Metabolic Classrooms

For decades, Alzheimer’s disease was blamed on amyloid plaques in the brain. But a growing body of research suggests the disease may actually be driven by impaired brain metabolism and insulin resistance—sometimes called “Type 3 diabetes.”

Why do some lean populations have diabetes rates similar to countries with high obesity? The answer isn’t just body weight — it’s how and where fat is stored. In this Metabolic Classroom, Dr. Ben Bikman explains how ethnicity, fat cell size, and distribution shape metabolic risk far beyond BMI.

Bile doesn’t just digest fat. Bile acids act like hormones that regulate liver fat, blood sugar, insulin sensitivity, energy expenditure, and inflammation.

Nearly half of heart attack patients have normal LDL cholesterol. Research shows insulin resistance and the triglyceride-to-HDL ratio may be stronger predictors of cardiovascular risk.

Exercise doesn’t just strengthen muscles—it triggers a powerful molecular messaging system. Extracellular vesicles released during exercise deliver signals throughout the body that improve insulin sensitivity, reduce inflammation, and enhance metabolic health.

Insulin resistance isn’t just a hormone or calorie problem—it’s a cellular energy problem. Inside your cells, a molecule called NAD⁺ acts like a rechargeable battery for metabolism. When excess glucose causes that battery to stay “overcharged,” energy flow slows, mitochondria struggle, and insulin signaling begins to break down.

Aging isn’t random. At the cellular level, it’s regulated by powerful signaling pathways that determine whether your cells are focused on growth or repair. Two of the most important of

Prefer to listen without the ads? Become a Ben Bikman Insider. For decades, nicotine has been treated as a scientific villain, largely because of its association with smoking. And to be

Glucagon is insulin’s metabolic opposite—but it rarely gets the attention it deserves. While insulin drives energy storage, glucagon signals the body to release and burn stored fuel. Contrary to common belief, glucagon doesn’t burn fat by pulling it directly from fat cells in humans. Instead, its primary fat-burning action happens in the liver, where it suppresses fat creation, increases fat oxidation, and supports ketone production when insulin is low. Understanding the balance between insulin and glucagon is key to improving metabolic health and sustainable fat loss.

LPS-driven inflammation may be a hidden cause of insulin resistance and fatty liver. In this Metabolic Classroom lecture, Dr. Ben Bikman explains how gut permeability fuels metabolic disease — and what strengthens the gut barrier.

Men experience a real hormonal decline called andropause—but unlike female menopause, much of it is driven by metabolism, not age. Here’s how testosterone changes, why insulin resistance and body fat accelerate the decline, and what men can do to support healthy hormonal function.

Omega-3s do far more than support heart health. Research shows that the long-chain forms—EPA and DHA—enhance fat burning, improve mitochondrial function, and amplify muscle growth and recovery. Here’s how these powerful fatty acids influence metabolism and body composition.

Ketones are often seen as backup fuel, but the heart tells a different story. In this article and full lecture, Dr. Ben Bikman explains how ketones support the cardiovascular system as high-octane fuel, reduce the heart’s workload, calm inflammation, protect against oxidative stress, and improve vascular function. When we look at the biochemistry and physiology—not the diet debates—ketones emerge as powerful allies for heart health.

Plant and animal proteins behave very differently inside the body. From amino acid profiles and digestibility to antinutrients and heavy metals, their metabolic impact is not interchangeable. Here’s what the science shows.

Men and women display distinct patterns in fat metabolism and ketone production, driven by hormonal, enzymatic, and adipose-tissue differences. Estrogen enhances fat mobilization and hepatic ketogenesis, while testosterone favors glycolytic pathways. Recognizing these sex-based distinctions refines how we interpret metabolic data and design nutrition strategies in research and clinical settings.