Gibbledygook's anti-viral log

Tell us what you are using to treat your MS-- and how you are doing.

Razavi, Chan et al Sensing autoimmunity in T1 Diabetes

Postby gibbledygook » Fri Jul 25, 2008 5:25 am

Right, I have now an article by Razavi, Chan et al from Trends in Molecular Medicine Vol 13 No 10 and entitled "Sensing Autoimmunity in T1 Diabetes". In it they say
"When capsaicin is applied to neonatal animals, there is permanent and complete degeneration of TRPV1+ sensory nerves in the periphery. NOD Mouse islets and surrounding exocrine tissue contain many small caliber TRPV1+ neurons, which are also removed by neonatal capsaicin treatment. Unexpectedly, this resulted in protection fromislet inflammation and diabetes, despite unabated loss of self-tolerance and islet autoimmunity in peripheral lymphoid organs [24]. The deletion of sensory neurons thus prevents islet tiissue access and disease, but other abnormalities, possiby intrinsic to the immune system, govern the priming and reactivity to classical Type 1 diabetes target autoantigens".
So this, albeit neo-natal capsaicin treatment stops diabetes. I don't know where Yale got the opposite (described above) from.

Furthermore, I have now substantially read the 2006 article by Shazani, Chan et al (TRPV1+ Sensory Neurons Control Beta Cell Stress and Inflammation in Auto Immune Diabetes) and their concluding remarks include the following:

Elimination of TRPV1+ neurons by capsaicin, transient functional normalization by acute local substance P injection, or replacement with wild-type trpv1 in ldd4 congenics has the same, islet-specific outcome: normalized insulin sensitivity and abrogation of insulitis, despite unimpeded generation of autoreactive lymphocytes that can transfer disease to untreate NOD hosts.


I think I can ignore the alarmingly incorrect Yale piece! It's simply not true that Razawi et el say anything like the elimination of TRPV1+ neuronal cells by large injections of capsaicin leads to the continuation of the autoimmune process. They say quite the opposite. Yale nuls points, gibbledygook dix points!

28/7/08
On reflection I think I am being unfair to Yale. The autoreactive T cells are obviously still there but the diabetes is annulled. So the disease is cured but the auto-immunity continues. Still, the main thing is that capsaicin relieves the damaging effects of the auto-immunity. I think the Yale wording frightened me as I had understood the research to have said that capsaicin cures diabetes, which it does but it doesn't stop the autoimmunity. I wonder if capsaicin delivered throughout the body might do so....!
Last edited by gibbledygook on Mon Jul 28, 2008 3:34 am, edited 3 times in total.
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Fight fire with fire, cont.:

Postby gibbledygook » Sun Jul 27, 2008 12:56 pm

The anti-inflammatory neuropeptide somatostatin is reduced in MS patients:

1: Biol Psychiatry. 1999 Aug 15;46(4):551-6. Links
Cerebrospinal fluid somatostatin, mood, and cognition in multiple sclerosis.Roca CA, Su TP, Elpern S, McFarland H, Rubinow DR.
Behavioral Endocrinology Branch, National Institute of Mental Health, Bethesda, Maryland, USA.

BACKGROUND: Cerebrospinal fluid (CSF) somatostatin (SS) levels have been shown to be decreased in multiple sclerosis (MS) during relapse as well as in disorders characterized by depression or cognitive impairment. Since MS is often associated with depression and cognitive impairment, we examined both the effect of course of illness on CSF SS as well as the variance in SS attributable to associated features (e.g., depression or cognitive impairment). METHODS: Fifteen patients with chronic progressive MS participating in a 2-year cyclosporine trial underwent lumbar punctures for CSF SS at baseline and at 12 and 24 months. Additionally, patients were evaluated by neuropsychological testing, and physical disability and mood ratings. Baseline CSF SS levels were also obtained in a group of control subjects (n = 10). RESULTS: At baseline, CSF SS levels were lower in MS patients than control subjects (p < .001). Decreased CSF SS at 24 months was correlated with decreased cognitive performance on several measures and was best and significantly predicted by cognitive deterioration at 24 months. CONCLUSIONS: Our data support those from previous studies that found lower levels of CSF SS in MS during relapse and suggest that changes in CSF SS are related to the process responsible for diminished cognitive function in MS.

PMID: 10459406 [PubMed - indexed for MEDLINE]

Related ArticlesPredicting quality of life in multiple sclerosis: accounting for physical disability, fatigue, cognition, mood disorder, personality, and behavior change. [J Neurol Sci. 2005] Low somatostatin content in cerebrospinal fluid in multiple sclerosis. An indicator of disease activity? [Acta Neurol Scand. 1980] Mitoxantrone: a review of its use in multiple sclerosis. [CNS Drugs. 2004] CSF nitric oxide metabolites are associated with activity and progression of multiple sclerosis. [Neurology. 2004] The influence of immunomodulation on psycho-neuroimmunological functions in benign multiple sclerosis. [Neuroimmunomodulation. 2004] » See all Related Articles...
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vanilloids, such as capsaicin looks like they upregulate this neuropeptide:

1: Neuropeptides. 2004 Dec;38(6):377-84. Links
Forty years in capsaicin research for sensory pharmacology and physiology.Szolcsányi J.
Department of Pharmacology and Pharmacotherapy, University Medical School of Pécs, Szigeti u 12, H-7624 Pécs, Hungary. janos.szolcsanyi@aok.pte.hu

Capsaicin, the pungent ingredient of chilli peppers has become a "hot" topic in neuroscience with yearly publications over half thousand papers. It is outlined in this survey how this exciting Hungarian research field emerged from almost complete ignorance. From the initial observation of the phenomenon of "capsaicin desensitization", a long-lasting chemoanalgesia and impairment in thermoregulation against heat, the chain of new discoveries which led to the formulation of the existence of a "capsaicin receptor" on C-polymodal nociceptors is briefly summarized. Neurogenic inflammation is mediated by these C-afferents which are supplied by the putative capsaicin receptor and were termed as "capsaicin sensitive" chemoceptive afferents. They opened new avenues in local peptidergic regulation in peripheral tissues. It has been suggested that in contrast to the classical axon reflex theory, the capsaicin-sensitive sensory system subserves a "dual sensory-efferent" function whereby initiation of afferent signals and neuropeptide release are coupled at the same nerve endings. Furthermore, in the skin at threshold stimuli which do not evoke sensation elicit already maximum efferent response as enhanced microcirculation. In isolated organ preparations large scale of new type of peptidergic capsaicin-sensitive neurogenic smooth muscle responses were revealed after the first one was described by ourselves on the guinea-pig ileum in 1978. Recently the "capsaicin receptor" has been cloned and it is now named as the "transient receptor potential vanilloid 1" (TRPV1). Hence, capsaicin research led to the discovery of the first temperature-gated ion channel gated by noxious heat, protons, vanilloids and endogenous ligands as anandamide, N-oleoyldopamine and lipoxygenase products. Another recent achievement is the discovery of a novel "unorthodox" neurohumoral regulatory mechanism mediated by somatostatin. Somatostatin released from the TRPV1-expressing nerve endings reaches the circulation and elicits systemic antiinflammatory and analgesic "sensocrine" functions with counter-regulatory influence e.g. in Freund's adjuvant-induced chronic arthritis. Nociceptors supplied by TRPV1 and sst4 somatostatin receptors has become nowadays promising targets for drug development.
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1: Pharmacol Ther. 2006 Nov;112(2):440-56. Epub 2006 Jun 9. Links
Inhibitory effect of somatostatin on inflammation and nociception.Pintér E, Helyes Z, Szolcsányi J.
Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, University of Pécs, H-7624 Pécs, Szigeti u. 12, Hungary. erika.pinter@aok.pte.hu

The present review focuses on promising new opportunities for anti-inflammatory and analgesic therapy. The theoretical background is an original observation based on our own experimental results. These data demonstrate that somatostatin is released from capsaicin-sensitive, peptidergic sensory nerve endings in response to noxious heat and chemical stimuli such as vanilloids, protons or lipoxygenase products. It reaches distant parts of the body via the circulation and exerts systemic anti-inflammatory and analgesic effects. Somatostatin binds to G-protein-coupled membrane receptors (sst(1)-sst(5)) and diminishes neurogenic inflammation by prejunctional action on sensory-efferent nerve terminals, as well as by postjunctional mechanisms on target cells. It decreases the release of pro-inflammatory neuropeptides from sensory nerve endings and also acts on receptors of vascular endothelial, inflammatory and immune cells. Analgesic effect is mediated by an inhibitory action on peripheral terminals of nociceptive neurons, since circulating somatostatin cannot exert central action. Somatostatin itself is not suitable for drug development because of its broad spectrum and short elimination half life, stable, receptor-selective agonists have been synthesized and investigated. The present overview is aimed at summarizing the physiological importance of somatostatin and sst receptors, pharmacological significance of synthetic agonists and their potential in the development of novel anti-inflammatory and analgesic drugs. These compounds might provide novel perspectives in the pharmacotherapy of acute and chronic painful inflammatory diseases, as well as neuropathic conditions.
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Fighting fire with fire

Postby gibbledygook » Mon Jul 28, 2008 3:51 am

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. suzutani@fmu.ac.jp

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.
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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.
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1: Trends Pharmacol Sci. 2004 Feb;25(2):67-71. Links

Comment in:
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.
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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. m-miyake@kirin.co.jp

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.
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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.
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or

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]
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Postby gibbledygook » Wed Jul 30, 2008 8:59 am

I have obviously overloaded my regimen section with pubmed abstract citations so that my entry is now a pain in the proverbial to read. I hope that if I add a few small entries like this that the whole thing will shrink to be a better format.

Anyway Cureo is right about spacing out the capsaicin throughout the meal. I particularly liked the description of the capsaicin as "depth charges"! Well done cureo! Yesterday I took my 2.4g of capsaicin at breakfast and lunch with one 600mg pill at the beginning of the meal and one at the end. Last night I had very little leg twitchiness.

Today I received my pack of salvia miltiorrhiza, for which there are pub med entries above. I am taking 1.8g of these a day.

I think I need a pub med holiday! I seem to have copied vast tracts of PubMed onto my regimen section. 8O

I'm particularly curious about the similarity between canine distemper virus and the beta 2 adrenoceptors missing on astrocytes in MS patients and the paradoxical increase of these receptors on primary progessive and secondary progressive monocytes. It's as though these are making up for the missing receptors in the astrocytes. Those pesky astrocytes are a problem.

Anyway fingers crossed the format returns to more legible.
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,
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Postby mrhodes40 » Wed Jul 30, 2008 9:39 am

Alex was your leg twitchiness less than it is usually on capsaicin or are you saying the capsaicin is reducing your twitchiness overall?

I like the abstracts, but they are kind of drinking from a firehose, you have to kind of study it to understand where you are going with it.
You are doing reat work on it all!
marie
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Postby gibbledygook » Thu Jul 31, 2008 9:38 am

Hi Marie,

The leg twitchiness in the first two weeks of capsaicin treatment was normal (ie hardly any), then when I was trying out a brand of astragalus in combination with the capsaicin, curcumin and skullcap I had a night of terrible spasms. Initially I put this down to the astragalus but I think the capsaicin has also been increasing the tingling and twitchiness over the last two weeks after having stopped the astragalus. Indeeed since just eating the capsaicin at breakfast and lunch I've had no twitchiness and much less tingling at night so I think the capsaicin can definitely irritate the damaged nerves so it's best to consume in the day, especially as it can make one feel rather awake at night when the "depth charges" kick in. I'm definitely enjoying an improvement since starting with it especially the bladder, spasticity and bowel, even the strength in my legs when exercising seems noticeably improved. And this during the hot, humid season in London. Maybe I could manage Singapore after all. :)

My chinese doctor just said that he wouldn't use astragalus for autoimmune patients so I guess that night of bad spasms was something to do with this immune "tonifier".

I've just received from pubmed some jatoba from iherb which is one of the herbs in one (of the many) pubmed citations above so I'll be giving that a go shortly.

By the way, thank you whoever shortened my urls to make my regimen more legible! I must learn to do this myself. :roll:
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,
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Still feeling better

Postby gibbledygook » Fri Aug 08, 2008 8:48 am

I continue to enjoy significantly better bladder, bowel and right leg motor function which is far less stiff than before. Unfortunately my left leg achilles tendon is playing up again so I'm not confident about trying a long walk as this may put too much strain on the left leg.
I haven't managed to maintain 2.4g of the capsaicin depth charges as I had a very severe loosening of the bowels so I'm back down to 1.8g daily or one 600mg tablet with every meal. These are ideally a protein meal, so I've been eating a lot of soft-boiled eggs for breakfast. The capsaicin has increased the night spasms but they calm down when I take extra curcumin. I continue to take about 7.2g of the life extension extra strong curcumin, slightly more skullcap at 6g with a different cheaper brand from herbal extracts plus, 1.2g salvia miltiorrhiza, bioperine 30mg. I have also increased my vitamin d to 5000 units a day and take about 1.5g of calcium/magnesium pills and NAC about 1.2g a day. And 30g of the chinese tea. These are the only things I take with real consistency.
The chinese tea has now changed and includes the following:
4.4g rehmannia preparata,
2.93g rehmannia raw
2.93g of gentiana macrophyllae,
3.66g ligustri lucidi fructus,
2.93g angelica sinensis,
2.93g salvia miltiorrhiza,
2.2g paeoniae radix,
2.2g liquidambaris fructus,
2.93g corni fructus,
2.2g jujubae fructus.

I must say this particular tea is pretty revolting to taste.

1: J Pharm Pharmacol. 2007 Sep;59(9):1279-85. Links
Fructus Ligustrum lucidi inhibits inflammatory mediator release through inhibition of nuclear factor-kappaB in mouse peritoneal macrophages.An HJ, Jeong HJ, Um JY, Park YJ, Park RK, Kim EC, Na HJ, Shin TY, Kim HM, Hong SH.
College of Oriental Medicine, Institute of Oriental Medicine, Oriental Medical Science Center, Kyung Hee University, 1-Hoegi-Dong, Dongdaemun-Gu, Seoul 130-701, Republic of Korea.

Fructus Ligustrum lucidi (FLL) is a widely used herbal medicine for the treatment of a variety of pathologies. We have investigated the anti-inflammatory mechanism of FLL in mouse peritoneal macrophages. FLL exerted an anti-inflammatory action through inhibition of lipopolysaccharide (LPS)-induced tumour necrosis factor (TNF)-alpha production in mouse peritoneal macrophages. The maximal inhibition rate of TNF-alpha production by FLL (0.5 mg mL(-1)) was 60.88 +/- 0.30%. In the inflammatory process, nitric oxide (NO) and prostaglandin E(2) (PGE(2)) increased in peritoneal macrophages. FLL decreased the protein level of NO and PGE(2) in LPS-stimulated mouse peritoneal macrophages. In addition, FLL inhibited nuclear factor-kappaB activation and IkappaB-alpha degradation by the decrease in IkappaB-alpha phosphorylation. Our study suggested that FLL reduced inflammation via an important molecular mechanism, which might explain its beneficial effect in the regulation of inflammatory reactions.

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Postby gibbledygook » Tue Aug 26, 2008 10:58 am

I'm back from the Austrian purge where there was no alcohol, no caffeine and not much food for two weeks but plenty of sun and calcium/magnesium drink. To my delight I discovered that the calcium/magnesium drink significantly alleviates the burning sensation from the capsaicin and so could happily take 3g a day. As suggested by my osteopath I started about 2 weeks ago to walk with much more pressure on the bad leg and have switched my cane to support my good leg. If I hadn't done this I could report that my walking was significantly better. Before the switch I walked through the airport at Stansted for about 1km or so it seemed with very little difficulty which impressed my partner a great deal. So I'm very bullish on the old phenols.
On return a few days ago I got my latest blood work which revealed a worrying increase in iron in the blood. Nothing of course to do with the egregious quantities of red wine consumed before the purge. I've ordered some milk thistle just in case.
For the last 2 days I suffered a very curious twitching sensation in my left pelvic area. Yesterday I stopped the capsaicin after breakfast to see if this might be contributing and today I haven't experienced this. So it seems like the capsaicin was maybe doing something there. I guess if I try the capsaicin tomorrow and the twitching reappears then it would be logical to blame it for this phenomenon. The twitching wouldn't bother me so much except that I'm trying to get and possibly am pregnant and I worry about herbs causing uterine contractions etc. And as capsaicin is so bioactive in me then I guess it may have a profound effect down there. ho hum. Several days before I know it would be safe to take capsaicin again.
Hope everyone's had a good summer.
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,
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Postby gibbledygook » Sat Aug 30, 2008 8:13 am

On Wednesday I backed off the capsaicin to 1.2g daily and then increased the salvia miltiorrhiza to 3.6g a day and switched from the new chapter skullcap to the herbalextractsplus skullcap which is in a higher dose and so now I take 7.2g of skullcap a day. Since doing this the pain in my left leg has drastically gone down as has any twitchiness at night and my walking has improved considerably; I just walked at least 800meters on a hot and humid morning in Marlow on my partner's arm but not really needing it. I've had no further twitchiness in my pelvis area so may increase the capsaicin cautiously.
I have also received some rehmannia caps from herbal extracts plus and have ordered some peony, nettle and a couple of others for allergy and MS. I'm really beginning to appreciate the efficacity of herbs. :)
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,
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Postby gibbledygook » Sun Aug 31, 2008 5:57 am

Well, I've done the pregnancy test and thankfully, in a way, I'm not pregnant this time around. Considering how low my progesterone levels are this isn't surprising and I shall now get some progesterone supplements from the doctor to deal with these low levels. I'm quite glad that I'm not as I've only just discovered the benefits of increasing the skullcap and salvia levels. I am enjoying really significant bladder control and walking benefits from this switch only last week. It seems incredible. I now no longer need to void the bladder manually and yesterday evening I went out with boots and heels and didn't need the toilet throughout the hour and a half at dinner where I drank water and a glass of wine. Having double checked the quantities the above mentioned figures require changing. My regime consists of approximately 7.2g of curcumin from life extension (has been more when spasms bad), 10.8g of skullcap, 7.8g salvia, 1.2g capsaicin (has been more and will try to up to 2.4g), 30mg bioperine, 3g green tea extract, 600mg milk thistle and plenty of calcium and magnesium, 5000 iu of vit d, n acetyl carnitine, selenium. More irregularly I also take inosine, vit b complex, alpha lipoic, omega 3, zinc and quercetin. I feel strongly that the improvements this week are from the increased skullcap and salvia and not the green tea which I had taken in large quantity before but never had noticed any improvements. I think the increased salvia may be the most important. Am very pleased with the MS at the moment. Less impressed with endocrinal situation! Indeed I have just added 50mg of pregnenolone to see if this has any effect on the progesterone. oh, and back on the disgusting chinese tea tomorrow. :(
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,
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Postby schnittke » Mon Sep 01, 2008 7:42 am

Glad to hear that you are doing so much better on this regimen. How many of the life Extension Curcumin tabs are you taking. Just curious as
the info on the bottle states that each dose is equivalent to 2772 mg of regular curcumin. Thanks!
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Postby gibbledygook » Mon Sep 01, 2008 1:45 pm

I'm taking about 18 pills a day of the life extension. In the past when I had night spasms I sometimes took another 3 or 6 pills to calm the spasms down which it seems to have always done. This is expensive and I may switch to the much cheaper brand of herbalextractsplus now that I've found extra relief from their skullcap and salvia. The tingling and spasms are right down from when I started taking these last two about a week ago.
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,
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Re: Gibbledygook's anti-viral log

Postby NHE » Mon Sep 01, 2008 5:30 pm

gibbledygook wrote:I'm taking about 18 pills a day of the life extension. In the past when I had night spasms I sometimes took another 3 or 6 pills to calm the spasms down which it seems to have always done. This is expensive and I may switch to the much cheaper brand of herbalextractsplus now that I've found extra relief from their skullcap and salvia.

Thanks for the link to that retailer. What's interesting is that their price for 600 capsules of 95% curcuminoid extract is actually quite a bit less than their price for 1 lb of bulk powder. If their capsules really are 600 mg, then 600 capsules would provide 360 g which would be $200.34 if you paid their bulk price. However, they only want $108.10 for that quantity. That's a price per lb. of $136.20 not $252.43 (surely I can't be the only one who has noticed this).

NHE
Last edited by NHE on Tue Sep 02, 2008 3:16 am, edited 1 time in total.
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Postby gibbledygook » Tue Sep 02, 2008 12:38 am

I'm afraid I hadn't noticed! But they are lot cheaper - I've now ordered the 600 capsule pots for the salvia, skullcap and capsaicin. It's great not having to order small pots. The only annoying thing for me is their lack of Latin plant names in the search function.
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,
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Postby gibbledygook » Wed Sep 03, 2008 2:24 pm

Well, what a busy day I've had. I went to see the doctor about fertility problems and we looked through some of the hormone levels which have been tested recently. I suspect that I may have adrenal insufficiency due to low corticotropin-releasing hormone which may have been depleted by the capsaicin treatment and this may be a problem for trying to get pregnant. So whilst the pollen season is now over I shall stop taking the capsaicin and just stick to the curcumin, skullcap, salvia, rehmannia, disgusting Chinese tea, DHEA, pregnenolone and a new Chinese herbal formula, Er Xian Tang concoction for hormonal imbalance. from the Sen on the King's Road. Apparently the Er Xian Tang is very warming like chilli so I was warned against eating chilli on top of this concoction. The Chinese are amazing. They just look at one's tongue and tell you to avoid warming herbs!!! Amazing. I'll see a fertility expert in October and see where my hormones are then.

Thursday 4th September, 2008
Well, the Chinese herbalist was right. The Er Xian Tang was unsuitably warming for me in that it had an almost immediate effect of increasing dramatically the tingling in my legs. I shall return to the doctor today and listen to her suggestions instead of insisting that my research is right!! I think she thought I was a mixture of damp, cold and warm in the heart!!! Whatever that means. So today I restarted the 25mg DHEA and continue the pregnenolone 50mg and stick with the old rehmannia, curcumin, salvia and scutelleria. I haven't noticed any difference with the pregnenolone for the last 5 days since starting that so I guess that it is okay. Fingers crossed the DHEA is also ok.
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,
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