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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:

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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:

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.

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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:

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

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