in the last 4 years, almost everytime i fly, i have some issues...some worse than others.
The study posted yesterday is very exciting new research into how MS lesions are formed. The researchers used autopsy brain material and performed a variety of tests to conclude that the injury to the brain was initiated and sustained by oxidative damage. They are not exactly sure why this is happening. But it is.
Why does this study matter?
It matters because it is yet another study showing that t-cells are reacting to cellular death in the brain. They are not initiating the damage. The immune system response is secondary. Oxidative stress comes first.
Now, for my theory, and the theory of many others looking at CCSVI--
If CCSVI is indeed the cause of MS, this is exactly what we would expect to occur in the MS brain.
CCSVI can create an hypoxic, or low oxygen environment in the brain, due to hypoperfusion (slowed blood flow through brain tissue.) This is very different than a stroke, or ischemic vascular event when there is an infarct, or a localized area of tissue death due to lack of oxygen. You'll note in the study that the researchers excluded brain tissue from their study where they could detect an infarct. Diffuse cerebral hypoxia is a slower event. It is harder to quantify, because it takes longer for damage to accrue. An infarct is like an explosion, diffuse cerebral hypoxia is like a slow boil.
The best example I can think of is what happens to the brain when we go to high altitude. I've written many times that it was Jeff's behavior at high altitude that started me on this trail. We were avid hikers, and the times that we went to extreme altitude, Jeff would become almost incapacitated as we reached the summit. He needed to lie down and recover. After one particularly high ascent as part of a day hike in the alps in Switzerland, he needed to spend the next day in the hotel, to recover. He had trouble walking and stayed in bed that day. It worried me, but he was back to normal the next day, so we forgot about it. It was 15 years later, after a week at high altitude in Salt Lake City for a film festival, he returned home to LA to get his first major MS flare and eventual diagnosis.
It's very important to note that the brain is eventually able to adjust to high altitude, and for those who live there full-time, the body develops strategies to oxygenate red blood cells more completely. What happened to Jeff--diffuse cerebral hypoxia due to temporary exposure to altitude--was because he was used to living at sea level. His body didn't have time to acclimate...and something happened. It was not a normal response to altitude sickness. I believe that is because his body was already compromised with slowed venous drainage due to two malformed jugular veins and a stenotic dural sinus, his reaction to lowered oxygen was more severe...I believe he was having the first of his many MS attacks. When he was finally diagnosed in his 40s, he had over 20 cerebral lesions...6 were fresh and many were older.
Here is some research on what happens to the brain at high altitude:
High altitude exposure results in decreased partial pressure of oxygen and an increased formation of reactive oxygen and nitrogen species (RONS), which causes oxidative damage to lipids, proteins and DNA.
(Note that this is almost exactly what the researchers noted in the MS brain tissue due to oxidative damage)
Exposure to high altitude appears to decrease the activity and effectiveness of antioxidant enzyme system. The antioxidant system is less in brain tissue and is very much susceptible to hypoxic stress. The aim of the present study was to investigate the time dependent and region specific changes in cortex, hippocampus and striatum on oxidative stress markers on chronic exposure to hypobaric hypoxia. The rats were exposed to simulated high altitude equivalent to 6100 m in animal decompression chamber for 3 and 7 days. Results indicate an increase in oxidative stress as seen by increase in free radical production, nitric oxide level, lipid peroxidation and lactate dehydrogenase levels. The magnitude of increase in oxidative stress was more in 7 days exposure group as compared to 3 days exposure group. The antioxidant defence system such as reduced glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD) and reduced/oxidized glutathione (GSH/GSSG) levels were significantly decreased in all the three regions. The observation suggests that the hippocampus is more susceptible to hypoxia than the cortex and striatum. It may be concluded that hypoxia differentially affects the antioxidant status in the cortex, hippocampus and striatum.
CCSVI could create this exact situation.
It's why I created the Endothelial Health program, to combat oxidative stress and strengthen the blood brain barrier. That's why we're all fighing to get people tested and treated for CCSVI.
So, that's why I get excited when I see a study that notes oxidative stress creating MS lesions. Not just 'cause it means "I'm right..." but because it's pointing to the TRUE means of how MS harms the brain and spine, and that's going to help move this research forward, to help more patients.
It's a terrific paper to bring to a neurologist, especially one who is still claiming that it's the crazed immune system causing the damage in the MS brain and spine. If that's true than why the slowed perfusion? Why the oxidative stress? These are the questions we need answered. Before any more toxic immune altering drugs are designed and billions more spent on the wrong disease model....we need to know WHY.
I hope this makes a bit more sense of the research, and explains why I search pubmed for these kinds of papers. Off to church. Have a lovely Sunday, all.