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Apr 2

Editorial: No Trp, no B: surprising connectivity of diet, microbiome, aging, and adaptive immunity – Journal of Leukocyte Biology (subscription)

Ben Franklin quipped: In this world nothing can be said to be certain, except death and taxes; whereas todays polymaths might shudder in attempts to explain modern politics, interest abounds in current efforts that are starting to move the needle on lifespan. Modern medicine and public health practices have contributed an increase in life expectancy of >2-fold in the United States since Franklins era, as well as an increase of 8 y in the past 50 y and a 44% increase in the number of U.S. centenarians from 2000 to 2014 [1]. Can specific interventions that target aging push this progress even further?

Insights from biomedical research as to the molecular basis of aging have been used to generate treatments designed to slow aging or increase healthspan (i.e., healthy golden years). For example, clinical trials of nicotinamide mononucleotide are underway [2], and metformin, used to treat diabetes, is being tested in the Targeting Aging with Metformin study [3]. CR as an anti-aging intervention predates testing of these compounds and has been studied extensively in rodents and other model organisms. Clinical studies are in progress [4], but the jury is still out as to whether CR might be effective for humans.

The featured paper (Tryptophan restriction arrests B cell development and enhances microbial diversity in WT and prematurely aging Ercc1/7 mice) by van Beek et al. [5] reduces the complexity of CR interventions by feeding mice a diet only lacking Trp, as TR also delays aging of mice. This study breaks

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Editorial: No Trp, no B: surprising connectivity of diet, microbiome, aging, and adaptive immunity - Journal of Leukocyte Biology (subscription)

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