Cpn exploits a variety of mechanisms to thwart our immune system. There is one mechanism that is particularly important and can be countered by over the counter supplements. Cpn targets niacin metabolism. In doing so it leads to impaired T-cell function, low melatonin, low serotonin, low tryptophan, low niacin all of which can present as depression, fatigue and insomnia, all familiar symptoms in Chronic Fatigue, Fibromyalgia and a host of Cpn related disorders.
Niacin therapy has been used safely for the treatment of hypercholesterolemia for decades, just the same, niacin levels should be increased slowly to minimize flushing and liver enzymes should be monitored. Expect some endotoxin release (as organisms die) as niacin is increased. Endotoxin release will lower nitric oxide levels temporarily and lead to cold hands and feet and possibly increased muscle aches in the initial stages of niacin treatment. You have to build up gradually on niacin as ingestion causes a flush like a hot flash. This reaction abates as you get used to the increased levels, and you can increase (UP TO???) the dose as tolerance develops.
Eventually time-released niacin can be used after niacin tolerance is established, but this form of niacin can be harder on the liver. Just be careful and make sure your doctor is monitoring liver enzymes and CBC every month or so until tolerance is well established. Unfortunately Niacinamide, ("No Flush Niacin") does not appear to be as effective.
Adding herbs that increase nitric oxide synthase (NOS) activity can also be helpful and can lead to improved immune function and warmer extremities. Garlic, ginseng, & ashwagandha all increase the activity of NOS and may be synergistic in combination with niacin. Increasing nitric oxide usually decreases FM related muscle pain and anxiety. One of the following articles supports the use of niacin for chronic headache (Mayo Clinic article) and another links infection with Cpn to disruption of niacin metabolism and immune evasion.Make sure that you are taking a good multivitamin daily when doing battle with Cpn. Nutritional demands are increased significantly by increased exposure to the endotoxin that is released from dying organisms. Biochemicals made by the the body to fight Cpn are made at the expense of tryptophan, niacin, melatonin, and serotonin all of which also are needed to fight Cpn in other ways. Supplementation with niacin and melatonin should make life more difficult for Cpn.
Best wishes to all of those who striving to be a bad host to Cpn. The last two articles document the effects of nitric oxide and melatonin on Cpn.
Mayo Clin Proc. 2003 Jun;78(6):770-1.
Sustained-release niacin for prevention of migraine headache.
Velling DA, Dodick DW, Muir JJ.
Division of Pain Management Mayo Clinic, Scottsdale, Ariz 85259, USA.
Considerable advances in the diagnosis and treatment of migraine headache have occurred during the past decade, but treatment options for acute migraine attacks have expanded at a faster rate than those for prophylaxis. We describe a patient whose migraine headaches responded dramatically to sustained-release niacin as preventive treatment. Niacin is not generally considered to be effective for migraine prevention. However, low plasma levels of serotonin have been implicated in migraine pathogenesis, and niacin may act as a negative feedback regulator on the kynurenine pathway to shunt tryptophan into the serotonin pathway, thus increasing plasma serotonin levels. Sustained-release niacin merits further study as a potentially useful preventive therapy for migraine headache.
PMID: 12934790 [PubMed - indexed for MEDLINE]
Can J Microbiol. 2005 Nov;51(11):941-947.
Effect of nitric oxide on the growth of Chlamydophila pneumoniae.
Carratelli CR, Rizzo A, Paolillo R, Catania MR, Catalanotti P, Rossano F.
Chlamydophila pneumoniae is an important human intracellular pathogen; however, the pathogenesis of C. pneumoniae infection is poorly understood and the immune control mechanism versus host cells is not completely known. The role of the nitric oxide (NO) synthase pathway in inhibiting the ability of C. pneumoniae to infect macrophage J774 cells and the ability of NO to damage isolated C. pneumoniae were investigated. Exposure of infected cultures to recombinant murine gamma interferon (MurIFN-γ) resulted in increased production of NO and reduced viability. Addition of 2-(N,N-diethylamino)-diazenolase-2-oxide before infection of J774 cells or during chlamydial cultivation released NO, both resulting in a reduction in the viability of C. pneumoniae in a dose-dependent way. These results indicate that immune control of chlamydial growth in murine macrophage cells may trigger a mechanism that includes NO release with effects on the multiplication of the microorganism, thus suggesting that NO may play a role in preventing the systemic spread of Chlamydia.
PMID: 16333333 [PubMed - as supplied by publisher]
J Antimicrob Chemother. 2005 Nov;56(5):861-8. Epub 2005 Sep 19.
Serotonin and melatonin, neurohormones for homeostasis, as novel inhibitors of infections by the intracellular parasite chlamydia.
Rahman MA, Azuma Y, Fukunaga H, Murakami T, Sugi K, Fukushi H, Miura K, Suzuki H, Shirai M.
Department of Microbiology, Yamaguchi University School of Medicine, 1-1-1, Minamikogushi, Ube, Yamaguchi 755-8505, Japan.
OBJECTIVES: Chlamydiae are obligate intracellular bacteria, causing a variety of diseases, i.e. pneumonia, sexually transmitted disease, conjunctivitis and zoonosis. Tryptophan depletion by interferon-gamma (IFN-gamma) is the most important host defence system against chlamydial infection. Thus chlamydial tryptophan metabolism is thought to play key roles for IFN-gamma resistance, persistent infection and host/tissue tropisms. We tested tryptophan derivatives for activity against chlamydia-infected cells. METHODS: Rates of chlamydial infection and sizes of the inclusions were evaluated by in vitro infection using three Chlamydiaceae species, Chlamydia trachomatis, Chlamydophila pneumoniae and Chlamydophila felis, which show significant divergence of tryptophan synthesis genes and different susceptibilities to IFN-gamma. RESULTS: Melatonin and serotonin, which are recognized as neural hormones for maintenance of organism homeostasis, reduced chlamydial infection but not other bacterial growth tested here. Unlike IFN-gamma, melatonin limited infection of all three chlamydiae and the effects were not recovered by tryptophan supplementation. Melatonin treatment only of host cells could diminish infection and the infection reduction was neutralized by a pertussis toxin, an inhibitor of G proteins. Ligands of melatonin and serotonin receptors also hampered infection. CONCLUSIONS: Inhibition mechanisms of chlamydial infection by melatonin and serotonin appear to be different from those of IFN-gamma and involve specific G-protein-coupled receptors. Melatonin is deemed to inhibit early progression of the chlamydial development cycle, such as establishment of intracellular infection and/or conversion from elementary body to reticulate body. Utilization of melatonin, serotonin or their derivatives may be advantageous for harmless prevention of chlamydial infection.
PMID: 16172105 [PubMed - in process]