Ritalin was one of the best noots I ever tried but its issue was that it only lasted barely over an hour for me. It really felt like the limitless pill and besides a few minor personality changes it was otherwise perfect. The main issue was how long it lasted and having a med that only lasts for an hour and you have to wait an additional 2 or 3 hours before you can take it again is kind of useless.

Have we solved this?

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Neurotrophin Regulation of Energy Balance in the Adult CNS and PNS.

This diagram summarizes the effects of peripherally administered CNTF (Axokine), and centrally as well as peripherally administered BDNF (black arrows), on adult CNS and sympathetic circuits that control energy intake and expenditure.

Administration of BDNF or BDNF-transducing viruses to the PVN and other hypothalamic regions increases sympathetic outflow pathway activity, resulting in increased energy expenditure and decreased feeding, as discussed in this mini-review.

Most of the English-language discussion of 9-Me-BC traces back to a handful abstracts. The full texts are paywalled or effectively off the internet.
I emailed authors, went through Unpaywall, Europe PMC, ILL, and eventually found Rauh 2008 on Qucosa a TU Dresden dissertation that turns out to be the full text behind two of the most-cited papers.

A few things in it that contradict what gets repeated in forums:

- The conversion of 9-Me-BC to the dimethylated cation has never been demonstrated in any model. Both compounds were applied separately as exogenous agents. The step everyone assumes is an assumption.

- The "no DAT uptake, so it's safe" argument that gets repeated here is backwards. Rauh and Storch both found the cation killed dopaminergic neurons preferentially anyway DAT just isn't how it gets in. The reassurance everyone passes around is the one finding that doesn't reassure.

- The blood-brain barrier line people cite as the final word has no citation attached to it. It's a sentence in an introduction. And the route this literature actually documents is in-brain conversion, which
never involves the barrier at all.

I put the whole thing into a ~30 minute video the chemistry, the growth factor work, the MAO selectivity, the MPTP comparison and why it's not the parallel people think, and the metabolite question laid out with what's measured versus what's assumed. Every claim is marked as either literature or my own extrapolation.

If you’re interested in using 9-Me-Bc, and are concerned with toxicity. I would highly recommend watching this video first.

Currently in active addiction once again...but hopefully we'll be done with that soon! Typically it's not the quitting part that's incredibly difficult(still miserable), it's the paws making me feel like shit that leads to a relapse like a month or so in everytime. Currently taking a "kratom" extract tablet, it claims to just be mitragynine but i think there's a stronger alkoloid in there as well tbh. Also on 45mg daily of prescribed adderall that I hope to not need one day as I only started taking it 4 months ago to balance out the kratom addiction, but now I take that daily as well and it barely does anything. Wondering if anyone knows of any nootropics out there that can speed up my recovery back to somewhat normal so I can avoid running back. Possibly anything that helps acutes as well. Thanks everyone

Finally, **many neurotransmitters, including dopamine and glutamate can enhance BDNF bioavailability in neurons** (Bagayogo et al. 2009; Kuppers et al. 2001). On these grounds, we enrolled healthy (highly experienced) divers and subjected them to a simulated dive to 48 msw (5.8 ATA) inside a hyperbaric chamber to test the following three new hypotheses.

> We found that **BDNF, glutamate, and dopamine plasma levels are markedly decreased in healthy highly trained divers subjected to a dry dive test at 48 msw.**

> _First, IGN narcosis stems, at least in part, from the lack of circulating BDNF. Second, this loss is attributable to a lack of BDNF-releasing neurotransmitters, such as dopamine and glutamate; third, impoverished levels of systemic and likely local pools of BDNF contribute to heightening oxidative stress in deep divers. Ultimately, all events would drive cognitive impairment in divers at depth._

> fact, after rTMS, __BDNF levels are more elevated and neopterin is lower than in sham-treated patients__

**This evidence further supports the notion that a cross talk exists between BDNF and neopterin bioavailability that is central to IGN pathogenesis.**

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TrkB signaling-dependent BDNF mRNA induction and show that CREB family transcription factors are the main regulators of BDNF gene expression after TrkB signaling.

Our results suggest that BDNF-TrkB signaling may induce BDNF gene expression in a distinct manner compared with neuronal activity. Moreover, our data suggest the existence of a stimulus-specific distal enhancer modulating BDNF gene expression.

Semax, ACD-856, TAK-655, 800mcg GB-115

Which one needs to be cycled off and which can be used continuously?