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Nathan Goodyear

Homocysteine Lowering and Cardiovascular Events after Acute Myocardial Infarction - NEJM - 0 views

www.nejm.org/...NEJMoa055227

NORVIT trial homocysteine vitamin B12 B6 folic acid CVD cardiovascular disease MI stroke strokes events

shared by Nathan Goodyear on 25 Jul 12 - No Cached
  • Nathan Goodyear on 25 Jul 12
     
    NORVIT trial showed that vitamin B12, B6, and folic acid reduced homocysteine levels by 27%, however it did not lower MI, stroke,or mortality rate.  ONe variable to consider is the polypharmacy of the study group ie.  they were taking statins, beta blockers, diuretics, coumadin... so was the lack of change in mortality the result of polypharmacy?  And was the polypharmacy blocking the increased CVD risks associated with elevated homocysteine that would have been treatable with vitamin B12, B6, and folic acid.
Nathan Goodyear

High serum testosterone is associated with... [J Am Coll Cardiol. 2011] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...21982312

Testosterone low T therapy treatment men CVD cardiovascular disease

shared by Nathan Goodyear on 31 Jul 12 - No Cached
  • Nathan Goodyear on 31 Jul 12
     
    Testosterone inversely associated with CV events in men.  Low T is not just for ED, but should be a part of CVD prevention.
Nathan Goodyear

Sex steroids and cardiovascular disease Yeap BB - Asian J Androl - 0 views

www.ajandrology.com/article.asp

cardiovascular disease CVD sex estradiol carotid intima-media thickness hormones hormone men Testosterone estrogen

shared by Nathan Goodyear on 15 Jan 14 - No Cached
  • Levels of SHBG are higher in older men, therefore levels of free T decline more steeply than total T as men's age increases.
  • calculations based on mass action equations may not reflect precisely free T measured using a reference method
  • free T declines more steeply with age than total T in both cross-sectional [35] and longitudinal studies, [36] as does free E2 in comparison to total E2
  • ...22 more annotations...
  • T may slow development of or progression of atherosclerosis by modulating effects on insulin resistance, inflammation, endothelial function, preclinical atherosclerosis or the vasculature.
  • these cross-sectional and longitudinal studies support a relationship between low circulating T with CIMT and higher E2 with its progression
  • lower levels of T are biomarkers for aortic vascular disease
  • circulating free T was negatively associated with the presence of AAA
  • luteinizing hormone (LH) was positively associated.
  • low levels of total or bioavailable T were associated with aortic atherosclerosis manifested as calcified deposits detected by radiography
  • Men with total or free T in the lowest quartile had increased adjusted ORs for PAD defined as ABI <0.90, as did men with free E2 in the highest quartile of values
  • The apparent association of SHBG with intermittent claudication reflects the correlation of total T with SHBG, while the contribution of E2 to risk of PAD remains unclear
  • men with total T in the lowest quartile of values (<11.7 nmol l−1 ) experienced an increased incidence of stroke or transient ischemic attack
  • lower total T with increased incidence of CVD events
  • cohort studies in mostly older men have supported the association of lower androgen levels with higher mortality
  • lower total or free T levels were associated with mortality in older men, but with discordant results for cause-specific mortality and for associations of E2
  • several large studies identifying lower endogenous levels of total or free T as independent predictors of all-cause or CVD-related deaths in middle-aged and older men
  • T exhibits anti-inflammatory effects, enhances flow-mediated brachial artery reactivity, and reduces arterial stiffness
  • Short-term T therapy had a beneficial effect on exercise-induced myocardial ischemia in middle-aged men with coronary artery disease or chronic stable angina, [95],[96],[97] and reduced angina frequency in older men with diabetes and coronary artery disease
  • T therapy resulted in an increase in treadmill test duration and time to ST segment depression
  • there are interventional studies supporting a protective effect of exogenous T against myocardial ischemia in men with coronary artery disease
  • employ conservative doses
    • Nathan Goodyear
      Nathan Goodyear on 16 Jan 14
       
      This dosing is 100 fold higher then peak production of a  young man at 20-22.
  • Observational studies indicate that lower levels of endogenous T in older men are associated with the presence of carotid atherosclerosis, aortic and peripheral vascular disease, and incidence of CVD events and mortality
  • Interventional studies have shown beneficial effects of exogenous T on vascular function and on exercise-induced myocardial ischemia in men with coronary artery disease
    • Nathan Goodyear
      Nathan Goodyear on 16 Jan 14
       
      the therapies employed in these studies were massively overdosed.
  • Nathan Goodyear on 15 Jan 14
     
    Nice review of all the sex hormones and their relationship to CVD in men.  
Nathan Goodyear

Inflammatory cause of metabolic syndrome via brain stress and NF-κB - 0 views

www.ncbi.nlm.nih.gov/...PMC3314172

metabolic syndrome TLR cytokines hypothalamus brain neurology metabolic syndrome NF-kappaB DIO diet induced obesity over nutrition nutrition inflammation

shared by Nathan Goodyear on 09 Jul 13 - No Cached
  • Mechanistic studies further showed that such metabolic inflammation is related to the induction of various intracellular stresses such as mitochondrial oxidative stress, endoplasmic reticulum (ER) stress, and autophagy defect under prolonged nutritional excess
  • intracellular stress-inflammation process for metabolic syndrome has been established in the central nervous system (CNS) and particularly in the hypothalamus
  • the CNS and the comprised hypothalamus are known to govern various metabolic activities of the body including appetite control, energy expenditure, carbohydrate and lipid metabolism, and blood pressure homeostasis
  • ...56 more annotations...
  • Reactive oxygen species (ROS) refer to a class of radical or non-radical oxygen-containing molecules that have high oxidative reactivity with lipids, proteins, and nucleic acids
  • a large measure of intracellular ROS comes from the leakage of mitochondrial electron transport chain (ETC)
  • Another major source of intracellular ROS is the intentional generation of superoxides by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase
  • there are other ROS-producing enzymes such as cyclooxygenases, lipoxygenases, xanthine oxidase, and cytochrome p450 enzymes, which are involved with specific metabolic processes
  • To counteract the toxic effects of molecular oxidation by ROS, cells are equipped with a battery of antioxidant enzymes such as superoxide dismutases, catalase, peroxiredoxins, sulfiredoxin, and aldehyde dehydrogenases
  • intracellular oxidative stress has been indicated to contribute to metabolic syndrome and related diseases, including T2D [72; 73], CVDs [74-76], neurodegenerative diseases [69; 77-80], and cancers
  • intracellular oxidative stress is highly associated with the development of neurodegenerative diseases [69] and brain aging
  • dietary obesity was found to induce NADPH oxidase-associated oxidative stress in rat brain
  • mitochondrial dysfunction in hypothalamic proopiomelanocortin (POMC) neurons causes central glucose sensing impairment
  • Endoplasmic reticulum (ER) is the cellular organelle responsible for protein synthesis, maturation, and trafficking to secretory pathways
  • unfolded protein response (UPR) machinery
  • ER stress has been associated to obesity, insulin resistance, T2D, CVDs, cancers, and neurodegenerative diseases
  • brain ER stress underlies neurodegenerative diseases
  • under environmental stress such as nutrient deprivation or hypoxia, autophagy is strongly induced to breakdown macromolecules into reusable amino acids and fatty acids for survival
  • intact autophagy function is required for the hypothalamus to properly control metabolic and energy homeostasis, while hypothalamic autophagy defect leads to the development of metabolic syndrome such as obesity and insulin resistance
  • prolonged oxidative stress or ER stress has been shown to impair autophagy function in disease milieu of cancer or aging
  • TLRs are an important class of membrane-bound pattern recognition receptors in classical innate immune defense
  • Most hypothalamic cell types including neurons and glia cells express TLRs
  • overnutrition constitutes an environmental stimulus that can activate TLR pathways to mediate the development of metabolic syndrome related disorders such as obesity, insulin resistance, T2D, and atherosclerotic CVDs
  • Isoforms TLR1, 2, 4, and 6 may be particularly pertinent to pathogenic signaling induced by lipid overnutrition
  • hypothalamic TLR4 and downstream inflammatory signaling are activated in response to central lipid excess via direct intra-brain lipid administration or HFD-feeding
  • overnutrition-induced metabolic derangements such as central leptin resistance, systemic insulin resistance, and weight gain
  • these evidences based on brain TLR signaling further support the notion that CNS is the primary site for overnutrition to cause the development of metabolic syndrome.
  • circulating cytokines can limitedly travel to the hypothalamus through the leaky blood-brain barrier around the mediobasal hypothalamus to activate hypothalamic cytokine receptors
  • significant evidences have been recently documented demonstrating the role of cytokine receptor pathways in the development of metabolic syndrome components
  • entral administration of TNF-α at low doses faithfully replicated the effects of central metabolic inflammation in enhancing eating, decreasing energy expenditure [158;159], and causing obesity-related hypertension
  • Resistin, an adipocyte-derived proinflammatory cytokine, has been found to promote hepatic insulin resistance through its central actions
  • both TLR pathways and cytokine receptor pathways are involved in central inflammatory mechanism of metabolic syndrome and related diseases.
  • In quiescent state, NF-κB resides in the cytoplasm in an inactive form due to inhibitory binding by IκBα protein
  • IKKβ activation via receptor-mediated pathway, leading to IκBα phosphorylation and degradation and subsequent release of NF-κB activity
  • Research in the past decade has found that activation of IKKβ/NF-κB proinflammatory pathway in metabolic tissues is a prominent feature of various metabolic disorders related to overnutrition
  • it happens in metabolic tissues, it is mainly associated with overnutrition-induced metabolic derangements, and most importantly, it is relatively low-grade and chronic
  • this paradigm of IKKβ/NF-κB-mediated metabolic inflammation has been identified in the CNS – particularly the comprised hypothalamus, which primarily accounts for to the development of overnutrition-induced metabolic syndrome and related disorders such as obesity, insulin resistance, T2D, and obesity-related hypertension
  • evidences have pointed to intracellular oxidative stress and mitochondrial dysfunction as upstream events that mediate hypothalamic NF-κB activation in a receptor-independent manner under overnutrition
  • In the context of metabolic syndrome, oxidative stress-related NF-κB activation in metabolic tissues or vascular systems has been implicated in a broad range of metabolic syndrome-related diseases, such as diabetes, atherosclerosis, cardiac infarct, stroke, cancer, and aging
  • intracellular oxidative stress seems to be a likely pathogenic link that bridges overnutrition with NF-κB activation leading to central metabolic dysregulation
  • overnutrition is an environmental inducer for intracellular oxidative stress regardless of tissues involved
  • excessive nutrients, when transported into cells, directly increase mitochondrial oxidative workload, which causes increased production of ROS by mitochondrial ETC
  • oxidative stress has been shown to activate NF-κB pathway in neurons or glial cells in several types of metabolic syndrome-related neural diseases, such as stroke [185], neurodegenerative diseases [186-188], and brain aging
  • central nutrient excess (e.g., glucose or lipids) has been shown to activate NF-κB in the hypothalamus [34-37] to account for overnutrition-induced central metabolic dysregulations
  • overnutrition can present the cell with a metabolic overload that exceeds the physiological adaptive range of UPR, resulting in the development of ER stress and systemic metabolic disorders
  • chronic ER stress in peripheral metabolic tissues such as adipocytes, liver, muscle, and pancreatic cells is a salient feature of overnutrition-related diseases
  • recent literature supports a model that brain ER stress and NF-κB activation reciprocally promote each other in the development of central metabolic dysregulations
  • when intracellular stresses remain unresolved, prolonged autophagy upregulation progresses into autophagy defect
  • autophagy defect can induce NF-κB-mediated inflammation in association with the development of cancer or inflammatory diseases (e.g., Crohn's disease)
  • The connection between autophagy defect and proinflammatory activation of NF-κB pathway can also be inferred in metabolic syndrome, since both autophagy defect [126-133;200] and NF-κB activation [20-33] are implicated in the development of overnutrition-related metabolic diseases
  • Both TLR pathway and cytokine receptor pathways are closely related to IKKβ/NF-κB signaling in the central pathogenesis of metabolic syndrome
  • Overnutrition, especially in the form of HFD feeding, was shown to activate TLR4 signaling and downstream IKKβ/NF-κB pathway
  • TLR4 activation leads to MyD88-dependent NF-κB activation in early phase and MyD88-indepdnent MAPK/JNK pathway in late phase
  • these studies point to NF-κB as an immediate signaling effector for TLR4 activation in central inflammatory response
  • TLR4 activation has been shown to induce intracellular ER stress to indirectly cause metabolic inflammation in the hypothalamus
  • central TLR4-NF-κB pathway may represent one of the early receptor-mediated events in overnutrition-induced central inflammation.
  • cytokines and their receptors are both upstream activating components and downstream transcriptional targets of NF-κB activation
  • central administration of TNF-α at low dose can mimic the effect of obesity-related inflammatory milieu to activate IKKβ/NF-κB proinflammatory pathways, furthering the development of overeating, energy expenditure decrease, and weight gain
  • the physiological effects of IKKβ/NF-κB activation seem to be cell type-dependent, i.e., IKKβ/NF-κB activation in hypothalamic agouti-related protein (AGRP) neurons primarily leads to the development of energy imbalance and obesity [34]; while in hypothalamic POMC neurons, it primarily results in the development of hypertension and glucose intolerance
  • the hypothalamus, is the central regulator of energy and body weight balance [
  • Nathan Goodyear on 09 Jul 13
     
    Great article chronicles the biochemistry of "over nutrition" and inflammation through NF-kappaB activation and its impact on the brain.
Nathan Goodyear

Response to Media Reports Associating Testosterone Treatment with Greater Heart Attack ... - 0 views

www.lef.org/...-Greater-Heart-Attack-Risk.htm

low T Testosterone CVD cardiovascular disease men male hormone hormones

shared by Nathan Goodyear on 15 Nov 13 - No Cached
  • Nathan Goodyear on 15 Nov 13
     
    Life extesnsions rebuttal to recent JAMA study.  There was several significant flaws in that study and thus limited evidence can be gained by that study.  In fact, I find no useful clinical information from that study. In the rebuttal, there are flaws. The reference the low serum T after treatment and correctly discuss aromatase activity.  But they fail the mention that the less than optimal serum T is likely the result of the high aromatase activity in these men.  Age, stress, and weight are primary causes of increases estrogen production in these men.  These would be why likely high estrogen production occurred and less than optimal serum T resulted.   And, increased E2 will cause an increase in CRP which can precipitate CVD events.
Nathan Goodyear

Beneficial and Adverse Effects of Testosterone on the Cardiovascular System in Men - 0 views

jcem.endojournals.org/...4300.abstract

low T Testosterone male men hormone hormones cardiovascular aging

shared by Nathan Goodyear on 14 Nov 13 - No Cached
  • Nathan Goodyear on 14 Nov 13
     
    pubmed review of 33 years finds mix bag on low T. Low T clearly associated with increased hypertension, dyslipidemia, atherosclerosis, thrombosis, cardiac dysfunction, and CV events.  Studies on Testosterone therapy in resolution of these dysfunctions are low.  This article claims there is a lack of evidence.  That is not true.  
Nathan Goodyear

Chronic distress and acute vascular stress r... [J Hum Hypertens. 2013] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...24284381

low T Testosterone cortisol stress cardiovascular disease blood pressure male men hormone hormones

shared by Nathan Goodyear on 29 Nov 13 - No Cached
  • Nathan Goodyear on 29 Nov 13
     
    Low T and high cortisol associated with increased ischemic events and elevated blood pressure.
Nathan Goodyear

Testosterone Supplementation in Heart Failure - 0 views

circheartfailure.ahajournals.org/...315.abstract

low T Testosterone therapy CHF heart failure cardiovascular men male hormone hormones

shared by Nathan Goodyear on 03 Dec 13 - No Cached
  • Nathan Goodyear on 03 Dec 13
     
    Meta-analysis finds no increase in adverse cardiovascular events in men with CHF and on Testosterone therapy.
Nathan Goodyear

Testosterone and Cardiovascular Risk in Men: A Systematic Review and Meta-analysis of R... - 0 views

www.sciencedirect.com/...S0025619611609646

testosterone cardiovascular therapy Low T men male hormone hormones

shared by Nathan Goodyear on 03 Dec 13 - No Cached
  • Nathan Goodyear on 03 Dec 13
     
    meta-analysis of 30 studies finds no significantly increased Odds ratio of Testosterone therapy and increased cardiovascular events.  Better translated--no increased risk with Testosterone therapy.
Nathan Goodyear

Blood Lead Below 0.48 μmol/L (10 μg/dL) and Mortality Among US Adults - 0 views

circ.ahajournals.org/...1388.full

Pb lead cardiovascular disease mortality

shared by Nathan Goodyear on 18 Sep 14 - No Cached
  • Nathan Goodyear on 18 Sep 14
     
    Lead levels lead to increased risk of cardiovascular events at lower than previous thought levels.  Levels as low as 2mcg/dl found to be associated with increased cardiovascular mortality.  This equates to 38% of Americans.  The author concludes with this statement, "Although a 10-fold decline in blood lead levels has occurred in the United States in recent decades, current levels remain orders of magnitude higher than in pre industrialized times".
Nathan Goodyear

A reverse J-shaped association of leisure time physical activity with prognosis in pati... - 0 views

heart.bmj.com/...heartjnl-2013-305242

exercise endurance training CHD CAD coronary heart disease cardiovascular

shared by Nathan Goodyear on 16 May 14 - No Cached
  • Nathan Goodyear on 16 May 14
     
    Increased risk of cardiovascular events and all-cause mortality is highest in the least active population in those with coronary heart disease.  However, those with the highest, strenuous physical activity were also at increased risk--though less than the inactive group.
Nathan Goodyear

[Androgenic deficit and its treatment in stroke male patients with diabetes mellitus ty... - 0 views

www.researchgate.net/...with_diabetes_mellitus_type_II

low T Testosterone hypogonadism diabetes type II diabetes stroke therapy treatment men male hormone hormones

shared by Nathan Goodyear on 13 May 14 - No Cached
  • Nathan Goodyear on 13 May 14
     
    Small study of 154 men post 1rst stroke finds a reduction in a second ischemic stroke with Testosterone therapy.  That equals a 7.1% risk of secondary stroke in the Testosterone treated group (diagnosed with low T) versus 16.6% in the untreated group.  Testosterone was started one week after the first stroke event.
Nathan Goodyear

Testosterone Deficiency, Cardiac Health, and Older Men - 0 views

www.hindawi.com/...143763

low T Testosterone obesity type II diabetes diabetes health wellness metabolic syndrome lipids cholesterol hypogonadism TDS testicular dysgenesis syndrome men male hormone hormones prostate cancer

shared by Nathan Goodyear on 12 May 14 - No Cached
  • Studies have shown pharmacological doses of testosterone to relax coronary arteries when injected intraluminally [39] and to produce modest but consistent improvement in exercise-induced angina and reverse associated ECG changes [40]. The mechanism of action is via blockade of calcium channels with effect of similar magnitude to nifedipine
    • Nathan Goodyear
      Nathan Goodyear on 12 May 14
       
      This directly refutes the recent studies (3) that Testosterone therapy increases cardiovascular events.
    • Nathan Goodyear
      Nathan Goodyear on 13 May 14
       
      Testosterone acts as a calcium channel blocker inducing vasodilation.
  • men with chronic stable angina pectoris, the ischaemic threshold increased after 4 weeks of TRT and a recent study demonstrates improvement continuing beyond 12 months [
  • Exercise capacity in men with chronic heart failure increased after 12 weeks
  • ...36 more annotations...
  • Studies have shown an inverse relationship between serum testosterone and fasting blood glucose and insulin levels
  • Medications such as chronic analgesics, anticonvulsants, 5ARIs, and androgen ablation therapy are associated with increased risk of testosterone deficiency and insulin resistance
  • Women with T2D or metabolic syndrome characteristically have low SHBG and high free testosterone
    • Nathan Goodyear
      Nathan Goodyear on 12 May 14
       
      This stands in polar opposite of that with men.
  • Hypogonadism is a common feature of the metabolic syndrome
  • The precise interaction between insulin resistance, visceral adiposity, and hypogonadism is, as yet, unclear but the important mechanisms are through increased aromatase production, raised leptin levels, and increase in inflammatory kinins
  • levels of testosterone are reduced in proportion to degree of obesity
  • Men should be encouraged to combine aerobic exercise with strength training. As muscle increases, glucose will be burned more efficiently and insulin levels will fall. A minimum of 30 minutes exercise three times weekly should be advised
  • Testosterone increases levels of fast-twitch muscle fibres
  • By increasing testosterone, levels of type 2 fibres increase and glucose burning improves
  • Weight loss will increase levels of testosterone
  • studies now clearly show that low testosterone leads to visceral obesity and metabolic syndrome and is also a consequence of obesity
  • In the case of MMAS [43], a baseline total testosterone of less than 10.4 nmol/L was associated with a greater than 4-fold incidence of type 2 diabetes over the next 9 years
  • There is high level evidence that TRT improves insulin resistance
  • Low testosterone predicts increased mortality and testosterone therapy improves survival in 587 men with type 2 diabetes
  • A similar retrospective US study involved 1031 men with 372 on TRT. The cumulative mortality was 21% in the untreated group versus 10% ( ) in the treated group with the greatest effect in younger men and those with type 2 diabetes
  • the presence of ED has been shown to be an independent risk factor, particularly in hypogonadal men, increasing the risk of cardiac events by over 50%
  • A recent online publication on ischaemic heart disease mortality in men concluded optimal androgen levels are a biomarker for survival
  • inverse associations between low TT or FT (Table 2) and the severity of CAD
  • A recent 10 year study from Western Australia involving 3690 men followed up from 2001–2010 concluded that TT and FT levels in the normal range were associated with decreased all-cause and cardiovascular mortality, for the first time suggesting that both low and DHT are associated with all-cause mortality and higher levels of DHT reduced cardiovascular risk
  • TDS is associated with increased cardiovascular and all-cause mortality
  • The effect of treatment with TRT reduced the mortality rate of treated cohort (8.4%) to that of the eugonadal group whereas the mortality for the untreated remained high at 19.2%
  • hypogonadal men had slightly increased triglycerides and HDL
  • Men with angiographically proven CAD (coronary artery disease) have significantly lower testosterone levels [29] compared to controls ( ) and there was a significant inverse relationship between the degree of CAD and TT (total testosterone) levels
  • TRT has also been shown to reduce fibrinogen to levels similar to fibrates
  • men treated with long acting testosterone showed highly significant reductions in TC, LDL, and triglycerides with increase in HDL, associated with significant reduction in weight, BMI, and visceral fat
  • Low androgen levels are associated with an increase in inflammatory markers
  • In the Moscow study, C-reactive protein was reduced by TRT at 30 weeks versus placebo
  • In some studies, a decline in diastolic blood pressure has been observed, after 3–9 months [24, 26] and in systolic blood pressure
  • A decline was noted in IL6 and TNF-alpha
  • No studies to date show an increase in LUTS/BPH symptoms with higher serum testosterone levels
  • TRT has been shown to upregulate PDE5 [65] and enhance the effect of PDE5Is (now an accepted therapy for both ED and LUTS), it no longer seems logical to advice avoidance of TRT in men with mild to moderate BPH.
    • Nathan Goodyear
      Nathan Goodyear on 12 May 14
       
      What about just starting with normalization of Testosterone levels first.
  • Several meta-analyses have failed to show a link between TRT and development of prostate cancer [66] but some studies have shown a tendency for more aggressive prostate cancer in men with low testosterone
    • Nathan Goodyear
      Nathan Goodyear on 12 May 14
       
      And if one would have looked at their estrogen levels, I guarantee they would have been found to be elevated.
  • low bioavailable testosterone and high SHBG were associated with a 4.9- and 3.2-fold risk of positive biopsy
  • Current EAU, ISSAM, and BSSM guidance [1, 2] is that there is “no evidence TRT is associated with increased risk of prostate cancer or activation of subclinical cancer.”
  • Men with prostate cancer, treated with androgen deprivation, develop an increase of fat mass with an altered lipid profile
  • Erectile dysfunction is an established marker for future cardiovascular risk and the major presenting symptom leading to a diagnosis of low testosterone
Nathan Goodyear

Histamine and mucosal mast cells in interstitial cystitis. - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...2750582

IC interstitial cystitis histamine mast cells bladder

shared by Nathan Goodyear on 12 May 15 - No Cached
  • Nathan Goodyear on 12 May 15
     
    Interstitial cystitis is a histamine/mast cell mediated event.
Nathan Goodyear

Review of health risks of low testosterone and testosterone administration - 0 views

www.ncbi.nlm.nih.gov/...PMC4391003

low Testosterone low T Testosterone men male hormone hormones health

shared by Nathan Goodyear on 28 Apr 15 - No Cached
  • Hypogonadism may be defined either as serum concentration of T (either total T, bioavailable T or free T) or as low T plus symptoms of hypogonadism
  • The Baltimore Longitudinal Study on Aging reported the incidence of total serum T < 325 ng/dL to be 20% for men in their 60s, 30% for men in their 70s and 50% for men over 80
  • The Massachusetts Aging Male Study reported that 12.3% of men aged 40 to 70 had a total serum T of < 200 ng/dL with 3 or more symptoms of hypogonadism
  • ...19 more annotations...
  • The Boston Area Community Health Study reported that 5.6% of men aged 30 to 70 were hypogonadal, as defined by total serum T < 300 ng/dL; or, free serum T < 5 ng/dL plus 3 or more symptoms of hypogonadism
  • In a health screening project among 819 men in Taiwan, the prevalence of hypogonadism (total serum T < 300 ng/dL) ranged from 16.5% for men in their 40s, 23.0% for men in their 50s, 28.9% for men in their 60s, and 37.2% for men older than 70 years of age
  • The prevalence of hypogonadism among men in Taiwan is higher than the prevalence reported in the Massachusetts Male Aging Study
  • CAG repeat sequence, within the androgen receptor (AR). Rajender et al[12] reviewed over 30 studies on the AR trinucleotide repeat and infertility
  • suggestion that CAG repeat length may determine androgen responsiveness, this issue is not clearly settled
  • reported prevalence of low T in older men range from 5.6% to 50%
  • Those in the hypogonadal group (n = 4269) had direct health care costs, that exceeded the eugonadal group (n = 4269) by an average of $7100 over the course of the observation window
  • higher economic burden and presence of co-morbidities for hypogonadism
  • minor to moderate improvements in lean mass and muscle strength
  • increased bone mineral density
  • modest enhancement in sexual function
  • reduced adiposity
  • lessening of depressive symptoms
  • Meta-analyses of clinical TRT trials as of 2010 have identified three major adverse events resulting from TRT: (1) polycythemia; (2) an increase in prostate-related events; and (3) and a slight reduction in serum high-density lipoprotein (HDL) cholesterol
  • polycythemia (> 3.5-fold increase in risk
  • TRT produced a 40% prostate enlargement in older hypogonadal male Veterans over 12 mo
  • no published analysis has reported measurable increases in prostate cancer risk or Gleason score in men undergoing TRT, or in hypogonadal men with a history of prostate cancer undergoing TRT
  • the prostate which highly expresses the type II 5α-reductase enzyme. Inhibition of this enzyme via finasteride (a type II 5α-reductase inhibitor) or dutasteride (a dual type I and II 5α-reductase inhibitor) reduces circulating DHT 50%-75% and > 90%, respectively[47], and reduces prostate mass[48] and prostate cancer risk
  • Normally estradiol partially regulates testosterone levels, at the hypothalamus, blunting LH and FSH release from the pituitary. As a selective estrogen receptor modulator, CC interrupts this pathway, and consequently there is a greater stimulation for the production of testosterone in Leydig cells
    • Nathan Goodyear
      Nathan Goodyear on 28 Apr 15
       
      this would only apply if E1 and/or E2 levels were elevated, which the authors make no mention of.
  • Nathan Goodyear on 28 Apr 15
     
    to be read
Nathan Goodyear

Roles of Testosterone Replacement in Cardiac Ischemia-Reperfusion Injury. - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...26015457

Testosterone cardiovascular disease cardiovascular disease heart health hormone hormones

shared by Nathan Goodyear on 04 Jun 15 - No Cached
  • Nathan Goodyear on 04 Jun 15
     
    Only abstract available here.  Authors of this review conclude, in a review of the current literature of Testosterone therapy and heart ischemia/reperfusion injury, that chronic, physiologic Testosterone therapy has positive cardiovascular protection whereas acute Testosterone has increased adverse events.  This is likely the difference between preventative and reactive medicine.
Nathan Goodyear

Thieme E-Journals - International Journal of Sports Medicine / Abstract - 0 views

www.thieme-connect.de/...DOI

endurance athletes endurance exercise endurance sports inflammation gut CRP IL-6 IL-1beta TNF-alpha IL-10 sports

shared by Nathan Goodyear on 23 Jun 15 - No Cached
  • Nathan Goodyear on 23 Jun 15
     
    Ultra endurance athletic events associated with significant increase in systemic inflammation due to damaged gut.
Nathan Goodyear

Effect of testosterone treatment on cardiac biomarkers in a randomized controlled trial... - 0 views

www.ncbi.nlm.nih.gov/...26120052

low T low Testosterone BNP troponin CVD cardiovascular disease men diabetes Testosterone inflammation

shared by Nathan Goodyear on 13 Aug 15 - No Cached
  • Nathan Goodyear on 13 Aug 15
     
    40 week study finds that low Testosterone is associated with increased 10 risk of cardiac adverse events.  This was also associated with elevated BNP and hs-cardiac Troponin.  The study found that Testosterone therapy did decrease BNP, though not statistically significant; no effect on hs-cardiac troponin was found.
Nathan Goodyear

Effects of Self-Selected Mass Loss on Performance and Mood i... : The Journal of Streng... - 0 views

journals.lww.com/...ss_Loss_on_Performance.18.aspx

wrestlers rapid weight loss

shared by Nathan Goodyear on 23 May 11 - No Cached
  • Nathan Goodyear on 23 May 11
     
    rapid weight loss in wrestlers pre-event causes increased mood effects and confusion
Nathan Goodyear

Testosterone Dose-Response Relationships with Cardiovascular Risk Markers in Androgen-D... - 0 views

press.endocrine.org/...jc.2013-4160

testosterone cardiovascular women female hormone hormones CVD disease

shared by Nathan Goodyear on 19 May 14 - No Cached
  • Nathan Goodyear on 19 May 14
     
    Study finds no worsening in cardiovascular biomarkers in women on Testosterone.  The women in this study were chose due to low Testosterone.  Testosterone was given IM at 4 different doses.  This is in contrast to other studies that have looked at endogenous Testosterone level.  Studies have shown increasing endogenous T levels in women is associated with increased CVD.  Studies on exogenous are lacking.  This points to limited risk associated with CVD and T therapy in women.   One caveat.  Two of the authors of this study have ties to the maker of the Testosterone enanthate used in this study.  Why is this important?  Prior studies have shown significant decrease in adverse event reporting in those funded by pharma--bias.
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