How To Reverse Insulin Resistance Through Diet, Exercise & Sleep - Found My Fitness with Dr Ben Bikman

Insulin Resistance: A Common Root Cause of Chronic Disease

Dr. Ben Bikman, a professor of cell biology, advocates the view that insulin resistance is a common root cause for most chronic diseases. It is implicated in type 2 diabetes, obesity, Alzheimer's, fatty liver disease, infertility, and even breast and prostate cancers. Insulin is a powerful hormone that affects virtually every cell in the body. Rather than treating individual diseases as separate issues, Dr. Bikman suggests addressing insulin resistance as a "common soil hypothesis" to simplify the clinical approach. This perspective highlights that insulin resistance is not the sole contributor to these conditions but is an undeniable factor.

Limitations of the Glucose-Centric Medical Paradigm

Modern clinical care often operates under a "glucose-centric paradigm," focusing primarily on blood glucose levels to monitor metabolic health. However, this approach can miss the early stages of insulin resistance. Insulin resistance is characterised by elevated insulin levels, where the body works harder to keep glucose in check, often maintaining normal glucose levels initially. Because glucose remains normal, this early phase of insulin resistance often "flies under the clinical radar". Dr. Bikman argues that if insulin levels were routinely measured, the earliest signs of metabolic problems could be detected sooner, allowing for earlier intervention. Ignoring high insulin levels can also lead to treatments, such as giving insulin therapy to type 2 diabetics, which may control glucose but can paradoxically "kill them faster" due to hyperinsulinemia and worsening insulin resistance.

Detecting Insulin Resistance

• Fasting Insulin Levels: A fasting insulin level of six microunits per milliliter or less is considered excellent, while levels in the mid-to-high teens or 20s indicate a metabolic issue.
• Continuous Glucose Monitors (CGMs): While CGMs measure glucose, not insulin, they can reveal dynamic glucose changes. If glucose levels do not return to normal within approximately two hours after consuming a carbohydrate-heavy meal, it suggests a problem.
• Skin Markers: The skin can serve as a "window to the metabolic soul". Two common signs around the neck are:
  • Acanthosis Nigricans: Darker pigmentation and a "crinkled tissue paper texture" of the skin folds.
  • Skin Tags: Small, mushroom-stalk-like growths of skin, often found around the neck or armpits. Both of these are strong indicators of insulin resistance and tend to disappear as insulin sensitivity improves.
• Triglyceride to HDL Ratio: A ratio of less than 1.5 is a strong indicator of good metabolic health and is a better predictor of cardiovascular risk than LDL cholesterol.
• Uric Acid Levels: Lower levels of uric acid have been linked to longer and healthier lives.

Causes of Insulin Resistance: Fast vs. Slow

• Fast Insulin Resistance: This type can develop within hours and resolve quickly if the stimulus is removed. Key primary stimuli include:
  • Stress Hormones: Elevated cortisol or epinephrine (adrenaline) can cause acute insulin resistance. Chronic sleep deprivation, for example, increases cortisol and epinephrine, leading to insulin resistance.
  • Inflammation: Increased inflammatory cytokines or autoimmune diseases can rapidly induce insulin resistance.
  • Too Much Insulin: Paradoxically, excessive insulin itself can lead to insulin resistance.
• Slow Insulin Resistance: This develops progressively over years and typically originates in the fat tissue. It is linked to specific lipids, particularly ceramides. Unlike inert triglycerides (stored fat), ceramides actively block the insulin signal at various points. All primary fast stimuli (stress, inflammation, excess insulin) are known to induce ceramide biosynthesis.

Insulin's Role in Fat Accumulation

Insulin plays a critical role in fat storage beyond blood sugar regulation. Dr. Bikman states that a fat cell cannot grow large without both elevated insulin and sufficient calories. Insulin acts as a signal to fat cells, telling them when to store energy and, more powerfully, inhibiting the breakdown of fat (lipolysis). This is demonstrated by the practice of some individuals with type 1 diabetes who deliberately underdose insulin to remain thin, despite suffering severe metabolic consequences like ketoacidosis. When insulin levels are consistently low, the body experiences metabolic advantages such as a higher metabolic rate (burning an extra 200 to 500 calories daily) and increased ketone excretion, which wastes calories through breath and urine.

Dietary and Lifestyle Factors Affecting Insulin Resistance

• Refined Carbohydrates and Sugars: These are identified as a primary problem, especially when consumed in processed foods ("bags and boxes with barcodes"), as they lead to significant insulin spikes. Fructose, while not directly eliciting an insulin response, can be converted to glucose and should be moderated by individuals with existing metabolic issues.
• Saturated Fats: While cell studies show palmitate (a saturated fat) can cause insulin resistance via ceramides, human studies indicate a more nuanced picture. In a low-carbohydrate diet, high saturated fat intake does not appear to cause insulin resistance because the body primarily produces saturated fat (palmitate) from *carbohydrates* in the liver. However, a combination of a high-carb and high-saturated fat diet is considered the "worst" for insulin resistance and cardio-metabolic health.
• Seed Oils (Linoleic Acid): Refined seed oils in concentrated and heated forms are considered pathogenic, not necessarily linoleic acid from natural sources. Natural sources often contain protective omega-3s and vitamin E, which prevent harmful peroxidation. Excessive linoleic acid can push fat cells towards unhealthy hypertrophy (swelling) rather than hyperplasia (multiplication).
• Meal Frequency and Timing: A high-carb diet with frequent snacking throughout the day (multiple small meals) is detrimental. Instead, fewer meals (two to three per day) with controlled carbohydrates, consumed earlier in the day, are recommended. Critically, avoiding eating for three to four hours before bed is essential, as late-night snacking spikes blood sugar, activates the sympathetic nervous system, and can lead to hypoglycemia during sleep, disrupting sleep quality.
• Exercise: While diet is paramount for metabolic health, exercise is crucial for strength, capability, and building muscle, which acts as a "great glucose consumer". Strength training is highly recommended, even in short bursts to failure, for improving insulin sensitivity. "Exercise snacks" (10-15 minutes of physical activity after a main meal) can significantly blunt glucose spikes.
• Sleep Deprivation: Even one night of poor sleep can induce insulin resistance by increasing stress hormones like cortisol and epinephrine. The use of caffeine to combat sleepiness can further exacerbate this by raising epinephrine levels.

Environmental Factors and Medications

• Environmental Toxins: Air pollution (particulate matter from diesel exhaust, cigarette smoke, and vaping) and plasticizers (e.g., BPA) have been shown to promote fat cell expansion and insulin resistance, even in calorie-controlled diets. Vaping particles, specifically, may be worse for mitochondrial outcomes than cigarette smoke. However, these are generally considered a "lower tier concern" compared to diet and exercise.
• Commonly Prescribed Medications:
  • Statins: Can increase the risk of type 2 diabetes (especially in women by 50%), Alzheimer's, and certain cancers by interfering with cholesterol synthesis and mitochondrial function.
  • Corticosteroids: Used for inflammation, these drugs can cause rapid weight gain by activating stress pathways that lead to insulin resistance and increased fat storage.
  • Atypical Antipsychotics: Many drugs with an "apne" suffix (e.g., olanzapine) promote weight gain, likely by inducing central insulin resistance in the hypothalamus, which reduces satiety signals.

Strategies for Reversing Insulin Resistance

Insulin resistance can be reversed, with significant improvements seen in as little as 90 days. Recommended strategies include:

• Dietary Control: Focus on "controlling carbs, prioritizing protein, and not fearing the fat" that naturally accompanies protein. Emphasise whole fruits and vegetables, while being mindful of sugary or starchy varieties for individuals with diabetes.
• Meal Timing: Consolidate calorie intake to earlier in the day and avoid eating for three to four hours before bedtime. This helps extend the overnight fasting period, allowing insulin levels to drop and improving insulin sensitivity.
• Exercise: Engage in regular physical activity, with a strong recommendation for strength training. Short bursts of activity (10-15 minutes) after meals can significantly reduce glucose spikes.
• Supplements:
  • Berberine: An effective supplement for improving insulin sensitivity.
  • Apple Cider Vinegar: The acetic acid in apple cider vinegar can reduce hepatic glucose production and activate AMPK, a pathway similar to that stimulated by exercise, thereby improving glucose control and insulin sensitivity. Taking a couple of tablespoons before a starchy meal can significantly lower glucose curves.
  • Exogenous Ketones: These act as signaling molecules and can improve metabolic markers, enhance satiety, and aid in fat burning and mitochondrial uncoupling.

Fat Storage and its Metabolic Impact

The way the body stores fat significantly impacts metabolic health, influenced by genetics, ethnicity, and sex.

• Hyperplasia vs. Hypertrophy:
  • Hyperplasia: The multiplication of fat cells, leading to more, but smaller, fat cells. This is generally associated with better metabolic health and is more common in Caucasians, Blacks, and women.
  • Hypertrophy: The enlargement of existing fat cells, leading to fewer, but larger, fat cells. These "sick fat cells" become insulin resistant to limit further growth, become hypoxic (low oxygen), and release pro-inflammatory cytokines. This process leads to the "spillover" of free fatty acids and ceramides, causing ectopic fat deposition (fat in places it shouldn't be, like the liver) and widespread inflammation. Hypertrophic fat storage is more common in East Asians, South Asians, Middle Easterners, and men, who may exhibit significant metabolic complications even at a lower body mass index.
• Visceral Fat: This fat, located around internal organs, primarily grows through hypertrophy due to the limited space in the visceral cavity. As a result, it is highly pro-inflammatory and strongly linked to chronic diseases like cancer and cardiovascular disease. Visceral fat cells are more responsive to breakdown signals from epinephrine, meaning intense exercise and cold therapy can be particularly effective in reducing it.
• Weight Loss: Successful weight loss involves shrinking the size of fat cells, not necessarily reducing their number. Procedures like liposuction, which remove fat cells but don't change the size of the remaining ones, do not lead to improved metabolic health outcomes.

GLP-1 Agonist Drugs (Ozempic/Wegovy)

GLP-1 agonists, such as Ozempic and Wegovy, are a class of drugs increasingly used for weight loss and diabetes management. Dr. Bikman, who has followed GLP-1 research for decades, expresses concerns about their current widespread use and high dosages.

• Mechanism of Action: Initially used as anti-diabetic drugs, GLP-1 agonists work by inhibiting glucagon release from alpha cells, thereby helping to lower blood glucose. At higher doses, they delay gastric emptying and slow intestinal peristalsis, causing food to remain in the stomach longer, which discourages further eating and activates central satiety centers in the brain. GLP-1 does not directly stimulate insulin release in humans.
• Concerns and Side Effects: The current high doses are considered "too much of a good thing". Side effects include chronic burping, nausea, stomach discomfort, and altered absorption of other medications (e.g., birth control) or nutrients. A significant concern is the loss of fat-free mass (muscle and bone) alongside fat during weight loss, potentially due to poor nutrient absorption or a direct catabolic effect of the drug at higher doses. High doses have also been correlated with severe adverse effects, including a doubled risk of blindness, a threefold increased risk of major depression, and a doubled risk of suicidal behavior and anxiety.
• Proposed Use: Dr. Bikman suggests that the best use of these drugs, if at all, is through micro-dosing and cycling. The goal should be to help individuals change their eating habits, particularly cravings for refined carbohydrates, rather than being seen as a magic bullet for weight loss. This approach aims to "rewire" habits over about 90 days, with the intention of eventually cycling off the drug once habits are established. He notes that some individuals lack a robust natural GLP-1 response to carbohydrates, making them more prone to overeating carbs, for whom a low dose could be beneficial.

Insulin, Glucose, and Aging

Metabolic health is a strong predictor of longevity, with insulin sensitivity and optimal glucose control being key.

• Insulin's Role in Aging: Insulin promotes aging through chronic mTOR activation and strong inhibition of autophagy, a catabolic process essential for cellular cleanup and recycling. While mTOR activation is necessary for muscle and bone growth, persistent activation by high insulin levels can be detrimental.
• Glucose's Pathogenicity: Although Dr. Bikman emphasizes insulin, glucose is also pathogenic through several mechanisms.
  • Glycation: High glucose levels lead to the irreversible alteration of proteins and other molecules (glycation), forming Advanced Glycation End Products (AGEs). These AGEs can compromise tissue structure (e.g., skin, blood vessel lining) and activate inflammatory pathways.
  • Sorbitol Pathway: Excess glucose can be diverted into the sorbitol pathway, where it is converted into sorbitol. Sorbitol accumulates in cells, leading to osmotic stress, water influx, and potentially cell bursting. This mechanism contributes to complications like macular degeneration, retinopathies, and nephropathies.
• Intervention Paradox: Focusing solely on lowering glucose in type 2 diabetics by increasing insulin can lead to worse outcomes, including increased risk of heart disease and cancer, despite improved glucose numbers. This highlights that high insulin itself is a major problem, distinct from the absence of insulin in type 1 diabetes where insulin therapy is life-saving.

Chapters

00:00:00 Introduction
00:01:33 Can you be insulin resistant with normal glucose levels?
00:05:13 Can glucose monitors detect hidden insulin resistance?
00:06:43 What your skin reveals about insulin resistance
00:08:07 Why is insulin resistance behind so many chronic diseases?
00:12:28 Does obesity cause insulin resistance, or vice versa?
00:19:20 Insulin’s surprising roles beyond blood sugar control
00:20:18 What’s driving weight gain—insulin or calories?
00:27:12 Do saturated fats cause insulin resistance?
00:33:44 Why refined carbs amplify risks from saturated fat
00:36:46 Fructose vs. refined sugar—which spikes insulin more?
00:37:43 High-carb vs. keto—which diet controls hunger better?
00:42:09 Why low-carb diets might provide a metabolic advantage
00:44:18 Does exercise give you metabolic ‘wiggle room’?
00:48:42 Why strength training beats cardio for insulin sensitivity
00:50:45 Should you lower insulin before cutting calories?
00:53:54 Does meal frequency drive insulin resistance?
00:57:14 Is nighttime snacking giving you insomnia?
00:59:06 Can a sugary breakfast lead to overeating later?
01:04:01 Does late-night eating disrupt sleep more than blue light?
01:05:41 Can one bad night’s sleep trigger insulin resistance?
01:09:31 Can air pollution cause weight gain?
01:13:23 Vaping vs. smoking—which is worse for metabolic health?
01:14:45 Can statins and antidepressants trigger weight gain?
01:17:30 How to reverse insulin resistance in 90 days
01:24:07 Does apple cider vinegar really lower blood sugar?
01:28:01 Ketone supplements—are the metabolic benefits real?
01:33:42 Why some ethnicities get diabetes without obesity
01:41:36 How oversized fat cells trigger metabolic chaos
01:46:36 Do seed oils silently promote insulin resistance?
01:49:52 Seed oils—always harmful or only when heated?
01:55:43 Fat, muscle, or liver—where does insulin resistance start?
02:01:29 Do fat cells shrink or disappear with weight loss?
02:04:13 Are shrunken fat cells still insulin resistant?
02:05:23 Can exercise and cold therapy specifically shrink visceral fat?
02:06:48 Injecting insulin for muscle, are the risks worth it?
02:09:53 Are drugs like Ozempic a shortcut or solution for obesity?
02:16:20 Are current GLP-1 agonist doses too high?
02:17:10 Microdosing GLP-1 drugs, a solution for carb cravings?
02:23:08 Do these medications cause muscle loss, or is it poor nutrition?
02:25:38 Do GLP-1 agonist benefits extend beyond weight loss?
02:27:49 Could these treatments actually promote longevity?
02:33:20 The dark side of GLP-1 drugs—can they trigger depression?
02:36:39 Insulin vs. glucose—what really drives accelerated aging?
02:41:42 How high glucose levels damage cells—from glycolysis to sorbitol
02:43:48 How insulin shuts down your body’s stress defences
02:48:23 Which biomarkers best predict biological ageing?
02:52:13 One simple breakfast change to lower insulin
02:54:27 Does eating dinner early improve insulin sensitivity?