Magnesium & Mental Health

Do you want to improve your mental performance? Learn how all major functions of our brain & nerves need magnesium, and why deficiency is linked to mental & nerve diseases.

++ Page Overview

This master page looks at all of magnesium’s roles in brain & nerve health[1] and includes a solutions section to help you restore and maintain healthy magnesium levels.

  1. Magnesium fuels our brain and nerves
  2. Magnesium develops our brain and nerves
  3. Magnesium develops our skills, intelligence and memory
  4. Magnesium protects our nerves and brain cells
  5. Magnesium creates new brain cells
  6. Magnesium facilitates nerve signalling
  7. Magnesium deficiency leads to mental and nervous system diseases (depression, Alzheimer’s, Parkinsons, Multiple Sclerosis, ADHD, etc.)

Before the solutions section, we take look at how modern farming and environmental stress levels have made it difficult to get enough magnesium from diet alone.

++ Helpful tip
This page has a lot of powerful info to help you resolve your problems. 

If you’re busy or want to understand things better, please read each section’s quick summary.

1. Magnesium fuels our brain & nerves...
Our brain and nerves are made of long thin cells called neurons which have branches at one end for receiving electric signals, and a terminal station at the other end for sending the signals to the next neuron.

This passing of electric signals along sequences of neurons is what allows us to think, perform vital functions and experience life with our senses.

Because our neurons are used so intensely non-stop, they need large amounts of energy. Neurons get energy by converting dietary sugar (glucose) into energy molecules called ATP (adenosine triphosphate)[2-4].

Both phases of this energy production need magnesium:

  1. First, our neurons need to absorb this glucose. This depends on the hormones insulin and glucagon, whose very creation[5-9] and function both require magnesium. [10-18]
  2. Second, our neurons now convert the glucose into energy molecules called ATP. This conversion is also a magnesium-dependent process. [19-23] In fact, each of the trillions of ATP molecules in your body needs to be bound to magnesium in order to be active.[24]

Magnesium and mental health and performance are linked at the most basic level: Our brain and nerves need magnesium for their energy.

In addition to their fuel, we also need magnesium for the physical development and maintenance of our brain and nerves:

1. Summary
Our brain and nerves are made of cells called neurons whose transmission of electric signals regulates our body and facilitates our five senses.

Neurons need magnesium to convert the food we eat into usable energy molecules called ATP. Low magnesium means low energy levels. 

2. Magnesium develops our brain & nerves...
During pregnancy, as the baby’s cells replicate & multiply, they begin to then differentiate (transform) into more specific cells. Out of the baby’s trillions of cells, 100 billion of them differentiate into neurons: the cells that make up our brain and nerves.

Both the cellular replication, AND differentiation into neurons requires magnesium:

  1. Replication: For a cell to replicate, it first needs to make a copy of its DNA. This process uses DNA polymerase, a magnesium-dependent enzyme[25]
  2. Differentiation: The newly replicated cell now engages a process called protein synthesis which transforms it into a neuron. This process is also magnesium-dependent. [5-9]

We see again how magnesium and mental health are related at a fundamental level:

Magnesium is critical for the initial creation and development of our neurons: the cells that make up the infrastructure of our brain and nerves. 

2. Summary
Our body develops and repairs our brain and nerves by replicating and developing neurons. 

This happens via protein synthesis, a process which requires magnesium.

3. Magnesium develops our skills and intelligence...
Protein synthesis occurs when a cell assembles the amino acids from the food we ate into special proteins. Hence the term protein synthesis: The synthesis (creation) of proteins. 

Our neurons also use the process of protein synthesis for their daily repair and growth. This is because proteins are what give our cells and thus our organs their structure and function.

One example of how protein synthesis happens in our neurons is after exercise. During exercise our brain sends signals along a pathway of connected neurons. This pathway starts from our brain and ends up at our muscles, where the signal activates them. If the signalling between neurons reaches a high-enough point, it strengthens their connectionsand thus our ability to perform the exercise. 

This strengthening of neurons and their connections is called long-term potentiation, and protein synthesis is the process by which it happens [26], which we now know is a process that needs magnesium.

(Long-term potentiation is exactly how we become better at the things we practice. When you hear “practice makes perfect,” think of long-term potentiation, facilitated by magnesium and protein synthesis.)

Want to improve your skills? Long-term potentiation:

However in order for long-term potentiation to take place, special receptors on our neurons called NMDA receptors must be activated.[27,28] Their activation allows an influx of positive charge into the neuron, which facilitates long-term potentiation. The critical factor is:

The NMDA receptor is regulated by magnesium. [29-32] Magnesium sits bound to the receptor, preventing its over-stimulation which can otherwise damage and kill the neuron.

Magnesium’s NMDA regulation of long-term potentiation allows us to selectively strengthen the neural connections involved in the tasks we practice most (practice makes perfect), while preventing the unnecessary development of other less used neural connections which we may not want to strengthen (such as the connections that are activated when we are stressed or angry).

In fact, improper NMDA regulation and its resulting over-activation has been linked with the development of various mental disorders including epilepsy. [33]

As we continue to look at our mental health and performance, we see that magnesium is critical for both NMDA receptor function and the protein synthesis needed for developing our skills via long-term potentiation. 

Magnesium helps make us smarter

Long-term potentiation makes us better at physical tasks, and mental ones: As we engage mental tasks, they activate various parts of our brain and the neurons in those areas send signals between each other in the same way that musculo-skelatal neurons do during exercise. Similarly, repetition of these mental tasks and their neuron signalling stimulates long-term potentiation, thus making that area of our brain better at what it does.

Because long-term potentiation requires protein sysnthesis (which requires magnesium), we see how increasing our mental skills (in response to consistently practicing these skills) requires magnesium in the short and long term. [34]

Magnesium also helps us improve our skill set by facilitating memory formation (which happens largely during REM sleep).[35] Magnesium does this via its role in creating DHEA from cholesterol[36-38]. DHEA is a powerful youth-preserving hormone which increases our REM sleep, thus increasing the window of opportunity for memory formation.[39]

Deep sleep (slow wave sleep) is even more critical to memory formation,[40-44] and magnesium supplementation is known to increase our deep sleep[45], thus increasing the opportunity for memory formation and boosting overall mental function.

3. Summary
The reason practice makes us better, is because the constant use of our neurons results in long-term potentiation: 

When our neurons and their connections grow stronger via protein synthesis.

The more we use the specific neurons for the task we practice, the more they grow, making us better. Remember: we need magnesium for this protein synthesis!

Long-term potentiation also works in response to repeated mental tasks.

We need magnesium to become better at physical tasks, and to become smarter.

Magnesium also helps boost our REM and Slow wave-sleep, which are both critical for memory development.

4. Magnesium protects and repairs nerves...
Our brain and nerve cells incur damage from oxidative stress and inflammation. When we experience these two for extended (chronic) periods of time, they lead to physical deterioration, malfunction and almost all major forms of disease. Magnesium is key in preventing and reducing both of these types of damage:

Magnesium vs oxidative damage

Much oxidative damage occurs when iron builds up in our cells (and thus tissues)[46,47] instead of circulating in our blood. Free iron in our cells rapidly oxidizes. This is another way of saying that it causes our tissues to rust.

Magnesium prevents this toxic build-up of iron in our tissues via its role in the creation and function of an enzyme called ceruloplasmin.[48] This enzyme loads iron from our cells onto the transporter molecules that carry it in our blood.[49,50] When our ceruloplasmin doesn’t work, iron builds up in our nerve and brain cells, leading to high rates of oxidative stress and physical damage. As we will discover in section 7, this leads to various forms of debilitating nervous and mental diseases.

Magnesium vs inflammation

All cells including neurons experience inflammation from stress. This can be environmental or psychological stress, the stress of oxidative damage, or simply the stress from daily wear-and-tear. Because neurons engage our environment, psyche, and daily use more than any other cells, they also incur more stress and inflammation.

Fortunately our body makes molecules called anti-oxidants to fight inflammation. Apart from Carbon Dioxide, our most abundant anti-oxidant is glutathione, whose creation requires magnesium-dependent ATP [51,52] which helps explain why magnesium and glutathione levels are related.[53,54]

In fact magnesium has such powerful anti-inflammatory properties that it directly reduces the death of neurons[55], while its deprivation causes their inflammatory death.[56]

This is why higher magnesium intake is shown to result in healthier people with less inflammation [57,58] and why magnesium deficiency is associated with a wide array of diseases.[59-63]

Magnesium’s anti inflammatory effects are so powerful that it has even been shown to stimulate the regeneration of a crushed sciatic nerve.[64] 

Simply put magnesium keeps our brain and nerves healthy by fighting inflammation, preventing neuronal damage and death, and repairing our neurons. What is even more fascinating, is the creation of new neurons in mature adults:

4. Summary
Excess iron in our neurons causes RUST and damage in our brain & nerves. Magnesium stops this: it keeps iron flowing in our blood instead of building up in our cells.

Magnesium also prevents damage and mental disease by fighting inflammation, and making antioxidants. 

It also directly reduces the death of our neurons and helps regenerate them.

5. Magnesium creates new brain cells...
Only a decade ago it was believed that we could not make new neurons. This meant that as our brain and nerve cells died, their numbers and our mental force declined permanently.

This belief is now altered as evidence has emerged that neurogenesis – the creation of new brain cells in adults – is a real phenomenon that takes place in adult brains of animals including humans. [65-68] While this is a new field of study that requires more research, initial findings are both promising and empowering.

What is critical, is that the creation of new neurons requires DNA replication and protein synthesis, which as we already know are both magnesium-dependent. Neurogenesis is impossible without magnesium.

6. Magnesium and nerve signalling...

Magnesium & neurotransmitters

In addition to our neurons’ development, protection and repair, magnesium is also critical to their function, ie: their ability to transmit electric signals throughout our body so we can experience the world with our five senses and react accordingly.

Besides regulating NMDA receptors[69], magnesium is needed for several other parts of our nerve signalling. To better understand, let’s look at how neurons send signals:

  1. Neuron A sends a messenger molecule called a neurotransmitter, to neuron B.
  2. The neurotransmitter interacts with neuron B’s receiving branches (dendrites).
  3. This creates an electric signal that passes from neuron B’s receiving end to its terminal end.
  4. When this signal arrives at the terminal end, it stimulates neuron B to send neurotransmitters towards the dendrites of the next neuron in the nervous pathway. So the process continues.

As we can see here, our nerves and brain could not function without these chemical messengers called neurotransmitters. 

Magnesium is critical here because neurotransmitters are – or contain – proteins which are made via protein synthesis, a process which we already know needs magnesiumThis leads to another component of nerve function for which magnesium and protein synthesis are needed:

Magnesium & nerve insulation

Our neurons receive neurotransmitters via their dendrites, and they send neurotransmitters from their terminals.  The long body of the neuron along which the electric signal travels from the dendrites to the terminals, is called the axon.

The axons of our nerves have a special coating called the myelin sheath, which insulates them from electrically active molecules and facilitates their transmission of these electric signals. Magnesium is critical to the formation and maintenance of the myelin sheath:

The myelin sheath is nearly 40% water. The remaining portion is 70-85% cholesterol [70] and 15-30% protein called myelin basic protein.[71]

We already know that proteins – including myelin basic protein – need magnesium to be made via protein synthesis. Yet magnesium is also involved in the regulation of cholesterol production via a pathway known as the Mevalonate pathway. [72,73]

Magnesium and mental health & performance are thus linked in another vital way: the facilitation of proper nervous signalling via magnesium’s role in our neurons’ myelin sheath.

Simply put, magnesium is needed for every major component of our mental and nervous health and function.

6. Summary
Our neurons use neurotransmitters to send their signals. We need magnesium to make these molecules.

Magnesium also regulates receptors on our neurons which facilitate the healthy passing of signals.

Magnesium also helps create & protect  our myelin sheath: the material that helps our neurons pass signals.

7. Magnesium deficiency & Mental aging/disease:

Simple logic tells us that if our brain and nerves need magnesium daily for:

  1. physical repair and maintenance,
  2. protection from inflammation and prevention of neuron death,
  3. synthesizing neurotransmitters & myelin sheath and transmitting electric signals,
  4. becoming stronger and smarter with practice,

then it becomes very clear that being deficient in magnesium for long enough can eventually lead to some form of debilitating disease of our brain and nerves. Below we look at magnesium deficiency’s relations to epilepsy, Alzheimer’s, Parkinson’s, Multiple Sclerosis, depression, ADHD, headaches & migraines, and other nervous system disorders.

Magnesium deficiency & epilepsy...
We know that magnesium’s role in regulating NMDA receptors is critical to the health of our brain and nerve cells. When this system fails and the receptors are over-activated, the development of epilepsy and other disorders may ensue.[33,74]

Magnesium also prevents degenerative mental diseases like epilepsy by helping our brain detoxify, via its role in the production of one of our most potent anti-oxidants: melatonin.

Melatonin is known for its sleep-inducing effects, however it is an extremely potent anti-inflammatory agent [75-78], with especially protective and beneficial effects on the central nervous system[79,80] in the short and long term.[81]

Our body makes melatonin by converting the amino acid tryptophan into serotonin and then into melatonin. This process requires several nutrient co-factors, including zinc, vitamin b6, and magnesium. [82,83]. This helps explain why magnesium deficiency can result in lower melatonin levels [84,85] and insomnia, and why magnesium supplementation improves primary insomnia. [86]

Magnesium deficiency & Alzheimer's...
Alzheimer’s is strongly linked with the build-up of beta-amyloid plaque in our brain and nerves.[87-90] New research also shows that beta amyloid exerts its neurotoxic effects before the build-up of plaque, via its binding to special PirB receptors on our neurons. [91]

This continued receptor-binding destroys the connections between our neurons, resulting in our inability to form memories – a primary characteristic of Alzheimer’s. How is magnesium deficiency related to the development of Alzheimer’s disease?

Magnesium is involved in melatonin and glutathione production, which both reduce the toxic effects of beta amyloid in our brain and nerve cells. [92-96] This helps explain why they’ve both been shown as beneficial to Alzheimer’s patients [97,98] and proposed as therapies.

Magnesium deficiency has been linked with Alzheimer’s since the 1990s [99,100] and studies now show a prevalence of magnesium deficiency in Alzheimer’s patients [101], with especially low levels in their brain[102] and cerebrospinal fluid. [103] 

While it’s no surprise that magnesium is shown to slow the progression of Alzheimer’s [104], and protect mental function in Alzheimer’s victims [105], preventative action is still the best option. Magnesium supplementation also helps prevent mental diseases and degeneration because of its role in preventing iron toxicity (ceruloplasmin), as high levels of iron are linked with neurodegenerative diseases like Alzheimer’s.[106-108]

Magnesium deficiency & Parkinson's...
Parkinson’s is the second most common mental disease after Alzheimer’s and they share several factors. Both are debilitating, both can result in dementia and both have a degree of beta amyloid plaque build-up [109,110]. 

Hence magnesium’s role in preventing beta amyloid toxicity (via glutathione and melatonin production) means that magnesium supplementation can serve as a preventative measure against the development of Parkinson’s.

Parkinson’s-specific research also identifies the buildup of molecules called alpha-synuclein as one of the primary correlations and problems of the disease. [111-113] Magnesium has been shown to play a very direct role in reducing the harmful build-up of alpha-synuclein.[114]

Findings also show that alpha-synuclein works together with dopamine, and calcium channels to cause the death of neurons in Parkinson’s.[115] This highlights the preventative power of magnesium in Parkinson’s because magnesium regulates calcium channels in all kinds of cells [116-122, 19], while also regulating dopamine levels in our cells.[123]

The importance of magnesium’s regulation of calcium has also been brought to light in a recent study which has linked calcium supplementation to brain lesions.[124] Similarly, magnesium’s regulation of iron (via its role in ceruloplasmin function) is another critical factor in prevention, because high levels of iron in our brain are also linked with Parkinson’s. [125]

Simply put, magnesium seems to reduce the main problematic factors in our nerve and brain cells which lead to Parkinson’s disease, which in turn helps explain why magnesium supplementation is shown to protect suffering and toxic neurons found in Parkinson’s disease. [126-128]

Magnesium deficiency & Multiple Sclerosis...
Remember our neurons’ myelin sheath? It’s the protective insulating material that surrounds their long bodies. Well, in multiple sclerosis, patients lose their ability to move because their nerves cannot properly transmit signals to do things like activate muscles to facilitate movement. A main cause of this inability of neurons to transmit signals is the degeneration of their myelin sheath. [129] As we have already learned, magnesium is needed for the process of protein synthesis which makes our myelin sheath’s main protein:  myelin basic protein.

Furthermore, several studies also reveal beta amyloid as a problematic molecule yet again, because it binds to white tissue:[130] findings suggest that beta amyloid plays a role in our neurons’ de-myelination by reducing myelin basic protein, which is a white tissue. [131,132] Thus magnesium helps prevent multiple sclerosis because its role in glutathione and melatonin production reduces beta amyloid which otherwise destroys our myelin sheath.

Magnesium’s key role in iron regulation is also once again a factor in prevention, as iron dysregulation is also linked with the development of multiple sclerosis,[133] as well as the development of another nerve-degenerating and debilitating disorder called Friedreich Ataxia.[134]

Even more specifically, magnesium has been shown to protect oligodendrocytes: the cells that manufacture our nerves’ myelin sheath.[135,136]  It is then no surprise that low levels of magnesium are found in multiple sclerosis patients [137-138].

Multiple sclerosis is extremely debilitating and maintaining healthy magnesium levels is critical in the prevention of this life-altering condition.

Magnesium, depression, anxiety, ADHD, migraines etc...
The first beneficial effects of magnesium supplementation on depression were observed nearly 100 years ago. [139] Perhaps the simplest connection between magnesium deficiency and problems in mood and depression can be found when we look at three important neurotransmitters: serotonin, dopamine and GABA.

Abnormal levels of these neurotransmitters, and/or the over-excitation of their receptors is found in depression, and it is widely accepted that magnesium is involved in the regulation and/or synthesis of all three.

This helps explain why low levels of magnesium in the cerebrospinal fluid of our nervous system are associated with depression and suicide. [140] Furthermore magnesium imbalance is often observed in people with depression[141-145], and higher dietary intake of magnesium is associated with lower depression symptoms.[146]

Very low magnesium intake has an even higher association with depression, and this is especially seen in young adults.[147] What is particularly astounding is that magnesium supplementation has been shown to reverse major depression in as fast as 7 days[148].

Magnesium deficiency is also strongly correlated with migraines and headaches [149,150] which is why supplementation has been shown to help substantially[151-153]. In fact magnesium infusion often eliminates symptoms instantly[154], with some scientists even concluding that:

“all migraine patients should be treated with magnesium.”

It comes as no surprise that magnesium deficiency is related to a variety of other mental problems which magnesium supplementation has been shown to help with, including anxiety[155], irritability and aggression[156-160], ADHD [161-166], suicidal ideationinsomnia, postpartum depression, and abuse of cocaine, alcohol and tobacco.[144] Researchers who have assessed these findings have concluded that:

“The possibility that magnesium deficiency is the cause of most major depression and related mental health problems including IQ loss and addiction is enormously important to public health and is recommended for immediate further study.”

These same findings also highlight that magnesium is low in our food and water supply. Now that we see just how critical magnesium is to the structure, fuel, and function of our brain and nerves, it becomes even more important to be aware of how our modern environments are impacting our ability to maintain healthy magnesium levels:

8. Why Our Magnesium Levels Are Now Dropping:

Figure 1 is a general representation of the trends of the three primary factors that affect the magnesium levels in our body everyday. The fourth line represents the human body’s ability to make its own magnesium, which will always stay at zero.

  1. Total environmental stress that drains our magnesium
  2. Magnesium in our soil and healthy foods
  3. Our intestine’s ability to absorb magnesium from food and pills

Our adrenals (stress glands) are magnesium-dependent. Stress depletes magnesium, and inflames our intestine, hindering absorption of dietary magnesium. (Even a healthy gut only absorbs 30-40% of a food’s magnesium.)

This means our brain & nerves are competing for their magnesium not only with our other vital functions, but also with increasing amounts of environmental stress and poor intestinal Mg absorption.

A magnesium deficiency graph that shows how our magnesium intake has declined since 1950, while our sources of magnesium depletion have increased. The depletion of our soils and the increasing environmental stress show us that we can no longer get enough magnesium without supplementation. This strengthens the importance of magnesium and mental health.
A magnesium deficiency graph that shows how our magnesium intake has declined since 1950, while our sources of magnesium depletion have increased. The depletion of our soils and the increasing environmental stress show us that we can no longer get enough magnesium without supplementation. This strengthens the importance of magnesium and mental health.
  1. Total environmental stress that drains our magnesium
  2. Magnesium in our soil and healthy foods
  3. Our intestine’s ability to absorb magnesium from food and pills

Our adrenals (stress glands) are magnesium-dependent. Stress depletes magnesium, and inflames our intestine, hindering absorption of dietary magnesium. (Even a healthy gut only absorbs 30-40% of a food’s magnesium.)

This means our brain & nerves are competing for their magnesium not only with our other vital functions, but also with increasing amounts of environmental stress and poor intestinal Mg absorption.

Summary & Solutions:

Summary: Magnesium necessary to mental health

All the main functions of our brain & nerves depend on magnesium:

  • Energy production
  • Physical repair and maintenance
  • Fighting inflammation and preventing death of brain cells
  • Creation of neurotransmitters and myelin sheath
  • Regulation and transmission of nerve signals
  • Increase in skill and intelligence from practice

It is simply impossible to have a healthy brain and nervous system if we are deficient in magnesium. The longer we are deficient, the worse the damage grows. Because our modern world makes it very difficult to get enough magnesium from diet, magnesium supplementation is often advised for therapeutic and preventative mental health measures.

 

Solutions: Safe & smart magnesium restoration

To restore magnesium levels effectively and thus increase your nervous system and whole-body health, several measures can be taken:

  1. Eat a magnesium-smart diet and avoid the tricky magnesium-rich foods.
  2. Use a natural, quality magnesium-chloride supplement to restore whole-body magnesium levels via trans-dermal absorption.
  3. Take a magnesium-taurate or a magnesium l-threonate supplement which are both helpful for mental health.
  4. Make efforts to reduce the environmental, psychological and physical factors that cause stress and thus deplete magnesium from your body.

Click here to learn more about the various types of magnesium supplements, including magnesium chloride, magnesium-taurate and magnesium L-threonate.

Click here to learn more about magnesium deficiency and the rest of your body parts.

++ References
    1.  Magnesium in the Central Nervous System https://www.adelaide.edu.au/press/titles/magnesium/magnesium-ebook.pdf
    2. Carbohydrate burning: 10 Steps of glycolysis  http://biology.about.com/od/cellularprocesses/a/aa082704a.htm
    3. Carbohydrate Burning: Citric acid cycle https://en.wikipedia.org/wiki/Citric_acid_cycle
    4. ATP production: Oxidative phosphorylation https://en.wikipedia.org/wiki/Oxidative_phosphorylation
    5. The linkage between magnesium binding and RNA folding.  http://www.ncbi.nlm.nih.gov/pubmed/11955006
    6. Bidentate RNA-magnesium clamps: on the origin of the special role of magnesium in RNA folding.  http://www.ncbi.nlm.nih.gov/pubmed/21173199
    7. A thermodynamic framework for the magnesium-dependent folding of RNA.  http://www.ncbi.nlm.nih.gov/pubmed/12717727
    8. RNA-magnesium-protein interactions in large ribosomal subunit.  http://www.ncbi.nlm.nih.gov/pubmed/22712611 
    9. A recurrent magnesium-binding motif provides a framework for the ribosomal peptidyl transferase center.  http://www.ncbi.nlm.nih.gov/pubmed/1927918
    10. Magnesium improves the beta-cell function to compensate variation of insulin sensitivity: double-blind, randomized clinical trial.(While magnesium’s role in the beta cell’s actual release of insulin is less established than its role in the beta cells creating insulin, this study makes ground on the overall impact of magnesium on beta cells).  http://www.ncbi.nlm.nih.gov/pubmed/21241290
    11. Intracellular magnesium and insulin resistance. http://www.ncbi.nlm.nih.gov/pubmed/15319146
    12. Magnesium in Human Health and Disease. http://www.springer.com/gp/book/9781627030434  or  see this excerpt:    https://books.google.ca/books?id=iUCx1dwWr7kC&pg=PA132&lpg=PA132&dq=tyrosine+kinase+Mg&source=bl&ots=y2ITN0DdKo&sig=d9F3WRCchZ2_2wQhvW9fe2faqtk&hl=en&sa=X&ved=0ahUKEwj7jJ3fxdTMAhVM1oMKHQDFAKkQ6AEIYzAJ#v=onepage&q=tyrosine%20kinase%20Mg&f=false
    13. Oral magnesium supplementation improves insulin sensitivity in non-diabetic subjects with insulin resistance. A double-blind placebo-controlled randomized trial. http://www.ncbi.nlm.nih.gov/pubmed/15223977
    14. The insulin receptor: structure, function, and signaling. http://www.cogsci.ucsd.edu/~mboyle/COGS163/pdf-files/W2-AR-The%20insulin%20receptor%20structure,%20function%20and%20signaling.pdf
    15. Insulin Signaling and the Regulation of Glucose Transport. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1431367/
    16. Regulation of GLUT4 and Insulin-Dependent Glucose Flux. http://www.hindawi.com/journals/isrn/2012/856987/
    17. Molecular Basis of Insulin-stimulated GLUT4 Vesicle Trafficking. http://www.jbc.org/content/274/5/2593.full
    18. Sustained activation of insulin receptors internalized in GLUT4 vesicles of insulin-stimulated skeletal muscle. http://www.ncbi.nlm.nih.gov/pubmed/11078443
    19. Biochemistry of magnesium http://www.uwm.edu.pl/jold/poj1532010/jurnal-16.pdf
    20. Magnesium regulation of the glycolytic pathway and the enzymes involved. http://www.ncbi.nlm.nih.gov/pubmed/2931560
    21. Thiamine and magnesium deficiencies: keys to disease.  http://www.ncbi.nlm.nih.gov/pubmed/25542071
    22. THE EFFECT OF MAGNESIUM DEFICIENCY ON OXIDATIVE PHOSPHORYLATION  http://www.jbc.org/content/228/2/573.full.pdf
    23. Section: “ELEMENTS OF MAGNESIUM BIOLOGY” Subsection: 1.13 Synthesis and activity of enzymes http://www.mgwater.com/durex01.shtml
    24. Magnesium metabolism. A review with special reference to the relationship between intracellular content and serum levels. http://www.ncbi.nlm.nih.gov/pubmed/3056314
    25. Critical role of magnesium ions in DNA polymerase beta’s closing and active site assembly.  http://www.ncbi.nlm.nih.gov/pubmed/15238001
    26. Protein synthesis is required for the enhancement of long-term potentiation and long-term memory by spaced training. http://www.ncbi.nlm.nih.gov/pubmed/12037179
    27. NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD) http://cshperspectives.cshlp.org/content/4/6/a005710.full
    28. Activation Mechanisms of the NMDA Receptor http://www.ncbi.nlm.nih.gov/books/NBK5274/
    29. Influence of external magnesium ions on the NMDA receptor channel block by different types of organic cations. http://www.ncbi.nlm.nih.gov/pubmed/22261381
    30. The mechanism of magnesium block of NMDA receptors  http://www.sciencedirect.com/science/article/pii/S1044576584710128
    31. NMDA Receptor Function and Physiological Modulation http://brain.phgy.queensu.ca/pare/assets/Neurobiology2.pdf
    32. Permeation and block of N-methyl-D-aspartic acid receptor channels by divalent cations in mouse cultured central neurones.  http://www.ncbi.nlm.nih.gov/pubmed/2451020
    33. The NMDA receptor complex as a therapeutic target in epilepsy: a review. http://www.ncbi.nlm.nih.gov/pubmed/22056342
    34. A novel role for protein synthesis in long-term neuronal plasticity: maintaining reduced postburst afterhyperpolarization.  http://www.ncbi.nlm.nih.gov/pubmed/20335469
    35. Memory consolidation during sleep: interactive effects of sleep stages and HPA regulation. https://www.ncbi.nlm.nih.gov/pubmed/17853075
    36. Consider Magnesium Homeostasis: III: Cytochrome P450 Enzymes and Drug Toxicity.  http://online.liebertpub.com/doi/abs/10.1089/pai.1994.8.7
    37. Biochemistry. 5th edition. Section 26.4Important Derivatives of Cholesterol Include Bile Salts and Steroid Hormones. http://www.ncbi.nlm.nih.gov/books/NBK22339/
    38. Hormonal regulation of cytochrome P450 enzymes, cholesterol side-chain cleavage and 17 alpha-hydroxylase/C17-20 lyase in Leydig cells.  http://www.ncbi.nlm.nih.gov/pubmed/2160293
    39. DHEA administration increases rapid eye movement sleep and EEG power in the sigma frequency range. https://www.ncbi.nlm.nih.gov/pubmed/7840167
    40. Impaired declarative memory consolidation during sleep in patients with primary insomnia: Influence of sleep architecture and nocturnal cortisol release. https://www.ncbi.nlm.nih.gov/pubmed/16876140/
    41. The Role of Slow Wave Sleep in Memory Processing. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2824214/
    42. Slow-wave sleep and the consolidation of long-term memory. https://www.ncbi.nlm.nih.gov/pubmed/20509828
    43. Midlife decline in declarative memory consolidation is correlated with a decline in slow wave sleep. https://www.ncbi.nlm.nih.gov/pubmed/17522024?dopt=Abstract&holding=npg
    44. The whats and whens of sleep-dependent memory consolidation. https://www.ncbi.nlm.nih.gov/pubmed/19251443
    45. Oral Mg(2+) supplementation reverses age-related neuroendocrine and sleep EEG changes in humans. https://www.ncbi.nlm.nih.gov/pubmed/12163983
    46. Iron, Free Radicals, and Oxidative Injury. http://jn.nutrition.org/content/134/11/3171S.full.pdf+html
    47. Ferrotoxic Disease: The Next Great Public Health Challenge. http://clinchem.aaccjnls.org/content/clinchem/60/11/1362.full.pdf
    48. Reconstitution of ceruloplasmin by the Cu(I)-glutathione complex. Evidence for a role of Mg2+ and ATP. https://www.ncbi.nlm.nih.gov/pubmed/8567646
    49. The Role of Ceruloplasmin in Iron Metabolism. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC322742/pdf/jcinvest00228-0276.pdf
    50. Multi-Copper Oxidases and Human Iron Metabolism. http://www.mdpi.com/2072-6643/5/7/2289/htm
    51. Glutathione Biosynthesis.  https://en.wikipedia.org/wiki/Glutathione
    52. Glutathione Synthesis in Human Erythrocytes http://www.ncbi.nlm.nih.gov/pmc/articles/PMC442063/
    53. Role of magnesium in glutathione metabolism of rat erythrocytes. http://www.ncbi.nlm.nih.gov/pubmed/7062145
    54. Effects of Glutathione on Red Blood Cell Intracellular Magnesium http://hyper.ahajournals.org/content/34/1/76.full
    55. The effect of magnesium on oxidative neuronal injury in vitro. http://www.ncbi.nlm.nih.gov/pubmed/9422349
    56. Magnesium deprivation decreases cellular reduced glutathione and causes oxidative neuronal death in murine cortical cultures. http://www.ncbi.nlm.nih.gov/pubmed/11164781
    57. Magnesium Intake in Relation to Systemic Inflammation, Insulin Resistance, and the Incidence of Diabetes  http://care.diabetesjournals.org/content/33/12/2604.abstractijkey=f923c1120dc6636d93fa39d29c797bee45949288&keytype2=tf_ipsecsha
    58. Dietary magnesium intake is inversely associated with serum C-reactive protein levels: meta-analysis and systematic review:  http://www.ncbi.nlm.nih.gov/pubmed/24518747
    59. Magnesium in Man: Implication for Health and Disease http://physrev.physiology.org/content/95/1/1.full
    60. Magnesium in Health and Disease: http://link.springer.com/chapter/10.1007%2F978-94-007-7500-8_3
    61. Magnesium Deficiency: A Cause of Heterogenous Disease in Humans: http://www.magtabsr.com/content/dr-resources-pdfs/Magnesium-Deficiency-A-Cause-of-Heterogenous-Disease-in-Humans.pdf
    62. Magnesium in Prevention and Therapy  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4586582/#B5-nutrients-07-05388
    63. Hypomagnesemia is Associated with Increased Mortality among Peritoneal Dialysis Patients.  http://www.ncbi.nlm.nih.gov/pubmed/27023783
    64. Magnesium supplement promotes sciatic nerve regeneration and down-regulates inflammatory response. http://www.ncbi.nlm.nih.gov/pubmed/21609904
    65. Does your brain produce new cells? https://www.theguardian.com/science/neurophilosophy/2012/feb/23/brain-new-cells-adult-neurogenesis
    66. Adult neurogenesis produces a large pool of new granule cells in the dentate gyrus. https://www.ncbi.nlm.nih.gov/pubmed/11406822
    67. Short-term and long-term survival of new neurons in the rat dentate gyrus. https://www.ncbi.nlm.nih.gov/pubmed/12717714
    68. Murine Features of Neurogenesis in the Human Hippocampus across the Lifespan from 0 to 100 Years  http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0008809
    69. NMDA receptor function, memory, and brain aging http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181613/
    70. High cholesterol level is essential for myelin membrane growth http://www.nature.com/neuro/journal/v8/n4/full/nn1426.html
    71. Multiple Sclerosis: A Coordinated Immunological Attack against Myelin in the Central Nervous System http://www.cell.com/cell/abstract/S0092-8674(00)81107-1?_returnURL=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0092867400811071%3Fshowall%3Dtrue
    72. Mevalonate pathway https://en.wikipedia.org/wiki/Mevalonate_pathway
    73. Comparison of Mechanism and Functional Effects of Magnesium and Statin Pharmaceuticals http://www.mgwater.com/statin.shtml
    74. The NMDA receptor in epilepsy http://www.oxfordscholarship.com/view/10.1093/acprof:oso/9780192625021.001.0001/acprof-9780192625021-chapter-17
    75. Melatonin Metabolism in the Central Nervous System http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3001211/
    76. Anti-inflammatory actions of melatonin and its metabolites, N1-acetyl-N2-formyl-5-methoxykynuramine (AFMK) and N1-acetyl-5-methoxykynuramine (AMK), in macrophages. http://www.ncbi.nlm.nih.gov/pubmed/15975667
    77. Melatonin and its relation to the immune system and inflammation. http://www.ncbi.nlm.nih.gov/pubmed/11268363
    78. Melatonin expresses powerful anti-inflammatory and antioxidant activities resulting in complete improvement of acetic-acid-induced colitis in rats. http://www.ncbi.nlm.nih.gov/pubmed/20676767
    79. Oxidative damage in the central nervous system: protection by melatonin http://www.sciencedirect.com/science/article/pii/S0301008298000525
    80. Melatonin and mitochondrial dysfunction in the central nervous system http://www.sciencedirect.com/science/article/pii/S0018506X12000517
    81. Antiinflammatory Activity of Melatonin in Central Nervous System http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3001216/
    82. The Magnesium Factor – melatonin biosynthesis – oxidative stress, pg 172. https://books.google.ca/books?id=BuW6xwqlQfkC&pg=PA172&lpg=PA172&dq=melatonin+biosynthesis+magnesium&source=bl&ots=vaxoOEyveq&sig=hwjGTCJch53S_NIo6Te8zvJHRww&hl=en&sa=X&ved=0ahUKEwiXwJGExKvOAhVE9x4KHToeAe0Q6AEIQjAF#v=onepage&q=melatonin%20biosynthesis%20magnesium&f=false
    83. Role of cellular magnesium in health and human disease. http://www.ncbi.nlm.nih.gov/pubmed/14766364
    84. Dietary factors and fluctuating levels of melatonin. http://www.foodandnutritionresearch.net/index.php/fnr/article/view/17252/23292
    85. Dietary magnesium deficiency decreases plasma melatonin in rats. http://www.ncbi.nlm.nih.gov/pubmed/17172005
    86. The Effect of Melatonin, Magnesium, and Zinc on Primary Insomnia in Long-term Care Facility Residents in Italy: A Double-blind, Placebo-controlled Clinical Trial http://www.medscape.com/viewarticle/736096
    87. Alzheimer’s Disease and the β-Amyloid Peptide http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2813509/
    88. The amyloid cascade-inflammatory hypothesis of Alzheimer disease: implications for therapy. http://www.ncbi.nlm.nih.gov/pubmed/24052108
    89. Soluble amyloid beta peptide concentration as a predictor of synaptic change in Alzheimer’s disease. http://www.ncbi.nlm.nih.gov/pubmed/10487842
    90. The amyloid cascade-inflammatory hypothesis of Alzheimer disease: implications for therapy. http://www.ncbi.nlm.nih.gov/pubmed/24052108
    91. Scientists reveal how beta-amyloid may cause Alzheimer’s https://med.stanford.edu/news/all-news/2013/09/scientists-reveal-how-beta-amyloid-may-cause-alzheimers.html
    92. Mechanism of neuroprotection of melatonin against beta-amyloid neurotoxicity. http://www.ncbi.nlm.nih.gov/pubmed/21354274
    93. Melatonin ameliorates amyloid beta-induced memory deficits, tau hyperphosphorylation and neurodegeneration via PI3/Akt/GSk3β pathway in the mouse hippocampus http://onlinelibrary.wiley.com/doi/10.1111/jpi.12238/abstract
    94. Melatonin reduces hippocampal beta-amyloid generation in rats exposed to chronic intermittent hypoxia. http://www.ncbi.nlm.nih.gov/pubmed/20654588
    95. Beta-amyloidolysis and glutathione in Alzheimer’s disease http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3640603/
    96. γ-glutamylcysteine (GGC)-mediated upregulation of glutathione levels can ameliorate toxicity of natural beta-amyloid oligomers in primary adult human neurons http://www.alzheimersanddementia.com/article/S1552-5260(13)02682-4/abstract
    97. Elevation of glutathione as a therapeutic strategy in Alzheimer disease http://www.sciencedirect.com/science/article/pii/S0925443911002262
    98. Beneficial effects of melatonin in experimental models of Alzheimer disease http://www.nature.com/aps/journal/v27/n2/abs/aps200613a.html
    99. Dementias: the role of magnesium deficiency and an hypothesis concerning the pathogenesis of Alzheimer’s disease. http://www.ncbi.nlm.nih.gov/pubmed/2092675
    100. Magnesium depletion and pathogenesis of Alzheimer’s disease http://www.mgwater.com/dur16.shtml
    101. Altered ionized magnesium levels in mild-to-moderate Alzheimer’s disease.  http://www.ncbi.nlm.nih.gov/pubmed/21951617
    102. Disturbances of magnesium concentrations in various brain areas in Alzheimer’s disease. http://www.ncbi.nlm.nih.gov/pubmed/11008926/
    103. Magnesium Status in Alzheimer’s Disease: A Systematic Review. https://www.ncbi.nlm.nih.gov/pubmed/26351088
    104. Magnesium ions show promise in slowing progression of Alzheimer’s disease in mice  https://www.sciencedaily.com/releases/2015/12/151201115043.htm
    105. Magnesium protects cognitive functions and synaptic plasticity in streptozotocin-induced sporadic Alzheimer’s model.  http://www.ncbi.nlm.nih.gov/pubmed/25268773/
    106. Iron, brain ageing and neurodegenerative disorders. www.nature.com/nrn/journal/v5/n11/full/nrn1537.html
    107. Three-dimensional tomographic imaging and characterization of iron compounds within Alzheimer’s plaque core material. https://www.ncbi.nlm.nih.gov/pubmed/18560134
    108. Ferritin levels in the cerebrospinal fluid predict Alzheimer’s disease outcomes and are regulated by APOE. www.nature.com/articles/ncomms7760
    109. Prevalence of amyloid-beta deposition in the cerebral cortex in Parkinson’s disease. http://www.ncbi.nlm.nih.gov/pubmed/12518303
    110. Striatal beta-amyloid deposition in Parkinson disease with dementia. http://www.ncbi.nlm.nih.gov/pubmed/18219254\
    111. The alpha-synucleinopathies: Parkinson’s disease, dementia with Lewy bodies, and multiple system atrophy. http://www.ncbi.nlm.nih.gov/pubmed/11193145
    112. Parkinson’s disease dementia: convergence of α-synuclein, tau and amyloid-β pathologies. http://www.nature.com/nrn/journal/v14/n9/full/nrn3549.html
    113. Evidence for α-synuclein prions causing multiple system atrophy in humans with parkinsonism http://www.pnas.org/content/112/38/E5308.full.pdf
    114. Magnesium inhibits spontaneous and iron-induced aggregation of alpha-synuclein. http://www.ncbi.nlm.nih.gov/pubmed/11850416
    115. Parkinson’s: Neurons Destroyed By Three Simultaneous Strikes https://www.sciencedaily.com/releases/2009/04/090429132222.htm
    116. Magnesium: Nature’s physiologic calcium blocker. http://www.ahjonline.com/article/0002-8703(84)90572-6/references
    117. Magnesium: An update on physiological, clinical and analytical aspects. http://www.sciencedirect.com/science/article/pii/S0009898199002582
    118. Extracellular magnesium and calcium blockers modulate macrophage activity. http://www.ncbi.nlm.nih.gov/pubmed/27160489
    119. Effects of magnesium on inactivation of the voltage-gated calcium current in cardiac myocytes. http://www.ncbi.nlm.nih.gov/pubmed/2559140
    120. Magnesium Inhibits Norepinephrine Release by Blocking N-Type Calcium Channels at Peripheral Sympathetic Nerve Endings. http://hyper.ahajournals.org/content/44/6/897.full
    121. Magnesium Inhibition of Ryanodine-Receptor Calcium Channels: Evidence for Two Independent Mechanisms. https://www.researchgate.net/publication/14121015_Magnesium_Inhibition_of_Ryanodine-Receptor_Calcium_Channels_Evidence_for_Two_Independent_Mechanisms
    122. Calcium–magnesium interactions in pancreatic acinar cells. http://www.fasebj.org/content/15/3/659.abstract
    123. Magnesium ion augmentation of inhibitory effects of adenosine on dopamine release in the rat striatum. http://www.ncbi.nlm.nih.gov/pubmed/9201762
    124. Elevated brain lesion volumes in older adults who use calcium supplements: a cross-sectional clinical observational study. https://www.ncbi.nlm.nih.gov/pubmed/24787048
    125. Genetics of iron regulation and the possible role of iron in Parkinson’s disease. https://www.ncbi.nlm.nih.gov/pubmed/18675357
    126. Dietary intake of antioxidant vitamins and risk of Parkinson’s disease: a case–control study in Japan. http://onlinelibrary.wiley.com/doi/10.1111/j.1468-1331.2010.03088.x/abstract
    127. Magnesium exerts both preventive and ameliorating effects in an in vitro rat Parkinson disease model involving 1-methyl-4-phenylpyridinium (MPP+) toxicity in dopaminergic neurons. http://www.sciencedirect.com/science/article/pii/S000689930702971X
    128. The selective toxicity of 1-methyl-4-phenylpyridinium to dopaminergic neurons: The role of mitochondrial complex I and reactive oxygen species revisited. https://www.scopus.com/record/display.uri?eid=2-s2.0-0033934847&origin=inward&txGid=0
    129. Multiple Sclerosis: A Coordinated Immunological Attack against Myelin in the Central Nervous System http://www.cell.com/cell/abstract/S0092-8674(00)81107-1?_returnURL=http%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0092867400811071%3Fshowall%3Dtrue
    130. Amyloid Proteins and Their Role in Multiple Sclerosis. Considerations in the Use of Amyloid-PET Imaging http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4814935/
    131. Focal demyelination in Alzheimer’s disease and transgenic mouse models. http://www.ncbi.nlm.nih.gov/pubmed/20198482
    132. The absence of myelin basic protein promotes neuroinflammation and reduces amyloid β-protein accumulation in Tg-5xFAD mice. http://www.ncbi.nlm.nih.gov/pubmed/24188129
    133. The role of iron dysregulation in the pathogenesis of multiple sclerosis: an Egyptian study. https://www.ncbi.nlm.nih.gov/pubmed/18408021
    134. Major targets of iron-induced protein oxidative damage in frataxin-deficient yeasts are magnesium-binding proteins. https://www.ncbi.nlm.nih.gov/m/pubmed/18280258/
    135. NMDA receptors are expressed in oligodendrocytes and activated in ischaemia. https://www.ncbi.nlm.nih.gov/pubmed/16372011
    136. Magnesium sulfate protects oligodendrocyte lineage cells in a rat cell-culture model of hypoxic-ischemic injury. https://www.ncbi.nlm.nih.gov/pubmed/26699082
    137. Magnesium concentration in plasma and erythrocytes in MS. http://www.ncbi.nlm.nih.gov/pubmed/7572055?dopt=Abstract
    138. Comparative findings on serum IMg2+ of normal and diseased human subjects with the NOVA and KONE ISE’s for Mg2+. http://www.ncbi.nlm.nih.gov/pubmed/7939388?dopt=Abstract
    139. Magnesium concentration in brains from multiple sclerosis patients. http://www.ncbi.nlm.nih.gov/pubmed/2353567?dopt=Abstract
    140. Magnesium in depression. http://www.ncbi.nlm.nih.gov/pubmed/23950577
    141. Aminergic Studies and Cerebrospinal Fluid Cations in Suicide. http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.1986.tb27901.x/abstract
    142. Electrolytes in blood in endogenous depression. http://www.ncbi.nlm.nih.gov/pubmed/5027529
    143. Calcium and magnesium concentrations in affective disorder: difference between plasma and serum in relation to symptoms. http://www.ncbi.nlm.nih.gov/pubmed/2618774
    144. Plasma and erythrocyte electrolytes in affective disorders. http://www.ncbi.nlm.nih.gov/pubmed/6222090
    145. Evolution of blood magnesium, sodium and potassium in depressed patients followed for three months. http://www.ncbi.nlm.nih.gov/pubmed/1299790
    146. Magnesium and depression: a systematic review.  http://www.tandfonline.com/doi/abs/10.1179/1476830512Y.0000000044?mobileUi=0&journalCode=ynns20
    147. Magnesium Intake and Depression in Adults. http://www.jabfm.org/content/28/2/249.full
    148. Rapid recovery from major depression using magnesium treatment. http://www.ncbi.nlm.nih.gov/pubmed/16542786
    149. Role of magnesium in the pathogenesis and treatment of migraine. http://www.ncbi.nlm.nih.gov/pubmed/19271946
    150. Deficiency in serum ionized magnesium but not total magnesium in patients with migraines. Possible role of ICa2+/IMg2+ ratio. http://www.ncbi.nlm.nih.gov/pubmed/8486510
    151. Role of magnesium in the pathogenesis and treatment of migraines. http://www.ncbi.nlm.nih.gov/pubmed/9523054
    152. Intravenous magnesium sulphate relieves migraine attacks in patients with low serum ionized magnesium levels: a pilot study. http://www.ncbi.nlm.nih.gov/pubmed/8549082
    153. Efficacy of intravenous magnesium sulfate in the treatment of acute migraine attacks. http://www.ncbi.nlm.nih.gov/pubmed/11251702
    154. Why all migraine patients should be treated with magnesium. http://www.ncbi.nlm.nih.gov/pubmed/22426836
    155. Latent tetany and anxiety, marginal magnesium deficit, and normocalcemia. http://www.ncbi.nlm.nih.gov/pubmed/1164868
    156. Type A behavior and magnesium metabolism. http://www.ncbi.nlm.nih.gov/pubmed/3523058
    157. Plasma magnesium levels in a population of psychiatric patients: correlations with symptoms.http://www.ncbi.nlm.nih.gov/pubmed/7800167
    158. Magnesium deficiency alters aggressive behavior and catecholamine function. http://www.ncbi.nlm.nih.gov/pubmed/3365326
    159. Stimulant-like effects of magnesium on aggression in mice. http://www.ncbi.nlm.nih.gov/pubmed/2880351
    160. The Shipley Project: Treating Food Allergy to Prevent Criminal Behaviour in Community Settings.http://www.tandfonline.com/doi/abs/10.1080/13590849862311
    161. Magnesium in Prevention and Therapy Section: ADHD http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4586582/
    162. The effects of magnesium physiological supplementation on hyperactivity in children with attention deficit hyperactivity disorder (ADHD). Positive response to magnesium oral loading test. http://www.ncbi.nlm.nih.gov/pubmed/9368236/
    163. Magnesium VitB6 intake reduces central nervous system hyperexcitability in children. http://www.ncbi.nlm.nih.gov/pubmed/15466962/
    164. Improvement of neurobehavioral disorders in children supplemented with magnesium-vitamin B6. I. Attention deficit hyperactivity disorders. http://www.ncbi.nlm.nih.gov/pubmed/16846100/
    165. Improvement of neurobehavioral disorders in children supplemented with magnesium-vitamin B6. II. Pervasive developmental disorder-autism. http://www.ncbi.nlm.nih.gov/pubmed/16846101/
    166. [Effect of MAGNE-B6 on the clinical and biochemical manifestations of the syndrome of attention deficit and hyperactivity in children]. http://www.ncbi.nlm.nih.gov/pubmed/16579066/

MgHealth.org 2017 Ι This website is designed by the artists at sitechild.com  Contact us at info@sitechild.com