ofonorow wrote:We have countless examples of people who have reversed their heart disease, (
http://practicingmedicinewithoutalicense.com/#TESTIMONY) much of it from optometrist Sydney Bush's CardioRetinometry - evidence from pcitures of the microscopic retinal arteries. He watches to formation of "atheromas" in these arteries - and their dissappearce. Dr. Bush noted that calcification's can take up to a year to reverse.
I agree that the disappearance of calcification in the eye can be a sign of reversal in calcification. However, I now don't believe that the Centimeters of calcified plaque (up to 80% of my abdominal aorta just above its bifurcation diagnosed 6 years ago) are that easily cleared like the one from microscopic arteries.
Used my recent visit to an optometrist to inquire about calcification of my arteries in the eye but he couldn't find even a trace - though the stenosis at my abdominal aorta still has the same extent! Which doesn't must mean much more than if microscopic calcifications already need up to a year to clear, centimeters may take many more years than humans are given.
Also my CIMT has increased from 1.3mm to 1.5 within 2 years. But then I also don't give to much credibility to those measurement of living and pulsating organic matter. For example, my ABI has been the worst when my pain-free walking distance (from intermittent claudication) has been the best, and vis-versa (300 meter versus 2 hours).
Here is my take on "growing new arteries" (johnwen?). Medical doctors and cardiologists are taught that atherosclerotic plaques are irreversible. They only grow, narrowing the arteries. So if greater blood flow is detected, they need something to explain it and have borrowed "angiogenesis" from cancer research to explain the increased blood flow. I just think this is hogwash and the increased blood flow is simply the reversal of CVD (narrowing/plaques) in the existing arteries.
I try to imagine how an artery would grow? It would be quite a trick, as there would either be a lot of internal bleeding, or something would "puncture" it after it somehow attached to its end point. ( I think we know (thank you John Beard) that cancers obtain blood using an enzyme (like trypsin) that eats through tissue, like the early placenta (trophoblast) "eats" through the uterus (womb) to obtain blood for the fetus.)
So how could I explain the vast improvement of my pain-free walking distance, since the extent of my main stenosis remained exactly the same?
I think there are many factors, but one could be angiogenesis. Take for example this MRI pic taken at my diagnosis:
At my last sonography I saw for the first time the 2 small arteries branching off just above the stenosis extending with each pulse much more than ever before. Therefore I have do assume these to have overtaken at least some of the workload of the main.