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Nathan Goodyear

Body Fat Distribution and Cortisol Metabolism in Healthy Men: Enhanced 5β-Red... - 0 views

jcem.endojournals.org/...4924.long

cortisone cortisol obesity overweight men 11-betaHSD type 1 5-alpha reductase metabolism

shared by Nathan Goodyear on 13 Mar 12 - No Cached
  • Nathan Goodyear on 13 Mar 12
     
    increased 11-betaHSD type 1 and increased 5-alpha reductase activity found to be associated with generalized obesity in men.  Both indicate increased cortisone to cortisol production.  
Nathan Goodyear

Sexual dimorphism in cortisol secretion starts after age 10 in healthy children: urinar... - 0 views

ajpendo.physiology.org/...E970

cortisol metabolites metabolism hormone hormones

shared by Nathan Goodyear on 23 May 14 - No Cached
  • Nathan Goodyear on 23 May 14
     
    good discussion of cortisol metabolite excretion in children.
Nathan Goodyear

http://www.biomed.cas.cz/physiolres/pdf/prepress/932627.pdf - 0 views

www.biomed.cas.cz/...932627.pdf

resistance training exercise resistance Testosterone cortisol men obese obesity hormone hormones

shared by Nathan Goodyear on 02 Sep 14 - No Cached
  • Nathan Goodyear on 02 Sep 14
     
    good discussion of the effects of resistance training on Testosterone and cortisol in obese men.  The literature is more more clear on the effects of resistance training on healthy men, but the evidence in obese men is less clear--likely due to the disrupted metabolism.
Nathan Goodyear

Glucocorticoids and 11beta-hydroxysteroid... [Minerva Endocrinol. 2007] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...17912154

cortisol 11-betaHSD1 obesity metabolic syndrome

shared by Nathan Goodyear on 14 Mar 12 - No Cached
  • Nathan Goodyear on 14 Mar 12
     
    Dysregulation of 11-betaHSD1 plays significant role in metabolic syndrome.  Decreased 11-betaHSD activity is found in the liver and increased 11-betaHSD1  is found in peripheral fat.  Take home: 11-betaHSD1 activity and cortisol metabolism differs in different tissue
Nathan Goodyear

Excessive Sugar Consumption May Be a Difficult Habit to Break: A View From the Brain an... - 0 views

press.endocrine.org/...jc.2014-4353

sugar sucrose brain hippocampus aspartame cortisol saliva salivary hormone hormones

shared by Nathan Goodyear on 20 Apr 15 - No Cached
  • Nathan Goodyear on 20 Apr 15
     
    Only abstract available here, but sugar in the form of sucrose found to lower cortisol.  Increased activity in the hippocampus was evident in the sucrose arm of this study.  Both of these activities will lead to stress induced food addictions--particularly of sugar.  Sugar is highly addictive and should be especially avoided in children.  Of note, this study followed the cortisol levels through saliva.
Nathan Goodyear

Dietary Macronutrient Content Alters Cortisol Metabolism Independently of Body Weight C... - 0 views

jcem.endojournals.org/...4480.long

cortisol 11-betaHSD1 low carb diet low carb carbohydrates metabolism macronutrients

shared by Nathan Goodyear on 07 Oct 13 - No Cached
  • Nathan Goodyear on 07 Oct 13
     
    Extra-adrenal cortisol production is increased by 11-Beta-HSD1 via low Carb diet.  This is counter to that seen in mice studies.  The fat content of the diet could explain this.  This study looked at men.
Nathan Goodyear

Kent Holtorf: Long Term Weight Loss - More Than Will Power? - 0 views

www.huffingtonpost.com/...-weight-loss---m_b_192933.html

leptin reverse T3 weight loss

shared by Nathan Goodyear on 09 Mar 11 - No Cached
  • which is a major reason for the regaining of lost weight with dieting as well being the mechanism behind stress induced weight gain (it is not due to increased cortisol).
  • f greater than 10, it demonstrates there is a degree of leptin resistance contributing to an inability to lose weight
  • that it is difficult to lose weight with leptin resistance. High carbohydrate diets and in particular high-fructose corn syrup is shown to significantly increase leptin resistance and is a likely mechanism that high fructose corn syrup is associated with obesity
  • ...9 more annotations...
  • inactive thyroid hormone called thyroxine
  • it is problem inside the cell that the inactive T4 is not converted to T3 but rather to a mirror image of T3 called reverse T3. The reverse T3 has the opposite effect of T3, blocking the effects of T3 and lowering rather than increasing metabolism.
  • Studies are showing that stress and dieting (especially yo-yo dieting) can set this hormone into action as well as chronic illness such as diabetes, chronic fatigue syndrome and fibromyalgia.
  • As soon as the body senses a reduction in calories, the production of reverse T3 is stimulated to lower metabolism
  • With chronic dieting or stress, the body often stays in this "starvation mode" with elevated levels of reverse T3 and decreased levels of T3, which is a major reason for the regaining of lost weight with dieting as well being the mechanism behind stress induced weight gain (it is not due to increased cortisol).
  • which is a major reason for the regaining of lost weight with dieting as well being the mechanism behind stress induced weight gain (it is not due to increased cortisol).
  • which is a major reason for the regaining of lost weight with dieting as well being the mechanism behind stress induced weight gain (it is not due to increased cortisol).
  • Studies are showing that such standard testing will miss 80% of thyroid dysfunction
  • ree T3/reverse T3 ratio
  • Nathan Goodyear on 09 Mar 11
     
    Fantastic review by Dr. Holtorf on reverse T3, leptin, and weight loss
Nathan Goodyear

Acute and delayed effects of a single-dose inject... [Metabolism. 1998] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...9781636

TSH thyroid TSH suppression IL-6 cytokine inflammation inflammatory

shared by Nathan Goodyear on 01 Feb 13 - No Cached
  • Nathan Goodyear on 01 Feb 13
     
    IL-6 is known to stimulate the HPA and increase cortisol production.  Both, IL-6 and cortisol can decrease TSH production.
Nathan Goodyear

Salivary cortisol and testosterone responses to resistance and plyometric exercise in 1... - 0 views

www.nrcresearchpress.com/...apnm-2015-0668

resistance training exercise testosterone cortisol hormones male hormones

shared by Nathan Goodyear on 16 May 16 - No Cached
  • Nathan Goodyear on 16 May 16
     
    Study of 12-14 y/o boys found increased Testosterone after resistance training and plyometric exercise.  Cortisol did increase after plyometric, but not resistance exercise.
Nathan Goodyear

Cortisol Measures Across the Weight Spectrum: The Journal of Clinical Endocrinology & M... - 0 views

press.endocrine.org/...JC.2015-2078

obesity overweight cortisol saliva salivary obese hormones anorexia women

shared by Nathan Goodyear on 28 Sep 15 - No Cached
  • Nathan Goodyear on 28 Sep 15
     
    Study looked at serum and salivary obesity in women: found that low cortisol was found in anorexia and class I obese women compared to normal weight women and that class II obesity was associated with hypercortisolism.
Nathan Goodyear

Out-Patient Screening for Cushing's Syndrome: The Sensitivity of the Combination of Cir... - 0 views

jcem.endojournals.org/...878

hormones hormone saliva testing salivary cortisol

shared by Nathan Goodyear on 20 Nov 10 - No Cached
  • Nathan Goodyear on 20 Nov 10
     
    salivary cortisol recommended for evaluating Cushing's syndrom
Nathan Goodyear

Effect of metoclopramide--a dopaminergic blocker a... [Acta Endocrinol (Copenh). 1985] ... - 0 views

www.ncbi.nlm.nih.gov/...4002999

cortisol T4 T3 rT3

shared by Nathan Goodyear on 14 Mar 11 - No Cached
  • High levels of cortisol may be responsible for the altered TT4 peripheral metabolism to TT3 and rT3 in these patients.
  • Nathan Goodyear on 14 Mar 11
     
    elevated cortisol blocks T4 to T3 conversion and increases rT3 production
Nathan Goodyear

Acute Suppression of Circulating Testosterone Levels by Cortisol in Men: The Journal of... - 0 views

press.endocrine.org/...jcem-57-3-671

Cortisol Testosterone stress men male hormone hormones

shared by Nathan Goodyear on 02 Apr 15 - No Cached
  • Nathan Goodyear on 02 Apr 15
     
    Cortisol inhibits Testosterone production in men.
Nathan Goodyear

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

jme.endocrinology-journals.org/...R51.full

metabolic endotoxemia obesity insulin resistance cardiovascular disease LPS inflammation

shared by Nathan Goodyear on 04 Aug 14 - No Cached
  • 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
  • ...37 more annotations...
  • 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.
  • Nathan Goodyear on 04 Aug 14
     
    Very nice updated review on Metabolic endotoxemia
Nathan Goodyear

http://www.cell.com/trends/endocrinology-metabolism/pdf/S1043-2760(00)00301-5.pdf - 0 views

www.cell.com/...S1043-2760(00)00301-5.pdf

fat adipose tissue aromatase cortisol leptin hormones obesity

shared by Nathan Goodyear on 29 Sep 16 - No Cached
  • Nathan Goodyear on 29 Sep 16
     
    Fat is a very active organ.  Increased aromatase due to cortisol.  Good review of Leptin signaling as well.  
Nathan Goodyear

JCI - Reduced activity of 11β-hydroxysteroid dehydrogenase in patients with c... - 0 views

www.jci.org/12745

11-betaHSD cortisol hormone hormones

shared by Nathan Goodyear on 23 May 14 - No Cached
  • Nathan Goodyear on 23 May 14
     
    good discussion of 11beta-HSD in cortisol metabolism
Nathan Goodyear

Cambridge Journals Online - Proceedings of the Nutrition Society - Fulltext -... - 0 views

journals.cambridge.org/...displayFulltext

11-betaHSD1 metabolism obesity energy cortisol nutrition

shared by Nathan Goodyear on 08 Oct 13 - No Cached
  • Nathan Goodyear on 08 Oct 13
     
    Peripheral 11Beta-HSD1 plays critical role in fat metabolism and energy utilization.  Good discussion on the role that extra-adrenal 11Beta-HSD1 plays in metabolism
Nathan Goodyear

http://www.dishlab.org/pubs/TomiyamaDallmanPMresponse2010.pdf - 0 views

www.dishlab.org/...iyamaDallmanPMresponse2010.pdf

cortisol cortisone cortisol:cortisone shunt cortisol: cortisone shuttle metabolism cortisol:cortisone

shared by Nathan Goodyear on 03 Jun 14 - No Cached
  • Nathan Goodyear on 03 Jun 14
     
    Great editorial on the complex metabolism of the cortisol:cortisone shunt.
Nathan Goodyear

Altered Cortisol Metabolism in Polycystic Ovary Syndrome: Insulin Enhances 5α... - 0 views

jcem.endojournals.org/...5907.short

PCOS women lean 11-betaHSD1 5-alpha-reductase androgens testosterone insulin syndrome

shared by Nathan Goodyear on 25 Apr 12 - No Cached
  • Nathan Goodyear on 25 Apr 12
     
    lean women with PCOS found to have reduced 11 beta-HSD1 and increased 5 alpha reductase activity.  This, in part, is associated with the elevated cortisol and androgens in these women.
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