Aspirin is one of the most commonly used NSAIDs, which are drugs used to reduce inflammation, usually temporarily. Many doctors even advise older patients to take baby aspirin to ward off heart disease. Here, I will argue that taking aspirin is a bad thing if you have chronic pain, and you might not want to take it at all (especially considering that there are many other anti-inflammatory alternatives, both natural and synthetic).

My argument comes out of two convincing studies plus one dumb theory I just made up.  The first study looked at people with fatty livers and tested how leaky their intestines became after taking aspirin, compared to people without a fatty liver. The reason they performed this study is that the causes of fatty liver (specifically conditions called NAFLD and NASH…meaning liver fat that is not caused by drinking too much alcohol and killing your liver) are not well understood. If you are obese, you can get fat infiltration into your liver, but it doesn’t always happen. Lots of nutrients and disease states are involved.

Now let me tell you why this study is cool. They found that both patients with fatty liver and without fatty liver had more stuff leaking through their small intestines after taking aspirin (note: at experimental doses, to induce a response). But those with fatty liver had more leaking in their large intestine (aka colon) as well. Not only that, but people with fatty liver ended up having higher endotoxin levels (endotoxins are released when certain bacteria die). You don’t want these endotoxins to leak through your intestine wall and get into your blood, no sir. That would probably lead to your body having to fight said endotoxins and produce inflammation.

So why is this important for fatty liver? Well, getting fat into the liver isn’t the worse thing in the world, but when you add inflammation and tissue scarring, bad things happen. Endotoxin may cause inflammation around that area, which could take you from fatty liver (which about a quarter of people in the US have) to a diseased fatty liver. In summary: having fatty liver means your colon is more susceptible to the bad effects of aspirin. Now combine those results with this study, which showed that patients with fatty liver have more small intestinal bacterial overgrowth, and you’ve got a bad recipe for gut health–both small intestine and large intestine. (Note, however, that this study did not find an increase in intestinal permeability or endotoxin, but did find high inflammation levels).

Okay, that’s all good. But why is this important for chronic pain? Well, first of all, you want a healthy liver if you have chronic pain. People with chronic pain tend to take more medications than the average person. Drugs are detoxified by the liver. You don’t want a damaged liver to get more damaged. Second, and perhaps more importantly, the liver controls much of the body’s metabolism. Screw up the liver, and you may have a hard time burning fats very well, you might be on the road to diabetes, and you might have a hard time dealing with disease because of these things. That is the path to the dark side. Systemic inflammation is tough to control, and is seriously implicated in some of the more confusing pain conditions.

These are only some of the things we know about aspirin’s disadvantages…I’ve also got a half-baked theory that taking too much aspirin can be bad in other ways. For example, Reye’s syndrome is a rare disease in children that is often associated with aspirin use, and can lead to anything from headaches and vomiting to death. Aspirin might be implicated in this because it can damange mitochondria–the energy powerhouses in our cells. While normal doses of aspirin surely don’t do much in this regard, I need to do more research as to how exactly long term aspirin use affects our cells. Also, taking opioid pain killers makes you constipated, and you don’t want to be constipated at the same time that you have an overload of dead bacterial waste products in your gut.

So in conclusion…be careful about what drugs you take. Aspirin is not benign.


  1. I think gut permeability is definitely a factor in fatty liver disease- both NAFLD and alcohol-related (my speciality is more in the later-  both academically and recreationally). It’s interesting what factors can protect against this (or perhaps we should more fairly say “what factors contribute to this”). There are a couple nice papers in the ALD realm that show that dietary saturated fats are protective against alcohol-induced fatty liver (if I remember correctly, this was first shown in the 80s), and they recently linked the protective effects of saturated fat to decreased gut permeability (and an associated decreased circulating LPS) in comparison to PUFA-fed pair-fed animals. In the non-alcoholic liver disease realm, there have been a few interesting papers that you might enjoy given their focus on another popular (but oh-so-dastardly) analgesic: acetaminophen.  These papers show that acetaminophen toxicity is exacerbated by dietary PUFA- I expect there’s be similar findings with Aspirin!

    (I can dig out refs if you’re interested)

  2. I am wondering about not just ASA but other NSAIDS which those of us with chronic pain are VERY familiar with as an adjunct to other pain meds or as a stand alone in hopes of skipping other pain meds. In my previous life when I was a hospice and palliative care nurse, I often had the difficult task of educating patients on the possible benefits of prescription pain meds when all else had failed and those folks had lost most all of quality of life due to their pain…more important in my way of thinking with my hospice patients who had a shorter time line predicted in which to love/engage/enjoy their life. One approach I would use was to tell them that they should be just a skeptical and careful of their over the counter meds as any that I would tell them about. And a family member of mine developed anemia from too much ibuprofen and folks are ALWAYS taking too much acetaminophen too. I use many approaches (meds, hypnosis, US, etc) to mitigate my pain all towards my end goal of having more quality of life and greater engagement with my loved ones. Like walking a razor’s edge some times, but it is what it is. Good post for sure and more to follow I know!

  3. I wonder if taking 5-10mg of K2 (as recommended by Ray Peat/Danny Roddy) would help prevent leakiness by counteracting the blood thinning effects of aspirin? In lower (not experimental) doses of aspirin and always being sure to take it with K2, I wonder if the same negative effects would show up?

    The fact that aspirin breaks down into salicylic acid, and that being largely responsible for many of its benefits, also makes me wonder if similar compounds (like orthosilicic acid as found in BioSil) would share the same benefits, and could be reasonably used as safer alternatives. BioSil is actually something I’ve been seriously considering adding to my supplement regimen and I’d like to know if you’ve ever heard of it before.

    As for the negative effects of aspirin in general, I’ve been trying to understand why exactly the negative effects come about. What action does aspirin take in the body that makes it potentially dangerous? By understanding that, we might find the best ways to counteract these negative effects to safely get the positive results with the least risk possible. Or, as I said before, simply find a safer alternative that functions similarly to aspirin without the associated risks.

    Very cool site, by the way!

    • “What action does aspirin take in the body that makes it potentially dangerous?”

      Aspirin is a salicylate, and salicylates inhibit the krebs cycle, something Ray Peat never mentions.

      “Salicylates act directly on the respiratory center, causing hyperpnea and tachypnea, which leads to a respiratory alkalosis. Metabolic acidosis results from several mechanisms, including the ability of salicylate to block alpha ketoglutaric dehydrogenase and succinic acid dehydrogenase. This blockage interrupts the tricarboxylic acid (Kreb’s) cycle and mitochondrial oxidation. “


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