Way above my head - in every direction!
The relevance is, I feel, very much that someone is looking. Hypotheses are being examined. And the tools of mathematics are being applied.
We can all see petrol will burn if you light a dish of it. But modern, high-efficiency/high-performance engines work as well as they do because extremely sophisticated mathematical techniques have been applied to the issue.
That is, we might be fairly convinced of a gut/thyroid connection in Hashimoto's but seeing more than that needs a lot of detailed work. Hopefully, this paper, the model developed, and work by others, will result in an understanding which enables us to see how to address the issues.
Simulation model for Hashimoto's Autoimmune Thyroiditis disease
Marcela Salazar-Viedma 1 , Juan Gabriel Vergaño-Salazar 2 , Luis Pastenes 1 3 , Vivian D'Afonseca 4
Affiliations
• PMID: 34496027
• DOI: 10.1210/endocr/bqab190
Abstract
Hashimoto's Thyroiditis (HT) is a pathology which often causes a gradual thyroid insufficiency in affected patients due to the autoimmune destruction of this gland. The cellular immune response mediated by T helper lymphocytes TH1 and TH17 can induce the HT disease. In this pathologic condition, there is an imbalance between the TH17 and Treg lymphocytes as well as a gut microbiota dysfunction. The objective of this work was to describe the interactions of the cell subpopulations that participate in HT. To achieve this goal, we generated a mathematical model that allowed the simulation of different scenarios for the dynamic interaction between thyroid cells, the immune system, and the gut microbiota. We used a hypothetical-deductive design of mathematical modeling based on a system of ordinary differential equations, where the state variables are the TH1, TH17 and Treg lymphocytes, the thyrocytes and the bacteria from gut microbiota. This work generated a compartmental model of the cellular immune response occurring in the thyroid gland. It was observed that TH1 and TH17 lymphocytes could increase the immune cells activity, as well as activate effector cells directly and trigger the apoptosis and inflammation processes of healthy thyrocytes indirectly. Likewise, the model showed that a reduction in Treg lymphocytes could increase the activity of TH17 lymphocytes when an imbalance of the gut microbiota composition occurred. The numerical results highlight the TH1, TH17 and bacterial balance of the gut microbiota activities as important factors for the development of Hashimoto's Autoimmune Thyroiditis disease.
Keywords: T helper cells; autoimmune hypothyroidism; dynamic systems; gut microbiota; mathematical modeling; thyrocytes.
pubmed.ncbi.nlm.nih.gov/344...
Full paper available as a PDF - currently as an accepted manuscript (double-spaced and liable to be edited):