How Do Pain Relievers Work George Zaidan
Translator: Ido Dekkers
Reviewer: Ariana Bleau Lugo
Say you’re at the beach,
and you get sand in your eyes.
How do you know the sand is there?
You obviously can’t see it,
but if you are a normal, healthy human,
you can feel it,
that sensation of extreme discomfort,
also known as pain.
Now, pain makes you do something,
in this case, rinse your eyes
until the sand is gone.
And how do you know the sand is gone?
Exactly. Because there’s no more pain.
There are people who don’t feel pain.
Now, that might sound cool, but it’s not.
If you can’t feel pain, you could
get hurt, or even hurt yourself
and never know it.
Pain is your body’s early warning system.
It protects you from the world
around you, and from yourself.
As we grow, we install pain detectors
in most areas of our body.
These detectors
are specialized nerve cells
called nociceptors
that stretch from your spinal cord
to your skin, your muscles, your joints,
your teeth and some
of your internal organs.
Just like all nerve cells,
they conduct electrical signals,
sending information from wherever
they’re located back to your brain.
But, unlike other nerve cells,
nociceptors only fire if something
happens that could cause
or is causing damage.
So, gently touch the tip of a needle.
You’ll feel the metal,
and those are your regular nerve cells.
But you won’t feel any pain.
Now, the harder you push
against the needle,
the closer you get
to the nociceptor threshold.
Push hard enough,
and you’ll cross that threshold
and the nociceptors fire,
telling your body to stop doing
whatever you’re doing.
But the pain threshold isn’t set in stone.
Certain chemicals can tune nociceptors,
lowering their threshold for pain.
When cells are damaged,
they and other nearby cells
start producing these tuning
chemicals like crazy,
lowering the nociceptors'
threshold to the point
where just touch can cause pain.
And this is where over-the-counter
painkillers come in.
Aspirin and ibuprofen
block production of one class
of these tuning chemicals,
called prostaglandins.
Let’s take a look at how they do that.
When cells are damaged, they release
a chemical called arachidonic acid.
And two enzymes called COX-1 and COX-2
convert this arachidonic acid
into prostaglandin H2,
which is then converted
into a bunch of other chemicals
that do a bunch of things,
including raise your body temperature,
cause inflammation
and lower the pain threshold.
Now, all enzymes have an active site.
That’s the place in the enzyme
where the reaction happens.
The active sites of COX-1 and COX-2
fit arachidonic acid very cozily.
As you can see, there is no room to spare.
Now, it’s in this active site
that aspirin and ibuprofen do their work.
So, they work differently.
Aspirin acts like a spine
from a porcupine.
It enters the active site
and then breaks off,
leaving half of itself in there,
totally blocking that channel
and making it impossible
for the arachidonic acid to fit.
This permanently deactivates
COX-1 and COX-2.
Ibuprofen, on the other hand,
enters the active site,
but doesn’t break apart
or change the enzyme.
COX-1 and COX-2 are free
to spit it out again,
but for the time
that that ibuprofen is in there,
the enzyme can’t bind arachidonic acid,
and can’t do its normal chemistry.
But how do aspirin and ibuprofen
know where the pain is?
Well, they don’t.
Once the drugs are in your bloodstream,
they are carried throughout your body,
and they go to painful areas
just the same as normal ones.
So that’s how aspirin and ibuprofen work.
But there are other dimensions to pain.
Neuropathic pain, for example,
is pain caused by damage
to our nervous system itself;
there doesn’t need to be
any sort of outside stimulus.
And scientists are discovering
that the brain controls
how we respond to pain signals.
For example, how much pain
you feel can depend on
whether you’re paying attention
to the pain, or even your mood.
Pain is an area of active research.
If we can understand it better, maybe
we can help people manage it better.