16 replies to this topic

[nebben]

Hi

Which one is better?

What are dis-/advantages for each?

Thankful for any help

nebben

[chomsky]

I would suggest a third option: simple L-Tyrosine.

N-acetyl-L-Tyrosine isn't absorbed very well:

Hepatology. 1995 Apr;21(4):923-8.

Utilization of tyrosine-containing dipeptides and N-acetyl-tyrosine in hepatic failure.

Druml W, Hubl W, Roth E, Lochs H.

Department of Medicine III, Vienna General Hospital, Austria.

The impact of hepatic dysfunction on the elimination and hydrolysis of three potential tyrosine sources for total parenteral nutrition, the dipeptides L-alanyl-L-tyrosine (Ala-Tyr) and glycyl-L-tyrosine (Gly-Tyr), and N-acetyl-L-tyrosine (Nac-Tyr) were evaluated in six patients with hepatic failure (five chronic, one acute) and seven healthy subjects. In controls, whole-body clearance (Cltot) of Ala-Tyr was higher than of Gly-Tyr (3,169 +/- 214 vs. 1,780 +/- 199 mL/kg/min, P < .01), and both exceeded clearance of Nac-Tyr (309 +/- 29 mL/kg/min, P > .01). Both dipeptides were hydrolyzed and released tyrosine immediately. In hepatic failure, elimination and hydrolysis of Ala-Tyr and Gly-Tyr were comparable to controls, but Cltot of Nac-Tyr was reduced (236 +/- 26 mL/kg/min). Neither in controls nor in patients an increase in plasma tyrosine concentration was seen after Nac-Tyr, and the major part of Nac-Tyr infused was lost in urine. The Cltot of tyrosine as evaluated after Ala-Tyr infusion (with the immediate release of tyrosine) was severely reduced in hepatic failure (152.7 +/- 38.4 vs. 484.4 +/- 41.4 mL/kg/min, P < .001) and half-life (kle) was retarded from 14.4 +/- 1.4 to 90.2 +/- 32.2 minutes (P < .03). The authors conclude that acute and chronic hepatic dysfunction does not affect elimination and hydrolysis of the dipeptides Ala-Tyr and Gly-Tyr and the constituent amino acids are released immediately. Nac-Tyr elimination was not grossly affected by hepatic failure, but neither in healthy subjects nor in hepatic failure patients was an increase of tyrosine seen. Both dipeptides but not Nac-Tyr may serve as a tyrosine source in parenteral nutrition. Moreover, by its rapid hydrolysis, the use of Ala-Tyr, for the first time, enables a simple rapid nonisotope evaluation of tyrosine kinetics for assessment of liver function.

L-Dopa is controversial -

Problem 1: Absorption. L-Dopa is is converted to dopamine in both the blood and brain via decarboxylase ezymes. Taking L-Dopa without a decarboxylase inhibitor (e.g. Carbidopa) may just increase peripheral dopamine without significant elevations in the CNS.

Problem 2: Neurotoxicity. A well documented condition called "Levodopa-induced dyskinesias" (LID) is assoicated with the side effects of levodopa therapy:

J Neural Transm. 2005 Mar;112(3):359-91. Epub 2004 Dec 22.

Levodopa-induced dyskinesia in Parkinson's disease.

Brotchie JM, Lee J, Venderova K.

Toronto Western Research Institute, MC 11-419, Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada. brotchie@uhnres.utoronto.ca

Levodopa-induced dyskinesias (LID) are abnormal involuntary movements that develop progressively with repeated dopamine replacement therapy in Parkinson's disease (PD). The pathophysiology of LID comprises many functionally-related abnormalities in neurotransmission which lead to abnormalities in the rate, pattern and synchronisation of neuronal activity within and outside the basal ganglia. In this review, we discuss the significance of the problem of LID, options currently available for avoiding and treating LID, recent advances in understanding the mechanisms responsible for the generation of LID once it has been established. In particular the discussion relates to the mechanisms underlying LID seen while levodopa is exerting its peak anti-parkinsonian actions, as it is this component of LID that is best modelled in animals and, to date, best understood. We do not aim to discuss the mechanisms by which LID is established and evolves, often termed priming, with repeated treatment, though this is an important area that has also witnessed significant advances recently (for recent review, see Blanchet et al., 2004). Finally, we define, where possible, the rationale for multiple novel therapeutic approaches that might help resolve the problem of LID.

L-Dopa shouldn't be taken, IMO, unless a disease-state (e.g Parkinson's) is being treated. Otherwise the side-effects far outweigh the supposed benefits to healthy humans.

I would stick with regular L-Tyrosine - it is cheaper, safer, and probably more effective than the other two pre-cursors.

[nebben]

What is the difference between the Tyrosines?
Are they all for human consumption?
Do they work as transmitter booster?


L-tyrosine
N-Acetyl-L-tyrosine
®-(-)-Nalpha-Benzyl-Nbeta-BOC-O-benzyl-D-hydrazinotyrosine
(S)-(+)-Nalpha-Benzyl-Nbeta-BOC-O-benzyl-L-hydrazinotyrosine
L-Tyrosine ethyl ester hydrochloride
BOC-D-Tyrosine
BOC-L-Tyrosine
N-Glycyl-L-tyrosine hydrate
N-Acetyl-L-phenylalanyl-3,5-diiodo-L-tyrosine
N-Benzoyl-L-tyrosine ethylester
O-Benzyl-L-tyrosine
D-Tyrosine
3-Nitro-L-tyrosine
N-(2-Chloroacetyl)-L-tyrosine
L-Tyrosine methyl ester hydrochloride
3,5-Diiodo-L-tyrosine dihydrate
O-Methyl-L-tyrosine
DL-Tyrosine
3-Fluoro-DL-tyrosine
L-Tyrosine hydrazide
DL-alpha-Methyltyrosine
L-Tyrosine methyl ester
DL-m-Tyrosine
3-Iodo-L-tyrosine
N-Acetyl-L-tyrosine ethyl ester monohydrate
3-Amino-L-tyrosine dihydrochloride monohydrate

Edited by nebben, 14 February 2006 - 11:18 PM.

[Bghead8che]

What is the difference between the Tyrosines?
Are they all for human consumption?
Do they work as transmitter booster?


L-tyrosine
N-Acetyl-L-tyrosine
®-(-)-Nalpha-Benzyl-Nbeta-BOC-O-benzyl-D-hydrazinotyrosine
(S)-(+)-Nalpha-Benzyl-Nbeta-BOC-O-benzyl-L-hydrazinotyrosine
L-Tyrosine ethyl ester hydrochloride
BOC-D-Tyrosine
BOC-L-Tyrosine
N-Glycyl-L-tyrosine hydrate
N-Acetyl-L-phenylalanyl-3,5-diiodo-L-tyrosine
N-Benzoyl-L-tyrosine ethylester
O-Benzyl-L-tyrosine
D-Tyrosine
3-Nitro-L-tyrosine
N-(2-Chloroacetyl)-L-tyrosine
L-Tyrosine methyl ester hydrochloride
3,5-Diiodo-L-tyrosine dihydrate
O-Methyl-L-tyrosine
DL-Tyrosine
3-Fluoro-DL-tyrosine
L-Tyrosine hydrazide
DL-alpha-Methyltyrosine
L-Tyrosine methyl ester
DL-m-Tyrosine
3-Iodo-L-tyrosine
N-Acetyl-L-tyrosine ethyl ester monohydrate
3-Amino-L-tyrosine dihydrochloride monohydrate

Ditto on the question. I assume Acetyl form would be best. Of all the choices which is preferred and why? Anyone know?

-Brian

[StrangeAeons]

your body develops tachyphalaxis to levodopa. It stops working within a year. Aside from that, it's a very very crude mechanism. If you're going to tweak your neurotransmitters, try some degree of selectivity.

[yoyo]

get some selegiline.

[Bghead8che]

get some selegiline.

Does anyone know the difference between the listed forms of Taurine? Which is bes?

[graatch]

I've used L-DOPA and PEA both worked well together or by themselves. L-DOPA 250-500 mg is usually noticeable in an hour or so. PEA 1-2 grams at once works in about 30 min or less.

L-DOPA would be the logical best choice for a dopamine precursor over L-Tyrosine.
PEA would also be the logical best choice over D-phenylalanine provided you dosed it high enough or added 1 mg of deprenyl.

Hi Steve.

[ortcloud]

Also consider vitamin d which rapidly increases the in‑vitro genetic expression of tyrosine hydroxylase (the rate‑limiting enzyme for the catecholamine biosynthesis)

[tripletandem]

I think PEA and deprenyl would cause the cheese effect.

no tyramine in PEA, no tyramine=no cheese effect. Regardless, you would have to take a substantial amount of deprenyl ( >10mg ) to even arrive at a minimal risk range for the "cheese effect". I hear good things about this combo, I'd check it out.

[mouse pad]

L-Dopa can also induce psychosis, and cause schizophrenic-like symptoms. I wouldn't take it.

[tripletandem]

Regarding selegiline and PEA, under 10mg\daily and however much PEA you want to take (within reason) seems not to be dangerous at all. At least as far as blood pressure\hypertension concerns. Relatively large amounts of the latter have been ingested with (15mg or less of) the former with no discernable effect on blood pressure or heart rate (in healthy individuals not more than 20lbs overweight). Also, based on my own personal reseach l-tyrosine in a normally functioning human body is the preferred route to replenish depleted dopamine stores (provided that is the only problem with your dopamanergic system).

[tripletandem]

Sorry I figure proper etiquette would be to post some study
http://www.ei-resour...hylamine-(pea)/

I don't know if I did that right, I'm kinda new at this. Anyways just google phenylethylamine+selegiline+depression. A million studys pop up to check out.

Edited by chrono, 24 October 2010 - 02:36 PM.
fixed link

[graatch]

no tyramine in PEA, no tyramine=no cheese effect. Regardless, you would have to take a substantial amount of deprenyl ( >10mg ) to even arrive at a minimal risk range for the "cheese effect"

PM
Regarding selegiline and PEA, under 10mg\daily and however much PEA you want to take (within reason) seems not to be dangerous at all. At least as far as blood pressure\hypertension concerns. Relatively large amounts of the latter have been ingested with (15mg or less of) the former with no discernable effect on blood pressure or heart rate (in healthy individuals not more than 20lbs overweight).

"Cheese effect" isn't the right term, but MAO-B inhibition = PEA not deaminated, as you note.

FWIW, 20mg of PEA with a MAO-B dose of deprenyl is almost too much for me. This is not a wild outlier in my view, looking at some of the n=1 experiences people have posted on various forums.

I hear good things about this combo, I'd check it out.

FWIW, that dose (again, 20mg with 5mg deprenyl) gives me an extremely jittery euphoria, like shitty cocaine, which lasts all of about 20 minutes followed by a fuzzy crash. Not for me. The studies that were done are indeed promising. I'd start with a low dose though, if you try it.