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 Medicine, 95(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 (
1,000 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 particle. Perspectives in biology and medicine, 27(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.
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.
