Since late 2016 we have entered the age of disclosures! Fasten your mental safety belt and enjoy the ride! Heretic

Saturday, December 29, 2018

Mechanism behind omega-6 seed oil triggering autoimmune diseases


Summary. The study proved the following mechanism on mice may be triggering diseases such as muscular dystrophy, rheumatoid arthritis, atherosclerosis and lupus:

1. Dietary omega-6 seed oils produces NHE,

2. NHE binds to aminoacids from the DNA, then

3. immune system reacts against that and produces antibodies against NHA and against the DNA

4. immune system attacks and destroys body's own DNA and the cells die!

First read this, to understand what NHE is:
4-Hydroxynonenal (NHE)



4-Hydroxynonenal is generated in the oxidation of lipids containing polyunsaturated omega-6 acyl groups, such as arachidonic or linoleic groups,
Special attention must also be paid to cooking oils used repeatedly in caterings and households, because in those processes very high amounts of OαβUAs are generated and they can be easily absorbed through the diet.

And then read this:

"Protein-bound 4-Hydroxy-2-nonenal
THE JOURNAL OF BIOLOGICAL CHEMISTRY VOL. 282, NO. 35, pp. 25769 –25778, August 31, 2007



Several lines of evidence indicate that the nonenzymatic oxidative modification of proteins and the subsequent accumulation of the modified proteins have been found in cells during aging and oxidative stress and in various pathological states, including premature diseases, muscular dystrophy, rheumatoid arthritis, and atherosclerosis. Our previous work suggested the existence of molecular mimicry between antibodies raised against hydroxy-2-nonenal (HNE)-modified protein and anti-DNA autoantibodies, a serologic hallmark of systemic lupus erythematosus (SLE). In the present study, we investigated the possible involvement of HNE-modified proteins as the endogenous source of the anti-DNA antibodies.


4-Hydroxy-2-nonenal (HNE), one of the most prominent lipid peroxidation-specific aldehydes, is believed to be largely responsible for the cytopathological effects observed during oxidative stress (4, 5). HNE exerts these effects because of its facile reactivity with biological materials, including proteins (Fig. 1) (5). Upon reaction of the protein, HNE specifically reacts with nucleophilic amino acids, such as cysteine, histidine, and lysine, to form stable Michael addition adducts possessing the cyclic hemiacetal structure (5). Previously, we raised the anti-HNE monoclonal antibodies (mAbs), which enantios-electively recognized the (R)-HNE-histidine Michael adducts (11), and unexpectedly found that the sequence of an anti-HNE mAb was highly homologous to the anti-DNA autoantibodies (12). In addition, we characterized the ability of the mAb to recognize DNA and identified the 4-Oxo-2-nonenal (ONE)-modified 2′-deoxynucleoside (7-(2-oxo-heptyl)-substituted 1,N2-etheno-type 4-oxo-2-nonenal-2′-deoxynucleoside) as an alternative epitope. Based on these findings, we proposed the hypothesis that post-translational protein modification with lipid peroxidation products, such as HNE, could serve as an immunological trigger for the production of anti-DNA autoantibodies in autoimmune diseases.

[thanks @TuckerGoodrich]


Larcana said...

My thought is that, in each individual, the damage presents differently due to time and genetic effect. Epigenetics . This would explain why some are affected early and other late in life.

Stan Bleszynski said...

Hi Larcana,

Yes, and also immune-related responses seems to be highly threshold-dependent, that is there is no symptoms and no damage until a certain limit of the trigger concentration is exceeded then the full blast hits the body. It is probably also aggravated by the mathematical collapse effect (in automation we call it positive feedback effect). Once the damage to DNA occurs and exceeds a certain threshold there is a run-away (a sudden "snap") effect when the dying tissue causes and accelerates a further immune response. The time signature of the response is therefore different from a typical metabolic damage caused for example by carbohydrates or some poison, when the body can cope until the rate of the damage (or consumption of the poison) is below the body auto-repair & regeneration speed. In this case the time signature is different and more gradual. Stan

JC said...

This is off topic. There may be some problems with K2 supplementation.

Stan Bleszynski said...

Hi JC,

I remember seeing studies that correlate vitamin K2 intake with reduced risk of cardiovascular events, by a large factor, bigger than 20% as in just calcium score tests.

Dr. Brewer objections are probably not consistent with cardiological practice, for example Dr. Agatston and others who reported correlation between rising calcium score and increasing risk, which does not seem to support the theory that soft less calcified plaque would be more dangerous.

Though theoretically, a decrease in calcium score may be due to either leaching of calcium from a plaque area that does not diminish in size and gets softer, therefore more dangerous. Or, due to a shrinkage of the entire plaque spot, which would be beneficial.