Psycho-Babble Medication Thread 884577

Shown: posts 1 to 13 of 13. This is the beginning of the thread.

 

Sustained stimulation with L-Tyrosine + Nardil

Posted by myco on March 9, 2009, at 10:30:17

Interesting note on L-Tyrosine with Nardil:

I've been toying with tiny dosages of L-Tyrosine (100-150mg; even these are too high) to augment Nardil (75mg). This stuff appears to build up quite nicely...I imagine with disrespect or ignorance one could wind up in trouble with this stuff on a maoi and not even know it until days down the road. Taken at 100mg twice a day for 3 days straight (that was 4 days ago that I stopped), I am still feeling mild stimulatory effects in my system...some irritability and insomnia goes along with it...actually broke my nice sleep pattern I had going there for awhile. Since we know that tyrosine will deplete seratonin, I will toy next with tiny bits of 5-htp to try to "cancel" out the effect. Logically, I can't see why it wouldnt work since I suspect the NE effect is the ongoing stimulation here.

Any thoughts?

myco

 

Re: Sustained stimulation with L-Tyrosine + Nardil

Posted by bulldog2 on March 9, 2009, at 13:41:31

In reply to Sustained stimulation with L-Tyrosine + Nardil, posted by myco on March 9, 2009, at 10:30:17

> Interesting note on L-Tyrosine with Nardil:
>
> I've been toying with tiny dosages of L-Tyrosine (100-150mg; even these are too high) to augment Nardil (75mg). This stuff appears to build up quite nicely...I imagine with disrespect or ignorance one could wind up in trouble with this stuff on a maoi and not even know it until days down the road. Taken at 100mg twice a day for 3 days straight (that was 4 days ago that I stopped), I am still feeling mild stimulatory effects in my system...some irritability and insomnia goes along with it...actually broke my nice sleep pattern I had going there for awhile. Since we know that tyrosine will deplete seratonin, I will toy next with tiny bits of 5-htp to try to "cancel" out the effect. Logically, I can't see why it wouldnt work since I suspect the NE effect is the ongoing stimulation here.
>
> Any thoughts?
>
> myco

You might want to try l-phenylalanine. That way you also get some pea.

 

5-HTP confirmed to lower Tyrosine stimulation myco

Posted by myco on March 9, 2009, at 16:06:12

In reply to Sustained stimulation with L-Tyrosine + Nardil, posted by myco on March 9, 2009, at 10:30:17

I added a wee bit (~20mg) of 5-htp this morning and it has successfully taken a bite out of the ongoing stimulation from tyrosine.

I think this confirms the inverse relationship between dopamine/norepinephrine and seratonin.

The combination of these two (L-Tyrosine & 5-HTP) in very small doses work well as augments for Nardil, at least in this trial. I think one of the benefits of these two is that they are easily adjustable for a best ratio of effect. I've also been reading that 5-htp should be taken with an aromatic L-amino acid decarboxylase such as EGCG (a catechin in green tea/extract) to prevent seratonin synthesis in the blood (as opposed to the brain).


---------

> Interesting note on L-Tyrosine with Nardil:
>
> I've been toying with tiny dosages of L-Tyrosine (100-150mg; even these are too high) to augment Nardil (75mg). This stuff appears to build up quite nicely...I imagine with disrespect or ignorance one could wind up in trouble with this stuff on a maoi and not even know it until days down the road. Taken at 100mg twice a day for 3 days straight (that was 4 days ago that I stopped), I am still feeling mild stimulatory effects in my system...some irritability and insomnia goes along with it...actually broke my nice sleep pattern I had going there for awhile. Since we know that tyrosine will deplete seratonin, I will toy next with tiny bits of 5-htp to try to "cancel" out the effect. Logically, I can't see why it wouldnt work since I suspect the NE effect is the ongoing stimulation here.
>
> Any thoughts?
>
> myco

 

Re: Sustained stimulation with L-Tyrosine + Nardil bulldog2

Posted by myco on March 9, 2009, at 16:09:37

In reply to Re: Sustained stimulation with L-Tyrosine + Nardil, posted by bulldog2 on March 9, 2009, at 13:41:31

> You might want to try l-phenylalanine. That way you also get some pea.

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

Hey Bulldog,

What advantages does PEA have? I havent got there yet really. How do you use it properly, where does it fit in biochemically etc..


 

Re: Sustained stimulation with L-Tyrosine + Nardil

Posted by bulldog2 on March 9, 2009, at 16:55:37

In reply to Re: Sustained stimulation with L-Tyrosine + Nardil bulldog2, posted by myco on March 9, 2009, at 16:09:37

> > You might want to try l-phenylalanine. That way you also get some pea.
>
> -------------
>
> Hey Bulldog,
>
> What advantages does PEA have? I havent got there yet really. How do you use it properly, where does it fit in biochemically etc..
>
>
>
>
>
>
>

There's been experiments with l-phenyalanine and low dose selegiline. Apparently pea has ad properties. It's a nice feel good chemical that is found in chocolate. So with l-phenyalanine you would get conversion to tyrosine and pea.
However since pea is related to amphetemine make sure you can use l-phenyalanine with nardil with bp problems.

 

Re: 5-HTP confirmed to lower Tyrosine stimulation

Posted by desolationrower on March 9, 2009, at 21:55:27

In reply to 5-HTP confirmed to lower Tyrosine stimulation myco, posted by myco on March 9, 2009, at 16:06:12

> I added a wee bit (~20mg) of 5-htp this morning and it has successfully taken a bite out of the ongoing stimulation from tyrosine.
>
> I think this confirms the inverse relationship between dopamine/norepinephrine and seratonin.
>
> The combination of these two (L-Tyrosine & 5-HTP) in very small doses work well as augments for Nardil, at least in this trial. I think one of the benefits of these two is that they are easily adjustable for a best ratio of effect. I've also been reading that 5-htp should be taken with an aromatic L-amino acid decarboxylase such as EGCG (a catechin in green tea/extract) to prevent seratonin synthesis in the blood (as opposed to the brain).
>
>
>
>
> ---------

i don't know why it was written that would help...if you stop 5ht synthesis in the gut, you also stop it in the brain. EGCG passes the bbb...carbidopa doesn't thats why it is used

-d/r

 

Re: 5-HTP confirmed to lower Tyrosine stimulation desolationrower

Posted by myco on March 9, 2009, at 22:36:57

In reply to Re: 5-HTP confirmed to lower Tyrosine stimulation, posted by desolationrower on March 9, 2009, at 21:55:27

I've read the opposite in a few studies...seems EGCG doesn't pass the blood brain barrier at all...merely inhibits AADC in the gut resulting in lower periferal seratonin and dopamine.

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

> i don't know why it was written that would help...if you stop 5ht synthesis in the gut, you also stop it in the brain. EGCG passes the bbb...carbidopa doesn't thats why it is used
>
> -d/r

 

Re: 5-HTP confirmed to lower Tyrosine stimulation myco

Posted by myco on March 9, 2009, at 22:43:32

In reply to Re: 5-HTP confirmed to lower Tyrosine stimulation desolationrower, posted by myco on March 9, 2009, at 22:36:57

AADC's (I know of 3 thus far) act both in the periphery and in the cns.

See:

Turner et al. 2006. Seratonin a la carte: Supplementation with the seratonin precursor 5-hydroxytryptophan. Pharmacology & Therapeutics. Mar;109(3):325-38.

in press version available for free here:
(http://www.uoregon.edu/~ablackwe/Documents/5-HTP.Pharm.Therap.pdf)


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

> I've read the opposite in a few studies...seems EGCG doesn't pass the blood brain barrier at all...merely inhibits AADC in the gut resulting in lower periferal seratonin and dopamine.
>
> ------------
>
> > i don't know why it was written that would help...if you stop 5ht synthesis in the gut, you also stop it in the brain. EGCG passes the bbb...carbidopa doesn't thats why it is used
> >
> > -d/r
>
>

 

Re: 5-HTP confirmed to lower Tyrosine stimulation myco

Posted by myco on March 9, 2009, at 22:48:22

In reply to Re: 5-HTP confirmed to lower Tyrosine stimulation myco, posted by myco on March 9, 2009, at 22:43:32

In fact by inhibiting AADC's in the gut you actually increase sythesis of dopamine and seratonin in the cns. There is no detrimental effect I can see based on the results i've looked at.

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


> AADC's (I know of 3 thus far) act both in the periphery and in the cns.
>
> See:
>
> Turner et al. 2006. Seratonin a la carte: Supplementation with the seratonin precursor 5-hydroxytryptophan. Pharmacology & Therapeutics. Mar;109(3):325-38.
>
> in press version available for free here:
> (http://www.uoregon.edu/~ablackwe/Documents/5-HTP.Pharm.Therap.pdf)
>
>
> ----------------
>
> > I've read the opposite in a few studies...seems EGCG doesn't pass the blood brain barrier at all...merely inhibits AADC in the gut resulting in lower periferal seratonin and dopamine.
> >
> > ------------
> >
> > > i don't know why it was written that would help...if you stop 5ht synthesis in the gut, you also stop it in the brain. EGCG passes the bbb...carbidopa doesn't thats why it is used
> > >
> > > -d/r
> >
> >
>
>

 

Re: 5-HTP confirmed to lower Tyrosine stimulation myco

Posted by myco on March 9, 2009, at 23:42:29

In reply to Re: 5-HTP confirmed to lower Tyrosine stimulation myco, posted by myco on March 9, 2009, at 22:48:22

I hope I dont get in trouble for the 4th post here but....

The idea that inhibiting AADC in the gut to boost effects in the cns is actually the basis for therapy strategies to increase bioavailability of medications. My next nardil experiment will be conducted with green tee extract in slowly increasing doses taken with nardil (same time) on an empty stomach with the cofacter for AADC's (vit B6).

See (for a good new study on this d/r):

Nagai et al. 2009. Inhibitory Effects of Herbal Extracts on the Activity of Human
Sulfotransferase Isoform Sulfotransferase 1A3 (SULT1A3). Biol Pharm Bull. Jan;32(1):105-9.

link:

(http://www.jstage.jst.go.jp/article/bpb/32/1/105/_pdf)


myco

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


> In fact by inhibiting AADC's in the gut you actually increase sythesis of dopamine and seratonin in the cns. There is no detrimental effect I can see based on the results i've looked at.
>
> --------------
>
>
> > AADC's (I know of 3 thus far) act both in the periphery and in the cns.
> >
> > See:
> >
> > Turner et al. 2006. Seratonin a la carte: Supplementation with the seratonin precursor 5-hydroxytryptophan. Pharmacology & Therapeutics. Mar;109(3):325-38.
> >
> > in press version available for free here:
> > (http://www.uoregon.edu/~ablackwe/Documents/5-HTP.Pharm.Therap.pdf)
> >
> >
> > ----------------
> >
> > > I've read the opposite in a few studies...seems EGCG doesn't pass the blood brain barrier at all...merely inhibits AADC in the gut resulting in lower periferal seratonin and dopamine.
> > >
> > > ------------
> > >
> > > > i don't know why it was written that would help...if you stop 5ht synthesis in the gut, you also stop it in the brain. EGCG passes the bbb...carbidopa doesn't thats why it is used
> > > >
> > > > -d/r
> > >
> > >
> >
> >
>
>

 

Re: 5-HTP confirmed to lower Tyrosine stimulation

Posted by desolationrower on March 10, 2009, at 1:46:00

In reply to Re: 5-HTP confirmed to lower Tyrosine stimulation myco, posted by myco on March 9, 2009, at 23:42:29

Absorption and distribution of tea catechin, (-)-epigallocatechin-3-gallate, in the rat.

Nakagawa K, Miyazawa T.

Food Chemistry Laboratory, Faculty of Agriculture, Tohoku University, Sendai, Japan.

To investigate the absorption and metabolism of an anticarcinogenic tea catechin, (-)-epigallocatechin-3-gallate (EGCg), in rats, a newly developed chemiluminescence-detection high-performance liquid chromatography (CL-HPLC) method was employed and the EGCg concentrations in blood plasma, liver, brain, small intestinal mucosa and colon mucosa were determined before and after EGCg administration. The recovery of EGCg, extracted consecutively with ethyl acetate and methanol, was 86.1% from plasma and 64.5-74.2% from the tissue samples. The EGCg concentrations of plasma and tissue samples from the control rat (before EGCg administration) were all below the detection limit (< 0.002 nmol/mL, 0.002 nmol/g), but 60 min after a single oral administration of EGCg (500 mg/kg body weight), the levels increased, reaching 12.3 nmol/mL in plasma, 48.4 nmol/g in liver, 0.5 nmol/g in brain, 565 nmol/g in small intestinal mucosa and 68.6 nmol/g in colon mucosa. The EGCg levels found in the tissues corresponded to 0.0003-0.45% of ingested EGCg. The results indicate that tea catechin, EGCg, is absorbed from the digestive tract, with the intestinal mucosa the most enriched of the organelles. This may explain the potent antioxidant function of EGCg in inhibiting colon mucosal phospholipid hydroperoxidation in the prevention of rat colonic carcinogenesis.

Neuroprotection and neurorescue against A&#946;toxicity and PKC-dependent release of non-amyloidogenic soluble precursor protein by green tea polyphenol (-)- epigallocatechin-3-gallate
Yona Levites, Tamar Amit, Silvia Mandel, and Moussa B. H. Youdim

E-mail contact: Youdim{at}Tx.Technion.ac.il

Green tea extract and its main polyphenol constituent (-)-epigallocatechin-3-gallate (EGCG) possess potent neuroprotective activity in cell culture and mice model of Parkinsons disease. The central hypothesis guiding this study is that EGCG may play an important role in amyloid precursor protein (APP) secretion and protection against toxicity induced by &#946;-amyloid (A&#946;). The present study shows that EGCG enhances (~6-fold) the release of the non-amyloidogenic soluble form of the amyloid precursor protein (sAPP&#945;) into the conditioned media of human SH-SY5Y neuroblastoma and rat pheochromocytoma PC12 cells. sAPP&#945; release was blocked by the hydroxamic acid-based metalloprotease inhibitor Ro319790, which indicated mediation via &#945;-secretase activity. Inhibition of protein kinase C (PKC) with the inhibitor GF109203X, or by down-regulation of PKC, blocked the EGCG-induced sAPP&#945; secretion, suggesting the involvement of PKC. Indeed, EGCG induced the phosphorylation of PKC, thus identifying a novel PKC-dependent mechanism of EGCG action by activation of the non-amyloidogenic pathway. EGCG is not only able to protect, but it can rescue PC12 cells against the &#946;-amyloid (A&#946;) toxicity in a dose-dependent manner. In addition, administration of EGCG (2 mg/kg) to mice for 7 or 14 days significantly decreased membrane-bound holoprotein APP levels, with a concomitant increase in sAPP&#945; levels in the hippocampus. Consistently, EGCG markedly increased PKC&#945; and PKC&#949; in the membrane and the cytosolic fractions of mice hippocampus. Thus, EGCG has protective effects against A&#946;-induced neurotoxicity and regulates secretory processing of non-amyloidogenic APP via PKC pathway.

Wide distribution of [3H](-)-epigallocatechin gallate, a cancer preventive tea polyphenol, in mouse tissue

M Suganuma, S Okabe, M Oniyama, Y Tada, H Ito and H Fujiki
Saitama Cancer Center Research Institute, Japan. masami@saitama-cc.go.jp

The increasing recognition of green tea and tea polyphenols as cancer preventives has created a need for a study of their bioavailability. For this purpose, we synthesized [3H] (-)-epigallocatechin gallate ([3H]EGCG) with a specific activity of 48.1 GBq/mmol and directly administered the solution into the stomachs of CD-1 female or male mice. Radioactivity in the digestive tract, various organs, blood, urine and feces was measured with an oxidizer at various times after administration and significant radioactivity was found in the previously reported target organs of EGCG and green tea extract (digestive tract, liver, lung, pancreas, mammary gland and skin), as well as other organs (brain, kidney, uterus and ovary and testes) in both sexes. Incorporation of radioactivity in the cells was confirmed by microautoradiography. Within 24 h, 6.6 (females) and 6.4% (males) of total administered radioactivity was excreted in the urine and 37.7 and 33.1% in feces. HPLC analysis of urine from both sexes revealed that 0.03-0.59% of administered [3H]EGCG, along with at least five metabolites, was excreted. In addition, we found that a second, equal administration to female mice after a 6 h interval enhanced tissue levels of radioactivity in blood, brain, liver, pancreas, bladder and bone 4-6 times above those after a single administration. These results suggest that frequent consumption of green tea enables the body to maintain a high level of tea polyphenols and this paper is the first pharmacological evidence of a wide distribution of [3H]EGCG in mouse organs, indicating a similar wide range of target organs for cancer prevention in humans.

I don't see any mention of EGCG/green tea in the first study, and the second on is in reference to some phase II enzyme affecting Dopamine, which is not the same as l-dopa/5-htp. And, theres like a million studies on green tea improving outcomes of various measure of brain health.

-d/r

 

Re: 5-HTP confirmed to lower Tyrosine stimulation desolationrower

Posted by myco on March 10, 2009, at 11:24:58

In reply to Re: 5-HTP confirmed to lower Tyrosine stimulation, posted by desolationrower on March 10, 2009, at 1:46:00

I'm not sure exactly what your referring to based on what I had posted...I just woke up here lol and bear with me as i'm a pharm noob and still learning

The reason I'm looking at this is a theory I have that i'm investigating regarding increasing bioavailability of nardil.

SULT1A3 (Nagai et al.) catalyzes the sulfation (I think thats the right way to say it) of dopamine and ritodrine in the intestine...inhibiting or acting as a detoxifying enzyme for many compounds of similar structure.

Since EGCG (an aromatic L-amino acid decarboxylase - AADC) from green tea has been shown to inhibit the activity of SULT1A3 in the intestine thus increasing bioavailability (inhibiting peripheral formation) of dopamine and ritodrine (Natai et al.) in the CNS, it could be possible that it could also increase bioavailability of Nardil. Not many studies have looked at phenelzine in this way that I know of.

If you look at the general structure of dopamine and ritodrine you will see that they are very similar to phenelzine (pointed out to me by Larry Hoover). It's quite possible that SULT1A3 has an unknown effect on the breakdown of phenelzine (recall all the complaints of the "new" nardil and it's "subpar" effect - I believe issues with absorption and bioavailability). Larry also confirmed the possibility of this theory actually working.

I'm struggling a lil bit with the idea of totally understanding this, have emailed some research docs and still no response yet, but I think there is something here to be looked at.

Myco


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

> Absorption and distribution of tea catechin, (-)-epigallocatechin-3-gallate, in the rat.
>
> Nakagawa K, Miyazawa T.
>
> Food Chemistry Laboratory, Faculty of Agriculture, Tohoku University, Sendai, Japan.
>
> To investigate the absorption and metabolism of an anticarcinogenic tea catechin, (-)-epigallocatechin-3-gallate (EGCg), in rats, a newly developed chemiluminescence-detection high-performance liquid chromatography (CL-HPLC) method was employed and the EGCg concentrations in blood plasma, liver, brain, small intestinal mucosa and colon mucosa were determined before and after EGCg administration. The recovery of EGCg, extracted consecutively with ethyl acetate and methanol, was 86.1% from plasma and 64.5-74.2% from the tissue samples. The EGCg concentrations of plasma and tissue samples from the control rat (before EGCg administration) were all below the detection limit (< 0.002 nmol/mL, 0.002 nmol/g), but 60 min after a single oral administration of EGCg (500 mg/kg body weight), the levels increased, reaching 12.3 nmol/mL in plasma, 48.4 nmol/g in liver, 0.5 nmol/g in brain, 565 nmol/g in small intestinal mucosa and 68.6 nmol/g in colon mucosa. The EGCg levels found in the tissues corresponded to 0.0003-0.45% of ingested EGCg. The results indicate that tea catechin, EGCg, is absorbed from the digestive tract, with the intestinal mucosa the most enriched of the organelles. This may explain the potent antioxidant function of EGCg in inhibiting colon mucosal phospholipid hydroperoxidation in the prevention of rat colonic carcinogenesis.
>
> Neuroprotection and neurorescue against A&#946;toxicity and PKC-dependent release of non-amyloidogenic soluble precursor protein by green tea polyphenol (-)- epigallocatechin-3-gallate
> Yona Levites, Tamar Amit, Silvia Mandel, and Moussa B. H. Youdim
>
> E-mail contact: Youdim{at}Tx.Technion.ac.il
>
> Green tea extract and its main polyphenol constituent (-)-epigallocatechin-3-gallate (EGCG) possess potent neuroprotective activity in cell culture and mice model of Parkinsons disease. The central hypothesis guiding this study is that EGCG may play an important role in amyloid precursor protein (APP) secretion and protection against toxicity induced by &#946;-amyloid (A&#946;). The present study shows that EGCG enhances (~6-fold) the release of the non-amyloidogenic soluble form of the amyloid precursor protein (sAPP&#945;) into the conditioned media of human SH-SY5Y neuroblastoma and rat pheochromocytoma PC12 cells. sAPP&#945; release was blocked by the hydroxamic acid-based metalloprotease inhibitor Ro319790, which indicated mediation via &#945;-secretase activity. Inhibition of protein kinase C (PKC) with the inhibitor GF109203X, or by down-regulation of PKC, blocked the EGCG-induced sAPP&#945; secretion, suggesting the involvement of PKC. Indeed, EGCG induced the phosphorylation of PKC, thus identifying a novel PKC-dependent mechanism of EGCG action by activation of the non-amyloidogenic pathway. EGCG is not only able to protect, but it can rescue PC12 cells against the &#946;-amyloid (A&#946;) toxicity in a dose-dependent manner. In addition, administration of EGCG (2 mg/kg) to mice for 7 or 14 days significantly decreased membrane-bound holoprotein APP levels, with a concomitant increase in sAPP&#945; levels in the hippocampus. Consistently, EGCG markedly increased PKC&#945; and PKC&#949; in the membrane and the cytosolic fractions of mice hippocampus. Thus, EGCG has protective effects against A&#946;-induced neurotoxicity and regulates secretory processing of non-amyloidogenic APP via PKC pathway.
>
> Wide distribution of [3H](-)-epigallocatechin gallate, a cancer preventive tea polyphenol, in mouse tissue
>
> M Suganuma, S Okabe, M Oniyama, Y Tada, H Ito and H Fujiki
> Saitama Cancer Center Research Institute, Japan. masami@saitama-cc.go.jp
>
> The increasing recognition of green tea and tea polyphenols as cancer preventives has created a need for a study of their bioavailability. For this purpose, we synthesized [3H] (-)-epigallocatechin gallate ([3H]EGCG) with a specific activity of 48.1 GBq/mmol and directly administered the solution into the stomachs of CD-1 female or male mice. Radioactivity in the digestive tract, various organs, blood, urine and feces was measured with an oxidizer at various times after administration and significant radioactivity was found in the previously reported target organs of EGCG and green tea extract (digestive tract, liver, lung, pancreas, mammary gland and skin), as well as other organs (brain, kidney, uterus and ovary and testes) in both sexes. Incorporation of radioactivity in the cells was confirmed by microautoradiography. Within 24 h, 6.6 (females) and 6.4% (males) of total administered radioactivity was excreted in the urine and 37.7 and 33.1% in feces. HPLC analysis of urine from both sexes revealed that 0.03-0.59% of administered [3H]EGCG, along with at least five metabolites, was excreted. In addition, we found that a second, equal administration to female mice after a 6 h interval enhanced tissue levels of radioactivity in blood, brain, liver, pancreas, bladder and bone 4-6 times above those after a single administration. These results suggest that frequent consumption of green tea enables the body to maintain a high level of tea polyphenols and this paper is the first pharmacological evidence of a wide distribution of [3H]EGCG in mouse organs, indicating a similar wide range of target organs for cancer prevention in humans.
>
> I don't see any mention of EGCG/green tea in the first study, and the second on is in reference to some phase II enzyme affecting Dopamine, which is not the same as l-dopa/5-htp. And, theres like a million studies on green tea improving outcomes of various measure of brain health.
>
> -d/r

 

Re: 5-HTP confirmed to lower Tyrosine stimulation myco

Posted by myco on March 10, 2009, at 11:40:36

In reply to Re: 5-HTP confirmed to lower Tyrosine stimulation desolationrower, posted by myco on March 10, 2009, at 11:24:58

If you were wondering how 5-htp fits into this from what I was going on about earlier....5-htp is given with carbidopa (another AADC - like EGCG from green tea). Carbidopa has been studied well so I was using the studies of 5-htp and AADC's, in general, to develope my idea. Thats all. Not sure if that fits into your confusion on what I was getting at.

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


> I'm not sure exactly what your referring to based on what I had posted...I just woke up here lol and bear with me as i'm a pharm noob and still learning
>
> The reason I'm looking at this is a theory I have that i'm investigating regarding increasing bioavailability of nardil.
>
> SULT1A3 (Nagai et al.) catalyzes the sulfation (I think thats the right way to say it) of dopamine and ritodrine in the intestine...inhibiting or acting as a detoxifying enzyme for many compounds of similar structure.
>
> Since EGCG (an aromatic L-amino acid decarboxylase - AADC) from green tea has been shown to inhibit the activity of SULT1A3 in the intestine thus increasing bioavailability (inhibiting peripheral formation) of dopamine and ritodrine (Natai et al.) in the CNS, it could be possible that it could also increase bioavailability of Nardil. Not many studies have looked at phenelzine in this way that I know of.
>
> If you look at the general structure of dopamine and ritodrine you will see that they are very similar to phenelzine (pointed out to me by Larry Hoover). It's quite possible that SULT1A3 has an unknown effect on the breakdown of phenelzine (recall all the complaints of the "new" nardil and it's "subpar" effect - I believe issues with absorption and bioavailability). Larry also confirmed the possibility of this theory actually working.
>
> I'm struggling a lil bit with the idea of totally understanding this, have emailed some research docs and still no response yet, but I think there is something here to be looked at.
>
> Myco
>
>
>
>
> ------------------
>
>
>
> > Absorption and distribution of tea catechin, (-)-epigallocatechin-3-gallate, in the rat.
> >
> > Nakagawa K, Miyazawa T.
> >
> > Food Chemistry Laboratory, Faculty of Agriculture, Tohoku University, Sendai, Japan.
> >
> > To investigate the absorption and metabolism of an anticarcinogenic tea catechin, (-)-epigallocatechin-3-gallate (EGCg), in rats, a newly developed chemiluminescence-detection high-performance liquid chromatography (CL-HPLC) method was employed and the EGCg concentrations in blood plasma, liver, brain, small intestinal mucosa and colon mucosa were determined before and after EGCg administration. The recovery of EGCg, extracted consecutively with ethyl acetate and methanol, was 86.1% from plasma and 64.5-74.2% from the tissue samples. The EGCg concentrations of plasma and tissue samples from the control rat (before EGCg administration) were all below the detection limit (< 0.002 nmol/mL, 0.002 nmol/g), but 60 min after a single oral administration of EGCg (500 mg/kg body weight), the levels increased, reaching 12.3 nmol/mL in plasma, 48.4 nmol/g in liver, 0.5 nmol/g in brain, 565 nmol/g in small intestinal mucosa and 68.6 nmol/g in colon mucosa. The EGCg levels found in the tissues corresponded to 0.0003-0.45% of ingested EGCg. The results indicate that tea catechin, EGCg, is absorbed from the digestive tract, with the intestinal mucosa the most enriched of the organelles. This may explain the potent antioxidant function of EGCg in inhibiting colon mucosal phospholipid hydroperoxidation in the prevention of rat colonic carcinogenesis.
> >
> > Neuroprotection and neurorescue against A&#946;toxicity and PKC-dependent release of non-amyloidogenic soluble precursor protein by green tea polyphenol (-)- epigallocatechin-3-gallate
> > Yona Levites, Tamar Amit, Silvia Mandel, and Moussa B. H. Youdim
> >
> > E-mail contact: Youdim{at}Tx.Technion.ac.il
> >
> > Green tea extract and its main polyphenol constituent (-)-epigallocatechin-3-gallate (EGCG) possess potent neuroprotective activity in cell culture and mice model of Parkinsons disease. The central hypothesis guiding this study is that EGCG may play an important role in amyloid precursor protein (APP) secretion and protection against toxicity induced by &#946;-amyloid (A&#946;). The present study shows that EGCG enhances (~6-fold) the release of the non-amyloidogenic soluble form of the amyloid precursor protein (sAPP&#945;) into the conditioned media of human SH-SY5Y neuroblastoma and rat pheochromocytoma PC12 cells. sAPP&#945; release was blocked by the hydroxamic acid-based metalloprotease inhibitor Ro319790, which indicated mediation via &#945;-secretase activity. Inhibition of protein kinase C (PKC) with the inhibitor GF109203X, or by down-regulation of PKC, blocked the EGCG-induced sAPP&#945; secretion, suggesting the involvement of PKC. Indeed, EGCG induced the phosphorylation of PKC, thus identifying a novel PKC-dependent mechanism of EGCG action by activation of the non-amyloidogenic pathway. EGCG is not only able to protect, but it can rescue PC12 cells against the &#946;-amyloid (A&#946;) toxicity in a dose-dependent manner. In addition, administration of EGCG (2 mg/kg) to mice for 7 or 14 days significantly decreased membrane-bound holoprotein APP levels, with a concomitant increase in sAPP&#945; levels in the hippocampus. Consistently, EGCG markedly increased PKC&#945; and PKC&#949; in the membrane and the cytosolic fractions of mice hippocampus. Thus, EGCG has protective effects against A&#946;-induced neurotoxicity and regulates secretory processing of non-amyloidogenic APP via PKC pathway.
> >
> > Wide distribution of [3H](-)-epigallocatechin gallate, a cancer preventive tea polyphenol, in mouse tissue
> >
> > M Suganuma, S Okabe, M Oniyama, Y Tada, H Ito and H Fujiki
> > Saitama Cancer Center Research Institute, Japan. masami@saitama-cc.go.jp
> >
> > The increasing recognition of green tea and tea polyphenols as cancer preventives has created a need for a study of their bioavailability. For this purpose, we synthesized [3H] (-)-epigallocatechin gallate ([3H]EGCG) with a specific activity of 48.1 GBq/mmol and directly administered the solution into the stomachs of CD-1 female or male mice. Radioactivity in the digestive tract, various organs, blood, urine and feces was measured with an oxidizer at various times after administration and significant radioactivity was found in the previously reported target organs of EGCG and green tea extract (digestive tract, liver, lung, pancreas, mammary gland and skin), as well as other organs (brain, kidney, uterus and ovary and testes) in both sexes. Incorporation of radioactivity in the cells was confirmed by microautoradiography. Within 24 h, 6.6 (females) and 6.4% (males) of total administered radioactivity was excreted in the urine and 37.7 and 33.1% in feces. HPLC analysis of urine from both sexes revealed that 0.03-0.59% of administered [3H]EGCG, along with at least five metabolites, was excreted. In addition, we found that a second, equal administration to female mice after a 6 h interval enhanced tissue levels of radioactivity in blood, brain, liver, pancreas, bladder and bone 4-6 times above those after a single administration. These results suggest that frequent consumption of green tea enables the body to maintain a high level of tea polyphenols and this paper is the first pharmacological evidence of a wide distribution of [3H]EGCG in mouse organs, indicating a similar wide range of target organs for cancer prevention in humans.
> >
> > I don't see any mention of EGCG/green tea in the first study, and the second on is in reference to some phase II enzyme affecting Dopamine, which is not the same as l-dopa/5-htp. And, theres like a million studies on green tea improving outcomes of various measure of brain health.
> >
> > -d/r
>
>


This is the end of the thread.


Show another thread

URL of post in thread:


Psycho-Babble Medication | Extras | FAQ


[dr. bob] Dr. Bob is Robert Hsiung, MD, bob@dr-bob.org

Script revised: February 4, 2008
URL: http://www.dr-bob.org/cgi-bin/pb/mget.pl
Copyright 2006-17 Robert Hsiung.
Owned and operated by Dr. Bob LLC and not the University of Chicago.