Salicylic acid vs. aspirin

[Foreigner]

I'm interested in taking aspirin as a longevity supplement but I need to consider this carefully. First of all, I want to find pure powdered aspirin, and not take the OTC stuff with fillers in it. But also, I am concerned about my GI. It's common advice from doctors that people with GI inflammation should avoid NSAIDs, but after looking at the studies those claims are based on, they all involve giving rodents 40-50x the equivalent human dose. Some people in my IBD community have even said that it helps their inflammation. So I am keen to experiment, just a little.

What I really want to know is, what is the big difference between aspirin and salicylic acid? As far as I can tell, it's just an acetyl group? Does this make it more shelf stable, or something? Feel free to explain this biochemically if you have the know-how.

The reason why I want to know is because salicylic acid is much more easy to find than pure aspirin. Some user reports online say that saicylic acid is more likely to cause GI problems and is therefore more appropriate to topical use, but it all seems so anecdotal. Another aspect is that aspirin apparently shows more COX-2 activity, which is more aligned with what I would want it for. But salicylic acid is so readily available and cheap, I am so tempted.

Thoughts? TIA

 

[Skorpio]

The acetyl group sets aspirin apart from other NSAIDs (including salicylic acid). Non aspirin NSAIDs are competitive inhibitors of the COX enzymes. They bind tightly, inhibit enzyme function then unbind and the enzyme resumes it's normal function. Aspirin on the other hand acetylates the active site on these enzymes, which inhibits them until they are broken down and replaced by new COX enzmes. (this effect is particularly significant in platelets, as they do not synthesize protein, aspirin can over time cause inhibition of platelet COX1 while exerting lower effects in the rest of the body).

The difference between salicylic acid and aspirin in terms of GI issues could very well be due to differences in COX 2/COX1 affinity (not sure how different they are, will do research at a later point). COX1 causes GI issues by down regulating the production of protective mucus in the gut, allowing acid to damage cells (among other effects, such as it's effect on platelets where COX activation allows for clotting factors to bind the platelets and activate each other much more efficiently/quickly than if they were just floating loose in the blood).

What aspects of longevity are you looking for? Is it the cardiac effects or anti inflammatory effects?

 

[allone]

vitamin C + aspirin = no GI issues.

have you ever used google btw??

 

[thegreenhand]

vitamin C + aspirin = no GI issues.

have you ever used google btw??

Let’s try to keep it civil and polite please

Foreigner has indicated that he already has tried browsing online for information before coming here, so yes he has ‘used google’

 

[Foreigner]

The acetyl group sets aspirin apart from other NSAIDs (including salicylic acid). Non aspirin NSAIDs are competitive inhibitors of the COX enzymes. They bind tightly, inhibit enzyme function then unbind and the enzyme resumes it's normal function. Aspirin on the other hand acetylates the active site on these enzymes, which inhibits them until they are broken down and replaced by new COX enzmes. (this effect is particularly significant in platelets, as they do not synthesize protein, aspirin can over time cause inhibition of platelet COX1 while exerting lower effects in the rest of the body).

The difference between salicylic acid and aspirin in terms of GI issues could very well be due to differences in COX 2/COX1 affinity (not sure how different they are, will do research at a later point). COX1 causes GI issues by down regulating the production of protective mucus in the gut, allowing acid to damage cells (among other effects, such as it's effect on platelets where COX activation allows for clotting factors to bind the platelets and activate each other much more efficiently/quickly than if they were just floating loose in the blood).

What aspects of longevity are you looking for? Is it the cardiac effects or anti inflammatory effects?

Do you mean the suppression of COX1 by competitive inhibition (or acetylation) downregulates mucus production, or the activity of COX1 without inhibition does this? I wasn't clear.

I'm looking for anti-inflammatory effects. It also has positive impacts on mitochondrial respiration.

vitamin C + aspirin = no GI issues.

have you ever used google btw??

I have very low tolerance for vitamin C orally if it's not present as part of a food. I can't take ascorbic acid on its own, it causes diarrhea, even in small quantities.

 

[Skorpio]

Do you mean the suppression of COX1 by competitive inhibition (or acetylation) downregulates mucus production, or the activity of COX1 without inhibition does this? I wasn't clear.

COX1 drives the mucus production.

Inhibition, either competitive or covalent will inhibit the production of this mucus.

This was the reason companies sought to develop COX2 selective inhibitors (while overlooking the cardiovascular risk of selectively inhibiting COX2).

 

[Foreigner]

COX1 drives the mucus production.

Inhibition, either competitive or covalent will inhibit the production of this mucus.

This was the reason companies sought to develop COX2 selective inhibitors (while overlooking the cardiovascular risk of selectively inhibiting COX2).

Thanks for the clarification. This is giving me second thoughts about the aspirin idea. With IBD, there is already insufficient mucus being produced, which is why microbes in the bowel cause inflammation. The mucosa is less intact. I suspect that COX2 inhibition would increase risk.

My problem is in the colon though and it seems that aspirin is mainly metabolized before that point. I have no stomach issues to speak of.

 

[Skorpio]

Thanks for the clarification. This is giving me second thoughts about the aspirin idea. With IBD, there is already insufficient mucus being produced, which is why microbes in the bowel cause inflammation. The mucosa is less intact. I suspect that COX2 inhibition would increase risk.

My problem is in the colon though and it seems that aspirin is mainly metabolized before that point. I have no stomach issues to speak of.

COX1, not COX2 inhibition causes negative GI effexts.

The GI effects of aspirin and other NSAIDs still exist when the drugs are administered IV. This demonstrates that the GI effects are not driven by the local maximum of drug concentration in the stomach due to the aspirin pill dissolving, but the perfusion of the organ by aspirin containing blood.

However this seems like an issue with significant nuance (regarding aspirin either helping or hurting IBD). Do you have any history taking aspirin and tolerating it /reacting poorly to it?

 

[Foreigner]

COX1, not COX2 inhibition causes negative GI effexts.

The GI effects of aspirin and other NSAIDs still exist when the drugs are administered IV. This demonstrates that the GI effects are not driven by the local maximum of drug concentration in the stomach due to the aspirin pill dissolving, but the perfusion of the organ by aspirin containing blood.

However this seems like an issue with significant nuance (regarding aspirin either helping or hurting IBD). Do you have any history taking aspirin and tolerating it /reacting poorly to it?

I have no history with it at all. I've never taken it, not even once.

It sounds like the enzyme inhibition effect is systemic and not local, from what you're saying. In which case I'd have to proceed with caution. Maybe I could take a baby dose to start.

 

[Skorpio]

I have no history with it at all. I've never taken it, not even once.

It sounds like the enzyme inhibition effect is systemic and not local, from what you're saying. In which case I'd have to proceed with caution. Maybe I could take a baby dose to start.

That sounds like the best way to go.

At the end of the day cells turn over proteins quite quickly usually, so the effect won't be super duper long lasting.

Biggest risk would be causing some issue that occurs via a self sustaining process (such as getting an ulcer that provides inflammatory stimuli beyond the point the drug is removed).

I would certainly reccomend taking a small dose and waiting at least a week or two to assess how you feel. I think with your inflammatory issues, extreme hesitancy is the safest way to approach trying a potentially risky treatment.

 

[sekio]

I would recommend using a NSAID like naproxen or ibuprofen for inflammation; they tend to produce fewer GI disturbances IME.