Reversing Arterial Blockage: Experimental Regimen That Worked For Man Facing Amputation of His Lower Legs
Reversing Arterial Blockage: Experimental Regimen That Worked For Man Facing Amputation of His Lower Legs
Reversing Arterial Blockage: Experimental Regimen That Worked For Man Facing Amputation of His Lower Legs
SUPPLEMENTS
PADMA BASIC - sources & comparison prices:http://www.bestdeal.com/search/landing/query/padma+basic/s/google/koid/6234666013/gkaid/61679560/adid/206645236
0/gkyid/1164695747/?query=padma+basic&gclid=COjOj63ogrACFQFeTAodHVs8jg
LAY-LEVEL ARTICLE ON PADMA:
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http://www.scribd.com/doc/158030311/TIBETAN-VASOACTIVE-HERBAL-BLEND-PADMA28
NOTA BENE: Back in the mid 1990s I placed PADMA in graduated levels in chow fed to guinea pigs with
induced blood vessel blockage and observed a reversal of plaque (High dose worked quickest).
Traditional dose: 3 tablets 1 hour before or 2 hours after meals.
Vitamin D3 + K2: http://www.iherb.com/Now-Foods-Vitamin-D-3-K-2-1-000-IU-45-mcg-120-Vcaps/10056
Suggested dose: 1 capsule with meals. Check with MD or DO to see if contraindicated.
Krill Oil: http://www.iherb.com/Now-Foods-Neptune-Krill-1000-60-Softgels/22675 1 softgel after
breakfast and 1 softgel after lunch or dinner
Neem: 440-500 mg capsules. 2 capsules 3 x daily with or after meals. One low cost source
http://www.iherb.com/Organix-South-TheraNeem-Organix-Neem-Leaf-90-VCaps/17641
Apple pectin: 700-1g (1000 mg) capsules. 1 to 2 capsules with or after meals. One low cost source is
http://www.iherb.com/Now-Foods-Apple-Pectin-700-mg-120-Capsules/361
DRUGS
Tetracycline: Advisability of using this and, if OK, safe dose to be determined solely by a licensed
physician (MD or DO)
NOTE: I have no commercial or other interest in any firm linked to above or below, and
get no concessions or favors of any kind from linking to them or their products.
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ADDITIONAL READING
http://www.sciencedaily.com/releases/2013/02/130227151254.htm - Lipid Researcher, 98, Reports
On the Dietary Causes of Heart Disease
COMMENT: You gotta love a guy who works in his lab sporting a bolo!
Fred A Kummerow
Burnsides Research Laboratory, Department of Comparative Biosciences, College of Veterinary
Medicine, University of Illinois, 1208 W. Pennsylvania Avenue, Urbana, IL 61801, USA
Received November 26, 2012; Accepted January 23, 2013; Epub February 17, 2013; Published February
27, 2013
Abstract: Despite major public health efforts, coronary heart disease continues to be the leading cause
of death in the United States. Oxidized lipids contribute to heart disease both by increasing deposition
of calcium on the arterial wall, a major hallmark of atherosclerosis, and by interrupting blood flow, a
major contributor to heart attack and sudden death. Oxidized cholesterol (oxysterols) enhances the
production of sphingomyelin, a phospholipid found in the cellular membranes of the coronary artery.
This increases the sphingomyelin content in the cell membrane, which in turn enhances the interaction
between the membrane and ionic calcium (Ca2+), thereby increasing the risk of arterial calcification.
Patients undergoing bypass surgery had greater concentrations of oxysterols in their plasma than
cardiac catheterized controls with no stenosis, and had five times more sphingomyelin in their arteries
than in the artery of the placenta of a newborn. The oxysterols found in the plasma of these patients
were also found in the plasma of rabbits that had been fed oxidized cholesterol and in frying fats and
powdered egg yolk intended for human consumption. Together these findings suggest that oxysterols
found in the diet are absorbed and contribute to arterial calcification. Oxidized low-density lipoprotein
(OxLDL) further contributes to heart disease by increasing the synthesis of thromboxane in platelets,
which increases blood clotting. Cigarette smoke and trans fatty acids, found in partially hydrogenated
soybean oil, both inhibit the synthesis of prostacyclin, which inhibits blood clotting. By increasing the
ratio of thromboxane to prostacyclin, these factors interact to interrupt blood flow, thereby
contributing to heart attack and sudden death. Levels of oxysterols and OxLDL increase primarily as a
result of three diet or lifestyle factors: the consumption of oxysterols from commercially fried foods
such as fried chicken, fish, and french fries; oxidation of cholesterol in vivo driven by consumption of
excess polyunsaturated fatty acids from vegetable oils; and cigarette smoking. Along with the
consumption of trans fatty acids from partially hydrogenated vegetable oil, these diet and lifestyle
factors likely underlie the persistent national burden of heart disease. (AJCD1211005).
Address correspondence to: Dr. Fred A Kummerow, Burnsides Research Laboratory, 1208 W.
Pennsylvania Avenue, Urbana, IL 61801, USA. Tel: 217-344-6380; Fax: 217-333-7370; E-mail:
[email protected]
http://www.ncbi.nlm.nih.gov/pubmed/22566693
J Biol Chem. 2012 May 7. [Epub ahead of print]
Limonoid Compounds Inhibit Sphingomyelin Biosynthesis by Preventing CERT-dependent Extraction of
Ceramides from the Endoplasmic Reticulum.
Hullin-Matsuda F, Tomishige N, Sakai S, Ishitsuka R, Ishii K, Makino A, Greimel P, Abe M, Laviad EL,
Lagarde M, Vidal H, Saito T, Osada H, Hanada K, Futerman AH, Kobayashi T.
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Source
RIKEN, Japan;
Abstract
In order to identify novel inhibitors of sphingomyelin (SM) metabolism, a new and selective highthroughput microscopy-based screening based on the toxicity of the SM-specific toxin, lysenin, was
developed. Out of a library of 2011 natural compounds, the limonoid, 3-chloro-8-hydroxycarapin-3,8hemiacetal (CHC), rendered cells resistant to lysenin by decreasing cell surface SM. CHC treatment
selectively inhibited the de novo biosynthesis of SM without affecting glycolipid and glycerophospholipid
biosynthesis. Pretreatment with brefeldin A abolished the limonoid-induced inhibition of SM synthesis
suggesting that the transport of ceramide (Cer) from the endoplasmic reticulum (ER) to the Golgi
apparatus is affected. Unlike the Cer transporter (CERT) inhibitor HPA-12, CHC did not change the
transport of a fluorescent short chain Cer analog to the Golgi apparatus or the formation of fluorescent
and short chain SM from the corresponding Cer. Nevertheless CHC inhibited the conversion of de novo
synthesized Cer to SM. We show that CHC specifically inhibited the CERT-mediated extraction of Cer
from ER membranes in vitro. Subsequent biochemical screening of 21 limonoids revealed that some of
them, such as 8-hydroxycarapin-3,8-hemiacetal (HC) and gedunin [Neem spp. AGP] which exhibits
anti-cancer activity, inhibited SM biosynthesis and CERT-mediated extraction of Cer from membranes.
Model membrane studies suggest that HC reduced the miscibility of Cer with membrane lipids and thus
induced the formation of Cer-rich membrane domains. Our study shows that certain limonoids are novel
inhibitors of SM biosynthesis and suggests that some biological activities of these limonoids are related
to their effect on the ceramide metabolism.
PMID: 22566693
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