Michael Ristow

Michael Ristow (b April 24, 1967) is a German physician.

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.

Main topic of Ristow’s interest is a common 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 has described a genetic mutation associated with extreme human obesity that was cited several hundred times in the scientific literature.

Later Ristow’s laboratory has, possibly for the first time, provided direct evidence for the so-called Warburg hypothesis and its relation to cancer. Specifically Ristow has shown that forced metabolic activity and respiration of small intracellular organelles named mitochondria efficiently blocks cancer growth as anticipated by Otto Heinrich Warburg as early as in 1924.

More recently Ristow has extended the relevance of mitochondrial metabolism by demonstrating that increased activity of these intracellular organelles due to impaired metabolism of the nutritive sugar glucose extends life span and prevents aging of a model organism, the worm Caenorhabditis elegans. This extension occurs (completely unexpectedly) by increasing oxidative stress due to increased mitochondrial activity. Most importantly the life-extending effect of the low-sugar diet is abolished by various antioxidants, suggesting that induction of oxidative stress may be required for health and extended life expectancy.

This latter process has been previously named mitohormesis or mitochondrial hormesis on a purely hypothetical basis, an suggests that increased mitochondrial activity and specifically generation of oxidative stress due to this metabolic increase exert positive biological effects ultimately promoting health and prevent aging. These findings significantly question the free radical theory of aging by Denham Harman, and provide a mechanistic basis for the questionable use of antioxidants in humans.