The wrinkle model requires compression—there has to be some squeezing from the sides. Botox kills the facial muscles which do the squeezing. (I haven’t actually researched this, just an educated guess, but one reason gears-level models are important is that they let us make pretty darn good educated guesses.)
No, botox doesn’t “kill muscles”. It paralyses muscles by disrupting nerve signals to that muscle.
“botox” uses the neurotoxin produced by the bacterium Clostridium botulinum (which also causes botulism).
I haven’t actually researched this, just an educated guess, but one reason gears-level models are important is that they let us make pretty darn good educated guesses
Research is easy to do.
Guesses could be deadly when talking about neurotoxins, and definitely not appearing ‘educated’ in this case.
I can only go on the words that are used so I’m not sure, but I didn’t consider “kill” might be being used metaphorically on a rationality website.
Especially when the poster then describes it as an educated guess based on a model that lets us make “darn good educated guesses” and admits they did not even type ‘how does botox work’ into a search engine.
Kudos to the OP for the post but we’re moving into bio-medical sciences (my background) so there are “facts” out there. Is it not better to use the knowledge that is available than making guesses?
Our model of rationalists does have to account for them being normal-ish humans who speak the language in common use around them. “Kill” is in common usage for disabling something, temporarily or permanently, without specifying mechanism; e.g. one can kill the lights or the music or wasteful spending or careless use of lanuguage on internet forums. Granted, it’d be quite prudent to avoid such use in Biology contexts. Given this is a rationality forum, what do you think is reasonable likelyhood for misunderstanding caused by sloppy use of language vs major oversights in subject matter research like you’re suggesting above? I’d be very surprised if it was less than 10:1. How much does that differ from your estimate elsewhere?
[Genuinely interested in peoples’ thought process during an exchange like above from a “how do we manage to talk past eachother even in a good faith rational discourse?” angle]
I would not predict that in general—loss of muscle is a major hallmark of aging, and I would expect that to have some impact. But I doubt that any age-related difference in muscle activity matters much for wrinkles.
Also, this isn’t just about facial wrinkles. The same model applies to wrinkles on the hands, elbows, etc.
The best source I’ve seen on the topic is this Physiological Reviews article (I’ve read other sources as well, but didn’t keep around links for most of them).
Reversibility is specifically addressed—age-related muscle loss (aka sarcopenia) is not really reversible. There are things people can do at any age to add muscle (e.g. exercise), but muscle is lost if exercise/diet/etc is held constant. Masters athletes are a visible example of this.
Also, it’s not just skeletal muscle. For example, the pupil muscle squeezes the lens of the eye to adjust focus. In old age, that muscle loses mass, resulting in slower focusing speed. (Source: Physiological Basis of Aging and Geriatrics; the chapter on the eye is one of the best in the book). And of course there’s loss of muscle mass in various sphincters, resulting in e.g. incontinence and other digestive problems. None of those muscles are suffering from lack of use.
Looking into the term sarcopenia (I avoided it earlier as it seemed inconsistently used and I was getting confused mass +/- function loss) here’s some snippets and thoughts.
ArticleIn his closing comments to a scientific congress in 1989, Dr. Irwin Rosenberg suggested that one way to bring greater attention to the issue of the decline in muscle mass with ageing was to give it a Greek name. Although two terms were suggested (“sarcomalacia” being the other one), “sarcopenia” was the term adopted by the field …
unfortunately in recent years the term has increasingly come to be synonymous with its operational definitions … the term sarcopenia is appearing in other clinical literature in which muscle atrophy is present but ageing per se is not the cause.
Among the most widely observed histological features of ageing muscle is its remarkable fiber size heterogeneity.
… the available evidence strongly implicates sporadic and repeating cycles of denervation-re-innervation in the histopathology of ageing muscle
Primary loss of muscle mass versus secondary loss of muscle mass after loss of innervation—paresis/paralysis—loss of function—atrophy. From what I’ve read sarcopenia is a secondary loss of muscle, and I’d classify sphincter incompetence as an innervation issue rather than a primary loss of muscle mass issue. No idea if/what the significance of distinguishing between primary and secondary is but something to be aware of.
Fascinating subject, my initial comment was poorly worded/wrong depending on what age “ageing” begins—I was thinking 30+ where loss of muscle may be noted but reversed (quickly found article) but by 60+ sarcopenia with strict definition occurs. Another article I found: sarcopenia v. non-sarcopenia.
(Just enjoying being able to interact on LW as so much stuff goes straight over my head!)
One of the main questions I haven’t found a satisfying answer to yet is whether denervation/renervation is causal for sarcopenia. Apparently a huge amount of resources went into imaging neuromuscular junctions for a while—the physiological reviews article I linked spends half the article on the topic—but that seems to be driven by historical accident more than anything. After wading through a ton of it I still haven’t seen any decisive evidence on whether denervation is the main cause of muscle atrophy, or muscle atrophy causes nerve atrophy. It sounds like either is sufficient to cause the other experimentally, but it’s not clear which actually comes first in aging. (And of course research is made difficult by authors sometimes making statements about causality which their data/experimental procedure doesn’t actually establish.)
If this would be an effective model of wrinkles, why does giving a people botox seem to remove wrinkles?
The wrinkle model requires compression—there has to be some squeezing from the sides. Botox kills the facial muscles which do the squeezing. (I haven’t actually researched this, just an educated guess, but one reason gears-level models are important is that they let us make pretty darn good educated guesses.)
No, botox doesn’t “kill muscles”. It paralyses muscles by disrupting nerve signals to that muscle.
“botox” uses the neurotoxin produced by the bacterium Clostridium botulinum (which also causes botulism).
Research is easy to do.
Guesses could be deadly when talking about neurotoxins, and definitely not appearing ‘educated’ in this case.
Are you sure they weren’t using kill metaphorically?
I can only go on the words that are used so I’m not sure, but I didn’t consider “kill” might be being used metaphorically on a rationality website.
Especially when the poster then describes it as an educated guess based on a model that lets us make “darn good educated guesses” and admits they did not even type ‘how does botox work’ into a search engine.
Kudos to the OP for the post but we’re moving into bio-medical sciences (my background) so there are “facts” out there. Is it not better to use the knowledge that is available than making guesses?
Our model of rationalists does have to account for them being normal-ish humans who speak the language in common use around them. “Kill” is in common usage for disabling something, temporarily or permanently, without specifying mechanism; e.g. one can kill the lights or the music or wasteful spending or careless use of lanuguage on internet forums. Granted, it’d be quite prudent to avoid such use in Biology contexts. Given this is a rationality forum, what do you think is reasonable likelyhood for misunderstanding caused by sloppy use of language vs major oversights in subject matter research like you’re suggesting above? I’d be very surprised if it was less than 10:1. How much does that differ from your estimate elsewhere?
[Genuinely interested in peoples’ thought process during an exchange like above from a “how do we manage to talk past eachother even in a good faith rational discourse?” angle]
If I understand your model, then you would predict that the facial muscle activity of older people is similar to that of younger people?
I would not predict that in general—loss of muscle is a major hallmark of aging, and I would expect that to have some impact. But I doubt that any age-related difference in muscle activity matters much for wrinkles.
Also, this isn’t just about facial wrinkles. The same model applies to wrinkles on the hands, elbows, etc.
Interesting. Have you anything to back that statement up?
I don’t think describing muscle loss as a major hallmark of ageing is accurate.
Muscle loss does occur as we age—likely due to lack of use, poor diet (and lower testosterone in men) since the effect can be reversed.
The best source I’ve seen on the topic is this Physiological Reviews article (I’ve read other sources as well, but didn’t keep around links for most of them).
Reversibility is specifically addressed—age-related muscle loss (aka sarcopenia) is not really reversible. There are things people can do at any age to add muscle (e.g. exercise), but muscle is lost if exercise/diet/etc is held constant. Masters athletes are a visible example of this.
Also, it’s not just skeletal muscle. For example, the pupil muscle squeezes the lens of the eye to adjust focus. In old age, that muscle loses mass, resulting in slower focusing speed. (Source: Physiological Basis of Aging and Geriatrics; the chapter on the eye is one of the best in the book). And of course there’s loss of muscle mass in various sphincters, resulting in e.g. incontinence and other digestive problems. None of those muscles are suffering from lack of use.
Exercise increases the size of individual muscle cells but not their number. When muscle cells die it doesn’t replenish them.
Looking into the term sarcopenia (I avoided it earlier as it seemed inconsistently used and I was getting confused mass +/- function loss) here’s some snippets and thoughts.
Primary loss of muscle mass versus secondary loss of muscle mass after loss of innervation—paresis/paralysis—loss of function—atrophy. From what I’ve read sarcopenia is a secondary loss of muscle, and I’d classify sphincter incompetence as an innervation issue rather than a primary loss of muscle mass issue. No idea if/what the significance of distinguishing between primary and secondary is but something to be aware of.
Fascinating subject, my initial comment was poorly worded/wrong depending on what age “ageing” begins—I was thinking 30+ where loss of muscle may be noted but reversed (quickly found article) but by 60+ sarcopenia with strict definition occurs. Another article I found: sarcopenia v. non-sarcopenia.
(Just enjoying being able to interact on LW as so much stuff goes straight over my head!)
One of the main questions I haven’t found a satisfying answer to yet is whether denervation/renervation is causal for sarcopenia. Apparently a huge amount of resources went into imaging neuromuscular junctions for a while—the physiological reviews article I linked spends half the article on the topic—but that seems to be driven by historical accident more than anything. After wading through a ton of it I still haven’t seen any decisive evidence on whether denervation is the main cause of muscle atrophy, or muscle atrophy causes nerve atrophy. It sounds like either is sufficient to cause the other experimentally, but it’s not clear which actually comes first in aging. (And of course research is made difficult by authors sometimes making statements about causality which their data/experimental procedure doesn’t actually establish.)