Dr. Benjamin Bikman

Associate Professor of Cell Biology and Physiology, BYU

Insulin resistance • cardiometabolic disease • bioenergetics

3Episodes
234 minAnalysed
1Topic
Last reviewed: Mar 20, 2026·Credential: PhD (Bioenergetics, East Carolina University)·First indexed: Mar 20, 2026

About the expert

Focus: Insulin resistance and metabolic disease

Benjamin Bikman is an associate professor at Brigham Young University, where he studies the relationship between insulin resistance and cardiometabolic disease. He holds a PhD in Bioenergetics from East Carolina University and completed postdoctoral training in metabolic disorders at Duke-NUS Medical School. He is co-founder of HLTH Code and Insulin IQ, and author of Why We Get Sick (2020).

Why this matters

BYU metabolic researcher who frames insulin resistance as the connector across multiple cardiometabolic conditions. The insulin-resistance-as-cardiovascular-driver framing is broadly mainstream; the carbohydrate-insulin model as the primary driver of obesity is still actively contested in the energy-balance literature. Bikman has commercial exposure (co-founder of HLTH Code and Insulin IQ, author of Why We Get Sick), which is relevant context when he is the source of a specific protocol or substance recommendation, although it does not itself invalidate the underlying physiology he discusses. Strongest on mechanism; worth pairing with conventional clinical-outcome evidence when the conversation moves from mechanism to recommended daily protocol. In his glucagon lecture he treats low insulin, reached mainly through low-carb eating, as the bigger lever for fat burning than glucagon itself, which is his interpretation rather than established weight-loss guidance.

Filter by species:

Episodes with Dr. Benjamin Bikman

A Sugar Substitute That’s Good For You? The Science Behind Allulose - with Dr. Bikman
Dr. Benjamin Bikman, a Brigham Young University metabolic researcher, explains the mechanistic case for allulose — a rare sugar that does not appear to spike insulin and may activate GLP-1 and AMPK pathways. Replacing fructose with allulose may reduce uric acid production in mechanistic models, with potential downstream effects on insulin sensitivity, fat oxidation, and possibly brain ketone availability. The episode is mechanism-rich and the substitution argument is biologically plausible; large clinical-outcome trials remain limited, so the practical framing is sweetener-of-choice for people who already use sweeteners, not a stand-alone metabolic intervention.
53 minHuman
Explore episode →
The Fastest Way to Lose Fat Nobody Tells You This!
Insulin resistance may sit under several chronic conditions, and lowering insulin can support fat burning. The carbohydrate-insulin model adds nuance to the calorie-balance view rather than replacing it. The strongest practical levers are not exotic: lower-carb whole foods, more protein, strength training, and meal timing.
158 minHuman
Explore episode →
What is glucagon, and why does it matter for weight loss?
Most weight-loss talk focuses on insulin, but its partner hormone, glucagon, is getting new attention. Glucagon is one of the key hormones that helps keep fuel available when you are not eating: it mainly acts on the liver, telling it to release stored glucose and, in the right conditions, to burn fat and make ketones. Because it can raise fat burning and energy use in the liver, some experimental obesity drugs are being designed to add a glucagon effect on top of GLP-1. It is a genuinely interesting piece of metabolism, but not a switch most people need to manage themselves.
23 minHuman
Explore episode →