40 replies to this topic

[Finn]

SCT-ers in the USA report higher efficacy on symptoms from Evekeo and Adderall, than they do from MPH or D-AMP

 

 

 

Google can't find anything about Evekeo in reddit/r/sct , and when it comes to people comparing Adderall and Dexedrine, I could find only person, he reported better morning fog clearing for Adderall. On the other hand, some people preferred Vyvanse over Adderall. There also seems to be ADHD-I who prefer Dexedrine over Adderall in reddit and addforums so it is somewhat mixed bag.

 

 

 

The two stimulant-drugs DL-AMP and D-MPH have both shown theoretically higher affinity for Norepinephrine than their more commonly prescribed brethren, whom show a higher affinity for Dopamine - this is why I theorize that these should be more effective - they are of course also the ONLY drugs I have yet to actually trial, so there's really no choice but to go for them anyway.

 

 

L-AMP and D-AMP have pretty much safe effect on NE, D-AMP has much stronger effect on DA though than L-AMP

 

 

 

In general, the stimulants appear to level out their benefits at very low dosages, 10-18 mg of MPH, 2,5-5 mg of D-AMP, and after this threshold, they only cause negative effects.

 

 

 

 

You were slow or ultra-slow CYP2D6? Amphetamine is metabolized by CYP2D6.

 

In rats, CYP2D1 is their equivalent for CYP2D6. 

 

 

http://europepmc.org...act/med/9833017

 

Effect of CYP2D1 inhibition on the behavioural effects of d-amphetamine.

 

 

In vivo, quinine (20 mg/kg) and budipine (10 mg/kg) increased the plasma area under the curve of AMP 4-fold and 3.6-fold respectively,

 

 

 

 

 

 

https://www.longecit...e-2#entry809865

 

Those were for rats. So when assuming 60 kg human, the human equivalent doses are roughly 3 mg and 10 mg for D-AMP and 10 mg and 30 mg for L-AMP. Somewhat annoying that 30 mg curve for D-AMP and 3 mg equivalent curve for L-AMP were not plotted, would have shown more comparison points for those two.

 

As you can see 10 mg curves for both L-AMP and D-AMP, and 30 mg curve for L-AMP are pretty similar when it comes to NE. Beyond certain point, NE just doesn't want to go up, safety/feedback mechanisms kick in hard, this might explain why ADHD-I don't get much out of larger doses.  Considering that you benefit most of doses 2.5-5 mg, and considering that being slow CYP2D6 with possibly 3-4 fold higher AUC, you probably have effectively already reached that "10 mg NE cap" with your 2.5-5 mg D-AMP dose.

 

 

 

Edited by Finn, 20 May 2018 - 07:06 AM.

[Mind_Paralysis]

You had some very interesting points today Finn, and I thank you for them.

 

In truth, I have known most of what you say, and considered it already, I have just blinded myself somewhat to some of your points, simplified things, since it felt safer, more hopeful to do so.

I shall ponder them more closely and try to come up with a reasonable response and a new plan of attack on my problems soon.

 

 

I can say that I'm hesitant to use an MAOI though... they do have their reputation, although as I have also been informed, that reputation is somewhat unfair.

 

Btw, what would you say about a combination like this, instead?

 

Moclobemide

Atomoxetine

Dexamphetamine

 

Yeah? As I understand it, NRI's can actually be used to neutralize the dietary restrictions on MAOI's, and this is more or less imperative for me - because my absentmindedness and forgetfulness could easily be the death of me, as I would be much more likely to FORGET which compounds and substances I cannot ever ingest.

 

(on another note... are there even selective TYRAMINE-targeting compounds? Not sure if reuptake inhibition or enhancement would be the key there though, admittedly)

 

https://www.longecit...o-diet-worries/

 

 

Hmm... it might be necessary to add even Guanfacine to the mix, to make sure there is NO bloodpressure increase here... that'd be a hell of a lot of drugs! But I digress... if one looks at my list on the first page, the combo of THREE different ADHD-drugs was more or less what worked the best.

[Mind_Paralysis]

Btw, Finn - could you by chance help me out with something else?

 

I've been trying to read up on the Default Mode Network, and specifically which DRUGS deactivate this network the most - what I find is an immense amount of drugs which do affect it in one way or another, but nothing on which ones that deactivate it the MOST... no head-to-head placebo-controlled studies that actually studies the switch-off effects induced, to see which ones lead to activation of other networks more.

 

If there are no such studies, then perhaps you could hypothesize a bit about which ones are the most plausible? OR... help me in my search in finding the professor in Neurology whom could possibly be the person to ask about this - SOMEone very talented that has devoted their entire life towards the study of the DMN must be out there - SOMEone MUST be the expert on this network!

 

Really, this network is involved in so many things, and have been theorized to exist for so long that someone must be an expert by now.

[Finn]

 

I can say that I'm hesitant to use an MAOI though... they do have their reputation, although as I have also been informed, that reputation is somewhat unfair.

 

Btw, what would you say about a combination like this, instead?

 

Moclobemide

Atomoxetine

Dexamphetamine

 

Yeah? As I understand it, NRI's can actually be used to neutralize the dietary restrictions on MAOI's, and this is more or less imperative for me - because my absentmindedness and forgetfulness could easily be the death of me, as I would be much more likely to FORGET which compounds and substances I cannot ever ingest.

 

(on another note... are there even selective TYRAMINE-targeting compounds? Not sure if reuptake inhibition or enhancement would be the key there though, admittedly)

 

https://www.longecit...o-diet-worries/

 

 

Hmm... it might be necessary to add even Guanfacine to the mix, to make sure there is NO bloodpressure increase here... that'd be a hell of a lot of drugs! But I digress... if one looks at my list on the first page, the combo of THREE different ADHD-drugs was more or less what worked the best.

 

Tyramine pressor effect is grows exponentially relative to the MAO-inhibition, the amount of tyramine required for 30 mm Hg or higher systolic bb increase with moclobemide, 240 mg of tyramine,  is 16 times higher than with phenelzine (15 mg of tyramine)and almost half of what it is on placebo (495 mg), you can't really get tyramine induced fatal hypertensive crisis with MOC, unless you overdose a lot so that MAO-B gets also inhibited. One junkie without prescription, who got pills from someone in his drug circles, overdosed with dozen(s) of tablets, then drank a half bottle of whiskey, also might have done coke but not traces of it blood anymore, so not sure, is the only person who has managed to get "food/drink induced" fatal hypertensive crisis from it.

 

 

Amphetamines are kinda risky with MAOIs, even with reversible and selective ones. 

Edited by Finn, 21 May 2018 - 01:56 PM.

[Finn]

Btw, Finn - could you by chance help me out with something else?

 

I've been trying to read up on the Default Mode Network, and specifically which DRUGS deactivate this network the most - what I find is an immense amount of drugs which do affect it in one way or another, but nothing on which ones that deactivate it the MOST... no head-to-head placebo-controlled studies that actually studies the switch-off effects induced, to see which ones lead to activation of other networks more.

 

If there are no such studies, then perhaps you could hypothesize a bit about which ones are the most plausible? OR... help me in my search in finding the professor in Neurology whom could possibly be the person to ask about this - SOMEone very talented that has devoted their entire life towards the study of the DMN must be out there - SOMEone MUST be the expert on this network!

 

Really, this network is involved in so many things, and have been theorized to exist for so long that someone must be an expert by now.

 

 

Spoiler

David Healy - The Creation of Psychopharmacology

 

In the nineteenth century, what was called the uric acid diathesis became one of the dominant concepts in medicine. Uric acid, a breakdown product of urea, was thought to accumulate to excess in some patients and in so doing to cause a number of disorders, from gout and rheumatism to cardiac disorders and what were later recognized as manic-depressive disorders. --

 

 

The discovery that lithium dissolves urate stones set the scene for its use for a wide range of conditions, in almost exactly the same way that the fact that methylene blue stained nerve cells provided a rationale to try it in the treatment of nervous disorders.

 

The effects of lithium on urates quickly gave rise to an industry in lithium waters in both the United States and Europe. --

 

This widespread use of lithium led to the discovery by Carl Lange in the 1880s that it had prophylactic effects in manic-depressive disorders. --

 

Between 1880 and 1900, Carl and his brother Frederick managed an asylum where they treated hundreds of patients with manicdepressive disorders using lithium and reported favorable results. Their experience was not unique. William Hammond at Bellevue Hospital in New York also used it to treat mood disorders in the 1870s and reported good results. Yet the use of lithium died out by 1900, and had to be rediscovered in the 1950s. If it worked, why did its use die out? At the end of the century, the uric acid diathesis was discredited, and with it went the theoretical rationale that underpinned treatment with lithium. Despite the fact that it worked, with no rationale for its use medical practitioners lost confidence in it. As the uric acid diathesis became incredible, the treatment became incredible also, and people were left to wonder how they could have thought such a treatment would work. Clearly, there is a delicate balance between the effects a treatment has and the reasons practitioners give as to why it works. Exactly the same thinking was later to underpin the use of Prozac, as we shall see.

 

This story summarizes pretty well contributions of theory to psychopharmacology. 

 

 

I'd say psychopharmacology is pretty experimental science, serendipitous discoveries and then further exploration around those. Really nothing significant has been discovered based on correct theoretical understanding, theory has contributed mainly to marketing. We don't really understand how antidepressants truly work, both doctors and patients feel less uncomfortable when given some sort of explanation.

 

"Hyperconnectivity of the default network has been linked to rumination in depression" so I would guess most antidepressants have potential to affect it in desirable way. I would recommend going more for experimental result data based, rule-of-thumb based approach than elaborate theory crafting.

 

Example:

 

Patient appears to get strong side effects from medications, might need to stay on drug for decades so mild side effect profile desirable, patient unlikely to abuse MDMA or cough syrups (dxm, codeine,etc.), try moclobemide which has one of mildest side effect profiles. 

Edited by Finn, 29 May 2018 - 02:08 PM.

[Mind_Paralysis]

Here is Barkley's latest version of his SCT lecture from February 16th of this year.

 

https://psych.vcu.ed...sentations.aspx

 

Echo360 version

https://ess.echo360....bb-0fda7ebb0a9d

m4v video version

https://ess.echo360....b0a9d/media.m4v

 

Interesting stuff related to possible causes of SCT and treatments starts at around 50 minutes, Echo360 scene/slide number 29. The beginning is pretty much just discussion of why SCT is separate disorder, classifications of ADHD subtypes etc.

 

I've been going through this link again, more closely, and I found the note Barkley makes this note regarding an article in SCIENTIFIC AMERICAN: MIND -magazine, about case-series of ruminative patients, whom were successfully treated for attention deficits?

 

The article supposedly talks about drugs commonly used for ruminative disorders, having an effect on a kind of attention-deficit that's very, very similar to SCT.

 

Can someone help me track this article down? It would help in analysing the drugs mentioned in these treatment-series, and make narrowing down my next treatment-option more manageable.

 

The mention is around the 01:01:51 mark - aka scene 37.

 

 

Meanwhile, a small update - I've managed to get screen-dumps and information from the computer-system used for licensed drug prescription, the one which my Dr. is having trouble with, and have started to try and write a completion /complimentory /motivating note for my Dr - it covers the drugs I've used, the combinations, and how long I trialled the drugs/combinations.

 

If I ever actually get this license, then it will be THE MOST well-earned, TRUE license in human history! No man has sacrificed as much as I have for his drugs... no man has ever truly dug in this deep into the system.

 

If I get it... I will have earned more than my keep.

[Mind_Paralysis]

So, I went through issues, well, summaries of them, of Scientific American: Mind magazine, on their official site, pretty much every issue in 2015 and 2014, which should be the time-span in question which Barkley mentions in the Echo-video, and I couldn't find any plausible article! : [

Nothing that seems to cover precisely what he speaks of... A series of cases with people afflicted with pathological mind-wandering, and how various clinicians treated their attentive symptoms - which drugs and combos they used.

 

Damn... Well, time to message both Barkley and the editors of Mind, I believe!

[mosspa]

I'm not sure I understand the OP's original post.  Adderall IS a 75%/25% racemic mixture of salts (four, I think) of the dextro(d)- levo(l)-enantiomers of amphetamine.  I understand that it is less commonly prescribed in Europe than in the USA, but I have trouble believing that it is totally unavailable. 

Edited by mosspa, 03 October 2018 - 09:29 PM.

[Keizo]

In Sweden you could contact https://www.dr-olalundin.com/

that's the only place I know of (through hearsay) that has considered to put or put patients on Adderall here in Sweden. Probably not worth the time and effort. 

[davis89x]

Hi @Mind_Paralysis  I am wondering how is your's situation now. Did you tried thearcine?

[Mind_Paralysis]

I'm not sure I understand the OP's original post.  Adderall IS a 75%/25% racemic mixture of salts (four, I think) of the dextro(d)- levo(l)-enantiomers of amphetamine.  I understand that it is less commonly prescribed in Europe than in the USA, but I have trouble believing that it is totally unavailable. 

In my region, it's almost unavailable. It can be had though, through a complex process of special licensing, not a lot of people are bound to get that though, since there's a local racemic small-scale production, also a special license, but much cheaper than imported Adderall.

Apparently Adderall will be coming to my region sometime next year though, if all goes according to plans. HOWever... Evekeo is bound to be a better fit, since that's generally the drug for peeps which haven't responded to either Dexamp or Adderall - it contains MORE levoamphetamine, a 50/50 mix - the local variation is also a 50/50 mix.

 

 

In Sweden you could contact https://www.dr-olalundin.com/

that's the only place I know of (through hearsay) that has considered to put or put patients on Adderall here in Sweden. Probably not worth the time and effort. 

 

It would have been, but I've already been in contact with his office, and he's retiring actually! So he's not taking on any new patients, and will be shutting down his practise in the coming years.

 

 

Hi @Mind_Paralysis  I am wondering how is your's situation now. Did you tried thearcine?

 

My situation is looking up somewhat actually - I've managed to get a trial for Dextro-Methylphenidate, Focalin, and thanks to some MORE, annoying, cumbersome handwringing, it seems as if I've actually GOT a Racemic Amp trial coming up!

 

(I had to help my doc with the new computer-system they're using for these special licenses in my region...I think we've got it now.)