Tuesday, September 24, 2013

How long you can live: Determination through the genes! DO YOU KNOW YOUR FOXO3 VARIANT?

Many patients that I meet these days stress during my interview with them that their own parents died of "old age".  Meaning that there seems to be a certain finality to life of humans.  There will be a time when despite good care and prevention, human life will end.  Patients deny their parents died of heart failure, stroke or any other cause but "old age" as if at some point we are doomed to a programmed death.  Inquisition into people who live longer (more then a hundred years) point to the existence of a gene, a particular variant FOXO3 (see below).  DO YOU KNOW YOUR FOXO3 VARIANT?
Evidence abounds now that how long we shall live is encrypted in our genes, but no one seems to rush to offer this option of an approach to care because it is not as simple as that!  But I still believe that for proper "advance directives" preparation of this information should be included as we gauge our sens of survival!   At the individual cellular level, basically this FOXO3,4,6 upregulates BIM and PUMA (wild animal in us keeping us alive!) and downregulates (FLIP) to slow programmed cellular death (Apoptosis).  The interesting thing is this FOX ability to work is very tightly linked to energy!  Yes, when you touch the FOXO, Galactose and Insulin metabolisms come right at you! As if telling you if you monitor me closely (as in Biomarkers) you may know what FOXY is doing.  In other words, the GALT gene is a good Biomarker of FOXO3.  And may tell you the status of cancer cells! (think carefully) during and after treatments!"
A variant of FOXO3 has been shown to be associated with longevity in humans. It is found in most centenarians across a variety of ethnic groups around the world.[7][8] The homologous genes daf-16 in the nematode C. elegans and dFOXO in the fruit fly are also associated with longevity in those organisms."
DAF-16 is the sole ortholog of the FOXO family of transcription factors in the nematode Caenorhabditis elegans.[1] DAF-16 is notable for being the primary transcription factor required for the profound lifespan extension observed upon mutation of the insulin-like receptor daf-2.[2] Moreover, the tractability of C. elegans as a model and interest in teasing out this conserved aging-associated genetic pathway allowed the intricacies of Insulin and Insulin-like growth factor (IGF) Signaling (IIS) to be thoroughly characterized primarily through studies using this model organism.[3]wikipedia

 "The expression of GALT is controlled by the actions of the FOXO3 gene. The absence of this enzyme results in classic galactosemia in humans and can be fatal in the newborn period if lactose is not removed from the diet. The pathophysiology of galactosemia has not been clearly defined.[1]wikipedia"
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