I know that it has been referred to many times on this forum, but somewhere out there is a paper debunking the risks of low TSH in terms of osteoporosis and atrial fibrillation, unless TSH is ultra low. I am miserably failing to find it!
Please can anyone help me with a link to it?
Thanks
Written by
fred1e
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Professor Hoermann is one of the group of people that diogenes works with. In case you, or other readers, weren't aware of this, diogenes is Dr John Midgley, who is one of Thyroid UK's medical advisors.
Diogenes is so Knowledgeable and so very informative/sharing with our thyroid journey. We ought to clone him. His open mindedness and out of the *BOX* thinking makes him a breath of fresh air. His constant research to in-better thyroid patients lives is in measurable. I am very Grateful to have and know him on our forum.
See first reply to this healthunlocked.com/thyroidu... post , contains links to other discussions and a link to : Serum Thyroid-Stimulating Hormone Concentration and Morbidity from Cardiovascular Disease and Fractures in Patients on Long-Term Thyroxine Therapy
Context: For patients on T4 replacement, the dose is guided by serum TSH concentrations, but some patients request higher doses due to adverse symptoms.
Objective: The aim of the study was to determine the safety of patients having a low but not suppressed serum TSH when receiving long-term T4 replacement.
Design: We conducted an observational cohort study, using data linkage from regional datasets between 1993 and 2001.
Setting: A population-based study of all patients in Tayside, Scotland, was performed.
Patients: All patients taking T4 replacement therapy (n = 17,684) were included.
Main Outcome Measures: Fatal and nonfatal endpoints were considered for cardiovascular disease, dysrhythmias, and fractures. Patients were categorized as having a suppressed TSH (≤0.03 mU/liter), low TSH (0.04–0.4 mU/liter), normal TSH (0.4–4.0 mU/liter), or raised TSH (>4.0 mU/liter).
Results: Cardiovascular disease, dysrhythmias, and fractures were increased in patients with a high TSH: adjusted hazards ratio, 1.95 (1.73–2.21), 1.80 (1.33–2.44), and 1.83 (1.41–2.37), respectively; and patients with a suppressed TSH: 1.37 (1.17–1.60), 1.6 (1.10–2.33), and 2.02 (1.55–2.62), respectively, when compared to patients with a TSH in the laboratory reference range. Patients with a low TSH did not have an increased risk of any of these outcomes [hazards ratio: 1.1 (0.99–1.123), 1.13 (0.88–1.47), and 1.13 (0.92–1.39), respectively].
Conclusions: Patients with a high or suppressed TSH had an increased risk of cardiovascular disease, dysrhythmias, and fractures, but patients with a low but unsuppressed TSH did not. It may be safe for patients treated with T4 to have a low but not suppressed serum TSH concentration.
Title : Serum Thyroid-Stimulating Hormone Concentration and Morbidity from Cardiovascular Disease and Fractures in Patients on Long-Term Thyroxine Therapy
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