384 replies to this topic

[rwac]

J Biol Chem. 2010 Mar 26. [Epub ahead of print]
Inhibition of Hsp70 by methylene blue affects signaling protein function and ubiquitination and modulates polyglutamine protein degradation.
Wang AM, Morishima Y, Clapp KM, Peng HM, Pratt WB, Gestwicki JE, Osawa Y, Lieberman AP.

According to this paper MB inhibits HSP70 at concentrations of a few uM.

... methylene blue inhibits the ability of the purified Hsp90/Hsp70-based chaperone machinery to enable ligand binding by the glucocorticoid receptor and ... this effect is due to specific inhibition of Hsp70.

The glucocorticoid receptor binds to cortisol, and inhibiting it might cause something akin to cortisol-resistance, leading to high cortisol levels (incidentally, I have been tested and I have high cortisol levels). This can then lead to high blood sugars/fat accumulation, etc. Time to reduce dosage for me, I've been taking 500 mcg/day.

Yikes.

Edited by rwac, 12 May 2010 - 10:28 PM.

[Sillewater]

I was meaning to back-calculate at what dosage that occurs. But haven't had the time. So maybe I'll stick with the 60mcg.

[rwac]

I was meaning to back-calculate at what dosage that occurs. But haven't had the time. So maybe I'll stick with the 60mcg.

It's not that easy. What makes it hard is that MB concentrates in more metabolically active areas, like cancers, brain, liver, etc.

[Sillewater]

geddarkstorm reported low blood pressure. Doesn't cortisol resistance lead to high blood pressure?

[rwac]

geddarkstorm reported low blood pressure. Doesn't cortisol resistance lead to high blood pressure?

I don't know how cortisol affects blood pressure, but I have low blood pressure too.

[Sillewater]

Have you considered a ketogenic diet for your grandfather, it might help quite a bit.

Sorry missed this.

I have definitely considered it but the only problem is my grandmother thinks not eating carbs will kill you, so she will not let him eat no starchy foods. She apparently thinks yams and squashes are superfoods that he has to eat every day multiple times a day. As many people of the Alzheimer's forums know there's always someone in your way when you want to help.

[rwac]

Sorry missed this.

I have definitely considered it but the only problem is my grandmother thinks not eating carbs will kill you, so she will not let him eat no starchy foods. She apparently thinks yams and squashes are superfoods that he has to eat every day multiple times a day. As many people of the Alzheimer's forums know there's always someone in your way when you want to help.

I suppose then, that there's no chance of getting your grandfather to fast for a couple of days and enter full blown ketosis to see if that helps him.

[Sillewater]

Definitely not, already tried.

[Lufega]

geddarkstorm reported low blood pressure. Doesn't cortisol resistance lead to high blood pressure?

I don't know how cortisol affects blood pressure, but I have low blood pressure too.

http://en.wikipedia....ortisol#Effects

Scroll down to where it says "additional effects"

<LI>It increases blood pressure by increasing the sensitivity of the vasculature to epinephrine and norepinephrine. In the absence of cortisol, widespread vasodilation occurs.

[rwac]

http://en.wikipedia....ortisol#Effects

Scroll down to where it says "additional effects"

<LI>It increases blood pressure by increasing the sensitivity of the vasculature to epinephrine and norepinephrine. In the absence of cortisol, widespread vasodilation occurs.

However, MB seems to increase cortisol, and paradoxically reduce blood pressure. I don't know how that would work. (Or atleast both Geddarkstorm and me somehow got low blood pressure)

[tintinet]

http://www.painjourn...e/S0304-3959(10)00061-8/abstract

Non-sequitur, but interesting.

[rwac]

Beneficial network effects of methylene blue in an amnestic model Penny D. Riha, Julio C. Rojas and F. Gonzalez-Lima

Abstract

Posterior cingulate/retrosplenial cortex (PCC) hypometabolism is a common feature in amnestic mild cognitive impairment and Alzheimer's disease. In rats, PCC hypometabolism induced by mitochondrial dysfunction induces oxidative damage, neurodegeneration and memory deficits. USP methylene blue (MB) is a diaminophenothiazine drug with antioxidant and metabolic-enhancing properties. In rats, MB facilitates memory and prevents neurodegeneration induced by mitochondrial dysfunction. This study tested the memory-enhancing properties of systemic MB in rats that received an infusion of sodium azide, a cytochrome oxidase inhibitor, directly into the PCC. Lesion volumes were estimated with unbiased stereology. MB's network-level mechanism of action was analyzed using graph theory and structural equation modeling based on cytochrome oxidase histochemistry-derived metabolic mapping data. Sodium azide infusions induced PCC hypometabolism and impaired visuospatial memory in a holeboard food-search task. Isolated PCC cytochrome oxidase inhibition disrupted the cingulo–thalamo–hippocampal effective connectivity, decreased the PCC functional networks and created functional redundancy within the thalamus. An intraperitoneal dose of 4 mg/kg MB prevented the memory impairment, reduced the PCC metabolic lesion volume and partially restored the cingulo–thalamo–hippocampal network effects. The effects of MB were dependent upon the local sub-network necessary for memory retrieval. The data support that MB's metabolic-enhancing effects are contingent upon the neural context, and that MB is able to boost coherent and orchestrated adaptations in response to physical alterations to the network involved in visuospatial memory. These results implicate MB as a candidate intervention to improve memory. Because of its neuroprotective properties, MB may have disease-modifying effects in amnestic conditions associated with hypometabolism.

Cognitive enhancers for anxiety disorders Stefan G. Hofmann, Jasper A.J. Smits, Anu Asnaani, Cassidy A. Gutner and Michael W. Otto

Available online 4 December 2010.

Abstract
Cognitive-behavioral therapy is an effective intervention for anxiety disorders. However, a significant number of people do not respond or only show partial response even after an adequate course of the treatment. Recent research has shown that the efficacy of the intervention can be improved by the use of cognitive enhancers that augment the core learning processes of cognitive-behavior therapy. This manuscript provides a review of the current state of cognitive enhancers for the treatment of anxiety disorders.


Research highlights
<a name="sp0020">►We review agents that might act as cognitive enhancers for cognitive-behavioral therapy for anxiety disorders in humans. ►We review d-cycloserine, cortisol, catecholamines, nutrients, botanicals, methylene blue, and endocannabinoids as possible cognitive enhancers. ►d-cycloserine is the most promising agent to augment extinction learning in animals and cognitive-behavioral therapy in humans. ►We examine the mechanism of cognitive enhancers and explore the role of genetic modulation.

[stephen_b]

I hadn't seen this study discussed before (sorry if I missed it), which has some in vivo results.

Alternative mitochondrial electron transfer as a novel strategy for neuroprotection, PMID 21454572, 6 May 2011.

Neuroprotective strategies, including free radical scavengers, ion channel modulators, and anti-inflammatory agents, have been extensively explored in the last 2 decades for the treatment of neurological diseases. Unfortunately, none of the neuroprotectants has been proved effective in clinical trails. In the current study, we demonstrated that methylene blue (MB) functions as an alternative electron carrier, which accepts electrons from NADH and transfers them to cytochrome c and bypasses complex I/III blockage. A de novo synthesized MB derivative, with the redox center disabled by N-acetylation, had no effect on mitochondrial complex activities. MB increases cellular oxygen consumption rates and reduces anaerobic glycolysis in cultured neuronal cells. MB is protective against various insults in vitro at low nanomolar concentrations. Our data indicate that MB has a unique mechanism and is fundamentally different from traditional antioxidants. We examined the effects of MB in two animal models of neurological diseases. MB dramatically attenuates behavioral, neurochemical, and neuropathological impairment in a Parkinson disease model. Rotenone caused severe dopamine depletion in the striatum, which was almost completely rescued by MB. MB rescued the effects of rotenone on mitochondrial complex I-III inhibition and free radical overproduction. Rotenone induced a severe loss of nigral dopaminergic neurons, which was dramatically attenuated by MB. In addition, MB significantly reduced cerebral ischemia reperfusion damage in a transient focal cerebral ischemia model. The present study indicates that rerouting mitochondrial electron transfer by MB or similar molecules provides a novel strategy for neuroprotection against both chronic and acute neurological diseases involving mitochondrial dysfunction.

I would be interested to see what doses they used in rats.

StephenB

[malbecman]

Here is the material and methods paragraph that mentions the dose they used. Dont forget, this is IP dosing so completely different (more bioavailable) than what one might get
by ingesting MB.

"Effect of MB on a Rotenone Model of PD

Rats were assigned to three groups. Control animals received vehicle infusion and daily saline injection (Veh/Sal; n = 6–8); a second group received rotenone infusion at a dose of 5 mg/kg/day and daily saline injection (ROT/Sal; n = 8–11); and the third group received rotenone infusion (5 mg/kg/day) and MB injection at a dose of 500 μg/kg/day (ROT/MB; n = 8–10). Vehicle or rotenone was infused via Alzet osmotic minipumps that were filled with vehicle or rotenone dissolved in vehicle (equal volumes of dimethyl sulfoxide and polyethylene glycol). Pumps containing vehicle or rotenone were sterilized with UV irradiation and implanted subcutaneously in the back. Intraperitoneal injections were administered with normal saline or MB (500 μg/kg/day), diluted in normal saline to 500 μl of final volume. "

I hadn't seen this study discussed before (sorry if I missed it), which has some in vivo results.

Alternative mitochondrial electron transfer as a novel strategy for neuroprotection, PMID 21454572, 6 May 2011.

Neuroprotective strategies, including free radical scavengers, ion channel modulators, and anti-inflammatory agents, have been extensively explored in the last 2 decades for the treatment of neurological diseases. Unfortunately, none of the neuroprotectants has been proved effective in clinical trails. In the current study, we demonstrated that methylene blue (MB) functions as an alternative electron carrier, which accepts electrons from NADH and transfers them to cytochrome c and bypasses complex I/III blockage. A de novo synthesized MB derivative, with the redox center disabled by N-acetylation, had no effect on mitochondrial complex activities. MB increases cellular oxygen consumption rates and reduces anaerobic glycolysis in cultured neuronal cells. MB is protective against various insults in vitro at low nanomolar concentrations. Our data indicate that MB has a unique mechanism and is fundamentally different from traditional antioxidants. We examined the effects of MB in two animal models of neurological diseases. MB dramatically attenuates behavioral, neurochemical, and neuropathological impairment in a Parkinson disease model. Rotenone caused severe dopamine depletion in the striatum, which was almost completely rescued by MB. MB rescued the effects of rotenone on mitochondrial complex I-III inhibition and free radical overproduction. Rotenone induced a severe loss of nigral dopaminergic neurons, which was dramatically attenuated by MB. In addition, MB significantly reduced cerebral ischemia reperfusion damage in a transient focal cerebral ischemia model. The present study indicates that rerouting mitochondrial electron transfer by MB or similar molecules provides a novel strategy for neuroprotection against both chronic and acute neurological diseases involving mitochondrial dysfunction.

I would be interested to see what doses they used in rats.

StephenB

[DbCooper]

Anybody know if MB can be absorbed through the skin? In college a few of my wrestling team mates swore it prevented ringworm.

[stephen_b]

Anybody know if MB can be absorbed through the skin? In college a few of my wrestling team mates swore it prevented ringworm.

It has a molecular weight of 319, so I think it would work, if you don't mind looking like a smurf.

[niner]

Anybody know if MB can be absorbed through the skin? In college a few of my wrestling team mates swore it prevented ringworm.

It doesn't need to be absorbed through the skin to prevent ringworm. Ringworm is a fungal infection of the skin, and methylene blue is an antifungal compound, or at least that's how it's used in aquaria. The infection is probably in the top layers of the skin, where immune surveillance is not as good, so if the MB soaks into the superficial layer, that would probably do the trick. Just from looking at the molecule, I'd say it has a pretty good chance of being systemically available transdermally. The problem is, you would have no idea what dose you were actually getting systemically. Since dose is important here, and very small quantities are involved, it would be better to use it orally. At least that way, you won't look like a smurf.

[maxwatt]

Anybody know if MB can be absorbed through the skin? In college a few of my wrestling team mates swore it prevented ringworm.

It has a molecular weight of 319, so I think it would work, if you don't mind looking like a smurf.

You could apply it to the sole's of your feet...

[sdxl]

You could apply it topically with ascorbic acid without looking like a smurf.

[aaron43]

Methylene Blue is not a spermacide, it affects the mobility rate during the time of administration. It doesn't kill the boys, it just slows them down for the time being, its not a compromising issue.
Also I included that thread in those posts of links i put, it just on pg 4 or something like that. I found that forum incomplete as well, it has really good information but it I feel it lacks the anecdotal evidence that it needs to make a more common nootropic. That's what I'm trying to do with this thread.

[aaron43]

I found this interesting...

Methylene blue facilitates the extinction of fear in an animal model of susceptibility to learned helplessness

I know there can never be concrete statistical evidence of this occuring 100% of the time, but through subjective reviews it could be discovered

[Raptor87]

I found this interesting...

Methylene blue facilitates the extinction of fear in an animal model of susceptibility to learned helplessness

I know there can never be concrete statistical evidence of this occuring 100% of the time, but through subjective reviews it could be discovered

Holy shit! What is the pharmaceutical name of Methylene Blue? Why not order the drug instead and cut the dosage?

Along with CBT, hippocampal renewal and rewiring you amygdala (which is one explanation to the fear- relief) then this drug would be of great benefit.

[Raptor87]

I found this interesting...

Methylene blue facilitates the extinction of fear in an animal model of susceptibility to learned helplessness

I know there can never be concrete statistical evidence of this occuring 100% of the time, but through subjective reviews it could be discovered

Holy shit! What is the pharmaceutical name of Methylene Blue? Why not order the drug instead and cut the dosage?

Along with CBT, hippocampal renewal and rewiring you amygdala (which is one explanation to the fear- relief) then this drug would be of great benefit.

http://en.wikipedia....e_blue#Medicine
http://en.wikipedia...._methylene_blue

New methylene blue (also NMB) is an organic staining agent used in diagnostic cytopathology and histopathology, typically for staining immature red blood cells. It is closely related to methylene blue, an older stain already in wide use.

New methylene blue is toxic. Skin contact or inhalation should be avoided.

I wonder if Urised is still available for online order?

[aaron43]

More studies:

Methylene blue improves brain oxidative metabolism and memory retention in rats.

Methylene blue restores spatial memory retention impaired by an inhibitor of cytochrome oxidase in rats.

Extinction memory improvement by the metabolic enhancer methylene blue.

STRIATAL NEUROPROTECTION WITH METHYLENE BLUE

Edited by aaron43, 21 June 2011 - 07:00 PM.

[s123]

Methylene blue intercalates in the DNA so it should probably cause insertion and/or deletion mutations. When exposed to white light (e.g. in your skin) it produces ROS such as singlet oxygen (directly in the neighborhood of your DNA). Many evidence shows that methylene blue + white light induces mutations and causes lipid peroxidation.

Methylene blue plus visible light, in the presence of oxygen, induced lipid peroxidation in rat liver microsomes, as assessed by the formation of thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides and the loss of membrane-bound enzymes. Peroxidation was enhanced by deuteration of the buffer and inhibited by scavengers of singlet oxygen (1O2) and Superoxide (O2 ). The damage induced seemed to be mainly due to Type II involving 1O2 and to a lesser extent Type I reactions with O2 and hydroxyl radical (* OH) as intermediates. Nicotinamide or vitamin B3, an endogenous metabolite occurring at high concentrations in tissues, had a relatively high rate constant of 1.8 × 108M−1s−1 with 1O2 and had a significant inhibitory effect on lipid peroxidation induced by photosensitization. This effect was both time- and concentration-dependent, high inhibition being associated with millimolar concentrations. Chemically related endogenous compounds like tryptophan and isonicotinic acid also had significant inhibitory properties. Similar protective effects were observed with natural antioxidants such as β-carotene, canthaxanthin, lipoic acid, glutathione, α-tocopherol and to a lesser extent ascorbic acid. Nicotinamide was a more effective antioxidant than ascorbic acid. It also showed a similar inhibitory effect against NADPH-ADP-Fe3+-induced lipid peroxidation. Our results suggest that nicotinamide had significant ability to protect against photosensitization-induced cytotoxicity and cell damage and that it may do so by its ability to react with 1O2 and other reactive oxygen species.

http://www.sciencedi...009279795036539

Exposure to methylene blue (MB) plus light mediates formation of large levels of 8-hydroxyguanine in DNA. The amount of 8-hydroxy-2′-deoxyguanosine (8-OHdG) present in DNA increased as the amount of MB concentration increased throughout the 2 to 200 μ range studied and was dependent on light exposure. As the time of light exposure increased so did the 8-OHdG content to levels of about 750 8-OHdG/105 deoxyguanosine after 15 min of light exposure when MB was at 20 μ . Even though previous research has demonstrated that hydroxyl free radicals formed from a variety of sources mediate 8-OHdG formation in DNA, inclusion of mannitol, superoxide dismutase, catalase, and desferal in the MB plus light experiments demonstrated that these scavengers of oxygen free radical intermediates or precursors caused either no change or an increase in the 8-OHdG content of DNA exposed to MB plus light. These results appear to rule out the direct role of oxygen free radical intermediates in the primary events involved in the MB plus light mediated formation of 8-OHdG in DNA. Oxygen was essential to cause MB plus light mediated 8-OHdG formation in DNA. It was noted that when the reaction was carried out where the deuterium oxide content had been increased to 100%, the amount of 8-OHdG formed in DNA increased about threefold over that observed when comparable reactions were carried out in pure H2O. Use of the singlet oxygen scavenger 2,5-dimethylfuran has yielded variable results on the MB plus light mediated formation of 8-OHdG in DNA. The data taken collectively clearly indicate that MB plus light mediates 8-OHdG formation in DNA. The D2O data and the requirement for oxygen suggest that singlet oxygen may be an intermediate.

http://www.sciencedi...003986189901677

In aerobic conditions, visible light irradiation of fixed eukariotic chromosomes in dilute solutions of dyes dramatically alters chromosomal structure. Our results indirectly suggest that singlet oxygen, an electronically excited and therefore reactive form of oxygen, which is produced by visible light in the presence of methylene blue, may be responsible for chromosomal alteration.

http://www.sciencedi...045603980900317

Methylene blue trihydrate has a variety of biomedical and biologically therapeutic applications. Groups of 50 male and 50 female rats and mice were administered methylene blue trihydrate in 0.5% aqueous methylcellulose solution by gavage at doses of 0, 5, 25, or 50mg/kg bw/day (rats) or 0, 2.5, 12.5, and 25mg/kg bw/day (mice), 5 days per week for 2 years. In rats survival of all dosed groups was similar to that of the vehicle controls, whereas mice exhibited a dose-dependent increase in survival. Rats receiving 25 and 50mg/kg bw/day and mice receiving 25mg/kg bw/day developed mild anemia. The incidences of pancreatic islet cell adenoma and adenoma or carcinoma (combined) were increased in all dosed groups of male rats, but increases were statistically significant in 25mg/kg bw/day males only and the dose-response was non-linear. There was a corresponding increase in the incidence of pancreatic islet cell hyperplasia but statistically significant only in the 50mg/kg bw/day male rats. There were no significant increases in neoplastic transformation observed in the mice; however, positive trends were noted for adenoma or carcinoma (combined) of the small intestine and malignant lymphoma.

http://www.ncbi.nlm....pubmed/19804809

[Raptor87]

Does the drug alter DNA?

[aaron43]

Does the drug alter DNA?

Methylene Blue and New Methylene Blue are different. They are relatives, NMB is the toxic relative to Methylene Blue. http://en.wikipedia...._methylene_blue

[aaron43]

Methylene blue intercalates in the DNA so it should probably cause insertion and/or deletion mutations. When exposed to white light (e.g. in your skin) it produces ROS such as singlet oxygen (directly in the neighborhood of your DNA). Many evidence shows that methylene blue + white light induces mutations and causes lipid peroxidation.

Methylene blue plus visible light, in the presence of oxygen, induced lipid peroxidation in rat liver microsomes, as assessed by the formation of thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides and the loss of membrane-bound enzymes. Peroxidation was enhanced by deuteration of the buffer and inhibited by scavengers of singlet oxygen (1O2) and Superoxide (O2 ). The damage induced seemed to be mainly due to Type II involving 1O2 and to a lesser extent Type I reactions with O2 and hydroxyl radical (* OH) as intermediates. Nicotinamide or vitamin B3, an endogenous metabolite occurring at high concentrations in tissues, had a relatively high rate constant of 1.8 × 108M−1s−1 with 1O2 and had a significant inhibitory effect on lipid peroxidation induced by photosensitization. This effect was both time- and concentration-dependent, high inhibition being associated with millimolar concentrations. Chemically related endogenous compounds like tryptophan and isonicotinic acid also had significant inhibitory properties. Similar protective effects were observed with natural antioxidants such as β-carotene, canthaxanthin, lipoic acid, glutathione, α-tocopherol and to a lesser extent ascorbic acid. Nicotinamide was a more effective antioxidant than ascorbic acid. It also showed a similar inhibitory effect against NADPH-ADP-Fe3+-induced lipid peroxidation. Our results suggest that nicotinamide had significant ability to protect against photosensitization-induced cytotoxicity and cell damage and that it may do so by its ability to react with 1O2 and other reactive oxygen species.

http://www.sciencedi...009279795036539

Exposure to methylene blue (MB) plus light mediates formation of large levels of 8-hydroxyguanine in DNA. The amount of 8-hydroxy-2′-deoxyguanosine (8-OHdG) present in DNA increased as the amount of MB concentration increased throughout the 2 to 200 μ range studied and was dependent on light exposure. As the time of light exposure increased so did the 8-OHdG content to levels of about 750 8-OHdG/105 deoxyguanosine after 15 min of light exposure when MB was at 20 μ . Even though previous research has demonstrated that hydroxyl free radicals formed from a variety of sources mediate 8-OHdG formation in DNA, inclusion of mannitol, superoxide dismutase, catalase, and desferal in the MB plus light experiments demonstrated that these scavengers of oxygen free radical intermediates or precursors caused either no change or an increase in the 8-OHdG content of DNA exposed to MB plus light. These results appear to rule out the direct role of oxygen free radical intermediates in the primary events involved in the MB plus light mediated formation of 8-OHdG in DNA. Oxygen was essential to cause MB plus light mediated 8-OHdG formation in DNA. It was noted that when the reaction was carried out where the deuterium oxide content had been increased to 100%, the amount of 8-OHdG formed in DNA increased about threefold over that observed when comparable reactions were carried out in pure H2O. Use of the singlet oxygen scavenger 2,5-dimethylfuran has yielded variable results on the MB plus light mediated formation of 8-OHdG in DNA. The data taken collectively clearly indicate that MB plus light mediates 8-OHdG formation in DNA. The D2O data and the requirement for oxygen suggest that singlet oxygen may be an intermediate.

http://www.sciencedi...003986189901677

In aerobic conditions, visible light irradiation of fixed eukariotic chromosomes in dilute solutions of dyes dramatically alters chromosomal structure. Our results indirectly suggest that singlet oxygen, an electronically excited and therefore reactive form of oxygen, which is produced by visible light in the presence of methylene blue, may be responsible for chromosomal alteration.

http://www.sciencedi...045603980900317

Methylene blue trihydrate has a variety of biomedical and biologically therapeutic applications. Groups of 50 male and 50 female rats and mice were administered methylene blue trihydrate in 0.5% aqueous methylcellulose solution by gavage at doses of 0, 5, 25, or 50mg/kg bw/day (rats) or 0, 2.5, 12.5, and 25mg/kg bw/day (mice), 5 days per week for 2 years. In rats survival of all dosed groups was similar to that of the vehicle controls, whereas mice exhibited a dose-dependent increase in survival. Rats receiving 25 and 50mg/kg bw/day and mice receiving 25mg/kg bw/day developed mild anemia. The incidences of pancreatic islet cell adenoma and adenoma or carcinoma (combined) were increased in all dosed groups of male rats, but increases were statistically significant in 25mg/kg bw/day males only and the dose-response was non-linear. There was a corresponding increase in the incidence of pancreatic islet cell hyperplasia but statistically significant only in the 50mg/kg bw/day male rats. There were no significant increases in neoplastic transformation observed in the mice; however, positive trends were noted for adenoma or carcinoma (combined) of the small intestine and malignant lymphoma.

http://www.ncbi.nlm....pubmed/19804809

This should answer your question: http://www.longecity...ue/page__st__20
The sun doesn't produce enough energy for what you have said to happen.
Read pg 2,pg 3, it answers your question

[aaron43]

Does the drug alter DNA?

Im sorry, I responded to the wrong quote on my response to brainfogged. The answer is no, this is from pg 2 of the link I provided. It can alter DNA given circumstances, but these are usually extreme cirumstances and unlikely.

My previous post made simple:

**Visible light isn't powerful enough energy-wise to penetrate skin and cause dna or chromosomal damage.
***Then there was a proceeding argument about light to the retinas, if that would cause damage. Then it was answered that in the studies the light used caused dna damage a high energy wavelength, much more powerful than the sun, and that we don't even look at the sun at its strongest point directly. We always look at light from reflective resources.
****Then there was an even more proceeding argument which i forget was, but was answered with: The studies used in dna damage, or toxic events, are much much many times fold higher than what the recommended nootropic dose is. And the drug is still safe enough to be used in many medical settings at much higher without concern. And I'd assume in a patient room there is plenty of visible light.

"This photosensitization thing seems quite absurd, to me anyways. MB isn't something brand new. It's been around for ages, used at concentrations way beyond 100nM (~1mg!) in humans and no ill "photosensitization" effects have been reported to my knowledge. Considering ~200mg of MB is used routinely for methylhemoglobinemia, and anywhere from ~733mg (12mg/kg/day) to ~1,500mg (24mg/kg/day) in humans is used to treat malaria with few ill effects (the minimal dosage needed to see any toxic effect what so ever from MB is estimated around 600mg from the rat toxicological studies)... Yeah, I'm sorry, but these studies with crayfish neurons (sunlight is actually 137 mW/cm2 at nigh noon, staring directly into the sun; so the crayfish study used three times the amount of energy that sunlight has, and you already can't stare directly into the sun, MB notwithstanding) and fungi (which used mM amounts of MB in their study) just don't cut it for me. Also, do we even know what doses were used in PMID: 6603875? They did say that vitamin E completely stopped any photosensitization by MB, and considering the issue is singlet oxygen production, which is made constantly all the time in our bodies, including our eyes, I really don't worry - the human body is quite apt at not only dealing with but actually using super oxide for a variety of signals.

I have no doubt, and this is only my opinion, that you have nothing to worry about with your retina and MB at these doses, what so ever. Not to mention humans have a better antioxidant system than most creatures on this planet, and even many mammals, our retinas are not prone to failure by any direct "sensitization" effect, and retinas can heal quite well. It's only if you lose the optic nerve or degenerate the retina faster than it can heal (usually this is genetic) that you run into trouble; and I'm afraid MB at these dosages just isn't going to be able to do that. You'll lose your lens long before retina trouble, more likely than not, since the lens is one of the very rare things that aren't turned over."

Edited by chrono, 11 October 2011 - 08:35 PM.

[Raptor87]

Does the drug alter DNA?

Im sorry, I responded to the wrong quote on my response to brainfogged. The answer is no, this is from pg 2 of the link I provided. It can alter DNA given circumstances, but these are usually extreme cirumstances and unlikely.

"This photosensitization thing seems quite absurd, to me anyways. MB isn't something brand new. It's been around for ages, used at concentrations way beyond 100nM (~1mg!) in humans and no ill "photosensitization" effects have been reported to my knowledge. Considering ~200mg of MB is used routinely for methylhemoglobinemia, and anywhere from ~733mg (12mg/kg/day) to ~1,500mg (24mg/kg/day) in humans is used to treat malaria with few ill effects (the minimal dosage needed to see any toxic effect what so ever from MB is estimated around 600mg from the rat toxicological studies)... Yeah, I'm sorry, but these studies with crayfish neurons (sunlight is actually 137 mW/cm2 at nigh noon, staring directly into the sun; so the crayfish study used three times the amount of energy that sunlight has, and you already can't stare directly into the sun, MB notwithstanding) and fungi (which used mM amounts of MB in their study) just don't cut it for me. Also, do we even know what doses were used in PMID: 6603875? They did say that vitamin E completely stopped any photosensitization by MB, and considering the issue is singlet oxygen production, which is made constantly all the time in our bodies, including our eyes, I really don't worry - the human body is quite apt at not only dealing with but actually using super oxide for a variety of signals.

I have no doubt, and this is only my opinion, that you have nothing to worry about with your retina and MB at these doses, what so ever. Not to mention humans have a better antioxidant system than most creatures on this planet, and even many mammals, our retinas are not prone to failure by any direct "sensitization" effect, and retinas can heal quite well. It's only if you lose the optic nerve or degenerate the retina faster than it can heal (usually this is genetic) that you run into trouble; and I'm afraid MB at these dosages just isn't going to be able to do that. You'll lose your lens long before retina trouble, more likely than not, since the lens is one of the very rare things that aren't turned over."


My Experience with Methylene Blue

My first day: I bought Methylene blue from the aquarium last night. Prepared it, a 60 microgram solution, its very easy thing to do , you just need a eye dropper, a few cups and a measuring glass.

When I took it I felt great energy. My thoughts were easily facilitated, it was as if I got the stereotypical "this is how I am usually supposed to feel" feeling. Which this could actually be the case because its increasing metabolism in the places of your brain that need it.

This nootropic has a different feel to it. I can say it definitely takes away social anxiety no problem, because it feels like your young again, where your whole world is focused on what's in front of you. That was the biggest effect I noticed. The second biggest thing I noticed, is the learning after the fact process. I could say that MB does help with thinking while doing a task due to the relaxed nature of how you feel which I just described as reduced social anxiety, but I would say that the biggest nootropic effect is after the fact learning. I felt when I would read or do something, after I am done, I feel like I fully understand the subject thoroughly and can implement it from there on out, whether it is a life lesson or an academic lesson or even a logical lesson. I would say that methylene blue facilitates the idea "fool me once shame on you, fool me twice shame on me" but without the fool me twice, because the MB facilitated the full understanding of the subject after the first try. Sort of..kind of..like selectively putting what is in your long term memory. Ask me more questions, if you ask me a question Ill be able to answer it instead of me just rambling. MB also definetly increases the energy department, I have in the past always felt tired when I knew I shouldn't or I would get tired much faster than other people, and I feel like MB kicks that completely out the door. Not only do you get the energy from optimal mitochondrial processing, but I feel like most people get tired quickly due to stress, and it seems as if it eliminates stress (or makes stress not seem as monumental as people can make it) thus facilitating more energy with a relaxed state of mind.

There are more effects I will continue to right about when I come across them again. Im taking 60 micrograms right now each dosing, and I dose periodically, mostly 4 hours apart, we'll see what happens.

Smoking marijuana and Methylene Blue - Very Nice, I guess you can describe it as how people would idealize the typical marijuana experience: (no nervousness, boosted creativity, mood increase, and talkative)

I would also be interested if I could see the difference in ratio of compound to side effects of methylene blue compared to an adderall or even an SSRI that people are likely to be prescribed

Great answer! It´s so cheap also! But Im not buying something from an aquarium- shop, the bottles are so badly labelled! And then there is the dosing issue.

But it would be fun to retrain yourself and live normally. I have panic attacks and nothing has helped! I keep training everyday for the situation and have done so for 11 years, somehow my brain doesn't understand what's dangerous and what's not!.

Not even when I was on Efexor which is used for panic- attacks, it cured my severe anxiety but the panic remained.

But when a car hit me, I felt nothing! The driver was screaming, shaking and talking jibberish. I just told him to calm down. I got up, said that I was ok and limped away to a date. The date laughed at me because I was full of groceries!

So if there were better studies and minus the side- effects, then I would try it out.

Edited by Brainfogged, 22 June 2011 - 02:33 PM.