Chronic, excessive exposure, and accumulation of neurotoxic agents such as heavy metals (lead, mercury, cadmium), mefloquine (Lariam), and food additives such as monosodium glutamate (MSG) and aspartame cause neurotoxicity and brain damage. This chemical-induced brain damage closely resembles the pathophysiology of classical traumatic brain injury (TBI) with decreased cognitive function, neurodegeneration, and increased psychiatric manifestations (depression, anxiety, sleep disturbances, and irritability). Current evidence supports a strong causal relationship between military-related exposure to specific neurotoxins, and the development of serious medical conditions and higher rates of suicide among service members. To address this current deficit in military healthcare, it’s recommended that efficacious, non-toxic, neuroprotective and neuro-regenerative agents such as highly bioavailable magnesium, nutritional lithium, zinc, selenium, boron, ascorbate, tocopherols, heavy metal chelators, and glutathione precursors such as N-acetyl-cysteine (NAC) be immediately employed as a “protective shield” and to support critical healing processes in the brain and nervous system.
Neurotoxicity is a term used to describe the neurochemical and neurophysiological changes caused by specific toxic agents. These changes can include negative effects on cognition, memory, mood, and sleep along with increased sensitivity to emotional and physiological stress. In today’s world, we are continuously exposed to toxins from multiple sources: the environment, diet, certain drugs, heavy metals, oxidative stress, and occupational hazards. While all people are at risk of toxicity – military service members are a population with some of the highest rates of occupational exposure to neurotoxic agents such as heavy metals (e.g. lead, mercury, cadmium), prescription drugs (e.g. mefloquine), blast waves, and dietary neurotoxins such as aspartame from food sources commonly consumed by military service members.
In addition to chemical toxins and physical injuries that induce brain trauma – nutritional deficiencies play a fundamental role in the progression and severity of the injury – and directly impact healing. A 2014 study published in Nutritional Neuroscience found that important brain nutrients (e.g. magnesium, vitamin C, folate) were frequently deficient in the diets of patients being treated for traumatic brain injury, which resulted in the “worst mean neurobehavioral scores for those patients not meeting the estimated average requirements .”
Particulate pollution is also a major concern. Dust and air quality studies in both Iraq and Afghanistan have shown unsafe levels of lead, other heavy metals, industrial pollutants, and depleted uranium . Other countries where service members are deployed to such as Pakistan, Yemen, Saudi Arabia, and Central African Countries are known for being some of the most polluted areas in the world. Many service members are suffering from unexplained illness – also known as “Gulf War Syndrome” – and health care providers repeatedly fail to perform the proper tests for these well-known toxic influences.
Service members are frequently exposed to unsafe levels of toxic substances from constant immersion into highly polluted, austere environments under extreme stress conditions with inadequate sleep, poor nutrition, along with chronic and continual use of antibiotics putting the service member at a higher risk of toxin exposure.
Another source of heavy metal exposure is the dirt and dust at firing ranges and shoot houses. Service members who explosively breach in these highly-contaminated areas are at greater risk of heavy metal poisoning, neurotoxicity, and cancer . These toxins build up on equipment and uniforms which soldiers take home and wash with their family members’ clothing – potentially contaminating the home and affecting the entire family. The human body was not designed to protect itself from the extremely high lead levels service members are routinely exposed to in their occupational environment. Heavy metals such as lead, cadmium, and mercury induce oxidative stress, and deposit in the brain and nervous system where they promote tissue injury, and increased systemic and neural inflammation. In addition, medications, such as quinolones, fluoroquinolones or antifungals, may put a soldier at increased risk for renal failure when exposed to heavy metals .
Heavy Metal Toxicity
Service members who conduct training in “live-fire” shoot houses and dirt flat ranges are at an increased risk of exposure to high levels of lead, tin, and copper . These environments cause excess particle amounts of heavy metals to be inhaled, ingested, and absorbed into soldiers while they conduct training. Excessive exposure to toxic metals leads to acute and chronic cellular dysfunction and classical symptoms of toxicity. The kidneys are the first target organ of heavy metal toxicity due to their ability to reabsorb and accumulate divalent metals (e.g. lead, mercury, cadmium]. The degree of damage by heavy metals depends on the nature, the dose, and the route and duration of exposure . Due to toxin uptake and partitioning to more metabolically active tissues, routine blood tests are not a reliable measure. Such tests are incapable of providing an accurate assessment of the body burden due to chronic exposure to heavy metals since these metals are sequestered and stored in fat, tissues, organs, and bones .
It’s been known for centuries that lead has detrimental effects on the brain and nervous system. Today, we know that lead (Pb2+) displaces calcium (Ca2+) in essential metabolic functions, crosses the blood-brain barrier (BBB), and preferentially accumulates in specialized glial cells known as astrocytes, which serve a myriad of vital homeostatic functions in the brain including regulation of neurotransmitter (e.g. glutamate) and extracellular potassium concentrations – both of which are essential for the propagation of actions potentials and neuronal firing .
There are approximately 1 trillion neurons in the central nervous system, with glial cells such as astrocytes accounting for about 90% of the total cells. Four main types of glia exist: astrocytes, oligodendrocytes, ependymal cells and microglia. The astrocytes – the “guardian angels” of the neurons and synapses – are the most common, and are so named because of their abundant long, thin projections which give them a starry look. Astrocytes perform critical housekeeping functions such as supplying neurons with nutrients, energy-rich molecules and neurotransmitter precursors essential for healthy neuronal function, and removes excess neurotransmitters (e.g. glutamate or GABA) from the synapse, so the next signal will be properly received and transmitted . Astrocyte processes surround all synapses and perform essential functions in maintaining the fluid, ion, pH, and neurotransmitter homeostasis of the synaptic interstitial fluid – critical for healthy synaptic transmission. Astrocytes also play a major role in controlling where and when our brain’s all-important synapses will form .
Lead, Calcium, and Vitamin D
Lead exposure is one of the greatest exposures to service members next to prescription drugs and explosive blasts. Lead is a well-described, neurotoxic heavy metal that increases oxidative stress, tissue inflammation, and damages sensitive cellular structures such as cell membranes and DNA. When deposited into the bones, brain, or other tissues, it can cause cancer and in some cases encephalopathy. According to a 2009 Veteran’s Affair study, elevated bone lead concentrations were associated with 2.5-fold increase in mortality, a 6-fold increase in cardiovascular mortality, and an 8-fold increase in ischemic heart disease .
Vitamin D plays a crucial role in the absorption of lead because the body thinks lead is calcium. Since lead and calcium share the same 2+ charge, the body does not recognize the difference between the two ions, and absorbs and stores lead in the place of calcium in bone and throughout the body. Calcium channels control the nervous system and conductivity of transmissions across nerves. If lead is in the system it can negatively impact the function of calcium channels and the resulting conductivity . As a well-known cognitive suppressing agent – lead exposure by altering this conductivity – can slow the service member’s mental and physical processes.
If a service member is on an intensive repletion protocol to correct a vitamin D deficiency, and is consuming 10-50,000 iu of vitamin D3 per day while working at a firing range and exposed to high levels of lead – the following protocol is recommended. Since vitamin D greatly enhances Ca2+ absorption – Pb2+ absorption will also increase  unless calcium (e.g. citrate or carbonate) is supplemented to competitively inhibit lead absorption [11-14] via their common uptake channel – the divalent metal transporter (DMT1) [15, 16]. Considering that many service members are vitamin D deficient – careful consideration should be given to service members who work or train at firing ranges regularly. To prevent both acute and chronic lead poisoning – Vitamin D supplementation should always be accompanied with supplemental calcium and magnesium (for calcium balance) to decrease gastrointestinal lead absorption.
Tests for Heavy Metal Exposure
A Complete Metabolic Analysis, Male Hormone Panel, and DMSA challenge test – via urinalysis – will show the effects of recent exposure to heavy metals, which invariably correlate with the clinical symptoms and degree of neurotoxicity. The absorption and accumulation of heavy metals can block vital metabolic functions such as the body’s primary energy producing pathway (i.e. Krebs Cycle) and also interferes with endocrine functions throughout the body, especially the hypothalamus, pituitary, adrenal axis (HPA) and hypothalamus, pituitary, thyroid axis (HPT) . The HPA axis controls every function in the nervous system. If this system is damaged, the inevitable consequence is a multitude of symptoms (e.g. chronic fatigue, brain fog, depression, anxiety, sleep disturbances, hormone imbalance) and chronic illness.
The biological half-life of lead in blood is 28-36 days in the blood and approximately 10- 30+ years in bone. Lead has a preferential affinity for bone tissue, where it is sequestered and hidden from detection. Therefore, unless the soldier was exposed to high levels of lead within 36 days, its presence would not be revealed in serum tests. The National Institutes of Health (NIH) utilize the dimercaptosuccinic (DMSA) challenge test for chronic heavy metal exposure and X-Ray Fluorescence (XRF), a non-destructive analytical technique to scan bone for chronic lead exposure. Free erythrocyte protoporphyrin (FEP) level may be useful in demonstrating the degree of biological abnormalities that exist from chronic lead exposure. Elevated blood lead levels (BLL) are associated with the development of microcytic anemia, and low serum iron and ferritin .
Lead Poisoning and Increased Cancer Incidence in the Military
Military personnel are experiencing increased rates of various forms of cancer. A 2009 study found that prostate cancer rates are twice those of the general population, and breast cancer rates are 20-40% higher among service members . A 2006 study found that rates for cervical, prostate, and vulvar cancers were significantly higher for U.S. Air Force active duty personnel than the general population . The incidence of thyroid cancer is also significantly higher among active duty U.S. military personnel .
A close inspection of the toxins service members are commonly exposed to offers substantial insight into this growing problem. Military personnel are often exposed to a wide variety of environmental toxins including dangerous levels of lead (a probable human carcinogen), and are deployed to countries that have high amounts of environmental pollutants in the air and soil. Lead and other heavy metals are inhaled and ingested into the lungs where lead is released to the blood and distributed throughout the body, and can be absorbed through the skin when conducting training. These metals are found in the primers, propellants, the rounds, and even the barrels of the weapons that the bullets travel through. The cloud of smoke that comes out of the barrel every time a weapon is fired contains particles of these metals. Heavy metals are widely known to disrupt the central nervous system, metabolism and cause renal failure .
Many of lead’s toxic properties are due to its ability to mimic or compete with calcium. Lead has a dual impact on the release of neurotransmitters by increasing spontaneous neurotransmitter release (non-productive neuronal firing), while decreasing stimulated release. Lead also negatively affects the synthesis of heme for red blood cell production . Lead inhibits DNA repair and acts synergistically with other mutagens, potentiating their negative effects in the body . The symptoms of lead poisoning include renal failure, limb weakness or numbness, hypertension, loss of memory, vision, headache, decreased cognitive function, and behavioral problems and sexual dysfunction . These symptoms are consistent with TBI because both TBI and lead toxicity involve neurotoxicity.
Service members may more successfully detox at home because the foods they need to assist the body are widely available. Soldiers cannot detox when they are deployed outside the continental United States (OCONUS) because the foods they eat are missing the necessary building blocks needed for normal detoxification processes. Fresh whole foods (preferably organic, pesticide, and chemical free) rich in antioxidants and glutathione precursors are an absolute requirement for proper detoxification (i.e. elimination) of heavy metals and other exogenous toxins.
Soldiers do not receive any antioxidants in the processed foods they consume on deployments. Processed foods are often full of preservatives (e.g. benzoates) and neurotoxic agents such as synthetic food colors (e.g. Red #40) and excitotoxic sweeteners (e.g. aspartame) and flavoring agents . The human body has a very limited reserve of the body’s primary antioxidant, glutathione, which requires a constant intake of adequate sulfurous amino acids (e.g. cysteine) to maintain sufficient levels for necessary antioxidant defenses. Once glutathione – and other supporting antioxidants are depleted (e.g. vitamin C, E, polyphenolic antioxidants) – the body loses its primary antioxidant and heavy metal defense shield – making it much more susceptible to cancer and chronic disease .
Traumatic Brain Injury
Traumatic brain injury (TBI), either physically or chemically induced increases oxidative stress, inflammation, and brain injury. When a service member experiences a TBI, their glutamatergic system gets upregulated for up to sixty minutes. Excitatory amino acids (EAAs) exceed healthy limits, and become toxic. The first 10 days following a TBI, known as the “acute phase, the following excitotoxic events occur: terminal membrane depolarization along with excessive release of excitatory neurotransmitters (i.e. glutamate, aspartate) leading to over-activation of N-methyl-D- aspartate (NMDA), α-amino-3-hydroxy-5-methyl-4-isoxazolpropionate (AMPA), and voltage-dependent Ca2+ and Na+ channels. Subsequent Ca2+ and Na+ influx leads to an increase in catabolic intracellular processes and a high level of oxidative stress .
The next stage, known as the “subacute phase” (> 10 days; < 1 year post-injury) is characterized by tissue damage and the beginning of Wallerian degenerative processes if healing is not progressing. The axon response to injury and secondary insults is followed by the process of Wallerian degeneration, which begins as a potentially reversible phase of intra-axonal damage, and proceeds to further axon fragmentation and demyelination of intact axons. These elements of axon and myelin pathology present opportunities for repair, though if no healing techniques are employed (e.g. biochemical restoration, nutrient therapeutics, hyperbaric oxygen) cell death is often the result . The “chronic phase” of post-concussion is diagnosed as persistent (> 1 year and ongoing) and by the severity of the trauma with symptoms such as chronic and progressive cognitive impairment, depression, anxiety, sleep disturbances, and progressive neurodegeneration and decline occurring years after the injury [28, 29]. At this point, cell death has occurred, and cognitive function and processing speed is invariably compromised.
An individual who has more exposure to blasts, blows to the head or hard landings with a parachute is at greater risk for neurodegenerative brain disease. Heavy breachers and assaulters are at the highest risk of developing complications with blast exposures. This mechanism of injury is apparent in NFL players and boxers and is known as encephalopathy. Encephalopathy is well-known and found in dead soldiers and athletes who commit suicide . This form of degenerative brain disease is caused by repetitive blows to the head. This is something to be considered with heavy breaching and static line jumping. Every jarring motion of the brain inside of the skull can turn on the glutamate and calcium activating neural circuitry. The severity of the acceleration and deceleration of the brain inside the skull determines the length of time these systems remain activated.
The quinoline antimalarial, mefloquine used prophylactically for soldiers abroad is another neurotoxic agent soldiers are having to contend with. When levels in the brain exceed a certain threshold, mefloquine becomes an insidious and damaging neurotoxin. The reason that effects differ is most likely due to genetic and metabolic differences among soldiers, along with body composition and mass differences . Mefloquine accumulates in tissue, rather than in the circulation, and as a result may only be effective if taken 7-9 weeks prior to entering a country with high malaria threat . Mefloquine neurotoxicity affects the brainstem and limbic system and may induce long-term or sometimes permanent mental health and neurological symptoms, including personality change, irritability, cognitive deficits, disequilibrium and visual disturbances. Due to its ability to cause neurological injury (i.e. brain trauma) – mefloquine neurotoxicity has a very similar clinical picture to that of classical TBI and PTSD [31-35].
One of the principles axioms in the field of toxicology is: “it’s the dose that makes the poison.” Though, with that said, some substances have greater potential to create toxicity than others. Mercury is one such substance. There are three forms of mercury that we are exposed to in our diet and environment: elemental (e.g. liquid or vapor), inorganic (e.g. HgCl2), and organic (e.g. methymercury). Each has its own profile of toxicity.
Symptoms of methyl-mercury poisoning include: detrimental effects on cognitive thinking, memory, attention, language, fine motor skills, impairment of speech, hearing, walking, muscle weakness, loss of peripheral vision, and “pins and needles” feelings, usually in the hands, feet, and around the mouth. Symptoms of prolonged or acute exposure to elemental mercury include: tremors, emotional changes (e.g. mood swings, irritability, nervousness, excessive shyness), insomnia, neuromuscular changes (e.g. weakness, muscle atrophy, twitching), headaches, disturbances in sensations, changes in nerve responses, and poor performance on tests of mental function.
Another form of organic mercury, ethyl-mercury – found exclusively in the synthetic preservative, thimerosal – has been shown to be 50 times more toxic than methyl-mercury, and contains 49.55% mercury by mass .
Two of the most insidious excitotoxins (ie. neurotoxins) in our food supply today are aspartame and monosodium glutamate (MSG)[24, 37-42]. There are currently over 6,000 consumer products containing aspartame, and thousands of that contain MSG in its many forms (e.g. autolyzed yeast, glutamate, glutamic acid, hydrolyzed protein, monopotassium glutamate, monosodium glutamate, textured protein, yeast extract, yeast food, yeast nutrient, flavors, and flavorings). The mechanism of toxicity of MSG is a very straight forward one – elevation of extracellular glutamate and excitotoxicity from overstimulation of the body’s primary excitatory glutamate receptor, the N-methyl-D-aspartate receptor (NMDA-R)[38-42].
Aspartame’s mechanism of toxicity is a bit more complex, and is driven by the following six components: phenylalanine, aspartic acid, methanol, formaldehyde, formic acid, and diketopiperazine (DKP) – and the list of adverse effects associated with its use is truly staggering and include: fatigue, depression, anxiety, seizures, headaches, migraines, tachycardia, breathing difficulties, irritability, weight gain, metabolic syndrome, tinnitus, numbness, dizziness, endocrine disruption (ie. Graves’ Disease), development of phobias, vision problems, night terrors, sleep apnea, and sleep disturbances [41, 42].
From a biological and toxicological perspective all of these adverse effects make perfect sense given the fact that aspartame is 10% methanol by weight, which is quickly converted (i.e. oxidized) to formaldehyde, and then to formic acid in the liver. Both formaldehyde and formic acid are “neuro-irritants”, disruptive to normal cellular function, and display biological toxicity at relatively low levels. Much like lead, formaldehyde is a carcinogen and neurotoxin that binds to proteins and receptors in the brain and nervous system interfering with their function. Both are very reactive chemical species, promoting cellular dysfunction, oxidative stress, and neuro-inflammation.
Chemically speaking, aspartame is a dipeptide composed of the two amino acids, phenylalanine and aspartic acid, with a conspicuous “o-methyl” group at one end of the molecule. It is this latter component that makes it especially toxic to the brain, eyes, and all nervous tissue. When consumed or heated to 85 ℉, aspartame quickly breaks down (i.e. hydrolyzes) into the two excitatory amino acids, phenylalanine and aspartic acid , and methyl alcohol (methanol). In a 1980 study published in Neurobehavioral Toxicology, Olney et al reported “conspicuous hypothalamic damage” (i.e. brain damage) in mice from the voluntary ingestion of glutamate and aspartate, similar to the feeding behavior of many consumers today . This study further substantiated previous studies demonstrating the ability of glutamate and aspartate to destroy neurons in the brains of various animal species [39, 40].
One can of diet soda contains approximately 180 mg of aspartame, which is equivalent to 8.2 packets of aspartame sweetener (e.g. Nutrasweet, Equal). Each packet contains 22 mg of Aspartame, and releases 2.2 mg of methanol per packet. The EPA classifies methanol as a “cumulative poison due to the low rate of excretion once it is absorbed”, and recommends an upper allowable limit of consumption for methanol of 7.8 mg per day. Heavy users of aspartame-containing products can consume as much as 250 mg of methanol daily or approximately 32 times the EPA limit .
Chewing gum is perhaps one of the most unsuspecting, and insidious sources and “delivery systems” of this neurotoxic poison. When an individual chews gum containing aspartame –the highly vascularized oral mucosa (i.e. lingual, sublingual, buccal tissues) in the mouth becomes saturated with this chemical – which is absorbed directly into the bloodstream and carried within seconds to the brain.
Processed foods containing monosodium glutamate (MSG) and aspartame are harmful to people who have TBI, nervous system disorders, or metabolic disorders. These toxins cause over-activation of the body’s primary excitatory receptor system (NMDA-R), producing neuronal degeneration, excitotoxicity, and eventual cell death. Two of the body’s natural neurotransmitters are aspartate and glutamate. MSG and aspartame contain highly potent, synthetic forms of these natural neurotransmitters and cause excitotoxicity and neuronal damage when consumed in large amounts [20, 39-42]. Individuals with acute or chronic mercury or lead poisoning, or a predisposition for depression, anxiety, or mood disorders will experience greater adverse effects to these chemicals than those without a pre-existing health condition. These foods or chemicals should not be consumed by an individual having any type of neurological condition or brain-related injury because they can increase the effects of the initial injury. Metabolism, genetics, size (i.e. body mass) and body composition will cause people to have greater or lesser effects [40-42].
Nutrient Deficiencies in Traumatic Brain Injury
Magnesium is rapidly depleted following brain trauma [43, 44], which further contributes to the pathophysiology of the trauma (e.g. increased oxidative stress, inflammation, excitotoxicity, cell death). Replenishing levels to normal values have been shown to prevent and reverse neurological injury . A 2004 review article titled, “Magnesium therapy and recovery of function in experimental models of brain injury and neurodegenerative disease”, reported that magnesium therapy was “effective in facilitating recovery of function and exhibits very robust and unique effects” .
Magnesium deficiency promotes inflammation, increasing levels of several pro-inflammatory mediators such as Substance P, TNF-α, IL-1, and IL-6, and has also been shown to promote insulin resistance, Type -2 diabetes, and metabolic syndrome [47, 48]. Magnesium acts as the brain’s primary inhibitory ion – functioning as the “brakes” – whereas calcium (influx) serves as the “accelerator” or activator. Though, magnesium isn’t the only nutrient that is depleted during trauma or the chronic stress that precedes and follows injury. Trauma and stress increase the body’s requirement for all essential nutrients especially those required in neuro-repair and healing. These include the full range of vitamins (e.g. A, B-complex, C, D, E, essential fatty acids, DHA, EPA), and trace minerals that reduce oxidative stress, and promote neuro-regeneration and the formation of new neurons (i.e. neuro-genesis) such as lithium and zinc.
Lithium is another critically important nutrient in neuroprotection, neurogenesis, and healing processes in the brain and nervous system. Lithium works as a companion nutrient with magnesium and zinc, and is needed for vitamin B12 and folate utilization. Lithium, magnesium and zinc increase the body’s natural antioxidant defense systems (e.g. SOD, GPx, catalase), and are essential in preventing NMDA receptor over-activation (i.e. hyperactivity). In the 2014 review article, “Lithium to the Rescue”, the authors’ state, “There is now a substantial understanding of how lithium can strengthen and protect the brain .” A portion of its beneficial effects reside in its ability to modulate the NMDA receptor, but in large part it is lithium’s inhibition of an enzyme called glycogen synthase kinase-3 (GSK3) that is governing its wide-ranging activity [50, 51]. Inhibition of GSK3 protects brain cells from a wide range of assaults, including oxidative stress, DNA damage, impairment of mitochondrial function, and excitotoxicity [52, 53].
Along with magnesium and lithium, zinc is also needed in higher amounts for healing and repair, and to counteract losses by injury and chronic stress. Zinc has been shown to have anti-depressive, anxiolytic activity (i.e. stress-reducing), and works alongside magnesium and lithium in various body systems [54-56, 57]. Like magnesium and lithium deficiency – zinc deficiency increases oxidative stress, NMDA receptor dysfunction (over-activity), and contributes to general inflammation  while zinc supplementation can reverse this. Symptoms of zinc deficiency include delayed wound healing, frequent infections, mental fatigue, learning difficulties, low testosterone, and neurosensory disorders [54, 56].
The human body requires a broad-spectrum of macro- and micronutrients that support a multitude of essential processes and protective functions. Thanks to the invaluable contributions of Gerhard N. Schrauzer PhD, Linus Pauling PhD, Jonathan V. Wright MD, John A. Myers MD, and many others – we now have strong scientific and clinical evidence identifying more than 31 macro- and micronutrients essential for human health and well-being. Though not complete – these include, vitamins A, B1, B2, B3, B5, B6, B12, folate, C, D, E, F (essential fatty acids), K1, K2, calcium, magnesium, phosphorus, potassium, sodium, and trace minerals: boron, chromium, cobalt (B12), copper, iodine, iron, lithium, nickel, manganese, molybdenum, selenium, silicon, strontium, vanadium, and zinc [58-68]. Evidence also exists for the essentiality of arsenic in the metabolism of the amino acid, methionine and in the synthesis of spermidine and spermine, and S-adenosylmethionine decarboxylase  – and the trace element, silver in eye function and visual acuity .
Comprising just 3% of the body’s total mass, the brain has the highest energy requirement of all human tissues – up to 20% of the body’s total energy consumption and contains 25% of the body’s neuroprotective, hormone-precursor, cholesterol – a direct reflection of the brain’s enormous metabolic demands [71, 72].
Hormones Imbalances and Testosterone Deficiency
Hormone imbalances and testosterone deficiency are another major problem facing many who have suffered brain traumas – whether chemically or physically induced – and the solution may reside in this little known, yet essential trace element. Boron, like magnesium, zinc, and lithium is deficient in most diets (i.e. Standard American Diet = 1 mg/d) – yet has powerful anti-inflammatory and neuroprotective effects (> 3 mg/d), and is essential for healing .
A 2011 study by Naghii et al investigating the effects of boron (10 mg/d) in 8 healthy adult males – reported a dramatic reduction in three key inflammatory biomarkers (e.g. hs-CRP, IL-6, TNF-α) – with a 50% decrease in hs-CRP – following one week of supplementation. Equally significant was their finding on free testosterone, which increased by an impressive, 28.3% . The increase in unbound free testosterone observed with boron supplementation may prove to be especially beneficial in males with stress- or trauma-induced testosterone deficiency.
Boron raises levels of antioxidant enzymes such as superoxide dismutase (SOD), catalase, and glutathione peroxidase, and protects against pesticide-induced oxidative stress and heavy-metal toxicity, while also demonstrating preventive and therapeutic effects in a number of cancers (e.g. prostate, cervical, lung cancer, and multiple and non-Hodgkin’s lymphoma). Dietary boron is inversely correlated with prostate cancer incidence. Prostate cancer was 52% lower in men whose diets provided greater than 1.8 mg per day of boron compared with those whose dietary intake was less than or equal to 0.9 mg/d .
Boron is essential in the body’s utilization of both magnesium and vitamin D. Boron supplementation increases magnesium absorption and retention, decreases arthritis pain, and through its anti-inflammatory activity and other neuroprotective effects improve brain function. Moreover, an adequate boron intake of ≥ 3 mg/d can help prevent and correct magnesium and vitamin D deficiency. In all of the studies conducted to date, a minimum threshold intake of 3 mg per day is required to unleash the myriad of boron’s beneficial effect .
To address the current deficit in military healthcare – in addition to an emphasis on proper testing (e.g. tox-screens, MRI/DTI, SPECT scans) – it’s recommended that strategies employing optimized levels of neuroprotective, neuro-regenerative nutrients such as highly bioavailable magnesium, lithium, zinc, selenium, boron, ascorbate, tocopherols, omega-3 fatty acids, heavy metal chelators, and glutathione precursors such as N-acetyl-cysteine (NAC) be immediately employed for their detoxifying and healing benefits on the brain and nervous system .
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