How icing works • Some thoughts on what icing is doing to tissue

In the aftermath of a flurry of inflammation research lately (see “An inflammatory problem,” parts one & two), I have tried to make better sense of icing. Icing is used wherever people suspect inflammation, but that includes at least three quite different biological situations:

1. true inflammation, where an immune system reaction makes sense (lacerations)
2. sterile injury, with an excessive immune response (bruises, muscle and ligament tears)
3. connective tissue degeneration, with little or no classic inflammation at all (repetitive strain injuries)

Icing is particularly popular as a treatment for repetitive strain injury, and I have prescribed it plenty myself. Why? Can ice actually help an injury that isn’t very “inflammatory” in the first place? This is an condensed excerpt from my updated icing article — if you want detail, skip on over there now and read that. Stay here for the skinny.

In case of inflammation

When tissue is damaged, the body responds with a complex array of chemical and neurological changes collectively known as inflammation. For instance, the capillaries widen in a big way to bring extra oxygen and nutrients to the area. They also “loosen,” becoming more permeable, to give immune system cells easy access to the injury. Most of the pain and discomfort of inflammation is due to the immune system reaction.

If the skin is broken, there is a risk of infection, and the immune system reaction is essential — a pure physiological goodness, finely-tuned by evolution to optimize recovery and minimize infection danger. Strictly speaking, if you to want to heal well, don’t interfere with this kind of inflammation!

If the skin isn’t broken, things are different! In this context, inflammation is an overreaction that causes collateral damage and excessive pain due to a weird glitch in biology. There is no need for the immune cells to get all fired up for a sterile, internal injury where there is no possibility of infection. Nevertheless, they do get fired up. It’s a reasonable goal to try to suppress it with ice (and anti-inflammatory medications like ibuprofen). Bet you didn’t know that. In this context, inflammation is an absurd overreaction that causes collateral damage and excessive pain for no good reason at all — a glitch in biology.Few people do — this is based on surprisingly new science.

Of course, immune system activity is not the only reason injuries hurt. Damaged and stressed cells put out many kinds of distress signals. As with most biological processes, our comfort is not really a priority. In fact, quite the opposite — inflammation has partly evolved to be painful. Cavemen didn’t have ibuprofen and ice, nor did they have the benefit of understanding inflammatory chemistry. In the big picture, super painful inflammation was good for our species: victims were encouraged to stay relatively still while inflammation ran its course like a fever!

But for modern humans, inflammation is … well, it’s overkill. We can afford to “turn it down.” We can ignore the warning of the inflammation to a point. Ice can only turn it down so much anyway, so there’s not risk of missing the pain alarm entirely! Cold slows metabolic activity, numbs nerve endings, constricts capillaries. It limits and controls inflammation. It makes it hurt less. It helps us get through the day. And that’s an especially good thing for sterile injuries, where the inflammation is largely pointless.

Where’s the fire?

And what if there’s not really not much inflammation? What if there’s no fire to put out? Does ice still have a role to play? Yes, some — but not because it’s “anti-inflammatory.”

What’s going on in a repetitive strain injury like runner’s knee or tennis elbow or Achilles tendinitis is painful degeneration — tissue rot, which has more in common with arthritis than inflammation. The chemistry of these situations is very different than classic inflammation, and in particular involves relatively little immune system activity. The most obvious implication of this is that treatments intended to suppress immune system activity — the anti-inflammatories — are obviously not going to work well. And indeed they don’t.

If ice can help a repetitive strain injury in any way beyond brief numbing — no one has ever actually proven it, or shown how it might work. However, it might stimulate miscellaneous minor tissue healing processes. Virtually any stimulatory input to the body, up to a point, can provoke a healthy, adaptive, tissue-building response. Maybe. (See Wolff’s Law). In broad strokes, that is probably the only plausible therapeutic mechanism of icing. Ice may simply be one of the easiest delivery systems for a bit of non-toxic stimulation — a way to stimulating tissue without overloading it, while simultaneously give some temporary pain relief from numbing.

It’s worth doing. The great advantages of ice as a treatment are not its impressive biological effects — which are unknown and unproven — but its thrift, ease, and safety: treatment options simply don’t get any more innocuous while still having some plausible mechanism of benefit. Therefore ice remains firmly on my “worth a shot” list for RSIs. However, it certainly isn’t “anti-inflammatory”!