The Metabolic Classroom with Dr. Ben Bikman

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.

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.

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

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/

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)

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

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.

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.)