Famotidine Is A Powerful Anti-serotonin Drug, Can Even Treat Serotonin Syndrome

[Regina]

Well, raising dopamine is a complex subject which certainly deserves a separate thread - I am sure there are several. I will like to quickly highlight few points I learned about dopamine:

Good dopamine levels and its proper metabolism is a wonderful thing.

Dopamine has to be broken down. Ideally, in a healthy person, most is broken down via MAO-A and COMT enzymes. If one or both of these are not working well, body will do one or two of the following things:
1.) it will create a new enzyme, MAO-B, which poorly breaks down dopamine, creating reactive oxygen species (ROS) and hydrogen peroxide in the process. This will cause neural damage and may even lead to Parkinson's in those individuals prone to it.
2.) it will up-regulate DBH enzyme that converts dopamine to noradrenaline / adrenaline. This can cause rapid conversion of dopamine to adrenaline, so by raising dopamine we end up with elevated adrenaline instead.

So, unless MAO-A and COMT enzymes are healthy, raising dopamine will cause problems, more or less, depending on the state of the factors involved.

Often, dopamine is reduced and replaced with serotonin as a harm-avoidance mechanism, a trade-off to prevent greater damage.

Dopamine agonist have merits, but also side-effects. I personally use some occasionally, but so far, low dose Selegiline has been the safest route for me, both from experience and understanding. When used in low dose, it inhibits MAO-B enzyme specifically.

I would consider selegiline myself to curb breaking down dopamine too much to NE. However, this description says selegiline increase cerebral nitric oxide and growth hormone: https://www.selegiline.com/

 

[sladerunner69]

Serotonin is the poor-man's substitute for dopamine. As perhaps, ego attempts to make up for a lack of self.

Why is serotonin so commonly prescribed for depression, then? Does serotonin feel good?

 

[Regina]

Well, raising dopamine is a complex subject which certainly deserves a separate thread - I am sure there are several. I will like to quickly highlight few points I learned about dopamine:

Good dopamine levels and its proper metabolism is a wonderful thing.

Dopamine has to be broken down. Ideally, in a healthy person, most is broken down via MAO-A and COMT enzymes. If one or both of these are not working well, body will do one or two of the following things:
1.) it will create a new enzyme, MAO-B, which poorly breaks down dopamine, creating reactive oxygen species (ROS) and hydrogen peroxide in the process. This will cause neural damage and may even lead to Parkinson's in those individuals prone to it.
2.) it will up-regulate DBH enzyme that converts dopamine to noradrenaline / adrenaline. This can cause rapid conversion of dopamine to adrenaline, so by raising dopamine we end up with elevated adrenaline instead.

So, unless MAO-A and COMT enzymes are healthy, raising dopamine will cause problems, more or less, depending on the state of the factors involved.

Often, dopamine is reduced and replaced with serotonin as a harm-avoidance mechanism, a trade-off to prevent greater damage.

Dopamine agonist have merits, but also side-effects. I personally use some occasionally, but so far, low dose Selegiline has been the safest route for me, both from experience and understanding. When used in low dose, it inhibits MAO-B enzyme specifically.

I think Selegiline is not Peat-friendly due to its promotion of nitric oxide:
L‐Deprenyl: nitric oxide production and dilation of cerebral... : NeuroReport

 

[TeslaFan]

I think Selegiline is not Peat-friendly due to its promotion of nitric oxide:
L‐Deprenyl: nitric oxide production and dilation of cerebral... : NeuroReport

Thank you for sharing that. I am not worried about NO as I take half the pill once per week.

 

[Dan W]

OK, I will see what I can do. It is OTC in the USA, so it should be fine to sell as a R&D product.

I foolishly started working on a famotidine comparison page before realizing you were going to make it obsolete. For what it's worth in the meantime, the name-brand Pepcid Maximum Strength (20mg) tablets look like the best option to me. Lot of downsides, but you at least avoid PEG and colloidal silica, and the small tablet size + higher dosage helps maximize your dosage-per-excipient.

I've never come across one of those pet/veterinary supply stores that doesn't ultimately require something from a vet when ordering. I'm not sure why aspirin seems to be an exception to that.

Anyone have a sense of whether we'd prefer famotidine to be delivered to the stomach vs the remaining digestive tract? It seems like the tablet formulations (and the antacids in the chewables) are designed to deliver the famotidine directly to stomach cells, but maybe we want to alter that process.

 

[Mito]

So, unless MAO-A and COMT enzymes are healthy, raising dopamine will cause problems, more or less, depending on the state of the factors involved.

What would be an indication that MAO-A and COMT enzymes are healthy or not healthy?

 

[TeslaFan]

What would be an indication that MAO-A and COMT enzymes are healthy or not healthy?

Good question. I did genetic and blood testing. I have homozygous SNPs on MAO-A gene, meaning I have predisposition to make less MAO-A enzyme. Therefore, my suspicion was that I have elevated serotonin, and that was confirmed by a blood test.
(Now, is it possible that my MAO-A enzymes are actually OK but I have SIBO instead? Theoretically, it is possible, but I doubt as I have been on antibiotics a few times, and serotonin drops just little under the upper limit due to reduction of bacterial endotoxin; it comes back to elevated levels within few weeks after treatment).

I also have homozygous SNPs on COMT gene, too, so I was suspecting slightly elevated catecholamines. The blood tests revealed undetectable dopamine, and normal / slightly elevated noradrenaline and adrenaline. That leads me to believe my DBH enzyme is overclocked, possibly as a compensation for low functioning MAO-A, which normally also breaks down dopamine.

 

[Nighteyes]

Good question. I did genetic and blood testing. I have homozygous SNPs on MAO-A gene, meaning I have predisposition to make less MAO-A enzyme. Therefore, my suspicion was that I have elevated serotonin, and that was confirmed by a blood test.
(Now, is it possible that my MAO-A enzymes are actually OK but I have SIBO instead? Theoretically, it is possible, but I doubt as I have been on antibiotics a few times, and serotonin drops just little under the upper limit due to reduction of bacterial endotoxin; it comes back to elevated levels within few weeks after treatment).

I also have homozygous SNPs on COMT gene, too, so I was suspecting slightly elevated catecholamines. The blood tests revealed undetectable dopamine, and normal / slightly elevated noradrenaline and adrenaline. That leads me to believe my DBH enzyme is overclocked, possibly as a compensation for low functioning MAO-A, which normally also breaks down dopamine.

What have you personally had success with in Regards to normalizing your dopamine without elevating noradrenaline? Do you use antiserotonin substanses?

 

[DaveFoster]

Famotidine before bed allows you to take more aspirin. That's why famotidine has such value.

 

[Regina]

Good question. I did genetic and blood testing. I have homozygous SNPs on MAO-A gene, meaning I have predisposition to make less MAO-A enzyme. Therefore, my suspicion was that I have elevated serotonin, and that was confirmed by a blood test.
(Now, is it possible that my MAO-A enzymes are actually OK but I have SIBO instead? Theoretically, it is possible, but I doubt as I have been on antibiotics a few times, and serotonin drops just little under the upper limit due to reduction of bacterial endotoxin; it comes back to elevated levels within few weeks after treatment).

I also have homozygous SNPs on COMT gene, too, so I was suspecting slightly elevated catecholamines. The blood tests revealed undetectable dopamine, and normal / slightly elevated noradrenaline and adrenaline. That leads me to believe my DBH enzyme is overclocked, possibly as a compensation for low functioning MAO-A, which normally also breaks down dopamine.

I had fairly wacky results of a catecholamine test. Undetectable dopamine but out of upper range noradrenaline. Haidut suggested that the enzyme that breaks down dopamine (into noradrenaline) was/is over-active and also that there are considerations with iron and copper that I need to test.

 

[TeslaFan]

What have you personally had success with in Regards to normalizing your dopamine without elevating noradrenaline? Do you use antiserotonin substanses?

I haven't had major success, nor a chance to observe meaningful difference in blood tests. I am still learning and searching for the right answer.

 

[TeslaFan]

I had fairly wacky results of a catecholamine test. Undetectable dopamine but out of upper range noradrenaline. Haidut suggested that the enzyme that breaks down dopamine (into noradrenaline) was/is over-active and also that there are considerations with iron and copper that I need to test.

My serum copper, ceruloplasmin, and copper RBC are all either low or below reference range on each test. I would encourage you to test yours.
I definitely feel better when supplementing copper, but I am afraid to do it too much as I am not sure if I am actually low on it, or it simply does not get utilized biologically and just gets loaded in the liver instead. I am trying to understand this better.

Dopamine and ceruloplasmin levels seem to be related, and are general markers of metabolic speed, just like TSH, but inversely related to it. (Elevated TSH - > low dopamine, low ceruloplasmin, and vice versa).

If we have similar biochemistry in this regard, it would be interesting to use that as ground base for further research.

 

[Regina]

My serum copper, ceruloplasmin, and copper RBC are all either low or below reference range on each test. I would encourage you to test yours.
I definitely feel better when supplementing copper, but I am afraid to do it too much as I am not sure if I am actually low on it, or it simply does not get utilized biologically and just gets loaded in the liver instead. I am trying to understand this better.

Dopamine and ceruloplasmin levels seem to be related, and are general markers of metabolic speed, just like TSH, but inversely related to it. (Elevated TSH - > low dopamine, low ceruloplasmin, and vice versa).

If we have similar biochemistry in this regard, it would be interesting to use that as ground base for further research.

Thanks skominac.
My TSH was quite low 1.4 (I think). But it was just one blood test many months ago. Time to test again and dig some more.

 

[Dan W]

Just a plug for Chris Masterjohn's podcast episode on copper, I found it really interesting:
https://chrismasterjohnphd.com/2017/02/03/manage-copper-status/

I ended up testing ceruloplasmin instead of serum copper because it was cheaper, but it was nice to understand the "why's" behind it. In my mind, if you suspect copper deficiency, it makes sense to test it first, correct any deficiency, and then test TSH.

 

[haidut]

I foolishly started working on a famotidine comparison page before realizing you were going to make it obsolete. For what it's worth in the meantime, the name-brand Pepcid Maximum Strength (20mg) tablets look like the best option to me. Lot of downsides, but you at least avoid PEG and colloidal silica, and the small tablet size + higher dosage helps maximize your dosage-per-excipient.

I've never come across one of those pet/veterinary supply stores that doesn't ultimately require something from a vet when ordering. I'm not sure why aspirin seems to be an exception to that.

Anyone have a sense of whether we'd prefer famotidine to be delivered to the stomach vs the remaining digestive tract? It seems like the tablet formulations (and the antacids in the chewables) are designed to deliver the famotidine directly to stomach cells, but maybe we want to alter that process.

It won't make it obsolete, some people still prefer the convenience of capsules/tablets. Mine would be liquid, as usual. So, please create that page.
I think that if used topically the effects on reducing gastric acid would be much less pronounced, while still affecting the intestinal cells that produce serotonin. Rubbing on the lower abdomen would probably be even more effective.

 

[haidut]

My serum copper, ceruloplasmin, and copper RBC are all either low or below reference range on each test

Have you tested iron, saturation, ferritin and transferrin? With copper values so low iron often is elevated as copper and iron can fill in for each other in most tissues. High iron is very intimately related to dopamine toxicity.

 

[haidut]

Just a plug for Chris Masterjohn's podcast episode on copper, I found it really interesting:
https://chrismasterjohnphd.com/2017/02/03/manage-copper-status/

I ended up testing ceruloplasmin instead of serum copper because it was cheaper, but it was nice to understand the "why's" behind it. In my mind, if you suspect copper deficiency, it makes sense to test it first, correct any deficiency, and then test TSH.

Peat once said he would like to see diet recommendations being guided by ceruloplasmin tests. He did not specify what he meant by that - does he think good diet would elevate or lower it. So, if somebody asks him it would help clarify one of those mysterious comments of his.

 

[Regina]

Peat once said he would like to see diet recommendations being guided by ceruloplasmin tests. He did not specify what he meant by that - does he think good diet would elevate or lower it. So, if somebody asks him it would help clarify one of those mysterious comments of his.

+1. I listened to the Masterjohn piece but would like to learn much more about what ceruloplasmin levels inform.

 

[Mito]

Good question. I did genetic and blood testing.

Have you ever done urine testing for neurotransmitters or do you think blood testing is superior?

 

[TeslaFan]

Have you tested iron, saturation, ferritin and transferrin? With copper values so low iron often is elevated as copper and iron can fill in for each other in most tissues. High iron is very intimately related to dopamine toxicity.

Thank you for asking!
I did.
These are the results:

TIBC: 314 ug/dL
UIBC: 252 ug/dL
Iron, Serum: 62 ug/dL
Iron, Saturation: 20 %
Ferritin, Serum: 89 ng/dL
Transferrin: 272 mg/dL

According to LabCorp ranges, these are all within them. On that same day, serum Copper was 68 ug/dL, which LabCorp marked as LOW, according to their range, which is: 72-166 ug/dL. Serum Ceruloplasmin was 17.7 mg/dL, which barely made it within the range of 16-31 mg/dL.

I did not test Copper RBC on this day, but 6 months prior the result was 0.55 ug/mL, which barely fits within the range of 0.5 - 1.0 ug/mL. On that same day, Copper Plasma was again marked LOW (0.64 ug/mL with the range: 0.8 - 1.75).

Thanks for any thoughts!