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Nathan Goodyear

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

  • 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
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  • 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.
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    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

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

  • strategies directed to preserve phospholipids in the plasma membrane such as the use of dietary docosahexaenoic acid (C22:6n-3; DHA)5 can have beneficial effects for post-TBI recovery
  • DHA is the most abundant polyunsaturated fatty acid (PUFA) in the brain
  • Curcumin provided in the diet before TBI can reduce oxidative damage and counteract TBI-related cognitive dysfunction.
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  • Our previous study indicated that n-3 fatty acids supplemented in the diet counteracted learning disability after TBI
  • There was a significant group effect on BDNF (F 4,25 = 5.229, P < .01 by ANOVA), and FPI reduced BDNF levels (50% of CTL, P < .01; Figure 1C), which was counteracted by DHA supplementation (90% of CTL, P < .05; Figure 1C). Curcumin also counteracted this reduction of BDNF
  • The combination of curcumin and DHA had a trend of greater effects in BDNF (117% of CTL; Figure 1C) compared with DHA or curcumin alone.
  • curcumin contributed to enhance the action of DHA, protecting against cognitive impairment, and these effects were associated with elevations in the BDNF receptor signaling
  • Our current results show that 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
  • The effects of the DHA diet and curcumin on cognitive enhancement were consistent with enhanced elevations in BDNF receptor signaling
  • effects of DHA and curcumin up to 2 weeks after TBI because this is the most critical period for the course of injury recovery because the brain is metabolically dysfunctional during this time
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    study that finds curcumin + DHA increased cognitive improvement after TBI within 2 weeks.  Good discussion of the proposed mechanism--increased BDNF.
Nathan Goodyear

Dietary Curcumin Supplementation Counteracts Reduction in Levels of Molecules Involved ... - 0 views

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    TBI leaves the mitochondria of the brain compromised.  The result is a compromise in the ability to produce energy leaving the brain limited in its ability to heal and or handle additional insults.  This animal study found curcumin able to provide preservation of the energy pathways post TBI.  This has implications on any neuro-insult, not just TBI
Nathan Goodyear

Stuck at the bench: Potential natural neuroprotective compounds for concussion - 0 views

  • Long-chain polyunsaturated fatty acids, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are highly enriched in neuronal synaptosomal plasma membranes and vesicles
  • The predominant CNS polyunsaturated fatty acid is DHA
  • effective supplementation and/or increased ingestion of dietary sources rich in EPA and DHA, such as cold-water fish species and fish oil, may help improve a multitude of neuronal functions, including long-term potentiation and cognition.
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  • multiple preclinical studies have suggested that DHA and/or EPA supplementation may have potential benefit through a multitude of diverse, but complementary mechanisms
  • pre-injury dietary supplementation with fish oil effectively reduces post-traumatic elevations in protein oxidation
  • The benefits of pre-traumatic DHA supplementation have not only been independently confirmed,[150] but DHA supplementation has been shown to significantly reduce the number of swollen, disconnected and injured axons when administered following traumatic brain injury.
  • DHA has provided neuroprotection in experimental models of both focal and diffuse traumatic brain injury
  • potential mechanisms of neuroprotection, in addition to DHA and EPA's well-established anti-oxidant and anti-inflammatory properties
  • Despite abundant laboratory evidence supporting its neuroprotective effects in experimental models, the role of dietary DHA and/or EPA supplementation in human neurological diseases remains uncertain
  • Several population-based, observational studies have suggested that increased dietary fish and/or omega-3 polyunsaturated fatty acid consumption may reduce risk for ischemic stroke in several populations
  • Randomized control trials have also demonstrated significant reductions in ischemic stroke recurrence,[217] relative risk for ischemic stroke,[2] and reduced incidence of both symptomatic vasospasm and mortality following subarachnoid hemorrhage
  • Clinical trials in Alzheimer's disease have also been largely ineffective
  • The clinical evidence thus far appears equivocal
  • curcumin has gained much attention from Western researchers for its potential therapeutic benefits in large part due to its potent anti-oxidant[128,194,236] and anti-inflammatory properties
  • Curcumin is highly lipophilic and crosses the blood-brain barrier enabling it to exert a multitude of different established neuroprotective effects
  • in the context of TBI, a series of preclinical studies have suggested that pre-traumatic and post-traumatic curcumin supplementation may bolster the brain's resilience to injury and serve as a valuable therapeutic option
  • Curcumin may confer significant neuroprotection because of its ability to act on multiple deleterious post-traumatic, molecular cascades
  • studies demonstrated that both pre- and post-traumatic curcumin administration resulted in a significant reduction of neuroinflammation via inhibition of the pro-inflammatory molecules interleukin 1β and nuclear factor kappa B (NFκB)
  • no human studies have been conducted with respect to the effects of curcumin administration on the treatment of TBI, subarachnoid or intracranial hemorrhage, epilepsy or stroke
  • studies have demonstrated that resveratrol treatment reduces brain edema and lesion volume, as well as improves neurobehavioral functional performance following TBI
  • green tea consumption or supplementation with its derivatives may bolster cognitive function acutely and may slow cognitive decline
  • At least one population based study, though, did demonstrate that increased green tea consumption was associated with a reduced risk for Parkinson's disease independent of total caffeine intake
  • a randomized, placebo-controlled trial demonstrated that administration of green tea extract and L-theanine, over 16 weeks of treatment, improved indices of memory and brain theta wave activity on electroencephalography, suggesting greater cognitive alertness
  • Other animal studies have also demonstrated that theanine, another important component of green tea extract, exerts a multitude of neuroprotective benefits in experimental models of ischemic stroke,[63,97] Alzheimer's disease,[109] and Parkinson's disease
  • Theanine, like EGCG, contains multiple mechanisms of neuroprotective action including protection from excitotoxic injury[97] and inhibition of inflammation
  • potent anti-oxidant EGCG which is capable of crossing the blood-nerve and blood-brain barrier,
  • Epigallocatechin-3-gallate also displays neuroprotective properties
  • More recent research has suggested that vitamin D supplementation and the prevention of vitamin D deficiency may serve valuable roles in the treatment of TBI and may represents an important and necessary neuroprotective adjuvant for post-TBI progesterone therapy
  • Progesterone is one of the few agents to demonstrate significant reductions in mortality following TBI in human patients in preliminary trials
  • in vitro and in vivo studies have suggested that vitamin D supplementation with progesterone administration may significantly enhance neuroprotection
  • Vitamin D deficiency may increase inflammatory damage and behavioral impairment following experimental injury and attenuate the protective effects of post-traumatic progesterone treatment.[37]
  • emerging evidence has suggested that daily intravenous administration of vitamin E following TBI significantly decreases mortality and improves patient outcomes
  • high dose vitamin C administration following injury stabilized or reduced peri-lesional edema and infarction in the majority of patients receiving post-injury treatment
  • it has been speculated that combined vitamin C and E therapy may potentiate CNS anti-oxidation and act synergistically with regards to neuroprotection
  • one prospective human study has found that combined intake of vitamin C and E displays significant treatment interaction and reduces the risk of stroke
  • Pycnogenol has demonstrated the ability to slow or reduce the pathological processes associated with Alzheimer's disease
  • Pcynogenol administration, in a clinical study of elderly patients, led to improved cognition and reductions in markers of lipid peroxidase
  • One other point of consideration is that in neurodegenerative disease states like Alzheimer's disease and Parkinson's disease, where there are high levels of reactive oxygen species generation, vitamin E can tend to become oxidized itself. For maximal effectiveness and to maintain its anti-oxidant capacity, vitamin E must be given in conjunction with other anti-oxidants like vitamin C or flavonoids
  • These various factors might account for the null effects of alpha-tocopherol supplementation in patients with MCI and Alzheimer's disease
  • preliminary results obtained in a pediatric population have suggested that post-traumatic oral creatine administration (0.4 g/kg) given within four hours of traumatic brain injury and then daily thereafter, may improve both acute and long-term outcomes
  • Acutely, post-traumatic creatine administration seemed to reduce duration of post-traumatic amnesia, length of time spent in the intensive care unit, and duration of intubation
  • At three and six months post-injury, subjects in the creatine treatment group demonstrated improvement on indices of self care, communication abilities, locomotion, sociability, personality or behavior and cognitive function when compared to untreated controls
  • patients in the creatine-treatment group were less likely to experience headaches, dizziness and fatigue over six months of follow-up
  • CNS creatine is derived from both its local biosynthesis from the essential amino acids methionine, glycine and arginine
  • Studies of patients with CNS creatine deficiency and/or murine models with genetic ablation of creatine kinase have consistently demonstrated significant neurological impairment in the absence of proper creatine, phosphocreatine, or creatine kinase function; thus highlighting its functional importance
  • chronic dosing may partially reverse neurological impairments in human CNS creatine deficiency syndromes
  • Several studies have suggested that creatine supplementation may also reduce oxidative DNA damage and brain glutamate levels in Huntington disease patients
  • Another study highlighted that creatine supplementation marginally improved indices of mood and reduced the need for increased dopaminergic therapy in patients with Parkinson's disease
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    great review of natural therapies in the treatment of concussions
Nathan Goodyear

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

  • 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
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  • 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
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    mouse study finds prolonged recovery in DHA deficient mice compared to controls.
Nathan Goodyear

Inhibitory Effect of Progesterone on Inflammatory Factors after Experimental Traumatic ... - 0 views

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    Now, this is in a rat TBI model; but progesterone was shown to reduce the inflammatory response post TBI. Particularily, through NF-kappa B inhibition.
Nathan Goodyear

Neuroendocrine disorders after... [J Neurol Neurosurg Psychiatry. 2008] - PubMed - NCBI - 0 views

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    The majority of people with PTHP after TBI remain undiagnosed.  The current thought, is that 25% of those with TBI have at least one pituitary hormone deficiency.  It does not have to be total pituitary failure.  Deficiencies can be isolated.
Nathan Goodyear

Progesterone and allopregnanolone reduce inflammatory cytokines after traumatic brain i... - 0 views

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    Abstract on listed here: but bioidentical progesterone and allopregnanolone (product of progesterone metabolism) shown to reduce inflammation after TBI.  This inflammation is what results in much of the post-TBI complications.
Nathan Goodyear

PsychiatryOnline | The Journal of Neuropsychiatry and Clinical Neurosciences | The Neur... - 0 views

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    Understanding the neuroendocrine effects of TBI. This article discusses all hormonal effects as a result of TBI.
Nathan Goodyear

Dietary Supplementation With the Omega-3 Fatty Acid Docosahe... : Neurosurgery - 0 views

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    Animal study finds pre-emptive DHA at 40 mg/kg reduced injury response during medically induced TBI.  Not only can DHA be used with TBI, but this study suggests it can be used in a prevention mode.
Nathan Goodyear

Prevalence of chronic hypopituitarism after blast concussion -- Wilkinson et al. 27 (1)... - 1 views

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    One of the first studies to look at PCS found that 42% of soldiers produced abnormally low hormone production following TBI one year after the injury.  This study highlights the potential pituitary dysfunction that can result from TBI.
Nathan Goodyear

Hypopituitarism after traumatic brain injury. - PubMed - NCBI - 0 views

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    TBI results in isolated or complete pituitary failure (PTHP) in up to 40% of those with TBI.  
Nathan Goodyear

Hypopituitarism after traumatic brain injury - 0 views

  • PTHP is observed in about 40% of patients with a history of TBI
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    post-traumatic hypopituitarism is found in 40% of those with TBI.  The severity does correlate with the increased likelihood of developing PTHP.  Isolated deficiencies have been found in PTHP.
Nathan Goodyear

The neurophysiology of brain injury. [Clin Neurophysiol. 2004] - PubMed - NCBI - 0 views

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    Just the abstract is available online, but the neurophysiology of brain injury is well discussed here.  This process takes time.  In fact, most TBIs are mild and often go unreported/unrecognized until neurological deficits begin.
Nathan Goodyear

Acute Glucocorticoid Deficiency and Diabetes Insipidus Are Common After Acute Traumatic... - 0 views

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    High rate (78%) of those post TBI have low cortisol levels due to damaged HPA axis.  Low cortisol levels post TBI are associated with an increase mortality rate and increased long-term HPA disruption.
Nathan Goodyear

Ketogenic Diet - Nutrition and Traumatic Brain Injury - NCBI Bookshelf - 0 views

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    good review of the impact of ketones on TBI.  The authors conclude that precursors to ketones may be the right approach to treatment.  This would be MCT's and ketones.
Nathan Goodyear

DIET, KETONES AND NEUROTRAUMA - 0 views

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    ketones to heal TBI?
Nathan Goodyear

http://www.jlr.org/content/early/2014/04/10/jlr.R046706.full.pdf - 0 views

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    Ketones for TBI?
Nathan Goodyear

Ketogenic Diet Prevents Alterations in Brain Metabolism in Young but not Adult Rats aft... - 0 views

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    ketones promote cerebral metabolic recovery after TBI.  Younger brains switch to ketone metabolism more readily compared to older brains.  Only abstract available here.
Nathan Goodyear

Fasting is neuroprotective following traumatic brain injury - Davis - 2008 - Journal of... - 0 views

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    short term fasting and ketosis provides neuroprotection and preserves mitochondria in animal TBI study.  This study found preventative effects of the ketones.
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