Instead of exercising, why not decrease the DAF 2 gene? (suggestions from the literature

"Decreased DAF-2 signaling also causes an increase in life-span." kimura et
 al! or is it the Insulin line
"Reduced signaling through the IGF type 1 (IGF-1) receptor increases life span in multiple invertebrate organisms. Studies on mammalian longevity suggest that reducing levels of IGF-1 may also increase life span."Lorenzini et al?

is it Mitochondrial activities as suggested by long et al:
"The traditional view of the role of mitochondria generated reactive oxygen species (ROS) in cellular aging...linked to "...."All of these appear to elicit mitochondrial retrograde signaling processes (defined as signaling from the mitochondria to the rest of the cell, for example, the mitochondrial unfolded protein response, or UPR^mt). The effects of mitochondrial retrograde signaling may even spread to other cells/tissues in a noncell autonomous manner by yet unidentified signaling mediators." long et al

are these some forms of cytokines ?

 It is assumed that such cytokine effect can act on FOXO3 in the substance Nigra:

"Parkinson's disease (PD) is characterized by the selective degeneration of neuronal populations presumably due to pathogenic interactions between aging and predisposing factors such as increased levels of α-synuclein. Here, we genetically modulate the activity of the transcription factor Forkhead box protein O3 (FOXO3) in adult nigral dopaminergic neurons" Pino et

It is assumed that such cytokine effect can act on FOXO3 in the substance Nigria:

if such cytokine is freed, they induces significant " consequences of their deregulation for tissue function and longevity." wang et al!

other researcher are focusing on UPR:

" In this review, we focus on the mitochondrial unfolded protein response (UPR^mt), a response to proteotoxic stress specifically in mitochondria, an organelle with a wide array of fundamental functions, most notably the harvesting of energy from food and the control of cell death." Jovaisaite et al!

THEY IMPLY THE LEVEL OF UPR COULD BE LINKED TO LIFESPAN
How this UPR is linked to Foxo3 or cytokine remains to be clarified...

Katoh et al
"Acceleration of ER-associated degradation in response to the accumulation of unfolded glycoproteins and insufficient interaction with calnexin/calreticulin in the ER lumen likely accounts for the increase of FOSs."
"C-fos but not c-jun expression was also suppressed in the diabetic group" Lu et al

could you follow age by level of c-FOS, we know here we are closer to Foxo3 in the epigenic area!


to be continued!........