I'll offer a contrarian view: longevity research, as in the current scope, is about as accurate and useful as Ray Kurzweil's predictions from the 90s.
Let's take caloric restriction, for instance, which is all the rage. Trouble is, all of the evidence we have is in mice or lesser animals, and the comparison is animals on caloric restriction against animals being force fed to the point of obesity. Let me repeat that: in research that shows caloric restriction increasing lifespan in animal models, they are not comparing to animals on a normal diet. So it's entirely plausible all this caloric restriction research findings is just confirmation of the fact that obesity shortens lifespans.
This isn't even touching on the point that correspondence between animal models and humans is abysmally bad. It's the best we have, but there's a very good reason drugs need to go through three stages of human testing after it's been proven successful in animals. With caloric restriction, we don't even have consistent positive results in monkeys, only in rodents.
Has any of this longevity stuff ever been tested in humans? Obviously not, since it would take many decades.
While I agree with the general sentiment that CR is probably not very useful for humans, I think you are either misinformed or exaggerating for the sake of generating a response.
Ad-libitum feeding is not force feeding. Noone goes and shoves the food into mice. The food is just available.
Ok, I'll concede that calling it force feeding is a bit tabloid, but the end result I described is undisputed - ad libitum feeding results in obesity in the control animals. Which indisputably muddies the waters for the results, since you don't know whether CR extends lifespans or AL feeding shortens lifespans in these animals.
The dog study you link also highlights another issue with this kind of research: they focus on osteoarthritis, i.e. cartilege in joints being worn out over time, since that was the most common chronic disease. This occurred equally often in both groups, but time until first treatment for this condition was 25% longer in the CR group. That's exactly what you expect just from the 25% reduced body mass of CR fed dogs which they report, since reduced body mass puts less stress on the joints. No attempt is made to account for this, it is not even mentioned as a confounding variable.
Taken together with the fact that they don't observe any significant increase in maximum lifespan of the CR fed dogs, it's again very unclear whether this is anything more than confirming the well-established result that when you inevitably get a chronic disease, higher body mass means you get sick faster.
I still haven't really figured out how CR is supposed to be sustainable. I am around BMI of 19, and have been as low as 17 (6'2", 133lb). I become extremely unhealthy when I don't eat enough. As far as I know, I can't eat less and maintain the same weight. CR would, for me, send me to the hospital. Is CR just another name for "lose weight"? Is it working towards a goal rather than a lifelong steady state of living?
A simple interpretation of CR would be:
“additional leanness from a normal body weight may add health and life span delaying the process of aging.”
Regarding BMI, rule of thumb is 20-ish.
CR in the NIA study reduces body weight by 25%, so the NIA CR “man equivalent” will have a BMI of 20.8 (in the lower half of the normal weight category)
I have the same body type. I've read about people doing CR who go from average body type to something like your or my body type (I was once 6' 135lb but I've gotten up to 150lbs lately).
As the OP say, there's very little basis to CR given you're talking mostly animals that are overeating and under exercising by default.
And mice are genetically uniform. CR has been partly tested on monkeys and other animals but it's a lot harder and results less conclusive.
> So it's entirely plausible all this caloric restriction research findings is just confirmation of the fact that obesity shortens lifespans.
Not entirely. It's accepted now that caloric restriction helps fighting cancer, so that effect alone means people following caloric restriction will live longer on average. Those feeding the cancers will simply die younger.
Rejuvenation therapies and treatments that slow the progression of aging won't be tested in humans by waiting to see. They will be tested using quick before/after measures of biomarkers of aging. Those biomarkers are under development, and numerous types exist somewhere in the slow scientific process of standardization and debate. Here applied to calorie restriction, for example:
"We obtained data from the National Institute on Aging CALERIE randomized trial through its public-access biobank (https://calerie.duke.edu/). The CALERIE trial randomized N = 220 nonobese adults to 25% caloric restriction (n = 145; 11.7% caloric restriction was achieved, on average) or to maintain current diet (n = 75) for 2 years. We analyzed biomarker data collected at baseline, 12-, and 24-month follow-up assessments. We applied published biomarker algorithms to these data to calculate two biological age measures, Klemera–Doubal Method Biological Age and homeostatic dysregulation. Intent-to-treat analysis using mixed-effects growth models of within-person change over time tested if caloric restriction slowed increase in measures of biological aging across follow-up. Analyses of both measures indicated caloric restriction slowed biological aging. Weight loss did not account for the observed effects. Results suggest future directions for testing of geroprotective therapies in humans."
That said, it is quite clear that research into provoking stress response isn't going to do much for longevity in humans, even while it may do useful things for long-term health in the same way as exercise and calorie restriction do. In addition to calorie restriction, growth hormone receptor knockout can be compared in mice and humans with Laron syndrome - the large gains in mouse life span don't occur in humans.
However, research into repairing the damage that causes aging is a whole different ball game. A completely different strategy, set of mechanisms, overall approach, and effect on the individual. A reversal of aging rather than a slight slowing of aging. We have no idea how results in mice will map to results in humans. So it is worth keeping an eye on the ongoing pilot trials and forthcoming larger trials of clearing senescent cells in human patients.
What you’re describing is not only the opposite of sound science and more likely to fool you than improve your life, but also a potentially hazardous money-grab. It is incredibly important not to fool yourself, to roughly paraphrase Feynman.
Caloric restriction makes you live longer, but apparently so does exercise. The problem is though that exercise costs calories so you will be consuming more. How to square this contradiction?
Let's take caloric restriction, for instance, which is all the rage. Trouble is, all of the evidence we have is in mice or lesser animals, and the comparison is animals on caloric restriction against animals being force fed to the point of obesity. Let me repeat that: in research that shows caloric restriction increasing lifespan in animal models, they are not comparing to animals on a normal diet. So it's entirely plausible all this caloric restriction research findings is just confirmation of the fact that obesity shortens lifespans.
This isn't even touching on the point that correspondence between animal models and humans is abysmally bad. It's the best we have, but there's a very good reason drugs need to go through three stages of human testing after it's been proven successful in animals. With caloric restriction, we don't even have consistent positive results in monkeys, only in rodents.
Has any of this longevity stuff ever been tested in humans? Obviously not, since it would take many decades.
Some pointers for further reading:
https://www.sciencedirect.com/science/article/pii/S089158491...
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3765579/