both obesity and low testosterone are also risk factors for neural dysfunction, including cognitive impairment [58–61] and development of AD
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in title, tags, annotations or urlRepublic Broadcasting Network » Bombshell Oxford Study: Less than 6% of "Appr... - 0 views
republicbroadcasting.org/...rt-their-benefits-harms-are-si
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Role of Glutathione in Cancer: From Mechanisms to Therapies - PMC - 0 views
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Tynor Foot Drop Splint Right-Left - 0 views
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Ankle Splint and Foot Drop Splint Stabilize Ankle Joint uphold the ankle joint easily fits into the feet foot drop splint flexible reduces the pressure on the ankle proper cushioning to the ankles Enhances comfort and walking pleasure
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Tynor Foot Drop Splint Right/Left Applications Prevention and correction of foot drop. Peripheral nerve paralysis. Nerve/Muscle damage. Ankle or Plantar flexion contracture. Functional Alignment of the foot. Post operative care. Burn patients. Tynor Foot Drop Splint Right/Left Features Effective foot lift. Strong leaf spring action. Customizable. Thin walled, worn in a shoe. Tynor Foot Drop Splint Right/Left Measurements Measure shoe size Size Chart - Sizes European American Small 34-36 2.8-4.4 Medium 37-39 5.3-6.8 Large 40-42 7.5-9.0
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John James a New Evidence Based Estimate of Patient Harms 2013 (1) - 0 views
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shared by Nathan Goodyear on 06 Oct 14
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The Benefits and Harms of Systemic T... [J Clin Endocrinol Metab. 2014] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...25279572
Testosterone women Postmenopause post-menopause female hormones hormone
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The Benefits and Harms of Systemic Dehydroepiandrosterone (DHEA) in Postmenopausal Wome... - 0 views
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Review of the data points to poor quality of evidence dealing with DHEA in post-menopausal women with normal adrenal function. Yet if DHEA is low, which is >95% produced by adrenals in women, then how can the adrenal function be "normal". The meta-analysis found no improvement in libido and/or sexual function, and no improvement in lipids, glucose, weight... was noted. Essentially not positive or negative effects were noted. Abstract only available here, so dosage is a question.
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shared by Nathan Goodyear on 28 Apr 15
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Diet-induced obesity and low testosterone increase neuroinflammation and impair neural ... - 0 views
www.ncbi.nlm.nih.gov/...PMC4190446
Testosterone neuroinflammation glia insulin resistance obesity diabetes brain CNS PNS inflammation low T low Testosterone TNF-alpha IL-1beta
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diet-induced obesity causes significant metabolic disturbances and impairs central and peripheral nervous systems.
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both obesity and low testosterone are linked with promotion of inflammatory pathways [70–72] and exert harmful actions on the central [73–75] and peripheral [29,76] nervous systems
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In general, obesity-related changes were worsened by low testosterone and improved by testosterone treatment; however, this relationship was not statistically significant in several instances. Further, our data suggest that a common pathway that may contribute to obesity and testosterone effects is regulation of inflammation
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fasting blood glucose levels were independently and additively increased by GDX-induced testosterone depletion and high-fat diet
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testosterone treatment significantly reduced fasting glucose under both the normal and high-fat diets, demonstrating potential therapeutic efficacy of testosterone supplementation
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fasting insulin, insulin resistance (HOMA index), and glucose tolerance, low testosterone tended to exacerbate and or testosterone treatment improved outcomes.
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testosterone’s effects likely do not indicate an indirect result on adiposity but rather regulatory action(s) on other aspects of metabolic homeostasis
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Prior work in rodents has shown diet-induced obesity induces insulin resistance in rat brain [63] and that testosterone replacement improves insulin sensitivity in obese rats [64]. Our findings are consistent with the human literature, which indicates that (i) testosterone levels are inversely correlated to insulin resistance and T2D in healthy [30,65] as well as obese men [66], and (ii) androgen therapy can improve some metabolic measures in overweight men with low testosterone
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it has been shown that TNFα has inhibitory effects on neuron survival, differentiation, and neurite outgrowth
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Our data demonstrate that low testosterone and obesity independently increased cerebrocortical mRNA levels of both TNFα and IL-1β
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many beneficial effects of testosterone, including inhibition of proinflammatory cytokine expression
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neuroprotection [80,81], are dependent upon androgen receptors, the observed effects of testosterone in this study may involve androgen receptor activation
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testosterone can be converted by the enzyme aromatase into estradiol, which is also known to exert anti-inflammatory [82] and neuroprotective [83] actions
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Since testosterone can affect glial function [86] and improve neuronal growth and survival [87–89], it was unexpected that testosterone status exhibited rather modest effects on neural health indices with the only significant response being an increase in survival in the testosterone-treated, high-fat diet group
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testosterone treatment significantly lowered TNFα and IL-1β expression to near basal levels even in obese mice, indicating a protective benefit of testosterone across diet conditions
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Testosterone status and diet-induced obesity were associated with significant regulation of macrophage infiltration
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a possible mechanism by which obesity and testosterone levels may affect the health of both CNS and PNS
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Study points to obesity and low Testosterone contribution of neuroinflammation. No effect of body weight was seen with TRT. This animal model found similar positive effects of TRT in insulin sensitivity. Obesity and low T increase inflammatory cytokine production: this study found an increase in TNF-alpha and IL-1beta and TRT reduced TNF-alpha and IL-1beta to near base-line. Testosterone is neuroprotective and this study reviewed the small volume of evaded that pointed to benefit from estradiol. Testosterone's effect on glial survival was positive but not significant. Obesity and low T were found to be associated with increased macrophage infiltration in the PNS with increased TNF-alpha and IL-1beta. Testosterone therapy improved peripheral neuropathy via its positive effects on nocicieption.
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shared by Nathan Goodyear on 29 Apr 15
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Clostridium scindens: a human gut microbe with a high potential to convert glucocortico... - 0 views
www.jlr.org/...2437.full
gut microbiota gut microbiome gut bacteria androgens hormones clostridium scindens
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During the enterohepatic circulation (EC), bile salts are synthesized in the liver, concentrated in the gallbladder, and function in the lumen of the small intestine to absorb dietary lipids and limit microbial growth at the site of nutrient uptake
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Bile acid 7α/β-dehydroxylating bacteria are organisms capable of converting primary bile acids made by the host to harmful secondary bile acids, deoxycholic acid, and lithocholic acid
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These bacteria normally comprise a small proportion of the gut microbiota (∼103–104/g wet weight) and consist of species within the genus Clostridium
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C. scindens and a small number of species belonging to the genus Clostridium are responsible for significant alterations in the human bile acid pool composition through bile acid 7α/β dehydroxylation
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bile acids play an important role in maintaining intestinal barrier function as antimicrobial agents in the small bowel (37, 38) and inducers of antimicrobial peptides
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Perturbations in the biliary bile acid pool composition can be indicative of hepatogastrointestinal diseases such as fat malabsorption (40), gallstones (3), gastrointestinal cancers (41), and possibly type II diabetes
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shared by Nathan Goodyear on 07 Oct 15
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Postmenopausal circulating levels of 2- and 16α-hydroxyestrone and risk of en... - 0 views
www.ncbi.nlm.nih.gov/...PMC3241553
estrogen metabolism 2-hydroxyestrone 4-hydroxyestrone estrogen metabolites cancer uterine cancer endometrial cancer hormones 2:16alpha-OHE1 2:16
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our results do not support the hypothesis that greater metabolism of oestrogen via the 2-OH pathway, relative to the 16α-OH pathway, protects against endometrial cancer. Indeed our results are more suggestive of an increase in risk, rather than a decrease, with higher levels of 2-OHE1
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women with a higher 2-OHE1 : 16α-OHE1 ratio did not have a decreased risk of endometrial cancer as compared with women with a lower ratio
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The findings from this first prospective epidemiological study of oestrogen metabolites and endometrial cancer are in line with results from prospective studies on breast cancer, another oestrogen-related cancer. None of the seven studies on breast cancer reported significant associations overall
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On the whole, prospective epidemiological data do not support the hypothesis that the 2-hydroxyestrogen pathway is protective, and the 16α-hydroxyestrogen pathway harmful, in hormone-dependent cancers
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Both 2- and 4-hydroxyestrogens are catecholestrogens, and it has been suggested that catecholestrogens increase risk of oestrogen-mediated cancers through direct genotoxic effects, rather than through stimulation of cell proliferation via binding to oestrogen receptors
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a significant increase in risk of breast cancer with levels of 2-OHE1 has also been reported previously, although it was limited to hormone receptor-negative tumours
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Diabetes Mellitus, Fasting Glucose, and Risk of Cause-Specific Death - NEJM - 0 views
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diabetes is associated with substantial premature death from several cancers, infectious diseases, external causes, intentional self-harm, and degenerative disorders, independent of several major risk factors
Who Says Smoking Pot is Illegal? - 1 views
Who Says Smoking Pot is Illegal? - 1 views
Who Says Smoking Pot is Illegal? - 1 views
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Exposure to volatile organic compounds and loss of pulmonary function in the elderly - 0 views
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is study suggests that exposure to toluene and xylene exert a harmful effect on pulmonary function by exacerbating oxidative stress in elderly people.
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Fructose: A Key Factor in the Development of Metabolic Syndrome and Hypertension - 0 views
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HFCS consists of fructose and glucose mixed in a variety of concentrations, but most commonly as 55% fructose and 45% glucose
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In the United States, HFCS and sucrose are the major sources of fructose in the diet, and HFCS is a major ingredient in soft drinks, pastries, desserts, and various processed foods
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fructose and glucose are metabolized in completely different ways and utilize different GLUT transporters
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In the liver, fructose bypasses the two highly regulated steps of glycolysis, catalyzed by glucokinase/hexokinase and phosphofructokinase both of which are inhibited by increasing concentrations of their byproducts. Instead, fructose enters the pathway at a level that is not regulated and is metabolized to fructose-1-phosphate primarily by fructokinase or ketohexokinase
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Fructokinase has no negative feedback system, and ATP is used for the phosphorylation process. As a result, continued fructose metabolism results in intracellular phosphate depletion, activation of AMP deaminase, and uric acid generation which is harmful at the cellular level
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Uric acid inhibits endothelial NO both in vivo and in vitro, [15] and directly induces adipocyte dysfunction
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Serum uric acid increases rapidly after ingestion of fructose, resulting in increases as high as 2 mg/dL within 1 hour
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Uncontrolled fructose metabolism leads to postprandial hypertriglyceridemia, which increases visceral adipose deposition. Visceral adiposity contributes to hepatic triglyceride accumulation, protein kinase C activation, and hepatic insulin resistance by increasing the portal delivery of free fatty acids to the liver
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Several reviews have concluded that intake of both fructose and HFCS by children and adults was associated with an increased risk of obesity and metabolic syndrome
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The Benefits and Harms of Systemic Testosterone Therapy in Postmenopausal Women With No... - 0 views
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Only abstract available. Meta-analysis of Testosterone therapy in post-menopausal women finds significant bias, some improvement in sexual function and cholesterol levels, yet safety and long-term data is significantly lacking. Take this with studies on endogenous Testosterone in women, significant caution needs to be followed with Testosterone in women. Only abstract available here.
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Oxidative Stress and Its Relationship With Adenosine Deaminase Activity in Various Stag... - 0 views
www.ncbi.nlm.nih.gov/...PMC3547448
Adenosine Deaminase ADA cancer breast cancer superoxide disumutase glutathione peroxidase oxidative stress inflammation
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Reduced SOD activity might be responsible for excessive accumulation of superoxide anions leading to increased free radical mediated injury. Increased free radical production has been shown to be responsible for chromosomal damage leading to mutagenecity, cell proliferation and carcinogenesis. SOD activity showed marked improvement after mastectomy indicating the lowering of oxidative stress.
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The increased production of reactive oxygen species causes oxidative stress leading to cell proliferation and hence increased inflammatory conditions
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Superoxide dismutase is an important antioxidant enzyme which decomposes the harmful superoxide anions into hydrogen peroxide thus protects the body from the action of free radicals
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Females suffering from breast cancer had significantly decreased Superoxide dismutase (SOD) and reduced glutathione (GSH) levels in comparison to normal females
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ADA seems to be a promising marker of inflammation in breast cancer thereby suggesting that it can be used as a diagnostic tool to detect the stage of breast cancer along with cytopathological studies
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In conclusion, our study confirmed the role of oxidative stress in the pathogenesis of breast cancer.
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Another potent antioxidant molecule is reduced glutathione. It acts as reductant which converts hydrogen peroxide into water and reduces lipid peroxidation products into their corresponding alcohols and thus mediates protective action.
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In the present study, significantly low SOD activity has been observed in female patients suffering from carcinoma breast both pre as well as post operative in comparison to healthy females.
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We observed significantly decreased SOD activity and GSH levels in patients belonging to clinical stage 4 as compared to those having stages 1, 2 or 3 of breast cancer.
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The compromised antioxidant defence system produces the oxidative stress which in turn creates the inflammatory response shown by concomitant increased adenosine deaminase (ADA) activity in female patients.
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Experimental and epidemiological evidences implicate the involvement of oxygen derived free radical in the pathogenesis of breast cancer.
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Antioxidant status was highly depressed in advanced stages of breast cancer as compared to initial stage.
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In the present study, significantly low GSH levels were observed in female patients of carcinoma breast as compared to normal females
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Walia et al. (1995) reported increased ADA activity in breast cancer patients as compared to age matched normal subjects.
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These free radicals are able to cause damage to membrane, mitochondria and macromolecules including proteins, lipids and DNA and actively take part in cell proliferation. This cascade in turn generates the inflammatory response and causes the progression of the disease.
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Marked oxidative stress in stage 4 of breast cancer indicated advancement of the disease, hence checking oxidative stress at initial stage could be helpful for controlling the progression of the disease.
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Adenosine deaminase enzyme (ADA) catalyzes the conversion of adenosine to inosine which finally gets converted to uric acid
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Study finds a reduction in SuperOxide Dismutase and Glutathione Perioxidase in advancing breast cancer. Cancer is a high oxidative stress disease that results in inflammation, mitochondrial dysfunction and proliferation. Adenosine Deaminase (ADA) is proposed to be another biomarker to assess tumor stage.
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Habits That Ruin Your Weight Loss Plan | Health Blog - 0 views
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Some Habits That Ruin Your Weight Loss Plan. Although we may follow a strict diet plan and hit the gym.., sometimes it becomes nearly impossible to get rid of those extra pounds... The problem lies with the seemingly harmless everyday habits that we have nurtured over the years and...
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While most of us are aware that eating cheesy sausages every day for breakfast is not really good for the waistline, there are many other subtle bad habits that keep on adding more pounds to our bodies. These habits are harmful because they have the potential to sabotage our weight loss plan.
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Pharmacologic ascorbic acid concentrations selectively kill cancer cells: Action as a p... - 0 views
www.pnas.org/...13604.full
IV vitamin C cancer ascorbic acid vitamin C H2O2 GPX glutathione Perioxidase
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Taken together, these data indicate that ascorbate at concentrations achieved only by i.v. administration may be a pro-drug for formation of H2O2, and that blood can be a delivery system of the pro-drug to tissues.
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These findings give plausibility to i.v. ascorbic acid in cancer treatment, and have unexpected implications for treatment of infections where H2O2 may be beneficial
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pharmacologic concentrations of ascorbate killed cancer but not normal cells, that cell death was dependent only on extracellular but not intracellular ascorbate, and that killing was dependent on extracellular hydrogen peroxide (H2O2) formation with ascorbate radical as an intermediate
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Our data show that ascorbic acid selectively killed cancer but not normal cells, using concentrations that could only be achieved by i.v. administration
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Ascorbate-mediated cell death was due to protein-dependent extracellular H2O2 generation, via ascorbate radical formation from ascorbate as the electron donor. Like glucose, when ascorbate is infused i.v., the resulting pharmacologic concentrations should distribute rapidly in the extracellular water space (42). We showed that such pharmacologic ascorbate concentrations in media, as a surrogate for extracellular fluid, generated ascorbate radical and H2O2. In contrast, the same pharmacologic ascorbate concentrations in whole blood generated little detectable ascorbate radical and no detectable H2O2. These findings can be accounted for by efficient and redundant H2O2 catabolic pathways in whole blood (e.g., catalase and glutathione peroxidase) relative to those in media or extracellular fluid
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ascorbic acid administered i.v. in pharmacologic concentrations may serve as a pro-drug for H2O2 delivery to the extracellular milieu
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H2O2 generated in blood is normally removed by catalase and glutathione peroxidase within red blood cells, with internal glutathione providing reducing equivalents
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The electron source for glutathione is NADPH from the pentose shunt, via glucose-6-phosphate dehydrogenase. If activity of this enzyme is diminished, the predicted outcome is impaired H2O2 removal causing intravascular hemolysis, the observed clinical finding.
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Only recently has it been understood that the discordant clinical findings can be explained by previously unrecognized fundamental pharmacokinetics properties of ascorbate
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Intracellular transport of ascorbate is tightly controlled in relation to extracellular concentration
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Intravenous ascorbate infusion is expected to drastically change extracellular but not intracellular concentrations
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For i.v. ascorbate to be clinically useful in killing cancer cells, pharmacologic but not physiologic extracellular concentrations should be effective, independent of intracellular ascorbate concentrations.
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There was no correlation with ascorbate-induced cell death and glutathione, catalase activity, or glutathione peroxidase activity.
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H2O2, as the product of pharmacologic ascorbate concentrations, has potential therapeutic uses in addition to cancer treatment, especially in infections
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Use of ascorbate as an H2O2-delivery system against sensitive pathogens, viral or bacterial, has substantial clinical implications that deserve rapid exploration.
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Recent pharmacokinetics studies in men and women show that 10 g of ascorbate given i.v. is expected to produce plasma concentrations of nearly 6 mM, which are >25-fold higher than those concentrations from the same oral dose
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As much as a 70-fold difference in plasma concentrations is expected between oral and i.v. administration,
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Complementary and alternative medicine practitioners worldwide currently use ascorbate i.v. in some patients, in part because there is no apparent harm
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We first investigated whether ascorbate in pharmacologic concentrations selectively affected the survival of cancer cells by studying nine cancer cell lines
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Clinical pharmacokinetics analyses show that pharmacologic concentrations of plasma ascorbate, from 0.3 to 15 mM, are achievable only from i.v. administration
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plasma ascorbate concentrations from maximum possible oral doses cannot exceed 0.22 mM because of limited intestinal absorption
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For five of the nine cancer cell lines, ascorbate concentrations causing a 50% decrease in cell survival (EC50 values) were less than 5 mM, a concentration easily achievable from i.v. infusion
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All tested normal cells were insensitive to 20 mM ascorbate.
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As ascorbate concentration increased, the pattern of death changed from apoptosis to pyknosis/necrosis, a pattern suggestive of H2O2-mediated cell death
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Apoptosis occurred by 6 h after exposure, and cell death by pyknosis was ≈90% at 14 h after exposure
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In contrast to lymphoma cells, there was little or no killing of normal lymphocytes and monocytes by ascorbate
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Ascorbate is transported into cells as such by sodium-dependent transporters, whereas dehydroascorbic acid is transported into cells by glucose transporters and then immediately reduced internally to ascorbate
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Whether or not intracellular ascorbate was preloaded, extracellular ascorbate induced the same amount and type of death.
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extracellular ascorbate in pharmacologic concentrations mediates death of lymphoma cells by apoptosis and pyknosis/necrosis, independently of intracellular ascorbate.
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Because these data implicated H2O2 in cell killing, we added H2O2 to lymphoma cells and studied death patterns using nuclear staining (19, 28). The death patterns found with exogenous H2O2 exposure were similar to those found with ascorbate
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For both ascorbate and H2O2, death changed from apoptosis to pyknosis/necrosis as concentrations increased
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Sensitivity to direct exposure to H2O2 was greater in lymphoma cells compared with normal lymphocytes and normal monocytes
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There was no association between the EC50 for ascorbate-mediated cell death and intracellular glutathione concentrations, catalase activity, or glutathione peroxidase activity
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H2O2 generation was dependent on time, ascorbate concentration, and the presence of trace amounts of serum in media
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whatever H2O2 is generated should be removed by glutathione peroxidase and catalase within red blood cells, because H2O2 is membrane permeable
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The data are consistent with the hypothesis that ascorbate in pharmacologic concentrations is a pro-drug for H2O2 generation in the extracellular milieu but not in blood.
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In patients with glucose-6-phosphate dehydrogenase deficiency, i.v. ascorbate is contraindicated because it causes intravascular hemolysis
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ascorbate, an electron-donor in such reactions, ironically initiates pro-oxidant chemistry and H2O2 formation
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data here showed that ascorbate initiated H2O2 formation extracellularly, but H2O2 targets could be either intracellular or extracellular, because H2O2 is membrane permeant
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More than 100 patients have been described, presumably without glucose-6-phosphate dehydrogenase deficiency, who received 10 g or more of i.v. ascorbate with no reported adverse effects other than tumor lysis