Cibus Medicina Est – 'Let Food Be Thy Medicine'

This article has since been published in both The War Kitchen Magazine (Issue 38) and the University of Sheffield Biology (APS) Magazine.

“If a newly discovered substance had aspirin’s anti-infective, anti-cancer, anti-stress, antioxidant and anti-inflammatory actions, it would be the most researched substance in history.” – Ray Peat, 2013

Aspirin is often viewed through a modern pharmaceutical lens, yet its origins are deeply rooted in ancient plant medicine. Derived from salicylic acid, a natural metabolite from willow bark and a variety of other plants, aspirin has been used for thousands of years to treat inflammation and pain. The Ancient Egyptians used willow leaves for a range of medicinal purposes, and even the Ancient Greek philosopher Hippocrates recommended infusions of willow bark to help reduce fever and ease pain during childbirth. Although Hippocrates wouldn’t have known about salicin (the raw compound in willow, which is metabolised into salicylic acid in the body), this nonetheless serves as a good example of the seemingly lost art of attentive observation. In the modern world of being told everything is either black or white, right or wrong, or this or that, we could all take a page (or quite a few) out of the Ancient Greeks’ book. The late Ray Peat articulated this well: “Perceive, think, act”.

Aspirin and WW1

It wasn’t until 1897 that chemist Felix Hoffmann, working for Bayer in Germany at the time, synthesised acetylsalicylic acid, creating the more stable and less irritating form of the compound we know today as aspirin. France had also been experimenting with salicylic acid derivatives at the time, but it was Hoffman’s addition of an acetyl group which made it a practical and marketable drug, an invention often mistakenly attributed to the French.

Aspirin was revolutionary during the early 20th century, not only because it was more effective and better tolerated than the other over-the-counter pain relievers, but also because it proved to be paramount in treating soldiers’ pain and fevers during WW1. Aspirin was even seen as so effective and important that the patent that Bayer had on aspirin at the time was prematurely broken by the Allied countries during the war. As part of wartime measures, Bayer’s German trademarks and patents were seized in Allied countries and companies in Britain, France, and the USA were allowed to produce and sell aspirin without Bayer’s permission. Aspirin also helped combat the 1918 influenza pandemic, being one of the main remedies widely available, and by the 1920s aspirin was a household staple and firmly established as a standard over-the-counter medicine.

Where did it go wrong?

However, aspirin’s status began to shift in the decades that followed. Aspirin became sold less and less, despite it still being the same-old effective compound. This can be predominantly attributed to the expiration of the patent on the synthesis of aspirin, allowing it to be mass-produced and cheaply made. As a result, aspirin brought in smaller profits, leading to reduced advertising and declining sales. In addition to this, the development of other pain relieving alternatives forced aspirin to slowly fade into obscurity, since pharmaceutical companies had more profitable, competing products to sell.

However, it wasn’t until the 1970s when aspirin had a renaissance. Scientists discovered that aspirin could do more than just kill pain. They found that aspirin could also reduce the risk of heart attacks and strokes, which would prove to be particularly beneficial given the rise in cardiovascular disease at the time (Dalen et al., 2014, Mahmood et al., 2014). A wave of studies followed, and researchers have been making novel discoveries ever since.

Aspirin’s effects

Beyond its common association with pain relief, aspirin’s effects extend to nearly every major biological system – a pharmacological Swiss Army knife. It is known to be anti-inflammatory, anti-cancer, anti-stress, pro-metabolic, neuroprotective, and liver-protective. In terms of hormone regulation and cellular metabolism, it has been shown to lower cortisol, excess lipolysis, aldosterone, excess oestrogen, serotonin, parathyroid hormone, prolactin, and both the formation of prostaglandins and lactic acid.

Aspirin’s most important role, though, may lie in its potent anti-inflammatory properties. It functions by blocking the cyclooxygenase (COX) enzymes, particularly COX-1 and COX-2, thus reducing production of the inflammatory prostaglandins derived from polyunsaturated fatty acids (PUFA). It’s this key mechanism which underpins many of its broader systemic effects.

Aspirin has also demonstrated cognitive-enhancing and mood-boosting effects. It is considered anti-fungal (biofilm-disruptive), an antioxidant, an antihistamine, antiviral, and anabolic. Beyond these, aspirin appears to have several lesser-known but still fascinating effects, such as preventing tooth decay, improving insulin sensitivity, increasing testosterone levels in men, and even extending lifespan.

Aspirin also exhibits a number of paradoxical effects. For example, it is an antioxidant that protects against lipid peroxidation. It can inhibit abnormal cell division, but promote normal cell division (Rothwell et al., 2011). One particularly interesting example of aspirin’s extraordinary effects is how salicylic acid is actually protective to the stomach, intestine, and other organs against the damage caused by other drugs. In the body, acetylsalicylic acid (aspirin) is broken down into acetic acid (found in vinegar) and salicylic acid (found in plants). And, “when aspirin was compared with other common anti-inflammatory drugs, it was found that the salicylic acid it releases protects against the damage done by the other drugs” – Ray Peat, 2006. (Ligumsky et al., 1985; Takeuchi et al., 2001).

For now, and for the future

Aspirin is still one of the most widely studied compounds in the world every year, despite being formulated almost 150 years ago. Even now, we are still uncovering more of aspirin’s remarkable effects. For example, last year research led by Georgi Dinkov showed that, with a combination of aspirin and vitamins B1/B3/B7, the team were able to completely cure 3 of 3 mice from a lethal human tumour (JeKo-1 cell line) with 100% lethality and no reported spontaneous regression. For context, a previous study tested this combination on the same tumour without the aspirin (only the B vitamins) and none of the mice survived, although the increase in tumour volume was perturbed.

And in only March of this year, a study was released showing that aspirin prevents metastasis—when a single cell breaks off from the original tumour into the bloodstream and, like a seed in the wind, spreads to other places in the body (Yang et al., 2025). Fortunately, the body has a mechanism to protect itself against metastasis in the form of T-cells. T-cells are able to recognise and destroy these cancerous cells. However, platelets that typically stop bleeding can suppress T-cells and prevent them from destroying these cancerous cells. Aspirin was observed to disrupt these platelets and allow the T-cells to “hunt down” the cancer cells, unleashing the T-cells onto the cancer.

Furthermore, a groundbreaking study was recently released, assessing the long term impacts of low dose aspirin on cancer prevention. It reviewed the cancer incidence from a whopping 1,506,525 people living in Hong Kong across 20 years, with 538,147 taking 80mg of aspirin per day (a very small dose), and the rest being the control group. The control group cohorts were ranked as being much healthier across the board than the aspirin group (15x fewer strokes, 12x fewer incidences of coronary heart disease, twice as less cases of hypertension etc). Over 10 years, aspirin users only had a slightly smaller prevalence of cancer (6.9% vs. 7.1%, however, those taking 80mg of aspirin for longer than 10 years had a significantly lower cancer risk (4.6% lower, p < 0.05). And remember, this is a 500,000-large group of people significantly less healthy than the control group. Aspirin users also had fewer deaths in total, fewer deaths from cancers, and a reduced risk of every cancer, besides bladder and leukemia. If you account for the poor health the aspirin group was already in at the start of the study, it cut cancer risk by around 50%, an enormous figure. 

Conclusion

Far from being a relic of early 20th-century medicine, aspirin continues to prove itself as one of the most versatile and powerful therapeutic agents discovered to date. Its transformation from an ancient herbal remedy to a marvel of modern medicine reflects not only its effectiveness at a biochemical level but also its evolutionary alignment with human physiology; the many “unexpected” beneficial effects of aspirin strongly suggest that it is acting on fundamental biological processes in a positive and coherent way. Aspirin blurs the line between drug and nutrient, synthetic and natural, and perhaps we’re only just beginning to understand the true scope of its potential. 

There hasn’t been a year since 2005, where fewer than 2,000 research papers have been published on aspirin, and the number is steadily growing as each year passes by. There seems to be a positive trend in this field of research, and partly from it emerges a collective pursuit of truly understanding the complexity of human physiology, led by the people, for the health of the people. A sizable proportion of the “Ray Peat sphere” on ‘X’ has been, and still is, a breeding ground for ideas and discussion about nutrition and bioenergetics, and is helping to accelerate this pursuit. As research continues to unveil aspirin’s effects, it challenges us to reconsider whether the most effective therapies might still lie in mother nature and the wisdom of the past.

References: 

General:

1. Takeuchi, K., Hase, S., Mizoguchi, H., Yusaku Komoike and Tanaka, A. (2001). Protection by aspirin of indomethacin-induced small intestinal damage in rats: mediation by salicylic acid. Journal of Physiology-Paris, 95(1-6), pp.51–57.
2. M. Ligumsky, Guth, P.H., J. Elashoff, Kauffman, G.L., Hansen, D. and Paulsen, G. (1985). Salicylic Acid Blocks Indomethacin-Induced Cyclooxygenase Inhibition and Lesion Formation in Rat Gastric Mucosa. Experimental Biology and Medicine, 178(2), pp.250–253. doi:https://doi.org/10.3181/00379727-178-42007.
3. Hippocrates (image taken from Connelly, D. (2014). A history of aspirin. [online] The Pharmaceutical Journal. Available at: https://pharmaceutical-journal.com/article/infographics/a-history-of-aspirin.)
4. Mahmood, S.S., Levy, D., Vasan, R.S. and Wang, T.J. (2014). The Framingham Heart Study and the epidemiology of cardiovascular disease: a historical perspective. The Lancet, 383(9921), pp.999–1008. doi:https://doi.org/10.1016/s0140-6736(13)61752-3.
5. Dalen, J.E., Alpert, J.S., Goldberg, R.J. and Weinstein, R.S. (2014). The Epidemic of the 20th Century: Coronary Heart Disease. The American Journal of Medicine, [online] 127(9), pp.807–812. doi:https://doi.org/10.1016/j.amjmed.2014.04.015.

Anti-cancer:

6. Rothwell, P.M., Wilson, M., Price, J.F., Belch, J.F., Meade, T.W. and Mehta, Z. (2012). Effect of daily aspirin on risk of cancer metastasis: a study of incident cancers during randomised controlled trials. The Lancet, [online] 379(9826), pp.1591–1601. doi:https://doi.org/10.1016/s0140-6736(12)60209-8.
7. ‌Mills, E.J., Wu, P., Alberton, M., Kanters, S., Lanas, A. and Lester, R. (2012). Low-dose Aspirin and Cancer Mortality: A Meta-analysis of Randomized Trials. The American Journal of Medicine, 125(6), pp.560–567. doi:https://doi.org/10.1016/j.amjmed.2012.01.017.
8. Arango, H.A., Icely, S., Roberts, W.S., Cavanagh, D. and Becker, J.L. (2001). Aspirin effects on endometrial cancer cell growth. Obstetrics and Gynecology, [online] 97(3), pp.423–427. doi:https://doi.org/10.1016/s0029-7844(00)01161-3.
9. Elwood, P.C., Morgan, G., Delon, C., Protty, M., Galante, J., Pickering, J., Watkins, J., Weightman, A. and Morris, D. (2021). Aspirin and cancer survival: a systematic review and meta-analyses of 118 observational studies of aspirin and 18 cancers. ecancermedicalscience, 15. doi:https://doi.org/10.3332/ecancer.2021.1258.
10. Lin, Q., Bai, M.-J., Wang, H.-F., Wu, X.-Y., Huang, M.-S. and Li, X. (2021). Aspirin-induced long-term tumor remission in hepatocellular carcinoma with adenomatous polyposis coli stop-gain mutation: A case report. World Journal of Clinical Cases, 9(24), pp.7189–7195. doi:https://doi.org/10.12998/wjcc.v9.i24.7189.
11. Wang, L., Zhang, R., Yu, L., Xiao, J., Zhou, X., Li, X., Song, P. and Li, X. (2021). Aspirin Use and Common Cancer Risk: A Meta-Analysis of Cohort Studies and Randomized Controlled Trials. Frontiers in Oncology, 11. doi:https://doi.org/10.3389/fonc.2021.690219.
12. Jiang, M.-C., Liao, C.-F. and Lee, P.-H. (2001). Aspirin Inhibits Matrix Metalloproteinase-2 Activity, Increases E-Cadherin Production, and Inhibits in Vitro Invasion of Tumor Cells. Biochemical and Biophysical Research Communications, 282(3), pp.671–677. doi:https://doi.org/10.1006/bbrc.2001.4637.
13. Yang, J., Yamashita-Kanemaru, Y., Morris, B.I., Contursi, A., Trajkovski, D., Xu, J., Patrascan, I., Benson, J., Evans, A.C., Conti, A.G., Al-Deka, A., Dahmani, L., Avdic-Belltheus, A., Zhang, B., Okkenhaug, H., Whiteside, S.K., Imianowski, C.J., Wesolowski, A.J., Webb, L.V. and Puccio, S. (2025). Aspirin prevents metastasis by limiting platelet TXA2 suppression of T cell immunity. Nature, [online] pp.1–10. 

Lowers cortisol:

1. Nixon, M., Wake, D.J., Livingstone, D.E., Stimson, R.H., Esteves, C.L., Seckl, J.R., Chapman, K.E., Andrew, R. and Walker, B.R. (2012). Salicylate Downregulates 11β-HSD1 Expression in Adipose Tissue in Obese Mice and in Humans, Mediating Insulin Sensitization. Diabetes, 61(4), pp.790–796. doi:https://doi.org/10.2337/db11-0931.
2. Rangasamy, S.B., Dasarathi, S., Pahan, P., Jana, M. and Pahan, K. (2019). Low-dose aspirin upregulates tyrosine hydroxylase and increases dopamine production in dopaminergic neurons: Implications for Parkinson’s disease. Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, [online] 14(2), pp.173–187. doi:https://doi.org/10.1007/s11481-018-9808-3.

Lowers serotonin:

1. Vitale, G., Pini, L.-A., Ottani, A. and Maurizio Sandrini (1998). Effect of Acetylsalicylic Acid on Formalin Test and on Serotonin System in the Rat Brain. General Pharmacology The Vascular System, 31(5), pp.753–758. doi:https://doi.org/10.1016/s0306-3623(98)00108-6.
2. Sandrini, M., Vitale, G., Dondi, M. and Pini, L.A. (1995). Effects of acetylsalicylic acid on serotonin brain receptor subtypes. General Pharmacology: The Vascular System, 26(4), pp.737–741. doi:https://doi.org/10.1016/0306-3623(94)00252-i.

Lowers prolactin:

1. Luigi Di Luigi, Guidetti, L., Romanelli, F., Baldari, C. and Conte, D. (2001). Acetylsalicylic acid inhibits the pituitary response to exercise-related stress in humans. Medicine and Science in Sports and Exercise, 33(12), pp.2029–2035. doi:https://doi.org/10.1097/00005768-200112000-00009.

Lowers excess lipolysis: 

1. Erman, A., Schwartzman, M. and Raz, A. (1980). Indomethacin but not aspirin inhibits basal and stimulated lipolysis in rabbit kidney. Prostaglandins, [online] 20(4), pp.689–702. doi:https://doi.org/10.1016/0090-6980(80)90108-2.

Lowers parathyroid hormone:

1. Alkhalaf, Z., Kim, K., Kuhr, D.L., Radoc, J.G., Purdue-Smithe, A., Pollack, A.Z., Yisahak, S.F., Silver, R.M., Thoma, M., Kissell, K., Perkins, N.J., Sjaarda, L.A. and Mumford, S.L. (2021). Markers of vitamin D metabolism and premenstrual symptoms in healthy women with regular cycles. Human Reproduction, 36(7), pp.1808–1820. doi:https://doi.org/10.1093/humrep/deab089.

Lowers aldosterone:

1. Snoep, J.D., Hovens, M.M.C., Pasha, S.M., Frölich, M., Pijl, H., Tamsma, J.T. and Huisman, M.V. (2009). Time-dependent effects of low-dose aspirin on plasma renin activity, aldosterone, cortisol, and catecholamines. Hypertension (Dallas, Tex. : 1979), [online] 54(5), pp.1136–42. doi:https://doi.org/10.1161/HYPERTENSIONAHA.109.134825.

Lowers prostaglandin formation:

1. Barnes, C.J., Hamby-Mason, R.L., Hardman, W.E., Cameron, I.L., Speeg, K.V. and Lee, M. (1999). Effect of aspirin on prostaglandin E2 formation and transforming growth factor alpha expression in human rectal mucosa from individuals with a history of adenomatous polyps of the colon. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, [online] 8(4 Pt 1), pp.311–5. Available at: https://pubmed.ncbi.nlm.nih.gov/10207634/.

Lowers lactic acid formation:

1. Ren, G., Ma, Y., Wang, X., Zheng, Z. and Li, G. (2022). Aspirin blocks AMPK/SIRT3-mediated glycolysis to inhibit NSCLC cell proliferation. European Journal of Pharmacology, [online] p.175208. doi:https://doi.org/10.1016/j.ejphar.2022.175208.

Pro-metabolic:

1. Mahmud, T., Rafi, S.S., Scott, D.L., Wrigglesworth, J.M. and Bjarnason, I. (1996). Nonsteroidal antiinflammatory drugs and uncoupling of mitochondrial oxidative phosphorylation. Arthritis & Rheumatism, 39(12), pp.1998–2003. doi:https://doi.org/10.1002/art.1780391208.
2. Meex, R.C.R., Phielix, E., Moonen-Kornips, E., Schrauwen, P. and Hesselink, M.K.C. (2011). Stimulation of human whole-body energy expenditure by salsalate is fueled by higher lipid oxidation under fasting conditions and by higher oxidative glucose disposal under insulin-stimulated conditions. The Journal of clinical endocrinology and metabolism, [online] 96(5), pp.1415–23. doi:https://doi.org/10.1210/jc.2010-1816.

Nootropic:

1. Ghosh, A., Dhumal, V.R., Tilak, A.V., Das, N., Singh, A. and Bondekar, A.A. (2011). Evaluation of nootropic and neuroprotective effects of low dose aspirin in rats. Journal of Pharmacology and Pharmacotherapeutics, 2(1), pp.3–6. doi:https://doi.org/10.4103/0976-500x.77079.

Mood booster:

1. Dominiak, M., Gędek, A., Sikorska, M., Mierzejewski, P., Wojnar, M. and Antosik-Wójcińska, A.Z. (2022). Acetylsalicylic Acid and Mood Disorders: A Systematic Review. Pharmaceuticals, 16(1), p.67. doi:https://doi.org/10.3390/ph16010067.

Neuroprotective:

1. Moro, M.A., J De Alba, A Cárdenas, J De Cristóbal, Leza, J.C., I Lizasoain, M.J.M Dı́az-Guerra, L Boscá and Lorenzo, P. (2000). Mechanisms of the neuroprotective effect of aspirin after oxygen and glucose deprivation in rat forebrain slices. Neuropharmacology, 39(7), pp.1309–1318. doi:https://doi.org/10.1016/s0028-3908(99)00226-9.
2. Gomes, I. (1998). Aspirin: a neuroprotective agent at high doses? The National medical journal of India, [online] 11(1), pp.14–7. Available at: https://pubmed.ncbi.nlm.nih.gov/9557513/.
3. ‌Asanuma, M., Nishibayashi-Asanuma, S., Miyazaki, I., Kohno, M. and Ogawa, N. (2001). Neuroprotective effects of non-steroidal anti-inflammatory drugs by direct scavenging of nitric oxide radicals. Journal of Neurochemistry, 76(6), pp.1895–1904. doi:https://doi.org/10.1046/j.1471-4159.2001.00205.x.

Pro-dopamine:

1. Aubin, N., Curet, O., Deffois, A. and Carter, C. (1998). Aspirin and salicylate protect against MPTP-induced dopamine depletion in mice. Journal of Neurochemistry, [online] 71(4), pp.1635–1642. doi:https://doi.org/10.1046/j.1471-4159.1998.71041635.x.

Liver protective:

1. F. Edward Boas, Brown, K.T., Ziv, E., Hooman Yarmohammadi, Sofocleous, C.T., Erinjeri, J.P., Harding, J.J. and Solomon, S.B. (2019). Aspirin Is Associated With Improved Liver Function After Embolization of Hepatocellular Carcinoma. American Journal of Roentgenology, [online] 213(3), pp.1–7. doi:https://doi.org/10.2214/ajr.18.20846.
2. Han, Y.-M., Lee, Y.-J., Jang, Y.-N., Kim, H.-M., Seo, H.S., Jung, T.W. and Jeong, J.H. (2020). Aspirin Improves Nonalcoholic Fatty Liver Disease and Atherosclerosis through Regulation of the PPARδ-AMPK-PGC-1α Pathway in Dyslipidemic Conditions. BioMed Research International, [online] 2020, p.7806860. doi:https://doi.org/10.1155/2020/7806860.
3. Simon, T.G., Henson, J., Osganian, S., Masia, R., Chan, A.T., Chung, R.T. and Corey, K.E. (2019). Daily aspirin use associated with reduced risk for fibrosis progression in patients with nonalcoholic fatty liver disease. Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association, [online] 17(13), pp.2776-2784.e4. doi:https://doi.org/10.1016/j.cgh.2019.04.061.

Anti-fungal (biofilm disruptive):

1. Trofa, D., Agovino, M., Stehr, F., Schäfer, W., Rykunov, D., Fiser, A., Hamari, Z., Nosanchuk, J.D. and Gácser, A. (2009). Acetylsalicylic acid (aspirin) reduces damage to reconstituted human tissues infected with Candida species by inhibiting extracellular fungal lipases. Microbes and Infection, [online] 11(14-15), pp.1131–1139. doi:https://doi.org/10.1016/j.micinf.2009.08.007.
2. Liu, X., Wang, D., Yu, C., Li, T., Liu, J. and Sun, S. (2016). Potential Antifungal Targets against a Candida Biofilm Based on an Enzyme in the Arachidonic Acid Cascade—A Review. Frontiers in Microbiology, 7. doi:https://doi.org/10.3389/fmicb.2016.01925.
3. Alem, M.A.S. and Douglas, L.J. (2004). Effects of Aspirin and Other Nonsteroidal Anti-Inflammatory Drugs on Biofilms and Planktonic Cells of Candida albicans. Antimicrobial Agents and Chemotherapy, 48(1), pp.41–47. doi:https://doi.org/10.1128/aac.48.1.41-47.2004.

Antihistamine:

1. Young, G. and Jewell, D. (1997). Antihistamines versus aspirin for itching in late pregnancy. PubMed. doi:https://doi.org/10.1002/14651858.cd000027.

Anti-oxidant:

1. Ellero-Simatos, S., Beitelshees, A.L., Lewis, J.P., Yerges-Armstrong, L.M., Georgiades, A., Dane, A., Harms, A.C., Strassburg, K., Guled, F., Hendriks, M.M.W.B., Horenstein, R.B., Shuldiner, A.R., Hankemeier, T., Kaddurah-Daouk, R. and Pharmacometabolomics Research Network (2015). Oxylipid Profile of Low-Dose Aspirin Exposure: A Pharmacometabolomics Study. Journal of the American Heart Association, [online] 4(10), p.e002203. doi:https://doi.org/10.1161/JAHA.115.002203.

Anabolic:

1. Chin, K.-Y. (2017). A review on the relationship between aspirin and bone health. Journal of Osteoporosis, [online] 2017, pp.1–8. doi:https://doi.org/10.1155/2017/3710959.

Antiviral:

1. Glatthaar-Saalmüller, B., Mair, K.H. and Saalmüller, A. (2016). Antiviral activity of aspirin against RNA viruses of the respiratory tract-an in vitro study. Influenza and Other Respiratory Viruses, 11(1), pp.85–92. doi:https://doi.org/10.1111/irv.12421.

Paradoxical effects: 

1. Rothwell, P.M., Fowkes, F.G.R., Belch, J.F., Ogawa, H., Warlow, C.P. and Meade, T.W. (2011). Effect of daily aspirin on long-term risk of death due to cancer: analysis of individual patient data from randomised trials. The Lancet, 377(9759), pp.31–41. doi:https://doi.org/10.1016/s0140-6736(10)62110-1.
2. Tewari, S., Kaushish, R., Sharma, S. and Gulati, N. (1997). Role of low dose aspirin in prevention of pregnancy induced hypertension. Journal of the Indian Medical Association, [online] 95(2), pp.43–4, 47. Available at: https://pubmed.ncbi.nlm.nih.gov/9357241/.

Tooth decay prevention:

1. Yuan, M., Zhan, Y., Hu, W., Li, Y., Xie, X., Miao, N., Jin, H. and Zhang, B. (2018). Aspirin promotes osteogenic differentiation of human dental pulp stem cells. International Journal of Molecular Medicine. doi:https://doi.org/10.3892/ijmm.2018.3801.

Stroke and DVT prevention:

1. Schrör, K. (1997). Aspirin and Platelets: The Antiplatelet Action of Aspirin and Its Role in Thrombosis Treatment and Prophylaxis. Seminars in Thrombosis and Hemostasis, [online] 23(04), pp.349–356. doi:https://doi.org/10.1055/s-2007-996108.
2. Lavu, M.S., Porto, J.R., Hecht, C.J., Acuña, A.J., Kaelber, D.C., Parvizi, J. and Kamath, A.F. (2024). Low-Dose Aspirin Is the Safest Prophylaxis for Prevention of Venous Thromboembolism After Total Knee Arthroplasty Across All Patient Risk Profiles. The Journal of bone and joint surgery. American volume, [online] 106(14), pp.1256–1267. doi:https://doi.org/10.2106/JBJS.23.01158.

Improving insulin sensitivity:

1. Yuan, M. (2001). Reversal of Obesity- and Diet-Induced Insulin Resistance with Salicylates or Targeted Disruption of Ikkbeta. Science, 293(5535), pp.1673–1677. doi:https://doi.org/10.1126/science.1061620.

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Increasing testosterone levels in men:

1. L. Di Luigi, Rossi, C., P. Sgrò, Fierro, V., Romanelli, F., C. Baldari and Guidetti, L. (2007). Do Non-Steroidal Anti-Inflammatory Drugs Influence the Steroid Hormone Milieu in Male Athletes? International Journal of Sports Medicine, 28(10), pp.809–814. doi:https://doi.org/10.1055/s-2007-964991.

Extending lifespan:

1. Berkel, C. and Cacan, E. (2021). A collective analysis of lifespan-extending compounds in diverse model organisms, and of species whose lifespan can be extended the most by the application of compounds. Biogerontology, 22(6), pp.639–653. doi:https://doi.org/10.1007/s10522-021-09941-y.