The Metabolic Classroom

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.

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

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/1BA884Ben'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.

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

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

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

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.comBen's favorite yerba maté and fiber supplement: https://ufeelgreat.com/usa/en/c/1BA884Ben'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.

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In this Metabolic Classroom lecture, Dr. Bikman explores GLP-1 receptor agonists (such as Ozempic and Mounjaro) and how to use them more effectively.Ben first explains how GLP-1 is naturally produced in the gut and helps regulate glucagon suppression, slows gastric emptying, and promotes satiety. However, he highlights research showing that individuals with obesity have a blunted GLP-1 response to carbohydrates, which may contribute to overeating. He suggests that GLP-1 drugs could be used more strategically—not just for general weight loss, but specifically to control carbohydrate cravings.While these drugs can promote rapid weight loss, they can also come with serious trade-offs, including mental health risks (depression, anxiety, and suicidal thoughts), lean mass loss (up to 40% of weight lost), diminishing effects over time, and digestive complications such as gastroparesis (stomach paralysis). He critiques the current high-dose, long-term approach to these medications, arguing that most people are not using them strategically and eventually regain lost weight—primarily as fat.Dr. Bikman proposes a better approach to using GLP-1 drugs that focuses on low-dose, short-term usage to help control carbohydrate cravings, rather than suppressing appetite completely.His four-step plan includes: (1) starting at the lowest effective dose, (2) engaging in resistance training to preserve muscle mass, (3) adopting a low-carb, high-protein diet, and (4) cycling off the drug after 3-6 months to assess whether cravings remain under control. He also discusses newer GLP-1/GIP dual agonists like Tirzepatide, which may be even more effective but still require careful usage.In closing, Ben emphasizes that GLP-1 drugs should be a tool, not a crutch.The ultimate goal should be to regain control over eating habits, build long-term dietary discipline, and use the drug only when needed. He encourages those considering these medications to work closely with their healthcare providers and approach them with a long-term metabolic health strategy in mind.Show Notes/References:For complete show notes and references referred to in this episode, 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 with Ben, ad-free Metabolic Classroom 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 Hosted on Acast. See acast.com/privacy for more information.

For this week's Metabolic Classroom lecture, Dr. Bikman focuses on natural ways to boost GLP-1 (Glucagon-Like Peptide-1), a powerful gut hormone involved in appetite control, blood sugar regulation, and metabolic health.Ben begins by explaining that GLP-1 is secreted in response to food intake, influencing glucagon suppression, slowing gastric emptying, and activating satiety centers in the brain. However, research shows that individuals with obesity tend to have a blunted GLP-1 response, particularly after consuming carbohydrates. This means that people with obesity may not experience the same level of fullness and appetite regulation, which can contribute to overeating.Dr. Bikman then discusses concerns with GLP-1 receptor agonist medications, such as Ozempic and Wegovy. While they effectively promote weight loss, they also come with significant downsides, including loss of lean mass (up to 40% of total weight lost), increased mental health risks (depression, anxiety, and suicidal thoughts), and a return of sweet cravings over time. Additionally, 70% of people discontinue these drugs within two years, often regaining weight—primarily as fat—due to muscle loss during treatment.He then presents natural methods to enhance GLP-1 production without drugs. His lab at BYU found that Yerba Mate significantly increases GLP-1 by 40-50%, likely due to its ferulic acid content and bitter taste receptors that also reduce sweet cravings. Allulose, a rare sugar, has also been shown to stimulate GLP-1 and improve glucose control, even in individuals with type 1 diabetes. Other natural boosters include a low-carbohydrate, protein-rich diet, which triples GLP-1 levels compared to a low-fat diet, collagen peptides, which enhance GLP-1 secretion and insulin sensitivity, and quality sleep, since poor sleep is linked to impaired GLP-1 signaling and increased hunger.Dr. Bikman concludes by emphasizing that leveraging diet and lifestyle changes is the most effective and sustainable way to improve GLP-1 levels, regulate appetite, and support long-term metabolic health. While GLP-1 medications may serve a purpose, particularly for those struggling with carbohydrate cravings, they come with risks that should not be ignored. Instead, strategies such as Yerba Mate, allulose, low-carb diets, collagen peptides, and better sleep can provide natural, lasting benefits without side effects.Show Notes/References:For complete show notes and references referred to in this episode, 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 with Ben, ad-free Metabolic Classroom 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 Hosted on Acast. See acast.com/privacy for more information.

Dr. Bikman's lecture this week explores the metabolic roles of bilirubin, a molecule typically associated with liver disease and jaundice but now emerging as a key player in metabolism, oxidative stress, and fat regulation.Bilirubin is produced from the breakdown of red blood cells and is transported to the liver, where it undergoes conjugation to become water-soluble and is then excreted into bile.While historically viewed as a waste product, recent research suggests that bilirubin plays a significant role in protecting against oxidative stress and inflammation, and may even contribute to metabolic flexibility and fat metabolism.One of bilirubin's most fascinating properties is its potent antioxidant effect. It neutralizes reactive oxygen species (ROS), helping to reduce oxidative stress—a key driver of chronic diseases, including insulin resistance, cardiovascular disease, and neurodegeneration. Bilirubin also acts as an anti-inflammatory agent, inhibiting key inflammatory pathways such as NF-kappa B, which is involved in obesity-related inflammation. Interestingly, individuals with Gilbert Syndrome, a genetic condition that causes mildly elevated bilirubin levels, have been shown to have a significantly lower risk of cardiovascular disease.Beyond its antioxidant and anti-inflammatory roles, bilirubin also influences fat metabolism. Studies suggest that bilirubin enhances mitochondrial function and thermogenesis, particularly in brown and beige fat, by increasing UCP-1 (uncoupling protein 1) expression, which helps the body burn fat more efficiently.Ben concludes by discussing ways to naturally increase bilirubin levels. Since bilirubin is excreted in bile, diets higher in fat may enhance enterohepatic recycling, allowing more bilirubin to re-enter circulation and exert its beneficial effects. While excessive bilirubin can be toxic, modestly elevated levels, as seen in Gilbert Syndrome, appear to provide metabolic advantages.This growing body of research challenges the outdated view of bilirubin as a mere waste product and suggests that it may be a crucial player in metabolic health.Show Notes/References:For complete show notes and references referred to in this episode, 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 with Ben, ad-free Metabolic Classroom 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 about becoming an Insider on our website: https://www.benbikman.com Hosted on Acast. See acast.com/privacy for more information.

Dr. Bikman's Metabolic Classroom lecture this week explores peptides and their effects on metabolism, fat loss, muscle growth, and overall health.Ben begins by defining peptides as short chains of amino acids that act as signaling molecules in the body. While some peptides occur naturally, others are synthetically developed for therapeutic purposes. He explains that peptides are gaining popularity in fitness, anti-aging, and metabolic health, influencing fat loss, muscle repair, insulin sensitivity, and even skin regeneration. He also introduces collagen peptides, highlighting their unexpected metabolic benefits, including their influence on GLP-1 and gut microbiome health.Ben then categorizes peptides based on their primary functions. For fat loss, peptides like CJC-1295 and Tesamorelin work by stimulating growth hormone and IGF-1, promoting fat breakdown while preserving muscle mass. Another peptide, Melanotan-2, originally known for increasing melanin, has been found to suppress appetite by affecting the melanocortin system. He also discusses peptides like Ipamorelin, which help enhance muscle recovery and growth by selectively increasing growth hormone secretion without affecting other pituitary hormones.In the anti-aging and skin health category, Thymosin Beta-4 stands out for its ability to enhance wound healing and tissue repair. Dr. Bikman also highlights the unexpected metabolic role of collagen peptides, explaining how they can increase GLP-1 levels, improve insulin sensitivity, and even activate AMPK, a crucial metabolic regulator involved in fat breakdown and cellular repair.Finally, he touches on how peptides are administered—most commonly via subcutaneous injections, though some peptides can be absorbed sublingually or applied topically.He cautions that not all peptides are created equal, warning against low-quality or counterfeit products. Ben emphasizes the need for high-quality sourcing and careful monitoring, as some peptides affect hormone levels and require medical supervision.Dr. Bikman concludes that peptides hold immense potential for metabolic health, fitness, and longevity, but should be used wisely and responsibly.Show Notes/References:For complete show notes and references referred to in this episode, 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 with Ben, ad-free Metabolic Classroom 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 about becoming an Insider on our website: https://www.benbikman.com Hosted on Acast. See acast.com/privacy for more information.

Learn more about becoming an Insider: https://www.benbikman.comIn this week's lecture, Dr. Bikman explores the metabolic origins of acne, challenging the conventional view that acne is purely a skin issue. While acne is often attributed to excess oil production, clogged pores, bacteria, and inflammation, Ben highlights how metabolic factors—especially insulin—play a significant role.Insulin directly stimulates sebaceous glands, increasing oil production, and also triggers the release of androgens (such as testosterone), further worsening acne. Additionally, insulin resistance promotes inflammation and hyperkeratinization, both of which contribute to acne severity.He explains that puberty naturally induces a state of insulin resistance, which helps drive growth and development. However, when combined with modern high-carbohydrate diets, this physiological insulin resistance can be exacerbated, leading to severe acne in some teenagers. He also discusses the role of insulin-like growth factor 1 (IGF-1), which is stimulated by high insulin levels and is known to increase sebum production and accelerate skin cell turnover, worsening acne conditions.Ben then presents compelling research on metabolic-based acne treatments, including the use of metformin, an insulin-sensitizing drug that has shown promise in reducing acne, particularly in conditions like PCOS. He also highlights dietary interventions, particularly low-carbohydrate and ketogenic diets, which have been found to significantly reduce acne severity by lowering insulin and improving skin health. One study found that young women on a ketogenic diet saw a 33% reduction in acne severity and a 50% improvement in skin quality within just 45 days.He concludes that acne is not just a cosmetic issue but a metabolic condition that can be managed through dietary and lifestyle changes. While conventional acne treatments address symptoms, tackling insulin resistance through proper nutrition provides a long-term solution. He encourages those struggling with acne to focus on cutting out refined carbohydrates, prioritizing protein, and embracing healthy fats to regulate insulin levels and improve skin health. Hosted on Acast. See acast.com/privacy for more information.

Learn more about becoming an Insider: https://www.benbikman.comIn this week's episode of the Metabolic Classroom lectures, Dr. Ben Bikman explores the metabolic impact of ADHD medications and whether ADHD itself has metabolic roots.Ben explains how stimulant medications (like Adderall and Ritalin) primarily work by increasing dopamine and norepinephrine, enhancing focus but also suppressing appetite and stimulating fat breakdown. This can lead to weight loss but may also contribute to binge eating episodes when the medication wears off. Non-stimulant ADHD medications (like Atomoxetine and Guanfacine) affect metabolism in different ways—some subtly improve insulin sensitivity, while others reduce fat breakdown, potentially leading to weight gain.Beyond medication, Dr. Bikman discusses ADHD as a possible metabolic disorder. Studies show that individuals with ADHD often have reduced glucose metabolism in the prefrontal cortex, the brain region responsible for attention and impulse control. He highlights research linking chronic sugar consumption to dopamine imbalances and brain energy instability, suggesting that modern dietary habits may be worsening ADHD symptoms.One potential solution? Ketones as an alternative brain fuel. Dr. Bikman shares research on the ketogenic diet as a therapy for ADHD, similar to its use in epilepsy and Alzheimer's disease. By shifting the brain's energy source from glucose to ketones, individuals may experience more stable brain function and improved focus. He concludes that ADHD may not just be a neurological condition—it could also be a metabolic issue, and targeting brain metabolism may offer new treatment possibilities.Show Notes/References:For complete show notes and references referred to in this episode, 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 with Ben, ad-free Metabolic Classroom 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 about becoming an Insider on our website: https://www.benbikman.com Hosted on Acast. See acast.com/privacy for more information.

Learn more about becoming an Insider: https://www.benbikman.comDr. Bikman's Metabolic Classroom lecture this week explores the physiological role and implications of GLP-1 (glucagon-like peptide-1) and the GLP-1 receptor agonist drugs used for type 2 diabetes management and weight loss.Ben begins by explaining GLP-1 as a hormone produced in the intestines in response to food. It plays a vital role in slowing gastric emptying, suppressing glucagon, and regulating appetite by signaling fullness to the brain. These mechanisms contribute to its effects on stabilizing blood sugar and enhancing insulin sensitivity.He then delves into GLP-1 receptor agonists, drugs that mimic GLP-1's actions, including semaglutide, liraglutide, and others marketed under brand names like Ozempic and Wegovy. These medications have gained fame for their weight loss efficacy, often leading to reductions in body weight by 15% or more.However, Ben emphasizes that weight loss involves not only fat but also lean mass, raising concerns about muscle loss and metabolic health. Additionally, he discusses the medications' side effects, including depression, anhedonia, and potential long-term complications like fat cell development and gallstones.The lecture also addresses the diminishing returns of these drugs over time, noting that their efficacy in reducing cravings and improving eating control tends to wane after prolonged use. Dr. Bikman highlights that education on healthy eating and resistance training is crucial for maintaining health outcomes, as reliance solely on medication can lead to unintended consequences, such as increased fat regain after discontinuation.Ben concludes by stressing the importance of combining these drugs with a low-carb diet and resistance training to minimize muscle loss and optimize long-term outcomes. He encourages using the lowest effective dose and underscores the need for lifestyle changes to complement pharmacological interventions.Show Notes/References:For complete show notes and references referred to in this episode, 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 with Ben, ad-free Metabolic Classroom 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 about becoming an Insider on our website: https://www.benbikman.com Hosted on Acast. See acast.com/privacy for more information.

Learn more about becoming an Insider: https://www.benbikman.comThis week, Dr. Bikman's lecture focuses on metabolic surgeries (also called bariatric surgeries), their mechanisms, and their impacts on weight loss and metabolic health.Ben begins by explaining the qualifications for these surgeries, which often serve as a last resort for individuals with severe obesity or comorbidities like type 2 diabetes. Common qualifications include a BMI of 40 or higher, or lower BMIs with conditions like hypertension or diabetes. These surgeries aim to address obesity and related health complications when traditional methods, like diet and exercise, fail.Dr. Bikman describes four primary types of metabolic surgeries: Roux-en-Y gastric bypass, sleeve gastrectomy, biliopancreatic diversion with duodenal switch, and adjustable gastric banding. He explains their procedures, including how they alter digestion, absorption, and stomach size, leading to weight loss through restriction and malabsorption. These surgeries also bring significant hormonal changes, such as increases in GLP-1 and reductions in ghrelin (hunger hormone), contributing to satiety and metabolic improvements.While these surgeries can dramatically improve insulin sensitivity, reduce glucagon levels, and improve conditions like type 2 diabetes, they come with risks. Nutrient deficiencies, surgical complications, dumping syndrome, and weight regain are significant concerns. Younger patients are particularly prone to weight regain, especially if they don't adopt sustainable eating habits. Dr. Bikman emphasizes the need for education on managing macronutrients and maintaining long-term behavioral changes.Ben concludes that metabolic surgeries can be a valuable tool for those with severe obesity and related complications. However, he warns of their limitations and advocates for coupling them with lifestyle changes to optimize long-term success.Show Notes/References:For complete show notes and references referred to in this episode, 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 with Ben, ad-free Metabolic Classroom 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 about becoming an Insider on our website: https://www.benbikman.com Hosted on Acast. See acast.com/privacy for more information.

In this Metabolic Classroom lecture, Dr. Bikman delves into the fascinating metabolic process of autophagy, the body's natural recycling system that maintains cellular health by breaking down and reusing damaged components.Ben explains how autophagy is essential for replacing malfunctioning organelles and proteins, thereby preventing diseases such as neurodegenerative disorders, cardiovascular conditions, and even some cancers. Autophagy also plays a crucial role in energy production during nutrient deprivation, highlighting its importance for survival and optimal cellular function.Dr. Bikman also discusses the relationship between autophagy and metabolic health, emphasizing how impaired autophagic activity in adipose tissue contributes to inflammation and insulin resistance in obesity. He explores its role in longevity, citing evidence that enhanced autophagy can improve health span and lifespan in animal studies.Additionally, Ben examines how factors like insulin, nutrient availability, and diets such as ketogenic diets regulate autophagy, with ketones having a direct effect on boosting this process.Throughout the lecture, Dr. Bikman underscores the need for balance in autophagy, warning against excessive or constant activation, whether through pharmacological means like rapamycin or mismanaged dietary habits, advocating instead for natural regulation via nutrient signals.Show Notes/References:For complete show notes and references referred to in this episode, 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 with Ben, ad-free Metabolic Classroom 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 about becoming an Insider on our website: https://www.benbikman.comBen's favorite yerba maté and fiber supplement: https://ufeelgreat.com/usa/en/c/InsulinIQBen'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)Other products Ben likes: https://www.amazon.com/shop/benbikmanphd Hosted on Acast. See acast.com/privacy for more information.

Learn more about becoming an Insider on our website: https://www.benbikman.comDr. Benjamin Bikman delves into the profound relationship between sleep and metabolic health, emphasizing the critical role sleep plays in maintaining insulin sensitivity and overall metabolic function.Ben explains that deep sleep is a restorative phase during which the body repairs cells, regulates hormones, and improves insulin sensitivity. Poor sleep, however, disrupts these vital processes, leading to hormonal imbalances that elevate cortisol levels and reduce melatonin production.Elevated cortisol, a stress hormone, promotes gluconeogenesis and insulin resistance, while insufficient melatonin—a hormone essential for regulating sleep—negatively impacts insulin sensitivity and glucose metabolism. This disruption creates a cycle of metabolic dysfunction, increasing the risk of conditions like type 2 diabetes and obesity.Dr. Bikman highlights actionable strategies to improve both sleep and metabolic health. He stresses the importance of avoiding high-glycemic meals before bed, minimizing exposure to blue light from screens, and maintaining consistent sleep schedules.He also discusses how ketones, especially in athletes after intense exercise, have been shown to improve sleep efficiency and REM sleep duration.For individuals struggling with sleep, Dr. Bikman explores the potential benefits of melatonin supplementation and exogenous ketones, underscoring the need for personalized approaches. By addressing evening habits and understanding the hormonal interplay between sleep and metabolism, individuals can take meaningful steps to enhance both sleep quality and metabolic health.This episode of The Metabolic Classroom provides valuable insights into how optimizing sleep can significantly improve overall well-being.Timestamps:(00:45) – Introduction to Sleep and Metabolic Health(01:22) – Why Sleep is Essential for Insulin Sensitivity(04:20) – How Cortisol Disrupts Sleep and Metabolism(08:10) – The Unexpected Role of Melatonin in Metabolism(19:35) – How Late-Night Eating and Blue Light Harm Sleep(23:40) – Can Exogenous Ketones Improve Sleep Quality?(28:20) – Practical Tips for Better Sleep and Metabolic Health Hosted on Acast. See acast.com/privacy for more information.

We sincerely apologize! During the livestream recording, we experienced some technical difficulties between 07:15 to 08:50. Thanks for your patience and understanding.Learn more about becoming an Insider on our website: https://www.benbikman.comDuring The Metabolic Classroom lecture this week, Dr. Bikman dives into the intricate relationship between salt- and water-regulating hormones and metabolic health.Starting with a discussion of the renin-angiotensin-aldosterone system (RAAS), he explains how hormones like angiotensin II, aldosterone, and antidiuretic hormone (ADH) are not only critical for regulating blood pressure but also significantly impact insulin sensitivity and fat cell dynamics. Angiotensin II promotes insulin resistance by increasing ceramide production, which blocks insulin signaling, while also enlarging fat cells and inhibiting their breakdown. Similarly, aldosterone exacerbates insulin resistance by enhancing ceramide levels and promotes both the growth and multiplication of fat cells. ADH complements these effects, particularly by inhibiting fat breakdown through its action on specific receptors.Ben emphasizes the counterintuitive finding that salt restriction, often prescribed to manage hypertension, can worsen insulin resistance, particularly in individuals with metabolic vulnerabilities. Studies highlight that reducing salt intake leads to increased fasting insulin levels, impaired glucose metabolism, and unfavorable lipid changes, such as reduced HDL cholesterol. Additionally, he warns that dehydration, much like salt restriction, activates these same hormonal pathways, compounding their metabolic effects.Dr. Bikman concludes with a reminder that interventions aimed at improving blood pressure should consider their broader metabolic implications, particularly for individuals predisposed to insulin resistance.Show Notes/References:For complete show notes and references referred to in this episode, 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 with Ben, ad-free Metabolic Classroom 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 about becoming an Insider on our website: https://www.benbikman.comTimestamps: (approximate)(01:13) Overview of Salt- and Water-Regulating Hormones(02:22) How Angiotensin II Influences Blood Pressure and Insulin Resistance(06:37) The Metabolic Effects of Angiotensin II on Fat Cells(11:22) Aldosterone's Role in Insulin Resistance and Fat Cell Growth(15:57) Metabolic Impacts of Antidiuretic Hormone (ADH)(29:02) The Counterintuitive Effects of Salt Restriction on Metabolic Health(33:13) The Role of Dehydration in Activating Metabolic Hormones(34:51) Conclusion: How Blood Pressure Hormones Influence Metabolic Health#MetabolicHealth #InsulinResistance #Hypertension #SaltAndHealth #BloodPressure #HormonesAndHealth #DrBenBikman #MetabolicSyndrome #LowCarbLife #Type2Diabetes #KetoLife #HealthyLifestyle #NutritionScience #MetabolismMatters #HealthEducation #FatCellBiology #InsulinSensitivity #SaltIntake #Dehydration #HealthTips Hosted on Acast. See acast.com/privacy for more information.

Learn more about becoming an Insider on our website: https://www.benbikman.comThis week in The Metabolic Classroom lecture, Ben focuses on the relationship between hypertension medications and metabolic health, providing a critical examination of their mechanisms and metabolic implications.He begins by highlighting the role of insulin resistance as a common root cause of both hypertension and metabolic disorders. Ben explains that while hypertension medications such as diuretics, beta blockers, ACE inhibitors, ARBs, and calcium channel blockers are often prescribed, they each have unique effects on insulin sensitivity and glucose metabolism, which can either mitigate or exacerbate metabolic dysfunction. Notably, some classes of these medications, like ARBs, may improve insulin sensitivity, while others, like beta blockers and diuretics, can impair it, leading to heightened risks for type 2 diabetes.Ben underscores the importance of addressing the root causes of hypertension—namely, insulin resistance—through lifestyle interventions like low-carbohydrate diets and fasting, which improve both blood pressure and metabolic health. He emphasizes the need for personalized treatment plans that consider the metabolic side effects of medications, advocating for strategies that tackle insulin resistance as a primary approach to improving overall health.Show Notes/References:For complete show notes and references referred to in this episode, 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 with Ben, ad-free Metabolic Classroom 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 about becoming an Insider on our website: https://www.benbikman.comBen's favorite yerba maté and fiber supplement: https://ufeelgreat.com/usa/en/c/InsulinIQBen'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)Other products Ben likes: https://www.amazon.com/shop/benbikmanphd#MetabolicHealth #Hypertension #BloodPressure #DrBenBikman #InsulinResistance #MetabolicScience #FatCellBiology #Diuretics #BetaBlockers #ACEInhibitors #CalciumChannelBlockers #BloodPressureMedications #HealthTips #DASHDiet #InsulinSensitivity #FatCells #KetogenicDiet #LowCarbLiving #HealthyLifestyle #HeartHealth Hosted on Acast. See acast.com/privacy for more information.

This week in The Metabolic Classroom, Ben explores the effects of a ketogenic diet on thyroid function, addressing concerns that lower thyroid hormone levels observed during the diet may indicate dysfunction.Dr. Bikman begins by explaining the hypothalamic-pituitary-thyroid (HPT) axis, a regulatory system that controls thyroid hormone production. The thyroid gland produces two primary hormones, T3 (triiodothyronine) and T4 (thyroxine), with T3 being the active form that influences metabolic processes. He emphasizes the concept of negative feedback within the HPT axis, explaining that normal TSH levels generally indicate a well-functioning thyroid, even if T3 levels are lower.Ben also reviews a commonly cited study that observed decreased T3 levels in individuals following a ketogenic diet. Despite the drop in T3, TSH levels remained normal, suggesting that the thyroid gland was not damaged but rather adapting to reduced metabolic demand. He introduces two key explanations: improved thyroid hormone sensitivity and reduced glucose metabolism. Improved sensitivity means that lower levels of T3 are sufficient to maintain metabolic functions, while reduced glucose consumption on a ketogenic diet lessens the body's need for thyroid hormone to regulate glucose uptake.The classroom lecture then delves into the concept of thyroid hormone resistance, a condition linked to metabolic disorders like obesity and type 2 diabetes. Dr. Bikman references studies showing that thyroid resistance is real and measurable, often associated with elevated TSH and thyroid hormones in individuals with metabolic syndrome. He speculates that a ketogenic diet may enhance thyroid sensitivity in these individuals, reducing the need for higher T3 levels.In conclusion, Dr. Bikman reassures those on a ketogenic diet that lower T3 levels do not necessarily indicate harm. If TSH levels are normal and no symptoms of hypothyroidism are present, the changes may reflect a healthy adaptation to the metabolic state induced by the diet.Show Notes/References:For complete show notes and references referred to in this episode, 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 with Ben, ad-free Metabolic Classroom Podcast episodes, show notes and references, Ben's Research Reviews Podcast sent to your inbox weekly, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews. You can learn more about becoming an Insider on our website: https://www.benbikman.comBen's favorite yerba maté and fiber supplement: https://ufeelgreat.com/usa/en/c/InsulinIQBen'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 exogenous ketone: https://www.americanketone.com (discount: Ben10) Hosted on Acast. See acast.com/privacy for more information.

In this week's episode of The Metabolic Classroom, Dr. Bikman delivers a comprehensive lecture on hormone replacement therapy (HRT), focusing on its role in addressing metabolic health challenges faced by women during menopause.The loss of estradiol causes fat to redistribute from healthier storage areas, like the hips and thighs, to the abdominal region, where larger fat cells become more insulin-resistant and pro-inflammatory. This shift contributes to systemic inflammation and elevates the risk of cardiometabolic diseases. Ben explains how HRT, particularly with estradiol, can mitigate these effects by improving insulin sensitivity, reducing inflammation, and promoting healthier fat storage patterns.He also addresses historical concerns about HRT, including risks of blood clots and cancer. Dr. Bikman explains that oral estrogens may slightly increase clotting risks due to their first-pass metabolism in the liver, but transdermal delivery methods like patches and gels do not carry this same risk. Regarding cancer, he highlights how older studies, such as the Women's Health Initiative, overstated the connection between HRT and breast cancer, particularly when using estrogen-only therapies. Ben emphasizes the importance of evaluating the absolute risks, which are relatively small.Beyond its metabolic benefits, HRT also shows promise in protecting against conditions like Alzheimer's disease. Ben discusses studies suggesting that HRT, when started early in menopause, may improve cognitive outcomes, preserve brain volume, and reduce the risk of Alzheimer's, particularly in women with the APOE4 gene. These findings suggest that timely HRT may support brain health alongside its other benefits.In conclusion, Ben underscores the substantial metabolic and overall health changes women face during menopause and the potential for HRT to improve quality of life, metabolic health, and long-term outcomes. He stresses the importance of individualized HRT plans tailored to each woman's unique circumstances, allowing for a nuanced approach to mitigating menopause-related challenges.visit https://www.benbikman.comBen's favorite yerba maté and fiber supplement: https://ufeelgreat.com/usa/en/c/InsulinIQBen'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)Show Notes/References:Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: support@benbikman.com with your request, and be sure to mention which Metabolic Classroom episode you are referring to, which in this case is “Episode 80 - Hormone Replacement Therapy in Women”. Hosted on Acast. See acast.com/privacy for more information.

During Dr. Ben Bikman's latest episode of The Metabolic Classroom lectures, Ben explores the metabolic effects of nicotine, emphasizing its influence beyond its addictive properties and its association with lung health and its connection to insulin resistance.Nicotine, a naturally occurring alkaloid found primarily in tobacco plants, is widely consumed through various products such as cigarettes, cigars, chewing tobacco, e-cigarettes, and nicotine replacement therapies like gums and patches. While most discussions on nicotine focus on its addictive qualities and respiratory impact, Ben highlights its significant effects on metabolism, including interactions with fat cells, insulin, and the nervous system.Nicotine primarily stimulates the sympathetic nervous system by increasing the release of catecholamines like epinephrine and norepinephrine. These stress hormones activate the “fight or flight” response, resulting in elevated heart rate, blood pressure, and metabolic rate.Nicotine's ability to increase lipolysis, the breakdown of stored fat into free fatty acids, often leads to temporary weight loss. However, its chronic use disrupts fat metabolism by impairing mitochondrial fat oxidation, leading to fat cell hypertrophy (enlargement). This enlargement, particularly in visceral fat, contributes to insulin resistance, fatty liver disease, and systemic inflammation.Ben also examines nicotine's role in insulin resistance through its activation of specific cellular pathways. Nicotine increases ceramide production, which disrupts insulin signaling by deactivating key proteins essential for glucose uptake. Additionally, nicotine activates receptors like RAGE (Receptor for Advanced Glycation End Products) and TLR4 (Toll-like Receptor 4), which further drive ceramide production and inflammation. This creates a self-perpetuating cycle that exacerbates metabolic dysfunction and promotes chronic insulin resistance.The classroom lecture highlights the paradoxical nature of nicotine's metabolic effects. While it temporarily enhances fat metabolism and weight loss, chronic exposure reverses these effects, promoting fat storage, inflammation, and severe insulin resistance. Ben emphasizes the metabolic risks associated with nicotine, especially in the context of rising vaping trends among younger populations. He concludes by urging greater awareness of nicotine's systemic effects, particularly its hidden role in metabolic health.visit: https://www.insuliniq.comBen's favorite yerba maté and fiber supplement: https://ufeelgreat.com/usa/en/c/InsulinIQBen'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)Show Notes/References:Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: support@insuliniq.com with your request, and be sure to mention which Metabolic Classroom episode you are referring to, which in this case is “Episode 79 - Nicotine and Insulin Resistance”. Hosted on Acast. See acast.com/privacy for more information.

For The Metabolic Classroom lecture this week, Dr. Bikman explores the often-overlooked effects of oxalates on human health, with a focus on their impact on metabolic, kidney, cardiovascular, gut, and joint health.Oxalates are natural compounds found in various plants, including leafy greens like spinach and kale, as well as certain nuts, seeds, grains, and legumes. They serve as a defense mechanism for plants against herbivores, as their high concentrations can cause irritation and reduce nutrient absorption. While often thought of as harmless, oxalates can act as “antinutrients” by binding to essential minerals such as calcium, magnesium, and iron, limiting their bioavailability and potentially leading to deficiencies.Oxalates form crystals with calcium, creating a compound known as calcium oxalate. When these crystals accumulate in the body, they can contribute to kidney stones—a problem that affects many people. Ben explains that calcium oxalate crystals make up about 80% of all kidney stones, underscoring the connection between oxalate consumption and kidney health. Individuals prone to kidney stones, particularly those consuming high-oxalate diets or taking high doses of vitamin C (which the body can convert to oxalates), may face a heightened risk.To mitigate oxalate-related health risks, Dr. Bikman suggests practical strategies, including reducing high-oxalate foods, ensuring adequate calcium intake to bind oxalates in the gut, staying hydrated to aid in oxalate excretion, and consuming fermented foods or probiotic supplements to support a healthy gut microbiome. He also highlights the importance of a balanced approach to vitamin C supplementation, as excessive intake may increase oxalate production in the body.visit: https://www.insuliniq.comBen's favorite yerba maté and fiber supplement: https://ufeelgreat.com/usa/en/c/InsulinIQBen'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)Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: support@insuliniq.com with your request, and be sure to mention which Metabolic Classroom episode you are referring to, which in this case is “Episode 78 - Oxalates & Metabolic Health”.#Oxalates #MetabolicHealth #KidneyStones #AntiNutrients #DrBenBikman #CalciumOxalate #GutHealth #Inflammation #JointPain #FermentedFoods #Microbiome #Probiotics #NutrientAbsorption #Metabolism #OxalatesInPlants Hosted on Acast. See acast.com/privacy for more information.

During this week's episode of The Metabolic Classroom, Dr. Bikman discusses the impact of microplastics on metabolic health, focusing on their effects on fat cells, insulin resistance, and blood vessel health.Microplastics—tiny plastic particles under five millimeters—are now ubiquitous in our environment, entering the body through food, water, air, and skin products. Their pervasiveness poses serious concerns due to their accumulation in human tissues and the release of harmful chemicals like BPA (bisphenol A) and phthalates, which disrupt normal hormone functions and lead to various health issues.Ben details how microplastics affect fat cell biology, particularly through BPA and phthalates, which mimic hormones like estrogen and testosterone, causing increased fat storage and even promoting fat cell growth and multiplication (hyperplasia and hypertrophy). This hormone disruption and fat cell expansion result in greater fat storage and elevated inflammation, contributing to insulin resistance, obesity, and chronic diseases like type 2 diabetes.Professor Bikman also explores how microplastics affect vascular health, citing studies that show microplastic particles in atherosclerotic plaques. These particles attract macrophages that attempt to remove the microplastics but instead form “foam cells,” which contribute to plaque formation and heighten the risk of cardiovascular disease.Ben concludes with recommendations to limit microplastic exposure, such as avoiding plastic containers for long-term water storage and choosing BPA-free, phthalate-free products, especially for food and beverages.visit: https://www.insuliniq.comBen's favorite yerba maté and fiber supplement: https://ufeelgreat.com/usa/en/c/InsulinIQBen'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)Show Notes/References:Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: support@insuliniq.com with your request, and be sure to mention which Metabolic Classroom episode you are referring to, which in this case is “Episode 77 - Microplastics & Metabolic Health: The Surprising Connection”.#Microplastics #MetabolicHealth #FatCells #DrBenBikman #BPA #Phthalates #InsulinResistance #ChronicInflammation #EndocrineDisruptors #HeartHealth #Atherosclerosis #PlasticsInHealth #Metabolism #HormoneDisruption #EnvironmentalHealth #MetabolicHealth Hosted on Acast. See acast.com/privacy for more information.

This week's episode of The Metabolic Classroom focuses on the potential of continuous glucose monitors (CGMs) as a valuable tool not only for individuals with diabetes but also for anyone interested in gaining deeper insights into their metabolic health.CGMs, which measure glucose levels continuously by detecting interstitial glucose, provide real-time feedback on how diet, exercise, stress, and sleep impact blood sugar, making them useful beyond their traditional application for managing diabetes.Dr. Bikman highlights studies that showcase the variability in individual glucose responses to the same foods, which can be attributed to factors like gut microbiome composition. Ben cites a prominent 2015 study from Israel that revealed individuals' glucose reactions to identical foods varied widely, showing the personal nature of glycemic responses and the role of CGMs in helping people manage their blood glucose variability.Another study, from Stanford University, further illustrates how CGMs can reveal “hidden” glucose spikes, leading people to make more informed dietary and lifestyle decisions.Dr. Bikman touches on the idea that, beyond personal use, CGMs have clinical benefits as well. Studies from the Scripps Research Institute and the Framingham Heart Study show that CGMs can detect early signs of prediabetes and diabetes in individuals who may otherwise go undiagnosed, providing a valuable tool for early intervention.While there are critiques about CGMs, including concerns about potential overemphasis on glucose levels, costs, and possible psychological impacts, Dr. Bikman asserts that the advantages—such as improving insulin sensitivity, reducing glycemic variability, and empowering users to make healthier choices—outweigh these concerns.Ben concludes by encouraging those curious about their metabolic health to consider CGMs as a practical tool for self-monitoring, with potential for significant long-term health benefits.visit: https://www.insuliniq.comBen'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)Show Notes/References:Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: support@insuliniq.com with your request, and be sure to mention which Metabolic Classroom episode you are referring to, which in this case is “Episode 76 - Using a Continuous Glucose Monitor (CGM) to Help You Improve Insulin Sensitivity”.#InsulinResistance #CGM #MetabolicHealth #BloodSugar #DrBenBikman #ContinuousGlucoseMonitor #InsulinSensitivity #GlycemicVariability #Microbiome #Prediabetes #SelfMonitoring #HealthTech #DiabetesPrevention #MetabolicInsights #NutritionalScience #Hyperglycemia #Glycation #HealthOptimization Hosted on Acast. See acast.com/privacy for more information.

In the recording of today's livestream episode of The Metabolic Classroom, Dr. Ben Bikman explores glucosamine's impact on both joint and metabolic health.Glucosamine, commonly used as a supplement to alleviate joint pain, especially in osteoarthritis, is an amino sugar that plays a role in cartilage formation. However, its effectiveness in improving joint health is debated, with some studies suggesting modest benefits, while others find it no better than a placebo.Dr. Bikman shifts the focus to glucosamine's metabolic effects, explaining that due to its structural similarity to glucose, glucosamine can enter cells via glucose transporters, particularly GLUT1 and GLUT2. Once inside cells, glucosamine can contribute to the production of UDP-GlcNAc, a molecule that interferes with insulin signaling, potentially leading to insulin resistance and elevated blood glucose levels. This effect is particularly concerning for individuals with underlying insulin resistance or a family history of type 2 diabetes.Ben refers to several studies, with most finding that glucosamine supplementation can impair insulin sensitivity and raise blood glucose levels in people with metabolic issues, while having little to no effect in metabolically healthy individuals.Dr. Bikman concludes by advising that glucosamine may not be worth the risk for people with metabolic health concerns, while for those who are metabolically healthy, it is likely safe to use. However, he stresses the importance of monitoring blood glucose levels if taking glucosamine and suggests other strategies for improving joint health, such as improving insulin sensitivity and reducing uric acid levels.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)visit: https://www.insuliniq.comReferences:Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: support@insuliniq.com with your request, and be sure to mention which Metabolic Classroom episode you are referring to, which in this case is “Episode 75 - Glucosamine and Metabolic Health: What You Need to Know.”#Glucosamine #MetabolicHealth #InsulinResistance #BloodSugar #JointPain #Osteoarthritis #DrBenBikman #CartilageHealth #GlucoseTransporters #HexosaminePathway #InsulinSensitivity #Supplements #HealthEducation #MetabolismMatters #ChronicDiseases #DiabetesPrevention #Inflammation #JointHealth #Hyperglycemia Hosted on Acast. See acast.com/privacy for more information.

In this episode of The Metabolic Classroom, Dr. Ben Bikman explores the metabolic implications of hyperglycemia, the condition of elevated blood glucose levels. He focuses on both the chronic effects, like those seen in diabetes, and the acute effects of glucose spikes, even from short-term dietary indulgences. Hyperglycemia, while often linked to insulin resistance and diabetes, also has a range of other negative consequences that can manifest even with occasional spikes.One of the key points Dr. Bikman discusses is the relationship between hyperglycemia and insulin. As glucose levels rise, insulin levels rise as well, which can lead to insulin resistance over time, forming a vicious cycle. He highlights studies showing that even a short-term increase in carbohydrate intake can significantly raise fasting insulin levels and triglycerides. These changes have direct consequences on metabolic health, including an increased risk for cardiovascular disease.Dr. Bikman also explains how hyperglycemia leads to oxidative stress, causing the overproduction of reactive oxygen species (ROS). This oxidative stress can damage proteins, lipids, and even DNA within cells. It also contributes to the formation of advanced glycation end products (AGEs), which are harmful compounds formed when glucose binds irreversibly to proteins, fats, or DNA. These AGEs are linked to various diseases such as retinopathy, kidney disease, and atherosclerosis.The lecture further explores how hyperglycemia damages the endothelium (the inner lining of blood vessels) and degrades the glycocalyx, a protective gel-like layer on the endothelium. This damage increases the risk of cardiovascular disease by making blood vessels more prone to atherosclerosis. Additionally, high blood glucose levels lead to the glycation and oxidation of LDL cholesterol, making it more dangerous and likely to contribute to plaque formation in arteries.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)visit: https://www.insuliniq.comReferences:Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: support@insuliniq.com with your request, and be sure to mention which Metabolic Classroom episode you are referring to. Hosted on Acast. See acast.com/privacy for more information.

This week, during the Metabolic Classroom lecture, Dr. Ben Bikman examines the metabolic consequences of medications used for mental health, such as antidepressants and anti-anxiety drugs. Ben highlights the close connection between mental health disorders like depression and anxiety with metabolic issues, particularly insulin resistance and type 2 diabetes. These medications, while effective for managing mental health symptoms, often lead to metabolic side effects such as weight gain and insulin resistance, complicating the relationship between mental and metabolic health.Dr. Bikman reviews key neurotransmitters—serotonin, dopamine, and norepinephrine—that influence both mental and metabolic functions. Serotonin helps regulate mood and appetite but can promote fat accumulation and inhibit fat breakdown. Dopamine is associated with pleasure and reward systems but also plays a role in regulating energy expenditure and fat metabolism. Norepinephrine, closely related to adrenaline, is involved in the body's stress response and can stimulate fat breakdown and thermogenesis.The lecture then shifts to the metabolic effects of common mental health medications, such as SSRIs, tricyclic antidepressants, and antipsychotics. While these drugs can stabilize mood, they are often linked to significant metabolic disturbances, including weight gain, insulin resistance, and cravings for carbohydrate-heavy foods. Ben notes that these medications may exacerbate underlying metabolic issues, potentially worsening the mental health conditions they are meant to treat.Dr. Bikman concludes by emphasizing the importance of addressing metabolic health when treating mental health disorders. He highlights the role of brain glucose hypometabolism, where insulin resistance in the brain may contribute to anxiety and depression. He suggests that improving metabolic health through approaches like ketogenic diets could potentially enhance mental health outcomes by better nourishing the brain and restoring neurotransmitter balance.https://www.insuliniq.com 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)References:Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: support@insuliniq.com with your request, and be sure to mention which Metabolic Classroom episode you are referring to.#MentalHealth #MetabolicHealth #Antidepressants #AnxietyMedications #WeightGain #InsulinResistance #DrBenBikman #MentalHealthMedications #DepressionTreatment #MetabolismMatters #HealthAndWellness #Neurotransmitters #Type2Diabetes #BrainHealth #SSRIs #Antipsychotics #FatMetabolism #MentalWellness #HealthyLiving #NutritionAndMentalHealth Hosted on Acast. See acast.com/privacy for more information.

In this lecture, Dr. Ben Bikman explores liposuction, highlighting its popularity and effects on body fat. While body fat serves important functions like energy storage and hormone regulation, liposuction only removes subcutaneous fat, leaving visceral fat untouched. Dr. Bikman emphasizes that fat cell size, not total fat, is key to metabolic health, and larger fat cells can lead to insulin resistance.Liposuction, though effective for quick fat removal, does not improve metabolic health or insulin sensitivity. Without lifestyle changes, patients often regain fat in different areas. He suggests that liposuction should be seen as a body contouring tool, not a health solution, but it may offer benefits for those with lipedema, improving pain and quality of life.https://www.insuliniq.comBen'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)Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: support@insuliniq.com with your request, and be sure to mention which Metabolic Classroom episode you are referring to. Hosted on Acast. See acast.com/privacy for more information.

In this week's episode of The Metabolic Classroom, Dr. Ben Bikman clarifies misconceptions about lactate metabolism, emphasizing that there is no lactic acid in the human body—only lactate.He explains that lactate is the end product of non-oxidative glycolysis, produced when cells, particularly muscles and red blood cells, require quick ATP energy. Dr. Bikman highlights that lactate production occurs during high-intensity activities where energy demand exceeds the capacity of mitochondria to generate ATP efficiently.Contrary to popular belief, lactate is not responsible for muscle soreness or fatigue.Ben delves into the history of lactate research, mentioning key contributors like Otto Meyerhoff, who identified lactate as a product of anaerobic metabolism, and Carl and Gerty Cori, who discovered the Cori cycle. This cycle demonstrates how lactate is recycled by the liver into glucose, which can then be used by muscles for energy. Lactate, once considered a waste product, is now understood to be an essential substrate for gluconeogenesis.Dr. Bikman introduces George Brooks' lactate shuttle theory, which reveals that lactate is a viable energy source that can be directly utilized by mitochondria for fuel. He explains that this discovery revolutionized the understanding of lactate, showing it can be oxidized within cells for energy production rather than merely being excreted as a waste product.Dr. Bikman also discusses lactate's potential in clinical contexts, such as traumatic brain injury (TBI) recovery, where lactate can serve as an alternative energy source for the brain when glucose metabolism is impaired. Moreover, he touches on how lactate influences fat cells, promoting mitochondrial uncoupling and aiding in fat burning, contributing to metabolic health. Ben suggests that continuous lactate monitoring could help identify mitochondrial dysfunction and predict type 2 diabetes risk.https://www.insuliniq.com 00:00 - Introduction to Lactate Metabolism01:09 - Lactic Acid vs. Lactate: Debunking the Myth02:16 - Glycolysis and Lactate Production04:23 - How Lactate is Produced in Muscles06:23 - Red Blood Cells and Lactate07:18 - History of Lactate Research: Otto Meyerhoff09:40 - The Cori Cycle: Lactate Recycled into Glucose13:54 - Lactate as a Viable Energy Source15:55 - George Brooks' Lactate Shuttle Theory18:44 - Lactate and Traumatic Brain Injury (TBI)20:55 - Lactate's Role in Fat Burning and Mitochondria23:58 - Lactate in Clinical Contexts: Metabolic Health25:09 - Continuous Lactate Monitoring and Mitochondrial Dysfunction28:59 - Lactate as a Predictor of Type 2 Diabetes29:59 - Conclusion: Lactate's Critical Role in Health and EnergyBen'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)References:Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: support@insuliniq.com with your request, and be sure to mention which Metabolic Classroom episode you are referring to. Hosted on Acast. See acast.com/privacy for more information.

In today's episode of The Metabolic Classroom, Dr. Ben Bikman delivers a lecture focusing on the drug rapamycin and its impact on longevity.The primary discussion revolves around the role of the protein complex mTOR (mammalian target of rapamycin) in the body's aging process. While rapamycin is often touted as a drug that can inhibit mTOR and thereby promote longevity, Ben emphasizes that much of this belief is based on animal studies and lacks solid human evidence. The mTOR pathway is involved in cell growth and protein synthesis, particularly in muscle tissue, making its inhibition controversial when it comes to aging and muscle maintenance.Dr. Bikman highlights that some research suggests reducing mTOR activity by lowering protein intake might promote longevity. However, he pointed out that for older populations, higher protein consumption is correlated with reduced mortality, particularly from animal protein sources. This is especially significant when considering muscle mass, which has been consistently linked to longer lifespan. Inhibiting mTOR might impair muscle growth and maintenance, making rapamycin problematic for those aiming to preserve muscle health as they age.In addition to discussing the potential benefits of rapamycin, Ben underscores its negative side effects, including immune suppression, increased triglycerides (which elevate the risk of heart disease), and the inhibition of muscle protein synthesis. He also raises concerns about the drug's ability to reduce testosterone levels and hinder reproductive health in both men and women. Given that reproduction is a key element of both evolutionary theory and many religious doctrines, Dr. Bikman questions the wisdom of using a drug that compromises reproductive function.Dr. Bikman concludes by connecting the role of insulin to mTOR activation. He argues that insulin has a much stronger effect on mTOR than dietary protein does, and prolonged elevated insulin levels, common in modern diets, keep mTOR constantly active. This chronic activation of mTOR may hinder longevity more than protein intake or rapamycin inhibition.Instead of relying on drugs like rapamycin, Ben suggests that reducing insulin levels through dietary interventions like fasting may be a more effective and natural way to manage mTOR activity and promote healthy aging.https://www.insuliniq.com My favorite meal-replacement shake: https://gethlth.com (discount: BEN10)My favorite electrolytes (and more): https://redmond.life (discount: BEN15)My favorite allulose source: https://rxsugar.com (discount: BEN20)References:Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: support@insuliniq.com with your request, and be sure to mention which classroom episode you are referring to.#Longevity #Rapamycin #AgingScience #mTOR #Healthspan #Autophagy #MuscleHealth #BenBikman #MetabolicHealth #HealthyAging #AntiAging #FastingBenefits #InsulinResistance #ImmuneHealth #ProteinSynthesis #HeartHealth #TestosteroneHealth #ReproductiveHealth #ScientificResearch #MetabolismMatters #BenBikman #DrBenBikman Hosted on Acast. See acast.com/privacy for more information.

In this episode of The Metabolic Classroom, Dr. Ben Bikman explores the topic of leaky gut syndrome, explaining how substances enter the body through the intestines and how the gut acts as a controlled gateway.While nutrients like amino acids, glucose, and fats are transported through the intestinal lining via a process called transcellular transport, problems arise when the tight junctions between the cells weaken. This can lead to harmful substances, including large molecules and microbes, passing into the bloodstream in a process known as paracellular transport.A key player in leaky gut syndrome is the molecule lipopolysaccharide (LPS), which comes from certain gut bacteria. Under normal conditions, LPS stays in the intestines and is expelled with waste, but when it enters the bloodstream due to leaky gut, it can trigger a chronic inflammatory response. This inflammation is linked to conditions like obesity, heart disease, and fatty liver disease. Bikman emphasized that even low levels of LPS in the blood can promote insulin resistance, further contributing to metabolic disorders.Several dietary and environmental factors can compromise the integrity of the gut barrier. Ben highlights the negative impact of fructose, which weakens tight junction proteins and promotes oxidative stress. Polyunsaturated fats from refined seed oils and gluten, especially in people with sensitivities, can also increase intestinal permeability. Additionally, chronic stress and alcohol consumption were identified as contributors to leaky gut.On a positive note, Dr. Bikman discusses strategies to improve gut health, such as consuming short-chain fatty acids (like butyrate), found in dairy and certain fibers. He also mentioned the potential benefits of saturated fats, particularly from dairy, which may promote gut healing. Lastly, Dr. Bikman shares the role of LDL cholesterol as a “scavenger” that helps remove harmful LPS from the blood, suggesting its misunderstood importance in immune health.https://www.insuliniq.com 00:00 Introduction to Leaky Gut01:52 How Substances Enter the Body Through the Gut03:58 Structure and Function of the Gut Lining07:07 Normal Transport vs. Leaky Gut Transport09:23 The Role of LPS in Leaky Gut and Inflammation11:41 How LPS Affects the Body12:45 Low-Grade Systemic Inflammation15:23 Cardiometabolic Consequences of Leaky Gut18:52 Dietary Triggers of Leaky Gut: Fructose and Seed Oils22:14 The Impact of Gluten and Stress on Gut Health24:05 Strategies to Improve Gut Health25:09 Short Chain Fatty Acids and Saturated Fats for Gut Healing28:08 The Role of LDL Cholesterol in Gut Health31:16 The Importance of Fiber and Probiotics33:32 The Rare Sugar Allulose and Gut Integrity35:23 Conclusion and Practical TakeawaysMy favorite meal-replacement shake: https://gethlth.com (discount: BEN10)My favorite electrolytes (and more): https://redmond.life (discount: BEN15)My favorite allulose source: https://rxsugar.com (discount: BEN20)Study references referred to are available upon request. Email: support@insuliniq.com Hosted on Acast. See acast.com/privacy for more information.

This episode of The Metabolic Classroom focuses on a deeper understanding of insulin's role in obesity, particularly through the lens of the fuel partitioning theory.This theory suggests that the way the body allocates energy between burning and storing it significantly influences weight gain and overeating. With obesity affecting over 700 million people worldwide, Dr. Bikman emphasizes the importance of understanding the broader health implications, including increased risks for chronic diseases like heart disease, type 2 diabetes, and certain cancers. He also notes the economic burden, highlighting how our current view of obesity is failing to make meaningful improvements.The lecture explores how the caloric view of obesity, which suggests that obesity is purely a result of consuming more calories than are burned, is overly simplistic. Dr. Bikman argues that hormonal influences, particularly insulin, are often overlooked in this view.He draws from a recent publication, “Trapped Fat: Obesity Pathogenesis as an Intrinsic Disorder in Metabolic Fuel Partitioning,” which emphasizes that hormonal signals like insulin play a critical role in whether the body stores or burns energy. Dr. Bikman points out that historical perspectives on obesity used to focus on hormones, but the caloric theory gained dominance after World War II.Through the discussion of various rodent models, such as the VMH lesion model and leptin-deficient animals, Dr. Bikman demonstrates how hormonal imbalances, particularly elevated insulin levels, can drive fat storage even in the absence of overeating. In these models, animals gain significantly more fat despite consuming the same number of calories as healthy controls. Dr. Bikman relates this to human analogs, like hypothalamic obesity and leptin resistance, explaining that these conditions similarly lead to obesity due to disrupted hormonal regulation, especially involving insulin.The final part of the lecture touches on how energy homeostasis and insulin resistance differ in individuals predisposed to obesity. Ben stresses that addressing insulin levels should be the primary strategy for reversing obesity. He concludes by highlighting how controlling insulin can increase metabolic rate and fat burning, allowing the body to waste energy through ketone excretion. He advises that focusing on reducing insulin rather than cutting calories is a more effective approach to long-term weight loss and health improvement.https://www.insuliniq.com My favorite meal-replacement shake: https://gethlth.com (discount: BEN10)My favorite electrolytes (and more): https://redmond.life (discount: BEN15)My favorite allulose source: https://rxsugar.com (discount: BEN20)References:Trapped fat: Obesity pathogenesis as an intrinsic disorder in metabolic fuel partitioning:https://pubmed.ncbi.nlm.nih.gov/38961319/ Hosted on Acast. See acast.com/privacy for more information.

In this episode of The Metabolic Classroom, Dr. Ken Berry and Dr. Ben Bikman discussed the critical role of endogenous insulin, the limitations of focusing solely on glucose levels, and the implications of common markers like A1C and uric acid in understanding metabolic health.Dr. Berry began by highlighting how many primary care physicians misunderstand the function of beta cells in type 2 diabetes, often believing that these cells “burn out” and stop producing insulin. Dr. Bikman clarified that in true type 2 diabetes, beta cells do not fail entirely; instead, insulin production often remains high or slightly decreases, which is still significantly higher than normal.The problem lies in the body's insulin resistance, not a lack of insulin production. Dr. Bikman emphasized the importance of measuring fasting insulin levels early in a patient's metabolic health journey, noting that levels above 6 microunits/mL can indicate potential problems.The conversation then shifted to the A1C test, a common marker used to assess blood glucose levels over time. Dr. Berry and Dr. Bikman discussed the limitations of A1C, particularly how it can be falsely elevated or decreased based on the lifespan of red blood cells. Longer-lived red blood cells can cause a falsely high A1C, even if glucose levels are normal, while short-lived red blood cells can lead to a falsely low A1C in the presence of hyperglycemia. Dr. Bikman suggested that while A1C has value, it should not be the sole marker for assessing metabolic health. He also pointed out that A1C does not account for the glycation caused by other sugars like fructose, which can lead to significant damage not reflected in A1C results.Dr. Berry raised concerns about the carnivore community, where some individuals see their A1C levels rise despite a healthy diet. Dr. Bikman explained that this could be due to longer-lived red blood cells resulting from a nutrient-rich diet. He recommended the fructosamine test as a better indicator of glucose glycation in these cases. The discussion also touched on the lack of tests for fructose and galactose glycation, leaving healthcare providers blind to the potential damage caused by high fructose intake, especially from fruit juices.The classroom discussion concluded with an exchange about uric acid, particularly its relationship with fructose metabolism. Dr. Bikman shared insights from his research showing that uric acid, which is produced during fructose metabolism, can contribute to insulin resistance and inflammation. However, he also noted that ketones, produced during a ketogenic diet, can inhibit the inflammation caused by uric acid, providing a potential explanation for why individuals on ketogenic diets may experience improved metabolic health despite elevated uric acid levels.https://www.insuliniq.com Learn more about Dr. Ken Berry: https://www.drberry.com/about #InsulinResistance #Type2Diabetes #DrBenBikman #DrKenBerry #A1CTest #FastingInsulin #UricAcid #CarnivoreDiet #Fructose #MetabolicHealth #KetogenicDiet #Inflammation #BetaCells #Endocrinology #BloodGlucose #ProperHumanDiet #HealthLecture #MetabolicClassroom #BiomedicalScience #InsulinIQMy favorite meal-replacement shake: https://gethlth.com (discount: BEN10)My favorite electrolytes (and more): https://redmond.life (discount: BEN15)My favorite allulose source: https://rxsugar.com (discount: BEN20) Hosted on Acast. See acast.com/privacy for more information.

In this episode of The Metabolic Classroom, Dr. Ben Bikman explores the metabolic effects of estrogens, particularly their role in glucose metabolism.Estrogens, mainly produced in the gonads, play a crucial role in regulating blood glucose by enhancing insulin sensitivity. Dr. Bikman explained that estrogens improve insulin signaling through pathways such as PI3 kinase and AKT, which are essential for glucose uptake in muscle and fat tissues. Additionally, estrogens activate AMP-activated protein kinase (AMPK), further promoting glucose uptake and maintaining healthy blood glucose levels.Estrogens also suppress glucose production in the liver by inhibiting key enzymes involved in gluconeogenesis, helping to prevent excess glucose release into the bloodstream. In contrast, progesterone decreases insulin sensitivity and promotes insulin resistance, counteracting some of estrogen's beneficial effects. This hormonal interplay affects glucose metabolism during the ovarian cycle, with estrogen-dominant phases being more favorable for glucose control.During menopause, the significant drop in estrogen levels leads to increased insulin resistance and shifts in fat storage, often resulting in more central fat accumulation. While hormone replacement therapy (HRT) can mitigate some of these changes, it comes with risks that need careful consideration. Ben emphasizes the significant role of estrogens in glucose metabolism and their broader impact on metabolic health, especially in women.https://www.insuliniq.com 01:19 - Overview of Estrogens and Progesterone02:20 - Cholesterol as the Precursor to Sex Hormones03:34 - The Role of Aromatase in Estrogen Production04:32 - Understanding the Family of Estrogens05:56 - Estrogens and Glucose Metabolism: Key Signaling Pathways06:54 - Insulin Signaling Pathway Overview08:57 - How Estrogens Enhance Insulin Sensitivity10:04 - The Role of AMPK in Glucose Uptake12:11 - Estrogens' Dual Mechanism in Regulating Glucose Levels13:18 - The Impact of Estrogens on Liver Glucose Production15:33 - Estrogens' Role in Suppressing Gluconeogenesis17:07 - Why Women Have Lower Risk of Type 2 Diabetes19:28 - Metabolic Effects During the Ovarian Cycle21:54 - Progesterone's Influence on Insulin Resistance and Fat Storage25:16 - The Shift in Fat Storage Patterns Post-Menopause26:16 - Hormone Replacement Therapy: Metabolic ConsiderationsPI3K activation leads to the phosphorylation of Akt, a key protein in glucose metabolism, which promotes the translocation of GLUT4 (glucose transporter type 4) to the cell membrane, facilitating glucose uptake into muscle and adipose tissue: https://www.sciencedirect.com/science/article/pii/S155041311930138X?via%3Dihub AMPK acts as an energy sensor and helps maintain cellular energy balance, which is crucial in regulating glucose and lipid metabolism: https://link.springer.com/article/10.1007/s12013-015-0521-z Progesterone increases blood glucose levels by enhancing hepatic gluconeogenesis. This effect is mediated by the progesterone receptor membrane component 1 (PGRMC1) in the liver, which activates gluconeogenesis pathways, leading to increased glucose production, especially under conditions of insulin resistance: https://www.nature.com/articles/s41598-020-73330-7 Hosted on Acast. See acast.com/privacy for more information.

Dr. Ben Bikman, a biomedical scientist and professor of cell biology, discusses the phenomenon of anabolic resistance.Anabolic resistance, primarily a problem associated with aging, refers to the reduced ability of muscles to synthesize protein in response to anabolic stimuli, such as protein intake and resistance exercise. This condition leads to a decline in muscle mass and function over time, contributing to a loss of physical capacity, increased risk of falls, and a greater dependency on others for daily living.Dr. Bikman emphasizes the importance of muscle mass for overall health. Beyond physical function, muscle plays a crucial role in metabolic regulation, particularly glucose metabolism and insulin sensitivity. Muscle acts as a “glucose sink,” helping to regulate blood glucose levels and maintain insulin sensitivity. Therefore, maintaining muscle mass is vital for preventing metabolic disorders and enhancing longevity and health span.Anabolic resistance is influenced by various age-related factors, including hormonal changes, reduced physical activity, insufficient protein intake, and chronic illnesses such as insulin resistance. The key intracellular signal involved in muscle protein synthesis is the mTOR1 pathway, which becomes less responsive with age and insulin resistance. Dr. Bikman also discusses the controversial use of rapamycin, a drug promoted by some longevity enthusiasts, which can inhibit mTOR1 and potentially exacerbate anabolic resistance and insulin resistance.To combat anabolic resistance, Dr. Bikman highlights the importance of dietary and exercise interventions. Older adults require higher protein intake, particularly high-quality protein sources rich in leucine, to stimulate muscle protein synthesis effectively. Additionally, resistance exercise is crucial, with a focus on going to muscle fatigue to promote maximal muscle protein synthesis. Dr. Bikman stresses the need for older adults to prioritize resistance exercise over aerobic exercise to maintain muscle mass and function.Dr. Bikman concludes by emphasizing the societal benefits of maintaining muscle mass and combating anabolic resistance. Strong, healthy, and independent individuals contribute to stronger communities and reduced economic burdens. By adopting proper dietary and exercise habits, individuals can improve their muscle health, enhance their quality of life, and increase their longevity.https://www.insuliniq.com 01:08 - Defining Anabolic Resistance02:15 - Impact of Aging on Muscle Protein Synthesis03:15 - Role of Anabolic Stimuli in Muscle Growth05:15 - Risks Associated with Loss of Muscle Mass06:17 - Muscle's Role in Metabolic Health07:19 - Muscle Mass and Longevity10:24 - Age-Related Factors: Hormones and Physical Activity11:10 - Biochemical Signaling and mTOR1 Pathway13:28 - Controversy Around Rapamycin and Longevity15:43 - Rapamycin's Impact on Muscle and Testosterone17:42 - Nutrient Sensing and mTOR1 Activation18:40 - Importance of Leucine in Protein Synthesis19:54 - Hormonal Regulation of mTOR120:55 - Consequences of Anabolic Resistance21:52 - Combating Anabolic Resistance: Dietary Strategies24:05 - Importance of High-Quality Protein Sources26:05 - Role of Resistance Exercise in Combating Anabolic Resistance28:55 - Exercise Protocols for Older Adults30:55 - Importance of Resistance Exercise Over Aerobic Exercise32:55 - Conclusion and Societal Benefits of Muscle HealthReferences:Due to character length constraints, references are not posted here. For a complete list, please email: support@insuliniq.com with your request. Hosted on Acast. See acast.com/privacy for more information.

Dr. Ben Bikman, professor of cell biology and metabolic scientist, delivers a lecture on the importance of fermentation and fermented foods from a metabolic perspective. He began by defining fermentation as the metabolic process where bacteria convert carbohydrates into organic molecules, emphasizing that bacteria primarily consume carbohydrates, not fats or proteins. Fermented foods such as dairy, vegetables, and beverages like kombucha and kefir are common examples. Fermentation not only changes the taste and texture of these foods but also has significant metabolic impacts.A key benefit of consuming fermented foods is the reduction in glycemic load, which helps control blood sugar and insulin levels. Dr. Bikman highlightes studies showing that fermented milk improves glycemic control and lipid profiles in people with type 2 diabetes. He pointed out the importance of choosing genuinely fermented products, such as real sourdough bread, which lower postprandial glucose levels compared to conventional bread.Dr. Bikman also discussed the production of short-chain fatty acids (SCFAs) during fermentation, such as acetate, propionate, and butyrate. These SCFAs have multiple health benefits, including improving gut health by maintaining gut barrier integrity, promoting an anti-inflammatory environment, and feeding gut cells. Additionally, SCFAs enhance metabolic functions, such as stimulating mitochondrial biogenesis and improving insulin sensitivity, which are crucial for overall metabolic health.Fermented foods also provide probiotics when consumed raw and unpasteurized. These beneficial bacteria can help balance the gut microbiota, improve digestion, and support immune function. Dr. Bikman emphasizes the importance of incorporating raw, fermented foods into the diet to reap these probiotic benefits.Lastly, Dr. Bikman introduced the concept of antinutrients, naturally occurring compounds in plant-based foods that can interfere with nutrient absorption. He explained that fermentation helps reduce the levels of antinutrients such as phytic acid, lectins, oxalates, and tannins, thereby enhancing the bioavailability of essential nutrients. He concludes by encouraging the incorporation of fermented foods into the diet as part of a strategy to control carbohydrate intake and improve metabolic health.https://www.insuliniq.com 01:00 – Overview of Fermentation02:00 – Definition and Examples of Fermented Foods04:00 – Benefits of Fermented Dairy: Kefir06:00 – Fermented Foods and Glycemic Control08:00 – Sourdough Bread vs. Conventional Bread10:00 – Introduction to Short-Chain Fatty Acids (SCFAs)12:00 – SCFAs and Gut Health13:00 – SCFAs and Metabolic Benefits15:00 – Probiotics in Fermented Foods16:00 – Importance of Raw, Unpasteurized Fermented Foods17:00 – Introduction to Antinutrients18:00 – Examples of Antinutrients: Phytic Acid, Lectins, Oxalates, Tannins20:00 – Fermentation's Role in Reducing Antinutrients#FermentedFoods #MetabolicHealth #DrBenBikman #Fermentation #GutHealth #Probiotics #ShortChainFattyAcids #GlycemicIndex #InsulinResistance #Kefir #Sauerkraut #Kimchi #Kombucha #HealthyEating #NutritionScience #DiabetesManagement #AntiNutrients #HealthyGut #Mitochondria #InsulinIQMy favorite meal-replacement shake: https://gethlth.com (discount: BEN10)My favorite electrolytes (and more): https://redmond.life (discount: BEN15)My favorite allulose source: https://rxsugar.com (discount: BEN20)References:(Due to character length constraints, references are not posted here. For a complete list, please email: support@insuliniq.com with your request.) Hosted on Acast. See acast.com/privacy for more information.

In this episode of The Metabolic Classroom, Dr. Bikman introduces the concept of the Randle Cycle, also known as the glucose fatty acid cycle, in a lecture aimed at providing a better understanding of metabolism. The Randle Cycle, first identified by Dr. Philip Randle and his colleagues in the 1960s, explores how cells decide between using glucose or fatty acids for fuel. Dr. Bikman emphasized that this cycle has been misinterpreted on social media and aims to clarify its relevance in metabolic functions and nutritional decisions.https://www.insuliniq.com 00:00 - Introduction to the Metabolic Classroom and Dr. Ben Bikman01:00 - Overview of the Randle Cycle (Glucose Fatty Acid Cycle)02:00 - Historical Background: Philip Randle's Research03:00 - Experimental Model: Perfused Rat Hearts04:00 - Key Terms: Glucose and Fatty Acids05:00 - Concept of Substrate Competition06:00 - Reciprocal Inhibition: Fats vs. Glucose08:00 - Fatty Acid Oxidation Process10:00 - Biochemical Pathways: Acetyl-CoA, NADH, and Pyruvate Dehydrogenase12:00 - Role of Citrate in Glycolysis Inhibition14:00 - Glucose Utilization and Malonyl-CoA16:00 - Insulin's Role in Fuel Selection18:00 - Insulin's Impact on Glucose and Fat Burning20:00 - Diabetes Case Study: Type 1 and Type 222:00 - Type 1 Diabetes: High Glucose and Fatty Acids24:00 - Ketones Production in the Liver26:00 - Type 2 Diabetes: Insulin Resistance and Metabolic Inflexibility28:00 - Insulin Resistance in Fat Cells30:00 - Metabolic Inflexibility in Type 2 Diabetes32:00 - Insulin Resistance in the Brain34:00 - The Impact on Hunger and Neurological Disorders36:00 - Conclusion: Importance of Insulin in Metabolic Health#Metabolism #RandleCycle #DrBenBikman #InsulinResistance #GlucoseMetabolism #FattyAcidOxidation #MetabolicHealth #DiabetesResearch #Ketosis #Type1Diabetes #Type2Diabetes #InsulinRole #CellBiology #NutritionalScience #MetabolicFlexibility #Ketones #GlucoseUtilization #FatBurning #BiomedicalScience #HealthLectureMy favorite meal-replacement shake: https://gethlth.com (discount: BEN10)My favorite electrolytes (and more): https://redmond.life (discount: BEN15)My favorite allulose source: https://rxsugar.com (discount: BEN20)References:https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/randle-cycle Insulin Regulation of Ketone Body Metabolism: https://onlinelibrary.wiley.com/doi/10.1002/0470862092.d0308The Effects of a Ketogenic Diet and Exercise Interventions on Cognitive Function: https://faseb.onlinelibrary.wiley.com/doi/10.1096/fasebj.31.1_supplement.lb810(Due to character length constraints, not every reference is posted above. For a complete list, please email: support@insuliniq.com with your request.) Hosted on Acast. See acast.com/privacy for more information.

Dr. Ben Bikman's lecture on leptin, delivered in his Metabolic Classroom series, highlights the hormone's critical role in metabolism. Leptin, primarily produced by white fat tissue, helps regulate energy balance by signaling the brain to suppress appetite and promoting mitochondrial biogenesis in muscle cells. Leptin levels correlate with body fat, and various factors like insulin and TNF alpha influence its production. Insulin significantly stimulates leptin secretion, highlighting a complex interplay between these hormones.Leptin resistance, a condition where the body fails to respond effectively to leptin despite high levels, is similar to insulin resistance and often occurs in individuals with higher body fat. This leads to compromised satiety signals, energy expenditure, and potential obesity. Dr. Bikman also explores leptin's broader effects on reproductive health, thyroid function, immune function, vascular health, and bone formation. These diverse roles underline leptin's significance in the body.A historical perspective reveals leptin's discovery in 1994 by Dr. Jeff Friedman's lab at Rockefeller University. They found that leptin played a crucial role in regulating body weight in mice. However, leptin injections in obese humans did not yield similar results, as most obese individuals already have high leptin levels, leading to the understanding that leptin resistance, not a lack of leptin, is the issue in obesity.The lecture concludes with practical insights on addressing leptin resistance, emphasizing the importance of controlling blood glucose and insulin levels, particularly through low-carb diets. This approach helps reduce leptin levels and improve leptin sensitivity, offering a pathway to better metabolic health and weight control. Hosted on Acast. See acast.com/privacy for more information.

Professor Ben Bikman discusses sarcopenic obesity, a condition involving obesity and muscle loss. This condition results from factors like sedentary lifestyles, aging, and metabolic disturbances. While obesity is common, sarcopenia typically affects the elderly, diseased, or very sedentary individuals. The combination of excessive fat and muscle loss makes sarcopenic obesity particularly challenging.Dr. Bikman explains the crucial role of muscle in blood glucose regulation. Muscle mass reduction impairs glucose control, leading to higher blood sugar levels and increased insulin resistance. Even a short period of bedrest can significantly reduce muscle mass and insulin sensitivity. Inflammation from enlarged fat cells also contributes to muscle loss and insulin resistance, creating a vicious cycle.Insulin resistance and sarcopenic obesity can both cause and result from each other. Insulin resistance impairs muscle protein synthesis and promotes fat cell growth, leading to further insulin resistance. Reduced muscle mass and increased fat cell size negatively impact metabolic health. Bikman stresses the importance of diet in managing sarcopenic obesity, advocating for a low-insulin diet by controlling carbs, prioritizing protein, and not fearing fats.To combat sarcopenic obesity, Dr. Bikman recommends proper nutrition and resistance training. Reducing insulin levels helps preserve muscle mass and promote fat loss. Resistance exercise is more effective than aerobic exercise for improving metabolic health. Consistent exercise and a controlled diet can help individuals manage or prevent sarcopenic obesity and improve metabolic health.[01:02] Understanding Fat Cell Size[02:07] Prevalence and Impact of Sarcopenic Obesity[05:02] Role of Muscle in Glucose Regulation[07:12] Effects of Bedrest on Muscle and Insulin Resistance[10:43] Insulin's Role in Muscle Protein Synthesis[16:04] Inflammation and Insulin Resistance[20:43] Sarcopenic Obesity Contributing to Insulin Resistance[24:41] Consequences of Sarcopenic Obesity[26:32] Solutions: Diet and Exercise for Sarcopenic Obesityhttps://www.insuliniq.com#MetabolicHealth #Sarcopenia #SarcopenicObesity #InsulinResistance #MuscleLoss #Obesity #HealthEducation #GlucoseControl #BloodSugar #InsulinSensitivity #MetabolicDisorders #HealthyAging #Inflammation #MuscleMass #FatLoss #NutritionTips #ExerciseScience #ResistanceTraining #LowCarbDiet #HealthTips #BenBikman #Metabolism #HealthyLifestyle #PreventDiabetes #FitnessEducation #DietAndExerciseStudies referenced found in YouTube show notes: https://youtu.be/iNmDbApK_FU Hosted on Acast. See acast.com/privacy for more information.

In this episode of The Metabolic Classroom Dr. Ben Bikman focused on the effects of alcohol on insulin resistance, emphasizing how ethanol, the main form of alcohol, influences the brain and metabolism. He highlighted that alcohol is primarily metabolized by the liver and can cause insulin resistance through both direct and indirect mechanisms. Dr. Bikman detailed the molecular pathways by which ethanol inhibits insulin signaling, notably by disrupting the insulin receptor substrate (IRS1) and increasing oxidative stress, which impairs insulin's ability to regulate glucose.Ben provided evidence from studies demonstrating ethanol's impact on insulin resistance at the cellular and whole-body levels. Research showed that ethanol consumption leads to higher insulin responses during glucose tolerance tests, indicating a reduced sensitivity to insulin. This phenomenon was observed in healthy humans who experienced a significant increase in insulin levels after consuming alcohol, suggesting a profound metabolic shift due to ethanol's presence.The lecture also covered indirect effects of alcohol on insulin resistance. Many alcoholic beverages contain high amounts of sugar, exacerbating insulin and glucose responses. Alcohol disrupts sleep quality, leading to poor metabolic outcomes and increased cortisol levels, which further contribute to insulin resistance. Additionally, ethanol competes with other metabolic substrates, leading to fat accumulation in the liver and elevated glucose and fat levels in the body.Dr. Bikman concluded by discussing the inflammatory response triggered by alcohol, particularly through the concept of a "leaky gut," where ethanol causes gaps in intestinal cells, allowing harmful substances like lipopolysaccharides (LPS) to enter the bloodstream and induce inflammation. This inflammation promotes ceramide production, further contributing to insulin resistance. Overall, Dr. Bikman emphasized the significant role of alcohol in metabolic health issues and encouraged mindfulness regarding alcohol consumption to mitigate these risks.01:10 - Alcohol and Metabolism02:18 - Direct Effects of Ethanol03:26 - Insulin Receptor Disruption06:38 - Whole-Body Impact08:37 - Ceramides and Insulin Resistance11:34 - Indirect Effects: Sugar13:31 - Indirect Effects: Sleep18:37 - Indirect Effects: Substrate Competition23:34 - Inflammation and Leaky GutStudies Referenced:(see notes on YouTube video: https://youtu.be/1aMuPTre1IU )https://www.insuliniq.com Hosted on Acast. See acast.com/privacy for more information.

In this episode of The Metabolic Classroom, Dr. Bikman, a biomedical scientist and professor of cell biology, delves into the concept of energy toxicity.He begins by explaining that energy toxicity attempts to explain why certain cells, particularly those capable of storing energy like muscle and liver cells, become insulin resistant. The primary idea is that when these cells accumulate excess energy, particularly in the form of triglycerides, they become resistant to further energy storage by becoming insulin resistant. He clarifies that this is closely related to lipotoxicity, where the stored fat itself, rather than glycogen, is seen as the main culprit for this condition.Ben notes that while the notion of energy toxicity encompasses both glucose and fats, triglycerides, a type of fat stored in muscle and liver cells, play a significant role. However, studies, such as one on endurance athletes, have shown that muscle triglycerides alone do not cause insulin resistance, leading to the concept of the “athlete's paradox.”Dr. Bikman further explores the biochemical pathways involved in insulin resistance, emphasizing that specific lipid intermediates, particularly diacylglycerols (DAGs) and ceramides, are more relevant than triglycerides in causing insulin resistance. DAGs disrupt the insulin signaling pathway by activating protein kinase C, while ceramides inhibit insulin signaling and affect mitochondrial function, increasing reactive oxygen species and contributing to insulin resistance.Ben challenges the notion of energy toxicity as a primary cause of insulin resistance, advocating instead for a focus on lipotoxicity and its mediators. He concludes that chronically elevated insulin levels, rather than the stored energy itself, are the main drivers of insulin resistance, suggesting that the term “insulin toxicity” might be more appropriate. This understanding is crucial for addressing what he identifies as the most common health issue worldwide—insulin resistance.01:16: Defining Energy Toxicity02:58: Lipotoxicity vs. Energy Toxicity06:20: Ectopic Fat Storage08:20: Triglycerides in Muscle Cells13:57: The Athlete's Paradox17:11: DAGs and Insulin Resistance19:26: Ceramides and Mitochondrial Function29:21: Insulin and Lipolysis33:59: High Insulin and Insulin ResistanceStudies Referenced:A phenomenon known as the “athlete's paradox”:https://academic.oup.com/jcem/article/86/12/5755/2849249 https://www.sciencedirect.com/science/article/abs/pii/S0165614717300962?via=ihubhttps://www.sciencedirect.com/science/article/pii/S0021925820859080?via=ihub https://www.jci.org/articles/view/43378 #MetabolicHealth #InsulinResistance #EnergyToxicity #Lipotoxicity #BenBikman #CellBiology #Triglycerides #DiabetesResearch #FatMetabolism #EctopicFat #KetogenicDiet #InsulinSensitivity #MitochondrialFunction #MetabolicClassroom #HealthScience #BiomedicalResearch #Endocrinology #Metabolism #HealthEducation #Type2Diabeteshttps://www.insuliniq.com Hosted on Acast. See acast.com/privacy for more information.

In this episode of The Metabolic Classroom, Dr. Bikman begins by emphasizing the critical role of insulin in regulating the body's use of fuel, and influencing whether nutrients are stored or burned.He highlights that food is a primary driver of insulin levels, but other factors like stress and sleep deprivation significantly impact insulin resistance.Stress, often exacerbated by poor sleep hygiene, leads to elevated levels of cortisol and epinephrine, which in turn increase blood glucose levels. Ben explains that going to bed on a full stomach can worsen sleep quality, further contributing to insulin resistance.Dr. Bikman discusses a study showing that restricting sleep to five hours per night for a week resulted in significant increases in cortisol and epinephrine, along with a notable decrease in insulin sensitivity. This chronic elevation of stress hormones due to poor sleep disrupts the natural circadian rhythm, causing a constant high level of cortisol, which not only hampers insulin function but also damages muscle, bone, and skin by promoting the breakdown of proteins for glucose production.Dr. Bikman advises improving sleep hygiene, such as reducing evening snacking and dimming lights, rather than relying on stimulants like caffeine, which can exacerbate cortisol levels and insulin resistance.00:57 - Impact of Stress on Insulin Resistance01:59 - Effect of Evening Eating on Sleep Quality02:59 - Study on Sleep Restriction and Insulin Sensitivity04:10 - Stress Hormones and Sleep Deprivation07:53 - Circadian Rhythm Disruption08:54 - Cortisol's Broader Effects10:45 - Advice on Improving Sleep HygieneStudies referenced in this episode:https://diabetesjournals.org/diabetes/article/59/9/2126/14525/Sleep-Restriction-for-1-Week-Reduces-Insulin https://pubmed.ncbi.nlm.nih.gov/20371664/ #InsulinResistance #MetabolicHealth #DrBenBikman #Nutrition #Health #SleepDeprivation #StressManagement #Hormones #Cortisol #HealthyEating #SleepHygiene #InsulinSensitivity #Glucose #CircadianRhythm #KetogenicDiet #DiabetesPrevention #HealthTips #Wellness #Caffeine #HealthyLifestylehttps://www.insuliniq.com Hosted on Acast. See acast.com/privacy for more information.

In this episode of The Metabolic Classroom, Dr. Bikman explores the history, science, and benefits of ketones, focusing on exogenous ketones.Ben highlights the significant benefits of ketones for brain health. He disputes the common belief that glucose is the brain's preferred fuel, citing research by Dr. George Cahill that indicates the brain relies heavily on ketones during fasting.The classroom also addresses the evolution and advantages of exogenous ketones. Early forms of exogenous ketones, like ketone salts, had limitations such as mineral imbalance and poor taste. Advances led to the development of ketone esters and bioidentical BHB, which are more effective and palatable. Exogenous ketones can help control appetite, reduce inflammation, and improve exercise performance. Despite initial concerns about their potential to be converted back into fat, Professor Bikman clarifies that this is not a risk, as the liver cannot reverse ketone production into fat.Overall, Dr. Bikman emphasizes that while ketones themselves offer numerous metabolic benefits, the primary advantage of a ketogenic state is maintaining low insulin levels, which supports fat burning and overall metabolic health. He encourages the use of exogenous ketones to enhance these benefits, particularly for managing cravings, improving physical performance, and supporting cognitive function.00:01 - Introduction to Ketones01:58 - Types of Ketones - Explanation of the three main types of ketones: acetoacetate, acetone, and beta-hydroxybutyrate.02:58 - Ketones and Blood Acidity - Discussion on how ketones can affect blood acidity and the distinction between ketosis and ketoacidosis.04:04 - Insulin's Role in Ketone Production - How insulin levels determine whether the body produces fat or ketones from acetyl-CoA.07:23 - Benefits of Low Insulin Levels - Overview of the metabolic benefits of low insulin levels, including improved fat burning and metabolic health.08:19 - Ketones and Brain Health - The positive effects of ketones on brain function and cognitive health, debunking the myth that glucose is the brain's preferred fuel.13:33 - Ketones and Physical Performance - Evidence that ketones improve physical performance and energy efficiency in muscle cells.17:31 - Anti-inflammatory Effects of Ketones - Ketones' role in inhibiting inflammation and their benefits for inflammatory disorders.Studies Referenced:Alzheimer's and Parkinson's (Cunnane et al., 2016): https://alzres.biomedcentral.com/articles/10.1186/s13195-021-00783-xKetones Elicit Distinct Alterations in Adipose Mitochondrial Bioenergetics: https://pubmed.ncbi.nlm.nih.gov/32872407/Ketogenic Diet Reduces Midlife Mortality and Improves Memory in Aging Mice: https://pubmed.ncbi.nlm.nih.gov/28877458/The Effects of Ketogenic Diet on Insulin Sensitivity and Weight Loss, Which Came First: The Chicken or the Egg?: https://pubmed.ncbi.nlm.nih.gov/37513538/ Learn more: https://www.insuliniq.com Hosted on Acast. See acast.com/privacy for more information.

In this episode of The Metabolic Classroom, Dr. Ben Bikman challenges the traditional view that saturated fats are the primary cause of atherosclerotic plaques and heart disease. He asserts that while plaques, or atheromas, in coronary arteries are composed partly of fats and foam cells, the exact process of plaque formation remains speculative. Dr. Bikman emphasizes that anyone claiming to know the definitive cause of plaque formation is likely overstating their knowledge. Foam cells, which are fat-laden macrophages, play a critical role in plaque development and are consistently present at the sites of these plaques.Dr. Bikman explains that inflammation is a significant factor in atherosclerosis, and C-reactive protein (CRP), a marker of inflammation, is a better predictor of heart disease than LDL cholesterol. He describes how macrophages engulf oxidized LDL cholesterol, turning into foam cells and secreting pro-inflammatory proteins like CRP. This process is driven by the presence of oxidized lipids, particularly those derived from omega-6 polyunsaturated fats such as linoleic acid, which are prevalent in modern diets due to the widespread use of vegetable oils.Ben highlights several studies to support his argument. A notable study from 1979 by Brown and Goldstein showed that macrophages only consume LDL cholesterol when it is oxidized, not in its native form. Another study from 1998 found that oxidized LDL containing specific bioactive lipids, nine and 13 HODE, is particularly problematic. These oxidized lipids are derived from linoleic acid, not from saturated or monounsaturated fats. Moreover, historical dietary studies, such as the Minnesota Coronary Experiment and the Sydney Diet Heart Study, revealed that participants consuming more polyunsaturated fats had higher mortality rates than those consuming saturated fats.To conclude, Dr. Bikman argues that the traditional belief that saturated fat causes heart disease is flawed. He points out that recent studies, including a correlational study published in the British Medical Journal, show that refined grains, not saturated fats, are more strongly linked to heart disease and overall mortality. He suggests that the real dietary culprit is the overconsumption of omega-6 polyunsaturated fats, particularly linoleic acid, found in processed foods. This shift in perspective underscores the importance of reevaluating dietary guidelines and focusing on the types of fats consumed.#HeartHealth #SaturatedFat #Atherosclerosis #Inflammation #InsulinResistance #LDLCholesterol #OxidizedLDL #FoamCells #Macrophages #BenBikman #MetabolicHealth #CholesterolMyths #LinoleicAcid #PolyunsaturatedFats #DietaryFats #CardiovascularResearchStudies referenced:Binding Site on Macrophages that Mediates Uptake in Degradation by Brown and Goldstein (1979): https://academic.oup.com/clinchem/article/46/6/829/5641219 Oxidized LDL Regulates Macrophage Gene Expression (1998): You can find more details on this study in resources like ScienceDirect and Cell Journal (you may need specific access or subscriptions to retrieve full texts).Strong Increase in Hydroxy Fatty Acids Derived from Linoleic Acid in Human Low-Density Lipoproteins of Atherosclerotic Patients (1998): https://www.sciencegate.app/document/10.1016/s0009-3084(97)00095-9 Learn more: https://www.insuliniq.com Hosted on Acast. See acast.com/privacy for more information.