The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 18 No. 8 • December 2015


A paper (Das, 2011) reviews changes with age that result in reduced levels of arachidonic acid and the long chain omega 3 fatty acids (found in fish oils) EPA and DHA and, consequently, low-grade systemic inflammation due to a reduced level of the important antiinflammatory, inflammation resolving molecules that are derived from them, lipoxins, resolvins, and protectins, respectively. It may surprise you to learn that arachidonic acid, which is the source of highly inflammatory prostaglandins, can also be converted to lipoxins, that have antiinflammatory effects. The chemical pathways are described in Das, 2011: “TNFalpha [tumor necrosis factor alpha, a major inflammatory cytokine] causes an immediate influx [to the inflamed tissues] of neutrophils concomitant with PGE2 [prostaglandin E2, a powerful inflammatory prostaglandin] and LTB4 [leukotriene B4] production, whereas during the phase of resolution of inflammation, an increase in LXA4, PGD2 [prostaglandin D2, which can function as an important antiinflammatory molecule via pulsatile release, as in the niacin flush] and its product 15 deoxydelta 12-14PGJ2 formation occurs that induces resolution of inflammation with a simultaneous decrease in PGE2 synthesis that stops neutrophil influx and enhances phagocytosis of debris.” The authors explain that this is a process in which there are two waves of release of arachidonic acid, one in which it and its metabolites are involved in inflammation and one in which they are involved in the resolution of inflammation. They note that high fat diets, trans-fat, and cholesterol block the action of the enzymes (delta5 and delta6 desaturases) that are required to produce GLA (gamma linolenic acid), DGLA (dihomogammalinolenic acid), AA (arachidonic acid) EPA, and DHA, thus exacerbating inflammatory conditions.


Another paper (McGahon, 1997) described how the age-associated decrease in membrane arachidonic acid (AA) observed in the dentate gyrus of the hippocampus of rats resulted in impaired long-term potentiation, an important process in learning and memory. Giving the aged animals a diet supplemented with arachidonic acid and its precursor, gamma-linolenic acid, resulted in reversal of the decreased membrane AA and sustained long term potentiation “indistinguishable from four month controls.”

We both take supplemental gamma linolenic acid.


  • Das. A defect in the activities of delta6 and delta5 desaturases and pro-resolution bioactive lipids in the pathobiology of non-alcoholic fatty liver disease. World J Diabetes. 2(11):176-88 (2011).
  • McGahon et al. The ability of aged rats to sustain long-term potentiation is restored when the age-related decrease in membrane arachidonic acid concentration is reversed. Neuroscience. 81(1):9-16 (1997).

Featured Product

FREE Subscription

  • You're just getting started! We have published thousands of scientific health articles. Stay updated and maintain your health.

    It's free to your e-mail inbox and you can unsubscribe at any time.
    Loading Indicator