I think there may be a nearly ideal way to learn. Gonna start trying it myself when I have time, for exams. Which is - exercise right before studying (aerobic training included) - then after studying, take a power nap. Both of these, individually, have been shown to boost recall and such, and it makes sense. You should get the benefits of both combined in this as well, as they work through different mechanisms of memory retention.

I was primed for this via pm, however I thought I'd post here. Just some thoughts I have on potential benefits of using marijuana in terms of memory storage.

THC binds to CB1 & CB2 receptors, both of which are G(i) coupled.. meaning they're inhibitory, and upon binding they subsequently decrease cAMP levels, and hence downstream effectors - PKA, CREB, etc.. of which CREB has HUGE roles in memory formation/LTP (long term potentiation), dendritic spine formation, etc.
So, it is easily clear that THC will impair short term memory & the storage of new long term memories, while high.

However, I think, examining the effects, THC may contribute to synaptic pruning via LTD (long term depression). This is an integral process, and in this case could be good. In essence, it ensures that your salient and well formed memories stay and are strengthened, whilst your weakly formed/unimportant memories will be forgotten. So, for someone in school (like me), constantly reading their school studies and various other biomedical studies, this is greatly beneficial. As I've continued to smoke, every night, I have noticed this as well.
My verbal fluency and memory for my studies have never been better (since they're salient to me), where I'll hardly read something and it's ingrained in my mind. On the flip though, I've noticed when it comes to simple things such as names, and generally other unimportant things I have trouble remembering it in any way. For me though, this is a good thing.. again, you decide what's salient, and I believe THC can help ensure that it stays, while the mumbo jumbo of the daily grind is forgotten.

Further, THC stays in your body for quite awhile. It also seems to act, subtly, as an ACHesterase inhibitor, thus increasing ACh levels circulating through the brain.. this can help the process of LTP, and thus THC could potentially contribute to long term memory storage more, after you're not high anymore.

About to just post a fewl studies I've read today and found interesting. Often times I can only get the abstract (unforunately, but working on getting full text for several).

"Leptin-Mediated Increases in Catecholamine Signaling Reduce Adipose Tissue Inflammation via Activation of Macrophage HDAC4"

http://www.sciencedirect.com/science/article/pii/S1550413114001296

- I find this particularly interesting, because leptin is pro-inflammatory. Leptin's effect on the SNS and leading to norepi/epi output is known, and it's generally known that those are anti-inflammatory, so no surprise there. I guess just add that to more positive effects of leptin. Decreasing adiposity and decreasing the inflammation in adipocytes, whilst also doing its myriad effects, of which include allowing inflammation and immune function systemically.

"PPARγ in Vagal Neurons Regulates High-Fat Diet Induced Thermogenesis"

http://www.sciencedirect.com/science/article/pii/S1550413114001193

- High fat diet leads to downexpression of ppar-gamma and increases thermogenesis. This is unexpected tbh. It says it may serve as a protection against diet induced weight gain, so a homeostatic mechanism basically. I don't know how to feel, however, after that study sometime last year basically saw that a high fat diet led to aberrant oscillations in the circadian rhythm and with that - ppar-gamma, which many were suspecting could increase fat gain. Perhaps this is suggesting that the oscillation observed, is simply a homeostatic mechanisms to prevent fat gain, so it may not be so negative after all? Simply surmise.

"Autophagy Is Required to Maintain Muscle Mass"

http://www.scopus.com/record/display.url?eid=2-s2.0-70449927247&origin=inward&txGid=A224C04F417BA53E5A5375CB4559EBA0.y7ESLndDIsN8cE7qwvy6w%3a1

- Something I've claimed before about the necessity of autophagy in muscle growth, not even going into its positive health effects.

"Reactive Oxygen Species Enhance Insulin Sensitivity"

http://www.scopus.com/record/display.url?eid=2-s2.0-70349512259&origin=inward&txGid=A224C04F417BA53E5A5375CB4559EBA0.y7ESLndDIsN8cE7qwvy6w%3a17

- In the face of all the negativity ROS gets, there's also this. By the way, this is how adiponectin increases insulin sensitivity. It induces an acute burst of ROS. This is also part of mitohormesis that I talk about.

Then, two full text reads on Sleep & cognitive function as well as synaptic plasticity. Very interesting.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3980112/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3896837/#!po=1.61290

A bit unrelated, but I've just been admitted to a research assistant's issuing in the main university (TAU) in the country. Economics dept.

This post was edited by Lightman on Apr 30 2014 02:45pm

Congratulations m9
Drop some Econ knowledge on us in here lolol

Not sure anyone will understand lol. It's either too dry mathematically or too complex logically.

Going through the first revision of my paper. Rather than just posting the abstract and the interesting studies, i'm going to post my full paper for HNF to read.

Just putting together a few things about coffee/caffeine that I've come across lately. Coffee da gawd liquid

"Coffee treatment prevents the progression of sarcopenia in aged mice in vivo and in vitro."

http://www.ncbi.nlm.nih.gov/pubmed/24269808

"Drinking coffee burns hepatic fat by inducing lipophagy coupled with mitochondrial β-oxidation"

http://onlinelibrary.wiley.com/doi/10.1002/hep.26736/abstract

And in the full text it says: "caffeine may inhibit PI3K-AKT and, in turn, inhibit mTOR to trigger autophagy by activating the ULK1 complex, which includes ULK1, Atg13, FIP200, and Atg101. Autophagy selectively removes excess LDs to generate FFAs. Decreased mTOR induces TFEB nuclear translocation by decreasing TFEB phosphorylation. TFEB up-regulates expression of autophagy and lysosomal genes, as well as PGC-1α and PPARα, which burn FFAs by increasing mitochondria β-oxidation. Thus, caffeine protects against fatty liver by coordinately inducing lipophagy and mitochondrial β-oxidation."

"Habitual consumption of coffee and green tea in relation to serum adipokines: a cross-sectional study"

http://link.springer.com/article/10.1007/s00394-014-0701-4

"Consumption of a dark roast coffee decreases the level of spontaneous DNA strand breaks: a randomized controlled trial"

http://link.springer.com/article/10.1007/s00394-014-0696-x

Can't wait m9.

Carbs immediately after exercise supported?

http://www.ncbi.nlm.nih.gov/m/pubmed/3132449/