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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:

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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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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:

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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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