Reinhard Stindl, Dr. med.

Image

Current Research

My research interests focus primarily on the capping structure at the end of eukaryotic chromosomes, called telomere. I am particularly interested in the phenomenon of telomere shortening and its implications for human disease and evolution.

The telomere story goes back to the Nobel laureate Barbara McClintock. She did some milestone experiments in the thirties, showing that linear chromosomes without telomeres are unstable and undergo breakage-fusion-bridge cycles, resulting in chromosomal aberrations. In 1961, Leonard Hayflick discovered the limited replication potential of human cells. Ten years later, Alexey Olovnikov proposed that this 'mitotic clock' results from the end replication problem of linear DNA molecules, leading to replicative telomere erosion.

The species clock hypothesis

In August 2001, I started to develop a new theory of species extinction. According to the species clock hypothesis, telomere erosion between generations of a species leads to a populationwide telomere crisis and finally extinction (or the appearance of a new chromosomal race). An indicator for extinction would be a rise in the incidence of e.g. cancer, vascular disease and diabetes; diseases which have been linked to short telomeres and exhausted tissue regeneration. Most importantly, fertility would go down in the population. The paper got published in 2004. What we currently see in humans, is an increase of the so-called age-associated diseases...even in the middle-aged!
Cancer: The telomere/aneuploidy/differentiation block model

The claim was made by the Robert A. Weinberg group that three defined genetic elements (1) suffice to produce a human malignant tumour. (However, after a while it turned out that the authors mistakenly introduced at least four “defined genetic elements”; instead of a large T vector and in addition to hTERT and H-ras, a vector containing the entire SV40 early region including small and large T was used (2).)
Peter Duesberg (University of California at Berkeley) challenged these experiments (3, 4). As a postdoctoral fellow in his lab, I found that 100% of the supposedly diploid tumour cells (HA1ER-2, HA1ER-3) contained unbalanced chromosome aberrations (5, 6, 7). Identical chromosomal rearrangements were present in a large fraction (up to 89%) of the cells, which cannot be explained by the “outgrow of aneuploid variants” (5, 7) - after just 1 week in cell culture. My letter to Cancer Research never got published. Since then, I`m convinced that unbalanced chromosomal aberrations play an essential role in the causation of epithelial cancer (=carcinoma). The paper 'Defining the steps that lead to cancer: ...' got published!

The telomere gender gap theory
In developed countries, the average gap in life expectancy between the sexes is 7 years. It has widened over the last decades, despite the trend of women copying the ‘unhealthy’ lifestyle of men. On average, women do have longer telomeres than men at the same age, although mean telomere length at birth does not show any sex-related differences. This is almost certainly a consequence of men being usually taller than women, although nobody has done an investigation yet. Clearly, a larger body requires more cell doublings, especially due to the ongoing regeneration of tissues over a lifetime. The paper got published in 2004.

News
Selected for Who's Who in Science and Engineering, 2006-2007 www.marquiswhoswho.com July 2006
I just don't know why ... but if it helps support my theory on telomere erosion and species extinction, I very much appreciate it.

Der Standard

NatureAustralia (pdf)

The Guardian

Der Standard (pdf)

NewScientist      pdf

The Guardian      pdf

VFWF Poster Award 2003

UC-Berkeley Press Release

Juni 2006

Spring 2005

April 2005

April 2004

April 2004

April 2004

Nov. 2003

Jan. 2001
Selected Publications

Beyond Medline: Stindl, R. Old fathers and long-telomered offspring: elongation of telomeres in the testes of older men versus transgenerational erosion of germline telomeres. Iranian Journal of Medical Hypotheses and Ideas 5, 8 (2011) Link   pdf

Li, R., Sonik, A., Stindl, R., Rasnick, D. & Duesberg, P. Aneuploidy vs. gene mutation hypothesis of cancer: Recent study claims mutation but is found to support aneuploidy. Proceedings of the National Academy of Sciences USA 97, 3236-41 (2000).  PubMed

Duesberg, P., Stindl, R. & Hehlmann, R. Explaining the high mutation rates of cancer cells to drug and multidrug resistance by chromosome reassortments that are catalyzed by aneuploidy. Proceedings of the National Academy of Sciences USA 97, 14295-14300 (2000).  PubMed

Duesberg, P., Stindl, R. & Hehlmann, R. Origin of multidrug resistance in cells with and without multidrug resistance genes: Chromosome reassortments catalyzed by aneuploidy. Proceedings of the National Academy of Sciences USA 98, 11283-11288 (2001).  PubMed

Stindl, R. Tying it all together: telomeres, sexual size dimorphism and the gender gap in life expectancy. Medical Hypotheses 62(1), 151-154 (2004).  PubMed   pdf

Stindl, R. Is telomere erosion a mechanism of species extinction? Journal of Experimental Zoology Part B: Molecular and Developmental Evolution 302B, 111-120 (2004).  PubMed   Link   pdf

Stindl, R. Defining the steps that lead to cancer: Replicative telomere erosion, aneuploidy and an epigenetic maturation arrest of tissue stem cells. Medical Hypotheses 71, 126–140 (2008).  PubMed   Link   pdf

image
Click to enlarge

Stindl, R., Stindl, W. Vanishing honey bees: Is the dying of adult worker bees a consequence of short telomeres and premature aging? Medical Hypotheses 75(4), 387-90 (2010). PubMed  pdf

Contact

Reinhard Stindl, Dr. med.

Currently at:
Alpharm GesmbH
Seb.-Kneippgasse 5-7
2380 Perchtoldsdorf, Austria

Email
If you got any questions or comments, please send me a mail!

Curriculum Vitae

www.stindl.info

This site is best viewed with Opera 9.23 or higher.

last updated : 1 April, 2012 21:33