Gibbledygook's anti-viral log

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

Doctor's best gingko

Postby gibbledygook » Tue Oct 21, 2008 7:45 am

The Doctor's Best gingko which was one of the cheaper pills on iherb seems more potent than the herbalextractsplus. I took 3grams yesterday and had no spasms and no pain on lying in bed prior to sleep. This is unusual. My right leg is quite stiff in the morning but soon loosens up. My feet feel quite different now from these last few weeks on gingko. So convinced am of the efficacity of gingko that I have stopped all the other herbs except 30mg bioperine and 3.6grams of curcumin. 8)

Chrysin may also be a good way to inhibit VEGF:
1: Mol Cancer Ther. 2007 Jan;6(1):220-6. Links
Chrysin inhibits expression of hypoxia-inducible factor-1alpha through reducing hypoxia-inducible factor-1alpha stability and inhibiting its protein synthesis.Fu B, Xue J, Li Z, Shi X, Jiang BH, Fang J.
The Institute for Nutritional Sciences, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.

Chrysin is a natural flavonoid and has been shown recently to have anticancer effects. However, the mechanisms that chrysin inhibits cancers are not well known. In this study, we investigated the effects of chrysin on expression of hypoxia-inducible factor-1alpha (HIF-1alpha) and vascular endothelial growth factor in human prostate cancer DU145 cells. Chrysin inhibited insulin-induced expression of HIF-1alpha by reducing its stability. Chrysin increases ubiquitination and degradation of HIF-1alpha by increasing its prolyl hydroxylation. In addition, chrysin interfered with interaction between HIF-1alpha and heat shock protein 90. Chrysin was also found to inhibit HIF-1alpha expression through AKT signaling. Inhibition of HIF-1alpha by chrysin resulted in abrogation of vascular endothelial growth factor expression. Finally, we showed that chrysin inhibited DU145 xenograft-induced angiogenesis in nude mice. Taken together, these results suggest that chrysin is a potent inhibitor of HIF-1alpha and provide a new sight into the mechanisms of chrysin against cancers.

PMID: 17237281 [PubMed - indexed for MEDLINE]
link
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Re: Doctor's best gingko

Postby CureOrBust » Wed Oct 22, 2008 12:01 am

gibbledygook wrote:The Doctor's Best gingko .... I took 3grams yesterday...
Is this the 120mg tablets? so you would of taken 25 tablets?
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Postby gibbledygook » Wed Oct 22, 2008 12:51 am

Yes! I have been taking 10 x 120mg tablets at various points during the day with 10mg of bioperine to aid absorption and washed down with a hot drink. I notice that about an hour later tingling is reduced although this could be some kind of psychosomatic influence. Yesterday I managed 4.8grams, so I took 10 pills before breakfast, lunch and supper and then last thing at night. I intend to continue with this for a while with no other supplements except curcumin to see how effective this is. I had a little bit of pain in the legs at night and a modest number of spasms but they were so modest I didn't need extra curcumin to calm them down.

Here's another herb which downregulates VEGF:
Artesunate (ART) is a semi-synthetic derivative of artemisinin extracted from the plant Artemisia annua is a safe and effective antimalarial drug. In the present investigation, ART was found also to inhibit angiogenesis in vivo and in vitro. The anti-angiogenic effect in vivo was evaluated in nude mice by means of human ovarian cancer HO-8910 implantation and immunohistochemical stainings for microvessel (CD31), vascular endothelial growth factor (VEGF) and VEGF receptor KDR/flk-1. Tumor growth was decreased and microvessel density was reduced following drug treatment with no apparent toxicity to the animals. ART also remarkably lowered VEGF expression on tumor cells and KDR/flk-1 expression on endothelial cells as well as tumor cells. The in vitro effect of ART was tested on models of angiogenesis, namely, proliferation, migration and tube formation of human umbilical vein endothelial cells (HUVEC). The results showed that ART significantly inhibited angiogenesis in a dose-dependent form in the range of 0.5~50 µmol/l. Additionally, the inhibitory effect of ART on HVUEC proliferation was stronger than that on Hela, JAR, HO-8910 cancer cells, NIH-3T3 fibroblast cells and human endometrial cells, indicating that ART was selectively against HUVEC. These findings and the known low toxicity of ART are clues that ART may be a promising angiogenesis inhibitor.

Copyright © 2004 S. Karger AG, Basel
link

From the general discussion going on over vascular health I am also now very interested in inhibiting platelet endothelial cell adhesion molecule (PECAM or CD31) as this is important in allowing T cells across the endothelium. Quercetin does this:

1: Acta Pharmacol Sin. 2001 Sep;22(9):857-60.Links
Effect of quercetin on adhesion of platelets to microvascular endothelial cells in vitro.Fan PS, Gu ZL, Liang ZQ.
Department of Pharmacology, Suzhou University, Suzhou Institute of Chinese Materia Medica, Suzhou 215007, China.

AIM: To study the effect of quercetin(Que) on the adhesion of platelets to microvascular endothelial cells (MVEC) isolated from human skin. METHODS: [3H]-adenine-labeled platelets were incubated with MVEC. Effect of Que on platelet endothelial cell adhesion molecular (PECAM) expression on MVEC was also evaluated using enzyme-linked immunosorbent assay (ELISA). RESULTS: Adhesion of platelet to MVEC reached to maximum at about 30 min. Que inhibited the adhesion of platelets to MVEC in a concentration-dependent manner. Que 5 micromol/L did not show any significant inhibition. When the concentration of Que increased to 10, 20, and 40 micromol/L, the inhibition rate increased to 10.5 %, 20.0 %, and 42.2 %, respectively. Pre-incubation of Que (10 - 40 micromol/L) with labeled platelets for 30 min also inhibited the adhesion but Que 5 micromol/L did not. The inhibition rate of Que 10, 20, and 40 micromol/L was 18.2 %, 29.8 %, and 65.3 % respectively. Expression of PECAM on the endothelial cells was decreased in a concentration-dependent manner when MVEC were treated with Que (10 - 40 micromol/L) for 12 h but Que 5 micromol/L did not significantly affect the expression. CONCLUSION: Que could inhibit the adhesion of platelets to MVEC. This effect may be related to decreased expression of PECAM on MVEC.

PMID: 11749871 [PubMed - indexed for MEDLINE]
link

We want some more angiopoietin-1!
1: Circ Res. 2000 Sep 29;87(7):603-7. Links
Angiopoietin-1 is an antipermeability and anti-inflammatory agent in vitro and targets cell junctions.Gamble JR, Drew J, Trezise L, Underwood A, Parsons M, Kasminkas L, Rudge J, Yancopoulos G, Vadas MA.
Vascular Biology Laboratory, Division of Immunology, Hanson Centre for Cancer Research, Institute of Medical and Veterinary Science and the University of Adelaide, South Australia. jennifer.gamble@imvs.sa.gov.au

Inflammation is a basic pathological mechanism that underlies many diseases. An important component of the inflammatory response is the passage of plasma components and leukocytes from the blood vessel into the tissues. The endothelial monolayer lining blood vessels reacts to stimuli such as thrombin or vascular endothelial growth factor by changes in cell-cell junctions, an increase in permeability, and the leakage of plasma components into tissues. Other stimuli, such as tumor necrosis factor-alpha (TNF-alpha), are responsible for stimulating the transmigration of leukocytes. Here we show that angiopoietin-1, a cytokine essential in fetal angiogenesis, not only supports the localization of proteins such as platelet endothelial cell adhesion molecule-1 (PECAM-1) into junctions between endothelial cells and decreases the phosphorylation of PECAM-1 and vascular endothelial cadherin, but it also strengthens these junctions, as evidenced by a decrease in basal permeability and inhibition of permeability responses to thrombin and vascular endothelial growth factor. Furthermore, angiopoietin-1 inhibits TNF-alpha-stimulated leukocyte transmigration. Angiopoietin-1 may thus have a major role in maintaining the integrity of endothelial monolayers.

PMID: 11009566 [PubMed - indexed for MEDLINE]
link

This Chinese formulat upregulates ang 1:
1: Zhong Xi Yi Jie He Xue Bao. 2008 May;6(5):508-11. Links
[Wenyang Huoxue Recipe up-regulates the expression of angiopoietin-1 mRNA in rats with chronic aristolochic acid nephropathy][Article in Chinese]


Wang HT, Wang YM, Liang YP, Liu YJ, Peng W.
Department of Nephrology, Putuo District Center Hospital, Shanghai 200062, China.

OBJECTIVE: To investigate the effects of Wenyang Huoxue Recipe (WRHXR), a compound traditional Chinese herbal medicine for warming yang and promoting blood flow, on the expression of angiopoietin mRNA in rats with chronic aristolochic acid nephropathy induced by Caulis Aristolochia Manshuriensis (CAM) decoction, and to explore the protection mechanism of WYHXR against kidney damage. METHODS: Twenty-eight male SD rats were randomly divided into normal control group, CAM group and WYHXR-treated group. Rats in the normal control group (n=8) and CAM group (n=10) were intragastrically administered with normal saline 10 ml/(kg.d) or CAM decoction 10 ml/(kg.d) respectively. Rats in the WYHXR-treated group (n=10) were intragastrically administered with WYHXR 30 g/(kg.d) and CAM decoction 10 ml/(kg.d). The expressions of Ang-l and Ang-2 mRNAs were detected by real-time reverse transcription polymerase chain reaction (RT-PCR) after 20-week treatment. RESULTS: Compared with the normal control group, the expression of Ang-l mRNA was significantly decreased, and the expression of Ang-2 mRNA was significantly increased in the CAM group (P<0.01). Compared with the CAM group, the expression of Ang-l mRNA was increased in the WYHXR-treated group (P<0.01). The expression of Ang-2 mRNA had no significant difference between the CAM group and the WYHXR-treated group (P>0.05). Renal pathology showed that renal damage in WYHXR-treated group was significantly reduced as compared with the CAM group. CONCLUSION: WYHXR can up-regulate the expression of Ang-l mRNA, which may be its action mechanism in protecting the kidneys.

PMID: 18471417 [PubMed - in process]
no definitive URL link available ie just http://www.ncbi.nlm.nih.gov/sites/entrez[/url]

And this concoction:
1: Zhongguo Zhong Xi Yi Jie He Za Zhi. 2008 Apr;28(4):343-7.Links
[Effect of buyang huanwu decoction on expressions of angiopoietin-1 and its receptor mRNA in brain of rat after intracerebral hemorrhage][Article in Chinese]


Zhou HJ, Tang T, Zhong JH.
Institute of Neurology, Xiangya Hospital, Central South University, Changsha.

OBJECTIVE: To investigate the mechanisms of Buyang Huanwu Decoction (BYHWD) by observing its effects on expressions of angiopoietin-1 (Ang-1) and the endothelial-specific receptor tyrosine kinase (Tie-2) mRNA in damaged region of rats' brain after intracerebral hemorrhage (ICH). METHODS: One hundred and sixty Sprague-Dawley rats were randomly divided into four groups, 10 in the normal control group, 60 in the sham-operative group, 60 in the ICH model group, and 30 in the BYHWD-treated group. The ICH model was established by injecting collagenase type VII 0.5 U stereotaxically into right globus pallidus. Animals in the BYHWD-treated group were administered orally with BYHWD, while animals in the sham-operative group and the ICH model group were administered orally with equal volume distilled water, and those in the normal control group drank water freely. The positional variations of the expression of Ang-1 and Tie-2 in the sham-operative group and the model group were assayed by immunohistochemistry on dayl, 4, 7, 14, 21 and 28 after modeling, in the meantime, the dynamic changes of Ang-1 and Tie-2 mRNA expressions in all groups were assayed by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: No significant expression of Ang-1 and Tie-2 in brain of rats in the normal or the sham-operative group was found during the experiment. In the model group, the Ang-1 and Tie-2 positive micrangio-segments appeared at the edge of clot on day 1 to day 4, they gradually penetrated to hematoma area from day 7; with Ang-1 and Tie-2 mRNA expressed from day 1, but very weak until day 4, showing no significant difference to that on day 1; thereafter, they increased gradually, and reached the peak on day 28 (P <0.05). While the two expressions in the BYHWD treated group reached the peak on day 21, and from day 7 to day 28, they were all significantly higher than those in ICH model group at the corresponding time points (P <0.01). CONCLUSION: BYHWD can promote the up-regulation of Ang-1 and Tie-2mRNA expressions in brain of intracerebral hemorrhagic rats, which might accelerate the angiogenesis in the reconstruction of microvascular network in the damaged zone, and thus facilitating the repairing of damaged tissue.

PMID: 18543490 [PubMed - in process]
link
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 Oct 22, 2008 4:37 am

I just tried to walk the 600meters to my local coffee shop. Unfortunately this wasn't nearly as easy as I thought it might have been and after about 400m my bad motor leg felt very stiff. What was also noticeable and good was that after sitting down the tingling rapidly disappeared. I wonder if the gingko will make walking harder at least initially. Perhaps the reduction in sensory disturbance, night spasms and the improvement in bladder and bowel function are the first improvements and the walking comes later. The walking felt very different and generally stiffer.

Looking at my diary I see I started gingko (5.4g) on the 7th October after my high dose salvia experiment went wrong and I started getting a stiffer leg than before. I then halve the dose of salvia to 7.2g on the 9th and much of the stiffness disappears within hours. There is no way I'd have even attempted a 600meter walk back then. I gradually further reduce the dose of salvia over the next week until on the 15th October after a walking/tingle test I realise that the gingko is stopping the tingling or appears to. This is when I reduce the salvia to 1.8g and start experimenting/concentrating on the gingko. I think what has happened is that too much salvia causes excessive vasodilation which is as bad as excessive vasoconstriction. Blood then leaked into the CNS causing more inflammation. My leg hasn't yet recovered from the excessive salvia insult.

Today I am increasing the ginkgo to 6g a day which 10 pills 5 times a day!!! This is the equivalent dose that the lab mice have been taking in various ginkgo experiments. I also note that ginkgo contains quercetin which inhibits PECAM and hence vascular permeability. Ginkgo also reduces endothelial VEGF and hence vascular permeability.

I keep forgetting to mention that since starting the high dose salvia treatment about 1 month and a half ago that my bladder and bowel function is much better.


1: Acta Pharmacol Sin. 2002 Oct;23(10):919-23.Links
Inhibitory effects of Ginkgo biloba extract on vascular endothelial growth factor in rat aortic endothelial cells.Zhang L, Rui YC, Yang PY, Qiu Y, Li TJ, Liu HC.
Department of Pharmacology, School of Pharmacy,The Second Military Medical University, Shanghai 200433, China.

AIM: To study the protective effects of Ginkgo biloba extract (GbE) against rat aortic endothelial cells (RAEC) damage induced by lysophosphatidylcholine (LPC). METHODS: Cell injury were determined by MTT assay and LDH release. Vascular endothelial growth factor (VEGF) protein production from RAEC was determined by enzyme-linked immunosorbent assay (ELISA). VEGF mRNA expression was examined by in situ hybridization and dot blot. RESULTS: GbE 0.01-1 microg/L prevented LPC-induced injury in cultured RAEC in a concentration-dependent manner. Cultured RAEC could express VEGF protein and VEGF mRNA was induced by LPC 5 mg/L. GbE could inhibit the expression of VEGF protein and VEGF mRNA in co-cultured RAEC with LPC. CONCLUSION: LPC could induce a strong expression of VEGF in RAEC. GbE could protect RAEC against the LPC-induced damage and downregulate VEGF protein and VEGF mRNA expression in cultured RAEC.

PMID: 12370096 [PubMed - indexed for MEDLINE]

link

1: Yao Xue Xue Bao. 2002 Feb;37(2):86-9.Links
[Expression of vascular endothelial growth factor in U937 foam cells and the inhibitory effect of drugs][Article in Chinese]


Yang PY, Rui YC, Zhang L, Li TJ, Qiu Y, Wang JS, Zhang WD.
Department of Pharmacology, Second Military Medical University, Shanghai 200433, China.

AIM: To study the expression of vascular endothelial growth factor (VEGF) in U937 foam cells and the inhibitory effect of salvianolic acid B and Ginkgo biloba extract in vitro. METHODS: U937 cells were incubated with 80 mg.L-1 oxidized low density lipoprotein (OX-LDL) for 48 h and a macrophage-derived foam cell model was established. The VEGF concentration in the media was determined by ELISA; the VEGF protein expression in cells was measured with immunohistochemistry; the VEGF mRNA level in cells was measured by in situ hybridization; the positive ratio detected by a morphometrical analysis system was used as the amount of the VEGF protein expression and the mRNA level. RESULTS: After U937 cells were incubated with OX-LDL, VEGF expression level increased greatly both in the cells and in the media. Salvianolic acid B and Ginkgo biloba extract were shown to remarkably inhibit the increase of VEGF. After treated with 10 micrograms/L-1 salvianolic acid B and Ginkgo biloba extract, the VEGF protein concentration in the media and positive ratio in the cells decreased compared with foam cells. After treated with 10 micrograms.L-1 salvianolic acid B and 100 micrograms.L-1 Ginkgo biloba extract, the VEGF mRNA level decreased measured by in situ hybridization. CONCLUSION: A high VEGF expression level was determined in U937 foam cells. Salvianolic acid B and Ginkgo biloba extract were found to inhibit VEGF expression significantly in U937 foam cells in vitro.

PMID: 12579948 [PubMed - indexed for MEDLINE]
link

1: Acta Pharmacol Sin. 2001 Sep;22(9):857-60.Links
Effect of quercetin on adhesion of platelets to microvascular endothelial cells in vitro.Fan PS, Gu ZL, Liang ZQ.
Department of Pharmacology, Suzhou University, Suzhou Institute of Chinese Materia Medica, Suzhou 215007, China.

AIM: To study the effect of quercetin(Que) on the adhesion of platelets to microvascular endothelial cells (MVEC) isolated from human skin. METHODS: [3H]-adenine-labeled platelets were incubated with MVEC. Effect of Que on platelet endothelial cell adhesion molecular (PECAM) expression on MVEC was also evaluated using enzyme-linked immunosorbent assay (ELISA). RESULTS: Adhesion of platelet to MVEC reached to maximum at about 30 min. Que inhibited the adhesion of platelets to MVEC in a concentration-dependent manner. Que 5 micromol/L did not show any significant inhibition. When the concentration of Que increased to 10, 20, and 40 micromol/L, the inhibition rate increased to 10.5 %, 20.0 %, and 42.2 %, respectively. Pre-incubation of Que (10 - 40 micromol/L) with labeled platelets for 30 min also inhibited the adhesion but Que 5 micromol/L did not. The inhibition rate of Que 10, 20, and 40 micromol/L was 18.2 %, 29.8 %, and 65.3 % respectively. Expression of PECAM on the endothelial cells was decreased in a concentration-dependent manner when MVEC were treated with Que (10 - 40 micromol/L) for 12 h but Que 5 micromol/L did not significantly affect the expression. CONCLUSION: Que could inhibit the adhesion of platelets to MVEC. This effect may be related to decreased expression of PECAM on MVEC.

PMID: 11749871 [PubMed - indexed for MEDLINE]

link
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 Oct 22, 2008 10:48 pm

Well, I didn't manage the 6g as I had a very unusual sensation when I was gearing up to take my last 1.2grams. Yesterday afternoon I took 1.2g at 15:30, another 1.2g at 18:30 and was about to take the last 1.2 at about 22:00 when I noticed that there was an odd feeling of great pressure in my brain. It was a sort of throbbing feeling. I surmised this was due to the ginkgo so backed off my extra dose. Shortly thereafter I had quite a few spasms. So this morning my leg felt good and smooth and I've just walked 5 minutes to the nearest shop for milk and the tingling was there after walking but has also calmed down quite rapidly. Good. Today I think I'll just be cautious and go back to 3grams. THREE is the magic number!!

I think that because ginkgo and salvia and other endothelial active herbs are so useful in MS that maybe large quantities are not necessary and that relatively modest quantities may be very effective. And certainly more modest quantities than I tend to go for! You'd never have known I was party central. 8)


I can't wait to try quercetin, horsechestnut etc too. I feel like a whole new world is opening up!

In fact I'm going to start taking horsechestnut today, after reading this little tit bit:
Horse Chestnut Uses

Aescin has the ability to decrease venous permeability, thereby decreasing swelling as a result of incompetent veins. Laboratory studies have shown that aescin can cause constriction of the veins and reduce the permeability of capillaries. [4] Because of these properties, horse chestnut is indicated for varicose veins and venous insufficiency, hemorrhoids, and phlebitis - a type of venous inflammation.



These venous-specific properties are the reason for horse chestnut's inclusion into several cosmetic formulations. [5] Additionally, horse chestnut extract appears to work as a weak diuretic agent, further enhancing its effects as a swelling reducer.

4 Dr. Duke's Phytochemical and Ethnobotanical Databases. www.ars-grin.gov/cgi-bin/duke/farmacy2.pl


It's interesting that an dysfunction of the platelets is being reported in Campath.
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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More horse chestnut

Postby gibbledygook » Thu Oct 23, 2008 1:47 am

I have decided to add the horse chestnut to the ginkgo as I'm too excited to stop!!!!

Of course this is not at all scientific but I am impatient to sort the vascular problems out and I think the combination is going to be spectacular. Fingers crossed.

Here's more horse chestnut research on angiogenesis and permeability etc:

1: Vascul Pharmacol. 2008 Jul 30. [Epub ahead of print] Links
Effect of beta-escin sodium on endothelial cells proliferation, migration and apoptosis.Wang XH, Xu B, Liu JT, Cui JR.
State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University 100083, Beijing China.

beta-Escin, the major active compound in extracts of the horse chestnut Aesculus hippocastanum seed, has shown clinically significant activity in chronic venous insufficiency (CVI). Our previous studies had shown that beta-escin sodium inhibited angiogenesis in chick chorioallantoic membrane (CAM) and in aortic disk assay. In this study, we explored the direct effect of beta-escin sodium on proliferation, migration and apoptosis in human umbilical vein endothelial cells (HUVECs) and ECV304 cells. Sulforhodamine B (SRB) assay showed that beta-escin sodium (10, 20, 40 mug/ml) inhibited endothelial cells (ECs) proliferation dose-dependently. beta-escin sodium also induced ECs apoptosis at 40 mug/ml. Cell migration was evaluated by an improved wound assay: barren spot assay. And the direct effect on cell motility excluding influence of cell proliferation was examined by High Content Screening (HCS, Cellomics) assay. The data indicated that beta-escin sodium suppressed ECs migration and cell motility. Western blot results suggested that beta-escin sodium acts on ECs possibly by increasing expression of thrombospondin-1 (TSP-1), and decreasing expression of PKC-alpha and activation of p44/42 mitogen-activated protein kinase (ERK) and p38 mitogen-activated protein kinase (p38 MAPK). Our findings give the evidence that beta-escin sodium might have potential anti-angiogenic activity via its direct effects on ECs.

PMID: 18718875 [PubMed - as supplied by publisher]
link

aescin seems to have contradictory effects:
1: Vascul Pharmacol. 2007 Jul;47(1):68-73. Epub 2007 Apr 21. Links
Endothelium protectant and contractile effects of the antivaricose principle escin in rat aorta.Carrasco OF, Vidrio H.
Department of Pharmacology School of Medicine, Universidad Nacional Autónoma de México, Apartado Postal 70297, 04510 Mexico, D.F. Mexico.

The triterpene saponin escin is the active component of the extract of seeds of Aesculus hippocastanum used in the treatment of chronic venous insufficiency. Escin is also used experimentally to increase membrane permeability in isolated cells. Since endothelial dysfunction is postulated to be involved in venous insufficiency, the possible endothelium-protectant effect of escin was explored in rat aortic rings, a model widely used to study such effects with cardiovascular agents. Escin enhanced endothelium-dependent relaxation induced by acetylcholine when such relaxation had been reduced by exposure to the superoxide ion generator pyrogallol. This effect was attributed to enhanced nitric oxide production by endothelial nitric oxide synthase, a calcium-dependent enzyme, activated by the increased endothelial cell permeability to calcium induced by escin. Another effect of escin thought to contribute to its therapeutic activity is its ability to produce venous contraction. The compound was found to induce concentration-related contraction also in rat aortic rings. This response was partially inhibited by removal of the endothelium or by preincubation with indomethacin, and was completely abolished by incubation in a calcium-free perfusion fluid. Contraction was considered to be due mainly to the aforementioned effect on calcium permeability, with some mediation by release of endothelial vasoconstrictor prostanoids. It was concluded that, in rat aorta, escin possesses an endothelium-protectant action and a direct contractile effect. The former could contribute to its beneficial effect in the treatment of venous insufficiency, while the latter could constitute a limiting side effect.

PMID: 17512261 [PubMed - indexed for MEDLINE]


here horsechesnut inhibits the reduction in VCAM and PECAM of an insult to the vasculature. Not sure that is good. Think we want to reduce both VCAM and PECAM.
1: Planta Med. 2007 Mar;73(3):285-8. Epub 2007 Feb 19.Links
Aescin protection of human vascular endothelial cells exposed to cobalt chloride mimicked hypoxia and inflammatory stimuli.Montopoli M, Froldi G, Comelli MC, Prosdocimi M, Caparrotta L.
Department of Pharmacology and Anaestesiology, University of Padova, Padova, Italy.

Human vascular endothelial cells (HUVECs) were exposed to CoCl2 as an in vitro model of hypoxia. Expression of VCAM-1 (vascular cell adhesion molecule), reduction of PECAM-1 (platelet endothelial cell adhesion molecule) and cytoskeletal changes without alterations in cell viability were observed. HUVECs were also exposed to Escherichia coli lipopolysaccaride (LPS) as an in vitro model of inflammation: significant IL-6 release was measured. Pre-treatment of HUVECs with aescin prevented, in a concentration-dependent fashion (0.1-1 microM), the action of CoCl2 on VCAM-1 and PECAM-1, also preserving endothelial cell morphology. Furthermore, aescin pre-treatment reduced IL-6 release from LPS-activated vascular endothelium.

PMID: 17310430 [PubMed - indexed for MEDLINE]
link

However this suggests a very positive action on the vasculature:
1: Eur J Pharmacol. 1996 Nov 14;315(2):227-33. Links
Effect of aescine on hypoxia-induced activation of human endothelial cells.Arnould T, Janssens D, Michiels C, Remacle J.
Laboratoire de Biochimie Cellulaire, Facultés Universitaires Notre dame de la Paix, Namur, Belgium.

Phlebotonic drugs are very often old drugs which improve symptoms in chronic venous insufficiency but their precise mechanism remains unclear. One reason for this lack of information is our poor understanding of the aetiology of the varicose vein. One hypothesis which is being more and more substantiated is that the origin of the disease lies in the activation of the endothelium during blood stasis, leading to a cascade of reactions which, in the long term, alter the structure of the vein wall. In this work, we tested aescine (Reparil i.v. form), a phlebotonic drug, in an in vitro model which mimics this situation, i.e. human endothelial cells exposed to hypoxic conditions. Aescine was shown to inhibit 2 important steps of the activation of endothelial cells incubated 120 min under hypoxia the decrease in ATP content, which is the starting point of the activation cascade, and the increase in the activity of phospholipase A2, an enzyme responsible for the release of precursors of inflammatory mediators. Hypoxia-activated endothelial cells also increase their adhesiveness for neutrophils. This process could also be prevented in a dose-dependent manner if endothelial cells were incubated in the presence of aescine. This inhibition was confirmed by morphological observations in scanning electron microscopy. All 3 effects were already evidenced at 100 ng/ml and were maximal at 750 ng/ml. These effects obtained at very low concentrations probably represent one of the main molecular and cellular mechanisms that underlie, among others, protection of the vessel wall. Objective criteria for our understanding of the preventive action of this phlebotonic drug are, thus, provided.

PMID: 8960888 [PubMed - indexed for MEDLINE]
link

here it reduces edema in the brain which is a feature of relapse:
To investigate the inhibiting effect of β-Aescin on nuclear factor-κB (NF-κB) activation and the expression of tumor necrosis factor-α (TNF-α) protein after traumatic brain injury (TBI) in the rat brain, 62 SD rats were subjected to lateral cortical impact injury caused by a free-falling object and divided randomly into four groups: (1) sham operated (Group A); (2) injured (Group B); (3) β-Aescin treatment (Group C); (4) pyrrolidine dithocarbamate (PDTC) treatment (Group D). β-Aescin was administered in Group C and PDTC treated in Group D immediately after injury. A series of brain samples were obtained directly 6 h, 24 h and 3 d respectively after trauma in four groups. NF-κB activation was examined by Electrophoretic Mobility Shift Assay (EMSA); the levels of TNF-α protein were measured by radio-immunoassay (RIA); the water content of rat brain was measured and pathomorphological observation was carried out. NF-κB activation, the levels of TNF-α protein and the water content of rat brain were significantly increased (P<0.01) following TBI in rats. Compared with Group B, NF-κB activation (P<0.01), the levels of TNF-α protein (P<0.01) and the water content of brain (P<0.05) began to decrease obviously after injury in Groups C and D. β-Aescin could dramatically inhibit NF-κB activation and the expression of TNF-α protein in the rat brain, alleviate rat brain edema, and that could partially be the molecular mechanism by which β-Aescin attenuates traumatic brain edema.
Keywords: Brain injuries, β-Aescin, Nuclear factor-κB, Tumor necrosis factor-α, Rats
link

Good for intestinal motility too. Interesting since starting the salvia/ginkgo I've really noticed improved gastrointestinal motility.

1: World J Surg. 2005 Dec;29(12):1614-20; discussion 1621-2. Links
Escin: inhibiting inflammation and promoting gastrointestinal transit to attenuate formation of postoperative adhesions.Fu F, Hou Y, Jiang W, Wang R, Liu K.
Department of Pharmacology, School of Pharmacy, Yantai University, Yantai, P.R., 264005, China. fufenghua@Sohu.com

Postoperative peritoneal adhesions are common, serious complications of general abdominal and gynecologic surgery that can lead to chronic abdominal pain, intestinal obstruction, and infertility. As yet, there are no ideal drugs that may be prescribed for patients to prevent adhesion formation effectively. In this study the effects of escin, a natural drug, on the various steps of adhesion formation were investigated. The effects of escin on increased vascular permeability induced by acetic acid in a mouse model of acute inflammation, granuloma formation in a subchronic inflammatory rat model, gastrointestinal transit in rats with intestinal paralysis, intestinal motility in postoperative patients, and postoperative adhesion formation in a rat model were observed. It was shown that escin could inhibit acute inflammation and granuloma formation, cause acceleration of gastrointestinal transit, help recover intestinal motility, and attenuate the formation of postoperative adhesions. The findings suggest that escin attenuates the formation of postoperative adhesions by inhibiting inflammation and promoting gastrointestinal transit. Thus it may be concluded that both inhibition of inflammation and increased gastrointestinal motility during the early postoperative period have a positive effect on decreasing the formation of adhesions.

PMID: 16311848 [PubMed - indexed for MEDLINE]
link

I like the idea of using horsechestnut as this is a plant that is probably suited to the higher latitude diseases.

Here's more good stuff:
1: Acta Pharmacol Sin. 2004 Jul;25(7):869-75.Links
Effects of sodium beta-aescin on expression of adhesion molecules and migration of neutrophils after middle cerebral artery occlusion in rats.Hu XM, Zhang Y, Zeng FD.
Institute of Clinical Pharmacology, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430030, China.

AIM: To investigate the effects of sodium beta-aescin on neutrophil migration and expression of adhesion molecules (ICAM-1 and E-selectin) after middle cerebral artery occlusion (MCAO) in rats. METHODS: Rats were pretreated with sodium beta-aescin for 7 d and then subjected to cerebral ischemia/reperfusion (I/R) injury induced by an MCAO. After a 2-h ischemia and a 24-h reperfusion, the infarct volume and neurological deficit were determined by the method of TTC staining and the Longa's score. The effect of sodium beta-aescin on the migration of neutrophils was evaluated by measuring the activity of myeloperoxidase (MPO) enzyme. The expressions of adhesion molecules were determined by immunohistochemistry and Western blot. RESULTS: Sodium beta-aescin significantly reduced the cerebral infarct volume and ameliorated the neurological deficit (P<0.05 or P<0.01). The MPO activity and the expressions of ICAM-1 and E-selectin in the vehicle-treated rats were increased significantly (P<0.01) after cerebral I/R. After treatment with sodium beta-aescin, the enzymatic activity of MPO and the expressions of these adhesion molecules were significantly reduced compared with the vehicle-treated group (P<0.05 or P<0.01). CONCLUSION: Sodium beta-aescin can attenuate brain injury, down-regulate the protein expressions of ICAM-1 and E-selectin, and reduce the migration of neutrophils after cerebral I/R.
PMID: 15210059 [PubMed - indexed for
link

1: Angiology. 2004 May-Jun;55 Suppl 1:S1-5. Links
Microcirculatory efficacy of topical treatment with aescin + essential phospholipids gel in venous insufficiency and hypertension: new clinical observations.Belcaro G, Cesarone MR, Dugall M.
Irvine2 Vascular Laboratory, Department of Biomedical Sciences, G. D'Annunzio University, Italy. cardres@pe.abol.it

Aescin + essential phospholipids (AEPL) topical gels are used for local treatment of venous and microcirculatory alterations (varicose veins, chronic venous insufficiency). Bruises, swelling, thrombophlebitis, and contusions are effectively treated with AEPL. Active ingredients are escinate and essential phospholipids (EPL). The aim of this new study was the evaluation of the efficacy of the effects of AEPL gel on the microcirculation in subjects with chronic venous insufficiency, venous hypertension (CVH), and venous microangiopathy. Patients were assessed measuring skin flux with laser-Doppler flowmetry (LDF). After 2 weeks of local treatment, all individual values (100%) were significantly decreased (p < 0.05), indicating an improvement in the microcirculation. In all treated patients, flux decreased at least 30% (indicating a decrease in the level of venous microangiopathy) (p < 0.05). Considering these observations, topical treatment with AEPL in areas of venous microangiopathy is beneficial, can prevent ulceration, and improves the skin healing processes.

PMID: 15156249 [PubMed - indexed for MEDLINE]
link

but this is less reassuring:
Responsiveness of human varicose saphenous veins to vasoactive agents.

Pharmacodynamics

British Journal of Clinical Pharmacology. 51(3):219-224, March 2001.
Brunner, Friedrich 1; Hoffmann, Christine 2; Schuller-Petrovic, Sanja 2
Abstract:
Aims : To test in vitro the constrictor and relaxation responsiveness of variously diseased segments of human saphenous vein from patients with varicose vein disease.

Methods : The vein segments were derived (i) from the inguinal saphenous vein (valvularly incompetent and slightly dilated; tissue A); (ii) from the distal end of the lower leg just above the medial ankle (competent; tissue B); (iii) from a tributary to the long saphenous vein just below the knee (dilated, incompetent and overtly varicose; tissue C). The contractile responses were tested with phenylephrine (an [alpha]-adrenergic receptor agonist) and aescin, a clinically used phlebotonic drug derived from horse chestnut extract. Relaxant responses were tested with acetylcholine and sodium nitroprusside.

Results : Both contractile agents contracted vein segments from the inguinal and ankle area with similar potency and efficacy, but were virtually without effect in the overtly varicose segments from the calf. E C50 values (molar concentration of the agonist that produces 50% of the maximum effect) in tissues A and B were 2.9 +/- 0.3 and 2.5 +/- 0.5 [micro]mol l-1 (phenylephrine) and 9.4 +/- 1.0 and 15.9 +/- 2.5 [micro]mol l-1 (aescin); the corresponding maximum effects (maximum effect, percent of KCl-induced contraction) were 76 +/- 3 and 70 +/- 4% (phenylephrine) and 70 +/- 2 and 71 +/- 3% (aescin) (P = NS in both cases for A vs B). In tissue C, the maximum effects were 5 +/- 5% (phenylephrine) and 10 +/- 7% (aescin) of KCl-induced contraction (not significantly different from zero). Acetylcholine-induced relaxation was similar for vein segments from locations A and B, whereas sodium nitroprusside was more effective in tissue B than A.

Conclusions : These findings support the notion that abnormalities within the venous wall affect venous smooth muscle contractility. Since competent and incompetent clinically normal vessels show normal contractile responses, whereas varicose vessels are not responsive to vasoactive drugs, it is likely that pharmacological treatment regimens are effective in early, but not in late stages of the disease.
link

The abstract isn't published but this looks very promising!!
1: Arzneimittelforschung. 1970 Jun;20(6):863-4.Links
[Studies of brain edema in the rat induced by triethyl tin sulfate. 6. Protective effect of aescin against the triethyl tin sulfate conditioned increase of permeability of blood-brain barrier]

link

BINGO!
1: Biol Pharm Bull. 1997 Oct;20(10):1092-5.Links
Effects of escins Ia, Ib, IIa, and IIb from horse chestnut, the seeds of Aesculus hippocastanum L., on acute inflammation in animals.Matsuda H, Li Y, Murakami T, Ninomiya K, Yamahara J, Yoshikawa M.
Kyoto Pharmaceutical University, Japan.

We investigated the effects of escins Ia, Ib, and IIb isolated from horse chestnut, the seeds of Aesculus hippocastanum L., and desacylescins I and II obtained by alkaline hydrolysis of escins on acute inflammation in animals (p.o.). Escins Ia, Ib, IIa, and IIb (50-200 mg/kg) inhibited the increase of vascular permeability induced by both acetic acid in mice and histamine in rats. Escins Ib, IIa, and IIb (50-200 mg/kg) also inhibited that induced by serotonin in rats, but escin Ia didn't. Escins Ia, Ib, IIa, and IIb (200 mg/kg) inhibited the hind paw edema induced by carrageenin at the first phase in rats. Escin Ia (200 mg/kg) and escins Ib, IIa, and IIb (50-200 mg/kg) inhibited the scratching behavior induced by compound 48/80 in mice, but escin Ia was weakest. Desacylescins I and II (200 mg/kg) showed no effect. With regard to the relationship between their chemical structures and activities, the acyl groups in escins were essential. Escins Ib, IIa, and IIb with either the 21-angeloyl group or the 2'-O-xylopyranosyl moiety showed more potent activities than escin Ia which had both the 21-tigloyl group and the 2'-O-glucopyranosyl moiety.

PMID: 9353571 [PubMed - indexed for MEDLINE]
link


Encore!!
1: Arzneimittelforschung. 1994 Jan;44(1):25-35.Links
Veinotonic effect, vascular protection, antiinflammatory and free radical scavenging properties of horse chestnut extract.Guillaume M, Padioleau F.
Lipha Group, Department of Pharmacology, Suresnes, France.

Horse chestnut extract (HCE), containing 70% escin, is the main active component of Veinotonyl 75. The aim of this work was to investigate pharmacological properties attempting to elucidate the efficacy of HCE in chronic venous insufficiency. Veinotonic and lymphagogue properties: HCE dose dependently contracts the canine saphenous isolated vein (cumulative doses 5 x 10(-8) to 5 x 10(-4) g/ml). Its action lasts more than 5 h. In the perfused canine saphenous vein, HCE (25-50 mg in bolus) increases the venous pressure of the normal vein and the pathological vein stenosed 8 days before, and the contractile response to noradrenaline is significantly potentiated. Moreover, during the perfusion in inverse direction of the blood stream, a clear contracting effect on the valves is also obtained with HCE. In the anaesthetized dog, HCE in situ improves the femoral vein compliance and opposes the venous distension obtained during clamping in a carotido-femoral perfusion with constant flow. In other respects, HCE significantly increases femoral venous pressure and flow, together with thoracic lymphatic flow, while respecting the arterial parameters (2.5 and 5 mg/kg i.v.). Vasculotropic action: HCE dose dependently diminishes the cutaneous capillary hyperpermeability induced either by injections of phlogistic agents as histamine and serotonin in the rat (100 to 400 mg/kg p.o.), or by an irritative agent (chloroform) application in the rabbit (50 to 300 mg/kg p.o. and 2.5 to 5 mg/kg i.v.). It significantly increases the vascular resistance in the guinea pig fed a scorbutigenic diet as measured by the petechia method (50 to 400 mg/kg p.o.). Antiedema and antiinflammatory properties: HCE decreases the formation of edemas induced in the rat's hind paw, one of lymphatic origin, the other of inflammatory origin (200 to 400 mg/kg p.o.). In an experimental model of pleurisy in the rat HCE suppresses plasmatic extravasation and leucocytes emigration into the pleural cavity (200 to 400 mg/kg p.o.; 1 to 10 mg/kg i.v.). It decreases the connective tissue formation in the subchronic model of inflammatory granuloma in the rat (400 mg/kg p.o. and 5-10 mg/kg s.c.). Antiradical mechanism of action both in vitro and in vivo: HCE dose dependently inhibits both enzymatic and non-enzymatic in vitro lipid peroxidation (5 x 10(-6) to 5 x 10(-4) g/ml).(ABSTRACT TRUNCATED AT 400 WORDS)

PMID: 8135874 [PubMed - indexed for MEDLINE]
link

et encore!!
1: Dtsch Med Wochenschr. 1986 Aug 29;111(35):1321-9.Links
[Effects of horse-chestnut seed extract on transcapillary filtration in chronic venous insufficiency][Article in German]


Bisler H, Pfeifer R, Klüken N, Pauschinger P.
The effect of horse-chestnut seed extract (standardized on aescin; Venostasin retard) was assessed in a randomized placebo-controlled crossover double-blind trial of 22 patients with proven chronic venous insufficiency by measuring the capillary filtration coefficient and the intravascular volume of the lower leg by venous-occlusion plethysmography. Three hours after taking two capsules of Venostasin (600 mg; each capsule containing 50 mg aescin) the capillary filtration coefficient had decreased by 22%, whereas after administration of an identical-looking placebo capsule it rose but slightly over three hours. The difference in the effect of Venostasin and placebo is statistically significant (P = 0.006). The intravascular volume was reduced 5% more after Venostasin than the placebo, but this is not statistically significant. It is concluded that Venostasin has an inhibitory effect on oedema formation via a decrease in transcapillary filtration and thus improves oedema-related symptoms in venous diseases of the legs.

PMID: 3527643 [PubMed - indexed for MEDLINE]
link
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 » Thu Oct 23, 2008 4:13 am

Have just done my 5 minute walk tingle test some 2 hours after my first 1.8g of horse chestnut. The walking seemed more fluid than the last test a few days ago and there was tingling afterwards but it is very mild. I reckon the combo of vein herbs and gingko/salvia type herbs are the way forward. My experience of too much salvia really makes me think that the problem is principally that of the vasculature and so everything to strengthen it must be undertaken. I have just ordered a supplement that combines horsechestnut, diosmin, hesperidin and a number of other herbs which are good for varicose veins and strengthening the vasculature. The horsechestnut I am currently using is from herbalextractsplus.
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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Bingo

Postby gibbledygook » Thu Oct 23, 2008 6:28 am

I have just done my 6 minute level 11 cross training with 600meters completed. There is now virtually no tingling in my left leg or knee. This is unprecedented. I have taken only 3.6g horse chestnut with the ginkgo now at 1.44g. This must be it.

Horse chestnut.
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 » Thu Oct 23, 2008 11:38 pm

gibbledygook wrote:Well, I didn't manage the 6g as I had a very unusual sensation when I was gearing up to take my last 1.2grams. Yesterday afternoon I took 1.2g at 15:30, another 1.2g at 18:30 and was about to take the last 1.2 at about 22:00 when I noticed that there was an odd feeling of great pressure in my brain. It was a sort of throbbing feeling. I surmised this was due to the ginkgo so backed off my extra dose. Shortly thereafter I had quite a few spasms.

I would be a little careful with high doses on Gingko.


Multiple sclerosis: Gingko biloba may offer relief to multiple sclerosis sufferers
Go easy
In their report, the UCLA researchers noted that they used the highest grade of GBE available. They didnt reveal a brand name, but they made the point that the quality of ginkgo supplements has been shown to vary widely.

This isnt the only concern when youre doing research to decide on a GBE supplement. Ginkgo biloba contains a toxic compound called ginkgolic acid which may cause gastrointestinal problems, headaches, and skin irritations for some users. Its generally accepted that 5 ppm is a safe maximum level for this acid. But some manufacturers dont list ginkgolic acid on their labels, so be sure to read content labels carefully.


If You Take Ginkgo Extract … Watch out for Ginkolic Acid
1) Safety: Watch Out for Ginkolic Acid!
Most people aren't aware that Ginkgo leaves contain a toxic compound, ginkgolic acid. Pharmaceutical-grade Ginkgo extract must contain 24% flavonoids, 6% triterpenes, and less than 5 parts per million of ginkgolic acid. But in the US, you can't be sure how much ginkgolic acid is in your product unless it is specifically stated on the label … and most manufacturers don't list it on the label. (And the sad fact is that many Ginkgo products contain more - much more ginkgolic acid than is considered safe.)

But they also have this
2) Effectiveness: Make Sure Your Ginkgo has a High Bilobalide Content to Get All the Benefits
New studies have shown that bilobalide, a unique phytochemical that is found only in Ginkgo, may prove to be one of the most significant breakthroughs in brain anti-aging. Bilobalide is a substance that recent research has shown:
induces important brain growth factors
* prevents cell death from amyloid protein—a culprit in Alzheimer's disease
* protects mitochondria, the tiny energy factories inside cells that provide the "spark of life"
* protects against Alzheimer's and other neurodegenerative disorders
* prolongs life span
works synergistically with the other compounds in Ginkgo
Buying a high-quality Ginkgo supplement that contains at least 3% bilobalide is very important, since the latest research shows bilobalide to be one of the major active components of the extract.4 But most companies don't tell you the amount that's in their product.


Of course, both web sites would happen to sell a recommended product.
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Butcher's Broom and other vascular aids

Postby gibbledygook » Fri Oct 24, 2008 2:48 am

I am enjoying a considerable reprieve from the tingling even after hot swimming pool excercise. This is doubtless due to the horsechestnut and hesperidin supplements which I now take in addition to the ginkgo and salvia, curcumin and scutellaria. I am now interested in a couple of other herbs for vascular integrity and then plan on a nice long research holiday. Fortunately many varicose vein supplements contain both horse chestnut and butcher's broom, gotu kola, grape seed extract, prickly ash and rutin.
1: J Pharmacol Sci. 2008 Oct;108(2):198-205.
Possible Mechanism of the Anti-inflammatory Activity of Ruscogenin: Role of Intercellular Adhesion Molecule-1 and Nuclear Factor-kappaB.Huang YL, Kou JP, Ma L, Song JX, Yu BY.
Department of Complex Prescription of TCM, China Pharmaceutical University, China.

Ruscogenin (RUS), first isolated from Ruscus aculeatus, also a major steroidal sapogenin of traditional Chinese herb Radix Ophiopogon japonicus, has been found to exert significant anti-inflammatory and anti-thrombotic activities. Our previous studies suggested that ruscogenin remarkably inhibited adhesion of leukocytes to a human umbilical vein endothelial cell line (ECV304) injured by tumor necrosis factor-alpha (TNF-alpha) in a concentration-dependent manner. Yet the underlying mechanisms remain unclear. In this study, the in vivo effects of ruscogenin on leukocyte migration and celiac prostaglandin E(2) (PGE(2)) level induced by zymosan A were studied in mice. Furthermore, the effects of ruscogenin on TNF-alpha-induced intercellular adhesion molecule-1 (ICAM-1) expression and nuclear factor-kappaB (NF-kappaB) activation were also investigated under consideration of their key roles in leukocyte recruitment. The results showed that ruscogenin significantly suppressed zymosan A-evoked peritoneal total leukocyte migration in mice in a dose-dependent manner, while it had no obvious effect on PGE(2) content in peritoneal exudant. Ruscogenin also inhibited TNF-alpha-induced over expression of ICAM-1 both at the mRNA and protein levels and suppressed NF-kappaB activation considerably by decreasing NF-kappaB p65 translocation and DNA binding activity. These findings provide some new insights that may explain the possible molecular mechanism of ruscogenin and Radix Ophiopogon japonicus for the inhibition of endothelial responses to cytokines during inflammatory and vascular disorders.

PMID: 18946195 [PubMed - in process]
link

1: Microvasc Res. 2008 May;76(1):66-72. Epub 2008 Mar 15. Links
Use of microcirculatory parameters to evaluate clinical treatments of chronic venous disorder (CVD).Lascasas-Porto CL, Milhomens AL, Virgini-Magalhães CE, Fernandes FF, Sicuro FL, Bouskela E.
Laboratory for Research in Microcirculation, Biomedical Center, State University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil. carmenporto@terra.com.br

OBJECTIVES: To evaluate changes on cutaneous microangiopathy in chronic venous disorder (CVD) after use of Cirkan [venotonic drug containing Ruscus aculeatus (plant extract), hesperidine methylchalcone (flavonoid) and vitamin C], elastic compression stockings (ECS) or no treatment for four weeks. PATIENTS AND METHODS: Fifty-five female patients (85 legs), 25 to 57 years, with at least one limb classified as C2,s or C2,3,s (CEAP classification), were allocated consecutively, according to entrance order, in these three groups. Ten healthy women age-matched were also investigated. Using orthogonal polarization spectral technique (noninvasive method), measurements of functional capillary density (FCD, number of capillaries with flowing red blood cells/mm(2)), capillary morphology (CM, % of abnormal capillaries/mm(2)) and diameters (mum) of dermal papilla (DDP), capillary bulk (DCB) and capillary limb (CD) were obtained on the medial perimalleolar region and later analyzed using CapImage software. RESULTS AND CONCLUSIONS: CVD patients showed significant changes on CD and CM compared to healthy subjects in agreement with our previous findings (J Vasc Surg 43:1037-1044, 2006). On Cirkan-treated patients, after 4 weeks, CD decreased on both limbs and CM improved on the left one, suggesting an amelioration of the chronic venous hypertension. No significant changes could be detected on other patient groups. These results confirm the existence of microcirculatory dysfunction in early stages of CVD, probably due to post-capillary hypertension, and further support the venotonic action of Cirkan.

PMID: 18423497 [PubMed - in process]
link

not so good as achillea
1: Acta Pol Pharm. 2006 Jul-Aug;63(4):277-80.Links
Anti-inflammatory activity of Achillea and Ruscus topical gel on carrageenan-induced paw edema in rats.Maswadeh HM, Semreen MH, Naddaf AR.
School of Pharmacy, Department of Pharmaceutical Technology, Al-Isra University, P.O. Box 961582, Code No. 11196 Amman, Jordan. maswadehhamza@hotmail.com

The anti-inflammatory activity of Achillea and Ruscus extracts was studied in comparison with diclofenac sodium topical gel (diclosal Emulgel), using the carrageenan induced paw edema model in Albino rats. Gel formulation was prepared containing 6% of each extract in gel base, namely sodium carboxymethylcellulose (NaCMC). The kinetics of drug release from the prepared formulation was studied separately in each case. Results showed that the release follows the Higuchi square root equation. The pharmacological screening revealed that the percent reduction of edema for Achillea extract and Ruscus extract were 48.1% and 18.8%, respectively, while diclosal Emulgel produced 47% reduction of edema.

PMID: 17203864 [PubMed - indexed for
link

inhibition of cox 2:
1: J Herb Pharmacother. 2004;4(2):11-8.Links
Inhibition of COX isoforms by nutraceuticals.Seaver B, Smith JR.
University of Montana, 441 S. 6th E., Missoula, MT 59812, USA.

Humans have two isoforms of Prostaglandin H Synthase or cyclooxygenase: COX-1 and COX-2. COX-1 is cytoprotective. COX-2 inhibitors reduce inflammation without the risk of ulceration and kidney damage. The ideal nutraceutical would inhibit COX-2 synthesis while preserving COX-1 synthesis. The hypothesis for this research was that COX inhibitors would fall primarily into three categories: COX-2 specific inhibition, non-specific inhibition (COX-1 and COX-2), and minimal inhibition. The human Cayman COX inhibitor screening assay was used to determine the inhibitory concentration 50 (IC50) of COX-1/ COX-2 activity of each nutraceutical. The assay was run, in duplicate, with three concentrations of a suspected inhibitor, a standard curve of eight concentrations, a non-specific binding sample, and a maximum binding sample. The inhibition and concentration of each sample was then put on a multiple regression best-fit line and the IC50 determined. For comparison, ibuprofen, rofecoxib, naproxen, and indomethacin were used. Positive results were seen for ipriflavone, resveratrol, MSV-60, amentoflavone, ruscus extract and notoginseng. Glucosamine, nexrutine, and berberine did not inhibit either isoform.

PMID: 15364641 [PubMed - indexed for MEDLINE
link

gonnae get me some bootcher's broom, ken
1: Int Angiol. 1999 Dec;18(4):306-12.Links
Effect of Ruscus extract and hesperidin methylchalcone on hypoxia-induced activation of endothelial cells.Bouaziz N, Michiels C, Janssens D, Berna N, Eliaers F, Panconi E, Remacle J.
Laboratoire de Biochimie et Biologie Cellulaire--Facultés Universitaires Notre-Dame de la Paix--Namur, Belgium.

BACKGROUND: Ruscus aculeatus extract and the flavonoid hesperidin methylchalcone (HMC) are drugs used in the treatment of chronic venous insufficiency. METHODS: In the present study, we investigated their effects on the activation of endothelial cells by hypoxia, a condition which mimics venous blood stasis. RESULTS: We observed that Ruscus extract was able to inhibit the activation of endothelial cells by hypoxia: the decrease in ATP content, the activation of phospholipase A2 as well as the subsequent increase in neutrophil adherence with a maximal protection obtained at 50 microg/ml. HMC was also able to inhibit the hypoxia-induced decrease in ATP content. Furthermore, the effects of Ruscus extract and of HMC on this decrease seem to be additive. CONCLUSIONS: The biochemical mechanism evidenced in this work might explain some of the beneficial therapeutic effects of these products in the treatment of chronic venous insufficiency patients.

PMID: 10811519 [PubMed - indexed for MEDLINE]
link

1: Clin Hemorheol Microcirc. 1997 Sep-Oct;17(5):385-8. Links
Antipermeability effects of Cyclo 3 Fort in hamsters with moderate diabetes.Svensjö E, Bouskela E, Cyrino FZ, Bougaret S.
Laboratório de Pesquisas em Microcirculação, State University of Rio de Janeiro, Brazil.

Ruscus aculeatus extract (the active principle of Cyclo 3 Fort) is used to increase venous tone in patients with venous disease. In these experiments, the effects of oral Cyclo 3 Fort on capillary permeability were studied in hamsters with moderate diabetes induced by two intraperitoneal injections of streptozotocin (40 mg/kg). Hamsters were treated with a placebo or Cyclo 3 Fort, 2, 10 or 50 mg/kg/day, for 4 weeks starting 3 days after induction of diabetes. Intravital microscopy of cheek pouch preparations was performed using fluorescein-labelled dextran (FITC-dextran) as a marker for plasma exudation (leak formation). Plasma levels of glucose were measured prior to experiments. Following preparation for intravital microscopy, each cheek pouch was subjected to two applications of histamine, 5 x 10(-6) M for 5 min at 30-minute intervals. Plasma exudation (number of leaks/cm2) was significantly reduced in animals receiving Cyclo 3 Fort at doses of 10 mg/kg or above. The mean number of leaks was 258 +/- 17 in the placebo group, compared with 253 +/- 12, 125 +/- 7 (p < 0.01) and 99 +/- 7 (p < 0.01) in animals receiving Cyclo 3 Fort, 2, 10 or 50 mg/kg, respectively. Blood glucose levels did not differ between groups. Thus, oral Cyclo 3 Fort inhibited histamine-induced plasma exudation in hamsters with mild diabetes without affecting the glycaemia.

PMID: 9502536 [PubMed - indexed for MEDLINE]
link
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 Oct 26, 2008 6:22 am

I realise now that because vascular problems are so central to my MS that the herbs salvia, ginkgo and horsechestnut need only be taken in really much lower doses than I have hitherto experimented with. This is because as I continually reduce the doses my walking improves and the absence of tingling remains. I have today taken only 480mg of ginkgo, 2.4g of salvia and 2.4g of horsechestnut and have just done the 5 minute walk/tingle test in a very warm flat with my jersey on. I am hot (temperature-wise)! I had a few very very minor tingles after the 5 minute walk. Amazing. And the walking was easier than the last few days. I really think that drugs for the vasculature are worth exploring. This will be my last update for a while as I have been overdoing the research and now just need to work out the optimal doses of the various vascular herbs. And the butcher's broom is arriving soon!
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 Oct 27, 2008 3:10 am

I have pared back the herbs to try to see more clearly what's what. I am now taking 960mg of ginkgo, 4.8g of salvia, 4.8g of curcumin and 30mg bioperine. My legs feel great! There is much less spasticity and tingling everywhere. Clearly I was overdoing it before. I am going to wait a few days before trying the horsechestnut and again in much lower dose than I first tried when I was taking about 11grams daily!!! My god, it's a wonder I haven't poisoned myself.
1: Altern Med Rev. 2001 Apr;6(2):126-40. Links
Hemorrhoids and varicose veins: a review of treatment options.MacKay D.
Thorne Research, 4616 SE 30th, Portland, OR 97202, USA. mackaynd@earthlink.net

Hemorrhoids and varicose veins are common conditions seen by general practitioners. Both conditions have several treatment modalities for the physician to choose from. Varicose veins are treated with mechanical compression stockings. There are several over-the-counter topical agents available for hemorrhoids. Conservative therapies for both conditions include diet, lifestyle changes, and hydrotherapy which require a high degree of patient compliance to be effective. When conservative hemorrhoid therapy is ineffective, many physicians may choose other non-surgical modalities: injection sclerotherapy, cryotherapy, manual dilation of the anus, infrared photocoagulation, bipolar diathermy, direct current electrocoagulation, or rubber band ligation. Injection sclerotherapy is the non-surgical treatment for primary varicose veins. Non-surgical modalities require physicians to be specially trained, own specialized equipment, and assume associated risks. If a non-surgical approach fails, the patient is often referred to a surgeon. The costly and uncomfortable nature of treatment options often lead a patient to postpone evaluation until aggressive intervention is necessary. Oral dietary supplementation is an attractive addition to the traditional treatment of hemorrhoids and varicose veins. The loss of vascular integrity is associated with the pathogenesis of both hemorrhoids and varicose veins. Several botanical extracts have been shown to improve microcirculation, capillary flow, and vascular tone, and to strengthen the connective tissue of the perivascular amorphous substrate. Oral supplementation with Aesculus hippocastanum, Ruscus aculeatus, Centella asiatica, Hamamelis virginiana, and bioflavonoids may prevent time-consuming, painful, and expensive complications of varicose veins and hemorrhoids.

PMID: 11302778 [PubMed - indexed for MEDLINE]
link

butcher's broom contracts the veins:
1: Int Angiol. 2000 Jun;19(2):176-83.Links
Pharmacological assessment of adrenergic receptors in human varicose veins.Miller VM, Rud KS, Gloviczki P.
Department of Surgery, Mayo Clinic and Foundation, Rochester, MN 55905, USA. miller.virginia@mayo.edu

BACKGROUND: Experiments were to characterize pharmacologically adrenergic receptors in human varicose veins to the natural transmitter norepinephrine and to an extract of Ruscus. METHODS: Greater saphenous veins and varicose tributaries from patients undergoing elective surgery for primary varicose disease and portions of greater saphenous veins from patients undergoing peripheral arterial reconstruction (control) were suspended for the measurement of isometric force in organ chambers. Concentration response curves were obtained to norepinephrine or the extract of Ruscus aculeatus in the absence and presence of selective antagonists of alpha, and alpha2 adrenergic receptors. RESULTS: Norepinephrine and Ruscus extract caused concentration-dependent contractions in all veins. Contractions to norepinephrine were greater in control veins than in varicose tributaries. Contractions to the extract were greater in varicose tributaries than in greater saphenous veins from varicose patients. Contractions to norepinephrine were reduced similarly by alpha and alpha2-adrenergic agonists in control and varicose veins but to a greater extent by alpha2-blockade in greater saphenous veins from varicose patients. Contractions to Ruscus extract were not reduced by alpha-adrenergic blockade in control veins but were reduced by alpha2-adrenergic blockade in varicose veins. CONCLUSIONS: These results suggest a differential distribution of alpha adrenergic receptors on greater saphenous veins from non-varicose patients compared to those with primary varicose disease. Venotropic agents from plant extract probably exert effects by way of multiple receptor and non-receptor mediated events.

PMID: 10905803 [PubMed - indexed for MEDLINE]
link

1: Clin Hemorheol Microcirc. 1997 Sep-Oct;17(5):385-8. Links
Antipermeability effects of Cyclo 3 Fort in hamsters with moderate diabetes.Svensjö E, Bouskela E, Cyrino FZ, Bougaret S.
Laboratório de Pesquisas em Microcirculação, State University of Rio de Janeiro, Brazil.

Ruscus aculeatus extract (the active principle of Cyclo 3 Fort) is used to increase venous tone in patients with venous disease. In these experiments, the effects of oral Cyclo 3 Fort on capillary permeability were studied in hamsters with moderate diabetes induced by two intraperitoneal injections of streptozotocin (40 mg/kg). Hamsters were treated with a placebo or Cyclo 3 Fort, 2, 10 or 50 mg/kg/day, for 4 weeks starting 3 days after induction of diabetes. Intravital microscopy of cheek pouch preparations was performed using fluorescein-labelled dextran (FITC-dextran) as a marker for plasma exudation (leak formation). Plasma levels of glucose were measured prior to experiments. Following preparation for intravital microscopy, each cheek pouch was subjected to two applications of histamine, 5 x 10(-6) M for 5 min at 30-minute intervals. Plasma exudation (number of leaks/cm2) was significantly reduced in animals receiving Cyclo 3 Fort at doses of 10 mg/kg or above. The mean number of leaks was 258 +/- 17 in the placebo group, compared with 253 +/- 12, 125 +/- 7 (p < 0.01) and 99 +/- 7 (p < 0.01) in animals receiving Cyclo 3 Fort, 2, 10 or 50 mg/kg, respectively. Blood glucose levels did not differ between groups. Thus, oral Cyclo 3 Fort inhibited histamine-induced plasma exudation in hamsters with mild diabetes without affecting the glycaemia.

PMID: 9502536 [PubMed - indexed for MEDLINE]
link

butcher's broom lowers edema:
1: Lymphology. 1996 Mar;29(1):29-35.Links
Treatment of secondary lymphedema of the upper limb with CYCLO 3 FORT.Cluzan RV, Alliot F, Ghabboun S, Pascot M.
Unité de Lymphologie, Hôpital Cognacq-Jay, Paris, France.

Fifty seven patients with secondary lymphedema of the upper limb after previous treatment for breast cancer were treated for 3 months with an extract of Ruscus + Hesperidin Methyl Chalcone (CYCLO 3 FORT) or placebo according to a double-blind protocol in the context of a controlled clinical trial. All patients also underwent manual lymphatic drainage twice a week for at least one month. With CYCLO 3 FORT, the reduction in volume of arm edema, the main assessment criteria, was 12.9% after 3 months of treatment as compared with a placebo (p=0.009). Decreased edema tended to be more marked in the forearm compared with the upper arm where excess fat deposition seemed to dominate over excess fluid accumulation. CYCLO 3 FORT was well tolerated with minimal adverse reaction.

PMID: 8721977 [PubMed - indexed for MEDLINE
link

1: J Cardiovasc Pharmacol. 1994 Aug;24(2):281-5.Links
Possible mechanisms for the inhibitory effect of Ruscus extract on increased microvascular permeability induced by histamine in hamster cheek pouch.Bouskela E, Cyrino FZ, Marcelon G.
Department of Physiology and Biophysics, University of Lund, Sweden.

Extract of Ruscus aculeatus is used in treatment of venous insufficiency. In the present study, we used the hamster cheek pouch preparation and investigated in vivo the effects of an alpha 1 and alpha 2 adrenoceptor antagonists, a calcium blocker, Ruscus extract, and their combination on increased microvascular permeability induced by histamine. Experiments were performed on male hamsters; 30 min after completion of the cheek pouch preparation, fluorescein-labeled dextran (molecular weight 150,000) was given intravenously (i.v.). Histamine, applied topically, increased the number of fluorescent vascular leakage sites from postcapillary venules, evidence of an increase in macromolecular permeability, which was quantified by ultraviolet light microscopy as the number of leaky sites in the prepared area. Prazosin (alpha 1-adrenoceptor antagonist), diltiazem (calcium blocker), and Ruscus extract applied topically dose-dependently inhibited the macromolecular permeability-increasing effect of histamine. Rauwolscine (alpha 2-adrenoceptor antagonist), also applied topically, had no effect on histamine-induced permeability increase. Inhibition of the histamine-induced permeability increase evoked by Ruscus extract could be blocked by prazosin and by diltiazem but not by rauwolscine. These results indicate that any variation in the transmembrane flux of calcium impairs formation of microvascular leaky sites by histamine. Our results show that Ruscus extract has a protective effect against the leakage of FITC-dextran in hamster cheek pouch after administration of histamine that is modulated by calcium and selectively by alpha 1-adrenoceptors.

PMID: 7526061 [PubMed - indexed for MEDLINE]

Related ArticlesInhibitory effect of the Ruscus extract and of the flavonoid hesperidine methylchalcone on increased microvascular permeability induced by various agents in the hamster cheek pouch. [J Cardiovasc Pharmacol. 1993] Effects of oral administration of purified micronized flavonoid fraction on increased microvascular permeability induced by various agents and on ischemia/reperfusion in the hamster cheek pouch. [Angiology. 1997] Possible mechanisms for the venular constriction elicited by Ruscus extract on hamster cheek pouch. [J Cardiovasc Pharmacol. 1994] ReviewThe hamster cheek pouch as a model in microcirculation research. [Eur Respir J Suppl. 1990] ReviewStructural and functional differentiation of microvascular endothelium. [Ciba Found Symp. 1980] » See Reviews... | » See All...
linl
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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Postby gibbledygook » Mon Oct 27, 2008 3:37 am

The histamine connection brings me back to luteolin:
1: Adv Exp Med Biol. 2007;601:423-30.Links
Mast cells, T cells, and inhibition by luteolin: implications for the pathogenesis and treatment of multiple sclerosis.Theoharides TC, Kempuraj D, Iliopoulou BP.
Department of Pharmacology, Internal Medicine and Biochemistry, Immunology Program, Tufts University School of Medicine, Tufts-New England Medical Center, Boston, MA, USA. theoharis.theoharides@tufts.edu

Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS) mainly mediated by Th1, but recent evidence indicates that Th2 T cells, mostly associated with allergic reactions, are also involved. Mast cells are involved in allergic and inflammatory reactions because they are located perivascularly and secrete numerous proinflammatory cytokines. Brain mast cells are critically placed around the blood-brain barrier (BBB) and can disrupt it, a finding preceding any clinical or pathological signs of MS. Moreover, mast cells are often found close to MS plaques, and the main MS antigen, myelin basic protein (MBP), can activate human cultured mast cells to release IL-8, TNF-alpha, tryptase, and histamine. Mast cells could also contribute to T cell activation since addition of mast cells to anti-CD3/anti-CD28 activated T cells increases T cell activation over 30-fold. This effect requires cell-to-cell contact and TNF, but not histamine or tryptase. Pretreatment with the flavone luteolin totally blocks mast cell stimulation and T cell activation. Mast cells could constitute a new unique therapeutic target for MS.

PMID: 17713031 [PubMed - indexed for MEDLINE
link
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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Postby gibbledygook » Mon Oct 27, 2008 4:36 am

Gotu kola
1: Angiology. 2001 Oct;52 Suppl 2:S55-9.Links
Treatment of edema and increased capillary filtration in venous hypertension with total triterpenic fraction of Centella asiatica: a clinical, prospective, placebo-controlled, randomized, dose-ranging trial.De Sanctis MT, Belcaro G, Incandela L, Cesarone MR, Griffin M, Ippolito E, Cacchio M.
Irvine Vascular Laboratory, St Mary's Hospital and Imperial College, London, UK.

The variation of capillary filtration rate (CFR), ankle circumference (AC), and ankle edema (AE) was evaluated in three groups of patients with venous hypertension (ambulatory venous pressure >42 mm Hg) and in a group of normal subjects before and after treatment for 4 weeks with total triterpenic fraction of Centella asiatica (TTFCA), a venoactive drug acting on the microcirculation and on capillary permeability. Group A (20 patients)was treated with TTFCA 60 mg thrice daily, group B (20 patients) was treated with 30 mg thrice daily; group C (12 patients) was treated with placebo; and group D (10 normal subjects) was treated with TTFCA 60 mg thrice daily in a randomized study. Capillary filtration rate was assessed by venous occlusion plethysmography, ankle edema by a new system called AET (ankle edema tester). Subjective symptoms of venous hypertension were assessed by an analogue scale line considering four symptoms: swelling sensation, restless lower extremity, pain and cramps, and tiredness. CFR, AC, and AE were significantly higher in patients in comparison with normal subjects. After 4 weeks of TTFCA treatment, there was a significant decrease of CFR, AC, and AET time in patients. This was also greater in the higher dose group. No significant change was observed in the placebo group and in normal subjects treated with TTFCA. Symptoms were also significantly improved in the two groups treated with the active drug according to the dose. No significant changes were observed in the placebo group. In conclusion, the improvement of signs and symptoms by TTFCA observed in patients with venous hypertension was well correlated with the improvement of CFR and ankle edema. Dose ranging showed that 180 mg/day is more effective in improving symptoms and CFR.

PMID: 11666125 [PubMed - indexed for MEDLINE]
link

Although there is much less stiffness in the leg today and yesterday on the lower ginkgo dose, I have noticed a slight return of asthmatic feelings which I haven't noticed at all since being on high dose ginkgo. I have also noticed about an hour ago a feeling of compression in the skull by the nose/sinus cavity. This is the same sensation I had when I went on a really high dose of ginkgo. I reckon that the sinuses are affected by the alterations in the blood flow and that it is reverting to as it was before high dose ginkgo.
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 » Tue Oct 28, 2008 3:07 am

Wow, the combination of lower doses of ginkgo and salvia is fantastic. My leg is so much less stiff it's quite extraordinary. I have just done my 5 minute 400meter walk to and from the shop and I have no tingles on sitting down. Standing up is much easier with much less stiffness. Today I have taken the same as yesterday, with 2x 120mg of ginkgo and 2x 600mg pills of salvia before breakfast. I shall repeat before lunch and supper and last thing at night. Even this may be too much! I may reduce the ginkgo to just one pill before each meal and last thing at night. I have today less feeling of head compression, at least for the moment. Last night I had some pain in the legs and some spasms which went after an extra dose of curcumin.

I'm pleased to see that a burst blood vessel on my left cheek has disappeared. Several years ago in a fit of vanity I tried to zap it with some kind of laser treatment which seemed to make it all the worse. Guess, I should have just gone to see the Chinese herbalists!

30/10/08
I have noticed since reducing the dosages that the night leg pain has made a bit of a return as have the spasms. I think I may start having a larger dose in the evening and will increase the salvia to 1.8g before supper this pm to see if this improves things.

I'm also rather sad to note, after my experience of the last 2 days and, frankly, of these last 4.5 years, that alcohol disrupts the vasculature in some way too. Whenever in the past I have drunk rather too much alcohol and am sobering up I get quite bad spasms. I think that when ethanol is in the system it acts as a vasodilator which is good but that its after-effects are that of vasoconstriction. I see on pubmed that ethanol has variable effects on the vasculature and this is a problem.
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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