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Need "Drano-like" remedy for arterial plaque

plaque

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#151 pamojja

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Posted 05 October 2016 - 05:22 PM

 An other one being happy with Pauling's therapy. :)  Was diagnosed a PAD 8 years ago due to a 80% stenosis at my abdominal aorta. Main debilitating symptom was intermittent claudication with a pain-free walking distance of merely 3-400 meters, at worse. Was certified a 60% disability because of that, usually such a severe blockage only gets worse.
 
Medically was only offered statins and aspirin for life, and a chirurgical replacement of the whole piece of aorta with Y-shaped goretex-like tubes. After carefully considering the possible benefits with it's risk - I choose Pauling's Therapy instead, and haven't regretted even for 1 day.
 
Though it took quite some time to completely get rid of intermittent claudication... In the beginning carefully and gradually increased the doses of vitamin C and l-lysine, and this way found that only once I crossed the threshold between a prevention and therapeutic dose (according to Pauling) after about 1 year, my walking distance increased substantially to 1 hour, 2 the second year. Then with a chronic bronchitis for a whole year decreasing down to 1/2 hour again. Before gradually going up till it was no more, 2 years ago.
 
True, I too don't have any evidence the plaque decreased. Only of the expansive revascularisation I'm sure. And I'm utterly pleased it was possible to overcome my disability this gentle way.

 

Linus Pauling "therapy" is not a therapy but a bad joke. No, Vitamin C and Lysine won't do anything to reduce atherosclerosis, and everybody who spends some time studying the pathophysiology of atherosclerosis will understand why it's hilarious nonsense. 

 

Keep joking, Dolph. Those who benefited know already much better. Just because it's never been tested in clinical trial doesn't mean it doesn't work. Pauling's Therapy is too easy to try, and to get confirmation it indeed is working.

 

But I completely disagree with RatherBeUnknown, that one could substantially reduce the ascorbic acid dose Linus Pauling differentiated from a preventive (3 vs. >6 g/d). Because in my experience improvement started with the therapeutic dose only.


Edited by pamojja, 05 October 2016 - 05:23 PM.

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#152 Darryl

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Posted 16 October 2016 - 01:24 AM

I've been going through the literature on plaque regression from the 1950s-1980s. Usually this occurs naturally with time when the animals are restored to normal, low-fat chow. But as an early example of attempts to use "Drano" like approaches, there's this:

 

Friedman et al, 1957. Resolution of aortic atherosclerotic infiltration in the rabbit by phosphatide infusion. Experimental Biology and Medicine95(3), pp.586-588.

 

I don't have access, but its described here:

 

To our knowledge, however, the first prospective, interventional study demonstrating substantial shrinkage of atherosclerotic lesions was performed in cholesterol-fed rabbits and reported in 1957. The dietary regimen raised total plasma cholesterol to around 26 mmol/l (glyph.gif1,000 mg/dl) and induced widespread lesions involving around 90% of the aorta. To mobilize tissue stores of cholesterol, animals received intravenous bolus injections of phosphatidylcholine (PC). After less than a week and a half of treatment, the remaining plaques were scattered and far smaller than initially, and three-quarters of arterial cholesterol stores had been removed.

 

 

 

Its works in other species, as well

 

Williams et al, 1984. Intravenously administered lecithin liposomes: a synthetic antiatherogenic lipid particlePerspectives in biology and medicine27(3), pp.417-431.

 

We propose that lecithin induces regression of experimental atherosclerosis by forming a synthetic antiadierogenic lipid particle, the lecithin liposome. We are proposing the following. Intravenously injected lecithin forms circulating liposomes, which take up cholesterol from many sources, including the arterial wall. In this way, lecithin liposomes become carriers ofendogenous cholesterol. These liposomes are gradually removed from the circulation by the liver, which catabolizes liposomes and excretes their cholesterol. Mobilization and excretion of endogenous cholesterol are further enhanced by the interactions of circulating liposomes with native lipoproteins and red blood cells. For example, circulating liposomes pick up apoproteins from native lipoproteins. Apoproteins directly augment the ability of liposomes to extract tissue cholesterol and may facilitate their catabolism by the liver. In addition, liposomes remove cholesterol from, and donate phospholipid to, native lipoproteins. These modifications may enhance the ability of native lipoproteins to extract cellular cholesterol and may reduce any further lipoprotein-mediated transport of cholesterol into the arterial wall. Finally, liposomes remove cholesterol from the membranes of red blood cells. Cholesterol-depleted red blood cells may act as additional intermediaries in the extraction of arterial cholesterol deposits. In the following sections, we first review the studies demonstrating regression of experimental atherosclerosis with intravenous administration of lecithin. We then examine the evidence diat lecidiin mobilizes tissue cholesterol by the formation of liposomes composed of lecithin and cholesterol, that these liposomes are disposed of by the liver, and interactions of liposomes with lipoproteins and red cells enhance these processes. Finally, we review literature from which we infer that die cholesterol of human atheromata may be susceptible to mobilization and excretion by intravenously administered liposomes. 
 
Regression of Expérimental Atherosclerosis with I.V. Lecithin
 
The cholesterol-fed rabbit is widely used as an experimental model of atfierosclerosis. In this model, rabbits fed on a diet containing 1-5 percent added cholesterol develop witthin 4—12 weeks deposits of cholesterol in many tissues, including the intima of large arteries. These intimal deposits remain die same size or even progress when the rabbits are returned to their usual cholesterol-free diet. In contrast, intravenous administration of lecithin preparations of varying purity (0.53 .5 g two to three times a week) resulted in rapid, substantial regression of the intimai lesions, with resolution in 1-4 weeks or after a total phospholipid dose of about 2-12 g. Lecithin-induced regression occurred even while the rabbits were maintained on die cholesterol-rich, adierogenic diet. Similar results were observed in other models. Experimental atherosclerosis produced in rabbits by a semisynthetic cholesterol-free diet rich in saturated fat regressed with infusions of lecithin. In baboons, the incidence and severity of experimental atherosclerosis, induced over 6 months by combining cholesterol feeding with injections of bovine serum albumin (to produce vasculitis and intimai injury), were significandy reduced by concurrent thrice-weekly infusions of polyunsaturated lecithin. Quail fed on a high-cholesterol diet for 3 months developed intimai deposits that resolved during 3 subsequent months of intravenous lecithin administration, despite continuation of the atherogenic diet. Extravascular cholesterol deposits in the subcutaneous tissues of rats regressed witth topical lecithin ...

 

 
 

 

 


Edited by Darryl, 16 October 2016 - 01:33 AM.

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#153 ta5

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Posted 16 October 2016 - 01:37 AM

[...]

 

...To mobilize tissue stores of cholesterol, animals received intravenous bolus injections of phosphatidylcholine (PC). After less than a week and a half of treatment, the remaining plaques were scattered and far smaller than initially, and three-quarters of arterial cholesterol stores had been removed.

 

 

There's been little followup.

 

Reminds me of Ray Kurzweil from 2006:

 

The body makes phosphatidylcholine, but very slowly, so over the decades the phosphatidylcholine in the cell membrane depletes, and the cell membrane gets filled in with inert substances, like hard fats and cholesterol, that basically don’t work. This is one reasons that cells become brittle with age. The skin in an elderly person begins to not be supple. The organs stop functioning efficiently. So it’s actually a very important aging process, and you can reverse that by supplementing with phosphatidylcholine. If you really want to do it effectively you can take phosphatidylcholine intravenously, as I do. Every week I have a I.V. with phosphatidylcholine. I also take it every day orally. So that’s one aging process we can stop today.

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#154 Adaptogen

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Posted 16 October 2016 - 02:37 AM

didn't see it mentioned in this thread, but I ran across an LEF study for their product, Arterial Protect: https://www.ncbi.nlm...pubmed/26496510

"This registry study revealed a significant increase in stability of plaques, indicated by an enhanced density of the plaques, following supplementation with the combination of Pycnogenol® and Centellicum®. As size and number of plaques was simultaneously reduced, the combination of the two plant extracts could be a safe option for prevention of cardiovascular events for patients with carotid plaques."

 

 

 


Edited by Adaptogen, 16 October 2016 - 02:41 AM.






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