Why Anti-Parasite Drugs May Work Against Cancer: Dr. Thomas Seyfried Reveals Emerging Mechanism
World-renowned cancer biologist Thomas Seyfried, PhD—a leading voice in the metabolic theory of cancer—has given one of his clearest explanations yet for why common anti-parasite medications such as mebendazole, fenbendazole, and possibly ivermectin have shown surprising anti-cancer activity in laboratory and clinical contexts.
For years, reports have circulated about these drugs suppressing tumour growth. But the mechanism remained unclear, and in some circles controversial. Seyfried now says: “We have a mechanism.”
Seyfried’s Key Insight: Parasites and Cancer Cells Share the Same Energy Weakness
In a recent discussion, Seyfried described taking a “deep dive” into why parasite drugs were producing anti-cancer effects:
“Mebendazole, fenbendazole—I did a dive on it and I said, why do parasite medications work against cancer cells? And it turns out that the parasites use mitochondrial substrate-level phosphorylation in the tissue … and mebendazole, fenbendazole kill these parasites.
So I tried it on the cancer cell and sure as hell, it targets the mitochondrial substrate and glycolysis.”
—Thomas Seyfried, PhD
His conclusion is striking:
Parasites rely on the exact same dysfunctional metabolic pathway that cancer cells rely on.
Both use a form of substrate-level phosphorylation (SLP)—a primitive, fermentation-based energy pathway that becomes dominant when mitochondria are damaged. This is the central claim of the metabolic theory of cancer: cancer is primarily a mitochondrial disease, forcing the cell to fall back to fermentative energy production.
Seyfried’s point is simple:
- Anti-parasite drugs kill parasites by choking off this energy pathway.
- Cancer cells rely on the same energy crutch.
- Therefore, these drugs can hit cancer cells even though cancer is not a parasite.
“So we have a mechanism now for why parasite medications are working, but cancer is not a parasite.”
The Ivermectin Question: Politics Delayed the Research
During the COVID-19 era, ivermectin became politically radioactive, and Seyfried openly acknowledges that he avoided engaging with ivermectin’s cancer-related mechanisms because of the political climate:
He didn’t want “to be associated with the politics around ivermectin.”
But others in the metabolic-nutrition field were not deterred.
Dr. Isabella Cooper Fills the Gap: Ivermectin Hits Mitochondrial Cell-Death Pathways
Dr. Isabella Cooper, PhD, a researcher in ketogenic science and hyperinsulinemia, explained to Seyfried the mechanism he chose not to investigate at the time:
“Ivermectin, it actually works on the mitochondrial cell-death pathway.”
—Dr. Isabella Cooper, PhD
This aligns with emerging literature suggesting that ivermectin can:
- Open mitochondrial permeability channels
- Trigger mitochondrial dysfunction specifically in cancer cells
- Induce apoptosis through ROS generation
- Suppress tumour energy metabolism
In other words: ivermectin may force damaged cancer mitochondria into programmed cell death, while leaving healthy mitochondria intact.
Convergence: Different Drugs, Same Target
What is striking is that these three unrelated drugs converge on mitochondrial energy metabolism—the Achilles heel of cancer cells:
- Mebendazole / Fenbendazole: Block parasite-type SLP energy pathways that cancer cells also exploit.
- Ivermectin: Pushes damaged mitochondria into apoptosis.
All three reinforce the metabolic theory of cancer:
target mitochondria → starve the tumour → restore energy control → trigger cell death.
The Bigger Picture: Cancer as a Metabolic Disease
These findings align with Seyfried’s broader argument that:
- Cancer is not driven primarily by random genetic mutations
- Mitochondrial dysfunction comes first
- Genetic instability comes second
- The most effective treatments target the cancer cell’s broken metabolism, not its DNA
Anti-parasite drugs, in Seyfried’s interpretation, are accidental metabolic therapies.
Conclusion
Seyfried’s latest clarification helps bring coherence to years of anecdotal reports and preliminary studies. While he stresses that anti-parasite drugs do not make cancer a parasite, their shared metabolic vulnerabilities appear to offer a credible explanation for their anti-cancer activity.
The door is now open for rigorous clinical trials that explore these medications not as fringe alternatives, but as potential mitochondrial-targeted adjuncts in cancer care.
World-renowned cancer biologist Thomas Seyfried, PhD, reveals “we have a mechanism now why parasite medications are working”.
Professor Thomas Seyfried: “Mebendazole, Fenbendazole [I] did a dive on it and I said, why [do] Parasite medications work against cancer cells, and it turns out that the parasites use mitochondrial substrate level phosphorylation in the tissue .. and mebendazol fenbendazol kill these parasites. So I tried it on the cancer cell and sure as hell, it targets the mitochondrial substrate and glycolysis”
Parasites rely on the EXACT same dysfunctional energy pathway cancer cells do and these drugs don’t care that cancer isn’t a parasite.
“So we have a mechanism now why parasite medications are working, but cancer is not a parasite”
Thomas Seyfried mentions avoiding researching Ivermectin because of political pressure during covid, but Dr. Isabella Cooper, PhD in Ketogenic Science and Hyperinsulinemia points out the mechanism for him:
“Ivermectin, it actually works on the mitochondrial cell death pathway”.
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