ASD & Dopamine

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Does anyone know whether ASD causes or is caused by low or high dopamine?
Or low or high Serotonin?
Are there any other neurotransmitters implicated in ASD?

Any good or bad experiences on SSRIs or antipsychotics or any other neuro drugs?

I can't find any hard evidence either way and want to know what issues I'm dealing with neurotransmitterly speaking

Thanks

People with ASD almost always have High Dopamine, usually well above normal range.

that makes sense, i did quite well on zyprexa a couple years ago except for the side effects. where did you find out ASDs have high dopamine?

I thought it was more complicated than that.

http://www.google.ca/url?sa=t&rct=j&q=a ... 1473,d.b2I

The article is more than I can understand. I have very little knowledge of brain chemistry. In one part of section 1.7.1 it seems to say that there are conflicting results between study. The author of this article found that Dopamine levels were lower in Autistic people but s/he also mentioned that other studies have found the opposite. It sounds like this is a student paper so I'm not sure how credible it is.

I'm wondering if it can be both. Some people on the spectrum have hypersensitivities and others have hyposensitivities. Dopamine is responsibile for regulating sensitivity and processing of information. Is it possible that hypersensitivities are the result of high/low dopamine levels and hyposensitivities are the result of the opposite?

What if people on the spectrum can be found on opposite extremes? One group has extremely high levels of dopamine while the other has extremely low levels?

well i read something that shows aspergers have lower dopamine leveks

http://www.wrongplanet.net/postt122615.html

"
What is serotonine?

Serotonine is a neurotransmitter that is generated when pleasure is experienced. Unlike dopamine levels, serotonine is generated at normal levels among people with Asperger's. However, since happinness and pleasure are correlated low levels of dopamine often imply low levels of serotonine and vice versa. It's hard to have fun when you're not happy and it's hard to be happy when you rarely have fun. "

that page also has 27 dopamine references as well

I've heard that many people with ASD also have ADHD, which I thought was associated with low dopamine levels. Otherwise, I'm not sure.

As for serotonin, I thought low levels are associated with depression. It's common in those with AS for sure, but you can take SSRIs for that.

I was on SSRIs for a while and it cured my depression. The side effects were annoying though so after my depression was cured, I went off of them.

Seems some studies show high Dopamine, while others show low Dopamine. Maybe some have high and others have low.

It's tricky.

So far there is evidence to suggest we have a higher than usual capacity in regards to dopamine. However - that capacity, often goes unused.
Basically if you had a NT and there "normal" capacity was about 100 (made up number here to demonstrate a point) - but they only used 80% of that capacity most of the time - this gives a nice balanced effect for brain chemistry. Our capacity seems to be much higher - something like 300 compared to their 100. So naturally we have more dopamine in our systems than NT's (over the normal mark)- but the problem is we also have a greater lack of it than they do because our capacity is so much more (probably about 50% lacking rather than 20% they do) - which results in symptoms of high dopamine capacity and low dopamine symptoms.

It's a similar but different story for serotonin. We simply don't have a "balance" for serotonin the way the normal population does. Of course the more dopamine in your system, it can either block you from storing serotonin, or simply can't balance the serotonin the more you dopamine is out. Low levels are assocatied with depression - most AS women show very low serotonin levels and are worse at processing and storing it than NT women.

Dang that sucks if true. but makes sense. and also sounds complicated. Can you elaborate more on the more capacity but more lack of it. Can you explain it a bit more, I am confused about it in regards to what it would look like if we observed people with more capacity but not enough of it? in contrast to say someone with high dopamine schizophrenia..

Sorry this is difficult stuff to explain while keeping it to laymans terms.

It's not enough simply to look at low dopamine or high dopamine. Neurotransmitters are an extremely complex and wonderful system when they work correctly. But because they are so complex, when things go wrong they really go wrong.

Dopamine is implicated in schizophrenia, ADD and ADHD - but all with very different results. This is because of the rather different way that neurotransmitters work. It is not necessary a case of simply increasing the level - blocking, stimulating or mimicking a neuroreceptor (a receptor obviously is different from a transmitter) will increase the level by proxy - yet you haven't actually increased the level, simply blocked, stimulated or mimicked one particular pathway, which increases the level to other systems of it's own accord. Because there are so many neuroreceptors, and all are reliant on different sets of chemicals, which one it affects significantly changes the effect it will have on you - as well as the way they interact with one another, causing further changes again. If you don't have enough of the right chemicals - which your body gets from a balanced diet - this plays havoc with your brain chemistry. Currently the fields responsible for this would rather hand out drugs (some warranted, some not) rather than encourage people to relearn the basics of a balanced diet.

Caffeine is a great example. Most people are aware that caffeine is a stimulant. What most aren't aware of - caffeine binds to another type of receptor (adenosine), which means your brain essentially allows your other natural stimulants - like dopamine - free reign. You haven't actually increased the level of dopamine, you have simply "disconnected the brakes" - as opposed to "putting your foot of the accelerator" - if you want to put it in terms of driving analogy's. As a result this blocks you from accessing serotonin for a time - and melatonin is made from serotonin in order to sleep - hence the sleeping issues with caffeine.

Other drugs - alcohol, amphetamines and cocaine - all primarily affect dopamine, yet all in very different ways. While overall it is the dopamine which is being affected, the way in which it is, matters - because that is the main difference causing the different results. The same way you see dopamine implicated in autism, schizophrenia, ADD and ADHD - yet all causing different results - it's because they work with different chemicals, receptors and pathways.

Hence I think you see the problem here - depending on which receptors can change our symptoms -enough for us to be classified as a group but with individual variation often being at extremes. Having a larger than normal capacity yet lacking the ability in many cases to fulfil it is generally what causes our issues. A lack of dopamine (or in our case not fulfilling it enough) tends to cause the following: exhaustion, little motivation, inattentiveness, an inability to focus, impulsiveness, forgetfulness, boredom, restlessness, resistance, and generally being uncooperative and unempathic. In an effort to correct this many of us seek out more stimulation or our preferred type of stimulation that won't overload our systems in amounts that generally annoy the people around us - essentially where stims and special interests come from. Also the reason video games are addictive and house chores aren't.

When you say "capacity" here, are you talking about the overall number of dopamine receptors? It makes sense that a mismatch between the dopamine baseline and the number of receptors would result in the feelings you describe and lead to people trying to increase dopamine production through stims and special interests. If people with ASDs tend to be born with more dopamine receptors that would mean that a lot of dopamine would have to be generated to bring about the positive feelings that come with a dopamine/receptor match.

But then there's this:

Dopamine regulation

from Wikipedia

This seems to say that there are a number of different types of dopamine recepetors and that some are upregulated by specific drugs while others are downregulated. And that too few dopamine receptors of certain types can drive people to addictive behaviours while too many of other types can drive people to addictive behaviors.

I tried to figure out from google which types of dopamine receptors would be in excess in ASDs but couldn't. Do you know? Or are you talking about something other than the number of receptors? I am very curious about dopamine and it does seem extensively studied. But all that extensive study means there is so very much information that even with the help of google I can't quite find out the specifics of how it relates to ASDs.

If there is a specific receptor that is in excess at birth, maybe there would be a way to specifically downregulate it too so as to avoid anhedonia and other unpleasant things. Or maybe not. I am so confused.

Atypical anti-psychotics work by affecting levels of dopamine release. This, in turn, may create up- or down-regulation. For example, in schizophrenia, there is lots of evidence that there is an excess of dopamine in certain areas of the brain. All anti-psychotics on the market now work primarily as dopamine antagonists, lowering the amount of dopamine that is available in the synapse. (Note that lowering dopamine amounts may work by less dopamine release from the pre-synaptic neuron, making the dopamine transporter, DAT, work more efficiently, etc.)

One reason tardive dyskinesia may occur with long-term anti-psychotic use is due to the brain's response to less dopamine. After a while, the brain "realizes" that the medication is making it so there's less dopamine available in the synapse. Its response may be to up-regulate receptors and become hyperstimulated by even low amounts of dopamine, leading to the unfortunate tics of TD. So, even if the patient stops taking anti-psychotics after developing tardive dyskinesia, the condition remains permanent due to the permanent changes in how the brain responds to dopamine. But the brain's first way to react to the lower dopamine levels caused by anti-psychotics is by developing Parkinsonian-like side effects, since Parkinson's is caused by dopaminergic neuron death in the substantia nigra. In fact, the main reason why the dopamine hypothesis of schizophrenia was first developed was by observing how Parkinson's patients could become psychotic on high doses of L-DOPA, and how schizophrenic patients often exhibited Parkinsonian-like side effects while taking their medication.

Traditional anti-psychotics, like Haldol and Thorazine, only work as D2 receptor antagonists. Most of the atypical anti-psychotics (e.g., Seroquel, Risperdal, Zyprexa) work as both D2 and D4 receptor antagonists AND serotonin antagonists. Abilify is one of the newest atypicals, and it works as a partial dopamine agonist, which is why it doesn't seem to have many extrapyramidal side effects to go along with it. Clozaril, the first atypical, has an extremely high amount of serotonin antagonism.

And keep in mind, too, that dopamine levels may be both abnormally high, abnormally low, and normal in the same individual, depending on what system you're looking at. (This has been found in schizophrenia, for instance. The anhedonia and poverty of speech associated with negative symptoms seem to be caused by a low amount of dopamine in one brain section. But we also know that positive symptoms seem to be caused by high amounts of dopamine in another brain section.) So, a goal of new drug developments is going to be the ability to "hone in" on one specific region of the brain, rather than having the medication affect all systems equally, including ones that may be working correctly.

If you're really into learning about dopamine, I highly recommend reading neuropharmacology/neurochemistry texts. A great intro neuro text is Biological Psychology by Kalat.

Thank you. I will do that. I took 3 semesters of neurology in college but that was 25 years ago so I no longer have my textbook, have forgotten much, and perhaps what I learned is now outmoded. I need to freshen up my knowledge.

Nevermind

Not sure if it's the AS or ADHD, as I have both and other things.

I took Effexor XR in the past (SSRI) & it helped to some extent for a while, especially with being calmer with a more balanced mood. I haven't taken it for a few years now & don't really miss its effects. I've taken Dexedrine IR for the last 2 years or so (ADHD stimulant, dopamine+) with great results *for me.* But again, I don't know if it's because of the ADHD vs. AS that it works as well as it does *for me,* as every person is going to have a bit of a different neuro-chemical makeup and each different pharmaceutical will have different results on them. ie before Dexedrine I tried a sample of Paxil I was given by my doc and after taking just one pill I knew there was no way I'd ever take another - it put me in a very very horribly dark depressed mindset. I had to remind myself that it was literally just a bad drug trip and would pass.

Sooo, there are good stories and bad.. and no way to know which exact pharmaceuticals may benefit you w/o trial & error. This is how they're prescribed for ADHD, too. People are encouraged to try a few different drugs for a few days each and see which ones works best for them, because we simply don't have the doctors and labs required to test everyone's brains and biological makeup in order to best select a drug.

That was very interesting, thank you.

As to the question of whether it's receptors - I honestly don't know. Nobody has looking at it in a systematic way before, they have been to busy trying to prove where ASD comes from rather than the simpler things we could focus on - some of the results we do have are contradictory and inconclusive at this point.

It could be receptors, but it could also be reuptake inhibitors. Perhaps a mixture of both?

I'm not sure about the specific receptors because again - it has not been studied conclusively. Currently most studies are focused on finding the cause of autism or finding a cure - very few are focused on the day to day workings that result in the symptoms we live with. Of course, either way - the difference between us and NT's does primarily point to a difference in the amount of receptors or reuptake inhibitors - in all probability, that difference comes from at least in part, an excess in testosterone during pre-natal development and pregnancy (combined with a range of other factors such as genetics, and more) which is what lead Baren-Cohen to his "extreme male brain theory" (By the way, I do not support this theory - but he does have a valid point for the essence of it). Dopamine is much more essential to men and actually relies on testosterone in order to create neurotransmitter itself (hence why possibly the level of testosterone in pre-natal development is contributing to affecting our receptors or reuptake inhibitors to give us that extra capacity)- most dopamine issues are seen primarily in men - things like ADD, ADHD, ASD and others are not an exception to this which suggests that this is really something we should be focusing on rather than ignoring.

One of the current issues with both SSRI's and ADHD medication is that once on it - especially on it long term - it interferes with our ability to produce the right amounts of neurotransmitters naturally and we end up producing too little or too much of them, which is why if you are on those long term you are supposed to come off them slowly in order to give your brain a chance to start normalizing the level of production again. Which means that while drugs may help while using them, they may also have more side effects long term than we are currently aware of. Especially in brains that are still growing this does not seem to be a smart idea to mess with that and we don't know how those kids who have been on them long term have reacted as a result of that usage during crucial stages of development yet.

Something I choose to experiment with personally was nutrition, after I observed a significant change in symptoms as a result of treating my medical condition. The interesting part was it didn't' just affect my medical condition, it affected my ASD symptoms too. After investigation, trial and error and experimenting - I managed to take my AS severity level from moderate to mild through the use of diet alone. It doesn't cure ASD of course, which will always be there, it simply brings my symptoms to a more manageable level. For example, instead of the usual 3 hours of people interaction per day, I can now handle 6 hours without overloading too badly - so for that to double without drugs suggests that this entire thing is much more treatable than it would seem from traditional literature if you know what you're doing.