3 votes
Posted 05 February 2013 - 05:01 PM
Cordyceps is a steriod promotor. Its basically hcg. Perhaps all these beneficial compunds are effective by lowering cortisol. Somebody try phosodylserine in high dose yet?
Posted 05 February 2013 - 09:11 PM
That would explain why Cordyceps makes me feel like THE MAN lol. Ashwagandha is potent cortisol-inhibitor but doesn't address the anhedonia issue so I don't think that's the case here..
Edited by nupi, 05 February 2013 - 09:13 PM.
Posted 05 February 2013 - 11:27 PM
Posted 06 February 2013 - 04:54 AM
Edited by Galaxyshock, 06 February 2013 - 05:03 AM.
Posted 06 February 2013 - 05:13 AM
Over the past few weeks, I've been mostly ignoring my anhedonia rather than obsessing over it, which helps me quite a bit.
Edited by Galaxyshock, 06 February 2013 - 05:18 AM.
Posted 07 February 2013 - 07:03 AM
Edited by Galaxyshock, 07 February 2013 - 07:28 AM.
Posted 07 February 2013 - 11:28 AM
Posted 07 February 2013 - 01:08 PM
Interesting, so I guess I will try Jiaogulan and Cordyceps (though that stuff is nasty even in capsules) in the morning and the afternoon. Not sure I need the Schisandra, as I don't feel like I am overstimulated at all. Still wondering where to best get Hordenine (iHerb does not seem to carry it)
. I'm guessing on continous use it can regulate adrenergic receptors so that one can actually get that surge of excitation we're missing, I've got real glimpses of it lately when hearing good songs or actually anticipating something.Edited by Galaxyshock, 07 February 2013 - 01:20 PM.
Posted 07 February 2013 - 07:51 PM
Edited by Dissolvedissolve, 07 February 2013 - 07:51 PM.
Posted 08 February 2013 - 03:38 AM
Posted 08 February 2013 - 04:15 AM
Posted 08 February 2013 - 05:06 AM
had any of you had experience with gotukola aka centella asiatica? seems it should be similar to bacopa for some aspects... im thinking of giving it a go
Edited by Galaxyshock, 08 February 2013 - 05:57 AM.
Posted 09 February 2013 - 09:47 AM
Edited by nupi, 09 February 2013 - 09:51 AM.
Posted 09 February 2013 - 10:14 AM
Edited by Galaxyshock, 09 February 2013 - 10:21 AM.
Posted 09 February 2013 - 02:26 PM
Do you chat up strangers or just start conversations with people you already know? This makes me wonder if a higher dose of schizandra would be effective in treating my AvPD...Edited by nupi, 09 February 2013 - 02:34 PM.
Posted 09 February 2013 - 03:17 PM
Posted 09 February 2013 - 04:29 PM
Edited by nupi, 09 February 2013 - 04:33 PM.
Posted 14 February 2013 - 11:10 PM
Posted 15 February 2013 - 01:08 AM
I started taking 500 mg of Trimethylglycine on February 12 and so far I haven't noticed any changes. How long should I give TMG a chance before giving up on it?
503 mg at 8:45 AM T+1 slight energy / motivation T+5 seemingly enhanced physical energy when walking 745 mg at 7:40 726 mg at 9:35 743 at 10:30 -2 day gap- (caffeine one day, armodafinil the next) 738 mg at 10:15 - with ~60 mg caffeine noted no crash for caffeine, but I was operating on ~10 hours of sleep and the caffeine dosage may have been too small to cause a crash 738 mg at 9:30 no effects noted
Edited by Dissolvedissolve, 15 February 2013 - 01:08 AM.
Posted 15 February 2013 - 01:38 AM
I noticed that too even tought about increased pheromone output.Mostly people in my class that I somewhat know.. Normally I just sit silent and barely mumble couple of words but lately it's been like a barrier was broken and I could talk about normal stuff without issues and enjoy it. Not spontaneously talking to strangers yet hehe but I feel like there's less and less preventing me to eventually do that if I wish. The social openity has also resembled as people giving me more looks, perhaps the "baseline" expression on my face has changed (well I'd say I have somewhat healthier appearance) or my behavior appears more friendly. Whatever it is, it's pretty good! Another thing is that let's say I play some game on computer and fail at something, I may express it spontaneously by curse word or smashing the table or something lol. So my behavior has become a bit more outward which is nice. These effects were a lot milder when I started using Schisandra so I'm thinking it's a "build-up" anti-depressant-like modulation. Could be some synergy with SJW or SSRI in your case.
Serotonin modulation of moth central olfactory neurons.
Kloppenburg P, Mercer AR.
Source
Institute of Zoology, University of Cologne, Cologne, Germany. peter.kloppenburg@uni-koeln.de
Abstract
In the tobacco hornworm, Manduca sexta, 5-hydroxytryptamine (5HT) acting at the level of the antennal lobes contributes significantly to changing the moth's responsiveness to olfactory stimuli. 5HT targets K(+) conductances in the cells, increasing the excitability of central olfactory neurons and their responsiveness to olfactory cues. Effects of 5HT modulation are apparent not only at the single cell level, but also in the activity patterns of populations of neurons that convey olfactory information from antennal lobes to higher centers of the brain. Evidence suggests that 5HT-induced changes in activity within neural circuits of the antennal lobes might also drive structural plasticity, providing the basis for longer-term changes in antennal lobe function.
Posted 15 February 2013 - 06:34 AM
So it's been almost 7 weeks since I started 1000 mg of Maca and 4 weeks since I started 500 mg of Rhodiola (3% rosavins) and the effects have stabilized. In the first 2 weeks of starting rhodiola I had a noticeable effect on anhedonia, but now it's very subtle.
Edited by Galaxyshock, 15 February 2013 - 06:42 AM.
Posted 15 February 2013 - 06:44 AM
Mucuna pruriens with methyldopa or cardidopa should fix this issue if its caused by dopaminergic issues but it seems straight forward like the anhedonia thread.Dopamine is closely associated with reward-seeking behaviors, such as approach, consumption, and addiction.[38] Recent research suggests that the firing of dopaminergic neurons is motivational as a consequence of reward-anticipation. This hypothesis is based on the evidence that, when a reward is greater than expected, the firing of certain dopaminergic neurons increases, which consequently increases desire or motivation towards the reward.[38] However, recent research finds that while some dopaminergic neurons react in the way expected of reward neurons, others do not and seem to respond in regard to unpredictability.[43] This research finds the reward neurons predominate in the ventromedial region in the substantia nigra pars compacta as well as the ventral tegmental area. Neurons in these areas project mainly to the ventral striatum and thus might transmit value-related information in regard to reward values.[43] The nonreward neurons are predominate in the dorsolateral area of the substantia nigra pars compacta which projects to the dorsal striatum and may relate to orienting behaviour.[43] It has been suggested that the difference between these two types of dopaminergic neurons arises from their input: reward-linked ones have input from the basal forebrain, while the nonreward-related ones from the lateral habenula.[43]
[edit]Animal studies
Clues to dopamine's role in motivation, desire, and pleasure have come from studies performed on animals. In one such study, rats were depleted of dopamine by up to 99 percent in the nucleus accumbens and neostriatum using 6-hydroxydopamine.[38] With this large reduction in dopamine, the rats would no longer eat of their own volition. The researchers then force-fed the rats food and noted whether they had the proper facial expressions indicating whether they liked or disliked it. The researchers of this study concluded that the reduction in dopamine did not reduce the rat's consummatory pleasure, only the desire to eat. In another study, mutant hyperdopaminergic (increased dopamine) mice show higher "wanting" but not "liking" of sweet rewards.[44] Mice who cannot synthesize dopamine are unable to feed sufficiently to survive more than a few weeks after birth, but will feed normally and survive if administered L-DOPA.[45]
Posted 15 February 2013 - 06:53 AM
Deoxyepinephrine, also known by the common names N-methyldopamine and epinine, is an organic compound and natural product that is structurally related to the important neurotransmittersdopamine and epinephrine. All three of these compounds also belong to the catecholamine family. The pharmacology of epinine largely resembles that of its "parent", dopamine. Epinine has been found in plants, insects and animals. It is also of significance as the active metabolic breakdown product of the prodrugibopamine, which has been used to treat congestive heart failure.[2][3]
Pharmacology
One of the most prominent pharmacological characteristics of epinine, its ability to raise blood pressure, was noted as early as 1910, by Barger and Dale, who reported that "methylamino-ethyl-catechol", as they called it, had about 1/7 x the pressor potency of epinephrine, but about 5 x the potency of dopamine ("amino-ethyl-catechol") in cat preparations.[14] The Buroughs Wellcome Co., for which Barger, Dale and Pyman (see "Chemistry" section) worked, subsequently marketed the hydrochloride salt of "methylamino-ethyl-catechol", under the name "epinine", as a substitute for epinephrine.[15] Tainter further quantified the pressor activity of epinine in atropine-treated and anesthetized intact cats, showing that doses of 0.02-0.2 mg, given i.v., were about 1/12 as active as l-epinephrine, but that the effect lasted about twice as long (~ 3 minutes), and was accompanied by an increase in pulse rate.[15]
Eventually, epinine was determined to be a non-selective stimulant of dopamine (DA) receptors, a-, and b-adrenoceptors, with the stimulation of D2 receptors leading to inhibition ofnoradrenergic and ganglionic neurotransmission. These studies, conducted using anesthetized animals, were amplified by van Woerkens and co-workers, who compared the effects of epinine and dopamine in unanesthetized pigs, so as to avoid any possible influences of an anesthetic. Drug doses were in the range of 1-10 μg/kg/min, administered by i.v. infusion over a period of 10 minutes. The results of these experiments showed that, in pigs, over the dose-range employed, epinine was more potent than dopamine as an agonist on D2, a-, and b2-receptors, but was weaker than dopamine as a D1-agonist. The b1-agonist effect of both compounds was weak or non-existent.[16]
Comparable studies, in which blood pressure, heart rate and serum prolactin levels were measured after the administration of 0.5-4 μg/kg/min of epinine by i.v. infusion over a 15 minute period to healthy humans, were reported subsequently by Daul and co-workers.[17] These investigators found that at lower doses (0.5 or 1.0 μg/kg/min), which produced plasma concentrations of 20-80 nM/L, epinine, in common with dopamine, caused a fall in prolactin level, but did not affect blood pressure or heart rate. At higher doses (2.0 or 4.0 μg/kg/min), epinine significantly increased both systolic and diastolic blood pressure, as well as heart rate. In contrast, dopamine caused an increase in systolic blood pressure and heart rate only. Both drugs increased diuresis and natriuresis - effects that are thought to be due to the activation of renal D1 receptors. It was concluded that at the lower doses, epinine and dopamine exerted their effects only at DA (D2) receptors, but did not activate a- or b-adrenoceptors. At the higher doses, epinine activated a-, b1- and b2-receptors to about the same extent, whereas dopamine showed only a mild stimulation of b1-receptors, without any effects on a- or b2-receptors. Additionally, it was observed that the effects of epinine were largely due to its direct action on receptors, while dopamine also produced some of its effects indirectly, by stimulating norepinephrine release.
Im quite skeptical of the above compounds being tested, mucuna is a neuroprotective form of ldopa but it probably wont work on its own as without a periphal conversion inhibitor there wont be much ldopa in the brain, it must work trough a differened mechanism.Pharmacology
Methyldopa has a dual mechanism of action:
- It is a competitive inhibitor of the enzyme DOPA decarboxylase, also known as aromatic L-amino acid decarboxylase, which converts L-DOPA into dopamine. Dopamine is a precursor for norepinephrine (noradrenaline) and subsequently epinephrine(adrenaline). This inhibition results in reduced dopaminergic and adrenergic neurotransmission in the peripheral nervous system. This effect may lower blood pressure and cause central nervous system effects such as depression, anxiety, apathy, anhedonia, and parkinsonism.
- It is converted to a-methylnorepinephrine by dopamine beta-hydroxylase (DBH). a-methylnorepinephrine is an agonist of presynaptic central nervous system a2-adrenergic receptors. Activation of these receptors in the brainstem appears to inhibit sympathetic nervous system output and lower blood pressure. This is also the mechanism of action of clonidine.
Posted 15 February 2013 - 07:02 AM
Youve got AvPD? thats usually only responsive to amphetamine, like ADHD and often comorbid with that too.
Posted 15 February 2013 - 07:12 AM
Im quite skeptical of the above compounds being tested, mucuna is a neuroprotective form of ldopa but it probably wont work on its own as without a periphal conversion inhibitor there wont be much ldopa in the brain, it must work trough a differened mechanism.
Edited by Galaxyshock, 15 February 2013 - 07:13 AM.
Posted 15 February 2013 - 07:55 AM
But you do enjoy social situations once you are in them? if thats the case and you got the confidence then this is your issue.
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