Michael Ristow

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Michael Ristow (b April 24, 1967) is a German medical researcher who has published influential articles on the metabolic basis of human diseases, including type 2 diabetes, obesity and cancer, as well as general aging processes. Amongst more than 50 peer-reviewed scientific publications, Ristow published a seminal article describing a genetic mutation associated with extreme human obesity. [1]

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.

Ristow’s laboratory has provided direct evidence supporting the so-called Warburg hypothesis. Specifically Ristow has shown that forced metabolic activity and respiration of mitochondria efficiently blocks cancer growth [2] as anticipated by Otto Heinrich Warburg as early as in 1924.

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. Interestingly, 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.[3]

Most importantly, Ristow's research further suggests that this is a mithormetic effect. Hormesis is a controversial concept in which it has been demonstrated that the induction of a stress can lengthen lifespan in some species. Ristow interpred his results thusly: 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. In 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.[3]

These findings bring into question the free radical theory of aging by Denham Harman, and provide a mechanistic basis to question the application of antioxidants to human health. [4]

[edit] References

  1. ^ Michael Ristow, M.D., Dirk Müller-Wieland, M.D., Andreas Pfeiffer, M.D., Wilhelm Krone, M.D., and C. Ronald Kahn, M.D. (October 1, 1998). "Obesity Associated with a Mutation in a Genetic Regulator of Adipocyte Differentiation". The New England Journal of Medicine 339 (14): 953–959. doi:10.1056/NEJM199810013391403. PMID 9753710. 
  2. ^ Tim J. Schulz, Rene Thierbach, Anja Voigt, Gunnar Drewes, Brun Mietzner, Pablo Steinberg, Andreas F. H. Pfeiffer and Michael Ristow (2006). "Induction of Oxidative Metabolism by Mitochondrial Frataxin Inhibits Cancer Growth: Otto Warburg Revisited". J. Biol. Chem. 281 (2): 977–981. doi:10.1074/jbc.M511064200. PMID 16263703. 
  3. ^ a b Schulz TJ, Zarse K, Voigt A, Urban N, Birringer M, Ristow M (2007). "Glucose restriction extends Caenorhabditis elegans life span by inducing mitochondrial respiration and increasing oxidative stress". Cell Metab. 6 (4): 280–93. doi:10.1016/j.cmet.2007.08.011. PMID 17908557. 
  4. ^ Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C (2007). "Mortality in randomized trials of antioxidant supplements for primary and secondary prevention: systematic review and meta-analysis". JAMA 297 (8): 842–57. doi:10.1001/jama.297.8.842. PMID 17327526. 

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