What's this "new" peptide we want to block?
It's called endothelin-1 or ET-1, and it's released by the astrocytes maintaining the endothelial layer of your blood brain barrier.
We've known about ET-1 for years. It's not only found in MS.
Endothelin-1 is raised in situations where there is endothelial distress. When endothelial cells are hurt by ischemia and oxidative stress, and nitric oxide levels are low. ET-1 creates vasoconstriction, is pro-inflammatory, pro-fibrotic and slows blood flow. Which would explain why it inhibits remyelination. Yet not one single press release on this exciting new MS discovery mentioned this important fact, or what causes ET-1 levels to be high in the first place.
As you might expect, plasma ET-1 levels are very high in ischemic stroke.
ET-1 released by astrocytes is seen after subarachnoid hemorrhage
Serum levels of ET-1 are used as a marker of cerebral ischemia
And Endothelin 1 serum levels are through the roof in people with MS----
The plasma ET-1 levels were, on average, 224% higher in the patients with MS than in the controls (p < 0.005). The mean ET-1 levels (mean +/- standard deviation [SD]) were 3.5 +/- 0.83 pg/mL (min 2.13, max 5.37 pg/mL) in patients with MS and 1.56 +/- 0.3 pg/mL (min 0.9, max 2.13 pg/mL) in healthy volunteers. Neither the different forms nor stages of MS had an influence on the results. The ET-1 level was also not correlated with the duration of the disease.
In fact, researchers have been looking at ET-1 for many years.
Here are some MS researchers that found that hypoperfusion in MS was related to ET-1 levels. They used an ET-1 inhibitor called Bosentan, which increased cerebral blood flow. (Bosentan is a high blood pressure medicine, which can be toxic to the liver.)
Why are MS researchers reticent to fully explore the connection of extracranial venous obstruction to hypoxic/ischemic conditions in the brain? I'm sure I don't need to reiterate this, but this ET-1 "breakthrough" may well be caused by Dr. Zamboni's discovery of restricted venous return.
The truth is, the best way to lower ET-1 levels might be to increase nitric oxide levels yourself.
High ET-1 levels are a sign that your nitric oxide supply is too low.
While we are waiting for that Breakthrough Drug! ™
here are some things you can do for free, on your own, to potentially increase your cerebral perfusion, remyelinate your brain, raise your NO levels and lower your ET-1 levels.
The present study suggests that exercise causes an increase in production of NO and a decrease in production of ET-1 in humans, which may produce beneficial effects (i.e., vasodilative and antiatherosclerotic) on the cardiovascular system.
EAT MORE FLAVONOIDS (fruits and veggies)
Epidemiological evidence demonstrates that diets rich in fruits and vegetables benefit heart and vascular health.(2–11) Molecularly, these beneficial effects of fruits and vegetables have been largely ascribed to their content in flavonoids. These compounds are synthesized in many edible plants and remain present when plants are processed to foods. Grapes and wine, cocoa and chocolate, black and green tea, and soy and soy-derived products, are among the most important sources of flavonoids in the human diet.
Dietary flavonoids, such as quercetin and (-)-epicatechin, can augment nitric oxide status and reduce endothelin-1 concentrations and may thereby improve endothelial function.
EAT MORE POLYUNSATURATED FATS (from nuts, seeds and fish)
Serum levels of ET-1 were positively correlated with saturated fatty acids (SFAs, r = 0.257; P = 0.025) and negatively correlated with polyunsaturated fatty acids (PUFAs, r = -0.319; P = 0.005). http://www.ncbi.nlm.nih.gov/pubmed/18702940
Here are some more ideas on how to address endothelial dysfunction. Always discuss any new health regimen with your own physician.
There are things we can control, and things we can't.
There are ways to boost your nitric oxide levels, lower you ET-1 levels and potentially improve your health. While researchers continue to look for ways to mediate the vascular connection to MS without mentioning or exploring the vascular connection to MS....