This Is MS Multiple Sclerosis Knowledge & Support Community

"hesperidin and its glycoside derivative diosmin have been the subject of extensive research for their potential to enhance vascular tone and facilitate circulation." 500 mg of diosmin and 100 mg of hesperidin, is called Diosvein by Swanson, and available on Amazon, without prescription.

It shows the general public in which direction the truth really lies.

As another example, under the presumption that reflux is worse when I put my head down, I have found that I'm dizzy to the point of falling in the shower, if I bend down with my head down. But I can do the same thing with no trouble, if I keep my neck straight and have my head up all the time. I believe the heat of the shower is making my blood thin enough that if I put my head down, venous blood will slow down or maybe reflux in my head, and that is what is making me dizzy.

Stuff like this, to me, feels like it reinforces the CCSVI story.

Hi Dania, Hi All,

This is a facinating thread!!

While reading the Sept/Oct AARP magazine this evening there I noticed there was an ad on page 69 for Vitacost.

It say’s for NEW customer’s of Vitacost there is a $10.00 Discount if you purchase $50 or more. The add says to enter the Promotional code MA94AR Plus it’s giving Free Shipping on orders over $49.

I hope I don’t sound like a commercial. It’s just that I LOVE a DEAL and I HATE paying for shipping!!! So I thought I’d pass this information along.

So sounds like a win/win situation for anyone who’s never used them and is in the market for supplements at the moment. Oh yeah, the offer is good through 9/30/11

Lora

I will also check the pro & cons mof taking Daflon with my doctor and post his answer.

One thing i've read in the Daflon info is that you can use it for maximum 3 months, why?

Robnl wrote:I will also check the pro & cons mof taking Daflon with my doctor and post his answer.

One thing i've read in the Daflon info is that you can use it for maximum 3 months, why?

Oh, no longer than 3 months and than you have to contact your doctor about longer use

I'm surprised that no one has made this connection before. Here is a link to a very informative Journal devoted to the venous valve and primary chronic venous disease.

http://www.medicographia.com/wp-content ... phia95.pdf

If we are operating on the theory that our MS is affected by venous hypertension of our cerebral veins then treatment effective on the same condition in the legs should naturally be considered.

I found this piece on p 149 "Daflon 500mg: Protective Against Venous Valve Failure" to be illuminating.

Perhaps this therapy, proven effective on CSVI elsewhere in the body, can help us get a "leg up on things" with our CCSVI? What I like about what I'm reading about Daflon so far is that it seems to be a relatively benign drug with few side effects and interactions that seems to be pretty effective.

Anecdotal evidence please STAT!

Jugular, wonderful find! I love posts that inform us. Knowledge is power and we are better equipped to make decisions. In that link it says that the valves are a problem. Dr Arata is convinced of this. Which comes first the venous hypertension which causes the valve problem? Interesting question. We know more now than when news came out with Dr Zamboni's discovery.

I think this is one case where real evidence is most required before the pw"MS" get really stoked.

The stuff does not sound as aggressive as Tysabri in its effect on leukocvte adhesion to the BBB, if it even has that effect, plus it does not modify leukocyte migration, but it is an anti-oxidant.

If it sounds too good to be true, is it? Sounds like it works really well on leg veins, but jugulars? azygus? Deep cerebrals? What if it works on veins with smooth muscles, but not on cerebral veins, because they don't have any? A lot of unknowns. Why 3 months? Side effects?

Wow, Jugular! Thank you!

The Venous Valve and Primary Chronic Venous Disease Journal, a French publication, is a must-read for all IRs doing valvuloplasty procedures. Unfortunately, some articles are written in French and need to be translated (I use Google-Translate, fwiw).

The Editorial to the Journal is titled, "Venous valve incompetence: the first culprit in the pathophysiology of primary chronic venous insufficiency" and was written by Dr. John Bergan of The Vein Institute of La Jolla Department of Surgery UCSD School of Medicine which is the same institution that conducted the Daflon 500 valve remodeling animal study (that I linked to) in which Dr. Bergan just so happens to be a named author.

I wonder if Dr. Bergan is still at UCSD? His email address is listed in the Journal as jbergan@ucsd.edu We need to find out if he's heard about CCSVI, and if not, we need to enlighten him. Perhaps someone from CCSVI Alliance could initiate contact with him? Maybe Dr. Hubbard (of San Diego, U.S.) might be interested in talking with him or with other doctors in the University of California at San Diego School of Medicine.

~~~~~~~~~~

ALL THE ARTICLES in the Journal are terrific and provide a very thorough overview of venous valves. Articles from embryology to venous disease in childhood to triggering mechanisms of venous valve incompetence to Daflon 500 to more areas of this research are covered. Read the Table of Contents -- it's extraordinarily comprehensive.

Dr. Françoise Pitsch of France wrote the terrific article, "DAFLON 500 MG: PROTECTIVE AGAINST VENOUS VALVE FAILURE" from which the below paragraph was taken:

Dr. Françoise Pitsch wrote:In most cases, venous hypertension is caused by reflux through incompetent venous valves.7 Examination of surgical specimens removed from limbs with chronic venous insufficiency and, more recently, the direct observation offered by angioscopy, has revealed lesions involving the venous wall, the valvular annulus, and the valve cusps.8,9 Failure of the valve and its annulus is responsible for progression of the disease via maintenance and further increase of venous hypertension. Immunohistochemical studies using monoclonal antibodies specific for monocytes and macrophages have demonstrated monocyte/macrophage infiltration into the valve leaflets and venous wall of patients with varicose veins (CEAP Class 2).10 Monoclonal antibody studies have found that leukocyte infiltration is greater within the base of the valve leaflets and in the proximal venous wall. Venous valves have been found to be prominent in regions of low shear stress with venous eddies and recirculation.11 It may be that these phenomena explain how the leukocytes are preferentially deposited in these regions.

I wonder if the "venous eddies" are the same as Dr. Sclafani's "funnels."

~~~~~~~~~~

Dr. G. W. Schmid-Schönbein of the U.S. (UCSD School of Medicine) wrote the terrific article, "Triggering mechanisms of venous valve incompetence" from which the below paragraph was taken:

G. W. Schmid-Schönbein wrote:A key event in CVD is the loss of the ability to properly close venous valves. Failure of valves may be brought about by dilation of the venous wall and the valvular annulus with remodeling of the valve leaflets, bulging and stretching of valve leaflets, commissural dilation, shortening, tearing and perforation of leaflets and, finally, complete destruction of the valve.31,32 Furthermore, ultrastructural and immunohistochemical studies of valves and the venous wall have revealed the presence of leukocytes adhering and transmigrating into the venous wall.17,33 The leukocyte infiltration of the venous parenchyma is accompanied by remodeling of the extracellular matrix, a process that may in part be responsible for the destruction of venous valves.

I could continue copying important sections from the Journal articles, but I'll stop here with the hope that everyone will read all the articles.

@happy poet, do not be concerned of the french, what you read was then translated into french.
But the idea of emailing the doctor is a great idea. Just found that he has retired from this clinic.
http://www.lajollaveincare.com/research/

thank you cheerleader, Dania, Jimmylegs..
this is great news. Since my venoplasty, mid June, my legs seem weaker and heavier(stamina improved, balance seems worse). Maybe Daflon or Zinc could help.
Does Daflon help with pain?? I have pain also and much pain in my calves.

Medicines can be very dangerous. This thread appears to recommend an over the counter medicine for pwMS who have CCSVI.
The papers quoted have used Daflon 500 for CVI not CCSVI. The drug is being used as a periferal vasoconstrictor not central vasodilator.

My professional advice is that pwMS do not use Daflon 500 unless it is under the supervision of a fully insured healthcare professional.

MarkW

MarkW wrote:under the supervision of a fully insured healthcare professional.

When I first read this sentence I thought the word that would follow "fully" would be "qualified," but your "fully insured" made me laugh a bit.

I completely agree with you. Each pw'MS' should consult with their fully qualified and fully insured doctor before taking Daflon 500.

If Daflon 500 is such a powerful vasoconstrictor, I'm surprised they would have even studied the drug in an effort to help combat venous hypertension. I wonder if the doctors who participated in the animal study felt that the vasoconstriction effects of Daflon 500 were mild enough not to matter or would not matter for some other reason. Would love to know what these doctors think of CCSVI. Hopefully someone will contact Dr. Bergan.

HappyPoet wrote:

Dr. Françoise Pitsch wrote:In most cases, venous hypertension is caused by reflux through incompetent venous valves.7 Examination of surgical specimens removed from limbs with chronic venous insufficiency and, more recently, the direct observation offered by angioscopy, has revealed lesions involving the venous wall, the valvular annulus, and the valve cusps.8,9 Failure of the valve and its annulus is responsible for progression of the disease via maintenance and further increase of venous hypertension. Immunohistochemical studies using monoclonal antibodies specific for monocytes and macrophages have demonstrated monocyte/macrophage infiltration into the valve leaflets and venous wall of patients with varicose veins (CEAP Class 2).10 Monoclonal antibody studies have found that leukocyte infiltration is greater within the base of the valve leaflets and in the proximal venous wall. Venous valves have been found to be prominent in regions of low shear stress with venous eddies and recirculation.11 It may be that these phenomena explain how the leukocytes are preferentially deposited in these regions.

I wonder if the "venous eddies" are the same as Dr. Sclafani's "funnels."

I think it's more the opposite. A funnel in CCSVI is when the healthy vein wall narrows like a funnel to the point where the stenosis is constricting flow. This makes it look like the healthy vein wall is stenosed when it is not. An eddy as described here sounds like a pooling of blood, not a narrowing.

Still very interesting. I agree with MarkW about seeing your doctor for guidance on prescriptions. I would think that a vasoconstrictor would hurt, not help, us.

http://ang.sagepub.com/content/52/1_suppl/S27.short
New Advances in the Understanding of the Pathophysiology of Chronic Venous Insufficiency

Geert W. Schmid-Schönbein, MD, PhD

Shinya Takase, MD

John J. Bergan, MD

Abstract

Chronic venous insufficiency (CVI) is inseparably linked to elevated venous pressure and is accompanied by vascular, dermal, and subcutaneous tissue damage and restructuring. Abundant evidence exists both in humans and in experimental models to suggest that the tissue damage may be initiated by generation of an inflammatory reaction. inflammatory indi cators include elevation of endothelial permeability; attachment of circulating leukocytes to the endothelium; infiltration of monocytes, lymphocytes, and mast cells into the connective tissue; and development of fibrotic tissue infiltrates and several molecular markers, such as growth factor or membrane adhesion molecule generation. Indicators of an inflammatory reaction are already detectable at early stages of CVI and may be involved in the development of primary venous valve dysfunction. One of the important questions is to identify trigger mechanisms for the inflammatory reaction in CVI. Current evidence suggests that, among several possible mechanisms (hypoxia, humoral stimulation), a shift in fluid shear stress from normal physio logical levels and endothelial distension under the influence of elevated venous pressure may serve as trigger mechanisms for inflammation.

The other component in Daflon 500 is Hesperidin, which is a vasodilator I think.
It's a citrus derived flavanoid, and is highly anti-inflammatory, anti-oxidant and a
powerful iron chelator, and some studies have shown it crosses the BBB.
It has been shown to help with metabolic syndrome, diabetes, stroke, haemarroids,
and varicose veins.

Does anyone have more info on hesperidin?