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Nathan Goodyear

Testosterone and glucose metabolism in men: current concepts and controversies - 0 views

joe.endocrinology-journals.org/...R37.full

Low T Testosterone metabolic syndrome MetS Diabetes men male glucose hormone hormones g

shared by Nathan Goodyear on 04 Feb 14 - No Cached
  • Around 50% of ageing, obese men presenting to the diabetes clinic have lowered testosterone levels relative to reference ranges based on healthy young men
  • The absence of high-level evidence in this area is illustrated by the Endocrine Society testosterone therapy in men with androgen deficiency clinical practice guidelines (Bhasin et al. 2010), which are appropriate for, but not specific to men with metabolic disorders. All 32 recommendations made in these guidelines are based on either very low or low quality evidence.
  • A key concept relates to making a distinction between replacement and pharmacological testosterone therapy
  • ...59 more annotations...
  • The presence of symptoms was more closely linked to increasing age than to testosterone levels
  • Findings similar to type 2 diabetes were reported for men with the metabolic syndrome, which were associated with reductions in total testosterone of −2.2 nmol/l (95% CI −2.41 to 1.94) and in free testosterone
  • low testosterone is more predictive of the metabolic syndrome in lean men
  • Cross-sectional studies uniformly show that 30–50% of men with type 2 diabetes have lowered circulating testosterone levels, relative to references based on healthy young men
  • In a recent cross-sectional study of 240 middle-aged men (mean age 54 years) with either type 2 diabetes, type 1 diabetes or without diabetes (Ng Tang Fui et al. 2013b), increasing BMI and age were dominant drivers of low total and free testosterone respectively.
  • both diabetes and the metabolic syndrome are associated with a modest reduction in testosterone, in magnitude comparable with the effect of 10 years of ageing
  • In a cross-sectional study of 490 men with type 2 diabetes, there was a strong independent association of low testosterone with anaemia
  • In men, low testosterone is a marker of poor health, and may improve our ability to predict risk
    • Nathan Goodyear
      Nathan Goodyear on 04 Feb 14
       
      probably the most important point made in this article
  • low testosterone identifies men with an adverse metabolic phenotype
  • Diabetic men with low testosterone are significantly more likely to be obese or insulin resistant
  • increased inflammation, evidenced by higher CRP levels
  • Bioavailable but not free testosterone was independently predictive of mortality
  • It remains possible that low testosterone is a consequence of insulin resistance, or simply a biomarker, co-existing because of in-common risk factors.
  • In prospective studies, reviewed in detail elsewhere (Grossmann et al. 2010) the inverse association of low testosterone with metabolic syndrome or diabetes is less consistent for free testosterone compared with total testosterone
  • In a study from the Framingham cohort, SHBG but not testosterone was prospectively and independently associated with incident metabolic syndrome
  • low SHBG (Ding et al. 2009) but not testosterone (Haring et al. 2013) with an increased risk of future diabetes
  • In cross-sectional studies of men with (Grossmann et al. 2008) and without (Bonnet et al. 2013) diabetes, SHBG but not testosterone was inversely associated with worse glycaemic control
  • SHBG may have biological actions beyond serving as a carrier protein for and regulator of circulating sex steroids
  • In men with diabetes, free testosterone, if measured by gold standard equilibrium dialysis (Dhindsa et al. 2004), is reduced
    • Nathan Goodyear
      Nathan Goodyear on 04 Feb 14
       
      expensive, laborious process filled with variables
  • Low free testosterone remains inversely associated with insulin resistance, independent of SHBG (Grossmann et al. 2008). This suggests that the low testosterone–dysglycaemia association is not solely a consequence of low SHBG.
  • Experimental evidence reviewed below suggests that visceral adipose tissue is an important intermediate (rather than a confounder) in the inverse association of testosterone with insulin resistance and metabolic disorders.
  • testosterone promotes the commitment of pluripotent stem cells into the myogenic lineage and inhibits their differentiation into adipocytes
  • testosterone regulates the metabolic functions of mature adipocytes (Xu et al. 1991, Marin et al. 1995) and myocytes (Pitteloud et al. 2005) in ways that reduce insulin resistance.
  • Pre-clinical evidence (reviewed in Rao et al. (2013)) suggests that at the cellular level, testosterone may improve glucose metabolism by modulating the expression of the glucose-transported Glut4 and the insulin receptor, as well as by regulating key enzymes involved in glycolysis.
  • More recently testosterone has been shown to protect murine pancreatic β cells against glucotoxicity-induced apoptosis
  • Interestingly, a reciprocal feedback also appears to exist, given that not only chronic (Cameron et al. 1990, Allan 2013) but also, as shown more recently (Iranmanesh et al. 2012, Caronia et al. 2013), acute hyperglycaemia can lower testosterone levels.
  • There is also evidence that testosterone regulates insulin sensitivity directly and acutely
  • In men with prostate cancer commencing androgen deprivation therapy, both total as well as, although not in all studies (Smith 2004), visceral fat mass increases (Hamilton et al. 2011) within 3 months
  • More prolonged (>12 months) androgen deprivation therapy has been associated with increased risk of diabetes in several large observational registry studies
  • Testosterone has also been shown to reduce the concentration of pro-inflammatory cytokines in some, but not all studies, reviewed recently in Kelly & Jones (2013). It is not know whether this effect is independent of testosterone-induced changes in body composition.
  • the observations discussed in this section suggest that it is the decrease in testosterone that causes insulin resistance and diabetes. One important caveat remains: the strongest evidence that low testosterone is the cause rather than consequence of insulin resistance comes from men with prostate cancer (Grossmann & Zajac 2011a) or biochemical castration, and from mice lacking the androgen receptor.
  • Several large prospective studies have shown that weight gain or development of type 2 diabetes is major drivers of the age-related decline in testosterone levels
  • there is increasing evidence that healthy ageing by itself is generally not associated with marked reductions in testosterone
  • Circulating testosterone, on an average 30%, is lower in obese compared with lean men
  • increased visceral fat is an important component in the association of low testosterone and insulin resistance
  • The vast majority of men with metabolic disorders have functional gonadal axis suppression with modest reductions in testosterone levels
  • obesity is a dominant risk factor
  • men with Klinefelter syndrome have an increased risk of metabolic disorders. Interestingly, greater body fat mass is already present before puberty
  • Only 5% of men with type 2 diabetes have elevated LH levels
  • inhibition of the gonadal axis predominantly takes place in the hypothalamus, especially with more severe obesity
  • Metabolic factors, such as leptin, insulin (via deficiency or resistance) and ghrelin are believed to act at the ventromedial and arcuate nuclei of the hypothalamus to inhibit gonadotropin-releasing hormone (GNRH) secretion from GNRH neurons situated in the preoptic area
  • kisspeptin has emerged as one of the most potent secretagogues of GNRH release
  • hypothesis that obesity-mediated inhibition of kisspeptin signalling contributes to the suppression of the HPT axis, infusion of a bioactive kisspeptin fragment has been recently shown to robustly increase LH pulsatility, LH levels and circulating testosterone in hypotestosteronaemic men with type 2 diabetes
  • A smaller study with a similar experimental design found that acute testosterone withdrawal reduced insulin sensitivity independent of body weight, whereas oestradiol withdrawal had no effects
  • suppression of the diabesity-associated HPT axis is functional, and may hence be reversible
  • Obesity and dysglycaemia and associated comorbidities such as obstructive sleep apnoea (Hoyos et al. 2012b) are important contributors to the suppression of the HPT axis
  • weight gain and development of diabetes accelerate the age-related decline in testosterone
  • Modifiable risk factors such as obesity and co-morbidities are more strongly associated with a decline in circulating testosterone levels than age alone
  • 55% of symptomatic androgen deficiency reverted to a normal testosterone or an asymptomatic state after 8-year follow-up, suggesting that androgen deficiency is not a stable state
  • Weight loss can reactivate the hypothalamic–pituitary–testicular axis
  • Leptin treatment resolves hypogonadism in leptin-deficient men
  • The hypothalamic–pituitary–testicular axis remains responsive to treatment with aromatase inhibitors or selective oestrogen receptor modulators in obese men
  • Kisspeptin treatment increases LH secretion, pulse frequency and circulating testosterone levels in hypotestosteronaemic men with type 2 diabetes
  • change in BMI was associated with the change in testosterone (Corona et al. 2013a,b).
  • weight loss can lead to genuine reactivation of the gonadal axis by reversal of obesity-associated hypothalamic suppression
  • There is pre-clinical and observational evidence that chronic hyperglycaemia can inhibit the HPT axis
  • in men who improved their glycaemic control over time, testosterone levels increased. By contrast, in those men in whom glycaemic control worsened, testosterone decreased
  • testosterone levels should be measured after successful weight loss to identify men with an insufficient rise in their testosterone levels. Such men may have HPT axis pathology unrelated to their obesity, which will require appropriate evaluation and management.
  • Nathan Goodyear on 04 Feb 14
     
    Article discusses the expanding evidence of low T and Metabolic syndrome.
Nathan Goodyear

JISSN | Full text | International Society of Sports Nutrition position stand: creatine ... - 0 views

www.jissn.com/6

creatine sports nutrition exercise

shared by Nathan Goodyear on 27 Jan 14 - No Cached
  • the energy supplied to rephosphorylate adenosine diphosphate (ADP) to adenosine triphosphate (ATP) during and following intense exercise is largely dependent on the amount of phosphocreatine (PCr) stored in the muscle
  • Creatine is chemically known as a non-protein nitrogen
  • It is synthesized in the liver and pancreas from the amino acids arginine, glycine, and methionine
  • ...26 more annotations...
  • Approximately 95% of the body's creatine is stored in skeletal muscle
  • About two thirds of the creatine found in skeletal muscle is stored as phosphocreatine (PCr) while the remaining amount of creatine is stored as free creatine
  • The body breaks down about 1 – 2% of the creatine pool per day (about 1–2 grams/day) into creatinine in the skeletal muscle
  • The magnitude of the increase in skeletal muscle creatine content is important because studies have reported performance changes to be correlated to this increase
  • "loading" protocol. This protocol is characterized by ingesting approximately 0.3 grams/kg/day of CM for 5 – 7 days (e.g., ≃5 grams taken four times per day) and 3–5 grams/day thereafter [18,22]. Research has shown a 10–40% increase in muscle creatine and PCr stores using this protocol
  • Additional research has reported that the loading protocol may only need to be 2–3 days in length to be beneficial, particularly if the ingestion coincides with protein and/or carbohydrate
  • A few studies have reported protocols with no loading period to be sufficient for increasing muscle creatine (3 g/d for 28 days)
  • Cycling protocols involve the consumption of "loading" doses for 3–5 days every 3 to 4 weeks
  • Most of these forms of creatine have been reported to be no better than traditional CM in terms of increasing strength or performance
  • Recent studies do suggest, however, that adding β-alanine to CM may produce greater effects than CM alone
  • These investigations indicate that the combination may have greater effects on strength, lean mass, and body fat percentage; in addition to delaying neuromuscular fatigue
  • creatine phosphate has been reported to be as effective as CM at improving LBM and strength
  • Green et al. [24] reported that adding 93 g of carbohydrate to 5 g of CM increased total muscle creatine by 60%
  • Steenge et al. [23] reported that adding 47 g of carbohydrate and 50 g of protein to CM was as effective at promoting muscle retention of creatine as adding 96 g of carbohydrate.
  • It appears that combining CM with carbohydrate or carbohydrate and protein produces optimal results
  • Studies suggest that increasing skeletal muscle creatine uptake may enhance the benefits of training
  • Nearly 70% of these studies have reported a significant improvement in exercise capacity,
  • Long-term CM supplementation appears to enhance the overall quality of training, leading to 5 to 15% greater gains in strength and performance
  • Nearly all studies indicate that "proper" CM supplementation increases body mass by about 1 to 2 kg in the first week of loading
  • short-term adaptations reported from CM supplementation include increased cycling power, total work performed on the bench press and jump squat, as well as improved sport performance in sprinting, swimming, and soccer
  • Long-term adaptations when combining CM supplementation with training include increased muscle creatine and PCr content, lean body mass, strength, sprint performance, power, rate of force development, and muscle diameter
  • subjects taking CM typically gain about twice as much body mass and/or fat free mass (i.e., an extra 2 to 4 pounds of muscle mass during 4 to 12 weeks of training) than subjects taking a placebo
  • The gains in muscle mass appear to be a result of an improved ability to perform high-intensity exercise via increased PCr availability and enhanced ATP synthesis, thereby enabling an athlete to train harder
  • there is no evidence to support the notion that normal creatine intakes (< 25 g/d) in healthy adults cause renal dysfunction
  • no long-term side effects have been observed in athletes (up to 5 years),
  • One cohort of patients taking 1.5 – 3 grams/day of CM has been monitored since 1981 with no significant side effects
  • Nathan Goodyear on 27 Jan 14
     
    Nice review of the data, up to the publication date, on creatine.
Nathan Goodyear

Annals of Internal Medicine | Long-Term Effects of Dihydrotestosterone Treatment on Pro... - 0 views

annals.org/article.aspx

DHT dihydrotestosterone prostate men male hormone hormones

shared by Nathan Goodyear on 06 Feb 14 - No Cached
  • Nathan Goodyear on 06 Feb 14
     
    DHT at 70 mg daily shown to have no adverse effects in the prostate of "healthy" men older than 50.  However, it did increase DHT metabolites (3 alpha androstane-diol and 3 beta androstane-diol), decreased LH, Testosterone, Estradiol, FSH, increased hemoglobin, creatinine, lean mass and decreased fat.
Nathan Goodyear

Gut microbe levels are linked to type 2 diabetes and obesity -- ScienceDaily - 0 views

www.sciencedaily.com/...140623141842.htm

gut microbiota dysbiosis diabetes obesity

shared by Nathan Goodyear on 25 Jun 14 - No Cached
  • Nathan Goodyear on 25 Jun 14
     
    Individuals with obesity and type II Diabetes been found to have significantly different gut bacteria populations compared to healthy individuals.  This is not new information.  The firmicutes:bacteroidetes ratio has been long known to be elevated in obese individuals vs those that are lean.  The question here is cause and effect.  Is the change in the bacterial population leading to obesity and type II diabetes?  Or is diabetes and obesity leading to changes in the bacterial population?  A heavy-laden carb diet is know to lead to a change to a more unhealthy gut bacterial population--maybe it is just a product of diet?  Maybe it is effected by vaginal delivery vs cesarean delivery?  Maybe breast feeding plays a role.  Maybe, all the above is required. The point is that the cause of obesity and type II diabetes may have its origins deep, deep in the...well you know. http://ow.ly/yqDML 
Nathan Goodyear

Diet-Induced Dysbiosis of the Intestinal Microbiota and the Effects on Immunity and Dis... - 0 views

www.ncbi.nlm.nih.gov/...PMC3448089

dysbiosis diet nutrition metabolic endotoxemia disease inflammation gut

shared by Nathan Goodyear on 27 Jul 14 - No Cached
  • The gut microbiota participates in the body’s metabolism by affecting energy balance, glucose metabolism, and low-grade inflammation associated with obesity and related metabolic disorders
  • Firmicutes and Bacteroidetes represent the two largest phyla in the human and mouse microbiota and a shift in the ratio of these phyla has been associated with many disease conditions, including obesity
  • In obese humans, there is decreased abundance of Bacteroidetes compared to lean individuals
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  • weight loss in obese individuals results in an increase in the abundance of Bacteroidetes
  • there is conflicting evidence on the composition of the obese microbiota phenotype with regards to Bacteroidetes and Firmicutes ratios
  • Bifidobacteria spp. from the phyla Actinobacteria, has been shown to be depleted in both obese mice and human subjects
  • While it is not yet clear which specific microbes are inducing or preventing obesity, evidence suggests that the microbiota is a factor.
  • targeted manipulation of the microbiota results in divergent metabolic outcomes depending on the composition of the diet
  • The microbiota has been linked to insulin resistance or type 2 diabetes (T2D) via metabolic syndrome and indeed the microbiota of individuals with T2D is also characterized by an increased Bacteroidetes/Firmicutes ratio, as well as an increase in Bacillus and Lactobacillus spp
  • It was also observed that the ratio of Bacteriodes-Prevotella to C. coccoides-E. rectale positively correlated with glucose levels but did not correlate with body mass index [80]. This suggests that the microbiota may influence T2D in conjunction with or independently of obesity
  • In humans, high-fat Western-style diets fed to individuals over one month can induce a 71% increase in plasma levels of endotoxins, suggesting that endotoxemia may develop in individuals with GI barrier dyfunction connected to dysbiosis
  • LPS increases macrophage infiltration essential for systemic inflammation preceding insulin resistance, LPS alone does not impair glucose metabolism
  • early treatment of dysbiosis may slow down or prevent the epidemic of metabolic diseases and hence the corresponding lethal cardiovascular consequences
  • increased Firmicutes and decreased Bacteroidetes, which is the microbial profile found in lean phenotypes, along with an increase in Bifidobacteria spp. and Lactobacillus spp
  • mouse and rat models of T1D have been shown to have microbiota marked by decreased diversity and decreased Lactobacillus spp., as well as a decrease in the Firmicutes/Bacteroidetes ratio
  • microbial antigens through the innate immune system are involved in T1D progression
  • The microbiota appears to be essential in maintaining the Th17/Treg cell balance in intestinal tissues, mesenteric and pancreatic lymph nodes, and in developing insulitis, although progression to overt diabetes has not been shown to be controlled by the microbiota
  • There is evidence that dietary and microbial antigens independently influence T1D
  • Lactobacillus johnsonii N6.2 protects BB-rats from T1D by mediating intestinal barrier function and inflammation [101,102] and a combination probiotic VSL#3 has been shown to attenuate insulitis and diabetes in NOD mice
  • breast fed infants have higher levels of Bifidobacteria spp. while formula fed infants have higher levels of Bacteroides spp., as well as increased Clostridium coccoides and Lactobacillus spp
  • the composition of the gut microbiota strongly correlates with diet
  • In mice fed a diet high in fat, there are many key gut population changes, such as the absence of gut barrier-protecting Bifidobacteria spp
  • diet has a dominating role in shaping gut microbiota and changing key populations may transform healthy gut microbiota into a disease-inducing entity
  • “Western” diet, which is high in sugar and fat, causes dysbiosis which affects both host GI tract metabolism and immune homeostasis
  • Nathan Goodyear on 27 Jul 14
     
    Nice discussion of how diet, induces gut bacterial change, that leads to metabolic endotoxemia and disease.
Nathan Goodyear

Reevaluation of the protein requirement in young men with the indicator amino acid oxid... - 0 views

ajcn.nutrition.org/...995.long

protein macronutrients nutrition diet men

shared by Nathan Goodyear on 21 Jul 15 - No Cached
  • the mean and population-safe protein requirements were estimated to be 0.93 and 1.2 g · kg−1 · d
  • diet containing 0.90 g · kg−1 · d−1 was at or above physiologic protein requirements for sedentary men
  • The current EAR recommendation and RDA for protein are 0.66 and 0.80 g · kg−1 · d−1, respectively. We believe that these recommendations are tentative because no long-term studies have suggested that these values would maintain nitrogen balance along with lean body mass, muscle mass, serum protein concentrations, immunity, functional capacity etc
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  • a series of long-term balance studies (67-69) showed that intake of the proposed safe allowance of 0.57 g (70) egg protein resulted in negative nitrogen balance, loss of lean body mass, and deteriorating serum protein and transferase values unless additional energy or nonessential nitrogen was supplied
  • The results of the present study suggest that the current EAR recommendations (0.66 g · kg−1 · d−1) and RDA (0.80 g · kg−1 · d−1) for protein are underestimated at 29% and 33%, respectively
  • Nathan Goodyear on 21 Jul 15
     
    study looked at protein requirements in 8 "healthy" men.  This study pointed to 1.2 g/kg/day as an appropriate daily dietary protein intake for healthy men.  This far exceeds levels per RDA.
Nathan Goodyear

Effect of Testosterone Treatment on Glucose Metabolism in Men With Type 2 Diabetes: A R... - 0 views

care.diabetesjournals.org/...2098.abstract

Testosterone treatment low subcutaneous fat visceral fat T glucose insulin resistance metabolism obesity diabetes men male hormone hormones

shared by Nathan Goodyear on 29 Jul 14 - No Cached
  • Nathan Goodyear on 29 Jul 14
     
    Only the abstract available in this publication.  Good study design.  No improvement in insulin resistance, glycemic control or visceral adiposity in obese men with type II diabetes.  The levels of inclusion were TT < 346, which would not meet the criteria put forth by other studies.  This study appeared to look at border line "low T" men with obesity and type II diabetes and found no direct glycemic control improvement.  An increase in lean muscle mass and decrease in subcutaneous fat was found.
Nathan Goodyear

Resistance training increases SHBG in overweight/obese, young men - 0 views

www.ncbi.nlm.nih.gov/...PMC3845495

resistance training overweight obesity obese men male hormone hormones SHBG free Testosterone Testosterone free androgen index

shared by Nathan Goodyear on 03 Sep 14 - No Cached
  • Nathan Goodyear on 03 Sep 14
     
    12 week study of obese  men in resistance training program finds increase in SHBG and resultant decrease in free Androgen index.  FAI is as a calculation of free Testosterone.  This is different in the studies in lean men which shows an increase in Testosterone. Here a different underlying metabolism is the result
Nathan Goodyear

Testosterone as Potential Effective Therapy in Treatment of Obesity in Men with Testost... - 0 views

www.ncbi.nlm.nih.gov/...PMC3296126

Testosterone low T low Testosterone men male hormone hormones obesity cardiovascular disease metabolic syndrome insulin resistance CVD Diabetes

shared by Nathan Goodyear on 23 Jan 15 - No Cached
  • Nathan Goodyear on 23 Jan 15
     
    Testosterone therapy in men with low T will improve lean body mass, some reduction in abdominal obesity, yet little effect in visceral obesity.
Nathan Goodyear

Growth hormone treatment in adults with Prader-Wil... [Endocrine. 2012] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...22081257

growth hormone growth hormone hormones Prader-Willi Syndrome fat

shared by Nathan Goodyear on 03 Aug 14 - No Cached
  • Nathan Goodyear on 03 Aug 14
     
    Thought GH in those with Prader-Willi Syndrome did not see an improvement in lipid and glucose metabolism, lean body mass increased and fat mass decreased.
Nathan Goodyear

Hyperandrogenism induces a proinflam... [J Clin Endocrinol Metab. 2014] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...24512496

androgens polycystic ovarian syndrome Testosterone DHEA androstenedione women inflammation TNF-alpha PCOS

shared by Nathan Goodyear on 05 Aug 14 - No Cached
  • Nathan Goodyear on 05 Aug 14
     
    Very insightful study.  Study looked at hyperadrogenism and inflammation in women on the orders of PCOS.  The study subjects did not have PCOS, but hyperandrogenism via 130 mg DHEA was associated with an increase in TNF-alpha in these lean o/w healthy women.  We know this is due to hyperandrogenism as elevated Testosterone, DHEA, and androstenedione were documented with treatment. Take home:  androgens promote inflammation in women.  I believe this has serious negative implications about the massive Testosterone doping that is occurring in women today.
Nathan Goodyear

Sarcopenia and Age-Related Endocrine Function - 0 views

www.hindawi.com/...cta

Testosterone low T low testosterone low T muscle mass sarcopenia aging

shared by Nathan Goodyear on 13 Aug 14 - No Cached
  • Nathan Goodyear on 13 Aug 14
     
    Good discussion of sarcopenia.  They article looked at the evidence of Testosterone and found the evidence pointed to improved lean muscle mass; but not a direct cause effect of low T and sarcopenia.
Nathan Goodyear

http://www.uclouvain.be/cps/ucl/doc/ir-ldri/images/BINDELS2013IJBCLB.pdf - 0 views

www.uclouvain.be/...BINDELS2013IJBCLB.pdf

dysbiosis gut flora gut gut microbiota muscle muscle mass

shared by Nathan Goodyear on 14 Apr 15 - No Cached
  • Nathan Goodyear on 14 Apr 15
     
    gut microflora and its impact on muscle loss/muscle growth.  Not just for lean versus fat evaluation.
Nathan Goodyear

THERAPY OF ENDOCRINE DISEASE: Testosterone supplementation and body composition: result... - 0 views

www.eje-online.org/...EJE-15-0262.abstract

low T low Testosterone Testosterone fat muscle mass metabolism body composition cholesterol triglycerides HDL men male hormones

shared by Nathan Goodyear on 19 Nov 15 - No Cached
  • Nathan Goodyear on 19 Nov 15
     
    new study finds Testosterone therapy in men with low T significantly reduces fat, increases lean muscle mass, and reduces fasting glucose and insulin levels.  Improvements in total cholesterol, triglycerides and HDL was also seen.  Only abstract available currently.
Nathan Goodyear

Effects of aromatase inhibition vs. testosterone in older men with low testosterone: ra... - 0 views

www.ncbi.nlm.nih.gov/...26588809

low T low Testosterone Testosterone testosterone therapy aromatase inhibitors aromatase inhibition aromatase inhibitor aromatase men male hormones strength muscle mass muscle bone mineral density

shared by Nathan Goodyear on 07 Dec 15 - No Cached
  • Nathan Goodyear on 07 Dec 15
     
    No surprise that Testosterone therapy improves Testosterone levels in men with low T, but aromatase inhibition (AI) did as well.  In this study, only lean mass increased compared to Testosterone therapy and placebo.  Strength increased in both Testosterone and AI.
Nathan Goodyear

Circulating 2-hydroxy and 16-α hydroxy estrone levels and risk of breast canc... - 1 views

www.ncbi.nlm.nih.gov/...PMC2562592

estrogen metabolism menopause post-menopause post menopause estrogen metabolite 2-OH-estrone 16-alpha-OH-estrone 2:16alpha-OH estrone breast cancer risk hormone hormones

shared by Nathan Goodyear on 21 Aug 14 - No Cached
  • 2-OH estrogens bind to the estrogen receptor (ER) with affinity equivalent to or greater than estradiol
  • previous prospective studies have not observed any significant associations with either 2-OH or 16α-OH estrone or the ratio of the two metabolites and breast cancer risk overall.
    • Nathan Goodyear
      Nathan Goodyear on 08 Oct 15
       
      whether that risk is increased or decreased
  • it has been hypothesized that metabolism favoring the 2-OH over the 16α-OH pathway may be inversely associated with breast cancer risk (28).
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  • they may act as only weak mitogens (14, 15), or as inhibitors of proliferation
  • No significant associations have been observed between 2-OH estrone and breast cancer risk
  • While 16α-OH estrone binds to the ER with lower affinity than estradiol, it binds covalently (18-20) and once bound, fails to down-regulate the receptor (21). Thus, 16α-OH estrone stimulates cell proliferation in a manner comparable to estradiol in ER+ breast cancer cell lines
  • In this large prospective study of 2-OH and 16α-OH estrone metabolites and breast cancer risk, we did not observe any significant associations overall with either individual metabolite or with the ratio of the two metabolites
  • we observed positive associations with 2-OH estrone and the 2:16α-OH estrone ratio among women with lower BMI and women with ER-/PR-tumors,
  • To date, several epidemiologic studies have examined the association between the 2-OH and 16α-OH estrogen metabolites and breast cancer risk with inconclusive results.
  • circulating estrogen levels have been associated more strongly with ER+/PR+ tumors than with ER-/PR- tumors
  • our results do not support the hypothesis that metabolism favoring the 2-OH estrone pathway is more beneficial to breast cancer risk than that favoring the 16α-OH estrone pathway
  • we observed significant positive associations of both 2-OH estrone and the 2:16α-OH estrone ratio with ER-/PR-tumors
  • Three (30, 32, 33) of four (30-33) studies observed RRs above 1 for the association between 16α-OH estrone and breast cancer risk (range of RRs=1.23-2.47); none of the point estimates was statistically significant though one trend was suggestive
  • based on animal studies, 2-OH estrone and the 2:16α-OH estrone ratio have been hypothesized to be inversely associated with breast cancer risk
  • No significant associations have been observed between 2-OH estrone, 16α-OH estrone, or the 2:16α-OH estrone ratio and breast cancer risk and the direction of the estimates is not consistent across studies.
    • Nathan Goodyear
      Nathan Goodyear on 08 Oct 15
       
      better worded is no consistent, significant associations.   There are some studies that point to the 16 catecholestrogen and increased cancer risk; limited studies show negative effects of 2 catecholestrogens on cancer risk and prospective studies available pretty much dispel the idea that the 2:16 ratio has an risk predictability.
  • we observed a suggestive inverse association with 16α-OH estrone and a significant positive association with the 2:16α-OH estrone ratio among lean women, suggesting possible associations in a low estrogen environment.
  • 16α-OH estrone increases unscheduled DNA synthesis in mouse mammary cells (27) and hence also may be genotoxic
  • Although 2-OH estrogens are capable of redox cycling, the semiquinones and quinones (i.e., the oxidized forms) form stable DNA adducts that are reversible without DNA destruction
  • In our population of PMH nonusers, we observed no associations with ER+/PR+ tumors, but significant positive associations with 2-OH estrone and the 2:16α-OH estrone ratio among women with ER-/PR- tumors
    • Nathan Goodyear
      Nathan Goodyear on 08 Oct 15
       
      one of the few studies to find this association between 2 catecholestrogens and the 2:16 ratio and ER-/PR-tumors
  • Animal and in vitro studies have shown that hydroxy estrogens can induce DNA damage either directly, through the formation of quinones and DNA adducts, or indirectly, through redox cycling and the generation of reactive oxygen species
    • Nathan Goodyear
      Nathan Goodyear on 08 Oct 15
       
      genotoxic via directe DNA adducts and indirectly via ROS; this is in addition to the proliferative effect
  • we observed a significant positive association between the 2:16α-OH estrone ratio and breast cancer risk among lean women
  • No significant associations have been observed with the 2:16α-OH estrone ratio
  • In the Danish study, no associations were observed with either ER+ or ER- tumors among PMH nonusers
  • significant positive associations with 2-OH estrone and the 2:16α-OH estrone ratio were observed among PMH users with ER+, but not ER-, tumors
  • it is possible that the genotoxicity of 2-OH estrone plays a role in hormone receptor negative tumors
  • 4-OH estrogens have a greater estrogenic potential than 2-OH estrogens, given the lower dissociation rate from estrogen receptors compared with estradiol (61), and are potentially more genotoxic since the quinones form unstable adducts, leading to depurination and mutation in vitro and in vivo
  • the balance between the catechol (i.e., 2-OH and 4-OH) and methoxy (i.e., 2-Me and 4-Me) estrogens may impact risk
  • Nathan Goodyear on 21 Aug 14
     
    The risks of estrogen metabolism are not clear cut.  Likely never will be due to the complexity of individual metabolism.  This study found no correlation between 2OH-Estrone and 2OH:16alpha-Estrone and breast cancer risk in ER+/PR+ breast cancer.  Translated: no benefit in breast cancer risk in 2OH-Estrone metabolism or increased 2OH:16alpha estrone metabolism.  There was a positive association between 2OH-Estrone and 2:16alpha-Estrone in women with ER-/PR- tumors and low BMI.
  • anonymous on 28 Oct 15
     
    pakistani sexy girls escort in dubai // russian sexy girsl escort in dubai // sexy girls in dubai // sexy girls escort in dubai //
rsf123

Where to buy: codeine | weed | mdma | pills | lean | fake note bills | coke | cocaine |... - 0 views

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started by rsf123 on 01 Jul 22 no follow-up yet
Nathan Goodyear

The role of short-chain fatty acids in the interplay between diet, gut microbiota, and ... - 0 views

www.ncbi.nlm.nih.gov/...PMC3735932

SCFA gut gut health diet nutrition metabolism gut flora gut microbiota

shared by Nathan Goodyear on 09 Nov 16 - No Cached
  • Acetate, propionate, and butyrate are present in an approximate molar ratio of 60:20:20 in the colon and stool
  • SCFAs might play a key role in the prevention and treatment of the metabolic syndrome, bowel disorders, and certain types of cancer
  • SCFA administration positively influenced the treatment of ulcerative colitis, Crohn's disease, and antibiotic-associated diarrhea
  • ...16 more annotations...
  • Gut bacteria in the cecum and large intestine produce SCFAs mainly from nondigestible carbohydrates that pass the small intestine unaffected
  • plant cell-wall polysaccharides, oligosaccharides, and resistant starches
  • inulin shifted the relative production of SCFAs from acetate to propionate and butyrate
  • age of approximately 3–4 years, when it becomes mature
  • SCFAs affect lipid, glucose, and cholesterol metabolism
  • colonocytes, the first host cells that take up SCFAs and which depend largely on butyrate for their energy supply
  • the microbiota educate the immune system and increase the tolerance to microbial immunodeterminants
  • the microbiota act as a metabolic organ that can break down otherwise indigestible food components, degrade potentially toxic food compounds like oxalate, and synthesize certain vitamins and amino acids
  • a large part of the SCFAs is used as a source of energy
  • The general idea is that colonocytes prefer butyrate to acetate and propionate, and oxidize it to ketone bodies and CO2
  • Exogenous acetate formed by colonic bacterial fermentation enters the blood compartment and is mixed with endogenous acetate released by tissues and organs (103, 104). Up to 70% of the acetate is taken up by the liver (105), where it is not only used as an energy source, but is also used as a substrate for the synthesis of cholesterol and long-chain fatty acids and as a cosubstrate for glutamine and glutamate synthesis
  • SCFAs regulate the balance between fatty acid synthesis, fatty acid oxidation, and lipolysis in the body.
  • Fatty acid oxidation is activated by SCFAs, while de novo synthesis and lipolysis are inhibited
  • obese animals in this study showed a 50% reduction in relative abundance of the Bacteroidetes (i.e., acetate and propionate producers), whereas the Firmicutes (i.e., butyrate producers) were proportionally increased compared with the lean counterparts.
  • increase in total fecal SCFA concentrations in obese humans.
  • In humans the distinct relation between the Firmicutes:Bacteroidetes ratio and obesity is less clear.
  • Nathan Goodyear on 09 Nov 16
     
    Great review of the role of SCFA in gut health and body metabolism
Nathan Goodyear

Effect of Tongkat Ali on stress hormones and psychological mood state in moderately str... - 0 views

www.ncbi.nlm.nih.gov/...PMC3669033

Tongkat Ali long jack cortisol stress testosterone hormone hormones

shared by Nathan Goodyear on 09 Mar 15 - No Cached
  • At the age of 60, testosterone levels are typically only 40-50% of youthful levels and may be lower
  • Eurycoma contains a group of small peptides referred to as “eurypeptides” that are known to have effects in improving energy status and sex drive in studies of rodents
  • The effects of tongkat ali in restoring normal testosterone levels appears to be less due to actually “stimulating” testosterone synthesis, but rather by increasing the release rate of “free” testosterone from its binding hormone, sex-hormone-binding-globulin (SHBG)
  • ...6 more annotations...
  • The current study found that daily supplementation with tongkat ali root extract (200 mg/day) improves stress hormone profile (lower cortisol; higher testosterone) and certain mood state parameters (lower tension, anger, and confusion)
  • tongkat ali supplementation (100 mg/day) improved lean body mass, 1-RM strength, and arm circumference to a significantly greater degree compared to a placebo group.
  • In a recent 12-week trial [46] of Eurycoma longifolia supplementation (300 mg/day), men (30–55 years of age) showed significant improved compared to placebo in the Physical Functioning domain of the SF-36 quality of life survey
  • sexual libido was increased by 11%
  • In men with low testosterone levels (average age 51 years), one month of daily supplementation with tongkat ali extract (200 mg/day) resulted in a significant improvement in serum testosterone levels and quality-of-life parameters
  • rise in cortisol and drop in testosterone is an early signal of “overtraining”
  • Nathan Goodyear on 09 Mar 15
     
    Tongkat Ali, commonly known as long jack, is found to reduce stress and increase Testosterone.  Stress is one of the common causes of low T in men.  It appears that long Jack functions as an adaptogen.
teremoso

To Maintain Body Fit, Used Fitness Equipment in Toronto - 2 views

While many of us are still experiencing economic challenges now, it's important to re-commit to health now more than ever. With Keystone Company raising premiums right and left, why not invest in t...

used fitness equipment toronto

started by teremoso on 21 May 12 no follow-up yet
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