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In the video
the benefit claimed for Daflon 500 is that it inhibits adhesion of leukocytes to the endothelium. That protects capillaries and valves according to the video. Daflon may be a vasoconstrictor but no mention is made of that in regard to the benefits it provides. The action of the leukocytes in the capillaries sounds like it could explain the autoimmune action of MS. Stopping that seems like a good idea, as does protecting the valves. Also I have to point out that Daflon 500 was given to Ginger, a woman who suffers from CVD, CCSVI and MS, with no adverse effects.

BTW most folks at this website are not opposed to ideas which are contrary to the mainstream medical view. If they were this forum on CCSVI would not exist.

David1949 wrote:In the video ... e=youtu.be the benefit claimed for Daflon 500 is that it inhibits adhesion of leukocytes to the endothelium. That protects capillaries and valves according to the video. Daflon may be a vasoconstrictor but no mention is made of that in regard to the benefits it provides. The action of the leukocytes in the capillaries sounds like it could explain the autoimmune action of MS. Stopping that seems like a good idea, as does protecting the valves. Also I have to point out that Daflon 500 was given to Ginger, a woman who suffers from CVD, CCSVI and MS, with no adverse effects.

BTW most folks at this website are not opposed to ideas which are contrary to the mainstream medical view. If they were this forum on CCSVI would not exist.

Nice post and great video. Whether Daflon 500 can help us or not, that's a great video demonstration of CSVI - at least a sister condition to CCSVI. I think Journey Into The Veins is a must see. Two thumbs way up! I think this is a better link though.

Bethr wrote: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?

http://www.ncbi.nlm.nih.gov/pubmed/21870429

It protects against ischemic reperfusion cerebral injury in rats.
We seem to be subject to ischemic-like injury, including possibly reperfusion injury, in CCSVI in MS.

Hesperidin also has a role in building or maintaining connective tissue. Not sure exactly.

I just spoke to someone from the company, Servier, (1-800-663-0839) that makes Daflon and was told, it is not available here in Canada. She suggested I ask my doctor for a sample.

Jugular thanks for pointing out the problem with my link. I fixed it now.

The fact it is not available here does not surprise me.

More on gravity: Cece I think was saying that the valves are different in the legs. Venous blood is normally going down from the brain, and up from the legs. Reflux is assisted by gravity in the legs, and opposed by it in the brain. Come to think of it, anything below heart level is the same way. Above the heart, though, if reflux happens it is against gravity, and toward the capillary bed. The shape of lesions shows something like that is happening. The blood-brain barrier, near sites of lesions, is being damaged when refluxed blood reaches it. If there are lesions below heart level they would be assisted by gravity and be shaped differently, because reflux would be from valves failing to hold the blood up, and would be more forceful than above the heart. In the legs, the thoracic or other pump is not necessary for reflux, because reflux is assisted by gravity. The same is true anywhere below the heart. (Everything changes in prone posture. Maybe that is why we sleep lying down: to recover from walking upright.)

Only because of the very low blood pressure in veins is reflux even possible without force from the heart, when gravity is draining the blood.

The fact that veins are in the middles of lesions makes perfect sense if they are being caused by refluxing blood.

It also makes sense to me that the action of Daflon on valves in the legs might be more beneficial for leg valve failure. It still might do some good for those above-the-heart valves, even though their failure might be worse below the heart.

Referring to the video

At approximately 1:30 into the video it explains how leukocytes can damage the endothelium. And at 2:50 it shows the leukocyte penetrating the endothelium of the capillary. If this happens in the brain it would cause a breach in the blood brain barrier. That’s the first thing that has to happen before an autoimmune attack on myelin can occur.

Yes it’s true that in the leg the valve fails open which results in higher pressure below the valve. But in CCSVI the valve fails shut which results in higher pressure above the valve. In either case the capillaries are exposed to higher pressure.

David1949 wrote:Referring to the video

At approximately 1:30 into the video it explains how leukocytes can damage the endothelium. And at 2:50 it shows the leukocyte penetrating the endothelium of the capillary. If this happens in the brain it would cause a breach in the blood brain barrier. That’s the first thing that has to happen before an autoimmune attack on myelin can occur.

That was one of the first intriguing things about CCSVI theory for me, that it actually explained the BBB breach.

Yes it’s true that in the leg the valve fails open which results in higher pressure below the valve. But in CCSVI the valve fails shut which results in higher pressure above the valve. In either case the capillaries are exposed to higher pressure.

Yes, and it fits with Dr. Tucker's ideas on reflux causing focal points of high pressure where the two waves (refluxing wave and incoming wave) combine.

The difference when it comes to medication is that a vasoconstrictor that helps tighten up veins to help them work against gravity may help the situation in the legs, but it does not seem as applicable in the neck in CCSVI. We do not want our neck veins any more constricted than they already are.

We do not want our neck veins any more constricted than they already are.

I read you well Cece; but if in the same process; the veins does not permeate (percolate or whatever); the result might still on the positive side?

Cece wrote:

David1949 wrote:Referring to the video

At approximately 1:30 into the video it explains how leukocytes can damage the endothelium. And at 2:50 it shows the leukocyte penetrating the endothelium of the capillary. If this happens in the brain it would cause a breach in the blood brain barrier. That’s the first thing that has to happen before an autoimmune attack on myelin can occur.

That was one of the first intriguing things about CCSVI theory for me, that it actually explained the BBB breach.

Yes it’s true that in the leg the valve fails open which results in higher pressure below the valve. But in CCSVI the valve fails shut which results in higher pressure above the valve. In either case the capillaries are exposed to higher pressure.

Yes, and it fits with Dr. Tucker's ideas on reflux causing focal points of high pressure where the two waves (refluxing wave and incoming wave) combine.

The difference when it comes to medication is that a vasoconstrictor that helps tighten up veins to help them work against gravity may help the situation in the legs, but it does not seem as applicable in the neck in CCSVI. We do not want our neck veins any more constricted than they already are.

With Daflon 500 mg, is the vasoconstrictor effect seems to be a small part of its mode of action and may not be a bad thing for us, perhaps?

Here is an article about Daflon 500 in phlebolymphology.org:

http://www.phlebolymphology.org/2009/11 ... on-500-mg/

In particular:

THE MECHANISM OF ACTION OF VENOACTIVE
DRUGS AND MPFF (DAFLON 500 MG)

Most venoactive drugs prolong the vasoconstrictor effect of noradrenaline on the vein wall, increasing venous tone, and thereby reducing venous capacitance, distensibility, and stasis. This increases the venous return and reduces venous pressure in patients suffering from CVD. Studies of the mechanism of action of MPFF have shown that it prevents or delays the occurrence of CVD by: (i) increasing venous tone (this results in restoration of normal blood flow, dispersion of red cell aggregates, and better oxygenation); (ii) improving capillary hyperpermeability and lymph flow thus protecting the microcirculation and decreasing the risk of edema; and (iii) inhibiting leukocyte adhesion to endothelial cells and the transmigration of leukocytes into the venous wall (an effect seen only with MPFF).

Apart from the ? that something that increases venous return in our legs may do the opposite to our heads, it seems to be targeted at the same sort of underlying pathology that may be causing us grief.

For more than 10 years it has been accepted that CVD is related to a primary failure of venous valves that are affected by inflammation.15,16 As a result, guidelines now mention that early pharmacological treatment directed towards preventing or inhibiting the inflammatory response at all stages of the disease may play a significant role in preventing or slowing the development and recurrence of the signs and symptoms of CVD.26 Key findings were those provided by the rat fistula model of venous hypertension with MPFF.15 In this model, venous hypertension caused by a femoral arterial-venous fistula resulted in the development of venous reflux and an inflammatory reaction in venous valves. In animals treated with MPFF there was a significant, dosedependent reduction in the reflux rate. MPFF also inhibited the expression of the endothelial cell adhesion molecules P-selectin and ICAM-1, reduced leukocyte infiltration, and decreased the level of apoptosis in the valves in a dose-dependent manner. These data suggest that in the rat model of venous hypertension, MPFF delays the development of reflux and suppresses damage to the valve structures by decreasing the interaction between leukocytes and endothelial cells.

And then there is the conclusion:

As a consequence of these findings, the most recent guidelines on the management of chronic venous disorders of the lower limbs have expanded the recommendations for the use of venoactive drugs following the realization that the beneficial effects of these agents is not just due to their effects on venous tone.

Maybe we're over-focused on vasoconstriction. Aspirin is also a vasoconstrictor, and yet it is sometimes prescribed as a long term means of preventing blood clots following venoplasty. The benefits outweigh the disadvantages.

With Daflon 500 the benefit is that it reduces adhesion of leukocytes to the endothelium. Now I'm not recomending that anyone run out and buy bootlegged Daflon to try it out. I'm just a jive engineer, not a doctor. But I think Daflon makes a good topic for discussion.

Yes, that is really interesting about the leukocyte adhesion reduction.

I also keep thinking in terms of pre-CCSVI treatment but we might need medications for post-CCSVI treatment. But what would they be?

Jugular, THANK YOU for keeping the ball rolling on digging up information. This reminds me of these first years when CCSVI was just becoming known, and lots of people would find--and still are finding--current and old research that would help support the theory of CCSVI.

We need more people to help search for information on Daflon -- I always thought we need to know how strong or weak Daflon's vasoconstriction effect is on veins...

Cece wrote:I would think that a vasoconstrictor would hurt, not help, us.

We haven't yet seen any scientific data that shows just how strong or weak Daflon 500 is as a vasoconstrictor--if you know of any such data, please share, thank you!

When you say "us" in the quote above, we need to differentiate between (what I call) "Valvular CCSVI" (annulus and leaflet stenoses) which comprises the MAJORITY of cases and "Non-Valvular CCSVI" which comprises the minority of cases (e.g., vein wall, high jugular, and compression stenoses).

Since the majority of pwCCSVI has stenoses of the valves, the important anti-valvular remodeling effect of Daflon has the potential to help a great many MS/CCSVI patients. The truth could be that the many beneficial effects of Daflon far outweigh its vasoconstriction effect. We just don't know yet how the cards will fall.

We should keep trying to find and critique scientific data before turning away too quickly from this promising compound that's easy to take and inexpensive ($.36/pill). Daflon 500 could be a very powerful adjunct to CCSVI procedures.

Just think of what this could mean--inhibition of a PROGRESSIVE INCREASE in valvular remodeling. In the history of CCSVI, has anything else like Daflon 500 ever been found that already has been shown in an animal study to decrease annular remodeling???

Hypothetical example:
Four months ago, Patient Y, who has "Valvular CCSVI," had her first CCSVI procedure with both IJV valves angioplastied. Improvements were short-lived. Her second procedure was done today with both IJV valves found to be 60% restenosed. Her IJV valves were angioplastied again, BUT THIS TIME, the patient will take Daflon to help slow/stop valvular remodeling and its associated reflux. After consultation with her doctor about all supplements, the patient will also take the vasodilators quercetin and bromelain to help offset whatever the vasoconstriction effect is of Daflon.

Patient Y could easily be you, Cece. The possibility of forestalling a third procedure or maybe even preventing one with Daflon is worth at least some amount of time spent investigating the compound before dismissing the possibility that the benefits of Daflon might outweigh its risk.

Cece, I'm very surprised you're not much more excited about Daflon, especially considering the above hypothetical. I'd love to see a study done immediately to answer the question of whether or not Daflon's anti-valvular remodeling benefit plus all its other benefits outweigh whatever its vasoconstriction effect might be.

I'd volunteer in a heartbeat for such a study because I have "Valvular CCSVI" with valvular restenosis that the anti-valvular remodeling of Daflon might slow/stop--I really don't want to have a third, or fourth, or fifth, or more procedures.

Patient Y is also benefiting from CCVBP (aka UCC) to relieve pressure on and compression of nerves, arteries, and veins which results in her benefiting from a multipronged strategy for a multifactorial disease that would look like this: 1) CCSVI venoplasty to decrease venous insufficiency and reflux, 2) Daflon 500 to decrease valvular remodeling and reflux, and 3) UCC to correct Atlas misalignment for proper CSF flow and decompression of nerves, arteries, and veins.

CCSVI had given me hope and several good improvements, but I restenosed six months after each valvuloplasty.

UCC still gives me hope because my properly adjusted Atlas resulted in a "notable" increase in my CSF flow and because my numb feet and 'MS' Hug symptoms are greatly relieved, 100% and 75%, respectively. I remain hopeful for even more improvements as time continues.

Daflon 500 is giving me a measure of new hope for my venoplastied IJV valves. Wish me luck with my Daflon 500 literature review (good links gladly accepted!) because the majority of pwCCSVI might benefit greatly and that thought alone, imo, is worth my effort.

If Daflon doesn't pan out, I'll continue to look for more hope and help for my ongoing neurological symptoms.

Cece, help us research this compound. Look at all the information that has been found so far--let's go find more! Let the hunt continue!

Edit in red

I always admire good writing, HappyPoet. Great post.

I wonder if anti-valvular remodeling means what you are suggesting. Yes, let's dig deeper.

I think I am still recovering from vacation and the start of the school year, I've missed half of this conversation and not understood the excitement.

HappyPoet wrote:If Daflon doesn't pan out, I'll continue to look for more hope and help for my ongoing neurological symptoms.

Amen brother.

Success is the ability to go from one failure to another with no loss of enthusiasm.

- Sir Winston Churchill