The "Concussion Doctor" Speaks.
In it, he played Bennet Omalu, M.D., a pathologist who fought to expose the extreme and potentially life-threatening dangers of a severe form of brain injury called chronic traumatic encephalopathy (CTE).
The movie was based on the true story of this medical hero who took on the National Football League and the medical establishment, which sought to discredit Dr. Omalu's findings and destroy his career.
Dr. Omalu's work eventually forced the NFL to implement changes aimed at helping protect players from long-term brain damage.
But there's more to this story.
While the toll among professional athletes is bad enough, it's dwarfed by the burden that millions of nonprofessional athletes--especially children and adolescents--will carry for the rest of their lives after suffering sports-related head injuries.
In his book, Truth Doesn't Have a Side, Dr. Omalu takes on this epidemic of traumatic brain injury (TBI) in the United States.
Even mild TBIs can cause headaches, fatigue, dizziness, sleep problems, and mood disorders. (1) It can also cause serious psychiatric disorders like depression, aggression, and increased risk of suicide. (2)
Despite the dangers--and the prevalence--mainstream medicine doesn't know much about the condition, and certainly doesn't have any ways to effectively treat it.
Fortunately, a number of innovative doctors are working to revolutionize the treatment of traumatic brain injury.
The NFL and Traumatic Brain Injury
In 2005, the prestigious journal Neurosurgery published Dr. Bennet Omalu's blockbuster report detailing his findings from the autopsy of Mike Webster. (3) This former player for the Pittsburgh Steelers died suddenly at age 50 in 2002 after struggling for years with progressive neurological symptoms.
After conducting the autopsy, Dr. Omalu concluded that Mike Webster suffered from a neurodegenerative disease as a result of repeated blows to the head. This condition, chronic traumatic encephalopathy, or CTE, is characterized by the accumulation of tau proteins in the brain, similar to Alzheimer's disease. (4)
In his conclusion, Dr. Omalu wrote, "This case highlights potential long-term neurodegenerative outcomes in retired professional National Football League players subjected to repeated mild traumatic brain injury." (3)
The backlash against Dr. Omalu was intense and instant. Worried about protecting its profits, the NFL immediately launched an organized and well-funded campaign to destroy him. First, the league pushed for retraction of his paper.
"To get a retraction, you need to successfully prove the researcher engaged in fraudulent behavior and generated false data," Dr. Omalu said. "They were pretty much labeling me a criminal."
To help bolster its case, Dr. Omalu said the NFL made a substantial grant to Boston University to fund research that would discredit him. At the same time, the medical establishment mobilized against Dr. Omalu and his research.
"They knew what they were doing," he said. "If they had succeeded, that would have been the end of me. I would have lost my license and my career would be over. But I defended myself and presented my data to a committee at the journal. A ruling was made that I had done nothing wrong."
Unfortunately for Dr. Omalu, his trials weren't over yet. Once his findings had been accepted and CTE described as a legitimate issue, the medical establishment launched a furious assault against him to discredit him personally and professionally. He was ostracized at every level of his profession, denied funding to continue his research, and he avoided conferences for fear of professional retaliation.
"I had to spend my own money because nobody would give me any to fund my research," he said. "They even enlisted the National Institutes of Health. Usually if someone introduces something new, the NIH will invite them to talk and see what they need. That didn't happen with me."
In fact, the narrative was "being rewritten" as the truth of his findings gained traction, and Dr. Omalu found himself being written out of the story.
"I was very confused," he said. "Why would they want to remove me? Other doctors were going around saying they were the first to publish this. In 2016, the NIH said it was the first to establish a diagnostic criteria for CTE. What about me? It was very difficult. I struggled with depression and contemplated suicide."
His enemies in the NFL and medical establishment stooped to the worst kind of smear campaign, he said.
"They used xenophobia against me because I'm a black guy and a foreigner," he said. "I wasn't a big name. I didn't have a big lab. I was working from my apartment and paying for my own research. But I believed the truth would prevail. It just took a foreigner from Nigeria to prove this was happening in America's biggest sport."
Ultimately, Dr. Omalu took his story to Hollywood, the only institution in America he thought was powerful enough to get the truth out about CTE and his story. "Will Smith didn't want to do the movie at first," he said. "But he did it to make the truth known. I'm deeply grateful to Hollywood, but it's still affecting me. I'm still being marginalized."
In 2016, Boston University rescinded its plans to give Dr. Omalu the prestigious Beyond Health Award. The school's reason? An interview Dr. Omalu gave in which he cited a potential conflict of interest at the school's Concussion Legacy Foundation and World Wrestling Entertainment, Inc., which is also struggling with the CTE question thanks to Dr. Omalu's pioneering work.
There's no way to know how many NFL players suffer from CTE because it can only be diagnosed post-mortem, but there's no debate it's widespread. The list of professional football players who have committed suicide or died of other causes and had CTE diagnosed at autopsy includes Andre Waters (2006), Junior Seau (2012), Ken Stabler (2016), Dave Duerson (2011), Ray Easterling (2012), and dozens more--including at least seven members of the Pro Football Hall of Fame. (5)
In fact, according to a 2017 study published in the Journal of the American Medical Association, the number of NFL players who suffer from CTE could be as high as 99%. The blockbuster study examined the donated brains of 111 NFL players and found evidence of mild to severe CTE in 110. It was found in every position, from placekicker to quarterback to linebacker. (6)
This means that playing in the NFL is, in terms of this specific affliction, more dangerous than fighting in Iraq, where tens of thousands of soldiers suffered mild traumatic brain injury (TBI).
WHAT YOU NEED TO KNOW
The Epidemic of Traumatic Brain Injury
* Thanks in large part to the efforts of Dr. Bennet Omalu, unwarranted neglect of the epidemic of severe brain injuries has finally received recognition and wide exposure in the media.
* Traumatic brain injury (TBI) and chronic traumatic encephalopathy (CTE), related to both professional and amateur sports players, is now being more frequently diagnosed, but medical understanding of the mechanisms involved in these injuries is lacking. Experts believe this lack of understanding has likely led to millions of undiagnosed cases and sufferers who therefore don't receive the treatment they need.
* TBI symptoms include fatigue, dizziness, sleep disorders, headaches, and mood disturbances. Changes in personality are sometimes observed, as well as behavioral and cognitive difficulties. Compared to the general population, patients with chronic traumatic encephalopathy are much more likely to commit suicide.
* Innovative treatments are being developed to help relieve the effects of chronic traumatic encephalopathy. These include the use of certain nutrients and hormone replacement therapy.
Why Children are More at Risk
While the link between chronic traumatic encephalopathy and professional football is new, the connection between sports and brain injury has been known for decades. (7) We are all familiar with famous boxer Muhammad Ali, who was diagnosed with Parkinson's disease in 1984 and publicly struggled with it for the rest of his life. (8)
But the risk is especially great for children and adolescents involved in sports.
A survey published in the journal Pediatrics estimated that 1.1 to 1.9 million children and adolescents under the age of 18 sustain a sports-related concussion every year. (9) And according to the American Association of Neurological Surgeons (AANS), sports-related injuries contribute to about 21% of all TBIs reported in American children and adolescents. (10)
In fact, TBI is the leading cause of sports-related fatality. (10)
As far back as 1957, the American Academy of Pediatrics issued a position paper warning that children should not engage in football, boxing, or wrestling out of a fear of head injury. (11) Almost 20 years later, the Lancet published an editorial saying it was "foolhardy" for people to engage in sports that have a risk of brain trauma. (12)
And now, with Dr. Omalu's new book, Truth Doesn't Have a Side, he is sounding the alarm once again.
"I don't think any child under 18 should play a high-impact, high-contact sport," he told Life Extension[R]. "That includes football, rugby, boxing, hockey, mixed-martial arts, and wrestling. The most important part of your life is your intellect, your intuition. If a game is meant to uplift your state of well-being, but actually robs you of your well-being, that is not a game. That is not a sport."
Many people might not realize that you don't have to suffer from a concussion to experience a traumatic brain injury.
"The focus on concussions alone is ridiculous," he says. "Concussion is a disease caused by TBI. The more important issue is subconcussive, repetitive injury. Every blow to the head causes brain injury. Every blow."
The bottom line, according to Dr. Omalu, is that there is no safe level of head trauma.
SHORT- AND LONG-TERM IMPACT OF TBI
A traumatic brain injury (TBI) is defined as an injury caused by brain trauma, whether it's from a blow to the head or from a piercing injury. They are categorized as mild, moderate, or severe on the Glasgow Coma Scale.
Concussions are a type of mild traumatic brain injury that results in symptoms, usually temporary, that may include headaches and confusion. (67,68) These can be caused by blows to the head such as in sports, falling, or accidents, or in the case of tens of thousands of soldiers in Iraq, exposure to blast waves from ordnance.
Symptoms of a mild traumatic brain injury may include brief loss of consciousness, headache, nausea, vomiting, and fatigue. (69) Most victims begin to recover from the acute injury within 24 hours while others experience persistent symptoms. And while some symptoms may occur soon after the injury, others can first appear weeks later. (70,71) While a CT scan might show localized swelling after a mild traumatic brain injury, many concussion sufferers show no abnormalities on MRI or CT scans. (72,73)
Unfortunately, this is only part of the picture. Once the acute phase ends, there is a chronic phase to the post-injury period that can last indefinitely. According to the American Academy of Family Physicians, up to 20% of people who suffer from mild traumatic brain injury will exhibit "persistent physical, cognitive, or behavioral symptoms" for years. These physical symptoms can include headaches, dizziness, nausea, and problems with coordination, sleep, vision, and hearing. (74)
Traumatic brain injury has been linked to a grim litany of psychiatric disorders, including personality changes, anxiety, aggression, depression, increased risk of suicide, and psychosis. (75)
The Search for Answers
Despite intense research into better understanding the neurobiological effects of mild TBI and concussion, there is no approved biomarker test used to diagnose it--and no consensus about exactly how mild TBI causes the long-term brain damage and cognitive deficits seen in so many soldiers and athletes. (13) This lack of agreement makes identification and treatment exponentially more difficult.
Most TBI cases are never reported, and few people get medical attention. Those who do are typically seen on an outpatient basis. (9)
Clearly, something has to change.
If there is a silver lining, it's that the increased focus on sports-related head trauma has spurred interest in novel approaches to limit the damage and help victims recover. There is no cure for CTE, but for the first time, innovative doctors are raising the hope of at least containing the damage.
DR. OMALU UNCOVERS FURTHER WRONGDOING
Dr. Bennet Omalu recently resigned from his position as chief medical examiner for San Joaquin County, California, due to what he sees as inappropriate police meddling in his work.
Dr. Omalu claims Sheriff-Coroner Steve Moore has "routinely" interfered with his investigations in an effort to protect police officers. He said the interference from the sheriff was so excessive that it nearly amounted to unlicensed medical practice.
In a statement given to the media, Dr. Omalu wrote that he had "observed long before this that the sheriff was using his political office as the coroner to influence the death investigation of persons who die while in custody or during arrest by the police."
Dr. Omalu's claims were backed up by his former assistant, forensic pathologist Dr. Susan Parson, who also resigned. Omalu and Parson have turned over detailed documents related to their allegations to county supervisors and the district attorney.
As one example of alleged misconduct, Dr. Omalu pointed to the case of a 26- year-old man who died after fighting with both police and civilians. Dr. Omalu ruled the death a homicide by blunt force trauma.
Afterward, he said, "The sheriff called me into his office and told me that he wanted to make it an accident since officers were involved. He said that I should amend my report and state that he died from the civilians and not the police officers."
In addition to numerous other cases, Dr. Omalu also cited a case from 2007 in which a man died during his arrest. "Information was intentionally withheld from me by the sheriff in order to mislead me from determining the case to be a homicide," he said. "The sheriff still went behind my back months later and changed the manner of death to an accident to minimize the seriousness of the case."
The San Joaquin County Medical Society has called on authorities to conduct a full investigation. The group's president, Dr. R. Grant Mellor, called the charges alarming and said, "Physician independence is paramount to avoid improper influence on the practice of medicine."
Hormones and Brain Injury
While mainstream medicine continues to struggle just to understand chronic traumatic encephalopathy, a number of physicians are looking to revolutionize treatment of traumatic brain injury.
Their focus is on hormone replacement therapy.
The National Institutes of Health database has dozens of studies showing the interaction between hormone status and TBI, yet virtually no mainstream doctors are using hormone therapy to address long-term damage caused by repeated TBI.
For example, there is a well-documented connection between reduced pituitary function and mild TBI. Specifically, studies have found hypopituitarism in 16% to 68% of patients. (14- 16) The more severe the injury, the worse the damage. (17)
The pituitary gland is responsible for producing critical hormones, including growth hormone and thyroid-stimulating hormone (TSH), as well as stimulating the production of sex hormones such estrogen and testosterone.
Because of the reduced pituitary function, patients with TBI often suffer from low growth-hormone levels and reduced production of gonadotropins (FSH and LH) and thyroid- stimulating hormone. (18,19) This reduction in growth hormone has been linked to increased abdominal obesity and metabolic alterations that are observable years after the original injury. (20)
Reductions in sex hormone levels after mild traumatic brain injury have been observed in mice. (21) In adolescent animals, repeated mild traumatic brain injury has been linked to hypogonadism in adulthood, as well as delayed puberty and erectile dysfunction. (22)
Research has shown that testosterone levels can be a good indicator of function in TBI patients. (23)
An animal study showed that treatment with estrogen reduced delayed swelling in the brain and intracranial pressure. (24) Estrogen has well-known neuroprotective and anti- inflammatory properties. (25,26)
These discoveries have prompted innovative physicians to investigate treating the long-term effects of TBI with hormone-replacement therapy. Among these groundbreaking doctors is Dr. Mark L. Gordon, who understood the importance of reduced pituitary function in this context years ago while treating a young man exhibiting signs of sports-induced brain injury. Today, he treats soldiers and athletes at his clinic, Millennium Health Centers, and hormone replacement is a vital part of his protocol.
Dr. Gordon's hormone-balancing approach relies on diligent testing, followed by physiological doses of vital hormones. The goal is to restore hormone levels to the middle of the optimal range, while carefully monitoring each patient for improvement. His results have earned him invitations to speak about hormone therapy at conferences on traumatic brain injury.
"For traumatic brain injury patients," Dr. Gordon told Life Extension, "any proper diagnosis and treatment protocol should begin with baseline testing of testosterone, growth hormone, thyroid, cortisol, insulin, and vitamin D."
AN OVERLOOKED MEDICAL HERO
This article does not fully relay the persecution and threats to his personal safety that Dr. Bennet Omalu endured by a medical establishment that was bought off by the NFL.
This article also does not fully describe the brilliant and painstaking research Dr. Omalu conducted that resulted in significant risk to his medical license, employment and immigration status.
History is laden with pioneers who defied conventional authority to advance medical science, often at great personal risk.
Identical situations exist today where effective means to save human lives exist, but are suppressed by a labyrinth of state and federal regulations that delay their introduction.
Reversing Brain Damage in Former Football Players
In 2014, William Faloon wrote an article in Life Extension Magazine[R] titled Outwitting our Aging Brain. It described how aging people suffer diminished brain blood-flow and what can be done to correct it.
In the box below is an excerpt from the article that describes a study showing reversal of traumatic brain injury clinical measures in response to a six-month treatment using specific nutrients:
Brain injuries are common in professional football players and severe cases sometimes make headline news stories. (27-29)
A clinical trial was conducted on 30 retired NFL players who demonstrated brain damage and cognitive impairment. They underwent baseline testing of cognitive function and brain perfusion as measured by SPECT imaging. (30)
Participants were encouraged to lose weight (if appropriate) and take the following supplements for six months:
Fish oil (30-33) 1,720 mg EPA 1,160 mg DHA Vinpocetine (34-39) 15 mg Ginkgo extract (40-45) 120 mg Alpha Lipoic Acid (46-49) 300 mg Acetyl L-Carnitine (48,50-52) 1,000 mg Huperzine A (53-55) 150 mcg N-acetyl-cysteine (56-60) 600 mg
The rationale behind using these nutrients was that they were individually shown to enhance blood flow, protect against free radicals, enhance brain-cell membrane structure, boost acetylcholine, enhance neuronal metabolic activity, and reduce chronic inflammatory markers.
After six months, the tests were repeated. There were statistically significant increases in scores of attention, memory, reasoning, information processing speed, and accuracy in these retired NFL players. The SPECT scan showed increased perfusion in areas throughout much of the brain. The researchers who conducted this trial concluded:
"This study demonstrates that cognitive and cerebral blood flow improvements are possible in this group with multiple interventions." (30)
Neurological trauma during football events accelerates brain aging. Life Extension members should be gratified to know that they have been taking most, if not all of the nutrients shown in this study to reverse brain damage in retired NFL players. This brain damage clearly linked hypoperfusion (reduced brain blood flow) with cognitive impairment.
The Gut-Brain Connection
Researchers are also beginning to understand the potential of using the "gut brain" to help treat TBI. (63) This is a layer of nerve cells in the digestive system known as the enteric nervous system (ENS) that is sometimes called the "second brain" or "gut brain."
The enteric nervous system functions independently of the central nervous system, secreting enzymes, immune system components, and hormones and relying on neurotransmitters identical to the ones used in the brain. (63,64)
Researchers used to think that communication between the central nervous system and the enteric nervous system was a one-way street, with the brain passing signals to the gut. (65) In more recent years, we have learned that communication is a two-way street and the ENS is in constant communication with the brain.
People with TBI show "structural damage to the GI tract." (66) This raises the possibility that treating the ENS/CNS axis by restoring normal gut flora, neurotransmitter function, and hormone production might reduce the risk of CTE and even help reduce symptoms of existing CTE.
When Dr. Bennet Omalu's autopsy report of Mike Webster was released in 2005, he was met with opposition from the National Football League (NFL)--but the league couldn't wish the issue away forever.
After years of denying the real-world trauma of players suffering from horrifying symptoms long after their playing days were over, the NFL finally admitted it had a concussion problem.
In late 2016, NFL Commissioner Roger Goodell announced the Play Smart Play Safe campaign, which included a $100 million pledge to study, prevent, and treat head injuries, the hiring of a Chief Medical Officer at the NFL, and increased focus on the league's concussion protocol. (76)
Football rule changes have been implemented in an effort to reduce blows to the head, but these will not eliminate the brain damage.
There has been an explosion in the recognition and diagnosis of TBI and CTE in recent years, both in professional sports and among the general population. Despite this wave of new cases, our understanding of the underlying mechanisms of traumatic brain injury and CTE remains primitive. As a result, millions of cases are likely not diagnosed and people don't receive proper treatment.
The effects of TBI can include headaches, fatigue, dizziness, sleep and mood disturbances, and cognitive, behavioral, and personality changes. The risk of suicide among people suffering from CTE caused by repeated mild TBIs is much higher than the normal population.
New research is helping us understand the link between TBI and disturbances in the endocrine system. Innovative doctors are using hormone replacement therapy, along with specific nutrients, to help reduce the effects of CTE and improve patients' quality of life.
If you have any questions on the scientific content of this article, please call a Life Extension[R] Wellness Specialist at 1-866-864-3027.
(1.) Laskowski RA, Creed JA, Raghupathi R. Frontiers in Neuroengineering Pathophysiology of Mild TBI: Implications for Altered Signaling Pathways. In: Kobeissy FH, ed. Brain Neurotrauma:
Molecular, Neuropsychological, and Rehabilitation Aspects. Boca Raton (FL): CRC Press/Taylor & Francis(c) 2015 by Taylor & Francis Group, LLC.; 2015.
(2.) Barnes SM, Walter KH, Chard KM. Does a history of mild traumatic brain injury increase suicide risk in veterans with PTSD? Rehabil Psychol. 2012;57(1):18-26.
(3.) Omalu BI, DeKosky ST, Minster RL, et al. Chronic traumatic encephalopathy in a National Football League player. Neurosurgery. 2005;57(1):128-34; discussion -34.
(4.) McKee AC, Cantu RC, Nowinski CJ, et al. Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury. J Neuropathol Exp Neurol. 2009;68(7):709-35.
(5.) Available at: https://www.nytimes.com/interactive/2016/02/03/sports/football/nfl-brain- disease-cte- concussions.html. (https://www.nytimes.com/interactive/2016/02/03/sports/football/nfl-brain- disease- cte-concussions.html) Accessed August 31, 2017.
(6.) Mez J, Daneshvar DH, Kiernan PT, et al. Clinicopathological Evaluation of Chronic Traumatic Encephalopathy in Players of American Football. Jama. 2017;318(4):360-70.
(7.) Omalu BI, DeKosky ST, Hamilton RL, et al. Chronic traumatic encephalopathy in a national football league player: part II. Neurosurgery. 2006;59(5):1086-92; discussion 92-3.
(8.) Available at: http://articles.latimes.com/1987-07-16/sports/sp- 4337_1_muhammad-ali. (http://articles.latimes.com/1987-07-16/sports/sp-4337_1_muhammad-ali) Accessed August 31, 2017.
(9.) Bryan MA, Rowhani-Rahbar A, Comstock RD, et al. Sports- and Recreation- Related Concussions in US Youth. Pediatrics. 2016;138(1).
(10.) Available at: http://www.aans.org/Patients/Neurosurgical-Conditions-and- Treatments/Sports-related- Head-Injury. (http://www.aans.org/Patients/Neurosurgical-Conditions-and- Treatments/Sports- related-Head-Injury) Accessed August 31,2017.
(11.) COMPETITIVE athletics: a statement of policy: report of the Committee on School Health, American Academy of Pediatrics. Pa Med J. 1957;60(5):627-9.
(12.) Brain Damage in Sport. The Lancet. 1976;307(7956):401-2.
(13.) Papa L, Edwards D, Ramia M. Frontiers in Neuroengineering Exploring Serum Biomarkers for Mild Traumatic Brain Injury. In: Kobeissy FH, ed. Brain Neurotrauma: Molecular, Neuropsychological, and Rehabilitation Aspects. Boca Raton (FL): CRC Press/Taylor & Francis (c) 2015 by Taylor & Francis Group, LLC.; 2015.
(14.) Klose M, Juul A, Poulsgaard L, et al. Prevalence and predictive factors of post-traumatic hypopituitarism. Clin Endocrinol (Oxf). 2007;67(2):193-201.
(15.) Salehi F, Kovacs K, Scheithauer BW, et al. Histologic study of the human pituitary gland in acute traumatic brain injury. Brain Inj. 2007;21(6):651-6.
(16.) Schneider HJ, Samann PG, Schneider M, et al. Pituitary imaging abnormalities in patients with and without hypopituitarism after traumatic brain injury. J Endocrinol Invest. 2007;30(4):Rc9-rc12.
(17.) Schneider HJ, Kreitschmann-Andermahr I, Ghigo E, et al. Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a systematic review. Jama. 2007;298(12):1429-38.
(18.) Dalwadi PP, Bhagwat NM, Tayde PS, et al. Pituitary dysfunction in traumatic brain injury: Is evaluation in the acute phase worthwhile? Indian J Endocrinol Metab. 2017;21(1):80-4.
(19.) Casano-Sancho P. Pituitary dysfunction after traumatic brain injury: are there definitive data in children? Arch Dis Child. 2017;102(6):572-7.
(20.) Giuliano S, Talarico S, Bruno L, et al. Growth hormone deficiency and hypopituitarism in adults after complicated mild traumatic brain injury. Endocrine. 2016.
(21.) Lopez-Rodriguez AB, Acaz-Fonseca E, Spezzano R, et al. Profiling Neuroactive Steroid Levels After Traumatic Brain Injury in Male Mice. Endocrinology. 2016;157(10):3983-93.
(22.) Greco T, Hovda DA, Prins ML. Adolescent TBI-induced hypopituitarism causes sexual dysfunction in adult male rats. Dev Neurobiol. 2015;75(2):193-202.
(23.) Young TP, Hoaglin HM, Burke DT. The role of serum testosterone and TBI in the in-patient rehabilitation setting. Brain Inj. 2007;21(6):645-9.
(24.) Kim H, Yu T, Cam-Etoz B, et al. Treatment of traumatic brain injury with 17alpha-ethinylestradiol-3-sulfate in a rat model. J Neurosurg. 2017;127(1):23-31.
(25.) Chakrabarti M, Das A, Samantaray S, et al. Molecular mechanisms of estrogen for neuroprotection in spinal cord injury and traumatic brain injury. Rev Neurosci. 2016;27(3):271- 81.
(26.) Brotfain E, Gruenbaum SE, Boyko M, et al. Neuroprotection by Estrogen and Progesterone in Traumatic Brain Injury and Spinal Cord Injury. Curr Neuropharmacol. 2016;14(6):641-53.
(27.) Casson IR, Viano DC, Powell JW, et al. Twelve years of national football league concussion data. Sports Health. 2010;2(6):471-83.
(28.) Available at: http://articles.latimes.com/2000/jun/09/sports/sp-39252. (http://articles.latimes.com/2000/jun/09/sports/sp-39252) Accessed December 19, 2017.
(29.) Available at: https://www.deseretnews.com/article/383760/CONCUSSIONS- FORCE-MERRIL- HOGE-TO-RETIRE.html. (https://www.deseretnews.com/article/383760/CONCUSSIONS- FORCE- MERRIL-HOGE-TO-RETIRE.html) Accessed December 19, 2017.
(30.) Amen DG, Wu JC, Taylor D, et al. Reversing brain damage in former NFL players: implications for traumatic brain injury and substance abuse rehabilitation. J Psychoactive Drugs. 2011;43(1):1-5.
(31.) Bazan NG, Musto AE, Knott EJ. Endogenous signaling by omega-3 docosahexaenoic acid-derived mediators sustains homeostatic synaptic and circuitry integrity. Mol Neurobiol. 2011;44(2):216-22.
(32.) Palacios-Pelaez R, Lukiw WJ, Bazan NG. Omega-3 essential fatty acids modulate initiation and progression of neurodegenerative disease. Mol Neurobiol. 2010;41(2-3):367-74.
(33.) Pu H, Guo Y, Zhang W, et al. Omega-3 polyunsaturated fatty acid supplementation improves neurologic recovery and attenuates white matter injury after experimental traumatic brain injury. J Cereb Blood Flow Metab. 2013;33(9):1474-84.
(34.) Santos MS, Duarte AI, Moreira PI, et al. Synaptosomal response to oxidative stress: effect of vinpocetine. Free Radic Res. 2000;32(1):57-66.
(35.) Gaal L, Molnar P. Effect of vinpocetine on noradrenergic neurons in rat locus coeruleus. Eur J Pharmacol. 1990;187(3):537-9.
(36.) Valikovics A. Investigation of the effect of vinpocetine on cerebral blood flow and cognitive functions. Ideggyogy Sz. 2007;60(7-8):301-10.
(37.) Vishnevskii AA, Korotkevich IG, Zhaparalieva Ch O. Membrane and functional effects of vinpocetine and tocopherol in rats with experimental cerebral ischemia. BiomedKhim. 2009;55(5):635-42.
(38.) Hadjiev D. Asymptomatic ischemic cerebrovascular disorders and neuroprotection with vinpocetine. Ideggyogy Sz. 2003;56(5-6):166-72.
(39.) Szilagyi G, Nagy Z, Balkay L, et al. Effects of vinpocetine on the redistribution of cerebral blood flow and glucose metabolism in chronic ischemic stroke patients: a PET study. J Neurol Sci. 2005;229-230:275-84.
(40.) Ahlemeyer B, Krieglstein J. Neuroprotective effects of Ginkgo biloba extract. Cell Mol Life Sci. 2003;60(9):1779-92.
(41.) DeKosky ST, Williamson JD, Fitzpatrick AL, et al. Ginkgo biloba for prevention of dementia: a randomized controlled trial. Jama. 2008;300(19):2253-62.
(42.) Ihl R. Effects of Ginkgo biloba extract EGb 761 (R) in dementia with neuropsychiatric features: review of recently completed randomised, controlled trials. Int J Psychiatry Clin Pract. 2013;17 Suppl 1:8-14.
(43.) Stoll S, Scheuer K, Pohl O, et al. Ginkgo biloba extract (EGb 761) independently improves changes in passive avoidance learning and brain membrane fluidity in the aging mouse. Pharmacopsychiatry. 1996;29(4):144-9.
(44.) Bridi R, Crossetti FP, Steffen VM, et al. The antioxidant activity of standardized extract of Ginkgo biloba (EGb 761) in rats. Phytother Res. 2001;15(5):449-51.
(45.) Chung HS, Harris A, Kristinsson JK, et al. Ginkgo biloba extract increases ocular blood flow velocity. J Ocul Pharmacol Ther. 1999;15(3):233-40.
(46.) Astiz M, de Alaniz MJ, Marra CA. The oxidative damage and inflammation caused by pesticides are reverted by lipoic acid in rat brain. Neurochem Int. 2012;61(7):1231-41.
(47.) Pershadsingh HA. Alpha-lipoic acid: physiologic mechanisms and indications for the treatment of metabolic syndrome. Expert Opin Investig Drugs. 2007;16(3):291-302.
(48.) Liu J, Head E, Gharib AM, et al. Memory loss in old rats is associated with brain mitochondrial decay and RNA/DNA oxidation: partial reversal by feeding acetyl-L-carnitine and/or R-alpha -lipoic acid. Proc Natl Acad Sci U S A. 2002;99(4):2356-61.
(49.) Maczurek A, Hager K, Kenklies M, et al. Lipoic acid as an anti- inflammatory and neuroprotective treatment for Alzheimer's disease. Adv Drug Deliv Rev. 2008;60(13-14):1463-70.
(50.) Wilson AD, Hart A, Wiberg M, et al. Acetyl-l-carnitine increases nerve regeneration and target organ Reinnervation--a morphological study. J Plast Reconstr Aesthet Surg. 2010;63(7):1186-95.
(51.) Long J, Gao F, Tong L, et al. Mitochondrial decay in the brains of old rats: ameliorating effect of alpha-lipoic acid and acetyl-L-carnitine. Neurochem Res. 2009;34(4):755-63.
(52.) Poon HF, Calabrese V, Calvani M, et al. Proteomics analyses of specific protein oxidation and protein expression in aged rat brain and its modulation by L-acetylcarnitine: insights into the mechanisms of action of this proposed therapeutic agent for CNS disorders associated with oxidative stress. Antioxid Redox Signal. 2006;8(3-4):381-94.
(53.) Wang J, Zhang HY, Tang XC. Huperzine a improves chronic inflammation and cognitive decline in rats with cerebral hypoperfusion. J Neurosci Res. 2010;88(4):807-15.
(54.) Zhang HY, Yan H, Tang XC. Non-cholinergic effects of huperzine A: beyond inhibition of acetylcholinesterase. Cell Mol Neurobiol. 2008;28(2):173-83.
(55.) Shang YZ, Ye JW, Tang XC. Improving effects of huperzine A on abnormal lipid peroxidation and superoxide dismutase in aged rats. Zhongguo Yao LiXue Bao. 1999;20(9):824-8.
(56.) Khan M, Sekhon B, Jatana M, et al. Administration of N-acetylcysteine after focal cerebral ischemia protects brain and reduces inflammation in a rat model of experimental stroke. J Neurosci Res. 2004;76(4):519-27.
(57.) Wang X, Svedin P, Nie C, et al. N-acetylcysteine reduces lipopolysaccharide-sensitized hypoxic-ischemic brain injury. Ann Neurol. 2007;61(3):263-71.
(58.) Pawlas N, Malecki A. Neuroprotective effect of N-acetylcysteine in neurons exposed to arachidonic acid during simulated ischemia in vitro. Pharmacol Rep. 2009;61(4):743-50.
(59.) Holmay MJ, Terpstra M, Coles LD, et al. N-Acetylcysteine boosts brain and blood glutathione in Gaucher and Parkinson diseases. Clin Neuropharmacol. 2013;36(4):103-6.
(60.) Hoffer ME, Balaban C, Slade MD, et al. Amelioration of Acute Sequelae of Blast Induced Mild Traumatic Brain Injury by N-Acetyl Cysteine: A Double-Blind, Placebo Controlled Study. PLOS ONE. 2013;8(1):e54163.
(61.) Kidd PM. Alzheimer's disease, amnestic mild cognitive impairment, and age- associated memory impairment: current understanding and progress toward integrative prevention. Altern Med Rev. 2008;13(2):85-115.
(62.) Kamphuis PJ, Scheltens P. Can nutrients prevent or delay onset of Alzheimer's disease? J Alzheimers Dis. 2010;20(3):765-75.
(63.) Goyal RK, Hirano I. The enteric nervous system. N Engl J Med. 1996;334(17):1106-15.
(64.) Nezami BG, Srinivasan S. Enteric nervous system in the small intestine: pathophysiology and clinical implications. Curr Gastroenterol Rep. 2010;12(5):358-55.
(65.) Mayer EA. Gut feelings: the emerging biology of gut-brain communication. Nat Rev Neurosci. 2011;12(8):453-55.
(66.) Sundman MH, Chen NK, Subbian V, et al. The bidirectional gut-brain- microbiota axis as a potential nexus between traumatic brain injury, inflammation, and disease. Brain Behav Immun. 2017.
(67.) Available at: http://bestpractice.bmj.com/best- practice/monograph/515.html. (http://bestpractice.bmj.com/best-practice/monograph/515.html) Accessed September 1, 2017.
(68.) Available at: http://www.aans.org/Patients/Neurosurgical-Conditions-and- Treatments/Concussion. (http://www.aans.org/Patients/Neurosurgical-Conditions-and- Treatments/Concussion) Accessed September 1, 2017.
(69.) Available at: http://www.mayoclinic.org/diseases-conditions/traumatic- brain- injury/basics/definition/con-20029302. (http://www.mayoclinic.org/diseases- conditions/traumatic- brain-injury/basics/definition/con-20029302) Accessed September 1, 2017.
(70.) Available at: https://www.nichd.nih.gov/health/topics/tbi/conditioninfo/Pages/symptoms.aspx. (https://www.nichd.nih.gov/health/topics/tbi/conditioninfo/Pages/symptoms.aspx) Accessed September 1, 2017.
(71.) Marshall S, Bayley M, McCullagh S, et al. Clinical practice guidelines for mild traumatic brain injury and persistent symptoms. Can Fam Physician. 2012;58(3):257-57, e128-40.
(72.) McCrory P, Johnston K, Meeuwisse W, et al. Summary and agreement statement of the 2nd International Conference on Concussion in Sport, Prague 2004. Br J Sports Med. 2005;39(4):195-204.
(73.) Available at: http://emedicine.medscape.com/article/92095-workup. (http://emedicine.medscape.com/article/92095-workup) Accessed September 1, 2017.
(74.) Mott TF, McConnon ML, Rieger BP. Subacute to chronic mild traumatic brain injury. Am Fam Physician. 2012;85(11):1045-51.
(75.) Fleminger S. Long-term psychiatric disorders after traumatic brain injury. Eur J Anaesthesiol Suppl. 2008;42:123-30.
(76.) Available at: https://www.playsmartplaysafe.com/commitment-letter/. (https://www.playsmartplaysafe.com/commitment-letter/) Accessed September 1, 2017.
Caption: Will Smith starred in the movie "Concussion," released in 2015 by Columbia Pictures.
Caption: Dr Bennet Omalu
|Printer friendly Cite/link Email Feedback|
|Title Annotation:||REPORT; Dr. Bennet Omalu|
|Date:||Mar 1, 2018|
|Previous Article:||Reduce Your Risk of Arterial Stiffness.|
|Next Article:||Vegan The Cookbook.|