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Nathan Goodyear

ScienceDirect - Journal of Diabetes and its Complications : Starvation diet and very-lo... - 0 views

  • The metabolic situation in extremely low-calorie diets may be comparable to that in starvation
  • increased insulin resistance in states of starvation and anorexia nervosa, with a concomitant role in stress hormones.
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    very-low-calorie diets, like found in the HCG diet, results in insulin resistance in many individuals, results in muscle mass loss, and results in many negative effects, including weight gain.
Nathan Goodyear

Diabetes - 0 views

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    Elevated LPS and metabolic endotoxemia associated with weight gain and type II diabetes
Nathan Goodyear

Exercise-associated hyponatremia: role of cytokines. - PubMed - NCBI - 0 views

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    study links rhabdomyolysis to exercise induced hyponatremia.  This article links the depletion of glycogen to muscle release of IL-6 leading to increase in ECW and thus hyponatremia. The abstract discusses fluid restriction vs hypertonic 3% NaCL to reverse the more severe cases.  The first signs are of weight gain and thus weight should be monitored.  Decreased renal output is also associated with EAH.  Altered mental status is an early sign.
wheelchairindia9

Heavy Duty Wheelchair - 0 views

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    Bariatric wheelchairs (often referred to as extra wide wheelchairs or heavy duty wheelchairs) are strong enough to accommodate almost any user. Just like lighter manual chairs, bariatric wheelchairs are all foldable and feature armrests and swing-away footrests - but they differ quite a bit in their construction. While lightweight wheelchairs often employ materials like aluminum or titanium alloy, a bariatric wheelchair is usually fashioned from steel. Karma 8020 X Heavy Duty Wheelchair: It comes with detachable swing away footrests. The wheel chair has flip-back armrests. It comes with centre of gravity adjustment. The wheel chair has wide profile casters. Seat Size 20'' inch & 22'' inch Total Weight 17 K.G. Heavy duty wheelchairs (often referred to as extra wide wheelchairs or bariatric wheelchairs) are sturdy enough to accommodate almost any user. Just their lighter cousins, manual chairs, heavy duty models all fold and feature arm rests and swing-away footrests - but they differ quite a bit in their construction. Heavy duty wheelchairs require more strength to push by the caregiver and by the user, if the chair is self-propelled. In some cases, it may be wise for the caregiver to ask for assistance from another person in order to push the wheelchair safely. Karma 8520 Heavy Duty Wheelchair: It comes with detachable swing away footrests. The wheel chair has flip-back armrests. It comes with centre of gravity adjustment. The wheel chair has wide profile casters. Seat Size 20'' inch & 22'' inch Total Weight 17 K.G. Features: Dual, reinforced steel cross braces. Supports individuals maximum weight. Reinforced steel frame provides added support. Heavy duty, nylon reinforced upholstery with a back carry pouch. Removable, reversible desk length arms. Adjustable leg support.
Nathan Goodyear

Minireview: Inflammation and Obesity Pathogenesis: The Hypothalamus Heats Up - 0 views

  • Leptin, secreted by adipocytes in proportion to body fat mass
  • The saturated fatty acid palmitate (16:0) induces NF-κB signaling through a TLR4-dependent mechanism
  • 18:0 (stearic) and longer saturated fatty acids as well as linolenic acid (18:3) increased proinflammatory cytokines, ER stress markers, and TLR4 activation
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  • (SOCS)-3. A member of a protein family originally characterized as negative feedback regulators of inflammation (13, 37), SOCS3 inhibits insulin and leptin signaling
  • IKKβ signaling in discrete neuronal subsets appears to be required for both hypothalamic inflammation and excess weight gain to occur during HF feeding
  • the paradoxical observation that hyperphagia and weight gain occur when hypothalamic inflammation is induced by HF feeding, yet when it occurs in response to systemic or local inflammatory processes (e.g. administration of endotoxin), anorexia and weight loss are the rule
  • , serves as a circulating signal of energy stores in part by providing feedback inhibition of hypothalamic orexigenic pathways [e.g. neurons that express neuropeptide Y and agouti-related peptide (AgRP)]
  • and stimulating anorexigenic neurons
  • signals from Toll-like receptors (TLRs), evolutionarily conserved pattern recognition molecules critical for detecting pathogens, amplified through signaling intermediates such as MyD88 activate the inhibitor of κB-kinase-β (IKKβ)/nuclear factor-κB (NF-κB), c-Jun N-terminal kinase (Jnk) and other intracellular inflammatory signals in response to stimulation by circulating saturated fatty acids
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    great read on the current understanding of how obesity and resultant inflammation disrupts hypothalamic function.
Nathan Goodyear

Cell Metabolism - Orexin Is Required for Brown Adipose Tissue Development, Differentiat... - 0 views

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    orexin plays a role in weight gain through regulation of brown fat differentiation.  Low brown fat predisposes one to obesity.  Higher brown fat increases metabolism and thus increases fat burning capacity
Nathan Goodyear

Inflammatory cause of metabolic syndrome via brain stress and NF-κB - 0 views

  • Mechanistic studies further showed that such metabolic inflammation is related to the induction of various intracellular stresses such as mitochondrial oxidative stress, endoplasmic reticulum (ER) stress, and autophagy defect under prolonged nutritional excess
  • intracellular stress-inflammation process for metabolic syndrome has been established in the central nervous system (CNS) and particularly in the hypothalamus
  • the CNS and the comprised hypothalamus are known to govern various metabolic activities of the body including appetite control, energy expenditure, carbohydrate and lipid metabolism, and blood pressure homeostasis
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  • Reactive oxygen species (ROS) refer to a class of radical or non-radical oxygen-containing molecules that have high oxidative reactivity with lipids, proteins, and nucleic acids
  • a large measure of intracellular ROS comes from the leakage of mitochondrial electron transport chain (ETC)
  • Another major source of intracellular ROS is the intentional generation of superoxides by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase
  • there are other ROS-producing enzymes such as cyclooxygenases, lipoxygenases, xanthine oxidase, and cytochrome p450 enzymes, which are involved with specific metabolic processes
  • To counteract the toxic effects of molecular oxidation by ROS, cells are equipped with a battery of antioxidant enzymes such as superoxide dismutases, catalase, peroxiredoxins, sulfiredoxin, and aldehyde dehydrogenases
  • intracellular oxidative stress has been indicated to contribute to metabolic syndrome and related diseases, including T2D [72; 73], CVDs [74-76], neurodegenerative diseases [69; 77-80], and cancers
  • intracellular oxidative stress is highly associated with the development of neurodegenerative diseases [69] and brain aging
  • dietary obesity was found to induce NADPH oxidase-associated oxidative stress in rat brain
  • mitochondrial dysfunction in hypothalamic proopiomelanocortin (POMC) neurons causes central glucose sensing impairment
  • Endoplasmic reticulum (ER) is the cellular organelle responsible for protein synthesis, maturation, and trafficking to secretory pathways
  • unfolded protein response (UPR) machinery
  • ER stress has been associated to obesity, insulin resistance, T2D, CVDs, cancers, and neurodegenerative diseases
  • brain ER stress underlies neurodegenerative diseases
  • under environmental stress such as nutrient deprivation or hypoxia, autophagy is strongly induced to breakdown macromolecules into reusable amino acids and fatty acids for survival
  • intact autophagy function is required for the hypothalamus to properly control metabolic and energy homeostasis, while hypothalamic autophagy defect leads to the development of metabolic syndrome such as obesity and insulin resistance
  • prolonged oxidative stress or ER stress has been shown to impair autophagy function in disease milieu of cancer or aging
  • TLRs are an important class of membrane-bound pattern recognition receptors in classical innate immune defense
  • Most hypothalamic cell types including neurons and glia cells express TLRs
  • overnutrition constitutes an environmental stimulus that can activate TLR pathways to mediate the development of metabolic syndrome related disorders such as obesity, insulin resistance, T2D, and atherosclerotic CVDs
  • Isoforms TLR1, 2, 4, and 6 may be particularly pertinent to pathogenic signaling induced by lipid overnutrition
  • hypothalamic TLR4 and downstream inflammatory signaling are activated in response to central lipid excess via direct intra-brain lipid administration or HFD-feeding
  • overnutrition-induced metabolic derangements such as central leptin resistance, systemic insulin resistance, and weight gain
  • these evidences based on brain TLR signaling further support the notion that CNS is the primary site for overnutrition to cause the development of metabolic syndrome.
  • circulating cytokines can limitedly travel to the hypothalamus through the leaky blood-brain barrier around the mediobasal hypothalamus to activate hypothalamic cytokine receptors
  • significant evidences have been recently documented demonstrating the role of cytokine receptor pathways in the development of metabolic syndrome components
  • entral administration of TNF-α at low doses faithfully replicated the effects of central metabolic inflammation in enhancing eating, decreasing energy expenditure [158;159], and causing obesity-related hypertension
  • Resistin, an adipocyte-derived proinflammatory cytokine, has been found to promote hepatic insulin resistance through its central actions
  • both TLR pathways and cytokine receptor pathways are involved in central inflammatory mechanism of metabolic syndrome and related diseases.
  • In quiescent state, NF-κB resides in the cytoplasm in an inactive form due to inhibitory binding by IκBα protein
  • IKKβ activation via receptor-mediated pathway, leading to IκBα phosphorylation and degradation and subsequent release of NF-κB activity
  • Research in the past decade has found that activation of IKKβ/NF-κB proinflammatory pathway in metabolic tissues is a prominent feature of various metabolic disorders related to overnutrition
  • it happens in metabolic tissues, it is mainly associated with overnutrition-induced metabolic derangements, and most importantly, it is relatively low-grade and chronic
  • this paradigm of IKKβ/NF-κB-mediated metabolic inflammation has been identified in the CNS – particularly the comprised hypothalamus, which primarily accounts for to the development of overnutrition-induced metabolic syndrome and related disorders such as obesity, insulin resistance, T2D, and obesity-related hypertension
  • evidences have pointed to intracellular oxidative stress and mitochondrial dysfunction as upstream events that mediate hypothalamic NF-κB activation in a receptor-independent manner under overnutrition
  • In the context of metabolic syndrome, oxidative stress-related NF-κB activation in metabolic tissues or vascular systems has been implicated in a broad range of metabolic syndrome-related diseases, such as diabetes, atherosclerosis, cardiac infarct, stroke, cancer, and aging
  • intracellular oxidative stress seems to be a likely pathogenic link that bridges overnutrition with NF-κB activation leading to central metabolic dysregulation
  • overnutrition is an environmental inducer for intracellular oxidative stress regardless of tissues involved
  • excessive nutrients, when transported into cells, directly increase mitochondrial oxidative workload, which causes increased production of ROS by mitochondrial ETC
  • oxidative stress has been shown to activate NF-κB pathway in neurons or glial cells in several types of metabolic syndrome-related neural diseases, such as stroke [185], neurodegenerative diseases [186-188], and brain aging
  • central nutrient excess (e.g., glucose or lipids) has been shown to activate NF-κB in the hypothalamus [34-37] to account for overnutrition-induced central metabolic dysregulations
  • overnutrition can present the cell with a metabolic overload that exceeds the physiological adaptive range of UPR, resulting in the development of ER stress and systemic metabolic disorders
  • chronic ER stress in peripheral metabolic tissues such as adipocytes, liver, muscle, and pancreatic cells is a salient feature of overnutrition-related diseases
  • recent literature supports a model that brain ER stress and NF-κB activation reciprocally promote each other in the development of central metabolic dysregulations
  • when intracellular stresses remain unresolved, prolonged autophagy upregulation progresses into autophagy defect
  • autophagy defect can induce NF-κB-mediated inflammation in association with the development of cancer or inflammatory diseases (e.g., Crohn's disease)
  • The connection between autophagy defect and proinflammatory activation of NF-κB pathway can also be inferred in metabolic syndrome, since both autophagy defect [126-133;200] and NF-κB activation [20-33] are implicated in the development of overnutrition-related metabolic diseases
  • Both TLR pathway and cytokine receptor pathways are closely related to IKKβ/NF-κB signaling in the central pathogenesis of metabolic syndrome
  • Overnutrition, especially in the form of HFD feeding, was shown to activate TLR4 signaling and downstream IKKβ/NF-κB pathway
  • TLR4 activation leads to MyD88-dependent NF-κB activation in early phase and MyD88-indepdnent MAPK/JNK pathway in late phase
  • these studies point to NF-κB as an immediate signaling effector for TLR4 activation in central inflammatory response
  • TLR4 activation has been shown to induce intracellular ER stress to indirectly cause metabolic inflammation in the hypothalamus
  • central TLR4-NF-κB pathway may represent one of the early receptor-mediated events in overnutrition-induced central inflammation.
  • cytokines and their receptors are both upstream activating components and downstream transcriptional targets of NF-κB activation
  • central administration of TNF-α at low dose can mimic the effect of obesity-related inflammatory milieu to activate IKKβ/NF-κB proinflammatory pathways, furthering the development of overeating, energy expenditure decrease, and weight gain
  • the physiological effects of IKKβ/NF-κB activation seem to be cell type-dependent, i.e., IKKβ/NF-κB activation in hypothalamic agouti-related protein (AGRP) neurons primarily leads to the development of energy imbalance and obesity [34]; while in hypothalamic POMC neurons, it primarily results in the development of hypertension and glucose intolerance
  • the hypothalamus, is the central regulator of energy and body weight balance [
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    Great article chronicles the biochemistry of "over nutrition" and inflammation through NF-kappaB activation and its impact on the brain.
Nathan Goodyear

Irvingia: Understanding the Risks of Leptin Resistance - Life Extension - 0 views

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    nice review on Leptin resistance and weight gain from LifeExtensions
Nathan Goodyear

Short Sleep Duration Is Associated with Reduced Leptin, Elevated Ghrelin, and Increased... - 0 views

  • Participants with short sleep had reduced leptin and elevated ghrelin
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    poor sleep reduces leptin and elevates ghrelin.  This will contribute to weight gain.
Nathan Goodyear

Muscle Strength, Body Composition, and Physical Activity in Women Receiving Chemotherap... - 0 views

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    Chemotherapy is associated with a decline in lean body mass.  This could play a role in increase weight, especially in pre menopause women.
Nathan Goodyear

Melatonin might help in controlling weight gain and preventing heart diseases associate... - 0 views

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    Melatonin helps in weight loss
Nathan Goodyear

Melatonin might help control weight gain and prevent heart disease associated with obesity - 0 views

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    Melatonin helps weight loss and improves cardiovascular disease risk factors
Nathan Goodyear

Green tea aqueous extract reduces visceral fat and... [Nutr Res. 2011] - PubMed result - 0 views

  • prevented visceral fat accumulation (17.8%
  • ecreased body weight gain (5.6%
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    Green tea  leads to 5.6% weight loss and 17.8% fat accumulation in animals fed high fat diet
Nathan Goodyear

The use of LeptiCore® in reducing fat gain and managing weight loss in patien... - 0 views

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    lepticor aids weight loss.
Nathan Goodyear

Gliadin Fragments and a Specific Gliadin 33-mer Peptide Close KATP Channels and Induce ... - 0 views

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    Mouse study finds that gluten diet increased weight gain by 20%, partly through increased insulin secretion.
Nathan Goodyear

Effects of selective serotonin reuptake inhibitors o... [Thyroid. 2009] - PubMed - NCBI - 0 views

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    Interesting study.  They found a "significant reduction of T(3) after 15 and 30 days" with SSRI use, yet their conclusion is SSRI is safe in hypothyroid.   The take is that part of the weight gain associated with SSRI use is through dysfunction of thyroid hormone production as the effects were also found with T4.
Nathan Goodyear

Androgen deprivation therapy in men with prostate cancer: how should the side effects b... - 0 views

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    Androgen deprivation therapy in men has been shown to worsen insulin resistance and precipitate type II Diabetes as well as stimulate weight gain.  This suggests a cause effect relationship between Testosterone and insulin sensitivity.  Other studies have pointed to a reciprocal decline in Testosterone due to hyperglycemia--both acute and chronic.   Androgen deprivation has a significant long list of cardiovascular risks and this should be discussed with the patient.
Nathan Goodyear

Nature Clinical Practice Endocrinology & Metabolism | Testosterone and ill-health in ag... - 0 views

  • Levels of total and bioavailable testosterone and SHBG were reported to be inversely correlated with the prevalence of the metabolic syndrome in men aged 40–80 years
  • as were total testosterone and SHBG in men aged 65–96 years
  • and in a cross-sectional analysis of a large cohort of non-diabetic men aged 70–89 years
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  • In longitudinal studies, decreased levels of total testosterone and SHBG predicted an increased incidence of metabolic syndrome in nonobese men
  • Free testosterone level is not associated with the prevalence of metabolic syndrome in middle-aged and older men
  • Levels of free, bioavailable and total testosterone are lower in men with T2DM than in age-matched controls,34, 35 and decreased total testosterone level predicts incident T2DM in middle-aged men.
  • men with T2DM commonly have low total or free testosterone levels
  • Total, bioavailable and free testosterone levels are inversely correlated with fasting insulin level and insulin resistance in middle-aged men without T2DM
  • total testosterone is positively correlated with insulin sensitivity in men with normal or impaired glucose tolerance or T2DM
  • low SHBG level is more strongly associated with metabolic syndrome than low total testosterone in aging men
  • the recognized association between low SHBG level and insulin resistance
  • Low levels of SHBG are also associated with smaller, denser LDL-cholesterol molecules in nondiabetic men,58 and were found to predict increased cardiovascular disease mortality in one study of older men
  • Low levels of SHBG might reflect obesity, insulin resistance and overall poor health
  • Compared with those who have normal testosterone levels, men aged 40 years or more with total testosterone levels <9.8 nmol/l or elevated LH level have greater CIMT
  • In men aged 73–94 years, total testosterone was inversely correlated with CIMT
  • a prospective analysis of men aged 73–91 years, progression of CIMT was not related to total testosterone level, but it was inversely related to free testosterone level
  • A study of men aged 55 years or more found that those with total and bioavailable testosterone levels in the highest tertile had a lower risk of severe aortic atherosclerosis (detected by radiography as abdominal aortic calcification) than those with the lowest testosterone levels.
  • a large study of men aged 69–80 years, those with total or free testosterone in the lowest quartile had increased odds of lower-extremity peripheral arterial disease
  • the possibility of reverse causation has to be considered, as systemic illness can result in decreased testosterone levels
  • previous case–control studies and longitudinal studies have failed to identify low testosterone levels as strong predictors of clinically significant coronary disease
  • Reviews of trials on testosterone therapy in men with either low or low-to-normal testosterone levels have not shown consistent beneficial effects either on lipid profiles or on actual cardiovascular events.24, 54, 55 These trials, however, have not been designed or powered to detect treatment-related differences in cardiovascular outcome
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    Declining Testosterone or low Testosterone is clearly associated with poor health in men.   Very nice review of the association between low Testosterone and metabolic dysfunction.  Low T is associated with increased metabolic syndrome, Diabetes, weight gain, insulin resistance...
Nathan Goodyear

Response to Media Reports Associating Testosterone Treatment with Greater Heart Attack ... - 0 views

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    Life extesnsions rebuttal to recent JAMA study.  There was several significant flaws in that study and thus limited evidence can be gained by that study.  In fact, I find no useful clinical information from that study. In the rebuttal, there are flaws. The reference the low serum T after treatment and correctly discuss aromatase activity.  But they fail the mention that the less than optimal serum T is likely the result of the high aromatase activity in these men.  Age, stress, and weight are primary causes of increases estrogen production in these men.  These would be why likely high estrogen production occurred and less than optimal serum T resulted.   And, increased E2 will cause an increase in CRP which can precipitate CVD events.
Nathan Goodyear

Effect of long-term dietary protein intake on g... [Diabetologia. 2000] - PubMed - NCBI - 0 views

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    Long-term high protein intake associated with increased gluconeogenesis.  In the presence of insulin resistance, this will promote weight gain.
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