these mice are an unusual strain and may be unsuitable as a model for humans.
jknosplr wrote:these mice are an unusual strain and may be unsuitable as a model for humans.
Due to genetic mapping some humans may be the exception to the rule also. I'm thinking that each case is unique to its self, i.e each human is its own chemistry set. When an predefined age is reached, a mapped genetic switch is turned on and the dieing process begins. One may prolong it by the hitting the correct concoction of supplemental intake but the hand writing is on the wall.
Saturated fat intake has increased some but for the most part I'm maintaining my regiment for the last three years. With the exception of taking statins, thinners, and BP meds. Doc indicated that statins will help calcify the plaques and in some cases reduce them, turn off the liver production of excessive cholesterol (tribal knowledge). Calcification is better than ruptures in my book.
Another though I had is the VC regiment may not stop the plaque growth once it starts but no new lesions would be formed after a time period of the being on the VC??. Reason I say this is during the Catheterization and placement of the stent in the Ramus artery no new lesions were noted that he could visually confirm in any of other artery's. There was one other plaque approx same age as the ruptured one which he did not touch due to insurance restrictions(obama health care that's unconstitutional in its finest hour) but no visibly new lesions, but then again only time will tell. As Fred Sanford says "its the big one!!" then its to late.
NOTE: The two lesions noted were present back in 06/26/2009, he indicated that they were insignificant at the time. They matured to be significant.
So who knows???
Thanks for the input Van
I am a bit perplexed that nobody is paying attention to the information on ferritin levels. If those levels are elevated and they don't take the measures I mentioned, everything else they do will be far less impactful on their CAD progression.
I have an appointment with the cardiologist on 3rd march 2011, I will request a Ferritin (iron Tox) test then along with the standard blood work. I will request a standard Cholesterol test as the VAP test measurements are some what in question.
Are there any current studies that confirm high ferritin levels are a contributing factor to CVD?
All I have found are studies from the circa 2000 that indicate one has nothing to do with the other, and or not enough data/studies has been collected/completed to prove the hypothesis..
Iron is a critical risk factor for CAD. Ferritin levels should be routinely checked. If they are greater than 25 ng/ml, I believe they should be vigorously treated. Above 400 ng/ml (still considered by some labs to be at the upper range of normal), consideration should be given to prescription chelation.
Phlebotomy helps a lot. It's a great idea to give as much blood as they will allow, which is usually 7 to 8 units annually. A far infrared sauna sweats outs a lot of iron, amazingly enough. Inositol hexaphosphate (IP6, phytate, phytic acid) is a great supplement. It avidly binds calcium, iron, and other mineral cations. This is best taken as 1 to 3 grams on a empty stomach daily. Great to take first thing in the morning or when you get up in the middle of the night to urinate. When taken with food, it just binds with a lot of the minerals in the food.
My review of the literature tells me that you are healthiest when your ferritin (storage form of iron) is as low as you can make it without making yourself anemic as well.
ofonorow wrote:Now, the question of fat-free/veg. diet as a treatment/cause for heart disease deserves its own thread, as we haven't really discussed this for years. So I will create a new topic based on 123xyz's post. http://www.vitamincfoundation.org/forum/viewtopic.php?f=11&t=8970
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