“Interestingly, SASP markers CCL-2/MCP-1 and IL-6 were found to be elevated in rapid agers compared to healthy agers. In addition, cystatin C (Evans et al., 2023) and C-reactive protein (CRP) were also elevated in rapid agers (Figure 4a,b). These data suggest that a subset of SASP and proinflammatory factors track with increased biological age independent of chronological age.”
https://onlinelibrary.wiley.com/share/2QA625QEICRNZXAYERBH?target=10.1111/acel.14104
Its an interesting paper, but I think suffers from a problem many papers suffer from. The body is not static. Biomarkers go up and down. Specifically IL-6/CRP goes up for a temporary infection and then goes down to a base line driven by sensecence. Hence if you simply take one measurement you will not get a proper picture of the underlying IL-6/CRP value.
Also
Consistent with our results, other studies have shown that upregulated HIF1α signaling impairs mitochondrial biogenesis and accelerates aging. Sirtuins are the main class of enzymes that destabilise HIF1α thereby promoting mitochondrial health during aging (Yuan et al., 2016). Similar to these reports, healthy agers positively associated with sirtuin signaling pathways, generally linked to longevity (Figure S2).
I think this just fits in with the conventional wisdom. HIF 1 alpha is upregulated by exercise. It is also upregulated by HBOT both of which are thought to have longevity benefits. We cannot have it both ways on this. I am not myself persuaded that the SIRTUINs (Class III HDACs) are miracle proteins.
I can see how this might apply with a high reading but wouldn’t it be meaningful if both metrics were very low?
That’s true. It all depends upon how accurate you want to be. I am in the sub 0.15 mg/L territory which is below the measurable threshold on the higher sensitivity tests. I would hence not be happy with 0.25mg/L without good reason.
Thinking about the evolutionary role of inflammation, I wonder if the harms of prolonged inflammation are described by some kind of J-curve where they begin to rise again (perhaps for different reasons) if inflammation drops below a certain level.