Ive been taking Adderall XR 30mg for about 3 years now, and i have found some tricks that can give you a good night's sleep. Some of these may work for you and some may not. However, they are all pretty simple and worth giving a try

1) No Caffine after 5 pm. Caffine increases the effect of Adderall
2) Eat shortly before you go to bed. It can be hard to sleep on an empty stomach. If I dont eat I will wake up at 3 in the morning starving. Eat even if you aren't hungry, chances are that you are hungry and your adderall is covering it up. Eat even if you had Dinner. I have found that the best thing to eat is a bowl of cereal, one that does not have a lot of sugar. When I am on adderall i can not be hungry at all but i have always found it easy to eat cereal. If you cant eat then drink milk. It has a mild tranquilizer in it.
3) Don't try to sleep with the TV on. That can keep your brain awake, try to concentrate on steady breathing or a constant sound. ie. a ceiling fan
4) Exercise in the evening. Days that I have lacrosse pratice i will pass out at 9:00. Staying fit is important for the physical health of Adderall takers but most importantly the mental health. Exercise has been a great cure for my adderall blues.
5) If you just can not sleep, then study, study, study. It will wear your brain down and after a while you will be so tired of studying that you will pass out with out even knowing it.
6) Dont take over the counter sleep aids. Drammamine, benedryl. They will falsely put you to sleep and you will feel even more tired it the next day. They also can affect your heart rate while on adderoll. You are mixing an upper with a downer and that can equal heart failure.
7)You may disagree with this - Get off the anti depressants, they never worked for me and they always kept me up

As someone who just started taking Adderall, thanks for the tips!

Melatonin was also helpful to me, and there is a study on PubMed showing particularily good efficacy for melatonin in ADHD subjects taking stimulant medication.

Some people with ADD take adderall as a sleep aid.

I've noticed both insomnia and an increased quality of sleep on Adderall. This is consistent with medical studies that show after a few weeks the same thing-- a tolerance is gained to the wakefulness promoting effect of the drug, and the lowered periodic limb movements (aka restless leg syndrome) result in a higher quality of sleep, as people with ADHD seem statistically much more likely to have lots of motor movement during sleep which negatively effects sleep quality.

I have a sleep tracker watch, which measures movements while sleeping, and the days I have more movements and sleep worse are when I get the least Adderall. After a drug holiday, the effect is very calming, relaxing feeling in my muscles, which isn't just psychosomatic as it clearly has an effect even while I'm unconcious...

I've noticed both insomnia and an increased quality of sleep on Adderall. This is consistent with medical studies that show after a few weeks the same thing-- a tolerance is gained to the wakefulness promoting effect of the drug, and the lowered periodic limb movements (aka restless leg syndrome) result in a higher quality of sleep, as people with ADHD seem statistically much more likely to have lots of motor movement during sleep which negatively effects sleep quality.

I have a sleep tracker watch, which measures movements while sleeping, and the days I have more movements and sleep worse are when I get the least Adderall. After a drug holiday, the effect is very calming, relaxing feeling in my muscles, which isn't just psychosomatic as it clearly has an effect even while I'm unconcious...
I wonder if that can be attributed to the amount of dopamine that is left sitting around in our brains as opposed to when we're not really on it?

well, it's not just a matter of dopamine, but of where the dopamine is exerting its effect. In the cortico-striatal regions where ADHD meds bind preferentially in ADDers (as opposed to the general population, where it binds in many places around the brain), it triggers frontal and prefrontal regions, many of which have an inhibitory effect on other regions in the brain. In addition, the brain no longer tries to compensate by pumping out more dopamine and flooding other areas.

So actually, Adderall can decrease dopamine and overal neurological activity in other regions of the brain. This is part of why it calms ADDers down.

Not only do I take it for sleep, but I've found that it tends to regulate my circadian rythms to the extent that missing sleep or sleeing in the afternoon can actually reset my body's clock to think that I should be sleeping on a different dose in the day (ie if I sleep through the afternoon from my 4:00 dose, my body treats the midnight dose like a morning dose and the 8:00 morning dose like an afternoon dose and the next 4:00 dose as the evening dose...of vice-versa, if I stayed up all night, by body would treat the 8:00 dose as the bedtime dose, go to sleep, and treat the 4:00 and midnight doses as the daytime ones). So not only does it work as a sleep aid for me, but it regulates my circadian rythms to the extent that it can even override sunlight and melatonin levels.

Hyperion, can you explain in monosyllabic words the way dopamine works in the ADHD brain or link to a "Dopamine for Dummies" post? The way it was explained to me was that there was an overall dopamine deficiency, and I hadn't realized it was related more to distribution. I remember reading a Weschler essay about Parkinson's disease, and being surprised to discover it seemed to have some similar causes as ADD (and effects, like inability to turn intention into action). But I suspect I have a 2nd grade understanding of it.

The best way to look at it is that dopamine is a just a chemical. It has no "true" meaning, no "universal" meaning. When it is in the synapse, or the region in between neurons, and it contacts a dopamine receptor, it tends to stimulate the cell whose receptor it is touching. If you release a large amount of dopamine in an area, it might excite nearby cells. The big picture effect is going to be determined by where in the brain this occurs.

The brain itself is not homogeneous. That is, it's not one big amorphous blob where every part does the same thing. Different regions are specialized for different tasks and the neurons in these regions will exert different effects when they are activated. Generally, when a neuron is stimulated enough, it fires off a load of whatever neurotransmitter it carried at other neurons. There is an obvious sexual metaphor that could be used, but this is a family board, so I'll let you just imagine it.

A deficit of dopamine in a region called the substantia nigra appears to correlate with the development of Parkinson's disease. It is thought that dopamine from this area activates neurons responsible for motor coordination and motion.

With ADHD, it is thought that dopamine (and its close chemical cousing norepinephrine) are lacking in critical regions in the front of the brain where the striatum and frontal lobe meet. This region, the prefrontal cortex, appears to be a crucial interface between two of the major divisions of the brain: the limbic system (older) and the neocortex (newer). The neocortex (or cerebral cortex) is the grey folded mass that we think of as the "brain" because in humans it is so large that it is most of our brain. The limbic system involves a number of smaller structures deeper in the brain. This includes structures like the amygdala, which is thought to be involved in aggression and fear, and the fight-or-flight system in general, or the thalamus and hippocampus, which are involved in short and long term memory, respectively. The hypothalamus appears to be involved in regulation of temperature and hormones. The limbic system is thought, as a generalization, to involve a lot of what we think of as "animal impulses," the irrational fear, jealousy, lust, hatred, etc. The cerebral cortex is what we associate with a lot of the "cognitive thinking" stuff, although to a large extent its role is to slow down the limbic system and regulate it.

This is one of the things that those frontal lobe areas appear to do, they seem to tell the limbic system to "stop, think, then act." They are sort of a filter for information. The limbic system is capable of functioning much faster on its own, but it is thought that certain responses are formed in regions of the limbic system, but pass through a feedback loop through the frontal lobe for "approval." No frontal lobe activity, and there will be little inhibition of the signal.

Dopamine in this situation is responsible for activating the frontal lobe regions. Lack of dopamine will result in lack of activity, which will result in lack of regulation and inhibition, which will result in an inability to pay attention or control one's impulses.

Now, in most ADDers, this lack of dopamine is localized to this prefrontal region. It occurs, essentially, because the dopamine drains too quickly from the synapses back into the cells. This is because, as experiments have shown, ADDers have an excess of a particular protein on the surface of those specific cells called a transport protein, which wisks the dopamine out of the synapse and back into the cell. With an overabundance of these things, dopamine levels in these synapses doesn't build up high enough, and the frontal regions don't get activated. Sometimes the brain will then try to pump out more dopamine to compensate, which floods the rest of the brain instead.

ADHD meds block these drains (methylphenidate) or cause them to work in reverse (amphetamines). In ADHD people, this corrects the problem at its core. Because these drugs bind to that protein (or to a receptor connected to it), they will bind in those regions preferentially in ADDers, because there are so many more of those proteins there, whereas for neurotypical people they will bind all over the brain.

When the drugs correct the problem, these regulatory regions then receive enough dopamine to function, and can send out their inhibitory signals to tell the rest of the brain to sit down and shut the hell up. These inhibitory signals are the brain's own way of lowering excess activity. In addition, the brain will no longer be pumping out excess dopamine and flooding other areas in an attempt to compensate.

Great post, Hyperion. I have one thing to possibly note though. You said, "ADHD meds block these drains (methylphenidate) or cause them to work in reverse (amphetamines). In ADHD people, this corrects the problem at its core. "

I'm not so sure the core of ADD is in the neurotransmitter level, but rather the cell chemical second messengers as well as signal transduction sequences. I believe that in the not so distant future when we have really begun to understand these processes, we will find the very roots of many diseases and a heck of a lot more.

Affecting whether or not the chemicals begin their sequence or not but not the fine details of the messenger chemicals in signals themselves seems crude by comparison, but this this is all the freedom you have using neurotransmitter modulation techniques.

Please let me know if i'm definitely wrong or missed something very crucial (ADD heh).

Well yeah, it's entirely possible that there are other things happening up and downstream as well. With "second messengers" (I assume you mean intracellular protein kinases?) and signal transduction (are you talking like disinhibition or just ion channels?), they're both affected by the actions that neurotransmitters and drugs exert upon the cell itself.

I wouldn't be surprised if there were more things going on with ADHD, especially as the entire brain is very interconnected, but what is currently known is that catecholamines (dopamine and norepinephrine) tend to excite neurons. The neurons in these regions which in most people light up during the functions that ADDers lack do not seem to get activated nearly as much in ADDers when they attempt these functions. ADDers have been observed to have lower levels of catecholamines in those regions, and they have been observed to have an overabundance of the protein that removes these chemicals from the synapse in that region. Finally, it has been observed that medications which block or reverse the removal of these neurotransmitters from the synapse tend to alleviate the symptoms of the disorder and also cause ADHD brains to more closely resemble non-ADHD brains on various brain scans.

So whether there is something deeper going on, or whether there are other issues involved elsewhere in the brain is certainly an interesting question and makes for some interesting speculation. In terms of what we can say for sure, though, I prefer to stick with observation and evidence.