dieting attempts cause weight gain via providing (misleading) information about the environment to the subconscious systems that control body mass
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shared by Nathan Goodyear on 07 Jan 14
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Steroid hormones in multiple sclerosis. [J Neurol Sci. 2005] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...15878598
MS multiple sclerosis multiple sclerosis hormone hormones pregnancy women Estriol E3 progesterone
shared by Nathan Goodyear on 07 Jan 14
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Pregnancy has a positive effect on MS patients, especially during the 3rd trimester. Rebound of MS increases in the postpartum period. Estriol is the dominant pregnancy estrogen. Progesterone is also produced at high levels. The withdrawal of these hormones in the postpartum period are likely to lead to this Rebound in MS.
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Long-Term Persistence of Hormonal Adaptations to Weight Loss - NEJM - 0 views
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An adaptive response to uncertainty can lead to weight gain during dieting attempts - 0 views
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Our model predicts that energy reserves should respond to repeated attempts to diet by weight cycling and becoming greater from one cycle to the next
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the very conditions that cause weight gain initially—a glut of food—causes further weight gain once cyclical dieting begins
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There is evidence that among weight cycling, people those who switch between dieting and binge-eating more frequently gain more weight
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yo-yo dieting leads to weight gain, in part, due to increase food intake in between the calorie restriction phases. The calorie restriction suppresses metabolic rate and results in muscle loss; both of which contribute to the rebound weight gain seen by so many.
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Weight Regain after a Diet-Induced Loss Is Predicted by Higher Baseline Leptin and Lowe... - 0 views
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Appetite-related hormones may play an important role in weight regain after obesity therapy.
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Subjects with higher plasma leptin and lower ghrelin levels at baseline could be more prone to regain lost weight
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shared by Nathan Goodyear on 09 Jul 11
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Beneficial effects of a long-term oral L-arginine treatment added to a hypocaloric diet... - 0 views
ajpendo.physiology.org/...E906.full
L-Arginine weight loss diet overweight obesity insulin-resistant diabetic patients
shared by Nathan Goodyear on 09 Jul 11
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L-arginine supplementation further decreased FM (P < 0.05) and waist circumference (P < 0.0001), preserving FFM (P < 0.03), and improved mean daily glucose profiles (P < 0.0001) and fructosamine (P < 0.03). Moreover, change in area under the curve of cGMP (second messenger of nitric oxide; P < 0.001), superoxide dismutase (index of antioxidant capacity; P < 0.01), and adiponectin levels (P < 0.02) increased, whereas basal endothelin-1 levels (P < 0.01) and leptin-to-adiponectin ratio (P < 0.05) decreased in the L-arginine group.
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L-Arginine helps to preserve muscle, while increase fat loss. This will help to prevent fat rebound in weight loss programs. Additionally, insulin resistance improved.
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Intravenous Ascorbate as a Tumor Cytotoxic Chemotherapeutic Agent - 0 views
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There is a 10 — 100-fold greater content of catalase in normal cells than in tumor cells
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induce hydrogen peroxide generation
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Ascorbic acid and its salts (AA) are preferentially toxic to tumor cells in vitro (6 — 13) and in vivo
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related to intracellular hydrogen peroxide generation
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only be obtained by intravenous administration of AA
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Preferentially kills neoplastic cells
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Is virtually non-toxic at any dosage
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Does not suppress the immune system, unlike most chemotherapy agents
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Increases animal and human resistance to infectious agents by enhancing lymphocyte blastogenesis, enhancing cellular immunity, strengthening the extracellular matrix, and enhancing bactericidal activity of neutrophils and modulation of complement protein
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Strengthens the structural integrity of the extracellular matrix which is responsible for stromal resistance to malignant invasiveness
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1969, researchers at the NCI reported AA was highly toxic to Ehrlich ascites cells in vitro
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In 1977, Bram et al reported preferential AA toxicity for several malignant melanoma cell lines, including four human-derived lines
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Noto et al reported that AA plus vitamin K3 had growth inhibiting action against three human tumor cell lines at non-toxic levels
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Metabolites of AA have also shown antitumor activity in vitro
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The AA begins to reduce cell proliferation in the tumor cell line at the lowest concentration, 1.76 mg/dl, and is completely cytotoxic to the cells at 7.04 mg/dl
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the normal cells grew at an enhanced rate at the low dosages (1.76 and 3.52 mg/dl)
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preferential toxicity of AA for tumor cells. >95% toxicity to human endometrial adenocarcinoma and pancreatic tumor cells (ATCC AN3-CA and MIA PaCa-2) occurred at 20 and 30 mg/dl, respectively.
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No toxicity or inhibition was demonstrated in the normal, human skin fibroblasts (ATCC CCD 25SK) even at the highest concentration of 50 mg/dl.
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the use of very high-dose intravenous AA for the treatment of cancer was proposed as early as 1971
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Cameron and Pauling have published extensive suggestive evidence for prolonged life in terminal cancer patients orally supplemented (with and without initial intravenous AA therapy) with 10 g/day of AA
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AA, plasma levels during infusion were not monitored,
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the long-term, oral dosage used in those experiments (10 g/day), while substantial and capable of producing immunostimulatory and extracellular matrix modulation effects, was not high enough to achieve plasma concentrations that are generally cytotoxic to tumor cells in culture
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This low cytotoxic level of AA is exceedingly rare
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5 — 40 mg/dl of AA is required in vitro to kill 100% of tumor cells within 3 days. The 100% kill levels of 30 mg/dl for the endometrial carcinoma cells and 40 mg/dl for the pancreatic carcinoma cells in Figure 2 are typical
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normal range (95% range) of 0.39-1.13 mg/dl
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1 h after beginning his first 8-h infusion of 115 g AA (Merit Pharmaceuticals, Los Angeles, CA), the plasma AA was 3.7 mg/dl and at 5 h was 19 mg/dl. During his fourth 8-h infusion, 8 days later, the 1 h plasma level was 158 mg/dl and 5 h was 185 mg/dl
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plasma levels of over 100 mg/dl have been maintained in 3 patients for more than 5 h using continuous intravenous infusion
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In rare instances of patients with widely disseminated and rapidly proliferating tumors, intravenous AA administration (10 — 45 g/day) precipitated widespread tumor hemorrhage and necrosis, resulting in death
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Although the outcomes were disastrous in these cases, they are similar to the description of tumor-necrosis-factor-induced hemorrhage and necrosis in mice (52) and seem to demonstrate the ability of AA to kill tumor cells in vivo.
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toxic effects of AA on one normal cell line were observed at 58.36 mg/dl and the lack of side effects in patients maintaining >100 mg/dl plasma levels
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Although it is very rare, tumor necrosis, hemorrhage, and subsequent death should be the highest priority concern for the safety of intravenous AA for cancer patients.
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Klenner, who reported no ill effects of dosages as high as 150 g intravenously over a 24-h period
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Cathcart (55) who describes no ill effects with doses of up to 200 g/d in patients with various pathological conditions
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following circumstances: renal insufficiency, chronic hemodialysis patients, unusual forms of iron overload, and oxalate stone formers
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Screening for red cell glucose-6-phosphate dehydrogenase deficiency, which can give rise to hemolysis of red blood cells under oxidative stress (57), should also be performed
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any cancer therapy should be started at a low dosage to ensure that tumor hemorrhage does not occur.
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patient is orally supplementing between infusions
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a scorbutic rebound effect can be avoided with oral supplementation. Because of the possibility of a rebound effect, measurement of plasma levels during the periods between infusions should be performed to ensure that no such effect takes place
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Every effort should be made to monitor plasma AA levels when a patient discontinues intravenous AA therapy.
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Older study, 1995, but shows the long-standing evidence that IVC preferentially is cytotoxic to cancer cells.`
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Gender and sex hormones in multiple sclerosis pathology and therapy - 0 views
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It is now well recognized that the disease manifestation is reduced in pregnant women with relapsing-remitting MS
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This occurs particularly during the third trimester when levels of estrogens (estradiol and estriol) and progesterone (see Table 2) are elevated up to about 20 times
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This seems well correlated with a decrease in active white matter lesions detected by MRI
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This clinical improvement is however followed by temporary rebound exacerbations at post-partum, when the hormone levels decline
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a shift from Th1 to Th2 immune response, expansion of suppressive regulatory T lymphocytes and decrease in the number of circulating CD16+ natural killer (NK)-cells
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Th1 lymphocytes secrete proinflammatory cytokines (e.g. IL-2, IFNgamma, lymphotoxin) while Th2 cells secrete anti-inflammatory cytokines (e.g. IL-4, IL-5, IL-10), which favor humoral-mediated responses
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Th2 cytokines are associated with down-regulation of Th1 cytokines and this Th2 shift is believed to provide protection from allograft rejection during pregnancy as well as from Th1-mediated autoimmune disease
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it is worth noting that the levels of other hormones with anti-inflammatory activity (1,25-dihydroxy-vitamin D3, norepinephrine, cortisol) also increase by 2 to 4 times during late pregnancy
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1,25-dihydroxy vitamin D3 induces regulatory T-cell function important for development of self-tolerance
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breast-feeding does not alter the relapse rate in women with MS
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Leptin is a pleiotropic hormone produced primarily by adipocytes but also by T lymphocytes and neurons
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Several lines of evidence indicate that leptin contributes to EAE/MS pathogenesis, influencing its onset and clinical severity, by acting as a proinflammatory cytokine which promotes regulatory T cell (Treg) anergy and hyporesponsiveness, resulting in increased Th1 (TNFalpha, INFgamma) and reduced Th2 (IL-4) cytokine production
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circulating leptin levels are increased in relapsing-remitting MS patients (men and women analyzed together) while the CD4+CD25+Treg population decreases
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As the leptin plasma concentrations are proportional to the amount of fat tissue, obese/overweight individuals produce higher levels of leptin
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Nielsen et al found that estradiol and progesterone exert neuroprotection against glutamate neurotoxicity, while MPA antagonizes the neuroprotective effect of estradiol and exacerbated neuron death induced by glutamate excitotoxicity
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very good review of the differences in MS and hormones between the sexes.
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shared by Nathan Goodyear on 17 Mar 15
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Therapeutic Testosterone Administration Preserves Excitatory Synaptic Transmission in t... - 0 views
www.jneurosci.org/...12312.long
Testosterone polyneuropathy MS multiple Sclerosis Estriol hormones autoimmune disease
shared by Nathan Goodyear on 17 Mar 15
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direct androgen receptor activation is not a mutually exclusive requirement of testosterone-mediated neuroprotection.
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Testosterone treatment after EAE induction restores synaptic transmission and corresponding synaptic protein levels within the hippocampus during EAE
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A growing body of evidence suggests that testosterone enhances hippocampal synaptogenesis
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This study demonstrates that testosterone treatment either before or after EAE disease induction partially restores deficits in synaptic transmission, preserves presynaptic and postsynaptic integrity, and prevents hippocampal pathology.
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treatment with a pregnancy estrogen, estriol, can prevent deficits in excitatory synaptic transmission in the hippocampus during EAE
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testosterone is important to the maintenance of normal synaptic spine density in the hippocampus
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estriol treatment was also capable of preserving levels of synaptic proteins that are known to orchestrate functional synaptic transmission within the hippocampus.
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Estriol is a therapeutic candidate in MS because it has widespread effects on the immune system and the CNS
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MS patients have significantly decreased relapse rates during the third trimester of pregnancy, when estriol levels are most elevated, and relapse rates rebound during the postpartum period coinciding with an abrupt decline in serum estriol levels
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In nonpregnant MS patients, estriol treatment has been shown to significantly reduce gadolinium-enhancing lesion number and volumes measured by MRI
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Testosterone restores/preserves nerve synapsis within the hippocampus in autoimmune demyelinating disease. Testosterone appears to have neuroprotection. The authors conclude that the majority of the protective effect was through aromatase activity.