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During this mini lecture, Dr. Bikman tackles the popular misconception that building muscle requires carbohydrates and insulin spikes. He begins by reframing insulin's role—not as a muscle-building hormone, but primarily as an anti-catabolic signal that helps prevent muscle breakdown.
Contrary to long-held beliefs, insulin doesn’t directly stimulate muscle protein synthesis, even at high levels. Instead, the real muscle-building heroes are essential amino acids, particularly leucine, which directly activate mTOR and stimulate muscle growth—even in the context of a low-carb, ketogenic diet.
Dr. Bikman emphasizes that amino acids not only promote protein synthesis but also prevent muscle degradation—effectively replicating and even exceeding insulin's effects. He then shifts the focus to ketones, especially beta-hydroxybutyrate (BHB), which offer unique metabolic advantages. Ketones reduce the brain’s demand for glucose, thereby preserving muscle-derived amino acids that would otherwise be converted into fuel. They also improve mitochondrial function and resilience, support anti-inflammatory signaling, and protect against muscle loss during aging, bedrest, or intense training.
Drawing on published studies and findings from his own lab, Ben discusses how BHB helps preserve lean muscle mass, enhance ATP production, and resist oxidative stress. Research in rodents and humans shows BHB’s muscle-protective effects extend to both performance enhancement and recovery. Finally, he addresses exogenous ketones as a potential supplement for those who want the benefits of ketones without following a strict ketogenic diet. Whether you’re an athlete or simply seeking longevity, Dr. Bikman makes a compelling case that a well-formulated low-carb, high-protein, ketogenic diet can be optimal for maintaining—and even building—muscle.
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 with Ben after the lecture, ad-free podcast episodes, show notes and references, and online, live Office Hours access with Dr Bikman. It also includes Ben’s Research Review Podcast, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews. Learn more: https://www.benbikman.com
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This week’s Metabolic Classroom lecture is a deep dive into the metabolic roots of migraines—a condition that affects millions but is rarely discussed through the lens of insulin resistance and energy dysregulation.
Dr. Bikman explains that migraines are more than just headaches; they’re complex neurological events often triggered by disruptions in how the brain accesses and uses energy. When the brain becomes insulin resistant, its ability to efficiently metabolize glucose falters, increasing susceptibility to migraines due to energy shortfalls and inflammation.
Ben outlines how factors like mitochondrial dysfunction, oxidative stress, and low serotonin—often seen in people with poor metabolic health—are strongly associated with migraine onset. He highlights how common triggers such as glucose spikes, hormonal fluctuations, and inflammation are not just surface-level issues but symptoms of deeper metabolic dysfunction.
The lecture also presents a compelling case for ketogenic diets and ketone supplementation as therapeutic strategies. Drawing from both historical and modern clinical studies, Dr. Bikman shows how ketones can bypass the broken glucose pathways in the insulin-resistant brain, offering a cleaner fuel that improves cellular energy and reduces inflammation. Ultimately, the lecture emphasizes the need to address the root metabolic imbalances to reduce both the frequency and severity of migraines.
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 with Ben after the lecture, ad-free podcast episodes, show notes and references, and online, live Office Hours access with Dr Bikman. It also includes Ben’s Research Review 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. Bikman explains how rare genetic forms of obesity—known as monogenic obesity—reveal deep insights into how the body stores fat and why the “calories in, calories out” model falls short.
He introduces three genetic conditions—leptin deficiency, POMC deficiency, and MC4R mutations—that disrupt appetite control and fat storage, all while keeping calorie intake the same. These disorders highlight how hormonal imbalances, especially chronically elevated insulin, play the decisive role in whether energy is stored or burned.
Ben walks through the hypothalamic POMC pathway, a brain circuit central to hunger and metabolism. Disruptions in this pathway don’t just make people feel constantly hungry; they reprogram the entire body to hoard calories as fat, even when calorie intake is strictly controlled. Animal and human studies consistently show that these conditions drive dramatic fat gain without an increase in food consumption, clearly separating energy intake from energy storage.
In all three conditions, the common endpoint is hyperinsulinemia—chronically elevated insulin levels—which drives fat storage and insulin resistance. Whether leptin is missing, POMC signals are silenced, or MC4R is defective, insulin surges as the body shifts into extreme conservation mode. This reinforces the idea that obesity is often less about willpower and more about hormonal signaling. Understanding these rare conditions sheds light on more common forms of obesity and reveals that insulin—not just calories—is the gatekeeper of fat storage.
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 with Ben after the lecture, ad-free podcast episodes, show notes and references, and online, live Office Hours access with Dr Bikman. It also includes Ben’s Research Review 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, Ben explores the fascinating metabolic effects of yerba mate, a traditional South American tea that’s gaining attention in scientific circles. Yerba mate contains a synergistic mix of bioactive compounds, including xanthines (like caffeine), chlorogenic acid, and saponins—all of which contribute to its wide-ranging health benefits. Dr. Bikman explains how this unique brew supports fat loss, improves mitochondrial efficiency, regulates appetite, and enhances insulin sensitivity.
Drawing from human and rodent studies, the lecture highlights yerba mate’s ability to increase fat oxidation, particularly when combined with exercise. It also activates AMPK, a critical energy-regulating enzyme, which promotes glucose uptake and mitochondrial biogenesis. One of the most intriguing effects of yerba mate is its stimulation of GLP-1—both directly through the gut and indirectly by modifying the gut microbiome—making it a natural, non-pharmaceutical way to enhance satiety and insulin regulation.
Dr. Bikman also discusses the underappreciated role of bitter taste receptors in the body—not just on the tongue, but also in fat cells and the gut. Yerba mate interacts with these receptors to influence hormone release (like CCK and PYY) and to promote thermogenesis in brown and beige fat, offering yet another pathway for metabolic support. Finally, he shares unpublished findings from his lab showing yerba mate’s impact on hepatic redox balance, adding to its reputation as a powerful metabolic ally.
Ben’s favorite yerba mate and fiber supplement: https://ufeelgreat.com/usa/en/c/1BA884
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In this Metabolic Classroom lecture, Ben explores the concept of anabolic resistance—the body’s reduced ability to build and maintain muscle in response to stimuli like protein intake and resistance training.
This phenomenon, often associated with aging, also affects individuals with obesity or a sedentary lifestyle. Because muscle health is directly tied to longevity, strength, insulin sensitivity, and independence, understanding and reversing anabolic resistance is critical for long-term metabolic health.
Dr. Bikman explains the key drivers of anabolic resistance: reduced anabolic hormone levels, impaired amino acid delivery, inflammation, and cellular changes such as insulin resistance and intramuscular lipid buildup. He emphasizes the central role of the mTOR signaling pathway in muscle protein synthesis, and how factors like age, obesity, and inactivity blunt this response—even when adequate nutrients and exercise are present.
The lecture ends with practical strategies to overcome anabolic resistance, including resistance training, high-leucine animal protein intake, creatine, omega-3s, vitamin D3, and even peptides. Ben stresses that building muscle isn’t just about looking good—it’s about preventing frailty, insulin resistance, and loss of independence. Resistance training is non-negotiable, and diet alone will never be enough to restore optimal muscle health.
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 with Ben after the lecture, ad-free podcast episodes, show notes and references, and online, live Office Hours access with Dr Bikman. It also includes Ben’s Research Review 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 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)
Other products Ben likes: https://www.amazon.com/shop/benbikmanphd
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In this episode of the Metabolic Classroom, Dr. Ben Bikman explores a surprising and controversial dietary trend: the “sugar diet.”
Despite its name, this diet isn’t built around candy and soda. Instead, it promotes a very high intake of simple carbohydrates—primarily from natural sources like fruit, honey, and juices—while restricting both protein and fat to below 10% of total calories. This unusual approach has been gaining popularity, especially among lean, athletic men, some of whom report improved energy, body composition, and insulin sensitivity.
Ben traces the diet's philosophical roots back to the 1930s rice diet used for managing kidney and heart disease, noting how both rely heavily on low-protein, high-carbohydrate intake. He reviews studies in both animals and humans showing that the key metabolic shifts—such as increased mitochondrial uncoupling, fat loss, and improved glucose control—may not be due to the sugar itself, but rather to the restriction of protein. This triggers a spike in FGF21, a liver hormone that enhances energy expenditure and metabolic health.
The lecture also examines the limitations of this approach. Dr. Bikman points out that the diet appears to work only under very specific conditions: in metabolically healthy individuals, especially men, with high physical activity levels. For others, particularly those prone to insulin resistance, food addiction, or poor satiety control, such a high-sugar diet could be problematic. He emphasizes that, as with all dietary interventions, context matters.
Ultimately, this lecture doesn’t promote the sugar diet but uses it as a lens to highlight the underestimated power of protein restriction in driving hormonal and mitochondrial adaptations. Dr. Bikman urges caution and encourages further exploration of how individual physiology responds to dietary extremes.
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 with Ben after the lecture, ad-free podcast episodes, show notes and references, and online, live Office Hours access with Dr Bikman. It also includes Ben’s Research Review 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 lecture, Ben challenges the conventional insulin-centric model of type 1 diabetes by introducing the “bi-hormonal hypothesis” proposed by Dr. Roger Unger.
While insulin deficiency is a defining feature of T1DM, Dr. Bikman emphasizes the overlooked role of glucagon in driving hyperglycemia, ketone production, and muscle wasting. In normal physiology, insulin from beta cells locally suppresses glucagon from alpha cells. But in type 1 diabetes, this local regulation is lost, allowing glucagon to run unchecked—even when blood glucose is high.
Ben explains how injected insulin, although lifesaving, can’t mimic the precise intra-islet insulin levels needed to suppress glucagon secretion. This mismatch helps explain why blood sugar control can remain elusive despite appropriate insulin use. Excess glucagon ramps up liver glucose output and ketogenesis, creating a more complex hormonal storm than insulin alone can calm.
The lecture also explores new therapeutic strategies—including glucagon receptor blockers and GLP-1 agonists—that may help suppress glucagon more effectively. Dr. Bikman urges a shift in perspective: instead of seeing diabetes as just a disease of insulin, it’s time to recognize its bi-hormonal nature and tailor treatment accordingly.
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 with Ben after the lecture, ad-free podcast episodes, show notes and references, online Office Hours access, Ben’s Research Review Podcast, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews. Learn more: https://www.benbikman.com
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This Metabolic Classroom lecture explores the often misunderstood world of nitrates and nitrites—compounds historically feared due to their association with processed meats.
Dr. Bikman presents a balanced examination of their biological role, historical use, and potential risks and benefits. While concerns remain over their conversion into carcinogenic nitrosamines (mainly in animal studies), the real-world human data is inconsistent and largely correlational. In fact, vegetables are the largest dietary source of nitrates—not processed meats.
Far from being mere preservatives, nitrates and nitrites play a key role in converting to nitric oxide in the body, which supports vascular health, mitochondrial function, and even insulin sensitivity. Human and animal studies suggest nitrates can improve mitochondrial efficiency, promote blood flow, and enhance insulin signaling via cyclic GMP and PKG pathways. They may also encourage the browning of fat tissue, supporting metabolic flexibility.
Despite the correlation-based cancer fears often cited in media and observational studies, Dr. Bikman emphasizes the importance of context, dose, and confounding variables. He argues that nitrates and nitrites are bioactive compounds with legitimate metabolic benefits—far from the health villains they’re often made out to be.
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 with Ben after the lecture, ad-free podcast episodes, show notes and references, online Office Hours access, Ben’s Research Review Podcast, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews. Learn more: https://www.benbikman.com
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This Metabolic Classroom lecture with Dr. Bikman explores how the loss of estradiol during menopause affects five key metabolic systems: the brain, muscles, mitochondria, fat tissue, and inflammation.
Each of these systems relies on estradiol for optimal function, and its decline contributes to increased risk for cognitive impairment, muscle loss, reduced mitochondrial function, increased visceral fat, and systemic inflammation.
Ketones—particularly beta-hydroxybutyrate (BHB)—can provide a partial compensatory effect in each system. In the brain, BHB supports glucose metabolism, reduces neuroinflammation, and enhances neuroplasticity. In muscles, ketones reduce protein degradation and improve mitochondrial function. At the mitochondrial level, BHB promotes mitochondrial biogenesis and helps reduce oxidative stress through NRF2 activation.
The lecture also outlines how ketones affect fat tissue by promoting mitochondrial uncoupling and upregulating thermogenic genes like UCP1. Additionally, BHB helps reduce inflammation by inhibiting the NLRP3 inflammasome. A final section reviews exogenous ketone strategies—salts, esters, acids, and MCTs—as potential tools to support women through menopause-related metabolic changes.
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 with Ben after the lecture, ad-free podcast episodes, show notes and references, online Office Hours access, Ben’s Research Review 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. Bikman explores the MTHFR gene and how common mutations can affect overall metabolic health. Ben explains the biochemical role of the MTHFR enzyme in the methylation cycle, its influence on homocysteine levels, and its downstream impact on DNA repair, neurotransmitter synthesis, and detoxification.
Ben also discusses how impaired MTHFR function contributes to oxidative stress and insulin resistance, particularly through its effect on the insulin receptor’s expression and membrane insertion. He draws attention to the connection between poor methylation and chronic conditions like fatigue, hormone imbalance, and even cardiovascular risk.
The lecture also provides practical strategies to support healthy methylation, including the use of methylated B vitamins (such as methylfolate and methylcobalamin), food sources like liver, and appropriate cooking methods for plant-based folate. His emphasis throughout is on using targeted nutrition and lifestyle choices to compensate for genetic vulnerabilities.
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 with Ben after the lecture, ad-free podcast episodes, show notes and references, online Office Hours access, Ben’s Research Review 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. Bikman breaks down the true nature and benefits of creatine—a molecule often misunderstood as merely a muscle-building supplement. Creatine plays a critical role in cellular energy production by helping regenerate ATP, especially in high-energy tissues like skeletal muscle and the brain. While our bodies produce creatine endogenously, supplementation can significantly enhance its availability and effects.
Ben discusses how creatine has been shown to improve physical performance, support brain health, and even influence glucose metabolism. It helps increase strength, power output, and recovery during resistance training. In the brain, it supports cognitive function and may protect against neurodegenerative conditions. For individuals with insulin resistance or type 2 diabetes, creatine can improve glucose uptake by enhancing GLUT4 translocation.
He also addresses common myths—especially the misconception that creatine damages the kidneys. Ben emphasizes that while creatinine levels may rise with supplementation, this does not indicate harm in healthy individuals. He further explains the potential gene-level benefits of creatine, such as improved expression of IGF-1 and myogenic regulatory factors related to muscle health.
The lecture concludes with practical advice on dosing and choosing the right form of creatine, noting that creatine monohydrate remains the most effective and well-studied option. Ben encourages its use not just for athletes but for anyone looking to support muscle, brain, or metabolic health.
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 with Ben after the lecture, ad-free podcast episodes, show notes and references, online Office Hours access, Ben’s Research Review Podcast, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews. Learn more: https://www.benbikman.com
#Creatine #BenBikman #MetabolicHealth #ATP #InsulinResistance #BrainHealth #MuscleRecovery #CreatineMonohydrate #CognitivePerformance #EnergyMetabolism #GlucoseControl #Neuroprotection #MitochondrialHealth #SarcopeniaPrevention #Type2Diabetes #Nootropics #SupplementScience #KidneyHealth #MuscleGrowth #HealthOptimization
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In this Metabolic Classroom lecture, Dr. Bikman dives into the science behind nattokinase, an enzyme derived from natto—a fermented soybean staple in Japan. Nattokinase has gained attention for its cardiovascular benefits, especially its ability to dissolve blood clots. Ben explains the enzyme’s key role in degrading fibrin, the primary structural protein in clots, and how it stimulates the body’s own clot-dissolving pathway by activating plasminogen. He compares its action to pharmaceutical blood thinners like Warfarin but notes nattokinase may work without the same bleeding risks.
Beyond clot dissolution, Ben explores nattokinase’s effects on atherosclerosis. He shares clinical trial results where nattokinase reduced plaque size and arterial wall thickness, even outperforming statins in some metrics. The enzyme also appears to improve lipid profiles, including lowering triglycerides and slightly boosting HDL. Though Ben remains skeptical of LDL as a reliable heart disease predictor, these lipid changes are seen as beneficial.
The lecture also touches on how nattokinase might support metabolic health. Some human and animal studies suggest the enzyme improves insulin sensitivity, possibly by activating lipoprotein lipase and hormone-sensitive lipase, both involved in fat metabolism. Rodent studies also hint at a role in reducing lipid peroxidation, potentially decreasing levels of oxidized LDL, a strong predictor of heart disease. However, Ben notes more human research is needed to confirm these findings.
Dr. Bikman ends the lecture by acknowledging the limitations of current nattokinase research, such as small study sizes, inconsistent dosing, and questions around supplement bioavailability. Despite these gaps, he finds the cardiovascular evidence promising and suggests those interested might consider trying natto—the whole food source—rather than a supplement. While not a magic bullet, nattokinase offers compelling support for vascular health and metabolic resilience.
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 with Ben after the lecture, ad-free podcast episodes, show notes and references, online Office Hours access, Ben’s Research Review 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 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://ketone.com/BEN30 (discount: BEN30)
Other products Ben likes: https://www.amazon.com/shop/benbikmanphd
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📢 Dr. Bikman’s Coaching Site, Insulin IQ: https://insuliniq.com
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In this episode of The Metabolic Classroom, Dr. Bikman critically examines the claims made in The China Study, a popular book advocating for a plant-based diet based on correlational data from the China-Cornell-Oxford Project. While the book suggests that animal protein causes cancer and chronic disease, Ben emphasizes that correlation is not causation and points out that many of the study’s conclusions are misleading or unsupported by the raw data.
For example, some regions with higher meat consumption actually had lower cancer mortality, and wheat flour consumption showed a stronger correlation with heart disease than meat intake.
He also scrutinizes the rat experiments used to bolster the study’s conclusions. These studies involved pairing a powerful carcinogen with isolated casein (a dairy protein), resulting in cancer growth. However, Ben highlights that whole dairy, including fats like CLA and butyrate, may actually protect against cancer. He explains how isolating one protein and ignoring other nutrients misrepresents the effects of real, whole food consumption.
Ben then shifts to mechanisms and dissects the mTOR pathway, often cited in arguments against animal protein. He presents data showing that insulin—not leucine—is a much more potent and sustained activator of mTOR. This undermines the idea that animal protein is uniquely harmful and suggests that refined carbohydrates, which spike insulin, are more concerning in cancer development.
In conclusion, Dr. Bikman encourages viewers not to fear animal protein, especially when consumed with its natural fats in whole foods. He urges people to scrutinize bold dietary claims and recognize that refined carbs, not protein, are more consistently implicated in disease. While The China Study may have popularized plant-based eating, its scientific foundation is far less solid than many assume.
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 with Ben after the lecture, ad-free podcast episodes, show notes and references, online Office Hours access, Ben’s Research Review 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 Metabolic Classroom lecture, Dr. Bikman unpacks the history, claims, and science behind the controversial HCG diet.
Originally popularized in the 1950s by Dr. Albert Simeons, the diet pairs daily HCG hormone injections with an extremely low-calorie diet (around 500 calories/day). Simeons claimed that HCG helps target problem fat areas, preserve muscle, and suppress hunger. Ben explains HCG’s legitimate role in pregnancy and medical uses (e.g., infertility and hypogonadism), but emphasizes that its weight loss effects are unproven in non-pregnant individuals.
Ben reviews numerous randomized controlled trials and meta-analyses, all of which consistently show that HCG provides no measurable benefit over placebo for weight loss, hunger suppression, or muscle preservation. Anecdotal success stories may stem from the extreme calorie restriction or a placebo effect, rather than any metabolic impact of HCG. He explains that even pregnancy-level HCG doses only mildly affect thyroid hormones and that therapeutic doses used in the diet are far too low to significantly alter metabolism or fat-burning.
Biochemical and in vitro studies show that HCG may stimulate fat cell growth, particularly in newborns and under high concentrations, but it does not increase lipolysis in adult fat tissue. This contradicts the idea that HCG helps “melt” fat from stubborn areas. Furthermore, its role in reducing hunger is more likely due to nausea or psychological commitment rather than true satiety signaling.
In conclusion, Dr. Bikman cautions against using HCG as a shortcut for weight loss. The extreme calorie restriction is effective but unsustainable and potentially harmful. He recommends lowering insulin by controlling carbohydrates as a healthier first step, emphasizing a protein-focused, low-carb approach over starvation and hormone injections. He encourages individuals to base their choices on rigorous science, not fad claims.
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: https://www.benbikman.com
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In this lecture, Dr. Bikman introduces lectins as harmful plant-derived proteins often found in carbohydrate-rich foods like legumes, grains, and nightshades. While these molecules serve as plant defense mechanisms, in humans they can bind to gut lining cells, disrupting tight junctions and increasing gut permeability (leaky gut). This disruption allows bacterial fragments (e.g., LPS) to enter circulation, triggering systemic inflammation, which in turn increases insulin resistance, autoimmune reactivity, and cardiometabolic risk.
Lectins are also molecular mimics, capable of binding to insulin receptors and partially triggering insulin-like effects. This can lead to inappropriate fat storage, lipogenesis, and eventually insulin resistance as receptors become desensitized. Some lectins, like wheat germ agglutinin (WGA), have been shown in studies to both mimic and interfere with insulin signaling in fat cells—promoting fat gain and metabolic dysfunction even independent of calories.
Lectins are linked to obesity, cardiovascular disease, fatty liver, and autoimmune disorders. They can increase inflammatory cytokines, damage liver mitochondria, promote oxidative stress, and worsen non-alcoholic fatty liver disease (NAFLD). In susceptible individuals, lectins can also drive autoimmune flares, with evidence pointing to their role in molecular mimicry, leading to the generation of autoantibodies and aggravated immune responses.
While cooking methods like pressure cooking or fermenting can reduce lectin levels by up to 95%, they are never fully eliminated. Dr. Bikman concludes that for individuals with autoimmunity, insulin resistance, gut issues, or cardiovascular risk, reducing lectin intake may be wise. Monitoring markers like CRP, fasting insulin, and blood glucose can offer clues to lectin sensitivity, and while more human studies are needed, the biological plausibility and clinical observations make a strong case for dietary caution.
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: 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://ketone.com/BEN30 (discount: BEN30)
Other products Ben likes: https://www.amazon.com/shop/benbikmanphd
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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:
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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:
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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
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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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