HoldsUp

Thomas Seyfried

Boston College

Thomas Seyfried, PhD, is a professor of biology at Boston College who specializes in the metabolic origins and treatment of cancer. He is the author of "Cancer as a Metabolic Disease" and co-developed the Glucose Ketone Index. His published research focuses on ketogenic metabolic therapy, mitochondrial metabolic theories of cancer, cellular fermentation mechanisms, and repurposed drug combinations for conditions such as glioblastoma.

26 claims checked on air: 4 context 5 contradicted 3 overstated 11 supported 3 unverified

What they said on air - contradicted

5 citing their own research

0:12:45contradictedlowtheir own paperEmily Kaplan and Dr. Seyfried: The oncology field must under

Mebendazole targets the glutaminolysis pathway to kill parasites and can kill cancer cells via the same metabolic target.

"We just published the mechanism in Purna's paper. We clearly showed that mebendazole targets the glutaminolysis pathway to kill the parasite, and also because the cancer cell is using the same pathway in part, then you—then you manage the cancers the same way." (said at 0:12:45)

Mebendazole's primary and well-established mechanism of action against parasites is the selective binding to helminth β-tubulin and disruption of microtubule polymerization, not targeting the glutaminolysis pathway. Similarly, in oncology research, its primary antitumor mechanism is described as the inhibition of tubulin polymerization alongside anti-angiogenic and signaling pathway alterations. While isolated preclinical studies have noted downstream metabolic effects such as glycolysis and glutaminolysis inhibition in specific glioma cell lines, glutaminolysis is not the recognized parasitic target or the primary antitumor mechanism.

0:33:00contradictedhighEmily Kaplan and Dr. Seyfried: The oncology field must under

About 50% of cancer deaths are caused by treatment-related complications rather than the cancer itself.

"And about 50% of people die from—they call it die from the complications of cancer. What's that? That's dying from the drugs that you use to treat the patient." (said at 0:33:00)

The claim that approximately 50% of cancer deaths are caused by treatment complications rather than cancer itself is contradicted by extensive epidemiological data and oncology clinical trials. The vast majority of cancer deaths are attributable to progressive underlying malignancy, metastatic disease, and tumor-associated organ failure. In population-based studies of metastatic cancer mortality, over 80% of deaths are directly due to the diagnosed cancer. Even in intensive treatment settings (such as pediatric oncology), treatment-related mortality accounts for roughly one-quarter of deaths, and in standard adult oncology regimens, treatment-related toxic death rates typically remain well below 5-10%.

0:51:00contradictedlowEmily Kaplan and Dr. Seyfried: The oncology field must under

Brain radiation increases extracellular glucose and glutamine levels, elevating blood sugar and upregulating cortisol in patients.

"They nuke people's brains freeing up massive amounts of glucose and glutamine and then are surprised... You irradiate a person, the blood sugar goes through the roof. Your whole body goes into a survival mode. Cortisol upregulated." (said at 0:51:00)

Clinical microdialysis studies in patients receiving cranial radiation for high-grade gliomas do not support the claim. Studies evaluating brain tumor extracellular fluid during radiotherapy found that extracellular glucose and glucose metabolites did not significantly increase. Furthermore, serum metabolome analysis found that circulating glutamine and other metabolites decreased rather than causing elevated blood sugar, and there is no evidence establishing that brain radiation induces systemic hyperglycemia via increased extracellular glucose and glutamine or cortisol upregulation.

1:05:24contradictedhighEmily Kaplan and Dr. Seyfried: The oncology field must under

All major cancer tumors ferment energy due to mitochondrial dysfunction, and no tumor grows uncontrollably without relying on a fermentation mechanism.

"We know that all major cancers that we have looked at, we have never found a tumor that's not fermenting as the result of mitochondrial dysfunction. We have never found that. I I Thomas Seyfried has a thousand reward for anybody to show us a tumor that's growing out of control not using a fermentation mechanism and we can't find any." (said at 1:05:24)

The claim reflects Otto Warburg's original 1920s hypothesis that cancer is fundamentally caused by irreversible mitochondrial dysfunction forcing cells into fermentation (aerobic glycolysis). Modern oncology and metabolic biochemistry have extensively refuted this universal generalization. Contemporary evidence demonstrates that mitochondria remain fully functional and intact in the vast majority of cancers. Many tumors maintain active mitochondrial oxidative phosphorylation (OXPHOS), some are predominantly OXPHOS-dependent, and metabolic plasticity allows tumors to utilize both pathways rather than relying exclusively on fermentation.

1:12:03contradictedhighEmily Kaplan and Dr. Seyfried: The oncology field must under

Omega-3 polyunsaturated fatty acids from fish oils lower triglycerides, whereas omega-6 polyunsaturated fatty acids are pro-inflammatory.

"So omega-6 versus omega-3s because the fish oils are polyunsaturated fatty acids and they're extremely healthy for you because we've seen triglycerides lowered. We did some big studies on this. But the omega-6 polyunsaturated fatty acids are pro-inflammatory." (said at 1:12:03)

While the first half of the claim is well-established—omega-3 fatty acids from fish oils reliably lower circulating triglyceride levels—the claim that omega-6 polyunsaturated fatty acids (PUFAs) are pro-inflammatory is contradicted by clinical evidence. Multiple systematic reviews and meta-analyses of randomized controlled trials demonstrate that dietary intake of omega-6 fatty acids (such as linoleic acid and arachidonic acid) does not increase systemic inflammatory markers (including CRP, TNF-alpha, and IL-6) in humans. The notion that omega-6 PUFAs promote inflammation is a mechanistic hypothesis that has not been supported by clinical intervention trials.

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