traumatic brain injury treatment with nootropics

Best Nootropics for Traumatic Brain Injury

David Tomen
Author:
David Tomen
23 minute read

Every day, 166 people in the USA die from traumatic brain injury (TBI) according to the Centers for Disease Control (CDC).[i] If you survive TBI, you can experience the effects for a few days. Or for the rest of your life.

TBI can result in impaired cognition and memory, loss of vision or hearing, personality changes and depression. Affecting not only those who suffered TBI but connected families and communities.

While decades of research and clinical studies have searched for pharmaceutical solutions to treat TBI, no prescription medication has been found.

As a result, millions are searching for and successfully using natural nootropic supplements to alleviate the symptoms of brain injury.

And yet, the US Food and Drug Administration put out a warning in 2014 telling consumers to ignore and avoid using dietary supplements for treating symptoms of TBI. The FDA news release claimed there was no scientific evidence to support claims that dietary supplements could in any way help an injured brain.[ii]

Turns out there is some truth in what they claim. Most of the clinical research on dietary supplements and traumatic brain injury have been done with animals. Very few have been conducted with human subjects dealing with TBI.

The thing is some of the nootropic supplements we’ll explore in this post have been used for thousands of years. Not treating TBI specifically. But the track record and user reports speak volumes.

The purpose of this post is to provide you with the latest scientific research on nootropic supplements and traumatic brain injury. You’ll learn how to recognize traumatic brain injury (including concussions).

You’ll see what happens in the human brain that’s injured. And we’ll also consider some nootropic supplements that have been scientifically, clinically shown to alleviate some of the symptoms of TBI.

But a cautionary note to start – traumatic brain injury, and even a concussion is serious. If you whacked your head hard enough that you feel some of the symptoms described in the next section, go immediately to the ER and get checked out for bleeding in your brain.

We’ll wait right here until you get back …

Recognizing Traumatic Brain Injury

Traumatic brain injury (TBI) is caused by a bump, blow or jolt to the head that disrupts normal function of the brain. Severity of traumatic brain injury can range from ‘mild’ TBI (i.e. a brief change in mental status or consciousness) to ‘severe’ TBI (i.e. extended period of unconsciousness or memory loss).

Most TBI’s are mild (mTBI) and commonly called concussions.[iii] One study in the UK found that mild TBI accounts for up to 80% of clinical traumatic brain injuries. But a simple concussion can result in cognitive impairment and white matter damage that may develop and persist for years.[iv]

Other research has shown that a concussion can result in behavioral changes, impairments in memory and attention, headache, and unsteadiness. Two or more concussions often result in severe brain injury (second impact syndrome) with a greater severity in symptoms and longer recovery time.traumatic brain injury treatment with nootropics

A study in Italy demonstrated how vulnerable the brain is after a single concussion (mTBI). A second mild concussion within 3 days resulted in profound metabolic abnormalities similar to those seen after a single severe TBI. Affecting acetyl-CoA, gene expression, neurotransmitters, and mitochondrial metabolism.[v]

Left unchecked, this type of brain injury often leads to earlier onset of age-related cognitive decline and dementia. I have conducted Personal Consultations within the last few months where traumatic brain injury led to early-onset Alzheimer’s or Parkinson’s Disease a few months after the  head injury.

The American Association of Neurology developed a grading system to help diagnose and treat concussions. Early symptoms (within a few minutes to a few hours) include lack of awareness, dizziness, headaches, nausea and vomiting. Later symptoms (days to weeks) include lower attention and concentration, persistent headaches, irritability, and sleep disturbances.[vi]

The key here is being able to recognize concussion or TBI and prevent a second injury. In sports, this means getting off the field and going into recovery rather than going back into play. It could mean the difference between quicker recovery to full health or a lifetime of cognition problems.

It also means the quicker you recognize the signs of concussion or TBI, you get medical help fast. And then identify which nootropic supplements you may want to try and support your recovery from TBI or concussion.

best nootropics for concussion

TBI and Concussion Effects on the Brain

A blow to the head immediately sets off a cascade of events in the brain. Effecting neuron depolarization, the release of excitatory neurotransmitters, ionic shifts, changes in glucose metabolism, altered cerebral blood flow and impaired axon function.[vii]

If this all sounds like Greek to you, stay with me and I’ll do my best to walk you through the neuroscience. As simply and basically as I can. This is important to help you understand specifically what you need to repair in your injured brain. And will help identify specifically which nootropics may help support that repair.

Traumatic brain injury or concussion starts with a disruption in neuron cell membranes and axon stretching. Causing an indiscriminate flux of ions through ion channels that were previously strictly regulated.[viii]

This process causes a widespread release of several different neurotransmitters, particularly the indiscriminate release of glutamate.[ix] Which is toxic when released in excess. Resulting in a further ionic flux.

Neuron mechanisms then work at maximum capacity to restore ionic balance which depletes brain cell energy stores.

As we step through each process in the brain that gets disrupted by traumatic brain injury, we can identify specific nootropics that may be able to target and assist in each of these problems.

Axon Injury

Traumatic brain injury often results in stretching of axons within the brain. Causing ionic flux and depolarization, calcium influx and swelling of mitochondria.[x] And neurofilament compaction (the skeletal structure that supports axons).traumatic brain injury definition

Neurofilament compaction can occur immediately after injury (5 mins. – 6 hours). And from 6 – 24 hours after you get knocked in the head, an influx of calcium can destabilize microtubules which are responsible for ions, proteins, amino acids and neurotransmitter movement into and out of the brain cell.

Axons extend from brain neurons to send messages to other neurons. The damage just described can interrupt this communication, result in axon blebbing (local swelling), and eventually the axon breaking off of the neuron.[xi]

Research has recently found that axon damage can also result from concussion (mTBI).[xii] And the damage can progress over a period of 4 – 6 weeks post-injury.

Axon damage from a concussion results in cognition problems. One study conducted in New York with 17 patients found cognitive impairment due to TBI and axon damage 8 months to 3 years after concussion![xiii]

We’ll look at nootropic supplements shown to support axon health and repair later in this post.

Cerebral Circulation

Studies have found that after TBI, cerebral blood flow decreases (hypoperfusion) the day of the injury. Day 1 – 3 blood flow in the brain increases too much (hyperemia). And days 4 – 15 after TBI, blood vessels constrict (vasospasm).[xiv] Meaning not enough blood flow to support brain cell repair and maintenance.

Cerebral blood flow and blood vessels can all be assisted with nootropics which we’ll explore in a minute.

Glutamate

When the brain is injured, neuron membranes deform. Resulting in excessive potassium release between neurons. This neuron membrane deformity also results in the release of excitatory neurotransmitters like glutamate. Which binds to NMDA and AMPA receptors and related ion channels.

The result is a widespread suppression of neurons and a condition resembling depression. Na+/K+ pumps (sodium and potassium) are activated to restore ionic balance. Because these pumps are ATP-dependent, and require high levels of glucose for metabolism, cellular energy stores are depleted.

This increase in metabolism occurs immediately and can last from 30 minutes to 4 hours after TBI.[xv] At the same time, oxidative metabolism is disrupted due to mitochondrial dysfunction.[xvi] IN turn depleting adenosine triphosphate (ATP) which brain cells use for energy.

Glucose and Mitochondria

Within 30 minutes of a concussion (mTBI), the use of glucose for metabolism rises well above normal levels. Hypometabolism (abnormally low metabolic rate) sets in after 6 hours which can last for up to 5 days.traumatic brain injury recovery

Hyperglycolysis (an increase in glucose utilization) followed by hypometabolism may last for months after moderate or severe TBI.[xvii]

NMDA channels are activated after TBI which result in a significant jump in Ca++ (calcium ions) which accumulate in mitochondria. Causing glucose oxidative dysfunction.

This oxidation is normally handled by antioxidants which prevent free radicals from damaging brain cells. With traumatic brain injury the antioxidants normally present in brain cells are insufficient to prevent brain cell damage or death (apoptosis).

Studies have found that metabolic markers such as the ATP/ADP ratio, NADH/NAD+ ratio, and N-acetylaspartate (NAA) levels all decrease after repeated concussions. Mitochondrial oxidative function is downregulated by as much as 10 days after injury.[xviii]

Animal studies have found that after TBI, the brain experiences a reduction in creatine (Cr), NAA, phosphatidylcholine (PC), and in the ATP/ADP ratio. And these findings were later confirmed in athletes with concussion.[xix] All of which can be helped with nootropics that we’ll explore later in this post.

NMDA Receptors

NMDA channels are associated with long-term potentiation (LTP) which is required for learning and the encoding of long-term memory.

It comes as no surprise that LTP is impaired after traumatic brain injury. Resulting is problems with memory. Problems with LTP manifest within 2 days of injury. And seems to recover within 7 – 15 days after injury. But LTP deficiency has been shown to last up to 8 weeks after TBI.[xx]

Nootropics to support NMDA receptor functionality and long-term potentiation will be explored in the next section of this post.

traumatic brain injury nootropic supplements

Nootropic Supplements for TBI or Concussion

Decades of research and clinical studies have shown that traumatic brain injury or concussion results in problems with ion balance, excess neurotransmitter activation, integrity of axons, brain cell energy metabolism and cerebral blood circulation.

This knowledge helps us identify nootropics from our List of Nootropics that can address each problem. And it turns out that several nootropics have been studied extensively specifically for treating the symptoms of traumatic brain injury. Particularly related to sports injuries.

If you’ve spent any time on Nootropics Expert®, it seems that most of the nootropics reviewed here could help repair and maintain an injured brain. So let’s narrow the list to supplements that have shown promise through therapeutic applications for TBI in actual clinical trials.

Creatine

As a nootropic, creatine is one of the most effective cognitive enhancers available. This non-essential amino acid is naturally synthesized in your liver, kidneys and pancreas. And used in your brain to provide a phosphate molecule to adenosine diphosphate (ADP) to produce adenosine triphosphate (ATP). ATP is the primary cellular fuel source created in brain cell mitochondria.

Studies have found that metabolic markers including the ATP/ADP ratio decrease due to traumatic brain injury. Part of the problem may be a drop in creatine from TBI.[xxi]

Maintenance of brain cell ATP levels is critical for the cellular energy required to maintain proper neuron membrane potential, ion gradients underlying brain signaling, intracellular calcium homeostasis, neurotransmission, and intracellular and intercellular signal transduction.[xxii]

A study in Greece worked with 30 children aged 1 – 18 years who suffered from TBI. The children were given 0.4 gr/kg of creatine per day for 6 months. The study found a reduction in post-traumatic amnesia, shorter intensive care stay, and improvements in recovery, communication, locomotion, sociability, personality and behavior and cognitive function.

The Greek study concluded that “administration of creatine may be beneficial to patients with traumatic brain injury”.[xxiii] Recommended dosage of Creatine for cognitive benefit is up to 5 grams per day.

DHA (Omega-3)

Omega-3 fatty acids (DHA & EPA) are important structural components of brain cell membranes. Modulating membrane fluidity, thickness, brain cell signaling and mitochondrial function.[xxiv]DHA Omega-3 for concussion and traumatic brain injury

DHA (docosahexaenoic acid) influences the phospholipid content of brain cell membranes increasing phosphatidylserine (PS) and phosphatidylethanolamine production and promoting neuron growth throughout your life.

Many clinical studies with animals have shown the DHA and/or EPA supplementation benefits for traumatic brain injury recovery. DHA has been shown to significantly reduce the number of swollen (blebbing), disconnected and injured axons when taken following traumatic brain injury.[xxv]

DHA is an antioxidant and anti-inflammatory,[xxvi] reduces AMPA-mediated cell death, reduces glutamate-induced toxicity, increases nitric oxide production for cerebral circulation, normalizes brain-derived neurotrophic factor (BDNF) levels, and generally helps restore brain cell homeostasis following TBI.

Despite all the positive animal research showing benefits of Omega-3’s and DHA in recovery from TBI, so far we have no human clinical trials to verify these benefits in humans.

But growing clinical experience by numerous health care professionals show that the brain needs to be saturated with high doses of Omega-3’s in order for the brain to heal after injury. Without sufficient DHA and EPA, healing is less likely to happen.[xxvii]

Green Tea

In 1998, a study was conducted in China including subjects from 12 provinces aged 35 – 60 years. In all, 14,212 people participated in this study to investigate the association between tea consumption and stroke.

The study concluded there was a 40% decreased risk of stroke in those who drank green, black or jasmine teas.[xxviii]green tea for concussion and traumatic brain injury

No human clinical trials have been done with green tea and traumatic brain injury. But the cognitive benefits of green tea are so profound, it must be included in this list of nootropics to benefit TBI and concussion.

TBI comes with severe oxidative stress, neuron injury, cerebral blood flow problems and inflammation. Green tea addresses all of these issues.

Green tea’s neuroprotective qualities include the flavonoid epigallocatechin-3-gallate (EGCG), the amino acid L-Theanine and methylxanthines which provide caffeine.

EGCG modulates nitric oxide and oxidative stress.[xxix] Green tea polyphenols potentiate nerve growth factor which is needed to regrow neurons.[xxx] L-Theanine delays neuronal cell death. EGCG is an anti-inflammatory and protects cell signaling pathways.

You can think of green tea as a fertilizer for nerve growth factor and L- Theanine as a silent hero that puts the brakes on neuronal cell death.

And EGCG reduces beta-amyloid mediated cognitive impairment and modulates tau pathology implicated in Alzheimer’s.[xxxi] And are associated with successive concussions or severe TBI.

We do have human studies showing that green tea extract and L-Theanine improves memory and brain theta wave activity which boosts cognitive alertness.[xxxii] A primary benefit in anyone dealing with a concussion.

Some professionals caution about the caffeine content in green tea when it comes to traumatic brain injury. But caffeine-mediated neuroprotection include reductions in neurological deficits, cerebral edema (brain swelling), brain cell apoptosis and protection from inflammation.[xxxiii]

Lithium Orotate

Glutamate toxicity plays a major role in brain damage from traumatic brain injury. Over-activity of glutamate on NMDA receptors causes apoptosis. Lithium inhibits this overactivity.

A study conducted by Dr. Peter Leeds and his team in 2014 states that lithium had “demonstrated robust beneficial effects in experimental models of Traumatic Brain Injury (TBI).

These include decreases in TBI-induced brain lesion, suppression of neuroinflammation, protection against blood-brain barrier disruption, normalization of behavioral deficits, and improvement of learning and memory, among others.”[xxxiv]

Lithium Orotate recommended dose is 5 mg 2 or 3-times per day. Naturopathic doctors suggest stacking Lithium Orotate with 1,000 mg of Omega-3 and 400 IU of Vitamin E (as mixed tocopherols). Excellent advice for anyone. Including those dealing with TBI or concussion.

N-Acetyl L-Cysteine (NAC)

N-Acetyl L-Cysteine (NAC) is a precursor of glutathione which is a potent antioxidant, anti-inflammatory and free radical scavenger. All problems that come with TBI. NAC also reduces irritability, anxiety and depression. Also associated with TBI.

A double-blind, placebo-controlled study was conducted with soldiers at a forward-deployed field hospital in Iraq. The soldiers in this study were dealing with mTBI after being exposed to blasts on the battlefield.

The soldiers were suffering from dizziness, hearing loss, headache, memory loss, sleep disturbances and neurocognitive dysfunction. All symptoms you may recall of concussion or mTBI.

The soldiers who were treated with N-Acetyl L-Cysteine (NAC) reported no symptoms after 7 days of supplementing with NAC. The researchers reported that “This is the first demonstration of an effective short term countermeasure for mTBI”.[xxxv]

Recommended dosage of NAC is 600 mg three-times per day.

Pine Bark Extract 

Pycnogenol® is a standardized extract of French maritime pine bark. This extract contains 65 – 75% proanthocyanidins (procyanidins).

Pine Bark Extract is a potent anti-inflammatory and one of the most powerful antioxidants currently known.[xxxvi] Both problems with traumatic brain injury.

Studies have shown that Maritime Pine Bark Extract is 50 – 100 times more potent than Vitamin E in neutralizing free radicals. And it helps recycle and prolong the activity of Vitamins C and E.

Pine Bark Extract helps reduce DNA damage caused by oxidation, inhibits proinflammatory gene expression, prevents glycation, inhibits brain cell membrane damage from free radicals, and reduces oxidative stress. And it can boost cerebral circulation by increasing nitric oxide activity.

I think we pretty much crossed off most of the symptoms associated with traumatic brain injury here. Recommended dosage of Pine Bark Extract is up to 300 mg per day.

Piracetam

Piracetam is a water-soluble ampakine nootropic in the racetam-family of compounds. The very first “nootropic”, Piracetam was developed by the father of nootropics, Dr. Corneliu Giurgea.

Piracetam modulates both AMPA and NMDA receptors. Both receptors as you may recall are negatively affected by brain trauma. It normalizes L-Glutamate and prevents the glutamate toxicity associated with traumatic brain injury.

Piracetam also increases cerebral blood flow. Reversing the symptoms caused by restricted blood flow after TBI.

A study conducted in Russia with 42 patients aged 12 – 18 dealing with severe traumatic brain injury symptoms for the past 1½ – 5 years. 20 patients received 1600 – 2400 mg of Piracetam daily for a month. The other 22 were used as controls.

The study concluded that Piracetam provided positive therapeutic effects on memory, attention, executive function and motor function. As well as speed of cognitive and motor performance.[xxxvii]

Recommended dosage of Piracetam is 1,600 mg 3-times per day for TBI.

Resveratrol

Resveratrol is a polyphenol stilbenoid and phytoalexin that certain plants produce in response to stress, such as injury or fungal infection. It’s a naturally occurring compound found most famously in red wine.

Resveratrol could be one of your best nootropics for controlling the damage done from TBI. Although no human studies have been conducted specifically with TBI victims.resveratrol for concussion and traumatic brain injury

This polyphenol increases brain-derived neurotrophic factor (BDNF) in the brain. BDNF has been called Miracle Gro for promoting repair and growth of new neurons. Resveratrol also increases cerebral blood flow.

Resveratrol as an anti-inflammatory is a potent inhibitor of TNF-α- and IL-1b-induced NF-kB activation. And it suppresses COX-2 by blocking NF-kB activation.

And Resveratrol prevents the release of toxic glutamate during a stroke. Even protecting the brain when administered 6 hours after stroke.[xxxviii] This sounds like a strong therapeutic candidate to be used within the first few hours of concussion to prevent further brain damage.

Pre-clinical studies have explored Resveratrol’s therapeutic effect on experimental TBI. Studies show it reduced neuron loss after TBI in animals. And improved locomotion, anxiety and memory.[xxxix]

Recommended dose of Resveratrol extract (99%) from Japanese Knotweed for brain damage caused by TBI and increasing cerebral blood flow is 250 – 500 mg.

Pramiracetam

Pramiracetam is a fat-soluble nootropic in the racetam-family of compounds. It was first synthesized by Parke-Davis scientists in the late 1970’s. In 1991, Pramiracetam was licensed to Cambridge Neuroscience Inc. And tested for restoring cognitive function after stroke or traumatic brain injury.

Pramiracetam increases nitric oxide activity in your brain. Which acts as a vasodilator which relaxes blood vessels. Improving cerebral blood flow which is a problem after TBI.

This nootropic also has a profound effect on the synthesis of acetylcholine. Which is critical for encoding new memories, concentration, cognition and neuroplasticity.

A study in Russia was conducted with 65 patients suffering from concussion. The researchers gave half the patients Pramiracetam and the other half received Piracetam.

Tests were carried out on the first, tenth and after thirty days. Both groups noted a considerable reduction in headaches, dizziness and nausea. But the Pramiracetam group reported better restoration of orientation, feeling and said it was more effective on amnesia.[xl]

Recommended dosage for Pramiracetam is 250 – 400 mg per day. For TBI you may go up to 1,500 mg per day.

Since this nootropic has a significant effect on acetylcholine, you should stack it with a choline supplement like Alpha GPC or CDP-Choline. And because it’s fat-soluble, take it with a tablespoon of unrefined, extra virgin coconut oil for absorption.

Oxiracetam

Oxiracetam is a water-soluble ampakine nootropic in the racetam-family of compounds. And in 1977, was the 3rd racetam nootropic to be developed.

Oxiracetam modulates both AMPA and NMDA receptors which prevents the glutamate toxicity associated with TBI. It also seems to prevent an imbalance of acetylcholine activity which should also benefit those recovering from brain injury.

Oxiracetam enhances protein kinase C (PKC) which affects M1 acetylcholine receptors. Oxiracetam even demonstrates the ability to repair these receptors when damaged. Such as from traumatic brain injury.[xli]

In a study done with Wistar rats dealing with TBI, researchers showed the rats who received Oxiracetam had significantly less brain impairment 7, 14 and 21 days after brain injury.[xlii]

While I don’t have access to any human trials with Oxiracetam and traumatic brain injury, this nootropic looks like a promising addition to any stack for someone recovering from TBI.

Recommended dosage of Oxiracetam is 750 – 1,500 mg per day split into two doses. Since this nootropic boosts acetylcholine in your brain, you should stack it with a good choline source like Alpha GPC or CDP-Choline.

Turmeric

Turmeric is one of the most studied herbs in Ayurvedic, Siddha, Unani and Chinese healing. This perennial shrub native to southern Asia has been used as medicine for at least 6,000 years.

Turmeric, or any one of its several active compounds including curcumin and Ar-turmerone undoes damage to your brain caused by depression, chronic stress and traumatic brain injury.

Turmeric and curcumin boosts neurogenesis, increases dendrites, repairs DNA, reduces inflammation, counters free radical damage, and boosts neurotransmitters when needed. All problems identified in TBI.

In one animal study, researchers in Germany found that Ar-turmerone, one of the many components extracted from turmeric, increased neural stem cells in the brain. Promoting the creation of new brain cells.[xliii]

Another study conducted at UCLA found that curcumin counteracts the outcome of traumatic brain injury on oxidative stress, synaptic plasticity and cognition.[xliv]

To obtain the cognitive benefits needed for healing traumatic brain injury, both Turmeric and Curcumin seem to be the best option. DolCas Biotch developed a standardized extract of turmeric containing curcumin-essential oil complex of 86% curcuminoids and 7-9% essential oils. Including the turmeric volatile oil Ar-turmerone. It’s called BCM95®.

If you choose a turmeric supplement containing BCM95®, follow the dosage directions on the label. Otherwise, recommended dosage for Turmeric extract (95% curcuminoids) is 750 mg 3-times per day.

B-Complex Vitamins

Any nootropic supplement stack used for traumatic brain injury or concussion recovery should include a high quality, bio-available B-Complex vitamin. Here’s why …

  • Vitamin B6 (Pyridoxine) – is needed to control inflammation caused by elevated homocysteine. It’s a cofactor in the synthesis of dopamine, epinephrine, GABA, norepinephrine and serotonin. Vitamin B6 has a direct effect on your immune system, gene transcription and expression and is involved in glucose regulation.
  • Vitamin B8 (Inositol) – helps boost serotonin and dopamine receptor density. Improves the effectiveness of all major neurotransmitters in your brain. Myo-inositol affects mRNA which regulates cell volume, controls cellular signaling, plays a role in DNA repair, is a component of brain cell membranes, regulates cell metabolism and energy consumption and affects long-term potentiation.
  • Vitamin B9 (Folate) – is involved in DNA and RNA synthesis, gene expression, amino acid synthesis and metabolism, and myelin synthesis and repair. Folate is required for synthesis of dopamine, epinephrine and serotonin.
  • Vitamin B12 (Methylcobalamin)Methylcobalamin, the type of B12 your body uses, is needed to control inflammation by regulating homocysteine, is a cofactor in the synthesis of dopamine, GABA, norepinephrine, and serotonin. And helps increase serotonin and dopamine levels which decrease anxiety, depression, fatigue and pain.

Choose a B-Complex that contains folate (not folic acid) and methylcobalamin (not cobalamin). I can’t imagine good recovery from traumatic brain injury or concussion without the assistance of the B-Vitamins.

concussion definition

Suggested Nootropic Stack for TBI or Concussion Recovery

The use of nootropic supplements and herbal remedies has become more common place. Particularly when it comes to quality recovery from traumatic brain injury or concussion.

So far, no pharmaceutical solution exists to your brain’s ability to repair from this type of injury.

When choosing nootropic supplements for your stack, do your best to select only high quality supplements from reputable manufacturers with a great track record and great customer reviews.

When it comes to plant-based nootropics, organics are best so you avoid contamination by heavy metals, and other toxins.

Follow dosage recommendations carefully to avoid side effects. And please do your homework and ensure each nootropic is not contraindicated with any of the prescription medicines you’re taking.

If I was personally dealing with concussion or traumatic brain injury, the first thing I’d do is go to the emergency room. And get checked out for bleeding in my brain.

When I got home, this is the nootropic stack I’d use, and you may want to consider as well. This is by no means medical advice. You should be consulting with your neurologist or neurosurgeon every step of the way when recovering from this type of injury.

Here’s a suggested nootropic stack to support ionic balance, neurotransmitter problems, axon damage, brain cell energy metabolism and cerebral blood flow.

  • Creatine
  • DHA (Omega-3)
  • Lithium Orotate
  • N-Acetyl L-Cysteine (NAC)
  • Pine Bark Extract
  • Turmeric (BCM95®) extract
  • B-Complex Vitamins
  • CDP-Choline

CDP-Choline is included because Pramiracetam boosts acetylcholine. And your brain needs more acetylcholine which is why you need to use a precursor like CDP-Choline. You could alternatively use Alpha GPC.

Find a green tea that you like and drink at least 4 cups per day. You could use a L-Theanine supplement. But you wouldn’t get the full benefit of all the cognitive health promoting properties of green tea.

I’d also highly recommend completely stop eating inflammation-producing foods or drink. This includes all processed food, grains, soft drinks and others. Do an Internet search for “inflammatory foods” for a full list.

It is possible to fully recover from traumatic brain injury. Not guaranteed of course. But the odds are stacked in your favor if you take action. And support your brain with what it needs to repair itself with nootropic supplements.

As an Amazon Associate I earn from qualifying purchases. This post may also contain other affiliate links and I will be compensated if you make a purchase after clicking on my links.

[i] “TBI: Get the Facts” Center for Disease Control and Prevention cdc.gov Retrieved February 11, 2022 (source)

[ii] Dallas M.E. “Dietary Supplements Can’t Treat or Cure Concussions” WebMD January 9, 2014 (source)

[iii] “Report to Congress on mild traumatic brain injury in the United States: steps to prevent a serious public health problem.”  Centers for Disease Control and Prevention (CDC) Atlanta (GA): Centers for Disease Control and Prevention; 2003.

[iv] Spain A., Daumas S., Lifshitz J., Rhodes J., Andrews P.J., Horsburgh K., Fowler J.H. “Mild fluid percussion injury in mice produces evolving selective axonal pathology and cognitive deficits relevant to human brain injury.” Journal of Neurotrauma. 2010 Aug;27(8):1429-38 (source)

[v] Vagnozzi R., Tavazzi B., Signoretti S., Amorini A.M., Belli A., Cimatti M., Delfini R., Di Pietro V., Finocchiaro A., Lazzarino G. “Temporal window of metabolic brain vulnerability to concussions: mitochondrial-related impairment–part I.” Neurosurgery. 2007 Aug;61(2):379-88 (source)

[vi] “Practice parameter: the management of concussion in sports (summary statement). Report of the Quality Standards Subcommittee.” Neurology. 1997; 48: 581–585 (source)

[vii] Giza, C.C. and Hovda, D.A. “The neurometabolic cascade of concussion.” Journal of Athletic Training. 2001; 36: 228–235 (source)

[viii] Farkas, O., Lifshitz, J., and Povlishock, J.T. “Mechanoporation induced by diffuse traumatic brain injury: an irreversible or reversible response to injury?.” Journal of Neuroscience. 2006; 26: 3130–3140 (source)

[ix] Katayama Y., Becker D.P., Tamura T., Hovda D.A. “Massive increases in extracellular potassium and the indiscriminate release of glutamate following concussive brain injury.” Journal of Neurosurgery. 1990 Dec;73(6):889-900. (source)

[x] Mata M., Staple J., Fink D.J. “Changes in intra-axonal calcium distribution following nerve crush.” Journal of Neurobiology. 1986 Sep;17(5):449-67. (source)

[xi] Povlishock J.T., Pettus E.H. “Traumatically induced axonal damage: evidence for enduring changes in axolemmal permeability with associated cytoskeletal change.” Acta Neurochirurgica Supplement. 1996;66:81-6. (source)

[xii] Spain, A., Daumas, S., Lifshitz, J., Rhodes J., Andrews P.J., Horsburgh K., Fowler J.H. “Mild fluid percussion injury in mice produces evolving selective axonal pathology and cognitive deficits relevant to human brain injury.” Journal of Neurotrauma. 2010; 27: 1429–1438 (source)

[xiii] Lipton M.L., Gellella E., Lo C., Gold T., Ardekani B.A., Shifteh K., Bello J.A., Branch C.A. “Multifocal white matter ultrastructural abnormalities in mild traumatic brain injury with cognitive disability: a voxel-wise analysis of diffusion tensor imaging.” Journal of Neurotrauma. 2008 Nov;25(11):1335-42. (source)

[xiv] Martin, N.A., Patwardhan, R.V., Alexander, M.J., Africk C.Z., Lee J.H., Shalmon E., Hovda D.A., Becker D.P. “Characterization of cerebral hemodynamic phases following severe head trauma: hypoperfusion, hyperemia, and vasospasm.” Journal of Neurosurgery. 1997; 87: 9–19 (source)

[xv] Yoshino, A., Hovda, D.A., Kawamata, T., Katayama Y., Becker D.P. “Dynamic changes in local cerebral glucose utilization following cerebral conclusion in rats: evidence of a hyper- and subsequent hypometabolic state.” Brain Research. 1991; 561: 106–119 (source)

[xvi] Verweij, B.H., Muizelaar, J.P., Vinas, F.C., Peterson P.L., Xiong Y., Lee C.P. “Mitochondrial dysfunction after experimental and human brain injury and its possible reversal with a selective N-type calcium channel antagonist (SNX-111)”. Neurological Research. 1997; 19: 334–339 (source)

[xvii] Bergsneider M., Hovda D.A., Shalmon E., Kelly D.F., Vespa P.M., Martin N.A., Phelps M.E., McArthur D.L., Caron M.J., Kraus J.F., Becker D.P. “Cerebral hyperglycolysis following severe traumatic brain injury in humans: a positron emission tomography study.” Journal of Neurosurgery. 1997 Feb;86(2):241-51. (source)

[xviii] Hovda, D.A., Yoshino, A., Kawamata, T., Katayama Y., Becker D.P. “Diffuse prolonged depression of cerebral oxidative metabolism following concussive brain injury in the rat: a cytochrome oxidase histochemistry study.” Brain Research. 1991; 567: 1–10 (source)

[xix] Vagnozzi, R., Signoretti, S., Tavazzi, B., Floris R., Ludovici A., Marziali S., Tarascio G., Amorini A.M., Di Pietro V., Delfini R., Lazzarino G. “Temporal window of metabolic brain vulnerability to concussion: a pilot 1H-magnetic resonance spectroscopic study in concussed athletes–part III.” ([discussion: 95–6]) Neurosurgery. 2008; 62: 1286–1295 (source)

[xx] Sanders M.J., Sick T.J., Perez-Pinzon M.A., Dietrich W.D., Green E.J. “Chronic failure in the maintenance of long-term potentiation following fluid percussion injury in the rat.” Brain Research. 2000 Apr 7;861(1):69-76. (source)

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Join The Discussion - 121 comments

Lauren
August 31, 2023

Hi there,
Thank you so much for such an incredible website and sharing your knowledge so freely! I’m blown away!
My story is so long but I’ll try and keep it as sort as possible. My 17 year old daughter did, I reckon, suffer a TBI when she was about 3 and she fell out of a trolley onto tiles hitting her head directly and was concussed. Had her in ER in 5 minutes [edited for length] I’ve left out a lot and tried to keep it short. If you have any advice whatsoever I would be so so grateful!!! Thank you again for all you do!

    David Tomen
    August 31, 2023

    Lauren, scroll up to the section called, “Suggested Nootropic Stack for TBI or Concussion Recovery“. I have a suggested nootropic stack in that section for TBI,.

      Lauren
      September 17, 2023

      Thanks… I was more wanting to find out what supplements are safe to be taking with Lithium and Arizofy. My daughter is already taking NAC, high dose fish oils, vits B and D and I was wondering specifically if I could add L-Tyrosine to help with her focus and energy?

        David Tomen
        September 22, 2023

        Lauren, Aripiprazole acts by modulating neurotransmission overactivity of dopamine. So chances are the drug will nullify the potential positive effects of L-Tyrosine. And the drug is moderately contraindicated with Lithium. But Lithium Orotate is such a micro dose of Lithium that is may not matter.

Surya
January 19, 2023

Which nootropic supports/promotes physical balance via the cerebellum?

Jason
January 1, 2023

Great article. I’ve been watching your reviews for almost a year now. You’ve responded and helped me with more than a few. I started coming to your page because I have memory issues, anger issues, mood swings, concentration and balance problems as well. I’ve had 10 concusions, 5 of which were considered severe as I was knocked unconscience, 3 caused short term blindness. 3 also resulted in skull fractures. First one was about 7 years of age (53 now) when I fell off of a picnic table onto concrete at school. Accompanying the concussions are 9 whiplashes, which have left me with constant neck pain which I’m sure doesn’t help the situation. 2 years ago I had a TIA and it further degraded my concentration, memory and I have a problem with balance when my eyes are closed.

After trying many different things, it seems alphaGPC, SAM-e, Sulforaphane, lithium orotate, selinium, NAC, ALCAR, iodine and a good multivitamin heavy on the Bs is finally producing benefits. The doc also has me on Lamotragine. It’s a lot but it keeps the, dare I say, .45 out of my hand. If I’m not mistaken, these drive the acetylcholine receptors the most by boosting sulpher and methionine levels. Correct me if I’m wrong there. I’ve tried boosting other neurotransmitter nootropics but nothing much else has worked. PS is next on the list if needed. I tried 5-htp and for about 2 weeks I was GREAT… then I crashed pretty much like you said in one of your videos.

I thank you for your help, it’s been a lifesaver. literally

    David Tomen
    January 13, 2023

    Jason, take a look at my suggested stack near the bottom of the above article. It may give you some ideas on what else you can try.

    But at 53 you should try raising your other neurotransmitters anyway. Because they all naturally decline with age even without the challenges you have been through. Dopamine declines by 10% per decade starting in your early 20’s. I suggest 500 mg L-Tyrosine twice per day, L-Tryptophan 500 mg before bed and 300 mg PharmaGABA before bed.

    And consider adding 400 mg magnesium chelate before bed, 1,000 mg DHA in the morning, and 100 mg Phosphatidylserine (PS) 3-times per day.

Max
October 20, 2022

Hello David. Your website is brilliant. Which nootropic would be best for repairing cognitive skill called Estimation if this skill was decreased by traumatic injury of prefrontal cortex?

    David Tomen
    October 22, 2022

    Max, it would depend on what kind of damage there is. If that is unknown then I suggest trying the stack I recommend above under the sub-title “Suggested Nootropic Stack for TBI or Concussion Recovery”.

Ann Richards
September 28, 2022

Hi,
I understand that nootropics need to be cycled. Would it make sense to cycle different nootropics on varying days of the week so that you can have something everyday.
Thank you

    David Tomen
    September 29, 2022

    Ann, who says “nootropics need to be cycled”? Because whomever said it doesn’t know how nootropics work.

Liz
September 25, 2022

Hello David, I am a great Fan of your work, and I also share your YouTube channel, on this occasion I ask for your help.
I am taking Potassium Bicarbonate, 1.3 Grams a Day (494 Mg of Elemental Potassium), and sporadically when I have a headache I take Ibuprofen,
I would like to know how much hours should I wait before taking Ibuprofen so that it does not interact with potassium supplementation?

-Finally, do you think it is safe to take this amount of Potassium all at once?, and how many times a Day do you recommend that amount (I Attached is the link to the supplement that I been consuming)

Nutricost-Potassium-Bicarbonate-Powder

    David Tomen
    September 26, 2022

    Liz, according to the National Institutes of Health here in the US human adults 19–50 years require 3,400 mg per day (men) and 2,600 mg (women).

    But there is some controversy over how much potassium is safe to take as a supplement. The FDA claims that any more than 99 mg per day of supplemental potassium have been associated with small-bowel lesions. This is their full explanation of dietary potassium (https://ods.od.nih.gov/factsheets/Potassium-HealthProfessional/)

    But I have not seen any contraindication between potassium and ibuprofen. Did I miss something?

      Liz
      September 26, 2022

      Hello David, Drugs.com says that Combining a Potassium Supplement with NSAIDS (Ibuprofen, etc) significantly increase potassium levels in the blood, I enclose the Link below,
      Without obligation David, how long would you wait before consuming Inuprofen after consuming the dose of Potassium bicarbonate that comes in the supplement that I mentioned? (494 Mg of Elemental Potassium), I did not find any recommended time anywhere, do you think 12 hours is enough?,
      I would greatly appreciate it

      https://www.drugs.com/drug-interactions/ibuprofen-with-potassium-chloride-1310-0-1912-0.html

      https://www.drugs.com/mtm/potassium-bicarbonate.html

        David Tomen
        September 27, 2022

        Liz, the half life of potassium is about 7 hours. So in 14 hours it should be cleared from your system.

        Jason
        January 1, 2023

        This is nice to know. I take 800 mg ibuprofen and 1000 tylenol twice a day for neck pain. I take it with my other suppliments which includes 3-400mg potasium. Guess I need to rethink my “stack”. It’s just I don’t get nearly enough potasium in my diet normally.

Yasin
August 22, 2022

Hello, thank your for your efforts of making this website. My question :

Can nootropics help with recovry from substance abuse like cocaine? Talking about sporadic use not hardcocre junkie. I would love to hear any opinion on that

    David Tomen
    August 23, 2022

    Yasin, there are a couple of supplements that help people detox from opiates. Including Black Seed Oil and Passionflower extract.

Michael
July 20, 2022

Hello David!

Everyone says about this delicate balance…

What is your daily Tyrosine – Tryptophan ratio?

    David Tomen
    July 20, 2022

    Michael, I personally use 1,000mg L-Tyrosine in the morning, 500 mg at noon and another 500 mg around 4 pm. And I use 500 mg L-Tryptophan about 90 mins. before bed.

    But that is what works for me. This will vary from person to person depending on how your system uses these precursors. And the other factor is age. As you get older you need more of these precursors because your system is not efficient in using them.

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