Most conversations about metabolism focus on what you eat or how much you move. But beneath those surface-level variables, a more fundamental story is unfolding — one governed by a single hormone that touches nearly every cell in your body. Dr. Benjamin Bikman, cell biologist and metabolic researcher at Brigham Young University, has spent more than a decade studying that hormone: insulin.
What he's found reshapes how we think about fat, energy, and the body's capacity to heal itself.
Insulin's primary role is deceptively simple: it signals your cells to store energy. When blood sugar rises, insulin rises in response, directing glucose and fatty acids into storage. This is normal physiology — the problem emerges when insulin remains chronically elevated.
High insulin does two distinct things to fat tissue. First, it drives adipogenesis — the conversion of stem cells into new fat cells. Second, it promotes lipogenesis — the filling of existing fat cells with stored lipid. You can't grow fat cells in a lab dish without insulin. Every biochemist knows this. And yet, Bikman notes, the role of insulin in human obesity is still routinely dismissed in favor of the simpler calorie narrative.
His benchmark is practical: if your fasting insulin is above roughly 8 mIU/L, your body is predominantly in storage mode — even while you sleep. Below that threshold, fat mobilization becomes the default. Diet, then, is not primarily about calories. It is about the hormonal signal those calories generate.
Beyond insulin itself, Bikman's research points to a class of bioactive lipids called ceramides as a critical link between chronic hyperinsulinemia and cellular dysfunction. Ceramides are not inherently harmful — every cell requires them. But when they accumulate excessively, the downstream effects are significant.
In muscle tissue — the body's primary glucose sink — ceramide accumulation forces mitochondria into a state of sustained fission: the healthy interconnected networks of mitochondria fragment and separate. The result is reduced ATP production, increased oxidative stress, and impaired insulin signaling. The muscle can no longer clear glucose efficiently, compounding the original problem.
What causes ceramide to accumulate? Two pathways: chronic inflammation, and high insulin itself. Hyperinsulinemia, independent of inflammation, activates ceramide biosynthesis — creating a self-perpetuating cycle. More insulin leads to more ceramides, which leads to more insulin resistance, which leads to more insulin.
Here is where the metabolic picture becomes particularly compelling for anyone interested in thermal protocols.
Brown adipose tissue is thermogenic fat — dense with mitochondria, designed not to store energy but to burn it as heat through a process called mitochondrial uncoupling. Newborns are rich in it. Adults retain depots throughout the thoracic cavity. And it is exquisitely sensitive to one signal: insulin.
When insulin arrives at brown fat cells, it binds to insulin receptors and delivers a clear instruction: slow down. Uncouple less. Start behaving like white fat. In Bikman's lab, brown fat cells exposed to insulin reduce their metabolic rate by approximately half. The thermogenic engine dims.
This is not a trivial effect. Brown fat activation contributes measurably to resting metabolic rate. The inverse relationship between fasting insulin and basal metabolic rate — documented as far back as Benedict and Joslin in the early twentieth century — reflects this mechanism precisely: higher insulin correlates with a lower metabolic rate, and not merely because of dietary restriction.
If insulin suppresses brown fat, what activates it? Cold exposure (discussed further here) is the well-established answer — but Bikman's research points to a second, underappreciated activator: ketones.
When the body enters a state of nutritional ketosis, circulating beta-hydroxybutyrate interacts with subcutaneous white adipose tissue in a remarkable way. Rather than storing energy, white fat cells begin to express uncoupling proteins and generate more mitochondria — behaving, functionally, like brown fat. This process is called beiging or beige adipogenesis.
The evolutionary rationale is elegant. Periods of food scarcity — historically coinciding with colder seasons — would naturally produce both ketosis and cold exposure simultaneously. The combination would prime the body to generate heat efficiently, even without abundant fuel. Seasonal carbohydrate availability in autumn (berries, starchy tubers) would prepare fat stores for winter, while winter itself would trigger the beiging mechanisms that sustain warmth through leaner months.
We have largely removed this seasonal rhythm from modern life. Temperature-controlled environments and year-round access to starchy foods mean the ancient feedback loop rarely engages. But it can be deliberately restored.
The science converges on a few clear principles:
The metabolic engine is not broken. It is responding precisely as designed — to the signals it receives. Shift the signals, and the engine shifts with them.