L
onge
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ity
Advocacy & Research for Unlimited Lifespans
29 votes
Posted 07 November 2015 - 09:43 PM
Hey Lostfalco thanks for the suggestions...galantamine used to be beneficial but since on my meds I had to totally rethink my supps program over the past year. I will try the butyric acid since I used to take resistant starch a couple of years ago.
Posted 09 November 2015 - 01:07 AM
Hey Falco!
Read the whole thread and have been lurking here for some time. Can you recommend the dosages of the aforementioned compounds?
Another reminder of interesting experimental ideas relating to massive memory enhancement if anyone is interested in trying them out. =)
1. tadalafil/sildenafil + zembrin
2. tadalafil + zembrin + sodium butyrate
3. tadalafil +zembrin + sodium butyrate + resistant starch/fiber
4. tadalafil + zembrin + sodium butyrate + resistant starch/fiber + ALCAR
Hey StabMe, glad you found some useful ideas in the thread! Sorry about the 87+ pages of thinking out loud. ha
Start with one substance at a time and start with low dosages. You can always adjust up from there.
tadalafil 2.5 to 5mg
zembrin 25mg (I'm honestly not a huge fan of zembrin but PDE4 inhibitors are currently hard to come by...make sure that you are familiar with its serotonin reuptake inhibiting properties)
sodium butyrate 600mg
resistant starch 1 to 2 tbsp
ALCAR 500mg
These are just starting doses and a fair amount of tweaking is almost certainly going to be required. =)
Edited by lostfalco, 09 November 2015 - 01:08 AM.
Posted 09 November 2015 - 06:57 AM
Bacopa is a possible HDAC inhibitor.
http://www.ncbi.nlm....pubmed/24610280
Cell Mol Neurobiol. 2014 May;34(4):577-89. doi: 10.1007/s10571-014-0042-0. Epub 2014 Mar 8.
Standardised extract of Bacopa monniera (CDRI-08) improves contextual fear memory by differentially regulating the activity of histone acetylation and protein phosphatases (PP1α, PP2A) in hippocampus.Contextual fear conditioning is a paradigm for investigating cellular mechanisms involved in hippocampus-dependent memory. Earlier, we showed that standardised extract of Bacopa monniera (CDRI-08) improves hippocampus-dependent learning in postnatal rats by elevating the level of serotonin (5-hydroxytryptamine, 5-HT), activate 5-HT3A receptors, and cyclic adenosine monophosphate (cAMP) response element binding (CREB) protein. In this study, we have further examined the molecular mechanism of CDRI-08 in hippocampus-dependent memory and compared to the histone deacetylase (HDACs) inhibitor sodium butyrate (NaB). To assess the hippocampus-dependent memory, wistar rat pups were subjected to contextual fear conditioning (CFC) following daily (postnatal days 15-29) administration of vehicle solution (0.5 % gum acacia + 0.9 % saline)/CDRI-08 (80 mg/kg, p.o.)/NaB (1.2 g/kg in PBS, i.p.). CDRI-08/NaB treated group showed enhanced freezing behavior compared to control group when re-exposed to the same context. Administration of CDRI-08/NaB resulted in activation of extracellular signal-regulated kinase ERK/CREB signaling cascade and up-regulation of p300, Ac-H3 and Ac-H4 levels, and down-regulation of HDACs (1, 2) and protein phosphatases (PP1α, PP2A) in hippocampus following CFC. This would subsequently result in an increased brain-derived neurotrophic factor (Bdnf) (exon IV) mRNA in hippocampus. Altogether, our results indicate that CDRI-08 enhances hippocampus-dependent contextual memory by differentially regulating histone acetylation and protein phosphatases in hippocampus.
Posted 09 November 2015 - 07:09 AM
LLLT + Pyruvate (pyruvate is an HDAC1 and 3 inhibitor) or Lactate
http://www.ncbi.nlm....pubmed/25966949
J Cereb Blood Flow Metab. 2015 Sep;35(9):1435-44. doi: 10.1038/jcbfm.2015.87. Epub 2015 May 13.
Low-level light in combination with metabolic modulators for effective therapy of injured brain.
Vascular damage occurs frequently at the injured brain causing hypoxia and is associated with poor outcomes in the clinics. We found high levels of glycolysis, reduced adenosine triphosphate generation, and increased formation of reactive oxygen species and apoptosis in neurons under hypoxia. Strikingly, these adverse events were reversed significantly by noninvasive exposure of injured brain to low-level light (LLL). Low-level light illumination sustained the mitochondrial membrane potential, constrained cytochrome c leakage in hypoxic cells, and protected them from apoptosis, underscoring a unique property of LLL. The effect of LLL was further bolstered by combination with metabolic substrates such as pyruvate or lactate both in vivo and in vitro. The combinational treatment retained memory and learning activities of injured mice to a normal level, whereas other treatment displayed partial or severe deficiency in these cognitive functions. In accordance with well-protected learning and memoryfunction, the hippocampal region primarily responsible for learning and memory was completely protected by combination treatment, in marked contrast to the severe loss of hippocampal tissue because of secondary damage in control mice. These data clearly suggest that energy metabolic modulators can additively or synergistically enhance the therapeutic effect of LLL in energy-producing insufficient tissue-like injured brain.
Edited by lostfalco, 09 November 2015 - 07:14 AM.
Posted 09 November 2015 - 06:27 PM
A quick reminder about the microbiome, epigenetics, and possible brain enhancement (this is a very new research area and there are many things yet to be discovered). For those of you who don't have time to sift through an 88 page thread. =)
I still take resistant starch every day.
http://www.ncbi.nlm....pubmed/25911232
Adv Appl Microbiol. 2015;91:1-62. doi: 10.1016/bs.aambs.2015.02.001. Epub 2015 Mar 11.
Microbiota regulation of the Mammalian gut-brain axis.
The realization that the microbiota-gut-brain axis plays a critical role in health and disease has emerged over the past decade. The brain-gut axis is a bidirectional communication system between the central nervous system (CNS) and the gastrointestinal tract. Regulation of the microbiota-brain-gut axis is essential for maintaining homeostasis, including that of the CNS. The routes of this communication are not fully elucidated but include neural, humoral, immune, and metabolic pathways. A number of approaches have been used to interrogate this axis including the use of germ-free animals, probiotic agents, antibiotics, or animals exposed to pathogenic bacterial infections. Together, it is clear that the gut microbiota can be a key regulator of mood, cognition, pain, and obesity. Understanding microbiota-brain interactions is an exciting area of research which may contribute new insights into individual variations in cognition, personality, mood, sleep, and eating behavior, and how they contribute to a range of neuropsychiatric diseases ranging from affective disorders to autism and schizophrenia. Finally, the concept of psychobiotics, bacterial-based interventions with mental health benefit, is also emerging.
Genes Brain Behav. 2014 Jan;13(1):69-86. doi: 10.1111/gbb.12109. Epub 2013 Dec 27.
Microbial genes, brain & behaviour - epigenetic regulation of the gut-brain axis.
To date, there is rapidly increasing evidence for host-microbe interaction at virtually all levels of complexity, ranging from direct cell-to-cell communication to extensive systemic signalling, and involving various organs and organ systems, including the central nervous system. As such, the discovery that differential microbial composition is associated with alterations in behaviour and cognition has significantly contributed to establishing the microbiota-gut-brain axis as an extension of the well-accepted gut-brain axis concept. Many efforts have been focused on delineating a role for this axis in health and disease, ranging from stress-related disorders such as depression, anxiety and irritable bowel syndrome to neurodevelopmental disorders such as autism. There is also a growing appreciation of the role of epigenetic mechanisms in shaping brain and behaviour. However, the role of epigenetics in informing host-microbe interactions has received little attention to date. This is despite the fact that there are many plausible routes of interaction between epigenetic mechanisms and the host-microbiota dialogue. From this new perspective we put forward novel, yet testable, hypotheses. Firstly, we suggest that gut-microbial products can affect chromatin plasticity within their host's brain that in turn leads to changes in neuronal transcription and eventually alters host behaviour. Secondly, we argue that the microbiota is an important mediator of gene-environment interactions. Finally, we reason that the microbiota itself may be viewed as an epigenetic entity. In conclusion, the fields of (neuro)epigenetics and microbiology are converging at many levels and more interdisciplinary studies are necessary to unravel the full range of this interaction.
Edited by lostfalco, 09 November 2015 - 09:18 PM.
Posted 10 November 2015 - 10:43 AM
Edited by abelard lindsay, 10 November 2015 - 10:44 AM.
Posted 10 November 2015 - 01:26 PM
Tons of good info in those pages, Falco 
I was wondering, if one finds obtaining tadalafil not easy, is there an alternative PDE5 inhibitor, that you would use in those combos? Artichoke, Forskolin, Quercetin? How do they stack with Zembrin?
I am having no problems ordering from iHerb: the delivery is fast and the package rarely gets seized by the customs. But if i try to order from online customs, the delivery rate is really low.
BTW, what is your current regimen? Still do lasering?
Hey StabMe, glad you found some useful ideas in the thread! Sorry about the 87+ pages of thinking out loud. ha
Start with one substance at a time and start with low dosages. You can always adjust up from there.
tadalafil 2.5 to 5mg
zembrin 25mg (I'm honestly not a huge fan of zembrin but PDE4 inhibitors are currently hard to come by...make sure that you are familiar with its serotonin reuptake inhibiting properties)
sodium butyrate 600mg
resistant starch 1 to 2 tbsp
ALCAR 500mg
These are just starting doses and a fair amount of tweaking is almost certainly going to be required. =)
Posted 10 November 2015 - 11:26 PM
Hey LostFalco,
Just curious on your opinon on dave asperys pqq compared to others (as his is quite expensive) but with statements like this :
"Unfair Advantage™ is the only product on the market today that delivers the active form that bypasses your stomach acid, ActivePQQ™. Suspended in a colloid so that it’s easily absorbed and fast acting, Unfair Advantage™ will turn the lights on for your mitochondria." - Dave Aspery, now I realise that dave aspery is a marketing person ( no disrespect to him I just understand that he runs a business).
Now im just curious as to this statment compared to for instance, the PQQ + Coq10 you suggested "http://www.amazon.co...uct_top?ie=UTF8".
Do you think it will still be effective?
Also, as far as the Led Lights go.. i once upon a time saw a post from you regarding cheap LED lights for the purpose low level light therapy, would this be the same thing you link to in your recommendations ?
"96 LED array: http://www.ebay.com/...=item232c0ac99b
48 LED array: http://www.ebay.com/...=item3a80a68672"
And im so sorry I know this stuff has probably been covered to death, if you would like id be more than happy to private message you instead, but i remeber you explaining how you get access to full articles instead of simply the abstract to medical studies. But im having a hard time locating them.
I Hope to not de rail the current theme of the thread by this post
Regards,
Posted 11 November 2015 - 12:56 AM
Speaking of Zembrin, Zembrin+forskolin (5mg of forskolin is about right, more might be uncomfortable) is one helluva combo. LostFalco, have you tried that yet? The only downside is it makes me a bit anti-social. I wish I could take a month, talk to no one, take that combo and work my way through some rather large technical books.
Taladafil gave me great erections and lowered my blood pressure, but was not a noticeable cognitive enhancer.
Hey Abelard, yeah I've tried zembrin + forskolin. Unfortunately, I haven't found a dose of forskolin that works well for me yet. I've tried dozens of doses and multiple brands...still working on it.
When did you take the tadalafil and what did you measure? There are some hints in the research indicating that it might be beneficial to take acetylcholine before studying, PDE5i right after studying, and PDE4i a few hours later. There is also the issue of the 'type' of memory that PDE5i might be expected to enhance, but that is a whole other can of worms....
Rodent study, choline deficit model, icv and oral
http://www.ncbi.nlm....pubmed/26027948
Neuropharmacology. 2015 Oct;97:233-9. doi: 10.1016/j.neuropharm.2015.04.019. Epub 2015 May 29.
PDE5 inhibition improves acquisition processes after learning via a central mechanism.
In previous studies, we have shown that phosphodiesterase type 5 inhibitors (PDE5-Is) can improve early consolidation of object memory. These conclusions were based on the timing of drug administration relative to the learning trial (i.e. before or after). However, there are very little pharmacological data available about the pharmacokinetic profile of orally administered PDE5-Is in the rat. Furthermore, there is still debate whether these effects are achieved via central or peripheral mechanisms and if acquisition processes are improved. In the current study, we tested the effects of the PDE5-I vardenafil in a cholinergic-deficit model and compared the effects after intracerebroventricular (ICV) versus oral (PO) administration. We found that PO vardenafil restored a scopolamine-induced memory impairment when dosed within 2 min after the learning trial while ICV vardenafil was able to restore memory when injected within 4 min after learning. Because the test trial was within 10 min after the learning trial, this suggests that these effects on object memory are related to acquisition processes that may still be ongoing in a time window after the learning trial. To further elucidate the extent of this acquisition window, we investigated the pharmacokinetic profile of vardenafil after PO administration where it was detected within 4 min post-dose. Taken together, our data suggest that PDE5 is involved in acquisition processes, which may linger for at least 4-6 min after learning. Further studies are needed to exclude that these effects could also be explained on basis of an effect on early consolidation processes. Additionally, the effectiveness of ICV-administered vardenafil provides further experimental evidence that PDE5-Is improve memory via a central mechanism.
http://www.ncbi.nlm....pubmed/17207788
Eur J Pharmacol. 2007 Mar 8;558(1-3):107-12. Epub 2006 Dec 1.
Time-dependent involvement of cAMP and cGMP in consolidation of object memory: studies using selective phosphodiesterase type 2, 4 and 5 inhibitors.
The present study investigated the time-dependent memory enhancing properties of three selective phosphodiesterase inhibitors (PDE-I) vardenafil (PDE5-I), rolipram (PDE4-I) and BAY 60-7550 (PDE2-I) in the object recognition task. In particular, the time-dependent involvement of cAMP and cGMP in memory consolidation was assessed by altering the time points of drug administration. Vardenafil (1 mg/kg, p.o.), rolipram (0.03 mg/kg, i.p.), and BAY 60-7550 (3 mg/kg, p.o.) were tested in rats with a 24 h delay between the learning and the test trial. The PDE-Is were administered at different time points, i.e. directly after, 1 h, 3 h and 6 h after the first trial. Using a 24 h interval, vardenafil only showed an effect on object memory when injected directly after trial 1, rolipram only showed an improvement when injected 3 h after trial 1 and BAY 60-7550 improved memory when injected either directly after or 3 h after trial 1. No treatment effects were found when the compounds were administered 1 h or 6 h after the first trial. Our results extend our previous data that different types of PDE-Is affect different stages of memory consolidation. Moreover, the present study provides further support that selective PDE-Is can influence memory consolidation in a time-dependent manner, assumingly by elevating central cAMP and cGMP levels.
Edited by lostfalco, 11 November 2015 - 12:59 AM.
Posted 11 November 2015 - 02:57 AM
Tons of good info in those pages, Falco
I was wondering, if one finds obtaining tadalafil not easy, is there an alternative PDE5 inhibitor, that you would use in those combos? Artichoke, Forskolin, Quercetin? How do they stack with Zembrin?
I am having no problems ordering from iHerb: the delivery is fast and the package rarely gets seized by the customs. But if i try to order from online customs, the delivery rate is really low.
BTW, what is your current regimen? Still do lasering?
Thanks, StabMe!
Your best bet for an herbal PDE5i is icariin. I did not have great results with it which is why I moved on to other PDE5i's. I think it's worth a try though.
I definitely still laser. =) My current regimen shifts a lot based on what I am experimenting with. Everything is so interrelated that it pretty much has to. Right now I'm testing BF-7 primarily.
http://www.ncbi.nlm....pubmed/24513083
Int J Neuropsychopharmacol. 2014 Jun;17(6):871-81. doi: 10.1017/S1461145713001533. Epub 2014 Feb 11.
Icariin, a phosphodiesterase-5 inhibitor, improves learning and memory in APP/PS1 transgenic mice by stimulation of NO/cGMP signalling.Phosphodiesterase-5 (PDE5) inhibitors are predominantly used in the treatment of erectile dysfunction, and have been recently shown to have a potential therapeutic effect for the treatment of Alzheimer's disease (AD) through stimulation of nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) signalling by elevating cGMP, which is a secondary messenger involved in processes of neuroplasticity. In the present study, the effects of a PDE5 inhibitor, icarrin (ICA), on learning and memory as well as the pathological features in APP/PS1 transgenic AD mice were investigated. Ten-month-old APP/PS1 transgenic mice overexpressing human amyloid precursor protein (APP695swe) and presenilin 1 (PS1-dE9) were given ICA (30 and 60 mg/kg) or sildenafil (SIL) (2 mg/kg), age-matched wild-type (WT) mice were given ICA (60 mg/kg), and APP/PS1 and WT control groups were given an isovolumic vehicle orally twice a day for four months. Results demonstrated that ICA treatments significantly improved learning and memory of APP/PS1 transgenic mice in Y-maze tasks. The amyloid precursor protein (APP), amyloid-beta (Aβ1-40/42) and PDE5 mRNA and/or protein levels were increased in the hippocampus and cortex of APP/PS1 mice, and ICA treatments decreased these physiopathological changes. Furthermore, ICA-treated mice showed an increased expression of three nitric oxide synthase (NOS) isoforms at both mRNA and protein levels, together with increased NO and cGMP levels in the hippocampus and cortex of mice. These findings demonstrate that ICA improves learning and memory functions in APP/PS1 transgenic mice possibly through the stimulation of NO/cGMP signalling and co-ordinated induction of NOS isoforms.
Posted 11 November 2015 - 03:03 AM
Hey LostFalco,
Just curious on your opinon on dave asperys pqq compared to others (as his is quite expensive) but with statements like this :
"Unfair Advantage™ is the only product on the market today that delivers the active form that bypasses your stomach acid, ActivePQQ™. Suspended in a colloid so that it’s easily absorbed and fast acting, Unfair Advantage™ will turn the lights on for your mitochondria." - Dave Aspery, now I realise that dave aspery is a marketing person ( no disrespect to him I just understand that he runs a business).Now im just curious as to this statment compared to for instance, the PQQ + Coq10 you suggested "http://www.amazon.co...uct_top?ie=UTF8".
Do you think it will still be effective?
Also, as far as the Led Lights go.. i once upon a time saw a post from you regarding cheap LED lights for the purpose low level light therapy, would this be the same thing you link to in your recommendations ?
"96 LED array: http://www.ebay.com/...=item232c0ac99b
48 LED array: http://www.ebay.com/...=item3a80a68672"
And im so sorry I know this stuff has probably been covered to death, if you would like id be more than happy to private message you instead, but i remeber you explaining how you get access to full articles instead of simply the abstract to medical studies. But im having a hard time locating them.
I Hope to not de rail the current theme of the thread by this post
Regards,
Hey Bluecheer, Dave's claims about pqq are not based on science. I've posted about this in his forums. =) http://forum.bulletp...ey/#entry129982
Those LEDs look like they should work.
I used to get free studies by going to a local university library, getting on the guest computers, accessing articles, and emailing them to myself. ha Don't tell on me. =) http://www.longecity...-10#entry597674
Posted 11 November 2015 - 03:24 AM
Thank you falco I appreicate it!
Yeah I thought so, its just when he makes claims like "The likely reason I didn’t feel any energy from large doses of PQQ over extended time is that PQQ is sold as the “stabilized” disodium salt form, because it’s more convenient for the manufacturer. Unfortunately, in humans, disodium salts precipitate when they are exposed to even small amounts of stomach acid."
And I couldnt find any evidence to how the pqq you recommended is synthesized, I got a little worried 
Yeah so, sorry but I was just curious if they were the ones in which you used? Because I remember you specifying that you knew a cheap source of them at a previous post.
And of course I wouldnt tell! Ive been dying to find out how you get all these studies! I have just been to lazy to post for so long, and as of late (and for the next few weeks) I dont think i will have time to syth through this maze of amazing studies and post to find that post.
Thoughts on prolonged use of Pregenelone>?
P.S i was curious to the source of your Modafinil, as I would like to try it again but.. took it before from a some what on relabile source and didnt feel much of anything.
Sorry for badgering, but do you think there is any real risk of prolonged use of taking daily amounts of PQQ, Coq10 & Alpha Lipoic Acid. Then ever going off them (Not that I wont to go off them, but im sure at some point in time my situation may not permit me to have access to them)
And if so how grand do you think the effects would be.
Regards,
Posted 11 November 2015 - 03:44 AM
And I couldnt find any evidence to how the pqq you recommended is synthesized, I got a little worried
Yeah so, sorry but I was just curious if they were the ones in which you used? Because I remember you specifying that you knew a cheap source of them at a previous post.
And of course I wouldnt tell! Ive been dying to find out how you get all these studies! I have just been to lazy to post for so long, and as of late (and for the next few weeks) I dont think i will have time to syth through this maze of amazing studies and post to find that post.
Thoughts on prolonged use of Pregenelone>?
P.S i was curious to the source of your Modafinil, as I would like to try it again but.. took it before from a some what on relabile source and didnt feel much of anything.
Sorry for badgering, but do you think there is any real risk of prolonged use of taking daily amounts of PQQ, Coq10 & Alpha Lipoic Acid. Then ever going off them (Not that I wont to go off them, but im sure at some point in time my situation may not permit me to have access to them)
You're very welcome, Bluecheer.
If Dave has randomized, double blind, placebo controlled evidence in humans backing his claims (about PQQ AND Unfair Advantage) then I'm all ears. Until then, I'm gonna keep my $59.95. Actually, I'd even pay attention to a rodent study or two. ha Currently, Unfair Advantage has exactly zero studies that I'm aware of.
I'm now a university student so I have unlimited access to full text studies. I'm like a kid in a candy store!
There were a handful of schizophrenic patients taking pregnenolone for 3+ years without problems in the literature. That's pretty much what I'm up to and I haven't noticed any issues at all.
Moda I got mainly through prescription. Tbh, I take moda VERY infrequently now...maybe once every month or two at most. It affects me differently now than it used to and I'm not sure exactly why at this point. It's kind of a bummer because I am fascinated by gap junction enhancement using moda but it just hasn't been working well for me in practice. Such is the nature of experimentation.
I don't see a huge risk in using PQQ, Coq10 and/or ALA fairly long term and then taking a break.
Edited by lostfalco, 11 November 2015 - 03:45 AM.
Posted 11 November 2015 - 03:59 AM
And I couldnt find any evidence to how the pqq you recommended is synthesized, I got a little worried
Yeah so, sorry but I was just curious if they were the ones in which you used? Because I remember you specifying that you knew a cheap source of them at a previous post.
And of course I wouldnt tell! Ive been dying to find out how you get all these studies! I have just been to lazy to post for so long, and as of late (and for the next few weeks) I dont think i will have time to syth through this maze of amazing studies and post to find that post.
Thoughts on prolonged use of Pregenelone>?
P.S i was curious to the source of your Modafinil, as I would like to try it again but.. took it before from a some what on relabile source and didnt feel much of anything.
Sorry for badgering, but do you think there is any real risk of prolonged use of taking daily amounts of PQQ, Coq10 & Alpha Lipoic Acid. Then ever going off them (Not that I wont to go off them, but im sure at some point in time my situation may not permit me to have access to them)
You're very welcome, Bluecheer.
If Dave has randomized, double blind, placebo controlled evidence in humans backing his claims (about PQQ AND Unfair Advantage) then I'm all ears. Until then, I'm gonna keep my $59.95. Actually, I'd even pay attention to a rodent study or two. ha Currently, Unfair Advantage has exactly zero studies that I'm aware of.
I'm now a university student so I have unlimited access to full text studies. I'm like a kid in a candy store!
There were a handful of schizophrenic patients taking pregnenolone for 3+ years without problems in the literature. That's pretty much what I'm up to and I haven't noticed any issues at all.
Moda I got mainly through prescription. Tbh, I take moda VERY infrequently now...maybe once every month or two at most. It affects me differently now than it used to and I'm not sure exactly why at this point. It's kind of a bummer because I am fascinated by gap junction enhancement using moda but it just hasn't been working well for me in practice. Such is the nature of experimentation.
I don't see a huge risk in using PQQ, Coq10 and/or ALA fairly long term and then taking a break.
Ah okay, Its probably to much money & time for studies, especially if the results arent surprisingly positive and money attracting for the product.
Ah lucky, may I enquire to what you are studying at the present moment?
Alright thanks, I thought i saw a post of yours specifying that everything you do (Experimental wise) you do it in reference to modafinil as that is your base of high cognition? ( I might be getting it a bit wrong).
Regards,
Edited by Bluecheer, 11 November 2015 - 04:00 AM.
Posted 11 November 2015 - 04:21 AM
Ah okay, Its probably to much money & time for studies, especially if the results arent surprisingly positive and money attracting for the product.
Ah lucky, may I enquire to what you are studying at the present moment?
Alright thanks, I thought i saw a post of yours specifying that everything you do (Experimental wise) you do it in reference to modafinil as that is your base of high cognition? ( I might be getting it a bit wrong).
Regards,
Yeah, studies are very expensive. The thing is, PQQ seems to be absorbed pretty well in humans. His claim that it doesn't absorb just doesn't seem in accord with the actual scientific data that we do have.
Studying information systems
Yeah, back when I wrote that about Moda it was true. For a long time it was my foundational supplement that I used to study other supplements (you're thinking of my "intelligence feedback loop"). You didn't get it wrong. =)
Edited by lostfalco, 11 November 2015 - 04:22 AM.
Posted 11 November 2015 - 04:29 AM
Yeah, studies are very expensive. The thing is, PQQ seems to be absorbed pretty well in humans. His claim that it doesn't absorb just doesn't seem in accord with the actual scientific data that we do have.
Studying information systems
Yeah, back when I wrote that about Moda it was true. For a long time it was my foundational supplement that I used to study other supplements (you're thinking of my "intelligence feedback loop"). You didn't get it wrong. =)
Ah okay must be quite interesting, (Intelligence feedback loop very nice phrase, coined your self I assume?) I am curious how much your priorities or Ideals (or whatever you want to call it) have changed sense first I scaned through your thread, I remeber a post with a message something on the lines of " The plan is to Enchance peoples minds and my own so that we can then use the advanced intelligence of our brains to tackle some of the greatest problems of humanity" Now thats paraphrasing and I may be quite off, but it was something to that effect.
I hope your goals are still as grand and positive for the rest of us as before.
Posted 11 November 2015 - 05:09 AM
Ah okay must be quite interesting, (Intelligence feedback loop very nice phrase, coined your self I assume?) I am curious how much your priorities or Ideals (or whatever you want to call it) have changed sense first I scaned through your thread, I remeber a post with a message something on the lines of " The plan is to Enchance peoples minds and my own so that we can then use the advanced intelligence of our brains to tackle some of the greatest problems of humanity" Now thats paraphrasing and I may be quite off, but it was something to that effect.
I hope your goals are still as grand and positive for the rest of us as before.
I have a bad habit of coining phrases. ha But, yeah that's mine.
Ideals are still very much the same! That's why I share instead of keeping all this to myself. =)
Edited by lostfalco, 11 November 2015 - 05:10 AM.
Posted 12 November 2015 - 09:55 PM
This is so cool. Definitely experiment until you find a fiber or fibers that work well for you. =)
http://www.ncbi.nlm....les/PMC3944646/
Clin Cancer Res. 2014 Feb 15;20(4):799-803. doi: 10.1158/1078-0432.CCR-13-2483. Epub 2013 Nov 22.
Molecular pathways: gene-environment interactions regulating dietary fiber induction of proliferation and apoptosis via butyrate for cancer prevention.
Gene-environment interactions are so numerous and biologically complicated that it can be challenging to understand their role in cancer. However, dietary fiber and colorectal cancer prevention may represent a tractable model system. Fiber is fermented by colonic bacteria into short-chain fatty acids such as butyrate. One molecular pathway that has emerged involves butyrate having differential effects depending on its concentration and the metabolic state of the cell. Low-moderate concentrations, which are present near the base of colonic crypts, are readily metabolized in the mitochondria to stimulate cell proliferation via energetics. Higher concentrations, which are present near the lumen, exceed the metabolic capacity of the colonocyte. Unmetabolized butyrate enters the nucleus and functions as a histone deacetylase (HDAC) inhibitor that epigenetically regulates gene expression to inhibit cell proliferation and induce apoptosis as the colonocytes exfoliate into the lumen. Butyrate may therefore play a role in normal homeostasis by promoting turnover of the colonic epithelium. Because cancerous colonocytes undergo the Warburg effect, their preferred energy source is glucose instead of butyrate. Consequently, even moderate concentrations of butyrate accumulate in cancerous colonocytes and function as HDAC inhibitors to inhibit cell proliferation and induce apoptosis. These findings implicate a bacterial metabolite with metaboloepigenetic properties in tumor suppression.
Edited by lostfalco, 12 November 2015 - 09:57 PM.
Posted 12 November 2015 - 10:15 PM
http://www.ncbi.nlm....les/PMC3481173/
J Neurochem. 2012 Nov;123 Suppl 2:108-15. doi: 10.1111/j.1471-4159.2012.07949.x.
Histone deacetylase inhibitors preserve function in aging axons.Aging increases the vulnerability of aging white matter to ischemic injury. Histone deacetylase (HDAC) inhibitors preserve young adult white matter structure and function during ischemia by conserving ATP and reducing excitotoxicity. In isolated optic nerve from 12-month-old mice, deprived of oxygen and glucose, we show that pan- and Class I-specific HDAC inhibitors promote functional recovery of axons. This protection correlates with preservation of axonal mitochondria. The cellular expression of HDAC 3 in the central nervous system (CNS), and HDAC 2 in optic nerve considerably changed with age, expanding to more cytoplasmic domains from nuclear compartments, suggesting that changes in glial cell protein acetylation may confer protection to aging axons. Our results indicate that manipulation of HDAC activities in glial cells may have a universal potential for stroke therapy across age groups.
http://www.ncbi.nlm....les/PMC3581211/
Diabetes. 2013 Mar;62(3):732-42. doi: 10.2337/db12-0548. Epub 2012 Oct 15.
Inhibition of class I histone deacetylases unveils a mitochondrial signature and enhances oxidative metabolism in skeletal muscle and adipose tissue.Chromatin modifications are sensitive to environmental and nutritional stimuli. Abnormalities in epigenetic regulation are associated with metabolic disorders such as obesity and diabetes that are often linked with defects in oxidative metabolism. Here, we evaluated the potential of class-specific synthetic inhibitors of histone deacetylases (HDACs), central chromatin-remodeling enzymes, to ameliorate metabolic dysfunction. Cultured myotubes and primary brown adipocytes treated with a class I-specific HDAC inhibitor showed higher expression of Pgc-1α, increased mitochondrial biogenesis, and augmented oxygen consumption. Treatment of obese diabetic mice with a class I- but not a class II-selective HDAC inhibitor enhanced oxidative metabolism in skeletal muscle and adipose tissue and promoted energy expenditure, thus reducing body weight and glucose and insulin levels. These effects can be ascribed to increased Pgc-1α action in skeletal muscle and enhanced PPARγ/PGC-1α signaling in adipose tissue. In vivo ChIP experiments indicated that inhibition of HDAC3 may account for the beneficial effect of the class I-selective HDAC inhibitor. These results suggest that class I HDAC inhibitors may provide a pharmacologic approach to treating type 2 diabetes.
Posted 12 November 2015 - 10:39 PM
One of the major themes of this thread is the massive interconnectivity between bioenergetics (mitochondria) and gene expression (DNA/epigenetics). Here's a very interesting theory about how the energy interacts with the information.
Note: I am NOT saying I necessarily agree with it...just that I find it interesting and will keep an eye on it moving forward. =)
Note 2: One of the major effects of LLLT is altering gene expression (of 111+ genes). http://www.photobiol...fo/Hamblin.html
http://www.ncbi.nlm....pubmed/26474928
Med Hypotheses. 2015 Oct 13. pii: S0306-9877(15)00375-8. doi: 10.1016/j.mehy.2015.10.004. [Epub ahead of print]
Mitochondrial emitted electromagnetic signals mediate retrograde signaling.
Recent evidence shows that mitochondria regulate nuclear transcriptional activity both in normal and cell stress conditions, known as retrograde signaling. Under normal mitochondrial function, retrograde signaling is associated with mitochondrial biogenesis, normal cell phenotype and metabolic profile. In contrast, mitochondrial dysfunction leads to abnormal (oncogenic) cell phenotype and altered bio-energetic profile (nucleus reprogramming). Despite intense research efforts, a concrete mechanism through which mitochondria determine the group of genes expressed by the nucleus is still missing. The present paper proposes a novel hypothesis regarding retrograde signaling. More specifically, it reveals the mitochondrial membrane potential (MMP) and the accompanied strong electromagnetic field (EF) as key regulatory factors of nuclear activity. Mitochondrial emitted EFs extend in long distance and affect the function of nuclear membrane receptors. Depending on their frequencies, EFs can directly activate or deactivate different groups of nuclear receptors and so determine nuclear gene expression. One of the key features of the above hypothesis is that nuclear membrane receptors, besides their own endogenous or chemical ligands (hormones, lipids, etc.), can also be activated by electromagnetic signals. Moreover, normal MMP values (about -140mV) are associated with the production of high ATP quantities and small levels of reactive oxygen species (ROS) while the hyperpolarization observed in all cancer cell types leads to a dramatic fall in ATP production and an analogous increase in ROS. The diminished ATP and increased ROS production negatively affect the function of all cellular systems including nucleus. Restoration of mitochondrial function, which is characterized by the fluctuation of MMP and EF values within a certain (normal) range, is proposed as a necessary condition for normal nuclear function and cancer therapy.
Edited by lostfalco, 13 November 2015 - 12:02 AM.
Posted 13 November 2015 - 04:21 AM
A quick little video reminding everyone how epigenetics works.
When you combine endosymbiosis with the microbiome it becomes very apparent how microbes run our lives. In fact, it could almost be said that we are made of microbes (I prefer thinking of myself as made of spacetime/fields as previously mentioned...but being made of microbes is another interesting way to think about what a human actually is).
Endosymbiosis: "eukaryotic cells originated as a symbiosis between separate single-celled organisms." https://en.wikipedia...i/Symbiogenesis
How do these three things relate? Our microbiome sends acetate, propionate, and butyrate to our cells which affect mitochondria and the nucleus (endosymbionts). It's microbes communicating with microbes...it's you.
Epigenetics
Endosymbiosis
Microbiome
Edited by lostfalco, 13 November 2015 - 05:02 AM.
Posted 13 November 2015 - 05:15 AM
A few mind-blowing quotes (for me at least =)). This beautifully ties together everything we've been talking about the past couple of years.
http://www.ncbi.nlm....pubmed/26187720
Full text pdf here: http://www.longecity...-84#entry742915
"Mitochondria regulate gene expression: At the subcellular level, mitochondria coordinate the func-tion of genes within the cell nucleus. In the same way that the brain regulates basic organ functions and behaviors, mitochondria impact fundamental cell functions and beha-viors including growth and differentiation [6,7], migration, autophagy, and death [8]. This is possible because mito-chondria are positioned, both topologically and functional-ly, in close proximity to the nucleus where they generate chromatin remodeling, epigenetic metabolites affecting gene expression (Figure 2). Signals from the totality of mitochondria within a cell can thus generate complex patterns of gene expression."
"Box 1. Mitochondria modulate neuronal synaptic function and animal behavior In neurons, neurotransmitter release by the presynaptic terminal requires mitochondrial ATP [67]. Because mitochondria contribute to synaptic vesicle release and recycling [68], the presence, absence, and movement of mitochondria in or out of the presynaptic terminal dynamically modulates neurotransmitter release [69]. Mitochondria also regulate spine morphogenesis and synaptic plasticity, and synaptic activity impacts mitochondrial positioning [70]. In the aging monkey brain dorsolateral prefrontal cortex, abnormal mitochon-drial shape (donut-shaped) within presynaptic terminals is asso-ciated with smaller active zone size, fewer docked synaptic vesicles, and impaired short-term memory [71]. The heteroplasmic mixture of two different mtDNA types in mice impairs memory retention and anxiety behavior [72]. In the honey bee, mitochondrial respiratory chain function in neurons, but not astrocytes, modulates aggressive behavior [73]. Mitochondrial dysfunctions also initiate and/or contribute to neurodegeneration [74,75]. Collectively, via their positioning, shape, and function, mitochondria are potent neuromo-dulators."
Edited by lostfalco, 13 November 2015 - 05:17 AM.
Posted 13 November 2015 - 06:38 PM
hey lostfalco, I actually posted a comment on here around a month ago or so, forgive me for nearly forgetting about it!
I had originally inquired as to what your experienced opinion was on the fact that nearly all of the literature and publications with regards to LLLT very specifically state that "nightly" treatments were given to the patients... I don't think I have read a single publication that states instructions of "2 days on, 1 day off"
I did see on thor's laser youtube channel a video which states that the benefits of laser were ameliorated after 2 weeks of daily use, but that 1 week of daily laser was more efficacious and superior to just 3 days of daily use. I don't know how to interpret this; should we not be doing 1 week on with a couple days off?
if the data shows that 1 week of daily use is superior to 3 days of daily use, then why are we all doing the 2 days on 1 day off ?
Posted 13 November 2015 - 09:36 PM
"...nearly all of the literature and publications with regards to LLLT very specifically state that "nightly" treatments were given to the patients..."
Hey crusader, thanks for your questions. Before I answer please reread the transcranial human studies and double check your facts. Dosing is far from a settled issue. =)
http://www.longecity...ts/#entry582938
Edited by lostfalco, 13 November 2015 - 09:42 PM.
Posted 14 November 2015 - 08:45 PM
Hi Falco, awesome thread. Lots of things in here to make you think.
To cut to the chase, I read on another forum that you have experience with Pinealon. I started a thread on it over here. Will you please be so kind to share a bit more detail on your experience?
Posted 14 November 2015 - 09:25 PM
Hi Falco, awesome thread. Lots of things in here to make you think.
To cut to the chase, I read on another forum that you have experience with Pinealon. I started a thread on it over here. Will you please be so kind to share a bit more detail on your experience?
Hey Nuke, no problem. Here's what I wrote about the peptide bioregulators (especially Cerluten and Pinealon) back in 2013/2014. I haven't taken them since then. Still waiting on corroborating research from multiple labs.
http://www.longecity...-56#entry633656
http://www.longecity...-56#entry633659
Posted 15 November 2015 - 02:32 AM
Some possible HDAC inhibitors to try:
1. ALCAR (donates acetyl groups) http://www.ncbi.nlm....pubmed/19755853
2. Resistant Starch (acetate, propionate, butyrate)
3. Triacetin http://www.longecity...-78#entry721627
4. Sodium Butyrate
5. Pyruvate
"Interestingly, pyruvate, butyrate, and propionate were identified as inhibitors of HDAC1 and HDAC3..."
http://www.ncbi.nlm....les/PMC3254183/
Crit Rev Biochem Mol Biol. 2011 Jun;46(3):181-99. doi: 10.3109/10409238.2011.557713. Epub 2011 Apr 5.
Metabolism as a key to histone deacetylase inhibition.
There is growing interest in the epigenetic mechanisms that are dysregulated in cancer and other human pathologies. Under this broad umbrella, modulators of histone deacetylase (HDAC) activity have gained interest as both cancer chemopreventive and therapeutic agents. Of the first generation, FDA-approved HDAC inhibitors to have progressed to clinical trials, vorinostat represents a "direct acting" compound with structural features suitable for docking into the HDAC pocket, whereas romidepsin can be considered a prodrug that undergoes reductive metabolism to generate the active intermediate (a zinc-binding thiol). It is now evident that other agents, including those in the human diet, can be converted by metabolism to intermediates that affect HDAC activity. Examples are cited of short-chain fatty acids, seleno-α-keto acids, small molecule thiols, mercapturic acid metabolites, indoles, and polyphenols. The findings are discussed in the context of putative endogenous HDAC inhibitors generated by intermediary metabolism (e.g. pyruvate), the yin-yang of HDAC inhibition versus HDAC activation, and the screening assays that might be most appropriate for discovery of novel HDAC inhibitors in the future.
http://www.ncbi.nlm....pubmed/18789002
Biochem J. 2009 Jan 1;417(1):379-89. doi: 10.1042/BJ20081132.
Colon cancer cells maintain low levels of pyruvate to avoid cell death caused by inhibition of HDAC1/HDAC3.Human colon cancer cells and primary colon cancer silence the gene coding for LDH (lactate dehydrogenase)-B and up-regulate the gene coding for LDH-A, resulting in effective conversion of pyruvate into lactate. This is associated with markedly reduced levels of pyruvate in cancer cells compared with non-malignant cells. The silencing of LDH-B in cancer cells occurs via DNA methylation, with involvement of the DNMTs (DNA methyltransferases) DNMT1 and DNMT3b. Colon cancer is also associated with the expression of pyruvate kinase M2, a splice variant with low catalytic activity. We have shown recently that pyruvate is an inhibitor of HDACs (histone deacetylases). Here we show that pyruvate is a specific inhibitor of HDAC1 and HDAC3. Lactate has no effect on any of the HDACs examined. Colon cancer cells exhibit increased HDAC activity compared with non-malignant cells. HDAC1 and HDAC3 are up-regulated in colon cancer cells and in primary colon cancer, and siRNA (small interfering RNA)-mediated silencing of HDAC1 and HDAC3 in colon cancer cells induces apoptosis. Colon cancer cells silence SLC5A8, the gene coding for a Na(+)-coupled pyruvate transporter. Heterologous expression of SLC5A8 in the human colon cancer cell line SW480 leads to inhibition of HDAC activity when cultured in the presence of pyruvate. This process is associated with an increase in intracellular levels of pyruvate, increase in the acetylation status of histone H4, and enhanced cell death. These studies show that cancer cells effectively maintain low levels of pyruvate to prevent inhibition of HDAC1/HDAC3 and thereby to evade cell death.
http://www.ncbi.nlm....pubmed/26057947
Exp Neurol. 2015 Sep;271:145-54. doi: 10.1016/j.expneurol.2015.06.008. Epub 2015 Jun 7.
Systemic pyruvate administration markedly reduces neuronal death and cognitive impairment in a rat model of Alzheimer's disease.
Alzheimer's disease (AD) is a major neurodegenerative disease of old age, characterized by progressive cognitive impairment, dementia and atrophy of the central nervous system. Amyloid-β (Aβ) oligomers are derived from proteolytic cleavage of amyloid precursor protein (APP) and recognized as the primary neurotoxic agents in AD. Pyruvate has a protective effect against Aβ oligomer-induced neuronal cell death and inhibition of long-term potentiation (LTP) in hippocampal slice cultures, leading us to investigate the effect of systemic pyruvateadministration in an intracerebroventricular Aβ oligomer infusion model. We found that sodium pyruvate (500mg/kg, intraperitoneally) improved neuron survival and sustained improvement in cognitive function as assessed by the Morris water maze. Pyuvate prevented the Aβ oligomer-induced inhibition of LTP and protein phosphatase 2A (PP2A) activation. Pyruvate suppressed the Aβ oligomer-induced poly[adenosine diphosphate (ADP) ribose] polymerase-1 (PARP-1) activity and ameliorated Aβ oligomer-induced decrease of NAD(+) level. Moreover, pyuvate, but not lactate, decreased reactive oxygen species (ROS) accumulation in hippocampus of Aβ1-42 oligomer-injection rat model. These results suggest that systemic pyruvate administration could significantly ameliorate Aβ oligomer-induced spatial learning and memory impairment by the improvement of neuron survival and prevention of LTP inhibition, and the beneficial effect of pyruvate could be linked, at least in part, to the elimination of ROS accumulation, prevention of PP2A activation, amelioration of NAD(+) level and suppression of PARP-1 activity.
http://www.ncbi.nlm....pubmed/15855333
Diabetes. 2005 May;54(5):1452-8.
Pyruvate administered after severe hypoglycemia reduces neuronal death and cognitive impairment.Hypoglycemia-induced brain injury is a significant obstacle to optimal blood glucose control in diabetic patients. Severe hypoglycemia triggers a cascade of events in vulnerable neurons that may culminate in cell death even after glucose normalization. A key event in this cascade is the activation of poly(ADP-ribose) polymerase-1 (PARP-1). Activated PARP-1 consumes cytosolic NAD, and because NAD is required for glycolysis, hypoglycemia-induced PARP-1 activation may render cells unable to use glucose even when glucose availability is restored. Pyruvate, however, can be metabolized in the absence of cytosolic NAD. Here we tested whether pyruvate could improve the outcome in rats subjected to insulin-induced hypoglycemia by terminating hypoglycemia with either glucose alone or glucose plus pyruvate. In the four brain regions studied--CA1, subiculum, dentate gyrus of the hippocampus, and piriform cortex--the addition of pyruvate reduced neuron death by 70-90%. Improved neuron survival was also observed when pyruvate delivery was delayed for up to 3 h. The improved neuron survival was accompanied by a sustained improvement in cognitive function as assessed by the Morris water maze. These results suggest that pyruvate may significantly improve the outcome after severe hypoglycemia by circumventing a sustained impairment in neuronal glucose utilization resulting from PARP-1 activation.
"The blood-brain barrier normally transports pyruvate at a rate much slower than glucose, but prior work suggests that significant pyruvate entry to the brain can be achieved by elevating plasma pyruvate concentrations..."
http://www.ncbi.nlm....pubmed/11588201
J Neurosci. 2001 Oct 15;21(20):RC171.
Protection by pyruvate against transient forebrain ischemia in rats.
Pyruvate has a remarkable protective effect against zinc neurotoxicity. Because zinc neurotoxicity is likely one of the key mechanisms of ischemic brain injury, the neuroprotective effect of pyruvate was tested in a rat model of transient forebrain ischemia. Control experiments in mouse cortical culture showed that pyruvate almost completely blocked zinc toxicity but did not attenuate calcium-overload neuronal death. Adult rats subjected to 12 min forebrain ischemia exhibited widespread zinc accumulation and neuronal death throughout hippocampus and cortex 72 hr after reperfusion. However, rats injected intraperitoneally with sodium pyruvate (500-1000 mg/kg) within 1 hr after 12 min forebrain ischemia showed almost no neuronal death. In addition, the mortality was markedly decreased in the pyruvate-protected groups (3.8%) compared with the NaCl-injected control group (58.1%). The neuroprotective effect persisted even at 30 d after the insult. The spectacular protection without noticeable side effects makes pyruvate a promising neuroprotectant in human ischemic stroke.
http://www.ncbi.nlm....les/PMC3160172/
J Neurosci. 2011 Jan 12;31(2):764-74. doi: 10.1523/JNEUROSCI.5052-10.2011.
HDAC3 is a critical negative regulator of long-term memory formation.
Gene expression is dynamically regulated by chromatin modifications on histone tails, such as acetylation. In general, histone acetylation promotes transcription, whereas histone deacetylation negatively regulates transcription. The interplay between histone acetyltranserases and histone deacetylases (HDACs) is pivotal for the regulation of gene expression required for long-term memory processes. Currently, very little is known about the role of individual HDACs in learning and memory. We examined the role of HDAC3 in long-term memory using a combined genetic and pharmacologic approach. We used HDAC3-FLOX genetically modified mice in combination with adeno-associated virus-expressing Cre recombinase to generate focal homozygous deletions of Hdac3 in area CA1 of the dorsal hippocampus. To complement this approach, we also used a selective inhibitor of HDAC3, RGFP136 [N-(6-(2-amino-4-fluorophenylamino)-6-oxohexyl)-4-methylbenzamide]. Immunohistochemistry showed that focal deletion or intrahippocampal delivery of RGFP136 resulted in increased histone acetylation. Both the focal deletion of HDAC3 as well as HDAC3 inhibition via RGFP136 significantly enhanced long-term memory in a persistent manner. Next we examined expression of genes implicated in long-term memory from dorsal hippocampal punches using quantitative reverse transcription-PCR. Expression of nuclear receptor subfamily 4 group A, member 2 (Nr4a2) and c-fos was significantly increased in the hippocampus of HDAC3-FLOX mice compared with wild-type controls. Memory enhancements observed in HDAC3-FLOX mice were abolished by intrahippocampal delivery of Nr4a2 small interfering RNA, suggesting a mechanism by which HDAC3 negatively regulates memory formation. Together, these findings demonstrate a critical role for HDAC3 in the molecular mechanisms underlying long-term memory formation.
Edited by lostfalco, 15 November 2015 - 03:03 AM.
Posted 16 November 2015 - 11:58 PM
Excellent thread and thanks for providing all this fantastic information!!! (finally read through most of it)
I was wondering if the diameter of the LED made any difference in the effectiveness of the laser as I haven't been able to find this info.
I have recently purchased: http://www.ebay.com....=STRK:MEBIDX:IT
The 96 LED array is 850nm but the led diameter is 10mm wheres the laser recommendations from lostfalco and a few other members all feature LED's with 5mm diameters.
Does this make a difference in the effectiveness/strength? Should I get one with 5mm diameter LED's?
Thanks for your response.
Posted 17 November 2015 - 01:17 AM
Excellent thread and thanks for providing all this fantastic information!!! (finally read through most of it)
I was wondering if the diameter of the LED made any difference in the effectiveness of the laser as I haven't been able to find this info.
Thanks, colourdeaf! You're a brave person for reading through this labyrinth. I'm glad you've found something useful.
The LED diameter should not make a huge difference. The device that you linked looks like it should work.
Posted 18 November 2015 - 04:32 AM
Hello my friends! End of the semester is coming quickly so I'm gonna take a little Longecity break and focus completely on school for a few weeks. Just wanted to let you know that BF-7 didn't make my brain explode or anything. =)
Talk to you guys soon!
-LF
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