We're on the verge of going in circles here first because all of these terms need to be defined, for example " normal aging." This is beyond the scope of both of us it seems because even science has not been able to define it entirely. Even this website, which has made an attempt to define the "problems" of aging is not definitive.
How many of the things on this list would Q's have to cause to create the overall effect of accelerated aging? They do cause cell loss, mitochondrial mutations, cancerous cells ( hypothetically), extracellular matrix stiffening, and the debris of cellular damage over a very short period of time. The issue isn't that these things occur because they do in all humans but that they happen at a rate that exceed our biomachinery's ability to fix them. That's aging, would you agree?
Radiation is analagous. We can't feel it, but it is creating disease states that certainly mimic accelerated aging. A little radiation we can deal with -- too much, over a shorter period of time, and we die.
What would FQ's have to be doing in addition to these biological events that would define "accelerated aging" to you?
I didn't see anything about ECM stiffening. It looks like they can induce MMP expression resulting in ECM breakdown at a faster rate than it's repaired, but that's not what you see in typical aged tissue. I don't think we need to define every possible aspect of "normal aging" to be able to talk about the differences between young and old tissue. The various problems that SENS deals with don't seem to be in dispute. I'd like to see a good model for aging reproduce many if not most of those. FQs can, in at least a small percentage of people, cause some cell loss, but not the kind of loss seen in aging. I don't think there's any evidence that they cause cancer, and the debris of cellular damage isn't that much of a problem in aging, in that it gets cleaned up reasonably quickly. While I agree that aging is at least in large part caused by damage that accrues faster than we can repair it, FQs mostly cause a different kind of damage, which is why I think it's not a good model for aging. If we were to propose a project aimed at repairing the damage found in people who were injured by FQs, that would be different. Some of that technology might carry over to people who were injured in a variety of other ways. Unfortunately, I think such a project would be well beyond our expertise and ability. It's also outside of the remit of our organization, which is supporting the goal of curing aging.
FQS/GWS is certainly part of the landscape of one's aging, and I think you're shopping time points. I don't think there are long term studies on this. But if there is short term cell loss beyond the discontinuation of the drug, wouldn't that trend continue until the damage was cleaned up? In any case, aging means curing all of the things that are going to bring us closer to death. Everyone ages differently and through different pathologies. I'm lactose/galactose intolerant, drinking it or eating other things I'm sensitive to will give me skin problems and all sorts of things that will increase oxidative stress and hasten my aging.
I do like the idea of using our technology/expertise to repair the aging caused by FQs, that is interesting. But at the same time, if we find that FQs cause accelerated aging and hastens death (as I expect it will, it can't be good to have mitos not producing enough power, a slower metabolism is a symptom and cause of aging), then we've done our mission and brought another community to our forum who will sympathize/empathize with our mission. That's the real opportunity here. If you've been suffering from something like this, you're going to want to get younger and see an improvement in your health, not just resume life in a more aged and dull condition. People should understand that they can have higher expectations. I think this falls into the advocacy part of our mission.