Concussion (mild TBI) Brain Food: A Review of Fish Oil, B-Complex and Protein (Amino Acid) Therapies

Concussion (mild Traumatic Brain Injury) Brain Food Treatment Research Summary:  Research shows that fish oil supplements if supplied before or after brain trauma aid in protecting cell membrane from damage and death. The Institute of Medicine research report shows that by immediately providing sufficient protein to brain damaged victims, mortality rates and Second Injury (damage surrounding the initial injury) can be significantly reduced.  Protein builds DNA, cell structures, and neurotransmitters. Researchers have found that Bcomplex vitamins are critical to maintaining reactions involved in the production of red blood cells, cell membrane, the myelin coating surrounding nerves fibers, and neurotransmitter production, making B-complex vitamins vital for nerve communication and brain function.   This report reviews these findings to encourage further evaluation and testing.  Home laboratory testing to monitor these nutrient levels should be evaluated.

High School Soccer Player Concussion Case Study:

As he jumped into the air, the soccer player was struck on the back of the head (posterior parietal, right side). He fell to the ground and lost consciousness for 10 – 15 seconds.  Afterwards, he felt normal and returned to play for 40 minutes. The next morning, the back of his head was swollen.  He described the pain as a “bad migraine”. The subject was lethargic and bright lights made him nauseous.  He experienced no balance nor vision problems.  Quick movements intensified his headache. He did not attend school, as it was difficult to concentrate, read, write, or spell.  He had memory difficulties. Bright light caused dizziness and irritated his headache.  He experienced no improvement of his condition during the first two weeks.

The third week post concussion, the subject began taking Fish Oil (600mg DHA+EPA, twice daily), B-complex (100mg/twice daily) , and Amino Acids (750mg/twice daily).  Feeling better, he attempted to attend school, but found himself “fading out”. At his physician’s office, he was unable to memorize colors or spell simple words.  Swelling was identified on the right side of his parietal lobe and left side of his frontal lobe.  He returned to school several days later for a few hours. He was unable to complete homework.  The third week he attended school part-time and on the fourth week, he attended full time. He felt “fairly normal”, however, continued to have difficulties with bright lights and could not recall elementary school memories.  He discontinued the vitamins at the end of the fourth week.

One year later, the subject suffered a minor concussion as the front of his head (right frontal lobe) struck a goal post.  His pupils were dilated.  He could remember colors and spell however, he was dizzy in bright light.  He discontinued play, but did not consider this event as serious as the previous. He took the vitamins for a few days and felt better.  The following year, he again hit his head during soccer season and took the vitamins for a couple days.

Since most concussions improve about the third to fourth week, it is difficult to determine whether fish oil, b-complex, and amino acids shortened recovery time. The subject believes that the improvements began with the vitamins.  He states that upon taking the vitamins, he felt like returning to school. Additional research would be more valuable should baseline, post concussion, and post treatment neurocognitive testing be completed with control and test groups.

Concussion – mild Traumatic Brain Injury Discussion:

The human brain is about the size of a cauliflower head with the density of medium soft cheese and can be easily sectioned with a spatula. The brain stem protrudes from the posterior-inferior surface sending commands up and down pathways and through relay centers to the pinky-sized spinal cord. The brain and spinal cord are surrounded by clear cerebral spinal fluid (CSF) and membranes which provide a shock absorber-like environment internal to the bony cranium and vertebrae.

When the cushion environment is disrupted by an “external mechanical force such as rapid acceleration or deceleration, impact, blast waves, or penetration by a projectile” (Maas AI, et al., 2008), a traumatic brain injury (TBI) results.  A mild TBI is referred to as a concussion.

TBIs are the leading cause of death/disability worldwide  (Alves OL, et al., 2001) and the number one cause of coma (Farag E, et al., 2011).   One third of TBI fatalities are firearm accidents (75% suicide) and another third are motor vehicle accidents (Leon-Carrion J, et.al., 2005). A total of 1.5 million people experience head trauma each year in the U.S. resulting in an annual cost exceeding $5.6 billion.  While most head injuries are mild (Cassidy JD, et al., 2004), the death rate to TBI is estimated at 21% by 30 days post injury (Greenwood, et al, 2003). The greatest number of TBIs occur in the male 15-24 age group (Hardman JM, et al., 2002) (Mass AI, et al., 2008). Sport and recreational activities in the U.S. alone may cause between 1.6 – 3.8 million TBIs each year (CDCP, 2007).  In addition, the military has seen a significant increase in TBIs. Approximately, 10-20% of veterans returning from the Middle East have experienced a TBI. The Department of Defense is conducting research to reduce the serious problems associated with these injuries and has requested a report from the Institute of Medicine (2011).

Clinically, a mild TBI or concussion is defined as post-traumatic amnesia of less than one day and a loss of consciousness between 0 -30 minutes (DOD TBI Task Force).  Symptoms include “headache, vomiting, nausea, lack of motor coordination, dizziness, and difficulty balancing” (Kushner D, 1998) along with “lightheadedness, blurred vision or tired eyes, ringing in the ear, bad taste in the mouth, fatigue or lethargy, and changes in sleep patterns.  Cognitive and emotional symptoms include behavioral or mood changes, confusion, and trouble with memory, concentration, attention, or thinking” (NINDS, 2008). Social behavior or emotional problems may also occur. Damage to the left side of the brain may involve speech, reading and writing difficulties.  Damage to the back of the brain may involve vision, balance, and coordination problems.

Current diagnostic techniques include neurological exam and neuro-imaging studies such as CT (CAT scan) or MRI (Magnetic Resonance Imaging).  CT scans are quickly completed in an emergency department. They are less expensive and better at showing bleeds than MRI  however, brain CT delivers a 1-2 millisievert dose of radiation.   MRI, which utilizes a magnetic field,  (no radiation exposure), delivers more detail of the brain and brain stem, but it is more time consuming and costly.  A CT of a more serious TBI may show hemorrhage, skull fracture, contusions (bruising), fracture, and/or edema (swelling).  An MRI of a more serious TBI, might show a shifting of brain structures, contusion, and hematoma. When blood exerts pressure upon the brain surface it can impair brain function. Interestingly, when brain tissue is seriously injured,  it appears to be cracked open on MRI, much like the appearance of a sponge that is torn open every 1-2 inches. The tears create fluid inlets, perhaps designed to bring nutrient rich CSF to the damaged areas.

A mild TBI or concussion will often show little damage on CT or MRI neuro-imaging studies, thus the increasing use of imPACT or CNS Vital Signs neurocognitive testing.  These computerized tests  have been more effective at assessing mild concussive damage by evaluating general mental functioning. To date, many athletic programs have been using them to compare pre and post injury results to determine ‘return to play’. Since they measure brain function in terms of verbal and visual memory, processing speed, reaction time, attention span, and non-verbal problem solving capabilities, neurocognitive testing has been successfully utilized to identify emotional and cognitive deficits related to mild TBIs.

When the brain is damaged, it immediately begins self repair. Raw materials are sought from nutrients in the blood supply and from CSF to rebuild the initial injury site.  When nutrient supply is insufficient, surrounding brain tissue may be broken down to supply substrate for reconstruction.

Damage apparent in adjacent tissue, has been defined as Second Injury and may result in more serious injury than the initial TBI (Park E, et al., 2008). When death results weeks later, it is typically caused by secondary damage (Ghajar J, 2000). In the past, this Second Injury has been commonplace and no therapy has been available to stop progression (Park E, et al., 2008). However, recent military studies found that by immediately supplying sufficient amounts of protein to the injured patient, Secondary Injury is significantly reduced (Institute of Medicine, 2011).  Providing omega-3 essential fatty acids (DHA/EPA) before injury or immediately after injury also reduces TBI damage (Mills JD, et al., 2011) (Wu A, et al., 2007).

Brain injury brings immune cells and fluids to the injury site, resulting in inflammation, but with the brain enclosed in the cranium there is minimal space to accommodate swelling.  The resultant increase in intracranial pressure may occlude blood vessels responsible for bringing oxygen and nutrients to brain cells and lymph vessels responsible for removing waste products (Scalea TM, 2005). Increased pressure can force the brain to herniate into spaces where it does not belong.  This renders the tissue non-functional and eventually will cause death.  A variety of anti-inflammatory medications are often utilized to diminish swelling.

Mild TBIs physically appear to resolve in 3 weeks and patients tend to return to normal activities.  Some patients have “physical, cognitive, emotional and behavioral problems such as headaches, dizziness, difficulty concentrating, and depression” (Parik S et al., 2007). Movement disorders, seizures, and substance abuse may also develop (Arlinghaus KA, et al., 2005). Depending upon the severity of the injury, the number of repeat injuries and the presence of adequate nutrients before and after the injury, the prognosis ranges from complete recovery to permanent disability, neurological disease or death. “Permanent disability is thought to occur in 10% of mild TBIs, 66% of moderate injuries, and 100% of severe injuries” (Frey LC, 2003). In many situations, particularly athletics, a second concussion may occur before the first concussion has healed.  This is of particular concern as multiple TBIs may have a cumulative effect (Kwasnica C, et al., 2008).

Brain Biochemistry:

As discussed in ‘The ERB Vision for Wellness‘ tab on this website, Dr. James Watson of Watson and Crick, the scientists who discovered the DNA double helix, tells us that to eliminate disease we must return to Biochemistry.  We expect that the many dedicated researchers referenced below would agree.  They have found that in Traumatic Brain Injury, nutrition matters.  Adequate supplies of the major tissue nutrients are critical.

In looking at a section of brain tissue, the lighter tan colored structures are called “white matter.” White matter consists of nerve fiber tracts or pathways traveling in both directions to and from the brain through the brainstem down the spinal cord and extending out to organs, arms, and legs.  A nerve can be up to four feet long. White matter nerve tissue is composed of essential fatty acids called omega-3s such as DHA (docosahexanoic acid) and EPA (eicosapentanoic acid).  Most nerve tissue contains a myelin coating.  The resistance created by this coating allows for impulse transmission at approximately 100m/sec ( 245 mph)! Nerve and myelin formation require B-complex vitamins.  The darker structures on a brain section are called  “gray matter.”  These are decision-making nuclei made from proteins composed of amino acid building blocks.  Proteins and amino acids formulate all structures, most noticeable of which are neurotransmitters.  Neurotransmitters are critical to brain function and communication throughout the body.

Essential Fatty Acids (DHA and EPA):

40% of brain tissue is essential fatty acids (DHA and EPA).   While EPA provides important anti-inflammatory actions (Sears B, 2011) and is included in supplements, 97% of the brain’s essential fatty acids are the 22 carbon chain,  Docosahexanoic Acid (DHA).  DHA is found in foods such as walnuts (ALA), microalgae, microplants, cod, salmon, mackerel, sardines, hake, caviar, herring, oysters, organ meats (liver), grass fed and finished beef, and fish oil or algae supplements.  Fish receive DHA from ocean phytoplankton (microalgae or microplants).  Cattle receive DHA from grass.  However, as we increasingly draw our food from farm-raised fish and grain-raised cattle, our dietary intake of DHA is being depleted, (Abel R, 2002).

Most humans consume an overabundance of vegetable oil and butters which contain no double bonds in their carbon chains.  DHA has six double bonds (22:6), one at every third carbon (omega-3 or n-3). In cell membrane, these double bonds allow the fatty acid to neutralize damaging free radicals.  In addition, the double bonds increase the fluidity properties of cell membrane which helps to protect the cell from trauma and cell death (apoptosis) (Eckert GP, et al., 2011). Proper cell communication and signaling is critical for brain function. Fifty percent of nerve cell plasma membrane is DHA (Collins C, et al., 2002) which is important in cell communication, neuronal survival, and growth.  DHA is found in three cell membrane phospholipids:  phosphytidylethnolamine, ethnolamine plasmalogens, and phosphatidylserine. Upon injury, these phospholipid pools are important reservoirs to reconstruct cell membrane (Chang CY, et al., 2009).  In the absence of dietary DHA, the brain will improvise and construct brain tissue from vegetable oil.  However, under traumatic conditions  vegetable oil fed rat brain falls apart, (Eckert  GP, et al., 2011) (Abel R, 2002).

Researchers found that in rats subject to TBI which then received 40mg/kg/day pharmaceutical grade fish oil rich in DHA and EPA for 30 days post TBI had more healthy nerve cells.  Essential fatty  acids  were shown  to be neuroprotective by reducing  the  number of  injured nerve axons, decreasing the level of inflammation,  and reducing oxidative stress and cell death (Mills JD et al., 2011). DHA fed to rats immediately post TBI was found to counteract cognitive decay, maintain membrane signaling function, and support the potential of DHA supplementation to reduce the effects of TBI. (Wu A, et.al 2011).  In addition, essential fatty acids DHA and EPA given to rats 4 weeks prior to TBI was found to help maintain brain homeostasis and reduce oxidative damage due to TBI (Wu A, et al., 2007). 

DHA and EPA have been found to improve the outcome of stroke studies of both rat and human models (Kong W, et.al) (Hagiwara H, et.al.).  Few human studies have been conducted using DHA as prophylaxis for TBI.  In 2006, 20 grams per day of omega-3 fish oil (CNN, 2012)  and hyperbaric oxygen treatment were used by Dr. Julian Bailes to treat the sole survivor of the West Virginia mining disaster, Randal McCloy, who suffered carbon monoxide poisoning. This patient now claims that his brain function is near normal.  Dr. Bailes and his colleagues have since published many research papers demonstrating the benefits of essential fatty acids and fish oil supplements.  In addition, “individual case reports using fish oil doses of 2-4 grams per day have been described, however sufficient human research is unavailable to recommend dosages”  (Maroon, JC and Bost J, 2011).

One new human case study was published in October 2012, when Peter Ghassemi convinced physicians to give his son Bobby, who was in a coma following a motor vehicle accident, omega-3 fish oil ( a similar dose to Randal McCloy).  Bobby  had a Glasgow Coma Score of 3 (scale 3 – 15), which Dr. Michael Lewis says that “a brick or piece of wood has a Glasgow Coma Score of 3. It’s dead.”  Peter Ghassemi, Bobby’s father, indicates that it was difficult to convince physicians to give their son fish oil.  They wanted to see 1000 case studies first, to prove its efficacy.  Eventually, physicians agreed.  Thanks to his father’s perserverance, Bobby has recovered today.  U.S. Army Colonel Lewis who recommended the therapy to Peter Ghassemi describes the therapy like this.  “If you have a brick wall and it gets damaged, wouldn’t you want to use bricks to repair the wall?  And omega-3 fatty acids are literally the bricks of the cell wall of the brain.”  (CNN,2012)

The textbook “Contemporary Nutrition” written by  Gordon M. Wardlaw and Anne M. Smith in 2013 tells us that EPA and DHA are slowly synthesized in the brain from alpha linoleic acid and can be found in “fatty fish such as salmon, tuna, sardines, anchovies, striped bass, catfish, herring, mackerel, trout or halibut “(listed highest to lowest omega-3 content) and in foods such as “canola and soybean oils, walnuts, flax seeds, mussels, crab and shrimp”.  The authors warn about high mercury levels in swordfish, shark, king mackerel, and albacore, and indicate that fish with low mercury levels include salmon, sardines, bluefish, herring and shrimp.  Eating fish twice each week is recommended.  Omega-3 fatty acids tend to act to reduce blood clotting and inflammation, while omega-6 foods tend to increase clotting and inflammation.  Vitamin K and calcium carbonate are also involved in the clotting process. “Fish oil capsules should be limited for individuals who have bleeding disorders, take anticoagulant medications, or anticipate surgery, because they may increase risk of uncontrollable bleeding and hemorrhagic stroke”.

Wardlaw and Smith recommend 1.6 grams per day of omega-3 fatty acids for men and 1.1 grams per day for women.  Elevated blood triglycerides are treated with 2 to 4 grams per day.  Omega 3 fatty acids have been found to reduce the inflammation of rheumatoid arthritis and help with behavioral disorders and cases of mild depression.  Freezing fish oil capsules helps to reduces the fishy after taste.  “2 tablespoons of flax seed per day is typically recommended as an omega-3 fatty acid source”.  Approximately 3 walnuts (6 halves) yields approximatley 1 gram of DHA.  Care should be taken to keep DHA sources refrigerated as they turn rancid easily.  For TBI patients on IV feeding it is important to investigate the quantity of DHA and EPA present in total parenteral nutrition.  One researcher takes approximately 1 gram of DHA/EPA through fish oil daily and regulates intake by the dryness/moistness of the skin.  In drier climates, she finds this daily intake amount must be doubled.  Mercury consumption in fish oil is a serious risk and mercury free alternatives should be explored.

More human studies are needed to establish the benefits/risks of DHA and EPA with TBI. Eventually these will come however, the bureaucracy is heavy, and the cost estimates of bringing a new drug to market varies from $500 million to $2 billion (Adams C, et al., 2006) (JHE, 2010). A bottle of fish oil, with a small profit margin, may not provide sufficient return on investment to entice investigation.  One subject with a fish oil allergy could mire the researching organization in million dollar legal proceedings for years to come. That said,  research studies are important for physicians to have as legal and medical support for their recommendations.  Given this climate, many individuals and their health care providers have taken on the responsibility to evaluate whether  fish oil supplements are a safe and worthwhile benefit or a risk addition to their diet.  By 2020, we expect clinicians and individual to measure and maintain their optimum DHA/EPA levels.

B Complex Vitamins:

Vitamin B is a vitamin complex  of B-1-thiamine, B-2 riboflavin, B-3 niacin, B-5 pantothenic acid, B-6 pyridoxine, B-9 folate, B12-cobalamin.  B complex vitamins are important for nerve, DNA and neurotransmitter synthesis,  and for cell energy production and metabolism.  The majority of the information cited below regarding the effects of B complex vitamins on brain function has been obtained from animal studies.

Thiamine (B1):

  • Required for red blood cells to carry oxygen (Combs GF Jr, et al., 2008)
  • Acetylcholine neurotransmitter production(Butterworth RF, et al., 2006)
  • Myelin synthesis in nerve cells (Butterworth RF, et al., 2006)
  • High school female RDA 1.0 mg/day, male 1.2 mg/day.
  • Adult RDA is 1.1 – 1.2 mg/day, Daily Value 1.5 mg/day, no upper limit set because water soluble and rapidly lost in urine, alcohol consumption reduces thiamin levels (Wardlaw, et.al., 2013)
Riboflavin (B2):
  • A component in all flavoproteins and  red blood cells (erythrocytes)
  • Reduced TBI lesions, edema, and improved outcome (Hoane MR, et al., 2005)
  • High school female RDA 1.0 mg/day, male 1.3 mg/day.
  • Adult RDA is 1.1 – 1.3 mg/day, Daily Value 1.7 mg/day, no upper limit set.  Alcohol consumption reduces riboflavin levels (Wardlaw, et.al., 2013)

Niacin (B3):

  • Involved in DNA repair, cholesterol, and energy production
  • Helps produce neurotransmitters in the adrenal gland
  • Reduces TBI lesion size and improves sensory, motor, cognitive, and behavioral recovery (Voner Haar C, 2011)
  • High school female RDA 14 mg/day, male 16 mg/day.
  • Adult RDA is 14 – 16 mg/day, Daily Value is 20 mg/day, upper limit is 35mg/day of nicotinic acid form. Alcohol consumption reduces niacin levels (Wardlaw, et.al., 2013)

Pantothenic Acid (B5)

  • Neurotransmitter acetylcholine production
  • Involved in signal transduction, and enzyme control
  • High school female and male 5 mg/day.
  • Adult Adequate Intake is 5 mg/day, Daily Value is 10 mg, no upper limit set (Wardlaw, et. al, 2013).

Pyridoxal Phosphate (B6):

  • Controls all amino acid metabolism  (Sahley BJ, 2002)
  • Red blood  cell and  antibody formation (Sahley BJ, 2002)
  • Dopamine and GABA neurotransmitter production
  • Nerve myelin sheath phospholipid production
  • High school RDA female 1.2 mg/day, male 1.3 mg/day.
  • Adult RDA is 1.3 – 1.7 mg/day, Daily Value is 2 mg, Upper Level is 100 mg/day based upon nerve damage.  Studies have shown that 2 – 6 grams/day of B-6 for 2 or more months can lead to irreversible nerve damage.  Symptoms of toxicity include walking difficulties and hand and foot numbness (Wardlaw, et. al, 2013)

Folate  (B9):

  • Required to synthesize, repair, and methylate DNA.
  • Provides neuroprotection in TBI (Naim MY, et al., 2010)
  • Important in rapid cell division and growth.
  • Production of healthy red blood cells and anemia prevention
  • Forms cell membrane phospholipids and receptors (Karakula H, et al.,2009) (Surtees R, 1998)
  • Prevents nerve damage and neural tube defects during development
  • Required for myelin regeneration (van Rensburg SJ, et al., 2006) (Guettat L, et al., 1997)
  • High school RDA female and male 400 mcg/day.
  • Adult RDA and Daily Value is 400 mcg/day,  pregnant women 600mcg/day  (important to prevent neural tube defects), Upper Level is 1 mg/day alcoholism and poor absorption reduces folate levels (Wardlaw, et.al., 2013)

Cobalamin (B12):

  •  Involved in blood formation.
  • Critical to DNA synthesis through folate regeneration
  • Formation of cell membrane phospholipids and receptors (Karakula H, et al., 2009) (Surtees R, 1998)
  • B12 supplementation partially resolved cognitive deficits and myelin imaging abnormalities (Chatterjee A, et.al., 1996) (Jongen JC, et al., 2001)
  • Improves cerebral and cognitive functions.  (Bourre JM, 2006)
  • Required for myelin synthesis (Hall CA, 1990) (van Rensburg SJ, et al, 2006) (Guettat L, et al., 1997)
  • Promotes nerve regeneration (Okada K, et al., 2010)
  • High school RDA female and male 2.4 mcg/day.
  • RDA is 2.4 mcg/day, Daily Value is 6 mcg/day, no Upper Limit set, stored in liver, 50% of dietary intake may be absorbed.  Nerve damage and anemia may result from insufficient intake.

There are 150mg time release (9-10 hours) capsules available for B complex.  All  B vitamins are water soluble and need to be replenished daily.  Vitamin B complex has an important  role  in  alleviating anxiety and lactic acid buildup.  Dietary supply may be inadequate under stress (Sahley BJ, 2002).

Protein (Amino Acids):

Linear chains of amino acids form proteins. Proteins produce nuclei in the brain, DNA,  cell membrane, enzymes, and neurotransmitters. Twenty amino acids are commonly identified.  All 20 amino acids need to present concurrently for protein synthesis to occur.  A problem may be that most foods do not provide all 20 amino acids concurrently as is provided by a 20 amino acid complex supplement.  More research needs to be completed on this topic.

Alanine – Precursor of neurotransmitter dopamine (Coxon KM, et al., 2005)

Arginine – Through agmantine, it is neuroprotective in trauma and ischemia models by significantly reducing  brain swelling volume and blood-brain barrier protection (Kim JH, et al., 2009)

Cysteine – Forms DNA double helix disulfide bonds

Glutamate – Important for calcium ion binding; may reduce blood glucose levels in the injured spinal cord reducing neurological impairment (Zhang TL, et al., 2010)

Glutathione – Critical to relieve oxidative stress in cells

Glycine – Important in red blood cell formation (Shemin D, et al., 1946); gives amino acid structures flexibility

Histidine – Used throughout the brain;  improves TBI outcome (Faden AI, et al., 1993) (Krusong K, et al., 2011)

Lysine – Important for connective tissue maintenance, and affects protein binding to phospholipid membranes (Blenis J, et al., 1993)

Methionine – The sole methyl donor in the central nervous system; increases S-adenylmethionine (SAMe) in CSF aiding in neurological disorder treatment (Chishty M, et al., 2002); forms Glutathione, important in reducing free radical-mediated traumatic injury  (Gidday JM, et al., 1999)

Phenylalanine – Produces chlorophenylalanine (CPA) which slowed the breakdown of the blood-brain barrier permeability, brain edema and blood flow; reduced the number of damaged and distorted nerve cells (Sharma HS, et al., 2000).

Proline – Maintains connective tissue (Bhattacharjee A, et al., 2005)

Serine – Acts as a neurotransmitter in the brain (Wolosker H, et al., 2008)

Taurine – Major component of brain tissue and muscle (Brosnan JT, 2006)

Threonine – A component of the serine/threonine kinase; neuroprotective following traumatic brain injury (Erlich S, et al.,2007)

Tryptophan – Precursor to neurotransmitter serotonin (Savelieva KV, et al., 2008); a modulator of serotonin which alters plasticity-related signaling pathways and matrix degradation (Penedo LA, et al., 2009)

Tyrosine – Precursor of the neurotransmitter dopamine, norepinephrine, epinephrine

Under prolonged stress or illness the body is unable to produce sufficient non-essential amino acids (Sahley BJ, 2002).  Trauma has been found to damage DNA and RNA, and to deplete neurotransmitters.  Neurological dysfunction is caused by traumatic brain injury (Cole J, et al., 2010

As amino acids are utilized for energy and substrate, they are oxidized to urea and carbon dioxide producing high levels of glutamate.  These high levels seen in the TBI patient can include oxidation of branched chained amino acids. Dietary consumption of Branched Chain Amino Acids (BCAAs) restored BCAA concentrations to normal, improved nerve cell communication, and reinstated cognitive performance after concussive brain injury (Cole J, et al., 2010). BCAAs and amino acid complex (protein) are available at nutrition stores.

The Institute of Medicine committee report of April 20, 2011 on Nutrition and Traumatic Brain Injury: Improving Acute and Subacute Health Outcomes in Military Personnel   found that supplying high levels of protein to the TBI patient within the first 24 hours severely reduced mortality.  This report calls for standardized protocols to require  a level of nutrition that represents more than 50 percent of the injured person’s total energy expenditure and provide 1 to 1.5 grams of protein per kilogram of body weight for two weeks. They expect this nutritional intervention limits the inflammatory response, thereby improving outcome.  Most importantly, in following this protein therapy, the detrimental secondary injury process was not apparent.

Protein needs of a sedentary adult are estimated at .8 grams/kilogram  or 56 grams/day for a 70-kilogram, 154lb man.  (Pounds/2.2 kilograms per pound * .8 grams/kilogram).   Protein needs of a football, power sport playing athlete are approximately 1.4 – 1.7 grams/kilogram for males and 1.1 – 1.5 grams/kilogram for females or 98-119 grams/day. Athletes in a strength training program can be recommended up to 2.0 grams of protein per kilogram per day, almost twice the RDA (Wardlaw, et. al., 2013).

The objective of this discussion has been to bring current research advancements to light given the realization that concussive TBIs cause damage and disease, such that this information may be further evaluated by the public, health care providers, and the medical research community.

Traumatic Brain Injury References:

Alves OL, Bullock R (2001). “Excitotoxic damage in traumatic brain injury”. In Clark RSB, Kochanek P. Brain injury. Boston: Kluwer Academic Publishers. p. 1. ISBN 0-7923-7532-7. Retrieved 2008-11-28.

Arlinghaus KA, Shoaib AM, Price TRP (2005). “Neuropsychiatric assessment”. In Silver JM, McAllister TW, Yudofsky SC. Textbook Of Traumatic Brain Injury. Washington, DC: American Psychiatric Association. pp. 63–65. ISBN 1-58562-105-6.

Center for Disease Control and Prevention, National Center for Injury Prevention and Control. “Traumatic brain injury” (http://www.cdc.gov/ncipc/factsheets/tbi.htm) 2007.

Cassidy JD, Carroll LJ, Peloso PM, Borg J, von Holst H, Holm L et al. (2004). “Incidence, risk factors and prevention of mild traumatic brain injury: Results of the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury”. Journal of Rehabilitation Medicine 36 (Supplement 43): 28–60. DOI:10.1080/16501960410023732. PMID 15083870.

Carlson K, Kehle S, Meis L, Greer N, MacDonald R, Rutks I, Wilt TJ, “The Assessment and Treatment of Individuals with History of Traumatic Brain Injury and Post-Traumatic Stress Disorder: A Systematic Review of the Evidence [Internet].” Washington (DC), Department of Veterans Affairs (US); 2009 Aug, VA Evidence-based Synthesis Program Reports

Department of Defense and Department of Veterans Affairs (2008). “Traumatic Brain Injury Task Force”. http://www.cdc.gov/nchs/data/icd9/Sep08TBI.pdf.

Farag E, Manno EM, Kurz A. (2011) “Use of hypothermia for traumatic brain injury: point of view” Minerva Anesthesiol. 2011 Mar;77(3):366-70. Epub 2011 Feb 1. PMID: 21283076

Frey LC (2003). “Epidemiology of posttraumatic epilepsy: A critical review”. Epilepsia 44 (Supplement 10): 11–17. DOI:10.1046/j.1528-1157.44.s10.4.x. PMID 14511389.

Furlow, B (2010 May-Jun). “Radiation dose in computed tomography.”. Radiologic Technology 81 (5): 437-50. PMID 20445138.

Ghajar J (September 2000). “Traumatic brain injury”. Lancet 356 (9233): 923–29. DOI:10.1016/S0140-6736(00)02689-1. PMID 11036909.

Greenwald BD, Burnett DM, Miller MA (March 2003). “Congenital and acquired brain injury. 1. Brain injury: epidemiology and pathophysiology”. Archives of Physical Medicine and Rehabilitation 84 (3 Suppl 1): S3–7. DOI:10.1053/apmr.2003.50052. PMID 12708551.

Hardman JM, Manoukian A (2002). “Pathology of head trauma”. Neuroimaging Clinics of North America 12 (2): 175–87, vii. DOI:10.1016/S1052-5149(02)00009-6. PMID 12391630. “TBI is highest in young adults aged 15 to 24 years and higher in men than women in all age groups.”

Kushner D (1998). “Mild traumatic brain injury: Toward understanding manifestations and treatment”. Archives of Internal Medicine 158 (15): 1617–24. DOI:10.1001/archinte.158.15.1617. PMID 9701095.

Kwasnica C, Brown AW, Elovic EP, Kothari S, Flanagan SR (March 2008). “Congenital and acquired brain injury. 3. Spectrum of the acquired brain injury population”. Archives of Physical Medicine and Rehabilitation 89 (3 Suppl 1): S15–20. DOI:10.1016/j.apmr.2007.12.006. PMID 18295644.

León-Carrión J, Domínguez-Morales Mdel R, Barroso y Martín JM, Murillo-Cabezas F (2005). “Epidemiology of traumatic brain injury and subarachnoid hemorrhage”. Pituitary 8 (3–4): 197–202. DOI:10.1007/s11102-006-6041-5. PMID 16508717.

Maas AI, Stocchetti N, Bullock R (August 2008). “Moderate and severe traumatic brain injury in adults”. Lancet Neurology 7 (8): 728–41. DOI:10.1016/S1474-4422(08)70164-9. PMID 18635021.

“NINDS Traumatic Brain Injury Information Page”. National Institute of Neurological Disorders and Stroke. 2008-09-15. Retrieved 2008-10-27.

Parikh S, Koch M, Narayan RK (2007). “Traumatic brain injury”. International Anesthesiology Clinics 45 (3): 119–35. DOI:10.1097/AIA.0b013e318078cfe7. PMID 17622833.

Park E, Bell JD, Baker AJ (April 2008). “Traumatic brain injury: Can the consequences be stopped?”. Canadian Medical Association Journal 178 (9): 1163–70. DOI:10.1503/cmaj.080282. PMC 2292762. PMID 18427091.

Salomone JP, Frame SB (2004). “Prehospital care”. In Moore EJ, Feliciano DV, Mattox KL. Trauma. New York: McGraw-Hill, Medical Pub. Division. pp. 117–8. ISBN 0-07-137069-2. Retrieved 2008-08-15.

Scalea TM (2005). “Does it matter how head injured patients are resuscitated?”. In Valadka AB, Andrews BT. Neurotrauma: Evidence-based Answers to Common Questions. Thieme. pp. 3–4. ISBN 3-13-130781-1.

Essential Fatty Acids References:

Abel R,  “The DHA Story, How Nature’s Super Nutrient Can Save Your Life”.  2002, ISBN 1-59120-001-6, (2002).

Adams C, Brantner V (2006). “Estimating the cost of new drug development: is it really 802 million dollars?”. Health Aff (Millwood) 25 (2): 420–8. DOI:10.1377/hlthaff.25.2.420. PMID 16522582.

CNN 2012   http://www.cnn.com/2012/10/19/health/fish-oil-brain-injuries/index.html

Eckert GP, Chang S, Eckmann J, Copanaki E, Hagl S, Hener U, Müller WE, Kögel D, “Liposome-incorporated DHA increases neuronal survival by enhancing non-amyloidogenic APP processing”.  Biochim Biophys Acta. 2011 Jan;1808(1):236-43. Epub 2010 Oct 29. PMID 21036142

Livestrong.com: http://www.livestrong.com/article/430423-how-many-omega-fish-oil-pills-should-you-take-a-day/

Mills JD,  Hadley K, Bailes JE, “Dietary Supplementation with the Omega-3 fatty acid Docosahexaenoic Acid in Traumatic Brain Injury”. Neurosurgery, 2011 Feb;68(2):474-81

Journal of Health Economics 2010 Study,  http://onlinelibrary.wiley.com/doi/10.1002/hec.1454/abstract

Sears, B (2011). “The fallacy of using DHA alone for brain trauma.” http://www.prweb.com/releases/concussion/brain_trauma/prweb4500964.htm

University of Maryland Medical System and University of Maryland Medical School:  Omega-3 fatty acids:  http://www.umm.edu/altmed/articles/omega-3-000316.htm

Wardlaw, Gordon M. and Smith, Anne M., “Contemporary Nutrition”, 2013, ISBN 978-0-07-340254-3, McGraw-Hill.

Vitamin B Complex References:

Bourre JM.  “Effects of nutrients (in food) on the structure and function of the nervous system: update on dietary requirements for brain. Part 1: micronutrients”.  Nutr Health Aging. 2006 Sep-Oct;10(5):377-85. PMID: 17066209

Butterworth RF, Thiamin. In: Shils ME, Shike M, Ross AC, Caballero B, Cousins RJ, editors. Modern Nutrition in Health and Disease, 10th ed. Baltimore: Lippincott Williams & Wilkins; 2006.

Chatterjee A, Yapundich R, Palmer CA, Marson DC, Mitchell GW. Neurology. “Leukoencephalopathy associated with cobalamin deficiency”, 1996 Mar;46(3):832-4. PMID: 8618695Acta Neurol Taiwan. 2009 Dec;18(4):231-41.

Chang CY, Ke DS, Chen JY, “Essential fatty acids and human brain”, Acta Neurol Taiwan. 2009 Dec;18(4):231-41.

Combs GF Jr., “The vitamins: Fundamental Aspects in Nutrition and Health. 3rd edition. Ithaca, NY: Elsevier Academic Press; 2000

Coxon KM, Chakauya E, Ottenhof HH et al. (August 2005). “Pantothenate biosynthesis in higher plants”. Biochemical Society Transactions 33 (Pt 4): 743–6. DOI:10.1042/BST0330743. PMID 16042590.

Guettat L, Gille M, Delbecq J, Depré A, “Folic acid deficiency with leukoencephalopathy and chronic axonal neuropathy of sensory predominance”.  Rev Neurol (Paris). 1997 Jun;153(5):351-3. PMID: 9296172

Hall CA, “Function of Vitamin B12 in the central nervous system as revealed by congential defects”, Am J Hematol. 1990 Jun;34(2):121-7

Hoane MR, Wolyniak JG, Akstulewicz SL, “Administration of riboflavin improves behavioral outcome and reduces edema formation an glial fibrillary protein expression after traumatic brain injury”, J Neurotrauma, 2005 Oct 22;(10):1112-22

Jongen JC, Koehler PJ, Franke CL, “Subacute combined degeneration of the spinal cord: easy diagnosis, effective treatment”, Ned Tijdschr Geneeskd. 2001 Jun 30;145(26):1229-33. PMID: 11455686

Karakuła H, Opolska A, Kowal A, Domański M, Płotka A, Perzyński J, “Does diet affect our mood? The significance of folic acid and homocysteine”  Pol Merkur Lekarski. 2009 Feb;26(152):136-41.

Naim MY, Friess S, Smith C, Ralston J, Ryall K, Helfaer MA, Marguiles SS, “Folic acid enhances early functional recovery in a piglet model of pediatric head injury”, Dev Neurosci. 2010;32(5-6):466-79. Epub 2011 Jan 5. PMID: 21212637

Okada K, Tanaka H, Temporin K, Okamoto M, Kuroda Y, Moritomo H, Murase T, Yoshikawa H. “Methylcobalamin increases Erk1/2 and Akt activities through the methylation cycle and promotes nerve regeneration in a rat sciatic nerve injury model.”, Exp Neurol. 2010 Apr;222(2):191-203. Epub 2010 Jan 4.

Surtees R, “Demyelination and inborn errors of the single carbon transfer pathway” Pediatr. 1998 Apr;157 Suppl 2:S118-21. PMID: 9587038

van Rensburg SJ, Kotze MJ, Hon D, Haug P, Kuyler J, Hendricks M, Botha J, Potocnik FC, Matsha T, Erasmus RT, “Iron and the folate-vitamin B12-methylation pathway in multiple sclerosis”, Metab Brain Dis. 2006 Sep;21(2-3):121-37. Epub 2006 May 26. PMID: 16729250

Vonder Haar C, Anderson G, Hoane MR, “Continuous nicotinamide administration improves behavioral recovery and reduces lesion size following bilateral frontal controlled cortical impact injury.”, Behav Brain Res, 2011 Oct 31;224(2):311-7.  Epub 2011 Jun 17.

Wardlaw, Gordon M. and Smith, Anne M., “Contemporary Nutrition”, 2013, ISBN 978-0-07-340254-3, McGraw-Hill.

Protein (Amino Acids) References:

Bhattacharjee A, Bansal M (March 2005). “Collagen structure: the Madras triple helix and the current scenario”. IUBMB Life 57 (3): 161–72. DOI:10.1080/15216540500090710. PMID 16036578.

Blenis J, Resh MD (December 1993). “Subcellular localization specified by protein acylation and phosphorylation”. Current Opinion in Cell Biology 5 (6): 984–9. DOI:10.1016/0955-0674(93)90081-Z. PMID 8129952.

Brosnan JT, Brosnan ME (June 2006). “The sulfur-containing amino acids: an overview”. The Journal of Nutrition 136 (6 Suppl): 1636S–1640S. PMID 16702333.

Chishty M, Reichel A, Abbott NJ, Begley DJ. “S-adenosylmethionine is substrate for carrier mediated transport at the blood-brain barrier in vitro.” Brain Res. 2002 Jun 28;942(1-2):46-50. PMID: 12031851

Jeffrey T. Cole, Christina M. Mitala, Suhali Kundu, Ajay Verma, Jaclynn A. Elkind, Itzhak Nissim,and Akiva S. Cohena, “Dietary branched chain amino acids ameliorate injury-induced cognitive impairment”,.Proc Natl Acad Sci U S A. 2010 January 5; 107(1): 366–371. Published online 2009 December 29. doi: 10.1073/pnas.0910280107 PMCID: PMC2806733

Erlich S, Alexandrovich A, Shohami E, Pinkas-Kramarski R. “Rapamycin is a neuroprotective treatment for traumatic brain injury.” Neurobiol Dis. 2007 Apr;26(1):86-93. Epub 2007 Jan 31.  PMID: 17270455

Faden AI, Labroo VM, Cohen LA. “Imidazole-substituted analogues of TRH limit behavioral deficits after experimental brain trauma.” J Neurotrauma. 1993 Summer;10(2):101-8.  PMID: 8411214

Gidday JM, Beetsch JW, Park TS. “Endogenous glutathione protects cerebral endothelial cells from traumatic injury.”  J Neurotrauma. 1999 Jan;16(1):27-36. PMID: 9989464

Instituteof Medicine committee report, Nutrition and Traumatic Brain Injury; Improving Acute and Subacute Health Outcomes in Military Personnel.  April 20, 2011.  http://www.nap.edu/openbook.php?record_id=13121&page=1

Kim JH, Lee YW, Park KA, Lee WT, Lee JE. “Agmatine attenuates brain edema through reducing the expression of aquaporin-1 after cerebral ischemia”, J Cereb Blood Flow Metab. 2010 May;30(5):943-9. Epub 2009 Dec 23. PMID: 20029450

Krusong K, Ercan-Sencicek AG, Xu M, Ohtsu H, Anderson GM, State MW, Pittenger C. “High levels of histidine decarboxylase in the striatum of mice and rats.” Neurosci Lett. 2011 May 16;495(2):110-4. Epub 2011 Apr 1. PMID: 21440039

Penedo LA, Oliveira-Silva P, Gonzalez EM, Maciel R, Jurgilas PB, Melibeu Ada C, Campello-Costa P, Serfaty CA. “Nutritional tryptophan restriction impairs plasticity of retinotectal axons during the critical period.”Exp Neurol. 2009 May;217(1):108-15. Epub 2009 Feb 10. PMID: 19416666

Sahley BJ (2002), “The Anxiety Epidemic”, ISBN: 1-889391-23-9

Savelieva KV, Zhao S, Pogorelov VM et al. (2008). Bartolomucci, Alessandro. ed. “Genetic disruption of both tryptophan hydroxylase genes dramatically reduces serotonin and affects behavior in models sensitive to antidepressants”. PloS ONE 3 (10): e3301. Bibcode 2008PLoSO…3.3301S. DOI:10.1371/journal.pone.0003301. PMC 2565062. PMID 18923670.

Sharma HS, Winkler T, Stålberg E, Mohanty S, Westman J. “p-Chlorophenylalanine, an inhibitor of serotonin synthesis reduces blood-brain barrier permeability, cerebral blood flow, edema formation and cell injury following trauma to the rat brain.” Acta Neurochir Suppl. 2000;76:91-5.  PMID: 11450100

Shemin D, Rittenberg D (1 December 1946). “The biological utilization of glycine for the synthesis of the protoporphyrin of hemoglobin”. Journal of Biological Chemistry 166 (2): 621–5. PMID 20276176.

Wardlaw, Gordon M. and Smith, Anne M., “Contemporary Nutrition”, 2013, ISBN 978-0-07-340254-3, McGraw-Hill.

Wolosker H, Dumin E, Balan L, Foltyn VN (July 2008). “D-amino acids in the brain: D-serine in neurotransmission and neurodegeneration”. The FEBS Journal 275 (14): 3514–26. DOI:10.1111/j.1742-4658.2008.06515.x. PMID 18564180.

Zhang TL, Zhao YW, Liu XY, Ding SJ. “Effects of L-lysine monohydrochloride on insulin and blood glucose levels in spinal cord injured rats”. Chin Med J (Engl). 2010 Mar 20;123(6):722-5.  PMI

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