Gibbledygook's anti-viral log

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

Postby cheerleader » Sat Nov 08, 2008 9:02 am

Gibs and Cure-
Planetary is the brand Jeff's been using for the last month. It looks kind of brownish/rust colored to me (smells like a fig newton mixed with dirt.)

He's still doing well, less fatigue, no new petechiae or vascular headaches. He only takes 1 tablet (1 g. salvia) , but is also taking curcumin, ginko, quercetin, EGCG and proteolytic enzymes...all blood thinners/vascular regulators.
AC
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby gibbledygook » Mon Nov 10, 2008 2:52 am

I must say I am now even more suspicious of the herbalextractsplus pills.

Yesterday I also added some quercetin (4g), some enzymes (a combination of pancreatin, papain, bromelain, trypsin, chymotrypsin and rutosid) and 100mg of pycnogenol to the ginkgo of (3x120mgx4daily), salvia (2x600mgx4) and curcumin (3x400mgx4daily). This was the 3rd day of our honeymoon and associated alcohol use with approx half a bottle consumed daily. Last night I had pretty dreadful spasms, much like on the last 2 days I added horsechestnut. I think the combination of ginkgo and alcohol is bad and counterproductive which with the new vasodilators results in worse spasms. I note from pubmed that alcohol has both vasodilatory and vasoconstrictive effects and that this interacts problematically with ginkgo. Booo! In fact being on the ginkgo has very recently made me more cautious on the top-ups (of alcohol). but not cautious enough! On a more positive note my bladder is much better, even with alcohol in the system in that there is much less urgency and I can now void much more without manual assistance. And the feeling of compression which I experienced a few days ago has dissipated even though I'm back on 3x120mg ginkgo 4 times daily. Ginkgo is definitely having an effect on me which seems negative when combined with alcohol, which is a pity as I do thoroughly enjoy a glass or three!
Last edited by gibbledygook on Mon Nov 10, 2008 7:35 am, edited 1 time in total.
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 CureOrBust » Mon Nov 10, 2008 4:39 am

gibbledygook, I know you have been explicitly tested for "Hughes Syndrome", but were you actually on ANY of your herbs at the time of the test? which may of hidden the issue? You could of been a "weak possitive" without the herbs.
MSRC on Hughes Syndrome
Q: How do you test for Hughes Syndrome?
A: There are two simple blood tests. Anticardiolipin Antibodies and Lupus Anticoagulant. If you have HS, it means your immune system is producing proteins, or antibodies, that make the blood far more stick than normal.

Q: Are the results of the blood test for Hughes Syndrome clear-cut?
A: The blood tests can give a range of results from 'weak positive' to 'strong positive' But we don't dismiss someone with a weak positive result. Also, only one of the two blood tests needs to be positive.

Q: Do diet and natural substances like gingko biloba, evening primrose oil, fish oils, garlic etc have the same blood-thinning effects as these drugs?
A: They have a mild effect but they certainly wouldn't get the same effect as the drugs. Anyone diagnosed with HS should definitely take one or other form of anticoagulant.
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Postby gibbledygook » Mon Nov 10, 2008 7:26 am

When I had the Hughes test I think I was on antibiotics and it was certainly a long, long time ago before I started the salvia and ginkgo which has been since summer 08. I wonder whether MS is just something very similar to Hughes. After all we have very high levels of a vasoconstrictor in our plasma.
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 cheerleader » Mon Nov 10, 2008 5:38 pm

Hey Alex,
Congrats on the nuptials and celebrations!! Very happy for you, and wish you both the best.

Jeff can't drink anymore...we had lots of champagne with friends the other night (after election results came in :!: ) He had bad muscle spasms and pain that night and the next day.

I agree that Hughes and MS are closely related. If all you had was Hughes, however, the blood-thinning herbs should make you all better, right? In MS, there continues to be a leakage thru the vessel wall (bacteria, c-reactive protein, iron, etc.) into tissue which sets the t-cells into attack mode. In healing the vessels, and thinning the blood, we hope to keep things from attacking the CNS.
Ac
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby CureOrBust » Tue Nov 11, 2008 3:28 am

cheerleader wrote:If all you had was Hughes, however, the blood-thinning herbs should make you all better, right?
Not by the doctors opinions.
MSRC wrote:A: They have a mild effect but they certainly wouldn't get the same effect as the drugs. Anyone diagnosed with HS should definitely take one or other form of anticoagulant.
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Postby gibbledygook » Tue Nov 11, 2008 6:52 am

I wouldn't describe the effects of the ginkgo and what I hope is salvia as particularly mild. I mean I can feel the herbs affecting the sites of damage in my legs after about 40minutes of taking them. I don't think doctors can actually state with any certainty what the effects of 1.4g daily of ginkgo is as they have not conducted any tests. Frankly, having just read Prospect magazine's article on Vioxxx, I'm going to struggle to have any trust in any pharmaceuticals for a very long time.

Yesterday I just added 300mg pycnogenol to the mix of 1.44g of ginkgo, 4.8g of salvia, 30mg bioperine, 4.8g curcumin, 7.2g of scutellaria and I had no spasms at all at night. I also again had some wine! Ooops! I'm on honeymoon. How do I stop drinking when I'm on a once in a lifetime holiday?! So maybe the day before yesterday when in addition to some pycnogenol I added 4g quercetin and 2 doses enzymes with wine it was one or other of these which caused such bad spasms. However I think the ethanol is a problem. Ethanol certainly has considerable effects on the endothelium and vasculature which may be quite disruptive particularly when treating the vasculature with ginkgo and salvia.
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 cheerleader » Tue Nov 11, 2008 3:52 pm

Well, this is ironic timing. Fax just came on Jeff's antiphospholipid testing. He's negative on Cardiolipin IgG autoantibodies (<11 GPL) , and negative on IgM autoantibodies (<10 MPL)...no Hughes Syndrome, but he certainly had coagulation issues. dang...still has MS...

Alcohol certainly changes blood flow Alex. Maybe a nice glass of wine? I know, it's your honeymoon!! What are you doing on the computer??

"...we suggest that impaired NOS-dependent responses of cerebral blood vessels during alcohol consumption may be related to an absence and/or an impaired metabolism of BH4 to uncouple eNOS. The uncoupling of eNOS in the endothelium of cerebral blood vessels may lead to endothelial dysfunction in alcohol-fed rats by a diminished production of nitric oxide and/or an increased production of superoxide anion to inactivate nitric oxide.
http://ajpheart.physiology.org/cgi/cont ... 81/5/H1863
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby gibbledygook » Sat Nov 15, 2008 8:40 am

Cheerleader, that article is absolutely FASCINATING. Maybe MS is a deficiency of tetrahydrobiopterin. Fascinating the way alcohol causes vasoconstriction which is the opposite to what I thought it did. Very interesting indeed. Thank you.
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 cheerleader » Sat Nov 15, 2008 11:25 am

gibbledygook wrote:Cheerleader, that article is absolutely FASCINATING. Maybe MS is a deficiency of tetrahydrobiopterin. Fascinating the way alcohol causes vasoconstriction which is the opposite to what I thought it did. Very interesting indeed. Thank you.


"Tetrahydrobiopterin deficiency is a rare disorder that increases the levels of several substances, including phenylalanine, in the blood. Phenylalanine is a building block of proteins (an amino acid) that is obtained through the diet. It is found in all proteins and in some artificial sweeteners. If tetrahydrobiopterin deficiency is not treated, phenylalanine can build up to harmful levels in the body, causing mental retardation and other serious health problems.
High levels of phenylalanine are present from early infancy in people with untreated tetrahydrobiopterin deficiency. Infants with this condition appear normal at birth, but medical problems ranging from mild to severe become apparent over time. The signs and symptoms of this condition can include mental retardation, progressive problems with development, movement disorders, difficulty swallowing, seizures, behavioral problems, and an inability to control body temperature."

hmm...neurological problems becoming apparent over time, movement disorders, swallowing issues, body temperature problems. You may be on to something, Gibs. A build up of phenylalanine? Are you home from your honeymoon? Still basking in marital bliss? :wink:
AC
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby gibbledygook » Sun Nov 16, 2008 6:22 am

Our honeymoon has been spent entirely at home which has been great because my husband immediately came down with a vicious cold and wouldn't have enjoyed being abroad at all.

I checked my phenylalanine levels for when I was first diagnosed and had a full amino acid test. They were low end of normal so I don't think we have a deficiency of the tetrahydrabiopterin or at least of the pathway which increases phenylalanine levels. However I can't help noticing how alcohol seems to modulate my tendency to spasm at night. With sufficient alcohol I get no spasms but sobre nights afterwards seem to bemuch worse for spasms.

I started the planetary herbals version of salvia a few days ago and take 2x 1.02grams 4 times daily or 8.15grams a day. I have found this salvia even better for bowel function than the herbalextractsplus of 4.8g a day but that could be the dosage. However at the same time this seems to have increased the effects the ginkgo for which the right dose seems to be something like 1x 120mg every 3 hours. I also continue with 3 x 400mg curcumin 4 times daily and 3 x 600mg scutellaria 4 times daily with bioperine.

I have a new Chinese tea which consists of the following:
rehmannia 2.63g
paeoniae radix 2.11g
angelica sinensis 2.63g
spatholobi caulis 3.16g
coicis semen 3.16g
chuanxiong rhizoma 1.05g
cyathulae radix 1.05g
persicae semen 1.05g
atractylodis macrocephelae 2.11g
salvia miltiorrhiza 2.11g
codonopsis radix 3.16g
dipsaci radix 1.58g
cynomoni herba 1.58g
drynariae rhizoma 1.58g

I shall try to investigate these further.
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 » Mon Nov 17, 2008 5:04 am

I must say, delightful though it is to have married my lovely kind partner about 10 days ago, the heavy alcohol consumption has completely disrupted my ginkgo/salvia experiment. It has been hard to gauge the correct amounts to take and I think it will require about a month of no alcohol and altering the ginkgo/salvia amounts for ever increasing improvements in neurological symptoms. However I remain impressed by the ability of the right amounts (when I get them) of these herbs to significantly improve my walking/spasms and pain. Yet I am also frustrated when my symptoms return to normal when I have taken either too little or too much and I don't really know which.

Yesterday I started to come down with my partner's week long feverish cold and had a rather sore throat. Somehow I ended up still being plied with 2 large glasses of red wine by our rather enthusiastic wine-making house guest. (Hopeless). Later I took some paracetemol tablets which contained phenylephrine. Here is something wikipedia says of this substance:

Phenylephrine is sometimes used as a vasopressor to increase the blood pressure in unstable patients with hypotension


I think that this stuff must be bad for the MS microvasculature since after taking these pills last thing at night I suffered the worse spasms I've had in many many months and had to take 2 zanaflex as the curcumin didn't help and even these 2 zanaflex didn't help and I was awake for most of the night. Only when I took some more salvia and ginkgo at 5am did I get off to a deeper sleep and the spasms calmed down.


Also the research below indicates that phenylephrine, a substance routinely put in pharmaceutical products is probably VERY BAD for MS. I become less and less impressed by the pharmaceutical industry with every second. Basically phenylephrine damages your heart tissue. So remember just to stick to hot water, lemon juice and whiskey next time you get flu as the night nurse type pills are full of ****.

1: Mol Pharmacol. 2008 Oct 24. [Epub ahead of print] Links
Phenylephrine-induced cardiomyocyte injury is triggered by superoxide generation through uncoupled eNOS and ameliorated by DY9836, a novel calmodulin antagonist.Lu YM, Han F, Shioda N, Moriguchi S, Shirasaki Y, Qin ZH, Fukunaga K.
Department of Pharmacology, Tohoku University Graduate School of Pharmaceutical Sciences.

The pathophysiological relevance of eNOS-induced superoxide production in cardiomyocyte injury following prolonged PE exposure remains unclear. The aims of this study were to define the mechanism of O2(.-) production by uncoupled eNOS and evaluate the therapeutic potential of a novel calmodulin antagonist, DY-9836, {3-[2-[4-(3-chloro-2-methylphenyl)-1-piperazinyl]ethyl]-5,6-dimethoxyindazole}, to rescue hypertrophied cardiomyocytes from PE-induced injury. In cultured rat cardiomyocytes, prolonged exposure for 96h to PE led to translocation from membrane to cytosol of eNOS and breakdown of caveolin-3 and dystrophin. When NO and O2(.-) production were monitored in PE-treated cells by DAF-FM and DHE, respectively, Ca(2+)-induced NO production elevated by 5.7-fold (p<0.01) after 48 h PE treatment and the basal NO concentration markedly elevated (16-fold; p<0.01) after 96 h PE treatment. On the other hand the O2(.-) generation at 96 h was closely associated with an increased uncoupled eNOS level. Co-incubation with DY-9836 (3 microM) during the last 48 h inhibited the aberrant O2(.-) generation near completely and NO production by 72% (P<0.01) after 96 h of PE treatment and inhibited the breakdown of caveolin-3/dystrophin in cardiomyocytes. PE-induced apoptosis assessed by TUNEL staining was also attenuated by DY-9836 treatment. These results suggest that O2(.-) generation by uncoupled eNOS likely triggers PE-induced cardiomyocyte injury. Inhibition of abnormal O2(.-) and NO generation by DY-9836 treatment represents an attractive therapeutic strategy for PE/hypertrophy-induced cardiomyocyte injury.

PMID: 18952768 [PubMed - as supplied by publisher]
makingmoneyfromsickpeopleiseasy

This research states that phenylephrine is a vasoconstrictor.

1: J Ethnopharmacol. 2008 Sep 27. [Epub ahead of print] Links
Endothelium-independent relaxation and contraction of rat aorta induced by ethyl acetate extract from leaves of Morus alba (L.).Xia M, Qian L, Zhou X, Gao Q, Bruce IC, Xia Q.
Department of Physiology, Zhejiang University School of Medicine, 388 Yuhangtang Road, Hangzhou 310058, China; Department of Physiology, Medical School, Jiaxing College, Jiaxing 314001, China.

AIM OF THE STUDY: Based on screening for vasoactive traditional Chinese medicinal herbs, the present study was performed to investigate the vasoactive effects of an ethyl acetate extract from leaves of Morus alba (L.) (ELM) on rat thoracic aorta and the mechanisms underlying these effects. MATERIALS AND METHODS: Isolated rat thoracic rings were mounted in an organ bath system and the effects of ELM on their responses were evaluated. RESULTS: ELM (0.125-32.000g/l) induced a concentration-dependent relaxation (P<0.01 vs. control) both in endothelium-intact and -denuded aortas precontracted by high K(+) (6x10(-2)M) or 10(-6)M phenylephrine (PE). In endothelium-denuded aortas, ELM at the EC(50) concentration reduced Ca(2+)-induced contraction (P<0.01 vs. control) after PE or KCl had generated a stable contraction in Ca(2+)-free solution. And after incubation with verapamil, ELM induced contraction in endothelium-denuded aortas precontracted by PE (P<0.01 vs. control); this was abolished by ruthenium red (P<0.01 vs. ELM-treated endothelium-denuded group; P>0.05 vs. control), but not by heparin (P>0.01 vs. ELM-treated endothelium-denuded group; P<0.01 vs. control). CONCLUSIONS: The results showed that ELM had dual vasoactive effects, and the relaxation was greater than the contraction. The relaxation was mediated by inhibition of voltage- and receptor-dependent Ca(2+) channels in vascular smooth muscle cells, while the contraction occurred via activation of ryanodine receptors in the sarcoplasmic reticulum.

PMID: 18948182 [PubMed - as supplied by publisher]
makingmoneyoutofsickpeopleiseasy
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 CureOrBust » Mon Nov 17, 2008 6:13 am

gibbledygook wrote:So remember just to stick to hot water, lemon juice and whiskey next time you get flu as the night nurse type pills are full of ****.
OR something like ABX's & Anti-virals. I know they work well for me. :) Without, I am in a more serious relapse situation.
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Postby gibbledygook » Tue Nov 18, 2008 4:00 am

I am now in full cold/flu mode with sore throat and odd temperature changes and sneezing fits. Curiously the dose of ginkgo/salvia that seemed pretty good yesterday is producing somewhat greater stiffness today. The dose yesterday was 240mg ginkgo with 1020mg salvia every 3 to 3.5 hours and 7 times in all. This works out at 1.68g of ginkgo and 7.140g of salvia. I had a few spasms at night and think I shall increase to 3 ginkgo this evening. Perhaps this increase in stiffness is owing to the effects of infection on the endothelium:
1: Atherosclerosis. 2005 Feb;178(2):345-50. Links
Acute inflammatory state during influenza infection and endothelial function.Marchesi S, Lupattelli G, Lombardini R, Sensini A, Siepi D, Mannarino M, Vaudo G, Mannarino E.
Internal Medicine Section, Department of Clinical and Experimental Medicine, University of Perugia, Italy. simonamarchesi@yahoo.it

Chronic inflammatory stimulus seems to contribute to atherosclerotic process. Several studies have established a relationship between infective agents as Chlamydia pneumoniae, herpes virus and cytomegalovirus and atherosclerotic lesions. Aim of this study was to investigate the effects of influenza infective state on endothelial function of healthy young subjects, expressed as brachial flow-mediated vasodilation (FMV) and soluble form of intercellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1). In 10 male subjects (mean age 35+/-14 years) exhibiting influenza symptoms for 3 days, we determined total cholesterol, high-density lipoproteins (HDL), low-density lipoproteins (LDL), triglycerides, sVCAM-1, sICAM-1 and brachial FMV. All subjects had an antibody pattern characteristic of influenza A or B virus infection. After 3 months brachial FMV was significantly increased (8.6+/-2.3% versus 11.5+/-3.2%; p<0.001), while HDL (46+/-10 mg/dL versus 49+/-9 mg/dL; p<0.05), sICAM-1 and sVCAM-1 were reduced (respectively: 488+/-105 ng/mL versus 340+/-127 ng/mL; p<0.001, 1710+/-80 ng/mL versus 1216+/-63 ng/mL; p<0.001). Univariate analysis showed a positive correlation between changes in CRP and sICAM-1 levels (r=0.95, p<0.001), a negative one between changes in sICAM-1 and brachial FMV (r=-0.65, p<0.05) and between CRP and brachial FMV (r=-0.64, p<0.05). This small study suggested that inflammatory state determined by viral agents may transitorily alter endothelial function in healthy subjects.
PMID: 15694944 [PubMed - indexed for MEDLINE]
link

1: Thromb Haemost. 2000 Aug;84(2):319-24. Links
Procoagulant activity of endothelial cells after infection with respiratory viruses.Visseren FL, Bouwman JJ, Bouter KP, Diepersloot RJ, de Groot PH, Erkelens DW.
Department of Internal and Vascular Medicine, University Medical Center Utrecht, The Netherlands. F.Visseren@digd.azu.nl

Influenza virus epidemics are associated with excess mortality due to cardiovascular diseases. There are several case reports of excessive coagulation during generalised influenza virus infection. In this study, we demonstrate the ability of respiratory viruses (influenza A, influenza B, parainfluenza-1, respiratory syncytial virus, adenovirus, cytomegalovirus) to infect lung fibroblasts and human umbilical vein endothelial cells in culture. All viral pathogens induced procoagulant activity in infected endothelial cells, as determined in a one-stage clotting assay, by causing an average 55% reduction in the clotting time. When factor VII deficient plasma was used clotting time was not reduced. The induction of procoagulant activity was associated with a 4- to 5-fold increase in the expression of tissue factor, as measured by the generation of factor Xa. Both experiments indicate that the procoagulant activity of endothelial cells in response to infection with respiratory viruses is caused by upregulation of the extrinsic pathway. Although both enveloped viruses and a non-enveloped virus (adenovirus) induced procoagulant activity in endothelial cells by stimulating tissue factor expression, the role of the viral envelope in the assembly of the prothrombinase complex remains uncertain. We conclude that both enveloped and non-enveloped respiratory viruses are capable of infecting cultured human endothelial cells and causing a shift from anticoagulant to procoagulant activity associated with the induction of tissue factor expression.

PMID: 10959707 [PubMed - indexed for MEDLINE]

link

Therefore need some artemisia scoporia which I can't find exactly at herbalextractsplus (just using them for reference) but can find lots of artemisia:
1: J Biomed Sci. 2003 Sep-Oct;10(5):518-25.Links
Scoparone inhibits tissue factor expression in lipopolysaccharide-activated human umbilical vein endothelial cells.Lee YM, Hsiao G, Chang JW, Sheu JR, Yen MH.
Department of Pharmacology, National Defense Medical Center, Taipei, Taiwan, ROC. ymlee@ndmctgh.edu.tw

Tissue factor (TF) is an important regulator and effector molecule of coagulation in various inflammatory states. In sepsis, expression of TF by activated endothelial cells leads to disseminated intravascular coagulation. Scoparone is extracted from the traditional Chinese herb ARTEMISIA SCOPARIA and is known to have potent anti-inflammatory properties. In the current studies, we examined the effects of scoparone on inhibiting lipopolysaccharide (LPS)-induced TF expression in cultured human umbilical vein endothelial cells (HUVECs). Flow-cytometric analysis revealed LPS (10 micro g/ml)-activated surface TF induction was concentration-dependently inhibited by scoparone (10-400 micro M). The concentrations of scoparone used in this study did not affect cell viability. The elevation of the procoagulant activity of TF by LPS was suppressed by scoparone. The LPS-induced superoxide formation was markedly decreased by scoparone. Messenger RNA expression of TF in LPS-activated HUVECs was also reduced by scoparone. Furthermore, scoparone did not significantly affect the IkappaBalpha degradation. Our results demonstrate that the inhibition of scoparone on LPS-induced TF expression in HUVECs may mediate by the mechanisms suppressing superoxide anion formation and TF transcription. Copyright 2003 National Science Council, ROC and S. Karger AG, Basel

PMID: 12928592 [PubMed - indexed for MEDLINE]
link

from herbalextractsplus
Botanical: Artemisia vulgaris
Family: Compositae (daisy) - Asteraceae (aster)
Other common names: Felon Herb, Cingulum Sancti Johannis, Saint John's Plant,

Common Artemisia, Wild Wormwood, Chinese Moxa, Sailor's Tobacco


or
Botanical: Artemisia absinthium
Family: Compositae (daisy)
Other common names: Absinthe, Green Ginger, Absinthium, Old Woman, Southernwood, Wormwood, Wermutkraut, Southern Wood


Now I actually have a small pot of this so I shall give it a whirl.


or jiaogulan:
1: Toxicol Appl Pharmacol. 2007 Jan 1;218(1):30-6. Epub 2006 Oct 25. Links
Gypenoside XLIX, a naturally occurring gynosaponin, PPAR-alpha dependently inhibits LPS-induced tissue factor expression and activity in human THP-1 monocytic cells.Huang TH, Tran VH, Roufogalis BD, Li Y.
Faculty of Pharmacy, University of Sydney, NSW 2006, Australia.

Tissue factor (TF) is involved not only in the progression of atherosclerosis and other cardiovascular diseases, but is also associated with tumor growth, metastasis, and angiogenesis and hence may be an attractive target for directed cancer therapeutics. Gynostemma pentaphyllum (GP) is widely used in the treatment of various cardiovascular diseases including atherosclerosis, as well as cancers. Gypenoside (Gyp) XLIX, a dammarane-type glycoside, is one of the prominent components in GP. We have recently reported Gyp XLIX to be a potent peroxisome proliferator-activated receptor (PPAR)-alpha activator. Here we demonstrate that Gyp XLIX (0-300 microM) concentration dependently inhibited TF promoter activity after induction by the inflammatory stimulus lipopolysaccharide (LPS) in human monocytic THP-1 cells transfected with promoter reporter constructs pTF-LUC. Furthermore, Gyp XLIX inhibited LPS-induced TF mRNA and protein overexpression in THP-1 monocyte cells. Its inhibition of LPS-induced TF hyperactivity was further confirmed by chromogenic enzyme activity assay. The activities of Gyp XLIX reported in this study were similar to those of Wy-14643, a potent synthetic PPAR-alpha activator. Furthermore, the Gyp XLIX-induced inhibitory effect on TF luciferase activity was completely abolished in the presence of the PPAR-alpha selective antagonist MK-886. The present findings suggest that Gyp XLIX inhibits LPS-induced TF overexpression and enhancement of its activity in human THP-1 monocytic cells via PPAR-alpha-dependent pathways. The data provide new insights into the basis of the use of the traditional Chinese herbal medicine G. pentaphyllum for the treatment of cardiovascular and inflammatory diseases, as well as cancers.

PMID: 17141290 [PubMed - indexed for MEDLINE]
link

From wikipedia:
Gynostemma pentaphyllum, also called jiaogulan (Chinese: 绞股蓝; pinyin: jiǎogǔlán, literally "twisting-vine-orchid") is an herbaceous vine of the family Cucurbitaceae (cucumber or gourd family) indigenous to the southern reaches of China, southern Korea and Japan. Jiaogulan is best known as an herbal medicine reputed to have powerful antioxidant and adaptogenic effects that increase longevity.

Western languages such as English and German commonly refer to the plant as jiaogulan. Other names include:[7]

Chinese: xiancao (仙草, literally "immortal grass"; more accurately "herb of immortality")
English: five-leaf ginseng, poor man's ginseng, miracle grass, fairy herb, sweet tea vine, gospel herb


from herbalextractsplus which supplies it:
Botanical: Gynostemma pentaphyllum
Family: Cucurbitaceae (gourd/squash)
Other common names: Southern Ginseng, Jiaogulan, Sweet Tea Vine, Gospel Herb,

Amachazuru (Japan), Dungkulcha (Korea)


or kudzu which increases TF activity although I'm not at all certain that this would be good in MS.
1: J Med Food. 2004 Spring;7(1):31-7. Links
Effect of kaikasaponin III obtained from Pueraria thunbergiana flowers on serum and hepatic lipid peroxides and tissue factor activity in the streptozotocin-induced diabetic rat.Choi J, Shin MH, Park KY, Lee KT, Jung HJ, Lee MS, Park HJ.
College of Pharmacy, Kyungsung University, Korea.

We investigated the effect of kaikasaponin III (KS-III) on Phase I and II enzymes and tissue factor (TF) activity to elucidate the pharmacological actions of this immunosuppressive saponin in the diabetic rat. This compound was obtained from the flower of Pueraria thunbergiana (Leguminosae) by chromatographic isolation. This crude drug (Puerariae Flos) has been used as a therapeutic agent for diabetes mellitus in traditional Korean medicine. KS-III prolonged the bleeding time and plasma clotting time in streptozotocin (STZ)-treated rats and increased the TF activity, suggesting that this compound has anti-thrombosis activity in STZ-induced rats. It also inhibited the formation of malondialdehyde (MDA) and hydroxy radicals in serum and liver, but promoted superoxide dismutase (SOD) activity. Low MDA concentrations and low xanthine oxidase and aldehyde oxidase activities were observed in the KS-III-treated rats, suggesting that such Phase I enzyme activities are the major source of lipid peroxidation. However, KS-III increased Phase II enzyme activities such as SOD, glutathione peroxidase, and catalase, suggesting the activation of free radical-scavenging enzymes. These results suggest that KS-III may exhibit its hypoglycemic and hypolipidemic effects by up-regulating or down-regulating antioxidant mechanisms via the changes in Phase I and II enzyme activities.

PMID: 15117550 [PubMed - indexed for MEDLINE]

Related ArticlesHypoglycemic and hypolipidemic effects of tectorigenin and kaikasaponin III in the streptozotocin-lnduced diabetic rat and their antioxidant activity in vitro. [Arch Pharm Res. 2000] Potent antimutagenic and their anti-lipid peroxidative effect of kaikasaponin III and tectorigenin from the flower of Pueraria thunbergiana. [Arch Pharm Res. 2002] Alternation of hepatic antioxidant enzyme activities and lipid profile in streptozotocin-induced diabetic rats by supplementation of dandelion water extract. [Clin Chim Acta. 2002] ReviewEffects of pineal peptide preparation Epithalamin on free-radical processes in humans and animals. [Neuro Endocrinol Lett. 2001] Review[Advances in the studies of saponins from Aralia] [Yao Xue Xue Bao. 1997] » See Reviews... | » See All...
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from herbalextractsplus:
Botanical: Pueraria lobata
Family: Fabaceae (legume)
Other common names: Kuzu, Pueraria, Gwat Gun, Ge Gan, Pueraria Root, Japanese Arrowroot


A staple in Japanese and Chinese herbal medicine, Kudzu has been a traditional treatment for stiff neck, headache, muscle tension and neurological conditions. For over two thousand years, Chinese physicians have relied on it to reduce alcohol abuse, relieve respiratory problems and counteract poisons.



we need some natural iron chelators:
1: Eur J Clin Invest. 2002 Mar;32 Suppl 1:84-90. Links
Iron chelation and hydroxyl radical scavenging reduce the inflammatory response of endothelial cells after infection with Chlamydia pneumoniae or influenza A.Visseren FL, Verkerk MS, van der Bruggen T, Marx JJ, van Asbeck BS, Diepersloot RJ.
Department of Internal and Vascular Medicine, Room F.02.126, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands. f.visseren@digd.azu.nl

BACKGROUND: Chronic low-grade inflammation is associated with increased risk of vascular diseases. The source of inflammation is unknown but may well be chronic and/or repetitive infections with microorganisms. Direct infection of endothelial cells (ECs) may also be a starting point for atherogenesis by initiating endothelial procoagulant activity, increased monocyte adherence and increased cytokine production. We hypothesized that iron-mediated intracellular hydroxyl radical formation after infection is a key event in triggering the production of interleukin-6 (IL-6) by ECs in vitro. METHODS: Cultured ECs were incubated with Fe(II) and Fe(III) or infected with Chlamydia pneumoniae or influenza A/H1N1/Taiwan/1/81 for 48 and 24 h, respectively. To determine the role of iron and reactive oxygen species, cells were coincubated with the H2O2 scavenger N-acetyl-l-cysteine, with the iron chelator deferoxamine (DFO) or with the intracellular hydroxyl radical scavenger dimethylthiourea (DMTU). After the incubation periods, supernatants were harvested for IL-6 determination. RESULTS: Incubating ECs with Fe(II) and Fe(III) resulted in increased IL-6 production. Similarly, infection with C. pneumoniae and influenza A also induced an IL-6 response. Coincubating ECs with DFO or DMTU blocked this response. Nuclear factor-kappaB activity was increased after infection and blocked by coincubation with DFO or DMTU. CONCLUSION: Cultured ECs respond to infection and iron incubation with increased production of IL-6. Iron, the generation of intracellular hydroxyl radical and NF-kappaB activity are essential in cellular activation, suggesting that reactive oxygen species generated in the Haber-Weiss reaction are essential in invoking an immunological response to infection by ECs.

PMID: 11886437 [PubMed - indexed for MEDLINE]
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time to load up on the green tea again. I have in the past taken high doses of green tea without noticing any positive or negative effect on my MS but maybe in conjunction with the ginkgo and salvia some good effects will occur.
1: J Neural Transm Suppl. 2006;(71):249-57.Links
Green tea catechins as brain-permeable, non toxic iron chelators to "iron out iron" from the brain.Mandel S, Weinreb O, Reznichenko L, Kalfon L, Amit T.
Eve Topf and US NPF Centers for Neurodegenerative Diseases and Department of Pharmacology, Faculty of Medicine, Technion, Haifa, Israel. mandel@tx.technion.ac.il

Evidence to link abnormal metal (iron, copper and zinc) metabolism and handling with Parkinson's and Alzheimer's diseases pathology has frequently been reported. The capacity of free iron to enhance and promote the generation of toxic reactive oxygen radicals has been discussed numerous times. Metal chelation has the potential to prevent iron-induced oxidative stress and aggregation of alpha-synuclein and beta-amyloid peptides. The efficacy of iron chelators depends on their ability to penetrate the subcellular compartments and cellular membranes where iron dependent free radicals are generated. Thus, natural, non-toxic, brain permeable neuroprotective drugs, are preferentially advocated for "ironing out iron" from those brain areas where it preferentially accumulates in neurodegenerative diseases. This review will discuss the most recent findings from in vivo and in vitro studies concerning the transitional metal (iron and copper) chelating property of green tea, and its major polyphenol, (-)-epigallocatechin-3-gallate with respect to their potential for the treatment of neurodegenerative diseases.

PMID: 17447435 [PubMed - indexed for MEDLINE
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anyone tried silicon?! I see that this can be bought at Iherb. I may purchase some.
1: Mult Scler. 2006 Oct;12(5):533-40. Links
Elevated urinary excretion of aluminium and iron in multiple sclerosis.Exley C, Mamutse G, Korchazhkina O, Pye E, Strekopytov S, Polwart A, Hawkins C.
Birchall Centre for Inorganic Chemistry and Materials Science, Lennard-Jones Laboratories, Keele University, Staffordshire, UK. c.exley@chem.keele.ac.uk

Multiple sclerosis (MS) is a chronic, immune-mediated, demyelinating disease of the central nervous system of as yet unknown aetiology. A consensus of opinion has suggested that the disorder is the result of an interplay between environmental factors and susceptibility genes. We have used a battery of analytical techniques to determine if the urinary excretion of i) markers of oxidative damage; ii) iron and iii) the environmental toxin aluminium and its antagonist, silicon, are altered in relapsing-remitting (RRMS) and secondary progressive MS (SPMS). Urinary concentrations of oxidative biomarkers, MDA and TBARS, were not found to be useful indicators of inflammatory disease in MS. However, urinary concentrations of another potential marker for inflammation and oxidative stress, iron, were significantly increased in SPMS (P<0.01) and insignificantly increased in RRMS (P>0.05). Urinary concentrations of aluminium were also significantly increased in RRMS (P<0.001) and SPMS (P <0.05) such that the levels of aluminium excretion in the former were similar to those observed in individuals undergoing metal chelation therapy. The excretion of silicon was lower in MS and significantly so in SPMS (P<0.05). Increased excretion of iron in urine supported a role for iron dysmetabolism in MS. Levels of urinary aluminium excretion similar to those seen in aluminium intoxication suggested that aluminium may be a hitherto unrecognized environmental factor associated with the aetiology of MS. If aluminium is involved in MS then an increased dietary intake of its natural antagonist, silicon, might be a therapeutic option.

PMID: 17086897 [PubMed - indexed for MEDLINE]
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milk thistle:
1: J Inorg Biochem. 2001 Jun;85(2-3):123-9. Links
Silybin, a new iron-chelating agent.Borsari M, Gabbi C, Ghelfi F, Grandi R, Saladini M, Severi S, Borella F.
Dipartimento di Chimica, Università di Modena, Via Campi 183-41100 Modena, Italy.

Silybin, a natural occurring flavolignan isolated from the fruits of Silibum marianum, has been reported to exert antioxidant and free radical scavenging abilities. It was suggested to act also as an iron chelator. The complexation and protonation equilibria of the ferric complex of this compound have been studied by potentiometric, spectrophotometric and electrochemical techniques. The formation of the complex silybin-Ga(III) in anhydrous DMSO-d6 has been studied by 1H NMR spectroscopy. Mass spectrometry and infrared spectroscopy on silybin-Fe(III) complex confirm all data obtained by 1H NMR spectroscopy. The experimental results show that silybin binds Fe(III) even at acidic pH. Different ternary complexes were observed at increasing methoxide ion concentration and their stability constants have been calculated. The results show the possible role of silybin in relation to the chelation therapy of chronic iron overload, as occurs in the treatment of Cooley's anemia.

PMID: 11410232 [PubMed - indexed for MEDLINE]
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chlorogenic acid (coffee)
1: Biosci Biotechnol Biochem. 1998 Jan;62(1):22-7. Links
Iron chelation by chlorogenic acid as a natural antioxidant.Kono Y, Kashine S, Yoneyama T, Sakamoto Y, Matsui Y, Shibata H.
Department of Life Science and Biotechnology, Faculty of Life and Environmental Science, Shimane University, Japan. ykono@life.shimane-u.ac.jp

Chlorogenic acid, a dietary antioxidant, effectively inhibited the iron-induced lipid peroxidation of bovine liver microsomes in a concentration-dependent manner. In the Fenton-type reaction, chlorogenic acid inhibited the production of the hydroxyl radical by iron-EDTA or iron-ADP, while iron plus chlorogenic acid did not generate the hydroxyl radical. The formation of an iron complex with chlorogenic acid was demonstrated by UV/vis absorbance spectroscopic, ESR and 1H-NMR studies. The ferric complex with chlorogenic acid was in the ferric high-spin state near rhombicity, and had no radical scavenging activity. The results indicate that chlorogenic acid prevented the formation of the hydroxyl radical by forming a chelate with iron whose complex cannot catalyze the Fenton-type reaction.

PMID: 9501514 [PubMed - indexed for MEDLINE]
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Chlorogenic acid is a family of esters formed between certain trans cinnamic acids and (-)-quinic acid[1] and is a major phenolic compound in coffee, found widespread in plants, and can be isolated from the leaves and fruit.[2] This compound, long known as an antioxidant, also slows the release of glucose into the bloodstream after a meal.[3]


My bladder and bowel have improved noticeably and I can now void the bladder without manual assistance although this isn't the case every time. The bowel is much more regular. I'm sure that this is down to the salvia/ginkgo. If only I could make the reductions in spasticity I can quite often feel with the ginkgo/salvia permanent![/url][/url][/quote]
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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gibbledygook
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kallikreins and MS

Postby gibbledygook » Tue Nov 18, 2008 10:02 am

1: Biol Chem. 2008 Jun;389(6):739-45. Links
Kallikreins are associated with secondary progressive multiple sclerosis and promote neurodegeneration.Scarisbrick IA, Linbo R, Vandell AG, Keegan M, Blaber SI, Blaber M, Sneve D, Lucchinetti CF, Rodriguez M, Diamandis EP.
Program for Molecular Neuroscience, Mayo Clinic College of Medicine, Rochester, MN 55905, USA. scarisbrick.isobel@mayo.edu

Tissue kallikrein KLK1 and the kallikrein-related peptidases KLK2-15 are a subfamily of serine proteases that have defined or proposed roles in a range of central nervous system (CNS) and non-CNS pathologies. To further understand their potential activity in multiple sclerosis (MS), serum levels of KLK1, 6, 7, 8 and 10 were determined in 35 MS patients and 62 controls by quantitative fluorometric ELISA. Serum levels were then correlated with Expanded Disability Status Scale (EDSS) scores determined at the time of serological sampling or at last clinical follow-up. Serum levels of KLK1 and KLK6 were elevated in MS patients (p<or=0.027), with highest levels associated with secondary progressive disease. Elevated KLK1 correlated with higher EDSS scores at the time of serum draw and KLK6 with future EDSS worsening in relapsing remitting patients (p<or=0.007). Supporting the concept that KLK1 and KLK6 promote degenerative events associated with progressive MS, exposure of murine cortical neurons to either kallikrein promoted rapid neurite retraction and neuron loss. These novel findings suggest that KLK1 and KLK6 may serve as serological markers of progressive MS and contribute directly to the development of neurological disability by promoting axonal injury and neuron cell death.

PMID: 18627300 [PubMed - indexed for
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1: Biosci Biotechnol Biochem. 2002 Sep;66(9):1859-64. Links
Anticoagulant from Taraxacum platycarpum.Yun SI, Cho HR, Choi HS.
Department of Biological Sciences and Immunomodulation Research Center, University of Ulsan, Korea.

An anticoagulant was purified from a Chinese herb, Taraxacum platycarpum. Its activity was heat-labile, and was decreased by incubation with subtilisin Carlburg or proteinase K, indicating that the active component was a protein. The protein had a molecular mass of 31 kDa by gel filtration and 33 kDa by sodium dodecyl sulfate polyacrylamide gel electrophoresis, so it probably was a monomer. When present at the concentration of 70, 255, and 873 nM, respectively, the protein doubled the thrombin time, prothrombin time, and activated partial thromboplastin time. It inhibited thrombin and kallikrein, but did not hydrolyze fibrinogen. The protein bound the anion-binding exosite of thrombin, competing with the fibrinogen binding site. In addition, the protein caused the murine macrophage cell line Raw 264.7 to produce cyclooxygenase-2, nitric oxide synthase, nitric oxide, and tumor necrosis factor-alpha.

PMID: 12400684 [PubMed - indexed for MEDLINE]
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from wikipedia:
Taraxacum is a large genus of flowering plants in the family Asteraceae. They are native to Europe, North America and Asia and two species, T. officinale and T. erythrospermum, are found as weeds worldwide.[1] ...Dandelions are thought to have evolved about thirty million years ago in Eurasia[8]


Top view of a dandelion head.They have been used by humans for food and herbalism for much of recorded history.

Dandelion contains luteolin, an antioxidant, and has demonstrated antioxidant properties without cytotoxicity


herbalextractsplus only supplies taraxacum officinale and this looks good for the CNS:


1: Immunopharmacol Immunotoxicol. 2000 Aug;22(3):519-30.Links
Taraxacum officinale inhibits tumor necrosis factor-alpha production from rat astrocytes.Kim HM, Shin HY, Lim KH, Ryu ST, Shin TY, Chae HJ, Kim HR, Lyu YS, An NH, Lim KS.
College of Pharmacy, Center of Oriental Medicinal Science, Wonkwang University, Iksan, Chonbuk, South Korea. hmkim@wonnms.wonkwang.ac.kr

Substance P (SP) can stimulate production of tumor necrosis factor-alpha (TNF-alpha) from astrocytes stimulated with lipopolysaccharide (LPS). The objective of the current study was to determine the effect of Taraxacum officinale (TO) on the production of TNF-alpha from primary cultures of rat astrocytes. TO (100 and 1000 microg/ml) significantly inhibited the TNF-alpha production by astrocytes stimulated with LPS and SP. Interleukin-1 (IL-1) has been shown to elevate TNF-alpha production from LPS-stimulated astrocytes while having no effect on astrocytes in the absence of LPS. We therefore examined whether IL-1 mediated inhibition of TNF-alpha production from primary astrocytes by TO. Treatment of TO (100 and 1000 microg/ml) to astrocytes stimulated with both LPS and SP decreased IL-1 production significantly. Moreover, the production of TNF-alpha by LPS and SP in astrocytes was progressively inhibited with increasing amount of IL-1 neutralizing antibody. Our results suggest that TO may inhibit TNF-alpha production by inhibiting IL-1 production and that TO has an antiinflammatory activity in the central nervous system.

PMID: 10946829 [PubMed - indexed for MEDLINE]
link[/quote]

coicis semen, which is in my latest tea:
1: East Afr Med J. 1995 Jan;72(1):51-5.Links
The effect on fibrinolytic system of blood plasma of Wister rats after feeding them with Coix mixed diet.Check JB, K'Ombut FO.
Department of Biochemistry, University of Nairobi, Kenya.

Experimental wister rats were fed on coix-mixed diet for 30 days in a view to study the effect of Coix feeding on the state of haemostatic mechanisms. Blood plasma which was obtained after cardiac puncture was analyzed for fibrinogen levels, euglobulin lysis time, fibrinolytic activity by protamin sulfate degradation and inhibitors of plasmin. These experimental models were set with a view to analyze situations mimicking processes associated with haemostasis and interpolate such situations in changes associated with the development of atherosclerosis. To study the plasma fibrinogen levels in experimental and control animals, spectrophotometric method was applied. Feeding the animals with coix-pellets mixed diet caused a decrease in fibrinogen levels as compared with controls. An overall decrease of this plasma protein was observed in both sexes. It was shown that euglobulin lysis time (ELT) was insignificantly changed in the experimental animals. However, fibrinolytic activity by degradation of protamin sulfate showed an increased fibrinolytic potential in experimental animals. In the same experimental models the analysis for the activity of inhibitors of plasmin showed no significant differences in mean values. It was found that coix has got vital nutritional value in lowering fibrinogen levels while at the same time creating a tendency of reducing fibrinolytic activity. More experiments should be conducted to show the possible mechanisms by which the observations can affect the development of atherosclerosis in man.

PMID: 7781558 [PubMed - indexed for MEDLINE]
link[/quote]
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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