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Nathan Goodyear

Clinical controversies in screening women for thyr... [J Midwifery Womens Health. 2006 ... - 0 views

  • In November 2002, the American Association of Clinical Endocrinologists (AACE) released new guidelines for clinical practice for the diagnosis and treatment of hyperthyroidism and hypothyroidism, which includes a new thyroid-stimulating hormone (TSH) reference range of 0.3 to 3.0 mIU/
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    TSH "screening" needs to be between 0.3 and 3 according to American Association of Clinical Endocrinologists
Nathan Goodyear

Subclinical Thyroid Dysfunction: A Joint Statement on Management from the American Asso... - 0 views

  • the potential benefits of early detection and treatment of subclinical thyroid dysfunction significantly outweigh the potential side-effects that could result from early diagnosis and therapy
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    Joint statement on early treatment of thyroid disease and subclinical thyroid dysfunction from The american association of clinical endocrinologists, the American Thyroid Association, and the Endocrine Society
Nathan Goodyear

Thyroid Replacement Therapy and Heart Failure - 0 views

  • A good biomarker of intracardiac TH signaling would be helpful but has not been identified. In the absence of such a marker, a rational, cautious therapeutic approach might be to restore and maintain over time biochemical euthyroidism as documented by normal circulating levels of TSH, FT4, and FT3.
  • a low-T3 state resulting from altered peripheral TH metabolism secondary to caloric restriction is associated with impaired cardiac contractility
  • Low-T3 syndrome is the central finding and defines the illness in a variety of acute and chronic severe nonthyroidal illnesses with cardiac origin, including MI, HF, and surgically treated cardiac disease.1 Low circulating levels of T3 in the absence of primary thyroid hypofunction have been found in 20% to 30% of patients with dilated cardiomyopathy.
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  • FT3 levels were inversely correlated to coronary artery disease
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    Great review of the current understanding of thyroid hormone metabolism in cardiac tissue.  Low T3 and increased rT3 (via increased D3 activity) is CLEARLY associated with poor cardiac performance and post MI and CHF is associated with poor outcomes.  T3 is critical in cardiac remodeling and recovery post MI.  T3 is actually a vasodilatory in the coronary arteries.   Why a endocrinologist would call rT3 useless only points to their ignorance of the literature.
Nathan Goodyear

Relationship of thyroid hormone levels and cardiov... [Endocrine. 2014] - PubMed - NCBI - 0 views

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    Patients with type II Diabetes and h/o of CVE  have higher rT3 in study.  The Endocrinologist that said reverse T3 is completely irrelevant needs to read more studies and stop listening to opinion.
Nathan Goodyear

Reverse T3 as a parameter of myocardial functi... [Int J Cardiol. 2010] - PubMed - NCBI - 0 views

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    Another study regarding reverse T3 that many Endocrinologists need to read.  In this study, the authors find that significantly higher reverse T3 levels were associated with myocardial function impairment (MFI) class IV.  This MFI class IV was also found associated with a decreased fT3/rT3.
Nathan Goodyear

Minireview: Cracking the Metabolic Code for Thyroid Hormone Signaling - 0 views

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    Here is a great review of thyroid hormone metabolism published in the very relevant journal Endocrinology.  The review describes the peripheral metabolism of the pro hormone T4 and the peripheral metabolism to free T3 and/or reverse T3 and the associated metabolic implications.  Why don't more endocrinologists read?This is an animal study.
Nathan Goodyear

Cellular and Molecular Basis of Deiodinase-Regulated Thyroid Hormone Signaling - 0 views

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    Anything and everything one would want to know regarding thyroid hormone signaling.  Doctors, especially endocrinologists, need to read this.  T4 is not or is ever inside target cells.  The enzymes, deiodinase types 1, 2, and 3, are what control the thyroid hormone at the cellular levels.  Deiodinase-2 is what generates T3 in the cytosol of the cell.  In contrast, deiodinase-3 is what generates rT3 which is inactive.  High Fat diet increases deiodinase-3.
Sundhar krishna

Pituitary Tumor Removal India at Affordable Cost - 0 views

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    Krishna Eye and Ent is one of the best hospital for skull base surgery India. We offer treatment for tumors like pituitary gland tumours, glomus tumors, cerebello pontine angle tumour and treatment for fungal sinusitis, endoscopic csf leak repair.
Nathan Goodyear

Biological functions and clinical implications of oestrogen receptors alfa and beta in ... - 0 views

  • ERα-positive cells respond to E2 with increased proliferation
  • ERβ was artificially introduced into these cells, E2-induced proliferation was inhibited
  • The proliferative response to E2 seems to be determined by the ratio of ERα/ERβ. The functions of ERβ in the breast are probably related to its antiproliferative as well as its prodifferentiative functions
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  • The risk of developing PC seems to be related to the diet
  • In the human prostate, ERβ is expressed in the basal epithelial cells and AR in the luminal epithelium.
  • For many years, DHT was considered to be the main hormone guiding prostate development and function. However, the idea was challenged when in 2001 Mahendroo et al. showed that mice in which both forms of 5α-reductase had been inactivated, have a normal functional prostate [50]. The question was then raised as to what is the real function of DHT in the prostate. In 1989 we hypothesized that DHT is a precursor of an oestrogen, 5α-androstane-3β,17β-diol (3β-Adiol) and that physiological levels of an oestrogen could be produced in the total absence of aromatase [51]. We later demonstrated that 3β-Adiol is abundant in the prostate and is a good natural ligand for ERβ
  • The overall effect of oestrogens in the immune system is determined by a balance between ERα and ERβ signalling
  • The hypothesis of our group is that ERβ plays an important role in regulating the differentiation of pluripotent haematopoietic progenitor cells whereas ERα induces proliferation
  • In tissues and cell lines of mammary epithelium for example, it has been noticed that E2 in the presence of ERα elicits proliferation, but in the presence of ERβ it inhibits proliferation
  • ERα and ERβ have distinctive tissue distributions and to the great surprise of endocrinologists [7] many tissues previously thought to be ‘oestrogen-insensitive tissues’ were found to be ERβ positive and oestrogen sensitive. The most notable of the ERα-negative ERβ-abundant tissues were the epithelium of the rodent ventral prostate [8], the granulosa cells of the ovaries [9] and the parenchyma of the lungs
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    Awesome article discusses the different balance of ER alpha and ER beta and the effects on tissue as it relates to proliferation versus differentiation.  This has clear implications in disease.  Physicians prescribing hormones without a knowledge and understanding of this are only causing potential harm to their clients.
Nathan Goodyear

Why Doesn't My Endocrinologist Know All of This? :: National Academy of Hypothyroidism - 0 views

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    Absolute must read!  How current medial practice lags way behind the scientific knowledge
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