Levothyroxine treatment and gastric juice pH in humans: the proof of concept
April 2022 Endocrine
DOI: 10.1007/s12020-022-03056-1
Camilla Virili,Giovanni Bruno,Maria Giulia Santaguida, Marco Centanni et al.
This downloadable paper demonstrates that insufficient stomach acidity interferes with T4 uptake.
Thankyou ... here's a link to it link.springer.com/article/1...
on a similar theme .. i was reading an older (2018) paper the other day by some of the sam authors... which touches on gastric acid (amongst many other things) .. so i will add it here for anyone who is searching for gastric acid implications on absorption academic.oup.com/edrv/artic...
(Gastrointestinal Malabsorption of Levothyroxine Camilla Virili, Alessandro Antonelli, Maria Giulia Santaguida, Salvatore Benvenga, Marco Centanni )
Thank you.
Thank you SO MUCH for this. It was someone clever on this forum that suggested low stomach acid or poor absorption might be behind my high dosage requirements, now on combined T3/T4. I'm getting some blood tests as a result. Same question as always - after 20 years of poorly responding to T4, why has this never been considered as possible in my case, leaving me to do the detective work and then find a doctor who will take it seriously? Thank you again.
I have a problem with the idea that stomach acid is the key issue.
First, yes, we have anecdotal, observational and (now) measured proof of an association between stomach acid and levothyroxine absorption.
But evidence from the chemists of the world identify that levothyroxine sodium is more soluble in alkaline solutions than acidic.
And evidence from physiologists identifies that absorption occurs after the stomach – in the jejunum and ileum. Both jejunum and ileum are around pH 7 to 8 (neutral to slightly alkaline).
Could it be that low stomach acid implies insufficiently alkaline jejunum and ileum? Rather than it being the acidity of the stomach itself that directly affects absorption?
Which would need some way of measuring pH in the jejunum and ileum.
I can imagine that the pH will vary depending on both the stomach acidity and when it is measured.
Looking at what is known, I deduce that low stomach acid causes poor digestion of food + bloating. This badly digested food passes into the small intestine relatively whole compared with proper stomach digestion. for example protein. Thus this can interfere with T4 uptake there (a malabsorption syndrome) as there is much more material to break down.
Agreed, this is certainly how I see it in my head... and appear to experience it in practice (ahem, it was food passing through me undigested with severe bloating that has convinced the GP to do blood tests).
Oh, I like this paper diogenes!
I know how much supplementing HCL + pepsin has helped make my thyroid meds work more effectively. Also reduced the amount I need to medicate, as well as reduce stomach bloating, infections, etc and I know my need for additional HCL is genuine by the sheer amount of it I can take.
It has been banned from OTC sales in America and is obviously contraindicated with peptic ulcers, or those on PPI's/H2 blockers but for many with hypothyroidism, HCL supplementation is paramount for well being to be gained as it is the low thyroid hormone reducing gut motility, and associated high/low cortisol levels that initiate low gastric acid and gut dysbiosis that stops good absorption, etc.
Scavenger Receptor Class B Member 1 Independent Uptake of Transthyretin by Cultured Hepatocytes Is Regulated by High Density LipoproteinBenefits of T3 on QoL in patients symptomatic on T4 onlyTSH is either a faulty indicator of treatment or if not, patients are often incorrectly treated by T4 (a logical challenge)Interference in the use of T4 as thyroid therapyThis is a good example of what present accepted assumptions are regarding T4 treatment, combination therapy re control by TSH levels
