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Michael Ristow

Michael Ristow
Born (1967-04-24) April 24, 1967 (age 49)
Lübeck, Germany
Nationality German
Fields Biochemistry
Institutions ETH Zurich, Switzerland
University of Jena, Germany
Harvard University, Cambridge
Joslin Diabetes Center, Boston
University of Cologne, Germany
Alma mater Ruhr University Bochum, Germany
Known for , metabolism

Michael Ristow (b April 24, 1967) is a German medical researcher who has published influential articles on biochemical aspects of metabolism and particularly the possibly health-promoting role of reactive oxygen species in diseases like type 2 diabetes, obesity and cancer, as well as general aging due to a process called .

Ristow was born in Lübeck in the North of Germany. He graduated at the University of Bochum in 1992 and received his M.D. from University of Bochum in 1996. He was appointed to the University of Jena in 2005 as a full professor in nutritional science, and is a full professor in energy metabolism at the ETH Zurich since 2013.

In 2007, Ristow’s group published evidence which could explain the basis of the observed extension of lifespan by restriction of sugar intake. In experiments on a model organism, the worm Caenorhabditis elegans, they found that lowering the availability of glucose extended the lifespan of the worms. It has been known since the 1930s that restricting calories while maintaining adequate amounts of other nutrients extends lifespan across a broad range of organisms. The mechanism has been proposed as a change in the activity of the sirtuins. Michael Ristow shows in his article that this effect can also occur independent of sirtuins, since worms deficient for sirtuins still show extended life span in states of sugar restriction.

Most importantly, Ristow's research suggests that this is a effect, as reviewed in.Hormesis is a controversial concept in which it has been demonstrated that the induction of a stress can lengthen lifespan in some species. Ristow's interpretation was that in response to a decrease in glycolytic energy production, the worms have to generate ATP by oxidative phosphorylation in the mitochondria, leading to increased production of reactive oxygen species. Due to a vacination-like response, the organism produces more defenses against oxidative stress, including increased production of catalase. Supplementation with antioxidants abolishes the increase in lifespan, and so does disruption of an AMP-kinase but not disruption of sirtuins.


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