Painkillers and Non Steroidal Anti Inflammatories (NSAIDS) are a part of all of our lives whether we train, or whether we are in pain. There are a lot of stories bandied around about the various types of painkiller – and this blog is not meant to be the be all and end all to the discussion. It came about as I happened to hear a podcast the other day with an injection trained physio- Dave Barker and thought that the information there would be really good to have the information in a written format somewhere.
Below is a summary of stuff that I gleaned from The Physio Matters Podcast. I believe it is pretty true to what was said, though any mistakes are probably mine and my interpretation of the discussion.
For the full podcast – have a listen here.
This is NOT in any way to be taken as a recommendation for taking particular pain killers for certain things and is most certainly NOT something that should be used as a substitute for a visit to a doctor or health professional.
Paracetamol is pretty complex and is (surprisingly) fairly poorly understood. Its main effect is on the Central Nervous System (binding to TRPA1 cells, if you must know)- but this was only discovered about 6 years ago. The main effect appears to be to make us feel less perturbed, but it also has an enhancing effect upon other drugs.
One of the main documented problems is that it quickly becomes toxic. Minimum and maximum levels are almost exactly the same. Paracetamol is metabolised by enzymes in the liver-, but the liver does not TOTALLY metabolise the drug. Because of this, over a period of time there is a gradual increase in toxicity within the liver. Not so great. It is useful to also think about the fact that alcohol is ALSO metabolised in the liver, so if you’re drinking WHILE taking paracetamol the liver is having to work harder than normal to metabolise both things as the same time…… hence why drinking and taking paracetamol is a bad idea.
500-600mg is the minimum effective dose and it has a half life of 1-2 hours, taking 1-2 days to reach a steady state. That being said, there is a lack of consistency in apparent effectiveness which is why patients often get stronger painkillers….. such as…..
Coedine which is actually benign in its pill form. However, it metabolises in the liver and becomes an opiate. The liver changes the product to a pain relieving drug, but about 10-15% of us are non-responders- we cannot metabolise coedine and it has absolutely no effect.
On the other side of the scale, 5% of people are hypermetabolisers and will have a much stronger reaction to the drug than others.
These two are classic short term painkillers and work in a good percentage of patients.
Now we get onto some slightly more heavy duty drugs….
Opioids such as fentanyl and morphine do not, it seems, work so well in chronic pain (though work pretty well in short term acute issues). There has been a massive increase in use of them in non-cancer paitents in recent years. If taken long term it seems that opiods have a reduced effect. This seems to be because the neurological pathways that opioids work on (decending inhibition) get exhausted, greater and greater volumes are needed to create the same pain relieving effect, which declines over time.
Tramadol is not an opioid… yet it does bind to opioid receptors. (it also has a post-synaptic effect f you really want to know…) That is pretty much all that was said about it – apart from this gem….
If you’re on tramadol and amatryptalin this creates an increase of seratonin and noradrenalin. This is not good. But I have no recollection as to why- if you’re interested drop me a line and I’ll do some more digging.
NSAIDS – ibuprofen, diclofenac and naproxen work on COX1 inhibitors which are neurotransmitters. These neurotransmitters also have a knock on effect to the prostaglandins in the stomach – essentially they stop working and gastric trauma is more likely. Funnily enough, from research we have found that in terms of pain relief we actually want to inhibit COX2 inhibitors – not COX 1 as they are much more effective for pain relief…. however, if we did that the knock on effect would be massive- and focussed on cardiovascular system, ending up with with a greater risk of strokes and heart attacks etc. Not so good. So that’s why we focus on COX1 inhibitors.
Side note for NSAIDS – In younger people, gastric problems are more likely as a side effect, but older people are more likely to have cardiovascular issues – (though historically this was due to diclofenac- naproxen is used more often these days and seems to be a better drug with fewer side effects).
Naproxen has some central and some antiinflammatory effects – both in the bloodstream and at the trauma area. It disrupts and attenuates the inflammatory response, it decreases pain but ALSO decreases the healing response which, if you have just been injured, is not such a great thing. Yes, you might be in pain and have large amounts of inflammation- but that inflammation is part and parcel of the healing process. Disrupting that in order to reduce inflammation might mean a longer time rehabbing.
Naproxen has a longer halflife than ibuprofen, meaning it doesn’t have to be taken as often.
- So the thing is don’t take anti-inflammatories in the first 24 hours as it will disrupt the beginning of the healing cycle.
- Taking prophylactic NSAIDS is NOT a good idea – it ends up being a psychological crutch… actually the risk of injury is increased, healing of microtrauma is decreased and remodelling is reduced as well.
- What we are aiming for is the minimum amount of drugs for the smallest amount of time.