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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

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

Chronic fatigue syndrome and mitochondrial dysfunction - 0 views

www.ncbi.nlm.nih.gov/...PMC2680051

mitochondria CFS fatigue chronic fatigues syndrome

shared by Nathan Goodyear on 18 Aug 14 - No Cached
  • Nathan Goodyear on 18 Aug 14
     
    Discussion of the mitochondrial role in chronic fatigue syndrome.  As the authors conclude, there is dysfunction, but whether the cause is primary or secondary or likely varies from individual to individual is yet undetermined.
  • Blu Electronic Cigarettes on 20 Aug 14
     
    very helpful post!
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

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

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

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

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

jcem.endojournals.org/...3545.full.pdf

CFS chronic fatigue syndrome adrenal fatigue cortisol therapy

shared by Nathan Goodyear on 12 May 12 - No Cached
  • Nathan Goodyear on 12 May 12
     
    This study reveals CFS to be low adrenal cortisol output problem. In this study, low dose cortisol (hydrocortisone) therapy improved symptoms of fatigue and improved the CRH adrenal stimulation of adrenal cortisol production.
Nathan Goodyear

A role for the body burden of aluminium in va... [Med Hypotheses. 2009] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...19004564

aluminum macrophagic myofasciitis macrophagic myofasciitis chronic fatigue syndrome

shared by Nathan Goodyear on 09 Oct 13 - No Cached
  • Nathan Goodyear on 09 Oct 13
     
    Aluminum, macrophagic myofasciitis, and chronic fatigue syndrome.
Nathan Goodyear

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

bjp.rcpsych.org/...136.full.pdf

chronic fatigue syndrome CFS salivary saliva cortisol hormone hormones fatigue

shared by Nathan Goodyear on 02 May 12 - No Cached
  • Nathan Goodyear on 02 May 12
     
    This study found suppressed am salivary cortisol in those with CFS.
Nathan Goodyear

Low-Dose Hydrocortisone for Treatment of Chronic Fatigue Syndrome, September 23/30, 199... - 0 views

jama.ama-assn.org/...1061.long

CFS cortisol hydrocortisone adrenal adrenals fatigue chronic fatigue syndrome

shared by Nathan Goodyear on 02 May 12 - No Cached
  • Nathan Goodyear on 02 May 12
     
    this study revealed symptom improvement with hydrocortisone treatment in those with CFS. Pre/post treatment was with serum cortisol and not salivary cortisol.  This is a weakness of the study.  The starting dosage of 25-30 mg hydrocortisone is high and with inadequate evaluation, this high dosage could have resulted in high dosage and adrenal suppression.  
Nathan Goodyear

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

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

leptin reverse T3 weight loss

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

Alterations in diurnal salivary cortisol rhyth... [Psychosom Med. 2008] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...18378875

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

shared by Nathan Goodyear on 02 May 12 - No Cached
  • Nathan Goodyear on 02 May 12
     
    Individuals with CFS found to have flattened salivary cortisol 4-point pattern and elevated IL-6.
Nathan Goodyear

Diurnal variation of adrenocortical activ... [Neuropsychobiology. 1998] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...9813459

CFS chronic fatigue syndrome adrenal adrenals adrenocortical activity fatigue

shared by Nathan Goodyear on 02 May 12 - No Cached
  • Nathan Goodyear on 02 May 12
     
    adrenocortical dysfunction found to play a role in CFS
Nathan Goodyear

Stuck at the bench: Potential natural neuroprotective compounds for concussion - 0 views

www.ncbi.nlm.nih.gov/...PMC3205506

concussions concussion natural therapies brain curcumin omega 3 resveratrol green tea EGCG EPA DHA vitamin E vitamin c vitamin D

shared by Nathan Goodyear on 20 Feb 16 - No Cached
  • Long-chain polyunsaturated fatty acids, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are highly enriched in neuronal synaptosomal plasma membranes and vesicles
  • The predominant CNS polyunsaturated fatty acid is DHA
  • effective supplementation and/or increased ingestion of dietary sources rich in EPA and DHA, such as cold-water fish species and fish oil, may help improve a multitude of neuronal functions, including long-term potentiation and cognition.
  • ...45 more annotations...
  • multiple preclinical studies have suggested that DHA and/or EPA supplementation may have potential benefit through a multitude of diverse, but complementary mechanisms
  • pre-injury dietary supplementation with fish oil effectively reduces post-traumatic elevations in protein oxidation
  • The benefits of pre-traumatic DHA supplementation have not only been independently confirmed,[150] but DHA supplementation has been shown to significantly reduce the number of swollen, disconnected and injured axons when administered following traumatic brain injury.
  • DHA has provided neuroprotection in experimental models of both focal and diffuse traumatic brain injury
  • potential mechanisms of neuroprotection, in addition to DHA and EPA's well-established anti-oxidant and anti-inflammatory properties
  • Despite abundant laboratory evidence supporting its neuroprotective effects in experimental models, the role of dietary DHA and/or EPA supplementation in human neurological diseases remains uncertain
  • Several population-based, observational studies have suggested that increased dietary fish and/or omega-3 polyunsaturated fatty acid consumption may reduce risk for ischemic stroke in several populations
  • Randomized control trials have also demonstrated significant reductions in ischemic stroke recurrence,[217] relative risk for ischemic stroke,[2] and reduced incidence of both symptomatic vasospasm and mortality following subarachnoid hemorrhage
  • Clinical trials in Alzheimer's disease have also been largely ineffective
  • The clinical evidence thus far appears equivocal
  • curcumin has gained much attention from Western researchers for its potential therapeutic benefits in large part due to its potent anti-oxidant[128,194,236] and anti-inflammatory properties
  • Curcumin is highly lipophilic and crosses the blood-brain barrier enabling it to exert a multitude of different established neuroprotective effects
  • in the context of TBI, a series of preclinical studies have suggested that pre-traumatic and post-traumatic curcumin supplementation may bolster the brain's resilience to injury and serve as a valuable therapeutic option
  • Curcumin may confer significant neuroprotection because of its ability to act on multiple deleterious post-traumatic, molecular cascades
  • studies demonstrated that both pre- and post-traumatic curcumin administration resulted in a significant reduction of neuroinflammation via inhibition of the pro-inflammatory molecules interleukin 1β and nuclear factor kappa B (NFκB)
  • no human studies have been conducted with respect to the effects of curcumin administration on the treatment of TBI, subarachnoid or intracranial hemorrhage, epilepsy or stroke
  • studies have demonstrated that resveratrol treatment reduces brain edema and lesion volume, as well as improves neurobehavioral functional performance following TBI
  • green tea consumption or supplementation with its derivatives may bolster cognitive function acutely and may slow cognitive decline
  • At least one population based study, though, did demonstrate that increased green tea consumption was associated with a reduced risk for Parkinson's disease independent of total caffeine intake
  • a randomized, placebo-controlled trial demonstrated that administration of green tea extract and L-theanine, over 16 weeks of treatment, improved indices of memory and brain theta wave activity on electroencephalography, suggesting greater cognitive alertness
  • Other animal studies have also demonstrated that theanine, another important component of green tea extract, exerts a multitude of neuroprotective benefits in experimental models of ischemic stroke,[63,97] Alzheimer's disease,[109] and Parkinson's disease
  • Theanine, like EGCG, contains multiple mechanisms of neuroprotective action including protection from excitotoxic injury[97] and inhibition of inflammation
  • potent anti-oxidant EGCG which is capable of crossing the blood-nerve and blood-brain barrier,
  • Epigallocatechin-3-gallate also displays neuroprotective properties
  • More recent research has suggested that vitamin D supplementation and the prevention of vitamin D deficiency may serve valuable roles in the treatment of TBI and may represents an important and necessary neuroprotective adjuvant for post-TBI progesterone therapy
  • Progesterone is one of the few agents to demonstrate significant reductions in mortality following TBI in human patients in preliminary trials
  • in vitro and in vivo studies have suggested that vitamin D supplementation with progesterone administration may significantly enhance neuroprotection
  • Vitamin D deficiency may increase inflammatory damage and behavioral impairment following experimental injury and attenuate the protective effects of post-traumatic progesterone treatment.[37]
  • emerging evidence has suggested that daily intravenous administration of vitamin E following TBI significantly decreases mortality and improves patient outcomes
  • high dose vitamin C administration following injury stabilized or reduced peri-lesional edema and infarction in the majority of patients receiving post-injury treatment
  • it has been speculated that combined vitamin C and E therapy may potentiate CNS anti-oxidation and act synergistically with regards to neuroprotection
  • one prospective human study has found that combined intake of vitamin C and E displays significant treatment interaction and reduces the risk of stroke
  • Pycnogenol has demonstrated the ability to slow or reduce the pathological processes associated with Alzheimer's disease
  • Pcynogenol administration, in a clinical study of elderly patients, led to improved cognition and reductions in markers of lipid peroxidase
  • One other point of consideration is that in neurodegenerative disease states like Alzheimer's disease and Parkinson's disease, where there are high levels of reactive oxygen species generation, vitamin E can tend to become oxidized itself. For maximal effectiveness and to maintain its anti-oxidant capacity, vitamin E must be given in conjunction with other anti-oxidants like vitamin C or flavonoids
  • These various factors might account for the null effects of alpha-tocopherol supplementation in patients with MCI and Alzheimer's disease
  • preliminary results obtained in a pediatric population have suggested that post-traumatic oral creatine administration (0.4 g/kg) given within four hours of traumatic brain injury and then daily thereafter, may improve both acute and long-term outcomes
  • Acutely, post-traumatic creatine administration seemed to reduce duration of post-traumatic amnesia, length of time spent in the intensive care unit, and duration of intubation
  • At three and six months post-injury, subjects in the creatine treatment group demonstrated improvement on indices of self care, communication abilities, locomotion, sociability, personality or behavior and cognitive function when compared to untreated controls
  • patients in the creatine-treatment group were less likely to experience headaches, dizziness and fatigue over six months of follow-up
  • CNS creatine is derived from both its local biosynthesis from the essential amino acids methionine, glycine and arginine
  • Studies of patients with CNS creatine deficiency and/or murine models with genetic ablation of creatine kinase have consistently demonstrated significant neurological impairment in the absence of proper creatine, phosphocreatine, or creatine kinase function; thus highlighting its functional importance
  • chronic dosing may partially reverse neurological impairments in human CNS creatine deficiency syndromes
  • Several studies have suggested that creatine supplementation may also reduce oxidative DNA damage and brain glutamate levels in Huntington disease patients
  • Another study highlighted that creatine supplementation marginally improved indices of mood and reduced the need for increased dopaminergic therapy in patients with Parkinson's disease
  • Nathan Goodyear on 20 Feb 16
     
    great review of natural therapies in the treatment of concussions
Nathan Goodyear

Promising role for Gc-MAF in cancer immunotherapy: from bench to bedside - 0 views

www.ncbi.nlm.nih.gov/...PMC5686300

nagalase Gc-MAF cancer

shared by Nathan Goodyear on 29 Jan 18 - No Cached
  • MAF precursor activity has also been lost or reduced after Gc-globulin treatment in some cancer cell lines
  • This appears to result from the deglycosylated ɑ-N-acetylgalactosaminidase (nagalase) secreted from cancerous cells
  • Nagalase has been detected in many cancer patients, but not in healthy individuals
  • ...31 more annotations...
  • Studies have shown that the production of nagalase has a mutual relationship with Gc-MAF level and immunosuppression
  • It has been demonstrated that serum levels of nagalase are good prognosticators of some types of cancer
  • The nagalase level in serum correlates with tumor burden and it has been shown that Gc-MAF therapy progresses, nagalase activity decreases
  • It has been shown that Gc-MAF can inhibit the angiogenesis induced by pro-inflammatory prostaglandin E1
  • The effect of Gc-MAF on chemotaxis or activation of tumoricidal macrophages is likely the main mechanism against angiogenesis.
  • Administration of Gc-MAF stimulates immune-cell progenitors for extensive mitogenesis, activates macrophages and produces antibodies. “This indicates that Gc-MAF is a powerful adjuvant for immunization.”
  • Cancer cell lines do not develop into tumor genes in mouse models after Gc-MAF-primed immunization (29-31) and the effect of Gc-MAF has been approved for macrophage stimulation for angiogenesis, proliferation, migration and metastatic inhibition on tumors induced by MCF-7 human breast cancer cell line
  • The protocol included: "a high dose of second-generation Gc-MAF (0.5 ml) administered twice a week intramuscularly for a total of 21 injections.”
  • Yamamoto et al. showed that the administration of Gc-MAF to 16 patients with prostate cancer led to improvements in all patients without recurrence
  • Inui et al. reported that a 74-year-old man diagnosed with prostate cancer with multiple bone metastases was in complete remission nine months after initiation of GcMAF therapy simultaneously with hyper T/NK cell, high-dose vitamin C and alpha lipoic acid therapy
  • It has also been approved for non-neoplastic diseases such as autism (41), multiple sclerosis (42, 43), chronic fatigue syndrome (CFS) (40), juvenile osteoporosis (44) and systemic lupus erythematous (45).
  • Gc-MAF has been verified for use in colon, thyroid (38), lung (39), liver, thymus (36), pancreatic (40), bladder and ovarian cancer and tongue squamous carcinoma
  • Prostate, breast, colon, liver, stomach, lung (including mesothelioma), kidney, bladder, uterus, ovarian, head/neck and brain cancers, fibrosarcomas and melanomas are the types of cancer tested thus far
  • weekly administration of 100 ng Gc-MAF to cancer at different stages and types showed curative effects at different follow-up times
  • this treatment has been suggested for non-anemic patients
  • Studies have shown that weekly administration of 100 ng Gc-MAF to cancer patients had curative effects on a variety of cancers
  • Because the half-life of the activated macrophages is approximately one week, it must be administered weekly
  • In vivo weekly intramuscular administration of Gc-MAF (100 ng) for 16-22 weeks was used to treat patients with breast cancer
  • individuals harboring different VDR genotypes had different responses to Gc-MAF and that some genotypes were more responsive than others
  • Administration of Gc-MAF for cancer patients exclusively activates macrophages as an important cell in adaptive immunity
  • Gc-MAF supports humoral immunity by producing, developing and releasing large quantities of antibodies against cancer. Clinical evidence from a human model of breast cancer patients supports this hypothesis
  • There is also evidence that confirms the tumoricidal role of Gc-MAF via Fc-receptor mediation
  • It is likely that the best therapeutic responses will be observed when the nutritional and inflammatory aspects are taken together with stimulation of the immune system
  • it should be noted that no harmful side effects of Gc-MAF treatment have been reported, even when it was successfully administered to autistic children
  • The natural activation mechanism of macrophages by Gc-MAF is so natural and it should not have any side effects on humans or animal models even in cell culture
  • Besides the Gc-MAF efficacy on macrophage activity, it can be a potential anti-angiogenic agent (28) and an inhibitor of the migration of cancerous cells in the absence of macrophages (47).
  • Activating or modifying natural killer cells, dendritic cells, DC, CTL, INF and IL-2 have all been recommended for cancer immunotherapy
  • It has been reported that nagalase cannot deglycosylate Gc-MAF as it has specificity for Gc globulin alone
  • inflammation-derived macrophage activation with the participation of B and T lymphocytes is the main mechanism
  • macrophages highly-activated by the addition of Gc-MAF can show tumoricidal activity
  • Previous clinical investigations have confirmed the efficacy of Gc-MAF. In addition to activating existing macrophages, Gc-MAF is a potent mitogenic factor that can stimulate the myeloid progenitor cells to increase systemic macrophage cell counts by 40-fold in four days
  • Nathan Goodyear on 29 Jan 18
     
    great review on Gc-MAF in cancer.  An increase in nagalase blocks Gc-protein to Gc-MAF activity leaving the host immune system compromised.
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