Yep, all the people observing benefits from carb restriction (including Kwasniewski) also restrict PUFAs with them at the same time.
Here is another paper demonstrating the expert's "derailed" thinking - their reversed causality suggests that it's H. pyroli which causes lipid peroxidation:
Levels of Malondialdehyde-Deoxyguanosine in the Gastric Mucosa
Relationship with Lipid Peroxidation, Ascorbic Acid, and Helicobacter pylori
Simon M. Everett1, Raj Singh, Chiara Leuratti, Kay L. M. White, Peter Neville, Darren Greenwood, Lawrence J. Marnett, Christopher J. Schorah, David Forman, David Shuker and Anthony T. R. Axon
Helicobacter pylori infection is associated with elevated gastric mucosal concentrations of the lipid peroxidation product malondialdehyde and reduced gastric juice vitamin C concentrations. Malondialdehyde can react with DNA bases to form the mutagenic adduct malondialdehyde-deoxyguanosine (M1-dG). We aimed to determine gastric mucosal levels of M1-dG in relation to H. pylori infection and malondialdehyde and vitamin C concentrations. Patients (n = 124) attending for endoscopy were studied. Levels of antral mucosal M1-dG were determined using a sensitive immunoslot-blot technique; antral mucosal malondialdehyde was determined by thiobarbituric acid extraction, and gastric juice and antral mucosal ascorbic acid and total vitamin C were determined by high-performance liquid chromatography. Sixty-four H. pylori-positive patients received eradication therapy, and endoscopy was repeated at 6 and 12 months. Levels of M1-dG did not differ between subjects with H. pylori gastritis (n = 85) and those with normal mucosa without H. pylori infection (n = 39; 56.6 versus 60.1 adducts/108 bases) and were unaffected by age or smoking habits. Malondialdehyde levels were higher (123.7 versus 82.5 pmol/g; P < 0.001), gastric juice ascorbic acid was lower (5.7 versus 15.0 µmol/ml; P < 0.001), and antral mucosal ascorbic acid was unchanged (48.0 versus 42.7 µmol/g) in H. pylori gastritis compared with normal mucosa. Multiple regression analysis revealed that M1-dG increased significantly with increasing levels of malondialdehyde, antral ascorbic acid, and total antral vitamin C. M1-dG levels were unchanged 6 months (63.3 versus 87.0 adducts/108 bases; P = 0.24; n = 38) and 12 months (66.7 versus 77.5 adducts/108 bases; P = 0.8; n = 13) after successful eradication of H. pylori. M1-dG thus is detectable in gastric mucosa, but is not affected directly by H. pylori.
SOURCE:
http://cebp.aacrjournals.org/cgi/content/full/10/4/369?hits=10&FIRSTINDEX=0&TITLEABSTRACT=gastric+mucosa&AUTHOR1=shuker&SEARCHID=1&gca=cebp%253B10%252F4%252F369&sendit=Get+All+Checked+Abstract%2528s%2529& |
Free Forum Hosting
Important Announcement
Prev Message
