'Best Nootropics for Traumatic Brain Injury'
https://nootropicsexpert.com/best-nootropics-for-traumatic-brain-injury
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 …
Table of Contents
o
Creatine
o
Pine Bark Extract (Pycnogenol®)
o
Turmeric
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.
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.
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).
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] Because
they run low on adenosine triphosphate (ATP) which
they use for fuel.
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.
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 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 linked to learning and formation of long-term memory.
It comes as no surprise that LTP is impaired after traumatic brain
injury. 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.
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.
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 fuel source powering 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.
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 (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]
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]
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.
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]
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) 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®)
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 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 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.
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 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 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 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.
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 help repair your
brain 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 (Pycnogenol®)
·
Pramiracetam
·
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
REFERENCES
[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)
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