Aspirin’s Many Benefits

Q What is your take on the use of a baby aspirin every day?

DANNIE, Chicago

A It has clearly been established that a daily baby aspirin (the acetylated version of the plant hormone salicylic acid, at 81 mg/day) can provide important cardiovascular benefits, although some individuals are sensitive to aspirin, in even low doses, for when it may cause gastrointestinal bleeding. To determine whether you are one of these, see your doctor.

A recently published paper1 explains more about the cardiovascular protection of aspirin by revealing that aspirin induces paraoxonase 1 (PON1, a molecule that is made in the liver and which circulates in association with Apo-A1 and HDL) and the Apo-A1 gene in mice.

PON1 has been found to protect against atherosclerosis and studies have shown that people who take aspirin have increased levels of PON1. PON1-deficient mice have been shown to be more susceptible to atherosclerosis.1 As well, low levels of HDL are positively correlated with low levels of PON1.1 It is interesting to note that the cardiovascular protective effects of HDL depend to a great extent on its content of Apo-A1 and PON1. HDL becomes less protective and even proatherogenic due to oxidative- and/or nitrative-stress-induced damage to Apo-A1 and PON1. This is probably a major reasons that it is not uncommon for people with normal levels of HDL and LDL to still have heart attacks.

Interestingly, in human and animal studies, a number of natural substances have also been found to increase PON1, including quercetin and catechin. In a liver culture study, resveratrol was reported to induce PON1 gene expression.1

Senescence, a state in which cells can no longer divide, has recently been discovered to be induced by oncogene (cancer-inducing gene) activation. This supports the theory that one function of senescence is to prevent the development of cancer.2

While senescent cells are alive and metabolically active, they do not function the same as nonsenescent cells.3 E.g., the capacity of endothelial cells (which line blood vessels) to generate nitric oxide decreases in senescence, which is not good because the suppression of oxidative stress or application of NO donors has been shown to delay the onset of replicative senescence in cell culture.4

This study also found that when human umbilical-vein endothelial cells in culture were incubated with aspirin, the activity of beta-galactosidase (a biomarker of senescence) was significantly decreased. But unlike aspirin, the use of ibuprofen and acetaminophen results in significant increases in beta-galactosidase activity. This is the case when a nitric oxide synthase inhibitor is added to the culture, abolished the aspirin-reduced beta-galactosidase activity. This demonstrates that the aspirin effect is mediated by nitric oxide.

Shortened telomeres and decreased levels of telomerase have also been shown to induce senescence. Yet, aspirin increases telomerase activity significantly, while ibuprofen and acetaminophen significantly reduce telomerase activity. As above, adding a nitric oxide synthase inhibitor to the culture with aspirin significantly blocked the effect of aspirin on telomerase activity, showing again the importance of nitric oxide.

The authors ventured, “It is conceivable and supported by recent observations that aspirin stimulates NO formation through its unique ability to trigger the synthesis of 15-epi-lipoxin A4. Aspirin is known to acetylate COX-2 within the endothelium, thus triggering 15-epi-lipoxin A4, which, in turn, elicits NO synthesis from both eNOS [endothelial nitric oxide synthase] and iNOS [inducible nitric oxide synthase].”4

Durk & Sandy have said (see “Aspirin Reduces Endothelial Cell Senescence,” Life Extension News, Volume 8 No. 4, October 2005) that they expect the above effect to be increased by use of an arginine supplement, especially if it contained choline and vitamin B5, because the latter two nutrients can be used to make acetylcholine, which activates eNOS conversion of arginine to nitric oxide.

References

  1. Jaichander et al. Induction of paraoxonase 1 and apolipoprotein A-1 gene expression by aspirin. J Lipid Res 49:2142-8 (2008).
  2. Braig et al. Oncogene-induced senescence as an initial barrier in lymphoma development. Nature 436:660-5 (2005); and Campisi. Suppressing cancer: the importance of being senescent. Science 309:886-7 (2005).
  3. Kletsas et al. The proinflammatory phenotype of senescent cells. Ann NY Acad Sci 1019:330-2 (2004).
  4. Bode-Boger et al. Aspirin reduces endothelial cell senescence. Biochem Biophys Res Commun 334:1226-32 (2005).

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