In this Metabolic Classroom lecture, Dr. Bikman dives into the central metabolic role of lipoprotein lipase (LPL)—a largely unsung but crucial enzyme that governs whether fat is burned or stored and even where it accumulates in the body.

LPL is anchored to capillary walls in tissues like fat, muscle, heart, and lactating mammary glands. It acts as a metabolic gatekeeper, hydrolyzing triglycerides from circulating lipoproteins (like chylomicrons and VLDL) into free fatty acids. Depending on the tissue, those fatty acids are either burned (e.g., in muscle) or stored (e.g., in fat cells). LPL activity is influenced by hormones, diet, age, exercise, and weight status, and it plays a role in both fat distribution and metabolic disease.

LPL expression is highly tissue-specific and hormonally regulated. For instance, insulin increases LPL in fat tissue (promoting fat storage) and suppresses it in muscle (reducing fat burning), whereas testosterone suppresses LPL in subcutaneous fat, especially in the buttocks and hips—explaining fat patterning differences between sexes. In contrast, estrogen increases LPL in subcutaneous areas, which supports healthier fat distribution in women. Interestingly, low-carb diets and exercise reverse this pattern, increasing muscle LPL and decreasing fat LPL, thus shifting the body into a fat-burning mode.

Ben also explains how weight loss impacts LPL expression. During weight loss, LPL activity in fat tissue tends to decline, but LPL gene expression can paradoxically increase, setting the stage for weight regain. He cites long-term studies showing that individuals with higher adipose LPL activity after dieting are more likely to regain fat. LPL in muscle tissue, however, increases after weight loss and exercise, supporting greater fatty acid oxidation. Thyroid hormone also influences LPL in both fat and muscle, revving up metabolism in hyperthyroid states and lowering LPL activity in hypothyroidism.

Finally, Ben links LPL to real-world clinical questions, including its role in insulin resistance, statin effects, thyroid hormone therapy, and sex hormone treatments like TRT. He emphasizes that LPL doesn’t just respond to metabolism—it helps define it, and that insulin is the dominant regulator of this enzyme.

Show Notes/References:

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

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

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

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

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

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

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

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

Show Notes/References:

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

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

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

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

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

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

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

Show Notes/References:

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

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

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

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

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

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

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

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

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

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

Show Notes/References:

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

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

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

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

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

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

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

Show Notes/References:

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

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

📢 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

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

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

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

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

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

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

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

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

Show Notes/References:

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

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