When taking any form of medication on a regular basis, you should always make an effort to understand how they work. This way, you will be in the best position to decide whether you want to carry on using that medication, you will know how to make the most of it and you will know how to avoid any negative side effects as best as possible.
Seeing as many of us will pop pain killers on a regular basis then, understanding how they work should be a top priority.
How Pain Works
To understand pain killers, it’s first necessary to understand pain itself. What makes us feel pain? Why do we experience it?
Essentially, the purpose of pain is to alert us to a problem. It’s pain that makes us remove our hand from the hot stove when we accidentally lean on it and it’s pain that tells us we need to take it easy when we have a stomach bug. Without pain, you would continue to exacerbate injuries and illnesses without realising it until the point where you eventually collapsed. So believe it or not, pain is actually a good thing.
What make us experience pain, are a particular nerve cells called nociceptor. These are found all along your spine, across your skin and even in some internal organs. Like all nerve cells, these conduct electrical signals and send information back to the brain. The difference though, is that nociceptors only fire when they are ‘excited’ enough – meaning that the level of stimulation is likely to also cause damage. If you lightly touch a needle you’ll feel metal, but if you push hard you’ll reach the ‘nociceptor threshold’ and the nociceptor will fire. This is your ‘pain threshold’.
Where the Drugs Come In
Different people have different pain thresholds, and interestingly this threshold can also be altered by using medication.
Certain chemicals are able to lower or heighten pain thresholds. One of the ‘tuning chemicals’ that increase the sensitivity of nociceptors is something called ‘prostaglandin’ (which also raises body temperature and causes other side effects), and this is responsible for making us more sensitive to pain. Prostaglandin is often increased when cells get damaged, because it is made from a chemical called arachidonic acid, which happens to be released by damaged cells.
Two enzymes, called ‘Cox-1’ and ‘Cox-2’, are responsible for converting this arachidonic acid into prostaglandin H2. Aspirin and Ibuprofin each work by blocking the action of Cox-1 and Cox-2 thereby preventing the creation of more prostaglandin. This means that you will still feel it when someone flicks you in the forehead, but chronic pain and general achiness will be reduced.
It’s also worth noting that Ibuprofen and Aspirin are both blood thinners, which can help to reduce swelling, but which might be an issue if you have low blood pressure already, or if you are also using other blood thinning medications and health supplements. Toxicity is possible in severely high doses.
Paracetamol works slightly differently from Aspirin and Ibuprofen, though the process is not completely understood. The generally belief is that it affects Cox-2 specifically, as well as inhibiting reuptake of anandamide, which is also responsible for increased activation of nociceptors.
Paracetamol is not a blood thinner, but when taken in very high doses can be toxic and place strain on the liver. Those with liver conditions or struggling with alcoholism should always check with doctors before using pain killers.