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Nathan Goodyear

The obesity epidemic and nonalcoholic fatty liver ... [Curr Gastroenterol Rep. 2008] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...18417045

obesity epidemic NAFLD non-alcoholic fatty liver disease children

shared by Nathan Goodyear on 19 Aug 11 - No Cached
  • Nathan Goodyear on 19 Aug 11
     
    obesity and non-alcoholic fatty liver disease are one in the same.
Nathan Goodyear

Nonalcoholic Fatty Liver Disease - 0 views

diabetes.diabetesjournals.org/...1844.short

nonalcoholic fatty liver disease metabolic syndrome

shared by Nathan Goodyear on 06 Apr 11 - No Cached
  • aracterized by clinical and laboratory data similar to those found in diabetes and obesity. NAF
  • We concluded that NAFLD, in the presence of normoglycemia and normal or moderately increased body weight, is ch
  • aracterized by clinical and laboratory data similar to those found in diabetes and obesity. NAF
  • ...1 more annotation...
  • LD may be considered an additional feature of the metabolic syndrome, with specific hepatic insulin resistance
  • Nathan Goodyear on 06 Apr 11
     
    Fatty Liver is component of Metabolic Syndrome
curetick

Walnut Benefits and Side Effects | How to Eat Walnuts - 0 views

curetick.com/lnut-benefits-and-side-effects

walnut_for_weight_loss walnut_health_benefits walnut_oil_during_pregnancy walnut_oil_for_skin

shared by curetick on 22 Feb 18 - No Cached
  • curetick on 22 Feb 18
     
    The walnut benefits can also be useful for weight loss purpose. The containing omega-3 inside the walnut have fatty acids with other substances into it. The 2.5 grams of 'ALA' per serving is found rich beneficial sources as the fatty acid. From studies among the women's observed that having a walnut at diet can be helpful for reducing the weight loss with greater efficiency. It also lowers the 'bad' levels of LDL cholesterol from the body. And the higher levels of 'HDL' cholesterol in a good manner as suggested by the doctors.
Nathan Goodyear

Causative role of gut microbiota in non-alcoholic fatty liver disease pathogenesis - 0 views

www.ncbi.nlm.nih.gov/...PMC3481143

metabolic endotoxemia inflammation non-alcoholic fatty liver NAFLD gut bacteria fatty liver disease

shared by Nathan Goodyear on 14 Jan 13 - No Cached
  • Nathan Goodyear on 14 Jan 13
     
    metabolic endotoxemia plays role in NAFLD.  Gut bacterial balance plays a role in NAFLD.
Nathan Goodyear

metabolic correction for attention deficit/hyperactivity disorder: A biochemical-physiological therapeutic approach - 0 views

functionalfoodscenter.net/...63028864.pdf

ADHD diet children pediatrics minerals vitamins essential fatty acids amino acids

shared by Nathan Goodyear on 13 Feb 13 - No Cached
  • Nathan Goodyear on 13 Feb 13
     
    This study of 116 patients diagnosed with ADHD, found that 80% could achieve improvement or "ameliorate" ADHD symptoms with supplementation with minerals, vitamins, amino acids, and essential fatty acids. I too have seen this in my practice. Maybe ADD/ADHD is simply a gut/dietary problem manifested in the brains of our children. That we treat with powerful drugs, that simply can be treated with dietary change
Nathan Goodyear

Minireview: Inflammation and Obesity Pathogenesis: The Hypothalamus Heats Up - 0 views

endo.endojournals.org/...4109.full

inflammation obesity overweight hypothalamus HPA

shared by Nathan Goodyear on 04 Oct 12 - No Cached
  • Leptin, secreted by adipocytes in proportion to body fat mass
  • The saturated fatty acid palmitate (16:0) induces NF-κB signaling through a TLR4-dependent mechanism
  • 18:0 (stearic) and longer saturated fatty acids as well as linolenic acid (18:3) increased proinflammatory cytokines, ER stress markers, and TLR4 activation
  • ...6 more annotations...
  • (SOCS)-3. A member of a protein family originally characterized as negative feedback regulators of inflammation (13, 37), SOCS3 inhibits insulin and leptin signaling
  • IKKβ signaling in discrete neuronal subsets appears to be required for both hypothalamic inflammation and excess weight gain to occur during HF feeding
  • the paradoxical observation that hyperphagia and weight gain occur when hypothalamic inflammation is induced by HF feeding, yet when it occurs in response to systemic or local inflammatory processes (e.g. administration of endotoxin), anorexia and weight loss are the rule
  • , serves as a circulating signal of energy stores in part by providing feedback inhibition of hypothalamic orexigenic pathways [e.g. neurons that express neuropeptide Y and agouti-related peptide (AgRP)]
  • and stimulating anorexigenic neurons
  • signals from Toll-like receptors (TLRs), evolutionarily conserved pattern recognition molecules critical for detecting pathogens, amplified through signaling intermediates such as MyD88 activate the inhibitor of κB-kinase-β (IKKβ)/nuclear factor-κB (NF-κB), c-Jun N-terminal kinase (Jnk) and other intracellular inflammatory signals in response to stimulation by circulating saturated fatty acids
  • Nathan Goodyear on 04 Oct 12
     
    great read on the current understanding of how obesity and resultant inflammation disrupts hypothalamic function.
Nathan Goodyear

Role of Gut Microbiota and Short Chain Fatty Acids in Modulating Energy Harvest and Fat Partitioning in Youth: The Journal of Clinical Endocrinology & Metabolism: Vol 0, No 0 - 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

Saccharomyces boulardii Administration Changes Gut Microbiota and Reduces Hepatic Steatosis, Low-Grade Inflammation, and Fat Mass in Obese and Type 2 Diabetic db/db Mice - 0 views

mbio.asm.org/...e01011-14.long

saccharomyces boulardii gut gut flora gut microbiota obesity inflammation fatty liver diabetes overweight fat mass

shared by Nathan Goodyear on 05 Jun 16 - No Cached
  • Nathan Goodyear on 05 Jun 16
     
    Saccharomyces boulardii found to reduce weight, fat mass, fatty liver, and inflammation in mice diabetes and obesity models.
Nathan Goodyear

The Mediterranean diet improves hepatic steatosis and insulin sensitivity in individuals with non-alcoholic fatty liver disease - 0 views

www.sciencedirect.com/...S0168827813001347

NAFLD nutrition non-alcoholic fatty liver mediterranean diet liver disease fatty liver

shared by Nathan Goodyear on 27 Apr 16 - No Cached
  • Nathan Goodyear on 27 Apr 16
     
    Mediterranean diet reduced insulin resistance and liver steatosis in those with NAFLD.
Nathan Goodyear

Adherence to the Mediterranean diet is associated with the severity of non-alcoholic fatty liver disease - 0 views

www.sciencedirect.com/...S0261561413002380

mediterranean diet nutrition NAFLD fatty liver insulin resistance liver disease non-alcoholic fatty liver

shared by Nathan Goodyear on 27 Apr 16 - No Cached
  • Nathan Goodyear on 27 Apr 16
     
    In those with NAFLD, mediterranean diet associated with reduced insulin resistance and reduced severity of liver disease; it did not resolve NAFLD
Nathan Goodyear

effects of beta-hydroxybutyrate on cognition in memory-impaired adults - 0 views

w.numedica.net/...Reger%202004.pdf

ketogenic diet ketone bodies ketosis Alzheimer's disease neurodegenerative disease MCT medium chain fatty acids

shared by Nathan Goodyear on 25 Jun 12 - No Cached
  • Nathan Goodyear on 25 Jun 12
     
    Those with Alzheimer's disease have associated dysfunction of glucose metabolism in the brain, particularly in the hippocampus. It has been reported that a ketogenic diet can improve cognitive function in these individuals. In this study, the ketone bodies were initiated through a diet high in medium chain fatty acids. The ketone bodies served as an alternative fuel source for the brain.
Nathan Goodyear

PPARs, Obesity, and Inflammation - 0 views

www.ncbi.nlm.nih.gov/...PMC1783744

obesity inflammation PPARs perioxisome proliferator-activated receptor

shared by Nathan Goodyear on 16 Jan 12 - No Cached
  • increase of 61% within 10 years
  • Many of the inflammatory markers found in plasma of obese individuals appear to originate from adipose tissue
  • obesity is a state of chronic low-grade inflammation that is initiated by morphological changes in the adipose tissue.
  • ...19 more annotations...
  • secretion of MCP-1, resistin, and other proinflammatory cytokines is increased by obesity, the adipose secretion of the anti-inflammatory protein adiponectin is decreased
  • the peroxisome proliferators- activated receptor (PPAR) family are involved in the regulation of inflammation and energy homestasis
  • natural agonists, including unsaturated fatty acids and eicosanoids
  • PPARα also regulates inflammatory processes, mainly by inhibiting inflammatory gene expression
  • upregulation of COX-2 is seen in alcoholic steatohepatitis and nonalcoholic steatohepatitis and has been directly linked to the progression of steatosis to steatohepatitis, the inhibitory effect of PPARα on COX-2 may reduce steatohepatitis
  • PPARα agonists have a clear anorexic effect resulting in decreased food intake, evidence is accumulating that PPARα may also directly influence adipose tissue function, including its inflammatory status.
  • PPARα may govern adipose tissue inflammation in three different ways: (1) by decreasing adipocyte hypertrophy, which is known to be connected with a higher inflammatory status of the tissue [3, 11, 59], (2) by direct regulation of inflammatory gene expression via locally expressed PPARα, or (3) by systemic events likely originating from liver
  • PPARγ is considered the master regulator of adipogenesis
  • Unsaturated fatty acids and several eicosanoids serve as endogenous agonists of PPARγ
  • PPARγ2, which is adipose-tissue specific
  • two different molecular mechanisms have been proposed by which anti-inflammatory actions of PPARγ are effectuated: (1) via interference with proinflammatory transcription factors including STAT, NF-κB, and AP-1
  • and (2) by preventing removal of corepressor complexes from gene promoter regions resulting in suppression of inflammatory gene transcription
  • diet-induced obesity is associated with increased inflammatory gene expression in adipose tissue via adipocyte hypertrophy and macrophage infiltration
  • PPARγ is able to reverse macrophage infiltration, and subsequently reduces inflammatory gene expression
  • Inflammatory adipokines mainly originate from macrophages which are part of the stromal vascular fraction of adipose tissue [18, 19], and accordingly, the downregulation of inflammatory adipokines in WAT by PPARγ probably occurs via effects on macrophages
  • By interfering with NF-κB signaling pathways, PPARγ is known to decrease inflammation in activated macrophages
  • Recent data suggest that activation of PPARγ in fatty liver may protect against inflammation
  • PPARs may influence the inflammatory response either by direct transcriptional downregulation of proinflammatory genes
  • anti-inflammatory properties of PPARs in human obesity
  • Nathan Goodyear on 16 Jan 12
     
    PPARs play pivotal in obesity.  PPARs appear to reduce the inflammatory cascade associated with obesity.  Downregulation of PPARs are associated with increased inflammation.  Natural PPARs include unsaturated fats and eicosanoids.
Nathan Goodyear

Access : FFA-Induced Adipocyte Inflammation and Insulin Resistance: Involvement of ER Stress and IKK|[beta]| Pathways : Obesity - 0 views

www.nature.com/...oby2010200a.html

FFA inflammation overweight obesity free fatty acids insulin resistance IKK-Beta endoplasmic reticulum stress

shared by Nathan Goodyear on 21 Dec 11 - No Cached
  • Nathan Goodyear on 21 Dec 11
     
    elevated FFA (free-fatty acids) shown to produce inflammation and insulin resistance through endoplasmic reticulum stress.  The main target in this pathway is IKK-Beta overexpression.
Nathan Goodyear

[Glutathione in the treatment of ch... [Recenti Prog Med. 1995 Jul-Aug] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...7569285

IV glutathione detoxification fatty liver disease NAFLD

shared by Nathan Goodyear on 10 Nov 11 - No Cached
  • Nathan Goodyear on 10 Nov 11
     
    high dose IV glutathione shown to reduce liver enzymes and thus liver cell damage in those with chronic fatty liver disease
Nathan Goodyear

Effects of supplementation with fish oil-derived n−3 fatty acids and γ-linolenic acid on circulating plasma lipids and fatty acid profiles in women - 0 views

www.ajcn.org/37.full

Omega-3 n-3 GLA fish oil cholesterol LDL fatty acids fish oil

shared by Nathan Goodyear on 23 Jul 12 - No Cached
  • Nathan Goodyear on 23 Jul 12
     
    mixture of omega-3 and GLA shown to statistically lower LDL.  The mixture that was statistically significant was 4:2.
Nathan Goodyear

Access : Nonalcoholic fatty liver disease: Microbiota in the pathogenesis of systemic autoinflammatory and metabolic disorders : Nature Reviews Endocrinology - 0 views

www.nature.com/...nrendo.2012.25.html

fatty liver disease NAFLD non-alcoholic fatty liver inflammation dysbiosis metabolic

shared by Nathan Goodyear on 02 Aug 12 - No Cached
  • Nathan Goodyear on 02 Aug 12
     
    Fascinating read of how inflammation as a direct result of dysbiosis in the gut contributes to the progression of NALFD.
Nathan Goodyear

When and how to evaluate mildly elevated liver enzymes in apparently healthy patients - 0 views

ccjm.org/195.full

elevated liver enzymes non-alcoholic fatty disease (NAFLD)

shared by Nathan Goodyear on 05 Mar 12 - No Cached
  • Nathan Goodyear on 05 Mar 12
     
    with an estimated 25% of Americans with non-alcoholic fatty liver disease (NAFLD), elevated liver enzymes are becoming a more common finding.  Nice review article on what the tests mean and what disease are underlying.
Nathan Goodyear

PLOS ONE: Effect of Marine-Derived n-3 Polyunsaturated Fatty Acids on C-Reactive Protein, Interleukin 6 and Tumor Necrosis Factor α: A Meta-Analysis - 0 views

www.plosone.org/...10.1371%2Fjournal.pone.0088103

inflammation omega 3 omega-3 n-3 CRP IL-6 TNF-alpha

shared by Nathan Goodyear on 14 Feb 14 - No Cached
  • Nathan Goodyear on 14 Feb 14
     
    meta-analysis finds that omega-3 fatty acids decrease CRP, IL-6, and TNF-alpha.
Nathan Goodyear

Synbiotic supplementation in nonalcoholic fatty liver disease: a randomized, double-blind, placebo-controlled pilot study - 0 views

ajcn.nutrition.org/...535.abstract

NAFLD non-alcoholic fatty liver synbiotics probiotic probiotics synbiotic fatty

shared by Nathan Goodyear on 18 Mar 14 - No Cached
  • Nathan Goodyear on 18 Mar 14
     
    small pilot study finds that synbiotics, probiotics and prebiotics, + lifestyle modifications work better than lifestyle modifications alone in NAFLD.
Nathan Goodyear

Nutrition & Metabolism | Full text | Fructose, insulin resistance, and metabolic dyslipidemia - 0 views

www.nutritionandmetabolism.com/...5

fructose metabolic syndrome metabolic syndrome insulin resistance obesity nutrition metabolism

shared by Nathan Goodyear on 16 Sep 13 - Cached
  • For thousands of years humans consumed fructose amounting to 16–20 grams per day
  • daily consumptions amounting to 85–100 grams of fructose per day
  • Of key importance is the ability of fructose to by-pass the main regulatory step of glycolysis, the conversion of glucose-6-phosphate to fructose 1,6-bisphosphate, controlled by phosphofructokinase
  • ...29 more annotations...
  • Thus, while glucose metabolism is negatively regulated by phosphofructokinase, fructose can continuously enter the glycolytic pathway. Therefore, fructose can uncontrollably produce glucose, glycogen, lactate, and pyruvate, providing both the glycerol and acyl portions of acyl-glycerol molecules. These particular substrates, and the resultant excess energy flux due to unregulated fructose metabolism, will promote the over-production of TG (reviewed in [53]).
  • Glycemic excursions and insulin responses were reduced by 66% and 65%, respectively, in the fructose-consuming subjects
  • reduction in circulating leptin both in the short and long-term as well as a 30% reduction in ghrelin (an orexigenic gastroenteric hormone) in the fructose group compared to the glucose group.
  • A prolonged elevation of TG was also seen in the high fructose subjects
  • Both fat and fructose consumption usually results in low leptin concentrations which, in turn, leads to overeating in populations consuming energy from these particular macronutrients
  • Chronic fructose consumption reduces adiponectin responses, contributing to insulin resistance
  • A definite relationship has also been found between metabolic syndrome and hyperhomocysteinemia
  • the liver takes up dietary fructose rapidly where it can be converted to glycerol-3-phosphate. This substrate favours esterification of unbound FFA to form the TG
  • Fructose stimulates TG production, but impairs removal, creating the known dyslipidemic profile
  • the effects of fructose in promoting TG synthesis are independent of insulinemia
  • Although fructose does not appear to acutely increase insulin levels, chronic exposure seems to indirectly cause hyperinsulinemia and obesity through other mechanisms. One proposed mechanism involves GLUT5
  • If FFA are not removed from tissues, as occurs in fructose fed insulin resistant models, there is an increased energy and FFA flux that leads to the increased secretion of TG
  • In these scenarios, where there is excess hepatic fatty acid uptake, synthesis and secretion, 'input' of fats in the liver exceed 'outputs', and hepatic steatosis occurs
  • Carbohydrate induced hypertriglycerolemia results from a combination of both TG overproduction, and inadequate TG clearance
  • fructose-induced metabolic dyslipidemia is usually accompanied by whole body insulin resistance [100] and reduced hepatic insulin sensitivity
  • Excess VLDL secretion has been shown to deliver increased fatty acids and TG to muscle and other tissues, further inducing insulin resistance
  • the metabolic effects of fructose occur through rapid utilization in the liver due to the bypassing of the regulatory phosphofructokinase step in glycolysis. This in turn causes activation of pyruvate dehydrogenase, and subsequent modifications favoring esterification of fatty acids, again leading to increased VLDL secretion
  • High fructose diets can have a hypertriglyceridemic and pro-oxidant effect
  • Oxidative stress has often been implicated in the pathology of insulin resistance induced by fructose feeding
  • Administration of alpha-lipoic acid (LA) has been shown to prevent these changes, and improve insulin sensitivity
  • LA treatment also prevents several deleterious effects of fructose feeding: the increases in cholesterol, TG, activity of lipogenic enzymes, and VLDL secretion
  • Fructose has also been implicated in reducing PPARα levels
  • PPARα is a ligand activated nuclear hormone receptor that is responsible for inducing mitochondrial and peroxisomal β-oxidation
  • decreased PPARα expression can result in reduced oxidation, leading to cellular lipid accumulation
  • fructose diets altered the structure and function of VLDL particles causing and increase in the TG: protein ratio
  • LDL particle size has been found to be inversely related to TG concentration
  • therefore the higher TG results in a smaller, denser, more atherogenic LDL particle, which contributes to the morbidity of the metabolic disorders associated with insulin resistance
  • High fructose, which stimulates VLDL secretion, may initiate the cycle that results in metabolic syndrome long before type 2 diabetes and obesity develop
  • A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, disturbs normal hepatic carbohydrate metabolism leading to two major consequences (Figure 2): perturbations in glucose metabolism and glucose uptake pathways, and a significantly enhanced rate of de novo lipogenesis and TG synthesis, driven by the high flux of glycerol and acyl portions of TG molecules coming from fructose catabolism
  • Nathan Goodyear on 16 Sep 13
     
    Fructose and metabolic syndrome.  Good discussion of the impact of high fructose intake and metabolic dysfunction.  This study also does a great job of highlighting the historical change of fructose intake.
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