4019 replies to this topic

[BieraK]

 

A showdown of epic proportions...LLLT vs. Pulsating Magnetic Field Therapy for lower back osteoarthritis. Looks like a draw!

 

Ok, I don't know how applicable this is for us but I thought it was interesting in light of recent experiments. =)

 

http://www.ncbi.nlm....pubmed/25763584

 

Pol Merkur Lekarski. 2015 Jan 25;38(223):26-31.

[Comparison of the effect of laser and magnetic therapy for pain level and the range of motion of the spine of people with osteoarthritis lower back].

[Article in Polish]

Zdrodowska B1, Leszczyńska-Filus M1, Leszczyński R1, Błaszczyk J2.

Author information

Abstract

Increased expression of degenerative disease of the lumbar spine is an onerous task, which reduces the efficiency of the activity and life of many populations. It is the most common cause of medical visits. In 95% of cases the cause of complaints is a destructive process in the course of degenerative intervertebral disc called a lumbar disc herniation. Protrusion of the nucleus pulposus causes severe pain and impaired muscle tone, often more chronic and difficult to master. Successful treatment of lumbar disc herniation constitutes a serious interdisciplinary problem. It is important to properly planned and carried out physiotherapy. Based on the number of non-invasive methods, to reduce muscle tension, mute pain and alleviation of inflammation. It is the treatment safe, effective, and at the same time, which is their big advantage, readily available and cheap. It is worth noting that not every method has the same efficiency. The question that the methods are effective in relieving pain and helping to effectively increase the range of motion led to a comparison of two methods - Low Level Laser Therapy (LLLT) and pulsating magnetic field therapy.

AIM: 

The aim of the study was to compare the efficacy of LLLT and pulsating magnetic field therapy in combating pain and increase range of motion of the spine of people with degenerative spine disease of the lower back.

MATERIALS AND METHODS: 

120 patients with diagnose lumbar disc herniation whit no nerve roots symptoms. Patients were divided into two Groups: A and B. Group A of 60 patients were subjected to laser therapy (λ=820nm, P=400mW, Ed=6-12 J/cm²) and the second Group B of 60 patients too, to pulsating magnetic fields procedures (5mT, 30 Hz, 15 minutes). Every patient before rehabilitation started and right after it has finished has undergone examination. Subjective pain assessment was carried out using a modified Laitinen questionnaire and Visual Analogue Scale of Pain intensity. Spine mobility was evaluated whit the Schober test and the Fingertip-to-floor-test. The obtained results were subjects to statistical analysis.

RESULTS: 

Research shows that both low energy laser and pulsating magnetic field physical attributes are effective methods for the treatment of pain and restricted mobility of the spine caused by disc herniation. Careful analysis emphasizes greater efficiency laser for pain. In contrast, a statistically greater improvement in global mobility of the spine, as well as flexion and extension of the lumbar recorded in group B, where the applied pulsating magnetic field.

CONCLUSIONS: 

Both laser and magnet therapy reduces pain and improves mobility of the spine of people with degenerative spine disease of the lower back. Comparison of the effectiveness of both methods showed a greater analgesic effect of laser treatment, and greater mobility of the spine was observed under the influence of pulsating magnetic field therapy.

 

:O This could be really good for my mother's osteoarthritis... This is the next level on healing technologies... For the first time in my life I'm feeling the recent advancement in technology fairly close and with an easy access .... but ironically, this technology like LLLT isn't new.

I think that LLLT+ICES can be applied in synergistic way, first LLLT for the ATP generation and the hormetic response, and then ICES for the anti-inflammatory effects. I think that LLLT could be bad if you have too much HIF-1alpha and VEGF and a bad response for counteract NF-kB... so ICES could enhance the body stress response.

The other idea that comes to my mind is the stem cell process behind these technologies, LLLT enhances stem cells and ICES interacts with stem cells also. Probably there are some risks with doing these two technologies, but the positive effects apparently can be much greater than the risks...


Effect of low-level laser therapy on mesenchymal stem cell proliferation: a systematic review.

Ginani F1, Soares DM, Barreto MP, Barboza CA.

Author information

 

Abstract

Low-level laser therapy (LLLT) has been used in several in vitro experiments in order to stimulate cell proliferation. Cells such as fibroblasts, keratinocytes, lymphocytes, and osteoblasts have shown increased proliferation when submitted to laser irradiation, although little is known about the effects of LLLT on stem cells. This study aims to assess, through a systematic literature review, the effects of LLLT on the in vitro proliferation of mesenchymal stem cells. Using six different terms, we conducted an electronic search in PubMed/Medline database for articles published in the last twelve years. From 463 references obtained, only 19 papers met the search criteria and were included in this review. The analysis of the papers showed a concentration of experiments using LLLT on stem cells derived from bone marrow, dental pulp, periodontal ligament, and adipose tissue. Several protocols were used to irradiate the cells, with variations on wavelength, power density, radiation time, and state of light polarization. Most studies demonstrated an increase in the proliferation rate of the irradiated cells. It can be concluded that the laser therapy positively influences the in vitro proliferation of stem cells studied, being necessary to carry out further experiments on other cell types and to uniform the methodological designs.

Just a comment: In the past the veins of my hands were always thin, it could hardly be noticed... but after LLLT the veins of my hands are bigger and with a clearly vassodilatory appearance, I can see the veins most of the time.... This is good or this is bad? I don't know.

Edited by BieraK, 25 March 2015 - 01:07 PM.

[Lucas N]

Dear @Lostfalco and other members.

 

Could you please share your current stack? Your core items inside the list above. I will really appreciate, without any further explanation, only what things are you taking/doing, and if possible in what dose. Best regards, and love this thread.

 

Vitamins & Minerals

 

Herbs

Mithocondrial

Neurosteroids

Stimulants

Racetams/Nootropics

Neurofeedback Devices

Laser Protocol

Diet

Exercise

Sleep Hacks

 

Drugs
 

Essential Oils

 

Other?
 

Edited by Lucas N, 25 March 2015 - 07:37 PM.

[BigPapaChakra]

 

 

My only experience thus far with PEMF are the EarthPulse v4.7 and 5.0. OpaqueMind has also used the v4.7 if I'm not mistaken and enjoyed it. My experience is only 'okay'. It has been mildly positive. I definitely find value in the EarthPulse, particularly the 5.0 with all the coils attached (to make it more powerful), but it hasn't changed my life as it has for others. I plan on getting some other PEMF units when I have the money, but I have no idea if I will use one of the many ICES techs, or something like the Lenyo Meridian, Lenyo Sleep System, QRS (more pricey), etc. I've also been contemplating going to a local clinic and paying for sessions with the DeltaPulse, a medical/sports professional unit.

 

Overall, though, I suspect this technology will prove to be extremely useful and potentially more potent than most other supplements, drugs, etc. It can cause direct epigenetic changes, modulate various transcription factors, and I suspect coming from the perspective of Gilbert Ling and Ray Damadian, it probably impacts the nano-protoplasm of a cell, protein unfolding, and more. Definitely something I want to mess around with a lot more. 

 

Thanks for the feedback, Papa. I remembered that you were going to test the EarthPulse out over a year ago. I was curious how it turned out for you. 

 

I'm still working my way through a lot of the literature on ICES/PEMF. Dr. Dennis seems to think that the mechanism of action consists of paracellular ion currents impacting some currently undiscovered cell surface ionic receptor. He thinks this functions as a sort of exercise mimicker. Have you come across anyone else that holds this position or is it peculiar to Dennis?  

 

 

I'm continuing my experiments with the EP as well. I remember one time I used it on the "Alert" setting directly under my head and it seemed to largely impact neuro-sensory processing. By that, I mean, vestibular capabilities coupled with proprioception. This makes sense in light of the research on PEMF, rTMS, and static magnets in Alzheimer's, TBI, and Parkinson's. Before I experiment with other devices/sources of PEMF, I'm going to start using the EP at the base of my skull more, perhaps around the cerebellum, and also my thyroid.

 

Also, yeah, some Japanese researchers have described what you're speaking about as "M.I.C.E. - magnetically induced cellular exercise". I suggest reading the work of Ling, Damadian, and Pollack. Their work on what cell architecture is truly like can elucidate the MOA of PEMF and ICES a lot better than the traditionally accepted fluid mosaic model of the "cell membrane". From my brief reading of the literature on multilayered polarized water in the cell, it's likely that pulsed electromagnetic fields directly impact protein extension into vicinal water, or perhaps even aiding in 'control' (for lack of a better term from my current understanding) of cardinal adsorbent sites. I think this would be profound because this would help make sense of all the research started in the early 1900's on bioelectricity and electrochemical control of organismic evolution and adaptation, in which bioelectric fields can cause mutations to an organism without much (or sometimes ANY) change to their DNA (for instance, giving an organism extra eyes or limbs or a denser cortex). 

 

I don't whatsoever enjoy the layout of the EarthPulse site, but I suggest checking it out because they have cited thousands of studies on PEMF, ICES, rTMS, etc. This is their bibliography just for Parkinson's: https://earthpulse.net/parkinsons.htmAlso download Dr. Becker's books on the site.

 

http://www.nature.co...wth-1.17087#/b1Bioelectric Signals Spark Brain Growth

 

^What's interesting about that is this research has been going on for over a century, by the likes of George Washington Crille and many Russian biophysicists set on conquering aging, yet researchers are now publishing papers on electromedicine that deal with facts that have already been known for a long time. 

[BigPapaChakra]

This is essentially synonymous with "structured water", which many call "quackery": http://revalesio.com...our-technology/seems like some scientists are picking up on the info that has been available for a long time. Phase II studies for MS and Asthma, Phase I for Parkinson's, Alzheimer's, and acute myocardial infarctions. 

[BigPapaChakra]

Let me know if this link works: http://novafile.com/tk3f7jkid7eo 

 

Handbook of Photomedicine by Michael R. Hamblin, PhD, and Ying-Ying Huang, MD

[mettmett]

Yes falco, I've also started taking tadaladil. I prefer a smaller dose as well since a full dropper gave me a head ache.
Its hard to say how much it has helped with memory. But, for what it's worth I do find myself having randomly vivid memories of things that I normally wouldn't. I haven't done any tests, but I can say with confidence that it has given me amazing pumps in the gym.

Overall I am liking it but so far I can't recommend it. That is subject to change though.. I'm only 4 days in.

Also it should be noted that due to life circumstances I am not getting near enough sleep. Thus further interfering with the memory aspect. The end.

[lostfalco]

GSK-3 and its relationship to CREB. Lithium and valproic acid are GSK-3 inhibitors. 

 

"Given that CREB phosphorylation by GSK3 abrogates its DNA binding activity8, it is plausible that GSK3 and nitric oxide signaling work in concert to control the duration and intensity of CREB-dependent transcription."

 

 

http://www.ncbi.nlm....pubmed/20648061

 

Nat Rev Neurosci. 2010 Aug;11(8):539-51. doi: 10.1038/nrn2870.

GSK3 signalling in neural development.

Hur EM1, Zhou FQ.

Author information

Abstract

Recent evidence suggests that glycogen synthase kinase 3 (GSK3) proteins and their upstream and downstream regulators have key roles in many fundamental processes during neurodevelopment. Disruption of GSK3 signalling adversely affects brain development and is associated with several neurodevelopmental disorders. Here, we discuss the mechanisms by which GSK3 activity is regulated in the nervous system and provide an overview of the recent advances in the understanding of how GSK3 signalling controls neurogenesis, neuronal polarization and axon growth during brain development. These recent advances suggest that GSK3 is a crucial node that mediates various cellular processes that are controlled by multiple signalling molecules--for example, disrupted in schizophrenia 1 (DISC1), partitioning defective homologue 3 (PAR3), PAR6 and Wnt proteins--that regulate neurodevelopment. 

 

 

 

 

http://www.ncbi.nlm....les/PMC3503340/

 

 

Published online 2012 Sep 24. doi:  10.1021/cn300110c

Glycogen Synthase Kinase 3 Inhibition Promotes Adult Hippocampal Neurogenesis in Vitro and in Vivo

Jose A. Morales-Garcia,† Rosario Luna-Medina,† Sandra Alonso-Gil,† Marina Sanz-SanCristobal,† Valle Palomo,‡Carmen Gil,‡ Angel Santos,§ Ana Martinez,*‡ and  Ana Perez-Castillo*†

Author information ► Article notes ► Copyright and License information ►

This article has been cited by other articles in PMC.

 

Go to:

Abstract

Glycogen synthase kinase-3 (GSK-3) is a serine/threonine kinase originally identified as a regulator of glycogen metabolism but it also plays a pivotal role in numerous cellular functions, including differentiation, cell cycle regulation, and proliferation. The dentate gyrus of the hippocampus, together with the subventricular zone of the lateral ventricles, is one of the regions in which neurogenesis takes place in the adult brain. Here, using a chemical genetic approach that involves the use of several diverse inhibitors of GSK-3 as pharmacological tools, we show that inhibition of GSK-3 induces proliferation, migration, and differentiation of neural stem cells toward a neuronal phenotype in in vitro studies. Also, we demonstrate that inhibition of GSK-3 with the small molecule NP03112, called tideglusib, induces neurogenesis in the dentate gyrus of the hippocampus of adult rats. Taken together, our results suggest that GSK-3 should be considered as a new target molecule for modulating the production and integration of new neurons in the hippocampus as a treatment for neurodegenerative diseases or brain injury and, consequently, its inhibitors may represent new potential therapeutic drugs in neuroregenerative medicine.

 

Edited by lostfalco, 29 March 2015 - 03:57 PM.

[lostfalco]

http://www.jneurosci...28/10/2576.long

 

J Neurosci. 2008 Mar 5;28(10):2576-88. doi: 10.1523/JNEUROSCI.5467-07.2008.

Synergistic neuroprotective effects of lithium and valproic acid or other histone deacetylase inhibitors in neurons: roles of glycogen synthase kinase-3 inhibition.

Leng Y1, Liang MH, Ren M, Marinova Z, Leeds P, Chuang DM.

Author information

Abstract

Lithium and valproic acid (VPA) are two primary drugs used to treat bipolar mood disorder and have frequently been used in combination to treat bipolar patients resistant to monotherapy with either drug. Lithium, a glycogen synthase kinase-3 (GSK-3) inhibitor, and VPA, a histone deacetylase (HDAC) inhibitor, have neuroprotective effects. The present study was undertaken to demonstrate synergistic neuroprotective effects when both drugs were coadministered. Pretreatment of aging cerebellar granule cells with lithium or VPA alone provided little or no neuroprotection against glutamate-induced cell death. However, copresence of both drugs resulted in complete blockade of glutamate excitotoxicity. Combined treatment with lithium and VPA potentiated serine phosphorylation of GSK-3 alpha and beta isoforms and inhibition of GSK-3 enzyme activity. Transfection with GSK-3alpha small interfering RNA (siRNA) and/or GSK-3beta siRNA mimicked the ability of lithium to induce synergistic protection with VPA. HDAC1 siRNA or other HDAC inhibitors (phenylbutyrate, sodium butyrate or trichostatin A) also caused synergistic neuroprotection together with lithium. Moreover, combination of lithium and HDAC inhibitors potentiated beta-catenin-dependent, Lef/Tcf-mediated transcriptional activity. An additive increase in GSK-3 serine phosphorylation was also observed in mice chronically treated with lithium and VPA. Together, for the first time, our results demonstrate synergistic neuroprotective effects of lithium and HDAC inhibitors and suggest that GSK-3 inhibition is a likely molecular target for the synergistic neuroprotection. Our results may have implications for the combined use of lithium and VPA in treating bipolar disorder. Additionally, combined use of both drugs may be warranted for clinical trials to treat glutamate-related neurodegenerative diseases.

 

Edited by lostfalco, 29 March 2015 - 04:11 PM.

[Kalliste]

I can't find any info on risks for the eyes, I've bought this device:

http://www.ebay.com/...984.m1423.l2649

 

What is a good protection for this? Can I just keep my eyes shut and look away? I've got Uvex Skyper glasses but I think those are mainly for blue light/UV. Are they any good even if they are not for exactly that laser light?

 

 

[lostfalco]

Hey Cosmicalstorm, I used these back when I was testing ebay lasers. 

 

http://www.longecity...e-8#entry592174

 

I'm not sure that they're completely necessary if you play it safe and keep the laser away from your eyes. 

Edited by lostfalco, 29 March 2015 - 05:08 PM.

[lostfalco]

Yes falco, I've also started taking tadaladil. I prefer a smaller dose as well since a full dropper gave me a head ache.
Its hard to say how much it has helped with memory. But, for what it's worth I do find myself having randomly vivid memories of things that I normally wouldn't. I haven't done any tests, but I can say with confidence that it has given me amazing pumps in the gym.

Overall I am liking it but so far I can't recommend it. That is subject to change though.. I'm only 4 days in.

Also it should be noted that due to life circumstances I am not getting near enough sleep. Thus further interfering with the memory aspect. The end.

Cool, mettmett. Keep me updated. 

 

I haven't noticed anything related to acquisition...but my retention seems to be improved. It'll be interesting to see how it works in the long run and in combination with other things. ALCAR and low dose Lithium Orotate seem like some interesting possibilities. 

[BieraK]

Another study of lithium with a relation to this thread:
http://www.ncbi.nlm....pubmed/19624390

Lithium-induced enhancement of mitochondrial oxidative phosphorylation in human brain tissue.

Maurer IC1, Schippel P, Volz HP.

Author information

 

Abstract

OBJECTIVES:

Extensive preclinical and clinical evidence suggests mitochondrial dysfunction in bipolar disorder. Studies of brain energy metabolism in bipolar disorder suggest an impairment of energy generation by mitochondrial oxidative phosphorylation. Lithium is an effective drug widely used in treating bipolar disorder, but its mechanism of action has remained uncertain. The aim of this study was to clarify the effect of lithium on mitochondrial oxidative phosphorylation.

METHODS:

We spectrophotometrically determined the activities of the respiratory chain complexes I + III [antimycin A-sensitive nicotinamide adenine dinucleotide (NADH) cytochrome c oxidorductase], complexes II + III (succinate cytochrome c oxidoreductase), succinate dehydrogenase, and complex IV [cytochrome c oxidase (COX)], and of the mitochondrial matrix enzyme citrate synthase in postmortem human brain cortex homogenates following exposure to lithium (up to 10 mM).

RESULTS:

Activities of complexes I + III and of complexes II + III were dose-dependently increased by lithium with maximum values at 1 mM (165%, p = 0.03, and 146%, p = 0.00002, of controls). Activity of succinate dehydrogenase remained unchanged up to 2 mM, but was raised at higher drug concentrations (maximum 220%, p = 0.01, of controls). In contrast, activity of COX was not significantly affected by the drug (decrease of 12% at 1 mM, p = 0.4).

CONCLUSIONS:

Our study suggests that lithium stimulates mitochondrial respiratory chain enzyme activities at clinically relevant concentrations. Lithium's effect on the mitochondrial respiratory chain presents further evidence of the pathophysiological significance of mitochondrial dysfunction in bipolar disorder. The effect may be relevant to the therapeutic efficacy of the drug by potentially reversing a disease-related alteration.

This can enhance the response to LLLT and produce a better adaptation to HIF-1a.

An interesting stack:
LLLT
Cordyceps (for cGMP increase)
Artichoke (For PDE4 inhibition... Zembrin/Kanna apparently is better because can cross the BBB)
Lithium Orotate
PQQ+CoQ10

Possible adds:
Low dose forskolin
Low dose Methylene Blue


What is the methylene blue dose used in photodynamic therapy? or in other words, what is the dose of methylene blue that can interact in a bad manner with LLLT?

I ask this because I was experimenting with doses of methylene blue after and before LLLT (Max 60 seconds with 850 nm)... the doses before where in the range of 60mcg - 180 mcg... and the dose before in the same range.
I've experience a better response to LLLT, I feel the fatigue and then the compensation with a very relaxed feeling....Is similar to my first LLLT sessions. Without MB is like I produce more ROS but not the sufficient ATP. 

[lostfalco]

More info on the mechanisms of lithium and valproate. 

 

http://www.ncbi.nlm....pubmed/24248060

 

Int J Mol Sci. 2013 Nov 15;14(11):22558-603. doi: 10.3390/ijms141122558.

Neuroprotective effects of psychotropic drugs in Huntington's disease.

Lauterbach EC1.

Author information

Abstract

Psychotropics (antipsychotics, mood stabilizers, antidepressants, anxiolytics, etc.) are commonly prescribed to treat Huntington's disease (HD). In HD preclinical models, while no psychotropic has convincingly affected huntingtin gene, HD modifying gene, or huntingtin protein expression, psychotropic neuroprotective effects include upregulated huntingtin autophagy (lithium), histone acetylation (lithium, valproate, lamotrigine), miR-222 (lithium-plus-valproate), mitochondrial protection (haloperidol, trifluoperazine, imipramine, desipramine, nortriptyline, maprotiline, trazodone, sertraline, venlafaxine, melatonin), neurogenesis (lithium, valproate, fluoxetine, sertraline), and BDNF (lithium, valproate, sertraline) and downregulated AP-1 DNA binding (lithium), p53 (lithium), huntingtin aggregation (antipsychotics, lithium), and apoptosis (trifluoperazine, loxapine, lithium, desipramine, nortriptyline, maprotiline, cyproheptadine, melatonin). In HD live mouse models, delayed disease onset (nortriptyline, melatonin), striatal preservation (haloperidol, tetrabenazine, lithium, sertraline), memory preservation (imipramine, trazodone, fluoxetine, sertraline, venlafaxine), motor improvement (tetrabenazine, lithium, valproate, imipramine, nortriptyline, trazodone, sertraline, venlafaxine), and extended survival (lithium, valproate, sertraline, melatonin) have been documented. Upregulated CREB binding protein (CBP; valproate, dextromethorphan) and downregulated histone deacetylase (HDAC; valproate) await demonstration in HD models. Most preclinical findings await replication and their limitations are reviewed. The most promising findings involve replicated striatal neuroprotection and phenotypic disease modification in transgenic mice for tetrabenazine and for sertraline. Clinical data consist of an uncontrolled lithium case series (n = 3) suggesting non-progression and a primarily negative double-blind, placebo-controlled clinical trial of lamotrigine.

 

Edited by lostfalco, 30 March 2015 - 01:26 AM.

[lostfalco]

 

Another study of lithium with a relation to this thread:
http://www.ncbi.nlm....pubmed/19624390

Nice find, BieraK. Thanks, man. 

 

I'll be interested to hear how PDE4 inhibition goes for you. I'm focusing more on PDE5 so it'll be cool to see how they compare. 

Edited by lostfalco, 30 March 2015 - 01:32 AM.

[Kalliste]

Hey Cosmicalstorm, I used these back when I was testing ebay lasers. 

 

http://www.longecity...e-8#entry592174

 

I'm not sure that they're completely necessary if you play it safe and keep the laser away from your eyes. 

 

I have ordered the laser and a pair of glasses that cover 808nm. Is there any topics in this very long thread that covers the use of a one-diode 808nm 200mw laser? How much focus to use and so on, I saw a youtube video of someone using it to etch things into tree panels

Edited by Cosmicalstorm, 30 March 2015 - 08:08 AM.

[Razor444]

San Pellegrino water has 0.2 mg of lithium per litre (liter). Not sure if that's a large enough dose to effect the sort of changes we're after.

[mettmett]

AN update on tadalifil:

It's going good.  I take it everyday except for Monday and Tuesday.  On those days I work on my website and I like the creative inspiration yerba mate gives me, so I risk combining them since yerba effects mao.  Since I've feel head pains at a full dropper's worth I definitely don't want to mix them together.

 

Ok so dosing:  The dropper when fully squeezed only fills halfway up.  So I'm assuming that is the full dose -25mg.  I take anywhere from 1/6 to 1/5 of that so ~5mg.  I plan on actually measuring it out soon.

 

The pumps in the gym are unmistakable.  Right now I would use the product just for that benefit alone.  At a low dose I don't notice any change in my erections, but I wasn't worried about that anyway.  I do notice an improvement in libido though.  I'm still finding myself remembering random stuff pretty vividly.  Hasn't positively or negatively influenced my short term memory at all.

BTW the website lostfalco recommends > superiorpeptides < is running a 45% off sale right now MMM45 is the code.  Good chance to test it out or buy it and test later.

Edited by mettmett, 31 March 2015 - 01:51 AM.

[mettmett]

This can enhance the response to LLLT and produce a better adaptation to HIF-1a.

An interesting stack:
LLLT
Cordyceps (for cGMP increase)
Artichoke (For PDE4 inhibition... Zembrin/Kanna apparently is better because can cross the BBB)
Lithium Orotate
PQQ+CoQ10

Possible adds:
Low dose forskolin
Low dose Methylene Blue


What is the methylene blue dose used in photodynamic therapy? or in other words, what is the dose of methylene blue that can interact in a bad manner with LLLT?

I ask this because I was experimenting with doses of methylene blue after and before LLLT (Max 60 seconds with 850 nm)... the doses before where in the range of 60mcg - 180 mcg... and the dose before in the same range.
I've experience a better response to LLLT, I feel the fatigue and then the compensation with a very relaxed feeling....Is similar to my first LLLT sessions. Without MB is like I produce more ROS but not the sufficient ATP. 

 

I've wondered about combining photosensitizers with LLLT.  I did do a couple applications of LLLT after consuming Saint John's Wort(a photosenstivity increaser).  It seemed like it was better than just LLLT by itself, but after reading about how they combine photosensitizers with lights to kill cancer cells I quit pursuing it further.

 

My theory was that if you could make the cells more sensitive to the light then you could apply the lasers for less time and receive the same effect of a longer application.  But I don't have any science to back that up and there is definitely a high risk for harming healthy cells.   

[lostfalco]

Since we are currently focused on 1) transcription factors and 2) opening chromatin so that those transcription factors can access genes...I thought it would be good to remind everyone of something that we talked about a year and a half ago. Acetate enhances histone acetylation AND inhibits HDACs (including HDAC2). One of the best ways to get more acetate is through feeding resistant starch to your microbiome. I may also have to look into glyceryl triacetate/triacetin. 

 

http://www.ncbi.nlm....pubmed/21359531

 

Mol Cell Biochem. 2011 Jun;352(1-2):173-80. doi: 10.1007/s11010-011-0751-3. Epub 2011 Feb 26.

Acetate supplementation increases brain histone acetylation and inhibits histone deacetylase activity and expression.

Soliman ML1, Rosenberger TA.

Author information

Abstract

Acetate supplementation increases brain, heart, and liver acetyl-CoA levels and reduces lipopolysaccharide-induced neuroinflammation. Because intracellular acetyl-CoA can be used to alter histone acetylation-state, using Western blot analysis, we measured the temporal effect that acetate supplementation had on brain and liver histone acetylation following a single oral dose of glyceryl triacetate (6 g/kg). In parallel experiments, we measured the effect that acetate supplementation had on histone deacetylase (HDAC) and histone acetyltransferase (HAT) enzymic activities and the expression levels of HDAC class I and II enzymes using Western blot analysis. We found that acetate supplementation increased the acetylation-state of brain histone H4 at lysine 8 at 2 and 4 h, histone H4 at lysine 16 at 4 and 24 h, and histone H3 at lysine 9 at 4 h following treatment. No changes in other forms of brain or liver H3 and H4 acetylation-state were found at any post-treatment times measured. Enzymic HAT and HDAC assays on brain extracts showed that acetate supplementation had no effect on HAT activity, but significantly inhibited by 2-fold HDAC activity at 2 and 4 h post-treatment. Western blot analysis demonstrated that HDAC 2 levels were decreased at 4 h following treatment. Based on these results, we conclude that acetyl-CoA derived from acetate supplementation increases brain histone acetylation-state by reducing HDAC activity and expression.

 

Edited by lostfalco, 31 March 2015 - 03:57 PM.

[BieraK]

 

This can enhance the response to LLLT and produce a better adaptation to HIF-1a.

An interesting stack:
LLLT
Cordyceps (for cGMP increase)
Artichoke (For PDE4 inhibition... Zembrin/Kanna apparently is better because can cross the BBB)
Lithium Orotate
PQQ+CoQ10

Possible adds:
Low dose forskolin
Low dose Methylene Blue


What is the methylene blue dose used in photodynamic therapy? or in other words, what is the dose of methylene blue that can interact in a bad manner with LLLT?

I ask this because I was experimenting with doses of methylene blue after and before LLLT (Max 60 seconds with 850 nm)... the doses before where in the range of 60mcg - 180 mcg... and the dose before in the same range.
I've experience a better response to LLLT, I feel the fatigue and then the compensation with a very relaxed feeling....Is similar to my first LLLT sessions. Without MB is like I produce more ROS but not the sufficient ATP. 

 

I've wondered about combining photosensitizers with LLLT.  I did do a couple applications of LLLT after consuming Saint John's Wort(a photosenstivity increaser).  It seemed like it was better than just LLLT by itself, but after reading about how they combine photosensitizers with lights to kill cancer cells I quit pursuing it further.

 

My theory was that if you could make the cells more sensitive to the light then you could apply the lasers for less time and receive the same effect of a longer application.  But I don't have any science to back that up and there is definitely a high risk for harming healthy cells.   

 

Yes, I think the same...with subsances like methylene blue and c60 the applicaton of LLLT seems to need less time.
.
But the problem with this is the type of light, for example according to this Methylene blue absorbs the light in the range of red light 580 - 700 nm.
http://www.longecity...-54#entry632100

 

And as I know, St John's Worth does no react with red and infrared light. The other important factor is the dose of Methylene Blue, apparently the dose used for kill cells (Photodynamic therapy) is higher compared to the mgc doses, would be interesting to know the MB dose used for the photodynamic therapy.

However in my experience there is an interaction between Methylene blue and LLLT... I've experienced different effects from MB after LLLT and MB before LLLT.  

[Razor444]

The potential use of histone deacetylase inhibitors in the treatment of depression

 

 

Abstract

Numerous preclinical studies demonstrate that changes in gene expression in the brain occur in animal models of depression using exposure to stress, such as social defeat and leaned helplessness, and that repeated administration of antidepressants ameliorates these stress-induced changes in gene expression. These findings suggest that alteration in gene transcription in the central nervous system in response to stress plays an important role in the pathophysiology of depression. Recent advances in epigenetics have led to the realization that chromatin remodeling mediated by histone deacetylase (HDAC) is closely involved in the regulation of gene transcription. In this context, we first review several preclinical studies demonstrating the antidepressant-like efficacy of HDAC inhibitors. We then suggest the efficacy of HDAC inhibitors in treatment-resistant depression based on the mechanism of action of HDAC. Finally, we discuss the possibility of using HDAC inhibitors in patients with treatment-resistant depression.

 

 

 

 table2.png   55.63KB   7 downloads

 

Edit: When Table 2 is copied from the paper, it doesn't keep its formatting. It's now attached as an image.

Edited by Razor444, 31 March 2015 - 11:11 PM.

[xls]

Lostfalco, any update on ICES?

[lostfalco]

Lostfalco, any update on ICES?

Hey xls, I'm currently in the middle of my tadalafil experiment so I'm holding off on ICES for a bit. I will definitely come back to it soon. 

[lostfalco]

AN update on tadalifil:

It's going good.  I take it everyday except for Monday and Tuesday.  On those days I work on my website and I like the creative inspiration yerba mate gives me, so I risk combining them since yerba effects mao.  Since I've feel head pains at a full dropper's worth I definitely don't want to mix them together.

 

Ok so dosing:  The dropper when fully squeezed only fills halfway up.  So I'm assuming that is the full dose -25mg.  I take anywhere from 1/6 to 1/5 of that so ~5mg.  I plan on actually measuring it out soon.

 

The pumps in the gym are unmistakable.  Right now I would use the product just for that benefit alone.  At a low dose I don't notice any change in my erections, but I wasn't worried about that anyway.  I do notice an improvement in libido though.  I'm still finding myself remembering random stuff pretty vividly.  Hasn't positively or negatively influenced my short term memory at all.

BTW the website lostfalco recommends > superiorpeptides < is running a 45% off sale right now MMM45 is the code.  Good chance to test it out or buy it and test later.

Thanks for the update, mettmett! Are you also noticing that you can remember a huge number of details from the previous day? This is the other primary effect that I've noticed in addition to my Anki studying. Of course, this is all very subjective. 

The potential use of histone deacetylase inhibitors in the treatment of depression

 

 

Thanks, Razor! 

[lostfalco]

San Pellegrino water has 0.2 mg of lithium per litre (liter). Not sure if that's a large enough dose to effect the sort of changes we're after.

It's probably a little on the low side but there is some (correlational) evidence that lithium in drinking water might help with depression and lower suicide rates. 

 

Lithium Orotate is also pretty damn cheap. http://www.swansonvi...ium-60-veg-caps

[lostfalco]

Dear @Lostfalco and other members.

 

Could you please share your current stack? 

 

Hey Lucas, check out Joe's Current Regimen for a monster stack involving all the elements you requested. http://selfhacked.co...urrent-regimen/

[lostfalco]

 

I have ordered the laser and a pair of glasses that cover 808nm. Is there any topics in this very long thread that covers the use of a one-diode 808nm 200mw laser? How much focus to use and so on, I saw a youtube video of someone using it to etch things into tree panels

 

I always used 320mW/cm2 as an irradiance limit and lasered primarily on EEG sites F3 and F4. I definitely prefer whole brain now.  http://www.longecity...e-3#entry583991

 

OpaqueMind lasered on these sites. 

http://www.longecity...e-8#entry590122

[lostfalco]

 

I'm continuing my experiments with the EP as well.

 

Also, yeah, some Japanese researchers have described what you're speaking about as "M.I.C.E. - magnetically induced cellular exercise". I suggest reading the work of Ling, Damadian, and Pollack.

 

http://www.nature.co...wth-1.17087#/b1Bioelectric Signals Spark Brain Growth

 

Looking forward to hearing your experiences, Papa. 

 

I'm familiar with Ling and Pollack. I'll have to look into Damadian. Thanks, man!

[lostfalco]

Glycerol triacetate is looking very interesting. Apparently, long term supplementation increased HAT activity (in rodents, of course). HATs transfer acetyl groups to histones and histone acetylation opens up genes to make them accessible to transcription machinery. In this case it reduced neuroinflammation...which is generally a very good thing. 

 

Glycerol triacetate is a food additive and shouldn't be too hard to purchase. http://en.wikipedia.org/wiki/Triacetin

 

http://www.jneuroinf.../content/9/1/51

 

Acetate supplementation modulates brain histone acetylation and decreases interleukin-1β expression in a rat model of neuroinflammation

Mahmoud L Soliman, Mark D Smith, Heidi M Houdek and Thad A Rosenberger^*

Abstract

Background

Long-term acetate supplementation reduces neuroglial activation and cholinergic cell loss in a rat model of lipopolysaccharide-induced neuroinflammation. Additionally, a single dose of glyceryl triacetate, used to induce acetate supplementation, increases histone H3 and H4 acetylation and inhibits histone deacetylase activity and histone deacetylase-2 expression in normal rat brain. Here, we propose that the therapeutic effect of acetate in reducing neuroglial activation is due to a reversal of lipopolysaccharide-induced changes in histone acetylation and pro-inflammatory cytokine expression.

 

Methods

In this study, we examined the effect of a 28-day-dosing regimen of glyceryl triacetate, to induce acetate supplementation, on brain histone acetylation and interleukin-1β expression in a rat model of lipopolysaccharide-induced neuroinflammation. The effect was analyzed using Western blot analysis, quantitative real-time polymerase chain reaction and enzymic histone deacetylase and histone acetyltransferase assays. Statistical analysis was performed using one-way analysis of variance, parametric or nonparametric when appropriate, followed by Tukey's or Dunn's post-hoc test, respectively.

 

Results

We found that long-term acetate supplementation increased the proportion of brain histone H3 acetylated at lysine 9 (H3K9), histone H4 acetylated at lysine 8 and histone H4 acetylated at lysine 16. However, unlike a single dose of glyceryl triacetate, long-term treatment increased histone acetyltransferase activity and had no effect on histone deacetylase activity, with variable effects on brain histone deacetylase class I and II expression. In agreement with this hypothesis, neuroinflammation reduced the proportion of brain H3K9 acetylation by 50%, which was effectively reversed with acetate supplementation. Further, in rats subjected to lipopolysaccharide-induced neuroinflammation, the pro-inflammatory cytokine interleukin-1β protein and mRNA levels were increased by 1.3- and 10-fold, respectively, and acetate supplementation reduced this expression to control levels.

 

Conclusion

Based on these results, we conclude that dietary acetate supplementation attenuates neuroglial activation by effectively reducing pro-inflammatory cytokine expression by a mechanism that may involve a distinct site-specific pattern of histone acetylation and histone deacetylase expression in the brain.

 

Edited by lostfalco, 01 April 2015 - 03:08 PM.

[lostfalco]

One of the most fascinating subjects on the planet...consciousness. I've been following Stanislas Dehaene for quite some time. He studies the neural correlates of human activities such as reading, doing mathematics, and consciousness. Highly recommended. 

 

 

 

Edited by lostfalco, 02 April 2015 - 06:54 PM.