Page 50 - summer2016

Glutamate is toxins, detrimental changes in the food supply Table 1) are particularly interesting. As it hap-

both essential and the loss of formerly protective lifestyle pens, glutamate is released in large amounts
after a TBI. While the brain has various
practices, few of us are lucky enough to have
and highly “unaltered physiology.” Thus instead of produc- mechanisms to restore glutamate homeostasis,
toxic at the ing a normal regenerative healing response, our neurodegenerative conditions and concussions
same time. impaired ability to recover quickly results in a impair glutamate clearance. The result—exces-
sive glutamate—then triggers a cascading series
“downward spiral of neurological demise.”
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Functional deficiencies and depletion of im- of damaging inflammatory effects. Thus, as the
portant brain nutrients are one of the key reasons body tries to heal by releasing glutamate, it sets
for our increased susceptibility to brain injury into motion a hyper-reactive excitatory response
and our compromised ability to heal. Common that damages the delicate neuronal tissue in the
deficiencies include sulfur, magnesium, zinc, vi- brain. These secondary effects turn out to be far
tamin D, B vitamins and omega-3 essential fatty more influential in determining the severity and
acids (EFAs)—especially docosahexaenoic acid outcome of concussion injury than the original
(DHA). Each of these functional deficiencies mechanical forces involved in the concussion.
has numerous downstream physiological conse- Neuroprotective omega-3 fatty acids can
quences related to brain injury and diminished decrease the toxic effects of glutamate. How-
brain resilience (see partial list in Table 1). ever, because of the widespread deficiency of
omega-3 fatty acids in the modern diet, this
GLUTAMATE TOXICITY neuroprotective action may not be readily avail-
Glutamate is the brain’s most abundant able to many concussion sufferers.
neurotransmitter, serving as a chemical mes-
senger that relays signals between neurons. SULFATE AND SULFATE TRANSPORTERS
Glutamate is needed for learning and memory Insufficient supplies of sulfate to the
and as an important source of energy, and is brain—or more precisely the cerebrospinal
involved in numerous aspects of normal brain fluid (CSF)—provide a central explanation
function and “many different and intercon- for many neurological disorders. (Sulfate is
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nected processes.” However, glutamate is the oxidized form of sulfur.) Impaired sulfate
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excitatory (brain-stimulating) as opposed to supply is a factor, for example, in Alzheimer’s
inhibitory (brain-calming), and it has somewhat disease, in part because adequate sulfate is
of a split personality: needed to remove potentially neurotoxic waste
“Glutamate has to be present in the right products and prevent oxidative damage. In the
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concentrations in the right places for the right case of concussion, Morley and Seneff suggest
time. Both too much and too little glutamate is that insufficient supplies of sulfate to the CSF
harmful. This implies that glutamate is both (caused by environmental and lifestyle factors)
essential and highly toxic at the same time.” 15 leave the delicate neuronal tissues in the brain
The issues surrounding omega-3 deficien- vulnerable to jarring. When there is insufficient
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cies, brain injury and glutamate toxicity (see sulfate in the brain, the neuronal tissues produce

TABLE 1. Functional nutritional deficiencies and their implications for brain injuries
DEFICIENCY OF: RESULTS IN:
Sulfur Impaired recycling of cellular debris and increased sensitivity to sudden impact
Magnesium Lower seizure thresholds
Zinc Increased protein misfolding comparable to that seen in Alzheimer’s disease
Vitamin D Increased likelihood of infectious agents in the brain
B vitamins Glutathione depletion and increased oxidative stress
Omega-3 fatty acids Increased glutamate toxicity
Adapted from Table 1 in Morley and Seneff, 2014. 11

50 Wise Traditions SUMMER 2016 Wise Traditions