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Nathan Goodyear

The use of estrogen in older women. [Clin Geriatr Med. 2003] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...14567012

estrogen HRT BHRT hormone hormones therapy women neurodegeneration Alzheimer's disease

shared by Nathan Goodyear on 14 Oct 13 - No Cached
  • Nathan Goodyear on 14 Oct 13
     
    Estrogen therapy in "older" women slows the physiologic effects of aging.  This study specifically highlights the effects of low estrogen and neurodegeneration of the brain.
Nathan Goodyear

Central nervous system disease in patients with macrop... [Brain. 2001] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...11335699

aluminum macrophagic myofasciitis macrophagic myofasciitis CNS disease central nervous system brain

shared by Nathan Goodyear on 09 Oct 13 - No Cached
  • Nathan Goodyear on 09 Oct 13
     
    Macrophagic myofasciitis and CNS disease. This study describes disease that mimics MS as a result of aluminum.
Nathan Goodyear

Reducing iron in the brain: a novel pharmacologic mechanism of huperzine A in the treat... - 0 views

www.sciencedirect.com/...S0197458013005721

Huperzine Huperzine-A brain Alzheimer's Alzheimers alzheimer's disease iron Fe disease

shared by Nathan Goodyear on 09 Apr 14 - No Cached
  • Nathan Goodyear on 09 Apr 14
     
    Huperzine reduces CNS iron.  This is in addition to the other neuroprotective effects of Huperzine A
Nathan Goodyear

Huperzine A ameliorates experimental autoimmune encephalomyelitis via the suppression o... - 0 views

www.sciencedirect.com/...S0014488612001550

Huperzine Huperzine-A MS multiple Sclerosis experimental autoimmune encephalopathy EAE inflammation autoimmune

shared by Nathan Goodyear on 09 Apr 14 - No Cached
  • Nathan Goodyear on 09 Apr 14
     
    Huperzine A reduces EAE, an experimental MS model.  Thus, huperzine A has a anti-inflammatory effect in the brain.  
Nathan Goodyear

Effects of the FITKids Randomized Controlled Trial on Executive Control and Brain Function - 0 views

pediatrics.aappublications.org/...e1063

children brain health cognition exercise fitness

shared by Nathan Goodyear on 07 Oct 14 - No Cached
  • Nathan Goodyear on 07 Oct 14
     
    After school fitness/exercise improved focus, attention, and cognition of children.
Nathan Goodyear

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

shared by Nathan Goodyear on 28 Apr 15 - No Cached
  • both obesity and low testosterone are also risk factors for neural dysfunction, including cognitive impairment [58–61] and development of AD
  • Levels of obesity and testosterone are often inversely correlated
  • 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
  • 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
  • fasting blood glucose levels were independently and additively increased by GDX-induced testosterone depletion and high-fat diet
  • testosterone treatment significantly reduced fasting glucose under both the normal and high-fat diets, demonstrating potential therapeutic efficacy of testosterone supplementation
  • fasting insulin, insulin resistance (HOMA index), and glucose tolerance, low testosterone tended to exacerbate and or testosterone treatment improved outcomes.
  • testosterone status did not significantly affect body weight
  • testosterone’s effects likely do not indicate an indirect result on adiposity but rather regulatory action(s) on other aspects of metabolic homeostasis
  • 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
  • it has been shown that TNFα has inhibitory effects on neuron survival, differentiation, and neurite outgrowth
  • Our data demonstrate that low testosterone and obesity independently increased cerebrocortical mRNA levels of both TNFα and IL-1β
  • Testosterone status also affected metabolic and neural measures
  • many beneficial effects of testosterone, including inhibition of proinflammatory cytokine expression
  • neuroprotection [80,81], are dependent upon androgen receptors, the observed effects of testosterone in this study may involve androgen receptor activation
  • testosterone can be converted by the enzyme aromatase into estradiol, which is also known to exert anti-inflammatory [82] and neuroprotective [83] actions
  • glia are the primary sources of proinflammatory molecules in the CNS
  • poorer survival of neurons grown on glia from mice maintained on high-fat diet
  • 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
  • significantly increased expression of TNFα and IL-1β in glia cultures derived from obese mice
  • 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
  • IL-1β treatment has been shown to induce synapse loss and inhibit differentiation of neurons
  • Testosterone status and diet-induced obesity were associated with significant regulation of macrophage infiltration
  • testosterone prevented and/or restored thermal nociception in both diet groups
  • a possible mechanism by which obesity and testosterone levels may affect the health of both CNS and PNS
  • Nathan Goodyear on 28 Apr 15
     
    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.
Nathan Goodyear

PLOS ONE: The Gut Microbiota and Developmental Programming of the Testis in Mice - 0 views

journals.plos.org/...article

hormone hormones Testosterone gut flora gut microbiome gut microbiota

shared by Nathan Goodyear on 30 Apr 15 - No Cached
  • The intra-testicular level of testosterone in GF mice was found to be significantly lower than in SPF and CBUT mice
  • This study establishes a novel role for the commensal gut microbiota in the regulation of testicular development and function
  • Absence of the normal microbiota influences the formation and the integrity of the BTB as well as the intra-testicular levels of testosterone and serum levels of LH and FSH.
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  • Nutritional, socioeconomic, lifestyle and environmental factors (among others) are involved in the regulation of normal spermatogenesis.
  • he gut microbiota is one such potential source of environmental factors/products that has developed an intimate symbiotic relationship with host's physiology.
  • Manipulation of the gut microbiotia through dietary modification, pre- and probiotics can therefore be beneficial for the host's reproductive health.
  • In the current study, colonizing GF mice with CBUT resulted in an increased sperm production, suggesting that bacterial products, e.g. of fermentation, directly or indirectly, can affect the testis.
  • the absence of gut microbiota influenced testosterone levels
  • A recent study demonstrated that dietary supplementation of the probiotics Lactobacillus reuteri increased and restored testosterone levels in aging mice
  • bacterial metabolites such as butyrate have been shown to increase the levels of LH [43] and FSH
  • This suggests that butyrate most likely regulates testosterone production at the testicular level by stimulation of gene expression in Leydig cells and with little or no effect at the pituitary- hypothalamic levels.
  • Nathan Goodyear on 30 Apr 15
     
    gut micro biome effects spermatogenesis, Testosterone production, and the brain-testicle-barrier.
Nathan Goodyear

A pyrazole curcumin derivative restores membrane homeostasis disrupted after brain trauma - 0 views

www.ncbi.nlm.nih.gov/...PMC3225197

brain trauma TBI curcumin lipid peroxidation

shared by Nathan Goodyear on 01 Nov 13 - No Cached
  • Nathan Goodyear on 01 Nov 13
     
    TBI associated with increased  4-Hydroxynonenal.  This is associated with increased lipid per oxidation.  Curcumin protects against this lipid peroxidation per this study.
Nathan Goodyear

Exercise normalizes levels of MAG and Nogo-A growth inhibitors after brain trauma - Chy... - 0 views

onlinelibrary.wiley.com/...20C0683F07B011D946D0062.f04t01

BDNF TBI traumatic brain injury exercise

shared by Nathan Goodyear on 01 Nov 13 - No Cached
  • Nathan Goodyear on 01 Nov 13
     
    exercise aids repair after TBI through BDNF.
Nathan Goodyear

The combined effects of exercise and foods in preventing neurological and cognitive dis... - 0 views

www.ncbi.nlm.nih.gov/...PMC3258093

diet nutrition exercise BDNF omega-3 omega 3 n-3 brain derived neurotrophic factor curcumin polyphenols neuroplasticity memory sugar saturated fats

shared by Nathan Goodyear on 01 Nov 13 - No Cached
  • The most prevalent types of cognitive impairments include disturbances in attention and learning and memory function
  • An association between BDNF and learning and memory was found when measuring the performance of rats on the Morris water maze task
  • exercise and BDNF have been associated with reducing depression and promoting cognitive enhancement.
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  • In addition to reducing oxidative stress and inflammation, DHA serves to improve neuronal function by supporting synaptic membrane fluidity
  • Curcumin has also been shown to protect the hippocampus and to counteract learning impairment
  • insufficient DHA in the brain can compromise neuronal function with subsequent effects on a broad range of neurological and behavioral faculties.
  • Nathan Goodyear on 01 Nov 13
     
    diet and exercise increases BDNF.  Diets rich in omega 3, curcumin, and polyphenols increase BDNF and thus increase neuroplasticity and associated cognition.   In contrast, sugar and saturated fats in crease oxidative stress and worsened spatial learning.  This study is a review.  
Nathan Goodyear

Effects of Elevation of Brain Magnesium on Fear Conditioning, Fear Extinction, and Syna... - 0 views

www.jneurosci.org/...14871.long

magnesium neuroplasticity brain

shared by Nathan Goodyear on 04 Nov 13 - No Cached
  • Nathan Goodyear on 04 Nov 13
     
    Magnesium, in this study Magnesium Threonate, shown to increase neuroplasticity
Nathan Goodyear

Brain-derived neurotrophic factor functions as a metabotrophin to mediate the effects o... - 0 views

www.ncbi.nlm.nih.gov/...PMC2805663

BDNF hippocampus memory brain MAPK

shared by Nathan Goodyear on 03 Nov 13 - No Cached
  • Nathan Goodyear on 03 Nov 13
     
    BDNF increased metabolic biomarkers, MAPK, in hippocampus.  This has implications in the treatment of learning disorders.  Exercise has consistently been shown to be the most significant mechanism to increase BDNF.
Nathan Goodyear

Acetyl-L-carnitine treatment increases choline ace... [Brain Res. 1994] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...8137174

Acetyl-L-carnitine carnitine brain acetylcholine nerve growth factor

shared by Nathan Goodyear on 04 Nov 13 - No Cached
  • Nathan Goodyear on 04 Nov 13
     
    Rat study, but acetyl-L-carnitine shown to increase nerve growth factor.  In addition, it increased acetylcholine activity.
Nathan Goodyear

Herbal Extracts and Phytochemicals: Plant Secondary Metabolites and the Enhancement of ... - 0 views

advances.nutrition.org/...32.full

herbs brain cognition memory

shared by Nathan Goodyear on 03 Nov 13 - No Cached
  • Nathan Goodyear on 03 Nov 13
     
    Good review of the current literature on herbs and improved cognitive function
Nathan Goodyear

An Overview of Brain-Derived Neurotrophic Factor and Implications for Excitotoxic Vulne... - 0 views

www.hindawi.com/...654085

BDNF brain derived neurotrophic factor

shared by Nathan Goodyear on 03 Nov 13 - No Cached
  • Nathan Goodyear on 03 Nov 13
     
    great review of BDNF and neurogenesis.
Nathan Goodyear

Brain-derived Neurotrophic Factor in Human Saliva: ELISA Optimization and Biological Co... - 0 views

www.ncbi.nlm.nih.gov/...PMC3046426

saliva BDNF brain derived neurotrophic factor

shared by Nathan Goodyear on 03 Nov 13 - No Cached
  • Nathan Goodyear on 03 Nov 13
     
    BDNF can be found and followed in saliva
Nathan Goodyear

The lighter side of BDNF | Regulatory, Integrative and Comparative Physiology - 0 views

ajpregu.physiology.org/...R1053

BDNF

shared by Nathan Goodyear on 11 Nov 13 - No Cached
  • Nathan Goodyear on 11 Nov 13
     
    Nice discussion of BDNF and cellular metabolism in different regions of the brain.  This article also points out the effects that BDNF has on feeding.
Nathan Goodyear

Branched Chain Amino Acid Supplementation for Patients with Cirrhosis | Clinical Correl... - 0 views

www.clinicalcorrelations.org/?p=3544

BCCA branched chain amino acids liver cirrhosis hepatitis amino acids

shared by Nathan Goodyear on 05 Oct 15 - No Cached
  • low level of BCAAs in patients with cirrhosis is hypothesized to be one of multiple factors responsible for development of hepatic encephalopathy
  • supplementation of BCAAs is thought to facilitate ammonia detoxification by supporting synthesis of glutamine, one of the non-branched chain amino acids, in skeletal muscle and in the brain as well as diminishing the influx of AAAs across the blood-brain barrier
  • oral BCAA supplementation is more useful in chronic encephalopathic patients than is parenteral BCAA supplementation in patients with acute encephalopathy
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  • malnutrition progressing to cachexia is another common manifestation of cirrhosis
  • Malnutrition can be mitigated with BCAA supplementation
  • Studies show that administration of amino acid formulas enriched with BCAAs can reduce protein loss, support protein synthesis, and improve nutritional status of patients with chronic liver disease
  • Leucine has been shown to be the most effective of the BCAAs because it acts via multiple pathways to stimulate protein synthesis
  • BCAAs metabolites inhibit proteolysis
  • Patients with cirrhosis have both insulin deficiency and insulin resistance
  • BCAAs (particularly leucine) help to reverse the catabolic, hyperglucagonemic state of cirrhosis both by stimulating insulin release from the pancreatic β cells and by decreasing insulin resistance allowing for better glucose utilization
  • Coadministration of BCAAs and glucose has been found to be particularly useful
  • BCAA supplementation improves protein-energy malnutrition by improving utilization of glucose, thereby diminishing the drive for proteolysis, inhibiting protein breakdown, and stimulating protein synthesis
  • Cirrhotic patients have impaired immune defense, characterized by defective phagocytic activity and impaired intracellular killing activity
  • another effect of BCAA supplementation is improvement of phagocytic function of neutrophils and possibly improvement in natural killer T (NKT) cell lymphocyte activity
  • BCAA supplementation may reduce the risk of infection in patients with advanced cirrhosis not only through improvement in protein-energy malnutrition but also by directly improving the function of the immune cells themselves
  • BCAA administration has also been shown to have a positive effect on liver regeneration
  • A proposed mechanism for improved liver regeneration is the stimulatory effect of BCAAs (particularly leucine) on the secretion of hepatocyte growth factor by hepatic stellate cells
  • BCAAs activate rapamycin signaling pathways which promotes albumin synthesis in the liver as well as protein and glycogen synthesis in muscle tissue
  • Chemical improvement with BCAA treatment is demonstrated by recovery of serum albumin and lowering of serum bilirubin levels
  • long-term oral BCAA supplementation was useful in staving off malnutrition and improving survival by preventing end-stage fatal complications of cirrhosis such as hepatic failure and gastrointestinal bleeding
  • The incidence of death by any cause, development of liver cancer, rupture of esophageal varices, or progression to hepatic failure was decreased in the group that received BCAA supplementation
  • Patients receiving BCAA supplementation also have a lower average hospital admission rate, better nutritional status, and better liver function tests
  • patients taking BCAA supplementation report improved quality of life
  • BCAAs have been shown to mitigate hepatic encephalopathy, cachexia, and infection rates, complications associated with the progression of hepatic cirrhosis
  • BCAAs make up 20-25% of the protein content of most foods
  • Highest levels are found in casein whey protein of dairy products and vegetables, such as corn and mushrooms. Other sources include egg albumin, beans, peanuts and brown rice bran
  • In addition to BCAAs from diet, oral supplements of BCAAs can be used
  • Oral supplementation tends to provide a better hepatic supply of BCAAs for patients able to tolerate PO nutrition as compared with IV supplementation, especially when treating symptoms of hepatic encephalopathy
  • Coadministration of BCAAs with carnitine and zinc has also been shown to increase ammonia metabolism further reducing the encephalopathic symptoms
  • Cirrhotic patients benefit from eating frequent, small meals that prevent long fasts which place the patient in a catabolic state
  • the best time for BCAA supplementation is at bedtime to improve the catabolic state during starvation in early morning fasting
  • A late night nutritional snack reduces symptoms of weakness and fatigability, lowers postprandial hyperglycemia, increases skeletal muscle mass,[25] improves nitrogen balance, and increases serum albumin levels.[26] Nocturnal BCAAs even improve serum albumin in cirrhotic patients who show no improvement with daytime BCAAs
  • Protein-energy malnutrition (PEM), with low serum albumin and low muscle mass, occurs in 65-90% of cases of advanced cirrhosis
  • hyperglucagonemia results in a catabolic state eventually producing anorexia and cachexia
  • BCAAs are further depleted from the circulation due to increased uptake by skeletal muscles that use the BCAAs in the synthesis of glutamine, which is produced in order to clear the ammonia that is not cleared by the failing liver
  • patients with chronic liver disease, particularly cirrhosis, routinely have decreased BCAAs and increased aromatic amino acids (AAAs) in their circulation
  • Maintaining a higher serum albumin in patients with cirrhosis is associated with decreased mortality and improved quality of life
  • the serum BCAA concentration is strongly correlated with the serum albumin level
  • Nathan Goodyear on 05 Oct 15
     
    great review of cirrhosis and BCCA supplementation.
Nathan Goodyear

Oxidative Stress and the Aging Brain: From Theory to Prevention - Brain Aging - NCBI Bo... - 0 views

www.ncbi.nlm.nih.gov/...NBK3869

stress oxidative aging mitochondria neurodegenerative disease

shared by Nathan Goodyear on 08 Feb 11 - No Cached
  • Nathan Goodyear on 08 Feb 11
     
    Must read on the free radical theory of aging to application of disease prevention as it relates to neurodegenerative disease
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