What Dr. Søberg is describing here is something I find genuinely elegant: your body doesn't trust a single pathway to keep you alive in the cold. It builds three. Cold receptors to the hypothalamus, hypothalamus to brown fat via noradrenaline. A direct signal from skin receptors to brown fat, bypassing the brain entirely. And then the muscles themselvesâwhen they start shivering, they send their own signal to brown fat, essentially saying "we need backup." Three parallel systems, all converging on the same tissue.
This is what evolutionary redundancy looks like in practice. When something matters enough for survival, the body doesn't leave it to chance. We see this same architectural principle in the research on heat shock proteins, in the immune cascade, in sleep pressure mechanisms. Multiple redundant systems, each capable of triggering the response independently. It suggests brown fat wasn't an afterthoughtâit was central.
The 2025 paper on brown fat thermogenesis and cold adaptation in humans aligns tightly with what Søberg describes here. The core consensus is solid: cold exposure upregulates uncoupling protein 1 in brown adipocytes, which decouples ATP synthesis from oxidative phosphorylationâessentially burning fuel to generate heat rather than store energy. The metabolic implications are substantial. One of the articles in the knowledge base puts it plainly: brown fat activation can increase metabolic rate comparable to muscle. That's not a marginal effect.
Where it gets more nuanced is the obesity data. A paper on brown adipose tissue in morbidly obese subjects found a blunted responseâtheir bodies didn't activate brown fat as effectively under cold exposure. Those with detectable brown fat showed meaningful increases in energy expenditure; those without it didn't respond at all. This is a crucial caveat. Brown fat isn't equally available to everyone, and the very people who might benefit most from its metabolic effects are the ones who have the least of it.
Most people try to suppress shivering. They get out, wrap up immediately, and wait for it to stop. I understand the instinctâit's uncomfortable. But Søberg's framing reorients this entirely. Shivering is hormesis. It's the contraction-driven signal that tells your muscle cells and brown fat cells: adapt. The more you allow this response without immediately suppressing it, the more your cells develop the capacity to produce and regulate heat efficiently.
The after-drop phenomenon she describes is real and worth understanding. When you exit cold water, your peripheral blood vesselsâwhich constricted to protect your coreâbegin to dilate. That cooler peripheral blood flows back toward the center. Core temperature can actually continue dropping for several minutes after you've left the water. This is why ending on cold and then warming up gradually matters. You're not just managing comfortâyou're completing a thermoregulatory cycle.
Cold exposure with shivering, not despite it. Get in, stay long enough to feel the full response, exit, and let the after-drop complete before aggressively warming. If you're targeting metabolic adaptationâinsulin sensitivity, brown fat development, baseline calorie burnâthis is your protocol. Regular exposure, moderate duration, allow the shiver. The knowledge base consistently shows that cold therapy improves glucose control across multiple mechanisms, and this is one of the primary drivers.
The surprising connection here is with the obese subjects study. Brown fat is trainable. Like any adaptive tissue, it responds to repeated stimulus. If your brown fat response is currently bluntedâwhether from years of thermal comfort or excess white adipose tissueâregular cold exposure is how you rebuild it. The pathway exists. You just have to use it.