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Upregulating Dopamine Receptors - ADHD problem

adhd dopamine sulbutiamine happy stack

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#31 Zenfood

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Posted 02 September 2014 - 10:52 AM

Area-1255
Now, just read it! (http://area1255.blog...h1h2h3-and.html)

 

Really interesting. You seem to have a lot of knowledge in these matters. Respect.

 

I am not sure if it would be a great thing to increase cAMP in my case? 

I have always felt that forskolin somehow actually is good for me. My motor skills improve while on it and I have better focus. However no euphoria or any good feelings on it. 

 

As I understand, methylphenidate activates cAMP in the prefrontal cortex, which is a good thing?
http://www.ncbi.nlm....pubmed/15890841

Whould combining forskolin and methylphenidate be a wise thing to try?

 

I am definitely going to order catuaba. Just not sure which one.

Abelard and Area-1255. Do you guys think that this would do?
http://www.iherb.com...15&sr=null&ic=5

Thanks!
 



#32 Area-1255

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Posted 02 September 2014 - 03:56 PM

Area-1255
Now, just read it! (http://area1255.blog...h1h2h3-and.html)

 

Really interesting. You seem to have a lot of knowledge in these matters. Respect.

 

I am not sure if it would be a great thing to increase cAMP in my case? 

I have always felt that forskolin somehow actually is good for me. My motor skills improve while on it and I have better focus. However no euphoria or any good feelings on it. 

 

As I understand, methylphenidate activates cAMP in the prefrontal cortex, which is a good thing?
http://www.ncbi.nlm....pubmed/15890841

Whould combining forskolin and methylphenidate be a wise thing to try?

 

I am definitely going to order catuaba. Just not sure which one.

Abelard and Area-1255. Do you guys think that this would do?
http://www.iherb.com...15&sr=null&ic=5

Thanks!
 

Forsklin would potentiate most ADHD drugs but given alone and with time it may allow for more leverage (in going off the drug) as one part in a "Re-Hab"cycle.  Which includes foskloin and histamine re-balancing. Interestingly, forskolin may actually be able to help

both low histamine and high histamine states, due to it's role as potent thermogenic and in bypassing receptors and instead is a direct activator of cAMP production.

In which that very same rehab cycle, which can be very effective in treating addiction, it also helps restore natual dopamine and adrenaline production.

 

Also stimulate drugs in general have limited usage in the long-term, not solely because of their pharmacodynamics,but also because

1.) Many receptors that stimulants target are the most prone to sensitization. (Alpha,1,adrenergic,Beta,adrenergic, DopamineD1 etc).

2.) The drugs lose their effectiveness altogether as to by starts enriching other methods of breakdown.

 

 

Thus, the only real way to get any kind of balance, is by hormone and histamine imbalance treatment.. 

Cortisol,ACTH,Estrogen, Testosterone,Vitamin D,pregnenolone, Progesterone (sigma2)..all of these affect downstream signaling and lay the groundwork in a particular direction (or directionS)...

 

 

SOURCES

 

http://www.ncbi.nlm....les/PMC3036556/

http://www.raysaheli.../forskolin.html

http://www.ncbi.nlm....pubmed/22654849

http://www.ucl.ac.uk/npp/research/tgs

 

 

 

 


Edited by Area-1255, 02 September 2014 - 04:04 PM.

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#33 NG_F

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Posted 03 September 2014 - 01:10 AM

Better You look out for something modulating i.e. that increase D2 mrna,than something that You have to use every day.

But since its genetically set, dont know.

You could try a MAO-B and/or MAO-A inhibitors. this works at least for me and "could" be safer than DRI.

 

The problem with 23andMe is that the result could distract from another problem.

This was IIRC the Reason why it was forbidden to diagnose Your results.

What if it turns out that You have a damaged dopamine system which is loosely related to the genetics ?

E.g. chronic stress is known to cause damage.

I would think about it.

 

I would advise You to stay away from Methylphenidate.

Prefrontal cortical and striatal transcriptional responses to the reinforcing effect of repeated methylphenidate treatment in the spontaneously hypertensive rat, animal model of attention-deficit/hyperactivity disorder (ADHD)

http://www.behaviora...content/10/1/17

 

Methylphenidate Exposure Induces Dopamine Neuron Loss and Activation of Microglia in the Basal Ganglia of Mice

http://www.plosone.o...al.pone.0033693

 

 

What do you suggest instead? I was taking Ritalin 10mgs/day but you have me concerned now. It's always a flip-flop here on the site. methylphenidate was purported here to be neuroprotective  in many threads for years.

 Would Vyvanse , Adderall  or dextroamphetamine be any safer on the brain long term?  I've never had any real focus with Wellbutrin, only scattered energy and slight anxiety.

 

Thanks in advance .



#34 Flex

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Posted 03 September 2014 - 07:42 AM

I´ve read that Methylphenidate alters 306 genes in the striatum and 252 of them were downregulated.

http://www.behaviora...content/10/1/17

http://www.longecity...e-3#entry680963

What would You think about it ?

 

I didnt look into the differences and the reports on Vyvanse Adderall  and Dextroamphetamine in particular,

but If You ask me Amphetamine seems to be even more problematic.

There are several threads where people report detrimental after a few months even within a moderate dose

like:

http://www.longecity...st/#entry666396

 

I dont want to scare You, but rather to warn. You have You own will and know whether You need it or not.

Basically I just want to prevent a bad awakening


Edited by Flex, 03 September 2014 - 07:46 AM.

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#35 Zenfood

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Posted 03 September 2014 - 02:08 PM

Hell. Makes sense, because my symptoms started getting worse after 12 months of methylphenidate use.
I took 36mg concerta + 20mg ritalin every day (5 days/w)

Just tried taking 10mg yesterday in one sitting and I experienced a crash and slight depressive symptoms.

 

Whenever I take 5mg twice a day I'm good. This is where I feel that it actually might improve my condition.

 

However, I just ordered Catuaba Bark Powder (100g)

 

Really lookin forward to it :)

 

Btw. Have you guys any idea what Maca does? I always feel good taking it and my libido goes up the roof - without being stimulating like Yohimbine HCL - which ultimately stresses me out and makes me crash. 

 

Tribulus Terrestris works well as well, since it's a MAOI.

 

I´ve read that Methylphenidate alters 306 genes in the striatum and 252 of them were downregulated.

http://www.behaviora...content/10/1/17

http://www.longecity...e-3#entry680963

What would You think about it ?

 

I didnt look into the differences and the reports on Vyvanse Adderall  and Dextroamphetamine in particular,

but If You ask me Amphetamine seems to be even more problematic.

There are several threads where people report detrimental after a few months even within a moderate dose

like:

http://www.longecity...st/#entry666396

 

I dont want to scare You, but rather to warn. You have You own will and know whether You need it or not.

Basically I just want to prevent a bad awakening

 


Edited by Zenfood, 03 September 2014 - 02:15 PM.


#36 Flex

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Posted 03 September 2014 - 03:11 PM

Maca is a faah inhibitor (afaik quiet potent). So it inhibits the degradation of endogenous canabinoids

This is the only thing what I know, apart from containing nearly all vitamins ( exept b12 as usual) and beeing an afrodisiac.

 

Here is an article about ADHD. It states that actually an increase of Adrenaline can cause ADHD and this could be decreased by Pycnogenol

But I cant say anything about its credibility, but I believe to read it somewhere too

 

Surprising Research Challenges Our Understanding of Norepinephrine Deficiency

http://www.naturalhe...ine-deficiency/

 

You could look also for stuff that inhibits Dopamine-β-Hydroxylase

But keep allways possible bloodthinning effects in mind:

 

Hypericin

Biochemical activities of extracts from Hypericum perforatum L. 1st Communication: inhibition of dopamine-beta-hydroxylase.

http://www.ncbi.nlm....pubmed/10083977

 

Xanthoangelol and 4-Hydroxyderricin Are the Major Active Principles of the Inhibitory Activities against Monoamine Oxidases on Angelica keiskei K.

http://www.ncbi.nlm....pubmed/24265870

 

Disulfiram

http://omicsonline.o...105.1000153.pdf

 

lettusic acid (?)

Lactuca satiυa L

http://www.google.co...7029076A1?cl=en


Edited by Flex, 03 September 2014 - 03:42 PM.


#37 NG_F

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Posted 04 September 2014 - 03:24 AM

I´ve read that Methylphenidate alters 306 genes in the striatum and 252 of them were downregulated.

http://www.behaviora...content/10/1/17

http://www.longecity...e-3#entry680963

What would You think about it ?

 

I didnt look into the differences and the reports on Vyvanse Adderall  and Dextroamphetamine in particular,

but If You ask me Amphetamine seems to be even more problematic.

There are several threads where people report detrimental after a few months even within a moderate dose

like:

http://www.longecity...st/#entry666396

 

I dont want to scare You, but rather to warn. You have You own will and know whether You need it or not.

Basically I just want to prevent a bad awakening

 

Thanks for the heads up Flex. I dont  need any messing about in my striatum at all , as I suffered a small hemorrhage in my left caudate nucleus in 2008.

  I have attention problems as well as some memory issues( Aquasition, Retention and Retrieval ) as well .

 

I'm currently taking zoloft (25mgs/day )  and some Noots- Cere, PRL-53, Phenylpiracetam, Coularacetam and Sulbutiamine.

 

 I'm also taking Modafanil as needed. I feel better on this, energy wise but not with my focus and my ability to complete mental tasks. 

 

I will stop the Ritalin and keep up with the Modafanil .The only problem is it effects my Benzo detox, as it's properties are very benzodiazepine antagonistic.

 

Any suggestions would greatly be appreciated  :)



#38 Zenfood

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Posted 04 September 2014 - 12:15 PM

I also decided to stop the methylphenidate.

 

Forgot to mention earlier that I have noticed improved eye vision. I should have perfect sight (LASIK operation 4 years ago), but the last year I have lost some eyesight on my right eye.

 

I started to notice perfect sight on both eyes on Ritalin.

 

I have tried Lipoic Acid + Grape Seed Extract, etc. because I thought I had oxidative stress in my retina.

So apparently it has something to do with blood flow or dopamine? I have some cayenne pepper and ginger and I'm going to take them and see how my vision is affected.

 

Flex:
"Adrenaline can cause ADHD and this could be decreased by Pycnogenol"
Really cool info. I have always felt calmer and more focused taking Grape Seed Extract (600-1200mg) and I think believe it should be equivalent to pycnogenol, because of the proanthocyanidin content.
 

 


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#39 FocusPocus

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Posted 05 September 2014 - 02:10 PM

I also decided to stop the methylphenidate.

 

Forgot to mention earlier that I have noticed improved eye vision. I should have perfect sight (LASIK operation 4 years ago), but the last year I have lost some eyesight on my right eye.

 

I started to notice perfect sight on both eyes on Ritalin.

 

I have tried Lipoic Acid + Grape Seed Extract, etc. because I thought I had oxidative stress in my retina.

So apparently it has something to do with blood flow or dopamine? I have some cayenne pepper and ginger and I'm going to take them and see how my vision is affected.

 

Flex:
"Adrenaline can cause ADHD and this could be decreased by Pycnogenol"
Really cool info. I have always felt calmer and more focused taking Grape Seed Extract (600-1200mg) and I think believe it should be equivalent to pycnogenol, because of the proanthocyanidin content.
 

 

Hi OP.

 

From someone else with ADD-Pi (also GAD) who seems to only benefit from 5mg Ritalin and nothing else,

 

Have you found an alternative to Ritalin with similar effects?


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#40 Zenfood

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Posted 08 September 2014 - 09:05 PM

Hey!

Maca is the only thing that has made me feel great and alive. 

 

Received my Catuaba Powder today. Tried 2g and later 4g today. Not sure if I noticed anything.

 

Going to take 5g on an empty stomach first thing in the morning tomorrow. I will  try Rio Amazon's Catuaba, 500mg 5:1 extract later.

 

My roommate, who also suffers from ADHD noticed improved focus and increased mood. He started do things he had been procrastinating for a while on 2g of it.

 

EDIT: Starting to think that I might be low in DHEA or something. Maca is supposed to increase DHEA levels (can't find any studies - just anecdotes).

 

I live in Finland and all hormone related supplements are banned here (Pregnenolone, DHEA, etc).

 

I will try to do a hormone panel test in the near future. However, I'll keep experimenting with Maca and Catuaba 'til then.

 

 

 

 


Edited by Zenfood, 08 September 2014 - 09:13 PM.


#41 Zenfood

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Posted 08 September 2014 - 11:26 PM

I found a very interesting thread:
https://www.drugs-fo...ad.php?t=244056

 

I've been drinking Gynostemma every morning for one month. Haven't noticed anything yet. I drink it, because it activates AMPK and lowers my Th2 as well.


Edited by Zenfood, 08 September 2014 - 11:26 PM.


#42 Area-1255

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Posted 08 September 2014 - 11:31 PM

I found a very interesting thread:
https://www.drugs-fo...ad.php?t=244056

 

I've been drinking Gynostemma every morning for one month. Haven't noticed anything yet. I drink it, because it activates AMPK and lowers my Th2 as well.

Some herbs take a while to build up to appreciable concentrations. Gymnostemma is one of those. Generally the herbs with stimulant ingredients are quicker, whereas adaptogens and classic tonics might take up to a week. Though Catuaba is usually something I notice within the first few days.


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#43 Bateau

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Posted 09 September 2014 - 03:36 AM

I found a very interesting thread:
https://www.drugs-fo...ad.php?t=244056

 

I've been drinking Gynostemma every morning for one month. Haven't noticed anything yet. I drink it, because it activates AMPK and lowers my Th2 as well.

 

All the studies in that thread are copy/pasted from my post here.

 

There's a few other studies that they missed that had some potential like the Stereospermum suaveolens, Uncaria rhynchophylla, and Ashwagandha. I never posted the ashwagandha study but it showed similar dose dependent repair of dopaminergic systems AFTER chemically induced parkinsons like Jiaogulan. Uncaria was similar but it was not dose dependent, there was much better results at smaller doses, this made the dose very practical though.

 

Although in vitro instead of the previous in vivo studies, Salidroside from Rhodiola shows some significant promise: http://www.ncbi.nlm.nih.gov/pubmed/24323403

and an in vivo study to back up assumptions: http://www.ncbi.nlm.nih.gov/pubmed/18054474 (Note: Rhodioloside = Salidroside)

 

@Area1255 Check out the data on tables 1-7 and figures 1-2 in the S. suavolens study, the data is pretty damn interesting IMO.

 

http://www.longecity...ic-supplements/

http://www.longecity...e-2#entry633447 (Here's where most of the data you're missing is)


Edited by Bateau, 09 September 2014 - 03:38 AM.

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#44 Zenfood

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Posted 09 September 2014 - 01:01 PM

OK. Thanks! I will continue with Gynostemma, Area-1255.
What do you notice from catuaba? 

 

Impressive, Bateau. Rhodiola has made me a bit happier in the past. However, the effect  is sometimes unpredictable.

However, it was standardized to 3% rosavins and 1% salidrosides. 
Maybe I should give this a try: http://www.herbosoph...5-salidrosides/

 

I have some Ashwagandha (Now Foods) laying around here as well. Not sure about dosing. 

I have to dive into the S. suavolens study and report back.
 

Also, what do you guys think about inositol for D2 receptor density?

 

------------------------------------------------------

THIS MORNING

I took these in a fasted state:
- 5g of Catuaba. Music sounded a bit better and mood was slightly improved. Still feeling unmotivated and want to be sedentary.
- 60 minutes later: Took 500mg of L-Phenylalanine. Slightly happier after 30 minutes.
- 30 minutes later: Took 500mg of L-Phenylalanine again and I really enjoy the music and feel decreased pain in my trapezius.
 
I got a small touch of how it feels to actually do things and a sense of getting rewarded. Like when I was a kid, I did my homework
and then my mom let me play my Super Nintendo. I was super excited after my home work was done.
 
As an adult, I just don't find motivation to do things even if the reward would be very tempting. Even if I'd manage to complete the task
in time and get the reward - the reward itself wouldn't be that enjoyable. 
 
So, I notice that my reward system got a bit activated. However, I'm still unmotivated and just want to sit. Almost like smoking weed and just wanting to relax and enjoy music/videos.
 
Also, I feel that I crave nicotine. Why?
I used to use snus (moist powder tobacco) for many years, which is placed under the upper lip for nicotine
absorption. I have noticed that nicotine has always made me a bit more happier, calmer and more focused.
 
----------------------------------------
 
I still think that Maca makes me feel better than catuaba. 
Right now I just feel that I would love to try catuaba with some nicotine (with or without L-tyrosine/L-phenylalanine).
 
I read a paper that Maca actually decreases cortisol. Maybe I have elevated cortisol levels? I always feel overwhelmed even
if I don't have things to do. If this is the case, it explains my dysthymia, anhedonia and why my memory is pretty bad (hippocampus size decreases with chronic/excess cortisol).
This could also explain why I'm sensitive to caffeine as well? 
 
How about circadian dysruption? I've had it since I was born.
 
To sum this up:
- I know that my brain craves dopamine
- I suspect lowered DHEA levels
- I probably have elevated cortisol levels (Therefore, no caffeine for me. Got Phosphatidyl Serine, gonna try it out)
 
-----------------------------------------
EDIT
 
Additional information from my gene test:
Carrier of one CYP1A2*1F allele; Slow Caffeine Metabolizer.One copy of the slow caffeine metaboliser SNP, and one copy of the fast version. This makes you more strongly affected by drinking coffee, as caffeine is broken down slower in the liver. Supposedly this increases the risk of heart attacks, although other studies show caffeine is generally good for the heart. It also makes caffeine more effective at preventing Breast Cancer, Alzheimer's Disease, and Parkinson's disease. Too much caffeine will shrink your breasts.
 
Gs157
more stimulated by coffee You appear to have a common genotype in the gene CYP1A2 which metabolizes coffee more slowly than some other forms. The same amount of caffeine will tend to have more stimulating effect on slow metabolizers than on fast metabolizers. Ciprofloxacin is also metabolized by CYP1A2, but is unclear if your genotype should influence its effect.
 
7x less likely to respond to certain antidepressants. This version of a blood brain barrier protein blocks many common antidepressants from entering the brain, including: amitriptyline (Elavil), citalopram (Celexa), paroxetine (Paxil), and venlafaxine (Effexor). That makes those antidepressants 7 times less effective.
 
I've been on citalopram and amitriptyline. Didn't do jack s%¤&.

Edited by Zenfood, 09 September 2014 - 01:59 PM.

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#45 Area-1255

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Posted 09 September 2014 - 04:48 PM

 

OK. Thanks! I will continue with Gynostemma, Area-1255.
What do you notice from catuaba? 

 

Impressive, Bateau. Rhodiola has made me a bit happier in the past. However, the effect  is sometimes unpredictable.

However, it was standardized to 3% rosavins and 1% salidrosides. 
Maybe I should give this a try: http://www.herbosoph...5-salidrosides/

 

I have some Ashwagandha (Now Foods) laying around here as well. Not sure about dosing. 

I have to dive into the S. suavolens study and report back.
 

Also, what do you guys think about inositol for D2 receptor density?

 

------------------------------------------------------

THIS MORNING

I took these in a fasted state:
- 5g of Catuaba. Music sounded a bit better and mood was slightly improved. Still feeling unmotivated and want to be sedentary.
- 60 minutes later: Took 500mg of L-Phenylalanine. Slightly happier after 30 minutes.
- 30 minutes later: Took 500mg of L-Phenylalanine again and I really enjoy the music and feel decreased pain in my trapezius.
 
I got a small touch of how it feels to actually do things and a sense of getting rewarded. Like when I was a kid, I did my homework
and then my mom let me play my Super Nintendo. I was super excited after my home work was done.
 
As an adult, I just don't find motivation to do things even if the reward would be very tempting. Even if I'd manage to complete the task
in time and get the reward - the reward itself wouldn't be that enjoyable. 
 
So, I notice that my reward system got a bit activated. However, I'm still unmotivated and just want to sit. Almost like smoking weed and just wanting to relax and enjoy music/videos.
 
Also, I feel that I crave nicotine. Why?
I used to use snus (moist powder tobacco) for many years, which is placed under the upper lip for nicotine
absorption. I have noticed that nicotine has always made me a bit more happier, calmer and more focused.
 
----------------------------------------
 
I still think that Maca makes me feel better than catuaba. 
Right now I just feel that I would love to try catuaba with some nicotine (with or without L-tyrosine/L-phenylalanine).
 
I read a paper that Maca actually decreases cortisol. Maybe I have elevated cortisol levels? I always feel overwhelmed even
if I don't have things to do. If this is the case, it explains my dysthymia, anhedonia and why my memory is pretty bad (hippocampus size decreases with chronic/excess cortisol).
This could also explain why I'm sensitive to caffeine as well? 
 
How about circadian dysruption? I've had it since I was born.
 
To sum this up:
- I know that my brain craves dopamine
- I suspect lowered DHEA levels
- I probably have elevated cortisol levels (Therefore, no caffeine for me. Got Phosphatidyl Serine, gonna try it out)
 
-----------------------------------------
EDIT
 
Additional information from my gene test:
Carrier of one CYP1A2*1F allele; Slow Caffeine Metabolizer.One copy of the slow caffeine metaboliser SNP, and one copy of the fast version. This makes you more strongly affected by drinking coffee, as caffeine is broken down slower in the liver. Supposedly this increases the risk of heart attacks, although other studies show caffeine is generally good for the heart. It also makes caffeine more effective at preventing Breast Cancer, Alzheimer's Disease, and Parkinson's disease. Too much caffeine will shrink your breasts.
 
Gs157
more stimulated by coffee You appear to have a common genotype in the gene CYP1A2 which metabolizes coffee more slowly than some other forms. The same amount of caffeine will tend to have more stimulating effect on slow metabolizers than on fast metabolizers. Ciprofloxacin is also metabolized by CYP1A2, but is unclear if your genotype should influence its effect.
 
7x less likely to respond to certain antidepressants. This version of a blood brain barrier protein blocks many common antidepressants from entering the brain, including: amitriptyline (Elavil), citalopram (Celexa), paroxetine (Paxil), and venlafaxine (Effexor). That makes those antidepressants 7 times less effective.
 
I've been on citalopram and amitriptyline. Didn't do jack s%¤&.

 

I find that a great deal of ingredients, drugs, supplements etc that take pathways down the Dopamine D2(2) generally (for whatever reason) end up interacting with serotonin 5-HT2A/2C - too many for it to be a coincidence - so much that it could be seen as a logical cross talk or common signaling pathway. 

Let's just think about the role of Dopamine D2 - a primary inhibiting role, and yet plays a role in functions many would deem to be more on the "stimulating" end. For example, it facilitates feelings of trust, love and is involved in general interest and behavioral sensitivity. 

Strongly though, and D2 receptors also have a role in keeping sex hormones going. (!) (!)

 

http://www.ncbi.nlm....pubmed/24345165

http://scientopia.or...he-d2-receptor/

http://www.nature.co...mp2012103a.html

 

 

But I wonder how many people stopped to think about a concept as simple as "negative feedback" ...because D2 receptors are actually auto receptors (D2S-Presynaptic) but probably not so much the D2L (Long Allele) - yet all of the D2 family is inhibitory upon adenylyl cyclase (and thus cAMP) and as most who understand this would know that there is almost ALWAYS some stimulation to follow inhibition (in order to maintain balance). Would it then make sense that activation of D2 elicits a compensation response that is mediated by the 5-HT2A receptors and other stimulatory serotonin receptors?

 

 

Here's a couple other good points, 

 

-Dopamine Agonists such as Cabergoline,Bromocriptine,Apomorphine also have various affinities for serotonin 5-HT2A (where they also act very potently) - coincidence?

-Inositol as seen prior has effect on BOTH 5-HT2A and D2 receptors densities.

-Many other drugs/chemicals that affect D2's also affect many serotonin subtypes (but namely the 5-HT2A/C) - LSD (!), and a few others.

-Interestingly, most dopaminergic drugs are of ergot/ergolamine family.

-Yet in the brain, there is almost ALWAYS a cross interaction of D2's and 5-HT2A/C's.

 

I have more looking to do, but just some research and some points for thought.

 

Keep in mind that 5-HT2A/2C blockade is suggested to be very helpful in depression, whereas D2 Blockade is NOT.

 

At least not in the context of using the normal drugs that inhibit D2 receptors (antipsychotics), however, agonists (activators) and potentiators of dopamine D2 activity have anti-depressant and anti anxiety effects.

In fact, Dopamine D2 receptor density correlates with alcohol intake, and because D2 activation leads to GABA release, less D2 activity leads to more alcohol intake and dependency. (!) (!!) (!!!)


Edited by Area-1255, 09 September 2014 - 04:52 PM.

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#46 Zenfood

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Posted 12 September 2014 - 09:03 PM

Dude. Awesome stuff!
Thanks for your input.

 

I have also concluded that I am histamine intolerant. Quercetin + EGCG is making me feel hella good.

Avoiding histamine foods too.

 

Also, I found this:
https://news.ycombin...item?id=8263515

Seems that methylphenidate is quite safe. I took 5mg sublingual today again and started reading a book. Still feeling great 8 hours later. Laser focus!

Catuaba didn't help me. But I have some 5:1 extract on the way. Going to try it and leave some feedback.

 

Luckily I quit alcohol three years ago. Never really enjoyed the effects from it.


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#47 Area-1255

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Posted 12 September 2014 - 09:31 PM

Dude. Awesome stuff!
Thanks for your input.

 

I have also concluded that I am histamine intolerant. Quercetin + EGCG is making me feel hella good.

Avoiding histamine foods too.

 

Also, I found this:
https://news.ycombin...item?id=8263515

Seems that methylphenidate is quite safe. I took 5mg sublingual today again and started reading a book. Still feeling great 8 hours later. Laser focus!

Catuaba didn't help me. But I have some 5:1 extract on the way. Going to try it and leave some feedback.

 

Luckily I quit alcohol three years ago. Never really enjoyed the effects from it.

Yep, you read my article on histamine..correct?



#48 Sciencyst

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Posted 13 September 2014 - 08:55 AM


 
To sum this up:
- I know that my brain craves dopamine
- I suspect lowered DHEA levels
- I probably have elevated cortisol levels (Therefore, no caffeine for me. Got Phosphatidyl Serine, gonna try it out)

 

 

In general, dopamine makes your brain crave reward, which itself is mediated by the opioid system.



#49 Area-1255

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Posted 13 September 2014 - 04:12 PM

 


 
To sum this up:
- I know that my brain craves dopamine
- I suspect lowered DHEA levels
- I probably have elevated cortisol levels (Therefore, no caffeine for me. Got Phosphatidyl Serine, gonna try it out)

 

 

In general, dopamine makes your brain crave reward, which itself is mediated by the opioid system.

 

Dopamine's interactions with the Opioid system..too much Opioid activity and you will feel numb...too little and it's like low adrenaline and / or low serotonin - they all interact - you seek sensations and "reward".

But don't be fooled, you NEED this reward circuitry in tact.

 

This is why people who get high off of opiates and monoaminergic enhancers....they lose zest and motivation in the long run - because what is there to accomplish when you are high all of the time?

If you give your brain artificial reward - you won't struggle to find another long-term goal...that's why I prefer not to be running on supraphysio- extramonomine -states all the time. Maybe on the weekend though ;)

Of course..then my rush will still come from something (someone) physical..primarily. lmao

 

"It's the psychology and our biology; if there is reward to be gained it's to be seen, if it comes from an artificial chemical then our brain no longer seeks reward, so by the common principles of how our brain works - we should expect to be short-circuited by the abuse of drugs."


Edited by Area-1255, 13 September 2014 - 04:14 PM.


#50 medievil

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Posted 13 September 2014 - 09:34 PM

Da transporters are dysregulated in adhd, simply increasing da or upregulates da receptor is not effective for add otherwise loops with cardidopa would work.

#51 medievil

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Posted 13 September 2014 - 09:41 PM

Keep in mind that 5-HT2A/2C blockade is suggested to be very helpful in depression, whereas D2 Blockade is NOT.

Only mildly helpful and only for melancholic depression that would make the most common depression atypical depression worse.


In general, dopamine makes your brain crave reward, which itself is mediated by the opioid system.

No da itself causes drug wanting but it's not simple in the way that simply increases da makes you crave drugs.

endorphins don't cause craving they are solely responsible for reward.

#52 Area-1255

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Posted 13 September 2014 - 11:59 PM

Keep in mind that 5-HT2A/2C blockade is suggested to be very helpful in depression, whereas D2 Blockade is NOT.

Only mildly helpful and only for melancholic depression that would make the most common depression atypical depression worse.


In general, dopamine makes your brain crave reward, which itself is mediated by the opioid system.

No da itself causes drug wanting but it's not simple in the way that simply increases da makes you crave drugs.

endorphins don't cause craving they are solely responsible for reward.

I already said the above about 5-HT2A/2C - did you copy it? lol

Dopamine does not make you crave reward, low dopamine levels and low adrenaline levels are associated with sensation seeking and risky activities. Though because adrenaline and serotonin have stronger effects on endorphins (namely 5-HT1A and Alpha-1-Adrenoreceptors) - low serotonin and low adrenaline gives the greatest sensation seeking "punch". But low dopamine as well - low dopamine leads to low GABA and problems with all kinds of other NT systems.



#53 medievil

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Posted 14 September 2014 - 12:14 AM

Yes I copied some sentences and replied under it, if it was me stating it would contradict myself and basically talk to myself, can be interesting to read but If I was talking to myself not it's not interesting if I say the same things as you.

Anyway, enough creative rambling of me haha.

Evidence that low da levels cause sensation seeking and risky behavor? that's what stimulants actually do, and da agonists can cause compulsive gambling.

Stims are the only thing working for my anhedonia, the last thing I want with my natural too low da levels is sensation seeking.

Endorphins Def do not make you seek out sensation, reward or whatever they just purely do one thing cause pleasure also endorphins regulate patience, ability to work towards long term goals and anxiolysis. herein just induces pure reward and is the only drug that makes you lie down the whole time as pleasure is directly stimulated, other drugs make you do stuff like talk or listen music as that induces endorphin reward, no need for that on herein as your passed the music inducing pleasure, you just induce the pleasure itself.

#54 Area-1255

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Posted 14 September 2014 - 12:51 AM

Yes I copied some sentences and replied under it, if it was me stating it would contradict myself and basically talk to myself, can be interesting to read but If I was talking to myself not it's not interesting if I say the same things as you.

Anyway, enough creative rambling of me haha.

Evidence that low da levels cause sensation seeking and risky behavor? that's what stimulants actually do, and da agonists can cause compulsive gambling.

Stims are the only thing working for my anhedonia, the last thing I want with my natural too low da levels is sensation seeking.

Endorphins Def do not make you seek out sensation, reward or whatever they just purely do one thing cause pleasure also endorphins regulate patience, ability to work towards long term goals and anxiolysis. herein just induces pure reward and is the only drug that makes you lie down the whole time as pleasure is directly stimulated, other drugs make you do stuff like talk or listen music as that induces endorphin reward, no need for that on herein as your passed the music inducing pleasure, you just induce the pleasure itself.

I never said endorphins make you seek out reward, you seek out reward to GET an endorphin rush - but low alpha-1-adrenergic activity and low serotonin LEADS to low endorphin - leading to you doing things to raise it.

 

Stimulants may help ahedonia, but I recommend getting your natural stimulant production going.

Histamine and DHT  ( in men ) are your natural stimulants.

As well as adrenaline and thyroid hormones (T4,T3 namely).

 

Therefore if you have normal histamine,DHT and Thyroid output you should NOT be addicted to Stims or dependent on them.

 

Just like low histamine and hypothyroidism is linked to Schizophrenia.

 

http://www.alternati...hizophrenia.htm

http://www.joanmathe...ler_coaster.htm

http://www.biobalanc....au/articles/54

 

http://area1255.blog...stamine-or.html

http://area1255.blog...sturbing_5.html

http://area1255.blog...h1h2h3-and.html

 

http://www.jneurosci...3/32/12982.full

http://www.ncbi.nlm....pubmed/20133675 (read!)


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#55 Mind_Paralysis

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Posted 20 September 2014 - 10:55 PM

Area-1255... I must ask, do you yourself have any form of ADHD? I ask, because I get the feeling that you don't and if so, you have probably missed a lot of the more recent research on this, and that research is more focused on the glutamatergic system, not the histaminergic. There's certainly a connection, since Histamine and glutamate are connected, but it doesn't appear to be a significant one.

 

I also get the feeling you've missed some of the key threads here on longecity regarding ADHD - the upregulating method of treatment have more or less been disproven, it only helps a very, very select few with their ADHD -problems.

 

Check out GetoutofBox's thread here on Longecity - he's one of the most talented amateur neuro-chemists I have ever met on the internet:

http://www.longecity...in-development/

 

 

In his thread, we explored most avenues of treatment, and came to the conclusion that the NMDA -network is altered/mutated among a huge percentage of the ADHD-suffering population - and that is also the current angle being investigated by the medical profession out there.

 

And considering that us ADHD-ers often have increased NMDA-activity, and common comorbid issues of allergies and asthma, I rather take issue with you suggesting Anti-histamines and NMDA as treatment for ADHD.

 

NMDA will most likely only worsen the problem for most of us, and Anti-histamines are completely without effect - many of us have tried many different anti-h's, as part of our treatment against allergies, and I can tell you this, not a one of us notice any improvement in attention on them - they just make you drowsy. As f*ck.

 

And I do believe I saw you mention increasing cAMP as a valid method of treating ADHD?? That's complete rubbish! Many, many ADHD-sufferers have naturally ELEVATED levels of cAMP in the PFC, leading to signal-distortion, and trouble with filtering out stimuli, so increasing cAMP is an incredibly stupid idea - it'll just make everything worse! Decreasing cAMP indirectly is actually one of the primary modes of effect of Intuniv ( guanfacin) as it is an Alpha-2-Agonist

 

 

ZENFOOD: These are compounds currently regarded as possible alternatives to Stimulants, check them out and make up your own mind as to which ones would benefit you.

 

Memantine - Is seeing rising use in the USA as treatment against ADHD, it's one of the very few compounds around that EXCLUSIVELY AGONISES THE D2-RECEPTOR. That's right. The very receptor you have an issue with.

The D2 -effect is very mild however, and the main mode of effect of Memantine is as a selective NMDA-antagonist. As you are probably aware, the NMDA-network is responsible for the communication between many centers in the brain, and helps keep the brain in balance - i.e, whenever you take a psychoactive substance such as Amphetamine, the NMDA-network takes note, and starts the process of de-regulating your Dopamine-receptors, resulting in tolerance building, and the brain keeping the same un-stimulated state, even when you take Amphetamine.

 

The most recent research in ADHD is showing increased NMDA -activity, possibly connected to lower levels of Kynurenic Acid in ADHD-sufferers. Kynurenic Acid is also the currently researched area of interest regarding Schizophreniacs, who have many symptoms working inversely to ADHD - HIGH Dopamine -levels, LOW NMDA activity, and sky-high levels of Kynurenic Acid.

 

"The Kynurenic Acid theory" for Schizophrenia is the most recent theory regarding that disease, and it links the dopamine and NMDA -theories together fairly nicely, as the NMDA -network seems to be altered among them, because of elevated Kynurenic Acid -levels, resulting in the NMDA-network failing to keep dopamine-levels in check, leading to haywire neuro-transmitters - resulting in, well... madness.

 

It would appear as if we ADHD-ers work in an inverted way, often less dramatically tho'. Low dopamine, high NMDA, low kynurenic acid, but not THAT much lower than the neurotypicals.

 

Memantine was originally intended as an Alzheimers-medication, since mutations in the metabotropic glutamate network ( which NMDA is a part of) appear to be at the root of at least part of the disease. Memantine was meant to decrease glutamate excitotoxicity, which is very high among those with Alzheimers-disease. It was found to be too weak however, it can't affect the NMDA-network enough to inhibit the toxicity, and thereby halt the disease.

 

However... increased NMDA-activity has been seen in a lot of other neurological disorders as well, and ADHD is one of them. The effect on ADHD was actually first noticed when it was used as treatment of Amphetamine-tolerance ( since Memantine antagonises the NMDA-receptors it also restores the effect of amphetamine and other psychoactives, by blocking the brain from blocking the effect of the drug)

 

And since Memantine has been shown to be effective, with a much better side-effect profile than stimulants, this then leads us to this compound...

 

NITRO-Memantine - this is an experimental research-chemical, currently in research for the treatment of Alzheimer. The docs really felt they were on to something with Memantine, so they gave it another whirl. By binding the memantine to a nitrate-group, they appear to have increased the effects of Memantine as an NMDA-antagonist many-fold. How many times? Hard to say, but it appears to be as much as 5-10 times. Now that's some strong stuff. The result is a chemical which can be used in smaller doses and appears to be less side-effect prown compared to Memantine, who already had a good side-effect profile. Memantine is known for causing brain-fog at incorrect doses, and can therefore be rather finicky in finding the right dose - not so with Nitromem, it's easier on the cognition when trying doses.

It also appears to affect more portions of the NMDA-network than Memantine, as recent rat-experiments show a REMARKABLE effect on autistic symptoms as well! Something which Memantine does not produce - this is of interest to us as well, since Authism Spectrum Disorders appear to be highly related to ADHD as well, it's not uncommon to have comorbid issues.

 

If everything pans out, Nitromemantine could be a one-shot bullet to your brain, removing your problems of ADHD, potential coordination issues, dyslexia, sensory disorders, authism-disorders, you f*cking name it.

We don't know much yet tho'... even the formulation is somewhat unknown at the time, since the company developing it has reportedly noted a clear effect on Alzheimer using a rat-model, they are keeping this one daaaamn close to the vest - they're not letting anything slip out until they're ready to cash in. If this truly works, they'll be richer than bloody Midas.

 

Memantine is available however, and may well be enough for many of us, we may not need as potent a chemical as Nitromemantine. Memantine has been reported to have an excellent anti-depressant effect as well, should be noted, so I definitely think you should try it - especially since it affects one of your mutated receptors DIRECTLY.

 

There are a few more options however, which you should check out:

 

Fasoracetam - the latest love-child of the Racetam-family, a high-potency variant which appears to be 10-15 times as powerful in effect as Piracetam. Fasoracetam has a very complex mode of effect, wherein it modulates cAMP, either lowering or increaseing it, depending on the situation in the brain, it seems. It also potentiates GABA and choline, leading to both an anti-depressant effect, as well as eliminating the need to suppliment with a choline-source while taking it. ( usually, racetams burn through your natural storages of choline, leading to brainfog if you don't supplement with choline - faso however, increases choline-levels on its own, meaning that you don't need to supplement - it fixes the deficiency itself! Remarkable.)

 

Fasoracetam is a potent Glutamate-agonist, and that appears to be its main mode of effect - however, some of the glutamate-receptors it agonises, in turn ANTAGONISES the NMDA-network! It's a very clever mode of effect. Fasoracetam was discovered to have potential therapeutic effect on ADHD very recently, via the Human Genome Project, as a Norwegian dr - Hakon Hakonarson, utilized genetic data on children with ADHD and discovered that certain portions of them have mutations within the metabotropic glutamate network, and then crossreferenced all known medical compounds that are connected to affecting those networks, and discovered that Fasoracetam was an already developed and known compound that affected glutamate -receptors.

 

Fasoracetam has an interesting point of convergence with Memantine here, since both of them were originally intended as treatment of Alzheimers, but found to be too weak to affect the symptoms. Coincidence? I think f***ing not.

 

They both affect the glutamate networks in the brain - they're both good sh*t for increasing cognition.

 

Fasoracetam is currently undergoing clinical trials to be used as a possible ADHD-medication and the study is almost complete - I e-mailed Hakonarson myself, and he informed me that he has found it effective for certain segments of the ADHD-population and will be publishing his findings early next year. Meanwhile, on this very forum, we have a thread where some of the members have been experimenting with Fasoracetam and reporting their findings. The results seem promising, a lot of the ones that suffer from ADHD reports significant improvement of symptoms, without the intense side-effects that stimulants give.

 

Intuniv ( time-released guanfacine) - A drug that is actually already a recognized and in-use medicine for treating ADHD. It works by agonising ( activating, increasing the effect of) something called the Alpha-2-adrenal receptors. These receptors are mostly located in your pre-frontal cortex, and help regulate the levels of neuro-transmitters in the PFC - they help you control your attention and behaviour. One of the ways they do this, is by decreasing the levels of cAMP in your PFC, allowing your other neuro-transmitters to reach their targets.

 

There's a direct correlation between the D2 -receptor which you have a mutation within, and cAMP - when the D2-receptor is activated, it actually antagonises cAMP, decreasing its levels, in order for specific signals to be translated more strongly.

May I ask which type of ADHD you have been diagnosed with? There is an interesting differentiation here, because the D4 -receptor, which is another dopamine-receptor, which is highly similar to the D2 version, has been linked to the Hypoactive version of ADHD - ADD. I myself am ADD, and my issues are primarily with motivation, not concentration. ( although I definitely have this as well. ) Much like the D2-receptor, the D4-receptor is activated by Dopamine, and then proceeds to decrease cAMP in the PFC, leading a nicely controlled and focused behaviour.

 

If you have mutations to any of these receptors, they may not decrease cAMP sufficiently, leading to signal-noise in the part of your brain that controls behaviour, meaning that you WON'T be able to control your behaviour, as your brain won't be able to sufficiently single out the most important signals - your attention will be going from one thing to the other constantly, unable to determine which stimuli is the most important one.

 

Intuniv is very effective for attention-control, and that's why it's becoming the primary weapon of choice for treating children with HYPERACTIVE adhd. It hardly affects motivation at all however, since that's not it's mode of effect - it increases focus.

 

Intuniv is a great addition to your methylphenidate-treatment as well, in the USA they are commonly combined, since Intuniv lowers the increased blood-pressure of methylphenidate, and meth clears up the sometimes tired feeling that Intuniv gives. Together, they synergize, removing each others weaknesses, and enhancing the strengths. I don't know if it's been cleared for use in Finland yet, but it's currently not in Sweden, where I reside... It has been scheduled for evaluation tho, and most likely it will be available in a year or two.

 

On a related note, there are actually other Alpha-2-agonists which have been noted to affect ADHD in a positive way, such as Cannabigerol - it is one of the compounds found in the marijuana-plant, and acts in a way nearly identical to guanfacine ( Intuniv).
This is most likely the reason why so many ADHD-ers find marijuana calming, as it somewhat clears the signal-noise in the PFC.

 

However... Cannabis also inhibits cognition, because of the many other psycho-active substances in it, which limits the usefulness of Cannabis in treating ADHD. Cannabigerol-levels in the strains used for drug-use is also much lower compared to other strains. The ones that seem to have the highest levels of Cannabigerol are the ones used for other, industrial purposes. If you can find a good strain of dietary hemp, and then test it for Cannabigerol-levels, then you have a pretty darn good cognitive enhancer there, and a good protein-supplement for that power-lifting as well, to BOOT! : D

 

 

In closing, feel free to check out my thread on ADHD, it's meant to be cover most aspects of the disease(s) so feel free to add your own 2 cents in there.

 

http://www.longecity...ception-thread/


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#56 Metagene

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Posted 23 September 2014 - 07:18 PM

 

 

Memantine - Is seeing rising use in the USA as treatment against ADHD, it's one of the very few compounds around that EXCLUSIVELY AGONISES THE D2-RECEPTOR. That's right. The very receptor you have an issue with.

The D2 -effect is very mild however, and the main mode of effect of Memantine is as a selective NMDA-antagonist. As you are probably aware, the NMDA-network is responsible for the communication between many centers in the brain, and helps keep the brain in balance - i.e, whenever you take a psychoactive substance such as Amphetamine, the NMDA-network takes note, and starts the process of de-regulating your Dopamine-receptors, resulting in tolerance building, and the brain keeping the same un-stimulated state, even when you take Amphetamine.

 

The most recent research in ADHD is showing increased NMDA -activity, possibly connected to lower levels of Kynurenic Acid in ADHD-sufferers. Kynurenic Acid is also the currently researched area of interest regarding Schizophreniacs, who have many symptoms working inversely to ADHD - HIGH Dopamine -levels, LOW NMDA activity, and sky-high levels of Kynurenic Acid.

 

"The Kynurenic Acid theory" for Schizophrenia is the most recent theory regarding that disease, and it links the dopamine and NMDA -theories together fairly nicely, as the NMDA -network seems to be altered among them, because of elevated Kynurenic Acid -levels, resulting in the NMDA-network failing to keep dopamine-levels in check, leading to haywire neuro-transmitters - resulting in, well... madness.

 

It would appear as if we ADHD-ers work in an inverted way, often less dramatically tho'. Low dopamine, high NMDA, low kynurenic acid, but not THAT much lower than the neurotypicals.

 

Memantine was originally intended as an Alzheimers-medication, since mutations in the metabotropic glutamate network ( which NMDA is a part of) appear to be at the root of at least part of the disease. Memantine was meant to decrease glutamate excitotoxicity, which is very high among those with Alzheimers-disease. It was found to be too weak however, it can't affect the NMDA-network enough to inhibit the toxicity, and thereby halt the disease.

 

However... increased NMDA-activity has been seen in a lot of other neurological disorders as well, and ADHD is one of them. The effect on ADHD was actually first noticed when it was used as treatment of Amphetamine-tolerance ( since Memantine antagonises the NMDA-receptors it also restores the effect of amphetamine and other psychoactives, by blocking the brain from blocking the effect of the drug)

 

And since Memantine has been shown to be effective, with a much better side-effect profile than stimulants, this then leads us to this compound...

 

 

 

 

Another problem with memantine is it also appears to antagonizes α3β2-nAChRs receptors on the sympathetic nerve terminals potentially causing  vertebrobasilar insufficiency in AD patients. 

 

 

 

Memantine, an NMDA receptor antagonist used for treatment of Alzheimer’s disease (AD), is known to block the nicotinic acetylcholine receptors (nAChRs) in the central nervous system (CNS). In the present study, we examined by wire myography if memantine inhibited α3β2-nAChRs located on cerebral perivascular sympathetic nerve terminals originating in the superior cervical ganglion (SCG), thus, leading to inhibition of nicotine-induced nitrergic neurogenic dilation of isolated porcine basilar arteries. Memantine concentration-dependently blocked nicotine-induced neurogenic dilation of endothelium-denuded basilar arteries without affecting that induced by transmural nerve stimulation, sodium nitroprusside, or isoproterenol. Furthermore, memantine significantly inhibited nicotine-elicited inward currents in Xenopous oocytes expressing α3β2-, α7- or α4β2-nAChR, and nicotine-induced calcium influx in cultured rat SCG neurons. These results suggest that memantine is a non-specific antagonist for nAChR. By directly inhibiting α3β2-nAChRs located on the sympathetic nerve terminals, memantine blocks nicotine-induced neurogenic vasodilation of the porcine basilar arteries. This effect of memantine is expected to reduce the blood supply to the brain stem and possibly other brain regions, thus, decreasing its clinical efficacy in the treatment of Alzheimer’s disease.

 

 

http://www.plosone.o...ne-0040326-g001

 

 

I had a couple great weeks before the side effects became too problematic. The experience gave me a better understanding of DCD and ADHD so no regrets in trying.


Edited by Metagene, 23 September 2014 - 07:19 PM.


#57 Zenfood

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Posted 25 September 2014 - 02:14 PM

Hey guys. Even if my responses might be relatively short, it doesn't mean that I don't appreciate your comments and your help. I actually do, deeply.

It's just that writing posts like these are mentally draining.

Sorry for being inactive for so long. I ordered some 5:1 catuaba and was supposed to receive it last Wednesday and I was eager to write a report.
But the imbecile sent me a standard extract... so I am going to return and receive a new one. Therefore no updates.

 

However, I have found something new that might be related to my cognitive decline and memory issues. I am 26 years old and my attention span is very bad (I tend to drift away and day dream) while watching a movie, talking to someone, etc. I forget simple and easy tasks. e.g. when I enter the kitchen: "What the hell was I supposed to do?" or when speaking to someone I have a hard time remembering words, it's always on the tip of my tongue. I also have social anxiety when meeting people. No, I don't get nervous. I am very funny, cocky, "alpha" and confident with others and I do not seek approval from anyone. It's just that I avoid bumping on people, because it is mentally draining.

 

This is not the "real me", because I have always been very popular amongst friends and girls all my life. If people ask me how I am and I answer them truthfully, they think I'm joking. They always counter with "But you look so healthy and you don't look sad at all to me. What you feel is normal." The only person that actually understands me is my girlfriend. My family knows that I am "broken", but they don't really understand it, because they have never been even slightly depressed (not that I am at the moment, but I was seriously depressed years ago - which probably damaged my neurons). My girlfriend knows and believes that I have more potential than being "couch-locked" reading studies and experimenting with supplements day in and day out - even though she met me when I was like this. She has seen glimpses of my happy, energetic and motivated inner being. "If you can't handle me at my worst, then you sure as hell don't deserve me at my best.” - Marilyn Monroe

I am very grateful that she puts up with my s***. She deserves so much better, but we both know that things will get better one day and I will show her what I'm capable of then. 

 

I have now used The Happy Stack (1000mg DHA, 250mg sublingual Uridine and 250mg Citicoline) with Noopept 3x10mg and Pramiracetam 2x300mg. These have had remarkable changes in my mood and memory. My cognitive skills are MUCH better. I do not miss the keys when typing as often as I used to. I can walk down the stairs with more confidence and ease, I now see in HD (Thank you Noopept) also, like my "visual fog" is gone and best of all I am more confident and my social anxiety is gone. I remember stuff and I feel that my synaptic plasticity is increasing. My patience and attention span is much better: I find it easier and actually fun to focus and meditate. This is better than smoking pot and I experience the same feelings: slight euphoria, more adventurous, more eager to learn things due to better memory. My libido has increased a lot too after only 4 days on this stack.

I think that bad memory and declined cognition causes anhedonia, etc. it's hard to be optimistic when you can't do basic stuff. Now I really feel that things are turning and s*** isn't hitting the fan all the time. I still have problem with motivation and fatigue. I popped one Modafinil today, but it doesn't help with the fatigue, I have only noticed more alertness and less social anxiety. However, brain fog and stuttering are undesired side effects I usually experience (yes, experiencing minor brain fog while writing now, even with prami+noopept, probably need to edit a lot). Doesn't remove the mental fatigue I experience. I bet that this has to do with histamine increase in the hypothalamus. Not going to touch that stuff again.

 

I have also been on a super strict anti-histamine diet for one week.Thank you Area-1255 and Joe from Selfhacked for opening my eyes.
I am following this: http://www.histamini...ist_HIT(EN).pdf

I have noticed that my histamine sensitivity has caused me sleep apnea (I checked this with my oximeter upon waking, it was super low, between 92-94%!) which of course causes fatigue and disrupts sleep, big time! I have probably suffered from this the last ten years without knowing it. I also make sure that my window is open during the night now. So, I have been taking Benadryl before sleep (managed to get a prescription! It's a great sleep aid) in order to block histamine and increase DAO enzymes up to 19%, and now I wake up with an oxygen level of 99%.

 

Anti-histamine diet, Benadryl and open window = Success

I also take EGCG+Quercetin (to name just a few supplements) twice daily, because they are antihistaminergic.

 

 

Stinkorninjor, awesome info! Trevligt att du också är svensk. Jag flyttade till Helsinki för ca. 18 månader sedan och blev diagnostiserad i Stockholm.

OK, back to English. They labeled me as "ADHD" and I didn't care to argue with them, because I just wanted the ritalin. I am not hyper at all. The only "hyper" thing about me is nail biting and restless swinging legs from time to time. I have never been impulsive or done stupid stuff. I always (over) analyze situations before entering them, which can make me passive and sedentary. I will get back on your post soon.

 

Just been thinking if all my troubles could actually stem from early stages of Parkinson's Disease? My symptoms are very similar to PD!
This is highly speculative, but is this why the Happy Stack and Noots are working so great for me?

I have a rare SNP that says:

0.9% Frequency

3x higher risk for PD
more info: 
http://www.snpedia.c...ex.php/Rs283413

 

P.S.
I am going to stay off the pramiracetam for a while soon and see what happens. Cycling is probably a good thing with this substance.
As for Noopept, I plan to stay on it for at least 6 months and then cycle. I will probably use the Happy Stack and drink Gynostemma/Jiaogulan tea for the rest of my life.


Edited by Zenfood, 25 September 2014 - 03:12 PM.

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#58 Zenfood

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Posted 25 September 2014 - 03:33 PM

I also had to add that the first time I took Noopept I really felt a "WOAH!" Sensation.  I also take one pill before sleep and it makes me remember my dreams now. I always take the pramiracetam separately from noopept, so I know the effect.

 

My girlfriend took one this morning and just got tired from it. I believe that it helps people with cognitive decline to get back to baseline, but not healthy people. She's a fitness instructor/dancer and is already super energetic with good memory, coordination and great mood.

 

More about Noopept. Interview with one of the creators:

http://smartdrugsmar...ovskaya-noopept


Edited by Zenfood, 25 September 2014 - 03:58 PM.


#59 Flex

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Posted 25 September 2014 - 04:39 PM

In regards of Piracetam :

http://selfhacked.co...egative_Reports

Oxidative Stress in a Model of Toxic Demyelination in Rat Brain: The Effect of Piracetam and Vinpocetine

http://link.springer...1064-011-0450-1

 

 

It could be the same or similair thing for Noopept.

According to some reports from longecity, some people have reported an impaired short term memory. 

 

Dont want to be a scaremonger, see it like a hint and invesatigate it to be on the safer-side.

 


Edited by Flex, 25 September 2014 - 04:44 PM.

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#60 Zenfood

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Posted 25 September 2014 - 04:47 PM

Thanks Flex. I am well aware of that article. I've read every article on that site at least twice.

 

Pramiracetam just feels right for me. You can also check Maija's comment on the first link. It helps with cognitive fatigue.

I'm going to cycle it from time to time and see what happens.

 

Noopept feels quite safe. That's why I'm willing to go 6 months with it. I've read a lot of reports from people that has used it for 6 months+ and quit cold turkey without any negative effects.

 

I would say that in my case it is worth the risk. However, if one is healthy I really don't think playing with racetams is a good idea.

 

 

"The protective ability of noopept most likely results from moderate suppression of oxidative stress and intracellular calcium influx, stabilization of mitochondrial function and reducing of apoptosis. Another possible mechanism by which this compound protects cells from amyloid toxicity may be related to the decrease of tau phosphorylation and, eventually, neurite stabilization and outgrowth."

 

This was released a couple of weeks ago.
Source: http://www.jbiomedsc...-014-0074-2.pdf

 


Edited by Zenfood, 25 September 2014 - 05:33 PM.

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