Hi everyone,
I check the site and the recent podcast to try and find an explanation to the study below but couldn’t find:
I think given the potential risk of exacerbating OA it is important to understand the background on this.
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Its an interesting study. Personally I think too much inhibition of mTORC1 is a problem as well as mTORC2. It may be that this restraint on growth exacerbates OA.
However, the study also needs to be done with intermittent rapamycin and also ideally with boron added to the Rapamycin group. I think the arguments for boron are so strong and the arguments against a low dose so weak that it is a bit of a no brainer for a control group in a test like this.
This, however, highlights the difficulty of testing when there are multiple potential interventions.
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Then there is also this research which seems to counter the study you posted, and its in an animal that is much closer to humans from a biological / evolutionary standpoint. But the first study posted in this thread also suggests that we should not ignore any increase in rapamycin induced hyperglycemia, should it happen to us (most people don’t report any issue like this).
RAPAMYCIN DELAYS BONE-RELATED HALLMARKS OF OSTEOARTHRITIS IN THE COMMON MARMOSE
adult rapamycin-treated marmosets display lower OA scores compared to control. Further, the age-associated increase in OA score trends to be delayed by rapamycin. Collectively, these data suggest rapamycin may be compressing the burden of OA to late life, which is consistent with the concept of healthspan extension.
https://www.oarsijournal.com/article/S1063-4584(22)00445-9/fulltext
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