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Nathan Goodyear

Androgens are bronchoactive drugs that act by relaxing airway smooth muscle and prevent... - 0 views

joe.endocrinology-journals.org/...1.abstract

low T Testosterone metabolites asthma dihydrotestosterone

shared by Nathan Goodyear on 09 Jul 14 - No Cached
  • Nathan Goodyear on 09 Jul 14
     
    Androgens relax smooth muscles of airways in men with asthma.  The metabolite 5beta-DHT was the most potent in this action.  This has implications in men with low T and asthma.  
Nathan Goodyear

Effects of 3-beta-diol, an androgen metabolite with intrinsic estrogen-like effects, in... - 0 views

www.biomedcentral.com/...1477-7827-4-51.pdf

5-beta androstanediol androgen metabolites ER beta ER-beta estrogen receptors ER

shared by Nathan Goodyear on 06 Jul 13 - No Cached
  • Nathan Goodyear on 06 Jul 13
     
    5-beta androstanediol doesn't have affinity for androgen receptors, but for estrogen receptors. Affinity for ER beta exceeds that for ER alpha.
Nathan Goodyear

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

joe.endocrinology-journals.org/...R47.full

testosterone hormone health disease hormones men male cardiovascular disease CVD

shared by Nathan Goodyear on 13 May 13 - No Cached
  • 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
  • Nathan Goodyear on 13 May 13
     
    Good deep look into the testosterone and CVD link.
Nathan Goodyear

New Frontiers in Androgen Biosynthesis and Metabolism - 0 views

www.ncbi.nlm.nih.gov/...PMC3206266

androgen androgens metabolites prostate cancer hormones

shared by Nathan Goodyear on 15 Jul 15 - No Cached
  • Nathan Goodyear on 15 Jul 15
     
    great article on androgen metabolism in the diseased prostate.
Nathan Goodyear

Activity and expression of progesterone metabolizing 5α-reductase, 20α-hydrox... - 0 views

www.ncbi.nlm.nih.gov/...PMC154104

progesterone metabolites breast cancer 5alpha-reductase 5-alpha pregnene 5-alpha pregnenes 4-pregnene 4-pregnenes

shared by Nathan Goodyear on 30 Jan 14 - No Cached
  • Exposure of human breast cell lines (MCF-7, MCF-10A, and ZR-75-1) to 5α-pregnanes results in changes associated with neoplasia, including increased proliferation and decreased attachment [1], depolymerization of F-actin [2] and decreases in adhesion plaque-associated vinculin
  • Exposure to 4-pregnenes results, in general, in opposite (anti-cancer-like) effects
  • 5αR1 has been detected in various androgen-independent organs, such as the liver and brain
  • ...10 more annotations...
  • 5αR2 has been found predominantly in androgen-dependent organs, such as epididymis and prostate
  • The 5α-pregnanes:4-pregnenes ratio was about 8-fold higher in tumorous than in nontumorous breast tissue after an 8-hour incubation with [14C]progesterone
  • Studies with breast cell lines, showing that 5α-pregnanes stimulate proliferation and decrease attachment of cells
  • both tissue and breast cell line studies suggest that an elevated level of progesterone 5α-reductase activity may be an indicator of breast tumorigenesis, regardless of presence or absence of ER and/or PR
  • 5αR1 is the main isoform expressed in human breast carcinomas [29] and that 5αR2 may not be associated with risk of breast cancer
  • the differences in 5α-pregnane production between the cells is due primarily to a difference in 5αR1 expression
  • As in the case of 5α-reductase activity, the presence or absence of ER and PR do not appear to be related to 5α-reductase expression.
  • the conversion of progesterone to the cancer promoting 5α-pregnanes is significantly higher in the human tumorigenic breast cell lines
  • lthough both 5αR1 and 5αR2 are expressed by these cells, the elevated 5α-reductase activity appears to be the result of significantly greater expression of 5αR1
  • Changes in progesterone metabolizing enzyme expression (resulting in enzyme activity changes) may be responsible for promoting breast cancer progression due to increased production of tumor-promoting 5α-pregnanes and decreased production of anti-cancer 20α – and 3α-4-pregnenes
  • Nathan Goodyear on 30 Jan 14
     
    balance of enzyme production between 5alpha-reductase and 20alpha-hydroxysteroid oxidoreductase and 3alpha(beta)-hydroxysteroid oxidoreductase play role in carcinogenesis and proliferation in the balance of production of progesterone metabolites. The 5alpha pregnenes are pro carcinogenic  and the 4-pregnenes are anti carcinogenic.
Nathan Goodyear

Associations between serum phthalates and biomar... [Environ Int. 2014] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...24583187

phthalates androgen receptors AR toxins hormones men male

shared by Nathan Goodyear on 04 Mar 14 - No Cached
  • Nathan Goodyear on 04 Mar 14
     
    Phthalates have both central inhibition and peripheral effects. This article highlights the peripheral anti-androgen effects of phthalates and phthalate metabolites. 
Nathan Goodyear

Promoting effects and mechanisms of action of androgen in bladder c... - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...9129932

bladder cancer bladder cancer Testosterone men male hormone hormones

shared by Nathan Goodyear on 04 Jan 15 - No Cached
  • Nathan Goodyear on 04 Jan 15
     
    Another animal study finds Testosterone plays a role in bladder cancer development.  The study used anti androgen and 5 alpha reductase inhibitor therapy to see if these add on therapies provided anything to ADR whether via castration or pituitary suppression--the answer was no.  The authors concluded that Testosterone played more of a role with AR versus the more active 5alpha-DHT metabolite.
Nathan Goodyear

The androgen metabolite 5alpha-androstane-3beta,17beta-diol (3betaAdiol) induces breast... - 0 views

www.researchgate.net/...aromatase_inhibitor_resistance

breast cancer aromatase aromatase inhibitors estradiol estrogen 3-beta androstanediol Testosterone DHT 3 beta HSD receptor receptors ER alpha ER-alpha ER beta ER-beta hormone hormones women

shared by Nathan Goodyear on 21 Jan 14 - No Cached
  • Nathan Goodyear on 21 Jan 14
     
    Great article!!  Nice discussion of the complexity of hormones.  Women on aromatase inhibitors can make estrogen from Testosterone.  This is important with estrogen sensitive cancer as in breast cancer.  This will occur via alternative pathways: Testosterone to DHT via 5 alpha reductase and then DHT to 3 beta androstanediol via 3 beta HSD.  3 beta androstanediol is a male hormone metabolite that binds to estrogen receptors.  The affinity is less than Estradiol, but appears to have a higher affinity for ER beta over ER alpha. 
Nathan Goodyear

Extranuclear Actions of the Androgen Receptor Enhance Glucose-Stimulated Insulin Secret... - 0 views

www.cell.com/...S1550-4131(16)30118-8

Testosterone low Testosterone low T hormones male hormones DHT dihydrotestosterone insulin AR androgen receptor Diabetes

shared by Nathan Goodyear on 18 May 16 - No Cached
  • Nathan Goodyear on 18 May 16
     
    only abstract available here. Mouse model finds possible explanation for low Testosterone and diabetes link.  Actually, the link is between the metabolite DHT and the AR. The activity of AR from DHT binding induces beta cell insulin secretion in the presence of glucose.  This is dependent on glucagon-like peptide 1 receptor activation also, which AR activation by DHT does in fact do.
Nathan Goodyear

Estrogen signaling and disruption of androgen metab... [Prostate. 2007] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...17075824

cadmium prostate cancer AR androgen receptors ER male hormone hormones men

shared by Nathan Goodyear on 06 Feb 14 - No Cached
  • Nathan Goodyear on 06 Feb 14
     
    Cadmium exposure/toxicity promotes prostate tumor growth and it does this via a AR independent process.  The authors propose that it is via estrogen receptors and estrogen signaling from DHT metabolites.
Nathan Goodyear

Analysis of Relations between serum levels of Epitestosterone, Estradiol, Testosterone,... - 0 views

www.biomed.cas.cz/...49_S113.pdf

PSA hormone hormones BPH Prostate cancer prostate cancer Epitestosterone men male aromatase Estradiol IGF-1

shared by Nathan Goodyear on 21 Aug 13 - No Cached
  • Nathan Goodyear on 21 Aug 13
     
    Great confusion exists in the medical profession about Testosterone and PSA and the health of the prostate. The conversion of Estrogen, whether E2 or E1, and other variables are responsible for increases in PSA while on Testosterone therapy. This study points out that Estradiol in men stimulates cell line growth of prostate cancer. In contrast, Epitestosterone, an androgen metabolite, has antiandrogen, inhibits this estrogen activity. Epitestosterone exists in an inverse relationship to Estradiol and IGF-1.
Nathan Goodyear

Aromatase and regulation of the estrogen-to... [Ann N Y Acad Sci. 2014] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...24684533

aromatase aromatase activity vitamin D estrone E1 inflammation RA rheumatoid arthritis

shared by Nathan Goodyear on 07 Apr 14 - No Cached
  • Nathan Goodyear on 07 Apr 14
     
    Study looked at inflammatory markers in RA.  The authors point to high aromatase activity, low androgens, and elevated estrone in synovial fluid as an indicator of a link between aromatase activity and inflammation production through E1 production.  The authors also point to the 16 alpha metabolite pathway as pro-inflammatory as well.  One very interesting point made by the authors is that vitamin D down regulates aromatase activity.  In addition to NK-kappaB inhibition, this may be another mechanism by which vitamin D reduces inflammation.
Nathan Goodyear

The safety of testosterone supplementation ther... [Nat Rev Urol. 2014] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...25069737

prostate cancer testosterone men male hormone hormones

shared by Nathan Goodyear on 30 Jul 14 - No Cached
  • Nathan Goodyear on 30 Jul 14
     
    Review, only abstract available--Testosterone therapy does not affect prostate size, intraprostatic Testosterone levels, or prostate cancer progression.  Carcinogenesis of the prostate is not a androgen driven process.  It is an aromatase process.  DHT metabolites can promote tumor growth via Estrogen receptors later, but initiation, via all accounts, occurs through aromatase expression and production of estrogen in the prostate.
Nathan Goodyear

Differential Effects of Dehydroepiandrosterone and Testosterone in Prostate and Colon C... - 0 views

press.endocrine.org/...en.2012-2249

testosterone prostate colon colon cancer cancer NGF nerve growth factor dhea dehydroepiandrosterone

shared by Nathan Goodyear on 19 Nov 14 - No Cached
  • Several studies indicate that DHEA may enhance cancer-promoting activities in several prostate cancer cell lines acting as agonist or antagonist for the intracellular AR
  • the estrogenic metabolites of DHEA, 5a-androstane-3b, 17b-diol (3b-Adiol) and E2 bind to estrogen receptors but not to AR
  • no specific receptor has been identified for DHEA
  • ...16 more annotations...
  • Different members of neurotrophins are expressed during cancer progression, suggesting their involvement in cell proliferation, anoikis protection, and malignancy
  • Regulation of the apoptotic machinery in prostate and colon cancer cells by testosterone occurs rapidly and is initiated at the plasma membrane level through specific membrane-binding sites not involving the classical cytoplasmic AR
  • testosterone exerts potent regulatory effects on prostate and colon cancer cell apoptosis
  • Testosterone increased cell death in a dose-dependent manner
  • testosterone antagonizes the prosurvival effects of DHEA in neuronal cells, blocking its binding to NGF receptors
  • treatment of cells with DHEA exerted a strong antiapoptotic effect,
  • Androgens hold a central role in prostate and colon cancer biology
  • elevated levels of DHEA or its sulfate ester DHEA-sulfate in young adults are associated to low incidence of androgen-dependent tumors
  • DHEA may play a protective role in young prostate
  • The decline of DHEA with aging may contribute to prostate cancer progression associated with advanced age
  • DHEA is an effective antiapoptotic factor, reversing the serum deprivation-induced apoptosis in prostate cancer cells (DU145 and LNCaP cell lines) as well as in colon cancer cells
  • NGF appears to exert similar antiapoptotic actions in both prostate and color cancer cells
  • exposure of prostate DU145 and colon Caco2 cancer cells to testosterone totally blocked the protective effects of both DHEA and NGF. These findings suggest that testosterone acts as an antagonist of DHEA and NGF
  • These findings support the hypothesis that testosterone may inhibit cancer cell growth by antagonizing the proliferative, antiapoptotic effects of endogenous factors, such as DHEA or NGF, in the case of prostate and colon cancer cells
  • intratumor hormonal microenvironment may play a critical role in tumor progression.
  • The paracrine interactions of androgens with locally produced NGF may define tumor cell fate
  • Nathan Goodyear on 19 Nov 14
     
    Full article of previously posted abstract.  Cancers are unique.  Not all cancers are alike.  Whether they are tissue specific or not, cancers are unique.  This article describes the uniqueness of DHEA and Testosterone cancer, with particular attention to colon.
Nathan Goodyear

Production of 3α-Androstanediol Glucuronide in Human Genital Skin - 0 views

jcem.endojournals.org/...711

DHT 3 alpha-androstanediol human androgens testosterone skin

shared by Nathan Goodyear on 22 Apr 13 - No Cached
  • Nathan Goodyear on 22 Apr 13
     
    DHT metabolite 3 alpha-androstanediol shown to be a good assessment of peripheral DHT action.
Nathan Goodyear

http://www.europeanurology.com/article/S0302-2838(08)01435-8/pdf/Oestrogens+and+Prostat... - 0 views

www.europeanurology.com/...el+Concepts+about+an+Old+Issue

prostate cancer estrogen 3-beta androstanediol DHT androgens Testosterone male men hormone hormones

shared by Nathan Goodyear on 20 Jan 14 - No Cached
  • Nathan Goodyear on 20 Jan 14
     
    Nice review of the proposed complex interaction between hormones and prostate cancer.  The complex nature of the development of cancer will likely eliminate the complete elucidation of the mechanism of prostate cancer.  However, there are many pieces that would favor: increased aromatase activity appears to play a significant role int he development of prostate cancer, clearly intraprostatic hormones are different than serum making serum evaluation of sex hormones irrelevant--the move should be to salivary hormones, and the growing knowledge of DHT metabolites in the protection of prostate cancer--3 beta androstanediol.
Nathan Goodyear

Hormones and prostate carcinogenesis: Androgens and estrogens Bosland MC, Mahmoud AM - ... - 0 views

www.carcinogenesis.com/article.asp

prostate cancer Testosterone DHT estrogen estradiol male hormone hormones

shared by Nathan Goodyear on 06 Feb 14 - No Cached
  • Nathan Goodyear on 06 Feb 14
     
    Testosterone, metabolites and prostate carcinogenesis.
Nathan Goodyear

Endocrinology of the Aging Male - 0 views

www.ncbi.nlm.nih.gov/...PMC3073592

aging male hormone hormones

shared by Nathan Goodyear on 30 Apr 13 - No Cached
  • All steps beyond the formation of pregnenolone take place in the smooth endoplasmic reticulum
  • Cytochrome P450 enzyme, CYP11A is located on the inner mitochondrial membrane and catalyses the rate limiting step of pregnenolone synthesis
  • Estrogen and related steroids, thyroid hormone and insulin increase SHBG levels.
  • ...21 more annotations...
  • SHBG decreases in response to androgens, and in the presence of hypothyroidism, and insulin resistance.
  • Plasma SHBG levels tend to increase with increasing age
  • The apparent metabolic clearance rate of testosterone is decreased in elderly as compared to younger men
  • Testosterone circulates predominantly bound to the plasma proteins SHBG and albumin, with high and low affinity respectively
  • Testosterone is secreted in a pulsatile fashion
  • Current clinical guidelines suggest at least two measurements
  • In adult men, there is a well-documented diurnal variation (particularly in younger subjects) in testosterone levels, which are highest in the early morning and progressively decline throughout the day to a nadir in the evening
  • In older men, the diurnal variation is blunted
  • it is standard practice for samples to be obtained between 0800 and 1100 h.
  • Testosterone and DHEA decline, whereas LH, FSH, and SHBG rise
  • DHT remains constant despite the decline of its precursor testosterone
  • Longitudinal studies show an average annual decline of 1–2% total testosterone levels, with decline in free testosterone more rapid because of increases in SHBG with aging
  • Massachusetts Male Aging Study (MMAS) data show DHEA, DHEAS, and Ae declining at 2–3% per year
  • DHT showed no cross-sectional age trend
  • Androstanediol glucuronide (AAG) declined cross-sectionally with age in the MMAS sample, at 0.6% per year
  • The EMAS data show that, consistent with the longitudinal findings of MMAS (Figure 1), the core hormonal pattern with increasing age is suggestive of incipient primary testicular dysfunction with maintained total testosterone and progressively blunted free testosterone associated with higher LH
    • Nathan Goodyear
      Nathan Goodyear on 01 May 13
       
      This author proves the point in the review of these two studies, that TT may remain constant in aging men, however, FT drops.
  • obesity impairs hypothalamic/pituitary function
  • Androgen deprivation in men with prostate cancer has been associated with increased insulin resistance, worse glycemic control, and a significant increase in risk of incident diabetes
  • Low serum testosterone is associated with the development of metabolic syndrome 116, 117 and type 2 diabetes. 118 SHBG has been inversely correlated with type 2 diabetes
  • Improvement in insulin sensitivity with testosterone treatment has been reported in healthy 121 and diabetic 122 adult men
  • In studies conducted in men with central adiposity, testosterone has been shown to inhibit lipoprotein lipase activity in abdominal adipose tissue leading to decreased triglyceride uptake in central fat depots. 123
  • Nathan Goodyear on 30 Apr 13
     
    great review of hormone changes associated with aging in men.
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
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