The Hard Science of Your Metabolism on Keto, Carnivore, and Carbs With Professor Ben Bikman of BYU
This interview features Professor Ben Bikman, a PhD researcher and metabolic scientist from BYU, whose work centers on insulin resistance, hyperinsulinemia, and the signaling properties of ketones. Listeners gain a rigorous scientific foundation for understanding why elevated insulin, not just high blood sugar, is a primary driver of chronic disease. Professor Bikman explains that insulin resistance is a two-sided coin: some cells stop responding to insulin while blood insulin levels simultaneously rise, and it is this hyperinsulinemia that causes much of the downstream damage seen in obesity, type 2 diabetes, infertility, and neurological decline.
A standout section covers how the two most common forms of infertility, erectile dysfunction and polycystic ovary syndrome (PCOS), stem from opposite sides of this coin. In men, insulin resistance prevents proper vasodilation, impairing blood pressure regulation and erectile function. In women, elevated insulin specifically suppresses the conversion of testosterone to estrogen in the ovaries, producing the hormonal imbalance that defines PCOS. Both conditions can improve dramatically when insulin is lowered through dietary change, which aligns with clinical observations of hormonal recovery on carnivore and low-carb diets.
Professor Bikman also unpacks the underappreciated role of ketones as signaling molecules, not just fuel. His lab has found that ketones activate receptors on fat cells that increase mitochondrial activity by two to three times, effectively raising metabolic rate without additional exercise. Separately, ketones inhibit the NLRP3 inflammasome, a master switch for systemic inflammation, explaining part of the anti-inflammatory benefit of ketogenic eating. He also addresses the fear of protein spiking insulin, clarifying that protein eaten without carbohydrates produces a proportionally greater glucagon response that offsets any modest insulin rise, making protein consumption safe and appropriate on a low-carb diet.
The conversation closes with a detailed look at Alzheimer's disease as a condition of brain insulin resistance, where the brain cannot access glucose yet is simultaneously blocked from receiving ketones by chronically high insulin. Supplementing with ketones has shown measurable cognitive improvement in affected individuals. Dr. Anthony Chaffee contributes his own experience as a former professional rugby player who performed at peak levels on a carnivore diet, and both discuss how the calories-in-calories-out model fails to account for insulin's control over metabolic rate, fat mobilization, and ketone excretion.
Key Takeaways
- Insulin resistance always comes paired with hyperinsulinemia; you cannot have one without the other, meaning chronically elevated insulin itself causes harm independent of blood sugar levels.
- PCOS can reverse on a low-carb or carnivore diet because lowering insulin removes the hormonal block that prevents ovaries from converting testosterone into estrogen, directly correcting the root hormonal imbalance.
- Erectile dysfunction may be the earliest clinical sign of insulin resistance in otherwise undiagnosed men, making fasting insulin testing a practical first diagnostic step rather than defaulting to testosterone testing.
- Ketones activate G-protein-coupled receptors on fat cells, increasing mitochondrial activity by two to three times and raising resting metabolic rate by roughly 300 calories per day, independent of any caloric burn from the ketones themselves.
- Eating protein with fat (and no carbohydrates) produces a glucagon response that equals or exceeds the insulin response, meaning protein does not meaningfully disrupt ketosis when consumed in a low-carb context.
- If you have been strictly carnivore or ketogenic for months and need to pass an oral glucose tolerance test, eating moderate carbohydrates for one to two days beforehand restores the first-phase insulin response and normalizes glucose clearance.
- Alzheimer's disease involves a brain that is insulin resistant and therefore cannot access glucose, while simultaneously being blocked from receiving ketones by high circulating insulin. Providing exogenous ketones (via diet or ketone esters) can partially restore cognition by bypassing this blockade.
- Infants reach 2 millimolar ketone levels within one hour of feeding, a level that takes a fat-adapted adult roughly 36 hours of fasting to achieve, indicating that nutritional ketosis is the biological default state for human brain development, not an unusual metabolic condition.
- Professor Ben Bikman on Insulin Resistance as the Root of Metabolic Disease
- Hyperinsulinemia, PCOS, and Erectile Dysfunction Explained
- Physiological Insulin Resistance on Low-Carb and Carnivore Diets
- Ketones as Signaling Molecules: Anti-Inflammatory and Metabolic Effects
- Does Dietary Protein Spike Insulin and Kick You Out of Ketosis?
- Ketosis Is Not Starvation: Brain Fuel, Fasting, and Human Metabolism
- Glucose vs Ketones: The Brain's Preferred Fuel and Infant Ketosis
- Plant Toxins and Carcinogens: Why Plants Are Trying to Kill You
- Carnivore Diet and Athletic Performance: Energy, Endurance, and Recovery
- Calories In Calories Out Is Wrong: How Low Insulin Drives Fat Loss
- Alzheimer's as Insulin Resistance of the Brain and Ketone Therapy
- Low-Fat Diets, Brain Atrophy, Depression, and the Cholesterol Myth
This is an auto-generated transcript from YouTube and may contain errors or inaccuracies.