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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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