76 replies to this topic

[Reformed-Redan]

bumpp

"Decreased tyrosine hydroxylase activity is not accompanied by change in responsiveness of dopaminergic receptors". -

http://www.ncbi.nlm..../pubmed/9423934

Edited by redan, 01 April 2012 - 06:46 PM.

[BioFreak]

Just to jump in on the tyrosine hydroxylase warning by abelard lindsay:
Its not a on or off switch that triggers the bad effects from too much tyrosine hydroxylase, it is a matter of "how much".

Dopamine deficient individuals could benefit from more tyrosine hydroxylase, within reason of course. In fact I bet that there is a genetic mutation that causes a underproduction of tyrosine hydroxylase, for which an artificial increase would be the perfect fix.

cAMP increases tyrosine hydroxylase. So the CILTEP stack seems to be a more potent activator of tyrosine hydroxylase by increasing camp (forskolin) and decreasing it's degradation (a pde 4 inhibitor) then each of those alone.

Just wanted to add the information to this thread since it has not been mentioned yet here.

And:

Chronic nicotine treatment leads to sustained stimulation of tyrosine hydroxylase gene transcription rate in rat adrenal medulla.
http://www.ncbi.nlm....pubmed/12538809

Nicotine is a powerful stimulant of the sympathoadrenal system, causing the release of peripheral catecholamines and activation of catecholamine biosynthesis. In previous reports, we have studied the mechanisms by which short-term nicotine treatment regulates tyrosine hydroxylase (TH) in adrenal medulla. In this report, we study the effects of chronic nicotine treatment on adrenal TH gene expression. Rats were injected with either saline or nicotine twice per day for up to 14 days. Chronic nicotine treatment elicited long-lasting, dose-dependent increases in the levels of adrenal TH mRNA, TH protein, and TH activity. In contrast, a single injection of nicotine elicited only a small increase in adrenal TH mRNA levels, which was transient and did not result in the induction of TH enzyme. Chronic nicotine administration also elicited a sustained increase in adrenal TH gene transcription rate, which persisted for up to 7 days after the final nicotine injection. This sustained transcriptional response correlated with a modest sustained increase in adrenal TH AP1 binding, but not in the levels of Fra-2 or other fos or jun proteins. These results demonstrate that repeated nicotine injections administered chronically over 1 to 2 weeks lead to sustained stimulation of the TH gene and consequent induction of TH gene expression in rat adrenal medulla. These studies support the hypothesis that chronic nicotine administration produces long-lasting cellular changes in adrenal medulla that lead to sustained transcriptional responses.

reserpine increases tyrosine hydroxylase also, which should come at no surprise, but it is pretty useless as it should only increase it as long as it depletes neurotransmitters.

Regulated expression of the tyrosine hydroxylase gene by epidermal growth factor.
http://www.ncbi.nlm....cles/PMC367973/

The addition of epidermal growth factor (EGF) to cultures of the rat PCG2 pheochromocytoma cell line increased the level of RNA coding for tyrosine hydroxylase (TH). A region of DNA containing 5'-flanking sequences of the TH gene was fused to a heterologous gene and transfected into a rat anterior pituitary cell line, GH4. The TH gene sequences from +27 to -272 contained information sufficient for the induction of TH by EGF. Two regions within this TH DNA were extensively homologous to the EGF regulatory element of the rat prolactin gene.

Edited by BioFreak, 06 January 2014 - 09:15 AM.

[BioFreak]

Pharmacology and neuroprotective properties of rasagiline.
http://www.ncbi.nlm..../pubmed/8988465

Rasagiline [R(+)-N-propargyl-1-aminoindane] is a selective irreversible inhibitor of MAO-B which is not metabolised to amphetamine-like derivatives. Like deprenyl, when given to rats in a dose selective for inhibition of MAO-B, it does not affect striatal extracellular fluid dopamine levels, but when administered chronically (21 days) it increased striatal microdialysate dopamine without reduction in deaminated metabolites. Similarly to deprenyl, rasagiline (10(-6)M) increased the percentage of tyrosine hydroxylase positive cells in a primary culture of rat fetal mesencephalic cells (6 days in culture). Rasagiline, but not deprenyl, also increased the number of neurons per field in this organotypic culture.

[BioFreak]

Biopterin is lowered in parkinson patients, which may lead to lower tyrosine hydroxylase:

Biopterin in Parkinson's disease
http://jnnp.bmj.com/...0/1/85.full.pdf

Tetrahydrobiopterin is an essential co-factor of
tyrosine hydroxylase, the rate-limiting enzyme in the
natural synthesis of dopamine. Levodopa therapy
by-passes this step. In Parkinsonian subjects, the
biopterin content of cerebrospinal fluid is reduced to
50% of that in control subjects,2 while in post mortem
striatal samples it is reduced by 80%.3 It
has been postulated that tetrahydrobiopterin
supplements might increase tyrosine hydroxylase
activity in Parkinsonian patients and boost endogenous
dopamine production.

Results
No significant difference was detected in any of the
cases, given either placebo or tetrahydrobiopterin.
No clinical impression of benefit nor trend towards
improvement was noted during treatment with tetrahydrobiopterin,
although two patients did report an
increased sense of well-being. There were no side
effects. All four patients subsequently responded well
to levodopa plus a decarboxylase inhibitor.

Maybe the dosage was not high enough since only two responded with increased wellbeing, but the sample size was too low anyways, and the question is how much this applies to non parkinson patients.

[BioFreak]

NADH increases tyrosine hydroxylase:
Monoaminergic neurotransmitters, their precursors and metabolites
in brains of Alzheimer patients
http://www.nadh-apot...er patients.pdf

In this
regard, the coenzyme nicotinamide adenine dinucleotide
(NADH) was found to increase tyrosine hydroxylase activity
and DA production in pheochromocytoma cells
[19]. NADH has also been applied to 17 AD patients and
all of the patients included in the trial exhibited a distinct
improvement of certain cognitive impairment [5]. The
clinical trial was mainly based on our biochemical findings
and confirms their importance.

[BioFreak]

Stress depletes catecholamines, which in turn increases tyrosine hydroxylase (which may deplete catecholamine precursors tyrosine and phenylalanine):

http://www.dtic.mil/.../u2/a507113.pdf

Under stressful conditions that activate
tyrosine hydroxylase, the rate-limiting enzyme that cata
lyzes the conversion of tyrosine to L-dopa, the enzyme
becomes more responsive to increased intraneural tyrosine
, whether through ingestion or injection of tyrosine
(1; 12). Animal studies have demonstrated that suppleme
ntal tyrosine increases brai
n levels of norepinephrine
(18; 23; 49) and dopamine (1).
...
The beneficial effects of tyrosine supplementation
reported in the present study are consistent with the
hypothesis that cold stress causes an
increase in the firing rate of catecholaminergic neurons and tyrosine
supplementation prior to stress increases syntheses of
the catecholamines required for optimal working
memory function. This hypothesis is supported by
studies demonstrating that brain catecholamines,
particularly norepinephrine and dopamine
, are depleted in certain regions of
the brain by exposure to a variety
of stressors (8; 17; 36) and that this depletion is associat
ed with decrements in cognitive performance (18; 46).
Administration of tyrosine, a precursor for the synthesi
s of dopamine and norepinephrine (48) has been shown
to prevent the stress induced depletion of brain norepinephrine and dopamine in CNS regions associated with
working memory (18; 19; 31).

Although interesting, it does not really help in increasing tyrosine hydroxylase because the increase is just the result of a feedback mechanism through a drop in baseline levels of catecholamines. Meaning if baseline levels are already too low, this feedback mechanism will only restore catecholamines up to this point.

[BioFreak]

Estrogens influence tyrosine hydroxylase:
The neuroprotective effects of estrogen on the aging brain
http://users.ox.ac.u...rontology_1.pdf

There is debate regarding the effect of estrogens on the
synthesis and breakdown of NA. Estrogens have been
reported to inhibit the enzyme tyrosine hydroxylase (which
is responsible for a step in dopamine, adrenaline and NA
synthesis) activity in the hypothalamus and striatum
(
Hersey et al., 1982
). However, others reported that
estrogens (1) increase tyrosine hydroxylase activity (
Beattie
et al., 1972
), (2) facilitate NA release (
Paul et al., 1979
), and
(3) decrease monoamine oxidase (a catabolic enzyme)
activity in rats (
Luine and McEwen, 1977
) and post-
menopausal women (
Klaiber et al., 1971
). Thus, estrogens
probably enhance adrenergic activity. This is important
because there is a link between the function of adrenergic
system and human cognition (
Walsh and Schiff, 1990
). For
example, inhibition of human noradrenergic neuron firing
and NA turnover is associated with reduced mental
performance (
Kugler et al., 1980
) and learning (
Frith et al.,
1985
).

And aerobic exercise could increase tyrosine hydroxylase:
Neuroplasticity of dopamine circuits after exercise: implications for central fatigue.
http://www.ncbi.nlm....Pubmed_RVDocSum

Habitual exercise increases plasticity in a variety of neurotransmitter systems. The current review focuses on the effects of habitual physical activity on monoamine dopamine (DA) neurotransmission and the potential implication of these changes to exercise-induced fatigue. Although it is clear that peripheral adaptations in muscle and energy substrate utilization contribute to this effect, more recently it has been suggested that central nervous system pathways "upstream" of the motor cortex, which initiate activation of skeletal muscles, are also important. The contribution of the brain to exercise-induced fatigue has been termed "central fatigue." Given the well-defined role of DA in the initiation of movement, it is likely that adaptations in DA systems influence exercise capacity. A reduction in DA neurotransmission in the substantia nigra pars compacta (SNpc), for example, could impair activation of the basal ganglia and reduce stimulation of the motor cortex leading to central fatigue. Here we present evidence that habitual wheel running produces changes in DA systems. Using in situ hybridization techniques, we report that 6 weeks of wheel running was sufficient to increase tyrosine hydroxylase mRNA expression and reduce D2 autoreceptor mRNA in the SNpc. Additionally, 6 weeks of wheel running increased D2 postsynaptic receptor mRNA in the caudate putamen, a major projection site of the SNpc. These results are consistent with prior data suggesting that habitually physically active animals may have an enhanced ability to increase DA synthesis and reduce D2 autoreceptor-mediated inhibition of DA neurons in the SNpc compared to sedentary animals. Furthermore, habitually physically active animals, compared to sedentary controls, may be better able to increase D2 receptor-mediated inhibition of the indirect pathway of the basal ganglia. Results from these studies are discussed in light of our understanding of the role of DA in the neurobiological mechanisms of central fatigue.

[BioFreak]

Substances needed for tyrosine hydroxylase to work:

calcium
NAD(P)H+H
folic acid
tyrosine of course
and tehydrobiopterin

If one of these is lacking, tyrosine hydroxylase can not do it's job.
Also, if there is not enough tyrosine hydroxylase, the conversion of tyrosine to l-dopa can not take place.

The tyrosine hydroxylase molecule includes iron, so iron deficiency may negatively influence tyrosine hydroxylase activity.

Tryosinase can replace tyrosine hydroxylase, although it is limited too and needed to degrade excess dopamine and l-dopa before they can become neurotoxic. So increasing tyrosine hydroxylase would definitely be better then using tyrosinase.

Edited by BioFreak, 06 January 2014 - 10:38 AM.

[Nobility]

Great posts,

But remember not to avoid good foods that contain Selenium, as everything has some function....
What I'm saying is, well in my opinion if I may some help to give some idea, as you stated that to avoid yeast...

But of course, don't avoid good foods that are high in Selenium such as certain fish ,etc...

[BioFreak]

Are you sure you posted in the right thread?

[Nobility]

Are you sure you posted in the right thread?

Hi,

Thank you very much for your post above mine, people and I learned a lot..

Yes, my reply was to the original post of the thread.

Thank You.

[chemicalambrosia]

Chronic nicotine treatment leads to sustained stimulation of tyrosine hydroxylase gene transcription rate in rat adrenal medulla.
http://www.ncbi.nlm....pubmed/12538809

Nicotine is a powerful stimulant of the sympathoadrenal system, causing the release of peripheral catecholamines and activation of catecholamine biosynthesis. In previous reports, we have studied the mechanisms by which short-term nicotine treatment regulates tyrosine hydroxylase (TH) in adrenal medulla. In this report, we study the effects of chronic nicotine treatment on adrenal TH gene expression. Rats were injected with either saline or nicotine twice per day for up to 14 days. Chronic nicotine treatment elicited long-lasting, dose-dependent increases in the levels of adrenal TH mRNA, TH protein, and TH activity. In contrast, a single injection of nicotine elicited only a small increase in adrenal TH mRNA levels, which was transient and did not result in the induction of TH enzyme. Chronic nicotine administration also elicited a sustained increase in adrenal TH gene transcription rate, which persisted for up to 7 days after the final nicotine injection. This sustained transcriptional response correlated with a modest sustained increase in adrenal TH AP1 binding, but not in the levels of Fra-2 or other fos or jun proteins. These results demonstrate that repeated nicotine injections administered chronically over 1 to 2 weeks lead to sustained stimulation of the TH gene and consequent induction of TH gene expression in rat adrenal medulla. These studies support the hypothesis that chronic nicotine administration produces long-lasting cellular changes in adrenal medulla that lead to sustained transcriptional responses.

Yet another reason to love nicotine as a nootropic...

[BioFreak]

Except that nicotine is a potential neurotoxin. For example in cholinergic Hb–IPN neurons.
http://www.sciencedi...161813X05000355

[Mind_Paralysis]

It's also a carcinogenic in and of itself (the carcinogenic effect of tobacco is a synergistic thing), so that decreases the usefulness of nicotine.

 

Also, devinthayer, I don't remember, but have we talked about which VERSION of ADHD that you have?

Also, whoever thought increasing cAMP was a good idea... it's not. cAMP also control signalling in the PFC, and increased levels have been reported in ADHD-individuals. The decreasing of cAMP through a feedback-loop from the Alpha-2-a receptors is actually the proposed mode of action of Guanfacine, an ADHD-medication.

 

The D4-receptors are also suspected to play a big role in ADHD, specifically variants that have more than 7 repeats - DRD4-vntr-7 is one of them. The D4-receptors interact with the NMDA-network, when signalled, and causes lowering of cAMP in the PFC at the exact moment it's necessary to increase the strength of particular signals.

 

So... with this in mind, you can see how increasing cAMP is a very stupid idea if you have ADHD.

 

Another note - caffeine increases cAMP in the PFC as well - so the increased vigor and energy it gives, is actually FALSE - it's masking the fact that it's also making you MORE inattentive. The end result on ADHD-cognition is either +- 0, or quite negative.

[thedevinroy]

Caffeine has a U shaped curve. At lower doses, it blocks adenosine receptors, no harm, no foul, but at higher doses it has a plethora of activities including PDE inhibition. We're talking like painful amounts though... jitters and headaches level to get Viagra like effects. Not that I've tried... Like not on purpose...

As far as ADHD, I'm on the inattentive side. Strattera was my NZT. Now, I'm trying out other things, since I've been unable to get the same clarity and upper level emotions on Stattera at a dose I'm comfortable with... it being hepatotoxic and all that.

I like the Huperzine A with Ashwagandha right now... just for remembering stuff and energy. Just a no go on the executive function aspect... Some racetams are okay so far.

Any little thing helps, but nothing comes close to external motivators. I'm talking harsh deadlines and threats and pressure to perform. And yeah that might be partially psychological, and I try to use that to my advantage to snap out of zombie mode, but it's equally chemical, too. The harder I try, the worse it gets.

Interesting fact, I was vaping for a long time. I cannot accurately say that I felt more up than down since the nic fits and ups and downs were pretty annoying. Sure, I can look back and say I was more confident and entertained, but it was a different part of my life. I'm thinking the nicotine is probably a bad idea, especially for expense purposes.

Thinking of trying a uridine supplement instead. Those seem to restore some dopamine function. Also, always to the green tea for providing a multitude of every day benefits including increased TH activity and neuroprotection of my dopaminergic neurons. I'll take that over a few puffs of vapor any day, no matter the flavor.

Edited by devinthayer, 27 June 2016 - 10:53 PM.

[PeopleProgrammer]

Bromantane is exactly what you are looking for. it upregulates tyrosine hydroxylase at a practically useful level without any of the sedation or anti-nootropic effects of mood stabilizers (ie, the histone deacetylase inhibitors). here is some reading and a collection of links on it: https://en.wikipedia...wiki/Bromantane

Edited by PeopleProgrammer, 02 July 2016 - 04:02 AM.

[Flex]

First off, those mentioned studies may not be checked or reviewed by any proefessionals. So it might work only in e.g. Rats, in vitro or not at all because the study is faulty, statisitacally not sigificant &etc.

The next thing would be to ask, whether the increase of the Tyrosine Hydroxylase (TH) is just of a short-termed duration

(because of e.g. regulatory negative feed-back loop in regards of Bromartane & etc.) or has indeed a modulatory long-term effect.

Obviously, be aware of pollution(heavy-metals, pesticides) of asiatic herbs. I for my self bought only "brand" products that are used by herbalists/TCM professionals like Sun Ten & sanjiu 999

but again no guarantee whteher its safe.

 

Seek an academic at e.g. sub reddits (/r/nootropics, askdrugnerds, psychiatry, maybe askscience and askadoctor) to examine/comment those concerns and stuides.

 

Jiaogulan (Gynostemma pentaphyllum)

17 Random Dopaminergic Supplements

http://www.longecity...ts/#entry630441

 

Catalpol attenuates MPTP induced neuronal degeneration of nigral-striatal dopaminergic pathway in mice through elevating glial cell derived neurotrophic factor in striatum.

http://www.ncbi.nlm....pubmed/20123001

 Catalpol = Rehmannia Glutinosa = chinese foxglove / Pin Yin = Sheng Di Huang

I had experienced some good effects with this but cant say whether it was because of Tyrosine Hydroxylase, Gdnf & etc.

 

Upregulating Dopamine Receptors - ADHD problem

http://www.longecity...em/#entry684515

Common flowering quince = Chaenomeles speciosa / Pin Yin = Mugua

 

9-me-β-carboline

9-me-BC Regeneration of dopaminergic neurons?

http://www.longecity...ns/#entry662128

 

and maybe You will find here some herbs that are worth researching for any effects on Tyrosine Hydroxylase

brainrepair topic

http://www.longecity...inrepair-topic/

Edited by Flex, 02 July 2016 - 03:48 PM.

[PeopleProgrammer]

ceretropic makes a very good quality bromantane with a 3rd party COA. its viable in the long term according to anecdotes such as those on reddit.

[thedevinroy]

Bromantane is exactly what you are looking for. it upregulates tyrosine hydroxylase at a practically useful level without any of the sedation or anti-nootropic effects of mood stabilizers (ie, the histone deacetylase inhibitors). here is some reading and a collection of links on it: https://en.wikipedia...wiki/Bromantane

When I first came across that adaptogen compound, I dismissed this as a possible drug that would ever have a semipermanent place in my cabinet due to the vertigo I got from Memantine, a drug with that same jungle gym looking subgroup. However, it seems those anticholinergic side effects in Bromantane may not occur in the same dosage ratio as Memantine.

Worth a second look for sure.

[thedevinroy]

First off, those mentioned studies may not be checked or reviewed by any proefessionals. So it might work only in e.g. Rats, in vitro or not at all because the study is faulty, statisitacally not sigificant &etc.
The next thing would be to ask, whether the increase of the Tyrosine Hydroxylase (TH) is just of a short-termed duration
(because of e.g. regulatory negative feed-back loop in regards of Bromartane & etc.) or has indeed a modulatory long-term effect.
Obviously, be aware of pollution(heavy-metals, pesticides) of asiatic herbs. I for my self bought only "brand" products that are used by herbalists/TCM professionals like Sun Ten & sanjiu 999
but again no guarantee whteher its safe.

Seek an academic at e.g. sub reddits (/r/nootropics, askdrugnerds, psychiatry, maybe askscience and askadoctor) to examine/comment those concerns and stuides.

Jiaogulan (Gynostemma pentaphyllum)
17 Random Dopaminergic Supplements
http://www.longecity...ts/#entry630441

Catalpol attenuates MPTP induced neuronal degeneration of nigral-striatal dopaminergic pathway in mice through elevating glial cell derived neurotrophic factor in striatum.
http://www.ncbi.nlm....pubmed/20123001
Catalpol = Rehmannia Glutinosa = chinese foxglove / Pin Yin = Sheng Di Huang
I had experienced some good effects with this but cant say whether it was because of Tyrosine Hydroxylase, Gdnf & etc.

Upregulating Dopamine Receptors - ADHD problem
http://www.longecity...em/#entry684515
Common flowering quince = Chaenomeles speciosa / Pin Yin = Mugua

9-me-β-carboline
9-me-BC Regeneration of dopaminergic neurons?
http://www.longecity...ns/#entry662128

and maybe You will find here some herbs that are worth researching for any effects on Tyrosine Hydroxylase
brainrepair topic
http://www.longecity...inrepair-topic/

Interesting. The article on Catalpol almost implies that GDNF is responsible for Tyrosine Hydroxylase transcription.

The 9-methyl-beta-carboline molecule is interesting since it is a molecule made from UV damaged DNA. I know that radiation, especially infrared, seems to be regenerative, and I wonder if it scares the body into working into a healthy stress mode. Hormetic, if you will.

[PeopleProgrammer]

devinthayer, I hate to burst your bubble but adaptogens do not exist. there is no magical drug or concept that can do no harm. a substance will always have a definite, quantifiable, and uniform effect. ie, SSRI's will always inhibit SERT. there is no drug that will only inhibit SERT when it would be beneficial or it "knows" to do so.

[thedevinroy]

devinthayer, I hate to burst your bubble but adaptogens do not exist. there is no magical drug or concept that can do no harm. a substance will always have a definite, quantifiable, and uniform effect. ie, SSRI's will always inhibit SERT. there is no drug that will only inhibit SERT when it would be beneficial or it "knows" to do so.

As naive as I sound, I assure you that I realize this is all biological alchemy. I only called it an adaptogen because that is how it is marketed in a certain country.

[Mind_Paralysis]

Devinthayer... have you tried Vyvanse (lisdexamphetamine) combined with Intuniv (guanfacine)?

 

I ask, because this combo is the only thing which legendary member of this board, GetOutofBox have tried that's given any appreciable benefit to his ADHD-PI/SCT symptoms.

 

As far as I can tell, yours, mine and his symptoms are all practically identical.

 

Vyvanse is the compound I have tried as of yet, that have given the most benefit. It's still waaay far off though - a lot more enhancement is needed until I am at baseline with neurotypicals. I am hoping to add Intuniv in the near future, to finally maybe get about... 60% or so reduction of symptoms.

More than that, is, I'm afraid, the best we can do at the moment.

 

 

Well, that, or find a genetic test that checks for VNTR-mutations, and see if you have DRD4-Vntr-7+, and if you do, then organize the group-buy for A-412,997 and see if that compound actually works.

 

(it's a super-selective stimulant which has litterally none of the side-effects of regular stimulants, the only noted side-effects being painful and prolonged erections. If you're a woman this is obviously not even a side-effect.)

Edited by Stinkorninjor, 05 July 2016 - 03:04 AM.

[PeopleProgrammer]

if you have truly intractable ADHD or depression, I 'd highly recommend Desoxyn. its kinda hard to get a script for but it is by far the best drug available. it makes vyvanse and adderall look like nothing. contrary to popular belief, if your dosage is less than ~40mg per day, the neurotoxicity is negligible. it actually only becomes statistically significant at very recreational doses, and even then the war-on-drugs agenda has heavily distorted and exaggerated it.

[Flex]

 

Interesting. The article on Catalpol almost implies that GDNF is responsible for Tyrosine Hydroxylase transcription.

The 9-methyl-beta-carboline molecule is interesting since it is a molecule made from UV damaged DNA. I know that radiation, especially infrared, seems to be regenerative, and I wonder if it scares the body into working into a healthy stress mode. Hormetic, if you will.

 

 

I understood it differently: 9-me-bc causes DNA damage by increasing UV damage ( kind of a magnifier)

The 9-me-bc itself is either from natural sources or maybe synthetic. I´m too lazy to take a look into the papers though
 

[thedevinroy]

Interesting. The article on Catalpol almost implies that GDNF is responsible for Tyrosine Hydroxylase transcription.

The 9-methyl-beta-carboline molecule is interesting since it is a molecule made from UV damaged DNA. I know that radiation, especially infrared, seems to be regenerative, and I wonder if it scares the body into working into a healthy stress mode. Hormetic, if you will.

I understood it differently: 9-me-bc causes DNA damage by increasing UV damage ( kind of a magnifier)
The 9-me-bc itself is either from natural sources or maybe synthetic. I´m too lazy to take a look into the papers though

https://www.ncbi.nlm...ubmed/23842892/

You are right. It is a photosensitizer. DNA damage increases when an excited beta carboline crashes into DNA making some funky purine oxidation and pyramidine dimers.

I doubt that DNA damage is the reason for the positive benefits. I mean yeah hormesis does work that way, sometimes, so maybe? Idk that would be weird.

Edited by devinthayer, 07 July 2016 - 05:26 PM.

[treonsverdery]

well, this suggestion would be better tried on mice, first.  you could take gamma-butyrolactone, https://en.wikipedia...a-Butyrolactone , a prechemical to the recreational drug GHB, before you sleep.  your body then responds to this producing more tyrosine hydroxylase, (reference http://www.ncbi.nlm..../pubmed/1360740 ) while you sleep, so then when you are awake you might be perkier, like on nicotine.

 

phrases from the pubmed thing  http://www.ncbi.nlm....pubmed/1360740 "decreased the dopamine (DA) content elevated by gamma-butyrolactone (GBL, 750 mg.kg-1, ip)" (kind of a huge dose)

 

so there is a slight possibility of new group of nootropics the sleep enhancers, that produce hyper well restedness, if taken while asleep.  Mg threonate doubles long term memory at lab mammals yet is likely to cause sleepiness, so there are possibly at least two hyperwellrestedness chemicals

 

it is apparently also the fluid at electrolytic capacitors (wikipedia) Hmmm. what are the other ingredients

Edited by treonsverdery, 07 July 2016 - 11:44 PM.

[Mind_Paralysis]

Devin... are you looking into the combos Focalin/Intuniv and Vyvanse/Intuniv?


As well as Metadoxin and Pyritinol?

These are the only compounds that have any recorded effect at SCT symptoms.

[thedevinroy]

well, this suggestion would be better tried on mice, first. you could take gamma-butyrolactone, https://en.wikipedia...a-Butyrolactone , a prechemical to the recreational drug GHB, before you sleep. your body then responds to this producing more tyrosine hydroxylase, (reference http://www.ncbi.nlm..../pubmed/1360740 ) while you sleep, so then when you are awake you might be perkier, like on nicotine.

phrases from the pubmed thing http://www.ncbi.nlm....pubmed/1360740 "decreased the dopamine (DA) content elevated by gamma-butyrolactone (GBL, 750 mg.kg-1, ip)" (kind of a huge dose)

so there is a slight possibility of new group of nootropics the sleep enhancers, that produce hyper well restedness, if taken while asleep. Mg threonate doubles long term memory at lab mammals yet is likely to cause sleepiness, so there are possibly at least two hyperwellrestedness chemicals

it is apparently also the fluid at electrolytic capacitors (wikipedia) Hmmm. what are the other ingredients

Arguably I could sleep better if I got more done before I went to sleep. I could wake up better knowing the morning was all mine, not spent feeling guilty about things I've been putting off.

[thedevinroy]

Devin... are you looking into the combos Focalin/Intuniv and Vyvanse/Intuniv?


As well as Metadoxin and Pyritinol?

These are the only compounds that have any recorded effect at SCT symptoms.

I'm open to those combos. Again, guanfacine and clonidine never helped, only made things worse. So I'm only open to it as a symptom reducer.

I'm a little sketched out about B vitamin analogues. Their effect seems too mysterious on a micro level to work on a macro level. Like I just don't understand how they work. Probably the same reason I resisted Piracetam analogues for so long... (That and aniracetam heavily sedated me and sent me into an unproductive rabbit hole for 3 hours every time.)