Aids: The Seleno-Enzyme Solution

[Guest guest]

AIDS: THE SELENO-ENZYME SOLUTION

 

AIDS is a consequence of HIV infection which causes deficiencies of the enzyme

glutathione peroxidase and its four components, yet this syndrome and viral

activity can be reversed with dietary supplementation.

Part 2 of 2

 

-----http://www.nexusmagazine.com/articles/aids.selenium2.html

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Extracted from Nexus Magazine, Volume 11, Number 2 (February-March 2004)

PO Box 30, Mapleton Qld 4560 Australia. editor

Telephone: +61 (0)7 5442 9280; Fax: +61 (0)7 5442 9381

From our web page at: www.nexusmagazine.com

 

by Harold D. Foster, PhD © 2003

Professor, Department of Geography

University of Victoria

PO Box 3050

Victoria, BC, V8W 3P5, Canada

Email: hfoster

Website: http://www.hdfoster.com

 

 

--

 

 

COROLLARY ONE: Deficiencies of Glutathione Peroxidase and its Components in

HIV/AIDS

There is strong evidence to show that HIV-seropositive individuals are deficient

in glutathione peroxidase. Gil and colleagues,54 for example, compared levels of

it in the blood of 85 HIV/AIDS patients with those in 40 healthy controls,

confirming the presence of a significant (p<0.05) reduction of the selenoenzyme

in the infected group. Beyond this, Batterham and co-workers55 showed that such

depressed glutathione peroxidase levels in men with HIV/AIDS could be raised by

supplementation with selenium and other antioxidants.

 

If Aumann and co-workers56 are correct, then HIV/AIDS patients should also be

very deficient in the four nutritional components that these researchers believe

are required by the body to produce glutathione peroxidase—namely, selenium,

cysteine, glutamine and tryptophan. There is certainly good evidence to prove

that such individuals are selenium deficient.

 

Several studies have documented declining plasma selenium levels in patients

with HIV/AIDS. Probably the most convincing of these was conducted by Baum and

co-workers57 in Florida. These researchers monitored 125 HIV-1–seropositive male

and female drug users in Miami over a period of 3.5 years. This study collected

data on CD4 T-cell count, antiretroviral treatment and plasma levels of vitamins

A, E, B6 and B12 as well as selenium and zinc. A total of 21 of these patients

died during the study. Only plasma selenium levels and CD4 T-cell counts could

have been used to predict which of the 125 patients would die, with selenium

levels being more accurate predictors than CD4 T-cell counts. The same research

group also monitored 24 HIV-infected children over a five-year period, during

which time half of them died of AIDS. As with adults, the lower their serum

selenium levels, the faster that death occurred.

 

It also appears as if the selenium deficiency seen in HIV/AIDS patients, as

expected, makes them more susceptible to Coxsackievirus infection. As a

consequence, myocardial infarctions are quite common even in relatively young

people who are HIV seropositive.59 In addition, autopsies often reveal that AIDS

patients60, 61 have been suffering from, and perhaps have died of, Keshan

disease—an endemic heart disease normally limited to the populations of regions

of extreme selenium deficiency.

 

HIV/AIDS patients also display low plasma levels of cysteine at every stage of

infection.62 Since this amino acid is one of the body's major sources of

sulphur, they are very deficient in it.63 Interestingly, depressed cysteine is

also characteristic of SIV-infected rhesus macaques.

Several researchers have documented glutamine deficiencies in HIV/AIDS

patients.65–67 Shabert and colleagues, for example, discovered that much of the

weight loss seen in individuals could be reversed by glutamine–antioxidant

supplementation.

 

If HIV is producing glutathione peroxidase for its own purposes and if this

selenoenzyme contains tryptophan, then HIV/AIDS patients should be deficient in

this amino acid. This appears to be the case. Werner and co-workers,68 for

example, have shown that, in male patients with advanced HIV infection,

tryptophan serum levels are less than half of those found in matched healthy

controls. Since tryptophan is required for the biosynthesis of both serotonin

and niacin, it is not surprising that their levels are also depressed in

patients with HIV/AIDS.69, 70

It is clear from the literature just cited that HIV/AIDS patients are indeed

very deficient in glutathione peroxidase and in the four components of this

selenoenzyme—namely, selenium, cysteine, glutamine and tryptophan. In short, the

clinical and scientific evidence supports the truth of corollary one.

 

 

COROLLARY TWO: Effective Treatment for HIV/AIDS Should Involve Correcting

Deficiencies of Glutathione Peroxidase and its Nutritional Precursors

There is a wealth of evidence that correcting one or more of the deficiencies of

selenium, cysteine, glutamine and tryptophan, which are characteristic of

HIV/AIDS, has significant health benefits. Selenium, for example, is a key

immunological enhancement agent that has a strong impact on lymphocyte

proliferation.

 

This relationship was confirmed by Peretz and co-workers,71 who monitored

enhanced lymphocyte response in elderly subjects given a daily 100-microgram

selenium supplement over a six-month clinical trial. This seems to be because

selenium is essential for lymphocytes—as shown by Porter and colleagues,72 who

demonstrated that plasma proteins carry selenium to lymphocytes which absorb it.

Further, Wang and co-workers73 have demonstrated that selenium enhances

lectin-stimulated T-lymphocyte proliferation and is an important modulator for

immune response. It is not surprising, therefore, that HIV/AIDS patients with

depressed plasma selenium also show T-lymphocyte abnormalities.74

 

There have been numerous clinical trials to explore the impact of cysteine

supplementation (usually given as N–acetylcysteine) on HIV/AIDS symptoms. De

Rosa and co-workers76 at Stanford University, for example, have shown that the

oral administration of N–acetylcysteine significantly replenished glutathione in

HIV-infected individuals. This is very significant, since subsequent research

has established that glutathione levels in HIV-positive patients is a predictor

of survival rates.77

 

As previously mentioned, cysteine is a significant source of sulphur and

HIV/AIDS patients are very deficient in this element. A trial carried out in

Germany by Breitkreutz and colleagues77 showed that N–acetylcysteine

supplementation helped to correct this sulphur deficiency while simultaneously

improving immunological functions in HIV/AIDS patients.

 

Glutamine is a major requirement of cells which are rapidly proliferating. As a

result there is a significant requirement for it in the digestive tract, where

it is essential for intestinal cell proliferation, intestinal fluid/electrolyte

absorption and mitogenic response to growth factors. Since glutamine deficiency

is so characteristic of HIV/AIDS, it is not surprising that patients typically

suffer badly from digestive malfunction and diarrhoea. It has been demonstrated

by Noyer and co-workers,78 at the Albert Einstein College of Medicine, that

glutamine therapy improves intestinal permeability in AIDS patients, although

the amount required to enhance intestinal absorption may be as much as 20 grams

per day.

Glutamine is also essential for muscle building; in HIV/AIDS patients,

deficiencies of it seem linked to loss of body cell mass. Shabert and his

colleagues79 have demonstrated that glutamine and antioxidant supplements can

reverse the weight loss typically seen in such patients, while Kohler and

co-workers80 also have shown that glycyl-glutamine improves lymphocyte

proliferation in AIDS patients.

 

I am not aware of any clinical trials conducted to test the impact of tryptophan

supplementation on HIV/AIDS. However, it is interesting to note that

antiretroviral drug therapy, designed to prevent HIV-1 replication, slows the

rate of tryptophan loss seen in seropositive individuals.81 Similarly, plasma

tryptophan levels can be increased in HIV-infected patients by nicotinamide

supplements.82 This is perhaps not surprising, given the close chemical

association between this nutrient and the tryptophan derivative, niacin.

 

Simply put, there is a great deal of evidence that HIV/AIDS patients are

typically deficient in glutathione peroxidase and its precursors—selenium,

cysteine, glutamine and tryptophan. Beyond this, it is clear from clinical

trials that survival rates and patients' symptoms are improved by

supplementation with such nutrients.

Indeed, one might go so far as to say it would be medical malpractice not to

give these nutrients to those who are HIV seropositive.

 

COROLLARY THREE: Reversing Deficiencies of the Precursors of Glutathione

Peroxidase Should Reverse the Symptoms of HIV/AIDS

The hypothesis presented here suggests that HIV/AIDS is a disease that is caused

by the combined deficiencies of glutathione peroxidase and its precursors. If

this is correct, then the symptoms normally associated with a deficiency of each

one of these substances ought to occur in AIDS patients. There is a wealth of

evidence that suggests this is the case.

 

Baum and co-workers83 have shown that adults and children dying of AIDS display

both depressed CD4 T-lymphocyte counts and very depleted plasma selenium stores.

This seems to be part of a positive feedback system, since one of the most

significant symptoms of selenium deficiency is a reduction of CD4 T-lymphocytes,

which occurs because this trace element is needed for their production. A

lowering of CD4 T-lymphocyte levels causes a drop in the efficiency of the

immune system, encouraging infection by other pathogens and resulting in a

further decline in selenium. I have termed this positive feedback system the

selenium CD4 T-cell tailspin.84

 

HIV/AIDS patients also often display a hypothyroid or low T3 (tri-iodothyronine)

syndrome.85 This seems to occur because selenium deficiency causes a reduction

in deiodinase, the enzyme required to convert T4 (thyroxine) to T3. It has been

further suggested that such a selenium deficiency abnormality of the thyroid may

be a significant factor in the AIDS wasting process.86

 

Selenium deficiency has been linked to depression in the general population.87,

88 It is not surprising, therefore, that this is also a characteristic of people

with HIV/AIDS.

It would appear, therefore, that at least three of the major symptoms of

HIV/AIDS—namely, depressed CD4 T-lymphocyte count, lowered tri-iodothyronine

production and depression—can be explained, at least in part, by the inadequate

selenium levels seen in such patients.

 

In 1981, Bunk and Combs89 described an experiment demonstrating that, in

chickens, selenium deficiency impaired the conversion of the S–amino acid

methionine into cysteine. It is highly likely that this is true for humans. If

it is, then, by encoding for the selenoenzyme glutathione peroxidase, HIV-1

causes a deficiency of cysteine in infected individuals in two distinct ways.

Firstly, the virus removes cysteine directly from the body as it replicates.

Secondly, it creates a selenium deficiency which impairs the conversion of

methionine to cysteine, so reducing the availability of the latter. Simply put,

HIV-1 both increases the demand for and reduces the supply of cysteine in

patients who are HIV-1 positive. Cysteine deficiency, in and of itself, has been

shown to be associated with depressed glutathione, poor wound and skin healing,

psoriasis, abnormal immune function and greater susceptibility to secondary

infections and cancers.90 All these characteristics of cysteine deficiency

are seen in HIV/AIDS patients.

 

Glutamine is a major nutrient required by rapidly proliferating cells and is of

particular significance in the digestive tract. Deficiencies cause abnormal

intestine permeability and digestive malfunction, often associated with

diarrhoea.91 Glutamine is also a favourite with body-builders, who use it in

large quantities to promote muscle growth. It is not surprising that muscle

protein wasting, therefore, is a symptom of glutamine inadequacy. Both diarrhoea

and muscle wasting are characteristics of HIV/AIDS.92

 

Tryptophan deficiencies, in and of themselves, have led to major health problems

in the past. Probably the worst of these was pellagra, which developed in

children eating diets high in corn. Maize is very deficient in tryptophan and so

such children quickly developed pellagra, which is thought to be due to a

co-deficiency of both tryptophan and its metabolite, niacin.93 As a consequence

of these two deficiencies, such individuals could not produce adequate

nicotinamide adenine dinucleotide and so developed pellagra. The symptoms of

this disease were known as " the four Ds " —namely, dermatitis, diarrhoea, dementia

and, ultimately, if not treated effectively, death.94 AIDS patients commonly

experience all such symptoms and also display inadequate levels of nicotinamide

adenine dinucleotide. This can be reversed, at least in vitro, by the

administration of nicotinamide.95

 

It would appear, therefore, that corollary three is correct and that the great

majority of the symptoms of HIV/AIDS (with the exception of those caused by

opportunistic pathogens) are a combination of symptoms seen in individuals who

are extremely deficient in glutathione peroxidase or in one or more of its

precursors.

 

COROLLARY FOUR: HIV-1 Seropositive Individuals Who Eat a Diet Elevated in

Selenium, Cysteine, Glutamine and Tryptophan Should Never Develop AIDS

Obviously, the easiest way to test the truth or otherwise of this fourth

corollary would be to arrange for a double-blind, placebo-controlled pilot study

in which half the HIV/AIDS patients are given injections of glutathione

peroxidase and supplements of selenium, cysteine, glutamine and tryptophan.

Unfortunately, geographers are not expected to develop new disease-related

hypotheses that have the potential for undermining genetic, biochemical and

clinical authority. As a result, I have been attempting to gain support for

testing this concept for more than two years. Given the enormous power of the

pharmaceutical industry and its lack of interest in the discovery of a cheap and

simple treatment for HIV/AIDS, it has not been an easy row to hoe. To date, all

I can point to are two AIDS patients who quickly reversed their major symptoms

when attempting to follow my suggested regime.96 Beyond this, there are research

teams in South Africa, Tanzania, Botswana and Morocco who have contacted me to

express a willingness to conduct such trials, should funding ever become

available.

 

CONCLUSIONS

Death from AIDS is a consequence of four nutritional deficiencies. Fortunately,

HIV infection does not need to be a death sentence because such deficiencies are

cheap and easy to reverse. And while the four nutrients won't eradicate HIV,

they activate the virus's own " warning system " , preventing its replication.

The genetic code of HIV includes a homologue for the essential human

selenoenzyme glutathione peroxidase. Paradoxically, this viral requirement for

selenium generally appears to restrict infection to individuals who, because of

a diet deficient in selenium or because of prior infection by other

selenium-encoding pathogens, are deficient in this trace element.

Unfortunately, the human population is becoming ever more susceptible to

infection by HIV-1 (and HIV-2 to a lesser extent) as well as other

selenoenzyme-encoding viruses because of acid rain, which reduces the

bioavailability of selenium.

To be replicated, HIV must compete with its host for glutathione peroxidase and

its four constituent nutrients—selenium, cysteine, glutamine and tryptophan. As

a consequence, replication of the virus gradually depletes seropositive

individuals of these substances. AIDS is the end product of these nutritional

declines, and most of its symptoms are caused by them. As a consequence, it is

likely that AIDS can be easily reversed by correcting such deficiencies.

To illustrate, glutathione peroxidase is one of the body's most significant

antioxidants. A lack of this selenoenzyme therefore accelerates free radical

damage and oxidative stress. Beyond this, having inadequate selenium and

cysteine undermines the immune system in a process that is accelerated by other

infectious pathogens. A deficiency of glutamine encourages muscle wasting and

digestive malfunction, while a lack of tryptophan and the compounds it

biosynthesises (such as niacin and serotonin) results in dermatitis, diarrhoea

and various neurologic and psychiatric symptoms including dementia.

Supplementation with the appropriate nutrients naturally reverses these

symptoms.

It is ironic, but not really surprising, that our continuous destruction of the

global ecosystem is promoting the spread of viral infections (and various

chronic degenerative diseases) that threaten humanity's domination of the

planet.

 

 

POSTSCRIPT (as at early January 2004)

Since I submitted this article for publication, I have learned of a small AIDS

trial that is taking place in Botswana.97 The trial is funded by a Canadian

vitamin company and is using the nutrient regimen suggested in my book. Here is

a quotation from the initial email report that I received in late September:

" I picked two candidates personally who have fully blown AIDS with relevant

symptoms like diarrhoea, skin rash, loss of weight and a lack of appetite. One

of these candidates has a severe complication of syphilis which has slowed his

recovery somewhat, but still, within two weeks of trials, his skin rash,

diarrhoea and fatigue have all but disappeared. The lady candidate gained 3 kg

in two weeks and now eats 'like a horse'. She resumed work last Tuesday after

several weeks of absence. I am gaining confidence in this treatment by the day

and I hope the same would apply to the remainder of the trial candidates…

" A lady who started the regimen three weeks back has just tested negative for

HIV, and her CD4 count has shot up from 500 to 700! " (It's unknown if this is

the same lady who ate " like a horse " !)

In the meantime, I have set up a small company, HD Foster Research Inc., which

is having the nutrients made up into a product called HELP. We are giving this

away to doctors who treat AIDS patients. The first taker is a physician in South

Africa, and I have mailed him enough treatment for 10 patients. The idea is to

find medical supporters who can vouch that the treatment works. Beyond this, the

small Canadian company that is using my treatment in Botswana (anecdotal

evidence suggests a 99% success rate in reversing AIDS) has spread its

activities into Zambia.

We have decided to produce a video in which I describe my theory of HIV/AIDS,

and which also shows patients recovering. We are looking for financial and other

assistance to do this. The idea is to give this away to TV stations in Africa

and elsewhere.

Recently I checked the progress of the two Victoria, BC, patients mentioned in

my book, who were dying of AIDS in 2001. They are now both in good health and

are back at work.

I have also had two more HIV/AIDS papers published in Chinese in the proceedings

of two different medical conferences held in Shanghai in November 2003. Two

additional papers have been accepted for publication in Chinese medical

journals. On 17 March I am scheduled to give a lecture on AIDS at the Centennial

AGM of the Association of American Geographers in Philadelphia.

Things are moving along. Hopefully, the world will soon know that the treatment

does indeed work. #8734;

 

 

 

Author's Note:

Readers wanting more detailed information about the HIV/AIDS environmental link

are directed to the website http://www.hdfoster.com, where they can download a

free copy of the book, What Really Causes AIDS.

 

 

 

About the Author:

Harold D. Foster, PhD, was born and educated in England. He specialised in

geology and geography, earning a BSc in 1964 from University College London and

a PhD in 1968 from London University. He is a Canadian by choice, and has been a

faculty member in the Department of Geography, University of Victoria, British

Columbia, Canada, since 1967.

 

A tenured professor, Dr Foster has authored or edited some 235 publications, the

majority of which focus on reducing disaster losses or identifying the causes of

chronic disease or longevity. He has published hypotheses on the origins of

numerous diseases including myocardial infarction, SIDS, cancer, diabetes,

schizophrenia, multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS),

Alzheimer's and Parkinson's diseases, and stroke.

 

His numerous books include: Disaster Planning: The Preservation of Life and

Property (Springer Verlag, New York, 1980); Reducing Cancer Mortality: A

Geographical Perspective (Western Geographical Press, Victoria, 1986); The

Ozymandias Principles: Thirty-one Strategies for Surviving Change (Southdowne

Press, Victoria, 1997); and What Really Causes AIDS (Trafford Publishing,

Victoria, 2002; see review in NEXUS 10/05). His new book, What Really Causes

Schizophrenia, is to be published by Trafford in late 2003.

 

Harold Foster is a member of the Explorers Club as well as several academic

organisations including The New York Academy of Sciences, The Royal Geographical

Society and The Royal Society of Literature. He is also the editor of both the

International and Canadian Western Geographical Series and is a member of the

boards of the Journal of Orthomolecular Medicine and the International

Schizophrenia Foundation.

 

He has been a consultant to numerous organisations, including the United Nations

and NATO, and to the governments of Canada, Ontario and British Columbia. He is

also a member of the Science Advisory Panel for the Healthy Water Association.

 

Every day, Dr Foster makes a point of taking at least the recommended daily

allowance of the known essential nutrients. He is also currently pursuing offers

for his suggested nutrient mixture to be produced for use in clinical trials

with AIDS patients. For a more detailed résumé, visit the website

http://www.hdfoster.com.

 

 

 

Endnotes

54. Gil, L. and others, " Contribution to characterization of oxidative stress in

HIV/AIDS patients " , Pharmacol Res 2003; 47(3):217-224.

55. Batterham, M. and others, " A preliminary open label dose comparison using an

antioxidant regimen to determine the effect on viral load and oxidative stress

in men with HIV/AIDS " , Eur J Clin Nutr 2001; 55(2):107-114.

56. Aumann, K.D. and others, " Glutathione peroxidase revisited – simulation of

the catalytic cycle by computer-assisted molecular modelling " , Biomed Environ

Sci 1997; 10(2-3):136-155.

57. Baum, M.K. and others, " High risk of HIV-related mortality is associated

with selenium deficiency, J Acquir Immune Defic Syndr Hum Retrovirol 1997;

15(5):370-374.

58. Campa, A. and others, " Mortality risk in selenium deficient HIV-positive

children " , J Acquir Immune Defic Syndr Hum Retrovirol 1999; 20(5):508-513.

59. Law, M. and others, " Modelling the 3-year risk of myocardial infarction

among participants in the Data Collection on Adverse Events of Anti-HIV Drug

(DAD) study " , HIV Med 2003; 4(1):1-10.

60. Dworkin, B.M., " Selenium deficiency in HIV infection and the acquired

immunodeficiency syndrome (AIDS) " , Chem Biol Interact 1994; 91(2-3):181-186.

61. Dworkin, B.M. and others, " Reduced cardiac selenium content in the acquired

immunodeficiency syndrome " , J Parenter Enteral Nutr (JPEN) 1989; 13(6):644-647.

62. Droge, W. and others, " Functions of glutathione and glutathione disulfide in

immunology and immunopathology " , FASEB J 1994; 8:1131-1138.

63. Breitkreutz, R. and others, " Improvement of immune functions in HIV

infection by sulfur supplementation: two randomized trials " , J Mol Med 2000;

78(1):55-62.

64. Droge, W. and others, " HIV-induced cysteine deficiency and T-cell

dysfunction – a rationale for treatment with N–acetylcysteine " , Immunol Today

1992; 13(6):211-214.

65. Shabert, J.K. and others, " Glutamine-antioxidant supplementation increases

body cell mass in AIDS patients with weight loss: a randomized double-blind

controlled trial " , Nutrition 1999; 15(11/12):860-864.

66. Noyer, C.M. and others, " A double-blind placebo-controlled pilot study of

glutamine therapy for abnormal intestinal permeability in patients with AIDS " ,

Am J Gastroenterol 1998; 93(6):972-975.

67. Kohler, H. and others, " Glycyl-glutamine improves in vitro lymphocyte

proliferation in AIDS patients " , Eur J Med Res 2000; 5(6):263-267.

68. Werner, E.R. and others, " Tryptophan degradation in patients infected by

human immunodeficiency virus " , Biol Chem Hoppe Seyler 1988; 369(5):337-340.

69. Murray, M.F, " Niacin as a potential AIDS preventative factor " , Med

Hypotheses 1999; 53(5):375-379.

70. Sidibe, S. and others, " Effects of serotonin and melanin on in vitro HIV-1

infection " , J Biol Regul Homeost Agents 1996; 10(1):19-24.

71. Peretz, A. and others, " Lymphocyte response is enhanced by supplementation

of elderly subjects with selenium-enriched yeast " , Am J Clin Nutr 1991;

53(5):1323-1328.

72. Porter, E.K. and others, " Uptake of selenium-75 by human lymphocytes in

vitro " , J Nutr 1979; 109(11):1901-1908.

73. Wang, R.D. and others, " Investigation of the effect of selenium on

T-lymphocyte proliferation and its mechanisms " , J Tongji Med Univ 1992;

12(1):33-38.

74. Baum, M.K. and others, " High risk of HIV-related mortality is associated

with selenium deficiency " , J Acquir Immune Defic Syndr Hum Retrovirol 1997;

15(5):370-374.

75. De Rosa, S.C. and others, " N–acetylcysteine replenishes glutathione in HIV

infection " , Eur J Clin Invest 2000; 30(10):915-929.

76. James, J.S., " NAC: First Controlled Trial, Positive Results " , AIDS Treatment

News 1996; 250:1-3, posted at http://www.aids.org/immunet/atn.nsf/

page/ZQX25002.html.

77. Breitkreutz, R., " Improvement of immune functions in HIV infection by sulfur

supplementation: two randomized trials " , J Mol Med 2000; 78(1):55-62.

78. Noyer, C.M. and others, " A double-blind placebo-controlled pilot study of

glutamine therapy for abnormal intestinal permeability in patients with AIDS " ,

Am J Gastroenterol 1998; 93(6):972-975.

79. Shabert, J.K. and others, " Glutamine-antioxidant supplementation increases

body cell mass in AIDS patients with weight loss: a randomized double-blind

controlled trial " , Nutrition 1999; 15(11/12):860-864.

80. Kohler, H. and others, op. cit.

81. Zangerle, R. and others, " Effective antiretroviral therapy reduces

degradation of tryptophan in patients with HIV-1 infection " , Clin Immunol 2002;

104(3):242-247.

82. Murray, M.F. and others, " Increased plasma tryptophan in HIV-infected

patients treated with pharmacologic doses of nicotinamide " , Nutrition 2001;

17(7-:654-656.

83. Baum, M.K., op. cit.

84. Foster, H.D., " AIDS and the 'selenium-CDR T cell tailspin': The geography of

a pandemic " , Townsend Letter for Doctors and Patients 2000; 209:94-99.

85. Bourdoux, P.P. and others, " Biochemical thyroid profile in patients infected

with the human immunodeficiency virus " , Thyroid 1991; 1:149.

86. Geelhoed-Duijvestijn, P.H. and others, " Effect of administration of growth

hormone on plasma and intracellular levels of thyroxine and tri-iodothyronine in

thyroidectomized thyroxine-treated rats " , J Endrocrin 1992; 133:45-49.

87. Hawkes, W.C. and others, " Effect of dietary selenium on mood in healthy men

living in a metabolic research unit " , Biol Psychiatry 1996; 39:121-128.

88. Finley, J.W. and others, " Adequacy or deprivation of dietary selenium in

healthy men: clinical and psychological findings " , J Trace Elem Exp Med 1998;

11:11-27.

89. Bunk, M.J. and others, " Evidence for an impairment in conversion of

methionine to cysteine in the Se-deficient chicken " , Proc Soc Ex Biol Med 1981;

167:87-93.

90. Braverman, E.R. (with C.C. Pfeiffer), The Healing Nutrients Within: Facts,

Findings and New Research on Amino Acids, Keats Publishing, New Canaan, 1987.

91. Rhoads, M., " Glutamine signalling in intestinal cells " , J Parenter Enteral

Nutr 1999; 23(5 Suppl):S38-40.

92. Ward, D.E., The AmFAR AIDS Handbook: the Complete Guide to Understanding HIV

and AIDS, W.W. Norton, New York, 1999.

93. Braverman, E.R., op. cit.

94. ibid.

95. Murray, M.F. and others, " HIV infection decreases intracellular nicotinamide

adenine dinucleotide (NAD) " , Biochem Biophys Res Commun 1995; 212(1):126-131.

96. Foster, H.D., 2000, op. cit.

97. Email to author, September 25, 2003.

_________________

 

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