Thomas Seyfried Explains Why Fenbendazole and Ivermectin Show Cancer-Fighting Potential
Thomas Seyfried Explains Why Fenbendazole and Ivermectin Show Cancer-Fighting Potential
In a short but powerful 30-second clip from the Thomas Seyfried YouTube channel, the renowned metabolic-therapy researcher lays out one of the clearest explanations yet for why antiparasitic drugs like mebendazole, fenbendazole, and similar compounds may have real anticancer potential. Speaking with characteristic directness, Seyfried states that these drugs hit two of cancer’s core energy pathways simultaneously: glycolysis and glutaminolysis. He emphasizes that cancer cells and parasites share a critical similarity — they both depend heavily on mitochondrial substrate-level phosphorylation, a primitive, fuel-scavenging mechanism that malignant cells rely on more than healthy ones.
Seyfried explains that when these drugs are used in the context of nutritional ketosis, their impact becomes even more pronounced. He describes them as “simple cheap-ass parasite drugs” that work because they exploit metabolic features shared between parasites and cancer cells. His conclusion is delivered without hesitation: “It works. It works really, really well.” While he acknowledges that the approach is not yet perfected, he stresses that the results show tremendous therapeutic promise with minimal toxicity, something rare in the landscape of cancer treatments.
Crashing Cancer’s Power Grid: How Fenbendazole Cuts Off Cancer’s Fuel Supply
Seyfried’s brief comments condense a substantial body of metabolic research into a few sentences. The fundamental idea is that cancer is, at its core, a disease of energy metabolism, not merely genetics. Tumor cells rely on two primary pathways for survival:
1. Glycolysis (Glucose Fermentation)
Cancer cells consume glucose at extreme rates to compensate for dysfunctional mitochondria. Fenbendazole and related benzimidazole drugs have been shown in preclinical studies to disrupt microtubules and impair glucose uptake, effectively throttling a tumor’s ability to produce ATP through glycolysis.
2. Glutaminolysis (Glutamine Fermentation)
When glucose is limited, cancer cells fall back on glutamine as a secondary fuel source. Seyfried explains that fenbendazole-like compounds also interfere with glutamine-driven ATP production, cutting off the backup system malignant cells depend on when glucose pathways are stressed.
Why Parasite Drugs Work: Shared Metabolic Vulnerabilities
Cancer cells and parasites both rely disproportionately on mitochondrial substrate-level phosphorylation—a primitive, emergency energy-generation mechanism. Healthy human cells use it minimally; cancer cells depend on it chronically.
Parasite drugs evolved to disrupt this exact process.
Cancer cells, by metabolic coincidence, get caught in the crossfire.
Why the Effect Is Stronger Under Ketosis
Nutritional ketosis reduces glucose availability and elevates ketones, which normal cells use efficiently but cancer cells cannot. When fenbendazole (and, in other clinical anecdotes, ivermectin) further disrupts glycolysis and glutaminolysis, the tumor is boxed into a metabolic corner with no viable energy source left. This creates a state of metabolic collapse, pushing cancer cells toward apoptosis while sparing healthy tissue.
Synergy With Ivermectin
While Seyfried mentions fenbendazole specifically, ivermectin has been shown in research to inhibit PAK1, suppress WNT/β-catenin signaling, and induce mitochondrial stress—all of which compound the metabolic vulnerabilities Seyfried describes.
Together, the two drugs may act as a dual blockade:
Fenbendazole: structure disruption + glucose/glutamine interference
Ivermectin: mitochondrial destabilization + survival-pathway inhibition
The result is a coordinated metabolic assault that aligns precisely with Seyfried’s metabolic theory of cancer.