Concussion Brain Food High School Athlete Dietary Survey





Background:  The Emergency Department is an opportune place to initiate treatment of traumatic brain injury (TBI). New nutrition oriented therapies are emerging in military operations to treat traumatic brain injury however, civilian medical centers have been less progressive in evaluating and adopting these therapies.

Purpose: In the civilian environment athletes are at high risk of mild traumatic brain injury (mTBI).  This study was designed to evaluate the dietary intake of nutrients important to brain function in the diets of athletic high school students.

Methods: A dietary survey was prepared to measure intake of foods containing omega-3 fatty acids, B-complex vitamins, amino acids (protein) and vitamin C which support brain tissue and neurotransmitter production. 71 students completed the survey.

Results: Athletic high school students report a diet averaging .67 g/day of omega-3 fatty acids. Given the recommended daily allowance (RDA) of .90 g/day for a 14-18 y/o sedentary female or male, this intake of omega-3 fatty acids appears inadequate.

Athletic high school students report a diet averaging a thiamin (B1) intake of .65 mg/day whereas the RDA for a sedentary 14-18 y/o and adult female is 1.0 mg/day and the RDA for a sedentary 14-18 y/o and adult male is 1.2 mg/day.  Thiamin (B1)  intake does not appear adequate for these athletes.

Riboflavin levels of 1.0 mg/day and 1.3 mg/day for sedentary females and males, respectively have been established.  Student athletes surveyed report  a diet averaging 1.56 mg/day.  These intake levels may be adequate for high school athletes.

Niacin levels of 14.0 mg/day and 16.0 mg/day for sedentary females and males, respectively have been established.  Student athletes surveyed were receiving an average daily intake of 14.21 mg/day.  These niacin intake levels may be adequate for the athletes.

Athletic high school students report a 3.43 mg/day intake of pantothenic acid (B5).  The RDA for sedentary females and males is 5.0 mg/day.  The athletes surveyed have an inadequate intake of pantothenic acid (B5).

Pyridoxal Phosphate (B6) levels of 1.2 mg/day and 1.3 mg/day have been established for sedentary females and males, respectively.  Our athletes average intake was 1.61 mg/day.  These pyridoxal phosphate levels may be adequate.

Athletic high school student intake of folate (B9) was an average of 313.02 mg/day. Established RDAs for sedentary females and males is 400 mg/day. The folate (B9) intake of the athletes surveyed is inadequate.

Cobalamin (B12) levels of 2.4 ug/day have been established. Surveyed athletes averaged 4.73ug/day.  Surveyed athlete’s intake appears more than adequate.

Athletic high school students report a diet averaging 57.5 g/day intake of protein which meets the RDA of a sedentary 14-18 y/o and adult female (46 g/day) and sedentary male (52 g/day).  However, an RDA for protein has been established requiring 67.5 g/day for an athletic adult female and 83.5 g/day for an athletic adult male. The current protein (amino acid) intake for the athletic high school student surveyed may not be adequate.  Additionally, a diet or supplement must contain all 20 amino acids concurrently for protein synthesis to occur. Protein synthesis stops when one amino acid is missing.

Conclusions:  Omega-3 intake in the student athletes surveyed appears inadequate.  The brain would manufacture brain tissue with omega-6 fatty acids, but without the additional double bonds present in the omega-3 fatty acids, the tissue would fall apart when concussed.

Thiamin (B1), pantothenic acid (B5), and folate (B9) intake does not appear adequate to meet sedentary high school student needs.  Without adequate thiamin, oxygen transport and the synthesis of myelin would diminish.  With a diet low in thiamin and pantothenic acid, acetylcholine neurotransmitter levels would fall.  DNA repair/synthesis and red blood cell production would be impaired given low folate levels.

Riboflavin (B2), niacin (B3), pyridoxal phosphate (B6) and cobalamin (B12) levels may be adequate in athletic high school students.  However, only 50-90% of B-complex vitamins are absorbed in the gastrointestinal system, thus actual availability levels may be less (Wardlaw & Smith, 2013)

The Food and Nutrition Board has established protein RDAs for sedentary individuals and specifically for athletes. The amino acid intake levels of the athletes surveyed do meet the sedentary RDA values, however intake does not meet the athletic RDA levels.  Interestingly the sedentary RDA protein levels have been increased by 50% for athletes.  However, increased RDA omega-3 and vitamin B-complex levels have not been established for athletes. Vitamin B complex provides the cofactors to metabolize amino acids.  Are sedentary levels of B complex and omega-3s sufficient in an athlete or could amino acid metabolites be trapped in athletes due to the lack of vitamin B co-factors?

Vitamin C  intake appears adequate to promote adrenal function and thus neurotransmitter production, although athletic RDAs have not been established.

If physical stress, mental stress, or brain injury requires additional omega-3 fatty acids, B-complex vitamins, and amino acids to promote healing, sufficient nutrients would not be available in the average diet of the athletes surveyed.

This survey is a patient dietary intake survey where the patients have been asked to recall intake over a typical week’s time.  Nutrient levels have been assigned from Nutrition Data given the food, multiplied by the quantity consumed, and computed for an average daily consumption. Thus, this survey provides an estimate of average daily brain food nutrient intake.  Laboratory measured patient blood/urine nutrient levels would be of greater accuracy and important to pursue in future research efforts.

Introduction to Brain Biochemistry and Nutrition:

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 made in the adrenal glands with help from vitamin C.  Neurotransmitters are critical to brain function and communication throughout the body.


Study Design: This survey listed common foods in each of the brain food nutrient categories of omega-3 fatty acids, B complex vitamins, proteins, and vitamin C, and questioned the students as to their weekly consumption of each food type.

Study Setting and Population:  A small high school athletics program participated in this survey.  The athletic trainer performs baseline, concussive, return to play neurocognitive testing of all athletes.  The school host a variety of high school sports, with the football and soccer programs producing 15-25 concussions per year ranging from mild to more severe.

Instrument Development and Data Collection: Surveys were distributed to high school students at their annual physical and athletics team sign up fair.  The surveys took approximately 5 minutes to complete and were turned in on site.

Measures and Statistical Analysis

We asked respondents to numerically estimate the number of times each food was consumed during a typical week.  Respondents were asked several other general questions about sports, homework hours and concussion history.

A numerical nutrient level was assessed for each food.  This value was multiplied by the number of times the food was consumed during the week and divided by the a 7 day week to determine an average nutrient consumption per food per day.


This Brain Food Survey has been developed to measure an average athletic high school student’s intake of omega-3 fatty acids, B-complex vitamins, amino acids and vitamin C.  It is expected that at least nutrient levels in accordance with the Recommended Daily Allowances (RDAs) are required for a healthy brain capable of healing a concussion (mild TBI) injury.

According to our survey the athletic high school student’s average daily intake of omega-3 fatty acids is  .67 g/day. Given the recommended daily allowance (RDA) of .90 g/day for a 14-18 y/o sedentary female or male, this intake is not adequate.

Athletic high school student intake of thiamin (B1) is .65 mg/day whereas the RDA for a sedentary, female, 14-18 y/o and adult is 1.0 mg/day and the RDA for a sedentary, male, 14-18 y/o and adult is 1.2 mg/day.  Thiamin intake may not be adequate.

Riboflavin levels of 1.0 mg/day and 1.3 mg/day for sedentary females and males, respectively have been established.  Our student athletes were receiving an average of 1.56 mg/day.  Riboflavin consumption appears adequate.

Niacin levels of 14.0 mg/day and 16.0 mg/day for sedentary females and males, respectively have been established.  Our student athletes were receiving an average of 14.21 mg/day.  These intake levels may be adequate.

Athletic high school student intake of pantothenic acid (B5) was an average of 3.43 mg/day.  The RDA for sedentary females and males is 5.0 mg/day.  Our athletes have an inadequate intake or pantothenic acid.

Pyridoxal Phosphate (B6) levels of 1.2 mg/day and 1.3 mg/day have been established for sedentary females and males, respectively.  Our athletes average intake was 1.61 mg/day.  These levels may be adequate.

Athletic high school student intake of folate (B9) was an average of 313.02 mg/day and established RDAs for sedentary females and males is 400mg/day. Our athletes’ intake is inadequate.

Cobalamin (B12) RDA levels of 2.4 ug/day have been established. Our athletes averaged 4.73ug/day.  Our athlete’s intake appears sufficient. However, gastrointestinal disorders may decrease secretion of intrinsic factor thereby decreasing colalbumin absorption.

The athletic high school students’ riboflavin, niacin, pyridoxial, and cobalamin appear adequate given the sedentary RDAs available.  However, vitamin B complex nutrients are said to be absorbed at a rate of only 50-90% and the prevalence of wheat lectins/gluten and other GI disturbances, the actual intake of these nutrients may be reduced.

The athletic high school student intake of an average of 57.5 g/day of protein meets the RDA of a sedentary 14-18 y/o and sedentary adult female (46 g/day) and sedentary male (52 g/day).  However, RDAs for protein have been established for an athletic adult female who requires 67.5 g/day and athletic adult male who requires 83.5 g/day. Current protein intake of the athletes surveyed may not be adequate.  All 20 amino acids must be consumed concurrently in the diet to enable protein synthesis. Missing amino acids will cause protein synthesis to stop.

Athletic high school student intake of vitamin C, ascorbic acid, was an average of 122mg/day.  Sedentary high school female student’s RDA is 65mg/day and male’s 75 mg/day.  Sedentary female adult RDA is 75mg/day and male 90mg/day.  Vitamin C intake appears more than adequate.

Athletic high school student intake of omega-3-fatty acids, thiamin, pantothenic acid, folate and amino acids are inadequate to sustain general sedentary nutrition and these low nutrients levels would appear to strain the body during increased physical stress, academic or social mental stress, and be most profoundly apparent during the body’s attempt to heal concussion.


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,, 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).

The Composition of Brain Tissue:

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.

In examining 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 brown structures on a brain section are called  “gray matter.”  These are decision-making nuclei made from proteins composed of amino acid building blocksAmino acids require B-complex vitamins to metabolizeProteins and amino acids formulate all structures, most noticeable of which are neurotransmitters.  Neurotransmitters are critical to brain function and communication throughout the body.  These neurotransmitters are produced in the adrenal glands which depend heavily on vitamin C and the amino acid methionine.

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 is found in foods such as walnuts, microalgae, microplants, cod, salmon, mackerel, sardines, hake, caviar, herring, oysters, organ meats (liver), grass fed and finished beef, and fish oil or algae supplementsFish receive DHA from ocean phytoplankton (microalgae or microplants).  Cattle produce ? make? DHA from grass.  However, as we increasingly draw our food from farm-raised fish and grain-raised cattle lacking grass to produce DHA, 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 the carbon chain.  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, DHA increases 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 that were subject to TBI and 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, 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, (Hagiwara H,, but few human studies have been conducted using DHA as prophylaxis for TBI.  In 2006, high doses of DHA and hyperbaric oxygen treatment were used by Dr. Julian Bailes to treat the sole survivor of the West Virginia mining disaster 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 perseverance, 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).

Eicosapentanoic Acid (EPA 20:5n-3?) is another essential fatty acid.  EPA is important in the synthesis of PGE (explain) and controls the thromboxine and leukotrine levels.  EPA is important in the metabolism of DHA.  Essential fatty acids (EFA) are among the most crucial molecules that determine the brain’s integrity and ability to perform. EFA are involved in the synthesis and functions of brain neurotransmitters.  Neuronal membranes contain phospholipid pools that are the reservoirs for the synthesis of specific lipid messengers on neuronal stimulation or injury.   (PMID 20329590). DHA and EPA maybe obtained through diet or supplements.

The textbook “Contemporary Nutrition” written by  Gordon M. Wardlaw and Anne M. Smith in 2013 tells us that EPA and DHA are only slowly synthesized in the brain from alpha linoleic acid but 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 approximately 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 on a daily basis regulates intake by the dryness/moistness of the skin.  In drier climates, she finds this daily intake amount must be doubled to maintain skin moisture. Mercury consumption in fish oil is a serious risk and mercury free alternatives should be explored.  Many manufacturers are now producing fish oil products which are molecularly distilled.

B Complex Vitamins:

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. 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.

Thiamine (B1) is required for oxygen to be transported in red blood cells (Combs GF Jr, et al., 2008), production of the neurotransmitter acetylcholine (Butterworth RF, et al., 2006), and synthesis of the myelin coating surrounding nerve cells (Butterworth RF, et al., 2006). High school female RDA  of thiamine is 1.0 mg/day and male 1.2 mg/day. Adult thiamine RDA is 1.1 – 1.2 mg/day, Daily Value 1.5 mg/day, and no upper limit has been set. Thiamin is water soluble and rapidly lost in urine. Alcohol consumption reduces thiamin levels (Wardlaw,, 2013).

Riboflavin (B2) is a component in all flavoproteins and  red blood cells (erythrocytes) and has been know to reduce TBI lesions, edema, and improve TBI outcome (Hoane MR, et al., 2005). High school female riboflavin RDA 1.0 mg/day, male 1.3 mg/day.  Adult riboflavin RDA is 1.1 – 1.3 mg/day, Daily Value 1.7 mg/day, no upper limit set.  Alcohol consumption reduces riboflavin levels (Wardlaw,, 2013)

Niacin (B3) is involved in DNA repair, cholesterol, and energy production. It helps produce neurotransmitters in the adrenal gland.  Niacin reduces TBI lesion size and improves sensory, motor, cognitive, and behavioral recovery (Voner Haar C, 2011).  High school female niacin RDA 14 mg/day, male 16 mg/day.  Adult niacin 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,, 2013)

Pantothenic Acid (B5) is  involved with 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). This vitamin is also involved with dopamine and GABA neurotransmitter production, and with the production of phospholipids for the myelin sheath.  High school RDA pyridoxal phosphate 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) is required to synthesize, repair, and methylate DNA, provides neuroprotection in TBI (Naim MY, et al., 2010), is important in rapid cell division and growth and the production of healthy red blood cells which prevents anemia. Folate forms cell membrane phospholipids and receptors (Karakula H, et al.,2009) (Surtees R, 1998), prevents nerve damage and neural tube defects during development and is 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,, 2013).  This alcoholism – folate – neural tube defects is critically important to women expecting to conceive.

Cobalamin (B12) is involved in blood formation, critical to DNA synthesis through folate regeneration, and important for the formation of cell membrane phospholipids and receptors (Karakula H, et al., 2009) (Surtees R, 1998). Cobalamin supplementation partially resolved cognitive deficits and myelin imaging abnormalities (Chatterjee A,, 1996) (Jongen JC, et al., 2001) and improved cerebral and cognitive functions  (Bourre JM, 2006). This vitamin is required for myelin synthesis (Hall CA, 1990) (van Rensburg SJ, et al, 2006) (Guettat L, et al., 1997) and promotes nerve regeneration (Okada K, et al., 2010). High school RDA colbalamin 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).

Vitamin B is a complex  of B-1-thiamine, B-2 riboflavin, B-3 niacin (niacinamide), B-6 pyridoxine, B12-cyanocobalamin, pantothenic acid, biotin, PABA, folic acid, choline and inositol.  All B vitamins are water soluble and they are not stored.  They must be supplied in sufficient amounts at all times.  This supply may be inadequate under stress. (Sahley p 94).

Vitamin B provides cofactors for reactions within the body particularly amino acid reactions.  B vitamin cofactors initiate the transfer of electrons, plus methyl, carbon, amino, carboxyl, acetyl, acyl,  and formyl groups.

The RDAs are Recommended Daily Allowances taken from the Dietary Reference Intakes, Food and Nutrition Board, Institute of Medicine, National Academics. The vitamin B complex nutrients surveyed above are absorbed at a rate of 50-90% (Wardlaw & Smith, 2013).  Due to the prevalence of gastrointestinal disorders present in the population, even the nutrients that appear to be consumed at adequate levels may not be sufficient.

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 must be present for protein synthesis.

Alanine is the precursor of neurotransmitter dopamine (Coxon KM, et al., 2005).

Arginine, through agmantine, 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 is important for calcium ion binding; may reduce blood glucose levels in the injured spinal cord reducing neurological impairment (Zhang TL, et al., 2010).

Glutathione is critical to relieve oxidative stress in cells.

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

Histidine is used throughout the brain, this amino acid improves TBI outcome (Faden AI, et al., 1993) (Krusong K, et al., 2011).

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

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

Phenylalanine produces chlorophenylalanine (CPA) which slowed the breakdown of the blood-brain barrier permeability, brain edema and blood flow and 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 is a major component of brain tissue and muscle (Brosnan JT, 2006).

Threonine is a component of the serine/threonine kinase and is neuroprotective following traumatic brain injury (Erlich S, et al.,2007).

Tryptophan is a 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 is a precursor of the neurotransmitter dopamine, norepinephrine, epinephrine.

Amino Acids essential amino acids are arginine, histidine, isoleucine, leucine, lysine, methionine, phyenylalanine, threonine, tryptophan, and valine.  These play a vital role in the brain’s function (Sahley p23).  Under prolonged stress or illness the body is unable to produce sufficient required non-essential amino acids  (Sahley p 22).   Amino acids are monomers polymerizing to produce proteins.  A multistep process requiring proteins as substrate and translation/transcription factors results in production of DNA and RNA.  Proteins also form neurotransmitters, enzymes and are components of cell membranes participating in cell signaling.

Trauma damages DNA and RNA, and depletes neurotransmitters.  Neurological dysfunction caused by traumatic brain injury results in profound changes in net synaptic efficacy, leading to impaired cognition.  The limbic hippocampus, a brain structure implicated in higher learning and memory, is often damaged in TBI.  Significant reductions are seen in the concentration of branched chain amino acids (BCAAs).  BCAAs  (leucine, isoleucine, alanine) are key amino acids involved in de novo glutamate synthesis.  Dietary consumption of BCAAs restored hippocampal BCAA concentrations to normal, reversed injury-induced shifts in net synaptic efficacy, and left to reinstatement of cognitive performance after concussive brain injury.   (Cole paper, Univ of Penn Dietary AA ameliorate cognitive impairment).

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 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.

A variety of single drugs have failed clinical trials to treat TBI, suggesting a role for drug combinations. Drug combinations acting synergistically often provide the greatest combination of potency and safety. (PMID 20824218) Recent preclinical studies suggest that neurorestorative strategies that promote neurogenesis, and synaptogenesis provide promising opportunities for treatment of TBI. (PMID 21155204).

The IOM committee’s report, Nutrition and Traumatic Brain Injury: Improving Acute and Subacute Health Outcomes in Military Personnel.  April 20, 2011.  Given the complexity of TBI and the current gaps in scientific knowledge, the committee could identify only one promising solution that can immediately improve treatment efforts: early feeding. Feeding protocols should be standardized to ensure the delivery of adequate levels of energy and protein to patients with severe TBI, and hospital intensive care units should include these protocols in their critical care guidelines. Specifically, the protocols should require providing, within the first 24 hours, a level of nutrition that represents more than 50 percent of the injured person’s total energy expenditure and provides 1 to 1.5 grams of protein per kilogram of body weight. This nutrition level should be continued for two weeks. Such nutritional intervention is likely to limit the person’s inflammatory response, which typically is at its peak during the first two weeks after an injury, and thereby improve the ultimate health outcome. Research has shown that feeding the severely injured soon after an injury is known to help in reducing mortality. (IOM report)

Based on findings about the physiological actions of nutrients and their effectiveness and safety from studies on animals and humans, the following nutritional interventions were identified as holding the most promise for improving TBI outcomes: the provision of or treatment with choline, creatine, n-3 fatty acids, and zinc. DOD should prioritize research on these interventions. (IOM report).


Athletic high school student intake of omega-3-fatty acids, thiamin, pantothenic acid, folate and amino acids are inadequate to sustain general sedentary nutrition and these low nutrients levels would appear to strain the body during increased physical stress, academic or social mental stress, and be most profoundly apparent during the body’s attempt to heal concussion.

Research to determine RDAs under physical stress, mental stress, athletics or injury would be important for neurological health now and in the future.  In addition, given our highly processed food, modified crops and farm raised fish and stockyard raised cattle, the average diet may not be providing nutrient levels anticipated.  There may also be interference in the diet caused by enhanced lectins and gluten found in grains attacking our immune systems.  The impact of these food modifications will be important to continue to assess.

To date our typical brain injury therapy has been anti-inflammatories.  Awareness of the basic nutrients required for a healthy brain are not generally well known to the medical, dietary, or public. Education as to the roles of these nutrients is critical to bring about a healthier populace. The brain injury brought on by concussion, disease, mental and physical stress may well be eliminated or repaired should adequate nutrients be provided to enable the amazing brain to make the necessary repairs.

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” ( 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”.

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.

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

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,

Sears, B (2011). “The fallacy of using DHA alone for brain trauma.”

University of Maryland Medical System and University of Maryland Medical School:  Omega-3 fatty acids:

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.

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

Institute of Medicine committee report, Nutrition and Traumatic Brain Injury; Improving Acute and Subacute Health Outcomes in Military Personnel.  April 20, 2011.

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.

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.

Mt Kilamanjaro at sunrise as seen from Mt. Meru, Tanzania Africa.

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