4 ms·

So this article seems to point to a neurodegenerative effect of Methylphenidate. I would caution against drawing conclusions from this study as of yet. MP has b

So this article seems to point to a neurodegenerative effect of Methylphenidate. I would caution against drawing conclusions from this study as of yet. MP has been used for decades and there does not seem to be a clinically evident effect of this sort. In order to derive clinical recommendations (like "stop taking ritalin") the potential damage has to be higher than that of all the "side effects" of ADHD, for example violence, depression and social problems. Which currently does not seem to be the case...

inmyunix 12y ago
"Nevertheless, this work supports studies [51], [57], [58], [59] that demonstrate that drugs shown to increase the levels of dopamine in the synaptic cleft can contribute to degenerative changes in the basal ganglia."
theonewolf 12y ago
This type of degenerative side effect though might especially express itself later in life: making you much more likely to develop say dementia earlier than a normal human. It's not like it would be an immediate side effect. Often brain damage chronically over time is not immediately visible.
- bayesianhorse 12y ago
  That effect should have been shown by now. I don't know of any studies specifically looking at this, but various global agencies require post-approval studies and monitoring which should have picked up on this. It's not like this drug is prescribed rarely or introduced very recently...
xkcd-sucks 12y ago
Traditional Parkinson's symptoms (problems w/ voluntary movement) only show up after 80-90% of dopaminergic neurons are gone. That's a whole lot of dead cells. Symptoms of pre-Parkinsonian dopaminergic neuron loss are (anhedonia, depression, psychiatric weirdness without movement disorder) are just beginning to be described, and it's very likely that stimulant use will be shown to cause pre-Parkinsonian symptoms in human populations once we know what to look for, and after somebody decides to spend tons of time and money investigating it. Maybe the appropriate clinical recommendation is to exercise caution with DAT ligands, and to use them as minimally as possible?
- bayesianhorse 12y ago
  So the mice showed 80% loss after what? One or two years of chronic use? How come people have taken this for twenty years and more and we didn't notice the Parkinson epidemic?
  - xkcd-sucks 12y ago
    The mice showed a ~20% loss at high dose. At the low dose, the mice showed no significant loss but were vulnerable to a sub-threshold dose of a toxin and toxin+MPH mice showed a ~20% loss. This is in figure 1, and in the discussion. Exactly what behavioral effects result from a 20% loss of DA neurons is still an open question. So, the clinical implication is that people on methylphenidate might be vulnerable to things (rotenone, heavy metals, etc) which aren't toxic to "normal" people.

inmyunix 12y ago

"Nevertheless, this work supports studies [51], [57], [58], [59] that demonstrate that drugs shown to increase the levels of dopamine in the synaptic cleft can contribute to degenerative changes in the basal ganglia."

theonewolf 12y ago

This type of degenerative side effect though might especially express itself later in life: making you much more likely to develop say dementia earlier than a normal human. It's not like it would be an immediate side effect. Often brain damage chronically over time is not immediately visible.

bayesianhorse 12y ago
That effect should have been shown by now. I don't know of any studies specifically looking at this, but various global agencies require post-approval studies and monitoring which should have picked up on this. It's not like this drug is prescribed rarely or introduced very recently...

xkcd-sucks 12y ago

Traditional Parkinson's symptoms (problems w/ voluntary movement) only show up after 80-90% of dopaminergic neurons are gone. That's a whole lot of dead cells. Symptoms of pre-Parkinsonian dopaminergic neuron loss are (anhedonia, depression, psychiatric weirdness without movement disorder) are just beginning to be described, and it's very likely that stimulant use will be shown to cause pre-Parkinsonian symptoms in human populations once we know what to look for, and after somebody decides to spend tons of time and money investigating it. Maybe the appropriate clinical recommendation is to exercise caution with DAT ligands, and to use them as minimally as possible?

bayesianhorse 12y ago
So the mice showed 80% loss after what? One or two years of chronic use? How come people have taken this for twenty years and more and we didn't notice the Parkinson epidemic?
- xkcd-sucks 12y ago
  The mice showed a ~20% loss at high dose. At the low dose, the mice showed no significant loss but were vulnerable to a sub-threshold dose of a toxin and toxin+MPH mice showed a ~20% loss. This is in figure 1, and in the discussion. Exactly what behavioral effects result from a 20% loss of DA neurons is still an open question. So, the clinical implication is that people on methylphenidate might be vulnerable to things (rotenone, heavy metals, etc) which aren't toxic to "normal" people.