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Subscribe to our NewsletterGet notified about the latest health news, coupons and promotions, and new products. The causes of a lack of magnesium can include dietary choices, availability of foods high in magnesium, as well as illness, use of certain pharmaceuticals, and genetic factors. Low magnesium can be hard to detect, so the first step to preventing magnesium deficiency is knowing its risk factors. The average American diet supplies less than two thirds of the magnesium required by the body.1 2 Yet each person is individual, not only in their intake of magnesium, but also in their ability to absorb and utilize this key mineral. The question of what causes low magnesium is in some ways easy to answer when examining modern eating habits.
It is not uncommon to find adults and children who state, “I don’t eat things that are green.” Fried foods such as chips and French fries have replaced healthy finger foods such as nuts and seeds.
Each of these common eating habits compounds to create a general lack of magnesium in the diet. Phosphates found in carbonated beverages such as dark-colored sodas bind magnesium, rendering it unusable by the body. In areas with high mineral water content, increased magnesium consumption has been shown to have positive effects on health. A symposium held by the World Health Organization in 2009 brought together scientists and medical professionals to review scientific evidence for the impact of calcium and magnesium in drinking water. The symposium made clear acknowledgement of the benefit of magnesium in drinking water to public health. The studies do show a [protective effect] between cardiovascular mortality and drinking-water magnesium. Water softening is often done to improve the household cleaning properties of water, yet doing so removes a valuable source of magnesium—one that can provide as much as 50% of the RDA in some parts of the world.
Increasingly, municipal water sources remove magnesium as a part of water treatment, though some municipal sources do re-supplement water supplies after softening. Contacting local government resources to determine the magnesium content of your water supply. Magnesium deficiency’s causes can also include supplementation of other competing vitamins and nutrients.
Yet widespread knowledge of the need for calcium is, unfortunately, not accompanied by a widespread knowledge of the need for magnesium. Among the known magnesium deficiency causes are prescription medications such as diuretics, antibiotics, painkillers and cortisone, which can deplete magnesium levels in the body by impairing absorption or by increasing excretion by the kidneys.
In cases of addiction or alcoholism, low intake and absorption can cause magnesium deficiency. Stressful conditions require more magnesium by the body, thus those experiencing these conditions are more susceptible to magnesium deficiency. These conditions not only increase the body’s need for magnesium, but also may reduce stomach acid levels, reducing the body’s ability to break down foods and supplements into an absorbable form.
The natural process of aging also reduces stomach acid levels and is associated with reduced absorption of magnesium. Learn about magnesium chloride, a highly soluble form of magnesium that supports healthy chloride levels in the GI tract. Digestive disorders such as Crohn’s disease, genetic diseases and other conditions may cause magnesium wasting by the kidneys or problems with absorption. Disorders such as these may be difficult to diagnose, though chronic deficiency symptoms such as muscle cramping, fatigue, irritability or high blood pressure may be an indication of magnesium depletion when accompanied by adequate dietary magnesium intake.
Due to an inability to accurately test body magnesium content, it is unknown exactly how many Americans are currently magnesium deficient, nor how many persons are deficient worldwide. Current tests focus on serum magnesium, which has been shown inadequate to pinpoint the existence or non-existence of a potential bodily deficiency.
Because of this difficulty in diagnosing magnesium deficiency, many doctors and health providers will consider not just test results and current symptoms, but also risk factors when addressing the possibility of magnesium deficiency.
By understanding the causes of a lack of magnesium, it’s possible for each of us to make proactive individual decisions on whether to supplement this commonly deficient essential mineral. For persons without kidney disease, magnesium supplementation has no side effects other than loose stools when taken orally, indicating a need to reduce dosage.2 And transdermal applications of magnesium avoid digestive problems entirely. Disclaimer: None of the above statements have been evaluated or approved by the Food and Drug Administration or the American Medical Association. All functions performed by the nervous system—from a simple motor reflex to more advanced functions like making a memory or a decision—require neurons to communicate with one another. The lipid bilayer membrane that surrounds a neuron is impermeable to charged molecules or ions.
A neuron at rest is negatively charged: the inside of a cell is approximately 70 millivolts more negative than the outside (?70 mV, note that this number varies by neuron type and by species). The resting membrane potential is a result of different concentrations inside and outside the cell. A neuron can receive input from other neurons and, if this input is strong enough, send the signal to downstream neurons. Potassium channel blockers, such as amiodarone and procainamide, which are used to treat abnormal electrical activity in the heart, called cardiac dysrhythmia, impede the movement of K+ through voltage-gated K+ channels. For an action potential to communicate information to another neuron, it must travel along the axon and reach the axon terminals where it can initiate neurotransmitter release. The synapse or “gap” is the place where information is transmitted from one neuron to another. When an action potential reaches the axon terminal it depolarizes the membrane and opens voltage-gated Na+ channels.
Fusion of a vesicle with the presynaptic membrane causes neurotransmitter to be released into the synaptic cleft, the extracellular space between the presynaptic and postsynaptic membranes, as illustrated in [link]. The binding of a specific neurotransmitter causes particular ion channels, in this case ligand-gated channels, on the postsynaptic membrane to open. Once neurotransmission has occurred, the neurotransmitter must be removed from the synaptic cleft so the postsynaptic membrane can “reset” and be ready to receive another signal. While electrical synapses are fewer in number than chemical synapses, they are found in all nervous systems and play important and unique roles. Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron, but often multiple presynaptic inputs must create EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential.
Brain-computer interface Amyotrophic lateral sclerosis (ALS, also called Lou Gehrig’s Disease) is a neurological disease characterized by the degeneration of the motor neurons that control voluntary movements. A relatively new line of research for helping paralyzed patients, including those with ALS, to communicate and retain a degree of self-sufficiency is called brain-computer interface (BCI) technology and is illustrated in [link]. Watch this video in which a paralyzed woman use a brain-controlled robotic arm to bring a drink to her mouth, among other images of brain-computer interface technology in action. Long-term depression (LTD) is essentially the reverse of LTP: it is a long-term weakening of a synaptic connection.
Neurons have charged membranes because there are different concentrations of ions inside and outside of the cell. After an action potential, the opening of additional voltage-gated ________ channels and the inactivation of sodium channels, cause the membrane to return to its resting membrane potential. An action potential travels along an axon until it depolarizes the membrane at an axon terminal. Foods like these were once common in diets around the world, but an increase in both food processing and the availability of enticing convenience foods with added fats and sugars has had its impact. A visit to the local supermarket finds cashiers unable to identify basic green vegetables such as kale, chard, and mustard greens, all high in magnesium. And millions around the world have entirely replaced their consumption of mineral-containing water with the consumption of carbonated beverages and coffee—drinks which actually reduce available magnesium through their high phosphate and sugar content and diuretic properties.
Today many people, especially women, supplement with calcium to prevent bone loss and osteoporosis. As a result, many are actively depleting their magnesium stores without realizing it—through their supplementation with calcium.
Complications such as liver disease, vomiting and diarrhea reduce body levels of magnesium, and treatment of addiction may in fact further complicate issues when withdrawal is experienced. Magnesium’s bioavailability is vulnerable to a reduction in hydrochloric acid, because many forms of magnesium must be broken down into an ionic form in the digestive tract to be used by the body. The level of absorption is also known to be affected by an individual’s state of health, as well as the presence of other minerals such as iron and calcium, which can impede magnesium absorption.
In these cases, extreme insulin deficiency leads to breakdown of compounds within the cells, releasing magnesium and excreting it from the body. Since only 1% of bodily magnesium is stored in the blood, low blood magnesium cause and effect does not necessarily overlap magnesium deficiency cause and effect.
The information provided on this site is intended for your general knowledge only and is not a substitute for professional medical advice or treatment for specific medical conditions. While humans use words and body language to communicate, neurons use electrical and chemical signals. These signals are possible because each neuron has a charged cellular membrane (a voltage difference between the inside and the outside), and the charge of this membrane can change in response to neurotransmitter molecules released from other neurons and environmental stimuli. To enter or exit the neuron, ions must pass through special proteins called ion channels that span the membrane. This voltage is called the resting membrane potential; it is caused by differences in the concentrations of ions inside and outside the cell.

Transmission of a signal between neurons is generally carried by a chemical called a neurotransmitter. The speed of conduction of an action potential along an axon is influenced by both the diameter of the axon and the axon’s resistance to current leak.
Synapses usually form between axon terminals and dendritic spines, but this is not universally true. The neurotransmitter diffuses across the synaptic cleft and binds to receptor proteins on the postsynaptic membrane.
Neurotransmitters can either have excitatory or inhibitory effects on the postsynaptic membrane, as detailed in [link]. This can be accomplished in three ways: the neurotransmitter can diffuse away from the synaptic cleft, it can be degraded by enzymes in the synaptic cleft, or it can be recycled (sometimes called reuptake) by the presynaptic neuron. The mode of neurotransmission in electrical synapses is quite different from that in chemical synapses. Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. The disease begins with muscle weakening and lack of coordination and eventually destroys the neurons that control speech, breathing, and swallowing; in the end, the disease can lead to paralysis. This technology sounds like something out of science fiction: it allows paralyzed patients to control a computer using only their thoughts. The technology can require many hours of training and long periods of intense concentration for the patient; it can also require brain surgery to implant the devices. Nodes of Ranvier allow the action potential to be regenerated at specific points along the axon.
Depolarization of the membrane causes voltage-gated Ca2+ channels to open and Ca2+ to enter the cell.
Whole and unrefined foods high in magnesium are becoming increasingly rare in the modern diet.
Alternate magnesium tests do exist, such as challenge testing, load testing, and the more recent ExaTest, but these are less commonly adopted by health professionals. Just like a person in a committee, one neuron usually receives and synthesizes messages from multiple other neurons before “making the decision” to send the message on to other neurons.
To understand how neurons communicate, one must first understand the basis of the baseline or ‘resting’ membrane charge. Ion channels have different configurations: open, closed, and inactive, as illustrated in [link].
If the membrane were equally permeable to all ions, each type of ion would flow across the membrane and the system would reach equilibrium. Transmission of a signal within a neuron (from dendrite to axon terminal) is carried by a brief reversal of the resting membrane potential called an action potential. Myelin acts as an insulator that prevents current from leaving the axon; this increases the speed of action potential conduction.
For example, when acetylcholine is released at the synapse between a nerve and muscle (called the neuromuscular junction) by a presynaptic neuron, it causes postsynaptic Na+ channels to open.
In an electrical synapse, the presynaptic and postsynaptic membranes are very close together and are actually physically connected by channel proteins forming gap junctions.
Additionally, one neuron often has inputs from many presynaptic neurons—some excitatory and some inhibitory—so IPSPs can cancel out EPSPs and vice versa. At that point, patients require assistance from machines to be able to breathe and to communicate.
There are various mechanisms, none fully understood, behind the synaptic strengthening seen with LTP.
In this situation, calcium that enters through NMDA receptors initiates a different signaling cascade, which results in the removal of AMPA receptors from the postsynaptic membrane, as illustrated in [link]. When a neuronal membrane is depolarized to at least the threshold of excitation, an action potential is fired.
They also save energy for the cell since voltage-gated ion channels and sodium-potassium transporters are not needed along myelinated portions of the axon.
The intracellular calcium influx causes synaptic vesicles containing neurotransmitter to fuse with the presynaptic membrane.
Two out of every three people you meet suffer from magnesium deficiency.The truly sad thing? Some ion channels need to be activated in order to open and allow ions to pass into or out of the cell. Because ions cannot simply cross the membrane at will, there are different concentrations of several ions inside and outside the cell, as shown in [link].
When neurotransmitter molecules bind to receptors located on a neuron’s dendrites, ion channels open.
In demyelinating diseases like multiple sclerosis, action potential conduction slows because current leaks from previously insulated axon areas. The neuron transmitting the signal is called the presynaptic neuron, and the neuron receiving the signal is called the postsynaptic neuron.
Calcium ions entering the cell initiate a signaling cascade that causes small membrane-bound vesicles, called synaptic vesicles, containing neurotransmitter molecules to fuse with the presynaptic membrane.
For example, some drugs that are given to Alzheimer’s patients work by inhibiting acetylcholinesterase, the enzyme that degrades acetylcholine. Signaling in electrical synapses, in contrast, is virtually instantaneous (which is important for synapses involved in key reflexes), and some electrical synapses are bidirectional. It is the net change in postsynaptic membrane voltage that determines whether the postsynaptic cell has reached its threshold of excitation needed to fire an action potential. Several special technologies have been developed to allow “locked-in” patients to communicate with the rest of the world.
Synaptic plasticity allows for these changes, which are all needed for a functioning nervous system.
One known mechanism involves a type of postsynaptic glutamate receptor, called NMDA (N-Methyl-D-aspartate) receptors, shown in [link].
The decrease in AMPA receptors in the membrane makes the postsynaptic neuron less responsive to glutamate released from the presynaptic neuron.
The neurotransmitter diffuses across the synaptic cleft and binds to receptors on the postsynaptic membrane. These ion channels are sensitive to the environment and can change their shape accordingly. The difference in the number of positively charged potassium ions (K+) inside and outside the cell dominates the resting membrane potential ([link]). At excitatory synapses, this opening allows positive ions to enter the neuron and results in depolarization of the membrane—a decrease in the difference in voltage between the inside and outside of the neuron. Note that these designations are relative to a particular synapse—most neurons are both presynaptic and postsynaptic. Synaptic vesicles are shown in [link], which is an image from a scanning electron microscope.
This depolarization is called an excitatory postsynaptic potential (EPSP) and makes the postsynaptic neuron more likely to fire an action potential. This inhibition of the enzyme essentially increases neurotransmission at synapses that release acetylcholine.
In addition to the ions that carry this current, other molecules, such as ATP, can diffuse through the large gap junction pores.
Electrical synapses are also more reliable as they are less likely to be blocked, and they are important for synchronizing the electrical activity of a group of neurons.
Together, synaptic summation and the threshold for excitation act as a filter so that random “noise” in the system is not transmitted as important information.
One technology, for example, allows patients to type out sentences by twitching their cheek. These recordings contain information from large populations of neurons that can be decoded by a computer. These receptors are normally blocked by magnesium ions; however, when the postsynaptic neuron is depolarized by multiple presynaptic inputs in quick succession (either from one neuron or multiple neurons), the magnesium ions are forced out allowing Ca ions to pass into the postsynaptic cell.
While it may seem counterintuitive, LTD may be just as important for learning and memory as LTP. In a chemical synapse, the action potential causes release of neurotransmitter molecules into the synaptic cleft. Depending on the specific neurotransmitter and postsynaptic receptor, this action can cause positive (excitatory postsynaptic potential) or negative (inhibitory postsynaptic potential) ions to enter the cell. Ion channels that change their structure in response to voltage changes are called voltage-gated ion channels.
When the membrane is at rest, K+ ions accumulate inside the cell due to a net movement with the concentration gradient. A stimulus from a sensory cell or another neuron depolarizes the target neuron to its threshold potential (-55 mV).
These unmyelinated spaces are about one micrometer long and contain voltage gated Na+ and K+ channels.
Release of neurotransmitter at inhibitory synapses causes inhibitory postsynaptic potentials (IPSPs), a hyperpolarization of the presynaptic membrane. Once released, the acetylcholine stays in the cleft and can continually bind and unbind to postsynaptic receptors.

For example, electrical synapses in the thalamus are thought to regulate slow-wave sleep, and disruption of these synapses can cause seizures. Other forms of BCI require the implantation of an array of electrodes smaller than a postage stamp in the arm and hand area of the motor cortex. Two processes in particular, long-term potentiation (LTP) and long-term depression (LTD) are important forms of synaptic plasticity that occur in synapses in the hippocampus, a brain region that is involved in storing memories. Next, Ca2+ ions entering the cell initiate a signaling cascade that causes a different type of glutamate receptor, called AMPA (?-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptors, to be inserted into the postsynaptic membrane, since activated AMPA receptors allow positive ions to enter the cell. The weakening and pruning of unused synapses allows for unimportant connections to be lost and makes the synapses that have undergone LTP that much stronger by comparison. Through binding to postsynaptic receptors, the neurotransmitter can cause excitatory or inhibitory postsynaptic potentials by depolarizing or hyperpolarizing, respectively, the postsynaptic membrane.
Voltage-gated ion channels regulate the relative concentrations of different ions inside and outside the cell. The negative resting membrane potential is created and maintained by increasing the concentration of cations outside the cell (in the extracellular fluid) relative to inside the cell (in the cytoplasm). Na+ channels in the axon hillock open, allowing positive ions to enter the cell ([link] and [link]).
Flow of ions through these channels, particularly the Na+ channels, regenerates the action potential over and over again along the axon.
For example, when the neurotransmitter GABA (gamma-aminobutyric acid) is released from a presynaptic neuron, it binds to and opens Cl- channels. This form of BCI, while more invasive, is very powerful as each electrode can record actual action potentials from one or more neurons.
So, the next time glutamate is released from the presynaptic membrane, it will have a larger excitatory effect (EPSP) on the postsynaptic cell because the binding of glutamate to these AMPA receptors will allow more positive ions into the cell. In electrical synapses, the action potential is directly communicated to the postsynaptic cell through gap junctions—large channel proteins that connect the pre-and postsynaptic membranes. The difference in total charge between the inside and outside of the cell is called the membrane potential. The negative charge within the cell is created by the cell membrane being more permeable to potassium ion movement than sodium ion movement.
Once the sodium channels open, the neuron completely depolarizes to a membrane potential of about +40 mV.
This ‘jumping’ of the action potential from one node to the next is called saltatory conduction. Cl- ions enter the cell and hyperpolarizes the membrane, making the neuron less likely to fire an action potential.
These signals are then sent to a computer, which has been trained to decode the signal and feed it to a tool—such as a cursor on a computer screen. The insertion of additional AMPA receptors strengthens the synapse and means that the postsynaptic neuron is more likely to fire in response to presynaptic neurotransmitter release. Rather than fertilizing with rich, vibrant compost, we treat the soil with synthetic fertilizers. In neurons, potassium ions are maintained at high concentrations within the cell while sodium ions are maintained at high concentrations outside of the cell. Action potentials are considered an "all-or nothing" event, in that, once the threshold potential is reached, the neuron always completely depolarizes. If nodes of Ranvier were not present along an axon, the action potential would propagate very slowly since Na+ and K+ channels would have to continuously regenerate action potentials at every point along the axon instead of at specific points.
This means that a patient with ALS can use e-mail, read the Internet, and communicate with others by thinking of moving his or her hand or arm (even though the paralyzed patient cannot make that bodily movement).
Some drugs of abuse co-opt the LTP pathway, and this synaptic strengthening can lead to addiction. The cell possesses potassium and sodium leakage channels that allow the two cations to diffuse down their concentration gradient.
Once depolarization is complete, the cell must now "reset" its membrane voltage back to the resting potential.
Nodes of Ranvier also save energy for the neuron since the channels only need to be present at the nodes and not along the entire axon.
Recent advances have allowed a paralyzed locked-in patient who suffered a stroke 15 years ago to control a robotic arm and even to feed herself coffee using BCI technology.
Fertilizer application begins the destruction of soil biodiversity by diminishing the role of nitrogen fixing bacteria and amplifying the role of everything that feeds on nitrogen. However, the neurons have far more potassium leakage channels than sodium leakage channels. This begins the neuron's refractory period, in which it cannot produce another action potential because its sodium channels will not open. Because more cations are leaving the cell than are entering, this causes the interior of the cell to be negatively charged relative to the outside of the cell. With less pore space and less of their sponge-like qualities, soils are less efficient at storing water and air. The actions of the sodium potassium pump help to maintain the resting potential, once established. Recall that sodium potassium pumps brings two K+ ions into the cell while removing three Na+ ions per ATP consumed. The diffusion of K+ out of the cell actually hyperpolarizes the cell, in that the membrane potential becomes more negative than the cell's normal resting potential. Water leeches through soils, draining away nutrients that no longer have an effective susbstrate on which to cling. The influence of dietary fat on jejunostomy output in patients with severe short bowel syndrome. As more cations are expelled from the cell than taken in, the inside of the cell remains negatively charged relative to the extracellular fluid. At this point, the sodium channels will return to their resting state, meaning they are ready to open again if the membrane potential again exceeds the threshold potential. With less available oxygen, the growth of soil microbiology slows, and the intricate ecosystem of biological exchanges breaks down.Magnesium is among the myriad of minerals lost to industrial agriculture practices. It should be noted that calcium ions (Cl–) tend to accumulate outside of the cell because they are repelled by negatively-charged proteins within the cytoplasm. Eventually the extra K+ ions diffuse out of the cell through the potassium leakage channels, bringing the cell from its hyperpolarized state, back to its resting membrane potential.
In it, they pegged city water supplies as one of the main culprits:Our human ancestors evolved in a world in which healthy drinking water came directly from streams, rivers, and lakes, rich in mineral content.
The human body became reliant on obtaining a considerable proportion of its daily mineral needs from natural water sources.Fast-forward to the twenty-first century.
Pesticides and other chemicals seeping into the water supply have made everyone suspicious of water quality.
As a result, municipal water-purification facilities have intensified their efforts to remove contaminants like lead, pesticide residues, and nitrates from drinking water. If you eat too much calcium, you actually hinder your absorption of magnesium.Studies indicate that taking a calcium supplement without enough magnesium can increase the shortage of both nutrients. You can buy pre-made magnesium oil online, or you could learn how to make magnesium oil at home.
Nutrition educator & author extraordinaire, she's also a rebel with a cause who enjoys playing in the rain, a good bottle of Caol Ila scotch, curling up with a page-turning book, sunbathing on her hammock, and watching her three children grow into young adults. Comments Peggy saysDecember 12, 2013 at 12:02 pm My family suffers from a variety of magnesium-deficiency ailments.
I’ve been feeding them magnesium-rich foods, and those of us with sturdy enough skin use mag oil and take epsom baths. But three of us have such tender skin that even soaking in an epsom salt bath breaks us out in an itchy rash that persists for days and mag oil applied anywhere on the body causes a raised rash.
My skin-sensitive family members right now rotate between taking Mag Citrate and Mag Glycinate.
It does taste bitter, but if it’s taken in cold water right after brushing, followed with some more cold water, there is no aftertaste whatsoever. My son is 4 and has SPD, he eats very few things (but he does eat tons of brown rice!) So I feel he is lacking lots of minerals and vitamins!
And the oil??Reply Kristen saysDecember 12, 2013 at 10:41 pm Yes, you can use Epsom Salt baths on toddlers and use a magnesium oil on them, too.
Reply Sue Sayers saysDecember 12, 2013 at 7:46 pm Can magnesium deficiencies be linked to hand tremors? Because the symptoms for deficiency are a good indication, certainly, but not conclusive if you have one that could be caused by something else. Also, the degree of deficiency would indicate the level of supplementation needed, don’t you think? We have been supplementing magnesium both orally and topically for several months and many symptoms have improved.

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