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  • BDD Moderators: Keif’ Richards | negrogesic

From 90mg adderall to 50mg vyvanse!!! WTF!

They are very effective for this purpose, as well as for the increase in prolactin that antipsychotics can cause. I would stick to the newer D2 selective ligands though as cabergoline is what's known as a "dirty" drug:

https://en.wikipedia.org/wiki/Dirty_drug

These aren't what you want if you're just looking to counteractp "just" a rise in prolactin, so cabergoline is a poor choice nowadays.

Ropinirole seems to me like the best choice, as cabergoline is dirty, and pramipexole is more selective for D3, and all the other ergot derivatives are all dripping with dirt and filth as well.
 
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They are very effective for this purpose, as well as for the increase in prolactin that antipsychotics can cause. I would stick to the newer D2 selective ligands though as cabergoline is what's known as a "dirty" drug:

https://en.wikipedia.org/wiki/Dirty_drug

These aren't what you want if you're just looking to counteractp "just" a rise in prolactin, so cabergoline is a poor choice nowadays.

Ropinirole seems to me like the best choice, as cabergoline is dirty, and pramipexole is more selective for D3, and all the other ergot derivatives are all dripping with dirt and filth as well.

I used cabergoline at .5mg 2x per week for about 7 years straight. When I got blood work on my prolactin my levels were less than zero and even after stopping cabergoline after seven years they remained less than zero for about three or four months but they are finally in normal range now. I wonder if it caused any permanent long-term side effects. I don't need to use any of those drugs anymore because I don't use steroids that increase prolactin anymore.

Pramipexole is nasty stuff if you take even .1 mg more than normal It can cause you to get extremely tired and fall asleep then two hours later wake up with an extreme burst of energy and it can cause a lot of flu like symptoms. I never liked that one.

P.S. I looked at the "dirty drug" link and didn't see cabergoline there.
 
Look at cabergoline's pharmacology, it doesn't need to be listed on the page: it doesn't give every example.

pramipexole causes those side effects because it is so D2 selective.

I never questioned or doubted cabergoline's efficacy - it is very effective as it is an extremely potent D2 ligand, it just happens to bind at many other alpha adrenergic and serotonergic and other dopaminergic sites as well, which pramipexole and ropinirole do not do - I simply stated it was "dirty".

cabergoline :

Binding profile[15][edit]

ReceptorBinding Affinity (Ki [nM])Action
5-HT1A20.0Agonist
5-HT1B479Unknown
5-HT1D8.71Unknown
5-HT2A6.17Agonist
5-HT2B1.17Agonist
5-HT2C692Agonist
α1A adrenergic288Unknown
α1B adrenergic60.3Unknown
α1D adrenergic166Unknown
α2A adrenergic12Unknown
α2B adrenergic72.4Antagonist
α2C adrenergic22.4Unknown
β1 adrenergic>10,000Unknown
β2 adrenergic>10,000Unknown
D1214Agonist
D2S0.62Agonist
D2L0.95Agonist
D30.79Agonist
D456.2Agonist
D522.4Unknown


compared to pramipexole:

Pramipexole acts as a partial/full agonist at the following receptors:[3][4]

 
If haloperidol counteracted cardiovascular effects of methamphetamine it means methamphetamine BINDS to the D2 receptors. D2 ligands LOWER BLOOD PRESSURE AND PULSE RATE

ie pramipexole or ropinirole. They are sedatives and cause hypotension and sleep attacks. They are GIRK channels and blocking them prevents potassium from entering the cell, causing DEPOLARIZATION.

I don't think you know that difference between agonists, antagonists, partial agonists, allosteric modulators, and so on. Or the different dopaminergic pathways in the brain. Cause what you're saying does not make sense.

I tried to teach you some things, but you don't want to be taught8(. So I'll peace out. Maybe in the future you'll be more open about these things. Go ahead and have the last word.:\
 
D2 is inhibitory. You need to do research. Only time it is excitatory is when the GIRK channel paradoxically opens T-type calcium channels. Where are you getting the idea that potassium promotes excitatory neurotransmission?

You just seem confused about the D2 receptor. I know what I am talking about, yet you on the hand never seem to explain a bloody thing... :)

D2 agonists. Just take a look at them. They are inhibitory agents. Pramipexole and ropinirole are sedatives.

Don't make me out to look stupid when I'm providing scientific evidence and facts and you are providing nothing meaningful to the conversation except denials to everything I say.
 
http://www.nature.com/npp/journal/v27/n5/full/1395957a.html

They are autoreceptors, just like the autoreceptors like the alpha 2 adrenergic. They are inhibitory, hence the actions of pramipexole and ropinirole.

These agents can cause their strange behavior and manic reactions for the same reason baclofen and GHB/phenibut can cause their hypomania: the g coupled inward rectifying potassium channels they activate is linked to low voltage gated calcium channels, and "low threshold spikes" of activity. The deinactivation of these GIRK channels causes depolarizations postsynaptically. This is the excitatory action you are thinking of.

Is it so hard to provide facts ho chi minh?

Haloperidol antagonized the cardiovascular effect of methamphetamine, meaning that by blocking the D2 receptor, they arrived at the conclusion that methamphetamine had activity at the receptor. This is what I was saying.

So don't imply I don't know what I was talking about. You know full well what I was saying.
 
If haloperidol counteracted cardiovascular effects of methamphetamine it means methamphetamine BINDS to the D2 receptors. D2 ligands LOWER BLOOD PRESSURE AND PULSE RATE

ie pramipexole or ropinirole. They are sedatives and cause hypotension and sleep attacks. They are GIRK channels and blocking them prevents potassium from entering the cell, causing DEPOLARIZATION.

Prami a sedative? It's a dopamine agonist. I beg to differ. One of the worst nights of my life was due to prami. lol


Also the whole time while feeling like shit, I'm pretty sure I've never had a harder erection in my life.
 
Only problem is I think the maximum allowance to 70 mg per day I'll have to ask him. Hopefully he can do something. Thanks

Reading your post in this thread, please take my advices as a fellow prescription vyvanse user:

If your doctor categorically will not go ovet 70 mg dose/day, you need to get a second opinion /change doctor.

It is true that studies have only examined doses up to 70 mg/day. All these studies have been on children. Children! You're a full grown man!

Also, when increasing your dose on Vyvanse it will take several days before full effect is exoerienced. At leadt 3-4 days, die to long half live. After 2 weeks you will know how a certain dose work, Vyvanse takes a long time to stabilise.

Also, diet affec Vyvanse much more than other adhd meds. Being a body builder I assume you get enough proteins with medication, so that should be ok.

The information in your Vyvance packet (huge paper sheet) should verify what I have said here about the dosage. It days that one should use caution about 70+ pr day. Also that only children have participated in study. You are probably twice the size of those participants.

Vyvanse willl help you much more if you dtay on a stable dose day to day. Atm you are obviously not on the right dose.
 
They have done short term and longer term (6 mos) studies in adults with the max of still 70mg. Im not saying some wont benefit from higher but I think the population that would is rather small.

What in your diet do you find is beneficial and how so?
 
They have done short term and longer term (6 mos) studies in adults with the max of still 70mg. Im not saying some wont benefit from higher but I think the population that would is rather small.

What in your diet do you find is beneficial and how so?

Ah, okay, thanks for the correction. I knew there were some studies on adults, but didn't know they finished yet.

The knowledge I found about Vyvanse and diet/health is a mix of scientific research and clinical exoeriences. The latter not being tested according to scientific methods, and I haven't found the research that some claims are referring to. I encourage sceptisism, at the same time I had to face the fact that these non-scientific claims from practicitioner(s) was all I had to go on.

Diet, short and easy explained;
Basically proteins, food that makes the accessibility of neurons good. Breakfast bring an important meal. My mess works better when I have a protein high breakfast together with meds, compared with cerials. It can be so little as 1 boiled egg, just get some proteins in your system. I experience food intake as much more significant on Vyvanse than on methylphenidate.

It is also suggested thay one avoid intake of c-vitamins a couple of hours prior/after taking Vyvanse. C-vitamins will shorten the effect of the meds. Not sure if this is due to the same principle why some amphetamine users drink citrus juice when trying to get clean/pass urine testing. I haven't tried this systematically to see if it's true, I just follow it.

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Edit: this isn't true, at least negligible. Did a little research after I posted. Only thing outside medical treatment strong enough to acidity urine is if you drink lots of cranberry juice. Glass of orange juice or vitamine c is not enough to make your urine more acid. Unless we're talking several gallons a day. Seems to be a misunderstanding leading to an urban myth.
###############

Vyvanse, being a pro drug, is depending on several transitions within the body, before the active drug is available in the brain. I've heard claims that one stage of Vyvanse and prozac uses the same path through the liver, making prozac block the Vyvanse uptake, diminishing the effect. Some type of Liver desease/malfunction can probably have same effekt, just guessing.

Huge deviations in digestion/bowl transition time can also cause a dimimished effect. If its 10 hours or 7 days, it will probably cause a different build up in the body, rather than the normal average about 20 hours. With a regular digestion/metabolism the medication will stay in body for days. Having a very slow digestion could cause dose to be imcrrased, while body levels slowly stack up too high over time. Not a doctor, pardon my lay man terms.

TL;DR: The more transitions, the more opportunities to something being screwd up temporarily or all the time, as body neds to break down molecules into the final desired connection.

Some guy (doctor) talked and wrote a lot about it. Not sure if science is saluting him, but he is very charismatic and makes a buck out of it, and seems to be endorsed of lots of Vyvanse users. Still, it's clinical try and error, not scientific evidence based (didn't read the book, so could be wrong, but believe it's a bit thin on scientific sources)
 
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The US shire site has the info in a pdf, which I coyld not quote on mobile. Missing some data graphs, The UK site has partly the same about Vyvanse studies (aka Elvanse) in adults:
Adult population

The effectiveness of Elvanse in the treatment of ADHD was established in a double-blind, randomised, placebo-controlled, parallel-group study conducted in 420 adult patients aged 18 to 55 years who met DSM-IV criteria for ADHD. Significant improvements in ADHD symptoms, based upon investigator ratings on the ADHD-RS with adult prompts total score, were observed for all Elvanse doses compared to placebo. Treatment with Elvanse significantly reduced the degree of functional impairment as measured by improvement on the CGI-I rating scale compared to placebo.

My interpretation:
Dosages was chosen ay random, not adjusted by symptoms.
All different dosages (30,50,70) increased measured function ability in their target group. Assuming most patients benefited, perhaps all, but that is not specified.


In addition, maintenance of effect was demonstrated in a double-blind, placebo-controlled, randomised withdrawal design study that enrolled adults (n=123) who met DSM-IV criteria for ADHD and who, at study entry, had been treated with Elvanse for a minimum of 6 months. A significantly lower proportion of patients treated with Elvanse met relapse criteria (8.9%) compared to patients receiving placebo (75.0%) in the double-blind randomised withdrawal phase. Relapse was defined as a ≥50% increase from randomisation in ADHD-RS-IV Total Score and a ≥ 2 point increase in CGI-S score relative to the CGI-S score at randomisation.

My interpretation:
Individual Optimized dose is not part of study. Given that patients had been on Vyvanse for at least 6 months, it is asumable that the patients had good effect of the Vyvanse. It is also asumable that it is patients that has had good effect within the doses 30-70 mg, as no studies have been done on patients finding optimized dose above 70 mg.

Selection criteria seems to be: adult, good effect on adhd symptoms of Vyvanse within range 30-70 mg.
Study tells us that these patients had a significant increase in ADHD symptoms when medicine was replaced with placebo.


Abuse liability studies

In a human abuse liability study, when equivalent oral doses of 100 mg lisdexamfetamine dimesylate and 40 mg immediate-release dexamfetamine sulphate were administered to individuals with a history of drug abuse, lisdexamfetamine dimesylate 100 mg produced subjective responses on a scale of “Drug Liking Effects” (primary endpoint) that were significantly less than dexamfetamine immediate release 40 mg. However, oral administration of 150 mg lisdexamfetamine dimesylate produced increases in positive subjective responses on this scale that were comparable to the positive subjective responses produced by 40 mg of oral immediate-release dexamfetamine and 200 mg of diethylpropion.

My interpretation :
Yeah, Vyvanse can get you high, but if you're given a choice you will prefer a different drug/stimulant to abuse.


I haven't read the full studies, but it's what I get from the overview.

There is also a study mentioned in the us info: adults with adhd using randomised doses to of placebo, 30,50 and 70 mg. Some 400 participants, study lasted 4 weeks. Meaning that they all started on 30 mg, and some went up 20 mg per week until they were on 50 or 70. Doses were chosen at random ( double blind study?). I belive mostly experience any increase in medication as pretty good the first week after. My doctor had me on a slower increase in dose, two weeks between, which I think was good. My point is: they all probably improved their symptoms in the study. Vyvanse side effects are very mild and neglible compared to the othet ADHD stimulants. But none of these studies say anything about patterns in indivudual adapted doses in adult ADHD patients.

Shire has excluded higher doses from the research, at least the ones they write about on Vyvanse pages. We just don't have the research.

Using knowledge from other Stimulant medication, and medication in general, I'm very open for the notion that adults may find they need larger doses than children. In Europe Shire express caution when exceeding 70 mg dose, due to lack of research. Not sure if they word it different from country to country, it could depend on local law or lawsuit practices (in the US).

Anecdotally I know a couple of adults on Vyvanse, both over 70 mg. Even I use 80 mg and I am a sensitive person in regard of medicine/drugs. I have a second diagnosis of ptsd, and it probably makes me need a higher dose due to interaction between diagnosis. Hope to reduce it over time.

Yes, I argue that many probably will benefit of a larger dose, but not myself. Perhaps that isn't too convincing...

I don't know if Vyvanse is less sensitive to mody mass than other medications (if positive effect follows a different curve than toxicity).

Some of you seem really gifted in this area, skilled in finding information. Really hope mote research comes through soon, and that you guys share it with the rest.
 
I knew that the 70mg dosage was only approved for children. somebody contradicted me on that. Knew I should have asked for a source -_- lol
 
https://files.acrobat.com/a/preview/b1493a22-4302-49ae-8448-658d8ecb330b

It seems up to 250mg the enzymatic liberation of the d-amp from LDX is not saturated with the d-amp concentration increasing linearly (and remarkably consistently between subjects) with dose. The safety of LDX in doses greater than 70mg is quite good as well. There are more patients with elevated BP and other CV markers with higher doses, especially at 150mg or more, but not so many that 70mg seems too low a max dose.


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4823324/#!po=67.0732

A nice review of LDX.
 
Prami a sedative? It's a dopamine agonist. I beg to differ. One of the worst nights of my life was due to prami. lol


Also the whole time while feeling like shit, I'm pretty sure I've never had a harder erection in my life.

It is a D2 agonist that displays sedative, hypotensive and bradycardic effects. You had such an erection due to low blood pressure. this is how ED pills work....

The dopamine agonists ARE sedatives... they work like the alpha 2 agonists like clonidine, tizindine, and guanficine... the d2 receptor is an inhibitory autorecptor that shuts off dopamine release just like the alpha 2 receptor shuts down norepinphrine release.

This receptor is not an excitatory, stimulating receptor; it reduces cAMP and increases potassium: these are all HIGHLY INHIBITORY ACTIOINS.

https://en.wikipedia.org/wiki/D2-like_receptor

http://plantbiotech.metu.edu.tr/plantbiotech/bio417/dopamine_receptors.pdf
 
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https://files.acrobat.com/a/preview/b1493a22-4302-49ae-8448-658d8ecb330b

It seems up to 250mg the enzymatic liberation of the d-amp from LDX is not saturated with the d-amp concentration increasing linearly (and remarkably consistently between subjects) with dose. The safety of LDX in doses greater than 70mg is quite good as well. There are more patients with elevated BP and other CV markers with higher doses, especially at 150mg or more, but not so many that 70mg seems too low a max dose.


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4823324/#!po=67.0732

A nice review of LDX.

Great links. Appreciated! Been reading for a couple of days now.

I'm not so scholared in this field, could you indulge me by explaining your comment in layman terms? I'm not sure if I understand it.

Also, reading up on the review of LDX, it seems like my experience of different day-to-day functioning are more likely to be caused by cormorbide diagnoses, rather than LDX absorption being affected by diet++. Very valuable information for me, as I'm now getting more and more certain I need supplementary medication to deal with non-ADHD symptoms, rather than further increase the LDX dosage.
 
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