The Big and Bangin' Pseudo-Advanced Drug Chemistry, Pharmacology and More Thread, V.2

[sibirianfox]

Sorry...
I just joined and was trying to reply to somebody's post...
For some reason in my response above, the person's quote is not listed.
I'm not sure what I did wrong. I cliqued on "Post quick reply".
Should it be "go advanced" if I want the quotes to show?
Tnx!

 

[yoyoman]

the doctors ended up waking him up from his coma for a minute using a shot of adrenaline... so he could say goodbye and people could say goodbye to him.... he died soon after... this seemed almost inhumane to me.... he was probably so confused suddenly waking up from adrenaline and finding himself in the ER... but i also had the thought that maybe if they coadministered vicodin and xanax with the adrenaline then maybe his body would have been able to handle the stress from the adrenaline and maybe nursed back to health

Why wouldn't they try methamphetamine or at least racemic amphetamine? That's the first thing that would pop into my mind if someone is slipping into a coma or is in one. IV amphetamines, meth being safer on the body you could crank the dose up pretty high (long half life, but whats the harm if it doesn't work).

I just don't get why they'd shoot him with adrenalin its like taking ephedrine to study everyday.

 

[Epsilon Alpha]

Why wouldn't they try methamphetamine or at least racemic amphetamine? That's the first thing that would pop into my mind if someone is slipping into a coma or is in one. IV amphetamines, meth being safer on the body you could crank the dose up pretty high (long half life, but whats the harm if it doesn't work).

I just don't get why they'd shoot him with adrenalin its like taking ephedrine to study everyday.

I think they've trailed it, this source (sketchy as hell) makes it sound like it works for some cases of mild damage.
http://www.comawakening.com/coma.html

 

[helium-4]

Given the drugs involved I would expect this to be a fairly textbook case of drug induced respiratory depression. The coma itself was likely caused because your friend stopped breathing while unconcious.
By the time coma has occured, brain tissue is almost always already dead and re-oxygenation will do nothing. Unless someone would have found him earlier to provide e.g. rescue breathing or an antidote, there is essentially no therapy for large-scale brain damage.

I had read somewhere that ketamine increased cerebellar blood flow some large amount. That said, I don't expect administering ketamine to a braindead patient will bring them back, or even help at all.

I think you should try to accept the facts, and take solace that your friend was feeling no pain when he passed on. There's nothing you really could have done.

And if ketamine or some other nada-antagonist was used they have to be used at a specific interval for a very short amount of time or the prolonged antagonism would result in a flood of glutamate post antagonism resulting in further brain damage. One of e problems with the studies involving ketamine and traumatic head injuries are poor procedures involving the administration of ketamine. I could pull up articles from my computer (on my iPad right now) if people were interested in further looks at this topic (ketamine for brain trama)

I think they've trailed it, this source (sketchy as hell) makes it sound like it works for some cases of mild damage.
http://www.comawakening.com/coma.html

I think some people put to much faith in episodes of house md were mircles happen all the time from experimental treatments

 

[helium-4]

^^ was purely out of curiosity



i think that's pretty rude of you

honestly i only met the dude once, i'm not going on like this out of some crazy grief stricken rage or something



and there never will be if every conversation like this is stifled

You are posting on a web forum to individuals who most likely don't have the capability to preform the research or have the time to come up with your hopes and dreams in a few lines of text to satisfy you (no offense to the professionals in ADD), you're not addressing a bunch of professional medical doctors or researchers who are working on tasks like this. I don't know what type of answer you are expecting to get. You can do reading on your own to find many of the expiremental processes being used like hyperthermia, various drugs prevent different stages of cell death, etc. but your most likely going to find articles showing no mircle therapy out there not showing the level of success for the desired results you'd like to see. Most experiments I've read have not had much success and still need years of research or in the case of some promising leads like ketamine, poor procedures in more realistic applications of the drug/combination of drugs with keteamine has slowed down the prospect of using ketamine in these type of situations due to poor results. Like I said a lot of the articles published using ketamine as a way to prevent further brain damage as well as induce synaptogenesis/neurogenesis show the opposite of the desired/expected response. Of course intiatially the nmda-antagonism slows cell death but in the higher phases of studies I've read the use of ketamine using their designed procedures caused further cell death making revival impossible. The timing of infusion as well as quantity administered needs to be done at a specific time pre/during/immediately (need to re read to articles to better explain the timing issue) after the traumatic injury took place. The infusion then needs to be halted to prevent a cascade of glutamate via a rebound effect produced by prolonged nmda-antagonism further speeding up apoptosis/cell death by the influx of Ca^2, Stimulating nitric oxide synthase leading to the production free radical ONOO- resulting further cascades of negative effects that produce further free radicals causing detrimental effects on the mitochondria within the cells as well as continue to increase the influx of Ca^2 and ONOO- along with many other damaging processes I'm not 100% knowledgable of.

When using ketamine for other therapies like inducing LTP the timing of administration is also important because like with trying to treat a tramautic brain injury, extended non competitive antagonism can cause the opposite of the desired effect to occur resulting in LTD, and all the lovely side-effects you see with dissociative abuses (poor memory retention/formation, Difficulty concentrating, inability to Learn new associated behaviors, difficulty with language/communication, Delusional thoughts, etc all easily seen when you read through the countless mxe threads). However if the administration and doses infused are dosed at certain time intervals LTP can be seen and ones ability to retain previously learned knowledge is increased, along with other potential benefits (reduction in stress/synaptogensis, potential therapeutic potentials in depression, forms of anxiety, OCD, and potentially others).

Sorry I kinda went one rant With the last paragraph as I find it very interesting and good to know for users "trying" to get the benefits from ketamine or other dissocitives like MXE as I feel to many like to pretend they are doing something positive to their brain where they are actually over using and doing the opposite. Sure different benefits like the anti-d qualities may still be seen with abusive dosing but interns of LTP or cognitive abilities I'd say not. End rant

 

[pharmakos]

thanks cloudy

I don't know what type of answer you are expecting to get.

i wasn't upset at any of the responses other than the "i think you should quit asking these questions and try to come to terms with your grief"

really had already put my grief behind me a few weeks ago

and questions are always okay imo, stifling questions in ADD is pretty contrary to the goal of the place i'd say

 

[nAON]

are there any drug therapies for coma that are intended to increase oxygen levels in the brain?

Look into Piracetam, apparently it's shown to help in decreasing negative effects of hypoxia in stroke victims.

 

[Jktm]

Sorry if this isn't even Pseudo-ADD material, but was curious as to what types of drugs/chemicals could be used to combat endogenous obesity from an extremely slow metabolism? I'm currently taking 75mg of IR phentermine daily and am eating around 1000 calories/day, but weight-loss comes slowly and has long plateaus that arise quickly once weight-loss has resumed, so I'm pretty sure it's not my appetite that is the issue. I know we aren't supposed to ask individualized questions such as this in ADD (or at least make your own thread for one), but I figured that there's probably many other people with this issue, so maybe it won't be a big deal.

 

[sekio]

There aren't very many drugs that raise metabolic rate in a "safe" way.

Two or three of the ones that come to me off the top of my head are D-methamphetamine, MDA/MDMA/Fenfluramine, and 2,4-dinitrophenol.

Meth is neurotoxic, the MDx and fenfluramines are likely cardiotoxic with long term use, and 2,4-dinitrophenol can cause all sorts of stupid side effects like caracts at a young age.

There is also the option of steroid therapy, but I am not very well-read into that book.

 

[Epsilon Alpha]

Sorry if this isn't even Pseudo-ADD material, but was curious as to what types of drugs/chemicals could be used to combat endogenous obesity from an extremely slow metabolism? I'm currently taking 75mg of IR phentermine daily and am eating around 1000 calories/day, but weight-loss comes slowly and has long plateaus that arise quickly once weight-loss has resumed, so I'm pretty sure it's not my appetite that is the issue. I know we aren't supposed to ask individualized questions such as this in ADD (or at least make your own thread for one), but I figured that there's probably many other people with this issue, so maybe it won't be a big deal.

It may be worth having your thyroid checked if your metabolism is that slow. If you come out with a low T3/T4 level you might want to talk to your doctor about supplementation.

Then there's steroids... Yeah it's a path I wouldn't recommend due to side effects, but that's beside the point.

 

[sekio]

Thyrioid and testosterone level tests are probably a good idea to have done by a Dr. - those are two big factors.

 

[Jktm]

I am a CPP so so the testosterone is definitely a possibility...I just wish my doc didn't charge extra for those labs... *sigh*

Thanks for the info guys...

 

[m060mm]

this source (sketchy as hell)
http://www.comawakening.com/coma.html

For truth.

I'm pretty sure he's a copypasta. The lack of organization and nonsequitor presentation.. and that background makes me nauseous after reading just a few lines.

Sorry if this isn't even Pseudo-ADD material, but was curious as to what types of drugs/chemicals could be used to combat endogenous obesity from an extremely slow metabolism? I'm currently taking 75mg of IR phentermine daily and am eating around 1000 calories/day, but weight-loss comes slowly and has long plateaus that arise quickly once weight-loss has resumed, so I'm pretty sure it's not my appetite that is the issue. I know we aren't supposed to ask individualized questions such as this in ADD (or at least make your own thread for one), but I figured that there's probably many other people with this issue, so maybe it won't be a big deal.

These guys' suggestions so far are pretty spot on. This is an endocrine disorder; treating the obesity itself, while beneficial to your overall health, is not the solution.

+1 to T3/T4, +1 to a whole HTPA axis assessment. Decline the MRI unless they really can't find anything with exhaustive blood work. (I'm considering cost, which you mentioned.) Insist on testing E2 early; you're giving me the impression that you have above average body fat. Even if you can control estrogen while you wait for conclusive results, it will help with your weight loss efforts and likely a lot of other side effects if it's in fact out of range. (Range being 10-30ng/dL; don't let them tell you 50-60 is ok.)

Congrats on being disciplined enough to stick to 1000/day but with all due, that is too low. Just my opinion after dealing with various comorbid conditions. I don't know your situation. I've had clients lose 100+ in a matter of six to nine months (no gimmicks so my numbers aren't jaw dropping) and keep it off. I'd say about 20% of them were hitting plateaus because they weren't eating enough. You need to build muscle to burn fat, look better and increase your basal metabolic rate, which is a factor many seem to underestimate.

Obviously you should consult your doctor before changing anything, but I think there are a few points worth discussing.

Best of luck!

edit: I went on the assumption that by CPP you meant precocious puberty. That's why I'm guessing your estrogen (or rather, T:E ratio) is off.

 

[Jktm]

CPP is Chronic Pain Patient lol...my bad...I was thinking my testosterone could have decreased from opioids...

And my sex/age is being questioned...20 year old dude lol...my brain is desensitized to estrogen lol...

 

[doppelgänger1]

Sorry if this isn't even Pseudo-ADD material, but was curious as to what types of drugs/chemicals could be used to combat endogenous obesity from an extremely slow metabolism? I'm currently taking 75mg of IR phentermine daily and am eating around 1000 calories/day, but weight-loss comes slowly and has long plateaus that arise quickly once weight-loss has resumed, so I'm pretty sure it's not my appetite that is the issue.

Too low calories intake will result in lower t3-bloodlevels and therfore lower calorie consumption. I don't know exactly, but 1000kcal sounds like to low to me.

 

[Jktm]

Another question from the pharmacology hopeful lol...

Does higher peak plasma concentrations of drugs necessitate increased receptor saturation (e.g. Would donating a pint of whole blood (or a unit of plasma for that matter) result in better response to pain medications)? I donate every 8 weeks regardless, but was wondering if taking the same dose of a medication after donating result in a stonger response than a dose taken a few hours before getting drained.

 

[sekio]

Not neccesarily.

If memory serves, decreasing blood volume will primarily affect drugs by decreasing the amount of water availiable for it to partition into, and decreasing e.g. albumin binding. (non-target binding) But dontaing a pint of 2 of blood won't really change gross parameters of drug efficacy and metabolism.

I would wager that a lot of the perceptible changes when yoiur blood is drained simply come from a loss of blood pressure & decrease in blood sugar. They're probably offset pretty easily by drinking some juice and waiting a little while. (hence why juice and cookies are a staple of blood drives)

 

[Jktm]

why is phentermine not an amphetamine? is it because the methyl group is on the second carbon as opposed to the amine?

I just notice the only difference in nomenclature between it an methampetamine is the placement of the methyl group...

 

[sekio]

Phentermine could be considered an amphetamine, it is alpha,alpha-dimethyl-phenethylamine,

The problem is, the alpha-carbon is a chiral center in amphetamine, and if it's in the wrong place it won't work... explaining phentermines (and L-amphetamine's) decreased potency.

 

[Jktm]

Ah, so it's that methyl group that fucks it up...

thanks for all the answers man...