The HIV-AIDS Titanic Hits its Own Iceberg

Beldeu Singh

By 1984, the proponents of HIV-causes AIDS claimed that they had “isolated” a new virus called the human immunodeficiency virus (HIV). It was said to be a retrovirus with an enzyme, reverse transcriptase [RT]. It is also said to be an enveloped virus although no one has seen its “budding process” under the electron microscope. It was stated to be the “probable cause of AIDS” and came to accepted as the causative agent of AIDS (Gallo RC, Montagnier L. The discovery of HIV as the cause of AIDS, New Engl J Med 2003;349:2283–5). It was made out to be a virulent pathogen that attacked the immune system (i.e. its white blood cells) and impaired it and later destroyed it leading to the establishment of opportunistic infections. Its spread, as an epidemic, however defies this possibility altogether.

This point is well put forth by Dr. Robert Root-Bernstein. Female prostitutes often have 200-300 sexual partners per year and are therefore assumed to have much higher rates of exposure to HIV and AIDS than the vast majority of heterosexuals. Many AIDS researchers assumed that female prostitutes would be the vectors (or means of transmission) of HIV and AIDS to the heterosexual community based on the fact that a single HIV-infected intravenous drug user or bisexual man could infect one female prostitute, who in turn could infect dozens or perhaps even hundreds of non-drug using heterosexual men. These men could, in turn, infect their other sexual partners, and an explosion of HIV and AIDS could occur among people without any obvious risk for AIDS. Paradoxically, no heterosexual epidemic has occurred and no evidence of female prostitutes transmitting HIV or AIDS into the heterosexual community exists for any Western nation. Transmission almost always seems to be drug related. In fact, sexual acquisition of HIV and AIDS among female prostitutes themselves is almost unknown in the absence of concomitant intravenous drug use. Cell-free viral particles have never been found directly in semen. In ‘American Journal of Epidemiology’ (Vol. 146, No.4), Nancy S. Padian et al reported: “We estimate that HIV infectivity for male-to-female transmission is low, approximately 0.0009 per contact, and that infectivity for female-to-male transmission is even lower.”

The HIV-causes AIDS hypothesis was devised to explain observations and to make predictions. Its predictions on how it would spread fails that hypothesis. Their first problem was due to the fact that they decided that they had indeed found an new virus in their supernatant solutions instead of isolating it through the process of reinfection of healthy cells and purifying it. Secondly, they decided that the particles in their supernatant were highly infective that targeted and killed T4 cell of the blood immune system. Let’s look at the other claims of the HIV hypothesis that were proposed to explain three observations:-

1. A decrease in a specific cell type, T4 lymphocytes
2. Opportunistic infections (OI), and
3. The high frequency of a malignancy, the Kaposi’s sarcoma (KS).

What defied the pathogenic cause of AIDS is that no other infectious agent causes such a diverse number of diseases. And it was further hypothesized that the HIV causes the syndrome indirectly. And then the titanic hits its iceberg. What is this indirect cause mechanism. The original causative idea that HIV kills the T4 cells and the consequent decrease in T4 cells (immune deficiency) leads to the appearance of the diseases which constitute the clinical syndrome. The decrease in T4 cells was stated to be the key factor of impairment of the immune system caused by the “HIV infection” and the diagnosis of AIDS.

AIDS studies run into other serious problems. Most researchers who use the test kits do not read the disclaimer on these test kits – that they cannot be used to diagnose and treat AIDS. Secondly, at one time it was said that these kits tested for the HIV antibodies and at other times they said that it tests for viral-specific proteins! A lot of people fail to realize that many of these studies are flawed because the so-called HIV was never isolated in accordance with the established steps in virology that require its purification and ability to reinfect healthy cells and to recover the virus from these infected cells. What Gallo has is only a supernatant that he has used to infect T4 cells that do not die upon his infecting them!. Finally, he talks about a p24 protein in his supernatant that has never been purified and never proven to be a HIV-specific protein. So, naturally, to make matters worse, many non-AIDS people test positive on these test kits and give a very large number of false positives.

So far, only “virus particles” have been noted or demonstrated. The presence of budding virus-like particles in human lymphoid cells used for HIV cultivation (VIIth International Conference on AIDS; 1991; Florence: O’Hara CJ, Groopman JE, Federman M, The ultrastructural and immunohistochemical demonstration of viral particles in lymph nodes from human immunodeficiency virus-related and non-human immunodeficiency virus-related lymphadenopathy syndromes, Hum Pathol 1988;19:545–9) support the possibility of AIDS as a latency disease associated with and triggered by oxidative stress (see: THE EPSTEIN-BARR VIRUS IN AIDS) but so far no one has observed the budding process under electron microscopy.

Later, they also claim that other cells act as HIV reservoirs, harboring intact viruses that may remain undetected by the immune system while it “targets” the cells of the immune system.

There is also no explanation on how an infected cell remains normal and remains undetected as an abnormal cell by NK cells or activated macrophages after the HIV incorporates its genetic material into the chromosomes of the cell. Such a virus, with such a capability, having a sophisticated enzyme system to incorporate its genetic material into the cells’ chromosomes and activate it later on into replicating itself cannot be so small and illusive that it avoids isolation and replication by other virologists. It must have a large amount of genetic material to be do all of those things but retroviruses as the fictitious Gallo-HIV is “gifted” with too little genetic material. Now the AIDS proponents observe only virus particles and may switch their hypothesis yet again – claiming that it is probably caused by virus particles or virus-like particles.

The retrovirus-like particles that have been seen in many non-infected cell lines used for “HIV isolation” including cord blood lymphocytes cannot be proven to be so by merely looking at their density 1.16 g/ml density in a sucrose gradient unless proven to be infective. So, even if they have an infective character in malnourished people and/or in people with chronic oxidative stress, it would a condition typifying oxidative stress and not a disease caused by virus infection as it was made out to be by the proponents of HIV-causes AIDS.

No particle of ‘HIV’ has ever been obtained pure, free of contaminants; nor has a complete piece of ‘HIV’ RNA (or the transcribed DNA) ever been proved to exist. Moreover, Dr David Ho admits that 99.8 per cent of putative ‘HIV particles’ are non-infectious; the remaining 0.2 per cent of ‘viral particles’, being defective, are not capable of replication. As a transmittable entity, ‘HIV’ could not survive in nature. This indicates that what we are calling ‘HIV’ is a misinterpreted, non-transmissible, endogenous epiphenomenon that should never have been classed as a virus. If particles are all that they observe, these particles may well come from a common virus such as the Epstein-Barr virus.

All of these have implications for insurers and in designing the AIDS cover and if there is no HIV virus, the insurers have collected premiums for a bogus pathogen. Some researchers claim 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). The biggest problem in medical science now is to show evidence of killing of T4 cells in AIDS patients by the HIV virus while Gallo is actually replicating the ‘virulent HIV’ in an immortalized lines of T4 cells for 22 years!.

We know that suppression of the immune system or impairing its function by low levels of natural antioxidants increases the risk of infections called opportunistic infections. Chronic oxidation stress and malnutrition are also factors, both singly and jointly that lead to immune suppression and lowering of white blood cell counts or even anaemia. There are studies that show decreases in T4 cells in drug users and if that condition persists, it leads to the development of AIDS. So, immune suppression precedes a positive antibody test (“HIV infection”) and not vice versa, which means that immune suppression is the cause of opportunistic infections and it is the cause of opportunistic infections. This point is well brought out by one study in drug users by Des Jarlias et al on “The relative risk for seroconversion among subjects with one or more CD4 count <500 cells/µl compared with HIV-negative subjects with all counts >500 cells/µl was 4.53” (Des Jarlais et al, CD4 lymphocytopenia among injecting drug users in New York City, J Acquir Immun Defic Syndr 1993;6:820–2).

Naturally, those with suppressed immune systems as indicated by relatively low T4 cell counts would be at a higher risk of infections. In another study, “low number of T4 cells was the highest risk factor for HIV infection” (Nicolosi et al, Incidence and risk factors of HIV infection: a prospective study of seronegative drug users from Milan and Northern Italy, 1987–1989. Epidemiology 1990;1:453–9). It appears that immune suppression leads to the development and progression of AIDS and that immunosuppression appears prior to an “HIV infection” was recognised by Montagnier as long ago as 1985. Depression in cell mediated immunity leads to AIDS. That is for sure but unfortunately, it is treated with drugs that further depress the immune system and can impair it to such an extent that it can cause the symptoms of AIDS! (see;ALTERNATIVES TO AZT IN AIDS PATIENTS).

In the Journal Of Infectious Diseases, Montagnier wrote that oxidative stress induces HIV replication! Since drugs cause oxidative stress, it would mean that these drugs are inducing HIV replication in “HIV-infected” patients. That is a paradox in treatment in modern medicine. If oxidative stress precedes HIV replication, then it means that there is sufficient oxidative stress to depress the immune system before the progression of AIDS. Their titanic is struck in the side.

If it is indeed true that the HIV replication is induced by oxidative stress, it is induced in people with chronic malnutrition and the answers in treatment and prevention strategies fall in natural antioxidant diets – not toxic drugs that generate free radicals in the body and cause oxidative stress.

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 mtDNA depletion activity explains muscular fatigue and muscular atrophy later on in its 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! It was labelled toxic by inhalation until a rushed trial turned it into ‘medicine’ to become a cornerstone in a multi-billion dollar industry. That medicine decreases T4 cells by killing them just as HIV was supposed to be doing! This fact, again has serious implications for health insurers.

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 means that natural antioxidants must be integrated into toxic therapies.

Chronic benzene poisoning results in great individual variation in signs and symptoms and includes lymphomas, myeloid leukemia, Hodgkin’s disease etc., much like in AIDS and mutagenesis due to severe free-radical damage. The cumulative effect of benzene and its derivatives takes a few to several years to develop and manifest, in most cases up to 10-12 years. Many drugs are benzene derivatives.

Free-radical damage reactions in cells produce toxic chemicals, destroy enzymes and kill cells. They also start chain reactions that are harmful to health and long term exposure to free-radicals can lead to chronic illness, chronic fatigue, cancers or early symptoms of aging. Benzene “burns out” the endocrine system and speeds up the aging process 100 fold, so in some AIDS cases the patients. The early cases of AIDS left a lasting impression of people who “died horrible deaths and looked like shriveled old men” due to immune system destruction caused by anaemia and leukocytopenia (see:AIDS, NON-HIV AIDS AND PRESCRIPTION AIDS). Excess free radicals always accelerate the aging process as well often interfering with healthy biochemical processes in the mitochondria.

Mitochondria are tiny structures within cells that convert the energy from food into a form that cells can use. Mitochondria also have a small amount of their own DNA. This genetic material is known as mitochondrial DNA or mtDNA. Mitochondrial DNA contains 37 genes. All of them are essential for normal mitochondrial function. Thirteen of these genes provide instructions for making enzymes involved in oxidative phosphorylation. Oxidative phosphorylation is a process that uses oxygen and simple sugars to create adenosine triphosphate (ATP). ATP is the cell’s main energy molecule to generate cellular energy that is used in the healthy biochemical pathways. The remaining genes carry instructions for making molecules called transfer RNAs (tRNAs) and ribosomal RNAs (rRNAs), which are chemical cousins of DNA. These types of RNA help assemble protein building blocks (amino acids) into functioning proteins. Hence, a block in the formation of ATP and proteins leads to fatigue and muscle wasting respectively. Free radical damage by ROS and the hydroxyl radical to the genetic material in mtDNA can lead to the development of cancers.

The matrix of mitochondria carries most of the respiratory enzymes of the citric acid cycle that are involved in the breakdown of sugars, proteins and fats for the production of ATP to generate cellular energy. Cells that require the most energy have high mitochondrial density. The cells of the brain, the skeletal muscles, the heart muscle and the eye contain the highest number of mitochondria (as many as 9,000 to 10,000 per cell) while the skin cells, which do not require much energy, contain only a few hundred of them. The heart also produces very high amounts of coenzyme Q10 which is an antioxidant enzyme that is effective in cell membrane repair and is important in ATP utilization to release energy for its continuous pumping activity.

Mitochondrial disorders can be acquired while under drug treatment. AZT treatment in AIDS patients has been shown to cause mtDNA depletion which in turn causes myopathic changes that are reversible upon termination of treatment. Chemotherapy agents such as fosfamide have been reported to decrease mitochondrial function. For mitochondria to reproduce themselves, a specific enzyme called gamma-DNA-polymerase or “pol-gamma” is required. Many drug medications have been found to interrupt pol gamma. Studies suggest that virtually all the nucleoside analog reverse transcriptase inhibitors (NRTIs) including AZT interrupt pol gamma to some extent. One study has already demonstrated that people given AZT had significant depletion of mitochondrial DNA in muscle tissue. So, free radical damage to mitochondria, whether by benzene and its derivatives or AZT or other toxic chemicals can cause the “chronic fatigue” and weight loss symptoms diagnosed in early AIDS patients.

Mitochondrial damage can possibly be a primary cause for low platelet count (thrombocytopenia), anaemia and low neutrophil count, regardless of HIV serostatus see:AIDS, NON-HIV AIDS AND PRESCRIPTION AIDS).

Mitochondrial damage means oxidative stress that impairs the cytochrome system in the mitochondria and free radical damage to its membranes as well as impairment of the MT protein system that binds the hydroxyl radical and transports it out of the mitochondria thus preventing oxidative damage within the mitochondria including oxidative damage to “pol-gamma” enzymes and mtDNA, whereby there is depletion of mitochondria in cells leading to fatigue and chronic fatigue. It excludes oxidative stress that merely lowers its ATP output.

”In order for mitochondria to reproduce themselves, a specific enzyme called gamma-DNA-polymerase, or “pol gamma” is required. Many medications have been found to interrupt pol gamma. Studies suggest that virtually all the nucleoside analog reverse transcriptase inhibitors (NRTIs) – such as AZT, 3TC, ddI, ddC, d4T, and abacavir – interrupt pol gamma to some extent. This disruption prevents the transport of long-chain fatty acids from being transported across the membrane wall into the mitochondria, where they are used as primary fuel and energy sources. As a result, fatty acids are dysfunctionally deposited and accumulated in muscle tissue. Without the cell’s main source of energy, the number of newly formed mitochondria drops, and therefore, cell function decreases and possibly even cells die (or apoptosis). Symptoms developed by an individual would depend upon the type of cell affected. However, the most common symptom is generalized, overall fatigue” (Brad S. Lichtenstein, Mitochondrial Damage, 2002, The Body, The Complete HIV/AIDS Resource).

Toxic medication has gained widespread use over the last 30 – 40 years and its prolonged 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) and 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 did not take analgesics. In the near future more evidence will come from studies to show that drugs cause certain diseases states to develop or otherwise increase the risk of developing disease conditions. Among them is expected the elevation of blood pressure in cardiovascular patients especially in geriatric patients and the elevation of blood glucose levels in diabetic patients when given antibiotics as these drugs also interfere in mitochondrial processes and possibly in the formation of coenzyme Q10 as well as in promoting mineral loss.

The only logical hypothesis is that toxic chemicals, whether or not they are approved for medication, if they generate free radicals in the body that decrease white blood cell count or kill T4 cells or damage the cell walls of cells of the immune system or the endocrine system and will promote the development of the AIDS condition. It results in immune deficiencies or immune disorders or damage to the genetic material in mitochondria and explains the variation of the symptoms of the AIDS and that also means there will be no such thing as an AIDS vaccine as predicted much earlier.

Remicade and Enbrel are drugs that possibly fall in this category as indicated by the contraction of TB in 12 patients in California and its risk in causing blood cancer. They provide a good example that like AZT, they weaken or impair the immune system sufficiently allowing drug-induced opportunistic infections (DIOIs) or interfere with the genetic material in cells to result in cancers. The worldwide rise of TB may in fact be DIOI-TB while HIV-linked TB is attributable to the ravaging effects of AZT on the immune system and due to the immunosuppressive drugs.

There is a worldwide rise of infectious diseases like TB that can be explained by impairment of cell mediated immunity or immunosuppression. “It dawns on me why tuberculosis -1.7 billion infected worldwide, 600 million cases annually, 2 million deaths, of which 95% are in developing countries; in Western countries less than 0.05% of the population is affected by the disease, of which more than 95% are homeless, alcoholics, IV-drug users, asylum seekers – ‘is an AIDS-defining illness’ “ (The Lancet editorial, July 6,1996).

The study of modern illnesses must consider the other point of disease states caused by oxidative stress that are similar to those caused by pathogens. Bacterial pneumonias and non-bacterial pneumocystis carinii pneumonia (PCP) is one such case. “Indeed, in the general population in Germany, for example, less than 1% of the population is affected by bacterial pneumonias. IV-drug users suffered more frequently from bacterial pneumonias long before AIDS came along for reasons well known to the venerable Virchow – unsatisfactory hygiene, malnutrition, bad housing etc., etc. The really important point, however, is that: IV-drug users classified as “HIV-infected” suffered from bacterial pneumonias, as a comprehensive study in Berlin has shown, whereas, non-bacterial pneumocystis carinii pneumonia (PCP) the most frequent “HIV associated respiratory disease” (and the most frequent “HIV associated disease” or “AIDS-defining illness” altogether in the West) does not, to all intents and purposes, feature at all in IV-drug users who are not homosexual (Heinrich Kremer, Acquired Iatrogenic Death Syndrome (AIDS), Heinrich Kremer, Pneumonias & Lung Diseases, Dec 1996). Homosexuals tend to use synthetic lubricants that absorb about 8 times faster through the anus than through the dermis and generate oxidative stress that can deplete natural vitamin C in lung tissue and in white blood cells and the decline in vitamin C levels compromises the function and role of the immune system. Natural vitamin C is not produced in the human body as it lost the glucoronic pathway about 18 million years ago during the course of evolution. Then, an antibiotic compounded the problem for this group of patients who became easily infected with a wide spectrum of microbes.

Co-trimoxazole was brought into clinical use in the early 1970s, i.e. more than 20 years ago. Individually, sulphamethoxazole and trimethoprim inhibited the growth of pathogens only, whereas both together as co-trimoxazole killed off a wide range of microbes. This was of great significance in the treatment of multiple infections of a minority of homosexuals in the large Western cities. The purpose of treatment in most cases was simply to suppress as quickly as possible the wide spectrum of microbial growth encountered in this group. Co-trimoxazole quickly became the wonder drug with specialist doctors and their homosexual patients in Western cities. But it produced a tragedy. Co-trimoxazole is a double-action folic acid inhibitor was used not only to treat but to prevent microbial infections (incredibly, often by self-administration), especially against the often refractory urinary tract and intestinal infections, and atypical pneumonias in this group of patients (see:Study Group AIDS Therapy, The role of antibiotics in the emergence of AIDS, 2001).

”Chemical antibiotics (e.g. sulphonamides, TMPSMX and Co-trimoxazole), that have been repeatedly administrated from 1970 on in any kind of infections, cause immunosuppression, and toxic effects like skin rash, nausea and vomiting, leukopenia, pancreatitis, hyperkalemia, thrombocytopenia, toxic metabolites and elevated levels of liver enzymes and methhaemoglobinemia and helped create resistant bacteria. By destroying bacteria in the gut they inhibit the production of immunoglobulins, needed for the body’s inner defences, and lay the body open to all sorts of bacterial, fungal and viral infections, including those associated with AIDS. By their strong oxidative effects they lead to a deficiency of glutathion molecules in cells, that is characteristic for the development of AIDS defining illnesses (Study Group AIDS Therapy, the role of antibiotics in the emergence of AIDS, 2001). Gut bacteria also produce butyric acid that has anti-cancer properties. Anti-virals also pose a similar problem.

Vancouver researchers found that tenofovir users were about three times more likely than abacavir users to develop higher-than-normal levels of creatinine in their blood. Another factor linked to having this problem was low CD4+ counts, roughly fewer than 150 cells. All in all, about 7 percent of tenofovir users in the Vancouver study developed some degree of kidney damage over an average of six months. A total of six patients had to stop taking tenofovir because of injured kidneys. Tenofovir may cause kidney damage by injuring the energy-producing parts of kidney tubules, called mitochondria, as does the nucleotide analogue adefovir. (Harris M et al, Nephrotoxicity of tenofovir DF. 12th Annual Canadian Conference on HIV/AIDS Research, April 10-13, Halifax. Abstract 168). This drug not only depresses white blood cell count but may also depress the mitochondrial density in cells and with ATP output falling below a critical level disrupts the healthy biochemical pathways in kidney cells and promoting the loss of minerals.

Tenofovir belongs to a group of drugs called nucleotide analogues, that also include adefovir (Hepsera) and cidofovir (Vistide). All three drugs are used to treat different viral infections. Other drugs that can cause kidney damage and dysfunction may include the following:

• Antifungals – amphotericin B (Fungizone) and related formulations of this drug.
• Antivirals – acyclovir (Zovirax), adefovir (Hepsera), cidofovir (Vistide), foscarnet (Foscavir), indinavir (Crixivan), Valtrex (valacyclovir).
• Antiparasite drugs – intravenous pentamidine.
• NSAIDS (non-steroidal anti-inflammatory agents) – acetaminophen (Tylenol), ibuprofen (Advil, Motrin), indomethacin (Indocid), naproxen (Naprosyn).
• Aminoglycoside antibiotics – amikacin (Amikin), gentamicin, paromomycin (Humatin), streptomycin, tobramycin.
• Other antibiotics – Septra (Bactrim, co-trimoxazole, trimethoprim-sulfamethoxazole).

Antibiotics kill microbial cells due to their function in inhibition in the synthesis of cell wall, inhibition of protein synthesis, injury to plasma membranes, inhibition in the synthesis of nucleic acids and inhibition in the synthesis of essential metabolites.

The degree of selective toxicity is expressed in terms of :

1. therapeutic dose, which is the amount of antibiotic needed for clinical treatment of an infection
2. toxic dose, the level at which the drug is toxic for the host.

The problem with antibiotics in the human biological system is that when these molecules enter the cells they are metabolised yielding hydrogen peroxide which must be converted into water and oxygen by the glutathione-catalase system. This additional biochemical activity can deplete the natural antioxidants in the body and a chronic decline in the levels of these enzymes can disrupt the healthy functioning of the tissues. Excess antibiotics will lead to a decline in output of the Krebs cycle leading to lower ATP output while it promotes mineral loss through the urine. Anti-cancer drugs are more toxic and can have more deleterious side-effects.

Dr. Penefsky and his collaborators have been researching to determine the effect of anticancer drugs on oxygen consumption by normal and cancerous cells. Dr. Penefsky and his collaborators have concluded that mitochondria are a common target for many anticancer drugs and that these effects on mitochondria are related to frequently observed adverse clinical responses (Harvey Penefsky, Ph.D., In collaboration with Abdul-Kader Souid, Karen A. Galvan and Kirk A. Tacka, Department of Pediatrics, State University of New York, Upstate Medical Center, Syracuse, New York).

While the purpose of administering anticancer drugs to patients is to kill the cancer cells, it is well known that many anticancer drugs in use today damage normal cells as well especially young healthy cells. Much of the damage results from interaction of the drugs with cell DNA, resulting in inhibition of protein synthesis and consequent cell death. Recently however, they found that anticancer drugs can inhibit cellular oxygen consumption both directly and indirectly (Souid AK, Tacka KA, Galvan KA, Penefsky HS, 2003, Immediate effects of anticancer drugs on mitochondrial oxygen consumption, Biochem Pharmacol. 2003 Sep 15;66(6):977-87,PMID: 12963484). They have found that cisplatin, a much-used anticancer agent containing platinum, indirectly inhibits mitochondrial oxidations by promoting the release from mitochondria of a critical component, cytochrome c. The effect of cisplatin on mitochondrial oxidations is delayed until significant amounts of cytochrome c are released. On the other hand, cyclophosphamide and anthracycline antibiotics, two other frequently-used anticancer agents, directly and immediately inhibit oxygen consumption in a dose-dependent manner (Tacka KA, Dabrowiak JC, Goodisman J, Penefsky HS, Souid AK, 2004, Effects of Cisplatin on Mitochondrial Function in Jurkat Cells, Chem Res Toxicol, 2004 Aug 16;17(8):1102-1111,PMID: 15310242).

Antibiotics and chemotherapy also deplete minerals in the body. These minerals are also critical in the catalytic function in the glutathione-catalase system that converts the hydrogen peroxide formed during metabolism of toxic drugs into water and oxygen. Such mineral loss exacerbates the health problems of cancer patients. Depletion of selenium leads to a drop in the production of glutathione. A critical drop in glutathione in cells itself can lead to apoptosis. A sharp decline in antioxidant enzyme levels in brain cells can lead to breathing difficulties and death. This problem in drug therapies points to the preference of natural biomolecules that have antibiotic and anti-cancer properties especially those that also have antioxidant properties as well as proper integration of natural antioxidants and bioavailable minerals after the administration of the drug.

It is well known that most antitumor agents induce apoptosis in cancer cells. Triggering of apoptosis by antitumor agents involves simultaneous or subsequent activation of death receptor systems, perturbation of mitochondrial function, and proteolytic processing of caspases, the death effector molecules of apoptosis. Recent advances have led to a widely accepted model that a conserved family of cysteine proteases (caspases) plays important roles in apoptosis (Nicholson et al, Identification and inhibition of the ICE/CED-3 protease necessary for mammalian apoptosis, Nature (Lond.), 376: 37-43, 1995).

Anti-cancer drugs such as MT-21 can induce the release of cytochrome c from the mitochondria that is necessary to activate caspase-9, and after this release has occurred there is a change in the membrane potential (Masahiko et al, MT-21 Is a Synthetic Apoptosis Inducer That Directly Induces Cytochrome c Release from Mitochondria, Cancer Research 60, 5214-5222, September 15, 2000). This is an important piece of information that explains the change in the membrane potential due to cytochrome c release from the mitochondria as all cancer cells develop a very high cell membrane potential (CMP). And it points to the possible use of natural antioxidant molecules and rapid free radical scavenging activity as possible interventions to remove the CMP and aid in the restoration of the cytochrome c levels in the mitochondria that can Aminoglycoside antibiotics – amikacin (Amikin), gentamicin, paromomycin (Humatin), streptomycin, tobramycin. eventually improve blood cell counts.

Research at the Broad Institute at Harvard University and the Massachusetts Institute also suggests that drugs like statins may interfere with processes in the mitochondria and lower ATP output (Nature Biotechnology, cf:NST p 44, March 2, 2008) producing strong decreases in cellular ATP while statins are known to interfere in the pathway that leads to the formation of coenzyme Q10 and any strong decreases of this enzyme in heart cells can pose a cardio-risk. An analysis of the diabetes drug, Avandia, in the New England Journal of Medicine reveals that it increased the risk of heart attacks while the FDA will require tougher warnings on diabetes drugs such as Avandia and Actos to strengthen warnings about a condition in which the heart does adequately pump blood (cf:NST p18, June 8, 2007).

Most of the adverse drug reactions (ADRs) are due to rapid increases of free radical activity that the natural antioxidant defense mechanism cannot cope with leading to massive oxidative damage to the natural antioxidant enzymes in cells, hormone and protein molecules, oxidative injury in the mitochondria, cell membranes, mitochondrial membranes and its cytochrome system and the MT protein system. Much of the fatigue and chronic fatigue symptoms are related to a depression in the production of the ATP and enzyme molecules and a suppression of the Krebs cycle in the mitochondria while oxidative damage to pol gamma enzymes and the genetic material in the mitochondria lead to cancer formation. Drug interference in mitochondrial functions and suppression of the production of ATP and coenzyme Q10 are factors in the development of AIDS symptoms while further oxidative damage to the cytochrome system and genes in the mitochondria precipitate the classic “AIDS-defining-illnesses”. AIDS is more of a “prescription disease” created by modern medical science (see:AIDS, NON-HIV AIDS AND PRESCRIPTION AID) that is attributable to the widespread use of toxic drugs especially the benzene derivatives and other drugs that interfere with folic acid and antioxidants in the body and in the mitochondria. And malnourished and geriatric patients are more susceptible to the side effects of drugs.

At the cellular and biomolecular levels, the adverse effects of drugs can be stated as follows:-

1. Suppression of the immune system directly or indirectly by loss of minerals and depletion of L-ascorbic acid.
2. Inhibition of cellular consumption of oxygen due to oxidative damage to the oxygen molecule.
3. Inhibition of phosphorylation and oxidative phosphorylation which is a metabolic pathway that uses energy released by the oxidation of nutrients to produce adenosine triphosphate (ATP). In general, excess free radicals generated by drugs interfere with the electron transfer processes essential in healthy biochemical pathways and can depress the formation of antioxidant enzymes as well.
4. Oxidative damage to cell membranes and mitochondrial membranes.
5. Oxidative damage that leads to the release of cytochrome c from the mitochondria and oxidative injury to the protonation process in its cytochrome system.
6. Oxidative damage to the MT protein system.

The number of deaths from adverse drug reactions has been growing steadily over the years as more and more toxic drugs get approval and these new drugs may not be better than previous one but may be more toxic and the number of such deaths has more than doubled since 1997. The annual cost of treating ADRs in the UK alone now stands at Pounds Sterling 466! This does not include the cost of treating AIDS patients whose condition was induced by long term use of drugs or excessive use of pharmaceutical drugs or drug-induced AIDS (DI-AIDS).

Modern medicine has entered its vicious cycle of treatment wherein it treats a condition or infection with toxic drugs that interfere with the processes in the mitochondria and/or suppress the immune function that produce new symptoms and these symptoms are then treated with other toxic drugs. This problem is here to stay with us because the health regulators periodically warn doctors about prescribing health supplements made from edible substances for health benefits as they insist that doctors must only deliver a pharmaceutical benefit. That is the new function of Health Ministries in modern societies.

There is some research on the administration of L-ascorbic acid in massive doses that markedly augments the effects of antibiotics and broadens their spectrum greatly. Presumably, lower doses of antibiotics are needed to eliminate the infection. It is an interesting area for further research. Additionally, L-ascorbic acid also prevents most, if not all, allergic reactions attributable to antibiotics and certainly manages these side-effects of toxic drugs by neutralizing the massive amounts of free radicals generated in the infected tissues when mitochondria are damaged. Natural vitamin C exhibits anti-histamine effects. Fruit juices with mandarin orange and carrots and red spinach will therefore become important in integrative medicine in the near future and as a therapeutic intervention in the field of biomolecular medicine but rapid free radical scavenging activity by extracts obtained in the nano form from fruits, flowers and vegetables (ediceuticals) appears to be the best option to treat ADRs.