Primary hypothyroidism (PHT) is associated with an increased risk for the development of atherosclerosis (AS) and other cardiovascular disorders. PHT induces atherosclerosis (AS) through the induction of endothelial dysfunction, and insulin resistance (IR). PHT promotes vasoconstriction and the development of hypertension. However, patients with subclinical PHT with normal thyroid hormones (THs) are also at risk for cardiovascular complications. In subclinical PHT, increasing thyroid stimulating hormone (TSH) levels could be one of the causative factors intricate in the progression of cardiovascular complications including AS. Nevertheless, the mechanistic role of PHT in AS has not been fully clarified in relation to increased TSH. Therefore, in this review, we discuss the association between increased TSH and AS, and how increased TSH may be involved in the pathogenesis of AS. In addition, we also discuss how L-thyroxine treatment affects the development of AS.
It seems everyone who is anyone is talking about this recently re-discovered connection. That is, everyone but actual medics who still are not ‘hearing’ this. I include endocrinologists and cardiologists!
At the moment I am pretty infuriated by this as it applies directly to me and my history.
OMG this has thrown me into a flat spin. It's stupid I know but I've never thought about what TSH is. I thought it was only relevant to indicate whether the thyroid needs a bit of a poke to produce T4. But of course the giveaway is the word "hormone". It's a bit shocking to read it's correlated to atherosclerosis. I've got endothelium dysfunction in the form of coronary microvascular angina and metabolic syndrome etc. I thought my subclinical hypothyroidism was OK as my T4 is not too awful - latest reading 15.4 (range 12 - 22) and my T3 is the highest it's ever been at 4.5 ( range 3.1 - 6.8) but maybe a rethink is needed. On the other hand the paper mentions that a case–controlled study observed that L-thyroxine treatment may aggravate ventricular dysfunction and pulmonary artery stiffness in patients with subclinical PHT. So I feel somewhat caught between a rock and a hard place. But thanks so much for bringing this paper to our attention.
Discussion of TSH - even in academic papers - tends to the ultra-simplistic end of the scale.
Which means that it is hard work trying to get a full picture of how TSH itself might affect us.
But I tend to be fairly calm about low TSH. By the time TSH drops to, say, 0.30, the amounts involved are really very small. So a further drop to 0.20, or 0.10, or whatever actually only needs a tiny change in quantity of TSH.
A high TSH, say 3.0 through 10.0, requires a massively greater amount of TSH to make that difference.
must admit , i didn't enjoy reading it either (while listening to the sound of intermittant pulsatile tinnitus and wondering about what exactly might be making that noise)
mind you ,i didn't understand much of it as i've never had any heart issues , I only got about a third of the way through before my brain gave out ..... so i've added it my random collection of 'papers about thyroid / heart that need a rainy day and a dictionary' . which i rediscovered the other day ,
it's here if you want some more heart stuff to read : healthunlocked.com/thyroidu... thyroid-disease-effects-on-heart-and-cardiovascular-system.-gps-told-keep-tsh-0.5-2-hypothyroidism-causes-raised-cholesterol
Thanks both (helvella and tattybogle). The paper does seem to skim over a huge range of other research and to follow all the links would mean disappearing down lots of rabbit holes for a long time. But it does make me think whether it's time to try to have a conversation with the GP. My TSH at latest reading is 4.58.
Thank you for this Helvella, it does take some absorbing.
The standout sentences for me were:
Although most laboratories have TSH reference around 0.4–4.5 mIU/L, based on the epidemiological survey, the National Academy of Clinical Biochemistry recommended that the TSH reference range should be 0.4–2.5 mU/L [48, 49].
It has been illustrated that TSH > 2.5mU/L is associated with IR and hyperinsulinemia in healthy Korean women [50]. TSH > 2.5mU/L increases the risk for the development of metabolic syndrome [50]. As well, even in euthyroid subjects, higher levels of TSH may be associated with the development of IR and hyperinsulinemia [50].
Moreover, TSH is also increased in patients with metabolic syndrome due to different causes including THs resistance, leptin resistance, and other neuroendocrine alterations [51].
Findings from different clinical studies observed that TSH is positively correlated with circulating leptin levels, IR, and visceral adiposity [50]. Therefore, monitoring of TSH may be required for dyslipidemia and cardiovascular diseases even in euthyroid patients.
The footnotes are as follows:
50. Oh J-Y, Sung Y-A, Lee HJ. Elevated thyroid stimulating hormone levels are associated with metabolic syndrome in euthyroid young women. Korean J Intern Med. 2013;28(2):180. 10.3904/kjim.2013.28.2.180. [Europe PMC free article] [Abstract] [CrossRef] [Google Scholar]
51. Teixeira PdFdS, Dos Santos PB, Pazos-Moura CC. The role of thyroid hormone in metabolism and metabolic syndrome. Ther Adv Endocrinol Metab. 2020;11:2042018820917869. 10.1177/2042018820917869. [Europe PMC free article] [Abstract] [CrossRef] [Google Scholar]
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This must surely be a game-changer for those who have been advocating for the upper reference in the range to be reduced and to do away with the subclinical definition (which has always struck me as strange if people are symptomatic).
48. D’Aurizio F, Metus P, Polizzi Anselmo A, Villalta D, Ferrari A, Castello R, et al. Establishment of the upper reference limit for thyroid peroxidase autoantibodies according to the guidelines proposed by the National Academy of Clinical Biochemistry: comparison of five different automated methods. Autoimmunity Highlights. 2015;6:31–37. 10.1007/s13317-015-0070-x. [Europe PMC free article] [Abstract] [CrossRef] [Google Scholar]
49. Meamar R, Feizi A, Aminorroaya A, Amini M, Nasri M, Tabatabaei A, et al. Thyroid stimulating hormone reference range: Iranian thyroid cohort study. Acta BioMedic. 2021;92(5):e2021283. [Europe PMC free article] [Abstract] [Google Scholar]
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This encapsulates the basic logical problem of diagnosis and treatment
Association of Thyroid Hormone Therapy With Quality of Life and Thyroid-Related Symptoms in Patients With Subclinical Hypothyroidism
