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The Nutrition InvestigatorThe health and nutrition blog by Dr. Roc Ordman.

Discovery about protein misfolding from Roc, Nutrition Investigator

by Roc (click here for full post)

Dear readers,

I am very excited about a new discovery described in the abstract that follows this explanation.  My friend Rolf Martin of blueberry fame helped me realize one theory of aging is that it is due to protein misfolding. When mRNA codes for proteins (translation) too rapidly or without the proper amino acids available, proteins are not synthesized correctly.  As we age, they form clumps in the cell, leading to senescent cells, that produce harmful signals leading to cancer, arthritis, etc.

        Blueberries, followed by a cup of green tea, slow the process of translation, reducing the rate of protein misfolding. The blueberries produce quercetin, and that preserves the EGCG in green tea, which slows translation.

      The abstract below shows that slowing translation is a primary effect of dietary restriction, which has long been known to slow the aging process and reduce age-associated disease.

     Conclusion: Getting quercetin and EGCG provides a benefit similar to dietary restriction, without the requirement of fasting for at least 12 hrs.

     Delight: This is especially good news to me, as MDR has invited me to develop a supplement, and June 1st I produced the first design, which includes quercetin and EGCG, and other ingredients that reduce protein misfolding, likely to increase healthspan.  I hope the production date will be scheduled by the time I give a presentation at the Linus Pauling Nutrition Conference August 14th.

    Below is the publication abstract:

“Diet restriction‐induced healthy aging is mediated through the immune signaling component ZIP‐2 in Caenorhabditis elegans”Abstract “Dietary restriction (DR) robustly delays the aging process in all animals tested so far. DR slows aging by negatively regulating the target of rapamycin (TOR) and S6 kinase (S6K) signaling pathway and thus inhibiting translation. Translation inhibition in C. elegans is known to activate the innate immune signal ZIP‐2. Here, we show that ZIP‐2 is activated in response to DR and in feeding‐defective eat‐2 mutants. Importantly, ZIP‐2 contributes to the improvements in longevity and healthy aging, including mitochondrial integrity and physical ability, mediated by DR in C. elegans. We further show that ZIP‐2 is activated upon inhibition of TOR/S6K signaling. However, DR‐mediated activation of ZIP‐2 does not require the TOR/S6K effector PHA‐4/FOXA. Furthermore, zip‐2 was not activated or required for longevity in daf‐2 mutants, which mimic a low nutrition status. Thus, DR appears to activate ZIP‐2 independently of PHA‐4/FOXA and DAF‐2. The link between DR, aging, and immune activation provides practical insight into the DR‐induced benefits on health span and longevity.”

Open access: https://onlinelibrary.wiley.com/doi/10.1111/acel.12982

While the study only dealt with C Elegans, the following lines from the conclusion apply well to humans: “Thus, we argue that increased immunity through the practice of DR is important to increased longevity and healthy aging. Furthermore, we propose that over‐feeding may suppress innate immunity, thereby accelerating aging.”

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