It is said that oxidized oil in general and Omega-3 specifically is bad for you if consumed in oxidized state. What are the scietific claims surrounding this?
asked byJohan_Lindn (115)
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on May 06, 2014
at 05:01 AM
Utilization of omega-3 unsaturated fats in fish oil has been accounted for to enhance the guess of a few perpetual incendiary ailments described by leukocyte aggregation, including atherosclerosis, systemic lupus erythematosus, psoriasis, provocative inside malady, and rheumatoid arthritis.1-4 Fish oil is likewise prescribed for medication of Iga nephropathy, the most well known manifestation of essential renal sickness around the world
on May 05, 2014
at 09:05 AM
Johan, you are not reading that science correctly. Omega3 and Omega6 compete for the same receptor sites in tissue. So the first part of the quoted research is saying that increasing doses of Omega-3 reduce the amount of Omega-6 arachidonic acid and its metabolites. Omega-6 is argued to be a very pro inflammatory fat, so reducing its concentration in tissue will reduce its negative side effects.
The second part of the quoted research is saying that some of the benefits of Omega-3 happen when you store it in tissue and it oxidizes *in your body tissue*. It's not saying that you should ingest rancid oil that already oxidized before you ingested it!!!!!!
The whole mechanism of action of polyunsaturated fats (Omega-3 and Omega-6) in the body is that you store them and then when they are needed they are oxidized.
on April 17, 2014
at 10:54 AM
By definition oxidized PUFAs are rancid. They smell bad to us as a result of evolution - to let us know that they're not fit for consumption.
on April 16, 2014
at 05:16 PM
On the contrary it seems,
"The acute effect of increasing doses of animal O3 is a reduction in arachidonic acid-derived inflammatory metabolites, increases in membrane permeability and anti-inflammatory molecules derived from EPA/DHA, as well as reduction in T-cell activation and antigenic stimulation. O3 also have direct effects: inhibition of LPS or lipopeptide-stimulated COX2 expression and LPS-induced NFkB activation (24,25). Interestingly, there is evidence that the anti-inflammatory effects seen for O3 are dependent on their oxidation. Oxidized EPA, but not unoxidized EPA, inhibits NFkB activation and expression of inflammatory molecules in a PPARa dependent manner, as well as chemotaxis (26,27,28). Oxidized, but not unoxidized DHA, inhibits polychlorinated biphenyl-induced NFkB activation and MCP-1 expression, effects probably mediated by its oxidation products (A4/J4 neuroprostanes) (29). Thus, it seems that contrary to what is believed, oxidation of O3 PUFA is necessary to mediate their beneficial biological effects."