Serum metabolomic analysis in patients with Hashimoto’s thyroiditis positive for TgAb or TPOAb: a preliminary study

[helvella]

Another interesting paper.

I have long believed that metabolomics might hold a key, or even a bunch of keys, to the impact of thyroid disorders. We know very well that some things are associated with high or low thyroid hormone levels but have little beyond that association.

Metabolomics might provide the finger to point at specific pathways and start to explain the actual routes of causation.

Over that, they might highlight issues which really do need to be looked it in those who have thyroid disorders.

For example:

notable changes were observed in … primary bile acid biosynthesis

And it has long appeared that bile issues are over-represented in those with thyroid issues. But pretty much everyone totally ignores that! At least a solid unwavering finger might result in people looking where it was pointing!

It is not an easy read. These things are almost never written with non-experts in mind. (Unfortunately, that includes most endocrinologists who are obviously rarely, if ever, metabolomics experts.). I’ve certainly found it tough getting through it. Nevertheless, it might well be worth a scan read - for as long as your eyes don’t glaze over.

Serum metabolomic analysis in patients with Hashimoto’s thyroiditis positive for TgAb or TPOAb: a preliminary study

Tao Luo, Xinyu Zhao, Xiao Jiang, Pengqian Li, Xiaotong Gu, Xingjie Xie & Haixia Liu 

Scientific Reports volume 15, Article number: 9945 (2025)

Abstract

Hashimoto’s thyroiditis (HT) is a prevalent autoimmune disorder, yet the metabolic abnormalities associated with HT and their relationship to antibody positivity remain poorly understood. This study aimed to characterize the distinct metabolic profiles associated with thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TgAb) positivity in female patients with HT. Serum metabolomic analysis was performed on 14 TPOAb-positive patients, 4 TgAb-positive patients, and 14 sex-matched healthy controls, evaluating a total of 225 metabolites. Partial least squares discriminant analysis (PLS-DA) revealed significant metabolic differences among the groups, identifying 36 key metabolites. Of these, 13 metabolites showed significant differences between the TPOAb-positive group and healthy controls, while 23 metabolites exhibited marked differences between the TgAb-positive group and controls. Further correlation analysis revealed a moderate positive association between TgAb and phenylacetyl-L-glutamine, while TPOAb was strongly correlated with LPC 16:0 sn-1. Additionally, metabolic pathway analysis showed significant activation of glycine, serine, and threonine metabolism in the TPOAb-positive group, whereas the TgAb-positive group exhibited enhanced activity in galactose metabolism. These findings suggest that TPOAb and TgAb positivity are associated with distinct metabolic profiles, reflecting their differential roles in metabolic pathways linked to Hashimoto’s thyroiditis. This study provides valuable exploratory evidence of metabolic abnormalities in HT under different antibody-positive states, laying the foundation for future large-scale investigations to elucidate the underlying mechanisms.

Open access

nature.com/articles/s41598-...

[Star13]

Interesting!Thanks for posting.

[RomerinSpring]

Thanks. These type of studies/research outcomes (sample size was still relatively small) highlight just how woefully limited, the medical understanding and treatment for thyroid disease currently is.

[helvella in reply to RomerinSpring]

Completely agree.

When I first came across thyroid disorders, I tried to understand what the actual hormone molecules do. What effect they have on the cells they enter.

Everything was expressed in terms of affecting metabolic rate. But almost nothing specific and detailed. Indeed, very little on precisely how thyroid hormones enter cells and what affects that process.

[Calceolaria in reply to helvella]

I read some of your posts on that I think. Amazing.

[flower365]

Wow, what a body of work. Thankyou.

[grumpyold]

This is an interesting read for me because I have always believed that my T2 diabetes was as a result of my Hashi's. I never fitted the profile for someone likely to become diabetic as my diet and exercise weren't unhealthy nor lacking. I didn't "deserve" T2 but medics look down on me as if I've been a doughnut eating couch potato for decades. Not fair🥺.

[Judithdalston]

interesting, especially as I was a TgAb only Hashimoto…. yet only ever recorded the high TgAb ( 779) once early in journey of overt hypothyroidism 20+ years ago. Within the following 7 years also had various ‘metabolic’ type diagnoses from diabetes to blocked bile duct etc, and now with Long Covid high BP/HR remains. I wish I could understand this paper rather better, and know what some of these metabolites actually do, especially in terms of the chicken and the egg situation…were metabolites off so got high TgAb, or in part the other way round, and could they still be off, perhaps to a lesser extent?

[Jgoodwin977]

Thanks for this, so do we produce more bile than average or less and we need to take bile salts to support?

[helvella in reply to Jgoodwin977]

I think the real lesson is that thyroid hormone needs to be right in order for everything to do with bile acid to work as it should.

The answer is not to take bile salts, or whatever else, but to get the thyroid hormone levels right for us.

I'm afraid I know far too little of this subject to have any idea if temporarily taking bile salts would be a good, or a bad, idea. And the paper is not really focussed on that. One or more of the papers referenced might provide better guidance.

[Jgoodwin977 in reply to helvella]

Thanks for clarifying

[jgelliss in reply to helvella]

👏👏👏👏