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finchloe121

5 Things You Need To Understand If You are Having Chronic Pain! - 0 views

www.pharmahealthonline.com/...if-you-are-having-chronic-pain

Health Pharmacy Medicicne

shared by finchloe121 on 24 Sep 22 - No Cached
  • finchloe121 on 24 Sep 22
     
    Chronic pain is a type of pain that usually lasts for weeks to months. This pain can come and go, and it can be anywhere in the body. Chronic pain can lead to anxiety, depression, and insomnia. Chronic pain is quite different from acute pain and there are some differences between the two types. People usually experience severe pain, when it is injured by a broken bone or a cut on the skin. This pain does not last long. Pain is not something that can be ignored. If it grows, it should be fixed. As fear and pain persist, one begins to think negatively. Long-term negative thoughts begin to form in his mind, a process called fear conditioning. This factor causes an increase in blood pressure and anxiety disorders. Chronic pain is difficult to treat, and results in increased pain, fear, and negative thoughts. Extreme levels of fear lead to more pain, and the cycle of pain threats can be difficult to break. One of the best pills used to treat body pain symptoms is Hydrocodone 325mg, which you can easily buy from any trusted online pharmacy, such as Pharma Health Online.
Nathan Goodyear

Chronic exposure to Low dose bacterial lipopolysaccharide inhibits leptin signaling in ... - 0 views

www.ncbi.nlm.nih.gov/...PMC4523075

LPS lipopolysaccharides leptin CCK cholecystokinin metabolism weight appetite diet nutrition inflammation

shared by Nathan Goodyear on 04 Oct 17 - No Cached
  • Obesity and models of obesity induced by ingestion of HF-diet in rodents are associated with chronically elevated circulating levels of LPS
  • chronic low-dose administration of LPS induces leptin-resistance in vagal afferent neurons and abolition of CCK-induced inhibition of food intake
  • HF fat feeding has been shown to enhance gastrointestinal permeability promoting the translocation of LPS to the circulation
  • ...9 more annotations...
  • LPS leads to an increase in SOCS3 expression [20]. SOCS3 is a negative regulator of leptin signaling
  • We observed a significant increase in energy intake in the LPS-treated rats
  • the data provides a mechanism linking changes in gut microbiota induced by ingestion of HF diets to dysregulation of food intake and body weight
  • SOCS3 is an important mechanism by which leptin resistance develops in vagal afferent neurons and coincides with the onset of hyperphagia
  • Chronic low-dose LPS treatment induced TLR4 activation and MyD88 signaling in vagal afferent neurons, associated with increased SOCS3 expression and reduced leptin-signaling, characterized by the absence of leptin-induced pSTAT3.
  • We demonstrate that this chronic low dose LPS is sufficient to induce leptin–resistance in vagal afferent neurons, reduced sensitivity to the satiating effects of CCK, and loss of vagal afferent plasticity
  • it suggests that the increase in food intake and body weight we observed at week 6 in the LPS treated rats may be caused by LPS-induced leptin resistance.
  • chronic LPS treatment of mice for four weeks increased body weight
  • chronic LPS treatment of mice for four weeks increased subcutaneous fat
  • Nathan Goodyear on 04 Oct 17
     
    Very interesting study.  High fat diet in rats induced gut flora change that resulted in LPS which induced appetite through leptin resistance and reduced cholecystokinin signaling.
Nathan Goodyear

Testosterone: a vascular hormone in health and disease - 0 views

joe.endocrinology-journals.org/...R47.full

testosterone hormone health disease hormones men male cardiovascular disease CVD

shared by Nathan Goodyear on 13 May 13 - No Cached
  • Testosterone has beneficial effects on several cardiovascular risk factors, which include cholesterol, endothelial dysfunction and inflammation
  • In clinical studies, acute and chronic testosterone administration increases coronary artery diameter and flow, improves cardiac ischaemia and symptoms in men with chronic stable angina and reduces peripheral vascular resistance in chronic heart failure.
  • testosterone is an L-calcium channel blocker and induces potassium channel activation in vascular smooth muscle cells
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  • Animal studies have consistently demonstrated that testosterone is atheroprotective, whereas testosterone deficiency promotes the early stages of atherogenesis
  • there is no compelling evidence that testosterone replacement to levels within the normal healthy range contributes adversely to the pathogenesis of CVD (Carson & Rosano 2011) or prostate cancer (Morgentaler & Schulman 2009)
  • bidirectional effect between decreased testosterone concentrations and disease pathology exists as concomitant cardiovascular risk factors (including inflammation, obesity and insulin resistance) are known to reduce testosterone levels and that testosterone confers beneficial effects on these cardiovascular risk factors
  • Achieving a normal physiological testosterone concentration through the administration of testosterone replacement therapy (TRT) has been shown to improve risk factors for atherosclerosis including reducing central adiposity and insulin resistance and improving lipid profiles (in particular, lowering cholesterol), clotting and inflammatory profiles and vascular function
  • It is well known that impaired erectile function and CVD are closely related in that ED can be the first clinical manifestation of atherosclerosis often preceding a cardiovascular event by 3–5 years
  • no decrease in the response (i.e. no tachyphylaxis) of testosterone and that patient benefit persists in the long term.
  • free testosterone levels within the physiological range, has been shown to result in a marked increase in both flow- and nitroglycerin-mediated brachial artery vasodilation in men with CAD
  • Clinical studies, however, have revealed either small reductions of 2–3 mm in diastolic pressure or no significant effects when testosterone is replaced within normal physiological limits in humans
  • Endothelium-independent mechanisms of testosterone are considered to occur primarily via the inhibition of voltage-operated Ca2+ channels (VOCCs) and/or activation of K+ channels (KCs) on smooth muscle cells (SMCs)
  • Testosterone shares the same molecular binding site as nifedipine
  • Testosterone increases the expression of endothelial nitric oxide synthase (eNOS) and enhances nitric oxide (NO) production
  • Testosterone also inhibited the Ca2+ influx response to PGF2α
  • one of the major actions of testosterone is on NO and its signalling pathways
  • In addition to direct effects on NOS expression, testosterone may also affect phosphodiesterase type 5 (PDE5 (PDE5A)) gene expression, an enzyme controlling the degradation of cGMP, which acts as a vasodilatory second messenger
  • the significance of the action of testosterone on VSMC apoptosis and proliferation in atherosclerosis is difficult to delineate and may be dependent upon the stage of plaque development
  • Several human studies have shown that carotid IMT (CIMT) and aortic calcification negatively correlate with serum testosterone
  • t long-term testosterone treatment reduced CIMT in men with low testosterone levels and angina
  • neither intracellular nor membrane-associated ARs are required for the rapid vasodilator effect
  • acute responses appear to be AR independent, long-term AR-mediated effects on the vasculature have also been described, primarily in the context of vascular tone regulation via the modulation of gene transcription
  • Testosterone and DHT increased the expression of eNOS in HUVECs
  • oestrogens have been shown to activate eNOS and stimulate NO production in an ERα-dependent manner
  • Several studies, however, have demonstrated that the vasodilatory actions of testosterone are not reduced by aromatase inhibition
  • non-aromatisable DHT elicited similar vasodilation to testosterone treatment in arterial smooth muscle
  • increased endothelial NOS (eNOS) expression and phosphorylation were observed in testosterone- and DHT-treated human umbilical vein endothelial cells
  • Androgen deprivation leads to a reduction in neuronal NOS expression associated with a decrease of intracavernosal pressure in penile arteries during erection, an effect that is promptly reversed by androgen replacement therapy
  • Observational evidence suggests that several pro-inflammatory cytokines (including interleukin 1β (IL1β), IL6, tumour necrosis factor α (TNFα), and highly sensitive CRP) and serum testosterone levels are inversely associated in patients with CAD, T2DM and/or hypogonadism
  • patients with the highest IL1β concentrations had lower endogenous testosterone levels
  • TRT has been reported to significantly reduce TNFα and elevate the circulating anti-inflammatory IL10 in hypogonadal men with CVD
  • testosterone treatment to normalise levels in hypogonadal men with the MetS resulted in a significant reduction in the circulating CRP, IL1β and TNFα, with a trend towards lower IL6 compared with placebo
  • parenteral testosterone undecanoate, CRP decreased significantly in hypogonadal elderly men
  • Higher levels of serum adiponectin have been shown to lower cardiovascular risk
  • Research suggests that the expression of VCAM-1, as induced by pro-inflammatory cytokines such as TNFα or interferon γ (IFNγ (IFNG)) in endothelial cells, can be attenuated by treatment with testosterone
  • Testosterone also inhibits the production of pro-inflammatory cytokines such as IL6, IL1β and TNFα in a range of cell types including human endothelial cells
  • decreased inflammatory response to TNFα and lipopolysaccharide (LPS) in human endothelial cells when treated with DHT
  • The key to unravelling the link between testosterone and its role in atherosclerosis may lay in the understanding of testosterone signalling and the cross-talk between receptors and intracellular events that result in pro- and/or anti-inflammatory actions in athero-sensitive cells.
  • testosterone functions through the AR to modulate adhesion molecule expression
  • pre-treatment with DHT reduced the cytokine-stimulated inflammatory response
  • DHT inhibited NFκB activation
  • DHT could inhibit an LPS-induced upregulation of MCP1
  • Both NFκB and AR act at the transcriptional level and have been experimentally found to be antagonistic to each other
  • As the AR and NFκB are mutual antagonists, their interaction and influence on functions can be bidirectional, with inflammatory agents that activate NFκB interfering with normal androgen signalling as well as the AR interrupting NFκB inflammatory transcription
  • prolonged exposure of vascular cells to the inflammatory activation of NFκB associated with atherosclerosis may reduce or alter any potentially protective effects of testosterone
  • DHT and IFNγ also modulate each other's signalling through interaction at the transcriptional level, suggesting that androgens down-regulate IFN-induced genes
  • (Simoncini et al. 2000a,b). Norata et al. (2010) suggest that part of the testosterone-mediated atheroprotective effects could depend on ER activation mediated by the testosterone/DHT 3β-derivative, 3β-Adiol
  • TNFα-induced induction of ICAM-1, VCAM-1 and E-selectin as well as MCP1 and IL6 was significantly reduced by a pre-incubation with 3β-Adiol in HUVECs
  • 3β-Adiol also reduced LPS-induced gene expression of IL6, TNFα, cyclooxygenase 2 (COX2 (PTGS2)), CD40, CX3CR1, plasminogen activator inhibitor-1, MMP9, resistin, pentraxin-3 and MCP1 in the monocytic cell line U937 (Norata et al. 2010)
  • This study suggests that testosterone metabolites, other than those generated through aromatisation, could exert anti-inflammatory effects that are mediated by ER activation.
  • The authors suggest that DHT differentially effects COX2 levels under physiological and pathophysiological conditions in human coronary artery smooth muscle cells and via AR-dependent and -independent mechanisms influenced by the physiological state of the cell
  • There are, however, a number of systematic meta-analyses of clinical trials of TRT that have not demonstrated an increased risk of adverse cardiovascular events or mortality
  • The TOM trial, which was designed to investigate the effect of TRT on frailty in elderly men, was terminated prematurely as a result of an increased incidence of cardiovascular-related events after 6 months in the treatment arm
  • trials of TRT in men with either chronic stable angina or chronic cardiac failure have also found no increase in either cardiovascular events or mortality in studies up to 12 months
  • Evidence may therefore suggest that low testosterone levels and testosterone levels above the normal range have an adverse effect on CVD, whereas testosterone levels titrated to within the mid- to upper-normal range have at least a neutral effect or, taking into account the knowledge of the beneficial effects of testosterone on a series of cardiovascular risk factors, there may possibly be a cardioprotective action
  • The effect of testosterone on human vascular function is a complex issue and may be dependent upon the underlying androgen and/or disease status.
  • the majority of studies suggest that testosterone may display both acute and chronic vasodilatory effects upon various vascular beds at both physiological and supraphysiological concentrations and via endothelium-dependent and -independent mechanisms
  • Nathan Goodyear on 13 May 13
     
    Good deep look into the testosterone and CVD link.
Nathan Goodyear

The Complex Role of Estrogens in Inflammation - 0 views

edrv.endojournals.org/...521.full

estrogens inflammation

shared by Nathan Goodyear on 14 Aug 12 - No Cached
  • These studies suggest inflammation-dependent up-regulation of ERβ relative to ERα.
  • up-regulation of ERβ relative to ERα under hypoxic conditions, which might lead to a preponderance of signaling through ERβ pathways
  • it seems that E2 at periovulatory to pregnancy levels inhibited proinflammatory cytokines from PBMCs
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  • it is clear that E2 can stimulate antibody production by B cells, probably by inhibiting T cell suppression of B cells
  • In cycling women, the largest quantities of Ig were detected before ovulation
  • In contrast, E2 at high concentrations leads to a suppression of B-lymphocyte lineage precursors
  • E2 at periovulatory to pregnancy serum levels is able to stimulate antibody secretion under healthy conditions but also in autoimmune diseases, whereas similar serum levels of E2 lead to a suppression of bone marrow B cell lineage precursors
  • In chronic inflammatory disorders, where B cells play a decisive role, E2 would promote the disease when autoaggressive B cells are already present, whereas chronically elevated E2 would inhibit initiation of an autoimmune disease when no such B cells are available. This might be a good reason why particularly B cell-dependent diseases such as SLE, mixed connective tissue disease (Sharp syndrome), IgA nephropathy, dermatitis herpetiformis, gluten sensitive enteropathy, myasthenia gravis, and thyroiditis appear in women in the reproductive years, predominantly, in the third or fourth decades of life
  • Th17 cells are thought to be the main responsible cells for chronic inflammatory tissue destruction in autoimmune diseases
  • IFN-γ, IL-12, and TNF were allocated to Th1 reactions
  • IL-4, IL-5, and IL-10 to Th2 responses
  • antiinflammatory T regulatory cells producing TGF-β and proinflammatory T helper type 17 cells (Th17) producing IL-17
  • no direct effects of estrogens on Th17 cells or IL-17 secretion have been described until now.
  • So-called Th17 cells producing IL-17 are the main T cells responsible for chronic inflammation.
  • Because IFN-γ has been allocated a Th17-inhibiting role (Fig. 1⇑), its increase by E2 at pregnancy doses and the E2-mediated inhibition of TNF must be viewed as a favorable effect in chronic inflammation
  • in humans and mice, E2 at periovulatory to pregnancy levels stimulates IL-4, IL-10, and IFN-γ but inhibits TNF from CD4+ T cells
  • In humans and mice, E3 and E2, respectively, at pregnancy levels inhibit T cell-dependent delayed type hypersensitivity
  • increased IL-4, IL-10, and IFN-γ in the presence of low TNF support an antiaggressive immune response
  • secretion of IL-1β is increased at periovulatory/proestrus to early pregnancy levels, whereas IL-1 secretion is inhibited at high pregnancy levels
  • The dichotomous effect of E2 on IL-1β and TNF at high and low concentrations is most probably due to inhibition of NF-κB at high concentrations
  • experiments with mouse and rat macroglial and microglial cells demonstrate that E2 at proestrus to pregnancy levels exerts neuroprotective effects by increasing TGF-β and by inhibiting iNOS and NO release, and reducing expression of proinflammatory cytokines and prostaglandin E2 production.
  • E2 at periovulatory to pregnancy levels inhibits NF-κB activation, which must be viewed as an antiinflammatory signal
  • It was shown that E2 concentrations equal to or above 10−10 m are necessary to inhibit NF-κB activation
  • important proinflammatory cytokines are typically inhibited at periovulatory (proestrus) to pregnancy levels of E2, which is evident for IL-6, IL-8, and TNF
  • low E2 concentrations were demonstrated to have no or even stimulatory effects
  • This renders a woman in the postmenopausal phase to a more proinflammatory situation
  • most in vitro studies demonstrated a stimulatory effect of E2 on secretion of IL-4, IL-10, and TGF-β typically at periovulatory to pregnancy levels
  • E2 at periovulatory to pregnancy levels has an ameliorating effect on chronic inflammatory diseases as long as B cell-dependent immunity or an overshooting fibrotic tissue repair process do not play a crucial pathogenic role. However, when the B cell plays an important role, E2 might even stimulate the disease process as substantiated by flare-ups in SLE during pregnancy
    • Nathan Goodyear
      Nathan Goodyear on 15 Aug 12
       
      SLE, mixed connective tissue disease (Sharp syndrome), IgA nephropathy, dermatitis herpetiformis, gluten sensitive enteropathy, myasthenia gravis, and thyroiditis
  • Short-term administration of E2 at pregnancy levels was shown to induce an inflammatory response specific to the lateral prostate of the castrated male rat
  • Nathan Goodyear on 14 Aug 12
     
    great review of the complex interaction between Estrogens and inflammation.  Reference here is in females.
Nathan Goodyear

Chronic stress impacts the cardiovascular system: animal models and clinical outcomes |... - 0 views

ajpheart.physiology.org/...H1476

chronic stress stress inflammation cardiovascular disease atherosclerosis NO nitric oxide oxidative stress cardiovascular heart

shared by Nathan Goodyear on 03 Sep 17 - No Cached
  • Nathan Goodyear on 03 Sep 17
     
    Chronic stress increases cardiovascular disease.  Of note, chronic stress reduces eNOS activity and NO bioavailability, increased lipid oxidation (oxLDL) via a reduction in antioxidant protection, increased pro-inflammatory cytokines, increased thrombosis and clotting risk, increased blood pressure and reduced HRV.
Nathan Goodyear

Chronic Traumatic Encephalopathy: Chronic Degenerative Disease - 0 views

turningpointnutrition.ca/...nt%201%20-%20CTE%20Chronic.pdf

CTE chronic traumatic encephalopathy sports athletes military head trauma TBI

shared by Nathan Goodyear on 07 Apr 12 - No Cached
  • Nathan Goodyear on 07 Apr 12
     
    Good discussion on chronic traumatic encephalopathy. CTE is a condition found in the military and sports related head trauma. This is usually the result of low, repetitive impact injuries to the brain. Though, genetic susceptibility is discussed as well.
Nathan Goodyear

Chronic Inflammation and Cytokines in the Tumor Microenvironment - 0 views

www.hindawi.com/...149185

inflammation cytokines tumor cancer inflammatory IL-6 IL-10 TNF-alpha

shared by Nathan Goodyear on 26 Jun 15 - No Cached
  • Nathan Goodyear on 26 Jun 15
     
    Acute inflammation is a response to an alteration induced by a pathogen or a physical or chemical insult, which functions to eliminate the source of the damage and restore homeostasis to the affected tissue. However, chronic inflammation triggers cellular events that can promote malignant transformation of cells and carcinogenesis. Several inflammatory mediators, such as TNF-α, IL-6, TGF-β, and IL-10, have been shown to participate in both the initiation and progression of cancer. In this review, we explore the role of these cytokines in important events of carcinogenesis, such as their capacity to generate reactive oxygen and nitrogen species, their potential mutagenic effect, and their involvement in mechanisms for epithelial mesenchymal transition, angiogenesis, and metastasis. Finally, we will provide an in-depth analysis of the participation of these cytokines in two types of cancer attributable to chronic inflammatory disease: colitis-associated colorectal cancer and cholangiocarcinoma.
Nathan Goodyear

Environmental Lead Exposure and Progression of Chronic Renal Diseases in Patients witho... - 0 views

www.nejm.org/...NEJMoa021672

EDTA chelation chronic renal insufficiency

shared by Nathan Goodyear on 15 Dec 10 - No Cached
  • Low-level environmental lead exposure may accelerate progressive renal insufficiency in patients without diabetes who have chronic renal disease. Repeated chelation therapy may improve renal function and slow the progression of renal insufficiency
  • Nathan Goodyear on 15 Dec 10
     
    EDTA chelation aids in lead induced chronic renal insufficiency
Nathan Goodyear

National Institutes of Health Pathways to Prevention Workshop: The Role of Opioids in t... - 0 views

annals.org/article.aspx

NIH opioids chronic pain pain health

shared by Nathan Goodyear on 16 Jan 15 - No Cached
  • Nathan Goodyear on 16 Jan 15
     
    NIH panel review finds little empirical evidence to support the use of opioids in chronic pain.
drreads

Chronic inflammation: symptoms, causes, treatment - Dr Reads - 0 views

www.drreads.com/...chronic-inflammation.html

inflammation chronic health

shared by drreads on 27 Sep 21 - No Cached
  • drreads on 27 Sep 21
     
    chronic inflammation
Nathan Goodyear

Alterations in Diurnal Salivary Cortisol Rhythm in a Population-Based Sample of Cases W... - 0 views

www.psychosomaticmedicine.org/...298.full

cortisol salivary saliva testing CFS chronic fatigue syndrome IL-6 inflammation

shared by Nathan Goodyear on 24 Apr 12 - No Cached
  • Nathan Goodyear on 24 Apr 12
     
    low flattened cortisol diurnal salivary pattern and elevated IL-6 found in chronic fatigue patients.  
Nathan Goodyear

Low-dose hydrocortisone in chronic fatigue syndrome: a randomised crossover trial : The... - 0 views

www.thelancet.com/...fulltext

CFS chronic fatigue syndrome hydrocortisone cortisol fatigue adrenal fatigue hypoadrenia adrenal insufficiency

shared by Nathan Goodyear on 01 May 12 - No Cached
  • Nathan Goodyear on 01 May 12
     
    low dose hydrocortisone therapy, 5-10 mg, shown to be effective short-term therapy in patients with chronic fatigue syndrome.  Additionally, and very important, this study found no adrenal function suppression at these doses.
Nathan Goodyear

Hypothalamo-Pituitary-Adrenal Axis Dysfunction in Chronic Fatigue Syndrome, and the Eff... - 0 views

jcem.endojournals.org/...3545.long

CFS chronic fatigue syndrome hydrocortisone cortisol fatigue adrenal fatigue hypoadrenia HPA adrenal insufficiency adrenal adrenals

shared by Nathan Goodyear on 01 May 12 - No Cached
  • We conclude that the improvement in fatigue seen in some patients with chronic fatigue syndrome during hydrocortisone treatment is accompanied by a reversal of the blunted cortisol responses to human CRH
  • These data further suggest that the hypocortisolism found in chronic fatigue syndrome may be secondary to reduced adrenal gland output.
  • 5-mg replacement dose of hydrocortisone, and the remainder 10 mg
  • Nathan Goodyear on 01 May 12
     
    low dose hydrocortisone therapy (defined as 5-10 mg), in this study, was used to treat CFS.  This study found an improvement in symptoms in these patients.  Additionally, low cortisol was found in these patients with CFS.  Their conclusion, was that low adrenal function is a component of CFS and low dose hydrocortisone therapy is an effective treatment.   Now, is the low cortisol as the result of increased metabolism as well?
Nathan Goodyear

Salivary cortisol response to awakening in chronic fatigue syndrome - 0 views

bjp.rcpsych.org/...136.long

saliva salivary cortisol chronic fatigue syndrome CFS testing morning cortisol

shared by Nathan Goodyear on 12 May 12 - No Cached
  • Nathan Goodyear on 12 May 12
     
    Low morning cortisol found in those with chronic fatigue syndrome.
Nathan Goodyear

Chronic Traumatic Encephalopathy in Athletes: Progressive Tauopathy following Repetitiv... - 0 views

www.ncbi.nlm.nih.gov/...PMC2945234

CTE chronic traumatic encephalopathy athletes concussion TBI head injury

shared by Nathan Goodyear on 07 Apr 12 - No Cached
  • Nathan Goodyear on 07 Apr 12
     
    discussion of chronic traumatic encephalopathy.  Good discussion of the neuropathological findings in 3 athletes.
Nathan Goodyear

Chronic traumatic encephalopathy in a National ... [Neurosurgery. 2005] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...15987548

CTE chronic traumatic encephalopathy football NFL concussions

shared by Nathan Goodyear on 07 Apr 12 - No Cached
  • Nathan Goodyear on 07 Apr 12
     
    chronic traumatic encephalopathy in football players is felt to play a role in the cognitive changes seen long-term.
Nathan Goodyear

Urinary Cortisol and Cortisol Metabolite Excretion in Chronic Fatigue Syndrome - 0 views

www.psychosomaticmedicine.org/...578.full

urinary cortisol metabolite metabolites saliva salivary hormone hormones CFS chronic fatigue syndrome

shared by Nathan Goodyear on 20 Feb 12 - No Cached
  • Nathan Goodyear on 20 Feb 12
     
    low cortisol is a frequent finding in chronic fatigue syndrome.  However, in the urine, the cortisol levels may be normal.  This is a reflection of increased metabolism of cortisol.  This is not a contradiction, but a metabolic effect.
Nathan Goodyear

Urinary Cortisol and Cortisol Metabolite Excretion in Chronic Fatigue Syndrome - 0 views

www.psychosomaticmedicine.org/...578.full.pdf

CFS chronic fatigue syndrome salivary saliva cortisol metabolism metabolization

shared by Nathan Goodyear on 13 Mar 12 - No Cached
  • Nathan Goodyear on 13 Mar 12
     
    It has been suggested in the literature that low salivary cortisol is a common finding in those with chronic fatigue. This study found no difference in the cortisol metabolite excretion. This would suggest that an increase metabolization of cortisol exists in those with CFS.
Nathan Goodyear

Molecular inflammation: Underpinnings of aging and age-related diseases 10.1016/j.arr.2... - 0 views

www.sciencedirect.com/...S1568163708000299

inflammation NF-KappaB aging disease ageing

shared by Nathan Goodyear on 23 Jan 12 - No Cached
  • Nathan Goodyear on 23 Jan 12
     
    chronic inflammation appears to be the major player in aging and age-related chronic diseases
Nathan Goodyear

Access : The role of exercise and PGC1|[alpha]| in inflammation and chronic disease : N... - 0 views

www.nature.com/...nature07206.html

inflammation exercise obesity overweight chronic disease

shared by Nathan Goodyear on 20 Dec 11 - No Cached
  • Nathan Goodyear on 20 Dec 11
     
    study shows increased activity and exercise delays onset of chronic disease.   Inactivity and obesity decreased the age of 
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