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John250

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  1. The entire amphetamine cascade is so complex it makes sense why it’s one of the most addictive drugs there is. After spending countless hours on wiki and selfdecode I pretty much got nowhere as the majority of things that help are changing gene expression. From what I’ve gathered you want to decrease expression of deltafosB while increasing expression of deltaJunD and the histone methyltransferase enzyme (EHMT2)(G9a) plus many other changes in gene expression. Of course that can’t be simple as it states: “Sufficiently overexpressing ΔJunD in the nucleus accumbens with v
  2. Thank you! Your a car fan I take it. Before my addiction I was into racing and tracking. I had a 2006 BMW M6 full bolt on around 575bph. Sold it when I opened a Nutrition store. In October I picked up another 2006 M6 and it had a 5.5l V10 13.2:1 high compression stroker on methanol put in. Rear diff went from a 3.62 to a 4.10. Carbon Fiber crankshaft, catless long tubes, fenders rolled to fit 315/30/20 drag radials,etc.. around 700bhp/600ft•lb/tq but hp/tq powerband on stock motor is around 6000-8250rpm. This powerband is 3000-7000rpm with redline at 8500. Haven’t even picked it up because of
  3. Thanks guys. The psychiatrist works at UCSD Executive Mental Health department and works Saturdays so I moved my appointment to tomorrow morning. I’m extremely nervous but it has to be done.
  4. I actually have an appointment on Monday with a new psychiatrist with 30+ years experience who specializes in neurology. I think I’m going to just come clean about how much I take, how I snort it and just tell him everything and just ask him for help and take whatever advice he gives me. Something I can reflect on right now which is really odd is I’ve never fought so hard for anything in my life. But I fought all the wrong reasons. I’ve been fighting so damn hard for like a year trying to fix myself just taking more and more amph or doing different things and researching or addin
  5. No that’s not what I’m saying. What I want to know is all of these horrible effects and downward path I want to know the mechanism causing it? Obviously it’s amphetamine because I was never this way before I started it and nothing else but what I’m curious on is what activity in my brain is causing this? Could this be depleted Serotonin? Imbalance of NE/DA (as my DBH gene shows I’m AA and I convert less NE and more DA. Or could my symptoms be from depleted dopamine since AMPH rapidly wears off and depleted DA and TH? I have a feeling it’s excessive DA in my mesolimbic pathway caus
  6. I keep seeing how Ibogaine works wonders for opiate and psychostimulant withdrawl. On selfhacked it states: “Inhibition of dopamine transporters: Ibogaine has the same effects on dopamine transporters, resulting in higher dopamine levels. Dopamine levels in addicted individuals are altered due to the excessive use of abused drugs, such as cocaine. Ibogaine can reset the dopamine levels to pre-addiction levels, without leading to a new addiction.” https://www.ncbi.nlm.nih.gov/pubmed/22451652/ The part that stands out the most is “Ibogaine can reset dopamine l
  7. Can someone explain this? I’ve seen this before when discussing therapeutic options for reducing drug cravings: “Tamoxifen has demonstrated some efficacy has a therapeutic for bipolar mania and is believed to exert these effects through inhibition of protein kinase C (PKC). As the symptoms of amphetamine treatment in rodents are believed to mimic the symptoms of a manic episode, many of the preclinical studies for this indication have demonstrated that tamoxifen inhibits amphetamine action. The amphetamine-induced increase in extracellular dopamine which gives rise to the ‘manic’ e
  8. Thanks everyone. No FMLA I run a private business{IFBB/Npc diet/training prep,etc..}. Hard to explain but I have many competitors and a few who were friends that know about my situation took advantage of it and basically stole a lot of my customers throughout my absence. Literally 10 hours total of work would catch me back up to where I could make an excuse to all my clients like I’m taking a 2 week vacation or something along those lines so I could detox but until I get those 10hrs caught up if I went to detox for 2 weeks on top of already being behind I would probably
  9. Unfortunately I’m already in that situation and have been about 4yrs now. I was prescribed up to 110mg/day Adderall in 2014 due to my size and metabolism but it was still negligent on the Dr’s part. I never even took it all I averaged about 60mg/day the first year and 1/2 then had a bad 4-6 months of 80-90mg. I developed a bad habit of snorting it which is good in a sense that I lost a good 25% of the drug but bad for the other obvious reasons. I went to new Dr. and came clean about the misuse and he switched me to 70mg Vyvanse which was rough as that’s only 28mg amphetamine so the jump from
  10. Yes I see what you are saying but I’m not necessarily referring to only increasing dopamine to get the benefits.i meant compounds that synergize that aren’t harmful themselves. Like the addition of theanine to caffeine,etc.. I have a bottle of Guanfacine from irc I got a long time ago but was afraid to use it because I’ve read several reports of fatigue being a big side effect of Guanfacine. Have you tried it and if so what did you notice, dosage, etc.?
  11. I have. I tried 200mg and then a low dose of 50mg. Each time I tried it was a few hours after my morning Vyvanse dose and I found it just gave me some brain fog and reduced amps cognitive positives. I feel there was probably a cross tolerance like there is when you add Wellbutrin with amp as they compete for DAT. However I haven’t tried Modafinil “before” amphetamine so maybe that will help. It’s odd how different methamphetamine is from amphetamine I’m very greatful I’m not hooked on meth because in several trials they tried giving methamphetamine users dextroampheta
  12. Well I guess if the person had no plans to quit it wouldn’t be worth it but during a taper it could be useful and speed it up. Say someone is used to needing 30mg amp to get up in the morning and function. Maybe with a PKC activator 20mg could let the person function the same. Or even if the end user didn’t plan to taper or quit they could reduce the dosage which would be overall less harmful. Like how let’s say 200mg caffeine+200mg theanine May give someone the same effects as 300-350mg caffeine. Your consuming less so less sides plus theanine is healthy. B
  13. So wouldn’t activating protein kinase C (PKC) increase the rewarding responses of amphetamines. Wouldn’t it make sense to find a PKC agonist or activator which would allow one to use less amphetamine yet reap the same rewarding effects?
  14. That makes sense. Here’s my problem with Amphetamine. There is no FDA withdrawl drug for it yet opiate users get methadone or suboxone, benzo’s get Gabapentin,etc.. all making the withdrawl easier yet nothing for amps. Amphetamine is also the easiest withdrawl of most drugs in terms of length of time and rare to have a risk of a seizure. But it’s by far the most debilitating fatigue and cognitive function leaving the user pretty much useless. However amphetamine, methamphetamine, coke and Nicotine all impact the brains main addiction pathway(deltafosB) far more than most other dr
  15. I’m probably reading this wrong but is it saying it reduces the dopamine and positives from amphetamines? If so I never understood why some studies would even list compounds that attenuated the “high” or positives of the drug. Like I read something about some NMDA antagonist that completely blocked all “positives” from amphetamines and it then said this antagonist could be useful for withdrawl. How? If your not feeling it your going to take more. You would think they would list compounds that synergize the drug not attenuate it.
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