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In this lecture, Dr. Bikman introduces lectins as harmful plant-derived proteins often found in carbohydrate-rich foods like legumes, grains, and nightshades. While these molecules serve as plant defense mechanisms, in humans they can bind to gut lining cells, disrupting tight junctions and increasing gut permeability (leaky gut). This disruption allows bacterial fragments (e.g., LPS) to enter circulation, triggering systemic inflammation, which in turn increases insulin resistance, autoimmune reactivity, and cardiometabolic risk.

Lectins are also molecular mimics, capable of binding to insulin receptors and partially triggering insulin-like effects. This can lead to inappropriate fat storage, lipogenesis, and eventually insulin resistance as receptors become desensitized. Some lectins, like wheat germ agglutinin (WGA), have been shown in studies to both mimic and interfere with insulin signaling in fat cells—promoting fat gain and metabolic dysfunction even independent of calories.

Lectins are linked to obesity, cardiovascular disease, fatty liver, and autoimmune disorders. They can increase inflammatory cytokines, damage liver mitochondria, promote oxidative stress, and worsen non-alcoholic fatty liver disease (NAFLD). In susceptible individuals, lectins can also drive autoimmune flares, with evidence pointing to their role in molecular mimicry, leading to the generation of autoantibodies and aggravated immune responses.

While cooking methods like pressure cooking or fermenting can reduce lectin levels by up to 95%, they are never fully eliminated. Dr. Bikman concludes that for individuals with autoimmunity, insulin resistance, gut issues, or cardiovascular risk, reducing lectin intake may be wise. Monitoring markers like CRP, fasting insulin, and blood glucose can offer clues to lectin sensitivity, and while more human studies are needed, the biological plausibility and clinical observations make a strong case for dietary caution.

Show Notes/References:

For complete show notes and references, we invite you to become an Insider subscriber. You’ll enjoy real-time, livestream Metabolic Classroom access which includes live Q&A after the lecture with Ben, ad-free podcast episodes, show notes and references, online Office Hours access, Ben’s Research Reviews Podcast, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews. Learn more: https://www.benbikman.com

Ben’s favorite yerba maté and fiber supplement: https://ufeelgreat.com/usa/en/c/1BA884

Ben’s favorite meal-replacement shake: https://gethlth.com (discount: BEN10)

Ben’s favorite electrolytes (and more): https://redmond.life (discount: BEN15)

Ben’s favorite allulose source: https://rxsugar.com (discount: BEN20)

Ben’s favorite health check-up for women: https://choosejoi.co/drben15 (discount: DRBEN15)

Ben’s favorite health check-up for men: https://blokes.co/drben15 (discount: DRBEN15)

Ben’s favorite exogenous ketone: https://ketone.com/BEN30 (discount: BEN30)

Other products Ben likes: https://www.amazon.com/shop/benbikmanphd

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In this Metabolic Classroom lecture, Dr. Bikman dives into the central metabolic role of lipoprotein lipase (LPL)—a largely unsung but crucial enzyme that governs whether fat is burned or stored and even where it accumulates in the body.

LPL is anchored to capillary walls in tissues like fat, muscle, heart, and lactating mammary glands. It acts as a metabolic gatekeeper, hydrolyzing triglycerides from circulating lipoproteins (like chylomicrons and VLDL) into free fatty acids. Depending on the tissue, those fatty acids are either burned (e.g., in muscle) or stored (e.g., in fat cells). LPL activity is influenced by hormones, diet, age, exercise, and weight status, and it plays a role in both fat distribution and metabolic disease.

LPL expression is highly tissue-specific and hormonally regulated. For instance, insulin increases LPL in fat tissue (promoting fat storage) and suppresses it in muscle (reducing fat burning), whereas testosterone suppresses LPL in subcutaneous fat, especially in the buttocks and hips—explaining fat patterning differences between sexes. In contrast, estrogen increases LPL in subcutaneous areas, which supports healthier fat distribution in women. Interestingly, low-carb diets and exercise reverse this pattern, increasing muscle LPL and decreasing fat LPL, thus shifting the body into a fat-burning mode.

Ben also explains how weight loss impacts LPL expression. During weight loss, LPL activity in fat tissue tends to decline, but LPL gene expression can paradoxically increase, setting the stage for weight regain. He cites long-term studies showing that individuals with higher adipose LPL activity after dieting are more likely to regain fat. LPL in muscle tissue, however, increases after weight loss and exercise, supporting greater fatty acid oxidation. Thyroid hormone also influences LPL in both fat and muscle, revving up metabolism in hyperthyroid states and lowering LPL activity in hypothyroidism.

Finally, Ben links LPL to real-world clinical questions, including its role in insulin resistance, statin effects, thyroid hormone therapy, and sex hormone treatments like TRT. He emphasizes that LPL doesn’t just respond to metabolism—it helps define it, and that insulin is the dominant regulator of this enzyme.

Show Notes/References:

For complete show notes and references, we invite you to become an Insider subscriber. You’ll enjoy real-time, livestream Metabolic Classroom access which includes live Q&A after the lecture with Ben, ad-free podcast episodes, show notes and references, online Office Hours access, Ben’s Research Reviews Podcast, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews.

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Dr. Ben Bikman opens this lecture with a comprehensive overview of fluoride’s history in public health, highlighting its original role in preventing dental cavities. However, he shifts the focus to its lesser-known systemic effects, particularly on metabolic health.

Ben emphasizes emerging evidence that chronic exposure to fluoride—from water, toothpaste, and other products—can disrupt fat cell function and insulin sensitivity, both key pillars of metabolic regulation.

Dr. Bikman explains how fluoride interferes with fat cell development by inhibiting PPARγ, a key regulator of adipogenesis. While this may initially seem beneficial (fewer fat cells), it actually leads to hypertrophic fat cells that are more insulin resistant and pro-inflammatory. Though human data is limited, epidemiological studies suggest a link between high fluoride exposure and abdominal obesity.

Fluoride’s impact extends to insulin resistance and pancreatic function. Rodent studies show impaired glucose tolerance and reduced insulin production following fluoride exposure. Mechanistically, this is due to oxidative stress damaging mitochondria in beta cells, impairing both insulin release and glucose uptake. Human studies—though sparse—have shown similar trends in high-fluoride areas with improvements upon fluoride reduction.

Ben also explores fluoride’s effects on mitochondrial function, liver health, brain development, and fertility. Mitochondrial damage in fat and liver cells impairs energy production and fat metabolism, potentially leading to fatty liver disease. In the brain, fluoride may lower IQ and disrupt thyroid function—especially harmful during development. In fertility, fluoride is linked to lower sperm count and hormone disruption in animal models. Dr. Bikman concludes by recommending avoiding fluoride in drinking water while acknowledging its limited role in dental care.

Show Notes/References:

For complete show notes and references, we invite you to become a Ben Bikman Insider subscriber. As a subscriber, you’ll enjoy real-time, livestream Metabolic Classroom access which includes live Q&A after the lecture with Ben, ad-free podcast episodes, show notes and references, online Office Hours access, Ben’s Research Reviews Podcast, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews. Learn more: https://www.benbikman.com

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In this Metabolic Classroom lecture, Dr. Ben Bikman explores the critical yet often overlooked role of fat tissue as an endocrine organ, not just a passive energy storage site.

Fat secretes dozens of bioactive hormones, collectively called adipokines, that influence everything from appetite and insulin sensitivity to inflammation and cardiovascular risk. He focuses primarily on leptin, adiponectin, and PAI-1 (plasminogen activator inhibitor-1), detailing how each one affects whole-body metabolism and health.

Leptin, produced by fat cells, signals the brain about the body’s energy stores, affecting long-term appetite and fertility more than immediate satiety. Paradoxically, individuals with obesity often have high leptin levels but suffer from leptin resistance, leading to persistent hunger and metabolic dysfunction. In contrast, adiponectin levels decrease as fat mass increases. Adiponectin plays a powerful protective role by enhancing insulin sensitivity, reducing inflammation, and promoting fat metabolism, making it a key marker of good metabolic health.

Ben also highlights PAI-1, a lesser-known adipokine secreted mainly by visceral fat, which inhibits the breakdown of blood clots, thereby raising cardiovascular disease risk. He further discusses other adipokines such as resistin, TNF-alpha, and angiotensinogen, which link excess fat mass to insulin resistance, inflammation, and hypertension.

Finally, he contrasts subcutaneous fat (more benign) with visceral fat (more harmful) and explains how brown fat offers unique metabolic benefits by promoting thermogenesis and thyroid hormone activation. The location and health of fat tissue matter just as much as its quantity.

Show Notes/References:

For complete show notes and references, we invite you to become a Ben Bikman Insider subscriber. As a subscriber, you’ll enjoy real-time, livestream Metabolic Classroom access which includes live Q&A after the lecture with Ben, ad-free podcast episodes, show notes and references, Ben’s Research Reviews Podcast, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews. Learn more: https://www.benbikman.com

#FatHormones #Leptin #Adiponectin #PAI1 #MetabolicHealth #FatLoss #InsulinResistance #Endocrinology #ObesityScience #SubcutaneousFat #VisceralFat #BrownFat #CardiovascularHealth #Inflammation #GlucoseControl #Ceramides #HormoneHealth #FatStorage #DrBenBikman #KetoScience

Ben’s favorite yerba maté and fiber supplement: https://ufeelgreat.com/usa/en/c/1BA884

Ben’s favorite meal-replacement shake: https://gethlth.com (discount: BEN10)

Ben’s favorite electrolytes (and more): https://redmond.life (discount: BEN15)

Ben’s favorite allulose source: https://rxsugar.com (discount: BEN20)

Ben’s favorite health check-up for women: https://choosejoi.co/drben15 (discount: DRBEN15)

Ben’s favorite health check-up for men: https://blokes.co/drben15 (discount: DRBEN15)

Ben’s favorite exogenous ketone: https://www.americanketone.com (discount: BEN10)

Ben’s favorite dress shirts and pants: https://toughapparel.com/?ref=40 (use BEN10 for 10% off)

Other products Ben likes: https://www.amazon.com/shop/benbikmanphd

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This week, Dr. Bikman dives deep into the metabolic role of cortisol, the body’s primary glucocorticoid. He explains that while cortisol is essential for survival—mobilizing energy during fasting or stress—chronically elevated levels can wreak metabolic havoc.

Cortisol is produced by the adrenal cortex under direction from the hypothalamic-pituitary-adrenal (HPA) axis. Its main role is to ensure energy availability, stimulating glycogen breakdown, muscle catabolism, and fat breakdown in specific depots. However, long-term cortisol elevation, such as in Cushing’s disease, leads to fat redistribution, muscle loss, insulin resistance, and increased risk of type 2 diabetes.

Cortisol’s metabolic effects are driven by its action on glucocorticoid receptors inside cells, activating genes like PEPCK and glucose-6-phosphatase that stimulate gluconeogenesis and increase blood sugar. It also indirectly causes insulin resistance by increasing ceramide accumulation, which interferes with insulin signaling in cells like muscle and fat. This, combined with glucose overproduction and muscle loss (the major glucose sink), creates a perfect metabolic storm: high blood sugar, high insulin, and reduced glucose uptake.

The hormone also affects fat storage patterns. Cortisol enhances fat accumulation in visceral (abdominal) fat while stimulating fat loss in subcutaneous regions like the limbs. It increases fat uptake by upregulating lipoprotein lipase and blocks fat breakdown by suppressing hormone-sensitive lipase, especially in the abdominal region. Yet cortisol alone isn’t enough to cause fat gain—insulin is still required. Ben illustrates this by showing how individuals with untreated type 1 diabetes have high cortisol and high appetite but still lose fat without insulin.

Lastly, cortisol influences the brain’s hunger and reward systems, increasing carbohydrate cravings through neuropeptide Y and dopamine signaling. Chronic stress or medical conditions that elevate cortisol can drive overeating and central obesity. In short, while cortisol is necessary, its chronic elevation leads to insulin resistance, fat redistribution, and loss of metabolic control.

Show Notes/References:

For complete show notes and references, we invite you to become a Ben Bikman Insider subscriber. As a subscriber, you’ll enjoy real-time, livestream Metabolic Classroom access which includes live Q&A after the lecture with Ben, ad-free podcast episodes, show notes and references, Ben’s Research Reviews Podcast, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews. Learn more: https://www.benbikman.com

#Cortisol #InsulinResistance #ChronicStress #GlucoseControl #MetabolicHealth #CushingsDisease #HormonalBalance #FatStorage #Ceramides #DrBenBikman #VisceralFat #FatLoss #SubcutaneousFat #BloodSugar #AppetiteRegulation #Type2Diabetes #Mitochondria #HPAaxis #CortisolAndCravings #FatDistribution

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In this lecture, Dr. Bikman presents a framework for understanding the two primary patterns of insulin resistance onset—what he terms “fast” and “slow” insulin resistance.

“Fast” insulin resistance happens quickly and can often be reversed just as rapidly. It’s typically triggered by three major factors: elevated insulin (from frequent carb consumption), stress hormones like cortisol and epinephrine, and inflammation (from infection, injury, or autoimmune activity). These triggers lead to the cellular accumulation of ceramides, which interfere with insulin signaling at the molecular level. The good news, he emphasizes, is that when these triggers are removed, the insulin resistance can often resolve quickly.

“Slow” insulin resistance, on the other hand, develops gradually and is more difficult to reverse. It begins in the fat cell, where prolonged exposure to insulin and excess calories causes hypertrophy—the fat cells get larger. As they grow, they become insulin resistant as a form of self-preservation, but this leads to a damaging cascade: elevated free fatty acids, chronic low-grade inflammation, and disruption of glucose control. Dr. Bikman describes how hypertrophic fat cells become hypoxic, triggering inflammation and impairing surrounding tissues.

Unlike the fast form, slow insulin resistance is rooted in long-term lifestyle habits and takes time to correct. The standard advice to “just cut calories” fails to address the core issue—chronically high insulin. Instead, Ben recommends that people first focus on lowering insulin through carbohydrate restriction, which naturally curbs hunger, boosts energy expenditure, and allows fat cells to shrink in a sustainable way.

He concludes that understanding whether your insulin resistance is fast or slow in origin can help shape more effective interventions. With better insight into the mechanisms—from ceramides to fat cell hypertrophy—comes better, more targeted strategies to improve metabolic health.

Show Notes/References:

For complete show notes and references, we invite you to become a Ben Bikman Insider subscriber. As a subscriber, you’ll enjoy real-time, livestream Metabolic Classroom access which includes live Q&A after the lecture with Ben, ad-free podcast episodes, show notes and references, Ben’s Research Reviews Podcast, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews. Learn more: https://www.benbikman.com

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During this week’s Metabolic Classroom lecture, Ben explores the metabolic power of cold therapy, explaining how brief, controlled exposure to cold can significantly enhance metabolic function.

He starts with a deep dive into brown adipose tissue (BAT), which is rich in mitochondria and burns calories to generate heat. Cold exposure activates BAT through norepinephrine, leading to mitochondrial uncoupling and energy expenditure without producing ATP. Interestingly, even white fat can be transformed into metabolically active “beige” fat, increasing thermogenesis.

Dr. Bikman then moves into how shivering muscle activity contributes to thermogenesis. Unlike BAT, muscle contraction generates heat while performing work. Shivering triggers glucose uptake, improves insulin sensitivity, and releases irisin, a hormone that stimulates thermogenic activity in fat tissue. He also discusses AMPK activation, which plays a key role in facilitating this glucose-burning process.

The lecture then highlights a series of hormones influenced by cold, including FGF21 and adiponectin, which boost fat oxidation, enhance insulin sensitivity, and promote mitochondrial biogenesis. Ben reflects on the broader role of the autonomic nervous system, emphasizing how cold therapy improves both sympathetic and parasympathetic function, promoting nervous system flexibility and resilience.

Dr. Bikman wraps up by comparing cold exposure methods—from face immersion and cold showers to cryotherapy and full-body ice baths. He strongly endorses full-body cold water immersion as the most effective strategy, especially when shivering occurs post-immersion. His personal recommendation is the Morozko Forge ice bath (he has no vested interest in this company), citing its sustained metabolic impact and practical benefit. He closes by urging viewers to consider cold therapy as a scientifically grounded tool to support overall metabolic health.

Show Notes/References:

For complete show notes and references, we invite you to become a Ben Bikman Insider subscriber. As a subscriber, you’ll enjoy real-time, livestream Metabolic Classroom access which includes live Q&A after the lecture with Ben, ad-free podcast episodes, show notes and references, Ben’s Research Reviews Podcast, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews. Learn more: https://www.benbikman.com

#ColdTherapy #IceBath #BrownFat #MetabolicHealth #InsulinResistance #Mitochondria #ShiveringThermogenesis #AMPK #Irisin #FGF21 #Adiponectin #FatLoss #GlucoseControl #HealthOptimization #AutonomicNervousSystem #BeigeFat #WeightLossTips #Hormones #Biohacking #BenBikman #drbenbikman

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Ben’s favorite yerba maté and fiber supplement: https://ufeelgreat.com/usa/en/c/1BA884

Ben’s favorite meal-replacement shake: https://gethlth.com (discount: BEN10)

Ben’s favorite electrolytes (and more): https://redmond.life (discount: BEN15)

Ben’s favorite allulose source: https://rxsugar.com (discount: BEN20)

Ben’s favorite health check-up for women: https://choosejoi.co/drben15 (discount: DRBEN15)

Ben’s favorite health check-up for men: https://blokes.co/drben15 (discount: DRBEN15)

Ben’s favorite exogenous ketone: https://www.americanketone.com (discount: BEN10)

Ben’s favorite dress shirts and pants: https://toughapparel.com/?ref=40 (use BEN10 for 10% off)

Other products Ben likes: https://www.amazon.com/shop/benbikmanph

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During this week’s Metabolic Classroom lecture, Dr. Ben Bikman explores the connection between seed oils—specifically linoleic acid—and insulin resistance, a growing area of interest and controversy in the metabolic health world.

Ben begins by detailing the historical rise of seed oils like soybean, corn, sunflower, and canola oil in the human diet. Once used for industrial purposes, they have now become the most common source of dietary fat, with soybean oil consumption increasing from zero to over 20 pounds per person per year in the U.S.. This rise coincides with a global increase in insulin resistance, prompting the question: Are seed oils to blame?

Dr. Bikman focuses on linoleic acid, the primary omega-6 polyunsaturated fat in seed oils, and differentiates between the fat itself and its oxidation products, such as 4-HNE and 13-HODE. He cites cell culture studies showing that unoxidized linoleic acid doesn’t impair insulin signaling, but its peroxidation products dramatically compromise insulin receptor function and glucose transport. Animal studies further support this by showing that diets high in linoleic acid lead to insulin resistance, obesity, and elevated inflammatory markers, while animals consuming fats like coconut oil fare much better.

However, when it comes to human studies, the picture becomes more complex. Some clinical trials suggest that diets high in polyunsaturated fats can improve insulin sensitivity—but these diets are almost always high in carbohydrates, and rarely test seed oils in a low-carb context. Dr. Bikman proposes a unifying theory: saturated fats may be more problematic when consumed alongside carbohydrates, because insulin shunts them into ceramide biosynthesis, a direct driver of insulin resistance. Linoleic acid, on the other hand, becomes dangerous when it undergoes peroxidation, especially in high oxidative stress environments or when used in cooking.

Ben concludes that context matters. Linoleic acid is present in all natural fats and can’t be avoided entirely—but its overconsumption through refined seed oils, particularly in fried foods or highly processed products, is likely harmful. He encourages consumption of natural fats from animals and fruits (like coconuts and olives), rather than industrial seed oils, especially for those concerned about metabolic health and insulin resistance.

Show Notes/References:

For complete show notes and references, we invite you to become a Ben Bikman Insider subscriber. As a subscriber, you’ll enjoy real-time, livestream Metabolic Classroom access which includes live Q&A after the lecture with Ben, ad-free podcast episodes, show notes and references, Ben’s Research Reviews Podcast, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews. Learn more: https://www.benbikman.com

Ben’s favorite yerba maté and fiber supplement: https://ufeelgreat.com/usa/en/c/1BA884

Ben’s favorite meal-replacement shake: https://gethlth.com (discount: BEN10)

Ben’s favorite electrolytes (and more): https://redmond.life (discount: BEN15)

Ben’s favorite allulose source: https://rxsugar.com (discount: BEN20)

Ben’s favorite health check-up for women: https://choosejoi.co/drben15 (discount: DRBEN15)

Ben’s favorite health check-up for men: https://blokes.co/drben15 (discount: DRBEN15)

Ben’s favorite exogenous ketone: https://www.americanketone.com (discount: BEN10)

Ben’s favorite dress shirts and pants: https://toughapparel.com/?ref=40 (use BEN10 for 10% off)

Other products Ben likes: https://www.amazon.com/shop/benbikmanphd

Hosted on Acast. See acast.com/privacy for more information.