Aspirin’s potential side effects may outweigh its use as a nootropic supplement.
For thousands of years, aspirin has been used in medicine to help minimize pain and handle fever side effects. Recent developments suggest the possibility of its use as a nootropic by means of:
- Enhancing cognition. Several studies have shown the potential of aspirin to improve memory and cognitive skills.
- Modulating inflammation. Aspirin’s ability to reduce inflammation may promote healthy brain vasculature.
- Protecting neurons. Neuroprotection may result from the medicine’s capacity to inhibit glutamate and subsequently reduced the risk of infarction.
An age-old medicine, acetylsalicylic acid, better known as aspirin, has been used to combat fever, pain, and inflammation, as well as in the management of numerous health conditions related to the heart. It is not only one of the most regularly consumed medications in the world, but also considered by WHO to be an essential medicine in a basic health system.1
Among nonsteroidal anti-inflammatory drugs (NSAIDs), aspirin is likely the most frequently used for medical practices, especially in cases of inflammation. The accepted mechanism behind the process is that aspirin chiefly inhibits cyclooxygenases (COXs) in order to modulate ion channels and nociceptors, similar to that of other nootropics.2 Taking into account that NSAIDs have been shown to decrease the risk of AD by 50%,3 aspirin is believed to possess prospects as a restorative agent in neurodegenerative disorders, like vascular dementia, specifically by targeting pathological pathways and clearing harmful peptides.45
Farther, aspirin employs complex pharmacological actions that may hinder dementia, including:
- Diminishing risk of ischemia
- Reducing inflammation
On the other hand, however, aspirin has negatively been tied to cerebral hemorrhages as a consequence of the blood thinning it causes through hindering prostaglandin action. The disparate workings of aspirin give it the potential to present either favorable or adverse nootropic effects.7
Aspirin’s direct role in battling vascular dementia is lacking in evidence
Since low-dose aspirin is well known to improve the prognosis of heart disease and stroke, most likely by stabilizing brain and heart blood flow while also minimizing clot formation within blood vessels, many medical doctors figure that it will also help in cases of vascular dementia.
A general review study of aspirin concerning vascular dementia revealed that there is actually no sound evidence suggesting that it helps people with vascular dementia.8 It is possible that vascular dementia is caused by a process that aspirin has no immediate role in. Those who use aspirin for vascular dementia should be aware of the many risks, including fatal hemorrhages, of taking it for extended periods of time.
How Aspirin May Help as a Nootropic
Aspirin’s strength seems to reside more in its capacity to shield neurons and act as an anti inflammatory than to boost cerebral function; it is not a brain-boosting smart drug.
Modulation of Inflammation
Inflammation involves a multi-faceted pathway that can harm neurons along the way. Fortunately, aspirin may be capable of stifling what is referred to as its neurotoxic cascade in three key areas:
- Cox-1: Aspirin may irreversibly inhibit cyclooxygenase (COX-1).
- Cox-2: Cox-2 enzyme activity may be modified by aspirin.
- Prostaglandin and thromboxane: Aspirin may suppress both compounds from stimulating inflammatory procedures.
Managing cox-1, cox-2, and prostaglandin with thromboxane pathways has positive anti-inflammatory and anti-platelet effects, which are particularly useful in atherosclerosis, heart problems, and stroke.9 Since comparable mechanisms underlie the pathophysiology of many neuropsychiatric complications, aspirin is a feasible candidate for secondary prevention via interrupting neurotoxic cascades.
Neuroprotection Against Glutamate
Interestingly, claims have been made that using aspirin to invoke chronic anti-inflammation may protect against the neurotoxicity triggered amino acid glutamate in both neuronal cultures as well as hippocampal slices. Aspirin purportedly wards off the induction of nuclear factor kappa beta (NF-κβ) by inhibiting glutamate at the site of its receptors.10 This result is at conflict with other studies, however, which suggest the opposing conclusion that activating NF-κβ prevents apoptosis of neuronal cells.
Aspirin’s Proposed Brain Benefits & Uses
The most common use of aspirin as a nootropic is in its prescription for cases of vascular dementia.
Beyond this, several groups are exploring the potential of using aspirin to boost mental performance.
- Improved spatial learning. One research group demonstrated aspirin markedly improving the performance of aged rats during hidden and visible platform trials of swimming in a maze. The improvement in both the speed of spatial learning and overall retention was impressive but only lasted 8 days.11 The underlying physiological mechanism behind the cognitive improvement still needs to be addressed.
- Memory retention. Aspirin administration significantly increased the retention of conditioned avoidance response compared to control through inhibition of serotonergic transmission. In other words, taking the medicine seemed to stop electroconvulsive shock (ECS) from the kind of conditioned memory loss that took place without aspirin.12
Aspirin + Piracetam: Another Synergistic Nootropic Stack?
There seems to be a forum buzz that aspirin and piracetam form a synergistic nootropic stack. This concept is often attributed to an 2013 Russian animal study in which researchers reported that aspirin plus piracetam was 15.7% more active than piracetam alone. Researchers attributed this apparent synergy to aspirin’s ability to enhance brain microcirculation, and suggested it may have neuroprotective activity. More on brain circulation nootopics
Research favors the probable capacity of aspirin to reinforce memory in animals as well as protect neurons. Salient nootropic benefits of aspirin include:
- Improving memory. In a neurotoxicity mouse model, both low and high doses of aspirin successfully improved short-term cognitive behavior via modulation of opioid systems in the cortex, which encompassed enhancements in spatial memory, extinction learning, and contextual memory.14
- Protecting neurons. When given before brain blood clots, aspirin significantly reduced not only infarction volume, but also glutamate release in ischemic rat brains by increasing ATP production.15
- Speeding up recovery. Walking track analysis and electrophysiological assessment determined that motor functional recovery in rats taking aspirin were better than that of the control. Axonal nerve regeneration was additional measured to be superior with aspirin.16
Aspirin studies demonstrate that it may possibly have a minor useful impact in brain health, but the data are sparse and at times inconclusive.
In this investigation, the cognitive decline of 3,809 seniors over the age of 65 was measured over the course of 3 years. There was no substantial effect on those who took aspirin, although the data show modest advantages in taking aspirin intermittently by influencing multi-infarction dementia.
- The study concluded that there is “little benefit of aspirin use on decline in cognitive function in an elderly population, although the data are consistent with a possible small beneficial effect associated with intermittent use.”17
For a period of 2 years, 310 adults with Alzheimer’s (AD) were observed for cognitive function after being given one 75 mg aspirin tablet a day in this randomized investigation. In people who took aspirin, mean mini-mental state examination (MMSE) score was 0.10 points higher and mean Bristol activities of daily living scale (BADLS) score was 0.62 points lower than in those who avoided aspirin. Out of those on aspirin, 8% had bleeds that led to hospitalization.
- The study concluded that “in patients with typical AD 2 years of treatment with low-dose aspirin has no worthwhile benefit and increases the risk of serious bleeds.”18
In this randomized, placebo-controlled, double-blind investigation, 3350 adults over the age of 50 years were examined after taking either 100 mg of aspirin per day or a placebo for a period of 5 years. No significant differences in change in cognitive ability or overall score were identified.
- The study concluded that “low dose aspirin does not affect cognitive function in middle aged to elderly people at increased cardiovascular risk.”19
For the most part, studies suggest not only the irrelevance of aspirin in terms of nootropic benefits, but also the bleeding threat it may pose. Room for continuing studies is certainly wanting, especially considering current research has focused almost exclusively on the elderly.
Dosage for Nootropic Use
Aspirin may be taken as a capsule with a glass of water:
- Typical dosage range 81 mg – 650 mg
- Average adult dosage 325 mg
- Extra strength dosage 500 mg
The supplement should neither be taken in combination with other N-SAIDS nor by those at risk of bleeding complications.
Supplements in Review Says
- Aspirin not recommended as a nootropic
We do not recommend aspirin as a nootropic. Although aspirin displays excellent inflammation modulating ability, the associated risks involved with taking it for routine supplementation outweigh the benefits. Animal studies have shown minor promise, but most research thus far highlights aspirin’s limited effect on cognitive function. Further studies are certainly concerning its ability to protect neurons and enhance memory may serve to clarify matters.
Try turmeric supplementation for similar and safer results. Aspirin is widely used as a temporary way to relieve symptoms associated with pain and fever. For cerebral-based anti-inflammatory effects, we suggest trying other nootropics, like turmeric, for similar and safer outcomes.
- WHO Model List of EssentialMedicines. World Health Organization. 2013 April;18:1-47. ↩
- Voilley N, et al. Nonsteroid anti-inflammatory drugs inhibit both the activity and the inflammation-induced expression of acid-sensing ion channels in nociceptors. J Neurosci. 2001;21:8026-33. ↩
- Stewart WF, et al. Risk of Alzheimer’s disease and duration of NSAID use. Neurology. 1997;48:626-32. ↩
- Hirohata M, et al. Non-steroidal anti-inflammatory drugs have anti-amyloidogenic effects for Alzheimer’s beta-amyloid fibrils in vitro. Neuropharmacology.2005;49:1088-99. ↩
- Medeiros R, et al. Aspirin-triggered lipoxin A4 stimulates alternative activation of microglia and reduces Alzheimer disease-like pathology in mice. Am J Pathol. 2013;182:1780-89. ↩
- Walters K, et al. Predicting dementia risk in primary care: development and validation of the Dementia Risk Score using routinely collected data. BMC Med. 2016;14:6. ↩
- Rands G, Orrell M. Aspirin for vascular dementia. Cochrane Database Syst Rev. 2000;4:CD001296. ↩
- Williams PS, et al. Aspirin for vascular dementia. Cochrane Database Syst Rev. 2000;4:CD001296. ↩
- Berk M, et al. Aspirin: a review of its neurobiological properties and therapeutic potential for mental illness. BMC Medicine. 2013 Mar 18;11(74):1-17. ↩
- Neuroprotective Agents. Jain KK. The Handbook of Neuroprotection. Springer Science & Business Media. 2011. ↩
- Smith JW, et al. Chronic aspirin ingestion improves spatial learning in adult and aged rats. Pharmacol Biochem Behav. 2002 Jan-Feb;71(1-2):233-8. ↩
- Ghosh A, et al. Evaluation of nootropic and neuroprotective effects of low dose aspirin in rats. J Pharmacol Pharmacother. 2011 Jan;2(1):3-6. ↩
- Lieberman HR, et al. The effects of caffeine and aspirin on mood and performance. J Clin Psychopharmacol. 1987 Oct;7(5):315-20. ↩
- Rizwan S, et al. Memory-enhancing effect of aspirin is mediated through opioid system modulation in an AlCl3-induced neurotoxicity mouse model. Exp Ther Med. 2016 May;11(5):1961-70. ↩
- De Cristobal J, et al. Neuroprotective effect of aspirin by inhibition of glutamate release after permanent focal cerebral ischaemia in rats. J Neurochem. 2001 Oct;79(2):456-9. ↩
- Cui Yi, et al. The neuroprotective effects of aspirin following crush injury to rat sciatic nerve. Int J Clin Exp Med. 2015;8(10):18185-90. ↩
- Sturmer T, et al. Aspirin Use and Cognitive Function in the Elderly. Am J Epidemiol. 1996;143(7):683-91. ↩
- Bentham P, et al. Aspirin in Alzheimer’s disease (AD2000): a randomised open-label trial. Lancet Neurol. 2008 Jan;7(1):41-9. ↩
- Price JF, et al. Low dose aspirin and cognitive function in middle aged to elderly adults: randomised controlled trial. BMJ. 2008;337:a1198. ↩