Diamant - Adamantane Solution For Lab/R&D

[KyleKingsly]

@KyleKingsly @haidut

Maybe relevant for some of those concerned about DAWS

J Psychiatr Pract. 2017 May;23(3):191-199. doi: 10.1097/PRA.0000000000000237.
The Role of Amantadine Withdrawal in 3 Cases of Treatment-Refractory Altered Mental Status.
Fryml LD1, Williams KR, Pelic CG, Fox J, Sahlem G, Robert S, Revuelta GJ, Short EB.

Amantadine, which was originally developed as an antiviral medication, functions as a dopamine agonist in the central nervous system and consequently is utilized in the treatment of Parkinson disease, drug-induced extrapyramidal reactions, and neuroleptic malignant syndrome. For reasons that are not entirely understood, abrupt changes in amantadine dosage can produce a severe withdrawal syndrome. Existing medical literature describes case reports of amantadine withdrawal leading to delirium, which at times has progressed to neuroleptic malignant syndrome. Amantadine withdrawal may be under-recognized by mental health clinicians, which has the potential to lead to protracted hospital courses and suboptimal outcomes. The goal of this case series is to highlight the role of amantadine withdrawal in the cases of 3 medically complex patients with altered mental status. In the first case, the cognitive side effects of electroconvulsive therapy masked acute amantadine withdrawal in a 64-year-old man with Parkinson disease. In the second case, a 75-year-old depressed patient developed a catatonic delirium when amantadine was discontinued. Finally, a refractory case of neuroleptic malignant syndrome in a 57-year-old patient with schizoaffective disorder rapidly resolved with the reintroduction of outpatient amantadine. These cases highlight several learning objectives regarding amantadine withdrawal syndrome: First, it may be concealed by co-occurring causes of delirium in medically complex patients. Second, its symptoms are likely to be related to a cortical and limbic dopamine shortage, which may be reversed with electroconvulsive therapy or reintroduction of amantadine. Third, its clinical presentation may occur on a spectrum and may include features suggestive of delirium, catatonia, or neuroleptic malignant syndrome.

"The common features among these cases suggest that risk factors for this withdrawal phenomenon may include being elderly, presence of advanced parkinsonism, and duration of amantadine therapy for longer than 1 year."

Thanks so much for the share @Koveras, that all makes sense and reflects what I might expect, however, that's not quite enough to convince me that dopamine agonists are safe. If you check search for dopamine agonist experiences on the social anxiety forum, you'll see that there are healthy people that used dopamine agonists for their anxiety for different periods, and some of them still got bad withdrawals. Risk factors mean that the risk factor is significantly increased, but it doesn't mean you won't get DAWS if you don't have any of them.

In addition, in any case, there's a high probability of dopamine receptor downregulation, as there is with indirect agonists like amphetamine, etc. It's a unsustainable and unwise course of supplementation for healthy people, imo.

 

[haidut]

@KyleKingsly @haidut

Maybe relevant for some of those concerned about DAWS

J Psychiatr Pract. 2017 May;23(3):191-199. doi: 10.1097/PRA.0000000000000237.
The Role of Amantadine Withdrawal in 3 Cases of Treatment-Refractory Altered Mental Status.
Fryml LD1, Williams KR, Pelic CG, Fox J, Sahlem G, Robert S, Revuelta GJ, Short EB.

Amantadine, which was originally developed as an antiviral medication, functions as a dopamine agonist in the central nervous system and consequently is utilized in the treatment of Parkinson disease, drug-induced extrapyramidal reactions, and neuroleptic malignant syndrome. For reasons that are not entirely understood, abrupt changes in amantadine dosage can produce a severe withdrawal syndrome. Existing medical literature describes case reports of amantadine withdrawal leading to delirium, which at times has progressed to neuroleptic malignant syndrome. Amantadine withdrawal may be under-recognized by mental health clinicians, which has the potential to lead to protracted hospital courses and suboptimal outcomes. The goal of this case series is to highlight the role of amantadine withdrawal in the cases of 3 medically complex patients with altered mental status. In the first case, the cognitive side effects of electroconvulsive therapy masked acute amantadine withdrawal in a 64-year-old man with Parkinson disease. In the second case, a 75-year-old depressed patient developed a catatonic delirium when amantadine was discontinued. Finally, a refractory case of neuroleptic malignant syndrome in a 57-year-old patient with schizoaffective disorder rapidly resolved with the reintroduction of outpatient amantadine. These cases highlight several learning objectives regarding amantadine withdrawal syndrome: First, it may be concealed by co-occurring causes of delirium in medically complex patients. Second, its symptoms are likely to be related to a cortical and limbic dopamine shortage, which may be reversed with electroconvulsive therapy or reintroduction of amantadine. Third, its clinical presentation may occur on a spectrum and may include features suggestive of delirium, catatonia, or neuroleptic malignant syndrome.

"The common features among these cases suggest that risk factors for this withdrawal phenomenon may include being elderly, presence of advanced parkinsonism, and duration of amantadine therapy for longer than 1 year."

Thanks. That's what I found as well - i.e. DAWS seems to be a risk only for a very small subset of people, using high doses typically reserved for very advanced conditions, and used for extended periods of time.
Interestingly, the abstract you posted shows that they gave amantadine (a dopaminergic chemical) to a person with shizophrenia and it kept him in remission. I find that highly ironic considering that schizophrenia is considered to be a dopamine-caused pathology and dopamine antagonists are the mainstream treatment for acute episodes. Recently, it has been found that Haloperidol (that the main drug of treatment for schizo) is also a serotonin antagonist, and on more than one 5-HT receptor. So, it is likely serotonin antagonism that treats psychosis, and that schizo is a serotonin-driven condition. That matches quite well with older studies and observations of people with carcinoid syndrome (and thus serotonin overload) exhibiting symptoms indistinguishable from acute psychosis in schizophrenics.

 

[charmer]

I am the person with autoimmune to voltage gate potassium channels with some brain inflammation after one or more forms of herpes infection. I have tried amantadine that I had available, which is 100 mg pills, which I split in 4 (25mg).

I didn't experience any dissociation, and initially I felt on a slightly more positive note. But just in day 2 it hit me with horrible myalgia around my body. I didn't see a connection at first and took it for 4 days. It only got worse. I felt really low and weepy.

Some additional factors we're I recently had a rituximab infusion (which rid of myalgia and my body felt so light at last). I also started talking amantadine right before peripe, which might have added to the symptoms.
My cortisol was also bottom low after corticosteroids they inject to avoid rituximab overreaction.

 

[mirc12354]

The effects became less pronounced after some time for me.
I also noticed that the taste changed. It first had a very distinctive, herb like taste, that I really liked. But after some time it just tasted like oil only.

Today I got a new bottle, and the taste is back again, and the effects as well. Not sure what is going on. I once put the bottle in the pocket of my trouser, to take with me to work, could that (the warmth of my body) somehow destroy the active ingredient?

I have taken orally everyday for three weeks. First two weeks 6 drops (10mg) in the AM and 6 drops in the PM. Most recent week only 6 to 10 drops in the PM.

....
The scent does seem to be getting less strong as I get to the end of the bottle, as another user noticed.

While Diamant being my favorite Idealabs supplement I also noticed this. Losing scent and potency over time (have product for 4 months ony)... how is this possible given all the saturation?

 

[haidut]

While Diamant being my favorite Idealabs supplement I also noticed this. Losing scent and potency over time (have product for 4 months ony)... how is this possible given all the saturation?

I don't think the adamantane degrades at all. The potency waning could be just from organism adapting to it and the same effects were seen with steroids and vitamins. I have tested the adamantaen and it actually stays undisturbed and undegraded for more than 18 months in vitamin E solution. You can take a week off and then resume and it should have the same effects as before. Some cycling may be needed with most supplements to avoid overadaptation.

 

[lifestyle]

I don't think the adamantane degrades at all. The potency waning could be just from organism adapting to it and the same effects were seen with steroids and vitamins. I have tested the adamantaen and it actually stays undisturbed and undegraded for more than 18 months in vitamin E solution. You can take a week off and then resume and it should have the same effects as before. Some cycling may be needed with most supplements to avoid overadaptation.

Do you know why contents at the end of a Diamant bottle would appear lighter in color and have substantially less camphor-like odor than the contents of a new bottle?

 

[haidut]

Do you know why contents at the end of a Diamant bottle would appear lighter in color and have substantially less camphor-like odor than the contents of a new bottle?

I have not seen this happening in any of the bottles. The bottle is air-tight and even as the content decreases here should not be much interaction of the contents with the real works. Sensitivity to camphor smell decreases with repeated exposure so it would be best to ask somebody not accustoms to camphor to smell the bottle towards the end and report what they sense.

 

[lifestyle]

I have not seen this happening in any of the bottles. The bottle is air-tight and even as the content decreases here should not be much interaction of the contents with the real works. Sensitivity to camphor smell decreases with repeated exposure so it would be best to ask somebody not accustoms to camphor to smell the bottle towards the end and report what they sense.

I have an bottle that is several months old next to a new bottle. They are markedly different. I always screwed the top on, but never made a point to really tighten it.

Several other commenters in this thread described the same experience. The end of a bottle just seems less potent. Is it possible this is due to separation?

 

[haidut]

I have an bottle that is several months old next to a new bottle. They are markedly different. I always screwed the top on, but never made a point to really tighten it.

Several other commenters in this thread described the same experience. The end of a bottle just seems less potent. Is it possible this is due to separation?

We use different amounts of tocopherol across batches so the color may be different between batches but the amount of adamantane is always the same. Again, I am not aware of adamantane degrading in any way. Given that is fully saturated it should last undefinitely but FDA says liquid products can only be advertised as having no more than 12 months of shelf life.

 

[Terma]

So in the end I couldn't make this work because it increased dependence on 5aDHP which needed to be halved.

I read this not long ago and it might provide a hint toward the reason:

Evidence for involvement of nitric oxide and GABAB receptors in MK-801- stimulated release of glutamate in rat prefrontal cortex

Collectively, these findings suggest the model illustrated in Figure 1. Under normal conditions, stimulation of NMDA receptors on GABAergic interneurons in the thalamus or hippocampus provides tonic inhibition of glutamatergic pyramidal neurons projecting to prefrontal cortex. NMDA receptor blockade results in a disinhibition of cortical glutamate release, thereby activating non-NMDA (AMPA/kainite) glutamate receptors expressed on cortical pyramidal neurons. Increased calcium influx through these receptors activates nitric oxide synthase within the cortical pyramidal neuron. Nitric oxide also diffuses retrogradely to the glutamate axon terminals projecting from hippocampus and thalamus, where it functions to sustain and enhance glutamate efflux through elevations of cGMP levels. In contrast, stimulation of cortical GABAB receptors inhibits nitric oxide formation, limiting glutamate release. Glutamate – nitric oxide interactions are therefore bi-directional in this model, with glutamate acting through non-NMDA glutamate receptors to stimulate nitric oxide production, and nitric oxide subsequently stimulating elevated glutamate release.

Won't post the diagram, it's terrible

If adamantane is sufficiently strong NMDA antagonist it might lead to increased glutamate release into AMPA/kainate receptors due to interneuron network described rather than NMDA. If this goes overboard, the nitric oxide they produce diffuses back into neurons releasing more glutamate (cyclical - i.e. bad headache).

In those studies baclofen GABAB agonist killed the excess glutamate, it seems through preventing nitric oxide release, or both, contribution of mechanisms is not very detailed. Baclofen and NOS inhibitor have additive effect.

In another study GABAA similarly controlled the baseline level of NO release from NMDA receptors (as an example, I'd suspect similar for AMPA/kainate), though the specifics are peculiar: GABAA, but not NMDA, receptors modulate in vivo NO-mediated cGMP synthesis in the rat cerebral cortex - ScienceDirect

The point is, strong NMDA antagonists actually lead to excitotoxicity hypothetically due to interneuron networks, what the threshold is I don't know; GABA(A/B) needed to make it sustainable, maybe nNOS (iNOS maybe, wasn't clear) inhibitors.

 

[Terma]

And sure, this is bound to come up: Plain (unmodified) Adamantane Is A Powerful Inhibitor Of NO Synthesis
But that regards iNOS, not nNOS. (there are other mechanisms with iNOS but I did not see them tie into this so far)

 

[Terma]

Something practical to go along with that:

Phencyclidine-Induced Behaviour in Mice Prevented by Methylene Blue

(well-known NMDA antagonist)

 

[Anders86]

Do Diamant increase levels of homocysteine as it has anti-cholinergic activity?

After a point I did not feel any rise in dopamine after administration, even combined with the BCAA-Phenylalanine combo. I do have the MTHFR mutation and felt great relief with some Choline, TMG and Folate. Have not tried Diamant since..

 

[Ron J]

Hey @haidut
If I remember correctly from other posts, adamantane can potentiate other substances; can it potentiate ATP and acetazolamide? And would those two be worth potentiating?

 

[Hans]

Anyone noticed burping from this? I take it orally and then get frequent burps that taste like adamantane.
@haidut any idea why this might be? Anti-viral activity happening in my gut?

 

[haidut]

Anyone noticed burping from this? I take it orally and then get frequent burps that taste like adamantane.
@haidut any idea why this might be? Anti-viral activity happening in my gut?

Probably just the tocopherol doing something to digestion. Other people reported burping from vitamin E before.

 

[haidut]

Hey @haidut
If I remember correctly from other posts, adamantane can potentiate other substances; can it potentiate ATP and acetazolamide? And would those two be worth potentiating?

I don't know, as it has not been tested. But I would suspect it can potentiate the latter as it has a decently long half life while the half life of ATP is just minutes.

 

[BlackSkull]

Greetings,

Salutations @haidut, your reputation precedes you.

Subject a 1/3 through the bottle of Diamant.

Subject started at 4 drops per day sublingually and last week switched to 8.

At first subject got headaches, but it cleared and subject’s head was clearer.

It did the same when subject upped to 8 drops, but is starting to clear.

Plus some other things.

 

[haidut]

Greetings,

Salutations @haidut, your reputation precedes you.

Subject a 1/3 through the bottle of Diamant.

Subject started at 4 drops per day sublingually and last week switched to 8.

At first subject got headaches, but it cleared and subject’s head was clearer.

It did the same when subject upped to 8 drops, but is starting to clear.

Plus some other things.

Thanks. Do you find that it potentiates the effects of other substances?

 

[BlackSkull]

Thanks. Do you find that it potentiates the effects of other substances?

The short answer is a resounding yes.

The long answer is that it potentiates many things.

Now that the tissues are saturated, the potentiation of other compounds is less noticeable as subject has reached a new homeostasis.

Other compounds include Andro, Gonadin, & Caffeine, specifically. Before reaching new homeostasis, subject displayed more intense and longer lasting manifestations of compounds, namely assertiveness and awareness.

**Disclaimer: Below is purely speculative : for more info research Varvara Ivanova, Russian parapsycologist and other related findings

However, subjects assertiveness should be defined as subject also engages in energy manipulation A.K.A working out, meditation, yoga, spirituality, and/or occultism.

Subject’s overall senses have potentiated, akin to a meditators 3rd eye, for example, suggesting greater opening and functioning of the soul, which is the human body and mind collectively.

Subject displays better ability to predict short-term events before they occur (only that subject is involved in) and feel others emotions and thoughts suggesting improved intuition, which is a spiritual phenomenon.

Some call this dissociation or schizophrenia and label it in a negative manner, but this labeling act is biased. Ancient Martial Artists trained this. Time travel and teleportation are a similar phenomenon, that of manipulating energy. Schizophrenia is nothing more than entering another dimension of time and space and not a permanent state. Medication is not needed unless one’s mind/soul is not strong enough to control it.

Therefore, regarding bodily function, this supplement should not be feared as the potentiation is merely an increase in one’s cellular vibrations and vitality.

Lastly, in the quest to increase subjects cellular vibrations to that of the speed of light (that of immortality A.K.A faster than the speed of time A.K.A permanently disease less) this supplement will definitely help.

However, I fear the only way to accomplish this feat may be through permanent DNA alteration, which seems like it will never be allowed.