Results From a Recent Rapamycin Life Span Study

There is some debate over whether rapamycin administration actually slows aging or only reduces cancer risk in mice: both sides argue the point from rigorous studies, but unlike many other compounds and methodologies the evidence for life extension in mice is strong and reproducible. These are debates over the cause of that life extension.

The recent paper quoted below comes from researchers who favor manipulation of mTOR as a way forward to treat aging, and who argue that rapamycin does slow aging. But again, from my point of view all such efforts to develop drugs to alter metabolism to modestly extend life are the slow, expensive road to a poor end result. We should be focused on building therapies to repair the damage that causes aging, an end result that is both of greater utility and can meaningfully help old people. There is not much use in a way to slow aging when you are already old.

Target of Rapamycin (TOR) is involved in cellular and organismal aging. Rapamycin extends lifespan and delays cancer in mice. It is important to determine the minimum effective dose and frequency of its administration that still extends lifespan and prevents cancer. Previously we tested 1.5 mg/kg of rapamycin given subcutaneously 6 times per two weeks followed by a two-week break. This intermittent treatment prolonged lifespan and delayed cancer in cancer-prone female FVB/N HER-2/neu mice.

Here, the dose was decreased from 1.5 mg/kg to 0.45 mg/kg per injection. This treatment was started at the age of 2 months (group Rap-2), 4 months (Rap-4), and 5 months (Rap-5). Three control groups received the solvent from the same ages. Rapamycin significantly delayed cancer and decreased tumor burden in Rap-2 and Rap-5 groups, increased mean lifespan in Rap-4 and Rap-5 groups, and increased maximal lifespan in Rap-2 and Rap-5 groups. In Rap-4 group, mean lifespan extension was achieved without significant cancer prevention.

The complex relationship between life-extension and cancer-prevention depends on both the direct effect of rapamycin on cancer cells and its anti-aging effect on the organism, which in turn prevents cancer indirectly. We conclude that total doses of rapamycin that are an order of magnitude lower than standard total doses can detectably extend life span in cancer-prone mice.



I know someone who has actually been on Rapamycin, I can tell you that they NOT keen to try it again.

It caused the activation of dormant herpes simplex virus in their face (on the lips and nose). Basically they got super painful cold sores from it (this person never normally got cold sores). By super painful, I mean just about needing really strong pain medication to get through the day painful.

Posted by: Jim at February 28th, 2014 9:02 AM

These were, as the abstract says, FVB/N HER-2/neu transgenic mice, which are extremely cancer-prone because they carry mutations in the same ErbB-2 oncogene that is targeted by Herceptin. This study may or may not tell us anything about the treatment of cancer generally, breast cancer generally, or HER2-positive breast cancer, but we can be quite confident in ignoring it as a clue about the use of rapamycin as a longevity/healthspan-enhancing drug in normal people without existing malignancy.

Posted by: Michael at March 1st, 2014 11:30 AM
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