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From The Work of Dr Heinrich Kremer on AIDS By John Kirkham In the absence of an English translation of Kremer’s book, the aim of this article is to present what I hope is an easily assimilable interpretation of Kremer’s work which makes clear the AIDS implications of vitally important medical research done after the enshrinement of the dogma that HIV causes AIDS.
Certain types of immune system cells (neutrophils and macrophages) eliminate microbes by producing nitric oxide (NO) gas. There must be a balance between NO gas-producing immune cells and those that do not produce NO gas. This balance between cellular and so-called humoral (antibody) immunity can be disturbed by non-infectious as well as infectious factors, and can lead to an acquired deficiency in cellular immunity (AIDS). Over-stimulation of an immune cell’s NO gas production that is either too strong or lasts too long leads to compensatory inhibition of NO gas production as a protective response and increased activation of antibody-producing cells. The end result can be an uninhibited rise in opportunistic microbes such as fungi, parasites, mycobacteria, and viruses within the body’s cells that would normally be eliminated without symptoms by NO gas.
During the NO gas defence process, cells, including NO gas producing cells, must be protected from potential damage and accelerated death caused by NO gas production and this is an important role of antioxidants. Nutritional intake must be sufficient to provide for the availability of antioxidants inside cells during this NO gas defence process and other NO inducing processes. If antioxidant supplies are insufficient or used up by various combinations of oxidising agents, toxic and pharmatoxic substances, malnutrition or lack of nutrition, foreign protein intake, chronic infections, lack of hormone regulation, emotional stress, etc. the NO gas production can no longer be neutralised sufficiently. This causes increased cell breakdown and cell-biology counter reactions to occur in immune cells and non-immune cells, the ultimate result of which is the effective switch off of immune cell NO gas production.
T-cells are particular types of cells important in cellular immunity. According to the Establishment, AIDS is the result of HIV decreasing a subset of T-cells known as CD4 cells, although it cannot explain how this happens. There are two types of CD4 cells: Th1 cells and Th2 cells (3). Th1 cells produce inflammatory immunological messenger chemicals (cytokines) such as gamma-interferon, that stimulate macrophages. Macrophages envelop invading microbes (a process called phagocytosis) and kill them using NO gas. Another important role of macrophages is the removal of dead and damaged cells and cell debris, again by phagocytosis. Th2 cells stimulate antibody production.
Under
conditions of persistent oxidative and nutritional stress the persistent
over-production of NO gas cannot be countered by an adequate supply
of antioxidants, particularly glutathione. The body responds to this
condition by releasing cortisol (an anti-inflammatory hormone) and reducing
the production of inflammatory cytokines by reducing the number of T-cells
that mature into Th1 cells, they mature into Th2 cells instead. These
Th2 cells migrate to the bone marrow where they stimulate antibody production,
hence the low T-cell count attributed to HIV. Once antibody production
exceeds an arbitrary threshold level, a positive HIV test occurs. Even
the use of recombinant (genetically engineered) proteins (never proven
to belong to HIV anyway) in the HIV test cannot prevent the binding
of non-specific antibodies, this is why the HIV tests called ELISA tests
use blood serum dilution factors. If the oxidative stress continues
unabated then the system responds by effectively switching off immune
cell NO gas production. This is called the Th1/Th2 switch. The human organism responds to various psychological, toxic, infectious, traumatic or nutritional stresses with an activation of the hypothalamus, the pituitary gland and the adrenal gland. The hypothalamus-pituitary-adrenals is called the neuroendocrine stress axis. This has survival value in “fight or flight” situations because it initiates reactions of the catabolic (cellular substance breakdown) metabolism in order to liberate energy quickly. The adrenal gland releases hormones called glucocorticoids and cortisol to contain inflammatory damage caused by this process, these hormones are natural glucocorticosterioids which suppress inflammatory cellular immune responses (11). A persistently raised cortisol level in the blood (known as hypercortisolism) impairs the cellular immune responses associated with Th1 cells. A high cortisol level causes Th2 cells to migrate to the bone marrow (4) where they activate antibody producing cells (B-cells). The activation of B-cells, and their subsequent antibody production, is also enhanced by cortisol (5). People who are at risk of getting AIDS have a persistent catabolic (cell breakdown) metabolism. For information on the important causal connection between AIDS and medical treatment with glucocorticosterioids you are referred to http://www.virusmyth.net/aids/data/mabcortico.htm
AIDS is primarily a result of persistent oxidative stress which manifests as a persistently low antioxidant level in general and of a particular protective chemical group, called a sulphydryl group, in particular. The sulphydryl (SH) groups are lost as a result of a chemical process called oxidation. The body provides sulphydryl groups in the form of glutathione. The sulphydryl groups (either from glutathione or its precursor cysteine) protect body structures by reacting with oxidising agents that would otherwise damage cells, the SH content of cysteine containing proteins is crucial for the transfer of oxygen through cell membranes. One effect of the loss of sulphydryl groups in cells is the polymerisation of a protein called actin which makes up the skeleton of cells. This leads to a weakening of the cell membrane which eventually kills the cell. It also activates nucleases (enzymes which breakdown DNA and RNA) and proteases (enzymes which breakdown proteins) within cells so that, with increased cell death, fragments of DNA, RNA and proteins reach the extracellular space in large amounts. Auto-antibodies generated against these cellular fragments can cause a false positive HIV test.
AIDS and the Drug Connection
Mitochondria are the energy factories of cells. Their DNA is not protected by the cell nucleus. There is no nuclear repair mechanism for mitochondrial DNA because mitochondria are outside the nucleus, they are dispersed within the fluid (known as the cytoplasm) surrounding the nucleus. Exposure to oxidising agents provides a source of harmful chemicals called free-radicals that can damage cells and mitochondrial DNA. The damage to mitochondrial DNA can be cumulative.
Treatment with nucleoside analogues (AZT, ddI, 3TC etc.) and with Septrin (Bactrim) and related antibiotics has a very adverse effect on mitochondria. As oxidising agents these drugs reduce oxygen transport into cells by oxidising thiol groups. This oxygen is needed for the production of ATP (the chemical fuel of the cell) in mitochondria in a proces called oxidative phosphorylation. In addition they inhibit the synthesis of mitochondrial DNA, which also decreases the production of ATP. The reduction of ATP leads to an increase in free-radicals, which are themselves highly reactive oxidisers. Once the level of ATP declines to a certain level and the molecules which normally remove harmful free-radicals are all used up, these excess free-radicals cause even more DNA damage and therefore an even greater reduction in ATP, more free-radicals and therefore even more DNA damage, a vicious circle. The cell initiates programmed cell death. This effect is particularly severe in rapidly maturing cells with high turnover, such as CD4 cells
A major group of oxidising agents are recreational drugs. Nitrite inhalents (poppers) are particularly severe oxidising agents promoting cell damage and antioxidant deficiency. The unprecedentedly high usage of nitrite inhalants (poppers) which were an integral part of the gay scene from about 1974 was an important contributor to early Western AIDS. Their use spread into the heterosexual community 4 or 5 years later. To quote Newell et al (6) “These products have been found to be profoundly immunosuppresive for human lymphocytes [immune system cells] in vitro” See also Hersh et al. (7) and Goedert et al. (8). In addition, the widespread homosexual use of particular benzene derived lubricants from 1978 onwards may have been a factor providing accelerated progression to AIDS in early cases due to bone marrow suppressive effects.
A major contributing factor to early Western AIDS was the use of Septrin (also known as Septra, Bactrim, Co-trimoxazole) with impunity from the early 1970s onwards to treat a wide range of microbial infections, mostly in promiscuous homosexuals, especially stubborn urinary tract infections, intestinal infections and atypical pneumonias.
Septrin is a combination of two substances, sulphamethoxazole and trimethoprim. Trimethoprim is used to treat leukaemia. It does this by killing white blood cells, which happen to be collectively the cells of the immune system! Sulphamethoxazole inhibits the synthesis of folic acid and trimethoprim inhibits the conversion of folic acid into tetrahydrofolate. Without tetrahydrofolate, essential precursors for new DNA cannot be synthesised. Inhibition of this essential metabolic pathway for growth, cell differentiation and division causes the faulty development of nucleic acids, enzymes and other proteins or ends this development completely. The damaging consequences for mitochondrial DNA are considerable because it does not benefit from nuclear DNA repair mechanisms. Septrin is used to treat PCP but the fungus causing PCP eventually develops resistance to Septrin.
In Africa a vicious circle can sometimes arise whereby persistent malnutrition and/or high exposure to chronic infections and inflammations causes antioxidant deficiency and suppression of cellular immunity leading to further chronic infection, compounded antioxidant deficiency and so on. This is AIDS in Africa.
AIDS-causing conditions in the west (Septrin, anti-HIV drugs, Poppers etc.) are generally more hostile to T-cells than AIDS causing conditions in Africa. For this reason PCP is quite rare in Africa (see notes 9 and 10) except in young children. This is partly because immature CD4 and CD8 cells (which mature in the thymus) are prone to destruction by cortisol but mature T-cells are resistant (12). The immature and inexperienced immune systems of young children are more vulnerable to such effects.
The vast majority of Western AIDS patients sooner or later get PCP, it is the typical AIDS defining disease in the West. The PC fungus is just as ubiquitous in Africa as it is in the West so if HIV were really the cause of AIDS, PCP would be as prevalent in African “AIDS patients” as it is the West. The prevalence of PCP in Africa will only start to resemble that in the West when Africans have been liberally showered with the “anti-HIV” poisons.
Summary
The loss of cellular immunity that characterises AIDS and renders the body open to opportunistic infections occurs as follows:
1. Damaging overproduction of NO gas is normally prevented by an adequate level of antioxidants, especially glutathione. Persistent oxidative and nutritional stress impairs this antioxidant protection and stimulates the catabolic metabolism.
2. Cortisol is produced to relieve inflammatory damage, suppress cellular immunity and stimulate the activity of Th2. More T-cells mature into Th2 than into Th1.
3. If the oxidative stress continues unabated immune cell NO-gas production shuts down.
4.
The increased cell debris produced by a combination of catabolic
(cell breakdown) processes, the concurrent reduction in Th1 type CD4
cells (which inhibits the activation of macrophages whose role is to
kill microbes and remove dead cells and cell debris) and the lack of
immune cell NO gas production provides ideal conditions for fungi such
as the PCP fungus which feed on cell debris. This increased cell debris
can also register as increased “viral load”. Conclusion
AIDS is a manifestation of a cumulative imbalance in fundamental and interrelated oxidative, metabolic and immunological processes caused by a variety of either direct or indirect oxidative and/or nutritional stressors. References and Notes
1. FASEB J., 1997, Vol. 11:1077-1089 2. Proc. Natl. Acad. Sci. USA, 1997, Vol. 94:1967-1972 3. Ann. Rev. Immunol., 1989, Vol. 7:145-173 4. Immunology, 1975, Vol. 28:669-680 5. Journal of Immunology, 1977, Vol 119(2):598-603 6. Pharmacotherapy, 1984, Vol. 4:284-291 7. Cancer Research, 1983, Vol. 43:1365-1371 8. Lancet, Feb 20, 1982, pp 412-416 9.
Quote from American Journal of Respiratory and Critical Care Medicine,
1994, Vol. 149(6):1591-1596 “Detailed investigations confirm the
rarity of PCP in Africa and highlight non-specific interstitial pneumonitis
as the predominant diagnosis” 11. Ann. Internal Med. 1976, Vol. 84:304-315 12. Medical Hypothesis 1996, Vol. 46:551-555
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