Which painkillers are okay to use if you have an autoimmune condition?
The fragile relationship between Hashimoto’s and painkillers
Pain is the most common cause of people visiting their healthcare providers. While an estimated 4 in 10 people in the USA suffer from chronic pain, only 1 in 4 of people taking painkillers achieve a full relief. This difference in the efficacy mostly does not come from one reason. Efficiency depends a lot on the genes and health conditions a person might have. In general, taking painkillers causes many — some very serious — side effects. The list of contraindications is usually quite long.
If you have an autoimmune disease, it is good to note the side effects you experience and mention them to your healthcare provider.
TYPES OF PAINKILLERS
On the market currently, there are three main types of painkillers:
Paracetamol (Acetaminophen: Tylenol®, Panadol®, Tipol®, Calpol® etc)→ used for mild and acute pain and fever.
NSAIDs (non-steroidal anti-inflammatory drugs) → used for stronger acute and mild chronic pain, such as after minor surgeries, peripheral pain, period cramps and similar.
Over the counter:
Advil®, Spalt®, Motrin®, Ibuprofen®
Aspirin®, Ascriptin®, Ecotrin®
Diclofenac (Cambia®, Cataflam®, Voltaren®)
For the full list, check: http://wb.md/2mG10u8
Narcotics (aka opioids)→ used mostly for strong and chronic pain, such as post surgery, massive injury, longer-lasting strong pain or in terminal diseases. All of them are highly addictive.
All narcotics are prescription- based:
Morphine, Codeine, endorphins, Oxycodone demerol, Methadone, Fentanyl, Tramadol etc.
NSAIDs countering inflammation
Most of the research on pain and autoimmune, inflammatory diseases was done on rheumatoid arthritis (RA) and psoriasis.
Aspirin and ibuprofen reduce inflammation in the body. This, in theory could work well for people having an autoimmune diseases. But, reducing inflammation is not the only effect on the body.
How do they work?
Aspirin and ibuprofen do not target one specific molecule or process in our body. These are so called “off target” effects, with some of the effects being less than desirable.
In their mechanism of action, they block the cyclooxygenases (COXs) enzyme family. The COX enzymes family has two enzymes: COX1 and COX2. COX1 promotes health of the stomach and intestine lining. COX 2 promotes inflammation, pain and fever.
Blocking COX1 causes the side effects, such as stomach ulcers, stroke, asthma, heart, liver and kidney problems. In addition, aspirin prevents blood clotting, and wound healing, making the process of inflammation last longer.
The problem of a leaky gut
The organs of our digestive system are protected with a single layer of cells. The protective cell layer separates the inside of the abdomen from the contents of the gut (food, bacteria). This is very important, because the content of the gut can start or increase the inflammation in case if they leak from the gut into the abdomen. This is the starting point of an autoimmune disease, where the immune system will get in contact with food particles and attack and destroy them, causing inflammation. This inflammation starts locally, but can spread fast throughout the entire body. At that point, the immune system will probably lose its oral tolerance too.
What to do?
NSAIDs are known to cause serious, and sometimes even fatal gastrointestinal (GI) bleeding and ulcers. If you develop upper abdominal pains, vomit blood, pass blood or black stools, stop taking NSAIDs and see your doctor immediately or go to the nearest healthcare provider.
Narcotics and autoimmune-driven inflammation
Narcotics, or opiates, can change our immune system. Their action is not fully understood. In most of the cases opiates will suppress the immune system, except in the case of endorphins. The way they do it is complex, and it involves them stimulating one type of immune cells, and the result depends on what type of immune balance there was before in the body. That means the activity of opiates will be very different in non-autoimmune patients and in autoimmune patients. It might be very different depending on the level of the current flare-up too.
There is further evidence that opioids might block the progression of certain autoimmune diseases through the regulation of growth and the amount of a certain type of immune cells, called B-lymphocytes. Most of the research so far was done in animal models, and confirmation of how it works in the humans is still missing.
Pain is an expanding market, currently worth 100+ billion US$. NSAIDs represent close to one third of this market, and they are the most used painkillers to treat mild to moderate level of acute pain.
There are several treatment options under research and clinical trials. Ask your healthcare provider if any of the options has shown good results and would be available for you (Esomeprazole® combined with Naproxen® and Famotidine® combined with Ibuprofen®). There are no results so far on how these combinations impact people with Hashimoto’s.
Although opioids seem to offer some promise of blocking an autoimmune response, their high addictive potential, as well as many additional side effects do not make them a silver bullet for both pain and autoimmune issues in the long run.
While painkillers mostly do not resolve the source of pain, as they only block pain signals in the brain, they do help with a normal day-to-day functioning of an individual.
People suffering from autoimmune diseases need to know which painkiller is good to use and will not cause or increase flare-ups, or contribute to a progressive worsening of the disease. In case of over the counter (OTC) painkillers, especially NSAIDs, please consult the pharmacist and ask for the specific side effects impacting the gut and make sure they know you have an autoimmune disease. In case of the prescribed painkillers make sure your healthcare provider knows you are diagnosed with Hashimoto’s, or any other condition. Do not overuse the painkillers, and if you can, talk to your healthcare provider at the first sign of a distress.
1. Arrieta MC, et al. Alterations in intestinal permeability, 2006
2. Wienecke T, et al. Paracetamol versus nonsteroidal anti-inflammatory drugs for rheumatoid arthritis, 2004
3. Fowler PD. Aspirin, paracetamol and non-steroidal anti-inflammatory drugs. A comparative review of side effects, 1987
4. Ramiro S, et al. Combination therapy for pain management in inflammatory arthritis (rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, other spondyloarthritis), 2011
5. Colebatch AN, et al. Safety of non-steroidal anti-inflammatory drugs, including aspirin and paracetamol (acetaminophen) in people receiving methotrexate for inflammatory arthritis (rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, other spondyloarthritis), 2011
6. Bushra R, et al. An overview of clinical pharmacology of Ibuprofen, 2010
7. Bjarnason I, et al. Effect of non-steroidal anti-inflammatory drugs and prostaglandins on the permeability of the human small intestine, 1986
8. Sacerdote P, et al. Experimental evidence for immunomodulatory effects of opioids, 2003
9. Zagon IS, et al. B lymphocyte proliferation is suppressed by the opioid growth factor-opioid growth factor receptor axis: Implication for the treatment of autoimmune diseases, 2011