When a TBI or any brain injury occurs, the body loses and has lessened capacity at operating at best capacity. A concussive injury leads to “inflammation, cellular damage, apoptosis, membrane disruption, axonal damage, mitochondrial dysfunction, hyper or hypo metabolism and increased susceptibility to repeat injury ( 1 ). To date, there is no effective treatment for a concussion. Concussion management thus far has focused on prevention (e.g., helmets, rule changes) and the philosophy of “rest, rest, rest” allowing symptoms to subside naturally before clearance to normal activity is approved ( 2 ). There are, however, certain things that can be done to improve brain function directly after an injury, and certain things to avoid to diminish the negative effects of TBIs.
Please keep in mind, this is just the research and a few things I’ve stumbled across in podcasts. Contact / consult your health care provider before implementing any of the below interventions.
what to do
- DHA + EPA: important for brain function and development, restoration of dopamine release (important for learning and memory / improve functional deficits), and significantly reduces the number of swollen, disconnected, and injured axons after a TBI. ( 1 & 4 )
- OMEGA-3 FATTY ACIDS: critical for optimal brain health and function, can protect against reduced plasticity and impaired learning, provide resistance to oxidative stress and decrease amount of brain injury created from a concussion ( 8 ).
- VITAMIN D + PROGESTERONE: By itself, vitamin D has not shown great promise for traumatic brain injuries, though in combination with progesterone, there are some promising results. In a rodent study, the combination of progesterone and vitamin D showed significantly reduced neuronal loss after a traumatic brain injury. In the two human-based studies, the combination of progesterone and vitamin D in patients with sTBI resulted in significantly improved outcomes, a better recovery rate, and a greater efficacy in reducing neuroinflammation ( 8 ). The cocktail of the two together is what can prevent injured neurons and their support cells from dying off over time ( 9 ).
- ZINC: total density of newly born cells was approximately 60% higher in zinc supplemented rats 1 week after TBI, and the results were maintained for 4 weeks after injury ( 14 ).
- MAGNESIUM: concentration declines for several days following injury, along with neurological deficits, so magnesium supplementation may be necessary following brain trauma. The fall in blood and brain magnesium levels often seen in TBI is associated with significantly worse prognosis in patients who experienced a continued decline in magnesium even when they were corrected within 24 h following injury, which means that supplementation is necessary for longer than a day after injury (4 ).
- CURCUMIN: Supplementation after a concussion improves membrane function, restored homeostasis, neuronal plasticity, synaptic plasticity, and neuronal signaling as well as reduce neural inflammation ( 8 ). It may counteract the negative effects of TBI on energy homeostasis and cognitive function, as shown in a study done in rats ( 10 ).
- RESVERATROL: Supplementation after a concussion can increase cell survival by suppressing autophagy and apoptosis as well as improve motor performance, visual spatial memory, and behavior ( 8 )
- CREATINE: Supplementation in children after sustaining a moderate to severe TB showed improved cognition, communication, self-care, personality, and behavior and significantly decreased headaches, dizziness, and fatigue ( 8 )
- VITAMIN E + VITAMIN C: When vitamin C is supplemented with vitamin E, there is a significantly less amount of brain injury. In one study, patients who presented with a Glasgow Coma Scale score less than or equal to 8 and had axonal injury and decreased mortality had increased Glasgow Outcome Scores if treated with vitamin E and decreased edema and lesion size if treated with vitamin C. ( 8 )
- S. BAICALENIS:supplementation decreased reactive oxygen species production, neuronal oxidative stress, apoptosis, neuronal cell damage, and motor and cognitive impairments. Animal models using S. baicalensis found that treatment with S. baicalensis decreased brain edema, inflammatory mediators, microglial activation, and cell death as well as increased overall neurological function ( 8 )
- CHOLINE: Dietary choline supplementation resulted in a modest degree of improvement in spatial memory after concussion, significant cortical tissue sparing, reduced brain inflammation, and normalized some TBI-induced deficits ( 11 )
- POTASSIUM ASPARTATE: In one study, researchers found that acute, post-injury administration of potassium aspartate (PA) markedly improved neurological sensorimotor function at 24 hours and 72 hours, and significantly lessened cortical lesion volume at 72 hours after TBI-induced CCI in rats. ( 12 )
- QUERCETIN:: Quercetin influences and protects mitochondrial structure, function and biogenesis. Quercetin also lessened the oxidative insult of mitochondria by enhancing the expressions and activities of antioxidant enzymes in a TBI model. ( 13 )
- GLUTATHIONE:: GSH depletion enhances oxidative stress. Proper GSH function depends on methylation processes, which need B vitamins, melatonin, as well as a properly functioning gut. (4 ).
- improved diet choices (especially those high in sugar and processed foods), infections and exposure to neurotoxic metals and pesticides/herbicides can worsen symptoms of TBI ( 4 )
- improved gut health: dysbiosis (an imbalance between good and bad gut bacteria in the colon), leads to further brain inflammation. (4 ) Disruption of gut flora leads to gut dysbiosis and in turn: increased inflammation and oxidative stress, hippocampus and amygdala damage, reduced levels of serotonin, dopamine, 5-hydroxytryptamine (5-HTP), melanin, and norepinephrine, damage to mitochondria, decreased absorption of zinc, decreased GSH, and decreased ability to detoxify toxins via the liver by destruction of CYP enzymes (4 )
- improved sleep: One theory for sleep is the enhanced removal of potentially neurotoxic waste products that accumulate in the awake CNS. Those with brain injuries often report disrupted sleep, which may further worsen the symptoms and negative effects of TBIs. (4 )
- fasting / ketogenic diet – One study found that fasting animals for 24 hr, but not 48 hr, after a moderate (1.5 mm), but not severe (2.0 mm), brain injury resulted in a significant increase in tissue sparing. This 24-hr fast also decreased biomarkers of oxidative stress and calcium loading and increased mitochondrial oxidative phosphorylation in mitochondria isolated from the site of injury. Insulin administration, designed to mimic the hypoglycemic effect seen during fasting did not result in significant tissue sparing after moderate CCI injury and in fact induced increased mortality at some injection time points. However, the administration of ketones resulted in increased tissue sparing after moderate injury. Fasting for 24 hour confers neuroprotection, maintains cognitive function, and improves mitochondrial function after moderate (1.5 mm) TBI. The underlying mechanism appears to involve ketosis rather than hypoglycemia. Therefore, a ketogenic diet may also be useful ( 16 )
- eat polyphenol rich foods: polyphenol-rich foods like blueberries leads to increased hippocampal plasticity and reverses cognitive and motor deficits. (4 )
- use noise canceling headphones: allow the noise in the brain to calm down ( 17 )
what not to do:
- using NSAIDs / anti-inflammatories: While using traditional anti-inflammatories like NSAIDs seems logical, it has been shown that chronic treatment with ibuprofen actually worsens the cognitive alterations in rodents exposed to an experimental TBI ( 2 )
- nothing at all: There seems to be a narrow window of opportunity wherein certain drugs can penetrate the BBB (Habgood et al., 2007) and gain access to the site of injury following a concussion. ( 2 )
- exposure to toxic metals: Aluminum toxicity is a documented cause of encephalopathy (brain inflammation) and aluminum, which is present in antiperspirants, high-sun protection factor (SPF) sunscreens, and antacids, bioaccumulates in the brain (4 ).
- eat food sprayed with herbicides / pesticides / glyphosate: exposure to food toxins especially glyphosate is a significant catalyst to nutrient functional deficiency, disrupted and dysfunctional homeostatic mechanisms as well as compromised gut health (4 ) Glyphosate disrupts cytochrome P450 (CYP) enzymes, interferes with several functions in the liver that would ultimately impact the brain. The liver depends upon CYP enzymes to activate vitamin D3, to produce CS and bile acids, and to detoxify other environmental toxins, including pharmaceutical drugs. (4 ) Glyphosate also disrupts CYP enzymes, which are needed both for proper detoxification maintenance and to activate vitamin D3, but of which are necessary for proper brain function. (4 )
- eat GMO foods: The increased consumption of packaged goods and processed foods, which are laden with GMO sourced ingredients and predominantly use omega-6 oils, further disrupts the ideal omega 3:6 ratio. The resulting relatively low omega-3 intake further reduces the amount of brain-supporting eicosapentaenoic acid (EPA) and more specifically DHA available in the diet. (4 )
- use testosterone: testosterone is contraindicated with a brain injury like a TBI ( 17 )
- take L-glutamine – too excitatory for the brain ( 17 )
- Ginkgo, turmeric, and high antioxidants, HBOT therapy, hyperbaric oxygen therapy, mitochondrial support through glutathione, coffee in the morning to increase ketosis, progesterone, 24-72 hours of fasting right after the injury, 30g fish oil once a brain bleed is ruled out, noise canceling headphones, True Dark glasses, 10 Unfair Advantages a day (Bulletproof product that’s another mitochondrial stimulant – an activated form of highly absorbable PQQ, bound to CoQ10), ice baths, cryotherapy, hyperbaric chambers ( 17 )
- While this isn’t a scientific study, JJ Virgin helped bring her son back from a severe brain injury. She utilized essential oils, fish oils, hyperbaric chambers, progesterone, vitamin D, avoided artificial sweeteners, GPC, Acetyl-L-carnitine, phosphatidylserine, ginkgo, and curcumin. She also did intrathecal stem cells transplant and recognized an odd outcome. When her son was waking up out of the brain injury, he was very violent. She did the intrathecal stem cells and the first three days are amazing, though when the neurological cells wake back up, they fire erratically, which sometimes results in violent behavior. It took all of these things together to see major progress with her son. ( 5 )
HAPPY BRAIN MATCHA!
- 2 cups boiling water
- 1 tbsp coconut butter (I used Pearl Butter brain butter – code lemons for 10% off)
- 1/2 tsp Bulletproof brain octane
- 1 tsp matcha
- 1 scoop Vital Proteins collagen
- 1/2 tsp Root and Bones reishi (code lemons for 15% off)
- 1/2 tsp Root and Bones chaga (code lemons for 15% off)
- few dashes of cinnamon
- optional: dollop of honey
( 1 ) Cernkovic Barrett, E., McBurney, M.I., & Ciappio, E.D. (2014). w-3 fatty acid supplementation as a potential therapeutic aid for the recovery form mild traumatic brain injury / concussion. Advances in Nutrition, 5, 268-277. doi: 10.3945/an.113.005280
( 2 ) Patterson, Z.R. & Holahan, M.R. (2012). Understanding the neuroinflammatory response following concussion to develop treatment strategies. Frontiers in Cellular Neuroscience, 6(58), doi: 10.3389/fncel.2012.00058
( 3 ) Lawrence, D.W. & Sharma, B. (2016). A review of the neuroprotective role of vitamin D in traumatic brain injury with impplicaitons for supplementation post-concussion. Brain Injury, 30(8), 960-968. doi: 10.3109/02699052.2016.1147081
( 4 ) Morley, W.A. & Seneff, S. (2014). Diminished brain resilience syndrome: A modern day neurological pathology of increased susceptibility to mild brain trauma, concussion, and downstream neurodegeneration. Surgical Neurology International, 5, 97. doi: 10.4103/2152-7806.134731
( 5 ) Fighting for Miracles. podcast. retrieved from: https://blog.bulletproof.com/fighting-miracles-jj-virgin-386/
( 6 ): Skolnick, B.E., Maas, A.I., Narayan, R.K., van der Hoop, R.G., MacAllister, T., Ward, J.D., Nelson, N.R., & Stocchetti, N. (2014). A clinical trial of progesterone for severe traumatic brain injury. The New England Journal of Medicine, 371, 2467-2476. doi: 10.1056/NEJMoa1411090
( 7 ): Wright, D.W., Yeatts, S.D., Silbergleit, R., Palesch, Y.Y., Hertzberg, V.S., Frankel, M., Goldstein, F.C., Caveney, A.F. … & Barsan, W.G. (2014). Very early administration of progesterone for acute traumatic brain injury. The New England Journal of Medicine, 371, 2457-2466. doi: 10.1056/NEJMoa1404304
( 8 ): Ashbaugh, A. & McGrew, C. (2016). The role of nutritional supplements in sports concussion treatment. Current Sports and Medicine Reports, 15(1), 16-19. doi: 10.1249/JSR.0000000000000219
( 9 ): Tang, H., Hua, F., Wang, J., Yousuf, S., Atif, F., Sayeed, I., & Stein, D.G. (2015). Progesterone and vitamin D combination therapy modulates inflammatory response after traumatic brain injury. Brain Injury, 1-10. doi: 10.3109/02699052.2015.1035330
( 10 ) Sharma, S., Zhuang, Y., Wu, A., Gomez-Pinilla, F. (2009). Dietary curcumin supplementation counteracts reduction in levels of molecules involved in energy homeostasis after brain trauma. Neuroscience, 161(4), 1037-1044. doi: 10.1016/j.neuroscience.2009.04.042
( 11 ) Guseva, M.V., Hopkins, D.M., Scheff, S.W., Pauly, J.R. (2010). Dietary choline supplementation improves behavioral, histological, and neurochemical outcomes in a rat model of traumatic brain injury. Journal of Neurotrauma, 25(8), 975-983. doi: 10.1089/neu.2008.0516.
( 12 ): Gu, Y., Zhang, J., Zhao, Y., Su, Y., & Zhang, Y. (2016). Potassium aspartate attenuates brain injury induced by controlled cortical impact in rats through increasing adenosine triphosphate (ATP) levels, Na+/K+-ATPase activity and reducing brain edema. Medical Science Monitor, 22, 4894-4901. doi: 10.12659/MSM.898185
( 13 ): Li, X., Wang, H., Gao, Y., Li, L., Tang, C., Wen, G., YAng, Y., … & Fan, Y. (2016). Quercetin induces mitochondrial biogenesis in experiemental traumatic brain injury via the PGC-1α signaling pathway. American Journal of Translational Research, 8(8), 3558-3566.
( 14 ): Cope, E.C., Morris, D.R., Gower-Winter, S.D., Brownsteine, N.C., Levenson, C.W. (2016). Effect of zinc supplementation on neuron precursor proliferation in the rat hippocampus after traumatic brain injury. Experimental Neurology, 279, 96-103. doi: 10.1016/j.expneurol.2016.02.017
( 15 ): Curtis, L. & Epstein, P. (2014). Nutritional treatment for acute and chronic traumatic brain injury patients. Journal of Neurosurgical Sciences, 58(3), 151-160.
( 16 ) Davis, L.M., Pauly, J.R., Readnower, R.D., Rho, J.M., & Sullivan, P.G. (2008). Fasting is neuroprotective following traumatic brain injury. Journal of Neuroscience Research, 86(8), 1812-1822. doi: 10.1002/jnr.21628
( 17 ) Asprey, D. (Dr. Jolene Brighton). (2017, June 30). On women’s health, post-birth control syndrome, and brain injuries [Audio podcast]. Retrieved from https://blog.bulletproof.com/womens-health-post-birth-control-syndrome-brain-injuries-dr-jolene-brighten-415/