PHARMACEUTICAL COMPENSATION WITH ASA or White Willow: ANTI-AGING PROTOCOL?

Updated: Jun 9, 2021

ASA versus White Willow Bark Extract

Original post: February 18, 2011



Aspirin or ASA, as I’ve outlined previously, works its cardiovascular preventive wonders by blocking COX activity, thereforethwarting production of the pro-inflammatory PGE2 and the clot-inducing thromboxane TXA2 (17, 18).


Acetaminophen, the active ingredient in Tylenol and other such pharmaceuticals, inhibits inflammation by retarding PGH (see Figure 13) activity (19). It’s through this chemistry that these pharmaceutical substances have powerful analgesic, anti-inflammatory, fever-reducing, and cough-suppressing activity, as well. In pharmaceutical reference guides such as


The Compendium of Pharmaceuticals and Specialties, ASA is said to “interfere with the production of prostaglandins in various organs and tissues through the acetylation of the enzyme cyclo oxygenase.”


In other words, when COX is acetylated, it’s inhibited and can’t catalyze the conversion of arachidonic acid into eicosanoid hormones that we tend to over-manufacture when our diets are unhealthy and our metabolisms malfunction. However, chronic overproduction and imbalance of these hormones can be alleviated in most of us with a little lifestyle change, the essence of the Ageless Performance program. The twisted nature of this chemistry impairs the free flow of our preprogrammed genetic health. As a result, we require the chemistry-bending assistance of the pharmaceutical blockers described above.


The activity of ASA isn’t the same as the natural salicylates found in herbs such as white willow bark and other herbal and food sources. In order for these natural salicylates to work the way ASA does, they must be acetylated, hence the name acetylsalicylic acid. Those thermogenesis promoting, fat-busting stacks that include white willow bark instead of ASA with the common caffeine and ephedrine sources don’t have the same effect as those that include ASA.


White willow bark salicylates can’t acetylate COX the same way ASA can and therefore aren’t able to arrest the activity similarly (20, 21). Interestingly studies have shown that ASA is metabolized eventually into salicylic acid in the body. The acetylsalicylate will acetylate COX, as we’ve seen, but the biochemical influence doesn’t end there. Salicylates do induce COX inhibition, as well, but not nearly with the potency of ASA. So how does the salicylate work?


In post-2000 studies salicylates were shown to down-regulate NF-kappa- B** activity (22). As noted earlier in this book, NF-kappa-B activity stimulates the genes that produce COX to promote the production of disease-instigating prostaglandins and thromboxanes. By inhibiting NF-kappa-B activity, COX-related gene activity is slowed down and COX activity is reduced, but through a different method than acetylation. ASA displays two rounds of activity in this system at two different levels— COX inactivation (by acetylation of the enzyme) and reduced COX production (by decreasing gene activity). It’s this NF-kappa-B down-regulation by white willow bark and other food sources of salicylates that provides milder anti-inflammatory activity but takes more time to induce than the more immediate inhibition by ASA acetylation. And it’s this NF-kappa-B suppression that prompts me to advocate long-term use of low doses of ASA— 20 to 25 mg daily.


The NF-kappa-B inhibition by low-dose ASA administration, in particular the salicylate, is likely due to antioxidant activity on the NFkappa-B complex that I mentioned earlier. In fact, studies have indicated that low-dose ASA can neutralize the hydroxyl radical in the biological system with much greater potency than ascorbic acid, glutathione, or cysteine (23). Antioxidants, as we know from the many studies previously cited, down-regulate NF-kappa-B, which is one way to maintain cellular health and biological age in a youthful state.


The prostaglandins we have to block in order to promote natural fat incineration are produced in extraordinary levels due to a metabolic imbalance that can exist at various levels in our bodies. This same imbalance causes chronic inflammation we can measure or feel, cardiovascular risks such as clotting that might or might not be apparent, but it also creates subclinical inflammation that we’re not aware of that can promote accelerated aging if it’s allowed to fester. Fix this common metabolic pathway and many health issues will miraculously rectify themselves and we can look and feel much younger. However, the reestablishment of balance might take a few months to instill and involves a lot more than low doses of ASA.


(** Nuclear-factor-kappa-B (NF-kappa-B): Regulates expression of genes, most of which encode proteins that play important role in immunity and inflammation; involved in brain function, particularly following injury and in neurodegenerative conditions such as Alzheimer’s disease.)


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