Alternatives to AZT in Aids Patients
Aids is a wholly a-typical epidemic. Its preference for intravenous drug users, people living in poor neighborhoods, gay white males and people of African descent of both sexes is an indication that the HIV virus must be a very selective virus indeed. Difficult to imagine how a virus distinguishes its victims in such a highly specific way unless ... yes, unless the epidemic is not virus based at all. To get an idea of how Aids testing selects for specific "risk groups", see Liam Scheff's “Knowing is Beautiful”.
Aids awareness promotional image
Abstinence from sex, condoms and anti-retroviral drugs are what's officially advocated to prevent the spread of Aids. Yet there are those who say that the immune deficiency seen in Aids is not of viral origin but is rather a matter of oxidative stress on the body's cells. In fact the elusive virus - its isolation has apparently never been proven in a peer-reviewed scientific paper - is not even present in many of the people who are diagnosed to have Aids.I invite you to read up about the validity of the non-specific tests, the non-infectious nature of the syndrome, and the highly toxic effects of the drugs prescribed to those unfortunate people who have been "diagnosed". To really get into this more deeply, just search "HIV" or "Aids" on this site - there is a google search window at the top of each page - and you will find a host of earlier articles that detail what I found while looking around. Start from there but by all means, please do your own research.
After a lot of suffering, it is time to move on from knowing about Aids and knowing what it isn't to actually doing something effective about it. Beldeu Singh, a writer and researcher in Malaysia, is summarizing those things that are strange in the HIV/Aids paradigm. He also suggests that there are ways to prevent and treat Aids by simple nutritional means. Of course his suggestions presuppose that the basic nutritional and hygienic needs such as a few proper meals a day and clean, drinkable water, have already been taken care of.
"African Aids" is largely due to malnutrition and endemic diseases. Our African brothers and sisters don't need anti-retroviral drugs as much as they need to be allowed to eat properly to start with, and to get clean water to drink. But assuming that those basic necessities are taken care of, what else can be done to prevent the development of Aids related illness? Let's see what Beldeu Singh has to say about that ...
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ALTERNATIVES TO AZT IN AIDS PATIENTS
(this article is part of a book in preparation)
The term AIDS first appeared in the Morbidity and Mortality Weekly Report (MMWR) of the Centers for Disease Control (CDC) in 1982 to describe ". . . a disease, at least moderately predictive of a defect in cell-mediated immunity, occurring with no known cause for diminished resistance to that disease" (CDC, 1982b). The initial CDC list of AIDS-defining conditions, which included Kaposi's sarcoma (KS), Pneumocystis carinii pneumonia (PCP), Mycobacterium avium complex (MAC) and other conditions, has been updated on several occasions, with significant revisions (CDC, 1985a, 1987a, 1992a). That is how the NIAID, the National Institute of Allergy and Infectious Diseases, has defined AIDS (see:The Definition of AIDS, The Relationship Between the Human Immunodeficiency Virus and the Acquired Immunodeficiency Syndrome, Sept 1995). Going by this definition - "moderately predictive of a defect in cell-mediated immunity, occurring with no known cause for diminished resistance" does not tie in with the "HIV causes AIDS" dogma and the administration of AZT and other toxic drugs and retrovirals. Those drugs will depress the blood immune cell counts while AIDS, in that definition, is only "moderately predictive of a defect in cell-mediated immunity."
"A defect in cell-mediated immunity, occurring with no known cause for diminished resistance to that disease" is totally absurd. Firstly, we know that there is no defect in the immune systems of AIDS patients. It is suppressed in the very early stages and later compromised and finally impaired to the extent that opportunistic infections set in and become established. It is certainly not a defect in cell-mediated immunity. And it is not a condition that occurs with "no known cause for diminished resistance to that disease." Drug toxicities are known to suppress the immune system and oxidative stress has been reported to aid the progresion of AIDS. Immune suppression is a condition, not a disease and certainly not a disease arising from a defect in cell mediated immunity. Suppression and defect are two worlds apart.
The case definition in adults and adolescents was expanded in 1993 to include HIV infection in an individual with a CD4+ T cell count less than 200 cells per cubic millimeter (mm3) of blood (CDC, 1992a). The current surveillance definition replaced criteria published in 1987 that were based on clinical conditions and evidence of HIV infection but not on CD4+ T cell determinations (CDC, 1987a). Surveillance definitions of AIDS have proven useful epidemiologically to track and quantify the recent epidemic of HIV-mediated immunosuppression and its manifestations. However, AIDS represents only the end stage of a continuous, progressive pathogenic process, beginning with primary infection with HIV, continuing with a chronic phase that is usually asymptomatic, leading to progressively severe symptoms and, ultimately, profound immunodeficiency and opportunistic infections and neoplasms (Fauci, 1993a). They remain committed to the pathogenic cause of AIDS, although after 26 years no one has seen the HIV and all that ever comes close to a viral cause may be attributable, in a certain percentage of AIDS patients, is a viral particle as observed by Montagnier, and that my be nothing more than a latency disease of EBV which is triggered by oxidative stress. So, there is still no case for a new whole virus and matters still point to the biochemical cause and oxidative stress in progression of the AIDS condition.
If at all there is also a viral link for AIDS in addition to the oxidative cause, it may be associated with oxidative stress involving the common EBV virus that can hide in cells of the immune system as a part of the viral genome bound to polymer actins that can become reactivated by excess hydrogen peroxide produced by cells during metabolic activity under oxidative stress, wherein the natural antioxidant enzymes (glutathione and catalase) are in low amounts and cannot convert all the hydrogen peroxide into water and oxygen as soon as it is formed. And the excess hydrogen peroxide breaks the chemical bonds that bind the polymer actins with the EBV viral genome activating it. Its like getting shingles after getting infected with chicken pox. And the administration of toxic drugs renders the situation more hopeless for the AIDS patient.
In the Journal Of Infectious Diseases (1997; 176;655-64), Montagnier wrote that “in AIDS pathogenesis oxidative stress is proposed as a metabolic alteration that favours disease progression by inducing both viral replication and apoptotic (cell) death. He claims to have “evidence that oxidative stress indeed induces, while antioxidants inhibit, HIV replication and apoptosis suggests the use of these molecules as an antiretroviral therapy to reduce cell death in AIDs patients.” Firstly, note that here we have Montagnier suggesting the use of antioxidants in AIDS patients to reduce apoptosis of T4 cells and as an antiretroviral therapy. The “oxidative stress induces HIV replication” assertion by Montagnier creates another paradox. AZT is toxic and generates severe oxidative stress, especially with prolonged use. AZT is a prescription drug and according to the manufacturer itself it causes symptoms that are indistinguishable from AIDS.
An article in the New England Journal of Medicine describes the muscle wasting caused by AZT and compared it to muscle wasting, called "myopathy", presumed to be caused by HIV. Their comments in the abstract are shocking: "We conclude that long-term therapy with Zidovudine can cause a toxic mitochondrial myopathy, which... is indistinguishable from the myopathy associated with primary HIV infection..."
After AZT had been licensed for human use, several independent studies reported that the drug is about 20 to 1000 times more toxic to human cells in culture than the manufacturer had claimed, i.e. that the half inhibitory doses (ID 50) ranged between 1 and 50 µM. In accordance with these results, life threatening toxicity including anemia, leukopenia, nausea, muscle atrophy, dementia, hepatitis and mortality, has been documented in humans treated with 20 to 60 µM AZT (Mir & Costello, 1988; Duesberg, 1992; Freiman et al., 1993; Tokars et al., 1993; Bacellar et al., 1994; Goodert et al., 1994; Seligmann et al., 1994).
Hence, it is not surprising that a British study found that AZT prophylaxis decreased survival and induced wasting syndrome, cryptosporidiosis, and cytomegalovirus infection, and the American MAC study shows that AZT increases the risk of pneumonia, one of the AIDS defining diseases.
AZT has effects of toxicity in animals and humans. “It produces excruciating headaches; severe nausea; muscular pain; wasting of the muscles; damage to kidneys and nerves; excruciating pains in the legs; encephalitis; severe anemia requiring transfusions to stay alive; lymphoma (cancer); cancer in 49% of cases, versus 2% incidence in non AZT group; liver damage; nail dyschromia (fingernails turn black); insomnia; impotence; dementia; mania; ataxia (failure of muscular coordination); seizures; alopecia (hair falls out). It is a fairly well established fact that AZT was designed to kill the bone marrow. It causes neutropenia or leukopenia (loss of white blood cells) or bone marrow aplasia and bone marrow toxicity. White blood cells are the basis of the immune system. T cells, granulocytes, those are all parts of the immune system. You kill those with AZT and the immune system is gone,” Harvey Bialy, Research editor Bio/Technology Science Journal.
A study on cardiovascular toxicology reports “AZT treatment increases superoxide (free radical) production” and “the effects of AZT on endothelium - dependent relaxation are eliminated by pretreatment with a free radical scavenger” (anti-oxidant) which proves that AZT toxicity is due to its free radical generating capacity. This study also provides the scientific inference that AIDS can be caused by superoxide free radicals and oxidative stress. In fact, AIDS is a free radical and oxidative stress induced condition that appears more easily in people with malnutrition associated with low organic selenium intake.
AZT is a poison that is cytotoxic. Originally developed for chemotherapy, it was never approved for use in humans because of its toxicity. It kills healthy cells by terminating the DNA synthesis in cells. Its mDNA depletion activity explains muscular fatigue and muscular atrophy later in long term use. AZT is confirmed to be carcinogenic in mice. In humans, AZT increases the risk of lymphomas by 50 times. AZT decreases white blood cells by killing young CD4 lymphocytes. It causes anemia, vomiting, lactic acidosis, fatigue, muscles wasting and lymphocytopenia and it stimulates leukemia – all the classic symptoms of AIDS!
The damage caused by AZT on the mitochondria and in mDNA depletion is due to its ability to generate superoxide free radicals. Clearly, AZT has free radical generating toxicity that destroys T4 cells and interferes with metabolism in the mitochondria by depleting antioxidants and antioxidant enzymes involved in the production the ATP energy molecules in mitochondria and utilization of ATP. While mitochondrial destruction causes chronic fatigue and muscle wasting, the immune system weakens due to depletion of glutathione and natural vitamin C and decrease in blood cell counts as young cells are killed and when these two symptoms coincide in the body it becomes very susceptible to opportunistic infections which become difficult to treat with other immunosuppressive or immunotoxic medications.
All the drugs used in AIDS patients are toxic and induce free radical damage. AZT is probably the most toxic of them. They generate oxidative stress as well as create oxidative injury to cells and going by what Montagnier wrote in the Journal Of Infectious Diseases, that oxidative stress induces HIV replication, it would mean that these drugs are inducing HIV replication in “HIV-infected” patients. That is simply astounding, indeed but medical authorities take no cognizance of it.
On one hand we understand that viral toxins can create oxidative stress and that appears to be the cause of secondary diseases eg carcinomas or leukemia, especially in cases of chronic infections but the Montagnier-HIV (M-HIV) is actually induced by oxidative stress and its replication is inhibited by antioxidants. This sounds more like a latency disease wherein a certain length of the viral genome forms a conjugate with a protein molecule produced by the T4 cell or cells of the immune system and can renter it without inhibition, only to be reactivated later on by oxidative stress that breaks the conjugate. Naturally, antioxidants would prevent such breakage and help prevent the latency disease (see: THE EPSTEIN-BARR VIRUS IN AIDS). If so, it cannot be a new virus, but one that is already a harmless passenger in many people. And if oxidative stress is a factor in the reactivation, it is nothing more than a problem of nutrition and antioxidant intake as a measure of curbing the AIDS problem.
The NIAID cites “recent studies that have demonstrated a substantial viral burden and active viral replication in both the peripheral blood and lymphoid tissues even early in HIV infection (Fox et al., 1989; Coombs et al., 1989; Ho et al., 1989; Michael et al., 1992; Bagnarelli et al., 1992; Pantaleo et al., 1993b; Embretson et al., 1993; Piatak et al., 1993). One group has reported that 25 percent of CD4+ T cells in the lymph nodes of HIV-infected individuals harbor HIV DNA early in the course of disease (Embretson et al., 1993). Other data suggest that HIV infection is sustained by a dynamic process involving continuous rounds of new viral infection and the destruction and replacement of over 1 billion CD4+ T cells per day (Wei et al., 1995; Ho et al., 1995)”.
Several mechanisms of CD4+ T cell killing have been observed in lentivirus systems in vitro and may explain the progressive loss of these cells in HIV-infected individuals (reviewed in Garry, 1989; Fauci, 1993a; Pantaleo et al., 1993a) (Table 2). These mechanisms include disruption of the cell membrane as HIV buds from the surface (Leonard et al., 1988) or the intracellular accumulation of heterodisperse RNAs and unintegrated DNA (Pauza et al., 1990; Koga et al., 1988). Evidence also suggests that intracellular complexing of CD4 and viral envelope products can result in cell killing (Hoxie et al., 1986: see; Mechanisms Of CD4+ T Cell Depletion).
The biggest problem in the gallo-HIV theory which says that a pathogenic virus attackes the T4 cells of the immune system is this:-
“If HIV is claimed to cause AIDS by killing T-cells, how is the mass production of HIV in immortal T-cell lines posseble, as shown in the patent of 1984, as source of HIV proteins for “AIDS tests” by Gallo/NIH, Weiss/Burroughs Wellcome (UK), and Montagnier/Pasteur?.”The NIAID, which is a component of the National Institutes of Health (NIH), supports the Gallo theory that CD4+ T cells, the cells depleted in AIDS patients, are primary targets of HIV because of the affinity of the gp120 glycoprotein component of the viral envelope for the CD4 molecule (Dalgleish et al., 1984; Klatzmann et al., 1984b; McDougal et al., 1985a, 1986). These so-called T-helper cells coordinate a number of critical immunologic functions. The loss of these cells results in the progressive impairment of the immune system and is associated with a deteriorating clinical course (Pantaleo et al., 1993a). In advanced HIV disease, abnormalities of virtually every component of the immune system are evident (Fauci, 1993a; Pantaleo et al., 1993a). They clearly assert that primary HIV infection is associated with a burst of HIV viremia and often a concomitant abrupt decline of CD4+ T cells in the peripheral blood (Cooper et al., 1985; Daar et al., 1991; Tindall and Cooper, 1991; Clark et al., 1991; Pantaleo et al., 1993a, 1994). The decrease in circulating CD4+ T cells during primary infection is probably due both to HIV-mediated cell killing and to re-trafficking of cells to the lymphoid tissues and other organs (Fauci, 1993a). And while they stick to the viral pathogenic cause that must produce the same disease in all infected persons, they also state that "HIV disease, however, is not uniformly expressed in all individuals" (see: Course Of HIV Infection, The Relationship Between the Human Immunodeficiency Virus and the Acquired Immunodeficiency Syndrome, Sept 1995).
Yet, in the same breath, they also claim that "HIV infects and kills CD4+ T lymphocytes in vitro, although scientists have developed immortalized T-cell lines in order to propagate HIV in the laboratory (Popovic et al., 1984; Zagury et al., 1986; Garry, 1989; Clark et al., 1991)". Now Gallo has something extremely exciting here. And rather interesting too. Simply because, if he tells us how he developed an immortalized line of T4 cell that are infected with HIV, he has a cure for HIV AIDS and he wins the Nobel Prize! So, inspite of the "several killing mechanisms observed" and that "HIV infection is sustained by a dynamic process involving continuous rounds of new viral infection and the destruction and replacement of over 1 billion CD4+ T cells per day " Gallo is actually replicating the virulent HIV in an immortalized lines of T4 cells for 21 years!
The HIV postulate for AIDS also claims that, once the virus infects CD4+ T cells, the virus’ genetic material is permanently integrated into the cell’s chromosomes, establishing permanent latency within infected cells. After infection, the HIV incorporates its genetic material into the host cell DNA. If a cell reproduces itself, each new cell also contains the integrated HIV genes. The virus can hide its genetic material for prolonged periods until the cell is activated and makes new viruses. So, its not an aggressive pathogen. And how do you culture HIV in an immortal line of T4 cells if it permanently integrates into the cell’s chromosome?
In order to say that a virus is the cause of a disease, it must be present in every case of the disease. The virus must be isolated and grown in a pure culture and used to reinfect a healthy host in which it replicates and causes the same disease. The virus must be recoverable and isolated from the experimentally reinfected host. This framework forms the classical postulates for disease causation, called the Koch Postulates.
Gallo was not able to isolate a "new virus" by applying the Koch postulates but clamied to have "isolated" a virus from the blood of one AIDS patient who was also suffering from leukemia. Without applying the classical Koch postulates, he went on to conclude that "HIV is the probable cause of AIDS. Today, we know that there are many AIDS patients who do not have such a virus and their condition is not a pathogenically caused but rather biochemically caused through oxidative stress that is caused by chemical stressors in certain population sub-groups or in populations who suffer chronic malnutrition or chronic oxidative stress.
The NIAID now says that "recent developments in HIV research provide some of the strongest evidence for the causative role of HIV in AIDS and fulfill the classical postulates for disease causation." It is a lucrative dogma that is not easy to let go and a liason has been set up to propagate it to the public (The Relationship Between the Human Immunodeficiency Virus and the Acquired Immunodeficiency Syndrome, Sept 1995).
Recent developments in HIV research provide some of the strongest evidence for the causative role of HIV in AIDS and fulfill the classical postulates for disease causation developed by Henle and Koch in the 19th century (Koch's postulates reviewed in Evans, 1976, 1989a; Harden, 1992). Koch's postulates have been variously interpreted by many scientists over the years. They claim that “one scientist who asserts that HIV does not cause AIDS has set forth the following interpretation of the postulates for proving the causal relationship between a microorganism and a specific disease (Duesberg, 1987)”:
1. The microorganism must be found in all cases of the disease. 2. It must be isolated from the host and grown in pure culture. 3. It must reproduce the original disease when introduced into a susceptible host. 4. It must be found in the experimental host so infectedThe Koch postulates are such simple rules that they require no interpretation unlike the provisions of a statute. They are clear and plain. The literal meaning does not warrant any intepretation.
The NIAID states that recent developments in HIV/AIDS research have shown that HIV fulfills these criteria as the cause of AIDS. All four postulates have been fulfilled in three laboratory workers with no other risk factors who have developed AIDS or severe immunosuppression after accidental exposure to concentrated HIVIIIB in the laboratory (Blattner et al., 1993; Reitz et al., 1994; Cohen, 1994c). Now accidental exposure to concentrates, without isolation is regarded by the AIDS posse as having fulfilled all the criteria that HIV is the cause of AIDS. Abandoning science and scientific rigors and substituting accidental exposures represents a real devotion to the HIV dogma as well as a considerable embarrassment to science.
Next they claim that they have in fact isolated the HIV. Improvements in co-culture techniques have allowed the isolation of HIV in virtually all AIDS patients, as well as in almost all seropositive individuals with both early- and late-stage disease (Coombs et al., 1989; Schnittman et al., 1989; Ho et al., 1989; Jackson et al., 1990). If so, what about all those AIDS patients who do not have a virus to link to their condition and what about the false seropositives? A close study of AIDS shows that there are people who test seropositive and show no symptoms of the disease and there are those who have AIDS but do not test positive. How can the HIV be found in almost all seropositive individuals when many individuals in a long list of conditions also test positive?
Christine Johnson, a researcher and author, compiled a long list of conditions documented in scientific literature to cause positives on HIV tests, and provides references for each condition. She cites 63 research papers by over 100 scientists. The list -
Anti-carbohydrate antibodies; Naturally-occurring antibodies; Passive immunization: receipt of gamma globulin or immune globulin (as prophylaxis against infection which contains antibodies); Leprosy; Tuberculosis; Mycobacterium avium; Systemic lupus erythematosus; Renal (kidney) failure; Hemodialysis/renal failure; Alpha interferon therapy in hemodialysis patients; flu vaccination; Herpes simplex I; Herpes simplex II; upper respiratory tract infection (cold or flu); Recent viral infection or exposure to viral vaccines; Pregnancy in multiparous women; Malaria; High levels of circulating immune complexes; Hypergammaglobulinemia (high levels of antibodies); False positives on other tests, including RPR (rapid plasma reagent) test for syphilis; Rheumatoid arthritis; Hepatitis B vaccination; Tetanus vaccination; Organ transplantation; Renal transplantation; Anti-lymphocyte antibodies; Anti-collagen antibodies (found in gay men, haemophiliacs, Africans of both sexes and people with leprosy); Serum-positive for rheumatoid factor, antinuclear antibody (both found in rheumatoid arthritis and other autoantibodies); Autoimmune diseases; Systemic lupus erythematosus, scleroderma, connective tissue disease, dermatomyositis Acute viral infections, DNA viral infections; Malignant neoplasms (cancers); alcoholic hepatitis/alcoholic liver disease; Primary sclerosing cholangitis; Hepatitis; "Sticky" blood (in Africans); Antibodies with a high affinity for polystyrene (used in the test kits); Blood transfusions, multiple blood transfusions; Multiple myeloma; HLA antibodies (to Class I and II leukocyte antigens); Anti-smooth muscle antibody; Anti-parietal cell antibody; Anti-hepatitis A IgM (antibody); Anti-Hbc IgM; Administration of human immunoglobulin preparations pooled before 1985; Haemophilia; Haematologic malignant disorders/lymphoma; Primary biliary cirrhosis; Stevens-Johnson syndrome; Q-fever with associated hepatitis; Heat-treated specimens; Lipemic serum (blood with high levels of fat or lipids); Haemolyzed serum (blood where haemoglobin is separated from the red cells); Hyperbilirubinemia; Globulins produced during polyclonal gammopathies (which are seen in AIDS risk groups); Healthy individuals as a result of poorly-understood cross-reactions; Normal human ribonucleoproteins; Other retroviruses; Anti-mitochondrial antibodies; Anti-nuclear antibodies; Anti-microsomal antibodies; T-cell leukocyte antigen antibodies; Proteins on the filter paper; Epstein-Barr virus; Visceral leishmaniasis and Receptive anal sex.Researchers estimate that only about 1 in 60,000 virions found using quantitative PCR were actually infectious, and that other studies have found as few as 1 in 10 million. The researchers were not able to culture any virus at all in more than half (35 of 66) patients, and people with no infectious virus at all had viral loads as high as 815,000 copies per milliliter. The study subjects had all tested positive on the ELISA and Western Blot antibody tests which are the two tests currently used to diagnose people as being HIV-positive, they all had high viral loads, and yet the majority of them had no culturable infectious units of HIV. This difficulty in finding active HIV particles has been encountered by many researchers who have tried to confirm the presence of HIV in people's blood (Chiodi 1988, Gallo 1984, Learmont 1992, Popovic 1984, Sarngadharan 1984, Schupbach 1984)(see:False Positive Viral Loads, What Are We Measuring? By Matt Irwin,2001).
“In 1990, of 20.2 million HIV tests done in Russia only 112 were confirmed and about 20,000 were false positives, 1991 saw some 30,000 false positives out of 29.4 million tests, with only 66 confirmations...in 1991 alone some 8000 false-positive results were reported in pregnant women, with only 6 confirmations [presumably with the Western Blot test]” (Voevodin A. HIV screening in Russia. Lancet. 1992;339:1548). We are a testing culture. Furthermore, any increase in the false positive rate could turn a screening program into a social catastrophe (see: Screening For HIV: Can We afford The False Positive Rate? The New England Journal Of Medicine, Vol. 317 No.4, July 23, 1987.
The problem with testing is that it leads to the administration of toxic drugs if the result is seropositive, even though the test kits carry a disclaimer that they cannot be used to diagnose and treat AIDS. Ironically, the treatment offered by modern medical science is a drug that is “toxic by inhalation” and can produce the same symptoms of AIDS! (see: The Azt Label; see: Drugs AIDS Patients Must Avoid).It is a demonstrable fact that there is a surprisingly high rate of false positives. This observation raises enough questions to advise caution regarding the current heavy reliance placed on tests when making treatment decisions for people "diagnosed" HIV-positive and to consider non-toxic alternatives as the first line of treatment.
There is strong evidence to show that HIV-seropositive individuals are deficient in glutathione peroxidase. Gil and colleagues 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 less than 0.05) reduction of the selenoenzyme in the infected group. Beyond this, Batterham and co-workers 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-workers 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 (see: AIDS - THE SELENO-ENZYME SOLUTION, Nexus Magazine, Volume 11, Number 2 (February-March 2004).
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 a more accurate predictor 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 (Nexus Magazine, Volume 11, Number 2 (February-March 2004). These studies may be properly interpreted to conclude that there is a deficiency in key antioxidant factors, namely selenium and glutathione that are indicators of oxidative stress and support the biochemical origin of the condition rather than that HIV causes depletion of glutathione. However, irrespective of the conclusion, the fact remains that antioxidant deficiencies are a critical factor in AIDS patients and in the progression of the disease, keeping in mind that glutathione levels are predictive of cell death and life expectancy. Cells die when their glutathione levels drop below 80%. Natural killer (NK) cells may become glutathione-depleted over time and immune response weakens as they lose the ability to recognize abnormal proteins on cancer cell surface. And there are many disease conditions associated with low glutathione levels. Overall, glutathione and natural vitamin C levels are important in the healthy functioning of the immune system. It enhances the body's natural immune activity involving the multiplication of lymphocytes and antibody production which requires normal levels of glutathione inside the lymphocytes (see: “Breakthrough In Cell-Defense" by Dr. Allan C. Somersall with Dr. Gustavo Bounous).
Palamara et al, investigated the effect of glutathione on the replication of human immunodeficiency virus (HIV) in chronically infected macrophages, a known reservoir of the virus in the body [AIDS Res Hum Retroviruses 1996 Nov 1;12(16):1537-41] Exogenous GSH strongly suppresses the production of p24gag protein as well as the virus infectivity. This is related to a dramatic decrease in both budding and release of virus particles from chronically infected cells (either macrophages or lymphocytes) This study suggests that GSH (glutathione) can interfere with late stages of virus replication and the suppression of virus replication by GSH is related to the selective inhibition of envelope glycoproteins. These results suggest a potential role of GSH taken in combination with other appropriate phytochemicals. But there is an enen more interesting study.
Herzenberg et al conducted in vitro studies that showed that low GSH levels both promote HIV expression and impair T cell function and they suggested a link between GSH depletion and HIV disease progression (Glutathione deficiency is associated with impaired survival in HIV disease, Proc Natl Acad Sci U S A. 1997 Mar 4;94(5):1967-72). Their clinical studies directly demonstrate that low GSH levels predict poor survival in otherwise indistinguishable HIV-infected subjects while, specifically, that GSH deficiency in CD4 T cells from such subjects is associated with markedly decreased survival 2-3 years after baseline data collection. This finding "establishes GSH deficiency as a key determinant of survival in AIDS patients and the unnecessary or excessive use of acetaminophen, alcohol, or other drugs known to deplete GSH should be avoided by HIV-infected individuals". And quite naturally, minerals that work with glutathione and enhance its antioxidant enzyme activity are equally important.
Sprietsma J.E. showed that the way in which the right amount of cysteine, glutathione (GSH), and copper and zinc ions made available in the right place at the right time and in the right form can prevent an unchecked multiplication of (AIDS) viruses in a more passive or active way forms the basis for the AIDS zinc-deficiency hypothesis (A-Z hypothesis) presented in this article [Med Hypotheses. 1999 Jun;52(6):529-38. Review] Comment in: Med Hypotheses. 2000 Nov;55(5):456-7. Zinc and copper ions that remain available in sufficient amounts via cysteine/GSH are effective natural inhibitors/combaters of (AIDS) viruses and thereby prevent the development of chronic virus diseases that can lead to AIDS, autoimmune diseases, (food) allergies and/or cancer. These ions are important for the efficient functioning of the glutathione-catalase antioxidant system that converts hydroxyl radicals into water and oxygen and also convert hydrogen peroxide into water and oxygen. Their biochemical activity that converts toxic radicals and chemicals into useful intracellular water and oxygen are key to healthy function of the cells and for the promotion of antioxidant-driven biochemical pathways in the body. Deficiencies of these antioxidant enzymes and ions result is free radical induced pathways that lead to the development of disease states and aid the progression of disease conditions.
There are researchers who have shown the existence of alternative treatment that is relevant to AIDS patients because it:-
1. Has strong antioxidant function that can remove oxidative stress effectively in the liver as well as in the blood tissue, 2. Improves endothelial function and therefore prevents the formation of superoxide in the endothelium and thereby prevents the formation of the highly reactive peoxynitrite radical by reacting with excess nitric oxide produced by endothelial dysfunction, which reduces the risk of oxidative stress that can oxidatively damage cell membranes, and 3. There are phytochemicals from dietary sources that inhibit viral integrase enzyme that is essential to the replication of the HIV (but how that could be proven when the HIV remains illusive and is not isolated, is a different matter, but that should not bother the AIDS posse, because they accept it as the cause of AIDS).Interestingly, all of the above health benefits are found in dietary sources or edible substances, including in a vegetable called artichoke. Artichoke leaf extracts have been shown to protect the liver, which also proves its possible use in integrated medicine involving drugs that have liver toxicities. The active ingredients in artichoke, namely caffeoylquinic acids such as cynarin also have antioxidant properties that can biochemically repair cell membranes and restore membrane integrity.
Oxidative damage to cell membranes, oxidative damage to mDNA, oxidative damage to the cytochrome system and depletion of coenzyme Q10 and in particular the depletion of glutathione leads to cell death.
Artichoke leaf extracts have also been demostrated to improve endothelial function which proves, at the biochemical level, that the antioxidants in the leaf extracts can effectively scavenge the superoxide in endothelial cells. This activity inhibits or prevents the formation of the peroxynitrite radical and the hydroxyl radical that can oxidatively damage cell membranes and mDNA and DNA respectively.
Interestingly, caffeoylquinic acids from artichoke have been “demonstrated to have potent activity against HIV” as “these compounds inhibit the HIV integrase enzyme which is essential to the virus’s ability to reproduce.”
Since medical science establishes a diagnosis in hospitals by seropositive test results using test kits that carry a disclaimer that they cannot be used to diagnose AIDS and certain other criteria such as depressed CD4 cell counts, anything that can be derived from dietary sources and found to be antioxidant in nature that can inhibit HIV replication while, at the same time reduce or remove oxidative stress (depending on the dosage) and improve immune cell function and increase blood cell counts would naturally merit serious medical attention as the first line of treatment. This is all the more significant as an approach in the face of the facts that AZT and retrovirals are toxic and can generate oxidative stress in the body while AZT is known to cause the same symptoms as seen in AIDS patients, including myopathy and immune suppression and it is immunotoxic to the extent that it can sufficiently suppress the immune system to lead to the establishment of opportunistic infections and cancers.
In a proper and comprehensive approach, the use of extracts of artichoke leaves must be logically augmented. Silymarin, from milk thistle, has been demonstrated to improve glutathione levels in liver cells by about 50% and in blood cells by about 35%. Silymarin has a much higher antioxidant activity than natural vitamin C or E. Raising glutathione levels improves free radical scavenging activity in cells and improves cell biochemistry that leads to improved cell function. Together with catalase, it improves the cell’s ability to scavenge hydroxyl radicals and also convert hydrogen peroxide formed during cell metabolism into water and oxygen both of which are important to healthy cell function.
Artichoke and milk thistle administration would result in improvement in the immune function of the body. This regime can be further augment by eggs, lime and citrus fruits and dried figs to broaden the range of dietary antioxidant intake. Selenium from eggs and brazil nuts is an important constituent of this regime as the role of selenium in reversing AIDS has already been shown. Selenium intake also helps to raise glutathione levels in cells. Research at Stanford University “now suggests that raising glutathione levels in patients extends lives even if CD4 count is low.” One way to augment natural antioxidant formulations for therapeutic and curative value is to use the superantioxidants together with the natural antioxidants that form the body’s natural antioxidant network system, such as alpha-lopic acid, coenzyme Q10, L-ascorbic acid, natural vitamin E etc etc.
Natural antioxidants that scavenge the superoxide, the peroxynitrite and hydroxyl radicals tend to boost immune cell function and slowly the whole systen begins to improve provided the amounts in the diet are sufficient to improve the function of the body’s natural antioxidant network system. Hence, the administration of a single natural antioxidant is not recommended. Methionine and cysteine from natural sources when taken together with foods rich in vitamin A, C and E can also effectively raise glutathione and catalase levels in cells. Pycnogenol from the bark of Pinus maritima can also be considered because it can scavenge both the peroxynitrite and hydroxyl radicals leading to improvements in immune function. A study in 1996, in which the immune systems of mice were suppressed with “retroviruses” such as “mouse-HIV” and by feeding ethanol, showed that pycnogenol intake can lead to a rebound of impaired immune systems with increased levels of NK cells and other cells of the immune system.
Natural beta-carotene reduces or inhibits the oxidation of lipids in the blood. Oxidized lipids tend to increase the risk of heart attacks as they can oxidatively damage the cell membranes in heart cells while depleting coenzyme Q10. Beta-carotene also scavenges the superoxide and can help improve endothelial function and improve immune function as levels of T4 cells and T8 cells improve with appropriate amounts in the diet. Natural beta-carotene, therefore forms an essential part of the anti-AIDS diet regime.
The picture is imcomplete without taking into account the role of medium chain fatty acids which leads us to cononut oil. Contrary to the propaganda in the west against tropical oils, coconut oil is not an artery-clogging oil. It does not contain long-chain fatty acids but only medium chain fattry acids (MCFA) – the same MCFA found in human breat milk. If I had my way, I would rename the coconut, known as Cocos nucifera to Cocos breastifera. MCFAs from natural sources have a special biochemistry in mammalian biological systems.
Coconut oil contains triglycerides which are broken down to monoglycerides and free fatty acids in the liver. If the body needs energy, these can be metabolized to yield energy, unlike long chain fatty acids that may end up as circulating lipoproteins that can get oxidixed in the blood and posed a risk to the heart or the cardiovascular system.
The monoglycerides, such as monolaurin and free fatty acids have antimicrobial properties as well. The most active are monolaurin and monocaprin. Coconout oil, in its natural form has no antimicrobial properties but these properties are found in the components after it is ingested in the body. These compounds can decrease viral loads by destroying the lipid coats of lipid coated viruses and by inactivation of enveloped viruses. Hence coconut must be integrated into the anti-AIDS diet.
The key points in designing alternative treatments is to first look for scientific evidence that would advance the general and specific ideas that are integral in the diagniosis and in the therapy put together from dietary sources or edible substances which must be based on sound research on the main phytochemicals involved while avoiding toxic drugs that can produce the same or similar symptoms in the the patients. In general prolonged use of toxic drugs can harm the quality of life while appropriate combinations of phytochemicals from food and edible sources can lead to improvements in the quality of life. But legally speaking, the point to advocate is this – if a treatment must be imposed especially after a doubtful diagnosis based on science that is frowned upon and the method also casts a serious doubt or a caution, then only phytochemical regimes from dietary sources or edible substances can be imposed and tried in preference to toxic medication especially the type of drugs to be avoided in that particular condition.
Toxic medication has gained widespread use and its prologed use in patients is fast becoming an issue in public health. For instance, the use of drugs in patients with heart disease that also inhibit the formation of coenzyme Q10 in the body will increase the risk of heart attacks and that becomes an issue in public health. US researchers say that “popular painkillers such as aspirin, ibuprofen and acetaminophen can raise blood pressure and thus raise the risk of heart disease among men” (Archives of Internal Medicine, 2002) is another example of drugs that cause concern in public health. These researchers reported that men who took such drugs for most days of the week were about one-third more likely to be diagnosed with high blood pressure than men not taking them and men who took paracetamol six or seven days a week were 34% more likely to be diagnosed with high blood pressure than men who dod not take anagesics. In the near future more evidence will come from studies to show that drugs cause ceretain diseases states to develop or otherwise increase the risk of developing disease conditions.
Of course, in the case of AZT the evidence is clear that it causes myopathy and other symptoms associated with AIDS. Hence, the greater and urgent need for alternatives.
Further References1. Gobhardt R, Antioxidative and Protective Properties of Extracts from Leaves of the Artichoke (Cynara scolymus L.) Against Hydroperoxide Induced Oxidative in Cultured Rat Hepatocytes, Toxicol Appl Pharmacol, 1997. 44(2);277-286.2. Lupatelli et al, Artichoke Juice Improves Endothelial Function in Hyperlipemia, Life Science, 2004;76(7):775-782.
3. Pristautz H., Cynarin in the Modern Treatment of Hyperlipemias, Weiner Medizinische Wocheschrift, 1975: 1223:705-709.
4. Michael Murray et al, The Encyclopedia of Healing Foods, Atria Books, Ny p 157.
5. David Highes, Journal of Laboratory and Clinical Medicine, March 1997; cf James Balch MD, The Superantioxidants, 1998, M Evans & Co Inc, NY, p128, 129.
6. James Balch MD, The Superantioxidants, 1998, M Evans & Co Inc, NY, p 100.
7. James Balch MD, The Superantioxidants, 1998, M Evans & Co Inc, NY, p 107.
8. Kritchevasky SB, Beta-carotene, carotenoids and the Prevention of Coronary Heart Disease, The Journal of Nutrition, 1999;129(1):5-8.
9. Hikina et al, The Antihepatoxic Actions of Flavolignans from Silybum marianum Fruits, Planta Medica, 1984, 50:248-250.
10. Hierholzer et al, In vitro effects of Monolaurin Compounds on Enveloped RNA and DNA viruses, 1982, Journal of Food Safety 4.
11. Isaacs and Thormar, The Role of Milk-derived Antimicrobial Lipids as Antiviral and Antimicrobial Agents, 1991, Immunology of Milk and the Neonate, edited by J Mestecky, Blair C and Ogra PL, NY, Plenum Press.
12. Isaacs et al, Addition of Lipases to Infant Formulas Produces Antiviral and Antibacterial Activity, Journal Of Nutritional Biochemistry 3.
13. Isaacs et al, Inactivation of Enveloped Viruses in Human Bodily Fluids by Purified Lipid, 1992, Annals of the New York Academy of Sciences 724.
14. Kabara JJ, Fatty acids and Derivatives as Antimicrobial Agents, The Pharmacological Effect of Lipids, American Oil Chemists Society.
15. Kabarra JJ, Antimicrobial Agents Derived from Fatty Acids, Journal of the American Oil Chemists Society 61.
16. Thormar et al, Inactivation of Enveloped Viruses and Killing of Cells by Fatty Acids and Monoglycerides, 1987, Antimicrobial Agents and Chemotherapy 31.
17. New Sunday Times, March 4, 2007, FOCUS p43.
- - -
Other articles by Beldeu Singh:THE EPSTEIN-BARR VIRUS IN AIDS
AIDS, NON-HIV AIDS AND PRESCRIPTION AIDS
DON’T QUESTION THE GALLO-HIV AIDS DOGMA
TOXIC RETROVIRALS: ALL AIDS PATIENTS ARE GUINEA PIGS
MOURNING DEATH BY AZT AND CELEBRATING GALLO's PROOF THAT HIV DOES NOT CAUSE AIDS
CAN I HAVE MY CHEMO SUPPLEMENT PLEASE!
(Scroll down one third of that page to find the title...)VACCINES, ANTIBODIES AND THE HIV RIDDLE
Flowers and Spices: Ayurveda or Toxic Chemotherapy?
Lead Toxicity, Free Radicals and AIDS: Is There a Connection?
CANCER AND MICRONUTRIENTS – IS THERE A CONNECTION WORTH EXPLORING?
There is no case for integrated medicine
Managing the Aging Process After Menopause
SYNTHETIC ANTIOXIDANTS ARE HARMFUL
WHY OMEGA-3 FISH OIL PROTECTS YOUR HEART AND BRAIN
DEVELOPMENT OF CANCER CELLS - GENETIC OR BIOCHEMICAL ORIGIN?
The Lazarus Effect or AIDS by Prescripton
THE POWER OF PSEUDO-SCIENCE IN AIDS DIAGNOSTICS
THERE WILL NEVER BE A VACCINE FOR HIV-AIDS
HEALTHY BODIES ARE NO GOOD TO BIG PHARMA
See also:
Mitochondrial DNA mutations can cause degenerative heart and muscle disease
A single change in the DNA of mitochondria – the cellular power plants that generate energy in all human cells – has been found to cause degenerative heart and muscle disease, according to University of California, Irvine researchers.As the mitochondrial DNA of our cells accumulates damage with age, the blueprints required to sustain energy production are lost, the body's equivalent of a brownout. The resulting age-related decline in cellular energy production ultimately leads to tissue and organ failure and the development of clinical disease or illness. Thus the accumulation of mtDNA damage may explain aging and the delayed-onset and progressive course of age-related diseases and aging.
Selenium pills 'may combat HIV'
The University of Miami found a lower HIV viral load in patients who took selenium supplements for nine months. Selenium deficiencies have been recorded in HIV patients, and evidence suggests the mineral can improve the function of the immune system.AIDS-defining illnesses: their causes and treatment
Study prompts concern about side effects of antiretrovirals
(link no longer active)
Metabolic abnormalities caused by side effects from antiretroviral drugs are becoming increasingly prevalent among Thais living with HIV/Aids, recent studies have found. According to a pilot study by Ramathibodi Hospital's Faculty of Medicine, published in the Journal of the Medical Association Thailand, the long-term toxicity of antiretroviral treatment has become more recognised through a variety of metabolic abnormalities including lipodystrophy, which affects body fat, and dyslipidemia, which affects the blood.
A recently released book:The Origin, Persistence and Failings of HIV/AIDS Theory
Thanks to enormous funding for educational programs, the whole world "knows" that HIV causes AIDS. But is what we know compatible with the facts? This book challenges the conventional wisdom on this issue. Collating and analyzing, for the first time, the results of more than two decades of HIV testing, it reveals that the common assumptions about HIV and AIDS are incompatible with the published data. Among the many topics explored are the failings of HIV testing, statistical evidence that HIV is neither sexually transmitted nor increasingly prevalent, and problems caused by the differing diagnostic criteria for AIDS around the world.
But how could everyone have been wrong for so long? This vital question, unaddressed in previous works questioning the HIV - AIDS connection, is central to this book. The author considers comparable missteps of modern science, and discusses how funding influences discovery in today's scientific circles.
Henry H. Bauer is Professor Emeritus of Chemistry & Science Studies and Dean Emeritus of Arts & Sciences at Virginia Polytechnic Institute & State University (Virginia Tech). He lives in Blacksburg, Virginia.
The book is available from McFarland and Amazon
posted by Sepp Hasslberger on Monday May 7 2007
updated on Wednesday November 17 2010URL of this article:
http://www.newmediaexplorer.org/sepp/2007/05/07/alternatives_to_azt_in_aids_patients.htm
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