Info for the more scientifically inclined | ADHD Information

[QUOTE=autumnstar]

Ok, I see what you're saying. I'd like to naturally be able to tackle this also, rather than dealing with drugs, the side effects, remembering to take them, etc. But what I struggle with is how to know what to naturally strive for.

I always thought I was normal. I thought everyone dealt with these distractions, racing thoughts, forgetfulness, miscommunications, etc. Since I've learned that 'normal' isn't this - I don't understand what 'normal' is. I would need to work with a 'normal' person to understand their differences to know what to work towards.

The other thought that pops up is, if it is (for lack of a better term right now) some kind of hormone imbalance that our brains aren't doing 'normally', wouldn't this hormone imbalance be like fighting an uphill battle?

One of the things that I recognized in myself was other women saying how bad their PMS is. I see myself there. My husband said that he always thought the PMS thing was a big excuse until he met me. He commented one time that he could see me not being able to control my irritation (it wasn't exactly anger but it was close) and watching me struggle with that. He couldn't imagine not being in control like that. And I've been reading alot of women say that during PMS, the meds don't seem to work. All you need is to be out of control of your emotions like that to understand that it can be a losing battle. But if the meds won't even work during PMS, that seems even more frustrating to be 'normal' most of the month then through back into that pit for a week each month.

Sorry for the ramble, autumnstar

[/QUOTE]

Arg, I just read something about this but damned if I can remember. It's the end of the quarter, I'm doing research for final papers and reading my fanny off!

Hormones are definitely a type of neurotransmitter but dopamine is a different kind and affects different receptors on different cells. Neurotrasmitters follow different paths in the brain. It's those paths (barring lesions--a physical impairment like a tumor or tissue atrophy or something) that affect behavior and thinking. Both nature (DNA and RNA) and nurture affect the pattern of neural transmission from nerve cell and region to other nerve cells and regions. Neuron paths are highly flexible. However... remember that one of the mandates of the brain is to conserve energy. Therefore, it takes a jolt to change a pattern. Introduction of drugs that affect the receptors will do it and so will conscious volition, practiced over time, as will natural chemicals obtained through the foods we eat.

You should read up on some heavy stuff about neurobiology and estrogen for a better understanding. Also, watch the very cool movie (out on DVD and available from Amazon or Target for ), "What the Bleep Do We Know." They explain neurotransmitters and receptors using very cool animation. Entertaining and eye-opening movie!

Here's what I'm reading from this- please help me out if you come from a background in neurobiology!!!

There is a particular gene (homozygous 10-rep allele at DAT1) that is found in kids with adhd. In these kids, the brain isnt doing what its supposed to with MPH.

The study looks at kids with different versions of this gene (adhd and non), how the kids respond to MPH (Ritalin) and what their brain scans look like with and without doses of MPH.

They found that when taking MPH (Ritalin), there was a higher level of blood flow in particular areas of the adhd kids' brains than in non adhd kids' brains.

Therefore, it looks like they may be able to use pharmacogenetics (study of how different variations of genes respond to differently to medications) and neuroimaging (the pics of the brain that show the blood flow) to see how various people's brains react to stimulants.

Anyone else????Those guys can't even spell floccinaucinahilipilification. floofthegoof38520.3834143519Hi Folks,

I know I don't usually post here (tend to lurk), but I might be of some help in this instance. . .

Methylphenidate= Ritalin.

The basics:

Neurons release neurotransmitters (chemicals), including dopamine and noradrenaline, to communicate with other neurons. In order to mantain a balanced concentration of neurotransmitter outside the neuron, you have to have a mechanism to get rid of the excess dopamine. What happens is the neuron that relesases dopamine also has a a dopamine transporter (DAT) which scoops up the excess dopamine and either recycles or gets rid of it.

Ritalin and amphetamine both work by increasing the amount of dopamine that hangs around outside of the neuron. Ritalin especially does this by blocking the DAT, preventing dopamine from getting scooped back into the neuron.

There is a gene that codes for the dopamine transporter; and like the gene that codes eye color, you can inherit different copies of this gene from either of your parents. Like eye color, there are a also number of variations in the structure of the transporter which slightly alter the efficiency at which it works and the ability of molecules to bind to it.

One of these variations (the 10-repeat allele), when inherited from both parents (homozygosity) seems to be associated with a different (possibly better?) response to Ritalin in patients with ADHD.

As for the implications of this study, it won't provide a diagnostic test for ADHD. What it might do is enable doctors to predict which drugs might work better for certain people, eliminating some of the guesswork. I.e. if you have a certain variation in your transporter, you may have a better chance of responding better to amphetamine that Ritalin.

Hope this was somewhat helpful and I didn't confuse you too much!

I will be reading this article when I get a chance to download it from work (can't access it from home), so if anyone has question feel free to ask.

-Tyger

(I'm both a researcher in the field and a sufferer of executive dysfunction of some kind or another)
Oh . . . sorry, wanted to give my opinion on the SPECT imaging again . . .

I understand people's reservations with Amen's use of SPECT imaging, but I also think there's a big difference between using an imaging technique to *diagnose* a condition, and using it as a tool to aid in the treatment of an already diagnosed condition. . .

If given a diagnosis of ADHD made by other means, you can by looking at the SPECT scans provide an accurate guess as to which medication has the best chance of working in the first instance, that's great! The big problem is that I have no published evidence to back me up, which is one of the reasons why I am so sceptical of Amen's claims. As far as I know, there is no work published in scientific journals that lend support to his claims.
uhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhhh

[QUOTE=ADHDMD]There is no test that a doctor can order to diagnosis you with ADHD. Genetic testing is a highly experimental test done only in special laboratories and is VERY expensive. ADHD remains a *clinical* diagnosis, which means only after an evaluation by a clinician experienced with ADHD do you know if you have it. The SPECT scanning recommended by Daniel Amen, MD is a bunch of baloney. There are minor differences in SPECT scanning among ADHD folks as a group, but it can't diagnosis individuals. Every ADHD expert and reputable organization is clear on this. Amen is the only doctor who thinks otherwise. Maybe someday we'll have a 'definitive' test, but truthfully most of the cases of ADHD just aren't that difficult for an experienced clinician to diagnosis. Things should get clearer as we get better Adult ADHD criteria and research in the future.[/QUOTE]

Are you open to some other information? What you just said is the same thing my own shrink told me, so I assume that's how you all are trained. However, I found some contradictory information when I was researching links between fibromyalgia and ADD and the name you just mentioned isn't striking a chord. Possible, but I don't think so without checking.

If you're interested, I'll look up what I found and post it. If you're not, I won't. God knows I've got enough to do.

For background, I'm just getting up to speed on the various scanning technologies (PET, fMRI, and MEG) so may have missed or misunderstood something. (Am planning to use brain scanning technology for my dissertation--probably post-doctoral research because of the cost. Leaning toward psychoneuroimmunology at this juncture. ADDer, heal thyself. Ha! )

There is no test that a doctor can order to diagnosis you with ADHD. Genetic testing is a highly experimental test done only in special laboratories and is VERY expensive. ADHD remains a *clinical* diagnosis, which means only after an evaluation by a clinician experienced with ADHD do you know if you have it. The SPECT scanning recommended by Daniel Amen, MD is a bunch of baloney. There are minor differences in SPECT scanning among ADHD folks as a group, but it can't diagnosis individuals. Every ADHD expert and reputable organization is clear on this. Amen is the only doctor who thinks otherwise. Maybe someday we'll have a 'definitive' test, but truthfully most of the cases of ADHD just aren't that difficult for an experienced clinician to diagnosis. Things should get clearer as we get better Adult ADHD criteria and research in the future.

The Myths that abound about the workings of the used chemicals to better manage the adhd brain are nicely exploded by your post on the genetics.

On the use of Spect Imaging to identify the most, individual case effective med is at this stage, a real wild frontier adventure. As you say, Not Enough clearly replication of findings in different centres to test possible validity. Scientific Journal Publication does not validate sufficiently as far as this Adult ADHDer is concerned. If we had say validation from differing cultural and ethnic perspectives then maybe it could be seriously considered and proposed.

TyGrr, Good to see U making such a valid contribution in our little corner. Thanks for the info and Ur time!

Sachetm,

The obviously clear findings of the "Amen" research are of themselves a vital step in the Neurobiology portrait of the ADHD brain. Why i am holding out on the multicentre/multiethnic replication for validity is because dispite the best efforts of Science the label of White/ Caucasion Afflicition is still being used in reference to ADHD in some parts of the Globe. As there is actually no justification for such a position I as an Adult ADHD with Dyslexia and Dyspraxia will always challange this until reasonable minds prove otherwise. The differences in the Prefontal Cortex between ADHDer and non ADHders is a facinating discovery and it is an article worth posting, if U can find it Sachetm. Unfortunately i do not have reference to it, Sorry! Sachetm on the Observation of Neuron firing patterns is there a Research Project in New Mexico. It was mentioned to me in passing but to date i have not found a method of getting any info on it.

Apologies to U for not explaining reason for my stance.

ryan195038524.4471296296Thanks Tygrr, I found your explanation to be very clear and helpful!!!

I just bought Dr. Amen's book, and in the images provided, the depressed pfc activity is clearly visible vs. a "normal" scan. Are you saying the data presented by him is an unrepresentative subset or something, and it is not that consistent in most cases?

[QUOTE=RandomUser]I just bought Dr. Amen's book, and in the images provided, the depressed pfc activity is clearly visible vs. a "normal" scan. Are you saying the data presented by him is an unrepresentative subset or something, and it is not that consistent in most cases? [/QUOTE]

On the validation of data the use of multicentre replication is healthier then taking a particular localised research universe and making claims for findings. The approach of carrying out the same piece of research in different parts of the world with universes of differering ethnic make up will be needed for validation. I know from monitoring research for the last seven years that the clearest consistency has been found with the use of Multicentre verification approach.

[QUOTE=ryan1950]

[/QUOTE]

Are you contending that variability may be in the imaging equipment itself as a variable or that brain physiology differs regionally. If the latter, I don't think that's consistent with neurobiology in general. If his sample size was too small or insufficiently heterogeneous that might slant things, but I'm having trouble grasping how regionality and ethnicity have anything to do with neurobiology. Could you explain your reasoning a bit more?

(I guess I'm going to have to go find that study I found previously, now, because I don't think it was this guy and it did claim that there were observed differences in the prefrontal cortex (think that was it) of the brain of someone w/ AD(H)D and without it. The study was done in relationship to fibromyalgia (or correlating it with AD(H)D--something like that I believe, because that's what I was looking at when I found it. Here's hoping I bookmarked it!

Just on an anectodotal level, there have to be physiological differences. Whether scanning is advanced enough at this point to show neuron firing patterns and neurotrasmitters produced is the question. I'm not sure what MEG shows vs. fMRI, but I've heard it does provide more detail. I think this will happen in the future but probably has a ways to go to get to the "right" level of detail. (Trying to avoid going to look for that study! )

Sorry for the ramble, autumnstar

Sachetm,

Excellent piece of research by you t.y. This particular project that you highlight is, if i am not wrong, being duplicated in other research centres globally and if as suspected the results found can be replicated it is another step on the road to finding exactly ADHD is chemically. Pheww That would be something to be "out of control" about. The fact that the hormonal changes at the end of the cycle are not mitigated by the meds is something i never considered as a man. Autumnstar, I can only start to imagen how frustrating that is for you after all the work you have done on yourself, Gess! we males need more education on it.

I know it's daunting. I don't understand half of it and am not motivated to go to some medical dictionary. However... the key thing I saw is that last sentence. There's some genetic link related or influenced by medication that affects the brain in specific ways for those with AD(H)D.

The reason I posted this is because I had a shrink tell me that there were no physical tests for AD(H)D. I knew he was wrong but didn't feel like arguing with him. (If he keeps up with that doctor arrogance thing, I'm dumping him. Assuming so far he was busy, tired, in a bad mood, or something else.) This is the second abstract I saw that mentioned this MPH thing, which I'm guessing may be some kind of neurotrasmitter. I have so much to learn to really understand neurobiology!

What I do know is that the brain is programmed (through DNA) to only recognize substances it can produce itself. Introducing them artifically (e.g., medications) is simply another way to change our neurobiology. The same things can almost always (giving myself an out here for that smartass who may come along) be accomplished by some form of self-training. It just takes longer and is often harder to accomplish. Ergo, if this neurotransmitter (assuming that's what this MPH stuff is) is lacking and can be enhanced through drugs (e.g., Ritalin), then how might that same effect be induced "naturally?"

Personally, this is where I think it gets interesting! (Unless I know so little I didn't get what this was saying at all!)

sachetm38519.8028240741

"The homozygosity of the 10-repeat allele at dopamine transporter gene (DAT1) seems to be associated with a poor response to methylphenidate (MPH) in children with attention-deficit/hyperactivity disorder (ADHD). This pilot study aimed to simultaneously assess polymorphisms at DAT1, response to MPH, and neuroimaging. Only ADHD children with at least a moderate response to MPH were included. Significantly higher regional cerebral blood flows assessed by single photon emission computerized tomography (SPECT) were detected in medial frontal and left basal ganglia areas in children with homozygosity for the 10-repeat allele at DAT1 gene (n = 4) than in children without this genotype (n = 4) (P < 0.05). These findings provide a preliminary connection between pharmacogenetics and neurobiological investigations on stimulant treatment of ADHD."

From: http://www.amenclinic.com/bp/abstracts/abstract_detail.php?r ecordid=1220

Implications, anyone?