just wondering how many people taking omeperazole are having problems with levothyroxine (converting T4 to T3 ) ?
omeperazole : just wondering how many people... - Thyroid UK
omeperazole
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Dunkenb
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helvellaAdministratorThyroid UK
Are you certain you are having problems converting? Rather than, say, absorption - of the levothyroxine and/or dietary components such as B12.
I’m on T3 but read this article on PPIs and H2 blockers that was interesting saying that they stop T4 conversion to T3
Well we're told not to consume our meds alongside food to not inhibit absorption, so I fail to see how lower stomach acid wouldn't have a similarity deleterious effect.
That said I heard people can get around this with glandulars and NDT by taking it with an acid like lemon juice or Acid Cider Vinegar, so perhaps the same might work when taking the levothyroxine of or taking HCI betaine beforehand.
Your stomach acid will still be weak even if you come off the PPI's, as presumably it is weak stomach acid that caused the reflux in the first place, so it isn't necessarily so that coming off them will increase conversion. It might be a bit better, but you have to weigh up the pro's and cons. It depends how bad the reflux is. T3 tends to help, but that can feel like more intense burning at first and not everyone can handle that.
The lowering of the amount of acid at one end of the digestive system has a knock on effect right through it. If you read the side effects of omeperazole, it can weaken bones , cause anemia and also disrupt T4 to T3 conversion via Deiodinase disruption
Sorry for the late reply!! I don't disagree with you, I hate the things, and can understand you wanting to get rid, sorry if it appears otherwise. But my point is that you still have to weigh up the pros and cons of stopping the PPI's. For e.g some people find that taking T3 and upping their levels of vitamins means they no longer get gerd symptoms and can safely dispense of the PPI's, but some people find they continue to experience gerd as silent reflux even after optimising all treatment (and some find a temporary worsening of gerd upon getting optimal) . Bearing in mind the possible complications of Barretts Oesophagus, some people may decide that they will continue taking their PPI'S whilst compensating for the side effects of reduced stomach acid as best they can.
I came off PPI'S myself, BUT I do still get fluctuating symptoms of Gerd with coughing and occasional choking. I wouldn't be surprised if I one day developed BO but that is a risk I have chosen to take. I used to take Zantac as an alterative, (I'm not sure what the real equivalent is it's definitely not Nexium) but when that disappeared I found a generic ranitidine in an old dying pharmacy and bought a lot, but I only ever used it very occasionally and stick to gaviscon tablets or licorice sweets on bad days mostly. Doctors can still prescribe ranitidine I think.
Can't see any mention of PPIs or H2 blockers on that link you've given.
However, it could be that taking PPIs reduces absorption of selenium. Selenium is necessary for conversion.
Did you start the T3 before or after you started the PPIs?
From the text “compounds known to affect deiodinases, including omeprazole, PTU, cimetidine, amphetamine, and glucocorticoids, which decrease 5-deiodinase activity”
Ive been on omeperazole for ten years and have to take liothyronine as my body isn’t converting Levo. I’m looking to get off of the omeperazole to see if T4 starts being converted to T3. GP’s seem to throw omeperazole at anyone with heart burn rather that deal with the causes.
If you are hypo then you are more likely to have low stomach acid, and the omeprazole is only making things worse. But doctors don't believe that low stomach acid is 'a thing'!
Silly me, I never thought to search for 'omeprazole', I was searching for 'PPIs' and 'H2 blockers'. lol
Somewhat old (1989 paper in 2011 publication). Massive doses to rats. Human doses are of the order of 10/20/40 milligrams once or twice a day. They gave rats (which probably weigh under one kilogram) doses up to 500 milligrams.
Even then, only a modest effect.
Studies on the effects of omeprazole on thyroid function in the rat
Journal of Pharmacy and Pharmacology, Volume 41, Issue 10, October 1989, Pages 733–735, doi.org/10.1111/j.2042-7158...
Abstract
The effects of omeprazole (an H+, K+-ATPase inhibitor) on thyroid parameters in rats have been examined. SK&F Wistar rats were dosed orally with omeprazole (up to 500 mg kg−1) or vehicle. Treatment for 7 or 14 days resulted in generally decreased plasma T3 concentrations in males (with little change or slight increases in females) and increased serum TSH concentrations (22%–68% increases). No changes were detected in thyroid 125I uptake or organification. Liver 5′-deiodinase activity was decreased in male rats after 7 days treatment. Thyroxine clearance was not altered after a single dose of omeprazole. In-vitro studies showed omeprazole to be only a weak inhibitor of TSH-stimulated 125I organification in cultured porcine thyrocytes. It is concluded that omeprazole has weak effects on the pituitary-thyroid-liver axis, its main action being to inhibit the peripheral deiodination of thyroid hormones.
So that last bit is what got me wondering about it’s affect on T4 to T3 conversion.
My sister who has been hypothyroid for about 35 years has also taken omeperazole for many years too. She has to have a high dose of levothyroxine but she has no problem with converting. However she does have a B12 deficiency which was/is caused by long term omeperazole use plus long term metformin use for type 2 diabetes.
