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Nathan Goodyear

Obesity and Severe Obesity Forecasts Through 2030 - 0 views

www.ajpmonline.org/...abstract

obesity

shared by Nathan Goodyear on 02 Jan 14 - No Cached
  • Nathan Goodyear on 02 Jan 14
     
    Obesity rates expected to top 50% of the population by 2030.  The Severe obesity rate is expected at 11%, which sounds better, but the rate currently sits at 6.3%.  Overalls, obesity is expected to increase by 33% with those in the severe category increasing by 130%.  These type of numbers require a refocus on out methods of curbing this trend, because our current gimmick-based therapies are not working
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

The ISME Journal - An opportunistic pathogen isolated from the gut of an obese human ca... - 0 views

www.nature.com/...ismej2012153a.html

obesity obese LPS endotoxin dysbiosis GI gut

shared by Nathan Goodyear on 20 Dec 12 - No Cached
  • Nathan Goodyear on 20 Dec 12
     
    LPS endotoxin found to increase obesity rates in mice.  The bacteria balance in the gut and the toxins they produce can contribute to the incidence of obesity.
Nathan Goodyear

Regulatory Mechanisms for Adipose Tissue M1 and M2 Macrophages in Diet-Induced Obese Mice - 0 views

diabetes.diabetesjournals.org/...2574.full

obesity overweight weight-loss M1 macrophage M2 ATM inflammation TNF-alpha IL-6

shared by Nathan Goodyear on 03 Jan 12 - No Cached
  • Nathan Goodyear on 03 Jan 12
     
    M1 macrophages (and a high M1/M2 ratio) promote inflammation and insulin resistance in obese individuals; This is in contrast to M2 macrophages.  Obese individuals will see a shift in M2 to M1.  The exact mechanism is yet unknown.  But M2 macrophages have been shown to resolve insulin resistance in this obese mice model
Nathan Goodyear

PLOS ONE: Probiotic Microbes Sustain Youthful Serum Testosterone Levels and Testicular ... - 0 views

journals.plos.org/...article

hormone hormones low T low Testosterone hypogonadism Testosterone probiotic L reuters probiotics Lactobacillus lactobacillus reuteri male aging

shared by Nathan Goodyear on 29 Apr 15 - No Cached
  • Studies in both humans and rodents, however, suggest that low testosterone is due to age-related lesions in testes rather than irregular luteinizing hormone metabolism
  • Various dietary factors and diet-induced obesity have been shown to increase the risk for late onset male hypogonadism and low testosterone production in both humans and mice
  • Testosterone deficiency and metabolic diseases such as obesity appear to inter-digitate in complex cause-and-effect relationships
  • ...28 more annotations...
  • dietary supplementation of aged mice with the probiotic bacterium Lactobacillus reuteri makes them appear to be younger than their matched untreated sibling mice
  • These results indicate that gut microbiota induce modulation of local gastrointestinal immunity resulting in systemic effects on the immune system which activate metabolic pathways that restore tissue homeostasis and overall health
  • all these studies we consistently observed that young and aged mice consuming purified L. reuteri organisms had particularly large testes and a dominant male behavior.
  • The testes of probiotic-fed aged mice were rescued from both seminiferous tubule atrophy and interstitial Leydig cell area reduction typical of the normal aging process. Preservation of testicular architecture despite advanced age or high-fat diet coincided with remarkably high levels of circulating testosterone. The beneficial effects of probiotic consumption were recapitulated by the depletion of the pro-inflammatory cytokine Il-17.
  • feeding of L. reuteri consistently increased the gonadal weights, consumption of a non-pathogenic strain of Escherichia coli (E. coli) K12 organisms did not affect testicular weight
  • mice with dietary L. reuteri supplements were rescued from diet-induced obesity and had normal body weight and lean physique
  • Despite the comparable numbers of ST profiles, we determined that testes from L. reuteri-treated mice had increased ST cross-sectioned profiles
  • the probiotic organism induced prominent Leydig cell accumulations in the interstitial tissue between the ST's
  • The probiotic-associated increase of interstitial Leydig cell areas was sustained with advancing age at 7 (CD vs CD+LR, P = 0.0025; CD+E.coli vs CD+LR, P = 0.0251) and 12 months
  • mice eating L. reuteri had profoundly increased levels of circulating testosterone regardless of the type of diet they consumed
  • blocking pro-inflammatory Il-17 signaling entirely recapitulates the beneficial effects of probiotics
  • previous studies we found that dietary probiotics counteract obesity [19] and age-related integumentary pathology [18] at least in part by down-regulating systemic pro-inflammatory IL-17A-dependent signaling
  • Testes histomorphometry and serum androgen concentration data were both suggestive of a probiotic-associated up-regulation of spermatogenesis in mice
  • Lactobacillus reuteri we discovered that aging male animals had larger testes compared to their age-matched controls
  • xamined testes of probiotic microbe-fed mice and found that they had less testicular atrophy coinciding with higher levels of circulating testosterone compared to their age-matched controls
  • Similar testicular health benefits were produced using systemic depletion of the pro-inflammatory cytokine Il-17 alone, implicating a chronic inflammatory pathway in hypogonadism
  • One specific aspect of this paradigm is reciprocal activities of pro-inflammatory Th-17 and anti-inflammatory Treg cells
  • Feeding of L. reuteri organisms was previously shown to up-regulate IL-10 levels and reduce levels of IL-17 [19] serving to lower systemic inflammation
  • insufficient levels of IL-10 may increase the risk for autoimmunity, obesity, and other inflammatory disease syndromes
  • Westernized diets are also low in vitamin D, a nutrient that when present normally works together with IL-10 to protect against inflammatory disorders
  • Physiological feedback loops apparently exist between microbes, host hormones, and immunity
  • The hormone testosterone has been shown to act directly through androgen receptors on CD4+ cells to increase IL-10 expression
  • studies in both humans and rodents suggest that hypogonadism is due to age-related lesions in testes rather than irregular LH metabolism
  • We postulate that probiotic gut microbes function symbiotically with their mammalian hosts to impart immune homeostasis to maintain systemic and testicular health [34]–[35] despite suboptimal dietary conditions.
  • Dietary factors and diet-induced obesity were previously shown to increase risk for age-associated male hypogonadism, reduced spermatogenesis, and low testosterone production in both humans and mice [2]–[4], [8]–[11], [14]–[17], phenotypic features that in this study were inhibited by oral probiotic therapy absent milk sugars, extra protein, or vitamin D supplied in yogurt.
  • Similar beneficial effects of probiotic microbes on testosterone levels and sperm indices were reported in male mice that had been simultaneously supplemented with selenium
  • L. reuteri-associated prevention of age- and diet-related testicular atrophy correlates with increased numbers and size of Leydig cells
  • the initial changes of testicular atrophy begin to occur in mice from the age of 6 moths onwards [7] and indicates that the trophic effect of L. reuteri on Leydig cells is a key event which precedes and prevents age-related changes in the testes of mice. This effect is reminiscent of earlier studies describing Leydig cell hyperplasia and/or hypertrophy in the mouse and the rat testis that were achievable by the administration of gonadotropins, including human chorionic gonadotropin, FSH and LH
  • Nathan Goodyear on 29 Apr 15
     
    Fascinating study on how the addition of Lactobacillus reuteri increased Testicular size, prevented testicular atrophy, increased serum Testosterone production and protected against diet-induced/obesity-induced hypogonadism.  This was a mouse model
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
  • ...21 more annotations...
  • 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

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

Effects of endocrine disruptors on obesity. [Int J Androl. 2008] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...18315718

obesity endocrine disruptors toxins toxicity

shared by Nathan Goodyear on 06 Apr 11 - No Cached
  • Most recently, obesity has been proposed to be yet another adverse health effect of exposure to endocrine disrupting chemicals (EDCs) during critical stages of development. Obesity is quickly becoming a significant human health crisis
  • The emerging idea of an association of EDCs and obesity expands the focus on obesity from intervention and treatment to include prevention and avoidance of these chemical modifiers.
  • Nathan Goodyear on 06 Apr 11
     
    Effects of endocrine disruptors on obesity.
Nathan Goodyear

European Journal of Clinical Nutrition - Effect of maternal n-3 long-chain polyunsatura... - 0 views

www.nature.com/...ejcn2014158a.html

nutrition n-3 omega 3 omega-3 fish oil pregnancy childhood obesity

shared by Nathan Goodyear on 22 Dec 14 - No Cached
  • It is estimated that approximately 30% of children and adolescents in the United States and about 15–30% of those in Europe can be classified as overweight or obese
  • An increasing body of evidence now suggests that the nutritional environment encountered in utero and the early postnatal life may elicit permanent alterations in adipose tissue structure or function and, thereby, programme the individual’s propensity to later obesity
  • The composition of fatty acids in the Western diets has shifted toward an increasing dominance of n-6 relative to n-3 LCPUFAs over the past decades.9,10 This shift is also reflected in the fatty acid composition of breast milk
  • ...8 more annotations...
  • Evidence from animal studies suggests that the n-6 LCPUFA arachidonic acid promotes adipose tissue deposition, whereas the n-3 LCPUFAs eicosapentaenoic acid and docosahexaenoic acid seem to exert an opposite effect
  • Overall, no effect of supplementation was found on BMI in preschool (<5 years) and school-aged (6–12 years) children
  • increased adiposity, once established in childhood, tends to track into adulthood
  • Many studies have shown that even children <2 years with a high BMI are at increased risk of developing obesity later in life
  • The acquisition of fat cells early in life appears to be an irreversible process
  • Evidence from cell culture and animal studies suggests that early exposure to n-3 LCPUFAs has the potential to limit adipose tissue deposition mainly by attenuating the production of the arachidonic acid metabolite prostacyclin, which has been shown to enhance adipogenesis
  • In conclusion, there is currently no evidence to support that maternal n-3 LCPUFA supplementation during pregnancy and/or lactation exerts a favourable programming effect on adiposity status in childhood
  • our systematic review highlights that most of the trials reviewed were prone to methodological limitations
  • Nathan Goodyear on 22 Dec 14
     
    Literature review finds limited data (9 studies, only 6 RCTs) of omega-3 during pregnancy.  No data was found that supported reduced obesity in children by mothers taking n-3 during pregnancy.  No harm was found either.  Data was sparse.   Take home: not enough data, no harm to pregnancy, children, thus if indications are present for mother, then recommend n-3.  At this point not studies have pointed to reduced obesity in children.
Nathan Goodyear

http://www.hairlosshelp.com/pdf/insulin.pdf - 0 views

www.hairlosshelp.com/...insulin.pdf

insulin SHBG Testosterone male men hormone hormones obese obesity

shared by Nathan Goodyear on 03 Mar 15 - No Cached
  • Nathan Goodyear on 03 Mar 15
     
    Men with Obesity are found to have lower SHBG and Testosterone levels.  This study found that suppression of insulin resulted in an increase in SHBG production from the liver in both obese and normal weight men.  Of note, the decrease in insulin resulted in a decrease in male Testosterone in both normal weight and obese men.
Nathan Goodyear

AMA Journals - The Perils of Marketing Weight Management Remedies and the Role of Healt... - 0 views

journals.ama.org/...jppm.13.031

obese obesity weight loss drugs weight loss weight management health

shared by Nathan Goodyear on 18 Nov 14 - No Cached
  • Nathan Goodyear on 18 Nov 14
     
    Do weight loss drugs reduce obesity or could they actually increase obesity rates? The search for gimmicks has created a dependance on weight-loss drug falsehoods that don't work long term.  Life style has been and continues to be the long term answer.  Weight-loss drugs actually are fueling the obesity trend due to a lack of metabolic solutions.   They work for the health of pharma profits, just not for the health of the patient.
Nathan Goodyear

Obesity Rates Increased in These 6 States - 0 views

www.livescience.com/rates-increase-six-states.html

obesity rates obese

shared by Nathan Goodyear on 21 Nov 14 - No Cached
  • Nathan Goodyear on 21 Nov 14
     
    New study finds previous obesity data woefully underestimating rates.  This study finds that obesity rates exceed 35% in Mississippi and West Virginia.
Nathan Goodyear

SHBG and testosterone are associated with inflammation in obese men - 0 views

www.endocrine-abstracts.org/...ea0032p761.htm

inflammation CRP cytokines obesity low T low Testosterone SHBG men male hormone hormones

shared by Nathan Goodyear on 07 Apr 15 - No Cached
  • Nathan Goodyear on 07 Apr 15
     
    Though, obesity is associated with increasing SHBG, inflammation (which is typically elevated in obesity) is negatively associated with SHBG.  CRP was used to evaluate inflammation in this study of obese men.  Testosterone was also negatively associated with inflammation in these men.
Nathan Goodyear

The Adipose Transcriptional Response to Insulin Is Determined by Obesity, Not Insulin S... - 0 views

www.cell.com/...S2211-1247(16)31014-2

obesity insulin resistance

shared by Nathan Goodyear on 23 Aug 16 - No Cached
  • Nathan Goodyear on 23 Aug 16
     
    Study disproves "healthy obesity".  The same underlying insulin resistance and altered transcription is present in "healthy obese" and obese individuals.  
Nathan Goodyear

http://www.nature.com/ijo/journal/v24/n2s/pdf/0801281a.pdf?origin=publication_detail - 0 views

www.nature.com/...0801281a.pdf

SHBG IR insulin resistance insulin Estrogen Estradiol obesity hormone hormones

shared by Nathan Goodyear on 02 Mar 15 - No Cached
  • Nathan Goodyear on 02 Mar 15
     
    Elevated insulin levels in men is associated with decreased liver production of SHBG and thus reduced SHBG levels.  Obesity is associated with decreased urinary cortisol in this study.  The authors found the low cortisol also contributed to the low SHBG as well. Low SHBG is associated with puberty, obesity, IR, hypothyroidism, and during androgen therapy.  SHBG is increased as a result of aging, short-term fasting, Estrogen, hyperthyroid, and liver disease.
Nathan Goodyear

International Journal of Obesity - Obesity is associated with impaired immune response ... - 0 views

www.nature.com/...ijo2011208a.html

obesity flu vaccine vaccinations influenza

shared by Nathan Goodyear on 10 May 16 - No Cached
  • Nathan Goodyear on 10 May 16
     
    flu vaccine not effective in obese individuals due to compromised CD8 cell activity; no surprise due to the fact that obesity is an inflammatory disease.
Nathan Goodyear

Role of Gut Microbiota and Short Chain Fatty Acids in Modulating Energy Harvest and Fat... - 0 views

press.endocrine.org/...jc.2016-1797

obesity gut gut flora gut microbiome gut microbiota butyrate firmicutes_bacteroidetes firmicutes bacteroidetes

shared by Nathan Goodyear on 22 Sep 16 - No Cached
  • Nathan Goodyear on 22 Sep 16
     
    gut bacteria differentiate obese versus non-obese.  Association found b/t firmicutes:bacteroidetes, increased Bacteroidetes, and Actinobacteria; in addition, acute, propionate, and butyrate (all medium chain fatty acids) were found to be associated with obesity.
Nathan Goodyear

Obesity and Gender influence cortisol secretion and metabolism in man - 0 views

jcem.endojournals.org/...1806.full.pdf

obesity obese overweight cortisol cortisone HPA

shared by Nathan Goodyear on 24 Apr 12 - No Cached
  • Nathan Goodyear on 24 Apr 12
     
    This study reveals the degree of metabolism dysfunction in obesity. This study suggests that cortisol metabolism is increased in obesity, which results in increased HPA activity resulting in increased peripheral cortisol production. The question to be asked: is serum, salivary, and urinary cortisol results revealing the same function of cortisol. The answer is no.
Nathan Goodyear

Annual Medical Spending Attributable To Obesity: Payer-And Service-Specific Estimates - 0 views

content.healthaffairs.org/...w822.short

Obese obesity costs cost medical costs

shared by Nathan Goodyear on 13 May 12 - No Cached
  • Nathan Goodyear on 13 May 12
     
    Obese individuals spend, on average, $1,400 more annually on medical costs than healthy individuals.  The costs associated with obesity have increased from $78.5 billion in '98 to $147 billion in '08.  
Nathan Goodyear

Evaluation of the effect of caloric restriction on... [Endocrine. 2008] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...19012000

BDNF obesity calorie restriction calorie-restriction neuroplasticity neurogenesis

shared by Nathan Goodyear on 25 Jun 12 - No Cached
  • Nathan Goodyear on 25 Jun 12
     
    In this study, weight loss through a calorie restriction diet, resulted in  an increase in BDNF.  The implications here is that obesity decreases BDNF, which is very important in neuroplasticity and neurogenesis.  Take home, obesity has negative effects on your brain. Remember that old commercial: "this is your brain on drugs".  Well, this is your brain with obesity.
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