PUFA Activates NF-kB, MUFA Does Not

[haidut]

This was an in vitro study but still pretty telling. Elevated NFkappaB is implicated in many disease, especially diabetes and cancer. As you can see both omega-3 and omega-6 have this effect. Vitamin E was protective against these effects of PUFA.

http://www.ncbi.nlm.nih.gov/pubmed/10548500

"...A 48-h incubation of cultured human fibroblasts with 5 x 10(-5) M oleic acid or polyunsaturated fatty acids (PUFA) from the (n-6) (linoleic, gamma-linolenic and arachidonic acids) or (n-3) (alpha-linolenic and eicosapentaenoic acids) series resulted in an enrichment of the cells with the introduced fatty acid. Cell enrichment with PUFA initiated a rise in the intracellular level of reactive oxygen species (ROS) and lipid peroxidation products (thiobarbituric reactive substances TBARS). Simultaneously, cell enrichment with all the studied PUFA induced an increase in AP1 and NFkappaB binding activity measured by electrophoretic mobility shift assay, whereas no significant effect was observed with the monounsaturated oleic acid. Furthermore, the antioxidants vitamin E (alpha-tocopherol) and N-acetyl cysteine prevented both the arachidonic acid-induced increase in intracellular ROS and TBARS, and the activation of AP1 and NFkappaB. These results indicate that the accumulation of PUFA from (n-6) and (n-3) series elicited an intracellular oxidative stress, resulting in the activation of oxidative stress-responsive transcription factors such as AP1 and NFkappaB."

 

[ddjd]

This was an in vitro study but still pretty telling. Elevated NFkappaB is implicated in many disease, especially diabetes and cancer. As you can see both omega-3 and omega-6 have this effect. Vitamin E was protective against these effects of PUFA.

Cellular enrichment with polyunsaturated fatty acids induces an oxidative stress and activates the transcription factors AP1 and NFkappaB. - PubMed - NCBI

"...A 48-h incubation of cultured human fibroblasts with 5 x 10(-5) M oleic acid or polyunsaturated fatty acids (PUFA) from the (n-6) (linoleic, gamma-linolenic and arachidonic acids) or (n-3) (alpha-linolenic and eicosapentaenoic acids) series resulted in an enrichment of the cells with the introduced fatty acid. Cell enrichment with PUFA initiated a rise in the intracellular level of reactive oxygen species (ROS) and lipid peroxidation products (thiobarbituric reactive substances TBARS). Simultaneously, cell enrichment with all the studied PUFA induced an increase in AP1 and NFkappaB binding activity measured by electrophoretic mobility shift assay, whereas no significant effect was observed with the monounsaturated oleic acid. Furthermore, the antioxidants vitamin E (alpha-tocopherol) and N-acetyl cysteine prevented both the arachidonic acid-induced increase in intracellular ROS and TBARS, and the activation of AP1 and NFkappaB. These results indicate that the accumulation of PUFA from (n-6) and (n-3) series elicited an intracellular oxidative stress, resulting in the activation of oxidative stress-responsive transcription factors such as AP1 and NFkappaB."

so would the NF-KB test be a good reflection of PUFA levels @haidut?

 

[haidut]

so would the NF-KB test be a good reflection of PUFA levels @haidut?

Any inflammatory biomarker, is usually a good reflection of PUFA status. Prostaglandins, leukotrienes, NO, CRP, ESR, etc are all good inflammatory biomarkers and the first 2 are a direct measure of PUFA overload as they are synthesized from arachidonic acid.

 

[tonto]

@haidut
Please look at these graphs, below, from this study, Insulin Resistance, Inflammation, and Serum Fatty Acid Composition. I'd like to know how you work through this type of article and see SFAs in a more favorable light than PUFA. Overall, I agree with you and am trying to understand how to read these papers. Evidence often seems mixed - perhaps O-6 to O-3 ratio impacts this? Perhaps the SFAs are enhancing a necessary immune response, whereas the PUFA is causing immune disruption? Thanks

 

[haidut]

@haidut
Please look at these graphs, below, from this study, Insulin Resistance, Inflammation, and Serum Fatty Acid Composition. I'd like to know how you work through this type of article and see SFAs in a more favorable light than PUFA. Overall, I agree with you and am trying to understand how to read these papers. Evidence often seems mixed - perhaps O-6 to O-3 ratio impacts this? Perhaps the SFAs are enhancing a necessary immune response, whereas the PUFA is causing immune disruption? Thanks
View attachment 9453

There have been a number of interventions studies with increasing omega-6 or SFA intake (through MCT/coconut oil in the diet) and the results show that SFA reduces inflammatory biomarkers. For me, intervention trials trump epidemiological studies. However, even in in the study you reference the abstract says that omega-6 and omega-3 are positively correlated with CRP.
"...Serum C-reactive protein was significantly associated with percent linoleic acid and eicosapentaenoic acid in nonsmoking men (P 0.03 and P 0.04, respectively) and with docosahexaenoic acid in nonsmoking women (r 0.46, P 0.0001). We constructed a multivariant regression analysis to predict circulating IL-6. Age, BMI, waist-to-hip ratio (WHR), smoking status, and the relation of saturated to -6 or saturated to -3 FAs were considered as independent variables separately in men and women. In overweight men, the ratio of saturated to -3 FAs (P 0.01), but not age, sex, BMI, WHR, or smoking status, independently contributed to 17% of IL-6 variance. In lean men, smoking status (P 0.02), but not the remaining variables, contributed to 8% of IL-6 variance."