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Meg Mangin R.N.
Research Team (on leave)
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Posted: Sun Jul 31st, 2005 03:40 |
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Can I use doxycycline instead of minocycline?
Tetracycline antibiotics are a group of broad spectrum antibiotics, indicated for use against many bacterial infections. They are so named for their four (“tetra-”) hydrocarbon rings (“-cycl-”) derivation (“-ine”).
"The tetracyclines are all different at the molecular level. Doxycycline is VERY different from minocycline. We don't use doxycycline, we use minocycline.
There are two reasons for this - one is that doxycycline doesn't kill as wide a range of bacteria as mino, the other is that doxycycline has an effect on the brain beyond its anti-bacterial effects. This is easy to verify, if, when you are in phase 3, you try a couple of 200mg pulses of doxy. The feeling you get is nothing like the herx you have endured for so long. And that feeling is addictive. As I withdrew from Doxy I had mental confusion which was quite unbelievable, and totally uncharacteristic of anything I felt while on the MP.
Short term (non MP) use of doxycycline (a month or so) will do no harm, but in the long term the species which are resistant to it will continue to proliferate and exacerbate the chronic disease.
There is a HUGE difference. I have seen people die on doxycycline, while they recover on minocycline and demeclocycline. Please understand that the Marshall Protocol may seem simple, but it has a lifetime of my own research behind it. Anything you change will likely get you into trouble. That is why the website is here, and the moderators will help you understand issues like this.
Here is a paper describing the extra features of minocycline.
http://www.postgradmed.com/issues/1997/04_97/cunha_1.htm
Note the following particularly:
1. Better lipid solubility -> better CNS and cellular penetration
2. Effectiveness against Staph, which is one of the strains contributing to these chronic diseases
Please understand that 99.9% of ID specialists do not fully understand the way that antibiotics work their magic on the pathogens' Genome, at the molecular level. Conversely, 99.9% of the material you will read about antibiotics is incomplete, and much is just guesswork.
Doxycycline has some effect on the brain which can promote a feeling of 'euphoria.' Additionally, it does not kill all the L-form species (it is not nearly as wide-spectrum as Minocycline) these are both dangerous (IMO) characteristics because they can make people prematurely think they have 'conquered' their infection.
It is crazy to talk about "Tetracycline alternatives." The complexity of antibiotic actions is way beyond your comprehension, and the comprehension of anybody who thinks in that way. Please use ONLY the FDA approved, decades-old, well studied, low-cost and perfectly-adequate antibiotics used in the MP, and only at the dosing levels we have been using in our cohort, and for which we have gathered safety data in Th1 patients."
Minocycline is a 30S bacterial ribosomal inhibitor,http://tinyurl.com/9r5hj so it preferentially inhibits protein synthesis of these bacterial pathogens. However, it can also inhibit mammalian protein synthesis to a degree, which we generally don't want to do...this can suppress the immune system and other important functions. So, we want just enough inhibition to block the pathogens ability to synthesize proteins without significantly inhibiting our own ability to synthesize proteins.
..Trevor..
Mar08 update:
Interesting that Staph aureus has been identified as a significant component of the microbiota in all three shotgun-genome studies to date. Minocycline's advantage over doxycycline is its ability to kill Staph spp. ..trevor..
See also The superiority of minocycline over other tetracyclines
Last edited on Wed Mar 26th, 2008 01:59 by Meg Mangin R.N.
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Nothing contained in this site is or should be considered, or used as a substitute for, medical advice, diagnosis or treatment by your physician.
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Meg Mangin R.N.
Research Team (on leave)
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Posted: Thu Sep 14th, 2006 03:03 |
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Tetracyclines are all different at the molecular level
(filelink)
The term 'tetracycline' refers to the 4 'benzene rings' of the chemical structure.
http://en.wikipedia.org/wiki/Tetracycline
Doxycycline is VERY different from minocycline. We don't use doxycycline, we use minocycline.
There are two reasons for this - one is that doxycycline doesn't kill as wide a range of bacteria as mino, the other is that doxycycline has an effect on the brain beyond its anti-bacterial effects. This is easy to verify, if, when you are in phase 3, you try a couple of 200mg pulses of doxy. The feeling you get is nothing like the herx you have endured for so long. And that feeling is addictive. As I withdrew from Doxy I had mental confusion which was quite unbelievable, and totally uncharacteristic of anything I felt while on the MP.
So that is the background info preparatory to answering your question  The MP antibiotics work by blocking the bacterial ribosomes from generating the proteins needed for the organisms to survive. The is also a little (quite small at the doses we are using) blockade of mitochondrial ribosomes within the host (us). Because we PULSE the antibiotic dosage, the blockade of mitochondrial ribosomes, which is strictly reversible and dosage-dependent, is only for a few hours every two days, producing minimal effects on the host-organism (us humans).
The affinity for mitochondrial RNA of all the antibiotics which have been found to be safe in man, is very much less than their affinity for the bacterial ribosomal RNA. For example, there is an antibiotic called Chloramphenicol, which is only used in extreme illness in Humans because it does have a significant effect on the mitochondria. However, the ability of the other antibiotics to kill bacteria far outweighs any minimal risk they have to the host.
The NIH did a study in Rheumatoid Arthritis for 4 years at 100mg of mino every 12 hours, and found no evidence of mitochondrial problems.
On the DVDs of the Chicago Conference I show 3-D models of a Bacterial Ribosome, showing where and how each antibiotic docks into the ribosomal RNA in order to prevent protein synthesis, and how the MP antibiotics do this synergistically, without the possibility of interaction.
Minocycline has direct action on the PXR receptor, and hence on 1,25-D, which probably explains its palliative activity in the AP (antibiotic protocol).
..Trevor..
Last edited on Wed Nov 5th, 2008 04:29 by Meg Mangin R.N.
____________________
Nothing contained in this site is or should be considered, or used as a substitute for, medical advice, diagnosis or treatment by your physician.
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