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Nathan Goodyear

Thyroid hormone action in mitochondria -- Wrutniak-Cabello et al. 26 (1): 67 -- Journal... - 0 views

  • Triiodothyronine (T3) is considered a major regulator of mitochondrial activity
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    T3 is major regulator of mitochondrial activity; not T4
Nathan Goodyear

Testosterone restores insulin sensitivity in patients with diabetes and hypogonadism | ... - 0 views

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    This is the abstract from oral presentation at AACE in Las Vegas from May.  Small study finds reduction in fat mass, increase in muscle mass, increase in insulin sensitivity, and reduction in inflammation signaling with Testosterone therapy in men with low Testosterone.  These men were type 2 diabetics.  This is consistent with prior published literature.  However, men without diabetes, this association is hard to reproduce. The degree of glucose control also effects the response to Testosterone therapy i.e. the worse the glucose control, the more the response from Testosterone.   Also of note, those men with hypogonatrophic hypogonadism had decreased insulin receptor expression, decreased insulin sensitivity, and decreased GLUT-4 expression versus eugonadal men.  Remember from prior studies, it is the conversion of Testosterone to DHT that increases GLUT-4 transcription, translocation, and expression.
Nathan Goodyear

Testosterone therapy not associated with myocardial infarction, stroke | Endocrinology - 0 views

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    Retrospective study finds no increase in new MI and/or stroke in men with Testosterone therapy.  There are some men that Testosterone therapy is cardioprotective and some that are not.
Nathan Goodyear

Short-term testosterone therapy failed to increase CV risk in women | Endocrinology - 0 views

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    24 week study of 71 women post-hysterectomy finds no increase in cardiovascular biomarkers.  Several problems with this study.  First, there was a large drop out--24%.  Second and most important, the women were pretreated with estrogen prior to Testosterone therapies were initiated.  Other studies have proposed that this protects cardiovascular risk in women on Testosterone.  Previous studies show increasing endogenous Testosterone is associated with increasing cardiovascular disease in women.   This study would be much better if no estradiol was prescribed.  That would give an unbiased view of Testosterone in post-hysterectomy women.  Not much can be taken from this study. If you doctor doesn't know this, find another doctor.  Inherent bias in this study as ties to the manufacturer of the Testosterone was disclosed. This study point to the inherent flaws in so much of the medical literature today.  Most would read the headlines and read no further, but the "further" dispels the headline as flawed.
Nathan Goodyear

http://joe.endocrinology-journals.org/content/208/2/97.full.pdf - 0 views

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    kisspeptins.
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

Testosterone at high concentrations interacts ... [Endocrinology. 1990] - PubMed - NCBI - 0 views

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    DHT binds to androgen receptor with higher affinity and stays bound with receptor up to 5 x longer.
Nathan Goodyear

Thyroid hormones act indirectly to increase sex hormone-binding globulin prod... - 0 views

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    Thyroid hormones stimulate SHBG levels.  
Nathan Goodyear

Testosterone: a metabolic hormone in health and disease - 0 views

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    Great, great read and review on the current understanding of testosterone and metabolic dysfunction. Very well referenced.
Nathan Goodyear

Testosterone: a vascular hormone in health and disease - 0 views

  • Testosterone has beneficial effects on several cardiovascular risk factors, which include cholesterol, endothelial dysfunction and inflammation
  • In clinical studies, acute and chronic testosterone administration increases coronary artery diameter and flow, improves cardiac ischaemia and symptoms in men with chronic stable angina and reduces peripheral vascular resistance in chronic heart failure.
  • testosterone is an L-calcium channel blocker and induces potassium channel activation in vascular smooth muscle cells
  • ...54 more annotations...
  • Animal studies have consistently demonstrated that testosterone is atheroprotective, whereas testosterone deficiency promotes the early stages of atherogenesis
  • there is no compelling evidence that testosterone replacement to levels within the normal healthy range contributes adversely to the pathogenesis of CVD (Carson & Rosano 2011) or prostate cancer (Morgentaler & Schulman 2009)
  • bidirectional effect between decreased testosterone concentrations and disease pathology exists as concomitant cardiovascular risk factors (including inflammation, obesity and insulin resistance) are known to reduce testosterone levels and that testosterone confers beneficial effects on these cardiovascular risk factors
  • Achieving a normal physiological testosterone concentration through the administration of testosterone replacement therapy (TRT) has been shown to improve risk factors for atherosclerosis including reducing central adiposity and insulin resistance and improving lipid profiles (in particular, lowering cholesterol), clotting and inflammatory profiles and vascular function
  • It is well known that impaired erectile function and CVD are closely related in that ED can be the first clinical manifestation of atherosclerosis often preceding a cardiovascular event by 3–5 years
  • no decrease in the response (i.e. no tachyphylaxis) of testosterone and that patient benefit persists in the long term.
  • free testosterone levels within the physiological range, has been shown to result in a marked increase in both flow- and nitroglycerin-mediated brachial artery vasodilation in men with CAD
  • Clinical studies, however, have revealed either small reductions of 2–3 mm in diastolic pressure or no significant effects when testosterone is replaced within normal physiological limits in humans
  • Endothelium-independent mechanisms of testosterone are considered to occur primarily via the inhibition of voltage-operated Ca2+ channels (VOCCs) and/or activation of K+ channels (KCs) on smooth muscle cells (SMCs)
  • Testosterone shares the same molecular binding site as nifedipine
  • Testosterone increases the expression of endothelial nitric oxide synthase (eNOS) and enhances nitric oxide (NO) production
  • Testosterone also inhibited the Ca2+ influx response to PGF2α
  • one of the major actions of testosterone is on NO and its signalling pathways
  • In addition to direct effects on NOS expression, testosterone may also affect phosphodiesterase type 5 (PDE5 (PDE5A)) gene expression, an enzyme controlling the degradation of cGMP, which acts as a vasodilatory second messenger
  • the significance of the action of testosterone on VSMC apoptosis and proliferation in atherosclerosis is difficult to delineate and may be dependent upon the stage of plaque development
  • Several human studies have shown that carotid IMT (CIMT) and aortic calcification negatively correlate with serum testosterone
  • t long-term testosterone treatment reduced CIMT in men with low testosterone levels and angina
  • neither intracellular nor membrane-associated ARs are required for the rapid vasodilator effect
  • acute responses appear to be AR independent, long-term AR-mediated effects on the vasculature have also been described, primarily in the context of vascular tone regulation via the modulation of gene transcription
  • Testosterone and DHT increased the expression of eNOS in HUVECs
  • oestrogens have been shown to activate eNOS and stimulate NO production in an ERα-dependent manner
  • Several studies, however, have demonstrated that the vasodilatory actions of testosterone are not reduced by aromatase inhibition
  • non-aromatisable DHT elicited similar vasodilation to testosterone treatment in arterial smooth muscle
  • increased endothelial NOS (eNOS) expression and phosphorylation were observed in testosterone- and DHT-treated human umbilical vein endothelial cells
  • Androgen deprivation leads to a reduction in neuronal NOS expression associated with a decrease of intracavernosal pressure in penile arteries during erection, an effect that is promptly reversed by androgen replacement therapy
  • Observational evidence suggests that several pro-inflammatory cytokines (including interleukin 1β (IL1β), IL6, tumour necrosis factor α (TNFα), and highly sensitive CRP) and serum testosterone levels are inversely associated in patients with CAD, T2DM and/or hypogonadism
  • patients with the highest IL1β concentrations had lower endogenous testosterone levels
  • TRT has been reported to significantly reduce TNFα and elevate the circulating anti-inflammatory IL10 in hypogonadal men with CVD
  • testosterone treatment to normalise levels in hypogonadal men with the MetS resulted in a significant reduction in the circulating CRP, IL1β and TNFα, with a trend towards lower IL6 compared with placebo
  • parenteral testosterone undecanoate, CRP decreased significantly in hypogonadal elderly men
  • Higher levels of serum adiponectin have been shown to lower cardiovascular risk
  • Research suggests that the expression of VCAM-1, as induced by pro-inflammatory cytokines such as TNFα or interferon γ (IFNγ (IFNG)) in endothelial cells, can be attenuated by treatment with testosterone
  • Testosterone also inhibits the production of pro-inflammatory cytokines such as IL6, IL1β and TNFα in a range of cell types including human endothelial cells
  • decreased inflammatory response to TNFα and lipopolysaccharide (LPS) in human endothelial cells when treated with DHT
  • The key to unravelling the link between testosterone and its role in atherosclerosis may lay in the understanding of testosterone signalling and the cross-talk between receptors and intracellular events that result in pro- and/or anti-inflammatory actions in athero-sensitive cells.
  • testosterone functions through the AR to modulate adhesion molecule expression
  • pre-treatment with DHT reduced the cytokine-stimulated inflammatory response
  • DHT inhibited NFκB activation
  • DHT could inhibit an LPS-induced upregulation of MCP1
  • Both NFκB and AR act at the transcriptional level and have been experimentally found to be antagonistic to each other
  • As the AR and NFκB are mutual antagonists, their interaction and influence on functions can be bidirectional, with inflammatory agents that activate NFκB interfering with normal androgen signalling as well as the AR interrupting NFκB inflammatory transcription
  • prolonged exposure of vascular cells to the inflammatory activation of NFκB associated with atherosclerosis may reduce or alter any potentially protective effects of testosterone
  • DHT and IFNγ also modulate each other's signalling through interaction at the transcriptional level, suggesting that androgens down-regulate IFN-induced genes
  • (Simoncini et al. 2000a,b). Norata et al. (2010) suggest that part of the testosterone-mediated atheroprotective effects could depend on ER activation mediated by the testosterone/DHT 3β-derivative, 3β-Adiol
  • TNFα-induced induction of ICAM-1, VCAM-1 and E-selectin as well as MCP1 and IL6 was significantly reduced by a pre-incubation with 3β-Adiol in HUVECs
  • 3β-Adiol also reduced LPS-induced gene expression of IL6, TNFα, cyclooxygenase 2 (COX2 (PTGS2)), CD40, CX3CR1, plasminogen activator inhibitor-1, MMP9, resistin, pentraxin-3 and MCP1 in the monocytic cell line U937 (Norata et al. 2010)
  • This study suggests that testosterone metabolites, other than those generated through aromatisation, could exert anti-inflammatory effects that are mediated by ER activation.
  • The authors suggest that DHT differentially effects COX2 levels under physiological and pathophysiological conditions in human coronary artery smooth muscle cells and via AR-dependent and -independent mechanisms influenced by the physiological state of the cell
  • There are, however, a number of systematic meta-analyses of clinical trials of TRT that have not demonstrated an increased risk of adverse cardiovascular events or mortality
  • The TOM trial, which was designed to investigate the effect of TRT on frailty in elderly men, was terminated prematurely as a result of an increased incidence of cardiovascular-related events after 6 months in the treatment arm
  • trials of TRT in men with either chronic stable angina or chronic cardiac failure have also found no increase in either cardiovascular events or mortality in studies up to 12 months
  • Evidence may therefore suggest that low testosterone levels and testosterone levels above the normal range have an adverse effect on CVD, whereas testosterone levels titrated to within the mid- to upper-normal range have at least a neutral effect or, taking into account the knowledge of the beneficial effects of testosterone on a series of cardiovascular risk factors, there may possibly be a cardioprotective action
  • The effect of testosterone on human vascular function is a complex issue and may be dependent upon the underlying androgen and/or disease status.
  • the majority of studies suggest that testosterone may display both acute and chronic vasodilatory effects upon various vascular beds at both physiological and supraphysiological concentrations and via endothelium-dependent and -independent mechanisms
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    Good deep look into the testosterone and CVD link.
Nathan Goodyear

Journal of Endocrinological Investigation - 0 views

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    Study finds that BMI is related to penile length
Nathan Goodyear

Journal of Endocrinological Investigation - 0 views

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    Testosterone levels fluctuate seasonally, with the peak production in the fall of the year.  Contrast that with LH, with it's peak in the spring of the year.  This study found that men with Klinefelter's syndrome had only seasonal fluctuations of testosterone, suggesting a testicular independent role.  This is a small study.  
Nathan Goodyear

Journal of Endocrinological Investigation - 0 views

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    Just an abstract, but the call for customized/individualized treatment strategies called for those with diabetes.  Medicine is moving to an individualized paradigm rather than a herd mentality.
Nathan Goodyear

Journal of Endocrinological Investigation - 0 views

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    The point of this post is not that the author concludes that metformin an statin therapy should be used in PCOS women on birth control with elevated cardiovascular risk; but that with struggling with PCOS should have cardiovascular risk assessment prior to starting birth control.  Again, back to the individualized approach paradigm.
Nathan Goodyear

Dose-dependent effects of vitamin D on transdifferentiation of skeletal muscle cells to... - 0 views

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    Dose dependent vitamin D impact on fat.  Low vitamin D concentrations associated with fat adipogenesis.  Higher vitamin D concentrations inhibited adipogenesis.
Nathan Goodyear

Acupuncture blocks cold stress-induced increases in the hypothalamus-pituitary-adrenal ... - 0 views

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    acupuncture decreases HPA sympathetic drive.  Acupuncture calms the HPA axis and relieves stress.  Granted this is in a rat model.
Nathan Goodyear

Journal of Endocrinological Investigation - 0 views

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    elevated autoimmune markers against the thyroid and an elevated TSH are both independent risk factors for thyroid malignancy in those with thyroid nodules.
Nathan Goodyear

Journal of Endocrinological Investigation - 0 views

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    TSH levels vary with weight.  TSH levels increase with increasing weight.
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