Famotidine Increases Glycogen, Improves Glucose Metabolism

haidut

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Several people on the forum have asked for measures on how to increase glycogen storage in the liver. Hypothyroid people have issues with glycogen storage and having a substance that can increase such storage would be helpful. It looks like famotidine is one such substance. It dose dependently increased glycogen storage. A human equivalent dose of 20mg doubled glycogen stores compared to controls and a 40mg dose quadrupled it. These are doses commonly recommended for every day famotidine use and should be fairly safe. Btw, famotidine also lowers blood sugar and the mechanism of action is likely the increased glycogen storage and uptake of glucose by the muscles.

http://www.ncbi.nlm.nih.gov/pubmed/22512725

"...Docking studies showed how famotidine is optimally fit within the binding pocket of GSK-3β via numerous attractive interactions with some specific amino acids. Experimentally, famotidine could inhibit GSK-3β (IC₅₀ = 1.44 μM) and increased significantly liver glycogen spares in fasting animal models. Moreover, a single oral dose of famotidine was shown to decrease the glycemic response curve after 75 g OGTT."
 

narouz

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You've posted other stuff about Famotidine before, haidut,
and I was very interested.
So I started taking about 20mg a day a week ago.
Of course...I'm taking a lot of other stuff.

In any case, I've been doing well.
I believe it reduces nitric oxide.
And there was something else about it I liked also, I think.

Oh...what I was trying to think of...enhanced liver function/healing.
Those are some good effects!
 

Peata

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I posted this in another thread, but I've been taking 20 mg. every morning and haven't had night issues since then. I don't have night terrors that wake me up in a fright, heart pounding, gasping, etc. Then I would have to eat something to calm down and get back to sleep. It made me dread night time for a while. But since the famotidine, no issues. I also think I can go longer in the day without food if needed. I haven't had the awful blood sugar issues while in the middle of shopping, for example. So, I guess famotidine works for me as described by haidut.
 

tara

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Along with the benefits to glycogen storage, does the reduction in stomach acid have the downside of worsening protein digestion?
 
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haidut

haidut

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tara said:
Along with the benefits to glycogen storage, does the reduction in stomach acid have the downside of worsening protein digestion?

I've always wanted an answer to this question as well, but I doctors seem unwilling to provide one. Most often I get the response that as long as the pancreas is producing enough protease and lipase, the reductions in stomach acid are nothing to worry about. Also, unlike PPI type of drugs the older H2 antagonists do not even reduce stomach acid that much. It looks like their beneficial effects are mostly due to protecting the gastric mucosa by reducing histamine levels there as well as increasing blood flow and stimulating parietal cell genesis. So they seem to be trophic to the GI tract and spur regeneration rather than simply block acid production like PPI.
 

tara

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haidut said:
tara said:
Along with the benefits to glycogen storage, does the reduction in stomach acid have the downside of worsening protein digestion?

I've always wanted an answer to this question as well, but I doctors seem unwilling to provide one. Most often I get the response that as long as the pancreas is producing enough protease and lipase, the reductions in stomach acid are nothing to worry about. Also, unlike PPI type of drugs the older H2 antagonists do not even reduce stomach acid that much. It looks like their beneficial effects are mostly due to protecting the gastric mucosa by reducing histamine levels there as well as increasing blood flow and stimulating parietal cell genesis. So they seem to be trophic to the GI tract and spur regeneration rather than simply block acid production like PPI.
Thanks Haidut.
 

NathanK

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haidut said:
Also, unlike PPI type of drugs the older H2 antagonists do not even reduce stomach acid that much. It looks like their beneficial effects are mostly due to protecting the gastric mucosa by reducing histamine levels there as well as increasing blood flow and stimulating parietal cell genesis.

I'm far from proficient at properly reading studies, but it appears that stomach acid is reduced by 60% when using, but within 48 hours things return to normal unlike newer medications which have high acid rebound causing ulcers. http://www.ncbi.nlm.nih.gov/pubmed/1685675

Again, I'm a neophite, but did you see where there are cases of famotidine causing aortic calcification even in light of other studies showing lowered PTH and tendonitis? I couldn't find studies showing this, but I see those cases may have been in people already afflicted with CVD and osteoporosis. I thought it might be worth noting.
 

burtlancast

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Shouldn't this work for people like Ray who always got migraines the day after skipping afternoon meals ?
I believe he blamed reduced glycogen storage.
 

NathanK

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NathanK said:
it appears that stomach acid is reduced by 60% when using, but within 48 hours things return to normal unlike newer medications which have high acid rebound causing ulcers. http://www.ncbi.nlm.nih.gov/pubmed/1685675

....did you see where there are cases of famotidine causing aortic calcification even in light of other studies showing lowered PTH and tendonitis? I couldn't find studies showing this, but I see those cases may have been in people already afflicted with CVD and osteoporosis. I thought it might be worth noting.
I further investigated this and I think the primary reasons that people with CVD and osteoporosis were developing aortic calcification is more than likely due to statins

In fact, famotadine does the opposite and reduces general body calcification deposits: http://www.ncbi.nlm.nih.gov/pubmed/22592911
Famotidine suppresses osteogenic differentiation of tendon cells in vitro and pathological calcification of tendon in vivo.
Heterotopic ossification or calcification follows any type of musculoskeletal trauma and is known to occur after arthroplasties of hip, knee, shoulder, or elbow; fractures; joint dislocations; or tendon ruptures. Histamine receptor H2 (Hrh2) has been shown to be effective for reducing pain and decreasing calcification in patients with calcifying tendinitis, which suggested that H2 blockers were effective for the treatment of tendon ossification or calcification. However, the detailed mechanisms of its action on tendon remain to be clarified.

Its no mystery to me why it has this effect if you piece together the other studies that show famotidine lowers PTH significantly

Here are pictures from the study showing the reduced bone calcification in mice:
http://www.researchgate.net/publication ... on_in_vivo

This is a chapter of a book that covers at least a dozen studies with famotidine:
https://books.google.com/books?id=5vL-s ... is&f=false
 

Dan W

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@haidut what do you think about these cases where famotidine raises prolactin?
I wonder if it only raises prolactin in special cases? I can't find the full text of the first one, but the second one is a single case of a woman accidentally taking a double dose of famotidine for 5 months, resulting in very high prolactin levels. They note:
We believe that the adverse effect observed in our case was caused by the sustained excessive intake of famotidine. Supporting this view are the disappearance of the hyperprolactinemia after discontinuation of famotidine, the positive MIF assay suggesting a cellular hypersensitivity mechanism, and the absence of other therapy.

They reference a contrasting study, though I haven't been able to find it:
By contrast, single intravenous doses of famotidine 20 mg were associated with significant decreases in serum prolactin. Furthermore, prolactin secretion was unaffected when famotidine was given orally at 40mg daily for 4 weeks in duodenal ulcer patients.
--
Hayakawa A, Ohe K, Miyoshi A, Marasawa S, Miwa T. Properties of famotidine in relation to safety. Ital J Gastroenterol 1984; 16: 174-76.

Here's a couple additional ones that don't seem to find a famotidine/prolactin link, at least short-term:
http://www.ncbi.nlm.nih.gov/pubmed/2877572
http://www.ncbi.nlm.nih.gov/pubmed/2866132
 

Velve921

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Would famotidine have a positive on effect on excessive urination? After 2 years of Peat ideals, I still can't get through the day without 120-150 grams of fat (6grams total of pufa)...if fat is too low then blood sugar is sluggish....if glycogen storage as an issue would thus be helpful.

I currently take 8mg of cyrpoheptadine before time and I still have to wake up 2-3x a night to urinate.
 

nullredvector

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Would famotidine have a positive on effect on excessive urination?

The most effective anti-excessive urination supp I have used is alpha lipoic acid 50-100mg daily. Seconds are sodium benzoate (lowers ammonia) and salt/lithium.
 

Dan W

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So a single dose is 20mg and a double is 40mg?
I'm not 100% sure, you could take their phrasing to mean either 80 or 160mg:
she received double the usual maximum dose of famotidine (80mg daily)

Double for 5 months raised prolactin but it didn't in the study?
I'm not sure what procedure they followed in the study, it could've been short-term. This was just a letter about something noticed in a patient, I'll PM you the full text.
 

Velve921

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The most effective anti-excessive urination supp I have used is alpha lipoic acid 50-100mg daily. Seconds are sodium benzoate (lowers ammonia) and salt/lithium.

Do you have anecdotal experience with ALA? If so what did you witness?

Is Pepcid something worth trying? What are common symptoms once consuming?
 

nullredvector

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Ala helps my mood a bit and decreases my urine output.

Pepcid was relaxing and promoted really good sleep but now I suspect it my be lowering my libido by raising prolactin - I could definitely be a special case here.
 

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