There was once a time when the cutting edge in pain relieving technology was a stick to bite down on. It was only when sticks ran short that people turned to pills. How do these work?
When it comes to stopping pain, there are some pills that manage it by deadening the entire area. They put a whole body part on lockdown, refusing to let any signal get out, numbing the whole place. It’s easy to see how those drugs stop pain. They stop everything. Other drugs are more selective. They screen the signals that go through the body, preserving feeling in a person’s aching head, or sore lower back, while blocking pain. How do they manage this?
Aspirin is probably the most well known pain killer. It was derived from willow and birch bark, and works by blocking a certain enzyme. Cyclooxygenase-2 is basically an alarm bell, ordering out the troops. It manufactures a chemical called prostaglandin, which – tattletale that it is – heads straight for the brain and lets the brain know that that particular area is in pain. This causes constant, annoying soreness in the region, even if nobody is moving it or poking it with a stick. Prostaglandin also stays busy around the area of the pain, telling the tissues nearby to release a lot of fluids. The tissues oblige, and the whole area puffs up like it’s trying to win an ugly context.
Aspirin – and Tylenol, and Celebrex, and Ibuprofen, and others – all belong to a class of drugs called COX-2 inhibitors. They enter the blood stream and seek out this enzyme. When they find it, they latch on tenaciously. When they stick to the enzyme, it’s unable work. When COX-2 is gummed up with pain killers, it can’t manufacture prostaglandin, keeping the area from becoming inflamed, and keeping any stray prostaglandin from running up a person’s spine to their head. Meanwhile, any other signals can go about their business uninterrupted.