This Is MS Multiple Sclerosis Community: Knowledge & Support

EAY to swallow supplement for those of us who tend not to like Tumeric in our food. A I was advised you can't take too much & it is GREAT for inflamation - I take this supplement a couple of times a day -Relegious!y Highly reccomend it to EVERYONE and yes - when I am excerbating - it turns this around - soo cool so affordable!

Has anyone experienced bladder problems while on green tea, and how did you get around this issue?

I have a supplement regime and have added green tea capsules to it on two occasions. On both of those occasions - they were years apart- I nearly immediately had a sharp increase in frequency and retention to the point where I needed to ICT at night. Within 3 days of stopping the green tea extracts the bladder went back to normal (for me!). I always took the green tea capsules in the morning.

Obviously I don't want to add to an already problematic MS bladder, but I DO want to add the benefits of green tea.

My supplements are:

6 x fish/epo capsules
1-2g vitamin c
Vitamin D3 - 4000IU
Cal/mag tablet +250g extra Mag
Multi-vitamin
4 x high acidophilous tablets
Ginkgo biloba (added this week)

Intermittantly:
Niacin
Zinc

_________________
~~~~~~~~~~~~~~~
Concussus Resurgo
~~~~~~~~~~~~~~~
RR-MS dx 1998 and Coeliac dx 2003
~~~~~~~~~~~~~~~
Copaxone, Cymbalta. EPO, Fish Oils, Vitamin D3 2000 IU daily, Cal/Mag/Zinc, Multivitamin/mineral, Co-Enzyme Q10, Probiotics, Milk Thistle.

After trying several times I have realised that green Tea actually makes me worse. i don't know if its because I am allergic to it or something but I get an increase of symptoms and new symptoms similar to a relapse everytime I drink it. I have tested this out on 3 different occasions.

I am drinking red clover tea and milk thistle tea now which seemto be helping me.

I would strongly suggest you drop STOP the Ginkgo biloba and replace it with some VINPOCETINE 10 mg treee times a day. It helps the voiding problem and it cures MS, makes you very smart and cures several other minor diseases.

Details and many boring abstracts/studies can be provided if requested.

I would prefer you do some of your own research at http://www.pubmed.gov

jackD

Thanks LR interesting to hear you also had a problem with green tea. I too have dropped it for the moment. Perhaps that's where it will stay for us! - I also take milk thistle extract every second week.

Jack D I am sure the moderator will remove your spam post.

_________________
~~~~~~~~~~~~~~~
Concussus Resurgo
~~~~~~~~~~~~~~~
RR-MS dx 1998 and Coeliac dx 2003
~~~~~~~~~~~~~~~
Copaxone, Cymbalta. EPO, Fish Oils, Vitamin D3 2000 IU daily, Cal/Mag/Zinc, Multivitamin/mineral, Co-Enzyme Q10, Probiotics, Milk Thistle.

JackD
I have read only a little on vinpocetine--will now do more research--but i do recall it says the 5 mg dose, once per day is best--for some reason, too much is bad--I will check further and post when find more info, but wanted you to be aware of this

and from the little i had read, it is a relatively new supplement, whereas Ginko has been around for 1000's of years in the chinese herbals--so there is a much longer track record, including postives and negatives, for Ginko than for vinpocetine.

If you have info at hand, would appreciate some posts on it.

Have fun with that research. I have lots of info on Vinpocetine.

That 5 mg mg dose is a joke. It must be part of the ad for the product. I.e To justify what they have for sale.

I guess if one was 100% healthy and was just taking it for some kind of wierd health insurance kind of thing that would make some limited sense.

30 mg per day is the standard therapeutic dose for almost all the conditions that it is reported to be of benefit.

Vinpocetine comes from the seeds of the PERIWINKLE plant family (Vinca minor to the flower people)

It has a VERY VERY VERY long history.

Periwinkle was listed as a medicinal agent in the De Materia Medica of the Greek physician Pedacius Diosorides, published during the first century.

I also have lots of VERY negative things to say about Ginkgo biloba. Basically it does not play well with other medications.

In fact it causes bleeding and strokes when taken with some other VERY common supplements. I have several ex-friends who did not believe me. Some are now dead STROKE! and some are "post stroke" that I just no longer keep in contact with.

I will post much more later tonight.

jackD

There is no doubt that Ginkgo biloba and Vinpocetine are very similiar in the good effects they have on a number of things.

I feel that Ginkgo biloba is probably quite safe and effective when taken as a sole agent for a number of things.

However MS folks tend to take many supplements that may bring out the dark side of Ginkgo biloba.

When you add a couple grams of omega-3s and some Vitamin E and and an aspirin plus a number of other innocent supplements the bleeding index goes off-the-scale.

The main point I am making is that Vinpocetine does the same good things and it's mechanisms of action is VERY VERY favorable to the MS condition.
Using it in place of Ginkgo biloba would make a lot of good sense as I will explain below.

The #1 positive thing about Vinpocetine is that it is a Phosphodiesterase inhibitor(Type I). Several Phosphodiesterase inhibitors(type IV) have been shown to be a very effective treatment for MS. However the side-effects were terrible.

There is new Phosphodiesterase inhibitor that was in the medical news that is under review as a treatment for MS based upon some good initial testing results.

The #2 great thing about Vinpocetine is it is a calcium channel regulator which reduces glutamate neurotoxicity and thus protects neurons from excess glutamate produced in MS brains.

In Europe Vinpocetine is the drug Cavinton.

One odd fact is that Vinpocetine is actually a derative of the alkaloid vincamine. Vinpocetine has much less side effects to vincamine and is twice as powerful.

jackD

I found? this little note on my old hard drive and will try to get more info.

jackD


VINPOCETINE HELPS MS PATIENTS
Exciting research with vinpocetine has been conducted on patients with multiple sclerosis. MS is a disease in which neural signals from the brain to the target muscle groups are obstructed because sclerotic plaques form in multiple locations along the nerve fibers and interrupt the signal transmission. As a result, the muscles weaken, and MS patients are often tired. In the later stages of the disease, they are often unable to walk, and they lose other motor skills as well.

MS patients treated with phosphodiesterase inhibitors, or PDEIs (see the sidebar for a description of phosphodiesterases and their inhibitors), exhibit a dramatic decrease in relapse rate.5 In a study published in the journal Multiple Sclerosis, 12 patients were treated with a cocktail of three different PDEIs, including 15 mg/day of vinpocetine, for an average of 499 days (1.4 years). The other two ingredients were the anti-Alzheimer's drug propentofylline and the antiasthma drug theophylline.

"Vinpocetine has the most clinical
promise for the management of
vascular insufficiencies
involving the brain."

Before the treatment, the patients averaged 3.1 relapses per year. During the treatment period, however, the incidence of relapses was much lower: only 0.92 per year. Seven of the 12 patients reported no relapses during the treatment period, three had a decreased incidence of relapses, and two had the same incidence as before. Since there were two other ingredients in the treatment formula, one can't say that vinpocetine alone was responsible for these results, but it likely played an important role in reducing the patients' relapse rates.

Another reason I take Vinpocetine is to help with my MS bladder problem. It really helps the rate of flow. It seems to help the smooth muscles contract in a more efficient (non-spastic manner).

jackD

World J Urol. 2001 Nov;19(5):344-50.

Phosphodiesterase 1 inhibition in the treatment of lower urinary tract dysfunction: from bench to bedside.
Truss MC, Stief CG, Uckert S, Becker AJ, Wefer J, Schultheiss D, Jonas U.

Urologische Klinik, Medizinische Hochschule, Hannover, Germany. truss.michael@mh-hannover.de

Anticholinergic drugs are currently the therapy of choice to treat urgency and urge incontinence. However, muscarinergic receptor blockers with adequate selectivity for detrusor smooth muscle are not available. Also, in contrast to the normal detrusor, the unstable detrusor neurotransmission seems to be at least partially regulated by non-cholinergic (NANC) pathways. These factors may explain the common side effects and the limited clinical efficacy of these compounds. Specific modulation of intracellular second messenger pathways offers the possibility of organ selective manipulation of tissue function, specifically contraction and relaxation of smooth musculature. Because of their central role in the intracellular regulation of smooth muscle tone phosphodiesterases (PDEs) are an attractive pharmacological targets. The PDE 5 specific inhibitor sildenafil (Viagra) has revolutionized the treatment of patients with erectile dysfunction. Numerous other PDE inhibitors are currently under investigation for the treatment of various disorders. We investigated the role of PDEs in human detrusor smooth muscle. Our data demonstrate the presence of five PDE isoenzymes in human detrusor and suggest, for the first time, that the cAMP pathway and the calcium/calmodulin-stimulated PDE (PDE 1) are of functional importance in the intracellular regulation in this tissue in vitro.

In addition. initial clinical data with the PDE 1 inhibitor vinpocetine in patients not responding to standard anticholinergic therapy indicate a possible role for vinpocetine in the treatment of urgency, urge incontinence and, possibly, low compliance bladder and interstitial cystitis.

The results of a larger randomized, double-blind, placebo-controlled, multicenter trial with vinpocetine show a tendency in favor of vinpocetine over placebo; however, statistically significant results were documented for one parameter only.

This might be due to the rather low dosage chosen and the small sample size. Further studies are necessary and currently underway to delineate the optimal dosage, indications and patient population. Modulation of intracellular key enzymes effecting second messenger metabolism, i.e. isoenzyme-selective PDE inhibition is a novel approach which possibly avoids the limitations of anticholinergic therapy in patients with lower urinary tract dysfunction.

PMID: 11760783 [PubMed - indexed for MEDLINE]



World J Urol. 2000 Dec;18(6):439-43.

Initial clinical experience with the selective phosphodiesterase-I isoenzyme inhibitor vinpocetine in the treatment of urge incontinence and low compliance bladder.

Truss MC, Stief CG, Uckert S, Becker AJ, Schultheiss D, Machtens S, Jonas U.

Department of Urology, Medizinische Hochschule Hannover, Germany. truss.michael@mh-hannover.de

Current pharmacological treatment modalities for urge incontinence and low compliance bladder are limited by a low clinical efficacy and the significant side effects of the standard drugs available.

Previous in vitro studies indicated a possible functional relevance of the intracellular phosphodiesterase (PDE)-1 isoenzyme in the regulation of human detrusor smooth muscle contractility.

We therefore investigated the effect of the PDE-1 inhibitor vinpocetine in nonresponders to standard pharmacological therapy. In 11/19 patients (57.9%) clinical symptoms and/or urodynamic parameters were improved.

Although these initial data are preliminary, they represent the first evidence that isoenzyme-selective PDE inhibition may be a novel approach to the treatment of lower urinary tract disorders.

PMID: 11204266 [PubMed - indexed for MEDLINE]

Here is the more techie stuff that explains HOW and WHY phosphodiesterase inhibitors like Vinpocetine help the MS condition.

#1 - suppresses the production of TNF-alpha and cytokines(mmp-9s).

#2 - promotes IL-10 production which lowers cytokines(mmp-9s)
Mult Scler. 1999 Apr;5(2):126-33.

jackD

Effects of phosphodiesterase inhibitors on cytokine production by microglia.

Yoshikawa M, Suzumura A, Tamaru T, Takayanagi T, Sawada M.

Department of Neurology, Nara Medical University, Kashihara, Japan.

Type III and IV phosphodiesterase inhibitors (PDEIs) have recently been shown to suppress the production of TNF-alpha in several types of cells.

In the present study, we have shown that all the types of PDEIs, from type I- to V-specific and non-specific, suppress the production of TNF-alpha by mouse microglia stimulated with lipopolysaccharide (LPS) in a dose-dependent manner.

Certain combinations of three different types of PDEIs synergistically suppressed TNF-alpha production by microglia at a very low concentration (1 microM).

Since some PDEIs reportedly pass through the blood-brain barrier (BBB), the combination of three PDEIs may be worth trying in neurological diseases, such as multiple sclerosis and HIV-related neurological diseases in which TNF-alpha may play a critical role.

Some PDEIs also suppressed interleukin-I (IL-I) and IL-6 production by mouse microglia stimulated with LPS.

In contrast, the production of IL-10, which is known to be an inhibitory cytokine, was upregulated by certain PDEIs.

The suppression of TNF-alpha and induction of IL-10 were confirmed at the mRNA level by RT-PCR. PDEIs may be useful anti-inflammatory agents by downregulating inflammatory cytokines and upregulating inhibitory cytokines in the central nervous system. (CNS).

PMID: 10335522 [PubMed - indexed for M

Vinpocetine is also a super antioxidant that reduces neuronal damage in pathological situations like Multiple Sclerosis.

jackD


Free Radic Res. 2000 Jan;32(1):57-66.

Synaptosomal response to oxidative stress: effect of vinpocetine.

Santos MS, Duarte AI, Moreira PI, Oliveira CR.

Department of Zoology and Faculty of Medicine, Center for Neurosciences of Coimbra, University of Coimbra, Portugal.

It has been suggested that reactive oxygen species (ROS) play a role in the neuronal damage occurring in ischemic injury and neurodegenerative disorders and that their neutralization by antioxidant drugs may delay or minimize neurodegeneration.

In the present study we examine whether vinpocetine can act as an antioxidant and prevent the formation of ROS and lipid peroxidation in rat brain synaptosomes. After ascorbate/Fe2+ treatment a significant increase in oxygen consumption (about 5-fold) and thiobarbituric acid reactive substances (TBARS) formation (about 7-fold) occurred as compared to control conditions.

Vinpocetine inhibited the ascorbate/Fe2+ stimulated consumption of oxygen and TBARS accumulation, an indicator of lipid peroxidation, in a concentration-dependent manner.

The ROS formation was also prevented by vinpocetine. Oxidative stress increased significantly the fluorescence of the probes 2',7'-dichlorodihydrofluorescein (DCFH2-DA) (about 6-fold) and dihydrorhodamine (DHR) 123 (about 10-fold), which is indicative of intrasynaptosomal ROS generation.

Vinpocetine at 100 microM concentration decreased the fluorescence of DCFH2-DA and DHR 123 by about 50% and 83%, respectively.

We conclude that the antioxidant effect of vinpocetine might contribute to the protective role exerted by the drug in reducing neuronal damage in pathological situations.

PMID: 10625217 [PubMed - indexed for MEDLINE]

I happen to know that one of the three PDEIs phosphodiesterase inhibitors was Vinpocetine because I got it from Nara Medical University, Medical Library. I will try to retreive it from my "dead" hard drive.

jackD


Mult Scler. 2000 Feb;6(1):56-8.

Drop in relapse rate of MS by combination therapy of three different phosphodiesterase inhibitors.

Suzumura A, Nakamuro T, Tamaru T, Takayanagi T.

Department of Neurology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-0813, Japan.

Phosphodiesterase inhibitors (PDEIs), when used in combination, synergistically suppress TNFalpha production by various cells and also suppress experimental demyelination at very low concentrations.

We conducted a pilot study to determine whether the combination of three PDEIs suppresses the relapse of MS at the usual therapeutic doses.

Of the 12 relapsing remitting MS, the mean relapse rate/year dropped remarkably (from 3.08+/-3.32 to 0.92+/-1.86) after PDEI treatment.

Seven out of 12 (58.3%) were relapse-free in the follow up period (499+/-142 days).

The combination of three PDEIs can be safe and useful strategy for the future treatment of MS. - 58

PMID: 10694847 [PubMed - indexed for MEDLINE]

Sorry but this just sounds too like a snake oil routine to me.
Cures MS!???


If anyone else would like to reply re. Green Tea and Bladder issues I'd very much like to hear your experiences.
Thanks[/quote]

_________________
~~~~~~~~~~~~~~~
Concussus Resurgo
~~~~~~~~~~~~~~~
RR-MS dx 1998 and Coeliac dx 2003
~~~~~~~~~~~~~~~
Copaxone, Cymbalta. EPO, Fish Oils, Vitamin D3 2000 IU daily, Cal/Mag/Zinc, Multivitamin/mineral, Co-Enzyme Q10, Probiotics, Milk Thistle.

The claim for "THE CURE FOR MS" is based upon the fact that the above study indicated the rate of lesion reduction with the three PDEIs (that included Vinpocetine) was 58%.

As I understand it the old BIG CRAB treatments showed only a 33% reduction at most.

I think any treatment that gets over a 50% reduction has a good claim to be a cure.

However I will confess that may be guilty of some, a tad, of HYPERBOLE in the claim. Maybe a big properly done study will find a 100% REDUCTION rate.

Since this is a supplement that will NEVER happen.

I will add that I take some Green Tea Extract.

I find that the LifeExtension Brand is quite potent and good.

I prefer their Decaffeinated MEGA GREEN TEA EXTRACT 98% Polyohenols 710.5 mg with 45% being EGCG 326.25 mg.

I also take a 200 mg L-Theanine capsule with it.

jackD

Theanine is an amino acid found in green tea that produces tranquilizing effects in the brain. In Japan, soft drinks and chewing gum are spiked with theanine for the purpose of inducing relaxation. Although theanine creates a feeling of relaxation, it doesn't shut down the brain. Studies on rodents show that theanine enhances the ability to learn and remember. By shutting off worry central, theanine appears to increase concentration and focus thought.
Theanine is different than kava-kava in that it doesn't cause drowsiness, just relaxation. Theanine increases GABA, while caffeine decreases it. GABA doesn't just relax, it also creates a sense of well-being. Theanine's ability to increase this brain chemical can literally put you in a better mood. Theanine also increases levels of dopamine, another brain chemical with mood-enhancing effects.

PROTECTING NEURONS
In studies on neurons in cell culture, theanine significantly reverses glutamate-induced toxicity. In vivo studies show the same effect in rodents. Glutamate-induced neuro-toxicity is a major cause of degenerative brain disease. Many Americans suffer from slightly elevated blood pressure, but don't know they have it. Chronic high blood pressure inflicts damage on the delicate cerebral vascular network and increases the risk of stroke. Theanine has been shown to help lower blood pressure.

Theanine readily crosses the blood-brain barrier . Studies show that theanine is a non-toxic, highly desirable mood modulator that can be enjoyed by everyone except babies.

Biol Pharm Bull. 2002 Dec;25(12):1513-8.

Neuroprotective effects of the green tea components theanine and catechins.
Kakuda T.

Central Research Institute, Itoen, Ltd, Shuzuoka, Japan.

The neuroprotective effects of theanine and catechins contained in green tea are discussed.

Although the death of cultured rat cortical neurons was induced by the application of glutamic acid, this neuronal death was suppressed with exposure to theanine.

The death of hippocampal CA1 pyramidal neurons caused by transient forebrain ischemia in the gerbil was inhibited with the ventricular preadministration of theanine.

The neuronal death of the hippocampal CA3 region by kainate was also prevented by the administration of theanine. Theanine has a higher binding capacity for the AMPA/kainate receptors than for NMDA receptors, although the binding capacity in all cases is markedly less than that of glutamic acid.

The results of the present study suggest that the mechanism of the neuroprotective effect of theanine is related not only to the glutamate receptor but also to other mechanisms such as the glutamate transporter, although further studies are needed.

One of the onset mechanisms for arteriosclerosis, a major factor in ischemic cerebrovascular disease, is probably the oxidative alteration of low-density lipoprotein (LDL) by active oxygen species. The oxidative alterations of LDL were shown to be prevented by tea catechins. Scavenging of *O(2)(-) was also exhibited by tea catechins.

The neuroprotective effects of theanine and catechins contained in green tea are a focus of considerable attention, and further studies are warranted.

PMID: 12499631 [PubMed - indexed for MEDLINE]