- To Change Your Mind - Details Matter
ADHD And Glutamate: Neurotransmitters Evolve
CoreBrain Training
October 30, 2010CorePsych Blog – Brief Kindle Updates
December 5, 2010
ADHD Challenges Involve More Than Dopamine and Norepinephrine– Thanks for this Guest Post from Lindsay Grude and Dr Kelly Olsen with the Research Team at NeuroScience up in Wisconsin.-
Common Sense
Attention deficit hyperactivity disorder (ADHD) is commonly associated with dysfunctional dopamine and norepinephrine neurotransmission, and most ADHD drugs target these neurotransmitters. [ed note: Intuniv, a new non-stimulant has added interest regarding the function of glutamate to the list of relevant ADHD neurotransmitters – and more about yet another one, PEA, in later postings.]
Glutamate Actions
Emerging research also implicates the neurotransmitter glutamate in the development of ADHD, likely due to its interaction with dopamine and norepinephrine. Current literature suggests that glutamate contributes to the development of ADHD through its interaction with dopamine neurotransmission. Â The striatum and prefrontal cortex, two regions of the brain that are implicated in ADHD, interact by exchanging dopamine and glutamate projections. Â The release of glutamate from the prefrontal cortex promotes responsiveness to external events, and elevations in glutamate signaling result in increased behavioral responsiveness to external events. Responding in a timely manner to changing stimuli is of course necessary, but excessive responsiveness may lead to constant shifting of attention. Â The striatum is likely the brain area that keeps this attention-shifting in check, as striatal dopamine released in the prefrontal cortex inhibits glutamate release from these neurons, thereby decreasing behavioral responsiveness to external stimuli.
As a result, inadequate dopamine neurotransmission from the striatum allows uncontrolled glutamate release, and the resultant excess glutamate signaling increases behavioral responsiveness to external stimuli, i.e. increases distractibility (Russell, 2003).
Following this line of reasoning, Ludolph et al. (2010) support the claim that excessive glutamate stimulation of the striatum from the prefrontal cortex results in the clinical manifestations of ADHD. Atomoxetine, a fairly new treatment for ADHD, was initially proposed to be effective through its support of norepinephrine transmission. However, Ludolph et al. found that the drug can also antagonize the N-methyl D-aspartate (NMDA) receptor, a type of glutamate receptor, and that this effect may have a role in atomoxetine’s success in treating ADHD.
Glutamate Relevance
It is also possible that a functional defect with glutamate receptors may contribute to the development of ADHD. In a study of spontaneously hypertensive rats (SHR), which are used as a model of ADHD, an abnormality in the NMDA receptor was found and thought to be a contributing factor to ADHD-related symptoms these rats display (Lehohla, 2003). SHRs have been used as an ADHD model to test glutamate α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors as well. Russell (2001) demonstrated in both SHR and control rats that glutamate injection into the prefrontal cortex caused norepinephrine release and determined that AMPA receptor stimulation on noradrenergic terminals was responsible.
More importantly, the study also found that the glutamate-stimulated release of norepinephrine was more pronounced in SHR compared to control rats. It is clear from the growing body of research that glutamate plays a role in the development of ADHD. Excessive glutamate release in the striatum increases behavioral responsiveness to external stimuli, and abnormalities in glutamate receptors have been associated with symptoms of ADHD.
However, the degree to which glutamate contributes to ADHD is yet unknown. It is imperative that future research explores this pathway, as the manipulation of dopamine and norepinephrine is simply not effective for everyone.  In the quest to develop more effective drugs to treat ADHD, glutamate will hopefully be more frequently spotlighted as a potential target.
———————————
Thanks to the NS team!
cp
———————————
References
РLudolph AG, Udvardi PT, Schaz U, Henes C, Adolph O, Weigt HU, Fegert JM, Boeckers TM, F̦hr KJ. Atomoxetine acts as an NMDA receptor blocker in clinically relevant concentrations. Br J Pharmacol. 2010 May;160(2):283-91.
– Lehola M, Kellaway L, Russell VA. NMDA receptor function in the prefrontal cortex of a rat model for attention-deficit hyperactivity disorder. Metab Brain Dis. 2004 Jun;19(1-2):35-42.
– Russell VA. Increased AMPA receptor function in slices containing the prefrontal cortex of spontaneously hypertensive rats. Metab Brain Dis. 2001 Dec;16(3-4):143-9.
– Russell VA. Dopamine hypofunction possibly results from a defect in glutamate-stimulated release of dopamine in the nucleus accumbens shell of a rat model for attention deficit hyperactivity disorder–the spontaneously hypertensive rat. Neurosci Biobehav Rev. 2003 Nov;27(7):671-82. Review.
Related articles
- Intuniv Answers: ADHD Neurotransmitters – Glutamate Matters (corepsychblog.com)
- Brain chemical finding could open door to new schizophrenia drugs (sciencedaily.com)
- When Memory Starts Working (thebeautifulbrain.com)
- Lab Discovery Could Lead to New Meds for Psychosis (psychcentral.com)
- How the ultimate smart phone sends text messages: Neurotransmitters. (didyouseemycrotch.wordpress.com)
- Pitfalls in the Diagnosis of Adult ADHD (brainposts.blogspot.com)
37 Comments
Hi Dr. Parker,
I was just wondering if you can shed any light on why MSG in foods can cause the food to be addicting. I have recently begun giving up foods with MSG, and I feel like I am experiencing a bit of a “withdrawal” feeling. I also watched a very interesting TED Talk by Dr. Katherine Reid on how a low glutamate diet helped reduce symptoms of autism in her daughter. (I know that is a very controversial topic, but I’m basically just wondering what happens in our brain when we consume foods containing MSG.) How does it impact dopamine? Your opinion would be much appreciated!
Kelly,
This link will help: http://neurotransporter.org/glutamate.html – And do take a look at the bottom of the next article on transporters. Transporters become subject to epigenetic change that can be measured and corrected through Walsh protocols: http://corepsych.com/walsh-resources.
cp
Memantine chemicals in the near future be used to treat ADHD?
Reha,
Already used, just not approved by the antiquated FDA. Acetyl Choline [ACh] will help w memory, and we use several supplements at CorePsych that significantly boost memory thru ACh as well as other precursors for executive functioning, Short answer: yes.
cp
Hi Dr.,
I am a 31 yo male with long-standing ADHD, which is most easily described as inattentive. I am an extremely capable and somewhat successful scientist (my critical reasoning abilities are extremely above average, though my retention, memory, and academic rigor are extremely below average), but my career progress has been severely hampered by ADHD. I suspect that I have some sort of food allergy, as complex carbohydrates have always left me tired, feeling short of breath and bloated/flushed, as well as completely unable to concentrate. This response has become more pronounced the older I have become. I have responded somewhat well to Strattera (though it induced sexual dysfunction). I am currently on Wellbutrin and Intuniv, which I can only say are completely required for me to be productive, though completely inadequate for a normal, healthy level of productivity. I feel as if there is an “activation potential” of anxiety and circumstance-induced hypomania that is required for me to be productive. Above this level of [what feels like adrenaline rush] I am extremely productive, below it I am embarassingly and unsustainably unproductive. I in the past have tended to abuse stimulants to some degree to lower said “activation potential”, though they can increase distractibillty via hypomania, and are probably only good in low levels if I am to write and get concentration dependent work done. I am shockingly easily addicted to coffee, drinking up to 30 cups a day when I am writing, with withdrawl symptoms when I miss a cup. I find it best to avoid it altogether now. I feel I am not making sufficient forward progress as a reliably productive person. I am writing all of these traits because they are outliers, and I hope that in some you recognize a familiar pattern, and can point me in the right direction to at least start the process of getting better. None of my doctors have had the willingness to treat my ADHD as anything but sub-clinically important, and my psychiatrist does not take a studied nor insightful approach to treatment. If it would help I would switch doctors if you could point me toward a physician/psychiatrist who can help me. I live/work in the north shore Boston/Boston metro west area.
Thanks,
Noah
Take a look at this ADHD FAQ piece it will give you specific direction on this complex presentation:
http://bit.ly/adhdfaq
Then watch my video playlist on gut and brain here: http://bit.ly/mindgut
And yes, we do consults in Boston all the time – long distance… see the CorePsych.com/Services page for details.
cp
[…] ADHD And Glutamate: Neurotransmitters Evolve (Dr. Charles Parker’s CorePsych blog) […]
Hi,
I am a 53 yo MD with debilitating ADHD which has gotten me on welfare. (Ask Gina Pera, she knows me)
My 80 mg q 4 hrs mg of Ritalin/day is not working much anymore (dosing was adjusted in 2007 by Bill Dodson with the help of TOVA (I “normalize” my TOVA (But not much my clinical) @ 40 g of Focalin q 4 hrs))
I have been trying NADH on top of that and must say I am getting some results… Hope it lasts.
Anyone else had any luck with it. I understand U need the patented formula for good gut delivery.
The iHerb.com one which U can get w/a discount ( use coupon OLA692 to get 5 US$ off and Yes, I do get a commission but it does seem to work.
Nicholas,
Sorry to be so very late getting back, been off my blogging schedule through vigorously planning a presentation in DC, and regrettably it just didn’t work out.
You, my friend, need a complete workup. You undoubtedly have a medical problem with challenging gut issues and really must do the “Transit Time” thing [Search here to find details]. You may, as many do out there in Stanford’s shadow, think that IgG is for the birds, but I use it all day everyday and have been having great success. When mixed with next understanding the NeuroScience findings, then we are home free. Don’t reply, but ask yourself: How many times a day do I go #2??
Happy to consult if you want to get into it, – and please say hello to g, she is a great woman, and tho we haven’t met I count her as a good friend and colleague.
Just reread your comment… welfare?? Please drop me a line off line and I will spend some time with you to get you pointed in the right direction.
cp
My 19 year old daughter had a horrific ski accident march of 2010. She smashed and broke both her femurs, tibia, tibia and humorous. Along with the multi long-bone fractures came a devastating result of massive fatty emboli in her brain (and lungs). It also came to light later that she did hit the back of her head enough to create a dent with cracks in her helmet. This was not discovered by any of the doctors or ski patrol as the other injuries were the focus. The miracle is that she has been recovering faster than anyone expected and she has insisted on resuming her college career (earlier than dr.’s think prudent) and has just begun a full load at a challenging college. Her word/speech area was definatly effected and it is showing up when she writes her papers- she has the concept, but the thoughts are not clear and word choices can be odd. She is also struggling with symptoms very ADD like-(not ADHA) before, she was an excellent student with no such symptoms. I have been trying to find any information about TBI and the Medications used for ADD and how they interact. SHe has had many typical TBI symptoms with regards to healing such as insomnia, mood swings, depression….BUT I am very happy to say, many of those symptoms disappeared with regular (high-level) chiropractics, acupuncture and cranial sacral. Excellent results for the other symptoms, but not for the areas needed to be a successful student. I would not consider ADD medication if it is known to have negative interactions with TBI sufferers…and even less is known about Fatty emboli patients. Last MRI looked good with the exception of a light foggy cloud-like area in a place the neurologist said made her brain look like and elderly persons…but that neurologist has been very, well, unhelpful beyond that (any great neurologist or neuropsychiatrist in the denver are…send my way!) Looking to see if I should pursue medication, and a new doctor relationship…
Erin,
Much literature exists on TBI and ADD, and using stimulant meds for the secondary ADD symptoms. I have several posts here including this one that drives more to the point on TBI and ADHD – just put ADHD and TBI in the Search Box for more info.
The latest for me, alluded to in that one link, is the value of neurotransmitter testing and correction which we can do long distance, no problem – if interested. Not many psychs using neurotransmitter precursors at this moment, but I predict they most will be in the next 5-10 yrs as I have seen some considerable improvements using NT testing with TBI. Just email Sarah on the Services page if interested in talking further.
cp
Dr. Parker, my 8-year-old son has been on Vyvanse for nearly 6 months – currently 50 mg – and we recently added a new 24-hour drug – Intuniv (currently 2 mg). For the past 2 days, I’ve followed the doctor’s suggestion to slowly decrease the Vyvanse to see how he does. Having trouble sleeping seems to be our biggest issue. I’ve been giving him Melatonin about 2 hours before bedtime and this seems to help him fall asleep, but he has been waking around 3-4 every morning complaining that he has been awake for awhile and can’t get back to sleep. He usually does, except last night he claims he didn’t sleep at all and was very tired and emotional. I sure hope that as I reduce the Vyvanse and rely more on the Intuniv that we can alleviate this big problem. But, I’ve read that a lot of parents complain that their children on Vyvanse have trouble sleeping. Before taking any of these medications, however, my son was a good sleeper. I’d like to know what you have to say about this, and any suggestions you might have. Thanks.
Beth,
Many more questions too lengthy to bring up here. Most importantly: sleep problems with Vyvanse most often mean one of two things – the dose is too high [therefore measure carefully DOE] or he has an associated underwater metabolic problem with the consequence of accumulating and metabolizing too slowly.
Intuniv often works very well with Vyvanse and they are quite compatible – not necessary to reduce Vyvanse unless it’s adjusted incorrectly.
cp
My ADHD son is 8 yrs old and diagnosed two yrs ago. We have been monkeying with medication for 2 yrs and still have issues. He is currently on Concerta 54mg. We have tried all other stimulants (except the patch) and Straterra. He does not tolerate short-acting meds. Concerta looses effectiveness after a few months and requires an increased dose. Then we’ll try other meds but always come back to Concerta because it’s best, when it’s working. He has zero appetite though. When he was diagnosed 25 months ago, he weighed 52 pounds. Today he weighs 50 pounds. He has grown an inch or so in height but the kids at school are starting to noticeably outgrown him — it’s not good. Besides not eating much, he’s picking at his fingers and chewing incessantly.
All of this makes me feel like it’s too much meds. But, lower doses of Concerta don’t provide enough hyperactivity and focus control for school. Adderall and Vyvanse both caused extreme mood and aggression issues that weren’t present at all before medication. Focalin caused some psychosis. (So did Celexa and Straterra when taken in conjunction with Concerta). Buspar caused the Concerta to not work when taken together.
Other things of note: he’s never had a problem sleeping (except on short-acting Focalin and Straterra). He is super-hyper in the mornings on the lower doses of the stimulant (more than before meds). He is gifted intelligence but has a writing disability and slow processing speed. He bounces around from a lack of proprioceptive input.
As for GI, he had an upper and lower GI test as an infant to rule out a pyloric stenosis. He was just found to have reflux and given a prescription for that. He hasn’t had any problem with reflux since he was a baby (that I can tell anyhow). When has was 2-3 yrs old, he had lots of problems potty training although his stool was normal. They put him on a laxative for a long time thinking it would make him run to the potty and learn that way but it didn’t help. To this day, he will soil himself from holding. But there’s absolutely not physical reason for it and he doesn’t do it every time so he’s not afraid of the toilet. This seems like a focus issue and not physical but I wonder since you talk so much about GI issues being related.
Does any of these point you in a certain direction? I don’t know where to go from here and his doc just wants to start adding mood meds. I don’t want to add meds to make original meds work. I want to get to the root of the issue and I want him to eat and grow.
Any advice would be welcome!
Penny,
Do review all the materials at my Testing Options page and consider IgG testing ASAP – if your guys can’t/won’t do it call my office for a consult… He has a narrow therapeutic window based upon immune system dysregulation until proven otherwise – almost classic in presentation.
cp
If the notion that an abnormality in glutamateric neurotransmission comes as a recent revelation to those charged with treating this disorder, I applaud Dr. Parker for having the courage to admit such an overt failing of logic amongst his colleages.
Its implications regarding the current understanding of this diagnosis amongst industry professionals are … not encouraging.
My subjective frustration notwithstanding, this site is certainly a great resource for patients like myself who are educating ourselves as a means of facilitating the treatment process. This cooperative effort has allowed my physician and I to drastically decrease medication dosages and eliminate altogether adjunctive therapy (Buproprion HCL) by introducing functional supplementation along the lines of NADH, Tyrosine, Omega-3 & B vitamins.
In my opinion, patients who are not working in tandem with those charged with treating them should be afforded no right to complain about an ineffective treatment protocol.
Pete,
We are clearly on the same path, and I strongly recommend that readers take a look at Pete’s views on Psychoneuroimmunology over at his site PeteSapper.com
Thanks for your kind remarks, look forward to bumping into you sometime out on the road. The devil is in the details, and it is foolish to assume that the public is unable to get the details when they must understand and ultimately make the choices for their own health care. Stay tuned, Pete, for the CoreBrain Training next year, it will be right up your alley, from SPECT and psychopharm to neurotransmitters and actually measuring neurotransmitters – 12 of them – and how to use them in everyday understanding of mind and body presentations. Sign up for the CoreBrain head’s up list to keep you posted here.
Best for the Holidays, 2011, and thanks again,
cp
I am a 30 year old college student who suffers from ADHD. I do very well in school while I’m on my stimulant medication, the problem is, no matter what medication I take nor no matter how much my DR. ups the dose I only get 6 or so hours of benefit, and as any one who has been to college knows, that just will not due. I’m at my wits end. I’ve been on almost all the major stim meds, even desoxyn, but after a few weeks I’m right back down to 6 hours. Even to obtain the 6 hours I have to take all kinds of supplements. Glutamine, Tyrosine, Taurine. I’m in a bind. I was hoping maybe you could shine some light on this before talk to my Dr. about switching meds again.
Chris,
Suggestions about meds require much more info than your comment provides. Dosages, types of meds, metabolic issues are all relevant as is protein breakfast. Take a look at this complimentary 20+ page White Paper on Precise Solutions for ADHD Meds and then get back.
cp
Hi there Dr. Parker,
So I no longer have the doubt that I posted about back in October. The meds definitely do help a lot — even though we still haven’t “finalized” yet. I can say this because I’ve had about a week or so of not taking anything and things have been much more difficult overall.
What they do help:
1) Initiation – it is nowhere near the battle with myself to begin working on tasks and to actually get more than one thing done in a day
2) To Do lists – I can actually sit down and make one, and the key here – have it be one that is reasonable and that I can actually accomplish rather than just having everything on it and being overwhelmed (subsequently avoiding the to do list, which is what I’ve always done)
3) Less getting side-tracked, impulsiveness – although I still get “hyper-focused” on non-important things, but am able to more easily (usually) break that…so that instead of stopping 6 hours later, I stop 30-50 minutes later than I planned.
4) General less confusion – I don’t have as many moments where there’s non-specific “stuff” in my head that makes it difficult for me to think. Also less restlessness, hyperactivity — I can think when I want to for the most part.
5) Maybe less worry — not sure about this one though. If I’m going to worry, I do – although it may be easier to work out of it.
6) Less frustration (especially on the road) — it’s like there’s more time for me to be able to actually change the thought that makes me angry, rather than just reacting immediately. I say this (strong, quick emotional reactions) is better…and it is…but it depends on the circumstances. Sometimes it’s not. But I can’t expect the meds to do everything —— right??!!
7) Sleep — I get to sleep more easily; actually go to bed at reasonable time and it takes less time to fall asleep.
8) Far less depression — even though this had improved to a certain extent before meds, and with a rocky start with the meds; I basically don’t have it as much when I take the meds. My theory is that since I’m getting done what I need/want to, it’s not failure after failure and I’m not so hard on myself. But the catch is that I still can be overall; and when I haven’t been taking the meds, the hit has been even harder than it was before I started.
So, is taking the meds really an answer??
And briefly, what they don’t help (which makes sense I guess): my estimation of time and how long things take, my organization of certain things, my doubts – not about whether the meds help now – but about whether or not I should be taking them.
Just wanted to share some of my experiences with you and your readers; and get your take on how I’m doing….Thank you!
anon3,
Your responses are quite typical when meds are adjusted correctly – good for you! And, yes depression is somewhat relieved when failure and struggle is diminished. It does sound, without more info, that you would benefit from more consistently taking the meds, that the possibility of a comorbid depression is somewhat complicating your progress, and the rebound is quite typical when you go back to your erstwhile level of functioning.
The last few lines suggest, without being more precise about DOE and dosing information, that your dose of stimulant might be slightly off. Just as I mentioned in another comment here on this posting I do suggest reading my complimentary White Paper for more information – available here at CorePsych Blog: Precise Solutions For ADHD Medications.
cp
Thanks 🙂
I’m sure you don’t recall, but in my previous post back in October I’d indicated that I take an immediate release and an extended release. I also have read your paper, as well as the book. The DOE on the extended is low – about 7-8 hours; and the DOE on the immediate is in the range of 4-6 (adjusted to be right about 5 or 5 1/2).
But like I said, right now I’m on nothing.
I guess my question/comment is, the meds can’t fix everything so how do you know if you should really take them at all?…even if it does help, which now I know it does.
I’m not one to take an easy way out, and even though I believe meds definitely have a place sometimes and that I personally have benefitted, I don’t know how to decide. Maybe that’s just my pride or my personality…or some aspect of adhd or depression….I wish it was easier to figure out.
anon3,
My criteria on the use question is pretty simple: if you need it and have sufficient trouble without it, use it. If you do see the larger picture and wish to take every step to remain off just using neurotransmitter chicken catchers, and simply want to grow your ranch with more chickens, then get the neurotransmitter testing, look at your immune system and neurotransmitters and see if you need neurotransmitter precursors – then add if you do.
cp
Hey Doc CP~
Hard to believe it been two months since Rachel has been in to see you. I wanted to let you know how she’s doing and perhaps get some feed back from you and your fellow professionals that participate in your Blogs… I have also invited Rachel’s attending Doc to feel free to add any thoughts she may have as well. I’m sure my (sp) grammar leaves much to be desired but hey, I’m a blue collar guy, ever learning in this path of life~ anyway…
Rachel (18yrs) is presently attending Hughes Center. As you well know, she has been diagnosed with numerous behavioral disorders as well as MR and Autism. I cant even begin to list them all but, please feel free to post your findings if you like. At present, the most predominant of these problems are Schizophrenic delusions, (I believe causing and resulting in) supersensitive anxiety and behavioral disorders. Her present medications are Ziprexa 15mg daily (5mg in the morning and 10mg in the afternoon) and, a daily dose birth control pill (which is very effective in easing the discomfort she has during her menstrual cycle). The positive results of this med are that Rachel’s cognitive state is (seemingly) not diminished; she is able to participate in group activities, have rational and articulated conversations and be more progressive in a learning environment. She is also able to identify and control these delusional manifestations to some extent but, she still has them regularly (and by her own description, they coerce her to inappropriate behaviors). I’ve also noticed that the “clicks” of pinching her lips along the length of her fingers and rolling her hair on her fingers are less pronounced as well. The negative results of this med are that Rachel has a constant sense of hunger and, as the med wears off, her delusions, anxiety sensitivity and negative behaviors seem greatly magnified.
The dialog with Rachel’s attending doctor (with the inputs of her previous doctor from Cumberland Hospital) has come to us agreeing that, while this med helps Rachel to some extent, it seems to only be masking the problem and that increasing dosages may not be helping. We are presently reviewing a number of options including; short term trials @ NIMH (in Bethesda, MA.) and 30 day Neurological diagnosis @ VTCC (in Richmond, VA.).
I definitely welcome your inputs since we will be returning to your care when Rachel achieves an outpatient level of treatment. So we’re clear on this, you have my authorization to post anything you like about Rachel in this forum except for her full name and Address and, I will be happy to put that in writing and bring it to your office if you need me to. We just need help… not fans! If Blogging about this can help us, or others in similar circumstances… cool… let’s do it~
Respectfully,
RD
RD-
Blue collar, pink collar, white or brown, we absolutely don’t discriminate on how you write or what you comment on…unless it’s a useless blast – but that’s not in your nature.
I do agree with your doc on the masking issue, we just need to find out what it’s masking!
Most outstanding about this comment, as have many of the readers at CorePsych Blog, is that you are reaching out and taking a risk, doing whatever you can to get your girl straight. I don’t want get into what your current docs should do [it’s just not appropriate], but I can tell you, without hesitation, that we will do anything we can to get more evidence on the table for your girl when she comes back to the office. I look forward to the neurotransmitter testing and IgG testing which I’m sure I brought up in the first visits, but think I recall couldn’t be accomplished because you were already on a path of more structure due to her significant regressions. My *guess* right here in front of you and the readers… she is a flaming case of immune dysfunction with a serious pro-inflammatory cytokine shower going on 24×7.
My bottom line: Let’s go ahead and talk about her progress and her problems here, perhaps post about it in anonymity with your feedback right up there for anyone to see and perhaps contribute to – and yes, would like you to sign a release in the office if you are looking for more feedback in this forum.
cp
My son, now 34, was 4.5 weeks premature and had respiratory distress syndrome at birth. He exhibited signs of moderate to severe ADHD throughout his school years. At 15 he developed an acute life-stealing case of Obsessive Compulsive Disorder. I won’t bore you with all the details of what we have gone through trying to find the right treatment and drugs for him. Just know that life stopped and did not restart for approximately 8-10 years. However, I can happily tell you that he is a successful entertainment attorney and LIFE IS GOOD! Except, all of the medication side effects…lethargy, sexual side effects, etc. He wants off the medicine. He has taken anafranil for 18 years (at times in combination with other meds, but always anafrani). I’ve been trying to do some research to see if getting off the drug is possible. I’ve found information on the OCD website regarding glutamate imbalance as a source of OCD. I was just wondering if untreated ADHD and the development of OCD are related. Any thoughts on this and / or any thoughts on getting off the meds?
Gay,
Absolutely related [OCD and ADHD], both issues covered vigorously in my new book, and directly related to glutamate challenges, as well as histamine, PEA, dopamine and norepinephrine – all measurable with NS testing outlined on this neuroscience page. My firm recommendation: he should consider NS testing to find out what the underlying biomedical challenges are.
cp
Gay,
One other thought that might sprinkle some more insight into the OCD/ADHD conundrum- both diagnosis are simply descriptions and describe an appearance of symptoms, one of my chief concerns about the insufficiency of the current outdated diagnostic codes as described in this CorePsych Blog post about the DSM 5.
And another point in this CorePsych YouTube video on Anxiety and ADHD.
cp
I found this topic interesting. I am reseaching the potential problems that may be associated with genetically modified plants, which promote a huge increase in the use of herbicides. Most GMO plants are modified to survive large doses of herbicides. What I have learned is that the major metabolite of glyphosate (the widest used herbicide in the US) is AMPA. In plants or grains the AMPA is more concentrated on the outer surface, such as the bran on grain but can be found present in all plant parts. AMPA is an excitory which acts very similar to glutamate. AMPA can work directly on the receptor ond also more recent studies in humans have shown that even a trace of AMPA can ramp up the effects of glutamate or other excitories as much as 15 times. When approving GMO plants for foods, the FDA only evaluates the unadulterated transformed plant. (unsprayed plants) They do NOT evaluate the fact that the intention of the end product is to survive high doses of chemical herbicides, (which is what the end consumer actually gets to eat.) So the only benefit of the GMO in the plant is to “survive the effects” and “conceal the appearance” of the chemical concentrations within themselves.
The EPA only evaluates the herbicide itself, not the metabolite (AMPA). In the EPA approvals for glyphosate, there have been NO neurological toxicity studies included. They also lack long term studies of the accumulated effects of the metabolites.
Original approvals were based on expected use volumes. The volumes of herbicide use have increased more than 20 fold with hundreds of millions of gallons of glyphosate being used annually on our foods. (Multiple sprayings on one crop)
Ph plays a strong role in the binding of AMPA. AMPA can concentrate in various tissues or bone of plants, animals etc.. I see a strong correlation to the increased use of herbicides and I suspect that residual AMPA will eventually be recognized to be directly linked with many neurological disorders.
Shawn,
You are very much on the right track and with some of the leading authorities in the field who regularly bring up pH as related to a variety of issues from immunity to neurotransmission. Herbicides are adding a significantly pathological variable that continues to need careful assessment from folks like yourself.
Thanks for weighing in – a best wishes with your continued work.
cp
Maybe this question isn’t answerable (yet), but….other than the fact that it’s believed genetics plays a role –
What causes ADHD? I know the manifestations can be because of innumerable reasons and that ADHD itself can be influenced either positively or negatively by these same reasons.(sleep, exercise, nutrition, allergies,thought patterns, sensitivities, hormones, free choice, etc…)
But what I want to know is, when considering ADHD as a neurological imbalance of certain neurotransmitters, what actually causes that?
Further, is there evidence that ADHD is truly more prevalent now than in the past? Or is it that it’s being identified better? Or is that people don’t want/”have time”/etc to work as hard to develop a healthy lifestyle for themselves and their children, and so they seek a diagnosis and subsequently medication? Or is it a combination of all of the above? How do you, as a practitioner, discern between these things? (Do most practitioners even try to discern between them?)
Thank you
Theresa,
The causes of ADHD are multiple and fill volumes – from genetic to environmental toxins to brain injury. We have better measuring tools, more effective molecular and cellular measurements that can specifically identify challenges down on the intracellular level.
Bottom line: stay tuned here for a series of presentations and a new website next year with more specific training modules on all of your questions – and interviews with leading authorities in brain physiology. No easy answers, but excellent new tools do provide better treatment targets and more consistent outcomes. Many people just want the meds, and the system is currently set that meds are the standard of care… but the meds are used quite frivolously by too many. See ADHD Medication Rules for more details.
cp
I’ve read the book, which is so incredibly helpful. Aside from that, I just want to know everything and I want to know it now…even though I recognize the lack of practicality and possibility in that statement. i guess there has to be a balance between remaining/seeking to be very knowledgeable and also accepting at some point “what is” — and being ok with that. I’m not there yet…Like I said, I want to know for certain why/how, so that this can make sense in my mind better — so that I can be confident it’s not (always) a personality flaw or my fault.
As a comparison, I’ve had relatives with different forms of cancer, and even that, we still don’t know what caused it…even though there is very clear physical evidence that there were tumors throughout the lymph system. (such evidence is clearer than tools at the disposal for diagnosing and treating problems like adhd — even when you include NT testing, allergy testing, and whatever else; they’re not diagnostic, but rather helpful in practice in that they provide clues to other contributors).
I want a clearer, concrete diagnostic method for all of these psychiatric problems. And I want to know the causes…not possible reasons for various manifestations, but the actual causes to the root of the problem.
Yet I cannot. I can’t even for the cancer…there’s the concrete diagnostic, but not the why (depending on the form of cancer). But for this (adhd etc…) there’s not a concrete diagnostic, which drives me absolutely crazy.
I feel like that’s what I need in order to be able to come to terms with it; a black and white, simple, yes or no. Intellectually though, I know life, medicine, and human beings are just not that simple. We are very complex and will always be learning more about the body and the brain, etc. How do I compromise/balance between what I know intellectually is reasonable and what I feel like I need and want in order to be ok with diagnosis and treatment?
The meds do help–a lot. Not perfect, but they definitely make a huge difference. I’ve noticed more lately (than I did when I posted that desperate message appealing for any consolation at the end of Oct) because now, before I go in for my next appointment, I have to choose if and when is the time that I will take the meds depending on the day’s responsibilities – since I don’t have enough coverage currently. So I’ve noticed those different responses. And I am one that does work very hard to have a healthy, balanced lifestyle..a strong work ethic, determination, self-discipline (sort of).
Hopefully soon, it (meds/dosoage/timing) will be really figured out, but I guess my bottom line question is (copied from above): How do I compromise/balance between what I know intellectually is reasonable and what I feel like I need and want in order to be ok with diagnosis and treatment?
Thank you for your willingness and commitment to sharing your knowledge and encouragement (from your experience) on this rocky road that I reluctantly travel. I know I’m not alone – have a very good therapist and pragmatic/knowledgeable doctor…but it’s helpful to have this blog too and know that there’s someone out there sharing their reliable information and experience to encourage those of us who need constant reassurance :/, even if live consultations & medical advice don’t follow.
Patiently (I hope and try) awaiting your words…whatever they may be. Thank you again.
Theresa,
Your inquiry is not unlike another comment on a different posting – so many wonder because the meds are given without a clear set of treatment objectives, as outlined in ADHD Medication Rules. So many need a clearer idea, a personalized, customized view of precisely what the targets are before starting meds. No matter how thoughtful and considerate your team people just want a better picture of why and how.
Without knowing you personally and digging into the details it is, regrettably, impossible for me here to give you the reassuring feedback you are seeking – do stay tuned here at CorePsych Blog, and do sign up for the CoreBrain training next Spring as I will be providing regular seminars/webinars to clarify these many issues. [You don’t have to be in the mental health field, some of the training will be for interested folks just trying, as you are, to figure out what works for them.]
cp
[…] This post was mentioned on Twitter by Dr Charles Parker, Michele Renee. Michele Renee said: RT @drcharlesparker ADHD And Glutamate: Neurotransm.. http://bit.ly/9gEC9N #ADD #medications #ADHD #Medications #disorder […]
Hi Dr. P,
Given this new line of thinking about ADHD and glutamate, could you comment on how this might relate to why guanfacine preparations are so calming to some while activating for others, and why Namenda/memantine is currently undergoing trials for ADHD (and autism)? I know this would likely involve some theorizing at this point, but your thoughts on this subject would be most welcome!
JB
JB,
Just a quick answer here, but covered extensively on all the CorePsych posts on Intuniv as so many find that med either excellent or challenging:
Glutamate can, just as any other neurotransmitter become diminished or elevated – and giving a glutamatergic product can either fill the tank or provide a relative overdose depending on that pre-existing, measurable, condition.
NMDA mimics the action of glutamate – see this link here for more info.
cp