Ways to Accelerate Biological Damage are Not Necessarily Interesting

If you spend time following life science research, you'll see a fair amount of work in which scientists remove a piece of biological machinery in laboratory animals so as to try to figure out what it does - the changes that occur in the studied animals will hopefully allow researchers to piece together the surrounding biology and place the machinery in the full context of what is already known. In many cases this reduces life span or accelerates the pace of some form of damage that normally increases with aging - but that outcome doesn't necessarily mean that the machinery removed is connected to aging in any significant way, or that it has any relevance to ways to slow aging and extend healthy life.

I'm sure, if you put your mind to it, you could think of a dozen ways to slowly ruin the type of machine you are most familiar with (clog up the spark plugs, remove the oil, pull out the filter head, and so forth), and few of them can be extrapolated the other way into ways to make a perfectly maintained machine last much longer than it normally does.

So it is with the biochemical machinery of life. The only true test of relevance to aging is to demonstrate that you can use the mechanism in question to extend life beyond the normal limits for a healthy individual in that species, or reduce some form of biological damage to levels far below what is normally the case at a given age. If all you are showing is that you can increase damage and shorten life span, then there's no doubt interesting science involved, but it's too soon to be getting excited.

This is why I think that the title and summary of a recent news item is absolutely wrong:

Researchers from the Universities of Bonn and Mainz have discovered a previously unknown function of the cannabinoid-1 receptor (CB1): it can protect against aging processes. Cannabinoids, such as THC (the active agent in Cannabis sativa) and endocannabinoids, and those formed by the body bind to the CB1 receptors. ... The animals in which the CB1 receptor had been switched off genetically [showed] clearly diminished learning and were less successful in their search for the platform. In addition, they showed a clear loss of nerve cells in the hippocampus, the researchers said.

The original paper, which is a matter of increasing damage only, has nothing but inference on how this applies to aging while CB1 is active and normally operational, and it's speculative to say that anything could come from this to move the needle in the opposite direction.

The reason I noticed this work at all is because it's possible that endocannabinoids are involved in calorie restriction in some way, based on work in nematode worms:

Not only have we been able to identify some of these molecules for the first time in the worm, but we have also been able to show they act as a signal of nutrient availability and ultimately influence the worm's lifespan. What makes this important is that the same molecules are present in both humans and C. elegans, so these molecules may play similar roles in both organisms. ... The molecules identified in the new study are N-acylethanolamines (NAEs), a group of signaling molecules derived from lipids that help indicate nutrient availability in the environment and maintain an animal's internal energy balance. [Researchers showed that] NAE abundance in the worm is reduced during periods of dietary restriction, and that NAE deficiency in the presence of abundant food is sufficient to extend the animal's lifespan. ... Importantly, this particular NAE is similar to endocannabinoids in mammals, which regulate many different physiological processes including nutrient intake and energy balance, as well as inflammation and neuronal function.

The CB1 paper above adds nothing much in the way of weight to that conjecture, however, and so I'd say it remains a fairly tenuous connection at this time. You'd need a study that shows extended life in mice through something very similar to NAE deficiency in worms, but engineered using endocannabinoids. So further research is required - and there are a great many more important things that researchers could be doing with their time.


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