The Metabolic Classroom with Dr. Ben Bikman

• The China Study Revisited - Science vs. Storytelling

  📢 Dr. Bikman’s Coaching Site, Insulin IQ: https://insuliniq.comand/or📢 Become an Insider, Ben’s website: https://www.benbikman.comIn 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 Hosted on Acast. See acast.com/privacy for more information.

  --------  

  20:54
• Does the HCG Diet Actually Work? What the Studies Really Say

  📢 Dr. Bikman’s Coaching Site, Insulin IQ: https://insuliniq.com📢 Become an Insider on Ben’s website: https://www.benbikman.comDuring 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 Hosted on Acast. See acast.com/privacy for more information.

  --------  

  27:23
• How Lectins Disrupt Insulin, Gut Health, and Immunity

  📢 Dr. Bikman’s Coaching Site, Insulin IQ: https://insuliniq.com📢 Become an Insider on Ben’s website: https://www.benbikman.comIn 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.comBen’s favorite yerba maté and fiber supplement: https://ufeelgreat.com/usa/en/c/1BA884Ben’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 Hosted on Acast. See acast.com/privacy for more information.

  --------  

  24:11
• How Lipoprotein Lipase (LPL) Determines Where Your Body Stores Fat

  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.

  --------  

  22:59
• The Metabolic Effects of Fluoride

  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.

  --------  

  19:06

More Health & Wellness podcasts

Trending Health & Wellness podcasts

About The Metabolic Classroom with Dr. Ben Bikman