The Metabolic Classroom with Dr. Ben Bikman

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

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

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

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

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

Show Notes/References:

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

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

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

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

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

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

Show Notes/References:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Show Notes/References:

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

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

📢 Learn more about becoming an Insider on Ben’s website: https://www.benbikman.com

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

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

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

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

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

Show Notes/References:

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

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

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

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

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

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

Show Notes/References:

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

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

📢 Learn more about becoming an Insider on Ben’s website: https://www.benbikman.com

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Show Notes/References:

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

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

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

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

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

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

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

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

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

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

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

(📢 NOTE: We apologize for the sound glitch starting at 2 minutes. Dr. Bikman’s lectures are recorded LIVE, and our production team didn’t want to interrupt him. 🙂 )

Dr. Ben Bikman’s Metabolic Classroom lecture this week explores fat metabolism and the differences between saturated, monounsaturated, and polyunsaturated fats. He begins by explaining that fat is more than just stored energy—it serves as fuel, structure, and biochemical signaling molecules. He categorizes fats based on saturation state, detailing how each type influences metabolism and health outcomes. Saturated fats (found in butter, coconut oil, and animal fat) are stable and non-reactive, making them efficient energy sources. Monounsaturated fats (found in olive oil and avocados) are slightly more flexible and commonly stored in fat cells. Polyunsaturated fats (PUFAs), such as omega-3 and omega-6 fats, play an important role in cell signaling but are highly prone to peroxidation, leading to inflammation and oxidative stress—especially when consumed from refined seed oils like soybean and corn oil.

Dr. Bikman then discusses how the body metabolizes and stores different fats. Long-chain saturated fats can be stored or burned for energy, while medium- and short-chain saturated fats (found in coconut oil and dairy) bypass traditional fat storage pathways and are rapidly burned for energy, often increasing ketone production. Monounsaturated fats (like oleic acid from olive oil) are the most abundant in human fat cells, showing the body's preference for this fat type. However, PUFAs, particularly linoleic acid from seed oils, are problematic because they are prone to peroxidation, contributing to inflammation and metabolic dysfunction.

Ben highlights research showing that high-carbohydrate diets increase the body's internal production of saturated fat, meaning even if someone avoids saturated fats in their diet, their liver will still create them from excess carbohydrates. He also explains that PUFAs, despite their risks, can be burned as energy, but their instability can cause oxidative damage. The key takeaway is that fat metabolism is dynamic, and insulin levels dictate whether fats are burned or stored. He concludes that natural, whole-food fats—especially saturated and monounsaturated fats—are the best choices for metabolic health, while high-PUFA seed oils should be avoided.

Show Notes/References:

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

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

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

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

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

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

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

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

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

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

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

In this Metabolic Classroom lecture, Dr. Bikman explores GLP-1 receptor agonists (such as Ozempic and Mounjaro) and how to use them more effectively.

Ben first explains how GLP-1 is naturally produced in the gut and helps regulate glucagon suppression, slows gastric emptying, and promotes satiety. However, he highlights research showing that individuals with obesity have a blunted GLP-1 response to carbohydrates, which may contribute to overeating. He suggests that GLP-1 drugs could be used more strategically—not just for general weight loss, but specifically to control carbohydrate cravings.

While these drugs can promote rapid weight loss, they can also come with serious trade-offs, including mental health risks (depression, anxiety, and suicidal thoughts), lean mass loss (up to 40% of weight lost), diminishing effects over time, and digestive complications such as gastroparesis (stomach paralysis). He critiques the current high-dose, long-term approach to these medications, arguing that most people are not using them strategically and eventually regain lost weight—primarily as fat.

Dr. Bikman proposes a better approach to using GLP-1 drugs that focuses on low-dose, short-term usage to help control carbohydrate cravings, rather than suppressing appetite completely.

His four-step plan includes: (1) starting at the lowest effective dose, (2) engaging in resistance training to preserve muscle mass, (3) adopting a low-carb, high-protein diet, and (4) cycling off the drug after 3-6 months to assess whether cravings remain under control. He also discusses newer GLP-1/GIP dual agonists like Tirzepatide, which may be even more effective but still require careful usage.

In closing, Ben emphasizes that GLP-1 drugs should be a tool, not a crutch.

The ultimate goal should be to regain control over eating habits, build long-term dietary discipline, and use the drug only when needed. He encourages those considering these medications to work closely with their healthcare providers and approach them with a long-term metabolic health strategy in mind.

Show Notes/References:

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

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For this week’s Metabolic Classroom lecture, Dr. Bikman focuses on natural ways to boost GLP-1 (Glucagon-Like Peptide-1), a powerful gut hormone involved in appetite control, blood sugar regulation, and metabolic health.

Ben begins by explaining that GLP-1 is secreted in response to food intake, influencing glucagon suppression, slowing gastric emptying, and activating satiety centers in the brain. However, research shows that individuals with obesity tend to have a blunted GLP-1 response, particularly after consuming carbohydrates. This means that people with obesity may not experience the same level of fullness and appetite regulation, which can contribute to overeating.

Dr. Bikman then discusses concerns with GLP-1 receptor agonist medications, such as Ozempic and Wegovy. While they effectively promote weight loss, they also come with significant downsides, including loss of lean mass (up to 40% of total weight lost), increased mental health risks (depression, anxiety, and suicidal thoughts), and a return of sweet cravings over time. Additionally, 70% of people discontinue these drugs within two years, often regaining weight—primarily as fat—due to muscle loss during treatment.

He then presents natural methods to enhance GLP-1 production without drugs. His lab at BYU found that Yerba Mate significantly increases GLP-1 by 40-50%, likely due to its ferulic acid content and bitter taste receptors that also reduce sweet cravings. Allulose, a rare sugar, has also been shown to stimulate GLP-1 and improve glucose control, even in individuals with type 1 diabetes. Other natural boosters include a low-carbohydrate, protein-rich diet, which triples GLP-1 levels compared to a low-fat diet, collagen peptides, which enhance GLP-1 secretion and insulin sensitivity, and quality sleep, since poor sleep is linked to impaired GLP-1 signaling and increased hunger.

Dr. Bikman concludes by emphasizing that leveraging diet and lifestyle changes is the most effective and sustainable way to improve GLP-1 levels, regulate appetite, and support long-term metabolic health. While GLP-1 medications may serve a purpose, particularly for those struggling with carbohydrate cravings, they come with risks that should not be ignored. Instead, strategies such as Yerba Mate, allulose, low-carb diets, collagen peptides, and better sleep can provide natural, lasting benefits without side effects.

Show Notes/References:

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

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Dr. Bikman’s lecture this week explores the metabolic roles of bilirubin, a molecule typically associated with liver disease and jaundice but now emerging as a key player in metabolism, oxidative stress, and fat regulation.

Bilirubin is produced from the breakdown of red blood cells and is transported to the liver, where it undergoes conjugation to become water-soluble and is then excreted into bile.

While historically viewed as a waste product, recent research suggests that bilirubin plays a significant role in protecting against oxidative stress and inflammation, and may even contribute to metabolic flexibility and fat metabolism.

One of bilirubin’s most fascinating properties is its potent antioxidant effect. It neutralizes reactive oxygen species (ROS), helping to reduce oxidative stress—a key driver of chronic diseases, including insulin resistance, cardiovascular disease, and neurodegeneration. Bilirubin also acts as an anti-inflammatory agent, inhibiting key inflammatory pathways such as NF-kappa B, which is involved in obesity-related inflammation. Interestingly, individuals with Gilbert Syndrome, a genetic condition that causes mildly elevated bilirubin levels, have been shown to have a significantly lower risk of cardiovascular disease.

Beyond its antioxidant and anti-inflammatory roles, bilirubin also influences fat metabolism. Studies suggest that bilirubin enhances mitochondrial function and thermogenesis, particularly in brown and beige fat, by increasing UCP-1 (uncoupling protein 1) expression, which helps the body burn fat more efficiently.

Ben concludes by discussing ways to naturally increase bilirubin levels. Since bilirubin is excreted in bile, diets higher in fat may enhance enterohepatic recycling, allowing more bilirubin to re-enter circulation and exert its beneficial effects. While excessive bilirubin can be toxic, modestly elevated levels, as seen in Gilbert Syndrome, appear to provide metabolic advantages.

This growing body of research challenges the outdated view of bilirubin as a mere waste product and suggests that it may be a crucial player in metabolic health.

Show Notes/References:

For complete show notes and references referred to in this episode, we invite you to become a Ben Bikman Insider subscriber. As a subscriber, you’ll enjoy real-time, livestream Metabolic Classroom access which includes live Q&A with Ben, ad-free Metabolic Classroom Podcast episodes, show notes and references, Ben’s Research Reviews Podcast, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews. Learn more about becoming an Insider on our website: https://www.benbikman.com

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Dr. Bikman’s Metabolic Classroom lecture this week explores peptides and their effects on metabolism, fat loss, muscle growth, and overall health.

Ben begins by defining peptides as short chains of amino acids that act as signaling molecules in the body. While some peptides occur naturally, others are synthetically developed for therapeutic purposes. He explains that peptides are gaining popularity in fitness, anti-aging, and metabolic health, influencing fat loss, muscle repair, insulin sensitivity, and even skin regeneration. He also introduces collagen peptides, highlighting their unexpected metabolic benefits, including their influence on GLP-1 and gut microbiome health.

Ben then categorizes peptides based on their primary functions. For fat loss, peptides like CJC-1295 and Tesamorelin work by stimulating growth hormone and IGF-1, promoting fat breakdown while preserving muscle mass. Another peptide, Melanotan-2, originally known for increasing melanin, has been found to suppress appetite by affecting the melanocortin system. He also discusses peptides like Ipamorelin, which help enhance muscle recovery and growth by selectively increasing growth hormone secretion without affecting other pituitary hormones.

In the anti-aging and skin health category, Thymosin Beta-4 stands out for its ability to enhance wound healing and tissue repair. Dr. Bikman also highlights the unexpected metabolic role of collagen peptides, explaining how they can increase GLP-1 levels, improve insulin sensitivity, and even activate AMPK, a crucial metabolic regulator involved in fat breakdown and cellular repair.

Finally, he touches on how peptides are administered—most commonly via subcutaneous injections, though some peptides can be absorbed sublingually or applied topically.

He cautions that not all peptides are created equal, warning against low-quality or counterfeit products. Ben emphasizes the need for high-quality sourcing and careful monitoring, as some peptides affect hormone levels and require medical supervision.

Dr. Bikman concludes that peptides hold immense potential for metabolic health, fitness, and longevity, but should be used wisely and responsibly.

Show Notes/References:

For complete show notes and references referred to in this episode, we invite you to become a Ben Bikman Insider subscriber. As a subscriber, you’ll enjoy real-time, livestream Metabolic Classroom access which includes live Q&A with Ben, ad-free Metabolic Classroom Podcast episodes, show notes and references, Ben’s Research Reviews Podcast, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews. Learn more about becoming an Insider on our website: https://www.benbikman.com

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Learn more about becoming an Insider: https://www.benbikman.com

In this week’s lecture, Dr. Bikman explores the metabolic origins of acne, challenging the conventional view that acne is purely a skin issue. While acne is often attributed to excess oil production, clogged pores, bacteria, and inflammation, Ben highlights how metabolic factors—especially insulin—play a significant role.

Insulin directly stimulates sebaceous glands, increasing oil production, and also triggers the release of androgens (such as testosterone), further worsening acne. Additionally, insulin resistance promotes inflammation and hyperkeratinization, both of which contribute to acne severity.

He explains that puberty naturally induces a state of insulin resistance, which helps drive growth and development. However, when combined with modern high-carbohydrate diets, this physiological insulin resistance can be exacerbated, leading to severe acne in some teenagers. He also discusses the role of insulin-like growth factor 1 (IGF-1), which is stimulated by high insulin levels and is known to increase sebum production and accelerate skin cell turnover, worsening acne conditions.

Ben then presents compelling research on metabolic-based acne treatments, including the use of metformin, an insulin-sensitizing drug that has shown promise in reducing acne, particularly in conditions like PCOS. He also highlights dietary interventions, particularly low-carbohydrate and ketogenic diets, which have been found to significantly reduce acne severity by lowering insulin and improving skin health. One study found that young women on a ketogenic diet saw a 33% reduction in acne severity and a 50% improvement in skin quality within just 45 days.

He concludes that acne is not just a cosmetic issue but a metabolic condition that can be managed through dietary and lifestyle changes. While conventional acne treatments address symptoms, tackling insulin resistance through proper nutrition provides a long-term solution. He encourages those struggling with acne to focus on cutting out refined carbohydrates, prioritizing protein, and embracing healthy fats to regulate insulin levels and improve skin health.

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In this week’s episode of the Metabolic Classroom lectures, Dr. Ben Bikman explores the metabolic impact of ADHD medications and whether ADHD itself has metabolic roots.

Ben explains how stimulant medications (like Adderall and Ritalin) primarily work by increasing dopamine and norepinephrine, enhancing focus but also suppressing appetite and stimulating fat breakdown. This can lead to weight loss but may also contribute to binge eating episodes when the medication wears off. Non-stimulant ADHD medications (like Atomoxetine and Guanfacine) affect metabolism in different ways—some subtly improve insulin sensitivity, while others reduce fat breakdown, potentially leading to weight gain.

Beyond medication, Dr. Bikman discusses ADHD as a possible metabolic disorder. Studies show that individuals with ADHD often have reduced glucose metabolism in the prefrontal cortex, the brain region responsible for attention and impulse control. He highlights research linking chronic sugar consumption to dopamine imbalances and brain energy instability, suggesting that modern dietary habits may be worsening ADHD symptoms.

One potential solution? Ketones as an alternative brain fuel. Dr. Bikman shares research on the ketogenic diet as a therapy for ADHD, similar to its use in epilepsy and Alzheimer’s disease. By shifting the brain’s energy source from glucose to ketones, individuals may experience more stable brain function and improved focus. He concludes that ADHD may not just be a neurological condition—it could also be a metabolic issue, and targeting brain metabolism may offer new treatment possibilities.

Show Notes/References:

For complete show notes and references referred to in this episode, we invite you to become a Ben Bikman Insider subscriber. As a subscriber, you’ll enjoy real-time, livestream Metabolic Classroom access which includes live Q&A with Ben, ad-free Metabolic Classroom Podcast episodes, show notes and references, Ben’s Research Reviews Podcast, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews. Learn more about becoming an Insider on our website: https://www.benbikman.com

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Dr. Bikman’s Metabolic Classroom lecture this week explores the physiological role and implications of GLP-1 (glucagon-like peptide-1) and the GLP-1 receptor agonist drugs used for type 2 diabetes management and weight loss.

Ben begins by explaining GLP-1 as a hormone produced in the intestines in response to food. It plays a vital role in slowing gastric emptying, suppressing glucagon, and regulating appetite by signaling fullness to the brain. These mechanisms contribute to its effects on stabilizing blood sugar and enhancing insulin sensitivity.

He then delves into GLP-1 receptor agonists, drugs that mimic GLP-1’s actions, including semaglutide, liraglutide, and others marketed under brand names like Ozempic and Wegovy. These medications have gained fame for their weight loss efficacy, often leading to reductions in body weight by 15% or more.

However, Ben emphasizes that weight loss involves not only fat but also lean mass, raising concerns about muscle loss and metabolic health. Additionally, he discusses the medications’ side effects, including depression, anhedonia, and potential long-term complications like fat cell development and gallstones.

The lecture also addresses the diminishing returns of these drugs over time, noting that their efficacy in reducing cravings and improving eating control tends to wane after prolonged use. Dr. Bikman highlights that education on healthy eating and resistance training is crucial for maintaining health outcomes, as reliance solely on medication can lead to unintended consequences, such as increased fat regain after discontinuation.

Ben concludes by stressing the importance of combining these drugs with a low-carb diet and resistance training to minimize muscle loss and optimize long-term outcomes. He encourages using the lowest effective dose and underscores the need for lifestyle changes to complement pharmacological interventions.

Show Notes/References:

For complete show notes and references referred to in this episode, we invite you to become a Ben Bikman Insider subscriber. As a subscriber, you’ll enjoy real-time, livestream Metabolic Classroom access which includes live Q&A with Ben, ad-free Metabolic Classroom Podcast episodes, show notes and references, Ben’s Research Reviews Podcast, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews. Learn more about becoming an Insider on our website: https://www.benbikman.com

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This week, Dr. Bikman’s lecture focuses on metabolic surgeries (also called bariatric surgeries), their mechanisms, and their impacts on weight loss and metabolic health.

Ben begins by explaining the qualifications for these surgeries, which often serve as a last resort for individuals with severe obesity or comorbidities like type 2 diabetes. Common qualifications include a BMI of 40 or higher, or lower BMIs with conditions like hypertension or diabetes. These surgeries aim to address obesity and related health complications when traditional methods, like diet and exercise, fail.

Dr. Bikman describes four primary types of metabolic surgeries: Roux-en-Y gastric bypass, sleeve gastrectomy, biliopancreatic diversion with duodenal switch, and adjustable gastric banding. He explains their procedures, including how they alter digestion, absorption, and stomach size, leading to weight loss through restriction and malabsorption. These surgeries also bring significant hormonal changes, such as increases in GLP-1 and reductions in ghrelin (hunger hormone), contributing to satiety and metabolic improvements.

While these surgeries can dramatically improve insulin sensitivity, reduce glucagon levels, and improve conditions like type 2 diabetes, they come with risks. Nutrient deficiencies, surgical complications, dumping syndrome, and weight regain are significant concerns. Younger patients are particularly prone to weight regain, especially if they don’t adopt sustainable eating habits. Dr. Bikman emphasizes the need for education on managing macronutrients and maintaining long-term behavioral changes.

Ben concludes that metabolic surgeries can be a valuable tool for those with severe obesity and related complications. However, he warns of their limitations and advocates for coupling them with lifestyle changes to optimize long-term success.

Show Notes/References:

For complete show notes and references referred to in this episode, we invite you to become a Ben Bikman Insider subscriber. As a subscriber, you’ll enjoy real-time, livestream Metabolic Classroom access which includes live Q&A with Ben, ad-free Metabolic Classroom Podcast episodes, show notes and references, Ben’s Research Reviews Podcast, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews. Learn more about becoming an Insider on our website: https://www.benbikman.com

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In this Metabolic Classroom lecture, Dr. Bikman delves into the fascinating metabolic process of autophagy, the body’s natural recycling system that maintains cellular health by breaking down and reusing damaged components.

Ben explains how autophagy is essential for replacing malfunctioning organelles and proteins, thereby preventing diseases such as neurodegenerative disorders, cardiovascular conditions, and even some cancers. Autophagy also plays a crucial role in energy production during nutrient deprivation, highlighting its importance for survival and optimal cellular function.

Dr. Bikman also discusses the relationship between autophagy and metabolic health, emphasizing how impaired autophagic activity in adipose tissue contributes to inflammation and insulin resistance in obesity. He explores its role in longevity, citing evidence that enhanced autophagy can improve health span and lifespan in animal studies.

Additionally, Ben examines how factors like insulin, nutrient availability, and diets such as ketogenic diets regulate autophagy, with ketones having a direct effect on boosting this process.

Throughout the lecture, Dr. Bikman underscores the need for balance in autophagy, warning against excessive or constant activation, whether through pharmacological means like rapamycin or mismanaged dietary habits, advocating instead for natural regulation via nutrient signals.

Show Notes/References:

For complete show notes and references referred to in this episode, we invite you to become a Ben Bikman Insider subscriber. As a subscriber, you’ll enjoy real-time, livestream Metabolic Classroom access which includes live Q&A with Ben, ad-free Metabolic Classroom Podcast episodes, show notes and references, Ben’s Research Reviews Podcast, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews. Learn more about becoming an Insider on our website: https://www.benbikman.com

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

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

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

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

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

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

Ben’s favorite exogenous ketone: https://www.americanketone.com (discount: Ben10)

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

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Dr. Benjamin Bikman delves into the profound relationship between sleep and metabolic health, emphasizing the critical role sleep plays in maintaining insulin sensitivity and overall metabolic function.

Ben explains that deep sleep is a restorative phase during which the body repairs cells, regulates hormones, and improves insulin sensitivity. Poor sleep, however, disrupts these vital processes, leading to hormonal imbalances that elevate cortisol levels and reduce melatonin production.

Elevated cortisol, a stress hormone, promotes gluconeogenesis and insulin resistance, while insufficient melatonin—a hormone essential for regulating sleep—negatively impacts insulin sensitivity and glucose metabolism. This disruption creates a cycle of metabolic dysfunction, increasing the risk of conditions like type 2 diabetes and obesity.

Dr. Bikman highlights actionable strategies to improve both sleep and metabolic health. He stresses the importance of avoiding high-glycemic meals before bed, minimizing exposure to blue light from screens, and maintaining consistent sleep schedules.

He also discusses how ketones, especially in athletes after intense exercise, have been shown to improve sleep efficiency and REM sleep duration.

For individuals struggling with sleep, Dr. Bikman explores the potential benefits of melatonin supplementation and exogenous ketones, underscoring the need for personalized approaches. By addressing evening habits and understanding the hormonal interplay between sleep and metabolism, individuals can take meaningful steps to enhance both sleep quality and metabolic health.

This episode of The Metabolic Classroom provides valuable insights into how optimizing sleep can significantly improve overall well-being.

Timestamps:

(00:45) – Introduction to Sleep and Metabolic Health

(01:22) – Why Sleep is Essential for Insulin Sensitivity

(04:20) – How Cortisol Disrupts Sleep and Metabolism

(08:10) – The Unexpected Role of Melatonin in Metabolism

(19:35) – How Late-Night Eating and Blue Light Harm Sleep

(23:40) – Can Exogenous Ketones Improve Sleep Quality?

(28:20) – Practical Tips for Better Sleep and Metabolic Health

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We sincerely apologize! During the livestream recording, we experienced some technical difficulties between 07:15 to 08:50. Thanks for your patience and understanding.

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During The Metabolic Classroom lecture this week, Dr. Bikman dives into the intricate relationship between salt- and water-regulating hormones and metabolic health.

Starting with a discussion of the renin-angiotensin-aldosterone system (RAAS), he explains how hormones like angiotensin II, aldosterone, and antidiuretic hormone (ADH) are not only critical for regulating blood pressure but also significantly impact insulin sensitivity and fat cell dynamics. Angiotensin II promotes insulin resistance by increasing ceramide production, which blocks insulin signaling, while also enlarging fat cells and inhibiting their breakdown. Similarly, aldosterone exacerbates insulin resistance by enhancing ceramide levels and promotes both the growth and multiplication of fat cells. ADH complements these effects, particularly by inhibiting fat breakdown through its action on specific receptors.

Ben emphasizes the counterintuitive finding that salt restriction, often prescribed to manage hypertension, can worsen insulin resistance, particularly in individuals with metabolic vulnerabilities. Studies highlight that reducing salt intake leads to increased fasting insulin levels, impaired glucose metabolism, and unfavorable lipid changes, such as reduced HDL cholesterol. Additionally, he warns that dehydration, much like salt restriction, activates these same hormonal pathways, compounding their metabolic effects.

Dr. Bikman concludes with a reminder that interventions aimed at improving blood pressure should consider their broader metabolic implications, particularly for individuals predisposed to insulin resistance.

Show Notes/References:

For complete show notes and references referred to in this episode, we invite you to become a Ben Bikman Insider subscriber. As a subscriber, you’ll enjoy real-time, livestream Metabolic Classroom access which includes live Q&A with Ben, ad-free Metabolic Classroom Podcast episodes, show notes and references, Ben’s Research Reviews Podcast, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews. Learn more about becoming an Insider on our website: https://www.benbikman.com

Timestamps: (approximate)

(01:13) Overview of Salt- and Water-Regulating Hormones

(02:22) How Angiotensin II Influences Blood Pressure and Insulin Resistance

(06:37) The Metabolic Effects of Angiotensin II on Fat Cells

(11:22) Aldosterone’s Role in Insulin Resistance and Fat Cell Growth

(15:57) Metabolic Impacts of Antidiuretic Hormone (ADH)

(29:02) The Counterintuitive Effects of Salt Restriction on Metabolic Health

(33:13) The Role of Dehydration in Activating Metabolic Hormones

(34:51) Conclusion: How Blood Pressure Hormones Influence Metabolic Health

#MetabolicHealth #InsulinResistance #Hypertension #SaltAndHealth #BloodPressure #HormonesAndHealth #DrBenBikman #MetabolicSyndrome #LowCarbLife #Type2Diabetes #KetoLife #HealthyLifestyle #NutritionScience #MetabolismMatters #HealthEducation #FatCellBiology #InsulinSensitivity #SaltIntake #Dehydration #HealthTips

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This week in The Metabolic Classroom lecture, Ben focuses on the relationship between hypertension medications and metabolic health, providing a critical examination of their mechanisms and metabolic implications.

He begins by highlighting the role of insulin resistance as a common root cause of both hypertension and metabolic disorders. Ben explains that while hypertension medications such as diuretics, beta blockers, ACE inhibitors, ARBs, and calcium channel blockers are often prescribed, they each have unique effects on insulin sensitivity and glucose metabolism, which can either mitigate or exacerbate metabolic dysfunction. Notably, some classes of these medications, like ARBs, may improve insulin sensitivity, while others, like beta blockers and diuretics, can impair it, leading to heightened risks for type 2 diabetes.

Ben underscores the importance of addressing the root causes of hypertension—namely, insulin resistance—through lifestyle interventions like low-carbohydrate diets and fasting, which improve both blood pressure and metabolic health. He emphasizes the need for personalized treatment plans that consider the metabolic side effects of medications, advocating for strategies that tackle insulin resistance as a primary approach to improving overall health.

Show Notes/References:

For complete show notes and references referred to in this episode, we invite you to become a Ben Bikman “Insider” subscriber. As a subscriber, you’ll enjoy real-time, livestream Metabolic Classroom access which includes live Q&A with Ben, ad-free Metabolic Classroom Podcast episodes, show notes and references, Ben’s Research Reviews Podcast, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews. Learn more about becoming an Insider on our website: https://www.benbikman.com

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

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

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

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

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

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

Ben’s favorite exogenous ketone: https://www.americanketone.com (discount: Ben10)

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

#MetabolicHealth #Hypertension #BloodPressure #DrBenBikman #InsulinResistance #MetabolicScience #FatCellBiology #Diuretics #BetaBlockers #ACEInhibitors #CalciumChannelBlockers #BloodPressureMedications #HealthTips #DASHDiet #InsulinSensitivity #FatCells #KetogenicDiet #LowCarbLiving #HealthyLifestyle #HeartHealth

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This week in The Metabolic Classroom, Ben explores the effects of a ketogenic diet on thyroid function, addressing concerns that lower thyroid hormone levels observed during the diet may indicate dysfunction.

Dr. Bikman begins by explaining the hypothalamic-pituitary-thyroid (HPT) axis, a regulatory system that controls thyroid hormone production. The thyroid gland produces two primary hormones, T3 (triiodothyronine) and T4 (thyroxine), with T3 being the active form that influences metabolic processes. He emphasizes the concept of negative feedback within the HPT axis, explaining that normal TSH levels generally indicate a well-functioning thyroid, even if T3 levels are lower.

Ben also reviews a commonly cited study that observed decreased T3 levels in individuals following a ketogenic diet. Despite the drop in T3, TSH levels remained normal, suggesting that the thyroid gland was not damaged but rather adapting to reduced metabolic demand. He introduces two key explanations: improved thyroid hormone sensitivity and reduced glucose metabolism. Improved sensitivity means that lower levels of T3 are sufficient to maintain metabolic functions, while reduced glucose consumption on a ketogenic diet lessens the body’s need for thyroid hormone to regulate glucose uptake.

The classroom lecture then delves into the concept of thyroid hormone resistance, a condition linked to metabolic disorders like obesity and type 2 diabetes. Dr. Bikman references studies showing that thyroid resistance is real and measurable, often associated with elevated TSH and thyroid hormones in individuals with metabolic syndrome. He speculates that a ketogenic diet may enhance thyroid sensitivity in these individuals, reducing the need for higher T3 levels.

In conclusion, Dr. Bikman reassures those on a ketogenic diet that lower T3 levels do not necessarily indicate harm. If TSH levels are normal and no symptoms of hypothyroidism are present, the changes may reflect a healthy adaptation to the metabolic state induced by the diet.

Show Notes/References:

For complete show notes and references referred to in this episode, we invite you to become a Ben Bikman “Insider” subscriber. As a subscriber, you’ll enjoy real-time, livestream Metabolic Classroom access which includes live Q&A with Ben, ad-free Metabolic Classroom Podcast episodes, show notes and references, Ben’s Research Reviews Podcast sent to your inbox weekly, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews. You can learn more about becoming an Insider on our website: https://www.benbikman.com

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

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

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

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

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

Ben’s favorite exogenous ketone: https://www.americanketone.com (discount: Ben10)

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In this week’s episode of The Metabolic Classroom, Dr. Bikman delivers a comprehensive lecture on hormone replacement therapy (HRT), focusing on its role in addressing metabolic health challenges faced by women during menopause.

The loss of estradiol causes fat to redistribute from healthier storage areas, like the hips and thighs, to the abdominal region, where larger fat cells become more insulin-resistant and pro-inflammatory. This shift contributes to systemic inflammation and elevates the risk of cardiometabolic diseases. Ben explains how HRT, particularly with estradiol, can mitigate these effects by improving insulin sensitivity, reducing inflammation, and promoting healthier fat storage patterns.

He also addresses historical concerns about HRT, including risks of blood clots and cancer. Dr. Bikman explains that oral estrogens may slightly increase clotting risks due to their first-pass metabolism in the liver, but transdermal delivery methods like patches and gels do not carry this same risk. Regarding cancer, he highlights how older studies, such as the Women’s Health Initiative, overstated the connection between HRT and breast cancer, particularly when using estrogen-only therapies. Ben emphasizes the importance of evaluating the absolute risks, which are relatively small.

Beyond its metabolic benefits, HRT also shows promise in protecting against conditions like Alzheimer's disease. Ben discusses studies suggesting that HRT, when started early in menopause, may improve cognitive outcomes, preserve brain volume, and reduce the risk of Alzheimer’s, particularly in women with the APOE4 gene. These findings suggest that timely HRT may support brain health alongside its other benefits.

In conclusion, Ben underscores the substantial metabolic and overall health changes women face during menopause and the potential for HRT to improve quality of life, metabolic health, and long-term outcomes. He stresses the importance of individualized HRT plans tailored to each woman’s unique circumstances, allowing for a nuanced approach to mitigating menopause-related challenges.

visit https://www.benbikman.com

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

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

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

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

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

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

Ben’s favorite exogenous ketone: https://www.americanketone.com (discount: Ben10)

Show Notes/References:

Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: support@benbikman.com with your request, and be sure to mention which Metabolic Classroom episode you are referring to, which in this case is “Episode 80 - Hormone Replacement Therapy in Women”.

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During Dr. Ben Bikman’s latest episode of The Metabolic Classroom lectures, Ben explores the metabolic effects of nicotine, emphasizing its influence beyond its addictive properties and its association with lung health and its connection to insulin resistance.

Nicotine, a naturally occurring alkaloid found primarily in tobacco plants, is widely consumed through various products such as cigarettes, cigars, chewing tobacco, e-cigarettes, and nicotine replacement therapies like gums and patches. While most discussions on nicotine focus on its addictive qualities and respiratory impact, Ben highlights its significant effects on metabolism, including interactions with fat cells, insulin, and the nervous system.

Nicotine primarily stimulates the sympathetic nervous system by increasing the release of catecholamines like epinephrine and norepinephrine. These stress hormones activate the “fight or flight” response, resulting in elevated heart rate, blood pressure, and metabolic rate.

Nicotine’s ability to increase lipolysis, the breakdown of stored fat into free fatty acids, often leads to temporary weight loss. However, its chronic use disrupts fat metabolism by impairing mitochondrial fat oxidation, leading to fat cell hypertrophy (enlargement). This enlargement, particularly in visceral fat, contributes to insulin resistance, fatty liver disease, and systemic inflammation.

Ben also examines nicotine’s role in insulin resistance through its activation of specific cellular pathways. Nicotine increases ceramide production, which disrupts insulin signaling by deactivating key proteins essential for glucose uptake. Additionally, nicotine activates receptors like RAGE (Receptor for Advanced Glycation End Products) and TLR4 (Toll-like Receptor 4), which further drive ceramide production and inflammation. This creates a self-perpetuating cycle that exacerbates metabolic dysfunction and promotes chronic insulin resistance.

The classroom lecture highlights the paradoxical nature of nicotine’s metabolic effects. While it temporarily enhances fat metabolism and weight loss, chronic exposure reverses these effects, promoting fat storage, inflammation, and severe insulin resistance. Ben emphasizes the metabolic risks associated with nicotine, especially in the context of rising vaping trends among younger populations. He concludes by urging greater awareness of nicotine’s systemic effects, particularly its hidden role in metabolic health.

visit: https://www.insuliniq.com

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

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

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

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

Show Notes/References:

Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: support@insuliniq.com with your request, and be sure to mention which Metabolic Classroom episode you are referring to, which in this case is “Episode 79 - Nicotine and Insulin Resistance”.

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For The Metabolic Classroom lecture this week, Dr. Bikman explores the often-overlooked effects of oxalates on human health, with a focus on their impact on metabolic, kidney, cardiovascular, gut, and joint health.

Oxalates are natural compounds found in various plants, including leafy greens like spinach and kale, as well as certain nuts, seeds, grains, and legumes. They serve as a defense mechanism for plants against herbivores, as their high concentrations can cause irritation and reduce nutrient absorption. While often thought of as harmless, oxalates can act as “antinutrients” by binding to essential minerals such as calcium, magnesium, and iron, limiting their bioavailability and potentially leading to deficiencies.

Oxalates form crystals with calcium, creating a compound known as calcium oxalate. When these crystals accumulate in the body, they can contribute to kidney stones—a problem that affects many people. Ben explains that calcium oxalate crystals make up about 80% of all kidney stones, underscoring the connection between oxalate consumption and kidney health. Individuals prone to kidney stones, particularly those consuming high-oxalate diets or taking high doses of vitamin C (which the body can convert to oxalates), may face a heightened risk.

To mitigate oxalate-related health risks, Dr. Bikman suggests practical strategies, including reducing high-oxalate foods, ensuring adequate calcium intake to bind oxalates in the gut, staying hydrated to aid in oxalate excretion, and consuming fermented foods or probiotic supplements to support a healthy gut microbiome. He also highlights the importance of a balanced approach to vitamin C supplementation, as excessive intake may increase oxalate production in the body.

visit: https://www.insuliniq.com

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

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

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

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

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

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

Ben’s favorite exogenous ketone: https://www.americanketone.com (discount: Ben10)

Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: support@insuliniq.com with your request, and be sure to mention which Metabolic Classroom episode you are referring to, which in this case is “Episode 78 - Oxalates & Metabolic Health”.

#Oxalates #MetabolicHealth #KidneyStones #AntiNutrients #DrBenBikman #CalciumOxalate #GutHealth #Inflammation #JointPain #FermentedFoods #Microbiome #Probiotics #NutrientAbsorption #Metabolism #OxalatesInPlants

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During this week’s episode of The Metabolic Classroom, Dr. Bikman discusses the impact of microplastics on metabolic health, focusing on their effects on fat cells, insulin resistance, and blood vessel health.

Microplastics—tiny plastic particles under five millimeters—are now ubiquitous in our environment, entering the body through food, water, air, and skin products. Their pervasiveness poses serious concerns due to their accumulation in human tissues and the release of harmful chemicals like BPA (bisphenol A) and phthalates, which disrupt normal hormone functions and lead to various health issues.

Ben details how microplastics affect fat cell biology, particularly through BPA and phthalates, which mimic hormones like estrogen and testosterone, causing increased fat storage and even promoting fat cell growth and multiplication (hyperplasia and hypertrophy). This hormone disruption and fat cell expansion result in greater fat storage and elevated inflammation, contributing to insulin resistance, obesity, and chronic diseases like type 2 diabetes.

Professor Bikman also explores how microplastics affect vascular health, citing studies that show microplastic particles in atherosclerotic plaques. These particles attract macrophages that attempt to remove the microplastics but instead form “foam cells,” which contribute to plaque formation and heighten the risk of cardiovascular disease.

Ben concludes with recommendations to limit microplastic exposure, such as avoiding plastic containers for long-term water storage and choosing BPA-free, phthalate-free products, especially for food and beverages.

visit: https://www.insuliniq.com

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

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

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

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

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

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

Ben’s favorite exogenous ketone: https://www.americanketone.com (discount: Ben10)

Show Notes/References:

Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: support@insuliniq.com with your request, and be sure to mention which Metabolic Classroom episode you are referring to, which in this case is “Episode 77 - Microplastics & Metabolic Health: The Surprising Connection”.

#Microplastics #MetabolicHealth #FatCells #DrBenBikman #BPA #Phthalates #InsulinResistance #ChronicInflammation #EndocrineDisruptors #HeartHealth #Atherosclerosis #PlasticsInHealth #Metabolism #HormoneDisruption #EnvironmentalHealth #MetabolicHealth

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This week’s episode of The Metabolic Classroom focuses on the potential of continuous glucose monitors (CGMs) as a valuable tool not only for individuals with diabetes but also for anyone interested in gaining deeper insights into their metabolic health.

CGMs, which measure glucose levels continuously by detecting interstitial glucose, provide real-time feedback on how diet, exercise, stress, and sleep impact blood sugar, making them useful beyond their traditional application for managing diabetes.

Dr. Bikman highlights studies that showcase the variability in individual glucose responses to the same foods, which can be attributed to factors like gut microbiome composition. Ben cites a prominent 2015 study from Israel that revealed individuals’ glucose reactions to identical foods varied widely, showing the personal nature of glycemic responses and the role of CGMs in helping people manage their blood glucose variability.

Another study, from Stanford University, further illustrates how CGMs can reveal “hidden” glucose spikes, leading people to make more informed dietary and lifestyle decisions.

Dr. Bikman touches on the idea that, beyond personal use, CGMs have clinical benefits as well. Studies from the Scripps Research Institute and the Framingham Heart Study show that CGMs can detect early signs of prediabetes and diabetes in individuals who may otherwise go undiagnosed, providing a valuable tool for early intervention.

While there are critiques about CGMs, including concerns about potential overemphasis on glucose levels, costs, and possible psychological impacts, Dr. Bikman asserts that the advantages—such as improving insulin sensitivity, reducing glycemic variability, and empowering users to make healthier choices—outweigh these concerns.

Ben concludes by encouraging those curious about their metabolic health to consider CGMs as a practical tool for self-monitoring, with potential for significant long-term health benefits.

visit: https://www.insuliniq.com

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

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

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

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

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

Ben’s favorite exogenous ketone: https://www.americanketone.com (discount: Ben10)

Show Notes/References:

Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: support@insuliniq.com with your request, and be sure to mention which Metabolic Classroom episode you are referring to, which in this case is “Episode 76 - Using a Continuous Glucose Monitor (CGM) to Help You Improve Insulin Sensitivity”.

#InsulinResistance #CGM #MetabolicHealth #BloodSugar #DrBenBikman #ContinuousGlucoseMonitor #InsulinSensitivity #GlycemicVariability #Microbiome #Prediabetes #SelfMonitoring #HealthTech #DiabetesPrevention #MetabolicInsights #NutritionalScience #Hyperglycemia #Glycation #HealthOptimization

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In the recording of today’s livestream episode of The Metabolic Classroom, Dr. Ben Bikman explores glucosamine’s impact on both joint and metabolic health.

Glucosamine, commonly used as a supplement to alleviate joint pain, especially in osteoarthritis, is an amino sugar that plays a role in cartilage formation. However, its effectiveness in improving joint health is debated, with some studies suggesting modest benefits, while others find it no better than a placebo.

Dr. Bikman shifts the focus to glucosamine’s metabolic effects, explaining that due to its structural similarity to glucose, glucosamine can enter cells via glucose transporters, particularly GLUT1 and GLUT2. Once inside cells, glucosamine can contribute to the production of UDP-GlcNAc, a molecule that interferes with insulin signaling, potentially leading to insulin resistance and elevated blood glucose levels. This effect is particularly concerning for individuals with underlying insulin resistance or a family history of type 2 diabetes.

Ben refers to several studies, with most finding that glucosamine supplementation can impair insulin sensitivity and raise blood glucose levels in people with metabolic issues, while having little to no effect in metabolically healthy individuals.

Dr. Bikman concludes by advising that glucosamine may not be worth the risk for people with metabolic health concerns, while for those who are metabolically healthy, it is likely safe to use. However, he stresses the importance of monitoring blood glucose levels if taking glucosamine and suggests other strategies for improving joint health, such as improving insulin sensitivity and reducing uric acid levels.

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

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

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

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

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

Ben’s favorite exogenous ketone: https://www.americanketone.com (discount: Ben10)

visit: https://www.insuliniq.com

References:

Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: support@insuliniq.com with your request, and be sure to mention which Metabolic Classroom episode you are referring to, which in this case is “Episode 75 - Glucosamine and Metabolic Health: What You Need to Know.”

#Glucosamine #MetabolicHealth #InsulinResistance #BloodSugar #JointPain #Osteoarthritis #DrBenBikman #CartilageHealth #GlucoseTransporters #HexosaminePathway #InsulinSensitivity #Supplements #HealthEducation #MetabolismMatters #ChronicDiseases #DiabetesPrevention #Inflammation #JointHealth #Hyperglycemia

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In this episode of The Metabolic Classroom, Dr. Ben Bikman explores the metabolic implications of hyperglycemia, the condition of elevated blood glucose levels. He focuses on both the chronic effects, like those seen in diabetes, and the acute effects of glucose spikes, even from short-term dietary indulgences. Hyperglycemia, while often linked to insulin resistance and diabetes, also has a range of other negative consequences that can manifest even with occasional spikes.

One of the key points Dr. Bikman discusses is the relationship between hyperglycemia and insulin. As glucose levels rise, insulin levels rise as well, which can lead to insulin resistance over time, forming a vicious cycle. He highlights studies showing that even a short-term increase in carbohydrate intake can significantly raise fasting insulin levels and triglycerides. These changes have direct consequences on metabolic health, including an increased risk for cardiovascular disease.

Dr. Bikman also explains how hyperglycemia leads to oxidative stress, causing the overproduction of reactive oxygen species (ROS). This oxidative stress can damage proteins, lipids, and even DNA within cells. It also contributes to the formation of advanced glycation end products (AGEs), which are harmful compounds formed when glucose binds irreversibly to proteins, fats, or DNA. These AGEs are linked to various diseases such as retinopathy, kidney disease, and atherosclerosis.

The lecture further explores how hyperglycemia damages the endothelium (the inner lining of blood vessels) and degrades the glycocalyx, a protective gel-like layer on the endothelium. This damage increases the risk of cardiovascular disease by making blood vessels more prone to atherosclerosis. Additionally, high blood glucose levels lead to the glycation and oxidation of LDL cholesterol, making it more dangerous and likely to contribute to plaque formation in arteries.

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

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

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

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

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

Ben’s favorite exogenous ketone: https://www.americanketone.com (discount: Ben10)

visit: https://www.insuliniq.com

References:

Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: support@insuliniq.com with your request, and be sure to mention which Metabolic Classroom episode you are referring to.

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This week, during the Metabolic Classroom lecture, Dr. Ben Bikman examines the metabolic consequences of medications used for mental health, such as antidepressants and anti-anxiety drugs. Ben highlights the close connection between mental health disorders like depression and anxiety with metabolic issues, particularly insulin resistance and type 2 diabetes. These medications, while effective for managing mental health symptoms, often lead to metabolic side effects such as weight gain and insulin resistance, complicating the relationship between mental and metabolic health.

Dr. Bikman reviews key neurotransmitters—serotonin, dopamine, and norepinephrine—that influence both mental and metabolic functions. Serotonin helps regulate mood and appetite but can promote fat accumulation and inhibit fat breakdown. Dopamine is associated with pleasure and reward systems but also plays a role in regulating energy expenditure and fat metabolism. Norepinephrine, closely related to adrenaline, is involved in the body’s stress response and can stimulate fat breakdown and thermogenesis.

The lecture then shifts to the metabolic effects of common mental health medications, such as SSRIs, tricyclic antidepressants, and antipsychotics. While these drugs can stabilize mood, they are often linked to significant metabolic disturbances, including weight gain, insulin resistance, and cravings for carbohydrate-heavy foods. Ben notes that these medications may exacerbate underlying metabolic issues, potentially worsening the mental health conditions they are meant to treat.

Dr. Bikman concludes by emphasizing the importance of addressing metabolic health when treating mental health disorders. He highlights the role of brain glucose hypometabolism, where insulin resistance in the brain may contribute to anxiety and depression. He suggests that improving metabolic health through approaches like ketogenic diets could potentially enhance mental health outcomes by better nourishing the brain and restoring neurotransmitter balance.

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

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

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

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

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

References:

Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: support@insuliniq.com with your request, and be sure to mention which Metabolic Classroom episode you are referring to.

#MentalHealth #MetabolicHealth #Antidepressants #AnxietyMedications #WeightGain #InsulinResistance #DrBenBikman #MentalHealthMedications #DepressionTreatment #MetabolismMatters #HealthAndWellness #Neurotransmitters #Type2Diabetes #BrainHealth #SSRIs #Antipsychotics #FatMetabolism #MentalWellness #HealthyLiving #NutritionAndMentalHealth

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In this lecture, Dr. Ben Bikman explores liposuction, highlighting its popularity and effects on body fat. While body fat serves important functions like energy storage and hormone regulation, liposuction only removes subcutaneous fat, leaving visceral fat untouched. Dr. Bikman emphasizes that fat cell size, not total fat, is key to metabolic health, and larger fat cells can lead to insulin resistance.

Liposuction, though effective for quick fat removal, does not improve metabolic health or insulin sensitivity. Without lifestyle changes, patients often regain fat in different areas. He suggests that liposuction should be seen as a body contouring tool, not a health solution, but it may offer benefits for those with lipedema, improving pain and quality of life.

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

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

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

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

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

Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: support@insuliniq.com with your request, and be sure to mention which Metabolic Classroom episode you are referring to.

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In this week’s episode of The Metabolic Classroom, Dr. Ben Bikman clarifies misconceptions about lactate metabolism, emphasizing that there is no lactic acid in the human body—only lactate.

He explains that lactate is the end product of non-oxidative glycolysis, produced when cells, particularly muscles and red blood cells, require quick ATP energy. Dr. Bikman highlights that lactate production occurs during high-intensity activities where energy demand exceeds the capacity of mitochondria to generate ATP efficiently.

Contrary to popular belief, lactate is not responsible for muscle soreness or fatigue.

Ben delves into the history of lactate research, mentioning key contributors like Otto Meyerhoff, who identified lactate as a product of anaerobic metabolism, and Carl and Gerty Cori, who discovered the Cori cycle. This cycle demonstrates how lactate is recycled by the liver into glucose, which can then be used by muscles for energy. Lactate, once considered a waste product, is now understood to be an essential substrate for gluconeogenesis.

Dr. Bikman introduces George Brooks' lactate shuttle theory, which reveals that lactate is a viable energy source that can be directly utilized by mitochondria for fuel. He explains that this discovery revolutionized the understanding of lactate, showing it can be oxidized within cells for energy production rather than merely being excreted as a waste product.

Dr. Bikman also discusses lactate’s potential in clinical contexts, such as traumatic brain injury (TBI) recovery, where lactate can serve as an alternative energy source for the brain when glucose metabolism is impaired. Moreover, he touches on how lactate influences fat cells, promoting mitochondrial uncoupling and aiding in fat burning, contributing to metabolic health. Ben suggests that continuous lactate monitoring could help identify mitochondrial dysfunction and predict type 2 diabetes risk.

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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: support@insuliniq.com 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.

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My favorite meal-replacement shake: https://gethlth.com (discount: BEN10)

My favorite electrolytes (and more): https://redmond.life (discount: BEN15)

My favorite allulose source: https://rxsugar.com (discount: BEN20)

References:

Due to character length constraints, references are not posted here. However, for a complete list, we respond quickly. Please email: support@insuliniq.com with your request, and be sure to mention which classroom episode you are referring to.

#Longevity #Rapamycin #AgingScience #mTOR #Healthspan #Autophagy #MuscleHealth #BenBikman #MetabolicHealth #HealthyAging #AntiAging #FastingBenefits #InsulinResistance #ImmuneHealth #ProteinSynthesis #HeartHealth #TestosteroneHealth #ReproductiveHealth #ScientificResearch #MetabolismMatters #BenBikman #DrBenBikman

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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.

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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: support@insuliniq.com

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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.

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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.

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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.

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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: support@insuliniq.com 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.

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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: support@insuliniq.com 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.

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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: support@insuliniq.com 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

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#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.

https://www.insuliniq.com

#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

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

#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. 

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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 

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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.

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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.

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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.

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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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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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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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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/

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What's the best way to lose body fat? That's the question at the center of a multi-billion dollar tug of war. But when we focus on the fundamentals of metabolism, the answer becomes clear. Dr. Ben Bikman and the Insulin IQ Team discuss the simple truth.

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We hear it all the time from the media, medical figures, and even well-intentioned friends and family. "Fatty foods will clog your arteries". But are fats themselves really to blame? Dr. Ben Bikman and the Insulin IQ Team explain what the science says about that.

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Does high insulin lead to more migraine headaches? Dr. Ben Bikman and the Insulin IQ team examine the evidence showing why people who suffer from migraines may want to reevaluate their nutrition and lifestyle to control insulin.

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Your brain uses more energy than any other organ in your body, but the type of fuel you give it is critical for lifelong mental health. This week join Dr. Ben Bikman and the Insulin IQ Team as they discuss the direct link between what you eat and how it affects your chances of getting Alzheimer's disease.

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When our lives get busy, oft times the first thing that we drop is our sleep schedule. This episode of the Metabolic Classroom is your wake up call. You cannot sacrifice sleep. This week Dr. Ben Bikman and the Insulin IQ team review why getting enough sleep is absolutely vital to your metabolic health.

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Metabolic disorders are a chief cause of female infertility. But what you may not now is that they also lead to male infertility. This week Dr. Ben Bikman and the Insulin IQ Team discuss why even young men need to be aware of how their reproductive health is affected by insulin resistance.

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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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There is so much debate regarding the best diet. This is a preview of a study that explored the efficacy of a low-fat vs. low-carb diet in people depending on their insulin resistance status. A simple takeaway: anyone can lose weight on a low-carb diet, but only insulin-sensitive people will lose weight on a low-fat diet.

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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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