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Drugs that kill off old cells may limit a body’s aging (arstechnica.com)
94 points by rbanffy 7 months ago | hide | past | web | favorite | 83 comments

Humans live a lot longer than other animals of our size and have a lot of adaptions to let us live longer that mice don't. Seemingly for this reason lots of aging reduction techniques that work for mice don't work in us. So don't get too optimistic about this result.

This increase in lifespan is relatively recent in evolutionary history too so it can't involve too many genes, but yes it appears likely that the low hanging fruit may have been picked already by evolution.

On the positive side we live a lot less than animals like the bowhead whale or the Greenland shark. There is a lot (in theory) that can be done.

> This increase in lifespan is relatively recent in evolutionary history too so it can't involve too many genes

It could if it was just an epigenetic switch that was flipped to turn back on an old and complex adaptation. (Which presumably saw regular-enough use through the aeons to avoid genetic drift "rusting" it.)

And I'm optimistic about reversing aging in the long run, actually. SENS[1] has some good ideas for eventually solving most things that aren't cancer. It's just that straightforwardish methods that work in mice don't ever seem to also work in humans and there have been a number of these. Maybe it'll work but until we see better evidence I think it's not worth worrying about this.


The vast majority of the increase in average life expectancy is the massive reduction in childhood and childbirth mortality. All of which is a direct result of the massive improvement in the quality of medical care in the 20th century. Not very much genetic impact (such a massive genetic shift would have had to happen in 2-3 generations globally. A genetic source of such a massive change would be incredibly geographically biased: while there has been more more migration in the last hundred year than at any prior point in history, a genetic change would require a complete spread through the source population)

The genetic change I am referring to is since we split from our common ancestors the chimps and gorillas. Our ageing rate has more than halved since this split. This has been so rapid and so recent that it can't involve that many genes.

We diverged from apes around 7 million years ago, so assuming a way higher than reasonable average generation time of 50 years gives you 140k generations. If we assume a more reasonable turn around (based on 15 being a marriage worthy age in Romeo and Juliet) we easily get around 300k generations. That’s actually quite a lot for evolution to play with.

The low hanging-fruit of longevity has been picked by modern science and technology.

Socrates lived to 71. Meanwhile today NPR reported that rubbish pickers in Mumbai live on average to 39.

The part that really called my attention is this one:

>>Cells pick up damage all the time, either through environmental exposures or simply as a byproduct of their normal metabolism. If the damage is sufficiently critical, the cell will respond by committing an orderly sort of suicide called apoptosis, which keeps it from causing any further problems. For lesser damage, there's a less drastic alternative called senescence, in which the cell remains active and contributes its normal functions to the organism's health, but it commits to no longer dividing.<<

Old people, lots of senescence cells no longer dividing, young people, lots of young cells still dividing. Aging kind of makes sense when looked at it this way. As long as cells are able to keep dividing you may be able to stay relatively young.

Knowing nothing else it seems that you must keep the number of senescence cells low to keep the effects of aging at bay. Of course, it is probably much more complicated than this. At a minimum this may be a piece of the puzzle to figure out long life.

The key aging problem is that DNA damage is accumulating over the lifetime. Some cells reach apoptosis, some reach senescence, some reach cancer, some keep on being normal for a while.

Culling senescent cells does not undo the accumulated damage. You are making room both for cancerous and normal cells. Normal cells are still damaged though. I'm guessing the net contribution is still positive, but the specter of cancer is still looming.

On the bright side, I hope that cancer can be managed purely mechanically. Imagine dropping by for your weekly ultra-targeted radiation therapy to kill this week's tumors before going for lunch.

Do you have a source on the claim, that accumulated DNA damage is key? As far as I know, DNA damage happens all the time, is usually no threat at youth, and the real problem is rather the ever increasing inability to repair, or kill defective cells with age. (Getting a tan comes from the signaling of DNA damage, so cells are well prepared for this, to some extent) This is were senescence becomes very important. It's not the senescent cells themselves that become cancerous, but other dysfunctional cells which can flourish in a "fog" brought on by senescence signaling havoc and intracellular trash, obstructing internal and external kill commands. The weakening immune system is part of this too. There are other parts which become cancerous just by chance, like the endless recombinations in antibody creation will ultimately result in rogue lymphocytes. But usually cells can detect damage and repair it, kill themselves when unable to, or get killed when misbehaving.

There’s this https://en.m.wikipedia.org/wiki/DNA_damage_theory_of_aging

Damage happens all the time, and unrepaired damage accumulated over the lifetime, hence aging.

You have an interesting point with prevalence of senescent cells can interfere with natural immune response to cancer.

Thanks. I think we meant the same, and it's rather a question where your argumentation's starting point is set, because Wikipedia concurs, that DNA damage is caused by decreasing repair or apoptosis.

Anyway, I think this is where some lifestyle fads can become interesting. Sure, there are definitely some aspects to aging that are unaffected by this, but I think better chances of reaching current max human age are in our hands somewhat. Balancing IGF1 and frequently giving the body a break to repair, kill, and remove trash, are sound targets IMHO. So for me that is: restriction of certein makros, in particular animal proteins and refined carbs, early and midlife to lower IGF1 (raising it seems beneficial in old people); short term fasting every now and then. Both have shown to increase apoptosis and repair. It's not even hard to do, if you stick to a blue zone typical diet (plantbased diets are associated with double digit reduction in overall cancer risk, which is huge considering lifetime death by cancer risk is 1/5) and have a daily fasting window of 13+ h (eg. Shown to reduce reoccurrence of breast cancer). I focused on cancer here, because intuitively it seems like a good marker for DNA maintenance.

"plantbased diets are associated with double digit reduction"

How about a source.

> Imagine dropping by for your weekly ultra-targeted radiation therapy to kill this week's tumors before going for lunch.

I suspect if we ever reach such a distant future, we'll consider most radiation therapy to be a very blunt and barbaric instrument (even if ultra-targeted) and use some kind of nanotechnology instead. Some engineered virus or bacterium or nanomachine that hunts down the carcinogenic cells.

Silly question: how difficult would it be to extract your DNA code into digital format and then create cells based on that digital formatted DNA and put them into your body?

Note: not at all a biologist as you can probably see from the way I phrase things :)

I imagine it'd be far easier to just extract existing stem cells from the body, freeze them, and then every once in a while wake them up, culture some, and re-seed the body with them.

I'd rather have my cells replaced with transistors - one by one. That way I might have a chance to outlive that radio made in 1960...

Can you imagine if one of the cures to aging is safely removing senescent cells from the body? I'm not going to say its easy by any means, but it does seem straightforward in an unexpected way ("right under our noses"). Very exciting times in biomedical research. My hope is that anti-aging quickly accelerates into an industry instead of basic research (requiring checks, balances, all that jazz to keep the snake oil salesman and quacks at bay), which should allow for orders of magnitude of funding to flow into finding protocols for treatment (from an aging populace).

Eagerly awaiting reasonattlm's take on this.

You have to be careful not to cause cancer in the process.

From what I read, a lot of the things the body does, which have aging as a side effect, are intended to block cells from becoming cancerous.

For example a senescent cell - it might be damaged, and if it dived it might become a cancer, so better stop it from dividing. But we still need it, so don't kill it off.

Now you might think - actually, let's kill it and let some other cell divide and replace it. But that creates more cell division, which are more opportunities for cancer.

Basically, it's a delicate balance.

I suspect a different balance is also possible (there are animals without cancer for example), but the hard part is you must change all the parts at once (into the new balance), and simply stopping one part of the process will cause cancer.

This is going to make the research very hand without truly understanding all the moving parts, and joining all the different treatments into a single working whole.

What's needed is a fast-living animal, that ages, and gets cancer, in the same way humans do. Then you can just experiment without understanding.

> What's needed is a fast-living animal, that ages, and gets cancer, in the same way humans do. Then you can just experiment without understanding.

A simulated human?

I'm pretty sure that we're very far from that. We can't even simulate relatively simple processes in timely manner.

And all the much-heralded advances in AI still produce email notifications that are kind of like those old Ad-lib games where the blanks get filled in by gobbledygook.

And after listening to one sleep-inducing waterfall video for a single long night of sleeping the next day about 2/3 of my Youtube homepage's suggestions are about soothing, meditative, nature videos... what a laugh.

Sadly, no. Cells are very complex. Whole multicellular organisms are even more complex. We don't have models nearly good enough to replace laboratory experiments with E. coli, much less good enough to replace medical trials with humans.

Do we need to understand anything about how a multicellular organism works, if we have 1. a working model of biology on the intracellular level, and 2. a working model of stereochemistry outside the cell, and use these to just "play out" cell division from an initial gamete within a simulated womb?

(I know that's A Lot of computing power, but maybe an algorithm like HashLife could make this possible by, say, 2100?)

If it's possible to do something like this at all, I think it must be based on techniques largely yet-to-be-discovered. To accurately model biology on the intracellular level, you need a "map" of the cell down to the molecular level, plus fast, general, highly accurate methods for simulating molecular-level chemistry.

For the chemical simulation side of things, it would take many centuries of continued Moore's Law progress to make today's most accurate algorithms for fully quantum chemistry run fast enough. And the wild ride of Moore's Law already appears to be closer to its end than its beginning. We'd need fundamental algorithmic breakthroughs to make it feasible without relying on better simulation hardware solving the problem. That might be possible, but I don't when/how/if such algorithms may appear.

On the problem of getting a ground-truth molecular map of a cell in the first place, we know that there are many gaps in current models. We're not sure where all of them are. Even if you had the fast, efficient, vast molecular simulation capacity I sketched above, it would still take a lot of experiment/simulation comparisons to be sure that all the biologically relevant features had been captured in the original model.

Even now I'm probably badly understating all the problems on the biology side. I worked at the interface of chemistry, biology, and chemical physics, but I was more familiar with the software/physics side of things. I learned just about enough biology to be useful in my role and to be grateful that even my most complicated debugging sessions didn't involve 3 billion years' worth of undocumented legacy code running on wet nanotechnology.

>>Can you imagine if one of the cures to aging is safely removing senescent cells from the body?

At a minimum it seems that we are on the right track. Pretty exciting times.

> Can you imagine if one of the cures to aging is safely removing senescent cells from the body?

Very rarely are things in biology so simple. Everytime we thought something was useless in the past (junk DNA, appendix, tonsils, ...) it turned out that removing it causes damage somewhere else.

What the evolutionary purpose of the senescence cells inhibiting other cells? I feel like it may be a "let's slow down until we heal" type thing, which would indicate there's other mechanisms at play that explains why they aren't being replaced as they should. I could be totally off the mark though.

Also, I just looked up how they test grip strength on mice. It's equal parts funny and sad.

Senescence is a tool of embryonic development repurposed to wound healing and cancer suppression. Cells need to be suppressed once the finger is done being built at the end and the edges, and senescent cells do that job. Cancerous tissue needs to be suppressed, and senescent cells are there to do that job.

The problem is not that senescent cells exist, it is that there is not 100% coverage of their removal after they do whatever the short-term job at hand happens to be. It is the lingering ones that cause the harm.

So it's their inability to be replaced that's the issue - some other mechanism is failing us. I suppose in the short term removing the cells "manually" would help.

Also, cells with long telomeres eventually senesce, just like the "one-time job" cells with short telomeres, even though the long-telomere cells would be better off apoptosing instead (as long as there's a source of more cells.)

For anyone else wondering about the grip strength test...


The mouse is placed on a little metal grid that is attached to a scale, and somebody pulls on its little tail until it loses its grip on the grid. This seems like something a sadistic gym teacher invented.

The paper: https://doi.org/10.1038/s41591-018-0092-9 The usual sources for bypassing journal paywalls will work.

The lifespan curves in the paper are very nice: same slope, shifted to the right all the way down to 100% cohort mortality. The 36% increase in remaining life span refers to the difference between 140 days and 190 days to 50% cohort mortality in the control and treated group respectively.

Senolytic approaches that clear some fraction of senescent cells are highly reliable when it comes to extending life span and reversing aspects of aging in mice. The drug combination used here, dasatinib and quercetin, is cheap: $100-200/dose if you are shopping carefully. It is being trialed by the non-profit Betterhumans at the moment in a 65+ year old human group. Dasatinib is a generic, so there is absolutely zero interest in anyone taking this into a development program, which is a shame. None of the later pharmaceuticals have yet demonstrated any better results in terms of percentage of senescent cells killed off, but FOXO4-DRI has essentially no side effects.

(If you are interested, dasatinib pharmacokinetics and side-effects are pretty well described. E.g. https://doi.org/10.1124/dmd.107.018267 )

Based on reporting from the self-experimentation community, and first principles arguments, senolytics are something to take once every few years, and don't expect to see noteworthy effects unless you are into high cancer risk years or have something like obesity or early arthritis going on, in which more than the usual count of senescent cells will be in place. Senescent cell contribution to aging most likely scales in the same way as cancer risk and for the same reason, loss of immunosurveillance.

Or you could wait for the human trial results to be published. Those will start to emerge next year for various senolytic candidates.

An interesting thought: compelling evidence for senescent cells to be an important contribution to aging has existed for 30+ years. The research community deliberately avoided engagement with treatment of aging as a medical condition from the 1970s to a decade or so ago. It took a lot of advocacy and people coming in from outside the research community to make that change. If that cultural black hole for development had not happened, how much sooner could simple pharmaceuticals have been discovered that significantly addressed aspects of aging in humans through selective destruction of senescent cells?

Another thought: there has been the usual foaming at the mouth over the past decade among those who decry rejuvenation therapies as the purview of the ultra-wealthy. Dasatinib and quercetin at $100-200/dose, at one dose every two years or so? That is much closer to the future of longevity science that this wild tale of massively expensive approaches hoarded by the rich.

Turmeric contains quercetin and it is cheap. Certified organic for $13/lb. Sorry I don't have time to go through the paper and figure out the dosage vs tumeric and consider the absorption rate/ability. I take it daily with Japanese Knotweed. I really appreciate your comment.

Quercetin on its own is not significantly senolytic. Only in combination with dasatinib. See:


Another argument against quercetin on its own having any significant effect is that it is widely used in large enough amounts. It would be well known by now if it had significant senolytic effects, because everyone with arthritis would have found their conditions meaningfully improved. That sort of thing doesn't escape notice for long.

How does a non-cancerous person obtain a chemo drug on a regular basis?

With money I suppose. Lots of.

Vitamin D causes autophagy.

There is another way that recently gets a lot of attention, and it is drug-free. It's called "fasting". The practice is very old (holy books speak of it). Only recently one of fasting's method has been understood as "autophagy", which means "self-eating". When your body is starved for nutrients it turns to it's own tissues, and eats the weak/unhealthy cells first.


The 2016 Nobel Prize for Physiology or Medicine was awarded to Japan’s Dr. Yoshinori Ohsumi for his discoveries of the underlying mechanisms of autophagy.

I found a lot of interest on YT for this topic, and related "fasting" topics. With alternative "healers" gaining huge following with treatments that include fasting. Note worthy are Dr Morse (mostly juice fasts) and the Master Fast System (mostly intermittent fasts). Also I see a lot of people doing long water-fasts in combination with strength training for rapid weight loss.

Its a very interesting subject to me, and I have done some experiments with it myself, not without results.

Would you have any nice references to the long-fast + strength training? Whenever I've tried longer than 3-day fasts, any sort of excess exercise would cause a significantly unpleasant feeling and light-headedness.

There is not too much scientific "papers" on this topic. But there's a guy named "Chris" on YT with a channel named "A Healthy Alternative" and he does interviews with people about their journey/progress/methods. I really like that channel for specifically this water-fast + strength training topic.

There is something about taking some salts/electrolites/minerals with your water at some point to counter some things like light-headedness.

Thanks for the suggestions! They're greatly appreciated.

Most welcome. I live for this stuff lately. It has empowered my a lot. "Kidney filtration", "mucoid plaque", "gall and liver stone purge"; and the names are Morse, MFS, Ehret, Spira. Search for the term just mentioned on YT - and do not follow blindly. I'm just getting started myself and already the results are amazing. There's also a lot about food when you are not fasting, and this more often IS backed by science (fasting is only recently picking up interest in the scientific comm); see names like: Greger(!), McDouggal, Fuhrman, Eisselstein, M. Klaper, Barbara Popper. The workout thing has also been very well researched (you do not need much time to get big results), here see the bodyweightfitness routine on reddit, and AthleanX. A couple of hours a week is all it takes. I do gym bouldering myself, as it is a more fun way to do strength training (and strength training give most bang for the hours). Good luck! I hope you get the same incredible results!

Oh, and check out Tim Shieff current videos, he's an athlete and now on a 35+ day water fast (prolly going for the biblical 40 days). Really cool guy also. He takes quite some inspiration from a guys named Shaun, who also documented some really long fasts lately.

Keto + intermittent fasting is a great combo. You just feel better and less bloated day to day.

The hypothesis I have heard is that fasting and keto both result in ketone bodies and ketone bodies result in the cellular optimization (culling old cells so not spent precious energy resources on less efficient older cells).

IF this is correct, it means keto and fasting both accomplish the same thing in terms of life extension, only with keto you get to eat bacon, steak and cabbage, spinach, brussel sprouts, etc rather than starve and be miserable. :D

Fasting have other benefits than keto: it activates your immune system, increase you hormone levels, allows many organs to rest and clean themself. On top of the ketose, you $ start a selective autophagy process that improves further the cellular optimization.

You can perfectly use both if you know what you are doing. They don't mutually exclude. Although day to day keto is a lot of fat and meat. You may want to favor the vegetable part of keto after a long fast for some time.

>Although day to day keto is a lot of fat and meat.

People who do keto do get a majority of their calories from fat, but a majority of long term ketors tend to eat mostly low NET carb vegetables by volume. For example, you could eat a whole small cabbage in a day and not fall outside macros that would allow for a ketogenic state.

>Fasting have other benefits than keto: it activates your immune system, increase you hormone levels, allows many organs to rest and clean themself.

I have seen studies that show many of these as the same benifits of keto. For example, NAFLD resolves within only slightly longer on keto than by fasting. Keto is pretty effective at resolving PCOS for example.

Now, it maybe the case that fasting is more actually effective, but keto unlike fasting is sustainable as a long term lifestyle (conserves LBM etc).

As you pointed out, intermittent fasting and keto are completely compatible.

Of course you can do both but why let that stop you assuming things that aren't true?

and neurons too?

I'm no keto fan. But it sure as hell works. My experience is that with fasting I do not feel so hungry. It seems that when my colon is empty, my hunger feeling also stops for a large part.

You might have already seen this BBC program, but if not I suspect you will enjoy it:


Hmmm... perhaps the "self-eating" is consuming those weakened cells. They may be the first to get consumed when the body needs the nutrients it's deprived of.

Yes, autophagy is selective. That's the main selling point of long duration fasting. But it's only half useful. You have to go back to regular eating with a balanced diet, otherwise you don't get as much benefits as you could since reconstruction needs quality building blocks.

> Yes, autophagy is selective.

Is it? How does it affect lean body mass and muscle mass?

It will always eat a bit of it, even sane muscle, the process is not perfect. But old cells and sick cells are prioritized. That's one reason it has benefits in combination with chemo therapy : the body will target the cancer cells. Not only those, but it's enough to help.

Same with weak joints, old muscle bruises, etc.

But again, eating properly after the fast is important to let the body rebuild what it destroyed.

what about brain cells?

I haven't read any study on brain cells specifically. My guess would be that the mechanism is the same and is not locally different according to the different body parts but i can't be sure.

I hear so much of this fasting hype lately. People seem to conveniently forget that you:

1. Lose all your muscle mass.

2. Suffer malnutrition.

3. Destroy your stomach lining due to too much acid building up.

All for zero proven benefit.

But hey, people like TDD too, so I don't hold it against you.

1. Lose all your muscle mass.

Given that fasting is always temporary, and that in one week of fasting you only consume 25% more proteins than an entire active day (remember you are supposed to rest while fasting), it's doubtful. Especially since fasting activate the production of growth hormones.

Not that you won't loose a little muscle. Of course you will on long fasts. But "all your muscle mass" is just plain silly.

Also it just doesn't happen with intermittent fasting: you tend to gain muscle.

2. Suffer malnutrition.

Malnutrition is a condition you get on the long run. Not on a few weeks on not eating a year. Besides, the improvement you get on your digestive systems after putting it to rest improve your ability to absorb nutriments after the fact, so if you follow a balanced nutrition after your fast, you should actually be better off.

And any fast minded person will tell you that what you eat after a fast is as much important as the fast itself. Once you empty the body, you gotta fill it with good things to allow it to rebuild clean what the autophagy removed.

3. Destroy your stomach lining due to too much acid building up.

Acid production stops after a few days because there is nothing to digest. The rare cases where people suffered from stomach lining were people with terrible eating habits that had acid problems already and went full throttle on fasting. Nobody knowledgeable about the practice would forget to tell you how important it is to prepare your body days or weeks before you fast. Especially if you are not used to it.

Have you ever read any study about fasting at all ?

Regarding your 3rd point, there was a recent study that made the rounds here finding that fasting may actually be beneficial to intestinal wall lining (but no word on stomach lining): http://news.mit.edu/2018/fasting-boosts-stem-cells-regenerat...

I do a three day fast about twice a year. I started it as a way to burn up weak white blood cells, so I get new fresh ones. This is also a common regimen for cancer patients, fasting before they start a new round of chemo.


I have anecdotal evidence that it helps, as I seem to get sick less than I used to.

Fair enough. I'm going to edit it.

> This is also a common regimen for cancer patients, fasting before they start a new round of chemo.

Yes, not only fasting has a positive effect on cancer, but it lower the side effects of the chemo.

Thanks! Edited mine too.

I also suffer from heartburn that started way before I ever fasted the first time. In contradiction to the poster you were responding to, I find that it goes away, not gets worse, when I'm fasting. As you say, the acid does seem to stop getting produced during fasting.

I don't know how you were fasting (or if you actually tried fasting)

I have been doing intermittent fasting 3 days a week, each time 24 hours, for 6 months. I've lost 35 pounds thus far.

1.) I am still doing the same weights as 6 months ago, some muscle groups even more. I make sure I have a protein shake after.

2.) I did blood testing for everything with my doctor 3 months ago and last week. My doctor says i'm perfectly healthy

3.) again, if you're eating alot of complex carbohydrates after fasting, or before, your stomach will have more acids. the key is to reduce your complex carbs as well

Your criticisms are valid, however given the audience I doubt most Americans would actually 'fast,' and instead would simply skip dinner, wake up actually-hungry instead of just salty-fat-hungry, and perhaps lose a few pounds.

Plus, light fasting (aka, skipping a couple of meals) actually feels really good!

The fasting hype is mostly short term intermitten fasting. That doesn't lead to muscle loss. Leangains by Martin Berkhan is the most famous system of muscle building that used fasted training.

You seem to be extremely misinformed, and everything you have said is demonstrably false.

Please stop spreading fear and ignorance if you haven't taken the time to do the research.

People also seem to conveniently forget that being overweight is a problem. Also, intermittent fasting has none of the downsides you've mentioned.

Exactly how long do you need to fast to "lose all muscle mass" and "suffer malnutrition". You mean continual intermittent fasting or just not eating for a long duration? Any sources on this?

I have been intermittent fasting (one to two 24 hour periods a week) for several months and have lost fat and increased muscle mass with really no negative side effects. The key is to lift weights to prevent muscle loss and to eat reasonably balanced diets (and enough calories) on non fasting-days. “Eat Stop Eat” has a good overview of the science behind it all (I have no association with the author)

I think you will need to source all those claims, all the evidence I've seen is to the contrary.

For 1. you can see MMA fighters cut weight and not 'lose all their muscle mass' so that one seems to have some pretty stark evidence against it. Not to mention that body builders routinely go on bulking and cutting cycles specifically to put on more muscle.

MMA fighters and bodybuilders do lose significant muscle mass during their cutting phase, not to mention dehydrating the shit out of themselves. It's not a healthy way to live, and it's not undertaken by these athletes unless strictly necesssry.

Fat goes first. Saying that a theoretical body builder who isn't even trying to make a certain weight loses 'significant' muscle is not something that's backed up by even common sense. If that were true, how does anyone end up with more muscle after they lose weight?

> It's not a healthy way to live, and it's not undertaken by these athletes unless strictly necesssry

That's not the discussion, this has nothing to do with whether fasting destroys muscle mass.

Do you have anything to back up your claim?

MMA cutting is a terrible example.

They try to rid their body of as much water as possible to lower their weight.

When we say fasting for health it usually means lots of water, but no calories.

You are completely missing the point.

It isn't that MMA cutting is healthy, it is that fat is burned first, not muscle. Fasting for a day here and there isn't going to make someone 'lose all their muscle mass'.

I am too lazy to reply to everyone making stuff up, but you went way, way overboard. Bulking is eating a calorie surplus, cutting is eating at a light calorie deficit, it has nothing to do with fasting.

When fighters cut just before weight in, they do so to make sure that they make their weight class cut off or they can't compete. This has nothing to do with fasting - they are forced to do it to stay in weight class, but at the very top of it (being as heavy as possible is overall a boon in the ring).

I'm not sure what exactly you are saying. Fighters rapidly lose fat weeks out from the fight and they don't lose muscle (then they lose water weight, which is irrelevant here).

The idea that you think 'fasting' loses muscle mass is an idea that is not backed up by any evidence. Fasting isn't a diet, it is about when you eat.

Also, you didn't source anything. Don't you think maybe the dozen people replying to you might be less likely to be 'making stuff up?'

Some people theorize that alcohol works in a similar way for the brain.

Ethical issues aside (which is essentially the biggest issue to be solved), I could see great value in applying some software methods to biology, among which something akin to unit testing.

What would be needed is a way to reliably test drugs in conditions as close to in vivo as possible (if going full SF, we can imagine full warehouses of human bodies that would be bred, preferably without brains for those aforementioned ethical issues -- unless you are creating a dystopia universe -- for the purpose of testing drugs, and harvesting organs). I cannot imagine how big an impact it would have on healthcare, biology and more general human body-related issues.

SF technologies like prosthetics, cryo-preservation/life support, stem cell regeneration, embryology and in vitro fetus development, cloning for "body parts", and countless others would suddenly seem a lot closer.

I don't think that kind of thing will happen any time soon, though. It may happen in the future if alternative technologies can't replace it (simulation, nanoscale engineering).

Such topics can quickly become extremely philosophical. I initially wrote a paragraph on what dying means to me (maybe fine with it), etc; on which I think I could go on for pages, but I think it would be better to stop here :)

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