Dr. Van Konynenburg had previous post a few times on a well established pattern of Accutane causing a hyperactive Glycine N-Methyltransferase (1-6).
http://forums.phoenixrising.me/inde...ed-depression-isotretinoin.12117/#post-206039
http://forums.phoenixrising.me/inde...h-can-you-pitch-in-on-this.16078/#post-257280
As Rich explains Glycine N-Methyltransferase which regulates the ratio of SAMe to SAH. If hyperactive in the way that the cited research says, SAMe is quickly converted to SAH, losing its methyl group to glycine.
I would agree that it would be tough to overcome that force to rebuild the methylation cycle without the right intervention.
Rich said that for some it was persistently in a locked increased activity/expression even after stopping Accutane. And noted that this enzyme is allosterically inhibited by Methyl-folate, as is documented in the literature (5-6).
I wonder if anyone on the board tried higher doses of methyl-folate this and what doses they tried? What was the outcome?
1. "All-trans-Retinoic Acid Rapidly Induces Glycine N-methyltransferase in a Dose-Dependent Manner and Reduces Circulating Methionine and Homocysteine Levels in Rats," http://nutrition.highwire.org/content/133/12/4090.full
2. "Retinoic Acid and Glucocorticoid Treatment Induce Hepatic Glycine N-Methyltransferase and Lower Plasma Homocysteine Concentrations in Rats and Rat Hepatoma Cells," http://jn.nutrition.org/content/133/11/3392.full
3. "Activation and induction of glycine N-methyltransferase by retinoids are tissue- and gender-specific," http://www.ncbi.nlm.nih.gov/pubmed/12054489
4. "Decreased plasma folate concentration in young and elderly healthy subjects after a short-term supplementation with isotretinoin," http://onlinelibrary.wiley.com/doi/...sCustomisedMessage=&userIsAuthenticated=false
5. "Inhibition of glycine N-methyltransferase by folate derivatives: implications for regulation of methyl group metabolism," http://www.sciencedirect.com/science/article/pii/S0006291X85800061
6. "Phosphorylation modulates the activity of glycine N-methyltransferase, a folate binding protein. In vitro phosphorylation is inhibited by the natural ligand," http://www.jbc.org/content/264/16/9638.full.pdf
http://forums.phoenixrising.me/inde...ed-depression-isotretinoin.12117/#post-206039
http://forums.phoenixrising.me/inde...h-can-you-pitch-in-on-this.16078/#post-257280
As Rich explains Glycine N-Methyltransferase which regulates the ratio of SAMe to SAH. If hyperactive in the way that the cited research says, SAMe is quickly converted to SAH, losing its methyl group to glycine.
I would agree that it would be tough to overcome that force to rebuild the methylation cycle without the right intervention.
Rich said that for some it was persistently in a locked increased activity/expression even after stopping Accutane. And noted that this enzyme is allosterically inhibited by Methyl-folate, as is documented in the literature (5-6).
I wonder if anyone on the board tried higher doses of methyl-folate this and what doses they tried? What was the outcome?
1. "All-trans-Retinoic Acid Rapidly Induces Glycine N-methyltransferase in a Dose-Dependent Manner and Reduces Circulating Methionine and Homocysteine Levels in Rats," http://nutrition.highwire.org/content/133/12/4090.full
2. "Retinoic Acid and Glucocorticoid Treatment Induce Hepatic Glycine N-Methyltransferase and Lower Plasma Homocysteine Concentrations in Rats and Rat Hepatoma Cells," http://jn.nutrition.org/content/133/11/3392.full
3. "Activation and induction of glycine N-methyltransferase by retinoids are tissue- and gender-specific," http://www.ncbi.nlm.nih.gov/pubmed/12054489
4. "Decreased plasma folate concentration in young and elderly healthy subjects after a short-term supplementation with isotretinoin," http://onlinelibrary.wiley.com/doi/...sCustomisedMessage=&userIsAuthenticated=false
5. "Inhibition of glycine N-methyltransferase by folate derivatives: implications for regulation of methyl group metabolism," http://www.sciencedirect.com/science/article/pii/S0006291X85800061
6. "Phosphorylation modulates the activity of glycine N-methyltransferase, a folate binding protein. In vitro phosphorylation is inhibited by the natural ligand," http://www.jbc.org/content/264/16/9638.full.pdf