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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