Benjamin Bikman isn't arguing that calories don't exist. He's arguing that hormones determine what your body does with them — and that insulin, specifically, is running the show in ways most metabolism conversations completely ignore.
The claim at the center of this work is blunt: insulin suppresses brown fat by roughly half. Not metaphorically. Measurably, in cell cultures, at the receptor level. You expose brown adipose tissue to insulin and it slows down, uncouples less, starts acting like its metabolically inert cousin. The engine doesn't disappear — it just dims. And if insulin stays chronically elevated, it stays dim.
That's the part that stopped me. We've spent years building cold exposure protocols specifically to activate thermogenesis. Ice baths, contrast therapy, deliberate cold shivering. All of it real, all of it effective. But if fasting insulin is consistently above 8 mIU/L, we're working against a hormonal headwind every single time.
Thomas Seager's work on cold plunge science, which we have in the knowledge base, makes a point that connects directly here: brown fat doesn't just generate heat in isolation. It communicates with the thyroid to regulate systemic metabolism. Without sufficient brown fat activity, there's nothing modulating that thyroid signal. Bikman's insulin research explains one reason why brown fat activity might be chronically blunted in the first place — not from cold avoidance, but from hormonal suppression.
Susanna Søberg's seasonal research also aligns with this. Her work on cold exposure improving glucose balance tracks with what Bikman describes: better insulin sensitivity means brown fat gets more freedom to operate. The mechanisms point in the same direction from different angles.
What Bikman adds that most cold exposure researchers don't discuss is ceramides — bioactive lipids that accumulate in muscle tissue when insulin stays high. As ceramide builds, mitochondria fragment. The energy-producing networks that healthy muscle depends on start to break apart. Glucose clearance drops. Insulin rises further to compensate. It's a self-reinforcing cycle, and cold exposure alone doesn't interrupt it.
Here's what I find most compelling: Bikman's evolutionary argument about seasonal co-occurrence. Historically, cold temperatures and food scarcity arrived together. The body expects both signals simultaneously — ketosis and cold — as a paired environmental cue. Ketones beiging white fat into thermogenic tissue, cold activating brown fat directly. These weren't meant to be separate interventions. They were designed to arrive at the same time.
We've separated them. We cold plunge in October after eating starchy meals. We try ketosis indoors in air conditioning. The signals that were meant to be additive arrive in isolation, and we wonder why results plateau.
Get insulin down first. That's dietary — reducing the carbohydrates that spike insulin most aggressively. Within 24 hours, the hormonal environment shifts. From there, cold exposure activates what insulin was suppressing. And if you can time periods of nutritional ketosis with your cold practice, you may be recreating the ancestral pairing that the body's thermogenic systems were actually built for.
Sequence matters here more than intensity. The engine is intact. It just needs the right conditions to run.