{"id":2760,"date":"2025-04-17T16:32:15","date_gmt":"2025-04-17T20:32:15","guid":{"rendered":"https:\/\/haidut.me\/?p=2760"},"modified":"2025-04-17T16:32:15","modified_gmt":"2025-04-17T20:32:15","slug":"just-2-3-tablets-same-dose-as-used-in-idealabs-cancer-studies-of-aspirin-daily-has-a-strong-anti-aging-effect","status":"publish","type":"post","link":"https:\/\/haidut.me\/?p=2760","title":{"rendered":"Just 2-3 tablets (same dose as used in IdeaLabs cancer studies) of aspirin daily has a strong anti-aging effect"},"content":{"rendered":"

There has been a consistent and well-funded effort by Big Pharma to convince the public that aspirin is a “dangerous” drug, with “unproven”\/”exaggerated” benefits and serious risks. That effort to drive down aspirin usage has been going on for decades, but it really picked up steam after 2020, when study after study showed that taking aspirin can greatly reduce the risks of both getting and dying fro COVID-19, as well as largely prevent the risk of developing the dreaded “long COVID” syndrome. Despite the concerted effort to drive down aspirin usage, recent studies have shown that about 2\/3 of the US population uses aspirin at least weekly for general disease prevention. The study below provides evidence that aspirin may not only be a panacea for many (all?) chronic diseases, but may also be a great anti-aging tool. The evidence for life-extension effects of aspirin is sparse, but almost a decade ago I posted about an aspirin analog being able to increase maximum (as opposed to average) lifespan by ~400%<\/strong><\/span>! The doses used in that study was equivalent to using less than 1g daily for a human.<\/p>\n

https:\/\/lowtoxinforum.com\/threads\/aspirin-pro-drug-from-willow-bark-extends-yeast-lifespan-by-almost-400.10141\/<\/a><\/p>\n

https:\/\/medicalxpress.com\/news\/2016-03-youngand-alive.html<\/a><\/p>\n

http:\/\/dx.doi.org\/10.18632\/oncotarget.7665<\/a><\/p>\n

Interestingly, the new study below demonstrates a robust anti-aging effect of aspirin in a higher organism (rats) using virtually the same dosage as the study published more than a decade ago. The new study also used aspirin, which is much more widely available and in more reliable formulations than willow bark (which is what the 2016 study above used). The human equivalent dose of aspirin in the new study was ~8.5mg\/kg daily, and it was administered orally. While such doses are considered “high” by most doctors, much higher doses (8g-10g daily) have been used in the past to treat inflammatory conditions such as rheumatoid arthritis and even those massive doses had few side effects except tinnitus. At a daily dose of 8.5mg\/kg even tinnitus is not likely to manifest as a side effect and for people concerned about bleeding risks, just a few milligrams (mg) of vitamin K daily may suffice to negate that risk. Interestingly, the study demonstrates that aspirin robustly decreases iNOS expression – the enzyme mainly responsible for the bulk of endogenous nitric oxide (NO) – and that elevated iNOS expression occurs with aging. This finding directly challenges the mainstream theory that NO is beneficial and that agents that increase its levels such as nitroglycerin, arginine, citrulline, etc are good for us. No wonder Big Pharma has made aspirin a target for a massive negative social campaign. A drug that may prevent and cure most chronic diseases, while challenging established medical dogma (e.g. iNOS\/NO) and also potentially extending lifespan, can make most pharma drugs obsolete.<\/p>\n

https:\/\/www.nature.com\/articles\/s41598-025-94566-1<\/a><\/p>\n

“…This study demonstrates that aspirin exhibits significant antiaging potential<\/strong><\/span> in aged rat models, as evidenced by its ability to attenuate oxidative stress through marked reductions in MDA levels, suppression of iNOS gene expression, and mitigation of DNA damage<\/strong><\/span>. Furthermore, histological and ultrastructural analyses revealed substantial improvements in buccal mucosal integrity, underscoring aspirin\u2019s protective role at the tissue and cellular levels<\/strong><\/span>. These results lay a critical foundation for future investigations into aspirin\u2019s mechanistic pathways and its broader role in promoting healthy aging.”<\/p>\n

“…There are numerous antiaging strategies, including diet and physical activity, but the most appealing one is reusing already approved drugs by the FDA, such as aspirin, statins, metformin, and rapalogs4<\/a><\/sup>. Aspirin is an already long studied and effective drug12<\/a><\/sup>. However, its antiaging mechanism remains ambiguous. Thus, in this study, the antiaging impact of aspirin was studied<\/strong><\/span>. To develop an aging model in the current work, systemic administration of D-galactose was applied6<\/a>,13<\/a><\/sup>. Accelerated aging using D-galactose mimics the natural aging process by increasing the production of advanced glycated end products, leading to activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-\u03baB), increasing reactive oxygen species (ROS) generation, mitochondrial breakdown, and apoptosis14<\/a>,15<\/a><\/sup>.<\/p>\n

In the herein study, MDA was selected as a marker for oxidative stress. It was proved by Gil et al. that plasma MDA level increased with aging<\/strong><\/span>16<\/a><\/sup>. This happens as it is produced by ROS reaction with polyunsaturated fatty acids leading to peroxidation of lipids17<\/a><\/sup>. Lipid peroxidation has significant consequences like loss of proliferation potential of cells, change of gene expression, and suppression of antioxidant enzymes. Consequently, oxidative stress accumulates, and aging occurs<\/strong><\/span>18<\/a><\/sup>. In the current work, the aging model group\u2019s MDA level was higher than the control group<\/strong><\/span>. This was in total harmony with prior work performed by Fan et al. and Zhou et al., who showed increased MDA levels in kidneys and brains of mice, respectively, upon D-galactose administration19<\/a>,20<\/a><\/sup>.<\/p>\n

On the other hand, it was found that aspirin decreased MDA levels compared to the aging model group<\/strong><\/span>. This came in harmony with Deng et al., who showed that aspirin provided a shielding effect against endothelial damage caused by low-density lipoprotein (LDL) injection21<\/a><\/sup>. They found that aspirin inhibited the increase in MDA blood levels caused by LDL<\/strong><\/span>. Moreover, in vitro work on endothelial cells cultured in high D-glucose levels showed that aspirin decreased ROS levels significantly<\/strong><\/span>22<\/a><\/sup>. Additionally, aspirin reduced hydrogen peroxide-induced oxidative stress<\/strong><\/span> in melanocytes in vitro23<\/a><\/sup>. This decrease in MDA levels in the aspirin group might be credited to the ability of aspirin to block the metabolism of arachidonic acid into prostaglandins, leading to a decrease in ROS generation that accompanies this process24<\/a><\/sup>. Moreover, aspirin can induce ferritin synthesis, which has antioxidant properties, thus reducing ROS formation<\/strong><\/span>25<\/a><\/sup>.<\/p>\n

In the current work, the iNOS gene was chosen as an oxidative stress and aging marker. This is because iNOS upregulation leads to increased production of nitric oxide, leading to peroxynitrite (ONOO) formation<\/strong><\/span>26<\/a><\/sup>. Increased ONOO formation has severe consequences like suppressing adenosine triphosphate (ATP) synthase, superoxide dismutase, and complexes I and II in the respiratory complex. Additionally, ONOO damages the membranes and DNA of the mitochondria<\/strong><\/span>. All this finally leads to oxidative phosphorylation, oxidative stress, and age-dependent reduction in ATP<\/strong><\/span> production27<\/a><\/sup>. In the current work, the aging model group\u2019s iNOS gene expression was greater than the control group<\/strong><\/span>. This was concomitant with prior studies in which D-galactose administration in mice caused increased iNOS expression20<\/a>,28<\/a><\/sup>.<\/p>\n

On the contrary, the aspirin group expressed lower levels of iNOS mRNA expression compared to the aging model group<\/strong><\/span>. This result was concomitant with prior work that proved that aspirin suppressed the expression of iNOS in lipopolysaccharide-induced macrophage activation29<\/a><\/sup>. Moreover, aspirin ameliorated intervertebral disc degeneration induced via percutaneous disc puncture in Sprague-Dawley rats by inhibiting iNOS expression<\/strong><\/span>30<\/a><\/sup>. Aspirin may have decreased iNOS mRNA expression via suppression of NF-\u03baB, which in turn inhibits M1 macrophage polarization. Decreased M1 macrophages ultimately decreases iNOS production29<\/a><\/sup>. Additionally, aspirin can activate adenosine monophosphate-activated protein kinase, resulting in diminished levels of iNOS, nitric oxide<\/strong><\/span>, and matrix metalloproteinases, which finally decrease oxidative damage30<\/a><\/sup>.<\/p>\n

The histological and ultrastructural examination of the buccal mucosa supported all the results mentioned above. The aging model group showed marked degeneration in epithelium and lamina propria of buccal mucosa as compared to the control group<\/strong><\/span>. These histological outcomes showed that D-galactose caused marked degeneration in rats\u2019 buccal mucosa. This was similar to Youssef\u2019s results, where aging led to the same degenerative changes in rats\u2019 buccal mucosa31<\/a><\/sup>. Moreover, Meng et al. demonstrated that gastric mucosa showed marked atrophy after D-galactose injection32<\/a><\/sup>. Moving to the ultrastructural analysis, this study showed that D-galactose caused keratinocyte degeneration and atypical nuclear morphology. Similar results were observed ultrastructurally upon normal aging in tongue epithelium of rats33<\/a><\/sup>. Moreover, Lopes et al. showed concomitant results34<\/a><\/sup>.<\/p>\n

However, in the aspirin-treated group, both histopathological and ultrastructural examinations were appealing, where aspirin protected the buccal mucosa<\/strong><\/span> against the deleterious effects of D-galactose. This agreed with Rahman et al.\u2019s study which showed that the skin of C57BL\/6 mice exposed to ultraviolet radiation showed decreased inflammatory cell infiltration upon daily oral administration of aspirin35<\/a><\/sup>. In the herein context, the prophylactic antiaging effect of aspirin on tissues may be accredited to the aspirin\u2019s antioxidant and anti-inflammatory properties<\/strong><\/span>. Aspirin can increase antioxidant genes expression like catalase and superoxide dismutase and inhibit NF-\u03baB. Inhibiting NF-\u03baB can decrease iNOS expression and ROS production, causing antioxidant and anti-inflammatory effects and thus preserving the tissues26<\/a>,36<\/a><\/sup>.<\/p>\n

The comet assay was performed in the current work as it can quantitatively detect DNA breakage and mutations37<\/a><\/sup>. In the current study, compared to the control group, the aging model group had a higher percentage of DNA breakage<\/strong><\/span> (% tail DNA). This was also shown in previous studies, which showed increased DNA breakage in the aging model group<\/strong><\/span> in cerebellum cells and immune cells in mice38<\/a>,39<\/a><\/sup>.<\/p>\n

In the present study, %DNA breakage (% tail DNA) was reduced in the aspirin group as compared to the aging model group<\/strong><\/span>. This coincided with a study performed by Dandah, who evaluated how aspirin affected lymphocytes taken from individuals with breast cancer. Using comet assay, they demonstrated that aspirin decreased DNA damage in lymphocytes in vitro40<\/a><\/sup>. Moreover, another study by Rahman et al. revealed that aspirin protected keratinocytes from ultraviolet radiation-dependent DNA damage by reducing 8-oxoguanine and cyclobutane pyrimidine dimers, markers of oxidative DNA damage<\/strong><\/span>, in keratinocytes and melanocytes in skin lesions35<\/a><\/sup>. Many mechanisms were introduced to explain the aspirin protective effect on DNA, including inhibition of cyclooxygenase enzyme and scavenging of ROS41<\/a><\/sup>. Furthermore, aspirin could directly inhibit tumor suppressor gene p53, which directly decreases DNA damage and increases cell survival<\/strong><\/span>40<\/a><\/sup>.”<\/p>\n","protected":false},"excerpt":{"rendered":"

There has been a consistent and well-funded effort by Big Pharma to convince the public that aspirin…<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[2],"tags":[101,326,994,12,2093,833,2076,298,891],"class_list":["post-2760","post","type-post","status-publish","format-standard","hentry","category-science","tag-aging","tag-aspirin","tag-dna","tag-inflammation","tag-inos","tag-lifespan","tag-mda","tag-no","tag-ros","wpcat-2-id"],"_links":{"self":[{"href":"https:\/\/haidut.me\/index.php?rest_route=\/wp\/v2\/posts\/2760","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/haidut.me\/index.php?rest_route=\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/haidut.me\/index.php?rest_route=\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/haidut.me\/index.php?rest_route=\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/haidut.me\/index.php?rest_route=%2Fwp%2Fv2%2Fcomments&post=2760"}],"version-history":[{"count":1,"href":"https:\/\/haidut.me\/index.php?rest_route=\/wp\/v2\/posts\/2760\/revisions"}],"predecessor-version":[{"id":2761,"href":"https:\/\/haidut.me\/index.php?rest_route=\/wp\/v2\/posts\/2760\/revisions\/2761"}],"wp:attachment":[{"href":"https:\/\/haidut.me\/index.php?rest_route=%2Fwp%2Fv2%2Fmedia&parent=2760"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/haidut.me\/index.php?rest_route=%2Fwp%2Fv2%2Fcategories&post=2760"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/haidut.me\/index.php?rest_route=%2Fwp%2Fv2%2Ftags&post=2760"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}