High Intensity Health  ·  Dr. Benjamin Bikman, PhD  ·  55 min

Key Takeaways: Insulin, Brown Fat & Ketones

Dr. Benjamin Bikman is a cell biologist at Brigham Young University whose research centers on insulin and its role in metabolic disease. This conversation covers the mechanisms by which insulin drives fat storage, suppresses thermogenic fat, and how both cold exposure and nutritional ketosis can restore metabolic function.

The Core Insights

• Insulin is the primary driver of fat accumulation. It promotes adipogenesis (creation of new fat cells from stem cells) and lipogenesis (filling existing fat cells). You cannot grow fat cells in the lab without insulin — and chronically elevated insulin means the body is perpetually in storage mode.
• Fasting insulin predicts your metabolic state. A fasting insulin above roughly 8 mIU/L means you are storing fat even during sleep and fasting periods. Most modern adults exceed this threshold.
• Ceramides link insulin to cellular damage. High insulin activates ceramide biosynthesis. Ceramides accumulate in muscle, force mitochondria into fragmented (fission) states, impair ATP production, and cause insulin resistance — completing a self-reinforcing cycle.
• Insulin suppresses brown fat by approximately half. Brown adipose tissue is your body's thermogenic engine — burning energy as heat. When insulin binds to brown fat cells, their metabolic rate drops by roughly 50%. This is a direct mechanism connecting chronic hyperinsulinemia to metabolic slowdown.
• Ketones activate the "beiging" of white fat. In a state of nutritional ketosis, beta-hydroxybutyrate signals subcutaneous white fat to behave like brown fat — producing more mitochondria and uncoupling them to generate heat rather than store energy. This expands thermogenic tissue without cold exposure.
• Cold exposure and ketosis are synergistic. Both activate similar thermogenic mechanisms. Combined, they may produce additive benefits — cold activating existing brown fat, ketones converting white fat into beige fat.
• The seasonal pattern is not accidental. Starchy carbohydrates are naturally abundant in autumn; cold and scarcity follow in winter. Bears become insulin-resistant before hibernation to store fat rapidly, then activate brown fat to sustain warmth during dormancy. Human physiology may follow a similar rhythm — one modern temperature control and year-round food availability have largely erased.
• Resistance training beats cardio for insulin sensitivity. Minute-for-minute, at lower training volumes (2–3 hours per week), resistance training improves insulin sensitivity more effectively than endurance training — primarily by expanding glucose-hungry muscle mass.

Practical Protocol

1. Prioritise insulin management through food quality. Reducing dietary carbohydrates — particularly refined and high-glycaemic sources — shifts the body out of chronic storage mode within 24 hours. This is the foundational lever; exercise amplifies it but cannot override it.
2. Add deliberate cold exposure. Ice baths or cold water immersion activate brown fat directly. Mild, sustained cold — enough to feel it genuinely — is required. A hot shower that ends cold is a start; dedicated cold immersion is more potent.
3. Explore periodic nutritional ketosis. Even brief periods of very low carbohydrate intake promote beiging of subcutaneous white fat and reduce ceramide accumulation. This need not be a permanent state — seasonal cycling may reflect the original human pattern.

Worth Remembering