Last week Dr. Ed Calabrese released a new paper arguing that Hermann Muller’s 1946 Nobel Prize in Medicine/Physiology was strategically awarded to promote eugenics. Ed’s historical analysis highlights the interplay between science, ideology, and institutional power in shaping public and scientific narratives
After World War II, eugenics became stigmatized due to its association with the Nazis, yet the 1946 prize was still awarded to Muller, as many of his nominators were still eugenics advocates.
Ethical objections aside, the scientific principles of eugenics were eventually discredited, but the celebration of Muller’s work had a lingering effect on regulatory policies and the environmental movement.
If you missed it, Dr. Calabrese was recently a guest on Episode Six of Emily Unleashed and we encourage you to watch the interview. Dr. Calabrese is considered by many to be “Mr. Hormesis,” and asserts that low doses of harmful substances like radiation or chemicals can actually have beneficial effects by stimulating adaptive responses in cells.
In contrast, the linear no-threshold (LNT) model, which traces back to Herman Muller’s work, assumes that even the smallest doses of radiation or carcinogens can cause harm, with no safe level of exposure. The LNT approach has dominated the shaping of public health policies, yet it is based on a flawed understanding of biology and ignores the body’s ability to repair damage from low-dose exposures.
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Metabolic health, medical education, and the case for bringing clinicians and coaches together
At the 2026 Unbreakable Health Retreat in Miami, Emily Kaplan hosted a panel with Bob Kaplan, Professor Thomas Seyfried, and Dr. Derek Lee on what it means to treat cancer as a metabolic disease. They discussed the glucose-ketone index (GKI), nutritional ketosis, and strategies aimed at restricting the fuels cancer cells depend on while considering how metabolic therapy can fit alongside standard cancer treatment.
The conversation also addressed the practical realities patients face when trying to pursue a metabolic approach within the conventional oncology system, including questions about nutrition, repurposed drugs, inherited cancer risk, and how to evaluate different treatment options. Seyfried and Lee connected these clinical questions back to mitochondrial dysfunction, fermentation, and the metabolic vulnerabilities that may offer additional targets for cancer treatment.
An abbreviated version of this discussion is available here, for free.
At the 2026 Unbreakable Health Retreat in Miami, Professor Thomas Seyfried presented the case that cancer is fundamentally a mitochondrial metabolic disease rather than primarily a genetic one. He contrasts the dominant somatic mutation theory with a metabolic model in which impaired mitochondrial respiration drives a shift toward fermentation, dysregulated cell growth, and the mutations commonly associated with cancer.
Citing the work of Otto Warburg and research from his lab at Boston College, Seyfried explains how cancer cells rely heavily on fermentable fuels—particularly glucose and glutamine—and why mitochondrial dysfunction sits upstream of many of the genetic abnormalities seen in tumors. He also discusses reactive oxygen species, altered cellular signaling, and the role of mitochondria in regulating cell growth and behavior.
The presentation then turns to the therapeutic implications of this model. Seyfried explains strategies aimed at placing tumor cells under metabolic stress by restricting the fuels they depend on, including ketogenic metabolic therapy and approaches targeting glucose and glutamine. For Seyfried, the therapeutic target follows directly from the biology: restrict the fuels cancer cells depend on, exploit their metabolic weaknesses, and treat mitochondrial dysfunction as the central feature of the disease.
An abbreviated version of this discussion is available here, for free.
MetFix and BSI Members can view the full 54-minute video.
