Reversing Wrinkled Skin And Hair Loss In Mice By Restoring Mitochondrial Function

[ddjd]

(BCAA) seem to induce mitochondrial biogenesis.

That's interesting. Where did you read about that

 

[Vinero]

That's interesting. Where did you read about that

Can a Power Booster Also Be a Longevity Booster | Life Extension

 

[Progesterone]

Can someone please tell me if this means MB is pro-erections or anti-erections:

"In rats, the intracavernous injection of drugs that act on the adenosine-3′5′-cyclic monophosphate (cAMP) and cGMP pathways revealed that neither cAMP nor drugs that stimulate adenylate cyclase activity induced any change in intracavernosal pressure [25]. In contrast, the intracavernosal injection of cGMP and SNP caused dose-dependent changes in intracavernous pressure that could be inhibited by methylene blue (a guanylate cyclase inhibitor). It was therefore concluded that cavernous smooth muscle relaxation in the rat is mediated by activation of guanylate cyclase and that the cAMP system only plays a minimal role [25]."

Nitric oxide and penile erection: Is erectile dysfunction another manifestation of vascular disease? | Cardiovascular Research | Oxford Academic

From what I understand, MB is pro-erections:

"
NO plays a major role in the physiological regulation of penile erection. NO elicits these effects through the activation of guanylate cyclase and the subsequent production of cGMP. Impaired NO activity appears to play an important role in the pathogenesis of erectile dysfunction. This impaired NO activity may be similar to that which occurs in other forms of vascular disease or in the presence of cardiovascular risk factors (e.g. smoking, dyslipidaemia, diabetes and hypertension).

The recent development of an effective, orally active, type V PDE inhibitor (sildenafil) provides a novel method of therapy for patients with erectile dysfunction. It achieves this by inhibiting the hydrolysis of cGMP, produced via the L-arginine-NO pathway."

"In contrast, the intracavernosal injection of cGMP and SNP caused dose-dependent changes in intracavernous pressure that could be inhibited by methylene blue (a guanylate cyclase inhibitor)"

"Another pathway that is potentially useful as a pharmacological target for the treatment of ED is the particulate guanylate cyclase (pGC).[32,77] This membrane-bound enzyme is the target for endogenous natriuretic peptides such as atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), C-type natriuretic peptide, and guanylin peptides such as uroguanylin (UGN). Three subtypes (A, B and C) have been identified with different affinities for the various peptides. Both ANP and UGN have been studied in vitro for their human corpus-cavernosum (HCC) relaxant capacities. Both were able to enhance relaxation of HCC strips versus vehicle in organ-bath experiments. This relaxant capacity of UGN (this experiment was not conducted with ANP) was mediated in large part by a rise in intracellular cGMP and was not influenced by the addition of L-NAME, a NOS inhibitor, nor by ODQ, a sGC specific inhibitor.[78] These results may hold promise for the future treatment of ED in patients who lack endogenous NO supply."

OR NOT... ????????

Methylene blue as a successful treatment alternative for pharmacologically induced priapism. - PubMed - NCBI

"Recent findings indicate methylene blue (MB), a guanylate cyclase inhibitor, to be a potential inhibitor of endothelial-mediated cavernous relaxation. This prompted us to assess the feasibility, use and effectiveness of MB in the treatment of priapism."

 

[ddjd]

Can someone please tell me if this means MB is pro-erections or anti-erections:

"In rats, the intracavernous injection of drugs that act on the adenosine-3′5′-cyclic monophosphate (cAMP) and cGMP pathways revealed that neither cAMP nor drugs that stimulate adenylate cyclase activity induced any change in intracavernosal pressure [25]. In contrast, the intracavernosal injection of cGMP and SNP caused dose-dependent changes in intracavernous pressure that could be inhibited by methylene blue (a guanylate cyclase inhibitor). It was therefore concluded that cavernous smooth muscle relaxation in the rat is mediated by activation of guanylate cyclase and that the cAMP system only plays a minimal role [25]."

Nitric oxide and penile erection: Is erectile dysfunction another manifestation of vascular disease? | Cardiovascular Research | Oxford Academic

From what I understand, MB is pro-erections:

"
NO plays a major role in the physiological regulation of penile erection. NO elicits these effects through the activation of guanylate cyclase and the subsequent production of cGMP. Impaired NO activity appears to play an important role in the pathogenesis of erectile dysfunction. This impaired NO activity may be similar to that which occurs in other forms of vascular disease or in the presence of cardiovascular risk factors (e.g. smoking, dyslipidaemia, diabetes and hypertension).

The recent development of an effective, orally active, type V PDE inhibitor (sildenafil) provides a novel method of therapy for patients with erectile dysfunction. It achieves this by inhibiting the hydrolysis of cGMP, produced via the L-arginine-NO pathway."

"In contrast, the intracavernosal injection of cGMP and SNP caused dose-dependent changes in intracavernous pressure that could be inhibited by methylene blue (a guanylate cyclase inhibitor)"

"Another pathway that is potentially useful as a pharmacological target for the treatment of ED is the particulate guanylate cyclase (pGC).[32,77] This membrane-bound enzyme is the target for endogenous natriuretic peptides such as atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), C-type natriuretic peptide, and guanylin peptides such as uroguanylin (UGN). Three subtypes (A, B and C) have been identified with different affinities for the various peptides. Both ANP and UGN have been studied in vitro for their human corpus-cavernosum (HCC) relaxant capacities. Both were able to enhance relaxation of HCC strips versus vehicle in organ-bath experiments. This relaxant capacity of UGN (this experiment was not conducted with ANP) was mediated in large part by a rise in intracellular cGMP and was not influenced by the addition of L-NAME, a NOS inhibitor, nor by ODQ, a sGC specific inhibitor.[78] These results may hold promise for the future treatment of ED in patients who lack endogenous NO supply."

OR NOT... ????????

Methylene blue as a successful treatment alternative for pharmacologically induced priapism. - PubMed - NCBI

"Recent findings indicate methylene blue (MB), a guanylate cyclase inhibitor, to be a potential inhibitor of endothelial-mediated cavernous relaxation. This prompted us to assess the feasibility, use and effectiveness of MB in the treatment of priapism."

No methylene blue will reduce errections. Nitric oxide and estrogen are both generally high during errections. My libido plummets when I'm on methylene blue.

One beer is estrogenic enough to get me excited though

 

[Progesterone]

No methylene blue will reduce errections. Nitric oxide and estrogen are both generally high during errections. My libido plummets when I'm on methylene blue.

One beer is estrogenic enough to get me excited though

Darn, that's no good, thx.

Are the hair benefits apparent at least?

 

[Mito]

"The first free radical that forms inside a cell is superoxide, and Methylene Blue binds to superoxide to fully reduce it to water.

Well Dr. Gonzalez-Lima claims MB reduces superoxide to to water but Travis says MB lowers the concentration of nitric oxide by converting it to superoxide. Maybe it depends on the concentration of MB? Haidut has posted that it requires a dose in the tens of milligrams of MB to scavenge nitric oxide. Famotidine Is A Powerful Scavenger Of Nitric Oxide (NO)

 

[Mito]

1mg-2mg a day in humans is not considered a large dose right?

I was referring to a large dose as tens of milligrams as Haidut had posted about that being the dose required for methylene blue to act as a nitric oxide scavenger. As for methylene blue reducing nitric oxide into superoxide and then peroxynitrite (per the @Travis post), I don’t know what concentration of methylene blue is required for methylene blue to generate peroxynitrite.

I think Ray has said that the optimal effects of MB on mitochondria are from ~1mg doses.

@Mito you believe MB is very beneficial for scalp hair, correct?

Probably anything that improves mitochondria function is beneficial for scalp hair. Some studies suggest methylene blue has the potential to improve some aspects of mitochondrial function.

 

[cats]

I was referring to a large dose as tens of milligrams as Haidut had posted about that being the dose required for methylene blue to act as a nitric oxide scavenger. As for methylene blue reducing nitric oxide into superoxide and then peroxynitrite (per the @Travis post), I don’t know what concentration of methylene blue is required for methylene blue to generate peroxynitrite.

I think Ray has said that the optimal effects of MB on mitochondria are from ~1mg doses.

Probably anything that improves mitochondria function is beneficial for scalp hair. Some studies suggest methylene blue has the potential to improve some aspects of mitochondrial function.

Maybe those events are not entirely mutually exclusive? If the pathway is methylene blue + nitric oxide = superoxide, followed by methylene blue + superoxide = water.

 

[Lejeboca]

I think Ray has said that the optimal effects of MB on mitochondria are from ~1mg doses.

Found a link to Peat's response about <1mg doses by way of haidut:

Here is where he says doses <1mg are optimal.

viewtopic.php?f=10&t=5344&p=69191&hilit=methylene+blue+therapeutic+effects#p69191

 

[JohnHafterson]

Glycine works:

Epigenetic regulation of the nuclear-coded GCAT and SHMT2 genes confers human age-associated mitochondrial respiration defects

 

[Captain_Coconut]

I’m pretty sure the various forms of SOD and its mimetics will also stop the oxidative stress cascade before superoxide has a chance to inflict damage. I have felt much greater pain relief and energy from copper aspirinate than I have from small to mega doses of M. Blue. The most I have noticed from MB is ocassional wired mental states, it has never helped me with pain.

 

[Pablo Cruise]

Back to Mitochondria LLL such as in the hairloss helmets has much data to support increased mitochondria function.

I take on occasion 100mg of MB for mood. I also took it for the brain as I was taking many tests. Did it help my brain, who knows. I can't say I have noticed any effect short term or other with its use upon my hair. I use reagent grade granules and make a 1% solution in water. (1gm in 100ml distilled water)