#Nutrition for #concussion – preliminary research results

Posted November 1st, 2011 in Concussion Nutrition by Rebecca Lane

If you know me, you know that I’m a hockey mom. The recent surge of interest in concussions in the media has started many organizations to develop protocols for getting athletes back to their game – various “return to play” rules have been written and are starting to be enforced. The OATA (Ontario Athletic Therapists Association) is also working on some protocols and asked if I might be interested in doing some research on nutrition for concussion (the # tags are for twitter.com as there is quite a group following information about #concussion for their children).

So here’s the first step in the process, writing about what I’ve found so far and outlining some of the questions I am hoping to find answers to. If you know the answers, or a great resouce where I might find the answers, to any of the questions PLEASE comment below. The more people involved, the better the results!

The following nutritional interventions were identified for review:

  1. Ketogenic Diets and/or Fasting for short periods – Ketogenic diets were originally developed in 1921 to treat epileptic children. They mimic biochemical changes associated with starvation or periods of limited food availability, and are composed of 80-90% fat, 10% protein and limited carbohydrates. In normal metabolism, carbohydrates in food are converted into glucose, which is the body’s preferred source of energy. Under some circumstances, like fasting, glucose is not available because the diet contains insufficient amounts of carbohydrates to meet metabolic needs. Consequently, fatty acid oxidation becomes favored, and the liver converts fat into fatty acids and ketone bodies that serve as an alternative fuel for brain cells. Based on the evidence presented, the ketogenic diet does hold some promise of effectiveness in improving the outcomes of TBI. There are indications that ketones may provide an alternative and readily usable energy source for the brain that might reduce its dependence on glucose metabolism, which may be impaired immediately following TBI. There is an absence of information on which forms of TBI – mild/concussion, moderate, severe, and penetrating – might benefit from such therapy. (Source: Nutrition and Traumatic Brain Injury: Improving Acute and Subacute Health Outcomes in Military Personnel, pp. 140-156) (More information available in this document: Neuroprotectice and Disease-modifying effects of the ketogenic diet)
    Questions: Duration? Long-term use in pediatric population has been associated with growth retardation, kidney stones, bone fractures (p. 141) Possible intermittent timing schedule? Effects of short-term fasting? For more info about ketogenic diets, click here.
  2. Antioxidants – During a TBI, damage to the brain can occur because of the generation of reactive oxygen species (which can be offset by the use of antioxidant therapy).  Oxidative stress is identified early after the initial injury, and compounds that intercept the production of reactive oxygen species could be beneficial for TBI outcomes. The use of single antioxidants has not been successful in treating oxidative-related diseases, so only consider a combination of vitamins A, C, E, all the B vitamins along with the minerals selenium and zinc.
    (Source: Nutritional Considerations in Traumatic Brain Injury, p. 608  [also pages 88-107 of the Department of Defence document above])
    Questions: Optimal dosage? and efficacy for children?
  3. Omega 3 fatty acids – fish oils and purified omega-3 fatty acids  have been proven to reduce inflammation within hours of continuous administration. For acute cases of TBI, it should be noted that there are intravenous fish oil formulations available in Europe, but these are not approved by the FDA. Continuous enteral (a way to provide food  through a tube placed in the nose,the stomach, or the small intestine) feeding with a feeding formula containing fish oil should provide equivalent effects for this purpose in the early phase of severe TBI when enteral access becomes available. (Source: Nutrition and Traumatic Brain Injury: Improving Acute and Subacute Health Outcomes in Military Personnel, p. 188-204)
    Questions: Should dosage be determined by weight, age, severity of TBI – or a combination of factors?  
  4. CDP-Choline – Choline has been shown to act as an anti-inflammatory and antioxidant in other diseases, and also to decrease calcium-mediated cell death, a feature of TBI. Choline has a critical role in neurotransmitter function because of its impact on acetycholine and dopaminergic function. Currently studies have only been done on animals, but they suggest that CDP-choline supplements increase dopamine receptor densities and can ameliorate memory impairment. It is suggested that CDP-choline may exert neuroprotective effects in an injured brain through its ability to improve phosphatidylcholine synthesis. (Source: Nutrition and Traumatic Brain Injury: Improving Acute and Subacute Health Outcomes in Military Personnel, p. 115-129)
    Questions: Optimal clinical dosage and duration of treatment? Further, the DoD will be monitoring the results of the Citicoline Brain Injury Treatment (COBRIT) trial, a human experimental trial examining the effect of CDP-choline and genomic factors on cognition and functional measures in severe, moderate, and complicated mild TBI. We’ll keep our eye on results from this trial.
  5. Creatine– Creatine, which is found in meat but is common in athletes’ dietary supplements, helps give the brain an intense and immediate hit of energy needed to help cells heal right after an injury. (Source:  http://www.theglobeandmail.com/news/world/americas/starve-a-fever-feed-a-concussion-speedy-feeding-offers-hope-of-better-healing/article1994021/)
    Military personnel are using creatine in the form of dietary supplements to increase strength and muscle mass. In the context of TBI, the committee found good evidence of improvements in cognition and behaviour from trials with creatine in children and adolescents. Although this evidence comes from long-term studies, treatment with creatine was started early after injury and may have influenced disease processes during the acute phase. In fact, creatine is thought to maintain mitochondrial energetics and improve cerebral vascular function, both of which are disrupted during the acute phase of TBI.  (Source: Nutrition and Traumatic Brain Injury: Improving Acute and Subacute Health Outcomes in Military Personnel, pp. 130-139)
    Questions: Timing of administration? Optimal dosage?
  6. Magnesium – Magnesium has a role in inhibiting the actions of the excitatory neurotransmitter glutamate by regulating calcium entry into the postsynaptic neuron, a process intimately related to a TBI event. Despite this seemingly neuroprotective action, there is no clear evidence that magnesium supplementation will affect TBI outcomes. (Source: Nutrition and Traumatic Brain Injury: Improving Acute and Subacute Health Outcomes in Military Personnel, pp. 157-187)
  7. Polyphenols – Few studies have been conducted to test their effectiveness in TBI, however their mechanism of action in protecting against cardiovascular and neurodegenerative diseases suggests that they warrant attention as neuroprotectants. Flavonoids are able to interact with neuronal signaling pathways critical in controlling neuronal survival – specifically selected for study were cucumin and resveratrol. (Source: Nutrition and Traumatic Brain Injury: Improving Acute and Subacute Health Outcomes in Military Personnel, pp. 205-226)
    Significant amounts of polyphenols – resveratrol, for example, which is found in red grapes, or curcumin, in yellow spices like turmeric – also helped keep inflammation down. (Source:  http://www.theglobeandmail.com/news/world/americas/starve-a-fever-feed-a-concussion-speedy-feeding-offers-hope-of-better-healing/article1994021/)
    Questions: Optimal dosage?
  8. Vitamin D – The role of vitamin D in the brain has only recently been recognized and is not well understood. Vitamin D and its receptor are thought to act by binding to DNA response elements that regulate gene transcription involved in cell proliferation, differentiation, and neural function in the brain. Vitamin D’s potential to increase resilience to TBI is supported by findings that vitamin D alone was also neuroprotective against animal models of stroke. Although there are only a few studies on vitamin D’s benefits for TBI treatment, the findings are promising and need to be evaluated further. (Source: Nutrition and Traumatic Brain Injury: Improving Acute and Subacute Health Outcomes in Military Personnel, pp. 227-232)
    Questions: Optimal dosage?
  9. Zinc – Zinc is an essential nutrient required for the function of many enzymes in the CNS. In the brain, zinc is released in the synaptic cleft where it modulates the activity of neuroreceptors. An excessive release of zinc can result in neural cell death. In the context of TBI, zinc deficiency might exacerbate the oxidative cascade that results in cell death.  (Source: Nutrition and Traumatic Brain Injury: Improving Acute and Subacute Health Outcomes in Military Personnel, pp. 233-246) Questions: Optimal dosage?

I hope that this has given you a starting point for finding answers to your questions about nutrition for concussion. I have skimmed most of the document, but only found the pdf of the entire document available online this morning! Many of the pieces will be hidden in here no doubt.

Dosage information as well as information for children, and adult timing and efficacy need to be researched further. As soon as I have answers, I’ll let you know. But much of the research is only available for these supplements regarding other neurological diseases, especially epilepsy.

There seems to be plenty of information about ketogenic diets for brain-disorders. While I think that immediately following the TBI, the focus should be on drinking water (which I just realized I didn’t mention at all above – every source recommends “Drinking plenty of water” – but give no idea of how much “plenty” is!) and eating glucose foods, once glucose metabolism starts to break down then ketones seem like the option for brain energy. Question, when does glucose metabolism break down after a TBI?

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