False dichotomy: Cryonics may fail (actually, will probably fail) to revive you. Or it may succed, and then you die anyway.
Robin Hanson uses an estimate of 5% here
It seems a quite optimistic estimate. Successful revival depends conjunctively on a large number of events, many of which are highly speculative (no damage from preservation, super duper nanotech) or outright implausible (cryo orgs not succumbing to organizational failure).
MNT isn’t strictly necessary. Anabolocytes, and other speculative genetically engineered cells. They are a little more likely than Freitas’ nanomedicine because, well, cells exist; which is not an argument that works for MNT.
There’s also whole-brain emulation, which doesn’t require nanotech to function—just slightly better scanners, substantially better neuroscience, and exponentially better computers.
We have plenty of models of neurons and some of them imitate neurons very well.
Eugene Izhikevich simulated an entire human brain equivalent with his model and he saw some pretty interesting emergent behaviour (Granted, the anatomy had to be generated randomly at every iteration, so we still need better computers).
That’s true, but we need to get it really, really close. Even relatively small statistical deviations from the behavior of the real neurons are probably intolerable. Besides, real neurons are not interchangeable: they have unique statistical biases and are influenced by a variety of factors not modeled by modern simulations, like neurotransmitter diffusion, glial activity, and subtle quirks of specific dendrites and axons.
Right now, even if you gave us a high-speed brain scanner, a high-speed computer, and an unlimited budget, we wouldn’t have the capability to interpret the image data the scanner produced, or even be quite sure which immunostains to use for the optical imaging to pin down the required details. I expect it to take at least five to ten years for us to get the theoretical details ironed out.
Vitrification seems to work pretty well, in terms of preserving relevant details. Observing some of those features is going to require an as-yet-not-fully-understood immunostaining process, but that’s under neuroscience. As far as the scanners go, the resolution is already adequate or near-adequate for most SEM technologies. It’s just a question of adding more beams and developing more automated methods, so the scanning can be more parallel.
PZ Meyers has unreasonably high standards for ‘relevant details.’ Demanding one millisecond total fixation time (with every atom being in precisely the same position as it was during life) is totally ridiculous. If you want to study intraneuron cell biology, sure, you need that, but for brain emulation, all you care about is the connection-ism of the network, and the long term statistical biases of particular neurons’ synaptic connections (plus glial traits, naturally), which is (probably) visible from features many orders of magnitude more durable than the kinds of data he’s talking about. Also, his comments about accelerating the speed of the network are kind of bizarrely ignorant, given how smart a guy he clearly is.
The only way the issues he mentions are problematic is if high-detail inter-neuron computing turns out to be necessary AND long-term state dependent, which the evidence suggests against (the blue brain project has produced realistic synchronized firing activity in a simulated neocortical column using relatively simple neuron models).
As far as a reference goes, there’s this study, in which they took a rat’s brain, vitrified it, and examined it at fine detail, demonstrating “good to excellent” preservation of gross cellular anatomy.
PZ Meyers has unreasonably high standards for ‘relevant details.’
Well, he’s a developmental biologist specialized in the vertebrate nervous system.
Demanding one millisecond total fixation time (with every atom being in precisely the same position as it was during life) is totally ridiculous. If you want to study intraneuron cell biology, sure, you need that, but for brain emulation, all you care about is the connection-ism of the network, and the long term statistical biases of particular neurons’ synaptic connections (plus glial traits, naturally), which is (probably) visible from features many orders of magnitude more durable than the kinds of data he’s talking about.
One millisecond fixation time might be an excessive requirement, but in order to perform an emulation accurate enough to preserve the self, you will probably need much more detail than the network topology and some statistics. Synapses have fine surface features that may well be relevant, and neurons may have relevant internal state stored as DNA methylation patterns, concentrations of various chemical, maybe even protein folding states. Some of these features are probably difficult to preserve and possibly difficult to scan.
EDIT:
As far as a reference goes, there’s this study, in which they took a rat’s brain, vitrified it, and examined it at fine detail, demonstrating “good to excellent” preservation of gross cellular anatomy.
Actually they vitrified 475 micrometre slices of the hippocampus of rat brains. It’s no mystery that small samples can be vitrified without using toxic concentrations of cryoprotectants.
Moreover, the paper says:
“Finally, all slices were transferred to the two wells of an Oslo-type recording chamber [ … ] and incubated with aCSF at 34–37 C for at least 1 h before being used in experiments.”
“Following initial incubation for 60 min or more at 35 C in aCSF to allow recovery from the shock of slice preparation, [ … ]”
I’m not a biologist so I might be missing something, but my understanding is that this means that somehow ischemia is not an issue here, while it certainly is when dealing with a whole brain.
One millisecond fixation time might be an excessive requirement, but in order to perform an emulation accurate enough to preserve the self, you will probably need much more detail than the network topology and some statistics. Synapses have fine surface features that may well be relevant, and neurons may have relevant internal state stored as DNA methylation patterns, concentrations of various chemical, maybe even protein folding states. Some of these features are probably difficult to preserve and possibly difficult to scan.
The surface details we can read with SEM, and we can observe chemical/protein concentrations through immunostaining and sub-wavelength optical microscopy (SEM and SWOM hybrid is my bet for the technology we wind up using). I don’t think there’s strong evidence for DNA methylation or protein state being used for long-term data storage. If evidence arises, we’ll re-evaluate then. But modern neuron models don’t account for those, and, again, function realistically, so they’re not critical for the computation. The details we’re reading likely wouldn’t have to be simulated outright—they would just alter the shape of the probability distribution your simulation is sampling from. A lot of the fine stuff is so noisy, it isn’t practical to store data in it. The stuff we know is involved we can definitely preserve. As a general rule, if the data is lost within minutes of death, it’s probably also lost during the average workday.
Actually they vitrified 475 micrometre slices of the hippocampus of rat brains. It’s no mystery that small samples can be vitrified without using toxic concentrations of cryoprotectants.
I honestly don’t think cryoprotectant damage is anywhere near the big problem here. I’m sure it does cellular damage, but it seems to leave cell morphology essentially intact, and isn’t reactive enough to really screw up most of the things we know we have to care about, in terms of cell state. Ischemia is a bigger problem, and one of my points of skepticism about non-standby cryonics. Four plus hours at room temperature simply seems too long. That said, as our understanding of cell death improves, we’re starting to notice that most brain death seems to be failure of the cells’ oxygen metabolisms, not failure of synaptic linkings. I’d like to see studies done on exactly how long it takes relevant neural details to begin to break down at room temperature. That said, flatlining cases suggest that there’s some reason to hope for the time being. I’d like to see the science done, in any case.
Eudoxia is referencing Mike Darwin’s idea of modifying white blood cells with arbitrarily-sophisticated biotechnology (we’re talking “you can design new organelles to spec” as a lower-level requirement) to do active cell repair, sucking up cell contents and yoinking nuclear genetic information from even very-damaged cells before digesting the old contents and replacing them. It’s an elaborate thought experiment with technical-looking diagrams that elides huge black boxes in its proposed mechanism. Basically it’s the idea of nanomedicine before the term was coined.
The original dichotomy is correct if you think about the consequences of cryonic success.
IF and only if cryonics succeeds, the world had developed the technology to restore you from a cracked, solid mass of brain tissue. (the liquid nitrogen will fracture your brain because it cools it below the glass transition point)
Also, as sort of a secondary thing, it has figured out a way to give you a new body or a quality substitute. (it’s secondary because growing a new body is technically possible, if unethical, today)
Anyways, this technical capacity means that almost certainly the technology exists to make backup copies of you. If this is possible, it would be also possible to keep you alive for billions of years, or some huge multiple of your original lifespan that it could be approximated as infinite.
You might consider these technical capabilities to be absurd, and lower that 5% chance to some vanishingly small number like many cryonics skeptics. However, one conclusion naturally falls from the other.
We’ve done body transplants in primates in the past. Hooking up the nerves is still tricky, but we could probably figure it out. Also, cloning one mammal is basically like cloning another. There’s really no doubt we could clone a human being if we really wanted to. The trick is that current cloning mechanisms have a very high failure rate, and nobody wants to deal with the pile of dead babies and fetuses that would come out of such a process.
Realistically, though, 3d tissue printing is probably the way to go. We can already do several organs that way, and resolution is essentially the only limit to being able to fabricate most of the rest.
We’ve done body transplants in primates in the past. Hooking up the nerves is still tricky, but we could probably figure it out.
One team did one head transplant with one monkey in the 1960s (it is said to have survived a day and a half). Reattaching a completely severed spinal cord is still impossible, not “tricky”—all attempts at head transplants have produced quadriplegics.
That’s just an example. I think that if society were far more tolerant of risks, and there was more funding, and the teams working on the problem were organized and led properly, then human patient successes would be seen in the near future.
Yes, that is part of it. I don’t think that the flat financial loss is the killer issue in many cases where an unproven method could work, or not. When doing nothing is acceptable, trying something becomes fraught with the risk of being blamed for the failure.
“Pascal’s wager” denotes several different fallacies, which are present in Pascal’s original argument.
Instrumentally, it refers to estimating expected utility based only on a possible outcome with an extremely large (positive or negative) payoff, without taking into account the fact that said outcome has an extremely small probability.
This is not quite right. The justification is that an action leading to certain negative consequences is not equivalent to inaction leading to the same consequences. Inaction is almost always acceptable, morally and legally. There are many obvious and non-obvious pitfalls in changing this attitude.
an action leading to certain negative consequences is not equivalent to inaction leading to the same consequences
True when comparing one actions with a non-conjugate declining-to-act (e.g. throwing someone off a building vs not saving someone from falling off a building)
In this case, we’re looking at a fear of ineffectiveness—the case where acting could produce the same effect as not doing that exact same thing.
And yet, from a consequentialist standpoint, there shouldn’t be. Regardless of potential pitfalls, this is unlikely to change: I suspect it’s “hardwired” into our psychology. But there is also a reverse tendency, especially on the part of the public attitude towards leaders, where it is better to be seen to be doing something rather than nothing. Even if it is not clear what action should be taken.
And yet, from a consequentialist standpoint, there shouldn’t be.
Only if your reasoning is extremely reliable in estimating the consequences of your action or inaction. Otherwise you may end up doing more harm by acting than you would by inacting (happens all the time). I am guessing that this is a part of what keeps people from acting.
I meant in the future. I think severe spinal cord damage is still a little beyond us right now. Though with the progress we’re making with stem cells, I’d guess we’re likely to take some steps on that front in the near-ish future.
During embryonic development, the nervous system begins as a single strip of specialized ectoderm, the neural plate, which folds on itself to form the neural tube that later becomes the spinal chord and the brain, while nerves grow out of it towards the other parts of the body. It never happens that two separate pieces of neural tissues become attached.
AFAIK, If you inject stem cells in the severed spine of a rat and play with growth chemical signals, you may get the formation of new neural tissue that makes more or less random connections with the existing tissue which may recover some function (if it doesn’t cause cancer), but that doesn’t seem to be a precise process.
I wonder whether the lizard tail regeneration involves the extension of a functional spinal chord.
I agree, but I did not want to overstate the case, so I used an estimate already provided in the forums. I certainly did not want the discussion to become about how likely recovery from cryonics is, and I am fairly happy with the results.
False dichotomy: Cryonics may fail (actually, will probably fail) to revive you. Or it may succed, and then you die anyway.
It seems a quite optimistic estimate. Successful revival depends conjunctively on a large number of events, many of which are highly speculative (no damage from preservation, super duper nanotech) or outright implausible (cryo orgs not succumbing to organizational failure).
MNT isn’t strictly necessary. Anabolocytes, and other speculative genetically engineered cells. They are a little more likely than Freitas’ nanomedicine because, well, cells exist; which is not an argument that works for MNT.
There’s also whole-brain emulation, which doesn’t require nanotech to function—just slightly better scanners, substantially better neuroscience, and exponentially better computers.
We have plenty of models of neurons and some of them imitate neurons very well.
Eugene Izhikevich simulated an entire human brain equivalent with his model and he saw some pretty interesting emergent behaviour (Granted, the anatomy had to be generated randomly at every iteration, so we still need better computers).
That’s true, but we need to get it really, really close. Even relatively small statistical deviations from the behavior of the real neurons are probably intolerable. Besides, real neurons are not interchangeable: they have unique statistical biases and are influenced by a variety of factors not modeled by modern simulations, like neurotransmitter diffusion, glial activity, and subtle quirks of specific dendrites and axons.
Right now, even if you gave us a high-speed brain scanner, a high-speed computer, and an unlimited budget, we wouldn’t have the capability to interpret the image data the scanner produced, or even be quite sure which immunostains to use for the optical imaging to pin down the required details. I expect it to take at least five to ten years for us to get the theoretical details ironed out.
It requires substantially better scanners, and a fixation process that preserves all the relevant features.
Vitrification seems to work pretty well, in terms of preserving relevant details. Observing some of those features is going to require an as-yet-not-fully-understood immunostaining process, but that’s under neuroscience. As far as the scanners go, the resolution is already adequate or near-adequate for most SEM technologies. It’s just a question of adding more beams and developing more automated methods, so the scanning can be more parallel.
Do you have any reference?
According to PZ Myers you can only do that with exceptionally small samples of tissue.
PZ Meyers has unreasonably high standards for ‘relevant details.’ Demanding one millisecond total fixation time (with every atom being in precisely the same position as it was during life) is totally ridiculous. If you want to study intraneuron cell biology, sure, you need that, but for brain emulation, all you care about is the connection-ism of the network, and the long term statistical biases of particular neurons’ synaptic connections (plus glial traits, naturally), which is (probably) visible from features many orders of magnitude more durable than the kinds of data he’s talking about. Also, his comments about accelerating the speed of the network are kind of bizarrely ignorant, given how smart a guy he clearly is.
The only way the issues he mentions are problematic is if high-detail inter-neuron computing turns out to be necessary AND long-term state dependent, which the evidence suggests against (the blue brain project has produced realistic synchronized firing activity in a simulated neocortical column using relatively simple neuron models).
As far as a reference goes, there’s this study, in which they took a rat’s brain, vitrified it, and examined it at fine detail, demonstrating “good to excellent” preservation of gross cellular anatomy.
Well, he’s a developmental biologist specialized in the vertebrate nervous system.
One millisecond fixation time might be an excessive requirement, but in order to perform an emulation accurate enough to preserve the self, you will probably need much more detail than the network topology and some statistics. Synapses have fine surface features that may well be relevant, and neurons may have relevant internal state stored as DNA methylation patterns, concentrations of various chemical, maybe even protein folding states. Some of these features are probably difficult to preserve and possibly difficult to scan.
EDIT:
Actually they vitrified 475 micrometre slices of the hippocampus of rat brains. It’s no mystery that small samples can be vitrified without using toxic concentrations of cryoprotectants.
Moreover, the paper says: “Finally, all slices were transferred to the two wells of an Oslo-type recording chamber [ … ] and incubated with aCSF at 34–37 C for at least 1 h before being used in experiments.”
“Following initial incubation for 60 min or more at 35 C in aCSF to allow recovery from the shock of slice preparation, [ … ]”
I’m not a biologist so I might be missing something, but my understanding is that this means that somehow ischemia is not an issue here, while it certainly is when dealing with a whole brain.
The surface details we can read with SEM, and we can observe chemical/protein concentrations through immunostaining and sub-wavelength optical microscopy (SEM and SWOM hybrid is my bet for the technology we wind up using). I don’t think there’s strong evidence for DNA methylation or protein state being used for long-term data storage. If evidence arises, we’ll re-evaluate then. But modern neuron models don’t account for those, and, again, function realistically, so they’re not critical for the computation. The details we’re reading likely wouldn’t have to be simulated outright—they would just alter the shape of the probability distribution your simulation is sampling from. A lot of the fine stuff is so noisy, it isn’t practical to store data in it. The stuff we know is involved we can definitely preserve. As a general rule, if the data is lost within minutes of death, it’s probably also lost during the average workday.
I honestly don’t think cryoprotectant damage is anywhere near the big problem here. I’m sure it does cellular damage, but it seems to leave cell morphology essentially intact, and isn’t reactive enough to really screw up most of the things we know we have to care about, in terms of cell state. Ischemia is a bigger problem, and one of my points of skepticism about non-standby cryonics. Four plus hours at room temperature simply seems too long. That said, as our understanding of cell death improves, we’re starting to notice that most brain death seems to be failure of the cells’ oxygen metabolisms, not failure of synaptic linkings. I’d like to see studies done on exactly how long it takes relevant neural details to begin to break down at room temperature. That said, flatlining cases suggest that there’s some reason to hope for the time being. I’d like to see the science done, in any case.
What are these?
I never heard of them and Google doesn’t yield meaningful results.
A special type of teacher’s password.
Eudoxia is referencing Mike Darwin’s idea of modifying white blood cells with arbitrarily-sophisticated biotechnology (we’re talking “you can design new organelles to spec” as a lower-level requirement) to do active cell repair, sucking up cell contents and yoinking nuclear genetic information from even very-damaged cells before digesting the old contents and replacing them. It’s an elaborate thought experiment with technical-looking diagrams that elides huge black boxes in its proposed mechanism. Basically it’s the idea of nanomedicine before the term was coined.
The original dichotomy is correct if you think about the consequences of cryonic success.
IF and only if cryonics succeeds, the world had developed the technology to restore you from a cracked, solid mass of brain tissue. (the liquid nitrogen will fracture your brain because it cools it below the glass transition point)
Also, as sort of a secondary thing, it has figured out a way to give you a new body or a quality substitute. (it’s secondary because growing a new body is technically possible, if unethical, today)
Anyways, this technical capacity means that almost certainly the technology exists to make backup copies of you. If this is possible, it would be also possible to keep you alive for billions of years, or some huge multiple of your original lifespan that it could be approximated as infinite.
You might consider these technical capabilities to be absurd, and lower that 5% chance to some vanishingly small number like many cryonics skeptics. However, one conclusion naturally falls from the other.
We don’t know how to reliably clone a human being, and we definitely don’t know how to transplant your brain into it or attach your head to it.
We’ve done body transplants in primates in the past. Hooking up the nerves is still tricky, but we could probably figure it out. Also, cloning one mammal is basically like cloning another. There’s really no doubt we could clone a human being if we really wanted to. The trick is that current cloning mechanisms have a very high failure rate, and nobody wants to deal with the pile of dead babies and fetuses that would come out of such a process.
Realistically, though, 3d tissue printing is probably the way to go. We can already do several organs that way, and resolution is essentially the only limit to being able to fabricate most of the rest.
One team did one head transplant with one monkey in the 1960s (it is said to have survived a day and a half). Reattaching a completely severed spinal cord is still impossible, not “tricky”—all attempts at head transplants have produced quadriplegics.
Wouldn’t this be tantamount to regrowing a transected spine? I’m not up-to-date on that area, but I don’t think we can do that yet.
We can and we can’t. Here’s an 11 year old article where rats successfully regained function : http://www.jneurosci.org/content/21/23/9334.abstract
That’s just an example. I think that if society were far more tolerant of risks, and there was more funding, and the teams working on the problem were organized and led properly, then human patient successes would be seen in the near future.
Isn’t that the funny thing? We’ll take a certain loss over a risk of the same exact loss. Sigh.
Isn’t it closer to “take a certain loss over a risk of the same exact loss, plus a whole lot of money”?
Yes, that is part of it. I don’t think that the flat financial loss is the killer issue in many cases where an unproven method could work, or not. When doing nothing is acceptable, trying something becomes fraught with the risk of being blamed for the failure.
That’s a Pascal’s wager argument.
What? No. Pascal’s wager is when you apply the rules of instrumental rationality to epistemic rationality.
Simply being willing to take risks to possibly get a better outcome, without warping your beliefs, is not the same thing at all.
“Pascal’s wager” denotes several different fallacies, which are present in Pascal’s original argument.
Instrumentally, it refers to estimating expected utility based only on a possible outcome with an extremely large (positive or negative) payoff, without taking into account the fact that said outcome has an extremely small probability.
This is not quite right. The justification is that an action leading to certain negative consequences is not equivalent to inaction leading to the same consequences. Inaction is almost always acceptable, morally and legally. There are many obvious and non-obvious pitfalls in changing this attitude.
True when comparing one actions with a non-conjugate declining-to-act (e.g. throwing someone off a building vs not saving someone from falling off a building)
In this case, we’re looking at a fear of ineffectiveness—the case where acting could produce the same effect as not doing that exact same thing.
And yet, from a consequentialist standpoint, there shouldn’t be. Regardless of potential pitfalls, this is unlikely to change: I suspect it’s “hardwired” into our psychology. But there is also a reverse tendency, especially on the part of the public attitude towards leaders, where it is better to be seen to be doing something rather than nothing. Even if it is not clear what action should be taken.
Only if your reasoning is extremely reliable in estimating the consequences of your action or inaction. Otherwise you may end up doing more harm by acting than you would by inacting (happens all the time). I am guessing that this is a part of what keeps people from acting.
I meant in the future. I think severe spinal cord damage is still a little beyond us right now. Though with the progress we’re making with stem cells, I’d guess we’re likely to take some steps on that front in the near-ish future.
Perhaps, but I don’t think it’s so easy.
During embryonic development, the nervous system begins as a single strip of specialized ectoderm, the neural plate, which folds on itself to form the neural tube that later becomes the spinal chord and the brain, while nerves grow out of it towards the other parts of the body. It never happens that two separate pieces of neural tissues become attached.
AFAIK, If you inject stem cells in the severed spine of a rat and play with growth chemical signals, you may get the formation of new neural tissue that makes more or less random connections with the existing tissue which may recover some function (if it doesn’t cause cancer), but that doesn’t seem to be a precise process.
I wonder whether the lizard tail regeneration involves the extension of a functional spinal chord.
I agree, but I did not want to overstate the case, so I used an estimate already provided in the forums. I certainly did not want the discussion to become about how likely recovery from cryonics is, and I am fairly happy with the results.