Big Freeze is much more likely to occur!
Back in junior high school in the 1960’s, we had to write a science fiction short story. Around that time, cryopreservation was just starting to hit the public radar—probably thanks to Robert Ettinger. I was hooked.
My story was about a guy (me, of course) who saved a decent chunk of money—maybe $100K—and arranged to be frozen at death. The twist was that when I was finally reawakened, it wasn’t just because of a medical breakthrough—it was the power of compounding interest. The money had grown so much over time that reviving me was economically justified. I woke up fabulously wealthy.
So yeah, cryonics and longevity have been on my mind a long time. Even back then I figured the best plan was: don’t die, stay invested, and let time do the rest.
Fast-forward to now, and I appreciate people like Brian Johnson pushing the edge on “don’t die” as a daily operating system—not just a Hail Mary. I was a pensive youth, already brooding on the long-term possibilities before I even had a checking account.
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Being frozen while the magic of compounding does it thing is the most spectacular story ever written by a junior high school student!!!
This is something that would make Warren Buffett proud.
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Watching my Dad die at 47 did it for me. Followed by reading Ray Kurzweil, though I don’t have hope for LEV, long healthspan and lifespan would be great.
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47 your dad was relatively young that sucks. But, in the rest of the world and our past for countless generations it was fairly normal to die in your 40’s or 50’s suddenly. And actually, it’s not all that uncommon to die in your 20’s from car accidents, drug overdose, or other modern ailments and disease. New technology, new ways to die it seems…often wonder if we really made any progress at all where it counts.
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That’s cool you started young when you got into this. Yeah, while I agree with others that immortality seems impossible in our lifetimes, I know for a fact that we live in a crazy world with insane possibilities made real, so I don’t discount the possibility.
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While I believe aging is inevitable, as is death, I do also believe that humans have genetic predispositions to longer life, or not. My 98 year old mother has severe dementia but is remarkably sound in body, still. And she never exercised, nor did she eat well. Her mother and sister, the same. But they all (as do I) seem to conform to what I think of as a “catabolic” or slow growth phenotype. And I may be wrong about this, but I think that the main mode by which rapamycin may extend life is by pushing away from the growth or anabolic toward the slowed growth catabolic. Since I am naturally positioned on the catabolic end of the spectrum, I decided not to take rapa. But I do try to behave well along all the dimensions, diet, sleep, exercise, BMI/calorie restriction, etc,
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I often find the long term trends helpful for my personal optimism. World in Data is my go to 
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But… don’t you think you could prevent dementia or alzheimer’s potentially using rapamycin. As you see it in your mom.
Matt Kaeberlein says using rapamycin before onslaught can prevent dementia and many cancers.
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Could Rapamycin prevent or delay Alzheimers? I would feel more persuaded if I could understand the mechanism of action – how does it prevent…? For example, I take Raloxifene, which is a selective estrogen reuptake modulator (“SERM”). It works by lodging in the estrogen receptors in the breast, thereby preventing estrogen from stimulating the breast cells. Since I had a very tiny, very indolent estrogen driven cancer, taking raloxifene makes sense – I understand how and why it is appropriate for me. It is also low risk and helps with bone remodeling. Similarly, snorting insulin seems to make sense for me personally since I have very low endogenous insulin, and research has shown that intranasal insulin can help the brain utilize glucose and can be neuro protective. So I understand why it might be protective and a good idea for me personally. And it is low risk.
I would love to understand how rapamycin might protect against Alzheimers. What is the mechanism? I think that if my major worries were cancer, a disease of overgrowth, I would take it. But Alzheimers – is sometimes called “type 3 diabetes”. And rapamycin can raise blood glucose. And I naturally have pre-diabetes level glucose.
I would really welcome inputs, vewpoints on this. Argue with me.
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You might want to research Dr. Ai-Ling Lin’s work on human clinical trials and rapamycin with the hippcampus benefits for those wqith APOE-4 genetic predespositoin for Azheimers.
Was earth shattering for those working with neurological issues like Alzheimers.
Ai-Ling Lin, PhD. - Vice Chair for Research, Radiology
Professor, Radiology and Biological Sciences
Professor, Institute for Data Science & Informatics
Roy Blunt NextGen Precision Health Building
University of Missouri
1030 Hitt Street
Columbia, MO 65212
Lab website: https://linbrain.com/
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Thanks for this. It does describe fairly convincingly how rapamycin might improve brain functioning – if you are APOE4. But says that these benefits are not necessarily there if you are not APOE4. I am APOE3/3.
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I couldn’t comment on rapamycin’s effect on Alzheimer’s (as i obviously don’t have Alzheimer’s) but I used to forget a lot. I did Rapa for about a year (and many other supplements) and nothing seemed to help with my memory. I would literally at times forget names of people I’ve been working with for last seven year LOL.i.e instead of asking the receptionist tell Bianca to come to my office I’d say tell the girl next to you come to my office. They would think I was doing it to be funny (lol) but it was literally that bad some days, some days It was better. Fast forward to couple months ago when I started taurine and my memory is so brisk that I can’t even believe it myself. Since Alzheimer’s has some of the same symptoms, I’d have to think that taurine must be on every person’s list who is concerned about memory loss, dementia, and maybe even Alzheimer’s. Again, this is n-1 but the effects were so significant that I had to mention it.
Alzheimer’s disease and the therapeutic effect of taurine
The neuroprotective effects of taurine have been shown to protect against various forms of dementia. Beresewicz-Haller et al. (2023) investigated the ability of taurine to improve cognition in a transgenic mouse model of AD. They administered taurine orally through drinking water to amyloid precursor protein (APP)/PS1 transgenic mice for six weeks. The results of the experiment showed that taurine treatment can improve the cognitive performance of the APP/PS1 mice without affecting their behavior in the Y-maze or passive avoidance test (Chen et al., 2019). In a transgenic AD mouse model, it has been shown that taurine has the ability to improve cognitive abilities. The insoluble fraction of amyloid beta (Aβ) in the cortex of APP/PS1 mice decreased when taurine was added, suggesting that it may help reduce cognitive impairment and Aβ-induced damage, as shown in Additional Table 1 (Kim et al., 2014). Taurine has been shown to block the neurotoxic effects of Aβ on rat hippocampal and cortical neurons in culture. Taurine supplementation may also protect central neurons from excitotoxicity caused by high concentrations of glutamate extracellularly. The neuroprotective effects of taurine are abolished by picrotoxin, an antagonist of GABA-A receptors. Neuronal death caused by Aβ in rat hippocampal and cortical areas can be prevented by GABA and muscimol, an agonist of the GABA-A receptor (Fontana et al., 2020). The use of taurine in the treatment of AD may be beneficial because of its ability to modulate GABA-A receptors and protect neurons from Aβ toxicity in AD-affected regions of the mammalian brain and from excitotoxicity (Paula-Lima et al., 2005). Taurine shows a beneficial role in AD by improving cognitive function in oligomeric Aβ mice. It restores acetylcholinesterase and acetylcholine transferase activities and inactivates microglia-dependent neuroinflammation to bypass dopaminergic neurons (Fontana et al., 2020).
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Found this as I was researching indolepropionamide
Indoles as essential mediators in the gut-brain axis. Their role in Alzheimer’s disease
https://www.sciencedirect.com/science/article/pii/S0969996121001522?via%3Dihub
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One of these indoles – IAA or indole-3-acetic acid / acetate – is the villain in this Nick Norwitz video (the hero is AKG):
I hope this guy isn’t just saying this to sell supplements with his affiliate link.
Not all indole molecules would be the same.
He is demonizing something shown to increase lifespan in fruit flies so we need more data instead of just dismissing it.
AKG does seem to be a healthy supplement however. I take AAKG, funnily enough I take it BECAUSE I want to increase indole production in the gut and this acts upstream from that.
Since an early age I witnessed family members and relatives with physical and mental ailments that made their lives difficult. Around the year 2000 after my father’s death I decided I would prefer to avoid those problems if possible. I wondered, “Would that be possible?” So, I started my first medical research around heart attacks and strokes. My goal has been and continues to be to maintain a physically fit and mentally capable body as long as possible with as short a period as possible for rapid decline and death. I want to enjoy the “golden years,” not suffer through them. If I can maintain health during my later years it may result in a longer life, but that is not the goal. And, “immortality?” No. That’s not going to happen!
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That’s interesting. Started taking Ca-AKG about a year ago for other reasons.
1gm per day. Fortunately it’s quite inexpensive, if you know a guy
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Didn’t have an impact in the ITP btw.
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That’s true. Fish oil also didn’t pan out, though may have increased healthspan of mice.
Then there’s aspirin to consider. In a 2004 ITP study a dose of 20 ppm saw a median male mouse life-extension (p=0.01); but with later doses in 2014 at 60 ppm and 200 ppm there was no effect. AKG could be similar to that.
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