Every time Icome across a report of some gene, protein, or hormone that is claimed to have the potential to make us live longer I am always very skeptical. Our bodies wear out and any effort to turn up the knob on activity in a type of cell or organ risks turning up the risk of cancer or some other disease that strikes when worn out cells are made to do more than they safely can do. This latest report provides an example. As the telomere caps on chromosomes wear down cells lose the ability to divide. So longer telomere caps good? Shorter telomere caps bad? Not that easy. Cells that can divide more times are cells that gain more chances to go cancerous.
New genomic research led by UC San Francisco scientists reveals that two common gene variants that lead to longer telomeres, the caps on chromosome ends thought by many scientists to confer health by protecting cells from aging, also significantly increase the risk of developing the deadly brain cancers known as gliomas.
The genetic variants, in two telomere-related genes known as TERT and TERC, are respectively carried by 51 percent and 72 percent of the general population. Because it is somewhat unusual for such risk-conferring variants to be carried by a majority of people, the researchers propose that in these carriers the overall cellular robustness afforded by longer telomeres trumps the increased risk of high-grade gliomas, which are invariably fatal but relatively rare cancers.
The research was published online in Nature Genetics on June 8, 2014.
A recurring theme at FuturePundit: If we could cure cancer we could run the risk of making cells able and eager to divide more times. The problem: On one hand, when aged cells replicate they run the risk of losing control and turning into cancer cells. On the other hand, we need cell replication in order to replace dead and damaged cells.
In undamaged cells long telomeres are good. In damaged cells restraints on cell divisions (and short telomeres are a restraint on cell division) protect against cancer.
“Though longer telomeres might be good for you as a whole person, reducing many health risks and slowing aging, they might also cause some cells to live longer than they’re supposed to, which is one of the hallmarks of cancer,” said lead author Kyle M. Walsh, PhD, assistant professor of neurological surgery and a member of the Program in Cancer Genetics at UCSF’s Helen Diller Family Comprehensive Cancer Center.
A story about how fasting seems to rejuvenate the immune system raises a similar question: Does a rejuvenated immune system as a result of fasting really reduce our risks of dying?
In the first evidence of a natural intervention triggering stem cell-based regeneration of an organ or system, a study in the June 5 issue of the Cell Stem Cell shows that cycles of prolonged fasting not only protect against immune system damage — a major side effect of chemotherapy — but also induce immune system regeneration, shifting stem cells from a dormant state to a state of self-renewal.
In both mice and a Phase 1 human clinical trial, long periods of not eating significantly lowered white blood cell counts. In mice, fasting cycles then “flipped a regenerative switch,” changing the signaling pathways for hematopoietic stem cells, which are responsible for the generation of blood and immune systems, the research showed.
Maybe some of those dormant old immune cells are genetically damaged and at risk of going cancerous. Maybe we are better off if we let cellular sleeping dogs keep sleeping.
What we need: the ability to tell cells with dangerous mutations to kill themselves. Cancers are the result of multiple dangerous mutations all happening in the same cell. If we could, say, send in gene therapy that would detect the risky pre-cancerous mutations and cause those cells to commit suicide (apoptosis for the biologically minded) then we could make our bodies safe enough for therapies that would turn up the knob on the healthy cells that aren't dividing enough.
|Share |||Randall Parker, 2014 June 08 08:04 PM|