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What if chronic pain is a feature, not a bug?

Paul Ingraham ARCHIVEDMicroblog posts are archived and rarely updated. In contrast, most long-form articles on PainScience.com are updated regularly over the years (see updates page).

Imagine someone immune to acute pain, anaesthetized but fully conscious. They can have teeth extracted without freezing, or even step on Lego with impunity. Miraculous! If you aimed a lit blowtorch at this amazing person’s back, the smell would be the first sign of trouble.

Is that a superpower? Or a disaster? If you compare this pain-free marvel to a normal human, who does better in life?

You don’t have to imagine it. Congenital immunity to pain is a rare but real condition, well-studied, and it’s definitely a “bug.” Acute pain is a critical sensory service; without it, we quickly accumulate injuries and infections that we don’t notice until it’s too late. People with CIP die young.

Thanks a bunch, biology — yet another unpleasant-but-necessary part of being human. As if taxes and TV remotes weren’t bad enough.

Chronic pain immunity

Now imagine a different kind of person: someone who is immune to chronic pain only. This comparison has to be a thought experiment, because no one’s immune to chronic pain exclusively, as far as we know.

Chronic pain is often described as a glitch, maybe even a disease in its own right — see central sensitization — like someone’s car alarm going off for an hour when it was really only needed for a minute (if that). If only we could shut off that alarm! It would dramatically improve the lives of a many tens of millions of miserable people.

Or would it? What if chronic pain is just as essential as acute pain, just over longer time-scales? What if they are actually exactly analogous, both “unpleasant but necessary” trade-offs?

Evolution and trade-offs

Evolution is chock-a-block with tradeoffs. Physiology has all kinds of tricks for saving our asses right now that have steep price tags that aren’t paid until much later. For instance, there are many fascinating examples of collateral damage from immune system activity, like osteoarthritis, which isn’t so much about physical wear-and-tear as lingering inflammation after fighting off infections. So our immune systems save our lives, but also make messes we don’t notice for decades. As awful as osteoarthritis can be, that’s a good deal. I don’t know anyone who would rather be killed by an infection at age twenty than have sore knees at sixty.

Acute pain is a complex phenomenon, but it’s nothing compared to the dizzying depth of chronic pain physiology. Chronic pain probably has many purposes, but there is certainly a clue in the phenomenon of neuroinflammation, standard equipment in animal biology. It kicks in to make us feel gross and fragile whenever we are menaced by disease or trauma.

Part of that system involves lowering our pain threshold (see Ji 2018), and that is almost certainly functional. It’s probably exactly analogous to how acute pain aborts risky behaviour, just in a more general way. The malaise and sensitivity of the neuroinflammatory state may be how biology doesn’t just guarantees that we rest and recover when we are most likely to need it.

In other words, it’s how the body says, “No! Sit the hell down! And stay there until you feel better!”

Why would we need to be warned that we’re sick?

Surely being sick itself is enough to know that we are sick? Surprisingly, it’s really not.

People wonder the same thing about acute pain: do we really need an obnoxious alarm system to tell us not to pet porcupines? Aren’t we smart enough to avoid them without pain? Or at least with much less extreme pain? But pain is a great teacher, and its harsh lessons are the entire reason that we know that dangerous things are dangerous! And there are also plenty of hazards that we feel coming before we can perceive them any other way.

Illness can be surprisingly subtle, often mostly asymptomatic … if not for the neuroinflammatory alarm system. It’s not a coincidence that the first warning sign of many serious diseases is usually just fatigue. It’s not that many diseases cause fatigue directly, it’s that fatigue is a standard reaction to most threats to the system.

In fact, most of what we think of as the symptoms of an illness is actually just our own body’s neuroinflammatory alarm system telling us that we are sick.

For instance, a sore throat is caused by the damage directly done by viruses to cells in the mucosa — it’s viral vandalism. The infection actually murders throat cells. But most other typical cold symptoms are caused by our immune response to the infection: congestion, post-nasal drip, sneezing, coughing, and so on… that’s all stuff we’re doing to fight the infection.

But that’s not all! When you feel just dreadful with a bad cold, the malaise is due to the neuroinflammatory alarm. The only way a respiratory tract infection can directly cause that kind of fatigue is if it gets so severe that it starts to impair your ability to breathe normally. Prior to that point, feeling gross is just a side effect of the immune system doing its job — not the effect of damage done by the virus itself.

“Why are you hitting yourself? Why are you hitting yourself?”

We “hit ourselves” with neuroinflammation so that we know we’re sick/injured and act accordingly. As with acute pain, it’s probably important — in an evolutionary context — that the alarm is too loud to ignore.

So acute pain modifies our behaviour on short time spans, which we know is critical to survival. I think it’s likely that some kinds of chronic pain are equally critical for modifying behaviour on longer time spans.

So it’s a feature, not a bug.

That’s not to say it’s always a “feature,” or even good thing — there might be many cases where the alarm is literally worse than the disease, and there might be many more where the alarm truly is a mistake.

 End of post. 
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