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Nathan Goodyear

Vitamin D status and ill health: a systematic review : The Lancet Diabetes & Endocrinology - 0 views

www.thelancet.com/...abstract

vitamin D vitamin d health

shared by Nathan Goodyear on 09 Dec 13 - No Cached
  • Nathan Goodyear on 09 Dec 13
     
    Another ill conceived conclusion by the authors.  IF you are going to study something, know everything about it.  They authors make a major statement about vitamin D, yet they seem to understand a basic understanding of vitamin dosing.  The authors stated that dosing 2,000 IU of vitamin D in those with levels < 50 provided no benefit.  That is of course correct, because 2,000 IU daily won't hold any levels stable, let alone increase levels to 70-80 where they need to be.  The authors of this study are stuck in the traditional RDC thinking here. What is interesting is that low vitamin D was associated with CVD, MS, dyslipidemia, inflammation, glucose dysmetabolism, infections, mood disorders, decline in cognition, impaired physical functioning, and all-cause mortality,  But, vitamin D supplementation is only good for bones.  The authors of this study make a mockery of medicine.
Nathan Goodyear

Targeting Synaptic Dysfunction in Alzheimer's Disease by Administering a Specific Nutri... - 0 views

iospress.metapress.com/...gg33167h46757165

alzheimer's disease Alzheimer's disease DHA EPA Folate B12 B6 vitamin E C vitamins brain

shared by Nathan Goodyear on 04 Dec 13 - No Cached
  • Nathan Goodyear on 04 Dec 13
     
    Combination of DHA, EPA, choline, phospholipids, Folate, B12, B6, vitamin C and E, and selenium improves memory and cognitive function in those with mild Alzheimer's disease.
Nathan Goodyear

Transdermal Testosterone Improves Verbal Learning and Memory in Postmenopausal Women No... - 0 views

onlinelibrary.wiley.com/...abstract

testosterone women memory brain menopause hormones hormone

shared by Nathan Goodyear on 29 Apr 14 - No Cached
  • Nathan Goodyear on 29 Apr 14
     
    study finds Testosterone improves cognitive function in postmenopausal women.  Was this due to aromatase activity and conversant to Estradiol?  Testing was limited in follow up.
Nathan Goodyear

Dietary curcumin counteracts the outcome of traum... [Exp Neurol. 2006] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...16364299

curcumin brain diet nutrition BDNF TBI memory

shared by Nathan Goodyear on 01 Nov 13 - No Cached
  • Nathan Goodyear on 01 Nov 13
     
    curcumin functions to reduce inflammation and free radicals.  Curcumin also increases BDNF post TBI, which will improve synaptic plasticity, cognition, and memory.  
Nathan Goodyear

Is Timing Everything? New Insights into Why the Effect of Estrogen Therapy on Memory Mi... - 0 views

endo.endojournals.org/...2570.full

estrogen therapy memory hormone therapy HRT BHRT Estradiol neurology brain women hormone hormones

shared by Nathan Goodyear on 06 Aug 13 - No Cached
  • Women who have an oophorectomy before the normal age at menopause show an increased risk for cognitive impairment or dementia later in life unless they are treated with estrogen until the normal age at menopause
  • SIRT1 has been implicated in the disruption of mitochondrial bioenergenetics in Alzheimer's disease and mild cognitive impairment
  • the increase in dementia observed with CEE/MPA rather than CEE alone suggests potential deleterious effects of MPA on brain function in older women
  • ...1 more annotation...
  • SIRT 1 as a potential mediator of the impact of E2
  • Nathan Goodyear on 06 Aug 13
     
    Early estrogen therapy in perimenopause and early menopause, with Estradiol, provides more health benefits than later therapy.  This article looked at Estrogen's effects on a woman's brain.  This likely has its origins in the change in estrogen receptors. The signal is not changing, but the reception of that signal is.  How else can one explain a different response to the same hormone dosage?
Nathan Goodyear

Dietary Strategy to Repair Plasma Membrane After Brain Trauma - 0 views

nnr.sagepub.com/...75.long

curcumin DHA TBI traumatic brain injury brain injury neuroinflammation BDNF brain derived neurotrophic factor brain

shared by Nathan Goodyear on 31 Aug 15 - No Cached
  • concussive brain injury is a major cause of neuropsychological disability in spite of no obvious neuronal death
  • TBI elicits oxidative damage to plasma membrane phospholipids
  • DHA is the most abundant polyunsaturated fatty acid (PUFA) in the brain, where the DHA-containing phospholipids contribute to plasma membrane biogenesis and receptor signaling
  • ...10 more annotations...
  • curcumin has potent anti-inflammatory and antioxidant activities that can function to reduce oxidative damage and cognitive deficits associated with neurological disorders
  • Curcumin provided in the diet before TBI can reduce oxidative damage and counteract TBI-related cognitive dysfunction
  • Our previous study indicated that n-3 fatty acids supplemented in the diet counteracted learning disability after TBI
  • curcumin contributes to enhance the effects of DHA on TBI by promoting phosphorylation of the BDNF receptor TrkB in the hippocampus
  • previous evidence indicates that curcumin10 and DHA5 counteract TBI-related learning disability by involving BDNF
  • Our findings indicate that curcumin counteracted the TBI-related reduction in n-3 DPA.
  • curcumin may promote the conversion of n-3 DPA to DHA
  • the combination of both nutrients has been reported to produce anti-inflammatory action
  • the enhanced actions of curcumin and DHA in reducing cholesterol levels could be interpreted as preservation of levels of phospholipids in the plasma membrane
  • curcumin and DHA may contribute to reduce inflammation associated with the action of cholesterol in the pathology of TBI.
  • Nathan Goodyear on 31 Aug 15
     
    Curcumin and DHA shown to protect against TBI through a reduction in inflammation and maintenance of brain phospholipid membranes.  BDNF is increases also.
Nathan Goodyear

Ibuprofen alters human testicular physiology to produce a state of compensated hypogona... - 0 views

www.pnas.org/...1715035115.full

ibuprofen Testosterone epigenetics hormones low Testosterone low T

shared by Nathan Goodyear on 09 Jan 18 - No Cached
  • The levels of LH in the ibuprofen group had increased by 23% after 14 d of administration
  • This increase was even more pronounced at 44 d, at 33%
  • We found an 18% decrease (P = 0.056) in the ibuprofen group compared with the placebo group after 14 d (Fig. 1A) and a 23% decrease (P = 0.02) after 44 d (Fig. 1C). Taken together, these in vivo data suggest that ibuprofen induced a state of compensated hypogonadism during the trial, which occurred as early as 14 d and was maintained until the end of the trial at 44 d
  • ...27 more annotations...
  • We first investigated testosterone production after 24 and 48 h of ibuprofen exposure to assess its effects on Leydig cell steroidogenesis. Inhibition of testosterone levels was significant and dose-dependent (β = −0.405, P = 0.01 at 24 h and β = −0.664, P &lt; 0.0001 at 48 h) (Fig. 2A) and was augmented over time
  • The AMH data show that the hypogonadism affected not only Leydig cells but also Sertoli cells and also occurred as early as 14 d of administration
  • Sertoli cell activity showed that AMH levels decreased significantly with ibuprofen administration, by 9% (P = 0.02) after 14 d (Fig. 1B) and by 7% (P = 0.05) after 44 d compared with the placebo group
  • Examination of the effect of ibuprofen exposure on both the ∆4 and ∆5 steroid pathways (Fig. 2B) showed that it generally inhibited all steroids from pregnenolone down to testosterone and 17β-estradiol; the production of each steroid measured decreased at doses of 10−5–10−4 M. Under control conditions, production of androstenediol and dehydroepiandrosterone (DHEA) was below the limit of detection except in one experiment with DHEA
  • Measuring the mRNA expression of genes involved in steroidogenesis in vitro showed that ibuprofen had a profound inhibitory effect on the expression of these genes (Fig. 3 B–D), consistent with that seen above in our ex vivo organ model. Taken together, these data examining effects on the endocrine cells confirm that ibuprofen-induced changes in the transcriptional machinery were the likely reason for the inhibition of steroidogenesis.
  • Suppression of gene expression concerned the initial conversion of cholesterol to the final testosterone synthesis. Hence, expression of genes involved in cholesterol transport to the Leydig cell mitochondria was impaired
  • A previous study reported androsterone levels decreased by 63% among men receiving 400 mg of ibuprofen every 6 h for 4 wk
  • We next examined the gene expression involved in testicular steroidogenesis ex vivo and found that levels of expression of every gene that we studied except CYP19A1 decreased after exposure for 48 h compared with controls
  • the changes in gene expression indicate that the transcriptional machinery behind the endocrine action of Leydig cells was most likely impaired by ibuprofen exposure.
  • Together, these data show that ibuprofen also directly impairs Sertoli cell function ex vivo by inhibiting transcription
  • ibuprofen use in men led to (i) elevation of LH; (ii) a decreased testosterone/LH ratio and, to a lesser degree, a decreased inhibin B/FSH ratio; and (iii) a reduction in the levels of the Sertoli cell hormone AMH
  • The decrease in the free testosterone/LH ratio resulted primarily from the increased LH levels, revealing that testicular responsiveness to gonadotropins likely declined during the ibuprofen exposure. Our data from the ex vivo experiments support this notion, indicating that the observed elevation in LH resulted from ibuprofen’s direct antiandrogenic action
  • AMH levels were consistently suppressed by ibuprofen both in vivo and ex vivo, indicating that this hormone is uncoupled from gonadotropins in adult men. The ibuprofen suppression of AMH further demonstrated that the analgesic targeted not only the Leydig cells but also the Sertoli cells, a feature encountered not only in the human adult testis but also in the fetal testis
  • ibuprofen displayed broad transcription-repression abilities involving steroidogenesis, peptide hormones, and prostaglandin synthesis
  • a chemical compound, through its effects on the signaling compounds, can result in changes in the testis at gene level, resulting in perturbations at higher physiological levels in the adult human
  • The analgesics acetaminophen/paracetamol and ibuprofen have previously been shown to inhibit the postexercise response in muscles by repressing transcription
  • Previous ex vivo studies on adult testis have indeed pointed to an antiandrogenicity, only on Leydig cells, of phthalates (41), aspirin, indomethacin (42), and bisphenol A (BPA) and its analogs
  • ibuprofen’s effects were not restricted to Leydig and Sertoli cells, as data showed that the expression of genes in peritubular cells was also affected
  • short-term exposure
  • In the clinical setting, compromised Leydig cell function resulting in increased insensitivity to LH is defined as compensated hypogonadism (4), an entity associated with all-cause mortality
  • compensated hypogonadic men present with an increased likelihood of reproductive, cognitive, and physical symptoms
  • an inverse relationship was recently reported between endurance exercise training and male sexual libido
  • AMH concentrations are lower in seminal plasma from patients with azoospermia than from men with normal sperm levels
  • inhibin B is a key clinical marker of reproductive health (32). The function of AMH, also secreted by Sertoli cells, and its regulation through FSH remain unclear in men
  • the striking dual effect of ibuprofen observed here on both Leydig and Sertoli cells makes this NSAID the chemical compound, of all the chemical classes considered, with the broadest endocrine-disturbing properties identified so far in men.
  • after administration of 600 mg of ibuprofen to healthy volunteers
  • 14 d or at the last day of administration at 44 d
  • Nathan Goodyear on 09 Jan 18
     
    ibuprofen alters genetic expression that results in decreased Testosterone production.
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.
  • ...23 more annotations...
  • 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

ω-3 Fatty Acid Supplementation as a Potential Therapeutic Aid for the Recover... - 0 views

advances.nutrition.org/...268.full

omega 3 DHA EPA fish oil TBI traumatic brain injury concussions concussion brain injury

shared by Nathan Goodyear on 30 Aug 15 - No Cached
  • There is a growing body of preclinical literature suggesting that ω-3 FAs, and DHA in particular, may play a therapeutic role in mTBI
  • the potential for ameliorating or possibly even preventing the complications associated with concussions
  • DHA is the predominant ω-3 FA present in the brain, and, consistent with this finding, DHA, and not EPA, has been demonstrated to be critical for brain development and cognitive function throughout life
  • ...7 more annotations...
  • the concentration of EPA in the brain is negligible (77–80), suggesting that EPA plays a limited role in mediating the beneficial effects of LCPUFA supplementation on mTBI pathology
  • the current state of the science regarding LCPUFA supplementation for the treatment of concussion is based primarily on animal models
  • there is evidence that the amount of DHA in brain tissue is decreased after mTBI (65, 66), suggesting an elevated need for DHA in mTBI recovery.
  • the well-established role of DHA in supporting the structure and function of the brain throughout the lifespan (26, 27, 46, 47, 53) provides encouragement that LCPUFAs may also prove beneficial in the context of concussion recovery.
  • no therapies are currently available to aid the recovery from this injury
  • Previously discussed reports outlining the use of ω-3 FAs in the recovery from severe TBIs (reviewed in Ref. 92) described the use of very-high doses of LCPUFAs (16.2 g/d EPA plus DHA) in the recovery of these patients
  • Within the context of mTBIs/concussions, translating a DHA intake used in several rat studies of mTBI recovery (40 mg ⋅ kg−1 ⋅ d−1 DHA) (57, 63, 64) using body surface area conversion methods (93) amounts to an estimated human intake of 387 mg/d DHA
  • Nathan Goodyear on 30 Aug 15
     
    nice review of the evidence of n-3, particularily DHA, in concussions and concussion recovery.
Nathan Goodyear

Longitudinal Assessment of Chemotherapy-Induced Alterations in Brain Activation During ... - 0 views

jco.ascopubs.org/...JCO.2013.53.6219.abstract

chemo brain chemotherapy brain cancer

shared by Nathan Goodyear on 03 Jun 14 - No Cached
  • Nathan Goodyear on 03 Jun 14
     
    Study reveals negatively altered brain activity, as visualized by functional MRI, after chemotherapy.  This is a small study, but it appears to be the first to prove that "chemo brain" is not just in a patients head--in fact, it is in their brain.
Nathan Goodyear

Hyperbaric oxygen therapy promotes neurogenesis: where do we stand? - 0 views

www.ncbi.nlm.nih.gov/...PMC3231808

hbot hyperbaric therapy hyperbaric brain TBI stroke neurogenesis neuorplasticity

shared by Nathan Goodyear on 18 May 17 - No Cached
  • Numerous in vivo and in vitro studies confirm that HBOT induces neurogenesis
  • HIF-1α is the principal mediator of cellular hypoxia adaptations
  • activated by hypoxia, HIF-1α causes the transcription of its regulated downstream genes, including erythropoietin (EPO) and VEGF which are known to promote neurogenesis
  • ...10 more annotations...
  • The safety of HBOT was also evaluated and it was pointed out that, if given at proper paradigms, like 1.5 ATA for 60 minutes, HBOT will not cause oxygen toxicity
  • Rockswold et al., on the other hand, found that HBOT might be potentially beneficial for severe TBI patients
  • McDonagh et al., concluded that there was insufficient evidence to establish the effectiveness of HBOT in the treatment of TBI
  • The first multicenter, randomized, double-blind, controlled trial in 2009 found that 40-hour HBOT of 24% oxygen at 1.3 ATM produced significant improvement in children's overall functioning, receptive language, social interaction, eye contact, and sensory/cognitive awareness compared to those received slightly pressurized room air
  • Another study in 2010 on 16 autism patients, adopting a similar treatment paradigm, showed no effect on a wide array of behavioral evaluations
  • To date, there is little evidence that HBOT causes malignant growth or metastasis. A history of malignancy should therefore not be considered as a contraindication for HBOT
  • HBOT enhances the production of reactive oxygen species (ROS) and causes oxidative stress in body tissues
  • Excessive accumulation of oxidative stress may contribute to neurodegenerative processes and cell death in the brain, as seen in diseases like Alzheimer's disease (AD) and Parkinson's disease (PD)
  • Hormesis
  • process that results in a functional improvement of cellular stress resistance, survival, and longevity in response to sub-lethal levels of stress
  • Nathan Goodyear on 18 May 17
     
    great review of hbot, brain injury, neuroplasticity and neurogenesis.
Nathan Goodyear

Chemistry and Structural Biology of Androgen Receptor - 0 views

www.ncbi.nlm.nih.gov/...PMC2096617

androgens Testosterone DHT dihydrotestosterone AR androgen receptors male hormones hormones

shared by Nathan Goodyear on 28 Sep 16 - No Cached
  • Healthy adult men typically produce approximately 3–10 mg of testosterone per day
  • circulating levels ranging from 300 to 700 ng/dL in eugonadal men
  • endogenous testosterone secretion is pulsatile and diurnal
  • ...15 more annotations...
  • highest concentration occurring at about 8:00 a.m. and the lowest at about 8:00 p.m.
  • Average serum concentrations and diurnal variation in testosterone diminish as men age
  • 40% is sequestered with high affinity to sex hormone-binding globulin (SHBG)
  • almost 60% is bound with low affinity to albumin
  • 2% as free, unbound hormone
  • 5α-DHT has even greater binding affinity to sex hormone-binding globulin than does testosterone
  • 5α-DHT is only about 5% as abundant in the blood as testosterone and is largely derived from peripheral metabolism of testosterone
  • Both 5α-reduction and aromatization are irreversible processes
  • Approximately 90% of an oral dose of testosterone is metabolized before it reaches the systemic circulation
  • there are three modes of action of testosterone. It may directly act through AR in target tissues where 5α-reductase is not expressed, be converted to 5α-DHT (5–10%) by 5α-reductase before binding to AR, or be aromatized to estrogen (0.2%) and act through the estrogen receptor
  • 5α-DHT is a more potent AR ligand than testosterone
  • has 2–10-fold higher potency than testosterone in androgen-responsive tissues
  • estrogen plays a major role in regulating metabolic process,74,75 mood and cognition,76 cardiovascular disease,77,78 sexual function including libido,79 and bone turnover in men
  • Free testosterone is considered the most “biologically active” form
  • testosterone is the major androgen that acts in the “DHT-independent” tissues, such as skeletal muscle, where 5α-reductase is not expressed or is expressed at a very low level
  • Nathan Goodyear on 28 Sep 16
     
    good review of androgens and AR.
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

Brain foods: the effects of nutrients on brain function - 0 views

www.ncbi.nlm.nih.gov/...PMC2805706

brain food nutrition cognition

shared by Nathan Goodyear on 03 Nov 13 - No Cached
  • Nathan Goodyear on 03 Nov 13
     
    Just a great article on the interaction between food, gut and the brain.
Nathan Goodyear

PLOS ONE: Depletion of Brain Docosahexaenoic Acid Impairs Recovery from Traumatic Brain... - 0 views

journals.plos.org/...article

DHA TBI traumatic brain injury omega 3 brain injury brain omega-3

shared by Nathan Goodyear on 31 Aug 15 - No Cached
  • The polyunsaturated fatty acids linoleic (LA, 18:2n-6) and linolenic acid (LNA, 18:3n-3) are essential fatty acids that cannot be synthesized by the body.
  • LNA serves as the precursor for long chain omega-3 fatty acids such as docosahexaenoic acid (DHA) while LA is converted into long chain omega-6 fatty acids such as arachidonic acid (AA)
  • DHA and AA are abundantly found in the brain, where these are stored mainly in membrane phospholipids
  • ...10 more annotations...
  • DHA has been shown to increase neurite outgrowth and synaptogenesis, and promotes glutamatergic neurotransmission through increase in glutamate receptor subunit expression
  • DHA has been shown to be converted to anti-inflammatory, proresolving and neuroprotective mediators, such as resolvins [7] and protectins
  • AA is converted by cyclooxygenases into 2-series prostaglandins and 4-series leukotrienes, most of which exert pro-inflammatory effects
  • Supplementation of DHA exerts neuroprotective effects and has been reported to afford protection from diffuse axonal injury [11] and mixed brain injury [12] as well
  • severe depletion of membrane DHA in the brain renders mice significantly more susceptible to TBI and impairs recovery following the injury
  • Omega-3 fatty acids may serve as nutraceutical agents and precondition the brain to make it more resilient to injury
  • it can be suggested that enriching DHA in the brain may be prophylactic and protective against brain injury
  • severe DHA deficiency in the brain impairs functional recovery from TBI in terms of vestibulo-motor and cognitive deficits
  • DHA deficiency further elevates TBI-induced production of SBDPs
  • less neurons were found around the injury site of DHA deficient brain after TBI compared to the omega-3 fatty acid adequate group
  • Nathan Goodyear on 31 Aug 15
     
    mouse study finds prolonged recovery in DHA deficient mice compared to controls.
Nathan Goodyear

Sex hormones and cognitive functioning in men. [Neuropsychobiology. 1987] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...3444523

testosterone DHT saliva salivary testing bioidentical

shared by Nathan Goodyear on 22 Nov 10 - No Cached
  • Nathan Goodyear on 22 Nov 10
     
    saliva testing and male hormones
Nathan Goodyear

Selenium and human health : The Lancet - 0 views

www.thelancet.com/...abstract

Selenium health

shared by Nathan Goodyear on 10 Nov 14 - No Cached
  • Low selenium status has been associated with increased risk of mortality, poor immune function, and cognitive decline
  • Higher selenium status or selenium supplementation has antiviral effects, is essential for successful male and female reproduction, and reduces the risk of autoimmune thyroid disease.
  • Prospective studies have generally shown some benefit of higher selenium status on the risk of prostate, lung, colorectal, and bladder cancers, but findings from trials have been mixed, which probably emphasises the fact that supplementation will confer benefit only if intake of a nutrient is inadequate
  • Nathan Goodyear on 10 Nov 14
     
    Selenium is a "U" shaped curve.  Abstract only available here.
Nathan Goodyear

Vitamin E reduces amyloidosis and improves cognitive function in Tg2576 mice following ... - 0 views

www.ncbi.nlm.nih.gov/...15255955

vitamin E TBI traumatic brain injury brain injury brain

shared by Nathan Goodyear on 21 Feb 16 - No Cached
  • Nathan Goodyear on 21 Feb 16
     
    animal model: vitamin E reduced brain lipid oxidation post TBI.
Nathan Goodyear

Sex hormones affect neurotransmitters and shape the adult female brain during hormonal ... - 0 views

www.ncbi.nlm.nih.gov/...PMC4335177

hormones neurotransmitters serotonin GABA dopamine estradiol progesterone glutamate

shared by Nathan Goodyear on 11 Jul 17 - No Cached
  • estrogen administration has been found to increase tryptophan hydroxylase
  • 5-HT2A mRNA levels in brain areas relevant for the control of mood, mental state and cognition (Sumner and Fink, 1998) and 5-HTT mRNA when administered for a longer period
  • n the other hand, estrogen treatment has also been observed to decrease mRNA related to serotonergic neurotransmission
  • ...4 more annotations...
  • Furthermore, acute estrogen administration decreases 5-HTT mRNA levels (Pecins-Thompson et al., 1998) and 5-HT1A mRNA levels and binding
  • assigning the effects of estrogen on serotonin to a homogenous functional class of stimulation or inhibition seems not to be feasible
  • Progesterone has been suggested to increase serotonergic neurotransmission via the regulation of the expression of serotonin-related genes and proteins
  • menopausal women gain less benefit from antidepressant treatments compared to women during their reproductive years
  • Nathan Goodyear on 11 Jul 17
     
    good review of the relationship of the sex hormones and neurotransmitters.
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