It's been nearly a whole month since I started taking capsaicin in addition to curcumin and skullcap. There is no doubt that it has had a noticeably good effect on my bladder and spasticity and bowel function. However there has also been a few nights, usually when I've smoked dope, when the pain in my left leg has returned with an alarming vengeance. Whenever I've smoked dope in the past, the pain has also increased so I shouldn't be too surprised especially as I think there is a common pathway between the vanilloid, capsaicin, and cannabinoids. I have also had bad night spasms on a couple of occasions recently; the first when I introduced a new brand of astragalus, the second after a week of inebriation, followed by a clean night and the third the same. Normally in the past when I've gone on holiday and had a drink every night and then not had a drink exactly the same bad attack of spasms occurs, so I shouldn't be too surprised. However I also think it likely that the capsaicin is having quite an impact on the old nervous system and I daresay that its effects aren't all benign, so I'm going to continue but with caution. I keep finding lots of information on capsaicin but i'm no clearer as to whether it is a good thing or not!
Given the above posted research on the involvement of the sensory/afferent nerves in autoimmune disease, I am wondering again about the varicella zoster virus which likes to remain dormant in precisely these types of nerves.
1: Phytother Res. 2003 Jun;17(6):609-13. Links
Anti-herpesvirus activity of an extract of Ribes nigrum L.Suzutani T, Ogasawara M, Yoshida I, Azuma M, Knox YM.
Department of Microbiology, Asahikawa Medical College, 2-1-1-1 Midorigaoka-Higashi, Asahikawa 078-8510, Japan. firstname.lastname@example.org
An extract of Ribes nigrum L., known as blackcurrant in Europe and Kurokarin(R) in Japan, has been used as an ingredient in a variety of foods and folk medicine. In this study, the anti-herpesvirus activity of this extract was examined in vitro. The extract inhibited herpes simplex virus type 1 attachment on the cell membrane completely at a 100-fold dilution, as well as the plaque formation of herpes simplex virus types 1 and 2, and varicella-zoster virus by 50% at a 400-fold dilution
or lower concentrations. This latter activity, which inhibits virus replication in cells, was due to the inhibition of protein synthesis in infected cells from the early stage of infection. Kurokarin is a possible candidate as a herbal medicine for herpesvirus infectious diseases. Copyright 2003 John Wiley & Sons, Ltd.
but then again the canine distemper virus looks like another very strong candidate
1: Neuroreport. 2001 Feb 12;12(2):191-4. Links
Disappearance of beta2-adrenergic receptors on astrocytes in canine distemper encephalitis: possible implications for the pathogenesis of multiple sclerosis.De Keyser J, Wilczak N, Walter JH, Zurbriggen A.
Department of Neurology, Academisch Ziekenhuis Groningen, The Netherlands.
It has been reported that astrocytes in the white matter of patients with multiple sclerosis (MS) lack beta2-adrenergic receptors. This abnormality might explain why astrocytes in active MS plaques aberrantly express major histocompatibility (MHC) class II molecules, which play an important role in the immunological cascade leading to myelin destruction. Canine distemper (CD) virus primarily infects astrocytes and causes a demyelinating disease in dogs that closely resembles MS. In control dogs, including three dogs with another inflammatory disease, beta2-adrenergic receptor immunoreactivity was observed on both neurons and astrocytes. In dogs with CD encephalitis, beta2-adrenergic receptors were present on neurons, but were absent on astrocytes in acute lesions, demyelinated lesions, and normal-appearing white matter. Similar to MS, several astrocytes in demyelinated lesions expressed MHC class II. These findings suggest that MS and the demyelinating stages of CD encephalitis have a common pathogenetic factor, and that the loss of astrocytic beta2-adrenergic receptors in MS might be induced by a viral infection of astrocytes.
1: Trends Pharmacol Sci. 2004 Feb;25(2):67-71. Links
Trends Pharmacol Sci. 2004 Jul;25(7):350-1; author reply 351-2.
Beta 2-adrenoceptor involvement in inflammatory demyelination and axonal degeneration in multiple sclerosis.De Keyser J, Zeinstra E, Mostert J, Wilczak N.
Department of Neurology, University Hospital Groningen, Hanzeplein 1, 9713 GZ Groningen, The Netherlands.
Relapses of multiple sclerosis (MS) are considered to be the clinical expression of acute T-cell-mediated inflammatory demyelinating lesions disseminated in the CNS, whereas disease progression seems to result from widespread axonal degeneration. The pathophysiology of both disease components is incompletely understood. Astrocytes in MS lack beta(2)-adrenoceptors, which via cAMP-mediated processes inhibit the expression of major histocompatibility (MHC) class II molecules and stimulate glycogenolysis in normal conditions. In a pro-inflammatory CNS environment this beta(2)-adrenoceptor defect might allow astrocytes to transform into facultative antigen-presenting cells that can initiate the inflammatory cascade. The same receptor defect might impair astrocytic glycogenolysis, which normally generates lactate that is transported to axons as an energy source. Failure of axonal energy metabolism might result in axonal degeneration through mechanisms that involve intra-axonal accumulation of Ca(2+) ions and mitochondrial dysfunction. If this hypothesis is correct, therapies designed to elevate cAMP levels in astrocytes should reduce or prevent both relapses and progression of MS.
How to inhibit MHC class II? Here's a herb I've never heard of:
1: J Immunol. 2006 May 15;176(10):5797-804. Links
Highly oligomeric procyanidins ameliorate experimental autoimmune encephalomyelitis via suppression of Th1 immunity.Miyake M, Sasaki K, Ide K, Matsukura Y, Shijima K, Fujiwara D.
Central Laboratories for Key Technology, Kirin Brewery, 1-13-5 Fukuura, Kanazawa, Yokohama-shi, Kanagawa 236-0004, Japan. email@example.com
Extracts of Jatoba, a South American herb, when injected i.p. into a mouse model of experimental autoimmune encephalomyelitis (EAE), inhibited the aggravation of clinical symptoms. At the same time, production of myelin oligodendrocyte glycoprotein Ag-specific IFN-gamma and TNF-alpha by spleen cells was markedly suppressed. After administration of Jatoba there was minimal evidence of the demyelination that is characteristic of the EAE model. Decreases in clinical scores were observed when Jatoba extracts were injected just before Ag. The purified active compounds are likely to be polyphenols that are absorbable to polyvinylpolypyrrolidone. The active compounds were polymerized polyphenol polymers (procyanidins) and at least five degrees of polymerization were necessary for activity. In addition, extracts of other plant materials containing such procyanidins had similar activity. After administration of highly polymerized procyanidins, there was a decrease in both dendritic and CD4(+) T cells. Although macrophages were increased in number, the expression of CD80 and MHC class II molecules was depressed indicating that the macrophages were immature. The results indicate that the suppression of development of EAE by the highly polymerized procyanidins resulted from an inhibition of Th1 and the effects might be associated with depression of Ag-presenting capability.
Maybe we need to some beta2 adrenoceptor agonists too:
1: J Neuroimmunol. 1995 Feb;56(2):201-6. Links
Beta-adrenergic agonists suppress chronic/relapsing experimental allergic encephalomyelitis (CREAE) in Lewis rats.Wiegmann K, Muthyala S, Kim DH, Arnason BG, Chelmicka-Schorr E.
Department of Neurology, University of Chicago, IL 60637.
Chronic/relapsing experimental allergic encephalomyelitis (CREAE) serves as an animal model for relapsing/remitting multiple sclerosis. Treatment with the beta-adrenergic agonist isoproterenol or the beta 2-adrenergic agonist terbutaline significantly suppressed both the first acute attack and the number of relapses in CREAE Lewis rats. The number of relapses was decreased even when treatment with beta-adrenergic agonist was started after the onset of the first acute attack of CREAE. beta-adrenergic receptor number was increased significantly on splenocytes from CREAE rats as compared to healthy controls or CFA-injected rats. Terbutaline treatment of CREAE rats lowered the splenocyte receptor number to normal values.
1: CNS Drugs. 2002;16(1):1-8.Links
Potential of beta2-adrenoceptor agonists as add-on therapy for multiple sclerosis: focus on salbutamol (albuterol).Makhlouf K, Weiner HL, Khoury SJ.
Center for Neurologic Diseases, Brigham & Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
The beta2-adrenergic receptor agonist salbutamol (albuterol) has been used for many years in the treatment of bronchospasm in patients with asthma. In this patient group, salbutamol is a relatively safe and inexpensive drug, and is easy to administer. Within the last few years, there has been increasing evidence that salbutamol might have immunomodulatory properties both in vitro and in vivo, in different animal models as well as in humans. This has led researchers to consider salbutamol as a potential therapy for several autoimmune diseases, including multiple sclerosis (MS). In this article, we review the literature presenting such evidence, and discuss the possible mechanisms by which salbutamol influences the immune system. We conclude that salbutamol might be an interesting add-on therapy in patients with MS and that further research is warranted.
PMID: 11772115 [PubMed - indexed for MEDLINE]
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,