4019 replies to this topic

[BieraK]

 

 

Excellent study thats a good news.

It is recent, hopefully soon we begin to see more studies about LLLT+CoQ10+PQQ or LLLT+C60

Also, without intending to advertise a product or make any kind of commercial profit, I will leave this here for those interested.

The ebay seller who had the low cost 100 pills of PQQ+CoQ10 combo has a site where he sells his products, I asked him by ebay for the product. I've bought mine there through Paypal

I mentions this because it seems he is no longer selling that product on ebay.
The site has other great products at an excellent cost.

 

The site: http://herbern.webs.com

 

You have 6 posts and post to a .webs store, I would not trust that at all. They claim to be a company, but use outlook as their email, don't even have their own website (.webs is free) and I don't see any CoAs.

 

 

Yes, you're right, I was also suspicious about the site. The same person on ebay sent me their website when I asked him about the PQQ+CoQ10 caps, after some thought I decided to take the risk, if I receive the product successfully that would be a good sign, I will upload a photo and write a comment if I feel an effect.

I think that a moderator may edit my post and just leave a statement like this: "contact the seller on ebay asking for his website at your own risk" and delete the link.... thats would be better for the safety of the members. (or delete the entire message)

On the other hand it seems appropriate that your distrust of the website. But your distrust me because of the number of my posts seems a bit exaggerated.

[resveratrol_guy]

Hello guys,

It's been a while since I wrote here. I'm still performing my LLLT regime and I've seen a solid results in long term memory, concentration, cognition and meta-cognition. 

 

I follow this topic for a year now- and I truly think it has started as one of the most innovative and profound brain-hacking discussion on this website. We need to push the theoretical discussion forward. The discussion about mitochondrial enhancers and signaling pathways was very interesting, but it's only one brick in the big question of how to hack your neuronal circuitry. And maybe It's only my take, but I think it's quite reasonable to presume that since the brain cells (and most of the other types of cells ) are working on ATP ( which is in the end of the day glucose ) - the question we really need to ask is how to increase the glucose (and oxygen) consumption of our brain cells.

 

I just came across a very interesting, and quite recent article about brain glucose consumption ( ref :  Bélanger, Mireille, Igor Allaman, and Pierre J. Magistretti. "Brain energy metabolism: focus on astrocyte-neuron metabolic cooperation." Cell metabolism14.6 (2011): 724-738. ). This article is doing a very good job in explaining the 'big-picture' regarding brain glucose consumption. One of the factors is, indeed, the mitochondrial. However, There are many esoteric factors we don't talk about- that might be a very interesting leads for further reading..

 

For these that don't have institutional access to the article, I attach here the most interesting piece 

 

This is way too interesting to ignore. Unfortunately, it seems like LLLT is sprayed all over Longecity. Would you care to elaborate on your results (got any test scores?) on what seems to be "the" LLLT thread over here?

[lostfalco]

Hey, what's up guys? Sorry I haven't been able to respond as much lately. School is pretty crazy right now. I should have a little more time to post in a week or two. 

 

In the meantime, I've been looking more into this (possible) connection that we talked about previously: molecular hydrogen increases ghrelin increases growth hormone. Very interesting.

 

http://www.ncbi.nlm....les/PMC4190751/

 

J Clin Diagn Res. 2014 Aug;8(8):MC13-7. doi: 10.7860/JCDR/2014/9863.4767. Epub 2014 Aug 20.

Ghrelin: ghrelin as a regulatory Peptide in growth hormone secretion.

Khatib N1, Gaidhane S2, Gaidhane AM3, Khatib M4, Simkhada P5, Gode D6, Zahiruddin QS7.

Author information 

 

Abstract

BACKGROUND: 

Ghrelin is a type of growth hormone (GH) secretagogue that stimulates the release of GH. It is a first hormone linking gastrointestinal-pituitary axis.

OBJECTIVE: 

This review highlights the interaction of ghrelin with GHRH and somatostatin to regulate the secretion of GH and intends to explore the possible physiological role of the ghrelin-pituitary-GH axis linkage system.

OBSERVATION: 

Ghrelin is highly conserved among species and is classified into octanoylated (C8:0), decanoylated (C10:0), decenoylated (C10:1) and nonacylated,ghrelin. Acylated ghrelin is the major active form of human ghrelin. The primary production site of ghrelin is the stomach, and it interacts with stomach ghrelin as well as hypothalamic GHRH and somatostatin in the regulation of pituitary GH secretion. Ghrelin stimulate GH release through the GHS receptor to increase intracellular Ca2+ ([Ca2+] levels via IP3 signal transduction pathway. Ghrelin is a specific endogenous ligand for the GHS receptor and provides a definitive proof of the occurance of a GHS-GHS receptor signalling system in the regulation of GH secretion.

CONCLUSION: 

Studies suggests that ghrelin is a powerful pharmacological agent that exerts a potent, time-dependent stimulation of pulsatile secretion of GH.

 

 

Another interesting study on ghrelin and memory.

 

http://www.ncbi.nlm....pubmed/25466701

 

Psychopharmacology (Berl). 2014 Dec 4. [Epub ahead of print]

Ghrelin increases memory consolidation through hippocampal mechanisms dependent on glutamate release and NR2B-subunits of the NMDA receptor.

Ghersi MS1, Gabach LA, Buteler F, Vilcaes AA, Schiöth HB, Perez MF, de Barioglio SR.

Author information 

 

Abstract

RATIONALE: 

Ghrelin (Ghr) is a peptide that participates in the modulation of several biological processes. Ghr administration into the hippocampus improves learning and memory in different memory tests. However, the possible mechanisms underlying this effect on memory have not yet been clarified.

OBJECTIVE: 

The purpose of the present work is to add new insights about the mechanisms by which Ghr modulates long-term memory consolidation in the hippocampus. We examined Ghr effects upon processes related to increased synaptic efficacy as presynaptic glutamate release and changes in the expression of the NR2B-subunits containing n-methyl-d-aspartate receptors (NMDAR), which are critical for LTP induction. We also attempted to determine the temporal window in which Ghr administration induces memory facilitation and if the described effects depend on GHS-R1a stimulation.

RESULTS: 

The present research demonstrated that Ghr increased glutamate release from hippocampal synaptosomes; intra-hippocampal Ghr administration increased NR2B-subunits expression in CA1 and DG subareas and also reversed the deleterious effects of the NR2B-subunit-specific antagonist, Ro 25-6981, upon memory consolidation and LTP generation in the hippocampus. These effects are likely to be the consequence of GHS-R1a activation.

CONCLUSION: 

According to the results above mentioned and previous findings, we can hypothesize some of the mechanisms by which Ghr modulates memory consolidation. At presynaptic level, Ghr stimulates glutamate release, probably by enhancing [Ca2+]i. At postsynaptic level, the glutamate released activates NMDAR while Ghr also mediates effects directly activating its specific receptors and increases NR2B-subunit expression.

 

Edited by lostfalco, 05 December 2014 - 05:24 AM.

[lostfalco]

Another very good review article on ghrelin and the brain.

 

http://www.sciencedi...969996114002575

 

Neurobiol Dis. 2014 Dec;72PA:72-83. doi: 10.1016/j.nbd.2014.08.026. Epub 2014 Aug 27.

Ghrelin: A link between ageing, metabolism and neurodegenerative disorders.

Stoyanova II.

Author information 

 

Abstract

Along with the increase in life expectancy over the last century comes the increased risk for development of age-related disorders, including metabolic and neurodegenerative diseases such as Alzheimer's, Parkinson's and Huntington's diseases. These chronic disorders share two main characteristics: 1) neuronal loss in motor, sensory or cognitive systems, leading to cognitive and motor decline; and 2) a strong correlation between metabolic changes and neurodegeneration. In order to treat them, a better understanding of their complexity is required: it is necessary to interpret the neuronal damage in light of the metabolic changes, and to find the disrupted link between the peripheral organs governing energy metabolism and the CNS. This review is an attempt to present ghrelin as part of molecular regulatory interface between energy metabolism, neuroendocrine and neurodegenerative processes. Ghrelin takes part in lipid and glucose metabolism, in higher brain functions such as sleep-wake state, learning and memory consolidation; it influences mitochondrial respiration and shows neuroprotective effect. All these make ghrelin an attractive target for development of biomarkers or therapeutics for prevention or treatment of disorders, in which cell protection and recruitment of new neurons or synapses are needed.

 

Edited by lostfalco, 05 December 2014 - 05:42 AM.

[Mustafa]

For me, If Hydrogen increases GH then that's pretty bad... GH is a stress hormone and it upregulates IGF-1. IGF-1 incentives cancer through obvious pathways (Angiogenesis mostly).There is also some hints that IGF-1 effect longevity through upregulating Daf-2, inhibiting FOXO. 

 

Off topic: I try to keep IGF-1, insulin and methionine to bare minmum. Hardest one to maintain low is methionine and arguably the most important one as I recall couple of studies have shown that by just reducing methionine, the subjects where able to gain the benefit of calorie restrictions without practicing calorie restrictions.

[hullcrush]

I've tried a little bit of LED therapy and I've realized I might be going way too high. 

I did about 20 minutes each on F3 and F4 positions three times, and I did not get sleepy. I did have immersive nightmares with almost enhanced audio and some peripheral weakness after. 

 

I'm using a 7 cm diameter 48 LED array applied to the forehead with a 12V power supply at 500mA, how many joules/cm2 is that delivering at 20 minutes? That seems high. I undoubtedly massacred my PFC. 

[BieraK]

I've tried a little bit of LED therapy and I've realized I might be going way too high. 

I did about 20 minutes each on F3 and F4 positions three times, and I did not get sleepy. I did have immersive nightmares with almost enhanced audio and some peripheral weakness after. 

 

I'm using a 7 cm diameter 48 LED array applied to the forehead with a 12V power supply at 500mA, how many joules/cm2 is that delivering at 20 minutes? That seems high. I undoubtedly massacred my PFC. 

I think that your a overdoing, 20 minutes its too much.

------------------------------------------------------------------------

I don't know if anyone has posted this before but googling HGF + laser in Longecity not appeared any results (HGF+Laser site:www.longecity.org).

Dihexa post caught my attention, I thought that might have some similarities with LLLT in relation to HGF, the MOA of Dihexa, and wound healing....  that idea was a result of this post: http://www.longecity...ndpost&p=659623


I looked over that and apparently LLLT enhances HGF, the dihexa mechanism!

"Miura et al. (1999) observed that following irradiation of the backs of Sprague-Dawley rats with linear polarized infrared laser, there was an upregulation of hepatocyte growth factor (HGF) and HGF activator expression."
https://books.google...llt hgf&f=false

unfortunately I do not have access to the study nor the book, if someone could get the Miura 1999 study would be very helpful.

Edited by Arsonista, 20 December 2014 - 04:55 AM.

[resveratrol_guy]

Hey lostfalco, I would just like to know how you would characterize your experience with LLLT since starting this thread. In particular, when do you feel that you peaked out, mentally? Or did you simply peak early, then plateau? (Obivously there are daily variances depending on sleep, diet, etc., so I'm talking more on a month-to-month level.) Did you start or stop any other regimens which might have significantly contributed to the results, apart from those discussed in your "current recommendations"?

 

Based on the original UT Austin studies, it would appear that LLLT is very dose-sensitive in its effects. While I'm assuming (hopefully correctly) that the therapy can be applied indefinitely many times, the time between applications and spatiotemporal profile of any given application can exert a huge effect on the benefits or lack thereof. Based on the fact that your recommendations haven't changed in several months, I'm assuming that the effects have been stable for you, but maybe I'm wrong.

 

Obviously quantitative data would be superior, but even just qualitative feedback like "I feel more literate" would be informative.

 

This isn't just idle curiousity on my part: my friend and I plan to use it as a followup to stem cell therapy for mental improvement.

Edited by resveratrol_guy, 04 January 2015 - 05:42 PM.

[AnygirlX]

I'm looking at purchasing 850nm LED lights (I don't know how to phrase this, but hopefully someone can interpret) but I don't know how powerful they need to be. Am I looking for a certain mW? If so what mW is it that I'm looking for? 

 

Thanks! 

[kentolpad]

I'm by no means an expert but i don't think you gotta watch out for the mw range. My led lights are not very powerful it's the number which makes them useful though. 

[lostfalco]

New selective HDAC2 Inhibitors showing promise! This is really exciting stuff. 

 

http://www.ncbi.nlm....pubmed/25642316

 

Chem Sci. 2015 Jan 1;6(1):804-815.

Kinetically Selective Inhibitors of Histone Deacetylase 2 (HDAC2) as Cognition Enhancers.

Wagner FF1, Zhang YL1, Fass DM2, Joseph N3, Gale JP1, Weïwer M1, McCarren P1, Fisher SL4, Kaya T1, Zhao WN5, Reis SA5, Hennig KM5, Thomas M1, Lemercier BC1, Lewis MC1, Guan JS3, Moyer MP1, Scolnick E1, Haggarty SJ5, Tsai LH3, Holson EB1.

Author information

 

Abstract

Aiming towards the development of novel nootropic therapeutics to address the cognitive impairment common to a range of brain disorders, we set out to develop highly selective small molecule inhibitors of HDAC2, a chromatin modifying histone deacetylase implicated in memory formation and synaptic plasticity. Novel ortho-aminoanilide inhibitors were designed and evaluated for their ability to selectively inhibit HDAC2 versus the other Class I HDACs. Kinetic and thermodynamic binding properties were essential elements of our design strategy and two novel classes of ortho-aminoanilides, that exhibit kinetic selectivity (biased residence time) for HDAC2 versus the highly homologous isoform HDAC1, were identified. These kinetically selective HDAC2 inhibitors (BRD6688 and BRD4884) increased H4K12 and H3K9 histone acetylation in primary mouse neuronal cell culture assays, in the hippocampus of CK-p25 mice, a model of neurodegenerative disease, and rescued the associated memory deficits of these mice in a cognition behavioural model. These studies demonstrate for the first time that selective pharmacological inhibition of HDAC2 is feasible and that inhibition of the catalytic activity of this enzyme may serve as a therapeutic approach towards enhancing the learning and memory processes that are affected in many neurological and psychiatric disorders.

 

Edited by lostfalco, 12 February 2015 - 04:22 AM.

[lostfalco]

A couple of quick refreshers on the beauty of HDAC2 inhibition. =)

 

http://www.ncbi.nlm....pubmed/23575838

 

J Neurosci. 2013 Apr 10;33(15):6401-11. doi: 10.1523/JNEUROSCI.1001-12.2013.

Loss of histone deacetylase 2 improves working memory and accelerates extinction learning.

Morris MJ1, Mahgoub M, Na ES, Pranav H, Monteggia LM.

Author information

 

Abstract

Histone acetylation and deacetylation can be dynamically regulated in response to environmental stimuli and play important roles in learning and memory. Pharmacological inhibition of histone deacetylases (HDACs) improves performance in learning tasks; however, many of these classical agents are "pan-HDAC" inhibitors, and their use makes it difficult to determine the roles of specific HDACs in cognitive function. We took a genetic approach using mice lacking the class I HDACs, HDAC1 or HDAC2, in postmitotic forebrain neurons to investigate the specificity or functional redundancy of these HDACs in learning and synaptic plasticity. We show that selective knock-out of Hdac2 led to a robust acceleration of the extinction rate of conditioned fear responses and a conditioned taste aversion as well as enhanced performance in an attentional set-shifting task. Hdac2 knock-out had no impact on episodic memory or motor learning, suggesting that the effects are task-dependent, with the predominant impact of HDAC2 inhibition being an enhancement in an animal's ability to rapidly adapt its behavioral strategy as a result of changes in associative contingencies. Our results demonstrate that the loss of HDAC2 improves associative learning, with no effect in nonassociative learning tasks, suggesting a specific role for HDAC2 in particular types of learning. HDAC2 may be an intriguing target for cognitive and psychiatric disorders that are characterized by an inability to inhibit behavioral responsiveness to maladaptive or no longer relevant associations.

 

 

http://www.ncbi.nlm....pubmed/19424149

 

Nature. 2009 May 7;459(7243):55-60. doi: 10.1038/nature07925.

HDAC2 negatively regulates memory formation and synaptic plasticity.

Guan JS1, Haggarty SJ, Giacometti E, Dannenberg JH, Joseph N, Gao J, Nieland TJ, Zhou Y, Wang X, Mazitschek R, Bradner JE, DePinho RA, Jaenisch R, Tsai LH.

Author information

 

Abstract

Chromatin modifications, especially histone-tail acetylation, have been implicated in memory formation. Increased histone-tail acetylation induced by inhibitors of histone deacetylases (HDACis) facilitates learning and memory in wild-type mice as well as in mouse models of neurodegeneration. Harnessing the therapeutic potential of HDACis requires knowledge of the specific HDAC family member(s) linked to cognitive enhancement. Here we show that neuron-specific overexpression of HDAC2, but not that of HDAC1, decreased dendritic spine density, synapse number, synaptic plasticity and memory formation. Conversely, Hdac2 deficiency resulted in increased synapse number and memory facilitation, similar to chronic treatment with HDACis in mice. Notably, reduced synapse number and learning impairment of HDAC2-overexpressing mice were ameliorated by chronic treatment with HDACis. Correspondingly, treatment with HDACis failed to further facilitate memory formation in Hdac2-deficient mice. Furthermore, analysis of promoter occupancy revealed an association of HDAC2 with the promoters of genes implicated in synaptic plasticity and memory formation. Taken together, our results suggest that HDAC2 functions in modulating synaptic plasticity and long-lasting changes of neural circuits, which in turn negatively regulates learning and memory. These observations encourage the development and testing of HDAC2-selective inhibitors for human diseases associated with memory impairment.

 

Edited by lostfalco, 12 February 2015 - 04:25 AM.

[kassem23]

I am not sure whether this has been posted yet, but this presentation included a study N=20 of healthy individuals and the effects of 1064 laser treatment. 

 

See here: http://dose-response...z-Lima_2014.pdf

[lostfalco]

Another promising epigenetic mechanism to keep an eye on...HAT Activators (I know we've talked about this a little before). 

 

http://www.jneurosci...3/26/10698.long

J Neurosci. 2013 Jun 26;33(26):10698-712. doi: 10.1523/JNEUROSCI.5772-12.2013.

A novel activator of CBP/p300 acetyltransferases promotes neurogenesis and extends memory duration in adult mice.

Chatterjee S1, Mizar P, Cassel R, Neidl R, Selvi BR, Mohankrishna DV, Vedamurthy BM, Schneider A, Bousiges O, Mathis C, Cassel JC, Eswaramoorthy M, Kundu TK, Boutillier AL.

Author information

Abstract

Although the brain functions of specific acetyltransferases such as the CREB-binding protein (CBP) and p300 have been well documented using mutant transgenic mice models, studies based on their direct pharmacological activation are still missing due to the lack of cell-permeable activators. Here we present a small-molecule (TTK21) activator of the histone acetyltransferases CBP/p300, which, when conjugated to glucose-based carbon nanosphere (CSP), passed the blood-brain barrier, induced no toxicity, and reached different parts of the brain. After intraperitoneal administration in mice, CSP-TTK21 significantly acetylated histones in the hippocampus and frontal cortex. Remarkably, CSP-TTK21 treatment promoted the formation of long and highly branched doublecortin-positive neurons in the subgranular zone of the dentate gyrus and reduced BrdU incorporation, suggesting that CBP/p300 activation favors maturation and differentiation of adult neuronal progenitors. In addition, mRNA levels of the neuroD1 differentiation marker and BDNF, a neurotrophin required for the terminal differentiation of newly generated neurons, were both increased in the hippocampus concomitantly with an enrichment of acetylated-histone on their proximal promoter. Finally, we found that CBP/p300 activation during a spatial training, while not improving retention of a recent memory, resulted in a significant extension of memory duration. This report is the first evidence for CBP/p300-mediated histone acetylation in the brain by an activator molecule, which has beneficial implications for the brain functions of adult neurogenesis and long-term memory. We propose that direct stimulation of acetyltransferase function could be useful in terms of therapeutic options for brain diseases.

 

http://www.ncbi.nlm....pubmed/20833281

Biochim Biophys Acta. 2010 Oct-Dec;1799(10-12):840-53. doi: 10.1016/j.bbagrm.2010.08.012. Epub 2010 Sep 15.

Tuning acetylation levels with HAT activators: therapeutic strategy in neurodegenerative diseases.

Selvi BR1, Cassel JC, Kundu TK, Boutillier AL.

Author information

Abstract

Neurodegenerative diseases, such as polyglutamine-related diseases, amyotrophic lateral sclerosis, and Alzheimer's disease are accompanied by transcriptional dysfunctions, leading to neuronal death. It is becoming more evident that the chromatin acetylation status is impaired during the lifetime of neurons, by a common mechanism related to the loss of function of histone acetyltransferase (HAT) activity. Notably, the HAT termed cAMP response element binding protein (CREB)-binding protein (CBP) was shown to display neuroprotective functions. Several other HATs have now been shown to participate in basic but vital neuronal functions. In addition, there is increasing evidence of several HATs (including CBP), as essential regulators of neuronal plasticity and memory formation processes. In order to counteract neuronal loss and/or memory deficits in neurodegenerative diseases, the current therapeutic strategies involve the use of small molecules antagonizing histone deacetylase (HDAC) activity (i.e. HDAC inhibitors). Although this strategy lacks specificity, some of these molecules display promising therapeutic properties. With the rapidly evolving literature on HATs and their respective functions in neuronal survival and memory formation, it seems essential to envisage direct stimulation of the acetyltransferase function as a new therapeutic tool in neurodegenerative diseases. In this review, we will highlight the present understanding and the future prospects of such therapeutic approach.

 

 

 

Edited by lostfalco, 27 February 2015 - 01:41 PM.

[boroda]

I am not sure whether this has been posted yet, but this presentation included a study N=20 of healthy individuals and the effects of 1064 laser treatment. 

 

See here: http://dose-response...z-Lima_2014.pdf

 

Unbelievable! Thank you

[kassem23]

Can someone please explain how J/cm^2 is calculated off of the following information. 

 

 

 

• Input power source: 12VDC ,0.5A

• Wavelength: 850nm

• Angle: 45°

• Diameter: 1.89inch

• Current: 370mA

• LED: 48, diameter 5mm

 

If I use conversion tools, I get 200J/cm^2, but that seems like a massive dose. Someone please advise?

 

It would be nice to know so I can calculate the appropriate dose and time of administration. 

 

Thank in advance!

[kassem23]

New calculations - 3.24W and 18mW/cm^2. So now that I know that irradiance (“intensity”) = 180mW/cm^2, then let’s say exposure time is 60 seconds, so that gives us - 180mW/cm^2 * 60s divided with 1000mW/W = 10,8 W*s = 10.8J/cm^2 is that correct?

 

[lostfalco]

Can someone please explain how J/cm^2 is calculated off of the following information. 

 

 

 

• Input power source: 12VDC ,0.5A

• Wavelength: 850nm

• Angle: 45°

• Diameter: 1.89inch

• Current: 370mA

• LED: 48, diameter 5mm

 

If I use conversion tools, I get 200J/cm^2, but that seems like a massive dose. Someone please advise?

 

It would be nice to know so I can calculate the appropriate dose and time of administration. 

 

Thank in advance!

Hey Kassem, which device do you have?

[lostfalco]

Holy crap!

 

http://www.medicalne...s/290127.php?tw

 

"It may sound like something from a horror movie, but at the American Academy of Neurological and Orthopedic Surgeons' 39th Annual Conference in Annapolis, MD, in June, an Italian surgeon will announce updated plans to conduct the first ever human head transplant, claiming the procedure could happen within the next 2 years."

 

I call dibs on this guy's body.  https://s-media-cach...9f0dd1a1ca8.jpg

Edited by lostfalco, 01 March 2015 - 03:06 AM.

[BieraK]

I am not sure whether this has been posted yet, but this presentation included a study N=20 of healthy individuals and the effects of 1064 laser treatment. 

 

See here: http://dose-response...z-Lima_2014.pdf

Of all the LLLT studies that I've seen, gonzalez-lima is one of the few that takes into account the hotmetic effects of LLLT... I've seen too much studies that starts with high doses of 20 min for example, and others studies with protocols of everday applications.

In this study they used 5 minutes of irradiation per spot, apparently is a good dose per week.

In my case I don't know what is the problem, the first doses of LLLT where great and effective, but after that I haven't felt the same effects, If I not take c60 I not feel the sleepy and oxygenated effect of LLLT in my brain.
I have a pain in the lower of my back, LLLT worked great the first times that I've used it in that location, goodbye to the pain, but for now LLLT is doing nothing for that I just only feel the vassodilatory effect but not the compensation that comes after the the stress response, the same for other parts of my body, like my legs, I feel the vasodilatory effects but not the after effects, I even feel the legs tired and uconfortable. I've never passed of the two mins for my head, and never passed of the 100 seconds in my body.

On the other hand this works great for gain muscle. 

Edited by BieraK, 01 March 2015 - 03:08 AM.

[kassem23]

 

Can someone please explain how J/cm^2 is calculated off of the following information. 

 

 

 

• Input power source: 12VDC ,0.5A

• Wavelength: 850nm

• Angle: 45°

• Diameter: 1.89inch

• Current: 370mA

• LED: 48, diameter 5mm

 

If I use conversion tools, I get 200J/cm^2, but that seems like a massive dose. Someone please advise?

 

It would be nice to know so I can calculate the appropriate dose and time of administration. 

 

Thank in advance!

Hey Kassem, which device do you have?

 

 

It should all be in the information there -- but it's this one, if you're curious what it looks like: http://www.ebay.de/i...E:X:AAQ:DE:1123

 

Also - quick question: Why do you administer the laser at night - would you not notice the effects more if you dosed in the morning, or does it still induce fatigue in you after many administrations? Do you recommend only doing it at night before sleep, hoping that the hormetic effects take place during the night and then waking up refreshed? Or how would you say it works in that regard?

 

Best wishes, and thanks in advance!

Edited by kassem23, 01 March 2015 - 12:34 PM.

[Overman]

Selling my vetrolaser:

http://m.ebay.com/it...9929?nav=SEARCH

[lostfalco]

http://www.ncbi.nlm....pubmed/25660059

 

Mech Ageing Dev. 2015 Feb 7;145C:39-50. doi: 10.1016/j.mad.2015.01.003. [Epub ahead of print]

Acetyl-l-carnitine increases mitochondrial protein acetylation in the aged rat heart.

Kerner J1, Yohannes E2, Lee K1, Virmani A3, Koverech A3, Cavazza C3, Chance MR2, Hoppel C4.

Author information

Abstract

Previously we showed that in vivo treatment of elderly Fisher 344 rats with acetylcarnitine abolished the age-associated defect in respiratory chain complex III in interfibrillar mitochondria and improved the functional recovery of the ischemic/reperfused heart. Herein, we explored mitochondrial protein acetylation as a possible mechanism for acetylcarnitine's effect. In vivo treatment of elderly rats with acetylcarnitine restored cardiac acetylcarnitine content and increased mitochondrial protein lysine acetylation and increased the number of lysine-acetylated proteins in cardiac subsarcolemmal and interfibrillar mitochondria. Enzymes of the tricarboxylic acid cycle, mitochondrial β-oxidation, and ATP synthase of the respiratory chain showed the greatest acetylation. Acetylation of isocitrate dehydrogenase, long-chain acyl-CoA dehydrogenase, complex V, and aspartate aminotransferase was accompanied by decreased catalytic activity. Several proteins were found to be acetylated only after treatment with acetylcarnitine, suggesting that exogenous acetylcarnitine served as the acetyl-donor. Two-dimensional fluorescence difference gel electrophoresis analysis revealed that acetylcarnitine treatment also induced changes in mitochondrial protein amount; a two-fold or greater increase/decrease in abundance was observed for thirty one proteins. Collectively, our data provide evidence for the first time that in the aged rat heart in vivo administration of acetylcarnitine provides acetyl groups for protein acetylation and affects the amount of mitochondrial proteins.

 

Edited by lostfalco, 03 March 2015 - 07:31 PM.

[lostfalco]

 

 

If I use conversion tools, I get 200J/cm^2, but that seems like a massive dose. Someone please advise?

 

It would be nice to know so I can calculate the appropriate dose and time of administration. 

 

Thank in advance!

 

It should all be in the information there -- but it's this one, if you're curious what it looks like: http://www.ebay.de/i...E:X:AAQ:DE:1123

 

Also - quick question: Why do you administer the laser at night - would you not notice the effects more if you dosed in the morning, or does it still induce fatigue in you after many administrations? Do you recommend only doing it at night before sleep, hoping that the hormetic effects take place during the night and then waking up refreshed? Or how would you say it works in that regard?

 

Best wishes, and thanks in advance!

 

Here's an article that will help you calculate dose. http://www.ncbi.nlm....les/PMC3288797/

 

Zawy has also done considerable work describing the elements involved in dose calculation. 

http://heelspurs.com/led.html#str

http://heelspurs.com/led.html#deep

http://heelspurs.com/led.html#skull

 

I hope those links help!

 

Administration at night or morning are both fine. Try both and see what works best for you. 

Edited by lostfalco, 03 March 2015 - 03:22 PM.

[rikelme]

Acetyl-l-carnitine increases mitochondrial protein acetylation in the aged rat heart.

 

 

Increased mitochondrial protein acetylation - a good, or a bad thing?

[neurokwarg]

I have finally worked my way through this gigantic thread; Lostfalco & co, you guys are awesome! This month i will be starting my own TULIP experience. However, i am still struggling on what device to get. 

 

http://www.amazon.co...AANG/ref=sr_1_1Light Relief device as recommended by Joe Cohen of Self Hacked

http://www.amazon.co...U/ref=sr_1_cc_2Nitecore CI6 IR Flashlight (850nm / 1500mW)

 

The IR flashlight is higher powered but only uses one LED. Is focused delivery more important vs. area coverage? What are your thoughts on this?

 

 

[lostfalco]

hmmm...I wonder if this would work on the brain? Probably not, but it's the first HDAC2 specific inhibitor I've been able to find in nature. Gotta keep looking! PCA is in a number of herbal medicines as well. 

 

http://www.ncbi.nlm....pubmed/23159608

 

Biochem Biophys Res Commun. 2013 Jan 4;430(1):381-6. doi: 10.1016/j.bbrc.2012.11.018. Epub 2012 Nov 14.

Protocatechualdehyde possesses anti-cancer activity through downregulating cyclin D1 and HDAC2 in human colorectal cancer cells.

Jeong JB1, Lee SH.

Author information

Abstract

Protocatechualdehyde (PCA) is a naturally occurring polyphenol found in barley, green cavendish bananas, and grapevine leaves. Although a few studies reported growth-inhibitory activity of PCA in breast and leukemia cancer cells, the underlying mechanisms are still poorly understood. Thus, we performed in vitro study to investigate if treatment of PCA affects cell proliferation and apoptosis in human colorectal cancer cells and define potential mechanisms by which PCA mediates growth arrest and apoptosis of cancer cells. Exposure of PCA to human colorectal cancer cells (HCT116 and SW480 cells) suppressed cell growth and induced apoptosis in dose-dependent manner. PCA decreased cyclin D1 expression in protein and mRNA level and suppressed luciferase activity of cyclin D1 promoter, indicating transcriptional downregulation of cyclin D1 gene by PCA. We also observed that PCA treatment attenuated enzyme activity of histone deacetylase (HDAC) and reduced expression of HDAC2, but not HDAC1. These findings suggest that cell growth inhibition and apoptosis by PCA may be a result of HDAC2-mediated cyclin D1 suppression.

 

Edited by lostfalco, 07 March 2015 - 12:28 AM.

[lostfalco]

Just sharing a little more research. =)

 

Sorry my responses have become so intermittent...life is a little crazy at the moment. Anyway, I figure that sharing a little inconclusive research is better than nothing for the moment. As you can see from my last few posts, I'm currently looking into ways to: 1) increase acetyl groups (ALCAR) and 2) inhibit the removal of those acetyl groups by HDAC2. 

 

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.

Preethi J1, Singh HK, Venkataraman JS, Rajan KE.

Author information

Abstract

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.

 

[lostfalco]

Another very interesting possibility...HDAC8 inhibitors. 

 

http://www.ncbi.nlm....les/PMC3625590/

 

Evid Based Complement Alternat Med. 2013;2013:514908. doi: 10.1155/2013/514908. Epub 2013 Mar 28.

NBM-T-L-BMX-OS01, Semisynthesized from Osthole, Is a Novel Inhibitor of Histone Deacetylase and Enhances Learning and Memory in Rats.

Yang YC1, Chen CN, Wu CI, Huang WJ, Kuo TY, Kuan MC, Tsai TH, Huang JS, Huang CY.

Author information

Abstract

NBM-T-L-BMX-OS01 (BMX) was derived from the semisynthesis of osthole, isolated from Cnidium monnieri (L.) Cuss., and was identified to be a potent inhibitor of HDAC8. This study shows that HDAC8 is highly expressed in the pancreas and the brain. The function of HDAC8 in the brain has not been adequately studied. Because BMX enhances neurite outgrowth and cAMP response element-binding protein (CREB) activation, the effect of BMX on neural plasticity such as learning and memory is examined. To examine declarative and nondeclarative memory, a water maze, a passive one-way avoidance task, and a novel object recognition task were performed. Results from the water maze revealed that BMX and suberoylanilide-hydroxamic-acid-(SAHA-) treated rats showed shorter escape latency in finding the hidden platform. The BMX-treated animals spent more time in the target quadrant in the probe trial performance. An analysis of the passive one-way avoidance results showed that the BMX-treated animals stayed longer in the illuminated chamber by 1 day and 7 days after footshock. The novel object recognition task revealed that the BMX-treated animals showed a marked increase in the time spent exploring novel objects. Furthermore, BMX ameliorates scopolamine-(Sco-) induced learning and memory impairment in animals, indicating a novel role of BMX in learningand memory.

 

[lostfalco]

A little epigenetics review. 

 

Edited by lostfalco, 08 March 2015 - 03:36 AM.