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Nathan Goodyear

Higher Serum Testosterone Concentration in Older Women is Associated with Insulin Resis... - 0 views

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    This study found that increasing Testosterone, as determined by serum, is associated with increased CVD, insulin resistance, and metabolic syndrome in postmenopausal women.  I believe that this massive Testosterone doping campaign that we are seeing in men and women is following the same patter seen with premarin and provera. 
Nathan Goodyear

Inverse Association of Testosterone and the Metabolic Syndrome in Men Is Consistent acr... - 0 views

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    Total Testosterone and SHBG inversely associated with Metabolic Syndrome.
Nathan Goodyear

Aging, Androgens, and the Metabolic Syndrome in a Longitudinal Study of Aging: The Jour... - 0 views

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    Study finds Total Testosterone and SHBG inversely associated with Metabolic Syndrome.  Free Testosterone and BMI were positively associated with MetS.
Nathan Goodyear

Mitochondrial oxidative stress and the metabolic syndrome - 0 views

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    Growing body of evidence points to mitochondria as an integral component in Metabolic Syndrome.
Nathan Goodyear

Hypogonadism and Metabolic Syndrome in Nigerian Male Patients With Both Type 2 Diabetes... - 0 views

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    Asian study finds Testosterone is inversely associated with increased central obesity, increased dyslipidemia, and metabolic syndrome in me with new diagnosis of type II diabetes and hypertension.  Men with metabolic syndrome, type II diabetes, and CVD must have appropriate hormone evaluation.
Nathan Goodyear

Clustering of metabolic and cardiovascular risk f... [Metabolism. 2014] - PubMed - NCBI - 0 views

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    When you look at PCOS in women, it is really just the early manifestation of Metabolic Syndrome.  PCOS no longer needs to be viewed through the prism of hormones and/or infertility but the means through which disease will walk.
Nathan Goodyear

Testosterone treatment improves metabolic syndrome-induced adipose tissue derangements - 0 views

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    Animal study of metabolic syndrome finds that Testosterone improves metabolic dysfunction in visceral adipose tissue.
Nathan Goodyear

Association of metabolic syndrome ... [Indian J Endocrinol Metab. 2014] - PubMed - NCBI - 0 views

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    Metabolic Syndrome is associated with CAD.  No surprise here, but increase in # of metabolic syndrome parameters was associated with increasing % of Triple vessel disease.   No surprise that MetS was associated with TNF-alpha, IL-6, IR, and hsCRP.
Nathan Goodyear

The association between hyperandrogenemia and the metabolic syndrome in morbidly obese ... - 0 views

  • a significant inverse relationship between HA and HDL-cholesterol levels which is in accordance with previous studies of women with PCOS
  • HA was associated with 61 % increased adjusted odds of MetS, and that this association was mainly driven by increased odds of dysglycemia and dyslipidemia
  • the prevalences of MetS, PCOS and HA were high among morbidly obese women <50 years of age
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  • Compared to women without HA, those with HA had significantly higher odds of having the MetS, which was mainly explained by the associations between HA and the lipid- and glucose components of the MetS
  • FTI-blood test might add value to the cardiovascular risk assessment of premenopausal women with morbid obesity
  • We calculated the free testosterone index (FTI) using the formula: FTI = 100 x serum testosterone (nmol/L) / sex hormone binding globulin (SHBG, nmol/L)
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    Another study that finds hyperandrogenism in women is associated with increased Metabolic Syndrome.  This study found obesity was associated with increased hyperandrogegism and Metabolic Syndrome irregardless of PCOS diagnosis or not.
Nathan Goodyear

11β-HSD1 inhibition ameliorates metabolic syndrome and prevents progression o... - 0 views

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    inhibition of 11beta-HSD1 improves metabolic syndrome and atherosclerosis.  This suggests that metabolic syndrome is associated with increase 11beta-HSD1 expression/activity.  Animal study
Nathan Goodyear

Akkermansia muciniphila and improved metabolic health during a dietary intervention in ... - 0 views

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    akkermansia muciniphila bacteria associated with improved metabolism following calorie restriction in obese adults.  Again, gut flora effects metabolism
Nathan Goodyear

Long-lived mitochondrial (Mit) mutants of Caenorhabditis elegans utilize a novel metabo... - 0 views

  • Our study suggests long-lived, genetically specified Mit mutants employ a novel metabolism and that life span may well arise as a function of metabolic state.
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    Mitchondria, metabolism,  and aging
Nathan Goodyear

Endogenous fructose production and metabolism in the liver contributes to the developme... - 0 views

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    Glucose increases fructose production in the liver through unregulated polyol pathway activity.  This aids the development of metabolic syndrome.  Carb restriction is important!  It is not just about what you give the body, but what the body does with it.
Nathan Goodyear

Prevalence of metabolic syndrome and... [J Diabetes Metab Disord. 2014] - PubMed - NCBI - 0 views

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    Startiling statistic: 11% of males 10-19 in Iran have metabolic syndrome and 7% of females of the same age have metabolic syndrome.
Nathan Goodyear

A causal role for uric acid in fructose-induced metabolic syndrome | Renal Physiology - 0 views

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    Article discusses the metabolic mechanism of fructose induced elevation of uric acid and the associated increased risk of metabolic syndrome.
Nathan Goodyear

Circulating Estrogen Metabolites and Risk for Breast Cancer in Premenopausal Women - 0 views

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    Epidemiologic study finds no association between increased 2OH-estrone metabolism and increased 2OH:16alphaOH-estrone metabolism and a reduction in breast cancer risk.
Nathan Goodyear

International Journal of Impotence Research - Obesity, low testosterone levels and erec... - 0 views

  • Studies have shown that ED may be an early biomarker of general endothelial dysfunction, atherosclerosis and CVD
  • testosterone treatment of hypogonadal young and older men improves sexual function, increases lean mass and decreases fat mass
  • In men with low serum testosterone (for example, <8 or 230 nmol l−1) with obesity, metabolic syndrome and diabetes mellitus, treatment with testosterone is warranted
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  • In obese middle-aged men, testosterone treatment reduced visceral adipocity, insulin resistance, serum cholesterol and glucose levels
  • testosterone replacement has a favorable impact on body mass, insulin secretion and sensitivity, lipid profile and blood pressure in hypogonadal men with the metabolic syndrome as well as type 2 diabetes mellitus
  • Testosterone significantly inhibits lipoprotein lipase activity, which reduces triglycerides uptake into adipocytes in the abdominal adipose tissue
  • testosterone treatment decreased endogenous inflammatory cytokines (tumor necrosis factor-α and IL-1β) and lipids (total cholesterol) and increased IL-10 in hypogonadal men
  • Testosterone treatment reduced leptin and adiponectin levels in hypogonadal type 2 diabetic men after 3 months of testosterone replacement
  • available data clearly show a relationship between obesity, low testosterone levels and ED
  • Obesity adversely affects endothelial function and lowers serum testosterone levels through the development of insulin resistance and metabolic syndrome
  • Metabolic disturbances as well as production of cytokines and adipokines by inflamed fat cells may be causal factors in the development of ED
  • The onset of ED and the associated risk of CVD may be delayed through lifestyle modifications that affect obesity, such as diet and exercise
  • Very low testosterone levels contribute to the development of ED in obesity, metabolic syndrome and type 2 diabetes mellitus
  • Obesity is associated with low total testosterone levels that can be explained at least partially by lower sex hormone-binding globulin (SHBG) in obese men
  • epidemiological studies have shown a negative correlation between BMI and total testosterone and to a lesser extent with free and bioavailable (biologically active) testosterone levels
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    Obesity is associated with low Testosterone and ED in men.
Nathan Goodyear

Fifty- two-Week Treatment With Diet and Exercise Plus Transdermal Testosterone Reverses... - 0 views

  • there appears to be a positive correlation between serum testosterone levels and insulin sensitivity in men across the full spectrum of glucose tolerance (Pitteloud et al, 2005), and this relationship is at least partially direct and not fully dependent on (changes in) elements of the MetS
  • supervised D&E alone led to significant improvements in testosterone concentrations, glycemic control, and components of the MetS
  • diet control, exercise, and testosterone supplementation may be beneficial in the management of men with T2D
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  • androgen-deprivation therapy in males with prostatic cancer may be associated with an increased risk for T2D, which may be caused by negative effects on insulin sensitivity
  • insulin sensitivity, measured by HOMA, improved in both groups and with a significantly greater degree when testosterone was added to supervised D&E
  • Fasting insulin concentrations, a good representative of insulin sensitivity, did show a significant correlation with changes in circulating androgen levels, an observation in support of Pitteloud et al (2005), who showed a direct relationship between insulin sensitivity and circulating testosterone concentrations using the hyper-insulinemic euglycemic clamp technique
  • 52 weeks of testosterone treatment also significantly improved circulation levels of adiponectin and hsCRP, key serum markers of insulin sensitivity and hepatic steatosis
  • The changes in both adiponectin and hsCRP were significantly correlated with the therapy-induced changes in bioavailable testosterone
  • a negative correlation was found between hsCRP levels and bioavailable testosterone
  • serum PSA concentrations did not differ between the 2 treatment groups, indicating that short-term testosterone administration appears to be acceptably safe
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    Study of men with metabolic syndrome and type II Diabetes finds that diet and exercise alone improved glucose control and metabolic syndrome components by 31%.  The addition of Testosterone therapy increased this % to 81%.
Nathan Goodyear

Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syn... - 0 views

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    Great article--only abstract available here.  Animal study finds that emulsifiers in process foods alters gut flora resulting in gut inflammation and obesity/metabolic syndrome.  Need an indictment against process foods--here you go.
Nathan Goodyear

Metabolic endotoxemia: a molecular link between obesity and cardiovascular risk - 0 views

  • Weight gain has been associated with a higher gut permeability
  • a high-fat diet promotes LPS absorption
  • higher concentrations of fatty acids impair intestinal barrier integrity
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  • The starting point for innate immunity activation is the recognition of conserved structures of bacteria, viruses, and fungal components through pattern-recognition receptors
  • TLRs are PRRs that recognize microbe-associated molecular patterns
  • TLRs are transmembrane proteins containing extracellular domains rich in leucine repeat sequences and a cytosolic domain homologous to the IL1 receptor intracellular domain
  • The major proinflammatory mediators produced by the TLR4 activation in response to endotoxin (LPS) are TNFα, IL1β and IL6, which are also elevated in obese and insulin-resistant patients
  • Obesity, high-fat diet, diabetes, and NAFLD are associated with higher gut permeability leading to metabolic endotoxemia.
  • Probiotics, prebiotics, and antibiotic treatment can reduce LPS absorption
  • LPS promotes hepatic insulin resistance, hypertriglyceridemia, hepatic triglyceride accumulation, and secretion of pro-inflammatory cytokines promoting the progression of fatty liver disease.
  • In the endothelium, LPS induces the expression of pro-inflammatory, chemotactic, and adhesion molecules, which promotes atherosclerosis development and progression.
  • In the adipose tissue, LPS induces adipogenesis, insulin resistance, macrophage infiltration, oxidative stress, and release of pro-inflammatory cytokines and chemokines.
  • the gut microbiota has been recently proposed to be an environmental factor involved in the control of body weight and energy homeostasis by modulating plasma LPS levels
  • dietary fats alone might not be sufficient to cause overweight and obesity, suggesting that a bacterially related factor might be responsible for high-fat diet-induced obesity.
  • This was accompanied in high-fat-fed mice by a change in gut microbiota composition, with reduction in Bifidobacterium and Eubacterium spp.
  • n humans, it was also shown that meals with high-fat and high-carbohydrate content (fast-food style western diet) were able to decrease bifidobacteria levels and increase intestinal permeability and LPS concentrations
  • it was demonstrated that, more than the fat amount, its composition was a critical modulator of ME (Laugerette et al. 2012). Very recently, Mani et al. (2013) demonstrated that LPS concentration was increased by a meal rich in saturated fatty acids (SFA), while decreased after a meal rich in n-3 polyunsaturated fatty acids (n-3 PUFA).
  • this effect seems to be due to the fact that some SFA (e.g., lauric and mystiric acids) are part of the lipid-A component of LPS and also to n-3 PUFA's role on reducing LPS potency when substituting SFA in lipid-A
  • these experimental results suggest a pivotal role of CD14-mediated TLR4 activation in the development of LPS-mediated nutritional changes.
  • This suggests a link between gut microbiota, western diet, and obesity and indicates that gut microbiota manipulation can beneficially affect the host's weight and adiposity.
  • endotoxemia was independently associated with energy intake but not fat intake in a multivariate analysis
  • in vitro that endotoxemia activates pro-inflammatory cytokine/chemokine production via NFκB and MAPK signaling in preadipocytes and decreased peroxisome proliferator-activated receptor γ activity and insulin responsiveness in adipocytes.
  • T2DM patients have mean values of LPS that are 76% higher than healthy controls
  • LPS-induced release of glucagon, GH and cortisol, which inhibit glucose uptake, both peripheral and hepatic
  • LPSs also seem to induce ROS-mediated apoptosis in pancreatic cells
  • Recent evidence has been linking ME with dyslipidemia, increased intrahepatic triglycerides, development, and progression of alcoholic and nonalcoholic fatty liver disease
  • The hepatocytes, rather than hepatic macrophages, are the cells responsible for its clearance, being ultimately excreted in bile
  • All the subclasses of plasma lipoproteins can bind and neutralize the toxic effects of LPS, both in vitro (Eichbaum et al. 1991) and in vivo (Harris et al. 1990), and this phenomenon seems to be dependent on the number of phospholipids in the lipoprotein surface (Levels et al. 2001). LDL seems to be involved in LPS clearance, but this antiatherogenic effect is outweighed by its proatherogenic features
  • LPS produces hypertriglyceridemia by several mechanisms, depending on LPS concentration. In animal models, low-dose LPS increases hepatic lipoprotein (such as VLDL) synthesis, whereas high-dose LPS decreases lipoprotein catabolism
  • When a dose of LPS similar to that observed in ME was infused in humans, a 2.5-fold increase in endothelial lipase was observed, with consequent reduction in total and HDL. This mechanism may explain low HDL levels in ‘ME’ and other inflammatory conditions such as obesity and metabolic syndrome
  • It is known that the high-fat diet and the ‘ME’ increase intrahepatic triglyceride accumulation, thus synergistically contributing to the development and progression of alcoholic and NAFLD, from the initial stages characterized by intrahepatic triglyceride accumulation up to chronic inflammation (nonalcoholic steatohepatitis), fibrosis, and cirrhosis
  • On the other hand, LPS activates Kupffer cells leading to an increased production of ROS and pro-inflammatory cytokines like TNFα
  • high-fat diet mice presented with ME, which positively and significantly correlated with plasminogen activator inhibitor (PAI-1), IL1, TNFα, STAMP2, NADPHox, MCP-1, and F4/80 (a specific marker of mature macrophages) mRNAs
  • prebiotic administration reduces intestinal permeability to LPS in obese mice and is associated with decreased systemic inflammation when compared with controls
  • Cani et al. also found that high-fat diet mice presented with not only ME but also higher levels of inflammatory markers, oxidative stress, and macrophage infiltration markers
  • This suggests that important links between gut microbiota, ME, inflammation, and oxidative stress are implicated in a high-fat diet situation
  • high-fat feeding is associated with adipose tissue macrophage infiltration (F4/80-positive cells) and increased levels of chemokine MCP-1, suggesting a strong link between ME, proinflammatory status, oxidative stress, and, lately, increased CV risk
  • LPS has been shown to promote atherosclerosis
  • markers of systemic inflammation such as circulating bacterial endotoxin were elevated in patients with chronic infections and were strong predictors of increased atherosclerotic risk
  • As a TLR4 ligand, LPS has been suggested to induce atherosclerosis development and progression, via a TLR4-mediated inflammatory state.
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    Very nice updated review on Metabolic endotoxemia
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