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Rethinking AIDS

"In regards to the complex of symptoms, together known as Aids or Acquired Immune Deficiency Syndrome, there exist to this very day a few misconceptions, which in this paper will be detailed and examined.


Since 1984 HIV is thought to be the probable cause but the definition of the syndrome has undergone many changes and will probably continue to do so.


It is surmised that the great majority of cases of HIV/Aids are sexually transmitted. Anal intercourse seems to carry the highest risk. Man to woman transmission is said to be more common than vice versa. Intravenous drug users are said to pass on the virus, when sharing needles. Children are infected through the placenta in utero. In the USA 60% of Aids cases are seen in homosexual men, 28% are intravenous drug users, 5% have heterosexual contact only, 1% have haemophilia or similar blood disorders and 3% have it from transfusion and 3% have received it in the womb. This pattern is similar in all western oriented societies, while in Africa and the Caribbean the pattern is overwhelmingly heterosexual.


The only tests available to determine infection is the tests for antibodies, which are said to be useless against HIV, so it is immediately assumed that if antibodies are detected that HIV infection is a fact and full blown Aids is only a matter of time.


Opportunistic infections are: candidiasis, pneumonia PCP, Herpes, cytomegalovirus CMV, toxoplasmosis, TBC, lymphoma and Kaposi’s sarcoma.


Haematological problems: thrombocytopenia (low platelet count), low white blood cell count, and anaemia.


The eyes can be affected and rheumatological problems, cardiovascular, renal and endocrine problems may be part of Aids.


The propositions brought forward, as to the cause and the origin, will be examined and a detailed investigation into the available literature on the subject presented here each under its respective heading.


In general there can be distinguished different theories that hold sway in different sections of the community, dependent on the orientation of its members. These theories will be set out below.

"Aids is caused by the Human Immuno Virus, which is a mutated form of Simian Immuno Virus, after the latter ‘jumped species’, due to the consumption of monkey flesh by indigenous Africans


Aids is caused by contaminated vaccines, made with cultures of monkey blood, with SIV mutating in the human body. (This is basically a variant of the first scenario)


Aids is caused by Biological Warfare research gone wrong. It is believed by some, that it has been released on purpose, to eradicate the male homosexual population.


All these scenarios take it for granted that HIV causes Aids.

Then there are the religious fanatics, who think it is the punishment of God, for those that live in sin.

I will examine the above-mentioned three theses or theories in a systematic manner. First the thesis will be presented. Then the antithesis, which lists the inconsistencies found, will be examined on their merits and demerits. Lastly the synthesis or conclusions of these theories will be drawn, and comparison with the reality of the sufferers examined to see if this is consistent with the theories.

Finally I will present what I consider a more realistic viewpoint, both scientifically and practically, and present possible treatments from the homoeopathic armamentarium.

Aids is caused by HIV.


HIV is the abbreviation of the Human Immuno deficiency Virus. It is classed among the Retroviruses, of which some 200 varieties are known, since research into the retroviruses started approximately 20 years ago. To date none of the other retroviruses are known to have caused any disease.


HIV is thought to be characterised by the breakdown and deterioration of the immune system. Crucial immune cells, called CD4+ T cells, or T helper cells, are disabled and die during the course of ‘infection’. It must be noted that these T cells are present in the blood of healthy people from 800-1200/ mm3. In people with full blown Aids these numbers have fallen below 200/mm3.


The symptoms listed, are intestinal tract infections or candida, pneumonia, skin rashes and in some cases Kaposi’s sarcoma, lymphoma or skin cancer. There is weight loss, sometimes neurological conditions and the involvement of other organs. There is often destruction of the lymph nodes, as they perform an important role in the immune response and the production of T cells.

Antithesis. Viruses do not and cannot cause disease.

A ‘viral disease’ is characterised by a high level of viruses in the blood of victims of full-blown cases. This is the case with all viral disease. Invariably this is noted only in full-blown cases. If we examine the blood of any person, we may find the virus in some cases, but never in disproportionate amounts. In fact the only method by which HIV can be discovered, is by testing for antibodies. The problem is that the blood is only investigated in those that are already sick, and that there is little chance or scope for the examination of ‘healthy’ subjects. This is however not at all important, because we are dealing with sick people and the healthy are of no concern to us.


What is important is that we must consider carefully what is being observed. In a full-blown case of disease we are looking at the disease ultimate. It is an end result. From the moment we entered primary school we have been taught that results are always different from causes, and this is scientific. In Viral disease we seem to throw this scientific principle out the window and declare that cause and result are one and the same thing. This is unscientific, to say the least. It has no place in any scientific discussion, least of all medicine, where lives are dependent on thorough scientific principles and procedures.

Anything that looks away from exactitude is unscientific. The physician must be classical; everything must be methodical. Science ceases to be scientific when disorderly application of the law is made,” says Kent (Lesser Writings pg. 645)


20 years of research has yielded 200 different retro viruses, of which little else is know than that they exist and that they do not cause any disease.



Why should HIV be the only exception?


An Aids test is among the most difficult, because the amount of HIV is one per billion cells, if one is a carrier and one per 100 million plus in full-blown Aids. The disproportionate low count cannot be held responsible for the severity of the disease. The best ‘test result’ is obtained by testing for antibodies.



Why is it presented in publications for the layman that the reverse of the above is true, i.e. that HIV is present by the billions?

Most doctors have gone crazy over the ‘vicious microbe’ as being the cause of disease and think the little fellows exceedingly dangerous,” says Kent. He continues:

As a matter of fact, the microbes are scavengers. I wonder if scientists reflect when they make statements about bacteria. Naturally they would say that the more bacteria the more danger, but this is not so. It is well known that shortly after death a prick from the scalpel is a serious matter. This is due to the ptomaines of the corpse; but when the cadaver has become green and filled with bacteria it is comparatively harmless. The microbe is not the cause of disease. We should not be carried away by these idle allopathic dreams and vain imaginations, but should correct the vital force. The bacterium is an innocent feller and if he carries disease, he carries the simple substance, which causes disease, just as an elephant would.” (Kent. Lesser Writings, pg. 663)


Therefore disease, considered as a thing separate from the living whole, from the organism and its animating vital force and hidden in the interior, be it of ever so subtle a character, is an absurdity that could only be imagined by minds of the materialistic stamp.” (Organon # 13)

And further:

The natural disease is never to be considered as a noxious material situated somewhere in the exterior or interior.” (Organon # 148)

“… Diseases are nothing more than alterations in the state of health of the individual, which express themselves by morbid signs.” (Organon # 19)


From these statements we can learn that viruses, bacteria and other microbial agents have nothing to do with the disease, and are not the cause. At best they are the concomitant symptom of the disease, appearing only when the disease is already full blown. We can also see that HIV, because of its low count, cannot be either the cause or a concomitant of disease, as its numbers are insufficient to have any effect or import on the disease.


If it is so that the microorganisms do not cause disease, we must look elsewhere for the cause of Aids. From the investigation conducted in West Africa and among the gay community, it has become evident that the consumption of antibiotics is much higher than among the average population.

“…. Medicines could never cure diseases if they did not have the power of altering the state of health…their curative power must be owing solely to this power they possess of altering the state of health.” (Organon # 19)

Much more frequent than the natural diseases associating with and complicating one another in the same body, are the morbid complications which the inappropriate treatment is apt to produce, by the long continued employment of unsuitable drugs.” (Organon # 41) In this respect Kent says:

We daily see that the antipathic and heteropathic methods have no permanence. By these means there are effected changes in the economy and changes in the symptoms but no permanent cure, the tendency being simply to the establishment of another disease, often worse than the first and without eradicating the first.” (‘Lectures on the philosophy’ pg. 90)


Thus Kent says:

We know very well that in the old school there is no plan laid down for acquiring a knowledge of medicines except by experimenting with them on the sick. This Hahnemann condemns as dangerous, because it subject the sufferers to hardship and because of its uncertainty.” (Lectures on the philosophy pg. 170)

Every real medicine acts at all times, under all circumstances, on every living being and produces its peculiar symptoms, distinctly perceptible if the dose be large enough (Organon # 32)

Medicinal substances act in the morbid changes they produce according to fixed eternal laws of nature to produce certain reliable disease symptoms, each according to its own peculiar character.” (Organon # 111)

“…It was never suspected that these histories of medicinal diseases would furnish the first rudiments of the true pure materia medica, which has until now consisted solely on false conjectures and fictions of the imagination.” (Organon # 110)

Let us investigate these statements from the Organon and the remarks that Kent has given in regards to these paragraphs. In order to furnish the material for this investigation we do not need the Homoeopathic Materia Medica, but the Pharmacopoeia of the allopathic drugs, as they form the rudimentary materia medica, as well as being tested exclusively on the sick.

We will do this investigation with the drugs that are known to cause symptoms - called side effects - which are similar to the disease under investigation, to ascertain whether there is a causal or other relation ship between them.

The “Essential Guide to Prescription Drugs 1997” gives us the following information:

Penicillin V

Introduced 1953 Prescription: USA: yes; Canada: Yes Available as generic: USA: Yes; Canada: Yes Class: Antibiotic, penicillins. Controlled Drug: USA: No; Canada: No

Benefits versus risks

Possible benefits: effective treatment of infections due to susceptible microorganisms.

Possible risks: Allergic reactions, mild to severe Superinfections, (yeast)

Principal uses

As a single drug product: used to treat responsive infections of the upper and lower respiratory tract, the middle ear and skin. Rheumatic fever; bacterial endocarditis

Combination therapy of animal bite wounds; stage one Lyme disease in children; dental abscesses

Usual adult dose range

Dosage based on sensitivity testing of the bacteria causing the infection, the severity of the infection and response of the patient. The total dosage should not exceed 7grams per day.

Possible Adverse Effects

Mild effects

Allergic reactions: skin rashes, hives and itching.

Irritation of the mouth and tongue; ‘black tongue,’ nausea, vomiting, mild diarrhea.


Serious Effects

Allergic reactions: Anaphylactic reactions, severe skin reactions, drug fever swollen painful joints, sore throat, abnormal bleeding or bruising.

Severe skin reactions, bulbous pemphigoid

hemolytic anemia, periarteritis nodosa, meningitis, porphyria, abnormal liver function.

Laboratory tests

Complete blood counts: decreased red cells. hemoglobin, white cells and platelets increased eosinophils.

Prothrombin time increased.

Liver function: increased aspartate aminotransferase (AST/GOT) and bilirubin.

Another example

In the Mims (1996) we read the following about the antibiotic Chloromycetin.


It belongs to the class of chloramphenicols.

Antibiotic, effective in a wide variety of bacterial infections. It possesses highly antimicrobial action, crosses tissue barriers readily and diffuses widely and rapidly through nearly all body tissues and fluids.

It is rapidly absorbed through the gastrointestinal tract, producing detectable concentrations in the blood, within one half hour after administration.

Because of this, we can see that what is usually seen as fatal, in the case of Aids and babies, can now be seen to be caused by other mechanisms.


Transport across the placental barrier occurs with somewhat lower concentration, and chloramphenicol is known to enter the cerebrospinal fluid. It is used for meningitis, typhoid fever, and other serious infections


Blood discrasias, including aplastic anaemia, overgrowth in fungi.

Adverse reactions

Haematological: as above in precautions. A reversible type of bone marrow depression, which is dose-related, may occur, with equally reversible type blood disorders. An irreversible type of bone marrow depression with a high mortality rate is not uncommon and is characterised by the appearance, weeks or months after therapy, of bone marrow aplasia or hypoplasia. The incidence of fatal cases is as high as 1 in 25.000 to 1 in 100.000, based on two dosage levels.

Dosage 50 mg/kg/day, in divided doses at six hourly intervals, is recommended. For the average person at 75 kg, this means that the average dose is 3,5 grams a day. In meningitis or with suspected resistant bacteria, this dose is often doubled, although the recommendation is to reduce this as soon as or when possible.

We shall now look at a few provings of antibiotics conducted by different homoeopaths around the world and collected in the Dictionary of Homoeopathic Materia Medica, by O.A.Julian. To be able to compare nicely we shall give the pathogenesis of Chloramphenicol first.

Pathogenesis of chloramphenicol

Mouth: bleeding gums, black pilous tongue

Digestive tract: nausea, vomiting. colic and diarrhea

Vascular system: aplasia anaemia, leucopoenia, thrombopoenia

Respiratory system: dyspnoea, suffocation.

Urinary system: dysuria, polyuria, hematuria

Locomotor system: many pains in the joints resembling rheumatological pains.

Skin: vesicular erythema, scarlatinaform eruptions, oedema, excessive perspiration, falling out of the hair.

Temperature: fever from 38 to 40 degrees

Next follows the pathogenesis of Penicillin

Digestive tract; mouth: bleeding gums; tongue: yellow brown, with imprint of teeth. Toothache; epigastric and umbilical cramps.

Vascular system: precordalgia, hypotension, oedema.

Respiratory system Angina, cough spasmodic, yellow expectoration, asthma.

Locomotor system pain aggravates, by movement; articular pains with oedema of muscles.

Skin eczema weeping, furuncles, warts, herpes, tuberous acne, impetigo.



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Comment by Vaikunthanath das Kaviraj. on September 26, 2012 at 11:24am

From Medscape Medical News
Childhood Antibiotics Linked to Inflammatory Bowel Disease
Troy Brown

September 24, 2012 - Children who received antianaerobic antibiotics in the first year of life had a 5.5-fold increased risk of developing inflammatory bowel disease (IBD) compared with those who were never exposed, according to a retrospective cohort study of more than 1 million children.

Matthew P.

 Kronman, MD, MSCE, an assistant professor of pediatric infectious diseases in the Division of Infectious Diseases at Seattle Children's Hospital and the University of Washington in Seattle, and colleagues presented their findings in an article published online September 24 in Pediatrics.

"We sought to examine the association between childhood antianaerobic antibiotic exposure and subsequent IBD development using a large population-based cohort, hypothesizing that exposure to antibiotics with anaerobic activity would be associated with the development of IBD," the authors write.

They analyzed data from 464 ambulatory practices in the United Kingdom that were participants in the Health Improvement Network. All children with at least 2 years of data from 1994 to 2009 were followed up between practice enrollment and IBD development, practice deregistration, 19 years of age, or death. The investigators excluded children with previous IBD.

A total of 1,072,426 patients provided 6.6 million person-years of follow-up. Of those patients, 748 (0.07%) developed IBD, for an overall incidence rate of 1.2/10,000 person-years. Of the 225,100 patients followed from birth, only 30 developed IBD, so meaningful analyses were not possible in this subgroup.

Among the 748 children who developed IBD, the median latency period between the first healthcare visit with a gastrointestinal diagnosis suspicious for IBD and the first IBD diagnosis was 3.9 months (interquartile range [IQR], 0.5 - 17.9 months), and 68.2% had latencies of 1 year or less. Fewer than 25% of the other children had diagnoses consistent with possible IBD within 5 years before censorship.

Exposure to Antibiotics

More than half (57.7%) of the patients received at least 1 antianaerobic antibiotic, defined as penicillin, amoxicillin, ampicillin, penicillin/b-lactamase inhibitor combinations, tetracyclines, clindamycin, metronidazole, cefoxitin, carbapenems, and oral vancomycin.

The patients took antianaerobic antibiotics for a median of 1 week (IQR, 0 - 2 weeks), with 42.3% receiving none, 31.9% receiving them for 1 to 2 weeks, and 25.8% receiving them for more than 2 weeks.

In both the unexposed and exposed groups, 0.07% of children developed IBD; however, the IBD incidence rates were 0.83/10,000 person-years in the unexposed group and 1.52/10,000 person-years in the exposed group, for an absolute risk increase of 0.69 cases/10,000 person-years and an 84% relative risk increase.

In univariate analysis, any antianaerobic antibiotic exposure was associated with developing IBD (P < .001, log-rank test), there was a dose-response effect (P < .001, log-rank test), and this association remained significant throughout childhood.

In their multivariate analysis, the investigators adjusted for family history of IBD, gender, chronic granulomatous disease, primary sclerosing cholangitis, and socioeconomic deprivation. They found that exposure by 1 year of age was associated with a 5.5-fold increased IBD risk (adjusted hazard ratio [aHR], 5.51; 95% confidence interval [CI], 1.66 - 18.28) compared with those never exposed, with IBD risks decreasing every 5 (aHR, 2.62; 95% CI, 1.61 - 4.25) and 15 (aHR, 1.57; 95% CI, 1.35 - 1.84) years.

Each course of antianaerobic antibiotics was associated with a 6% increased IBD hazard (aHR, 1.06; 95% CI, 1.04 - 1.08), and each week of exposure was associated with a 1% increase in hazard (aHR, 1.01; 95% CI, 1.00 - 1.02).

Exposure to more than 2 courses of antianaerobic antibiotics in the first year of life had a higher association with IBD development than exposure to 1 to 2 courses, with an aHR of 4.77 (95% CI, 2.13 - 10.68) vs 3.33 (95% CI, 1.69 - 6.58).

Exposure to any antibiotic, penicillins, broad-spectrum penicillins, and cephalosporins was associated with development of IBD, but exposure to macrolide, sulfonamide, and tetracycline were not.

Exposure to metronidazole or fluoroquinolones (2 potential IBD treatments) was associated with IBD development.

"[T]hese class-specific findings remained significant after re-setting the IBD outcome at the first metronidazole or fluoroquinolone prescription in the year before IBD diagnosis, suggesting that outcome misclassification was not significantly present," the authors write. Exposure to any fluoroquinolone (aHR, 2.09; 95% CI, 1.10 - 3.98]) and any metronidazole (aHR, 186.25; 95% CI, 10.86 - 3193.65) by 1 year of age.

Results were similar for the 2 IBD subgroups, Crohn's disease, and ulcerative colitis, but they did not vary with age. The primary outcome was not changed when sensitivity analysis was conducted by assigning all missing Townsend scores first in the highest and then in the lower deprivation category.

When sensitivity analysis was conducted using a 1-year latency period, the primary outcome's precision and magnitude were altered, but not its direction: any antianaerobic antibiotic exposure in the first year of life (aHR, 3.73; 95% CI, 1.17 - 11.84), each course of antibiotics (aHR, 1.03; 95% CI, 0.99 - 1.06), exposure to 1 to 2 courses of antibiotics (aHR, 2.18; 95% CI, 1.07 - 4.50), and exposure to more than 2 courses of antibiotics (aHR, 4.14; 95% CI, 1.74 - 9.87).

"Our study suggests that reduction in childhood antianaerobic antibiotic use may have the potential to help curb the rising incidence of childhood IBD. Many unanswered questions remain, however, such as whether specific difficult-to-culture organisms could play roles in either IBD pathogenesis or protection against IBD, and whether alteration of flora through antibiotic exposure alters the immune system directly," the authors write.

Sonia Michail, MD, an investigator at the Saban Research Institute of Children's Hospital Los Angeles, California, and an associate professor of clinical pediatrics at the Keck School of Medicine of the University of Southern California, commented on the study in an email interview with Medscape Medical News.

Dr. Michail was not surprised by the association between antibiotics and the development of IBD, but she was surprised by the strength of the association.

"This work further confirms the strong contribution of the gut microbiome towards the development of disease and suggests that perturbations of the gut microbiome at an early stage in life when the immune system is still developing may have an impact on disease incidence several years later. These findings fit well with what we now know about the effect of antimicrobial therapy on the gut microbiome," Dr. Michail said.

"This study highlights the importance of judicial use of antibiotics, especially in young infants and children at higher risk for developing [IBD] such as those with a strong family history of IBD. It adds yet another depth to the potential risk of using antimicrobial therapy in infants and children," Dr. Michail said.

Dr. Kronman received support for this study from a National Research Service Award Institutional Research Training grant at the Children's Hospital of Philadelphia in Pennsylvania, as well as a University of Pennsylvania Center for Education and Research on Therapeutics grant from the Agency for Healthcare Research and Quality. This work was also supported by a National Institutes of Health Clinical and Translational Science Award and was funded by the National Institutes of Health. One author has received research support from Merck and Company Inc for other projects and has served as a consultant for Pfizer Inc, HemoCue Inc, Merck and Company Inc, Cubist Pharmaceuticals, and Astellas Pharma US Inc. He has also received a lecture honorarium from Merck and Company Inc. Another author previously received research support from Sage Pharmaceuticals Inc for other projects. The remaining authors and Dr. Michail have disclosed no relevant financial relationships.
Pediatrics. Published online September 24, 2012. Abstract
Comment by Hans Weitbrecht on September 18, 2012 at 7:00pm

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