The story Andrew Sheridan tells is compelling not because it's dramatic — though it is — but because it illustrates something the research literature struggles to capture: the body's capacity for adaptation when you give it the right signals at the right time.
He came to thermal contrast out of necessity. Achilles tendon repair. Nerve damage. Thirty percent sensation in his foot five months post-surgery. Physical therapy wasn't moving the needle. So he started sitting in a 185-degree Finnish sauna, then dropping into a 45-degree cold plunge. And sensation came back.
The core claim here is that alternating heat and cold — what Thomas Seager calls "pendulating" between sympathetic and parasympathetic nervous system states — can stimulate nerve repair in ways that conventional rehabilitation cannot. That's a meaningful claim. And the biological plausibility is real.
The vasodilation that comes with heat exposure drives blood — and with it oxygen, nutrients, growth factors — to damaged tissues. Heat shock proteins, which Rhonda Patrick's work on sauna and longevity covers thoroughly, act as molecular chaperones. They don't just protect existing proteins; they facilitate repair. In the papers we have on thermal interventions and skeletal muscle adaptations, heat specifically enhances protein turnover — the mechanism by which damaged tissue rebuilds. Heat creates conditions for healing.
Cold does something different. Vasoconstriction reduces inflammation and swelling, which in acute nerve damage can actually impede healing if left unchecked. By cycling hot and cold, Sheridan wasn't just stimulating circulation in one direction — he was creating a pump effect. Flushing inflammatory byproducts out, drawing fresh blood back in. Repeat. The tissue responds.
We don't yet have robust randomized controlled trial data on thermal contrast therapy specifically for neuropathy. What we have is mechanistic plausibility, compelling case studies, and a growing body of research on individual thermal interventions in isolation. Seager's framing is exactly right: Sheridan was "on the leading edge of what would constitute a hypothesis for science." That's how many protocols enter the literature. Someone does something out of desperation. It works. Scientists reverse-engineer why.
The grounding piece Sheridan mentions — the idea of an "ozone bath" during a cold plunge — is more evocative than evidence-based. I'd hold that loosely. The thermal mechanisms are where the science is solid.
If you're recovering from injury — particularly soft tissue or nerve damage — thermal contrast deserves serious consideration as an adjunct to conventional rehabilitation. Not a replacement. An adjunct. The protocol Sheridan used isn't exotic: sustained heat followed by cold immersion, cycling through the sequence. Consistency over intensity. His results didn't come from a single session; they came from repeated, disciplined application over weeks.
Here's what surprised me most when I sat with this alongside the knowledge base: Sheridan wasn't trying to optimize his metabolism. He was trying to feel his foot again. But the research on brown adipose tissue shows that cold exposure activates UCP1 — the uncoupling protein that drives thermogenesis — which is linked to improved insulin sensitivity and metabolic resilience. The two goals share the same biological infrastructure. You can't target just the nervous system or just the metabolic system. When you introduce thermal contrast, the whole system responds. That's not a limitation. That's the point.