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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.com
Ben’s favorite yerba maté and fiber supplement: https://ufeelgreat.com/usa/en/c/InsulinIQ
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)
Show Notes/References:
Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: [email protected] 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
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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.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)
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: [email protected] 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
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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.com
References:
Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: [email protected] 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
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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.com
References:
Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: [email protected] with your request, and be sure to mention which Metabolic Classroom episode you are referring to.
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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: [email protected] 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
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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.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)
Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: [email protected] 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.
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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 Metabolism
01:09 - Lactic Acid vs. Lactate: Debunking the Myth
02:16 - Glycolysis and Lactate Production
04:23 - How Lactate is Produced in Muscles
06:23 - Red Blood Cells and Lactate
07:18 - History of Lactate Research: Otto Meyerhoff
09:40 - The Cori Cycle: Lactate Recycled into Glucose
13:54 - Lactate as a Viable Energy Source
15:55 - George Brooks' Lactate Shuttle Theory
18:44 - Lactate and Traumatic Brain Injury (TBI)
20:55 - Lactate’s Role in Fat Burning and Mitochondria
23:58 - Lactate in Clinical Contexts: Metabolic Health
25:09 - Continuous Lactate Monitoring and Mitochondrial Dysfunction
28:59 - Lactate as a Predictor of Type 2 Diabetes
29:59 - Conclusion: Lactate’s Critical Role in Health and Energy
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)
References:
Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: [email protected] 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.
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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: [email protected] 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
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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 Gut
01:52 How Substances Enter the Body Through the Gut
03:58 Structure and Function of the Gut Lining
07:07 Normal Transport vs. Leaky Gut Transport
09:23 The Role of LPS in Leaky Gut and Inflammation
11:41 How LPS Affects the Body
12:45 Low-Grade Systemic Inflammation
15:23 Cardiometabolic Consequences of Leaky Gut
18:52 Dietary Triggers of Leaky Gut: Fructose and Seed Oils
22:14 The Impact of Gluten and Stress on Gut Health
24:05 Strategies to Improve Gut Health
25:09 Short Chain Fatty Acids and Saturated Fats for Gut Healing
28:08 The Role of LDL Cholesterol in Gut Health
31:16 The Importance of Fiber and Probiotics
33:32 The Rare Sugar Allulose and Gut Integrity
35:23 Conclusion and Practical Takeaways
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)
Study references referred to are available upon request. Email: [email protected]
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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/
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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 #InsulinIQ
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)
Hosted on Acast. See acast.com/privacy for more information.
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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 Progesterone
02:20 - Cholesterol as the Precursor to Sex Hormones
03:34 - The Role of Aromatase in Estrogen Production
04:32 - Understanding the Family of Estrogens
05:56 - Estrogens and Glucose Metabolism: Key Signaling Pathways
06:54 - Insulin Signaling Pathway Overview
08:57 - How Estrogens Enhance Insulin Sensitivity
10:04 - The Role of AMPK in Glucose Uptake
12:11 - Estrogens' Dual Mechanism in Regulating Glucose Levels
13:18 - The Impact of Estrogens on Liver Glucose Production
15:33 - Estrogens' Role in Suppressing Gluconeogenesis
17:07 - Why Women Have Lower Risk of Type 2 Diabetes
19:28 - Metabolic Effects During the Ovarian Cycle
21:54 - Progesterone’s Influence on Insulin Resistance and Fat Storage
25:16 - The Shift in Fat Storage Patterns Post-Menopause
26:16 - Hormone Replacement Therapy: Metabolic Considerations
PI3K 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
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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 Resistance
02:15 - Impact of Aging on Muscle Protein Synthesis
03:15 - Role of Anabolic Stimuli in Muscle Growth
05:15 - Risks Associated with Loss of Muscle Mass
06:17 - Muscle's Role in Metabolic Health
07:19 - Muscle Mass and Longevity
10:24 - Age-Related Factors: Hormones and Physical Activity
11:10 - Biochemical Signaling and mTOR1 Pathway
13:28 - Controversy Around Rapamycin and Longevity
15:43 - Rapamycin's Impact on Muscle and Testosterone
17:42 - Nutrient Sensing and mTOR1 Activation
18:40 - Importance of Leucine in Protein Synthesis
19:54 - Hormonal Regulation of mTOR1
20:55 - Consequences of Anabolic Resistance
21:52 - Combating Anabolic Resistance: Dietary Strategies
24:05 - Importance of High-Quality Protein Sources
26:05 - Role of Resistance Exercise in Combating Anabolic Resistance
28:55 - Exercise Protocols for Older Adults
30:55 - Importance of Resistance Exercise Over Aerobic Exercise
32:55 - Conclusion and Societal Benefits of Muscle Health
References:
Due to character length constraints, references are not posted here. For a complete list, please email: [email protected] with your request.
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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 Fermentation
02:00 – Definition and Examples of Fermented Foods
04:00 – Benefits of Fermented Dairy: Kefir
06:00 – Fermented Foods and Glycemic Control
08:00 – Sourdough Bread vs. Conventional Bread
10:00 – Introduction to Short-Chain Fatty Acids (SCFAs)
12:00 – SCFAs and Gut Health
13:00 – SCFAs and Metabolic Benefits
15:00 – Probiotics in Fermented Foods
16:00 – Importance of Raw, Unpasteurized Fermented Foods
17:00 – Introduction to Antinutrients
18:00 – Examples of Antinutrients: Phytic Acid, Lectins, Oxalates, Tannins
20:00 – 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 #InsulinIQ
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. For a complete list, please email: [email protected] with your request.)
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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 Bikman
01:00 - Overview of the Randle Cycle (Glucose Fatty Acid Cycle)
02:00 - Historical Background: Philip Randle’s Research
03:00 - Experimental Model: Perfused Rat Hearts
04:00 - Key Terms: Glucose and Fatty Acids
05:00 - Concept of Substrate Competition
06:00 - Reciprocal Inhibition: Fats vs. Glucose
08:00 - Fatty Acid Oxidation Process
10:00 - Biochemical Pathways: Acetyl-CoA, NADH, and Pyruvate Dehydrogenase
12:00 - Role of Citrate in Glycolysis Inhibition
14:00 - Glucose Utilization and Malonyl-CoA
16:00 - Insulin’s Role in Fuel Selection
18:00 - Insulin’s Impact on Glucose and Fat Burning
20:00 - Diabetes Case Study: Type 1 and Type 2
22:00 - Type 1 Diabetes: High Glucose and Fatty Acids
24:00 - Ketones Production in the Liver
26:00 - Type 2 Diabetes: Insulin Resistance and Metabolic Inflexibility
28:00 - Insulin Resistance in Fat Cells
30:00 - Metabolic Inflexibility in Type 2 Diabetes
32:00 - Insulin Resistance in the Brain
34:00 - The Impact on Hunger and Neurological Disorders
36:00 - 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 #HealthLecture
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:
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.d0308
The 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: [email protected] with your request.)
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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.
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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 Obesity
https://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 #DietAndExercise
Studies referenced found in YouTube show notes: https://youtu.be/iNmDbApK_FU
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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 Metabolism
02:18 - Direct Effects of Ethanol
03:26 - Insulin Receptor Disruption
06:38 - Whole-Body Impact
08:37 - Ceramides and Insulin Resistance
11:34 - Indirect Effects: Sugar
13:31 - Indirect Effects: Sleep
18:37 - Indirect Effects: Substrate Competition
23:34 - Inflammation and Leaky Gut
Studies Referenced:
(see notes on YouTube video: https://youtu.be/1aMuPTre1IU )
https://www.insuliniq.com
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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 Toxicity
02:58: Lipotoxicity vs. Energy Toxicity
06:20: Ectopic Fat Storage
08:20: Triglycerides in Muscle Cells
13:57: The Athlete's Paradox
17:11: DAGs and Insulin Resistance
19:26: Ceramides and Mitochondrial Function
29:21: Insulin and Lipolysis
33:59: High Insulin and Insulin Resistance
Studies 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=ihub
https://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 #Type2Diabetes
https://www.insuliniq.com
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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 Resistance
01:59 - Effect of Evening Eating on Sleep Quality
02:59 - Study on Sleep Restriction and Insulin Sensitivity
04:10 - Stress Hormones and Sleep Deprivation
07:53 - Circadian Rhythm Disruption
08:54 - Cortisol’s Broader Effects
10:45 - Advice on Improving Sleep Hygiene
Studies 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 #HealthyLifestyle
https://www.insuliniq.com
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- Se mer
