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Nathan Goodyear

Cortisol Exerts Bi-Phasic Regulation of Inflammation in Humans - 0 views

www.ncbi.nlm.nih.gov/...PMC3186928

cortisol glucocorticoids inflammation hormones

shared by Nathan Goodyear on 12 Oct 16 - No Cached
  • GCs induce increased cellular expression of receptors for several pro-inflammatory cytokines including interleukin (IL)-1 (Spriggs et al. 1990), IL-2 (Wiegers et al. 1995), IL-4 (Paterson et al. 1994), IL-6 (Snyers et al. 1990), and IFN-g (Strickland et al. 1986), as well as GM-CSF
  • GCs have also been shown to stimulate effector cell functions including phagocytosis by monocytes (van der Goes et al. 2000), effector cell proliferative responses (Spriggs et al. 1990), macrophage activation (Sorrells and Sapolsky 2010), and a delay of neutrophil apoptosis
  • a concentration- and time-dependent range of GC effects that are both pro- and anti-inflammatory
  • ...13 more annotations...
  • basal (diurnal) concentrations of cortisol do not exert an anti-inflammatory effect on several pro-and anti-inflammatory mediators of the human immune inflammatory response
  • withdrawal of cortisol activity in vivo did not lead to increased inflammatory responsiveness of immune effector cells
  • maximal suppression of inflammation was achieved by a stress-associated, but still physiologic, cortisol concentration. There was no greater anti-inflammatory effect at higher cortisol concentrations (Yeager et al. 2005) although IL-10 concentrations continued to increase with increasing cortisol concentrations as we and others have shown
  • acutely, physiological cortisol concentrations are anti-inflammatory and, as proposed, act to limit over expression of an inflammatory response that could lead to tissue damage
  • Acutely, cortisol has anti-inflammatory effects following a systemic inflammatory stimulus (Figure 4). However, a cortisol concentration that acts acutely to suppress systemic inflammation also has a delayed effect of augmenting the inflammatory response to subsequent, delayed stimulu
  • 1) GCs can exert pro-inflammatory effects on key inflammatory processes and, 2) GC regulation of inflammation can vary from anti- to a pro-inflammatory in a time-dependent manner
  • The immediate in vivo effect of both stress-induced and pharmacological GC concentrations is to suppress concurrent inflammation and protect the organism from an excessive or prolonged inflammatory response
  • GCs alone, in the absence of an inflammatory stimulus, up-regulate monocyte mRNA and/or receptors for several molecules that participate in pro-inflammatory signaling, as noted above and in the studies presented here.
  • In humans, as shown here, if in vivo GC concentrations are elevated concurrent with an inflammatory stimulus, anti-inflammatory effects are observed
  • In sharp contrast, with a time delay of 12 or more hours between an increased GC concentration and the onset of an inflammatory stimulus, enhancing effects on inflammation are observed. These effects have been shown to persist in humans for up to 6 days
  • GC-induced enhancement of inflammatory responses is maximal at an intermediate concentration, in our studies at a concentration that approximates that observed in vivo following a major systemic inflammatory stimulus
  • In addition to enhanced responses to LPS, recently identified pro-inflammatory effects of GCs also show enhanced localization of effector cells at inflammatory sites
  • we hypothesize that pre-exposure to stress-associated cortisol concentrations “prime” effector cells of the monocyte/macrophage lineage for an augmented pro-inflammatory response by; a) inducing preparative changes in key regulators of LPS signal transduction, and b) enhancing localization of inflammatory effector cells at potential sites of injury
  • Nathan Goodyear on 12 Oct 16
     
    very interesting read on the effects of inflammation on cortisol and visa versa.
Nathan Goodyear

Lipoprotein(a) as a cardiovascular risk factor: ... [Eur Heart J. 2010] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...20965889

Lp(a) lipoprotein a cardiovascular risk disease CVD

shared by Nathan Goodyear on 06 Aug 14 - No Cached
  • Nathan Goodyear on 06 Aug 14
     
    Lp(a) is a useful biomarker in the overall assessment of those at moderate to high risk of CVD.
Nathan Goodyear

Oral spore-based probiotic supplementation was associated with reduced incidence of pos... - 0 views

www.wjgnet.com/...117.htm

probiotics spore probiotics LPS lipopolysaccharides IL-1beta inflammation gut gut bacteria gut flora gut health gut microbiome gut microbiota

shared by Nathan Goodyear on 05 Oct 17 - No Cached
  • Nathan Goodyear on 05 Oct 17
     
    Study finds spore probiotic for 30 days reduced LPS endotoxin by 42%, while the placebo group found a 36% increase.  As a result, and to no surprise, there was a significant drop in IL-beta.  Also, in the spore probiotic group, there was a 24% reduction in triglycerides.
Nathan Goodyear

Lipoprotein(a) Mass: A Massively Misunderstood Metric - Journal of Clinical Lipidology - 0 views

www.lipidjournal.com/...abstract

Lp(a) lipoprotein(a) heart health cardiovascular disease risk

shared by Nathan Goodyear on 26 Aug 14 - No Cached
  • Nathan Goodyear on 26 Aug 14
     
    Lp(a), especially the particle #, is highly associated with increased cardiovascular risk.
Nathan Goodyear

http://orthomolecular.org/library/jom/1992/pdf/1992-v07n01-p005.pdf - 0 views

orthomolecular.org/...1992-v07n01-p005.pdf

vitamin C CVD Pauling Linus Pauling Lp(a) cardiovascular disease hypertension

shared by Nathan Goodyear on 16 Jan 17 - No Cached
  • Nathan Goodyear on 16 Jan 17
     
    This is the unified paper theory of CVD and vitamin C as published by Pauling and Rath.  Vitamin C deficiency results in a decrease in the integrity and stability of the vascular wall.  Chronic deficiency results in in an increase in and accumulation of Lp(a) which leads to atherosclerotic plaques.
Nathan Goodyear

Lipoprotein(a) levels and long-term cardiovascular risk in the contemporary era of stat... - 0 views

www.ncbi.nlm.nih.gov/...PMC2936758

Lp(a) lipoprotein(a) cardiovascular disease risk heart health

shared by Nathan Goodyear on 26 Aug 14 - No Cached
  • Nathan Goodyear on 26 Aug 14
     
    Lp(a) found to highly correlate with obstructive coronary disease.
Nathan Goodyear

The gut-liver-axis: Endotoxemia, inflammation, insulin resistance and NASH - 0 views

www.journal-of-hepatology.eu/...abstract

metabolic endotoxemia obesity overweight LPS bifidobacterium inflammaiton gut insulin resistance

shared by Nathan Goodyear on 20 Jan 12 - No Cached
  • Nathan Goodyear on 20 Jan 12
     
    metabolic endotoxemia starts with what you eat.  Chronic over nutrition results in elevated LPS. This starts a cascade of events that results in inflammation.  A well balanced gut flora of bifidobacterium is one way to slow this trigger.
Nathan Goodyear

http://eurheartj.oxfordjournals.org/content/26/16/1633.full.pdf - 0 views

eurheartj.oxfordjournals.org/...1633.full.pdf

Lp(a) lipoprotein(a) cardiovascular disease risk heart health

shared by Nathan Goodyear on 26 Aug 14 - No Cached
  • Nathan Goodyear on 26 Aug 14
     
    Lp(a) associated with increased risk at levels > 30 in women.  The risk is double.
Nathan Goodyear

Selective increases of bifidobacteria in gut microflora improve high-fat-diet-induced d... - 0 views

dl-web.dropbox.com/...0DM%2C%20and%20endotoxemia.pdf

bifidobacterium flora LPS metabolic endotoxemia Diabetes DM type II obesity inflammation overweight weight-loss

shared by Nathan Goodyear on 20 Jan 12 - No Cached
  • Nathan Goodyear on 20 Jan 12
     
    decreased bifidobacterium gut flora results in increased absorption of LPS in high fat diets resulting in endotoxemia. This plays a significant role in diabetes
Nathan Goodyear

Metabolic endotoxaemia related inflammation is associated with hypogonadism in overweig... - 0 views

www.ncbi.nlm.nih.gov/...PMC5341351

Testosterone low Testosterone Low T obesity IL-6 overweight metabolic endotoxemia hypogonadism LPS

shared by Nathan Goodyear on 06 Apr 17 - No Cached
  • Nathan Goodyear on 06 Apr 17
     
    Study finds that inflammation that is the result of obesity in men (IL-6) negatively effects the leading cell and Sertoli cells in men.  Testosterone levels in these men correlated significantly with lipopolysaccharide binding protein.  This points to a negative correlation b/t LPS metabolic endotoxemia and low Testosterone.  Could Testosterone merely be the result of an unhealthy diet and gut?
Nathan Goodyear

Histochemistry and Cell Biology, Volume 127, Number 2 - SpringerLink - 0 views

www.springerlink.com/...yj35n4j531j67211

TLR TLR-4 toll-like receptors inflammtion obesity LPS lipopolysaccharides

shared by Nathan Goodyear on 19 Jan 12 - No Cached
  • Nathan Goodyear on 19 Jan 12
     
    Abstract only, but this study shows that the innate immunity plays a role in the development of obesity through the TLR.  LPS was shown to stimulate the inflammatory cascade through the TLRs
Nathan Goodyear

Preadipocytes Mediate Lipopolysaccharide-Induced Inflammation and Insulin Resistance in... - 0 views

endo.endojournals.org/...5340.full

LPS lipopolysaccharides inflammation obesity NF-KappaB insulin resistance IR

shared by Nathan Goodyear on 19 Jan 12 - No Cached
  • Nathan Goodyear on 19 Jan 12
     
    proposed model of how LPS stimulates NF-kappaB activation and the inflammatory cascade.  This plays a key role in the obesity epidemic.
Nathan Goodyear

Figure 2 : Targeting gut microbiota in obesity: effects of prebiotics and pro... - 0 views

www.nature.com/...nrendo.2011.126_F2.html

gut obesity probiotics metabolic endotoxemia LPS inflammation PPAR-gamma microbiota endocannabinoid system

shared by Nathan Goodyear on 18 Jan 12 - No Cached
  • Nathan Goodyear on 18 Jan 12
     
    nice diagram of proposed mechanism of how diet and gut microbiota can influence the production of PPAR-gamma inducing growth of adipose tissue.  Also proposes how LPS and the endocannabinoid system contributed to a leaky gut and thus the proposed "metabolic endotoxemia"
Nathan Goodyear

Dysregulated Innate Immune Responses in Young Children with Autism Spectrum Disorders: ... - 0 views

mercola.fileburst.com/...europsych%20--%20Jyonouchi.pdf

autism ASD LPS inflammation innate immune system gut gastrointestinal

shared by Nathan Goodyear on 29 Jan 12 - No Cached
  • Nathan Goodyear on 29 Jan 12
     
    Dysfunctions of the innate immune system, in the gastrointestinal system, in children with autism found. LPS found to be involved. Again, revealing a gut-brain connection in autism.
Nathan Goodyear

Succinate Dehydrogenase Supports Metabolic Repurposing of Mitochondria to Drive Inflamm... - 0 views

www.cell.com/...S0092-8674(16)31162-X

inflammation LPS macrophages lipopolysaccharide mitochondria energy ATP ROS

shared by Nathan Goodyear on 12 Oct 16 - No Cached
  • Nathan Goodyear on 12 Oct 16
     
    Fascinating study: inflammation via LPS induces pro-inflammatory move by macrophages that induces a change in mitochondria to increase inflammation and decrease ATP production.
Nathan Goodyear

ScienceDirect.com - Zentralblatt für Bakteriologie, Mikrobiologie und Hygiene... - 0 views

www.sciencedirect.com/...S0176672486801158

Lyme borrelia burgdorferi LPS lipopolysaccharides disease microbiology

shared by Nathan Goodyear on 18 Apr 12 - No Cached
  • Nathan Goodyear on 18 Apr 12
     
    Borrelia burgdorferi (lyme disease) shown to express LPS, just like dream negative bacteria.
Nathan Goodyear

Carvacrol, a component of thyme oil, activates PPARα and γ and suppresses COX... - 0 views

www.ncbi.nlm.nih.gov/...PMC2789773

essential oil essential oils LPS COX2 cox-2 cyclooxygenase inflammation thyme natural

shared by Nathan Goodyear on 29 Sep 14 - No Cached
  • Nathan Goodyear on 29 Sep 14
     
    essential oils inhibit LPS induced COX-2 activity.
Nathan Goodyear

Lipopolysaccharide-induced toll-like receptor 4 signaling enhances the migratory abilit... - 0 views

www.sciencedirect.com/...S0039606013001050

LPS lipopolysaccharides cancer

shared by Nathan Goodyear on 11 Sep 17 - No Cached
  • Nathan Goodyear on 11 Sep 17
     
    LPS stimulation induced increased mets potential in esophageal cell culture study.
Nathan Goodyear

Metabolic endotoxaemia - a potential novel link between ovarian inflammation and impair... - 0 views

www.tandfonline.com/...09513590.2014.994602

metabolic endotoxemia progesterone hormones LPS lipopolysaccharides gut inflammation luteal phase defect

shared by Nathan Goodyear on 22 Jun 17 - No Cached
  • Nathan Goodyear on 22 Jun 17
     
    Systemic LPS, metabolic endotoxemia, that is the result of inflammation originating out of the gut found to cause luteal phase dysfunction--low progesterone.  Now, we have the gut-hormone connection.
Nathan Goodyear

Lipopolysaccharide induces inflammation and facilitates lung metastasis in a ... - 0 views

www.ncbi.nlm.nih.gov/...25625500

LPS breast cancer angiogenesis VEGF

shared by Nathan Goodyear on 16 Aug 19 - No Cached
  • Nathan Goodyear on 16 Aug 19
     
    LPS found to increase breast cancer metastasis via increase in VEGF. It also increases NF-kappaB.
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