76 replies to this topic

[thedevinroy]

L-Tyrosine, the precursor to L-DOPA, is converted to L-DOPA via the enzyme Tyrosine Hydroxylase. This is the rate limiting factor in conversion from tyrosine to dopamine.

Decreasing Selenium Increases Dopamine Levels in Rats: http://www.ncbi.nlm..../pubmed/8600301

We have studied the turnover of dopamine, noradrenaline, and serotonin and their metabolites in hippocampus of adult female rats that were fed control or selenium-deficient diets during 15 days. Under these circumstances, there was an increase of dopamine turnover (4-fold) in rats fed with selenium-deficient diet with respect to controls and also an increase in the tyrosine hydroxylase activity (75.8%), which was the result of the increase of the amount of the enzyme (2-fold), without significant change in the phosphorylation of the tyrosine hydroxylase. In addition the glutathione peroxidase, glutathione reductase, catalase, and superoxide dismutase activities have been studied. After selenium-deficient diet, the enzymatic activities of superoxide dismutase and catalase did not show change with respect to the controls; however glutathione reductase and glutathione peroxidase significantly decreased 15% and 29%, respectively. It is concluded that the increase in dopamine turnover seems to be associated with the induction of tyrosine hydroxylase enzyme. In these conditions the decrease in antioxidant capacity may produce a cascade of events, which accelerates the degenerative process, since the increase in dopamine turnover produces an increase in oxygen radical by monoamine oxidase activity.

Stay away from yeast, I guess. And take a MAO-B inhibitor to prevent that free radical damage.

cAMP and Glucocorticoid steroids: http://www.ncbi.nlm..../pubmed/6113272

More From Pubmed: http://www.google.co...+hydroxylase%22

I believe certain stimulants also increase the activity of the enzyme, such as amphetamine and methylphenidate.

Thoughts?

Edited by devinthayer, 18 July 2011 - 09:31 PM.

[thedevinroy]

Also, I have to add... I only feel tyrosine working when taken with fruit or juice. I think it has to do with Vitamin C. To properly make dopamine and norepinephrine from precursors, I believe you needyou need NADH (B3 + ADP), Vitamin B6 (PLP), Vitamin C, and a methyl doner like TMG or SAMe.

Edited by devinthayer, 18 July 2011 - 09:26 PM.

[rwac]

Is it the vitamin C or the sugar causing an insulin response?

[thedevinroy]

Since insulin is more of a downer, I would say it is probably Vitamin C, which decreases insulin... if it is indeed insulin that caused an increase in vigilance, mood, and concentration and not Vitamin C as a co-factor in monoamine reactions.

[The Human Meteorite]

Tyrosine hydroxylase is hypothesized to be responsible for the increase in risk of schizophrenia caused by the toxoplasma gondii virus. Just putting that out there.

[thedevinroy]

Tyrosine hydroxylase is hypothesized to be responsible for the increase in risk of schizophrenia caused by the toxoplasma gondii virus. Just putting that out there.

Of course! Too much dopamine activity is associated with schizophrenia. Many antipsychotics treat this overload and "fix" the confusion. Dopamine is further converted into noradrenaline, adrenaline, and then metabolites. If my memory serves me correctly, schizophrenia is caused by the body's inability to break down or remove certain metabolites of the dopaminergic and adrenergic types caused by O-methylation into DMPEA and stuff. Tyrosine hydroxylase just adds an OH group to a phenyl ring, so... it's a bit further back in the process, but schizos have no more Catechol O-methyltransferase (http://www.ncbi.nlm....gov/pubmed/3250) than a normal person, so it does make sense that lowering dopamine levels would treat schizophrenia.

If you are a healthy individual, a slight increase in dopamine isn't going to make you schizophrenic, even over time. However, like I mentioned before, an MAO-B would be a good addition, in order to avoid too much L-DOPAC (http://en.wikipedia....enylacetic_acid).

Edited by devinthayer, 19 July 2011 - 03:05 AM.

[rwac]

Since insulin is more of a downer, I would say it is probably Vitamin C, which decreases insulin... if it is indeed insulin that caused an increase in vigilance, mood, and concentration and not Vitamin C as a co-factor in monoamine reactions.

No, I mean an insulin surge drives things into cells along with glucose, like creatine and protein.
Sugar creates an insulin surge.

[Delta Gamma]

BDNF and lithium have been shown to upregulate TH, and I used to have the full text for the second link before BL went off for maintenance.

http://www.ncbi.nlm..../pubmed/9523597
http://onlinelibrary...67020443.x/full
doi:10.1016/0006-8993(95)00215-C

[thedevinroy]

Since insulin is more of a downer, I would say it is probably Vitamin C, which decreases insulin... if it is indeed insulin that caused an increase in vigilance, mood, and concentration and not Vitamin C as a co-factor in monoamine reactions.

No, I mean an insulin surge drives things into cells along with glucose, like creatine and protein.
Sugar creates an insulin surge.

In that case, it could have been a group effort. The insulin from the sugar could have driven the vitamin C and tyrosine into my cells which then helped to make dopamine. Then the Vitamin C could have lowered insulin levels, causing more of a lift. Either way, fruit is good stuff along side of tyrosine.

[thedevinroy]

BDNF and lithium have been shown to upregulate TH, and I used to have the full text for the second link before BL went off for maintenance.

http://www.ncbi.nlm..../pubmed/9523597
http://onlinelibrary...67020443.x/full
doi:10.1016/0006-8993(95)00215-C

Do you take lithium? If so, do you take it before bed? I imagine it has somewhat of a stabilizing effect like GABA or magnesium, even at the nootropic dose.

[thedevinroy]

Lithium increases tyrosine hydroxylase levels both in vivo and in vitro. (http://www.ncbi.nlm..../pubmed/9523597)

Lithium, a simple monovalent cation, is the mainstay in the treatment of manic-depressive illness, but despite extensive research, its mechanism of action remains to be elucidated. Because lithium requires chronic administration for therapeutic efficacy and because its beneficial effects last well beyond its discontinuation, it has been postulated that lithium may exert major effects at the genomic level. We have previously shown that lithium, at therapeutically relevant concentrations, increases gene expression through the activator protein-1 (AP-1) transcription factor pathway in vitro. In the present study, we have sought to determine if lithium also increases the expression of endogenous genes known to be regulated by AP-1 and have therefore investigated the effects of lithium on tyrosine hydroxylase (TH) levels. Male Wistar rats were treated with LiCl for 9 days (subacute) or 4 weeks (chronic), and TH levels were measured in frontal cortex, hippocampus, and striatum using immunoblotting. Chronic (but not subacute) lithium treatment resulted in significant increases in TH levels in rat frontal cortex, hippocampus, and striatum. Lithium (1 mM) also increased TH levels in human SH-SY5Y neuroblastoma cells in vitro, indicating that lithium increases TH levels in both rodent and human tissues, likely via a direct cellular effect. These effects are compatible with (but likely not exclusively due to) an effect on the DNA binding of the 12-O-tetradecanoylphorbol 13-acetate response element to the AP-1 family of transcription factors.

That seems a bit high of a concentration. I think 1mM is one milli mole, which means 6.941mg of Lithium per liter. That's quite a bit more than the nootropic dose. Perhaps it also works at lower concentrations? I haven't the full text to see if they did tested effects of other concentrations, but I did find this abstract (http://www.ncbi.nlm....pubmed/10364437):

In the present study, several doses of lithium chloride were tested for their ability to induce the expression of tyrosine hydroxylase (TH) in neurons derived from a human teratocarcinoma cell line (hNT) after 5 and 10 days in vitro (DIV). Following immunocytochemical staining for tyrosine hydroxylase, the percentage of TH-positive neurons was determined and morphometric analysis, including mean soma profile area and neuritic length, was performed. hNT neurons responded to lithium treatment in a dose-dependent manner. In 5 DIV, the most effective dose of lithium chloride (1.0 mM) increased the number of TH-positive neurons approximately sixfold. In addition, both TH-positive hNT neuron mean soma profile area and neurite length were significantly larger than controls by 60 and 70%, respectively. Moreover, even after withdrawal of lithium chloride on day 5, the number of TH-positive neurons in 10 DIV cultures remained significantly increased. These data suggest that hNT cells are indeed responsive to lithium exposure and may serve as a continual source of TH-expressing neurons in new therapeutic approaches to degenerative brain disease.

Indeed! Note the last bold phrase, "may serve as a continual source of TH-expressing neurons". This sounds like lithium, over time, can cause a semi-permanent increase in dopamine levels. I'd like to see more in vivo studies, so I did a search and found something else interesting. Lithium treats and prevents Parkinson's (http://www.ncbi.nlm....pubmed/15111020):

Lithium has been reported to exert neuroprotective activity in several neuronal cell cultures and in vivo models against glutamate toxicity. Since this action was reported to be associated with alterations in the antiapoptotic Bcl-2 family proteins, the effect of chronic lithium diet on the ability of the parkinsonism neurotoxin, N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to deplete striatal dopamine in mice was determined. Mice were fed for with a diet containing 1.1, 2.2, 3.3, and 4.4 g/kg lithium chloride (LiCl) for 4 weeks, during which time serum levels of lithium were monitored. The 3.3 g/kg lithium diet gave serum level value very similar to what is observed in lithium therapy in man and the 4.4 g/kg well above this. At the end of this period the mice received 24 mg/kg MPTP i.p. once daily for 3 days. A direct relation was established with the increase in serum lithium and its ability to prevent MPTP induced depletion of striatal dopamine (DA) and its metabolites DPOAC and HVA. With the diet containing the highest lithiumconcentration there was an almost complete prevention of striatal dopamine depletion and the reduction in tyrosine hydroxylase activity and protein and it prevented the increase in dopamine turnover (DOPAC + HVA/DA) normally observed in MPTP treatment. Lithium did not interfere with the metabolism of MPTP, or with its brain uptake, since, the level of its monoamine oxidase (MAO) B derived metabolite, MPP+, in the striata of lithium and non-lithium treated mice were almost identical. Striatal Bcl-2 was significantly decreased, while Bax was increased in MPTP treated mice. Lithium treatment not only increased striatal Bcl-2 in control mice, but also prevented its reduction as induced by MPTP, and an opposing effect was seen with Bax. The neuroprotective action of lithium in this model of Parkinson's disease has been attributed to its antiapoptotic activity which among other factors includes induction of Bcl-2 and reduction of Bax.

Also I found this study where Lithium prevents Meth-induced reduction of tyrosine hydroxylase (TH) (http://www.ncbi.nlm....14/?tool=pubmed):

Previous studies found that Meth decreases TH staining as a marker for dopaminergic neurons (Deng et al. 2007). We investigated TH levels in the prefrontal cortex after Meth treatment with or without chronic pretreatment with lithium or VPA. We found that TH levels were significantly lower in prefrontal cortex after 1 d of Meth treatment, an effect that was prevented by pretreatment with lithium or VPA; this suggests that these agents protect against Meth-induced reductions in TH levels (Fig. 6). ß-actin was used as a loading control. Under similar conditions, we also investigated the general neuronal marker neuron-specific enolase (NSE). Levels of NSE and actin remained unchanged, suggesting that the effects of lithium and VPA on TH are relatively specific (data not shown).

Other than those few studies, I can't find much on lower doses of Lithium long term and it's effects on tyrosine hydroxylase.

Edited by devinthayer, 19 July 2011 - 06:07 PM.

[Delta Gamma]

BDNF and lithium have been shown to upregulate TH, and I used to have the full text for the second link before BL went off for maintenance.

http://www.ncbi.nlm..../pubmed/9523597
http://onlinelibrary...67020443.x/full
doi:10.1016/0006-8993(95)00215-C

Do you take lithium? If so, do you take it before bed? I imagine it has somewhat of a stabilizing effect like GABA or magnesium, even at the nootropic dose.

Never used lithium but I do have a strong interest in its pharmacology. J.Galt raved about it in the "amphetamine neurotoxicity reduction/prevention" thread at doses of what I'm guessing were about 20mg/day. I also have a friend who uses really low dose lithium for her depression and mood swings (40mg/day or something like that) and she's been happy with that dose for over a year now.

Unfortunately almost all the research on lithium focuses on chronic high dose lithium, but given the fact that differences in ground water concentrations of lithium can have a notable effect on large populations of people it definitely seems active at ~20mg a day. However, lithium does have several side effects which may limit its usefulness. But, its worth a shot if you've got a decent metabolism.

http://bjp.rcpsych.o...tract/198/5/346
http://www.unt.edu/h...Fs/Flanagan.pdf
http://www.ncbi.nlm....les/PMC3114818/

[thedevinroy]

Here is an interesting Study: http://www.ncbi.nlm....pubmed/15249143

Nicotinic and muscarinic acetylcholine receptors are essential for the long-term response of tyrosine hydroxylase gene expression to chronic nicotine treatment in rat adrenal medulla.

Nicotine induces tyrosine hydroxylase (TH) mRNA by interacting with nicotinic acetylcholine receptors (nAChRs) in cultured adrenal medullary cell systems; however, the mechanisms responsible for the induction of adrenal TH in response to systemically administered nicotine under in vivo conditions are more complex. In the present study, we tested whether nAChRs and muscarinic acetylcholine receptors (mAChRs) participate in the induction of adrenal TH observed after long-term treatment with nicotine. Chronic nicotine treatment (1.6 mg/kg, two daily injections spaced 12 h apart for 7 days) induced TH mRNA, TH protein and TH activity in rat adrenal medulla. This induction of TH gene expression was totally blocked when an antagonist of either nAChRs or mAChRs was administered prior to each nicotine injection. Repeated injections of the mAChR agonist bethanechol (5 mg/kg injected twice per day for 7 days) also produced increases in TH mRNA levels; however, TH protein levels and TH activity did not increase in response to bethanechol. In denervated adrenal glands chronic nicotine treatment did not lead to induction of either TH mRNA, TH protein or TH activity, whereas chronic bethanechol treatment led to induction of TH mRNA, but not TH protein or activity. These results suggest that agonist occupation of both nAChRs and mAChRs are essential for the complete response of TH gene expression to chronic nicotine treatment in rat adrenal medulla, but that stimulation of either cholinergic receptor by itself is not sufficient to elicit a full response. The results also suggest that both transcriptional and post-transcriptional mechanisms may potentially need to be regulated to induce TH protein in response to some stimuli.

Ahem... raising acetylcholine levels increases tyrosine hydroxylase.

That would explain a lot.

[QuantumTubule]

Dopamine is converted in vivo into SA 4503, food for thought.
GDNF increases TH positive neurons in certain circumstances........

[canz]

I just started 500mg of Tyrosine 3x per day in between meals, and noticed an increase in mood. ESPECIALLY in the morning when I eat two tangerines with my dose....explains alot. I think I'll eat a tangerine with each dose.

It kind of reminds me of when my buddies used to use LSD when I was younger they would carry around a bottle of orange juice claiming it creates greater effects of the LSD.

[thedevinroy]

Dopamine is converted in vivo into SA 4503, food for thought.
GDNF increases TH positive neurons in certain circumstances........

SA 4503 sounds like a trip. Sigma receptor agonist... like DMT and cocaine. Probably one of the metabolites schizophrenics are tripping on.

How might I go about increasing GDNF? Any nootropics OTC or herbal that do that?

[thedevinroy]

From http://www.ncbi.nlm..../pubmed/9011759:

Vitamin D increases expression of the tyrosine hydroxylase gene in adrenal medullary cells.


We examined expression of the 1,25-dihydroxyvitamin D3 [1,25-(OH)2 D3] receptors in chromaffin cells of the adrenal medulla and the effects of 1,25(OH)2 D3 on expression of the tyrosine hydroxylase (TH) gene. Accumulation of 1,25(OH)2 D3 in the nuclei of adrenal medullary cells, but not in the adrenal cortex, was observed in mice intravenously injected with radioactively labeled hormone. 1,25(OH)2 D3 produced concentration-dependent increases in the TH mRNA levels in cultured bovine adrenal medullary cells (BAMC). The maximal increases (2-3-fold) occurred at 10(-8) M 1,25(OH)2 D3. Combined treatment with 1,25(OH)2 D3 and 20 microM nicotine had no additive effect on TH mRNA levels suggesting that transsynaptic (nicotinic) and vitamin D (hormonal) stimulation of TH gene expression are mediated through converging mechanisms. Induction of TH mRNA by 1,25(OH)2 D3 was not affected by calcium antagonist TMB-8. By increasing expression of the rate limiting enzyme in the catecholamine biosynthetic pathway, 1,25-(OH)2 D3 may participate in the regulation of catecholamine production in adrenal chromaffin cells. This regulation provides mechanisms through which 1,25(OH)2 D3 may control response and adaptation to stress.

[manic_racetam]

So would it have a greater effect to supplement with L-tyrosine and increase levels of tyrosine hydroxylase or just supplement with pure L-Dopa?

Doesn't l-tyrosine just increase dopamine concentrations centrally, rather than in specific regions of the brain?

Don't know how I've overlooked this supplement for so long, just bought some today.

[QuantumTubule]

An interesting thing about GDNF is that it displays positive feedback to an extent. That is increased GDNF increase GDNF.
About increasing GDNF, i remember that Royal jelly does this, there are a few more. There is a great article about GDNF around on imminst.

[thedevinroy]

An interesting thing about GDNF is that it displays positive feedback to an extent. That is increased GDNF increase GDNF.
About increasing GDNF, i remember that Royal jelly does this, there are a few more. There is a great article about GDNF around on imminst.

Found a study on Royal Jelly and BDNF: http://www.jstage.js...69_800/_article

Oral Administration of Royal Jelly Facilitates mRNA Expression of Glial Cell Line-Derived Neurotrophic Factor and Neurofilament H in the Hippocampus of the Adult Mouse Brain.

Royal jelly (RJ) is known to have a variety of biological activities toward various types of cells and tissues of animal models, but nothing is known about its effect on brain functions. Hence, we examined the effect of oral administration of RJ on the mRNA expression of various neurotrophic factors, their receptors, and neural cell markers in the mouse brain. Our results revealed that RJ selectively facilitates the mRNA expression of glial cell line-derived neurotrophic factor (GDNF), a potent neurotrophic factor acting in the brain, and neurofilament H, a specific marker predominantly found in neuronal axons, in the adult mouse hippocampus. These observations suggest that RJ shows neurotrophic effects on the mature brain via stimulation of GDNF production, and that enhanced expression of neurofilament H mRNA is involved in events subsequently caused by GDNF. RJ may play neurotrophic and/or neuroprotective roles in the adult brain through GDNF.

Resveratrol increases BDNF: http://www.longecity...on-in-rat-brain

N-Acetyl-Serotonin increase BDNF: http://www.longecity...timulates-bdnf/

More on BDNF (suggests Lithium): http://www.longecity...ecule-to-watch/

Light Calorie Restriction increases BDNF: http://www.longecity...bdnf-in-humans/

IDRA-21 (supposedly) increases BDNF: http://www.longecity...post__p__461655

High Impact Running & DHA-enriched Diet: http://www.longecity...ediate-results/

Some Exercise (not a lot): http://www.longecity...ercise-addicts/

It seems that BDNF is something that needs balance and the most natural way of increasing it is to get outside a few times a week and "use yo boday". Basically, healthy people have more BDNF... they don't over eat and diet once in a while, and they exercise enough.

Nicotine is weird with BDNF/NGF: http://www.longecity...nicotine-patch/

N-Acetyl-Cysteine increases BDNF: http://www.longecity...tyl-l-cysteine/ (taken with TMG [TMG + NAC = SAMe], one guy reports overall increased energy and immunity, makes sense... he was one of the only ones who could really recommend it)

[thedevinroy]

So would it have a greater effect to supplement with L-tyrosine and increase levels of tyrosine hydroxylase or just supplement with pure L-Dopa?

Doesn't l-tyrosine just increase dopamine concentrations centrally, rather than in specific regions of the brain?

Don't know how I've overlooked this supplement for so long, just bought some today.

Some people like N-Acetyl-Tyrosine better for peripheral activity. Tyrosine and Dopa pass the BBB no problem. L-Dopa supplementation is not as effective, in my opinion, than increasing Tyrosine Hydroxylase activity OVER TIME. Yes, L-Dopa supplementation does give a boost, but many report its effects are temporary even with continued use.

L-Dopa is metabolized really fast by COMT and MAO-B. It also is converted really fast into dopamine, which cannot cross the BBB. If you supplement with tyrosine (or dark/red meat), then the tyrosine can cross the BBB, be converted by increased Tyrosine Hydroxylase, quickly converted to dopamine, and then hit a receptor or (even better) go into VMAT to be stored for prolonged use. L-Dopa would get metabolized fast and turned into dopamine, causing peripheral effects, then the effect would fade. The body gets used to the dopamine, and down regulates its receptors, causing tolerance.

Basically, I believe Tyrosine Hydroxylase induction to be the more well-rounded approach. Must people eat enough tyrosine, and it is a matter of enzyme regulation to really help its conversion. Tyrosine is also used in the thyroid. Some stimulating effects from tyrosine supplementations (usualyl in conjunction with iodine) will come from its conversion into thyroid hormones. Thus, a combined increase of tyrosine and tyrosine hydroxylase will keep the thyroid in balance.

The suspicion that L-Dopa is ineffective for the most part as a CNS stimulant and stays primarily as a peripheral stimulant that causes a faster tolerance (since more L-Dopa is needed to cross the BBB more frequently) is the reason I have chosen to create this thread, otherwise it would be easier. To prevent this metabolism, it is useful to take a peripheral inhibitor of dopamine synthesis like Carbidopa to ensure it crosses the BBB before it turns into dopamine. The existence of this drug is what caused my suspicion.

Edited by devinthayer, 15 October 2011 - 02:34 PM.

[Neurotik]

Would taking L-Tyrosine with loose-leaf green tea be an effective method of ingestion?

[abelard lindsay]

You want to increase Tyrosine Hydroxolase. It's easy just start huffing cat poo and give yourself Toxoplasmosa!

Besides you really don't want to do this. Why are you so focused on dopamine metabolism? Getting your dopamine metabolism going really fast is just going to cause psychotic symptoms. That's because dopamine turns into catecholamines like norepinephrine and adrenaline downstream which causes anxiety and agression and if you front load the system too much then the enzymes that reduce catecholamines are going to not be able to keep up and you are not going to be a happy camper.

Go ahead and take Tyrosine so your brain always has dopamine at the ready but don't alter your tyrosine hydroxylase level as that's an important bottleneck that keeps dopamine metabolism from getting out of control.

Oh yeah, if you don't believe me on the cat poo stuff (BTW, I'm not serious, just showing you what a dumb idea increasing Tyrosine Hydroxolase is since parasites do it to make mice attracted to cat pee):

The neurotropic parasite toxoplasma gondii increases dopamine metabolism.

Prandovszky E, Gaskell E, Martin H, Dubey JP, Webster JP, McConkey GA.

Source

Institute of Integrative and Comparative Biology, Faculty of Biological Sciences, University of Leeds, Leeds, United Kingdom.


Abstract

The highly prevalent parasite Toxoplasma gondii manipulates its host's behavior. In infected rodents, the behavioral changes increase the likelihood that the parasite will be transmitted back to its definitive cat host, an essential step in completion of the parasite's life cycle. The mechanism(s) responsible for behavioral changes in the host is unknown but two lines of published evidence suggest that the parasite alters neurotransmitter signal transduction: the disruption of the parasite-induced behavioral changes with medications used to treat psychiatric disease (specifically dopamine antagonists) and identification of a tyrosine hydroxylase encoded in the parasite genome. In this study, infection of mammalian dopaminergic cells with T. gondii enhanced the levels of K+-induced release of dopamine several-fold, with a direct correlation between the number of infected cells and the quantity of dopamine released. Immunostaining brain sections of infected mice with dopamine antibody showed intense staining of encysted parasites. Based on these analyses, T. gondii orchestrates a significant increase in dopamine metabolism in neural cells. Tyrosine hydroxylase, the rate-limiting enzyme for dopamine synthesis, was also found in intracellular tissue cysts in brain tissue with antibodies specific for the parasite-encoded tyrosine hydroxylase. These observations provide a mechanism for parasite-induced behavioral changes. The observed effects on dopamine metabolism could also be relevant in interpreting reports of psychobehavioral changes intoxoplasmosis-infected humans.

PMID: 21957440 [PubMed - in process] PMCID: PMC3177840 Free PMC Article

Edited by abelard lindsay, 15 October 2011 - 04:19 PM.

[thedevinroy]

Would taking L-Tyrosine with loose-leaf green tea be an effective method of ingestion?

People say they get the best effects on an empty stomach, but green tea probably won't add to your stomach volume too much protein or amino acids. You're in the clear.

[thedevinroy]

You want to increase Tyrosine Hydroxolase. It's easy just start huffing cat poo and give yourself Toxoplasmosa!

Besides you really don't want to do this. Why are you so focused on dopamine metabolism? Getting your dopamine metabolism going really fast is just going to cause psychotic symptoms. That's because dopamine turns into catecholamines like norepinephrine and adrenaline downstream which causes anxiety and agression and if you front load the system too much then the enzymes that reduce catecholamines are going to not be able to keep up and you are not going to be a happy camper.

Go ahead and take Tyrosine so your brain always has dopamine at the ready but don't alter your tyrosine hydroxylase level as that's an important bottleneck that keeps dopamine metabolism from getting out of control.

It was mentioned earlier about the Toxoplasmosa. I'm glad you brought the study forward to show everybody what things would be like if dopamine got too out of hand. Yes, too much dopamine will make you go insane and be agitated. In fact, many dopaminergics caution to discontinue use if manic symptoms occur.

I feel a little hurt by your tone. You have your right to your own opinion, just as I have a right to my own aspirations and hobbies. I have ADHD, so I constantly research ways of bettering myself, especially when common advice like exercise and diet falls incredibly short of any therapeutic effect psychotropics can give.

I believe 99.99% of people are not going to be complete idiots and try snuffing cat poo to get high or better themselves. I also believe that a good 99% of people are not going to become scizophrenic from reading advice on raising dopamine levels. Additionally, I believe that those who are not looking to increase their cognition through dopamine pathways will not take any advice. Lastly, this is knowledge, which anyone has a right to... it's online in library format in some places and some of the more intelligent words used in this conversation will prevent a portion of uneducated readers from making big mistakes via discouragement of continued reading, the "over my head" or "whatever..." effect.

This is a discussion, and I am not advising, nor have I advised anything dangerous on this thread. I also don't advise getting LSD. You never know how much you are going to get, so this is risky business.

Increasing tyrosine hydroxylase is helpful for those of us who perhaps live in an environment where a lack of attention, mood, concentration, and energy cause problems. By "increasing" I do mean inducing the enzyme via upregulation of genetic expression. I do not mean injecting the enzyme. I do not mean contracting a parasitic disease. I certainly wish to expose the healthiest ways of raising these levels, and the most natural ways as well as the most artificial ways. This is a discussion to compare and contrast each method, not a set of dramatic actions to go insane.

[thedevinroy]

I apologize if I took that a bit too seriously. I take a lot of understanding for granted. I have a tendency to assume people began with the knowledge I already have obtained, and the common viewer may be missing some core concepts in order to completely understand my research, advice, and conversation. I suppose this comes from growing up in an environment where most people my age were smarter than me in normal conversation. I absolutely marvelled at the conversations other people had. I learned something every day, and today I get asked how I know so much. Honking my own horn... better stop.

Anyway, sorry, dude. Kinda went overboard.

[Neurotik]

Would taking L-Tyrosine with loose-leaf green tea be an effective method of ingestion?

People say they get the best effects on an empty stomach, but green tea probably won't add to your stomach volume too much protein or amino acids. You're in the clear.

Thanks for the clarification. The reason I asked is because I am under the (perhaps false?) impression that green tea is an all-round good transport system for noots and herbs, assisting some in passing the blood-brain barrier, such as, say, Mucuna Pruriens, which requires a decarboxylase inhibitor. But perhaps that need not apply in the case of L-Tyrosine.

What I do know is that green tea is useful as a transport system in certain cases, I'm just unsure as to which ones.

[thedevinroy]

Would taking L-Tyrosine with loose-leaf green tea be an effective method of ingestion?

People say they get the best effects on an empty stomach, but green tea probably won't add to your stomach volume too much protein or amino acids. You're in the clear.

Thanks for the clarification. The reason I asked is because I am under the (perhaps false?) impression that green tea is an all-round good transport system for noots and herbs, assisting some in passing the blood-brain barrier, such as, say, Mucuna Pruriens, which requires a decarboxylase inhibitor. But perhaps that need not apply in the case of L-Tyrosine.

What I do know is that green tea is useful as a transport system in certain cases, I'm just unsure as to which ones.

Haha me neither. Pretty sure L-Tyrosine is a pretty well absorbed amino acid regardless.

[abelard lindsay]

With the cat poo thing I was just kidding around. I should have used more smileys.

Anyway, I think for ADD you should explore better regulating GABA. It's the inhibitory neurotransmitter and it can really help to slow down racing and distracting thoughts. It also helps in social situations by making a person more resistant to humiliation and allowing time to think things over before speaking instead of just blurting things out inapropriately. The important thoughts get through and the irrelevant ones get damped. It's a bit like turning the squelch knob up on your brain. I would stay away from any gaba-b agonists, as those are known to be addictive and cause receptor upregulation. Plain old GABA is pretty nice and gentle, since it doesn't cross the blood brain barrier very well. Too much GABA will make you sleepy but there is a sweet spot for sure. Picamilion is pretty nice too.

Devan, you should really check out Dr. Eric Braverman's "The Edge Effect". It's a great tour of neuroscience and filled with details about how neurochemistry can be directly affected by supplements, foods, drugs, etc. He also has some great tests to get a rough measure of your current brain chemistry levels and each individual's dominant neuro-chemistry that personality has formed around.

[thedevinroy]

Yes, GABA is indeed a great way to control hyperactivity. I think so much more consistent and controlled with Picamilon. It also gives me a soothing relaxing feeling that is absolutely lacking during a regular day. During social interactions, I highly recommend it to cut back on social anxiety. It is a magic bullet for that. Interviews, parties, etc. all go a little bit smoother with a little GABA (not a lot, or you'll be too drugged to function).

For that soothing controlled feeling, I prefer nicotine over GABAergics, but I only use the electronic cigarettes, which are not "addicting", and I just don't feel the urge to go out and buy them, so I'm always out. The lozenges are terrible and expensive... as do I imagine the gum is as well. With Huperzine A, the nicotine becomes VERY relaxing. Unfortunately, the effects are not long-lasting without menthol... and I never have any menthol around.

+1 for not taking my comments the wrong way and coming to the table with something new and constructive. Thanks.