Antibiotic trials for ALS are set up to fail

Because there have been many anecdotal reports of antibiotics helping ALS patients, there has been considerable interest in trying antibiotics for this condition. Clinical trials have been conducted, testing Ceftriaxone and Minocycline. It is however important to realize that these trials have never been based on the assumption that ALS is caused by a bacterium and that therefore, an antibiotic would be a suitable medicine. Instead, opponents of the bacterial etiology hypothesis of ALS have set up antibiotic trials to fail by insisting that any improvements of ALS symptoms would be due to anti-inflammatory properties of the antibiotic, or because of some assumed beneficial role in the metabolism of glutamates. The position that there exist chronic bacterial infections that can cause serious neurological syndromes is a highly dangerous one for one's career, and everything is done to avoid drawing such conclusions in research papers or starting a clinical trial under such assumption.

The trial's fatal flaws were its short treatment duration in regard to how long severe neuroborreliosis needs to be treated, as well as the insufficiently low dosages to treat neuroborreliosis and the murky way the dosages were lowered as soon as the patient experienced discomfort or deterioration. Because the dosing of the antibiotic was done in such a way, that as soon as a significant bacterial dieoff was achieved, the antibiotic was either withdrawn or its dosage reduced. From the study:

In our opinion, this makes the study useless to determine the efficacy of Minocycline against ALS caused by Neuroborreliosis, because: "The highest tolerated dose" is not a useable designation of quantity, and virtually guarantees that none of the ALS patients received a bactericidal or bacteriostatic dose, because before such a dose is attained in the CNS, extremely unpleasant dieoff effects will manifest themselves. As soon as these effects were deemed "adverse" by either patient or physician, the dose was lowered or the antibiotic was withdrawn for weeks at a time, inevitably resulting in complete treatment failure. The only effect that can reasonably be expected of such an experiment is to "stir up" the spirochetes - to cause some serious herxing but not to significantly lower the bacterial load. On the contrary, such an approach would likely result in more, not less cerebral inflammation, as a few spirochetal fragments would trigger an inflammatory immune response. Spirochetes would also tend to migrate to tissue with lower antibiotic serum concentration, causing damage to neurons, as they are often intracellular (embedded inside neurons).

Note how the study mentions that as soon as a serious Jarisch-herxheimer reaction would occur, the Minocycline would be stopped permanently. This approach guarantees that none of the ALS patients would ever improve, if the cause of their symptoms would be Lyme disease. On the contrary, it guarantees that some would deteriorate, as a result of the extra inflammation caused by the "waking up" of the immune system and the "shaking up" of the bacteria.

Oral Minocycline is even at the maximum dosages administered in the trial not to be expected to cure or even significantly alleviate the severe neurological damage of Neuroborreliosis. Chronic (antibiotic-resistant[1]) Lyme neuroborreliosis is amply documented in medical literature.[2]

We made a screen capture of the graph that showed the decline of the ALS patients treated with Minocycline versus the decline of an untreated control group: (The black "treatment end" line is ours)

This graph is used to justify the conclusion that Minocycline is harmful to ALS patients, because some ALS patients deteriorated much faster on Minocycline than without. As we already stated, the design of the study made it impossible for any ALS patients to be properly treated for Lyme neuroborreliosis, because as soon as a Jarisch-Herxheimer ("dieoff") reaction set in, treatment was either stopped permanently or temporarily, or dosing was reduced. What remains is the Jarisch-Herxheimer reaction, causing an accelerated demise of especially bulbar ALS patients, because their symptoms worsen due to the dieoff of Borrelia spirochetes in their brains.


1.  Dclaesson    Wednesday, August 15, 2012

Preaching to the Choir here....I KNOW some of the pathogens of lyme are leading to ALS and there are many who have died as a result. One veterinarian figured out on his death bed that his ALS was from lyme and he did save his son. Thank you for all you do and I am so sorry that you have been the target of much abuse by some others.

2.  KMDickson    Wednesday, August 15, 2012

Lyme and OspA exposure tolerize to mycoplasma, which seems to be the main driver of the ALS outcome of Lyme.
Meanwhile, OspA or exposure to shed (blebbed) borrelial antigens seems to activate EBV (IL-10 and TNF) which is the main cause of the MS outcome of Lyme.
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