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).
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shared by Nathan Goodyear on 01 May 12
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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
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Chronic fatigue syndrome and mitochondrial dysfunction - 0 views
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shared by Nathan Goodyear on 12 May 12
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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
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shared by Nathan Goodyear on 20 Feb 12
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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
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shared by Nathan Goodyear on 24 Apr 12
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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
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shared by Nathan Goodyear on 13 Mar 12
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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
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shared by Nathan Goodyear on 12 May 12
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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
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shared by Nathan Goodyear on 09 Oct 13
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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
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shared by Nathan Goodyear on 02 May 12
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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
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shared by Nathan Goodyear on 02 May 12
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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
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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.
SARS-CoV-2 infection triggers reactivation of latent viruses in people with chronic fat... - 0 views
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Kent Holtorf: Long Term Weight Loss - More Than Will Power? - 0 views
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f greater than 10, it demonstrates there is a degree of leptin resistance contributing to an inability to lose weight
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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
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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.
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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.
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As soon as the body senses a reduction in calories, the production of reverse T3 is stimulated to lower metabolism
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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).
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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).
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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).
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shared by Nathan Goodyear on 02 May 12
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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
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shared by Nathan Goodyear on 02 May 12
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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
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shared by Nathan Goodyear on 20 Feb 16
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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
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Long-chain polyunsaturated fatty acids, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are highly enriched in neuronal synaptosomal plasma membranes and vesicles
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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.
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multiple preclinical studies have suggested that DHA and/or EPA supplementation may have potential benefit through a multitude of diverse, but complementary mechanisms
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pre-injury dietary supplementation with fish oil effectively reduces post-traumatic elevations in protein oxidation
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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.
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DHA has provided neuroprotection in experimental models of both focal and diffuse traumatic brain injury
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potential mechanisms of neuroprotection, in addition to DHA and EPA's well-established anti-oxidant and anti-inflammatory properties
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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
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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
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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
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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
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Curcumin is highly lipophilic and crosses the blood-brain barrier enabling it to exert a multitude of different established neuroprotective effects
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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
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Curcumin may confer significant neuroprotection because of its ability to act on multiple deleterious post-traumatic, molecular cascades
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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)
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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
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studies have demonstrated that resveratrol treatment reduces brain edema and lesion volume, as well as improves neurobehavioral functional performance following TBI
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green tea consumption or supplementation with its derivatives may bolster cognitive function acutely and may slow cognitive decline
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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
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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
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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
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Theanine, like EGCG, contains multiple mechanisms of neuroprotective action including protection from excitotoxic injury[97] and inhibition of inflammation
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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
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Progesterone is one of the few agents to demonstrate significant reductions in mortality following TBI in human patients in preliminary trials
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in vitro and in vivo studies have suggested that vitamin D supplementation with progesterone administration may significantly enhance neuroprotection
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Vitamin D deficiency may increase inflammatory damage and behavioral impairment following experimental injury and attenuate the protective effects of post-traumatic progesterone treatment.[37]
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emerging evidence has suggested that daily intravenous administration of vitamin E following TBI significantly decreases mortality and improves patient outcomes
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high dose vitamin C administration following injury stabilized or reduced peri-lesional edema and infarction in the majority of patients receiving post-injury treatment
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it has been speculated that combined vitamin C and E therapy may potentiate CNS anti-oxidation and act synergistically with regards to neuroprotection
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one prospective human study has found that combined intake of vitamin C and E displays significant treatment interaction and reduces the risk of stroke
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Pycnogenol has demonstrated the ability to slow or reduce the pathological processes associated with Alzheimer's disease
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Pcynogenol administration, in a clinical study of elderly patients, led to improved cognition and reductions in markers of lipid peroxidase
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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
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These various factors might account for the null effects of alpha-tocopherol supplementation in patients with MCI and Alzheimer's disease
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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
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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
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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
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patients in the creatine-treatment group were less likely to experience headaches, dizziness and fatigue over six months of follow-up
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CNS creatine is derived from both its local biosynthesis from the essential amino acids methionine, glycine and arginine
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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
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chronic dosing may partially reverse neurological impairments in human CNS creatine deficiency syndromes
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Several studies have suggested that creatine supplementation may also reduce oxidative DNA damage and brain glutamate levels in Huntington disease patients
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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
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Promising role for Gc-MAF in cancer immunotherapy: from bench to bedside - 0 views
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MAF precursor activity has also been lost or reduced after Gc-globulin treatment in some cancer cell lines
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This appears to result from the deglycosylated ɑ-N-acetylgalactosaminidase (nagalase) secreted from cancerous cells
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Studies have shown that the production of nagalase has a mutual relationship with Gc-MAF level and immunosuppression
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It has been demonstrated that serum levels of nagalase are good prognosticators of some types of cancer
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The nagalase level in serum correlates with tumor burden and it has been shown that Gc-MAF therapy progresses, nagalase activity decreases
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It has been shown that Gc-MAF can inhibit the angiogenesis induced by pro-inflammatory prostaglandin E1
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The effect of Gc-MAF on chemotaxis or activation of tumoricidal macrophages is likely the main mechanism against angiogenesis.
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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.”
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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
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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.”
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Yamamoto et al. showed that the administration of Gc-MAF to 16 patients with prostate cancer led to improvements in all patients without recurrence
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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
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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).
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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
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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
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weekly administration of 100 ng Gc-MAF to cancer at different stages and types showed curative effects at different follow-up times
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Studies have shown that weekly administration of 100 ng Gc-MAF to cancer patients had curative effects on a variety of cancers
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Because the half-life of the activated macrophages is approximately one week, it must be administered weekly
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In vivo weekly intramuscular administration of Gc-MAF (100 ng) for 16-22 weeks was used to treat patients with breast cancer
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individuals harboring different VDR genotypes had different responses to Gc-MAF and that some genotypes were more responsive than others
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Administration of Gc-MAF for cancer patients exclusively activates macrophages as an important cell in adaptive immunity
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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
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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
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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
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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
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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).
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Activating or modifying natural killer cells, dendritic cells, DC, CTL, INF and IL-2 have all been recommended for cancer immunotherapy
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It has been reported that nagalase cannot deglycosylate Gc-MAF as it has specificity for Gc globulin alone
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inflammation-derived macrophage activation with the participation of B and T lymphocytes is the main mechanism
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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