steroid hormones typically interact with their cognate receptor in the cytoplasm for AR, glucocorticoid receptor (GR) and PR, but may also bind receptor in the nucleus as appears to often be the case for ERα and ERβ
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Communication between genomic and non-genomic signaling events coordinate steroid hormo... - 0 views
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This ligand binding results in a conformational change in the cytoplasmic NRs that leads to the dissociation of HSPs, translocation of the ligand-bound receptor to the nucleus
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In the nucleus, the ligand-bound receptor dimerizes and then binds to DNA at specific HREs to regulate gene transcription
- ...25 more annotations...
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the genomic effects of steroid hormones take longer, with changes in gene expression occurring on the timescale of hours
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Classical steroid hormone signaling occurs when hormone binds nuclear receptors (NR) in the cytoplasm, setting off a chain of genomic events that results in, among other changes, dimerization and translocation to the nucleus where the ligand-bound receptor forms a complex with coregulators to modulate gene transcription through direct interactions with a hormone response element (HRE)
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NRs have been found at the plasma membrane of cells, where they can propagate signal transduction often through kinase pathways
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Membrane-localized ER, PR and AR have been reported to modulate the activity of MAPK/ERK, phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), nitric oxide (NO), PKC, calcium flux and increase inositol triphosphate (IP3) levels to promote cell processes including autophagy, proliferation, apoptosis, survival, differentiation, and vasodilation
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ERα36, a 36kDa truncated form of ERα that lacks the transcriptional activation domains of the full-length protein. Membrane-localized ERα36 can activate pathways including protein kinase C (PKC) and/or mitogen activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) to promote the progression of various cancers
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G protein-coupled receptor 30 (GPR30), also referred to as G protein-coupled estrogen receptor (GPER), is a membrane-localized receptor that has been observed to respond to estrogen to activate rapid signaling
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androgen-mediated non-genomic signaling through this GPCR can modulate male fertility, hormone secretion and prostate cancer progression
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non-NR proteins located at the cell surface can bind to steroid hormones and respond by eliciting rapid signaling events
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Estrogens have been shown to induce rapid (i.e. seconds) calcium flux via membrane-localized ER (mER)
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ER-calcium dynamics lead to activation of kinase pathways such as MAPK/ERK which can result in cellular effects like migration and proliferation
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A similar crosstalk occurs between the receptor tyrosine kinase insulin-related growth factor-1 receptor (IGF-IR) and ERα. Not only does IGF-IR activate ERα, but inhibition of IGF-IR downregulates estrogen-mediated ERα activity, suggesting that IGF-IR is essential for maximal ERα signaling
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androgen-bound AR associates with the kinase Src at the plasma membrane, activating Src which then leads to a signaling cascade through MAPK/ERK
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However, Src can also increase the expression of AR target genes by the ligand-independent transactivation of AR
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estrogen modulated the expression of several genes including endothelial nitric oxide synthase (eNOS) via rapid signaling pathways
34More
Progesterone metabolites in breast cancer - 1 views
erc.endocrinology-journals.org/...717.full
progesterone metabolism tumor tumorigenesis cancer risk growth hormone hormones 5-beta-pregnanediol 5-alpha-pregnanediol 4-pregnenediol 5-alpha reductase
shared by Nathan Goodyear on 20 Feb 12
- No Cached
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P metabolites produced within breast tissues might be independently active hormones functioning as cancer-promoting or -inhibiting regulatory agents
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these P metabolites function as independent pro-or anti-cancer autocrine/paracrine hormones that regulate cell proliferation, adhesion, apoptosis and cytoskeletal, and other cell status molecules via novel receptors located in the cell membrane and intrinsically linked to cell signaling pathways
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only a fraction of all breast cancer patients respond to this estrogen-based therapy and the response is only temporary
- ...30 more annotations...
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P serves as the precursor for the major steroid hormones (androgens, estrogens, corticosteroids) produced by the gonadal and adrenal cortical tissues.
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These P-metabolizing enzymes included 5α-reductase, 5β-reductase, 3α-hydroxysteroid oxido-reductase (3α-HSO), 3β-HSO, 20α-HSO, 20β-HSO, 6α(β)-, 11β-, 17-, and 21-hydroxylase, and C17–20-lyase
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Reduction of P to 5α-pregnanes is catalyzed by 5α-reductase and the direct 5α-reduced metabolite of P is 5α-pregnane-3,20-dione (5αP). The 5α-reductase reaction is irreversible
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The two 4-pregnenes resulting from direct P conversion are 4-pregnen-3α-ol-20-one (3αHP) and 4-pregnen-20α-ol-3-one (20αHP), catalyzed by the actions of 3α-HSO and 20α-HSO respectively
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the P-metabolizing enzyme activities identified in human breast tissues and cell lines were: 5α-reductase, 3α-HSO, 3β-HSO, 20α-HSO, and 6α-hydroxylase
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In normal breast tissue, conversion to 4-pregnenes greatly exceeded the conversion to 5α-pregnanes, whereas in tumorous tissue, conversion to 5α-pregnanes greatly exceeded that to 4-pregnenes
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The results indicated that P 5α-reductase activity is significantly higher, whereas P 3α-HSO and 20α-HSO activities are significantly lower in tumor than in normal tissues
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he results showed that production of 5α-pregnanes was higher and that of 4-pregnenes was lower in tumorigenic (e.g. MCF-7) than in nontumorigenic (e.g. MCF-10A) cells (Fig. 3c⇑), while differences in ER/P status did not appear to play a role
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The 5α-pregnane-to-4-pregnene ratios were 7- to 20-fold higher in the tumorigenic than in the nontumorigenic cell lines
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altered direction in P metabolism, and hence in metabolite ratios, was due to significantly elevated 5α-reductase and depressed 3α- and 20α-HSO activities in breast tumor tissues and tumorigenic cells. It appeared, therefore, that changes in P-metabolizing enzyme activities might be related to the shift toward mammary cell tumorigenicity and neoplasia
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In vivo, changes in enzyme activity can result from changes in levels of the enzyme due to changes in expression of the mRNA coding for the enzyme, or from changes in the milieu in which the enzyme operates (such as temperature and pH, and concentrations of cofactors, substrates, products, competitors, ions, phospholipids, and other molecules)
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Overall, the enzyme activity and expression studies strongly suggest that 5α-reductase stimulation and 3α- and 20α-HSO suppression are associated with the transition from normalcy to cancer of the breast
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The level of expression of 5α-reductase is up-regulated by estradiol and P in the uterus (Minjarez et al. 2001) and by 5α-dihydrotestosterone (DHT) in the prostate
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Stimulation in cell numbers was also observed when cells were treated with other 5α-pregnanes, such as 5α-pregnan-3α-ol-20-one, 5α-pregnan-20α-ol-3-one, and 5α-pregnane-3α,20α-diol, whereas other 4-pregnenes such as 20α-HP and 4-pregnene-3α,20α-diol resulted in suppression of cell proliferation
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Stimulation of cell proliferation with 5αP and inhibition with 3αHP were also observed in all other breast cell lines examined, whether ER/P-negative (MCF-10A, MDA-MB-231) or ER/P-positive (T47D, ZR-75-1) and whether requiring estrogen for tumorigenicity (MCF-7, T47D) or not (MDA-MB-231), or whether they are nontumorigenic (
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αHP resulted in significant increases in apoptosis and decreases in mitosis, leading to significant decreases in total cell numbers. In contrast, treatment with 5αP resulted in decreases in apoptosis and increases in mitosis.
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The opposing actions of 5αP and 3αHP on both cell anchorage and proliferation strengthen the hypothesis that the direction of P metabolism in vivo toward higher 5α-pregnane and lower 4-pregnene concentrations could promote breast neoplasia and lead to malignancy.
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The studies showed that binding of 5αP or 3αHP occurs in the plasma membrane fractions, but not in the nuclear or cytosolic compartments
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separate high-specificity, high-affinity, low- capacity receptors for 5αP and 3αHP that are distinct from each other and from the well-studied nuclear/cytosolic P, estrogen, and androgen and corticosteroid receptors
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The studies thus provided the first demonstration of the existence of specific P metabolite receptors
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the receptor results suggest that the putative tumorigenic actions of 5αP may be significantly augmented by the estradiol-induced increases in 5αP binding and decreases in 3αHP binding.
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Estradiol and 5αP resulted in significant dose-dependent increases, whereas 3αHP and 20αHP each resulted in dose-dependent decreases in total ER
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In combination, estradiol + 5αP or 3αHP + 20αHP resulted in additive increases or decreases respectively in ER numbers.
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The data suggest that the action of 5αP on breast cancer cells involves modulation of the MAPK signaling pathway
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current evidence does not appear to support the notion that increased 5α-reductase activity/ expression might significantly alter androgen influences on breast tumor growth.
35More
Progesterone metabolites regulate induction, growth, and suppression of estrogen- and p... - 0 views
www.ncbi.nlm.nih.gov/...PMC3706910
progesterone metabolites metabolite 5-alpha pregnene 5-alpha pregnenes 5alpha-dihydroprogesterone 4-pregnene 4-pregnenes 3alpha-dihydroprogesterone breast cancer ER PR hormone hormones receptors estrogen
shared by Nathan Goodyear on 28 Jan 14
- No Cached
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in vitro studies had shown that the progesterone metabolites, 5α-dihydroprogesterone (5αP) and 3α-dihydroprogesterone (3αHP), respectively, exhibit procancer and anticancer effects on receptor-negative human breast cell lines
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Onset and growth of ER/PR-negative human breast cell tumors were significantly stimulated by 5αP and inhibited by 3αHP
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When both hormones were applied simultaneously, the stimulatory effects of 5αP were abrogated by the inhibitory effects of 3αHP and vice versa
- ...31 more annotations...
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Treatment with 3αHP subsequent to 5αP-induced tumor initiation resulted in suppression of further tumorigenesis and regression of existing tumors
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Tumorigenesis of ER/PR-negative breast cells is significantly enhanced by 5αP and suppressed by 3αHP, the outcome depending on the relative concentrations of these two hormones in the microenvironment in the breast regions
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The findings show that the production of 5αP greatly exceeds that of 3αHP in ER/PR-negative tumors and that treatment with 3αHP can effectively block tumorigenesis and cause existing tumors to regress
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hypothesis that a high 3αHP-to-5αP concentration ratio in the microenvironment may foster normalcy in noncancerous breast regions.
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Our previous in vitro studies had shown that breast tissues and cell lines readily convert progesterone to 5α-pregnanes, such as 5αP, and delta-4-pregnenes, such as 3αHP (Figure (Figure1),1), and that tumorous breast tissues [15] and tumorigenic breast cell lines [16] produce higher levels of 5αP and lower levels of 3αHP than do normal breast tissues and nontumorigenic cell lines
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The progesterone metabolism studies suggested that increases in 5αP and decreases in 3αHP production accompany the shift toward breast cell neoplasia and tumorigenicity
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In vitro studies on five different human breast cell lines showed that cell proliferation and detachment are significantly increased by 5αP and decreased by 3αHP
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the prevailing theory of hormonal regulation of breast cancer, as well as hormone-based therapies, revolves around estrogen and/or progesterone and ER/PR-positive breast cells and tumors.
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Not only do these "receptor-negative" breast cancers fail to benefit from current hormonal therapies, but they also generally exhibit more-aggressive biologic behaviors and poorer prognosis than the receptor-positive ones
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The results of the studies reported here show for the first time that the progesterone metabolites, 5αP and 3αHP, act as hormones that regulate ER/PR-negative breast tumor formation, growth, and regression
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The onset of the ER/PR-negative human breast cell tumors in mice was considerably accelerated, and the growth significantly stimulated, by just one or two applications of 5αP
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In contrast, 3αHP retarded onset of tumor formation, suppressed tumor growth, and inhibited or regressed existing 5αP-induced tumors
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When both hormones were administered simultaneously, the effects of one were abrogated by the effects of the other.
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The 5αPR and 3αHPR (which are associated with the plasma membranes of both ER/PR-positive [19] and ER/PR-negative [29] cells) are distinct from each other and from known ER, PR, androgen, and corticosteroid receptors, and lack affinity for other steroids, such as progesterone, estrogen, androgens, corticosteroids, and other progesterone metabolites
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Levels of 5αPR are upregulated by 5αP itself and estradiol, and downregulated by 3αHP in both ER/PR-positive and -negative cells
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ndications are that 5αP acts via the surface receptor-linked mitogen-activated protein kinase (MAPK; Erk1/2) pathway; 5αP significantly stimulates activation of Erk1/2 [30], increases the Bcl-2/Bax expression ratio [18] and actin depolymerization [31], and decreases expression of actin and adhesion plaque-associated vinculin [31], resulting in decreased apoptosis and increased mitosis and cell detachment
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3αHP appears to suppress protein kinase C (PKC), phospholipase C (PLC), Ca2+ mobilization (unpublished observations), and the Bcl-2/Bax expression ratio [18], and increases expression of the cell-cycle inhibitor p21 [18], resulting in increased apoptosis and decreased proliferation and detachment of breast cell lines.
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the tumors, which on average had about threefold higher concentrations of 5αP than the respective sera, and >10-fold higher 5αP than 3αHP levels
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Previous in vitro metabolism studies showed that human breast tumor tissues convert significantly more progesterone to 5α-pregnanes like 5αP and less to 4-pregnenes like 3αHP than do paired normal (nontumorous) tissues
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Similar differences in progesterone metabolism and enzyme gene expressions were observed between tumorigenic and nontumorigenic breast cell lines
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The current findings, along with the previous in vitro studies, suggest that the relative concentrations of 5αP and 3αHP in the breast microenvironment constitute important autocrine/paracrine determinants not only for tumorigenesis but also for potential regression of tumors and the maintenance of normalcy of ER/PR-negative breast cells/tissues.
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Evidence presented here shows that a high concentration of 5αP, relative to 3αHP in the microenvironment, promotes initiation and growth of tumors, whereas a higher concentration of 3αHP, relative to 5αP, suppresses tumorigenesis and promotes normalcy
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in the 3αHP-treated mice, the elevated 3αHP levels, relative to 5αP, in the microenvironment could have opposed progression to xenograft neoplasia by its inherent anticancer actions and the suppression of 5αP synthesis and 5αPR expression
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the opposing actions of the progesterone metabolites also appear to exert some control over the estrogen-regulated effects on breast cancer by their ability to modulate ER numbers in ER-positive cells
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because both ER/PR-negative and ER/PR-positive, as well as normal and tumorigenic human breast cell lines, have been shown to respond to 5αP and 3αHP in vitro, it is suggested that these endogenously produced progesterone metabolites may also play regulatory hormonal roles in ER/PR-positive breast cancers, as well as in the maintenance of normalcy in nontumorous breast tissues.
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The in vivo data provide further evidence that progesterone metabolites, such as 5αP and 3αHP, deserve to be considered as active hormones in their own right, rather than inactive waste products
1More
Oral estrogen antagonizes the metabolic actions of growth hormone in growth hormone-def... - 0 views
ajpendo.physiology.org/...E1191.long
oral estrogen oral estrogen HGH human growth hormone growth hormone IGF-1 hormone hormones therapy
shared by Nathan Goodyear on 19 Feb 13
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One really wonders if estrogen should ever be given orally at all. Though this study is small, this is consistent with other studies that show that estrogen therapy, particularly oral therapy interferes with growth hormone signaling and thus action. Oral estrogen decreases IGF-1, increases growth hormone binding protein, lowers metabolism and reduces protein metabolism as monitored by leucine turnover.
1More
Neuroprotection of Sex Steroids - 0 views
www.ncbi.nlm.nih.gov/...PMC3036837
hormones estrogen progesterone testosterone sex hormones brain neurology neuroprotection neuroprotective hormones hormone
shared by Nathan Goodyear on 10 Jul 12
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great article on sex hormones and neuroprotection. This article summarizes the research on estrogen, progesterone, and aromatase activity in in vitro and in vivo studies. Additionally, the study reviews the androgenic neuroprotection in men. Who has said that hormones are not needed post menopausal again? Maybe, that is the sign that they need the neuroprotective effect of hormones.
1More
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
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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.
20More
Longitudinal Effects of Aging on Serum Total and Free Testosterone Levels in Healthy Me... - 0 views
press.endocrine.org/...jcem.86.2.7219
low t low Testosterone Testosterone SHBG FAI free androgen index male hormone hormones aging obesity
shared by Nathan Goodyear on 30 Mar 15
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NUMEROUS CROSS-SECTIONAL INVESTIGATIONS have demonstrated lower concentrations of circulating testosterone (T) and/or free T in older men
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T levels decline at a more or less constant rate, with age, in men, with no period of accelerated decline
- ...15 more annotations...
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aging in men is associated with decreases in bone mineral density (BMD) (18, 19), lean body and muscle mass
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strength (22, 23) and aerobic capacity (24), as well as with increases in total and abdominal body fat, low-density lipoprotein cholesterol, and/or low-density lipoprotein/high-density lipoprotein cholesterol ratios (25, 26, 27, 28), all of which also occur in nonelderly hypogonadal men
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Most (1, 5, 6, 7, 8, 9), but not all (10, 11, 12), cross-sectional studies have demonstrated a decrease, with age, in total T in men
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total T, but not free T index, tended to decrease with greater BMI is consistent with prior studies showing that obesity is associated with decreases in both SHBG and total T, with an unchanged T-to-SHBG ratio
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The conventional definition for T levels is statistical (values more than 2 sd below the mean), rather than functional. Such a definition does not reflect clinical realities, such as the existence of characteristic individual set points for circulating hormone levels, below which one, but not another, individual may develop metabolic changes of hormone deficiency; nor does it address the concept of reserve capacity, the possibility that persons with hormone levels 2 sd below the population mean still may have adequate hormone concentrations to meet their metabolic needs.
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both T and free T index (a calculated value related to free or bioavailable T) decreased progressively at a rate that did not vary significantly with age, from the third to the ninth decades.
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contrasts with other studies showing diminished free, as well as total, T in with increasing total (48) or abdominal (49) obesity in men.
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Our analysis of date-adjusted T and free T index levels, by decade, showed that relatively high numbers of older men in this generally healthy population had at least one hypogonadal value (defined as below the 2.5th percentile for young men)
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The issue of how properly to define hypogonadism, or indeed any hormone deficiency, remains problematic
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The decrease in free T index was somewhat steeper than that of total T, owing to a trend for an increase in SHBG with age
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It would clearly be better to define the lower limit of normal for a hormone as: the blood level at which metabolic and/or clinical sequelae of hormone deficiency begin to appear, or the level below which definite benefits can be demonstrated for hormone supplementation for a significant proportion of the population
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an effect of aging to lower both total and bioavailable circulating T levels at a relatively constant rate, independent of obesity, illness, medications, cigarette smoking, or alcohol intake
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Article highlights the problems with the definition of low T. This article finds consistent decline in Total Testosterone and FAI with increasing age groups, with a significant portion of men > 60 meeting the required levels for "low T". This study found a decrease in total T and FAI at a consistent rate independent of variables, such as BMI. This study did find a decrease in SHBG and total T with obesity; in contrast to other studies.
1More
Salivary Sex Hormone Measurement in a National, Population-Based Study of Older Adults - 0 views
www.ncbi.nlm.nih.gov/...PMC2763516
hormone hormones saliva salivary estradiol progesterone testosterone DHEA testing
shared by Nathan Goodyear on 16 Oct 12
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Another study supports saliva hormone testing. This study involved 2,722 individuals and tested estradiol, progesterone, DHEA and testosterone in men and women. All of these are sex hormones. Someone needs to tell the insurance companies that the overwhelming evidence supports saliva hormone testing. But, that would mean they are even interested in the science.
1More
Hormone therapy and Alzheimer disease dementia: Ne... [Neurology. 2012] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...23100399
alzheimer disease dementia hormone HRT hormones Alzheimer's neurology
shared by Nathan Goodyear on 01 Nov 12
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study finds that HRT given as women transition through menopause has benefiical effect in people with Alzheimer's. However, when given years later, after menopause, no benefit is found. In fact, rates increased. Several flaws with this study. First, they used synthetic hormones, particularily progestins. Second, there seems to be no thought that the interpretation of the signal has changed. For example, we know that when men have low T, their estrogen receptor status changes from ER beta to ER alpha, which is more proinflammatory. Third, use bioidentical hormones and compare these to synthetic hormones.
1More
JAMA Network | Archives of Internal Medicine | Combined Estrogen and Testosterone Use a... - 0 views
archinte.jamanetwork.com/article.aspx
hormones synthetic bioidentical BHRT breast cancer estrogen testosterone
shared by Nathan Goodyear on 16 May 12
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this study revealed increased breast cancer risk in women on "estrogen" and "testosterone" therapy. Now, several problems here: first, are these synthetic hormone or bioidentical. Second, the dosages appear, in what is written, to be supra physiologic. Third, giving supra physiologic estradiol and testosterone will obviously create imbalances and growth potential. Fourth, how were the women evaluated prior to starting hormone therapy and then were they remonitered (unlikely), fifth, were hormone metabolites evaluated (too, also unlikely). This study has serious flaws and very little can be extrapolated other than: don't take supra physiologic hormone levels without appropriate evaluation. Enough said
1More
Hormonal aspects of overtraining syndrome: a systematic review | BMC Sports Science, Me... - 0 views
26More
Endocrinology of the Aging Male - 0 views
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Cytochrome P450 enzyme, CYP11A is located on the inner mitochondrial membrane and catalyses the rate limiting step of pregnenolone synthesis
- ...21 more annotations...
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SHBG decreases in response to androgens, and in the presence of hypothyroidism, and insulin resistance.
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The apparent metabolic clearance rate of testosterone is decreased in elderly as compared to younger men
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Testosterone circulates predominantly bound to the plasma proteins SHBG and albumin, with high and low affinity respectively
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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
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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
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Androstanediol glucuronide (AAG) declined cross-sectionally with age in the MMAS sample, at 0.6% per year
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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
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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
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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
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Improvement in insulin sensitivity with testosterone treatment has been reported in healthy 121 and diabetic 122 adult men
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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
1More
Regulation of mitochondrial biogenesis by thyroid hormone - 0 views
ep.physoc.org/...121.full.pdf+html
T3 mitochondria thyroid hormone receptors TRH thyroid hormone response elements TRE hormone thyroid
shared by Nathan Goodyear on 29 Jun 13
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1More
Sexual function and hormone profile in young adult men with idiopathic gynecomastia: Co... - 0 views
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somewhat flawed study in that they looked at serum sex hormones to evaluate men with gynecomastia compared to controls. A better eval would have been of saliva or blood spot. Free levels will show more subtle changes physiologically than will serum as to the sex hormones. The study did find decreased sexual function in the men with gynecomastia--indicating hormone issues not picked up by the serum.
1More
Effects of hormones on skin wrinkles and rigidity vary by race/ethnicity: fou... - 0 views
25More
PLOS ONE: Increased Risk of Non-Fatal Myocardial Infarction Following Testosterone Ther... - 0 views
www.plosone.org/...10.1371%2Fjournal.pone.0085805
Testosterone therapy cardiovascular disease men male hormones
shared by Nathan Goodyear on 30 Jan 14
- No Cached
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In men aged 65 years and older the RR was 2.19 (1.27, 3.77), while in men under age 65 years the RR was 1.17
- ...20 more annotations...
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For TT prescription, in men under age 65 years, the RR was 2.90 (1.49, 5.62) for those with a history of heart disease and 0.90 (0.61, 1.34) for those without
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In men aged 65 year and older, the RR was 2.16 (0.92, 5.10) for those with a history of heart disease and 2.21 (1.09, 4.45) for those without.
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Among men aged 65 years and older, we observed a two-fold increase in the risk of MI in the 90 days after filling an initial TT prescription
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Among younger men with a history of heart disease, we observed a two to three-fold increased risk of MI in the 90 days following an initial TT prescription and no excess risk in younger men without such a history
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Among older men, the two-fold increased risk was associated with TT prescription regardless of cardiovascular disease history
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our own findings appear consistent with a higher frequency of thrombotic events following TT prescription among men with more extensive coronary vascular disease.
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Our findings are consistent with a recent meta-analysis of placebo-controlled randomized trials of testosterone therapy lasting 12 or more weeks among mainly older men, which reported that testosterone therapy increased the risk of adverse cardiovascular-related events (OR = 1.54, 95%CI:1.09, 2.18), as well as serious adverse cardiovascular-related events (OR = 1.61, 95%CI:1.01, 2.56) which included myocardial infarction along with other conditions
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This association appeared unrelated to average baseline testosterone level (p = 0.70) but varied by source of funding (p = 0.03), with a stronger summary effect in a meta-analysis of studies not funded by the pharmaceutical industry (OR = 2.06, 95%CI:1.34, 3.17) compared with studies funded by the pharmaceutical industry
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the evidence supports an association between testosterone therapy and risk of serious, adverse cardiovascular-related events–including non-fatal myocardial infarction–in men
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there is some evidence that low endogenous testosterone levels may also be positively associated with cardiovascular events
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effects of endogenous and exogenous testosterone may differ. Exogenous testosterone (TT) is associated with physiologic changes that predispose to clotting and thrombotic disorders including increased blood pressure [18], polycythemia [19], reductions in HDL cholesterol [18], [20], and hyperviscosity of the blood and platelet aggregation. [20]–[23]; TT also increases circulating estrogens [24], [25] which may play a role in the observed excess of adverse cardiovascular-related events, given that estrogen therapy has been associated with this excess in both men and women
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Recently TT has been increasing extraordinarily rapidly, including among younger men and among those without hormone measurement
1More
The dialectic role of progesterone - 0 views
www.sciencedirect.com/...S0378512208003927
progesterone metabolites metabolism progesterone metabolites hormone hormones breast cancer
shared by Nathan Goodyear on 18 Jun 14
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Just the abstract available here. Article states the complexity of hormones found in hormone metabolism. I love the authors quote, "As steroid hormones are known to be converted to many other steroids occupying different receptors and thereby exerting various different effects..." Doesn't fit into the "know your numbers" marketing deception does it?
1More
Sex Steroid Hormone Levels and Body Composition in Men - 0 views
jcem.endojournals.org/...2442.abstract
hormone body composition hormones body composition Testosterone Estradiol E2 T SHBG
shared by Nathan Goodyear on 10 Jun 13
- No Cached
1More