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finchloe121

How To Diagnose And Defeat Insomnia In An Easy Manner! - 0 views

www.pharmahealthonline.com/...eat-insomnia-in-an-easy-manner

Health Pharmacy Medicine

shared by finchloe121 on 24 Sep 22 - No Cached
  • finchloe121 on 24 Sep 22
     
    Insomnia is a condition that prevents a person from getting peaceful and sound sleep for hours. It is a symptom that occurs due to various symptoms and causes. This sleep disorder affects people in different ways. If you suffer from insomnia, you may not be able to fall asleep or stay asleep. Cognitive behavioral therapy or CBT is a type of psychotherapy used to treat insomnia, anxiety disorders, depression, eating disorders, marital disorders, and quality of life. Cognitive-behavioral therapy focuses on changing individuals' negative thoughts because thoughts can primarily contribute to the construction of anxiety, depression, and emotional difficulties. Many people typically need at least 3-4 hours of sleep a night, but the average sleep time is 6-9 hours. This means that sleep duration and sleep cycles vary from person to person. The most important thing is to get enough sleep, no matter how long it takes. The best remedy to treat the symptoms of this disorder is to use OTC Zolpidem 5mg Tablets Online.
Nathan Goodyear

Omega-3 fatty acids as treatments for mental illness: which disorder and which fatty acid? | fats - 0 views

www.dietaryfiberfood.com/...atty-acid-mental-disorders.php

Omega-3 mood disorders depression bi-polar

shared by Nathan Goodyear on 15 Feb 11 - No Cached
  • The most convincing evidence for beneficial effects of omega-3 PUFA is to be found in mood disorders. A meta-analysis of trials involving patients with major depressive disorder and bipolar disorder provided evidence that omega-3 PUFA supplementation reduces symptoms of depression. Furthermore, meta-regression analysis suggests that supplementation with eicosapentaenoic acid may be more beneficial in mood disorders than with docosahexaenoic acid,
  • Nathan Goodyear on 15 Feb 11
     
    Omega-3 beneficial in depression and bi-polar clients
Nathan Goodyear

Kynurenine Pathway Metabolites in Humans: Disease and Healthy States - 0 views

www.la-press.com/and-healthy-stat-article-a1204

kynurenine pathway neurodegenerative disorders excitotoxicity ALS Parkinson's disease Alzheimer's mood disorder depression anxiety quinolinate picolinate disordered tryptophan metabolism

shared by Nathan Goodyear on 27 Oct 11 - No Cached
  • Nathan Goodyear on 27 Oct 11
     
    review of studies looking at kyneurenine pathway and it's contribution to neurodegenerative disorders and mood disorders
Nathan Goodyear

http://ac.els-cdn.com/S0303720713002426/1-s2.0-S0303720713002426-main.pdf?_tid=360bb0b2-d064-11e3-a7fe-00000aacb35f&acdnat=1398861637_afe2f36870f4686269eac5af8db43d69 - 0 views

ac.els-cdn.com/...2.0-S0303720713002426-main.pdf

endocrine disorders mitochondria disease biochemistry diabetes aging hypoparathyroidism hypothyroidism hypogonadism hormones

shared by Nathan Goodyear on 30 Apr 14 - No Cached
  • Nathan Goodyear on 30 Apr 14
     
    Very well done article that discusses the relationship between mitochondria and endocrine disorders.  Mitochondrial disorders cannot just include inherited mitochondriopathies, but acquired mitochondriopathies as well.
Nathan Goodyear

Effect of inositol on bulimia nervosa and binge ea... [Int J Eat Disord. 2001] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...11262515

inositol eating disorders binge

shared by Nathan Goodyear on 01 Jun 11 - No Cached
  • Inositol is as therapeutic in patients with bulimia nervosa and binge eating as it is in patients with depression and panic and obsessive-compulsive disorders
  • Nathan Goodyear on 01 Jun 11
     
    inositol effective in eating disorders, including binge eating
Nathan Goodyear

Inositol treatment of obsessive-compulsive disorde... [Am J Psychiatry. 1996] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...8780431

inositol depression panic obsessive-compulsive disorders

shared by Nathan Goodyear on 01 Jun 11 - No Cached
  • he authors conclude that inositol is effective in depression, panic, and obsessive-compulsive disorder
  • Nathan Goodyear on 01 Jun 11
     
    inositol effective in depression, panic, and obsessive-compulsive disorders
Nathan Goodyear

Double-blind, placebo-controlled, crossover trial of inositol treatment for panic disorder -- Benjamin et al. 152 (7): 1084 -- Am J Psychiatry - 0 views

ajp.psychiatryonline.org/...1084

inositol panic disorders anxiety

shared by Nathan Goodyear on 01 Jun 11 - No Cached
  • The authors conclude that inositol's efficacy, the absence of significant side effects, and the fact that inositol is a natural component of the human diet make it a potentially attractive therapeutic for panic disorder.
  • Nathan Goodyear on 01 Jun 11
     
    inositol proven effective in panic disorders
Nathan Goodyear

Evaluation, Diagnosis, and Treatment of Gastrointestinal Disorders in Individuals With ASDs: A Consensus Report - 0 views

pediatrics.aappublications.org/...S1.full

ASDs autism gastrointestinal disorder ASD

shared by Nathan Goodyear on 28 Jun 11 - No Cached
  • The consensus expert opinion of the panel was that individuals with ASDs deserve the same thoroughness and standard of care in the diagnostic workup and treatment of gastrointestinal concerns as should occur for patients without ASDs. Care providers should be aware that problem behavior in patients with ASDs may be the primary or sole symptom of the underlying medical condition, including some gastrointestinal disorders
  • Nathan Goodyear on 28 Jun 11
     
    ASD behavior problems may have underlying gastrointestinal disorders as the cause
Nathan Goodyear

Mood Disorders and Obesity: Understanding Inflammation as a Pathophysiological Nexus | Mohammad Alsuwaidan - Academia.edu - 0 views

www.academia.edu/..._as_a_Pathophysiological_Nexus

obesity overweight mood disorders depression anxiety weight loss' leptin adiponectin inflammation cytokines

shared by Nathan Goodyear on 22 Jan 13 - No Cached
  • Nathan Goodyear on 22 Jan 13
     
    good review of the interaction between the immune system and the neuroendocrine system in obesity and mood disorders.  
Nathan Goodyear

Salivary testosterone: Associations with depression, anxiety disorders, and antidepressant use in a large cohort study - 0 views

www.jpsychores.com/...abstract

saliva salivary low testosterone depression anxiety mood disorders

shared by Nathan Goodyear on 25 Apr 12 - No Cached
  • Nathan Goodyear on 25 Apr 12
     
    large study revealed that low salivary testosterone is associated with increased depression, anxiety, and other mood disorders.
Nathan Goodyear

PsychiatryOnline | The Journal of Neuropsychiatry and Clinical Neurosciences | Can Traumatic Brain Injury Cause Psychiatric Disorders? - 0 views

neuro.psychiatryonline.org/article.aspx

TBI traumatic brain injury psychiatric disorders depression anxiety schizophrenia insomnia

shared by Nathan Goodyear on 16 Feb 12 - No Cached
  • Nathan Goodyear on 16 Feb 12
     
    research, though limited, supports the hypothesis that TBI contributes to psychiatric disorders.
Nathan Goodyear

Nutritional therapies for mental disorders - 0 views

www.ncbi.nlm.nih.gov/...PMC2248201

vitamins nutritional therapy vitamin mood disorders depression anxiety bipolar shizophrenia OCD

shared by Nathan Goodyear on 26 Jun 12 - No Cached
  • Nathan Goodyear on 26 Jun 12
     
    Nutritional therapies for mood disorders.
Nathan Goodyear

Testosterone and glucose metabolism in men: current concepts and controversies - 0 views

joe.endocrinology-journals.org/...R37.full

Low T Testosterone metabolic syndrome MetS Diabetes men male glucose hormone hormones g

shared by Nathan Goodyear on 04 Feb 14 - No Cached
  • Around 50% of ageing, obese men presenting to the diabetes clinic have lowered testosterone levels relative to reference ranges based on healthy young men
  • The absence of high-level evidence in this area is illustrated by the Endocrine Society testosterone therapy in men with androgen deficiency clinical practice guidelines (Bhasin et al. 2010), which are appropriate for, but not specific to men with metabolic disorders. All 32 recommendations made in these guidelines are based on either very low or low quality evidence.
  • A key concept relates to making a distinction between replacement and pharmacological testosterone therapy
  • ...59 more annotations...
  • The presence of symptoms was more closely linked to increasing age than to testosterone levels
  • Findings similar to type 2 diabetes were reported for men with the metabolic syndrome, which were associated with reductions in total testosterone of −2.2 nmol/l (95% CI −2.41 to 1.94) and in free testosterone
  • low testosterone is more predictive of the metabolic syndrome in lean men
  • Cross-sectional studies uniformly show that 30–50% of men with type 2 diabetes have lowered circulating testosterone levels, relative to references based on healthy young men
  • In a recent cross-sectional study of 240 middle-aged men (mean age 54 years) with either type 2 diabetes, type 1 diabetes or without diabetes (Ng Tang Fui et al. 2013b), increasing BMI and age were dominant drivers of low total and free testosterone respectively.
  • both diabetes and the metabolic syndrome are associated with a modest reduction in testosterone, in magnitude comparable with the effect of 10 years of ageing
  • In a cross-sectional study of 490 men with type 2 diabetes, there was a strong independent association of low testosterone with anaemia
  • In men, low testosterone is a marker of poor health, and may improve our ability to predict risk
    • Nathan Goodyear
      Nathan Goodyear on 04 Feb 14
       
      probably the most important point made in this article
  • low testosterone identifies men with an adverse metabolic phenotype
  • Diabetic men with low testosterone are significantly more likely to be obese or insulin resistant
  • increased inflammation, evidenced by higher CRP levels
  • Bioavailable but not free testosterone was independently predictive of mortality
  • It remains possible that low testosterone is a consequence of insulin resistance, or simply a biomarker, co-existing because of in-common risk factors.
  • In prospective studies, reviewed in detail elsewhere (Grossmann et al. 2010) the inverse association of low testosterone with metabolic syndrome or diabetes is less consistent for free testosterone compared with total testosterone
  • In a study from the Framingham cohort, SHBG but not testosterone was prospectively and independently associated with incident metabolic syndrome
  • low SHBG (Ding et al. 2009) but not testosterone (Haring et al. 2013) with an increased risk of future diabetes
  • In cross-sectional studies of men with (Grossmann et al. 2008) and without (Bonnet et al. 2013) diabetes, SHBG but not testosterone was inversely associated with worse glycaemic control
  • SHBG may have biological actions beyond serving as a carrier protein for and regulator of circulating sex steroids
  • In men with diabetes, free testosterone, if measured by gold standard equilibrium dialysis (Dhindsa et al. 2004), is reduced
    • Nathan Goodyear
      Nathan Goodyear on 04 Feb 14
       
      expensive, laborious process filled with variables
  • Low free testosterone remains inversely associated with insulin resistance, independent of SHBG (Grossmann et al. 2008). This suggests that the low testosterone–dysglycaemia association is not solely a consequence of low SHBG.
  • Experimental evidence reviewed below suggests that visceral adipose tissue is an important intermediate (rather than a confounder) in the inverse association of testosterone with insulin resistance and metabolic disorders.
  • testosterone promotes the commitment of pluripotent stem cells into the myogenic lineage and inhibits their differentiation into adipocytes
  • testosterone regulates the metabolic functions of mature adipocytes (Xu et al. 1991, Marin et al. 1995) and myocytes (Pitteloud et al. 2005) in ways that reduce insulin resistance.
  • Pre-clinical evidence (reviewed in Rao et al. (2013)) suggests that at the cellular level, testosterone may improve glucose metabolism by modulating the expression of the glucose-transported Glut4 and the insulin receptor, as well as by regulating key enzymes involved in glycolysis.
  • More recently testosterone has been shown to protect murine pancreatic β cells against glucotoxicity-induced apoptosis
  • Interestingly, a reciprocal feedback also appears to exist, given that not only chronic (Cameron et al. 1990, Allan 2013) but also, as shown more recently (Iranmanesh et al. 2012, Caronia et al. 2013), acute hyperglycaemia can lower testosterone levels.
  • There is also evidence that testosterone regulates insulin sensitivity directly and acutely
  • In men with prostate cancer commencing androgen deprivation therapy, both total as well as, although not in all studies (Smith 2004), visceral fat mass increases (Hamilton et al. 2011) within 3 months
  • More prolonged (>12 months) androgen deprivation therapy has been associated with increased risk of diabetes in several large observational registry studies
  • Testosterone has also been shown to reduce the concentration of pro-inflammatory cytokines in some, but not all studies, reviewed recently in Kelly & Jones (2013). It is not know whether this effect is independent of testosterone-induced changes in body composition.
  • the observations discussed in this section suggest that it is the decrease in testosterone that causes insulin resistance and diabetes. One important caveat remains: the strongest evidence that low testosterone is the cause rather than consequence of insulin resistance comes from men with prostate cancer (Grossmann & Zajac 2011a) or biochemical castration, and from mice lacking the androgen receptor.
  • Several large prospective studies have shown that weight gain or development of type 2 diabetes is major drivers of the age-related decline in testosterone levels
  • there is increasing evidence that healthy ageing by itself is generally not associated with marked reductions in testosterone
  • Circulating testosterone, on an average 30%, is lower in obese compared with lean men
  • increased visceral fat is an important component in the association of low testosterone and insulin resistance
  • The vast majority of men with metabolic disorders have functional gonadal axis suppression with modest reductions in testosterone levels
  • obesity is a dominant risk factor
  • men with Klinefelter syndrome have an increased risk of metabolic disorders. Interestingly, greater body fat mass is already present before puberty
  • Only 5% of men with type 2 diabetes have elevated LH levels
  • inhibition of the gonadal axis predominantly takes place in the hypothalamus, especially with more severe obesity
  • Metabolic factors, such as leptin, insulin (via deficiency or resistance) and ghrelin are believed to act at the ventromedial and arcuate nuclei of the hypothalamus to inhibit gonadotropin-releasing hormone (GNRH) secretion from GNRH neurons situated in the preoptic area
  • kisspeptin has emerged as one of the most potent secretagogues of GNRH release
  • hypothesis that obesity-mediated inhibition of kisspeptin signalling contributes to the suppression of the HPT axis, infusion of a bioactive kisspeptin fragment has been recently shown to robustly increase LH pulsatility, LH levels and circulating testosterone in hypotestosteronaemic men with type 2 diabetes
  • A smaller study with a similar experimental design found that acute testosterone withdrawal reduced insulin sensitivity independent of body weight, whereas oestradiol withdrawal had no effects
  • suppression of the diabesity-associated HPT axis is functional, and may hence be reversible
  • Obesity and dysglycaemia and associated comorbidities such as obstructive sleep apnoea (Hoyos et al. 2012b) are important contributors to the suppression of the HPT axis
  • weight gain and development of diabetes accelerate the age-related decline in testosterone
  • Modifiable risk factors such as obesity and co-morbidities are more strongly associated with a decline in circulating testosterone levels than age alone
  • 55% of symptomatic androgen deficiency reverted to a normal testosterone or an asymptomatic state after 8-year follow-up, suggesting that androgen deficiency is not a stable state
  • Weight loss can reactivate the hypothalamic–pituitary–testicular axis
  • Leptin treatment resolves hypogonadism in leptin-deficient men
  • The hypothalamic–pituitary–testicular axis remains responsive to treatment with aromatase inhibitors or selective oestrogen receptor modulators in obese men
  • Kisspeptin treatment increases LH secretion, pulse frequency and circulating testosterone levels in hypotestosteronaemic men with type 2 diabetes
  • change in BMI was associated with the change in testosterone (Corona et al. 2013a,b).
  • weight loss can lead to genuine reactivation of the gonadal axis by reversal of obesity-associated hypothalamic suppression
  • There is pre-clinical and observational evidence that chronic hyperglycaemia can inhibit the HPT axis
  • in men who improved their glycaemic control over time, testosterone levels increased. By contrast, in those men in whom glycaemic control worsened, testosterone decreased
  • testosterone levels should be measured after successful weight loss to identify men with an insufficient rise in their testosterone levels. Such men may have HPT axis pathology unrelated to their obesity, which will require appropriate evaluation and management.
  • Nathan Goodyear on 04 Feb 14
     
    Article discusses the expanding evidence of low T and Metabolic syndrome.
Nathan Goodyear

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

www.ncbi.nlm.nih.gov/...PMC3314172

metabolic syndrome TLR cytokines hypothalamus brain neurology metabolic syndrome NF-kappaB DIO diet induced obesity over nutrition nutrition inflammation

shared by Nathan Goodyear on 09 Jul 13 - No Cached
  • 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
  • ...56 more annotations...
  • 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 [
  • Nathan Goodyear on 09 Jul 13
     
    Great article chronicles the biochemistry of "over nutrition" and inflammation through NF-kappaB activation and its impact on the brain.
Dr. Jennifer Martinick

Dr Jennifer Martinick - Warning about Hair Disorders - 0 views

speakerdeck.com/...k-warning-about-hair-disorders

Dr Jennifer Martinick

shared by Dr. Jennifer Martinick on 20 Nov 13 - No Cached
  • Dr. Jennifer Martinick on 20 Nov 13
     
    Dr Jennifer Martinick shares this informative slide show to spread awareness about Hair Disorders.
Nathan Goodyear

Tryptophan-Kynurenine Metabolism as a Common Mediator of Genetic and Environmental Impacts in Major Depressive Disorder: The Serotonin Hypothesis Revisited 40 Years Later - 0 views

www.ncbi.nlm.nih.gov/...PMC3021918

disordered tryptophan metabolism depression kynurenine pathway Tryptophan

shared by Nathan Goodyear on 26 Sep 13 - No Cached
  • Nathan Goodyear on 26 Sep 13
     
    Disordered tryptophan metabolism in depression
wheelchairindia9

Chair For Cerebral Palsy Child - 0 views

www.wheelchairindia.com/...Cerebral-Palsy-Wheelchair

cerebellum and the cortex common causes of brain damage cause like chicken pox or measles neurological problems are properly managed

shared by wheelchairindia9 on 12 May 15 - No Cached
  • wheelchairindia9 on 12 May 15
     
    Cerebral palsy (CP) is a group of conditions caused by medical abnormalities in the development of a fetus or the early life of a child. These lead to damage or delayed development in the brain. The disorder is permanent and, though it does not worsen with age, the level of functionality of a person with cerebral palsy varies widely: in some cases, effects may be very minor, while in others, movement is impaired to the extent that a wheelchair is required. Common complications associated with CP vary by the type of CP disorder but can include vision problems, seizures, learning disabilities, and issues speaking, writing, and performing other tasks. Cerebral palsy causes problems with muscle tone, movement, balance and/or coordination. Symptoms and effects range from mild to severe. In some infants, problems are evident soon after birth. In others, diagnosis comes in later infancy or toddlerhood. Cerebral Palsy Wheelchair Description: The model designed for cerebral palsy child only. Ultra light weight aluminium alloy frame. Seat Width 38 cms (15"). Net Weight: 18.5 kgs. Epoxy powder coated frame. Detachable arm rest & foot rest provided. Elevated and swinging foot rest. Elevated foot rest provided to elevate leg angle. Height adjustable and detachable head rest. Hydraulic reclining high back for a comfortable posture. Hydraulic adjustable seat angle. Detachable back and seat pad. Extra cushion upholstery provided to under arm, head & calg Foldable. Lever and paddle brakes provided. Safety belt provided. Maintenance free rear solid wheels. Cloth look like water proof upholstery. Anti wheels for better safety and stability. Extra cushion upholstery provided to under arm, head & leg Folding action. Lever and paddle brakes provided. Safety belt provided. Maintenance free rear solid wheels. Cerebral Palsy Wheelchair Recline system: Recline system provides kids with the most comfortable resting environment. It also allows stretching abdomin
Nathan Goodyear

Mitochondrial disorders - 0 views

brain.oxfordjournals.org/...2153.abstract

mitochondrial disorders

shared by Nathan Goodyear on 03 Mar 11 - No Cached
  • Nathan Goodyear on 03 Mar 11
     
    highly technical discussion on mitochondrial disorders
Nathan Goodyear

SpringerLink - Journal of Autism and Developmental Disorders, Volume 36, Number 3 - 0 views

www.springerlink.com/...8575wx07436024k5

gluten-free casein-free autism spectrum disorder ASD children pediatrics

shared by Nathan Goodyear on 06 Sep 11 - No Cached
  • Nathan Goodyear on 06 Sep 11
     
    Gluten-free and Casein-free diet in children with autism spectrum disorder shown to have improvement in some children
Nathan Goodyear

EDTA Chelation Therapy: Efficacy in Brain Disorders - 0 views

drcranton.com/...study4.htm

EDTA therapy brain disorders chelation

shared by Nathan Goodyear on 07 Jul 11 - No Cached
  • Nathan Goodyear on 07 Jul 11
     
    EDTA chelation benefits cerebral blood flow.  Has important implications in many brain disorders
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