anciendaze
Senior Member
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We certainly know from personal experience that people with bad cases of ME/CFS may suddenly start to behave like much older people, despite earlier active lives. We have regularly heard that cells from severe ME/CFS patients resemble those from much older people. We have also heard that cells from healthy people start to behave like cells from patients if placed in blood from patients. The obvious thought was that there is something in patients' blood that makes cells act old. Another logical possibility is that there is something in the blood of healthy people which keeps their cells acting young.
Research on molecular genetics from the University of Exeter has shown that, at least at the cell level, it is possible to make old (senescent) cells start acting like young cells. (There is a spelling mistake in the report not seen in the actual article. The natural biochemicals are called resveratrols, and those used to mimic them in this research are called resveralogues, analogues of resveratrol.)
At this point we naturally get into controversy over the role of chemicals in certain food items like red wine and their effect on longevity. Arguments have raged over the role of certain chemicals as antioxidants. My opinion has been that really powerful antioxidants might even be dangerous, if this were in fact the mechanism of action.
Resveratrols, (there are a number of different chemicals,) appear naturally in the skins of various berries like grapes, blueberries or cranberries to limit growth of fungi and molds which would consume the sugars found within. It seems obvious that they must act as chemical signals associated with sugar metabolism. This is the first example I've seen connecting such signals with changes in RNA splicing in human cells. The mechanism seems to be considerably trickier than previously assumed.
Now, I'll add a caution, there is no evidence that more is better in people who do not have a specific deficiency in biochemical signalling. This would explain the poor statistical results of previous studies on health effects of "antioxidants", if they were mixing people who did not need them with people who did, and probably studying the wrong mechanism of action.
I'll also add a speculation about why such a limiting mechanism should be so highly conserved in organisms as different as fungi and humans. One clear way of distinguishing runaway growth, as in infection or cancer, is by glucose metabolism of cells. Limiting these things has undoubted evolutionary benefits. Here's an example of current research.
Research on molecular genetics from the University of Exeter has shown that, at least at the cell level, it is possible to make old (senescent) cells start acting like young cells. (There is a spelling mistake in the report not seen in the actual article. The natural biochemicals are called resveratrols, and those used to mimic them in this research are called resveralogues, analogues of resveratrol.)
At this point we naturally get into controversy over the role of chemicals in certain food items like red wine and their effect on longevity. Arguments have raged over the role of certain chemicals as antioxidants. My opinion has been that really powerful antioxidants might even be dangerous, if this were in fact the mechanism of action.
Resveratrols, (there are a number of different chemicals,) appear naturally in the skins of various berries like grapes, blueberries or cranberries to limit growth of fungi and molds which would consume the sugars found within. It seems obvious that they must act as chemical signals associated with sugar metabolism. This is the first example I've seen connecting such signals with changes in RNA splicing in human cells. The mechanism seems to be considerably trickier than previously assumed.
Now, I'll add a caution, there is no evidence that more is better in people who do not have a specific deficiency in biochemical signalling. This would explain the poor statistical results of previous studies on health effects of "antioxidants", if they were mixing people who did not need them with people who did, and probably studying the wrong mechanism of action.
I'll also add a speculation about why such a limiting mechanism should be so highly conserved in organisms as different as fungi and humans. One clear way of distinguishing runaway growth, as in infection or cancer, is by glucose metabolism of cells. Limiting these things has undoubted evolutionary benefits. Here's an example of current research.
