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The "Deficits in attention, motor control and perception" -thread

adhd add sct concentration motivation dcd coordination perception

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#1 Mind_Paralysis

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Posted 01 August 2014 - 04:45 PM


This is the be-all, catch-all thread for the study, treatment, hypothesizing, and brainstorming regarding the neurological problem called "ADHD" - but with a caveat! It also includes the frequently co-morbid issues of motor control ( gross and minor), perception, and processing.

 

Very often, the sufferers of a variation of ADHD will tell you that they have more issues than the ones outlined as Classical ADHD. Often training and medication can only help some of the symptoms - because they are not stacked, not researched, or diagnosed correctly.

Well, here, we will strive to do so. If you have ADHD, in any form, caused either by the "classic" neuro-genetic mutations, or by some other genetic, internal, or external cause - then post your symptoms, your known causes, your DIAGNOSED disorders, and your SUSPECTED disorders, and together - we shall try and find stacks, tips, tests, and theories which might be helpful to all of us.

 

As such, I will here add a legend, which should help out in our research, regarding the disorders, the connections, the genetics, the potential treatment ( chemical, psychological, physiological, etc), and various compound which may be useful in treating the disorder(s).

 

-----------------------------------------

LEGEND OF ADHD!

-----------------------------------------

 

Disorders by Medical abbreviations:

-------------------------------------------------

ADHD - Attention Deficit Hyperactivity Disorder
A disorder leading to difficulties in attention (studying, learning), behavioural control ( emotions, social interaction), planning, and motivation. ( execution of said plans) 
 

The causes of ADHD can be many, and varied.

 

Classical ADHD, which is the most studied form - is often caused by changes in various neural networks, leading to faulty production or processing of important signal-transmitting chemicals in the brain.

 

Classical ADHD is most likely an almost completely neuro-genetic disorder, but various other genetic disorders can cause symptoms similar to Classical ADHD, but the root-cause can be one completely separated from neurological mutations.

 

The cause of the disorder can also be one of external trauma, as certain traumas to the brain, mild or severe, can cause symptoms that mimic the disorders caused by genetic mutations, through purely mechanical ( head-trauma, etc ) or developmental ( toxins, premature birth, etc) means.

 

Changes in the Pre-Frontal Lobe and mesolimbic pathway have been observed in those suffering from the disorder, and are the prime focus of research and theory regarding the disorder(s), at this time.

 

Variations of ADHD:

---------------------------

ADHD-PI - Attention Deficit Hyperactivity Disorder, Predominantly Inattentive

A variation of the disorder which features little to no hyperactivity, rather, the persons afflicted with this variation are often HYPO-active, meaning that they can be perceived as lazy, letargic, or simply disinterested, by the mainline population. The pathology is hypothetically differentiated in that it is predominantly caused by Mesolimbic Pathway dysfunction, and not PFC dysfunction.

 

ADHD-PH - Attention Deficit Hyperactivity Disorder, Predominantly Hyperactive

This variation has greater problems with hyperactivity behavioural control than the other variations, and seek constant stimulation and reward. They do not, however, have as severe difficulties with motivation as the other variations. The pathology is hypothetically differentiated in that it is predominantly caused by PFC dysfunction, and not Mesolimbic Pathway dysfunction.

 

ADHD-C - Attention Deficit Hyperactivity Disorder, Combined type

The most common variation of ADHD - which features difficulties in both behavioural control, attention, and motivation. Most persons diagnosed with ADHD will have a combination of symptoms, but will often "lean" towards either Inattention or Hyperactivity as the dominant symptom. Those with ADHD-C have a less clearly obvious dominant symptom, implying a combination of PFC and Mesolimbic Pathway dysfunction.

 

Link:

http://en.wikipedia.org/wiki/Adhd

----

 

DCD - Developmental Coordination Disorder

A developmental disorder with a greater comorbidity among those diagnosed with ADHD, than the greater population. Often called "clumsy child syndrome" or "Dyspraxia", it is characterized by a difficulty in executing complex gross motor movements. Theories regarding the neuro-pathology of the disease range from abnormalities in the Nigrostriatal pathway,
Substantia Nigra circuitry, and the Cerebellum, to the Caudate nucleus.

 

As of this time, no accepted theory for the nature of the disorder, exists.
----

 

 

Dysgraphia - A difficulty in executing motor-tasks of a more delicate manor, such as drawing or writing.

It is unknown whether there is a connection between DCD and Dysgraphia, even though both are diseases of motor-control. One can often be diagnosed with both, but one or the other may be more prominent, or even so subtly debilitating, that it is only barely diagnosed as a handicap. Never-the-less, both diseases prevent a person from reaching their full potential, in an increasingly competitive society - as such, both must be treated, and conquered, in order for the individual to be ALL that they can truly be.

----

 

 

Dyscalculia - A difficulty in solving and handling arithmetic mathematics, and a general difficulty in handling quantities of various kinds.

 

Link:

http://en.wikipedia....iki/Dyscalculia

 

----

 

-------------------------------

Medical abbreviations:

-------------------------------

PFC - Pre-Frontal Cortex

The region of the brain located behind your forehead. It controls impulses, emotions, planning, and many higher, complex functions.

 

http://en.wikipedia....efrontal_cortex


Edited by Stinkorninjor, 01 August 2014 - 04:56 PM.

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#2 Metagene

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Posted 25 August 2014 - 03:11 PM

I'm searching for alternatives to dual-n back, Cambridge brain science, etc. I have the unholy trinity of ADHD-PI/Dysgraphia/Dyscalculia so it's very little I won't try.

Effects of multitasking-training on gray matter structure and resting state neural mechanisms.

We investigated the effects of 4 weeks of MT-training on regional gray matter volume (rGMV) and functional connectivity during rest (resting-FC) in young human adults. MT-training was associated with increased rGMV in three prefrontal cortical regions (left lateral rostral prefrontal cortex (PFC), dorsolateral PFC (DLPFC), and left inferior frontal junction), the left posterior parietal cortex, and the left temporal and lateral occipital areas as well as decreased resting-FC between the right DLPFC and an anatomical cluster around the ventral anterior cingulate cortex (ACC).

http://www.ncbi.nlm....ccipital cortex

About mirror reading:

http://www.longecity...ǫnibɒɘя-ɿoɿɿim/

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#3 Mind_Paralysis

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Posted 25 August 2014 - 09:08 PM

Perhaps it's not dual-n-back alternatives you need, but rather, potentiation of the effects? If you take in some agents similar to NSI-189 and (-)-Clausenamide, while doing various brain-training, then perhaps it will work better?

Side-note - it would appear as if Fasoracetam actually stacks pretty well with NSI-189, no obvious side-effects so far. Perhaps a combo of those, WHILE you do brain-training, could be highly beneficial?

 

BTW! Know that you aren't alone in these problems, Metagene! =) My problems are, you guessed it... DCD/Dysgraphia ( these might be one and the same, since I do have problems wherein I've hit an artificial roof in my drawing, as well as in my karate-training), ADHD-PI and Dyscalculia.

I've had almost nothing to but B's and straight A's in my grades, all my life, EXCEPT sports and maths - recently did the College aptitude test here in Scandinavia as well, almost a 100%! On everything non-mathematical...

Yay...

 

Faso might be it tho'. It's supposed to be more effective if you have MORE mutations in the mGlur -network, than if you don't. Those are the groups it's being researched to help.


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#4 Metagene

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Posted 26 August 2014 - 08:55 PM

Fasoracetam is intriguing but I didn't want to take it while using 30mg of Adderall a day. I'm on 10mg memantine liquid solution as of yesterday . Only day two and I feel pretty great so far. :)

A guy on reddit noted the effects of (-)-Clausenamide on cortical density might not be related to learning. It would be nice to have more studies that back up those claims.

Yeah it looks like were in the same boat! It's good to see that you are proficient in other domains. I haven't had much success academically and usually learn things the hard way but there's hope I suppose lol.

#5 Mind_Paralysis

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Posted 27 August 2014 - 03:44 PM

I think you should consider decreasing the dose of Adderall when you're on Memantine as well, might not be necessary to take Adderall at all.

OR...! Even better... you could start phasing out the Adderall, and then be the FIRST to reveal what happens when you stack Faso and memantine! : D I actually think this combo could be interesting... they both interact with the glutamatergic network, they're both in investigation for use as ADHD  -medications - but one is an antagonist, and one is an agonist - so what happens when they stack?

 

I theorize, what's going to happen, is that Memantine is going to potentiate the faso, it's going to block the parts that activate the network, and make the deactivation stronger ( most of the receptors Faso agonise, actually block activity on the NMDA-receptors, down-stream, so in theory, they could stack. )



#6 Metagene

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Posted 27 August 2014 - 04:07 PM

Actually thought about asking my shrink to reduce the Adderall dosage to 25mg last visit because 30mg is not really better than 20mg 

 

You could be right, I think I'll try Faso + Memantine one weekend to see what happens. I have to be up at 3:00 am to get to work on week days and my work quality was always hit or miss before Adderall. If it wasn't a union job I might be jobless right now  :unsure:



#7 Mind_Paralysis

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Posted 27 August 2014 - 11:30 PM

Do you really need your doc to adjust your dose tho'? I do my own adjustments, because I hardly ever see the psychiatrist anyway, he's pretty much swamped.

I was on one 18 mg concerta-tab first, then automatically increased it to 18+18 mg after the first week, since I got tolerance pretty quickly ( 18 mg is the lowest dose, after all). After about two months I did my own automatic adjustment of dosage as well, and now I utilize a topper of a third 18 mg dose, if I feel that I need it, it varies. He lets me get away with this stuff, since he knows that I take both temporary, and longer breaks. Basically, I'm on a 1.5 week break right now, since I ran out of medicine, and I don't fill it up until I have another appointment with my psychologist.

 

Basically, if you have the pills, why not do the dosing yourself? You save a lot of time and problems that way - all you have to do is FIRST implement the change that you KNOW is going to be beneficial for you, and THEN talk to the Dr about implementing it. Most of the time they might well comply, so there's not necessarily an issue with this.

And hey, in this case, LOWERING the dose...? I'm pretty sure he's going to think it's a wise move. Just do it, man.

 

And definitely try Faso with mem! =) Just remember to do a bit of weaning off from the Adderall prior tho' - you need to be clean from the Amphetamine for this to work without issues. You can always slightly increase the Memantine while you go off the amphetamine, to compensate.

 

Sorry to hear you're having trouble with work btw. : ( I know the feeling, I was in a union-job myself, which wasn't going too well ( construction-electrician). Had I been diagnosed and medicated, the job might have gone better. The union was a big help tho'. Always unionise!


Edited by Stinkorninjor, 27 August 2014 - 11:33 PM.


#8 Metagene

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Posted 28 August 2014 - 08:24 PM

Work has improved considerably since I was diagnosed two years ago. It's hard to believe I stuck it just shy of a full decade. Mostly on sheer desperation and stubbornness though. Co-sign on union jobs.

I only have a 30 day supply of Adderall XR so it's not much trouble. I go to the psychiatrist every two months so he writes me an additional script.

Yeah same here too. Sometimes I see the APRN :P They mostly want to make sure I'm not losing too much weight then chat for a few minutes about my social life and what not.

I might decide to cut the cord completely if D-Deprenyl turns out to be a winner.

#9 Flex

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Posted 29 August 2014 - 08:04 PM

Found this in reddit/science. Maybe it could be helpful or at least interresting:

 

Dyslexic Readers Have Disrupted Network Connections in the Brain

Dyslexic readers showed decreased connectivity within the visual pathway as well as between visual and prefrontal regions, increased right-hemisphere connectivity, reduced connectivity in the visual word-form area, and persistent connectivity to anterior language regions around the inferior frontal gyrus.

This altered connectivity profile is consistent with dyslexia-related reading difficulties.

 

http://www.elsevier....ns-in-the-brain



#10 Mind_Paralysis

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Posted 04 October 2014 - 06:43 PM

Flex: Certainly an interesting link, since one of my comorbidities is Dyscalculia - a disorder closely related to Dyslexia. Not sure how to apply it directly to myself, but others looking into the thread might have dyslexia instead, and might come up with some idea to improve their issues.

 

On another, intersting note - I just read that the Angular Gyrus -portion of the brain is involved with not only mathematics, and implicated in Dyscalculia - but with attention and visual information as well!

Could a error in the Angular Gyrus then, coupled with ADHD, give a person not just Dyscalculia, but DCD as well? It seems there's a connection to movement there.

 

What do you guys say? Anybody with know-how in how the Angular Gyrus is connected to movement?

 

Trying to find a unifying element between my diagnoses here, you see - ADHD-PI-DCD-Dyscalculia.


Edited by Stinkorninjor, 04 October 2014 - 06:49 PM.


#11 Flex

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Posted 04 October 2014 - 08:45 PM

I´m not sure whether the angular cortex is exactly the same as paretial cortex, which plays a role in mathematical skills, but NSI-189 could or should be helpful

See my post at

Improving Mathematical skills with nootropic

http://www.longecity...ic/#entry674685

 

Admittely, its just a assumption from me, but perhaps there could be something interresting

 



#12 5IMON

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Posted 27 November 2014 - 01:42 PM

Stinkorninjor Check out my thread Ive just posted, I want your feedback

#13 Mind_Paralysis

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Posted 24 April 2015 - 10:57 AM

Flex: Very interesting. = ) May definitively be worth a look.

 

 

On to something completely different: I've been working on a hypothesis of the role of Kynurenic Acid in ADHD, and this is what I've got so far:

 

My recent studies have led me to believe that there might be a common recurring genetic polymorphism within variations on ADHD that involves problems with the processing or synthesis of Tryptophan into Kynurenic Acid – and the subsequent effect of a hyper-active

NMDA-network, leading both to cognitive deficits (primarily in executive function), and problems with compensation for deficits within the dopaminergic circuitry.

 

My basis for the hypothesis is that it in a seemingly elegant way binds together recent theories regarding the involvement of the NMDA-network in various CNS-disorders, as well as the efficiency of Memantine, a

non-competitive NMDA-antagonist in treating ADHD, with the observations of alterations with Tryptophan-metabolism in ADHD, and the potential therapeutic value of Ketogenic diets in the treatment of ADHD, as well as the observed disruptions of Circadian Rhytms within individuals afflicted with ADHD.

It all leads back to Kynurenic Acid – and its relationship to the

NMDA-network and the metabolism of Tryptophan.

 

 

A potential method of treatment could be supplementation with compounds which inhibit kynurenine hydroxylase – primarily the compound Nicotinylalanine.

 

Roberto Pelliciari of Italian neuroscience research had a patent for the use of Nicotinylalanine in the treatment of a wide variety of CNS –disorders, however he and his colleagues were unable to procure funding from pharmaceutical companies to start the development and testing of NAL and derivatives for the use in CNS-disorders.

 

 

 

 

Reference sources:
-----------------------------

1- Altered tryptophan and alanine transport in fibroblasts from boys with attention-deficit/hyperactivity disorder (ADHD): an in vitro study

http://www.ncbi.nlm....51/?tool=pubmed
 

2- Attention-deficit hyperactivity disorder (ADHD) and glial integrity: S100B, cytokines and kynurenine metabolism - effects of medication

http://www.behaviora.../content/6/1/29

 

3- Adult attention-deficit hyperactivity disorder is associated with alterations in circadian rhythms at the behavioural, endocrine and molecular levels.

http://www.ncbi.nlm....pubmed/22105622

 

4- Melatonin Effects in Methylphenidate Treated Children with Attention Deficit Hyperactivity Disorder: A Randomized Double Blind Clinical Trial

http://www.ncbi.nlm....les/PMC3428643/

5- Ketogenic diet increases concentrations of kynurenic acid in discrete brain structures of young and adult rats - Springer

http://link.springer...0702-011-0750-2

 
6- Cerebral Synthesis and Release of Kynurenic Acid: An Endogenous Antagonist of Excitatory Amino Acid Receptors

http://www.jneurosci...9/2965.full.pdf

 

7- Kynurenines in CNS disease: regulation by inflammatory cytokines

http://www.ncbi.nlm....les/PMC3915289/

 

8- The ketogenic diet causes a reversible decrease in activity level in

Long-Evans rats.

http://www.ncbi.nlm....pubmed/16750194

 

9- Effect of the ketogenic diet on the activity level of Wistar rats.

http://www.ncbi.nlm....pubmed/15585674

 

10- Ketogenic diet increases concentrations of kynurenic acid in discrete brain structures of young and adult rats

http://link.springer...2/fulltext.html

 

11- Inhibitors of kynurenine hydroxylase and kynureninase increase cerebral formation of kynurenate and have sedative and anticonvulsant activities.

http://www.ncbi.nlm..../pubmed/7969905

 

12- Nicotinylalanine increases the formation of kynurenic acid in the brain and antagonizes convulsions.

http://www.ncbi.nlm..../pubmed/1431895


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#14 zompy

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Posted 21 September 2016 - 12:19 PM

This actually feels the appropriate place to ask, I've been thinking I have ADD (focus troubles) for years. I have never been able to really study because I just lose focus and start thinking about other stuff for example. I have tried a lot of nootropics atm, even some trials with adderall/dexamphetamin but I am not sure what to do. I do not have a prescription for this, but I am uncertain if I want to have one anyway. I can imagine that using this stuff for years can have really negative impact. What do you think?



#15 Mind_Paralysis

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Posted 22 September 2016 - 07:27 AM

This actually feels the appropriate place to ask, I've been thinking I have ADD (focus troubles) for years. I have never been able to really study because I just lose focus and start thinking about other stuff for example. I have tried a lot of nootropics atm, even some trials with adderall/dexamphetamin but I am not sure what to do. I do not have a prescription for this, but I am uncertain if I want to have one anyway. I can imagine that using this stuff for years can have really negative impact. What do you think?

 

Using Amphetamine over a certain dosage - yes. Methylphenidate? No.

 

Methylphenidate has actually been proven to be neuroprotective, and the neurotoxic effects of Amphetamine are only visible with very high doses - 120-150 mg per day. The wast majority of patients stop at 20-50 mg of Amphetamine per day.

 

Now, it CAN have negative effects on you if you are ADD/SCT/CDD though - we do not respond as strongly as our hyperactive cousins to these stimulants - hence, we experience far more of the negative effects - and most of us have underlying anxiety-conditions as well - so, not a good combo.

 

Anyways, I truly, truly recommend getting a diagnosis - it will finally help you to understand certain things about yourself.

 

Now, regarding medication - I recommend Atomoxetine or Reboxetine - because recent studies have shown that where we dipher from ADHD is in the secondary cortex the most liked to the symptoms - for the ADHD-ers, this is the Striatum, they have a Fronto-Striatal disease. Dopamine is highly involved in that region, hence why dopaminergics work so well for them. For us though, the secondary region is the Superior Parietal Lobe - a completely different region, one which is instead mostly activated by... NOREPINEPHRINE!

 

Reboxetine and Atomoxetine are both NRI's - Norepinephrine Reuptake Inhibitors.

 

They will work, and they don't have any known long-term negative effects, all of the negatives are short-term.



#16 lourdaud

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Posted 22 September 2016 - 10:52 AM

 

This actually feels the appropriate place to ask, I've been thinking I have ADD (focus troubles) for years. I have never been able to really study because I just lose focus and start thinking about other stuff for example. I have tried a lot of nootropics atm, even some trials with adderall/dexamphetamin but I am not sure what to do. I do not have a prescription for this, but I am uncertain if I want to have one anyway. I can imagine that using this stuff for years can have really negative impact. What do you think?

 

Using Amphetamine over a certain dosage - yes. Methylphenidate? No.

 

Methylphenidate has actually been proven to be neuroprotective, and the neurotoxic effects of Amphetamine are only visible with very high doses - 120-150 mg per day. The wast majority of patients stop at 20-50 mg of Amphetamine per day.

 

Now, it CAN have negative effects on you if you are ADD/SCT/CDD though - we do not respond as strongly as our hyperactive cousins to these stimulants - hence, we experience far more of the negative effects - and most of us have underlying anxiety-conditions as well - so, not a good combo.

 

Anyways, I truly, truly recommend getting a diagnosis - it will finally help you to understand certain things about yourself.

 

Now, regarding medication - I recommend Atomoxetine or Reboxetine - because recent studies have shown that where we dipher from ADHD is in the secondary cortex the most liked to the symptoms - for the ADHD-ers, this is the Striatum, they have a Fronto-Striatal disease. Dopamine is highly involved in that region, hence why dopaminergics work so well for them. For us though, the secondary region is the Superior Parietal Lobe - a completely different region, one which is instead mostly activated by... NOREPINEPHRINE!

 

Reboxetine and Atomoxetine are both NRI's - Norepinephrine Reuptake Inhibitors.

 

They will work, and they don't have any known long-term negative effects, all of the negatives are short-term.

 

 

In the short run reboxetine and atomoxetine are amazing. Totally kills my ADHD and enhances my working memory like nothing else. But, these meds never go out of your system and you'll have elevated noradrenaline and cortisol levels 24/7. This can't be good and I'm sure this will have huge implications long term, on your immune system or whatever. Personally after going off reboxetine after two months use I was a complete wreck.
 



#17 Mind_Paralysis

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Posted 22 September 2016 - 02:06 PM

 

 

This actually feels the appropriate place to ask, I've been thinking I have ADD (focus troubles) for years. I have never been able to really study because I just lose focus and start thinking about other stuff for example. I have tried a lot of nootropics atm, even some trials with adderall/dexamphetamin but I am not sure what to do. I do not have a prescription for this, but I am uncertain if I want to have one anyway. I can imagine that using this stuff for years can have really negative impact. What do you think?

 

Using Amphetamine over a certain dosage - yes. Methylphenidate? No.

 

Methylphenidate has actually been proven to be neuroprotective, and the neurotoxic effects of Amphetamine are only visible with very high doses - 120-150 mg per day. The wast majority of patients stop at 20-50 mg of Amphetamine per day.

 

Now, it CAN have negative effects on you if you are ADD/SCT/CDD though - we do not respond as strongly as our hyperactive cousins to these stimulants - hence, we experience far more of the negative effects - and most of us have underlying anxiety-conditions as well - so, not a good combo.

 

Anyways, I truly, truly recommend getting a diagnosis - it will finally help you to understand certain things about yourself.

 

Now, regarding medication - I recommend Atomoxetine or Reboxetine - because recent studies have shown that where we dipher from ADHD is in the secondary cortex the most liked to the symptoms - for the ADHD-ers, this is the Striatum, they have a Fronto-Striatal disease. Dopamine is highly involved in that region, hence why dopaminergics work so well for them. For us though, the secondary region is the Superior Parietal Lobe - a completely different region, one which is instead mostly activated by... NOREPINEPHRINE!

 

Reboxetine and Atomoxetine are both NRI's - Norepinephrine Reuptake Inhibitors.

 

They will work, and they don't have any known long-term negative effects, all of the negatives are short-term.

 

 

In the short run reboxetine and atomoxetine are amazing. Totally kills my ADHD and enhances my working memory like nothing else. But, these meds never go out of your system and you'll have elevated noradrenaline and cortisol levels 24/7. This can't be good and I'm sure this will have huge implications long term, on your immune system or whatever. Personally after going off reboxetine after two months use I was a complete wreck.
 

 

 

Interesting.

 

Well, Atomoxetine is the verified ADD-recommended drug, so maybe that will work better for you? I kind of doubt it though, since Atomoxetine has KAPPA-agonism - in theory, this SHOULD make Atomoxetine the more taxing drug - because the norepinephrine tells your body that it is in an urgency - things must get done - however, the KAPPA-agonism tells your brain that you are also continously FAILING!

 

In essence, every day would feel like an unending nightmare of failure and stress, stress, stress - hence high cortisol.

 

Yet... the supposedly kinder drug, Reboxetine, CRACKED you??

 

Hmm... curious... very curious.

 

IF you were on the right dosage, I can't understand why... because our SCT-brains are in perpetual slow-motion, the lack of norepinephrine is TOTAL! That is what drives our cortisol up, up, up and away! In an attempt to increase norepinephrine and compensate for the deformities in our brains.

Truly, more norepinephrine, at the RIGHT dosage, simply cannot be unbeneficial then!

 

Are you a 100, HUNDRED percent certain that you were on the right dosage? In the case with Atomoxetine at least, the therapeutic window is ULTRA-easy to shoot past! Why? Because Atomoxetine's half-life is completely dependent on a single CYP2D6 enzyme - and, if like me, you have a mutation making you a ultra-slow metabolizer... then the properties of the drug are wildly altered...! 93% bioavailability! TEN, *TEN* times the half-life! TEN times the exposure to the drug!

 

To me, even 6 mg will IMMEDIATELY hit the therapeutic window! Onset of effect is a few mere days! Not weeks. Perhaps even hours...

 

However, the slightest mistake in dosing... will cost me. My. Very. *LIFE!* o.o

 

Because Atomoxetine's combined norepinephrine and kappa-agonism has earned it a skull on the packaging - SUICIDAL ideation! And what is my #1 secondary diagnosis? Why, it's Suicidal OCD!

True life or Death shall be my reward upon ingesting it...

 

 

Now, humorous dramatics aside... are you a 100% certain that you are not a slow metabolizer of Reboxetine, and you simply mis-shot your therapeutic window with about... oh... a Battleship or two?

 

I would try a rechallenge on a lower dosage imho, possibly with a bit of an antistressor-stack for the night! = )

Gabapentin and Magnesium-L-Threonate (real-deal nmda-antagonism) should cap any anxiety and difficulty sleeping to kingdom come. Perhaps add Valerian Root as well, and I see you positively freezing into low cortizol.


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#18 zompy

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Posted 28 September 2016 - 09:54 AM

 

This actually feels the appropriate place to ask, I've been thinking I have ADD (focus troubles) for years. I have never been able to really study because I just lose focus and start thinking about other stuff for example. I have tried a lot of nootropics atm, even some trials with adderall/dexamphetamin but I am not sure what to do. I do not have a prescription for this, but I am uncertain if I want to have one anyway. I can imagine that using this stuff for years can have really negative impact. What do you think?

 

Using Amphetamine over a certain dosage - yes. Methylphenidate? No.

 

Methylphenidate has actually been proven to be neuroprotective, and the neurotoxic effects of Amphetamine are only visible with very high doses - 120-150 mg per day. The wast majority of patients stop at 20-50 mg of Amphetamine per day.

 

Now, it CAN have negative effects on you if you are ADD/SCT/CDD though - we do not respond as strongly as our hyperactive cousins to these stimulants - hence, we experience far more of the negative effects - and most of us have underlying anxiety-conditions as well - so, not a good combo.

 

Anyways, I truly, truly recommend getting a diagnosis - it will finally help you to understand certain things about yourself.

 

Now, regarding medication - I recommend Atomoxetine or Reboxetine - because recent studies have shown that where we dipher from ADHD is in the secondary cortex the most liked to the symptoms - for the ADHD-ers, this is the Striatum, they have a Fronto-Striatal disease. Dopamine is highly involved in that region, hence why dopaminergics work so well for them. For us though, the secondary region is the Superior Parietal Lobe - a completely different region, one which is instead mostly activated by... NOREPINEPHRINE!

 

Reboxetine and Atomoxetine are both NRI's - Norepinephrine Reuptake Inhibitors.

 

They will work, and they don't have any known long-term negative effects, all of the negatives are short-term.

 

 

I am really curious if you have some science backed info about that. I have seen and heard a lot of people claiming methylphenidate is dangerous longterm. 

Thanks for the info so far, I will look into it, appreciate the informative posts from you :) 



#19 Catwoman

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Posted 28 September 2016 - 12:38 PM

Interesting thread. I have Dyscalculia (and of course OC-spectrum disorder). I wasn't diagnosed with ADD ever, but I have some characteristics. 



#20 zompy

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Posted 29 September 2016 - 11:56 AM

I am actually also wondering: I have read recommendations for memantine and fasoracetam, however in what dosage? Also since faso is quite expansive.



#21 Mind_Paralysis

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Posted 29 September 2016 - 12:41 PM

 

 

This actually feels the appropriate place to ask, I've been thinking I have ADD (focus troubles) for years. I have never been able to really study because I just lose focus and start thinking about other stuff for example. I have tried a lot of nootropics atm, even some trials with adderall/dexamphetamin but I am not sure what to do. I do not have a prescription for this, but I am uncertain if I want to have one anyway. I can imagine that using this stuff for years can have really negative impact. What do you think?

 

Using Amphetamine over a certain dosage - yes. Methylphenidate? No.

 

Methylphenidate has actually been proven to be neuroprotective, and the neurotoxic effects of Amphetamine are only visible with very high doses - 120-150 mg per day. The wast majority of patients stop at 20-50 mg of Amphetamine per day.

 

Now, it CAN have negative effects on you if you are ADD/SCT/CDD though - we do not respond as strongly as our hyperactive cousins to these stimulants - hence, we experience far more of the negative effects - and most of us have underlying anxiety-conditions as well - so, not a good combo.

 

Anyways, I truly, truly recommend getting a diagnosis - it will finally help you to understand certain things about yourself.

 

Now, regarding medication - I recommend Atomoxetine or Reboxetine - because recent studies have shown that where we dipher from ADHD is in the secondary cortex the most liked to the symptoms - for the ADHD-ers, this is the Striatum, they have a Fronto-Striatal disease. Dopamine is highly involved in that region, hence why dopaminergics work so well for them. For us though, the secondary region is the Superior Parietal Lobe - a completely different region, one which is instead mostly activated by... NOREPINEPHRINE!

 

Reboxetine and Atomoxetine are both NRI's - Norepinephrine Reuptake Inhibitors.

 

They will work, and they don't have any known long-term negative effects, all of the negatives are short-term.

 

 

I am really curious if you have some science backed info about that. I have seen and heard a lot of people claiming methylphenidate is dangerous longterm. 

Thanks for the info so far, I will look into it, appreciate the informative posts from you :)

 

 

I just want to say that I really, really want to report back on this, and give you the run-down - show you the studies which GetOutofBox (former legendary member of Longecity - THE man when it comes to neuropsychiatric disease) showed me, buut...

 

My CDD is currently making that impossible, lol!

 

But, I will give it a shot. Here we go.

 

First, you can read some discussion on the subject here:

 

Long-Term Use of Methylphenidate

http://www.addforums...ead.php?t=95991

 

Long-term Ritalin users, please come in

http://www.longecity...please-come-in/
 

Methylphenidate neurotoxic?

http://www.longecity...ate-neurotoxic/

 

This brand new data was actually new to me - but, it's still rather... iffy. Mainly because the neuroprotective evidence has more proof, while the neurotoxic has only been observed in this study. There's also the fact that no increased risk of Parkinsons has been noted with methylphenidate use, while with Amphetamine... there IS a risk!

 

 

Secondly, and more importantly, you can read these studies:

 

Methylphenidate exerts no neurotoxic, but neuroprotective effects in vitro.

https://www.ncbi.nlm...pubmed/16736241

 

Neuropharmacological Mechanisms Underlying the Neuroprotective Effects of Methylphenidate

https://www.ncbi.nlm...les/PMC2701286/

 

 

Prior to this new data, I would have said that MPH causes no primary damage, only secondary (because of the anxiogenic effects), and M-AMP and AMP were the neurotoxins.

 

Still, I gotta' admit... at the moment, it's not as clear any more.



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#22 Mind_Paralysis

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Posted 29 September 2016 - 12:48 PM

I am actually also wondering: I have read recommendations for memantine and fasoracetam, however in what dosage? Also since faso is quite expansive.

 

Memantine seems to vary - but it can be quite low - 2-4 mg seems like a good shot to aim for. Some where as high as 20 mg, but IMHO! those people were chasing a high.

 

Fasoracetam, well, I would say 25-50 mg seems to be the sweet-spot for most.

 

 

I'm not sure you should bother with Faso though - Dr. Hakon Hakonarson who did the study and trial of it as treatment of ADHD found that it was only a specific subset which would gain from it - kids and adults with... INTELLECTUAL DISABILITY.

 

Apparently, seems to be similar to severe negative symptoms in schiz and connected to mGlur 2-3 receptors in the Pre-Frontal Cortex.

 

You honestly don't strike me as the type... ; )

 

That said, I've tried Faso and can certainly recommend it as a decent nootropic - slightly stimulating, and it's definitely anxiolytic - it upregulates GABA-receptors.

 

When I trialled it, I would actually say it QUELLED a great deal of the anxiety I get from MpH! = ) So, pretty good stuff, but will mostly help very specific people.







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