I was on it for a few months along with another couple of drugs. Went through a couple of really bad weeks with dizziness before adjusting to it and then seemed the inflammation was better but did little else.
I have never taken Minocycline. I was on 400mg of Doxycycline, same family as Minocycline, for about a year. I got really sick when I first started, but the last several months on it I felt the best I have since getting sick over 24 years a go. I stopped taking it about two weeks a go because I want to be off everything when I take get the xmrv serological test. Not sure when it's going to be available though.
I'm not sure if a couple of months would be long enough.
I was much better last year on doxycyline and then minocycline for 6 months in total. I stopped them both and 3 months later had a bad relapse. Started doxy again (400 mg) and after 5 months was no better and stopped it while on LDN.
Since stopping LDN I've been on minocin (sustained release minocycline) and plaquenil for 4 weeks and I'm suddenly feeling very much worse, so it may be doing something. The symptoms have been intolerable so I'm stopping it for a while and going back on doxy.
I've come round to thinking that just because something doesn't work at one point in the illness, that doesn't necessarily mean it won't help at another stage. I think we may have an accumulation of different types of infections which have different life cycles and different forms, which need different treatments at different times.
Lyme patients often do well on minocin and they think it's better than minocycline.
It took awhile before I felt better on Doxycycline. I felt much worse first for a long time, until I finally started to feel better. I think after being sick for over 24 years antibiotics or antivirals may take awhile before I see improvements.
I was on Minocin for three years. Very bad die off the first few months but I strongly believe this is what has gotten me to a 7 and has allowed me to work. It didn't cure me but it helped. After Minocin I was on anti-virals for three months.
lIn the new study, molecular biologist Janice Clements of Johns Hopkins University in Baltimore and her colleagues infected human CD4 T cells with HIV in lab dishes, then added minocycline to some of these batches. After 24 hours, the minocycline-treated cells contained half as much HIV RNA as the other cells, suggesting the drug had inhibited the ability of the virus to replicate.
As expected, minocycline attenuated microglial activation as confirmed by decreased OX-42 immunoreactivity, normalized nitrite/nitrate levels in brain and significantly attenuated HO-1, eNOS and iNOS expression. These results indicate that the beneficial effect of minocycline on the neurological complications of ALF is mediated, at least in part, by reduction of oxidative/nitrosative stress.
Thanks for posting this. When I take minocin, I feel much, much better. At least for a while.
The problem is that I also seem to have lyme and/or other bacterial infections, which was the reason I started taking it in the first place. So, after feeling better, I start feeling much worse (herxheimer) because of the bacteria die-off. After a few days, I am a basket case. There is no doubt in my mind that minocin decreases inflammation before the herx kicks in. I try to explain all this to my doctor, but just doesn't seem to get it. I would take minocin just for the anti-inflammatory aspects if I could.
I doubt this is suppressing XMRV, but who knows. I have an open mind.
Hi all, I too felt worse when first starting Minocin but improved after 3 or 4 months. I was on it for three years. It works by evening out your immune system as well as dealing with bacterial infections. Be warned though, I developed some severe hyperpigmentation which improved but did not disappear after stopping. Also darkened my teeth, already dark by childhood tetracycaline. I am thinking of going back on it though. Interesting, my ANA went from 360 to nothing, zero. The doctor had never seen this.
Have you been tested for co-infections that play a role in ME/CFS/CFIDS? Micoplasma and Chlamydia P. are 2 that are prevelant is us, as well as all of the Lyme Panels (about 4-5 of them). If you respond to antibiotics, you might be feeling better because the co-infections are being treated. Doxycycline is normally used for 12-24 months to take care of these infections, I could not tolerate this antibiotic so they use 600 mg of Zithromax on me for 2 years. The Micoplasma Infection alone can make the patients' symptoms much, much worse in CFS/CFIDS. It is really important to get all of your tests run...HHV-6A, EBV, CMV, Lyme etc....plus all of the Piggy Back co-infections run as well. http://vlgonvalcyte.wordpress.com/
Researchers in Germany and at the University of Wisconsin have reported that minocycline either blocks the disease or lessens the severity of symptoms when used to treat laboratory rats afflicted with the animal equivalent to MS. In an article in Annals of Neurology, they reported on study results from four groups of rats, two of which received doses of the protein that causes autoimmune encephalomyelitis and two control groups, all of which were treated with minocycline. Whether the rats were treated before or at the onset of the disease, the minocycline lessened the severity of symptoms and blocked relapses. Later, it was found to have protected both the myelin sheaths and the nerve fibers in the rats' brains. Earlier, Finnish studies of stroke patients had shown that minocycline stopped the activation of microglial cells which patrol the brain and respond to immune events and are known culprits in MS and other nerve diseases.
Minocycline possesses anti-inflammatory properties independently of its antibiotic activity although the underlying molecular mechanisms are unclear. Lipopolysaccharide (LPS)-induced cytokines and pro-inflammatory protein expression are reduced by minocycline in cultured macrophages. Here, we tested a range of clinically important tetracycline compounds (oxytetracycline, doxycycline, minocycline and tigecycline) and showed that they all inhibited LPS-induced nitric oxide production. We made the novel finding that tigecycline inhibited LPS-induced nitric oxide production to a greater extent than the other tetracycline compounds tested. To identify potential targets for minocycline, we assessed alterations in the macrophage proteome induced by LPS in the presence or absence of a minocycline pre-treatment using 2-DE and nanoLC-MS. We found a number of proteins, mainly involved in cellular metabolism (ATP synthase ?-subunit and aldose reductase) or stress response (heat shock proteins), which were altered in expression in response to LPS, some of which were restored, at least in part, by minocycline. This is the first study to document proteomic changes induced by minocycline. The observation that minocycline inhibits some, but not all, of the LPS-induced proteomic changes shows that minocycline specifically affects some signalling pathways and does not completely inhibit macrophage activation.