Preventing and Treating Strokes with Hydrogen and Magnesium

Dr. Matthias Rath believes heart attacks and strokes are not true diseases but the result of nutritional deficiencies. "Heart disease is not caused so much by what you eat as by what you don’t eat."[1] Whatever we choose to believe or conceive, traumatic brain injury (TBI) and cerebral vascular events are usually devastating, yet because few in the mainstream listen to Dr. Rath, heart disease and strokes continue to mow down the public in excessive numbers.

Annually, in the United States, approximately 795,000 people suffer a stroke, of which 610,000 are first attacks. An estimated 7.2 million Americans age 20 or more report a history of stroke. Ischemic stroke is one of the most common sources of mortality in the world.

Researchers have been trying to find complementary therapies to treat ischemic stroke to improve its prognosis and expand the therapeutic window for reperfusion treatment. There are few treatments proven to ameliorate the brain damage and overall outcome in patients in the mainstream of medicine. But that would change if people listened to the research on hydrogen gas and high dosages of magnesium. 

This essay is about these two strong neuroprotective agents, which, when brought together, could turn the corner in both the prevention of strokes and their treatment. An ideal neuro-protectant would be non-toxic, easily administered, permeable at the blood-brain barrier (BBB), and offer protection at all stages of injury, including prophylaxis. Hydrogen gas fits the bill.

Hydrogen Gas is Essential for Stroke Patients

Every doctor and patient should know that hydrogen has many of the required characteristics for a successful neuroprotectant: it is easy to produce, diffuses rapidly through the lipid membranes, is inert and safe to administer, and reacts only with the most aggressive ROS. At the same time, it mediates multiple pathophysiologic pathways leading to apoptosis and cell death.

Hydrogen gas eliminates hydroxyl free radical and peroxynitrite anions producing a therapeutic effect in patients with ischemic stroke. Many studies have been published illustrating its anti-oxidative, anti-inflammatory, and anti-apoptotic effects. 

Numerous experimental evidence indicates that free radical formation in all forms of stroke damage was increased, leading to nutritive oxidative stress. There are several free radical production mechanisms during ischemia, including intracellular calcium overload, mitochondrial dysfunction, NMDAR-mediated excitotoxicity, and the release of inducible nitric oxide synthase. Excessive free radicals, such as ROS and hydroxyl radical, can damage cellular macromolecules and lead to autophagy, apoptosis, and necrosis of cells by affecting signaling pathways. Also, free radicals cause DNA damage and cellular aging.

The key to the success of hydrogen in stroke patients is mitigating the production of free radicals, which are the most important pathological mechanism of brain damage after stroke. Takedown the level of damaging free radicals, and we reduce brain damage. Hydrogen gas therapy targets hydroxyl radicals, which are considered the main trigger for free radical chain reactions.

One study showed that hydrogen eye drops directly decreased hydroxyl radicals in ischemia/reperfusion of retinas.[2] Hydrogen can also reduce 8-hydroxy-deoxyguanine, decreasing DNA oxidation.

In a clinical trial of 25 patients with cerebral ischemia, 3% hydrogen was administered by inhalation for one h of twice daily for seven days. Hydrogen concentration reached a plateau at 20 min, then it decreased to 10% of the plateau after 6–18 min of cessation of administration, in arterial and venous blood, respectively. Conclusion: There is increasing evidence from cellular, animal, and human studies suggesting that hydrogen can be administered safely as a neuroprotector during revascularization.

It is time for hydrogen to take center stage for stroke patients. Injections or IV drips of magnesium would also be called for and patients’ water infused with magnesium bicarbonates.

Magnesium for Prevention and Treatment of Stroke

Magnesium deficiency can cause metabolic changes
that may contribute to heart attacks and strokes.
National Institute of Health

When magnesium is present in water, life and health are enhanced. One of the main benefits of drinking plenty of magnesium-rich water is to prevent heart disease and stroke, even in children.   Dr. Jerry L. Nadler informs us that magnesium prevents blood vessels from constricting, thus warding off blood pressure rises, strokes, and heart attacks. Magnesium inhibits the release of thromboxane, a substance that makes blood platelets stickier."

A ten-year study of 2,182 men in Wales found that those eating magnesium-low diets had a 50 percent higher risk of sudden death from heart attacks than those eating one-third more magnesium. High magnesium eaters were only half as likely to have any cardiovascular incident such as non-fatal heart attacks, strokes, angina (chest pain), or heart surgery.[3]

A 2006 issue of the Journal of the American College of Nutrition published an article showing that as consumption of magnesium falls, the level of C-reactive protein goes up. C-reactive protein (CRP) is produced in the liver. It has emerged as a strong predictor of clinical events of cardiovascular diseases, such as heart attacks and stroke, even in cases where cholesterol levels may be normal.

In my practice the use of magnesium in the early
stages of a stroke has rendered the best results.
Dr. Al Pinto

The most effective stroke treatments are given within the first few hours after a stroke has occurred. With magnesium treatments, the trend toward a better functional outcome in patients at 30 days is seen when treatments are started 24 hours from onset versus controls.

Over a decade ago, in Los Angeles, California, the FAST-MAG trials had ambulance personal injecting magnesium quickly upon arrival when patients were having a stroke. The Field Administration of Stroke Therapy (FAST-MAG) was an NIH-NINDS-sponsored study whose goal is to evaluate field-initiated magnesium’s effectiveness and safety in improving the long-term functional outcome of patients with acute stroke.

This experimental trial addressed the crucial factor of delayed time to treatment, which has hindered all past human clinical trials of neuroprotective drugs.[4] The FAST-MAG Pilot Trial demonstrated that field initiation of magnesium in acute stroke is feasible, safe, and potentially productive. The basic design was to inject magnesium within 1-2 hours of the onset of stroke when the benefits of neuroprotective acute stroke therapies are likely to be greatest.

By utilizing field delivery via the ambulance, medical scientists were conducting the first neuroprotective study ever performed in the 0-2-hour window. Most stroke patients typically don’t receive treatment within these brief windows. Patients usually arrive at the hospital too late, and the consequences as such are great.

Researchers believe magnesium slows the chemical process that can kill 12 million brain cells per minute during an untreated stroke, leading to long-term disability and death. Every moment is crucial to the outcome. At least nine pre-clinical studies have examined systemic magnesium sulfate’s effect upon final infarct size in animal focal ischemic stroke models. Eight of the nine demonstrated substantial decreases in infarct size in treated animals, with reductions ranging from 26 to 61 percent.

Early studies using rats and mice showed that if given
at high concentrations, magnesium can decrease the area
of the brain that is permanently lost as a result of a stroke
Dr. Jose Vega

"How does magnesium protect the injured brain?" asks Dr. Vega. "The response to a lack of oxygen and nutrients (i.e., ischemia) by the brain includes a local release of chemicals that can damage brain cells even beyond the damage that can be expected by ischemia alone. Perhaps the most harmful of these chemicals is glutamate, an amino acid used in very low amounts by brain cells to communicate with each other. However, during a stroke, the massive amount of glutamate released produces a flood of calcium inside brain cells, which causes them to die. Magnesium is thought to have the ability to prevent glutamate from causing this flood of calcium in the cells, thus protecting them from premature death."

Dr. Tavia Mathers and Dr. Renea Beckstrand from Brigham Young University published in the Journal of the American Academy of Nurse Practitioners in 2009 that magnesium has been heralded as an ingredient to watch for in 2010 and noted that magnesium is helpful for reduction of the risk of stroke.[5]       

Dr. Saver and colleagues[6] investigated the neuroprotective effect of early magnesium infusion in ischemic or hemorrhagic stroke in the field; three-quarters of the infarct cohort were treated within two hours of onset and nearly one-third within one hour of onset. Dramatic early results were reported in the early-stage (42 percent of < 2-hour infarct patients) and good results in the 90-day global functional outcomes (69 percent of all patients and 75 percent of < 2-hour infarct patients).

Low CSF Mg+2 levels in patients with
acute ischemic stroke at admission
predicted a higher one-week mortality.[7]

An essential prerequisite for any pharmacological agent to offer significant brain neuronal protection during strokes is its ability to cross the blood-brain barrier freely. Several studies show that magnesium crosses this barrier in both animals and humans.[8] Magnesium ions cross the intact blood-brain barrier efficaciously so that intravenous magnesium sulfate significantly raises cerebrospinal fluid and brain extracellular fluid magnesium to supraphysiologic levels.

Dr. Jerry Nadler said, "Higher dietary intake of magnesium was among the factors associated with a reduced risk of stroke in men with hypertension. In a survey of almost 45,000 men ages 40-75, the overall risk of stroke was significantly lower for men in the highest quintile of intake of potassium, magnesium, and cereal fiber, but not of calcium, compared with men in the lowest quintile of intake."

Magnesium is an agent with actions on the N-methyl-D-aspartate (NMDA) receptor and has a low incidence of side effects. It may reduce ischemic injury by increasing regional blood flow, antagonizing voltage-sensitive calcium channels, and blocking the NMDA receptor. Systemically administered magnesium at doses that double physiological serum concentration significantly reduces infarct volume in animal models of stroke, with a window of up to six hours after onset and favorable dose-response characteristics when compared with previously tested neuroprotective agents.[9]