The Effect of Soy Phytoestrogen Supplementation on Thyroid Status and Cardiovascular Risk Markers in Patients with Subclinical Hypothyroidism: A Randomized, Double-Blind, Crossover Study
ABSTRACT There is concern whether soy phytoestrogens may affect thyroid function. If true, soy phytoestrogens may be expected to have a greater impact in subjects with subclinical hypothyroidism.
The primary aim was to determine the effect of soy phytoestrogen supplementation on thyroid function, with a secondary aim of assessing the effects on cardiovascular risk indices in patients with subclinical hypothyroidism.
We conducted a randomized, double-blind, crossover study in a tertiary care setting.
Sixty patients with subclinical hypothyroidism participated in the study.
Patients were randomly assigned to either low-dose phytoestrogen (30 g soy protein with 2 mg phytoestrogens, representative of a Western diet) or high-dose phytoestrogen (30 g soy protein with 16 mg phytoestrogens, representative of a vegetarian diet) supplementation for 8 wk, then crossed over after an 8-wk washout period.
The primary outcome was progression to overt hypothyroidism, with secondary outcome measures of blood pressure, insulin resistance, lipids, and highly sensitive C-reactive protein (hsCRP).
Six female patients in the study progressed into overt hypothyroidism with a standardized rate ratio of 3.6 (95% confidence interval, 1.9, 6.2) after 16-mg phytoestrogen supplementation. Both systolic and diastolic blood pressure decreased with 16 mg phytoestrogens, whereas systolic pressure alone decreased with 2 mg phytoestrogens. Insulin resistance (homeostasis model assessment of insulin resistance, 3.5 ± 0.09 vs. 2.6 ± 0.08; P < 0.02) and hsCRP (4.9 ± 0.04 vs. 3.9 ± 0.03; P < 0.01) decreased with 16 mg phytoestrogens. Lipid profile remained unchanged.
There is a 3-fold increased risk of developing overt hypothyroidism with dietary supplementation of 16 mg soy phytoestrogens with subclinical hypothyroidism. However, 16-mg soy phytoestrogen supplementation significantly reduces the insulin resistance, hsCRP, and blood pressure in these patients.
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ABSTRACT: Industrial chemical contaminants have a variable impact on the hypothalamic-pituitary-thyroid axis, this depending both on their class and on confounding factors. Today, mounting evidence is pointing to the role of environmental factors, and specifically EDCs, in the current distressing upsurge in the incidence of thyroid disease. The unease is warranted. These substances, which are nowadays rife in our environments (including in foodstuffs), have been shown to interfere with thyroid hormone action, biosynthesis, and metabolism, resulting in disruption of tissue homeostasis and/or thyroid function. Importantly, based on the concept of the "nonmonotonic dose-response curve", the relationship between dose and effect has often been found to be nonlinear. Thus, small doses can induce unpredictable, adverse effects, one case being polychlorinated biphenyls (PCBs), of which congener(s) may centrally inhibit the hypothalamic-pituitary-thyroid axis, or dissociate thyroid receptor and selectively affect thyroid hormone signaling and action. This means that PCBs can act as agonists or antagonists at the receptor level, underlining the complexity of the interaction. This review highlights the multifold activity of chemicals demonstrated to cause thyroid disruption. It also represents a call to action among clinicians to undertake systematic monitoring of thyroid function and registering of the classes of EDs and additionally urges broader scientific collaborations to clarify these chemicals' molecular mechanisms of action, substances whose prevalence in our environments is disrupting not only the thyroid but all life on earth.Endocrine 10/2014; 48(1). DOI:10.1007/s12020-014-0442-4 · 3.53 Impact Factor
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ABSTRACT: Background A number of recent advances in our understanding of thyroid physiology may shed light on why some patients feel unwell while taking levothyroxine monotherapy. The purpose of this committee was to review the goals of levothyroxine therapy, the optimal prescription of conventional levothyroxine therapy, the sources of dissatisfaction with levothyroxine therapy, the evidence on treatment alternatives, and the relevant knowledge gaps. We wished to determine whether there are sufficient new data generated by well-designed studies to provide reason to pursue such therapies and change the current standard of care. Methods Committee members identified 24 questions relevant to the treatment of hypothyroidism. The clinical literature relating to each question was then reviewed. Clinical reviews were supplemented, when relevant, with related mechanistic and bench research literature reviews, performed by our team of translational scientists. Ethics reviews were provided, when relevant, by a bioethicist. The responses to questions were formatted, when possible, in the form of a formal clinical recommendation statement. When responses were not suitable for a formal clinical recommendation, a summary response statement without a formal clinical recommendation was developed. For clinical recommendations, the supporting evidence was appraised, and the strength of the clinical recommendations was assessed, using the American College of Physicians (ACP) system. Results We reviewed the following therapeutic categories: i) levothyroxine therapy, ii) non-levothyroxine based thyroid hormone therapies, and iii) use of thyroid hormone analogs. The second category included thyroid extracts, synthetic combination therapy, triiodothyronine therapy, and compounded thyroid hormones. Conclusions We concluded that levothyroxine should remain the standard of care for treating hypothyroidism. We found no consistently strong evidence for the superiority of alternative preparations (eg. levothyroxine-liothyronine combination therapy, or thyroid extract therapy, or others) over monotherapy with levothyroxine, in improving health outcomes. Some examples of future research needs include: development of superior biomarkers of euthyroidism to supplement TSH measurements, mechanistic research on serum triiodothyronine levels (including effects of age and disease status, relationship with tissue concentrations, as well as potential therapeutic targeting), and long-term outcome clinical trials testing combination therapy or thyroid extracts (including sub-group effects) Additional research is also needed to develop thyroid hormone analogs with a favorable benefit to risk profile.Thyroid: official journal of the American Thyroid Association 09/2014; DOI:10.1089/thy.2014.0028 · 3.84 Impact Factor