditions and Minerals
THREE SERIOUS VIRAL INFECTIONS THAT
THE IMMUNOVA PRODUCTS MAY HELP ALLEVIATE:
3. HEPATITIS C
1. CHRONIC FATIGUE SYNDROME
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
· The host's immune system normally holds this latent infection
· 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.
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):
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
· 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 (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
Microscope picture of infected cell
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.)
five stages of HIV infection)
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
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 is absolutely necessary for the metabolism of selenium
(and vitamin B6). Both minerals are commonly reduced in
the majority of hepatitis C patients.
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
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
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-naïve
(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
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
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
Note that all four generic versions use the spelling 'alfa' and
not 'alpha' interferon
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,
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
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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