25 replies to this topic

[richards2324]

I believe my anxiety and depression are caused from low dopamine do to experiences I’ve had with two dopaminergic drugs (I had positive effects from wellbutrin and mucuna pruriens a Chinese bean with L-dopa in it) as I think a lot of other cases are too and that SSRI’s are overly prescribed medications that a lot of people don’t respond to. Dopamine increase motivation and reward and norepinephrine the byproduct of dopamine increases focus and concentration which all depressed people lack.  There are virtually no DRI’s other than research chemicals which I don’t understand their rarity(haven’t researched that a lot). I’m finding it extremely hard to find a safe longterm antidepressant that boosts dopamine, especially ones that are on the market.

 ( something like this)

 

Does anyone know what I could try if I was trying to boost my dopamine? Or does anyone know of any NDRI’s that have a stronger affinity for dopamine that would be effective and with a good half life(not Ritalin and the such either) or lastly, just normal NDRI’s(don’t want these because they have a tendency to increase anxiety long-term, I’ve tried Wellbutrin it didn’t work)? I’d prefer ones that are on the market but if someone can find ones off the market that are safe that’d be useful too.Is Amineptine(tricyclic, possible liver damage) a good NDRI? It prefers dopamine over norepinephrine. It has a short half life which could make it more addictive and less suitable for a longterm antidepressant. It’s hard to obtain and the source I have I wouldn’t know the purity of it as I can’t test it although it looks promising as an antidepressant.

 

I’m currently set on serzone ( an SNDRI and serotonin antagonist, possible liver damage 1 in 250,000 according to wiki don’t if that is correct), and the MAOI’s Parnate (works more on MAOI B then A), Nardil(works equally on MAOI A and B), selegiline(MAOI B). Also, dopamine agonists although I don’t know if they would be effective antidepressants. Overall, MAOI’s have the most drugs that boost dopamine, that are FDA prescribed, equally among the other neurotransmitters instead of norepinephrine more and such. The fact that even if they are MAOI type A they still boost dopamine equally, is how I take it, to the other monoamines (tyramine, serotonin, norepinephrine). There just aren’t a lot of NDRI’s, DRI’s, and triple reuptake inhibitors.

 

I just started modafinil as it's supposed to be a weak dopamine reuptake inhibitor but don't seem to be getting any results after 3 tabs(2 last night and one this morning).

 

List of MAOI’s:  http://mentalhealthd...ase-inhibitors/

 

List of some NDRI’s: http://mentalhealthd...ors-ndris-list/

 

-Focalin-This drug consists of the D-stereoisomer of methylphenidate (Ritalin) and was developed by the company Novartis as an ADHD medication. It functions by preventing reuptake of norepinephrine and dopamine and elicits a stimulant effect on the CNS. It is known to be well-tolerated and effective when used for attentional deficits and has also been considered as an adjunct strategy for treating certain cases of depression.

 

-Ethylphenidate –not sure if this is safe, read a lot about how it disagrees with the body, looking for a safe longterm antidepressant

This is a drug that functions as a psychostimulant and is considered relatively similar to methylphenidate (Ritalin) in its effects. It functions as a norepinephrine-dopamine reuptake inhibitor, with a stronger affinity for dopamine.

Nomifensine looks safe except for the risk of haemolytic anaemia to which the FDA withdrew approval for nomifensine on March 20, 1992 although it doesn’t prefer dopamine over norepinephrine

 

List of NDRIs according to wiki

The section only lists compounds that are selective for NET and DAT relative to the serotonin transporter (SERT). For a list of compounds that inhibit reuptake at all three transporters, see serotonin-norepinephrine-dopamine reuptake inhibitor.

Many NDRIs exist, including the following:

·         Amineptine (Survector, Maneon, Directim)

·         Bupropion (Wellbutrin)^[2]

·         Desoxypipradrol (2-DPMP)

·         Dexmethylphenidate (Focalin)

·         Difemetorex (Cleofil)

·         Diphenylprolinol (D2PM)

·         Ethylphenidate

·         Fencamfamine (Glucoenergan, Reactivan)

·         Fencamine (Altimina, Sicoclor)

·         Lefetamine (Santenol)

·         Methylenedioxypyrovalerone(MDPV)

·         Methylphenidate (Ritalin, Concerta, Metadate, Methylin, Rubifen, Stimdate)

·         Nomifensine (Merital)

·         O-2172

·         Oxolinic acid

·         Pipradrol (Meretran)

·         Prolintane (Promotil, Katovit)—experience- http://www.longecity...prolintane-hcl/

·         Pyrovalerone (Centroton, Thymergix)

·         Tametraline (CP-24,411)

·         WY-46824

[aconita]

I would suggest to focus first on lifestyle ad nutrition, exercise boost dopamine, a proper omega 3/6 ratio and sound nutrition helps too.

 

Drugs always comes with they array of unpleasant side effects, supplementing levodopa is not very safe even if it comes from mucuna, the only drug I am aware of that may help without causing too much damage is selegiline 2,5mg once a week.

 

Low testosterone and HGH may cause depression too, maybe it would be worth to check those out.

 

 

[richards2324]

I would suggest to focus first on lifestyle ad nutrition, exercise boost dopamine, a proper omega 3/6 ratio and sound nutrition helps too.

 

Drugs always comes with they array of unpleasant side effects, supplementing levodopa is not very safe even if it comes from mucuna, the only drug I am aware of that may help without causing too much damage is selegiline 2,5mg once a week.

 

Low testosterone and HGH may cause depression too, maybe it would be worth to check those out.

I've already tried diet and nutrition.  I think Mucuna is safe but it's  not working anyway.  If you boost testosterone it boosts your dopamine right?

[Adam Karlovsky]

Partially agreeing with aconinita, these are some things you can consider:

Some types of depression can go into spontaneous remission with the simple supplementation of nutrients such as 1.5g magnesium glycinate per day, or 200-2200mg of EPA in excess of DHA each day. There are many other examples, such as zinc, lithium, iron, calcium and chromium, so nutrition is not to be overlooked. It may be as simple as a serum mineral test, looking for minerals you are deficient or low in. And yes, having low hormone levels of testosterone can cause depressed mood, irritability and fearfulness, though most depressed people are not testosterone deficient. 

Meanwhile, loading up on dopamine and norepinephrine may be a naive strategy. For example, increasing norepinephrine may turn mild depression into productive crankiness, or it might offer a severely depressed person the 'mental energy' to actually commit suicide. A balanced and open approach is needed to tackle depression, and having someone monitor you is important.

I do know someone who has had success with amineptine and selegiline, but they've had to buy amineptine on the grey market, as they've no legal, local access to it. Having said that, I also know people who've had success with tianeptine and selegiline. As for modafinil, I would not expect modafinil to have much of an effect on depression, but it might make you less sleepy, and some depressed people have hypersomnia, and sleeping too much can exacerbate symptoms of depression. Or as mentioned above it could make you cranky productive, or increase your risk of suicide, if taken alone. Taken as part of a stack it might be a reasonable strategy, but I would hesitate to take large doses (more than 100mg per day) and rather focus on other treatments.

 

And of course exercise is a good treatment for the depressed, if they have the mental energy to do any. https://en.wikipedia...henylethylamine

Some further reading for those who are interested:
 

    Buspirone (Buspar) might seem more promising. It acts to desensitise the inhibitory autoreceptor 5-HT1A subtype of serotonin receptor, thereby modulating serotonin release and (sometimes) promoting a brightening of mood. Thus buspirone can be useful in anxious depressive states. Its active metabolite 1-PP is an anxiolytic 5-HT1A partial agonist too. Buspirone lacks the intellect-clouding effects of other clinical and alcoholic anti-anxiety agents. It's not a muscle relaxant. It's only mildly sedating. Yet buspirone's weak and equivocal effects on sub-types of dopamine function, while useful commercially for the purposes of touting its lack of "abuse-potential", mean buspirone isn't very exciting or popular. Crucially, unlike the benzodiazepines, it's not a fast-acting drug. Several weeks of use may pass before its dubious psychological benefits are felt. Researchers hope that newer 5-HT1A agonists in the pipeline will be more effective. Alas any therapeutic gain is likely to be modest.

    Amineptine (Survector) is a cleanish, (relatively) selective dopamine reuptake blocker. Higher doses promote dopamine release too. Amineptine is pro-sexual and liable occasionally to cause spontaneous orgasms. It is a mild but pleasant psychostimulant and a fast-acting mood-brightener. Unlike most other tricyclics, it doesn't impair libido or cognitive function. Unlike typical stimulants and other activating agents, it may actually improve sleep architecture. Scandalously, amineptine isn't licensed and marketed in Britain and America. For it is feared it might have "abuse-potential". FDApressure led to its withdrawal in Europe too. This drove amineptine onto the pharmaceutical grey market, discomfiting doctors and patients alike.

        Another "French" option is amineptine's cousin, tianeptine (Stablon). Tianeptine is a neuroprotective antidepressant that reverses the neuronal damage and lasting misery caused by uncontrolled stress. Chronic stress causes dysphoria by inducing corticotropin-releasing factor (CRF2) receptor stimulation of dynorphin release. The endogenous opioid peptide dynorphin activates the unpleasant kappa opioid receptors. Tianeptine acts both as a non-sedating anti-anxiety agent and a non-stimulating mood-brightener. Its use increases extracellular dopamine concentration in the nucleus accumbens and, at higher doses, in the frontal cortex. Uniquely in clinical medicine, tianeptine acts as a selective serotonin reuptake enhancer. Its puzzling efficacy as an antidepressant illustrates how little modern psychiatric medicine really understands about mind, mood and depression. Like other contemporary antidepressants, tianeptine's therapeutic action presumably depends on downstreamadaptations both between and within neurons occurring over a period of several weeks. Chronic tianeptine use reverses stress-induced hippocampal dendritric atrophy and amgydaloid dendritichypertrophy, which is just as nasty as it sounds. But the precise molecular mechanisms are obscure. Tianeptine/Stablon is not licensed in North America primarily because its patent has expired.

        A breakthrough in tianeptine research was announced in July 2014 with the unexpected discovery that tianeptine is a full agonist at the mu and delta opioid receptors with negligible effect at the kappaopioid receptors. Selective mu opioid agonists in the brain's twin "hedonic hotspots" typically induce euphoria. Selective kappa agonists typically induce dysphoria. The role of central delta opioid receptors is poorly understood. Dual activation of the mu and, less potently, the delta opioid receptors may be critical to tianeptine's mood-brightening and anxiolytic effect - a therapeutic action seemingly unaccompanied by the physiological tolerance and dependence that have plagued traditional opioids. All previous research into tianeptine may need to be re-evaluated in this light. More research is urgently needed.

  Depressive hypersomniacs who fare poorly on SSRIs, or can't get hold of amineptine or EC-licensed reboxetine, might consider trying a so-called eugeroic ("good arousal") agent instead. Alpha1-adrenergic agonists like adrafinil (Olmifon) and modafinil (Provigil, Alertec) are centrally-acting psychostimulants that can brighten mood and sharpen mental focus. They stimulate the noradrenergic post-synaptic receptors, increase glutamatergic transmission, and activate the wakefulness-promoting orexinergic neurons, thereby boosting alertness, memory, mood, motivation and energy. At sensible dosages, they are remarkably free of side-effects. Modafinil was licensed by the FDA as Provigil for the treatment of narcolepsy in Dec 1998; and in September 2003, an advisory panel to the FDA endorsedits use for treating shift work sleep disorder and sleep apnea. However, the significance of these prescribing indications is rapidly being eroded. Modafinil and adrafinil are now mainly used off-label as so-called lifestyle drugs.

  Agomelatine (Valdoxan, Melitor, Thymanax) is a novel antidepressant and anti-anxiety agent developed by Servier and licensed in the European Union in February 2009. A synthetic analogue of the natural hormone melatonin, agomelatine is a potent melatonin receptor agonist and a serotonin 5-HT2C receptor antagonist. Blockade of the neural 5-HT2C receptors enhances frontocortical adrenergic and dopaminergic transmission, potentially improving cognitive performance. In "animal models", agomelatine also reduces the adverse effects of stress on memory. By acting as a melatonin receptor agonist, agomelatine improves sleep quality. When taken once daily before bedtime, agomelatine doesn't cause daytime drowsiness and sedation like the old tricyclics; nor does its use kill libido like the SSRIs. Agomelatine is typically well tolerated and remarkably free from adverse side-effects at therapeutic dosages. Drug giant Novartis acquired the US rights to agomelatine from Servier in 2006. In July 2009, Novartis announced it was delaying submission for US regulatory approval another three years while it conducted additional Phase III trials. Development for the US market was discontinued altogether in October 2011. American consumers must now order agomelatine online or from Europe.

 

- The Good Drug Guide, http://biopsychiatry.com/ 

 

 

 

Edited by Adam Karlovsky, 21 January 2016 - 11:25 PM.

[aconita]

Neurotransmitters and hormones are related, therefore changing one will effect the other too, of course.

 

What about exercise?

[richards2324]

Neurotransmitters and hormones are related, therefore changing one will effect the other too, of course.

 

What about exercise

 

Working out doesn't do anything anymore that's how depleted my body is. I used to workout extremely hard. I'm a very healthy person I've done all I can health wise trust me.

[richards2324]

 

Partially agreeing with aconinita, these are some things you can consider:

Some types of depression can go into spontaneous remission with the simple supplementation of nutrients such as 1.5g magnesium glycinate per day, or 200-2200mg of EPA in excess of DHA each day. There are many other examples, such as zinc, lithium, iron, calcium and chromium, so nutrition is not to be overlooked. It may be as simple as a serum mineral test, looking for minerals you are deficient or low in. And yes, having low hormone levels of testosterone can cause depressed mood, irritability and fearfulness, though most depressed people are not testosterone deficient. 

Meanwhile, loading up on dopamine and norepinephrine may be a naive strategy. For example, increasing norepinephrine may turn mild depression into productive crankiness, or it might offer a severely depressed person the 'mental energy' to actually commit suicide. A balanced and open approach is needed to tackle depression, and having someone monitor you is important.

I do know someone who has had success with amineptine and selegiline, but they've had to buy amineptine on the grey market, as they've no legal, local access to it. Having said that, I also know people who've had success with tianeptine and selegiline. As for modafinil, I would not expect modafinil to have much of an effect on depression, but it might make you less sleepy, and some depressed people have hypersomnia, and sleeping too much can exacerbate symptoms of depression. Or as mentioned above it could make you cranky productive, or increase your risk of suicide, if taken alone. Taken as part of a stack it might be a reasonable strategy, but I would hesitate to take large doses (more than 100mg per day) and rather focus on other treatments.

 

And of course exercise is a good treatment for the depressed, if they have the mental energy to do any. https://en.wikipedia...henylethylamine

Some further reading for those who are interested:
 

    Buspirone (Buspar) might seem more promising. It acts to desensitise the inhibitory autoreceptor 5-HT1A subtype of serotonin receptor, thereby modulating serotonin release and (sometimes) promoting a brightening of mood. Thus buspirone can be useful in anxious depressive states. Its active metabolite 1-PP is an anxiolytic 5-HT1A partial agonist too. Buspirone lacks the intellect-clouding effects of other clinical and alcoholic anti-anxiety agents. It's not a muscle relaxant. It's only mildly sedating. Yet buspirone's weak and equivocal effects on sub-types of dopamine function, while useful commercially for the purposes of touting its lack of "abuse-potential", mean buspirone isn't very exciting or popular. Crucially, unlike the benzodiazepines, it's not a fast-acting drug. Several weeks of use may pass before its dubious psychological benefits are felt. Researchers hope that newer 5-HT1A agonists in the pipeline will be more effective. Alas any therapeutic gain is likely to be modest.

    Amineptine (Survector) is a cleanish, (relatively) selective dopamine reuptake blocker. Higher doses promote dopamine release too. Amineptine is pro-sexual and liable occasionally to cause spontaneous orgasms. It is a mild but pleasant psychostimulant and a fast-acting mood-brightener. Unlike most other tricyclics, it doesn't impair libido or cognitive function. Unlike typical stimulants and other activating agents, it may actually improve sleep architecture. Scandalously, amineptine isn't licensed and marketed in Britain and America. For it is feared it might have "abuse-potential". FDApressure led to its withdrawal in Europe too. This drove amineptine onto the pharmaceutical grey market, discomfiting doctors and patients alike.

        Another "French" option is amineptine's cousin, tianeptine (Stablon). Tianeptine is a neuroprotective antidepressant that reverses the neuronal damage and lasting misery caused by uncontrolled stress. Chronic stress causes dysphoria by inducing corticotropin-releasing factor (CRF2) receptor stimulation of dynorphin release. The endogenous opioid peptide dynorphin activates the unpleasant kappa opioid receptors. Tianeptine acts both as a non-sedating anti-anxiety agent and a non-stimulating mood-brightener. Its use increases extracellular dopamine concentration in the nucleus accumbens and, at higher doses, in the frontal cortex. Uniquely in clinical medicine, tianeptine acts as a selective serotonin reuptake enhancer. Its puzzling efficacy as an antidepressant illustrates how little modern psychiatric medicine really understands about mind, mood and depression. Like other contemporary antidepressants, tianeptine's therapeutic action presumably depends on downstreamadaptations both between and within neurons occurring over a period of several weeks. Chronic tianeptine use reverses stress-induced hippocampal dendritric atrophy and amgydaloid dendritichypertrophy, which is just as nasty as it sounds. But the precise molecular mechanisms are obscure. Tianeptine/Stablon is not licensed in North America primarily because its patent has expired.

        A breakthrough in tianeptine research was announced in July 2014 with the unexpected discovery that tianeptine is a full agonist at the mu and delta opioid receptors with negligible effect at the kappaopioid receptors. Selective mu opioid agonists in the brain's twin "hedonic hotspots" typically induce euphoria. Selective kappa agonists typically induce dysphoria. The role of central delta opioid receptors is poorly understood. Dual activation of the mu and, less potently, the delta opioid receptors may be critical to tianeptine's mood-brightening and anxiolytic effect - a therapeutic action seemingly unaccompanied by the physiological tolerance and dependence that have plagued traditional opioids. All previous research into tianeptine may need to be re-evaluated in this light. More research is urgently needed.

  Depressive hypersomniacs who fare poorly on SSRIs, or can't get hold of amineptine or EC-licensed reboxetine, might consider trying a so-called eugeroic ("good arousal") agent instead. Alpha1-adrenergic agonists like adrafinil (Olmifon) and modafinil (Provigil, Alertec) are centrally-acting psychostimulants that can brighten mood and sharpen mental focus. They stimulate the noradrenergic post-synaptic receptors, increase glutamatergic transmission, and activate the wakefulness-promoting orexinergic neurons, thereby boosting alertness, memory, mood, motivation and energy. At sensible dosages, they are remarkably free of side-effects. Modafinil was licensed by the FDA as Provigil for the treatment of narcolepsy in Dec 1998; and in September 2003, an advisory panel to the FDA endorsedits use for treating shift work sleep disorder and sleep apnea. However, the significance of these prescribing indications is rapidly being eroded. Modafinil and adrafinil are now mainly used off-label as so-called lifestyle drugs.

  Agomelatine (Valdoxan, Melitor, Thymanax) is a novel antidepressant and anti-anxiety agent developed by Servier and licensed in the European Union in February 2009. A synthetic analogue of the natural hormone melatonin, agomelatine is a potent melatonin receptor agonist and a serotonin 5-HT2C receptor antagonist. Blockade of the neural 5-HT2C receptors enhances frontocortical adrenergic and dopaminergic transmission, potentially improving cognitive performance. In "animal models", agomelatine also reduces the adverse effects of stress on memory. By acting as a melatonin receptor agonist, agomelatine improves sleep quality. When taken once daily before bedtime, agomelatine doesn't cause daytime drowsiness and sedation like the old tricyclics; nor does its use kill libido like the SSRIs. Agomelatine is typically well tolerated and remarkably free from adverse side-effects at therapeutic dosages. Drug giant Novartis acquired the US rights to agomelatine from Servier in 2006. In July 2009, Novartis announced it was delaying submission for US regulatory approval another three years while it conducted additional Phase III trials. Development for the US market was discontinued altogether in October 2011. American consumers must now order agomelatine online or from Europe.

 

- The Good Drug Guide, http://biopsychiatry.com/ 

 

 

 

 

so amineptine is feasible for a longterm solution?  I tried tianeptine for a day I didn't really like the affects of the serotonin I try to stay away from serotonin as I had really bad experience with Paxil withdrawal and Paxil didn't even make me feel any better the year I was taking it.

Edited by Adam Karlovsky, 21 February 2016 - 02:35 AM.

[Adam Karlovsky]

 

 

so amineptine is feasible for a longterm solution?  I tried tianeptine for a day I didn't really like the affects of the serotonin I try to stay away from serotonin as I had really bad experience with Paxil withdrawal and Paxil didn't even make me feel any better the year I was taking it.

 

Do not conflate Paxil (an SSRI and an NRI) with Tianeptine (a tricyclic SSRE that also selectively increases extracellular dopamine and is also a mu and delta opioid receptor agonist). They work very differently, and don't expect Tianeptine's effects to become apparent after a single dose, it takes 7 days minimum for initial improvements, and in some people 3-4 weeks. I doubt anything will 'cure' your depression with a single dose, stop expecting acute effects, that's setting yourself up for addiction, start looking for chronic effects instead.

But to answer your first question, I don't see why amineptine isn't a legitimate long term solution.

Edited by Adam Karlovsky, 22 January 2016 - 01:03 AM.

[aconita]

What about uridine monophosphate?

[richards2324]

What about uridine monophosphate?

http://www.powdercit...hosphate-powder

 

I supposed I could try this according to powder city it increases dopamine.

 

Research is also being conducted into the use of this supplement as a method to improve age related memory loss [9, 10] and mood [1]. It boosts mood by increasing levels of dopamine in the brain [1], which not only improves your mood but your motivation and energy as well

[richards2324]

 

 

 

so amineptine is feasible for a longterm solution?  I tried tianeptine for a day I didn't really like the affects of the serotonin I try to stay away from serotonin as I had really bad experience with Paxil withdrawal and Paxil didn't even make me feel any better the year I was taking it.

 

"Do not conflate Paxil (an SSRI and an NRI) with Tianeptine (a tricyclic SSRE that also selectively increases extracellular dopamine and is also a mu and delta opioid receptor agonist). They work very differently, and don't expect Tianeptine's effects to become apparent after a single dose, it takes 7 days minimum for initial improvements, and in some people 3-4 weeks. I doubt anything will 'cure' your depression with a single dose, stop expecting acute effects, that's setting yourself up for addiction, start looking for chronic effects instead.

But to answer your first question, I don't see why amineptine isn't a legitimate long term solution."

 

 

Tianeptine still releases serotonin so you will get a similar to an ssri in my opinion in that regard. I'm not expecting acute affects I just didn't like how it felt. As to the comment before this one I would prefer a dopamine boost over a norepinephrine boosts because I know norepinephrine can lead to anxiety.

Edited by Adam Karlovsky, 21 February 2016 - 02:37 AM.

[BasicBiO]

"Meanwhile, loading up on dopamine and norepinephrine may be a naive strategy. For example, increasing norepinephrine may turn mild depression into productive crankiness.."

 

This is precisely what Selegeline did for me.  Good initial boost that I appreciated, but then quickly elevated to outright pissiness..it was bad.

 

OP, my depression sounds like yours. I've lifted for over 20 years, my workouts are intense and depleting. This is compounded by my job which requires intense hiking.  Add familial and financial stress and pow, I was laid low for several years.  

 

Take it easy with your workouts, limit them to an hour.  Add in lots of B vitamins, selenium, zinc, chromium and use the form that is appropriate for your genotype. NSI-189 has helped me tremendously as has hormone replacement therapy.  The two go hand in hand for me and I feel like I've gone from feeling 70 years old to 35. I'm 43 at the moment.

 

Uridine also works well if you don't want to go the drug route. For me it provides an instant boost, but continuous use seems to up end my mood after a week or two. 

[richards2324]

"Meanwhile, loading up on dopamine and norepinephrine may be a naive strategy. For example, increasing norepinephrine may turn mild depression into productive crankiness.."

 

This is precisely what Selegeline did for me.  Good initial boost that I appreciated, but then quickly elevated to outright pissiness..it was bad.

 

OP, my depression sounds like yours. I've lifted for over 20 years, my workouts are intense and depleting. This is compounded by my job which requires intense hiking.  Add familial and financial stress and pow, I was laid low for several years.  

 

Take it easy with your workouts, limit them to an hour.  Add in lots of B vitamins, selenium, zinc, chromium and use the form that is appropriate for your genotype. NSI-189 has helped me tremendously as has hormone replacement therapy.  The two go hand in hand for me and I feel like I've gone from feeling 70 years old to 35. I'm 43 at the moment.

 

Uridine also works well if you don't want to go the drug route. For me it provides an instant boost, but continuous use seems to up end my mood after a week or two. 

Selegiline is just supposed to boost dopamine though right? It should effect norepinephrine only secondarily after it converts from dopamine to norepinephrine which shouldn’t cause the bad imbalanced effects of norepinephrine alone.

 

Do you still take NSI-189? I heard it is like wellbutrin I was wanting to try it. How does it make you feel? It’s supposed to work on dopamine right?

 

Continuous use of uridine stops working after a week or two ur saying?

Edited by richards2324, 17 February 2016 - 07:56 PM.

[Adam Karlovsky]

Tianeptine still releases serotonin so you will get a similar to an ssri in my opinion in that regard. I'm not expecting acute affects I just didn't like how it felt. As to the comment before this one I would prefer a dopamine boost over a norepinephrine boosts because I know norepinephrine can lead to anxiety.

 

No, it simply does not release serotonin, and does not have a similar effect to an SSRI.

 

 

A reuptake enhancer (RE), also sometimes referred to as a reuptake activator, is a type of reuptake modulator which enhances the plasmalemmal transporter-mediated reuptake of aneurotransmitter from the synapse into the pre-synaptic neuron, leading to a decrease in the extracellular concentrations of the neurotransmitter and therefore a decrease in neurotransmission.

The antidepressant tianeptine was once claimed to be a (selective) serotonin reuptake enhancer (SRE or SSRE), but the role of serotonin reuptake in its mechanism is doubtful. Tianeptine has no affinity to the serotonin transporter, neither increases nor decreases extracellular levels of serotonin in cortico-limbic structures of conscious rats, and it didn't show any other long-term effect on the serotonin pathway.^[1] Thus, tianeptine's role as an SSRE may have been the coincidence of a yet unknown mechanism of action.

- https://en.wikipedia...uptake_enhancer

Have a thorough read about tianeptine here, here and here.

[Finn]

I believe my anxiety and depression are caused from low dopamine do to experiences I’ve had with two dopaminergic drugs (I had positive effects from wellbutrin and mucuna pruriens a Chinese bean with L-dopa in it) 

 

 

so amineptine is feasible for a longterm solution?  I tried tianeptine for a day I didn't really like the affects of the serotonin I try to stay away from serotonin as I had really bad experience with Paxil withdrawal and Paxil didn't even make me feel any better the year I was taking it.

 

 

 

 

In animal studies, squirrel monkeys and rats could be induced to self-administer bupropion (Wellbutrin) intravenously, monkeys could be induced to self-administer modafini, etc. 

 

In general, dopaminergics tend to give nice feeling at least initially from the first dose to both animals and humans, regardless of their condition, that's why it is so easy to induce animals to self-administer them. So you responding to dopaminergics positively initially doesn't necessarily mean that they will cure your depression in long term. 

 

Not getting a good response from one serotonergic drug, Paxil, doesn't mean that other serotonergic drugs might not work for you. You should give antidepressants also some time, even if you feel somewhat weird on day 1, that doesn't mean that antidepressant doesn't work for you. But you shouldn't waste too much on time on any single antidepressant either. Why were you on Paxil  for a year if it was not helping you?

 

 

 

Edited by Finn, 21 April 2016 - 04:42 PM.

[richards2324]

 

I believe my anxiety and depression are caused from low dopamine do to experiences I’ve had with two dopaminergic drugs (I had positive effects from wellbutrin and mucuna pruriens a Chinese bean with L-dopa in it) 

 

 

so amineptine is feasible for a longterm solution?  I tried tianeptine for a day I didn't really like the affects of the serotonin I try to stay away from serotonin as I had really bad experience with Paxil withdrawal and Paxil didn't even make me feel any better the year I was taking it.

 

 

 

 

In animal studies, squirrel monkeys and rats could be induced to self-administer bupropion (Wellbutrin) intravenously, monkeys could be induced to self-administer modafini, etc. 

 

In general, dopaminergics tend to give nice feeling at least initially from the first dose to both animals and humans, regardless of their condition, that's why it is so easy to induce animals to self-administer them. So you responding to dopaminergics positively initially doesn't necessarily mean that they will cure your depression in long term. 

 

Not getting a good response from one serotonergic drug, Paxil, doesn't mean that other serotonergic drugs might not work for you. You should give antidepressants also some time, even if you feel somewhat weird on day 1, that doesn't mean that antidepressant doesn't work for you. But you shouldn't waste too much on time on any single antidepressant either. Why were you on Paxil  for a year if it was not helping you?

 

I'm positive I have low dopamine every time I took dopamine through wellbutrin, mucuna pruriens, and Sam-e my anxiety was removed and I felt relaxed again all 3 of which stopped working though. It's not just a nice feeling thing.

[Finn]

 

 

I believe my anxiety and depression are caused from low dopamine do to experiences I’ve had with two dopaminergic drugs (I had positive effects from wellbutrin and mucuna pruriens a Chinese bean with L-dopa in it) 

 

 

so amineptine is feasible for a longterm solution?  I tried tianeptine for a day I didn't really like the affects of the serotonin I try to stay away from serotonin as I had really bad experience with Paxil withdrawal and Paxil didn't even make me feel any better the year I was taking it.

 

 

 

 

In animal studies, squirrel monkeys and rats could be induced to self-administer bupropion (Wellbutrin) intravenously, monkeys could be induced to self-administer modafini, etc. 

 

In general, dopaminergics tend to give nice feeling at least initially from the first dose to both animals and humans, regardless of their condition, that's why it is so easy to induce animals to self-administer them. So you responding to dopaminergics positively initially doesn't necessarily mean that they will cure your depression in long term. 

 

Not getting a good response from one serotonergic drug, Paxil, doesn't mean that other serotonergic drugs might not work for you. You should give antidepressants also some time, even if you feel somewhat weird on day 1, that doesn't mean that antidepressant doesn't work for you. But you shouldn't waste too much on time on any single antidepressant either. Why were you on Paxil  for a year if it was not helping you?

 

I'm positive I have low dopamine every time I took dopamine through wellbutrin, mucuna pruriens, and Sam-e my anxiety was removed and I felt relaxed again all 3 of which stopped working though. It's not just a nice feeling thing.

 

 

Pharmaceutically induced euphoria can temporarily fix anxiety, depression and plenty of other psychiatric issues. The bad thing about euphoria is that it is by it's definition an unsustainable state so it will always end fast with any euphoria producing substance, and might only come back with long breaks in use or increase of dose (usually not recommended). When those 3 substances stopped working for you, it's not like their pharmacodynamic mechanisms stopped working for you, those dopamine levels just were not enough for you to produce euphoria anymore.

Edited by Finn, 23 April 2016 - 07:30 PM.

[richards2324]

so i need  a higher dose? I tried that with the mucuna pruriens and a tiny bit with the Sam-e. the wellbutrin didn't work the second time I took it no matter what the dose I took I went high enough.

[irony]

straight adderall XR has helped my depression and anxiety in lowish doses from 10-20mg.   Have you tried that?

Edited by irony, 24 April 2016 - 07:05 PM.

[Finn]

so i need  a higher dose? I tried that with the mucuna pruriens and a tiny bit with the Sam-e. the wellbutrin didn't work the second time I took it no matter what the dose I took I went high enough.

 

No. Euphoria experiences vary from individual to individual and especially with the "non-abusable"/"low abuse potential" stuff it is possible that you get euphoria only once. My point was that euphoria is not the long term solution it is just a nice boost at the beginning of the treatment. Also accept that it will end relatively fast, don't think the euphoria as the real fix, if you are not expecting the end of euphoria, the "counter placebo" effect created by the disappointment can give you feeling that the whole drug stopped working even though it didn't stop working. 

 

Depression is a malfunction mode of brain, some of this malfunction can even be seen through fmri, some about that, over-activity of certain regions of brain, causing certain thought patterns in the video below

 

 

Brain is pretty complex so there are multiple vastly different antidepressants that can kick the brain out of that malfunctioning mode, drugs effects varying from individual to another, kinda partially reboot the computer, but it isn't so complex that all stuff affecting neurotransmitters would be equally good, some routes are just overall not effective and that's why there are failed antidepressants like reboxetine. 

 

Working antidepressant kicks your brain out of the malfunction mode, when this malfunction mode that harmed your brain ends or becomes lesser, then starts neurogenesis, the natural healing process, the brain repairing the damage, all antidepressants induce neurogenesis. This will take time. You should give antidepressants generally about 2 months to start to work, then move to another if it doesn't work for you. Any instant cure is most likely just euphoria, which will pass, don't be too disappointed if it ends. 

 

There are virtually no DRI’s other than research chemicals which I don’t understand their rarity

 

 

There is reason for that, DRI isn't good sustainable solution for pretty much anything.

Edited by Finn, 25 April 2016 - 02:25 PM.

[richards2324]

straight adderall XR has helped my depression and anxiety in lowish doses from 10-20mg.   Have you tried that?

doesn't adderall cause adrenal fatigue or not at that low of a dose?

[richards2324]

 

so i need  a higher dose? I tried that with the mucuna pruriens and a tiny bit with the Sam-e. the wellbutrin didn't work the second time I took it no matter what the dose I took I went high enough.

 

No. Euphoria experiences vary from individual to individual and especially with the "non-abusable"/"low abuse potential" stuff it is possible that you get euphoria only once. My point was that euphoria is not the long term solution it is just a nice boost at the beginning of the treatment. Also accept that it will end relatively fast, don't think the euphoria as the real fix, if you are not expecting the end of euphoria, the "counter placebo" effect created by the disappointment can give you feeling that the whole drug stopped working even though it didn't stop working. 

 

Depression is a malfunction mode of brain, some of this malfunction can even be seen through fmri, some about that, over-activity of certain regions of brain, causing certain thought patterns in the video below

 

 

Brain is pretty complex so there are multiple vastly different antidepressants that can kick the brain out of that malfunctioning mode, drugs effects varying from individual to another, kinda partially reboot the computer, but it isn't so complex that all stuff affecting neurotransmitters would be equally good, some routes are just overall not effective and that's why there are failed antidepressants like reboxetine. 

 

Working antidepressant kicks your brain out of the malfunction mode, when this malfunction mode that harmed your brain ends or becomes lesser, then starts neurogenesis, the natural healing process, the brain repairing the damage, all antidepressants induce neurogenesis. This will take time. You should give antidepressants generally about 2 months to start to work, then move to another if it doesn't work for you. Any instant cure is most likely just euphoria, which will pass, don't be too disappointed if it ends. 

 

There are virtually no DRI’s other than research chemicals which I don’t understand their rarity

 

 

There is reason for that, DRI isn't good sustainable solution for pretty much anything.

 

well that's dissapointing that a DRI isn't sustainable I was thinking about ordering amineptine. There aren't that many drugs that provide dopamine I'm on nardil right now but it's not working at the max dose of 90 mg I was thinking of trying levodopa as I will die from lack of dopamine I'm positive of this I've been through hell and back an antipsychotic saved me the first time but It's not working now.  The norepinephrine kicked in a little on nardil though and that's helped me depression so I know i wanna get on an NRI also if nardil doesn't work all the way

[irony]

 

straight adderall XR has helped my depression and anxiety in lowish doses from 10-20mg.   Have you tried that?

doesn't adderall cause adrenal fatigue or not at that low of a dose?

 

 

I don't know.   Never heard of that being a problem though

[richards2324]

 

 

straight adderall XR has helped my depression and anxiety in lowish doses from 10-20mg.   Have you tried that?

doesn't adderall cause adrenal fatigue or not at that low of a dose?

 

 

I don't know.   Never heard of that being a problem though

 

 

 

hmm it's an amphetamine I thought it did that

 

 

[Finn]

 

 

There is reason for that, DRI isn't good sustainable solution for pretty much anything.

 

well that's dissapointing that a DRI isn't sustainable I was thinking about ordering amineptine. There aren't that many drugs that provide dopamine I'm on nardil right now but it's not working at the max dose of 90 mg I was thinking of trying levodopa as I will die from lack of dopamine I'm positive of this I've been through hell and back an antipsychotic saved me the first time but It's not working now.  The norepinephrine kicked in a little on nardil though and that's helped me depression so I know i wanna get on an NRI also if nardil doesn't work all the way

 

As her pharmacodynamics mechanism, dopamine reuptake inhibition is sustainable. But DRI alone isn't sustainable solution for pretty much anything.  On the first day when you felt that the Wellbutrin didn't work for you anymore, your dopamine reuptake inhibition was about the same as it was on the last day it worked, and stronger than on the first day it worked. Your body didn't just randomly disable Wellbutrin's mechanism's, your body adapted to to the results of the mechanism, and it didn't produce the mild euphoria anymore. It doesn't matter how you try to produce dopaminergic euphoria, your body adapts to the results, the mechanism that led to the results doesn't matter. The same with other dopaminergics that "stopped working for you". The mechanism didn't stop from working, rather your body adapted to  the results. 

 

http://global.britan...nce/homeostasis

Any system in dynamic equilibrium tends to reach a steady state, a balance that resists outside forces of change. When such a system is disturbed, built-in regulatory devices respond to the departures to establish a new balance; such a process is one of feedback control. All processes of integration and coordination of function, whether mediated by electrical circuits or by nervous and hormonal systems, are examples of homeostatic regulation.

 

 

Homeostatis, is overall nice, eventhough it prevents constant euphoria, it also prevents nasty stuff, Parkinson's disease might be caused by breakdown of dopamine homeostatis.

 

The problem is that you have confused the temporary relief brought by dopaminergic euphoria for a real solution, and you keep chasing it. It isn't going to work, just like you can't use of opioidergics to produce euphoria constantly and use that euphoria as solution for your issues. Your body adapts to the results. 

Edited by Finn, 29 April 2016 - 01:39 PM.

[richards2324]

 

 

 

There is reason for that, DRI isn't good sustainable solution for pretty much anything.

 

well that's dissapointing that a DRI isn't sustainable I was thinking about ordering amineptine. There aren't that many drugs that provide dopamine I'm on nardil right now but it's not working at the max dose of 90 mg I was thinking of trying levodopa as I will die from lack of dopamine I'm positive of this I've been through hell and back an antipsychotic saved me the first time but It's not working now.  The norepinephrine kicked in a little on nardil though and that's helped me depression so I know i wanna get on an NRI also if nardil doesn't work all the way

 

As her pharmacodynamics mechanism, dopamine reuptake inhibition is sustainable. But DRI alone isn't sustainable solution for pretty much anything.  On the first day when you felt that the Wellbutrin didn't work for you anymore, your dopamine reuptake inhibition was about the same as it was on the last day it worked, and stronger than on the first day it worked. Your body didn't just randomly disable Wellbutrin's mechanism's, your body adapted to to the results of the mechanism, and it didn't produce the mild euphoria anymore. It doesn't matter how you try to produce dopaminergic euphoria, your body adapts to the results, the mechanism that led to the results doesn't matter. The same with other dopaminergics that "stopped working for you". The mechanism didn't stop from working, rather your body adapted to  the results. 

 

http://global.britan...nce/homeostasis

Any system in dynamic equilibrium tends to reach a steady state, a balance that resists outside forces of change. When such a system is disturbed, built-in regulatory devices respond to the departures to establish a new balance; such a process is one of feedback control. All processes of integration and coordination of function, whether mediated by electrical circuits or by nervous and hormonal systems, are examples of homeostatic regulation.

 

 

Homeostatis, is overall nice, eventhough it prevents constant euphoria, it also prevents nasty stuff, Parkinson's disease might be caused by breakdown of dopamine homeostatis.

 

The problem is that you have confused the temporary relief brought by dopaminergic euphoria for a real solution, and you keep chasing it. It isn't going to work, just like you can't use of opioidergics to produce euphoria constantly and use that euphoria as solution for your issues. Your body adapts to the results. 

 

it could still work for like 5 years though or so right? i get that it's not a lifetime solution