Completely eliminated my severe anxiety symptoms with three supplements!
- Thread starter Hip
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it is an oral spray not a body spray- can you image?"You know when you've been Tangoed"
ahh ooops my bad, no Eau du Tumeric then but I guess you could still smell like a curry if it's oral. Yup I remember the advert LoL
A quick update - I'm still using NAG. I cant work out if it is having any anti anxiety effect for me, but it does seem to help me get over a broken gut much more quickly (I get this frequently, following a cold like virus) it's as if the lining gets ripped to shreds and NAG helps sort it out quick. Having said that about antianxiety, today is day 29 without a single benzo which is a remarkable difference compared to a few months ago when I was using 2 - 3 times a week (not considered high usage, but still enough to build tolerance!). So what I'm saying is, perhaps it's having more of an effect than I have given it credit for.
One thing I do really credit with helping me get out of the hole I was in at the first part of this year is the flaxseed oil. This is definitely doing something. I am also really pleased with the effect of Magnesium Malate. I'll often take one of those when I feel anxiety brewing and it seems to take the edge off.
I plan to try theanine next, in capsules. At the moment I'm getting it from sencha & matcha green tea and can feel that lift in mood and calming it is known for.
The Oolong GABA tea is still pretty good but after further experimentation, you definitely need to pulse it.
Can anyone recommend a good Turmeric supplement, say in capsule form? as I dont really want to buy bulk powder.
cheers
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Hey hip. I'm on a regimen of 75mg nortriptyline, 40mg lexapro and 80mg atOmoxetine for depression and ADHD. I want to add 10mg amiloride to the regimen but the leaflet says it's not recommended to take it with tricyclics or atomoxetine. It also says to avoid anti-psychotics. Was wondering whether I could just ignore the precautions and take it anyway?
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ey hip. I'm on a regimen of 75mg nortriptyline, 40mg lexapro and 80mg atOmoxetine for depression and ADHD. I want to add 10mg amiloride to the regimen but the leaflet says it's not recommended to take it with tricyclics or atomoxetine. It also says to avoid anti-psychotics. Was wondering whether I could just ignore the precautions and take it anyway?The
Hip
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Hi @sugamama, according to the interactions checker at drugs.com, the interaction between nortriptyline and amiloride is a moderate one (not a major one), which may lead to some lowered blood pressure.
Any particular reason for taking amiloride?
Any particular reason for taking amiloride?
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similar to you, anxiety, depression and denationalization. a comibination of two nri's and one ssri helps and am curious to know whether amiloride will increase the efficacy or improve the combination. any notable cognitive improvements since restarting it? i also feel complete remission from a hangover and am wondering if there's a glutaminergic element to the problem. considering trying ketamine. i'm also very sensetive to norepinephrine, running and cold showers severely disturb my cognition.
AngelM
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Thank you so much for the information. I happen to have the supplement NAG, but have never tried it. I believe my integrative medicine doc suggested it along with other supplements for CFIDS, but I didn't get around to trying it. I also keep turmeric on hand, and use it for cooking, but have never used it medicinally. I will buy some flaxseed oil, and I should be good to go. I find the association with sinusitis very interesting. For years I have had flare ups of CFIDS symptoms (didn't have a clue what was going on back then) but the flares always began with sinusitis and then followed a pattern. I knew there had to be a connection, but I couldn't for the life of me figure out what it was. Thank you again for the advice.
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@Hip I'm curious about something, I've been doing some reading on NAG and ordered some from Jarrow to give it a try.
Do you have any dopamine related issues? Specifically ANKK1 A1? Or general (DDD) Dopamine Deficient Depression?
I came across a study where they used GlcNAc to clean D2 receptors from Bovine to sample.
"Under optimal conditions about 65% of the applied D2 dopamine receptors bound to WGA-agarose and could be eluted with N-acetylglucosamine."
They determined D2 receptors were glycoproteins as a result. I haven't had a chance to dive into it, and studies and few and far between.
Do you have any dopamine related issues? Specifically ANKK1 A1? Or general (DDD) Dopamine Deficient Depression?
I came across a study where they used GlcNAc to clean D2 receptors from Bovine to sample.
"Under optimal conditions about 65% of the applied D2 dopamine receptors bound to WGA-agarose and could be eluted with N-acetylglucosamine."
They determined D2 receptors were glycoproteins as a result. I haven't had a chance to dive into it, and studies and few and far between.
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Also do you know of any mercury exposure you've come across? Have you had your mercury levels checked out?
"Mercury concentration in urine and urinary activity of N-acetyl-beta-D-glucosaminidase were determined in a group of 100 workers from an electrolysis workshop. The enzyme activities measured were twice as high as those of 100 control subjects. The difference was statistically significant. There was no correlation between urinary activity of N-acetyl-beta-D-glucosaminidase and mercury concentration in urine. The applicability of this biochemical-toxicological test in occupational health practice is discussed."
It's known that metabolites of NAG can chelate metals. Could be possible this increase in urinary protein excretion is a result of the increased demand and breakdown of n-Acetylglucosamine through N-acetyl-beta-D-glucosaminidase to remove heavy metals?
"Mercury concentration in urine and urinary activity of N-acetyl-beta-D-glucosaminidase were determined in a group of 100 workers from an electrolysis workshop. The enzyme activities measured were twice as high as those of 100 control subjects. The difference was statistically significant. There was no correlation between urinary activity of N-acetyl-beta-D-glucosaminidase and mercury concentration in urine. The applicability of this biochemical-toxicological test in occupational health practice is discussed."
It's known that metabolites of NAG can chelate metals. Could be possible this increase in urinary protein excretion is a result of the increased demand and breakdown of n-Acetylglucosamine through N-acetyl-beta-D-glucosaminidase to remove heavy metals?
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Also do you eat a lot of wheat?
Wheat germ agglutinin or WGA is a lectin that protects wheat (Triticum vulgaris) from insects, yeast and bacteria. An agglutinin protein, it binds to N-acetyl-D-glucosamine and Sialic acid.
WGA has been shown to be inflammatory in the brain and elsewhere, to cause leaky gut and impaired digestive function etc.
I'd imagine if someone isn't sufficient in NAG, or has deficient enzyme function to manufacture it in specific areas that WGA could do a lot of damage. It's in wheat, corn, rice, oats etc.
Wheat germ agglutinin or WGA is a lectin that protects wheat (Triticum vulgaris) from insects, yeast and bacteria. An agglutinin protein, it binds to N-acetyl-D-glucosamine and Sialic acid.
WGA has been shown to be inflammatory in the brain and elsewhere, to cause leaky gut and impaired digestive function etc.
I'd imagine if someone isn't sufficient in NAG, or has deficient enzyme function to manufacture it in specific areas that WGA could do a lot of damage. It's in wheat, corn, rice, oats etc.
Hip
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Mainly virally-triggered anhedonia, which was severe at one stage, but is a bit better now. Anhedonia is the inability to feel pleasure or reward from life's normally enjoyable activities; dopamine is thought to play a critical role anhedonia and the reward circuitry of the brain.
If find both anhedonia and my depression hard to treat, because dopaminergic antidepressants like MAO inhibitors (which used to boost my mood and enthusiasm enormously previously) stopped working for me after my brain was assaulted in quick succession by: a nasty organophosphate poisoning, a viral brain infection, and the development on ME/CFS.
Some of the dopaminergic drugs I have looked into and tried are listed in this post. Perhaps we can carry on this discussion about dopamine on that thread, which is more appropriate. ANKK1 A1 I don't know anything about.
I have not been checked for mercury, but there's nothing I can think of that would have exposed me to a major source. I've been gluten free for decades, as eating gluten would reliably-as-clockwork trigger a bout of depression in me 1 hour later, and the bout would last for 6 to 8 hours, and they clear. But since I developed ME/CFS, I seem to have lost my gluten sensitivity, although I still avoid gluten most of the time, just as a precaution.
No offense but I wish when people make posts like this they could explain it in more detail, this is about as vague as vague can be. Is this saying that NAG obliterates dopamine receptors? as far as I can tell "eluted" means to clean or remove. Or is it saying it resets them and therefore would help dopamine production?
Ive tried searching google and cant find much of anything. Curious as Im taking NAG as part of a gut protocol.
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D2 receptors are n linked glycoproteins. WGA-Agglutinin comes from wheat, corn, oats etc, it crosses the blood brain barrier and has affinity with several dopaminergic systems.
Small amounts of WGA are very pro-inflammatory. WGA can form a glycoprotein with NAG which causes even more damage.
In the study they used NAG to remove WGA from the receptors.
The original quote is describing a test tube manipulation which would have been undertaken to purify and characterise dopamine receptors.
Some type of extract from animal tissue (there is no link to the study so I can't say what), containing dopamine receptors solubilised from their membranes, was applied to a solid phase (agarose gel) which had WGA attached to it.
The lectin WGA recognises NAG, so any glycoproteins in the mixture containing NAG on the surface would bind to the gel and other substances pass through. The fact that a significant proportion of the dopamine receptors in the mixture bound to the gel indicates that they are glycoproteins containing NAG.
The bound receptor could then be eluted (released) from the gel by applying a vast excess of NAG which out-competed the binding of receptor to WGA.
This is a commonly used purification technique called affinity chromatography. A wide variety of substances can be immobilised on a gel support and used to select out substances which interact with them from a complex mixture. Some small molecule which also binds can then be applied in vast excess to recover the wanted bound substance which has now been considerably purified from the starting mixture.
The experiment says nothing whatsoever about the effect of NAG that you swallow on dopamine receptors in situ.
Rats fed very large amounts of WGA certainly show adverse effects on the gut and a certain amount of uptake into the blood, but the authors of the study note that the amount of WGA in a normal diet has not been found to be toxic.
Similarly WGA injected intravenously (again in considerable amounts) has been observed to cross the BBB - after all it was an experiment designed to illuminate the transcytosis pathway.
It is a big jump to go from these experimental situations to one which links dietary WGA to adverse effects on dopaminergic systems.
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@asymmetry - I noticed you started with a low dose of NAG initially. I'd like to do the same after trying it twice and apparently getting a pretty bad reaction but can't figure out how to do it! Did you just open the capsule and measure out the contents until you got the dose you wanted? And then take it with water or something?
Hip
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I came across that study recently, but thanks for posting it anyway. I have not fully digested the implications, but the basic story is that brain cells contain some of the highest amounts of NAG found in any cell of the body, and that increasing NAG levels in neurons reduces synaptic signaling, which in turn decrease hyper-excitability in the brain.
So NAG turns out to be a regulator of neuronal excitability.
This could explain why NAG has anti-anxiety effects: my biochemical theory of anxiety posits that anxiety is caused when neuroinflammation produces excess glutamate in areas of the brain that mediate anxiety (the "anxiety circuit" areas such as the amygdala); glutamate is an excitatory neurotransmitter, and may over-stimulate these "anxiety circuits" of the brain.
So by countering neuronal excitability, NAG will counter the over-stimulatory effects of glutamate in the "anxiety circuits", which in turn may lower anxiety.
eric_gladiator
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Hello, is it possible to combine any of these with hyper juan herb?
Hip
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What is hyper juan herb?