The Metabolic Classroom with Dr. Ben Bikman

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.

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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.

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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)

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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.

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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 )

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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

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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

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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 Ketones

01:58 - 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-x

Ketones 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/ 

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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 #CardiovascularResearch

Studies 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 

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This episode of The Metabolic Classroom is sponsored by RxSugar. Use this link to get 20% off: https://rxsugar.com/discount/BEN20

02:10 - Overview of Uric Acid: Explanation of what uric acid is and its origins from purine metabolism.

03:16 - Uric Acid and Hyperuricemia: Discussion on uric acid production, excretion, and the condition of hyperuricemia.

05:09 - Gout and Uric Acid Crystallization: How high uric acid levels lead to gout and kidney stones.

07:08 - Importance of Uric Acid in Metabolism: Why uric acid is important, its clinical relevance, and its connection to insulin resistance.

09:14 - Uric Acid and Inflammation: How uric acid causes systemic inflammation and contributes to insulin resistance.

12:27 - Sources of Uric Acid, Purines and Fructose: Detailed breakdown of purine and fructose metabolism leading to uric acid production.

16:31 - Fructose Metabolism and Uric Acid: The role of the liver in metabolizing fructose and its link to uric acid production.

22:47 - Pharmacological and Nutritional Interventions: Treatments like allopurinol and the benefits of allulose in reducing uric acid.

30:34 - Ketogenic Diet and Uric Acid: The effects of the ketogenic diet on uric acid levels and insulin sensitivity.

Summary:

In this episode of The Metabolic Classroom, Professor Bikman discusses the significance of uric acid, particularly its impact on insulin resistance. Uric acid, a byproduct of purine metabolism, is usually expelled through the kidneys. When production exceeds excretion, it leads to hyperuricemia, causing gout, kidney stones, and inflammation linked to insulin resistance.

Dr. Bikman explains that excessive uric acid activates inflammation pathways, producing ceramides that disrupt insulin signaling, leading to insulin resistance. He highlights the connection between fructose consumption and uric acid production, noting that unregulated fructose metabolism in the liver increases uric acid levels. This rise in fructose intake, rather than purine-rich foods, contributes to gout and metabolic issues.

To address this, Dr. Bikman discusses pharmacological interventions like allopurinol, which lowers uric acid levels but may have side effects. He also mentions allulose, a rare sugar that shows promise in reducing uric acid by enhancing its excretion. Despite potentially increasing uric acid, the ketogenic diet is noted for reducing inflammation and improving insulin sensitivity due to ketones.

Dr. Bikman concludes by emphasizing the importance of understanding uric acid's role in metabolic health and encourages further research and practical dietary interventions to manage uric acid levels, integrating pharmacological, nutritional, and lifestyle approaches to improve overall metabolic health.

Studies referenced in this episode:

https://pubmed.ncbi.nlm.nih.gov/24769205/

https://www.sciencedirect.com/science/article/abs/pii/S1933171115006063?via=ihub 

https://www.metabolismjournal.com/article/S0026-0495(65)80039-7/abstract 

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In this episode of The Metabolic Classroom, Professor Ben Bikman, an expert in metabolic research, discusses the debate surrounding saturated fat and its impact on insulin resistance.

Dr. Bikman addresses misconceptions about saturated fat perpetuated by proponents of plant-based diets, who often blame meat-based saturated fats for insulin resistance. He refers to his own 2011 research, highlighting the role of toll-like receptor four (TLR4) activation in inducing inflammation and insulin resistance, particularly stimulated by saturated fats.

Acknowledging limitations in his earlier work, Dr. Bikman transitions to discussing fat digestion and absorption, setting the stage for studies on the impact of dietary saturated fat on metabolic outcomes. He cites a study by Volk et al. (2014) contradicting the direct link between dietary saturated fat intake and plasma saturated fat levels. Further, he discusses research challenging the low-fat emphasis of diets like DASH, including a study by Chiu et al. (2016) showing comparable blood pressure reduction with a high-fat version.

The lecture also covers a meta-analysis by Choi et al. (2020) supporting the benefits of ketogenic diets high in saturated fat for glycemic control and insulin resistance.

Dr. Bikman emphasizes the importance of considering context, suggesting that saturated fat consumption without excessive carbohydrate intake may not necessarily lead to insulin resistance. However, he acknowledges studies indicating potential concerns with high saturated fat intake in hypercaloric, high-carb diets, advocating for balanced macronutrient consumption.

00:01 - Introduction of the topic of saturated fat and insulin resistance, highlighting common misconceptions and his expertise in the field.

02:33 - Role of TLR4: Research on toll-like receptor four (TLR4) activation and its connection to inflammation and ceramide synthesis, leading to insulin resistance.

07:05 - Fat Digestion Primer: Explanation of fat digestion in the small intestine, emphasizing the formation of chylomicrons for fat transport into the bloodstream.

11:55 - Study by Volk et al. (2014): Key study that challenges the idea of dietary saturated fat directly increasing plasma saturated fat levels, despite high consumption.

16:41 - High-Fat DASH Diet Study: Research comparing a high-fat version of the DASH diet to the standard low-fat version, highlighting similar blood pressure reduction but improved lipid profiles with the high-fat diet.

19:46 - Meta-analysis by Choi et al. (2020): Demonstrating the benefits of ketogenic diets, typically high in saturated fat, in improving glycemic control and insulin resistance.

21:40 - Historical Trends: The paradox of decreasing saturated fat consumption over time while insulin resistance rates have increased, suggesting a more complex relationship.

25:58 - Overfeeding Studies: Studies showing that overconsumption of carbohydrates, particularly refined sugars and starches, can increase liver fat and saturated fat production, contributing to insulin resistance.

27:09 - Study by Luukkonen et al. (2018): Study indicating that in a hypercaloric, high-carb diet, high saturated fat intake may worsen insulin resistance compared to high unsaturated fat intake.

28:06 - Conclusion: The need for nuanced understanding, context, and critical appraisal of research findings regarding the relationship between saturated fat, carbohydrate intake, and insulin resistance.

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#InsulinResistance #SaturatedFat #MetabolicHealth #NutritionScience #HealthEducation #DietaryMyths #CellBiology #ResearchInsights #FatDigestion #KetogenicDiet #CardiometabolicHealth #DASHDiet #Inflammation #MedicalResearch #HealthDebunked

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This episode of the Metabolic Classroom is sponsored by Redmond Real Salt. Use code BEN15 to get 15% off of their products: https://redmond.life

Summary:

In this lecture, Professor Ben Bikman explores the cardiometabolic effects of salt intake, detailing its role in electrolyte balance, fluid regulation, nerve function, muscle contractions, acid-base balance, and nutrient absorption. He explains the renin-angiotensin-aldosterone system (RAAS) and its response to low blood pressure or sodium levels, leading to sodium retention and water reabsorption in the kidneys. Dr. Bikman discusses how insulin influences salt handling by stimulating sodium reabsorption and increasing aldosterone production. He warns against the unintended consequences of salt restriction, such as elevated insulin levels and resistance, exacerbating metabolic syndrome and cardiovascular risk.

Shifting focus to fat cells, Dr. Bikman explains how aldosterone and angiotensin II affect fat cell growth and differentiation, promoting lipogenesis, inflammation, and fibrosis. He suggests salt restriction may contribute to obesity and insulin resistance. Discussing potential anti-obesity effects, he mentions angiotensin receptor blockers inhibiting angiotensin II signaling in fat cells.

Dr. Bikman stresses the complex interplay between salt, insulin, and fat cell biology, cautioning against oversimplified dietary recommendations. He encourages critical thinking about salt intake's impact on metabolic health and body composition, advocating for deeper understanding and knowledge sharing to improve health outcomes.

01:52: Importance of Salt in the Body - Overview of the essential role of salt, particularly sodium, in electrolyte balance, fluid regulation, nerve function, muscle contractions, acid-base balance, and nutrient absorption.

06:00: Biochemical Pathways of Salt Regulation - Detailed explanation of the RAAS cascade, involving renin, angiotensinogen, angiotensin-converting enzyme, angiotensin I and II, and aldosterone. Discussion of the physiological effects of angiotensin II, including vasoconstriction, thirst stimulation, and stimulation of aldosterone production.

09:48: Interaction Between Salt Regulation and Insulin - Exploration of the interaction between salt regulation pathways and insulin, including insulin's direct effect on sodium reabsorption in the kidneys and its modulation of the RAAS. Explanation of how salt restriction can lead to increased insulin levels and insulin resistance.

13:44: Consequences of Salt Restriction - Discussion of the negative health consequences of salt restriction, including increased insulin resistance and metabolic syndrome. Reference to studies showing the association between salt restriction and adverse metabolic outcomes.

17:58: Hypertension and Cardiovascular Health - Summary of the relationship between salt restriction, hypertension, and cardiovascular disease. Mention of anti-hypertensive medications targeting the RAAS, such as ACE inhibitors and angiotensin receptor blockers.

20:59: Metabolic Effects on Fat Cells - Transition to discussing the metabolic effects of salt-regulating pathways on fat cells. Explanation of how aldosterone and angiotensin II promote fat cell growth, differentiation, lipogenesis, inflammation, and fibrosis.

27:53: Conclusion and Takeaways - Recap of the lecture's key points, emphasizing the complex interplay between salt intake, insulin, and fat cell biology. Call to action for critical thinking about dietary recommendations and sharing of knowledge for informed decision-making.

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Dr. Ben Bikman, a biomedical scientist and expert in cell biology, welcomes his audience to a discussion on lipedema, a topic he’s been asked about frequently. He highlights the importance of addressing insulin resistance through diet.

Ben begins by providing a primer on adipose tissue, explaining its composition and the role of fat cells and fibroblasts. He delves into the structural changes in collagen within fat tissue, particularly in lipedema, where there's an overproduction of collagen leading to increased rigidity and compression on fat cells and nerves.

The lecture explores why lipedema predominantly affects women, linking it to hormonal changes, particularly increases in estrogen levels during puberty, pregnancy, and menopause. Ben explains how estrogen influences fibroblast activity, leading to excessive collagen production and fibrosis in lipedema.

The discussion then delves into the mechanisms of pain in lipedema, attributing it to both mechanical pressure on nerves and biochemical factors such as inflammation. Finally, Ben explores various treatment approaches, including compression therapy, manual lymphatic drainage, and low-carbohydrate diets, which have shown promise in reducing pain and improving quality of life in women with lipedema.

Throughout the lecture, Dr. Bikman emphasizes a paradigm shift in understanding lipedema as a disorder of connective tissue rather than fat cells alone, offering insights into its pathophysiology and potential therapeutic interventions. He concludes by highlighting recent research supporting the efficacy of low-carbohydrate diets in managing lipedema.

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01:59 - Adipocyte Structure

04:43 - Collagen Alterations in Lipedema

06:57 - Estrogen’s Role in Lipedema

10:10 - Mechanical Factors Contributing to Pain

11:07 - Biochemical Factors Contributing to Pain

14:11 - Therapeutic Interventions for Lipedema

23:27 - Impact of Low-Carbohydrate Diet on Pain Reduction

30:14 - Insights into Fat Cell Function and Hormonal Influence

37:31 - Summary

Effect of a low-carbohydrate diet on pain and quality of life in female patients with lipedema: a randomized controlled trial

The Benefits of Low-Carbohydrate, High-Fat (LCHF) Diet on Body Composition, Leg Volume, and Pain in Women with Lipedema

Dr. Bikman’s website

#Lipedema #Lipadema #LipedemaAwareness #Lipoedema #LipedemaSupport #LipedemaTreatment #LipedemaSurgery #LipedemaTherapy #LipedemaDiet #LipedemaLegs #InsulinResistance #InsulinResistanceAwareness #InsulinResistanceDiet #InsulinSensitivity #MetabolicSyndrome #Type2Diabetes #BloodSugarControl #InsulinResistanceSupport #HealthyLiving #diabetesprevention

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Dr. Ben Bikman discusses the intricate relationship between metabolic health and male infertility.

While metabolic health is often associated with conditions like obesity and diabetes, Dr. Bikman emphasizes its relevance to less obvious issues like male infertility. He notes that while the processes of reproduction differ between the sexes, they share a common metabolic core.

Ben highlights that infertility affects approximately 15% of couples trying to conceive, with men contributing to around 30% of cases. He explains the role of hormones like follicle-stimulating hormone (FSH) and luteinizing hormone (LH) in male reproductive function, detailing their influence on spermatogenesis and testosterone production.

The classroom lecture delves into how poor metabolic health, particularly insulin resistance, can disrupt testosterone production and lead to issues like erectile dysfunction and reduced sperm quality. Insulin resistance affects testosterone synthesis directly in the testes and indirectly by promoting aromatization, the conversion of testosterone into estrogen, leading to a vicious cycle of reduced testosterone and increased insulin resistance.

Dr. Bikman discusses various strategies to improve metabolic health and potentially alleviate male infertility, including dietary changes, medication such as insulin-sensitizing drugs like metformin, and exercise, particularly resistance training. He stresses the importance of addressing underlying metabolic issues to improve reproductive outcomes and suggests that prioritizing metabolic health before attempting reproduction is crucial.

In conclusion, Dr. Bikman underscores the interconnectedness of metabolic health and reproductive function, advocating for a holistic approach to addressing male infertility that focuses on improving insulin sensitivity and overall metabolic well-being.

00:00 - Introduction to metabolic health's relevance in male infertility

01:18 - Infertility statistics and men's contribution to the issue

02:37 - Hormonal role in male reproductive function: FSH and LH

03:53 - FSH and LH stimulation of spermatogenesis and testosterone

05:57 - Testosterone's functions in male fertility and maturation

08:04 - Nitric oxide's role in erectile function and its insulin connection

11:28 - How insulin resistance impacts testosterone production and erectile dysfunction

14:02 - Insulin resistance's effects on testosterone synthesis and aromatization

18:55 - Strategies to improve metabolic health and alleviate male infertility

26:38 - Conclusion: The link between metabolic health and reproductive function

#MaleInfertility #FertilityHealth #Metabolism #ReproductiveHealth #InfertilityAwareness #MenHealth #SpermHealth #HormonalHealth #NutritionForFertility #HealthTalk #MaleHealth #FertilityJourney #HealthyLiving #HolisticHealth

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In this lecture, Professor Ben Bikman delves into the metabolic aspects of female infertility, specifically focusing on the influence of insulin resistance. He begins by highlighting the high prevalence of infertility among women of reproductive age, with up to 15% affected globally, and particularly prevalent in regions with high rates of insulin resistance, such as Sub-Saharan Africa, South Asia, and the Middle East.

Insulin resistance, a condition where cells become less responsive to insulin, plays a crucial role in female infertility. Dr. Bikman explains that insulin resistance manifests in two main aspects: disrupted insulin signaling in cells and elevated blood insulin levels, known as hyperinsulinemia. These disruptions affect various stages of reproductive physiology, including oocyte development, ovulation, and implantation.

Dr. Bikman then provides a detailed explanation of the ovulatory cycle, emphasizing the interplay of hormones such as follicle-stimulating hormone (FSH), estradiol, and luteinizing hormone (LH) in regulating follicle growth, ovulation, and corpus luteum formation. He discusses how insulin resistance can interfere with this process, leading to poor oocyte quality, failed ovulation, and complications with implantation.

The lecture further explores conditions associated with insulin resistance and female infertility, notably polycystic ovary syndrome (PCOS). Dr. Bikman explains the Rotterdam criteria used for diagnosing PCOS, which include irregular ovulation, signs of hyperandrogenism, and ovarian cysts. He elucidates how insulin resistance contributes to the development of PCOS by inhibiting aromatase activity, leading to reduced estradiol production and disrupted ovulation.

Finally, Dr. Bikman discusses treatment approaches for PCOS, including the use of insulin-sensitizing medications like metformin and dietary interventions such as low-carbohydrate or ketogenic diets. He underscores the importance of addressing insulin resistance to improve ovulatory function and mitigate the most common form of female infertility.

(00:01) Introduction to Female Infertility and Metabolism

(01:14) Global Prevalence of Female Infertility and its Association with Insulin Resistance

(02:23) Understanding Insulin Resistance and its Impact on Female Reproductive Physiology

(05:30) The Ovulatory Cycle and the Role of Hormones in Reproduction

(11:14) Effects of Insulin Resistance on Oocyte Development and Ovulation

(13:27) Impact of Insulin Resistance on Implantation and Uterine Health

(17:19) Polycystic Ovary Syndrome (PCOS) and its Relationship with Insulin Resistance

(33:44) Treatment Approaches for PCOS: Medications and Dietary Interventions

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#pcos #pcosawareness #PCOSTips #PCOSJourney #PCOSCommunity #PCOSFight #PCOSWarrior #FertilityJourney #InfertilityAwareness #TTC #FertilityTips #FertilitySupport #InfertilitySupport #ConceptionJourney #FertilityTreatment #PCOSandFertility #InfertilityStruggle #PCOSAwarenessMonth #IVF #FertilityHealth #FertilitySuccessStories

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In this Metabolic Classroom episode, Dr. Bikman delves into the intricate dynamics of fatty liver disease, a prevalent metabolic problem affecting millions worldwide. Describing the liver as the “soccer mom” of metabolism due to its involvement in various metabolic processes, Ben emphasizes the liver’s central role in nutrient metabolism, particularly in handling fats.

Fatty liver disease, once primarily associated with alcohol consumption, has now become a widespread issue driven by metabolic factors. It progresses from simple fat accumulation to inflammation (non-alcoholic steatohepatitis or NASH), fibrosis, and potentially cirrhosis.

Insulin resistance, a key player in metabolic disorders, is dissected into two components: impaired insulin action and chronically elevated insulin levels (hyperinsulinemia). Dr. Bikman highlights the crucial role of insulin in driving fat accumulation in the liver, explaining that elevated insulin is necessary for the liver to store fat and prevent its breakdown, even in the presence of excess free fatty acids. He elucidates how insulin resistance in fat cells leads to increased release of fatty acids, exacerbating fat accumulation in the liver.

Dr. Bikman discusses two primary pathways contributing to fatty liver disease: uptake of free fatty acids from adipose tissue and de novo lipogenesis, the process of synthesizing new fat within the liver.

While elevated insulin primarily drives fat storage, Ben also addresses the independent roles of fructose and alcohol in promoting liver fat accumulation. Fructose metabolism in the liver and alcohol-induced disruptions in fat metabolism contribute significantly to fatty liver disease, even without the direct influence of insulin.

Finally, Dr. Bikman explores strategies for preventing or reversing fatty liver disease, emphasizing the importance of controlling carbohydrate intake to lower insulin levels and restrict fructose consumption. He contrasts pharmaceutical interventions with lifestyle modifications, advocating for dietary changes as a more effective and sustainable approach.

Throughout the Metabolic Classroom lecture, Ben empowers his audience with a deeper understanding of the metabolic underpinnings of fatty liver disease, encouraging them to share this knowledge and take proactive steps toward metabolic health.

#insulinresistance #metabolicsyndrome #metabolichealth #type2diabetes #type1diabetes #weightloss #intermittentfasting #intermittantfasting #fasting #lowcarb 

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In this lecture from the Metabolic Classroom, Dr. Ben Bikman, a biomedical scientist specializing in metabolism, delves into various strategies for fat loss.

He begins by highlighting the importance of understanding fat tissue dynamics, focusing particularly on hormones, drugs, and sex-specific effects. The main topic for the lecture is strategies for fat loss, which Bikman divides into three categories: drugs, surgical interventions, and lifestyle changes.

Bikman briefly revisits the topic of drugs for fat loss, emphasizing GLP-1 agonists and their mechanism of action in reducing cravings. He discusses their efficacy but also mentions potential side effects such as sexual dysfunction and the risk of regaining fat mass after discontinuation.

Moving on to surgical interventions, Bikman provides detailed explanations of bariatric surgeries including Roux-en-Y gastric bypass, laparoscopic adjustable gastric banding, laparoscopic sleeve gastrectomy, and biliopancreatic diversion with duodenal switch. Ben discusses their mechanisms, benefits, drawbacks, and potential complications, shedding light on the complexity and consequences of these procedures.

Next, Bikman explores liposuction, highlighting its cosmetic nature and its limited impact on metabolic health. He explains how liposuction removes fat cells from subcutaneous fat depots, which may lead to a rebound effect as remaining fat cells compensate by hypertrophying.

The lecture’s focus then shifts to lifestyle changes, particularly exercise and nutrition. Bikman emphasizes that exercise should be pursued for health and strength rather than solely for weight loss. He stresses the importance of nutrition in fat loss, advocating for strategies that prioritize lowering insulin levels through carbohydrate control, prioritizing protein, and not fearing dietary fat.

Bikman underscores the significance of managing insulin levels as a primary step in fat loss, followed by potential calorie control through structured fasting if necessary. He discusses the metabolic advantages of lowering insulin, including increased metabolic rate and ketone production.

Finally, Dr. Bikman briefly mentions alternate methods like sauna and cold plunge therapy, suggesting their potential contribution to fat loss, although empirical evidence is lacking. He concludes by emphasizing the importance of shrinking fat cells through proper lifestyle strategies, promoting overall metabolic health.

Throughout the lecture, Bikman’s teaching style is engaging and informative, providing insights into the complex interplay of hormones, physiology, and behavior in fat metabolism and weight management. 

Learn more at: https://www.insuliniq.com

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In this episode of the metabolic classroom, Dr. Ben Bikman takes the helm to explore the multifaceted role of fat tissue as an endocrine organ. He begins by challenging the conventional view of fat tissue as merely a storage depot for energy, emphasizing its crucial role in hormone production and regulation.

Dr. Bikman introduces the concept of endocrine organs and highlights the often overlooked status of fat tissue as one such organ. He discusses how fat tissue releases hormones into the bloodstream, exerting significant metabolic effects throughout the body.

The lecture delves into sex-specific differences in fat distribution and hormone production, with a focus on the influence of estrogen on fat storage and hormone levels in women. Dr. Bikman further explores the impact of menopause on fat tissue and hormonal changes, shedding light on how shifts in hormone production affect metabolism and fertility.

Leptin, the first discovered fat-derived hormone, is dissected in detail by Dr. Bikman, who elucidates its role in appetite regulation, metabolic processes, and fertility. He discusses how excess fat can lead to leptin resistance, compromising its effectiveness in metabolic regulation.

Other hormones such as adiponectin, estrogen, TNF alpha, plasminogen activator inhibitor 1 (PAI-1), and T3 are also explored for their metabolic effects and their association with fat cell size.

The lecture concludes with a focus on brown adipose tissue and its production of T3, highlighting its role in regulating metabolic rate, particularly in response to stimuli like cold exposure.

In summary, Dr. Bikman provides a comprehensive overview of the endocrine functions of adipose tissue, emphasizing the intricate relationship between fat cells and hormone regulation, with implications for metabolism, inflammation, and overall health.

00:01 - Introduction to Adipose Tissue as an Endocrine Organ

01:07 - Sex-Specific Differences in Fat Distribution

03:21 - Impact of Menopause on Fat Tissue and Hormone Production

05:45 - Endocrine Effects of Fat Distribution

07:58 - Role of Fat Tissue in Aromatization and Estrogen Production

10:13 - Impact of Fat Cell Size on Hormone Production

12:24 - Detailed Exploration of Leptin

14:45 - Examination of Adiponectin and its Metabolic Effects

18:17 - TNF Alpha and its Impact on Inflammation and Insulin Resistance

21:05 - Plasminogen Activator Inhibitor 1 (PAI-1) and its Implications for Clotting

22:16 - Brown Adipose Tissue and its Production of T3

24:30 - Conclusion and Summary

#insulinresistance #metabolicsyndrome #metabolichealth #type2diabetes #type1diabetes #weightloss #intermittentfasting #intermittantfasting #fasting #lowcarb 

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In this episode of The Metabolic Classroom, Professor Ben Bikman, a biomedical scientist specializing in diabetes, metabolism, and fat tissue, delves deeper into the topic of fat tissue, focusing specifically on its storage locations and the factors influencing them.

Dr. Bikman emphasizes the complexity and nuance of fat tissue beyond its commonly recognized role in energy storage, insulation, and cushioning, highlighting its function as an endocrine organ that produces various hormones and signals.

Ben begins by discussing the enzyme lipoprotein lipase (LPL), which plays a crucial role in fat storage by pulling fats off circulating triglyceride-rich lipoproteins in the bloodstream. He explains how the expression and activity of LPL are influenced by factors such as insulin, exercise, and sex hormones, particularly testosterone and estrogen.

The lecture explores how sex differences play a significant role in fat storage patterns, with males tending to store fat centrally around the abdomen due to increased LPL expression induced by testosterone, while females typically store more fat in subcutaneous depots such as the breasts, buttocks, and hips, influenced by estrogen. Ben also discusses the impact of menopause on fat storage, noting shifts towards central fat deposition in women as estrogen levels decline.

Additionally, Dr. Bikman touches on the effects of aging on fat storage, explaining how fat cell number tends to plateau in adulthood and decrease in older age, leading to hypertrophy (enlargement) of existing fat cells and potentially ectopic fat deposition in organs like the liver and pancreas.

The lecture concludes with Ben addressing the difference between hyperplasia (increased fat cell number) and hypertrophy (increased fat cell size) in subcutaneous and visceral fat depots, emphasizing the metabolic implications of storing fat in different locations. He also briefly mentions the influence of non-caloric signals, such as chemicals leached from plastics, on fat cell growth.

Overall, the lecture provides a comprehensive overview of the multifaceted nature of fat tissue storage, highlighting the interplay of hormonal, physiological, and environmental factors in shaping fat distribution and its metabolic consequences.

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In this week's episode of the Metabolic Classroom, Dr. Bikman delves into the complexities of fat tissue. The lecture aims to shift perspectives on fat beyond mere energy storage, highlighting its multifaceted roles in the body. Dr. Bikman encourages listeners to not only absorb the information but also become teachers themselves, spreading these insights and implementing practical changes.

The lecture begins with an exploration of the evolutionary role of fat, debunking misconceptions and emphasizing its importance in survival and early development. Dr. Bikman discusses theories like the expensive tissue hypothesis, shedding light on why humans are born with fat and its significance in brain growth.

Moving on, Dr. Bikman dives into the different types of fat and their storage mechanisms. He explains the distinctions between subcutaneous and visceral fat, emphasizing their impact on metabolic health. Additionally, he explores the metabolic behavior of fat tissue, distinguishing between white, brown, and beige fat and their implications for energy expenditure and storage.

The lecture concludes with a discussion on the genetic and environmental factors influencing fat storage. Dr. Bikman highlights the role of insulin and energy availability in fat accumulation, as well as the impact of diet and environmental chemicals. By understanding these factors, listeners gain insights into managing weight and promoting metabolic health. Until next time in the Metabolic Classroom, Dr. Bikman reminds his audience: more knowledge, better health.

#insulinresistance #metabolicsyndrome #metabolichealth #type2diabetes #type1diabetes #weightloss #intermittentfasting #intermittantfasting #fasting 

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In this week's episode of the Metabolic Classroom, Dr. Ben Bikman welcomes viewers to a discussion on commonly used cardiometabolic and weight loss drugs. The focus of this particular lecture is on drugs targeting heart disease, a leading cause of mortality globally. Dr. Bikman acknowledges the controversy surrounding cardiovascular drugs due to the severity of heart disease and the passionate advocacy for drug therapies.

The lecture begins with an overview of two main categories of cardiovascular drugs: those addressing blood pressure and those targeting cholesterol levels. Dr. Bikman explains the significance of blood pressure in cardiovascular health, emphasizing its correlation with heart attacks and hypertension. He delves into the physiological effects of high blood pressure, likening it to over-inflating a balloon and causing stress and damage to the inner lining of blood vessels.

Moving on to drugs that control blood pressure, Dr. Bikman highlights the potential impact on insulin resistance and mitochondrial function, crucial factors in heart disease risk. He discusses common classes of antihypertensive drugs such as beta blockers, ACE inhibitors, calcium channel blockers, and diuretics, detailing their mechanisms and side effects.

Transitioning to cholesterol-lowering drugs, Dr. Bikman discusses the controversy surrounding the assumption that cholesterol is solely responsible for heart disease. He challenges the oversimplified view of LDL cholesterol's role in plaque formation and suggests alternative paradigms, including the immune response to infections in blood vessels.

Dr. Bikman then discusses two classes of anti-cholesterol medications: PCSK9 inhibitors and statins. He explains how PCSK9 inhibitors increase LDL receptor expression to enhance LDL clearance and discusses potential side effects such as worsened insulin resistance and mitochondrial dysfunction. Finally, he explores the mechanism of statins in reducing cholesterol production and addresses controversies surrounding their use, including potential risks of developing type 2 diabetes and Alzheimer's disease.

#insulinresistance #metabolicsyndrome #metabolichealth #type2diabetes #type1diabetes #weightloss #intermittentfasting #intermittantfasting #fasting #lowcarb 

Learn more at: Insulin IQ

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In today's lecture, Dr. Bikman guides his audience through a comprehensive exploration of anti-diabetic drugs, shedding light on their mechanisms, implications, and the broader context of diabetes management. Kicking off the discussion, Dr. Bikman elucidated the prevalent glucose-centric paradigm in understanding diabetes, emphasizing its limitations, particularly in discerning the nuanced differences between type 1 and type 2 diabetes. He underscored the pivotal role of insulin deficiency in type 1 and insulin resistance in type 2 diabetes, setting the stage for a deeper dive into the intricacies of anti-diabetic medications.

The lecture commenced with an in-depth analysis of metformin, a cornerstone in diabetes treatment known for its efficacy in improving insulin sensitivity. Despite its widespread use, Dr. Bikman elucidated the persistent ambiguity surrounding metformin's cellular mechanisms, particularly concerning its impact on mitochondrial function. While acknowledging its beneficial effects, such as reducing hepatic glucose production, Dr. Bikman also highlighted the drug's gastrointestinal side effects and its potential to blunt mitochondrial adaptations to exercise.

Transitioning to insulin therapy, Dr. Bikman delineated its indispensable role in type 1 diabetes management but cautioned against its potential risks in type 2 diabetes, including weight gain and heightened cardiovascular, cancer, and Alzheimer's disease risks. He delved into the nuances of insulin secretagogues and thiazolidinediones, discussing their mechanisms and associated complications, such as increased cardiovascular risk and adverse effects on adipogenesis.

Further, Dr. Bikman explored GLP-1 agonists and SGLT2 inhibitors, elucidating their mechanisms of action and potential side effects, including an elevated risk of urinary tract infections with SGLT2 inhibitors and heightened ketogenesis. Before concluding, he briefly touched on amylin analogs, adding another dimension to the multifaceted landscape of anti-diabetic medications.

Dr. Bikman's lecture provided a comprehensive understanding of anti-diabetic drugs, transcending the traditional glucose-centric perspective and highlighting the complexities inherent in diabetes management. By navigating through the intricate mechanisms and implications of these medications, he empowered his audience with invaluable insights to navigate the complexities of diabetes treatment effectively.

#insulinresistance #metabolicsyndrome #metabolichealth #type2diabetes #type1diabetes #weightloss #intermittentfasting #intermittantfasting #fasting 

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In today's episode of The Metabolic Classroom, Dr. Ben Bikman delves into the fascinating topic of GLP-1, a hormone of significant interest in metabolic research. Dr. Bikman sets the stage by expanding the discussion beyond GLP-1 to include other incretions, defining them as a class of hormones produced by the small intestine. These hormones play crucial roles in nutrient metabolism, satiety, and hunger regulation.

The discovery of incretions stemmed from observations following gastric bypass surgeries, where elevated levels of these hormones were found in the bloodstream, leading to improvements in diabetes. Dr. Bikman highlights GLP-1's well-known effect on insulin secretion and glucagon suppression, which contribute to its ability to rapidly correct high glucose levels and improve diabetes. However, he notes the ongoing debate regarding GLP-1's direct insulin secretagogue effect in humans, contrasting findings from cell culture and animal models with recent human studies.

Moving beyond GLP-1, Dr. Bikman discusses other incretions like GIP, PYY, and cholecystokinin, outlining their roles in glucose regulation, appetite control, and digestion. He explores the pharmacological applications of GLP-1 agonists in managing diabetes and obesity, detailing various drugs and their mechanisms of action. Furthermore, he touches upon natural methods to enhance GLP-1 secretion, including dietary factors like protein, fat, and sugars. The session concludes with insights into the live Q&A session, emphasizing the dynamic interaction between science and audience participation in The Metabolic Classroom.

Learn more at: https://www.insuliniq.com 

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Beginning with a discussion on the evolution of these medications, Dr. Bikman emphasizes their significance in combating obesity-related health issues. He proceeds to analyze the mechanisms of popular weight loss drugs, such as Orlistat, Phentermine, and the combination of Phentermine with Topiramate, elucidating how each functions to aid weight loss.

While highlighting the benefits, Dr. Bikman doesn’t shy away from detailing the potential side effects, ensuring a comprehensive understanding for the audience. Moreover, he shares an intriguing scientific fact regarding lactate’s role in fat metabolism, adding depth to the discussion. Throughout, Dr. Bikman maintains a balance between scientific evidence and personal insight, fostering an engaging and informative session.

In discussing liraglutide’s mechanism of action, Dr. Bikman reveals its role as a GLP-1 receptor agonist, mimicking the actions of the incretin GLP-1. He then previews next week’s class dedicated to incretins and their use in weight loss drugs, including medications like wegovy and ozempic.

Liraglutide primarily promotes weight loss by reducing gastric emptying, leading to prolonged feelings of fullness and decreased appetite. Additionally, it inhibits glucagon, lowering blood glucose levels and subsequently increasing metabolic rate and fat burning. Dr. Bikman notes common side effects such as gastrointestinal discomfort and hints at potential risks of thyroid tumors associated with GLP-1 agonists.

Ben transitions to discussing semaglutide, another GLP-1 receptor agonist, and its similar effects on weight loss and side effects, including the possibility of ileus. He also touches on metformin’s off-label use for weight loss, its mechanisms involving AMPK activation and ATP inhibition, and its potential interference with exercise-induced mitochondrial benefits.

Learn more at: Insulin IQ

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In today's Metabolic Classroom, the discussion centers on addressing insulin resistance, marking the final part of a series that viewers are encouraged to catch up on if they haven't already. Previous episodes have delved into the nature, origins, and implications of insulin resistance, highlighting its association with various diseases. Despite the somber tone of these revelations, the current discussion offers a ray of hope by focusing on solutions to this pervasive issue, emphasizing its solvability and preventability.

Before delving into strategies for combating insulin resistance, Dr. Bikman takes a moment to outline methods for assessing one's own insulin resistance status, recognizing limitations in traditional approaches that solely focus on glucose levels. He stresses the importance of understanding insulin's broader role beyond glucose regulation, highlighting the significance of elevated insulin levels as an early indicator of resistance. The discussion moves to practical considerations, such as interpreting fasting insulin levels, with values below six suggesting insulin sensitivity, while higher readings may indicate varying degrees of resistance, requiring further evaluation.

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The focus of Dr. Bikman’s Metabolic Classroom today is to help us all better understand, “Why does insulin resistance matter?”

This week's Metabolic Classroom with Dr. Bikman delves into insulin resistance and its impact on health. Insulin resistance, involving impaired insulin function and elevated blood insulin levels, is explored as a key factor in chronic diseases. Dr. Bikman focuses on its crucial role in connecting obesity and type two diabetes, examining its effects on muscle tissue, the liver, and pancreatic alpha cells.

The delayed diagnosis of type two diabetes, due to a focus on glucose levels, is highlighted, with Dr. Bikman discussing the ongoing debate about which tissues become insulin resistant first. The complexities of insulin resistance in fat cells, muscles, the liver, and alpha cells of the pancreas are underscored.

Insulin resistance's effects on glucose clearance in muscle tissue and disruptions in the liver's glycogen storage and glucose regulation are explained. The discussion expands to its impact on pancreatic alpha cells, contributing to elevated blood glucose levels. Dr. Bikman explores the connection between insulin resistance and various health issues, including type 2 diabetes, fatty liver disease, Alzheimer's, hypertension, and infertility.

In examining these health conditions, Dr. Bikman challenges conventional views and emphasizes the role of insulin resistance. For instance, Alzheimer's is linked to metabolic factors, while hypertension is connected to insulin-driven mechanisms. The discussion also covers the influence of insulin resistance on infertility, affecting both erectile dysfunction and polycystic ovary syndrome (PCOS).

Dr. Bikman concludes by summarizing how insulin resistance influences these health conditions and highlights lifestyle modifications as a positive intervention. The upcoming discussion on clinically measuring insulin resistance and actionable steps is teased, urging viewers to share this knowledge for broader awareness.

Learn more at: Insulin IQ

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The focus of the classroom today is to help you better understand the origins of insulin resistance.

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The title for today is focusing on Insulin Resistance in the Metabolic Syndrome, and I could describe that another way, which is just kind of understanding metabolic health and that’s at the heart of what I wanted to focus on for the time that we have during the lesson itself.

Alright, so first of all, metabolic health. We’ve all heard the term metabolism a lot. It is a buzzword, it is a word that we hear perhaps too often and even to the point that it’s often misused. 

Metabolism, just to be very precise, is the balance of all of the chemical reactions that are happening in the body. There are biochemical reactions in every cell that are trying to build up molecules. Those are called anabolic reactions or anabolism, and there are chemical biochemical processes that are degrading molecules, breaking them down. That is catabolism and metabolism is the fusion or the balance of all of those things. The sum of all of those reactions.

Now with metabolic health, we’re starting to get more specific to the topic.

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Many people today are wary of discussions about leaky gut because there are so many questionable cures being sold without scientific evidence to support them. Let's talk about exactly what leaky gut is and how it's affected by what we eat.

Here are the resources that Ben references during the episode:

Source #1 - https://pubmed.ncbi.nlm.nih.gov/18000291/

Source #2 - https://aasldpubs.onlinelibrary.wiley.com/doi/full/10.1002/hep.30652

Source #3 - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6412740/

Source #4 - https://science.sciencemag.org/content/373/6553/eabe6729

Source #5 - https://pubmed.ncbi.nlm.nih.gov/27171436/

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One of the most persistent oppositions to a low carb diet is the idea that it can damage the kidneys. Let's dive into what the data really shows.

Here is the resource that Ben references during the episode:

Source #1 - https://pubmed.ncbi.nlm.nih.gov/30383278/

Source #2 - https://pubmed.ncbi.nlm.nih.gov/27346534/

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Many people claim that eating low-carb can actually make you insulin resistant. How can this be? The answer lies in the key difference between two types of insulin resistance; pathological versus physiological. Let's discuss what's really happening.

Here is the resource that Ben references during the episode:

Source #1 - https://academic.oup.com/jes/article/5/5/bvab049/6199842?login=true

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It’s estimated that up to 12% of women in the US are affected by fertility problems directly caused by insulin resistance. Join Dr. Ben Bikman, the Insulin IQ team, and special guest Dr. Steven Cowles, OBGYN, for a conversation on how insulin control is giving women hope to have the family they want.

Here is the resource that Ben references during the episode:

Source #1 - https://pubmed.ncbi.nlm.nih.gov/26225266/

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Here are the resources that Ben references during the episode:

Study #1 - https://care.diabetesjournals.org/content/25/2/364.short

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For our entire lives we’ve always heard that “healthy whole grains are an essential part of a balanced diet.” In light of what we now know about nutrition and insulin, does that statement hold up? Join Dr. Bikman and the Insulin IQ team for a conversation about the evidence.

Here are the resources that Ben references during the episode:

Study #1 - https://www.sciencedirect.com/science/article/abs/pii/0002934387900581?via%3Dihub

Study #2 - https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1651-2227.1987.tb10498.x

Study #3 - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4325021/

Study #4 - https://cdnsciencepub.com/doi/full/10.4141/cjas2012-017

Study #5 - https://academic.oup.com/ajcn/article/103/2/341/4564756?login=true

BYU Address - https://speeches.byu.edu/talks/benjamin-bikman/the-plagues-of-prosperity/

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Some of the most common diabetes drugs work in interesting ways. Let’s talk about some of the most common: SGLT inhibitors and GLP-1 receptor agonists.

Here are the resources that Ben references during the episode:

Study #1 - https://pubmed.ncbi.nlm.nih.gov/24917578/

Study #2 - https://pubmed.ncbi.nlm.nih.gov/30240793/

Study #3 - https://pubmed.ncbi.nlm.nih.gov/32827151/

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“Good” cholesterol? “Bad” cholesterol? Decades of unclear and misinterpreted science have led to widespread misunderstanding of this vital component of every cell in our bodies. Join Dr. Ben Bikman, special guest Dr. Bret Scher, and the Insulin IQ team as we distill down what you need to know about cholesterol.

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Despite sharing a name, type 1 and type 2 diabetes have surprisingly little in common. Let’s explore what they have in common and their many differences.

Here are the resources that Ben references during the episode:

Study #1 - https://www.endocrinology.org/endocrinologist/129-autumn18/features/endogenous-insulin-its-role-in-the-initiation-progression-and-management-of-diabetes

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Metformin is the most widely used drug to fight diabetes. Let’s talk about how it works and when it doesn’t work well.

Here are the resources that Ben references during the episode:

Study #1 - https://www.sciencedirect.com/science/article/abs/pii/S0891584910003874?casa_token=z96rcmkuc7YAAAAA:pxbbTkuPhL7Nop4oUECKmCq81Ev4Dc7z4XYvbaNMXLorp-F9p4nrHLo9bkUiIL0Trjv9EhNNGds

Study #2 - https://www.jci.org/articles/view/13505?content_type=full

Study #3 - https://europepmc.org/article/med/3817257

Study #4 - https://onlinelibrary.wiley.com/doi/full/10.1111/acel.13039

Study #5 - https://onlinelibrary.wiley.com/doi/full/10.1111/acel.12880

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A spike in glucose levels each morning can be startling, but it doesn’t need to be scary. To understand the dawn phenomenon, you need to understand hormones.

Here are the resources that Ben references during the episode:

Study #1 - https://www.nejm.org/doi/full/10.1056/nejm198811103191901

Study #2 - https://pubmed.ncbi.nlm.nih.gov/6389230/

Study #3 - https://pubmed.ncbi.nlm.nih.gov/2859524/

Study #4 - https://diabetes.diabetesjournals.org/content/45/8/1044

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Stress is an essential part of being human—we need a stress response. However, when stress is turned on indefinitely, metabolic health suffers.

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Sex hormones control many processes in the body and estrogens have multiple and diverse effects on telling the body where and how to store fat.

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We all know about leptin’s effects on hunger, but it’s involved in so much more. Let’s learn about this metabolic heavyweight.

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Dietary fiber enjoys a lofty position in the hallowed halls of dietary advice, but the truth is more complicated. Whether fiber is helpful or harmful depends on other factors.

Here are the resources that Ben references during the episode:

Study #1 - https://academic.oup.com/ajcn/article-abstract/59/6/1386/4715907

Study #2 - https://pubmed.ncbi.nlm.nih.gov/6259919/

Study #3 - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3435786/

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The brain is among the highest metabolic rate organs in the body. It needs a lot of energy, and it needs insulin’s help. When the brain becomes insulin resistant, we create an “energy gap” that stems from a genetic level.

Here are the resources that Ben references during the episode:

Study #1 - https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0144116

Study #2 - https://pubmed.ncbi.nlm.nih.gov/25147107/

Study #3 - https://alz-journals.onlinelibrary.wiley.com/doi/full/10.1002/alz.12310

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Within the field of nutrition, fewer topics are as hotly debated and defended as the view that red meat causes cancer. Let’s explore the data, keeping in mind that correlation is not causation.

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How glucose moves in and out of cells is important to understanding insulin resistance, fuel use, and more. Let’s learn about glucose transporters on cells and how they regulate glucose in the body.

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We’ve been told for decades that saturated fats cause plaques that block blood vessels. What if that’s wrong?

Study #1 - https://www.pnas.org/content/76/1/333.short

Study #2 - https://www.cell.com/fulltext/S0092-8674(00)81574-3#BIB40

Study #3 - https://pubmed.ncbi.nlm.nih.gov/9488997/

Study #4 - https://www.plefa.com/article/S0952-3278(12)00146-9/pdf

Study #5 - https://www.bmj.com/content/bmj/346/bmj.e8707.full.pdf

Study #6 - https://www.bmj.com/content/353/bmj.i1246

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While a calorie is certainly a calorie, overlooking the effect of those calories on insulin means we miss a piece of the metabolic puzzle. We’ll explore some studies that reveal what insulin does to metabolic rate in the body.

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A low-carb diet can do a lot of good things, but does it come at the expense of the thyroid? We’ll review the evidence and explore the relationship between thyroid and carbs.

Here are the resources that Ben references during the episode:

Study #1 - https://pubmed.ncbi.nlm.nih.gov/11167929/

Study #2 - https://pubmed.ncbi.nlm.nih.gov/6865775/

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When fat cells get too big rather than too many, they start to suffer. This week Dr. Ben Bikman and the Insulin IQ Team review the evidence for why this happens and what you can do about it.

Here are the resources that Ben references:

Source #1 - https://jim.bmj.com/content/64/5/989

Source #2 - https://pubmed.ncbi.nlm.nih.gov/30649347/

Source #3 - https://pubmed.ncbi.nlm.nih.gov/32398753/

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Are you worried about your fatty liver. This week Dr. Ben Bikman and the Insulin IQ Team explore what the sweet carbohydrate, fructose, does to liver fat.

Here are the three studies that Ben references during this session:

Source - #1 https://academic.oup.com/ajcn/advance-article/doi/10.1093/ajcn/nqaa332/6056215?fbclid=IwAR3K6hXW-NlQFWUdsnr0RcQuzgSatgJEosx_8Q3gE79VFL-XkLkYldeRD-c

Source - #2 - https://www.jci.org/articles/view/37385/figure/1

Source #3 - https://pubmed.ncbi.nlm.nih.gov/25825943/

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Are you eating enough salt to stay insulin sensitive? Dietary salt is too often viewed as something to avoid, but could eating too little salt actually make your metabolic problems worse? Dr. Ben Bikman and the Insulin IQ Team discuss what you need to know.

Here is the link referenced in this episode:

Source #1 - https://pubmed.ncbi.nlm.nih.gov/9589654/

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Long term restriction of calories seems like the simplest answer to losing weight; eat less weigh less, right? However, this approach the serious consequences that chronic calorie restriction has on your fat cells and hormones. This week Dr. Ben Bikman and the Insulin IQ Team explain the metabolic reasons why getting healthier is not just about calories.

Here is the link referenced in this episode:

Source #1 - https://pubmed.ncbi.nlm.nih.gov/3308961/

Learn more at Insulin IQ

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

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

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

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

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

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

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

Do low-carb diets spike cortisol and reduce muscle mass? The stress hormone cortisol is not something we want elevated for very long. If you've heard that a low-carb diet spikes cortisol levels, you may be concerned. This week Dr. Ben Bikman and the Insulin IQ team dive into a couple of studies on this important topic.

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At Insulin IQ, we get lots of questions from our clients and students about low-carb, high-fat eating and the thyroid.

In this episode of Dr. Bikman’s Metabolic Classroom, Ben discusses this topic with a couple of our Insulin IQ team members.

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Our friend, Dr. Bret Scher, MD writes, “A new study, published in the Journal of the American Medical Association (JAMA), shows no benefit from intermittent fasting. But, after taking a close look, it’s revealed that we should be cautious about how we interpret this conclusion.”

During our Insulin IQ LIVE stream on Monday, October 5, 2020 Dr. Ben Bikman shares his thoughts on the JAMA research.

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