Metabolic disease has quietly become one of humanity’s most pressing health crises, affecting billions worldwide.
Yet most people have never heard of insulin resistance—the root cause driving everything from Alzheimer’s to infertility.
In a recent wide-ranging conversation, Dr. Benjamin Bikman, a professor of physiology and developmental biology who earned his PhD in bioenergetics, explained how this single condition connects nearly every chronic disease plaguing modern society.
The discussion revealed why focusing on glucose levels misses the real problem—and how simple lifestyle changes can reverse decades of damage.
Jump to:
- What Bioenergetics Actually Means (And Why It Matters)
- Why Insulin—Not Glucose—Is The Real Problem
- Metabolic Disease Explained: Beyond The Fitness Industry Myths
- Understanding Insulin Resistance: The Two-Sided Coin
- Fat Cell Size Matters More Than Fat Mass
- Visceral Fat: The Most Dangerous Kind
- The Three Cardinal Causes of Insulin Resistance
- How To Measure Your Insulin Resistance
- Fat Cells: Hormone Factories Poisoning Your Blood
- Insulin Resistance and Brain Health
- Testosterone, Fertility, and Sexual Function
- GLP-1 Drugs: Promise and Problems
- Reversing Type 2 Diabetes Through Diet
- Practical Steps for Improving Insulin Sensitivity
- The Research That Still Needs Doing
- Why This Matters Now More Than Ever
What Bioenergetics Actually Means (And Why It Matters)
The term “bioenergetics” sounds esoteric, almost mystical. Dr. Bikman acknowledges this perception has become problematic.
There is in fact that term has been hijacked by like kind of guru spiritual wellness individuals where it really is like harnessing the energy like chakra in your body and it’s pretty discouraging. I put my head in my hands when I hear that.
In reality, bioenergetics represents a rigorous scientific discipline. Only three universities in the United States offer degrees in this field.
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The study combines biochemistry and physiology with heavy emphasis on mitochondria—the cellular powerhouses that convert nutrients into usable energy. This specialized knowledge allows researchers to understand how calories, nutrients, and metabolism intersect with diseases like obesity and diabetes.
It’s a hybrid but an amalgamation of looking at energy in a very biochemical sense which is things like calories, nutrients, how you burn things, how you build things and that is but all within the context again all within the context of biology and the cell.
Why Insulin—Not Glucose—Is The Real Problem
Standard medical practice obsesses over glucose levels. Every routine blood test measures glucose or hemoglobin A1C.
Insulin levels are almost never checked.
This represents a fundamental blind spot in modern medicine. Dr. Bikman argues that reframing metabolic health around insulin—not just glucose—would allow earlier detection and more effective treatment of chronic disease.
Our obsessive focus in zeroing in on glucose actually has us missing the more important marker because if we can reframe the paradigm to focus or at least include insulin, we not only detect these cardiometabolic chronic diseases much much sooner, but we also treat them much better.
The shift from infectious diseases to metabolic diseases represents one of modern medicine’s greatest challenges. Where previous generations worried about cholera and dysentery, today’s health threats stem from within.
Metabolic Disease Explained: Beyond The Fitness Industry Myths
The wellness industry has corrupted the term “metabolism” beyond recognition. Trainers promise to “jumpstart your metabolism” with superfoods or special supplements.
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These claims fundamentally misunderstand what metabolism actually means.
Scientifically, metabolism refers to the sum of all chemical reactions happening in cells at any moment. These reactions divide into two categories: anabolic reactions that build molecules, and catabolic reactions that break them down.
Metabolic health, then, relates directly to metabolic syndrome—a cluster of complications including elevated waist circumference, high blood glucose, elevated blood pressure, and abnormal blood lipids.
The metabolic syndrome used to be called the insulin resistance syndrome and now we’ve actually come to the cause of it all. If we can say metabolic health but be thinking what is your insulin resistance status now we are really talking about some productive terms.
The Upstream Driver of Chronic Disease
Consider how doctors typically diagnose and treat high blood pressure. They identify the condition, then immediately prescribe medication.
This approach treats symptoms while ignoring root causes.
If the clinician simply says to the patient you have high blood pressure then if it stops there if there is a period as you said then the next sentence is and here’s your prescription for a drug. If however we say you have high blood pressure which is a consequence of insulin resistance period. Now the next sentence is well this is a lifestyle problem.
One individual shared how this reframing changed everything. At 33 years old with 39% body fat, he received diagnoses for high blood pressure and pre-diabetes. When prescribed blood pressure medication, a health screening doctor offered different advice.
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The doctor suggested losing weight and improving diet instead of relying on medication for potentially five decades. Following this advice—losing over 50 pounds of fat—transformed every health marker. Blood pressure normalized. A1C levels improved dramatically. Triglycerides dropped from 150 to 75.
All without medication.
Understanding Insulin Resistance: The Two-Sided Coin
Insulin resistance ranks among the most common conditions worldwide, yet most people cannot define it accurately.
The condition has two distinct components. First, certain cells stop responding properly to insulin’s signals—they become resistant. Second, blood insulin levels rise much higher than normal, a state called hyperinsulinemia.
Insulin functions as a hormone—a chemical messenger telling cells what to do. Every single cell in the body contains insulin receptors, specialized docking stations where insulin binds to deliver instructions.
Every single cell of the body has insulin receptors on it. These little docking stations that are specific for insulin to come and dock and then tell the cell to do something. But again, with insulin resistance, some cells aren’t working particularly well.
This two-part definition explains how insulin resistance creates such diverse health problems. From Alzheimer’s disease to atherosclerosis, hypertension to infertility, the mechanism remains the same: insulin isn’t working properly, and levels have become chronically elevated.
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The Singapore Paradox: Why Thin Populations Get Sicker
Dr. Bikman conducted his postdoctoral research in Singapore, where he observed a startling phenomenon. Despite having far less obesity than the United States, Singapore struggles with higher rates of type 2 diabetes.
Walking Singapore’s streets reveals relatively few overweight individuals compared to American cities. Yet Singapore has ranked as high as number nine globally for diabetes prevalence, while the United States sits around number 70.
The explanation challenges conventional thinking about fat and health.
How we store fat actually matters much more than how much fat we’re storing.
Fat Cell Size Matters More Than Fat Mass
Different ethnic groups show dramatically different capacities for creating new fat cells. This genetic variation produces profound health consequences.
Blacks and whites make new fat cells more readily than most other ethnicities. This ability—called hyperplasia—allows fat storage in many smaller cells rather than forcing existing cells to grow larger.
East Asians and South Asians have limited potential to create new fat cells. Any weight gain forces fat into existing cells, making them increasingly large through hypertrophy.
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Small fat cells remain insulin sensitive and anti-inflammatory. Large fat cells become insulin resistant and promote inflammation.
You take an East Asian version of me and you put 10 pounds on that version of us and versus 10 pounds on this European version of us. We the European version, we just don’t look as good in our speedo. The East Asian version, we’ve got pre-diabetes and hypertension.
This concept of “personal fat threshold” explains why individuals tolerate different amounts of body fat before developing metabolic disease. Northern Europeans can carry significantly more fat before crossing into dangerous territory compared to East Asians.
Why Women Are Fatter Yet Healthier Than Men
Within the same ethnicity, females naturally carry more body fat than males due to sex hormone differences. Yet women consistently show better metabolic health than their male counterparts.
Estradiol and other female hormones promote both subcutaneous fat storage and new fat cell creation. Women therefore accumulate more but smaller fat cells, protecting against cardiometabolic problems despite higher overall body fat percentages.
Visceral Fat: The Most Dangerous Kind
The body stores fat in two primary locations: subcutaneous (beneath the skin) and visceral (between organs). Visceral fat poses far greater health risks.
Subcutaneous fat can expand outward, allowing new fat cell creation. Physical space constraints limit visceral fat expansion, forcing those cells to grow through hypertrophy alone.
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Ten pounds of visceral fat creates more metabolic damage than ten pounds of subcutaneous fat. Those enlarged visceral fat cells actively promote insulin resistance and inflammation.
Visceral fat cells are actually more problematic than subcutaneous fat cells. Visceral adipose because of the volume limit will only grow through hypertrophy. So those visceral adipocytes will not multiply because then you begin to physically compress too much.
Visceral fat also affects blood pressure through a specific mechanism. Elevated insulin forces kidneys to retain salt and water, increasing blood volume and consequently raising blood pressure.
The Three Cardinal Causes of Insulin Resistance
Dr. Bikman identifies three primary drivers of insulin resistance, ordered by importance and controllability.
Stress and Cortisol
Elevated stress hormones—epinephrine and cortisol—promote insulin resistance. Unfortunately, this lever proves difficult to control effectively.
Telling someone with high cortisol to “calm down” often increases their stress about being stressed, creating a counterproductive cycle.
Inflammation
Chronic inflammation drives insulin resistance, but like stress, it depends on variables often outside individual control. While important, it represents another slippery lever.
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Insulin Itself: The Most Powerful and Controllable Factor
Biology follows a fundamental principle: too much of something generally creates resistance to that something. Constant insulin elevation causes the body to become resistant to insulin’s signals.
Refined carbohydrates—starches and sugars—spike insulin more than any other food.
The average individual worldwide at this point from the Middle East to East Asia to Southeast Asia to North and South America and through Europe everywhere, the average individual spends every waking moment in a state of elevated insulin.
Modern eating patterns keep insulin chronically elevated. Breakfast spikes insulin. Mid-morning snacks spike it again. Lunch, afternoon snacks, dinner, and evening treats maintain this elevation throughout waking hours.
Insulin only normalizes several hours into sleep—assuming people actually sleep instead of snacking late into the night.
How To Measure Your Insulin Resistance
Most people never discover their insulin resistance status until serious complications develop. Dr. Bikman recommends several assessment methods.
Blood Tests: The Gold Standard
Request fasting insulin measurement at your next blood draw. Optimal levels fall below 6 microunits per milliliter. Single-digit readings indicate good insulin sensitivity.
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If doctors refuse to check insulin, examine lipid markers instead. Divide triglycerides by HDL cholesterol. Ratios below 1.5—ideally below 1.0—suggest good metabolic health.
Skin: The Metabolic Window
Visible skin changes often reveal insulin resistance before blood tests. Two conditions commonly appear around the neck:
- Acanthosis nigricans: Skin darkens in color and develops a crinkled, tissue-paper texture
- Skin tags: Small mushroom-stalk protrusions of skin, like tiny fingers poking upward
Both conditions can reverse quickly as insulin sensitivity improves, making them useful markers for tracking progress.
Fat Cells: Hormone Factories Poisoning Your Blood
Enlarged fat cells don’t simply store energy passively. They actively secrete harmful substances into the bloodstream.
Large fat cells release pro-inflammatory cytokines—hormones that promote systemic inflammation. This creates what researchers call “subclinical chronic inflammation,” a constant low-grade inflammatory state contributing to numerous diseases.
Small fat cells do the opposite, releasing anti-inflammatory hormones that protect health. The difference between small and large fat cells determines much of the health impact of carrying excess weight.
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Extra fat essentially creates a 24/7 drip feed of inflammatory chemicals into your system.
Insulin Resistance and Brain Health
Alzheimer’s disease is sometimes called “type 3 diabetes” for good reason. The brain suffers profoundly from insulin resistance.
Brain cells require insulin function to absorb adequate glucose for energy needs. When neurons become insulin resistant, they cannot access sufficient fuel despite abundant blood sugar.
Improving insulin sensitivity helps the brain in two ways. First, neurons regain ability to use glucose effectively. Second, lower insulin levels shift metabolism toward fat burning, producing ketones.
The brain loves ketones to put it in a silly way. In fact, if the brain has a preference for either glucose or ketones, it chooses ketones. If it has equal access to both from the blood, the brain overwhelmingly like 70% of its energy will start coming from ketones.
Multiple human studies show cognitive improvement when Alzheimer’s patients achieve ketosis. Ketone supplements rapidly improve performance on cognitive tests.
Testosterone, Fertility, and Sexual Function
Insulin resistance devastates reproductive health in both sexes through multiple mechanisms.
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Fat Tissue as Unwanted Ovaries
Fat cells express aromatase, an enzyme converting testosterone into estradiol (the primary estrogen). Insulin normally inhibits this conversion.
As men gain fat, their fat cells increasingly express aromatase. Larger, more numerous fat cells hijack testosterone, converting it to estrogen at accelerating rates.
We have a perspective which is that you’re fat because you are low T. In fact in most men it’s actually probably the exact opposite. You are low T because you have too much fat. And as you reduce your fat, you reduce the aromatization.
Weight loss preserves testosterone by reducing this unwanted conversion process. The testes produce adequate testosterone—fat cells just stop stealing and feminizing it.
Erectile Dysfunction: An Early Warning Sign
Insulin plays a crucial role in normal erectile function by stimulating nitric oxide production in blood vessel walls. Nitric oxide causes vasodilation—blood vessel expansion necessary for erections.
When insulin resistance develops, this mechanism fails. Blood vessels remain constricted, preventing adequate blood flow.
Research suggests erectile dysfunction may represent the earliest manifestation of insulin resistance in otherwise healthy men—appearing before other obvious symptoms.
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Female Infertility and PCOS
Polycystic ovary syndrome (PCOS) represents the most common cause of female infertility. Like male erectile dysfunction, it stems fundamentally from insulin resistance.
Insulin resistance disrupts ovarian hormone production, preventing normal ovulation cycles. Both the most common male and female fertility issues share the same metabolic root.
GLP-1 Drugs: Promise and Problems
Semaglutide (marketed as Ozempic and Wegovy) and similar drugs ending in “-glutide” mimic GLP-1, a hormone naturally produced in intestines.
GLP-1 affects metabolic health through several mechanisms. It helps control blood sugar by signaling the liver to retain glucose. At higher levels, it slows food movement through intestines and activates brain satiety centers.
The Fundamental Problem with Current Use
Dr. Bikman expresses strong reservations about how these drugs are currently prescribed.
I believe they’re used too readily for the wrong purpose and at too high of a dose. When we talk about these drugs, we talk about them as weight loss drugs and that may give the person this mistaken view that as long as they’re injecting, they’re good to go and they don’t need to worry about anything.
Current protocols produce profound side effects: severe nausea, depression, and increased suicidality. Seventy percent of users discontinue within two years—not because they achieved their goals, but because they prefer being overweight to feeling miserable.
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Studies show 200% increased risk of major depression and 100% increased risk of suicidal behavior at the two-year mark compared to placebo.
A Better Approach: Treating Carbohydrate Addiction
Research from 1996 revealed crucial differences in GLP-1 response between lean and obese individuals. After high-fat meals, both groups showed similar GLP-1 responses and satiety.
After high-carbohydrate meals, lean individuals experienced dramatic GLP-1 elevation lasting three hours. Obese individuals showed essentially no response—no statistical significance whatsoever.
If we are sitting at a table and we’re going out for pasta and garlic bread, someone is going to eat a certain amount of that and feel full in part because of GLP-1, someone’s going to eat a certain amount of that and not feel full and simply be looking around for the next plate of pasta and garlic bread.
This understanding suggests reframing these medications as tools for controlling carbohydrate cravings rather than generic weight loss drugs. A better protocol would involve:
- Lower “micro-doses” instead of maximum therapeutic doses
- 90-day cycles focused on habit formation
- Emphasis on learning different eating patterns
- Cycling off to assess whether new habits persist
- Cycling back on if cravings return after monitoring
This approach treats the underlying behavioral problem rather than just suppressing all interest in life activities.
Maybe the more honest view is that this drug reduces your interest in life and things that you used to be passionate about.
Reversing Type 2 Diabetes Through Diet
Type 1 diabetes requires lifelong insulin supplementation because the pancreas cannot produce it. Type 2 diabetes, however, responds dramatically to lifestyle intervention.
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Dr. Bikman’s research team published a study following 11 newly diagnosed type 2 diabetics. Without counting calories, subjects simply limited carbohydrate intake while eating unlimited protein and fat.
Within 90 days, all 11 reversed their diabetes by every clinical marker without medication.
Larger studies by organizations like Virta Health have replicated these findings. The implications are profound: type 2 diabetes fundamentally represents a carbohydrate intolerance problem.
This is a disease of you basically eating too much carbs and you just can’t control your blood sugar anymore and if you can’t control your blood sugar then let’s just eat less of it.
Practical Steps for Improving Insulin Sensitivity
The most controllable factor in insulin resistance is insulin itself—specifically, how often and how high it spikes.
Reduce Refined Carbohydrates
Starches and sugars spike insulin more dramatically than any other macronutrient. Reducing or eliminating these foods represents the single most powerful intervention.
For those struggling with carbohydrate cravings, Dr. Bikman acknowledges the addictive nature of these foods. Many conventional addiction markers apply: seeking, craving, inability to moderate, and regret after overconsumption.
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Abstinence is easier than perfect moderation. For some of us, we need to acknowledge I’m an addict to these carbs. And so it’s easier for me to never even start eating than it is to stop eating.
Time-Restricted Eating
Allowing insulin to normalize between meals and overnight proves crucial. Constant snacking maintains chronically elevated insulin throughout waking hours.
Monitor Sleep and Evening Eating
Dr. Bikman changed his own habits after seeing data from sleep monitors and continuous glucose monitors. Evening carbohydrate consumption caused blood sugar spikes followed by hypoglycemia during sleep.
Low blood sugar activates the sympathetic nervous system—preparing the body for physical activity precisely when it should be resting. This disruption destroyed sleep quality.
Avoiding glucose-spiking foods in evenings dramatically improved his sleep, which then cascaded into better overall health.
Artificial Sweeteners: Choose Wisely
Not all sweeteners affect insulin equally. Aspartame, stevia, monk fruit extract, and erythritol show minimal or no insulin response.
Some sugar alcohols can spike insulin mildly, potentially increasing hunger. Individual responses vary based on gut microbiome differences.
If you want something simple that actually works, this is one of the most effective tools I’ve used to build strength, conditioning, and endurance without needing a full gym setup.
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Allulose stands out as uniquely beneficial—it significantly increases GLP-1 and promotes satiety rather than hunger.
The Research That Still Needs Doing
Given unlimited research funding, Dr. Bikman would conduct weight gain studies rather than weight loss studies.
Current obesity research compares different weight loss diets. This approach introduces confounding variables because both low-fat and low-carb diets typically reduce total calorie and carbohydrate intake compared to baseline.
Researchers cannot determine whether results stem from calorie restriction or insulin reduction.
To answer the question better, we actually have to do a weight gain problem, which is try to make people fat and have them on two different diets. You’re going on a high carb version of this high calorie diet. You’re going on a ketogenic version, low carb, high-fat version, but it’s high calorie, and we’re going to see which one makes people fatter.
Such studies would definitively answer whether obesity primarily results from excess calories or hormonal dysregulation. Unfortunately, no pharmaceutical company will fund research showing that simply controlling carbohydrates works—there’s nothing to patent and sell.
Why This Matters Now More Than Ever
Insulin resistance has become one of the most common conditions worldwide, yet remains largely undiagnosed and misunderstood.
If you want something simple that actually works, this is one of the most effective tools I’ve used to build strength, conditioning, and endurance without needing a full gym setup.
- Full-body training with one weight using swings, squats, and presses
- Solid cast iron build that feels stable and lasts for years
- Comfortable grip that makes high-rep workouts easier to handle
The consequences extend far beyond weight and appearance. Brain health, fertility, sexual function, cancer risk, and lifespan all depend on metabolic health.
The good news? Insulin resistance remains largely controllable through lifestyle choices. Unlike genetic conditions or infectious diseases, this epidemic has solutions within individual reach.
Measuring fasting insulin, understanding personal fat thresholds, and reducing refined carbohydrate intake represent accessible first steps. The alternative—decades of medication treating symptoms while underlying metabolic dysfunction worsens—serves neither patients nor society.
As public health professionals increasingly discuss metabolic health, understanding what metabolism actually means becomes critical. The conversation has moved beyond fitness industry platitudes into hard science with profound implications for human health and longevity.
