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Is low-dose Dexedrine safe for a 4- or 5-year-old?

She is already on guanfacine. AFAIK, it hasn't really helped much yet, if any. I would HATE if they put her on nasty fucking drugs like bupropion or atomoxetine. Those are both trash drugs, and even made me FEEL gross and like my brain was truly being fucked with.
I love how much I am learning through this discussion. Thank you everyone for their support...it has been difficult and I know that my brother, sister-in-law, and neice especially will benefit from all of this.
 
She is already on guanfacine. AFAIK, it hasn't really helped much yet, if any. I would HATE if they put her on nasty fucking drugs like bupropion or atomoxetine. Those are both trash drugs, and even made me FEEL gross and like my brain was truly being fucked with.
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You're not the one who's supposed to be taking them. Everyone responds to drugs differently - they do work for some people. Try them and see.

e.g. Phenobarbital is a life saver for some epileptics but at the same time some people don't tolerate it well. Does that mean we shouldn't prescribe it at all?
 
sekio said:
I would rather see kids on low-ish doses of amphetamine or methylphenidate PRN for attention span purposes, than on broad spectrum, daily, antipsychotics or SNRIs.
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Really? Even though ADD is hardly a dangerous disease other than not being able to work? How about the high suicide rate of schizophrenics? Those three classes rarely go hand-in-hand.
 
Yes however untreated bi-polar oftentimes morphs into schizophrenia. And the use of anti-psychotics in children is not low.
 
To be fair, amphetamine really is almost a natural/endogenous compound. Beyond half-life, it's not much different than just supplementing trace amines.
 
Yet it induces a subsequent signalling cascade pretty far removed from those ordinarily encountered; little pharmacological adjustments can make large differences.

ebola
 
I can't really provide any evidence of what I'm about to say simply bc there's no research on the pharmacogenomics of trace amines, but barring gene transcription/expression, amph has the same pharmacodynamics as regular PEA. =/

Granted, pharmacogenomics can make a HUGE difference in the long run response to a drug, so I'm strictly talking about short term effects (24-hour timescale).

Edit: I can support my pharmacodynamics statement though - I even made a nice little diagram ;D

https://en.wikipedia.org/wiki/Amphetamine#Pharmacodynamics Purple lines=phenethylamine


Edit2: This is what is currently known about amph and human gene expression: stupidly long database hyperlink | link for any species

And just for the hell of it: here's the compound/gene expression link for CARTPT (expression is strongly induced by amphetamine)
 
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I think its prudent to add that, while TAAR1 function in monoamine systems is more or less understood at a functional level, the functions/roles of TAARs (particularly TAAR1 and TAAR2) outside the CNS aren't as clear atm. I read a research paper on TAAR1/TAAR2's role in human leukocyte chemotaxis a while back - phenethylamine is probably a ligand for TAAR2 in cells that regulate the immune system. No clue about amphetamine.

So...what I said is also strictly confined to pharmacodynamics in the CNS.
 
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I can't really provide any evidence of what I'm about to say simply bc there's no research on the pharmacogenomics of trace amines, but barring gene transcription/expression, amph has the same pharmacodynamics as regular PEA. =/

Granted, pharmacogenomics can make a HUGE difference in the long run response to a drug, so I'm strictly talking about short term effects (24-hour timescale).
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Right, but in this case, the pharmacokinetics make a huge difference, given how fast phenethylamine is usually chopped by MAO. All this is just to say that while amphetamine induces a cascade qualitatively similar to what's seen in endogenous processes, its effects are vastly quantitatively different, particularly in terms of downstream, more high level alteration in the function of neural circuits (where a qualitative difference is observed).

ebola
 
ebola? said:
Right, but in this case, the pharmacokinetics make a huge difference, given how fast phenethylamine is usually chopped by MAO. All this is just to say that while amphetamine induces a cascade qualitatively similar to what's seen in endogenous processes, its effects are vastly quantitatively different, particularly in terms of downstream, more high level alteration in the function of neural circuits (where a qualitative difference is observed).

ebola
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True enough. Doesn't really change the fact that it has the same monoaminergic pharmacodynamics though. =P
 
roger&me said:
sorry for the less than advanced reply but 4 year olds are supposed to be "adhd", they are little tiny kids. Being hyper and inattentive is the whole point of childhood, its how kids explore their environment and find out who they are.

Not trying to start a philosophical discussion here, but there is an element of insanity in giving powerful monoamine releasers to kids that young. Especially when the medical necessity of such a decision is dubious at best. Intuitively i find it very hard to believe that any child is at risk of suffering serious long term consequences as a result of not being treated for adhd. I find it much easier to believe that exposure to monoamine releasers during early brain development might have a deleterious effects on a child's physical and mental health.

If it were my child, i would look at the doctor like "are you crazy? This is a 4 year old we're talking about here".
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quoted for truth!!!!!!!!!!!!!!!!!!

stop drugging your children- can you not see that society is wrong for thinking this is the rational response to a 4 year old being active
 
I'm on 45 mg, and I think its a bad idea giving it to anyone that young because at that age, the brain is being still being formed, so you don't want the brain to form into a system thats dependent on an external substance to boost monoamine levels. Don't get me wrong now, the brain is always being formed and when you quit dexedrine, it gradually adapts but its harder for people who do drugs at earlier ages to get off them. They did a study on porn addiction (I couldn't be bothered looking for it, it was in a TED talk though should be easy to find) and analysed how long it takes for the brain to adapt to the lack of novelty (which causes dopamine release) after quitting hardcore porn, and older generations recovered quicker because the internet wasn't around when they were teenagers. I don't remember the exact figures, but people who started looking at hardcore porn as kids took around twice as long to fully adapt.
 
@frogwarrior: FYI I posed a similar argument about a page ago about getting the brain and it's chemistry household to 'rely' on a drug during the critical developmental stage, adapt, get used to, become dependent etc. but it apparently wasn't very well accepted.
 
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