Regina

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You know, I just had a hearing test (I'm 61), and it was the best they had ever measured in their office. I like to joke I didn't listen to that much rock and roll when younger - but maybe inner-ear stuff can actually mean hearing that's "too" good. I do have a problem filtering out noise - so perhaps it's all related.
me too. I was dyslexic as a child and I am very sensitive to sound (can hear the grass grow type). It did make me a good sound engineer. I can sound-proof just about anything. But I can't hear a word anyone says in a bar.
The pianist, Alfred Brendel, was said to have suffered from this greatly. He was well-known for canceling performances because he couldn't sleep in the hotel room because of noise.
 

Name1

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It is very minimally metabolized since it is such a stable chemical. Mostly acetylation and then excretion. Since it is so lipophilic, the half life is probably on the order of 24+ hours (as it is for the other derivatives) so it may be taken every other day or eve less often.
TGA eBS - Product and Consumer Medicine Information Licence
"...Amantadine is metabolised to a minor extent, principally by N-acetylation. Whether this metabolic pathway is affected by acetylator phenotype remains to be determined."
Presumably your product is not metabolized by N-acetylation since it does not have an amino group?
 

Name1

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"Many of the studies on those derivatives compared effects of adamantane to the new derivative and found them to be almost the same."


"The list of studies is a little light because I wanted to post only the studies known to be directly relevant to adamantane and not its derivatives. There over 5,000 studies on all adamantane derivatives and as I go through them slowly I will update the references section accordingly."

How are any of these studies directly relevant to adamantane when none of them study the effects of adamantane, only the effects of functionalized derivatives? None of the studies you have posted compare the effects of adamantane to its functionalized derivatives.
 

Rad

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Do you know if he says these are items a child can take long term? My oldest son has a lot of similar issues and I recall the delivery nurse said he passed the infant hearing test faster than any baby she had tested in the previous 25 years. I just ordered his book on amazon out of curiosity. Thank you for this tip.

Harold Levinson says that patients can be on the medications from 1 to 4 years. He says 1 out of every 5 will give a positive response. He starts on a quarter of the normal dose and will change medication if there are any side effects. I've wondered about do it yourself but I think that would be very difficult. He says he usually ends up on a combination of antimotion sickness meds and a stimulant. If no immunity or side effects develop then he continues it. He says 'in cases where long-term use causes immunity, the doctor need only make a slight change in medication to "restart" a favourable response.'

The treatment definitely has nothing to do with whether you can hear well or not. I myself have bat-like hearing. Being in the UK, there isn't anyone skilled in this method but I take my various supplements with an eye to any noticeable improvement. At least, when I remember.
 

Rad

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You know, I just had a hearing test (I'm 61), and it was the best they had ever measured in their office. I like to joke I didn't listen to that much rock and roll when younger - but maybe inner-ear stuff can actually mean hearing that's "too" good. I do have a problem filtering out noise - so perhaps it's all related.

Yep, I have bat-like hearing but from Dr.Levinson:

'When I say the inner-ear system, I am referring to the cerebellar-vestibullar system (CVS), a complex network comprised of the vestibullar system (the inner ear) and the cerebellum...Note that the inner ear is not to be confused with the middle ear, the small air-filled space between the eardrum and inner ear where our sense of hearing originates.'

He has talked about dyslexics and add/adhd peeps noticing improvements in their symptoms when they exercise. I certainly used to notice improvement doing martial arts involving tumbling and acrobatics when I was younger.

I think the he's talking about a fine tuning controller for the brain. Structures which not only control gross and fine motor control of the body but also of activities such as reading, writing, etc as well as stabilizing thoughts and emotions so the don't careen around your mind space ad enable you to hold them for perusal.

http://www.dyslexiaonline.com/treatment/treatment.html
 

sugarisgreat

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Harold Levinson says that patients can be on the medications from 1 to 4 years. He says 1 out of every 5 will give a positive response. He starts on a quarter of the normal dose and will change medication if there are any side effects. I've wondered about do it yourself but I think that would be very difficult. He says he usually ends up on a combination of antimotion sickness meds and a stimulant. If no immunity or side effects develop then he continues it. He says 'in cases where long-term use causes immunity, the doctor need only make a slight change in medication to "restart" a favourable response.'

The treatment definitely has nothing to do with whether you can hear well or not. I myself have bat-like hearing. Being in the UK, there isn't anyone skilled in this method but I take my various supplements with an eye to any noticeable improvement. At least, when I remember.
Great information. Thanks again.
 
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haidut

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How are any of these studies directly relevant to adamantane when none of them study the effects of adamantane, only the effects of functionalized derivatives? None of the studies you have posted compare the effects of adamantane to its functionalized derivatives.

The ones I posted on cortisol inhbition, HDAC inhbition and lipophilicity all compared adamantane to the derivatives as well and found it to be active. The dopaminergic, anti-serotonin, and NMDA antagonism effects of adamantane were confirmed in early 1960s and that is what led to the work on derivatives for Parkinson and AD. While not all studies are on adamantane directly, some of them are (as I mentioned above). Also, if you look at the structure of adamantane and compare it to amantadine, rimantadine and memantine you will see that the only difference is a single amino group, which (as the studies posted discussed) is there to make adamantane more water soluble and shorten the half-life, not to change its biological effects.
 

ThinkPerceive

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I was looking into half-life info (it's about 11 hours - so will accumulate over time if taken daily), and found this interesting article on "actoprotective" compounds. They are discussing orally consumed Bromantane, but the breakdown process happens on the Adamantane piece (6th position??) - so likely Adamantane is similar once absorbed. Interesting that elimination is through the adrenal gland? I didn't know that was a thing...

The drug is metabolized in the liver, but its elimination occurs mostly through the adrenal gland. Bromantane metabolism is characterized mainly by hydroxylation in the 6th position of the adamantan cycle. All of the determined metabolites can be found in urine, even in two weeks after administration of bromantane (this last fact is important for doping control) (Burnat et al., 1997).​

The Pharmacology of Actoprotectors: Practical Application for Improvement of Mental and Physical Performance

The Burnat article doesn't seem to be available anywhere (the Russian stuff seems to dead-end, even on Sci-Hub).

(edited to remove the second link - it was identical the one above!)
 
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I was looking into half-life info (it's about 11 hours - so will accumulate over time if taken daily), and found this interesting article on "actoprotective" compounds. They are discussing orally consumed Bromantane, but the breakdown process happens on the Adamantane piece (6th position??) - so likely Adamantane is similar once absorbed. Interesting that elimination is through the adrenal gland? I didn't know that was a thing...

The drug is metabolized in the liver, but its elimination occurs mostly through the adrenal gland. Bromantane metabolism is characterized mainly by hydroxylation in the 6th position of the adamantan cycle. All of the determined metabolites can be found in urine, even in two weeks after administration of bromantane (this last fact is important for doping control) (Burnat et al., 1997).​

The Pharmacology of Actoprotectors: Practical Application for Improvement of Mental and Physical Performance

The Burnat article doesn't seem to be available anywhere (the Russian stuff seems to dead-end, even on Sci-Hub). But this seemed interesting, about Actoprotectors in general.

The Pharmacology of Actoprotectors: Practical Application for Improvement of Mental and Physical Performance

Thanks. Yes, I like I said in my original post the early studies were all with adamantane and the basic properties like dopaminergic, antiserotonin, anticholinergic, anticortisol and anti-NMDA are all within the adamantane molecule. The subsequent derivatives were developed mainly as an attempt to control half-life and target specific organs/tissues. But still, there is probably nothing one of the simpler derivatives can do that adamantane cannot also achieve (perhaps in higher doses).
 

Squatrat

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Supposedly the Adam family can increase sensitivity to benzos and amphetamines while extending the half-lif of other chemicals. Do you think this drug would increase the halflife of vyvanse(medical meth)?
 

CoconutEffect

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Supposedly the Adam family can increase sensitivity to benzos and amphetamines while extending the half-lif of other chemicals. Do you think this drug would increase the halflife of vyvanse(medical meth)?
Do you have a citation or a legitimate source for that?
I've been interested in (memantine's) tolerance reducing abilities, specifically for benzos, but can only find anecdotal evidence and some bro science
 

Squatrat

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Do you have a citation or a legitimate source for that?
I've been interested in (memantine's) tolerance reducing abilities, specifically for benzos, but can only find anecdotal evidence and some bro science

I read some anecdotal evidence here and elsewhere on that net that memantine can be used to reduce tolerance to drugs. Im not an expert and thats why I ask Haidut.
 

Regina

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Yep, I have bat-like hearing but from Dr.Levinson:

'When I say the inner-ear system, I am referring to the cerebellar-vestibullar system (CVS), a complex network comprised of the vestibullar system (the inner ear) and the cerebellum...Note that the inner ear is not to be confused with the middle ear, the small air-filled space between the eardrum and inner ear where our sense of hearing originates.'

He has talked about dyslexics and add/adhd peeps noticing improvements in their symptoms when they exercise. I certainly used to notice improvement doing martial arts involving tumbling and acrobatics when I was younger.

I think the he's talking about a fine tuning controller for the brain. Structures which not only control gross and fine motor control of the body but also of activities such as reading, writing, etc as well as stabilizing thoughts and emotions so the don't careen around your mind space ad enable you to hold them for perusal.

http://www.dyslexiaonline.com/treatment/treatment.html
Oh yea. Aikido keeps a lot of symptoms at bay for me. The tumbling type movements simultaneous with the need to be mentally present in that moment disambiguates me.
 
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haidut

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Supposedly the Adam family can increase sensitivity to benzos and amphetamines while extending the half-lif of other chemicals. Do you think this drug would increase the halflife of vyvanse(medical meth)?

I have only seen studied on it being used to wean people off of strong opioids. To increase the half life it will have to be mixed with those drugs. Adamantane does not inhibit any drug metabolizing enzyme AFAIK, so it won't directly increase the half life of anything when taken separately. Bu if something was dissolved together with adamantane and given as a solution the adamantane would help it get inside the cells more easily and have stronger effects.
 

Squatrat

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Would taking diamat orally with a drug improve that drugs effects or would it actually have to be some kind of solution?
 

Name1

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The ones I posted on cortisol inhbition, HDAC inhbition and lipophilicity all compared adamantane to the derivatives as well and found it to be active. The dopaminergic, anti-serotonin, and NMDA antagonism effects of adamantane were confirmed in early 1960s and that is what led to the work on derivatives for Parkinson and AD. While not all studies are on adamantane directly, some of them are (as I mentioned above). Also, if you look at the structure of adamantane and compare it to amantadine, rimantadine and memantine you will see that the only difference is a single amino group, which (as the studies posted discussed) is there to make adamantane more water soluble and shorten the half-life, not to change its biological effects.

Can you show me specifically where in, for example, the study on HDAC inhibition (doi: 10.1016/j.bmcl.2013.03.002) the HDAC inhibition activity of unsubstituted adamantane (C10H16) is compared to the HDAC inhibition activity of substituted derivatives of adamantane?
 

Pointless

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I have only seen studied on it being used to wean people off of strong opioids. To increase the half life it will have to be mixed with those drugs. Adamantane does not inhibit any drug metabolizing enzyme AFAIK, so it won't directly increase the half life of anything when taken separately. Bu if something was dissolved together with adamantane and given as a solution the adamantane would help it get inside the cells more easily and have stronger effects.

It might even have to be bonded chemically to the drug like they did in this study.

Adamantane as a brain-directed drug carrier for poorly absorbed drug. 2. AZT derivatives conjugated with the 1-adamantane moiety. - PubMed - NCBI

I read some anecdotal evidence here and elsewhere on that net that memantine can be used to reduce tolerance to drugs. Im not an expert and thats why I ask Haidut.

It probably has to do with its NMDA antagonism, as those types of drugs are known to do that.
 
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