Any treatment that slows aging would show an effect in ordinary clinical trials, and no supplement has done so, says Morbid author Saul Newman
Any treatment that slows aging would show an effect in ordinary clinical trials, and no supplement has done so, says Morbid author Saul Newman
On October 20, Saul Newman, who won an Ig Nobel Prize for identifying errors in data on exceptionally long-lived people, answered questions from Reddit users. He discussed supplements, calorie restriction, epigenetic clocks, and conflicts of interest surrounding “blue zones,” regions with unusually high proportions of centenarians.
Newman bases his argument on Gompertz's law: after forty, the annual risk of death roughly doubles every eight years. On biological age, which he describes in terms of wear and tear on the body, he writes:
“If you reduced biological age by, say, eight years, the risk of dying from EVERYTHING would fall by half. That includes every disease that gets worse with age.”
The rate of aging is difficult to measure directly, he adds. Since age makes almost every disease worse, however, a treatment that slows aging would show up in trials as a treatment for everything. He says no supplement has shown this effect.
Newman gives this assessment of supplements containing NAD+, a molecule involved in cellular metabolism: “NAD+ supplementation did exactly what it promised biochemically, and had no effect at all on clinical outcomes.” He cites a review of 113 studies; a review of that size appeared in Ageing Research Reviews in 2026. It included 33 studies in humans and 80 in rodents. In humans, supplementation consistently raised NAD+ levels, while health effects varied and were often absent.
Calorie restriction extends lifespan in mice, but Newman suggests it may remove “external” causes of death unrelated to aging, which he compares to mousetraps:
“Adding or removing mousetraps (or risks like mousetraps) will shorten or lengthen a mouse's life without changing aging at all.”
A pooled analysis published in 2012 of experiments in yeast, worms, flies, and rodents found that dietary restriction extends lifespan by reducing both components of mortality: the component independent of age (“mousetraps”) and the component that increases with age.
Epigenetic clocks estimate biological age from chemical marks on DNA, a process called methylation. Newman writes: “Yes, DNA methylation predicts age. Your Amazon shopping habits predict it just as accurately or better.” Predicting age and changing it are different tasks, he adds. The authors of a 2024 paper in Nature Aging, including developers of these clocks, identified DNA sites likely to have causal links to age-related traits. Such sites were no more common among those used by current clocks than among other sites.
Discussing “blue zones,” Newman said he declined a paid trip to Sardinia because it seemed like a bribe: in his view, the company Blue Zones depends on questionable data showing unusually high proportions of centenarians. He says aging researchers Steven Austad and Jay Olshansky went on the trip, and that Austad subsequently published a paper challenging his work without declaring a conflict of interest and announced a partnership with the company.
In their 2025 response to critics of “blue zones”, Austad and his coauthor declared no conflicts of interest. In July, Olshansky told Australia's ABC that he and his colleagues had asked the founder of Blue Zones to fund a new institute. He sees no conflict of interest: “It doesn't affect the science.” In an article about Bolotana, Sardinia, published on October 5, he disclosed consulting fees for helping establish the institute. The American Federation for Aging Research (AFAR) launched the institute on October 13 in partnership with Blue Zones. Olshansky became chair of its advisory committee, and Austad, AFAR's scientific director, joined the committee.
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