I never learned much about Magnesium in the first few years of med school, which was a mistake, because it’s awesome.
Here I’ve tried to outline why it’s important and when to think about it in a clinical setting.
1. There’s loads of it
Magnesium is the ninth most abundant element in the universe, and the eleventh (by mass if you’re being pedantic) in your body. It’s required by every single cell as it is crucial to the basic nucleic acid chemistry that makes life possible, over 300 enzymes need it as a co-factor, and even ATP likes to hang out as a chelate of magnesium ions.
2. It’s useful as medicine
Magnesium has been used for many medicinal uses. It is a common laxative, antacid and it can stabilise muscle spasm in eclampsia. It increases production of prostaglandins and reduces that of thromboxane and angiotensin II. It also, in low doses, makes mineral water taste tart apparently (that was just for interest).
3. You can get it from loads of places
Clearly the ninth most abundant element in the universe isn’t going to be difficult to find, and you can find buckets of it in foods such as:
- Vegetables (given it’s crucial to chlorophyll, green stuff’s your best bet)
4. It does a lot of stuff in the body
Magnesium’s pretty busy in the world of metabolism. Most of it (60%) just chills in the bones, and the rest is mostly intracellular (20% in skeletal muscle). About 1% sits in the extracellular space, so clearly measuring your blood levels of magnesium isn’t going to tell you much about how much there is in your body.
It interacts with three major ions and their conduction channels:
Magnesium is required for the NaKATPase to function correctly in myocytes. Thus low magnesium means the sodium isn’t being pumped out and potassium isn’t being brought back in. This leads to a tachycardia and a predisposition to arrhythmias.
To begin with, magnesium inhibits potassium leaving the cell through its channels. This means that too little magnesium, and you’re going to start losing potassium from the kidneys, and develop hypokalaemia. So – if you have a patient who’s hypokalaemic, and they’re not responding to potassium supplementation, start thinking about magnesium! In addition, patients in DKA (diabetic ketoacidosis) should have their magnesium monitored, so that the hypokalaemia caused by insulin driving the potassium into the cells isn’t compounded by renal losses.
Magnesium suppresses release of calcium from the sarcoplasmic reticulum. This has several effects
- reduced muscle contraction
- reduced neuronal excitation through two mechanisms:
- blockage of NMDA glutamate receptors
- inhibition of acetylcholine release
- reduced production of parathyroid hormone
- interestingly mild reduction of magnesium stimulates PTH release, however
- severe drops in magnesium reduce PTH release
- reduces sensitivity of skeletal muscle to parathyroid hormone
Clinically this is important, as magnesium sulphate can be used as a bronchodilator in severe asthma.
As explained in point 4, you can have a normal blood magnesium while still being significantly deficient, and there isn’t really a reliable biomarker to measure. The best way to test whether someone is deficient is to load them with magnesium (a magnesium loading test… weirdly) and see how much of it they retain. If they hold onto more than 20%, they were definitely deficient in the first place. You’ve also just fixed the problem, so win win!
Symptoms of magnesium deficiency include:
- muscle cramps
- abnormal heart rhythm
- tremors and athetosis (fidgeting)
- extensor plantar reflex
It’s a scary list but it makes sense – the muscle cramps largely due to the increased calcium that results from low magnesium, and the potassium leakage from cells that occurs.
Reasons for low magnesium in the blood are put into three categories:
- not enough uptake
- redistribution into the cells
- too much loss
Magnesium is absorbed in the duodenum and secreted by the colon, so malabsorption or excessive throughput will prevent it being absorbed into the blood. Conditions such as Crohn’s or Ulcerative Colitis will cause hypomagnesaemia by causing diarrhoea.
Redistribution into the cells
Adrenaline and other catecholamines tend to shove magnesium ions into the cells. Thus after a heart attack, 80% of patients will have low serum magnesium. Drugs that cause intracellular shift of calcium will drag magnesium with it, so things like Digitalis are also a risk factor.
A huge cause of hypomagnesaemia is alcohol. 30% of alcoholics have low magnesium, as do 85% of those with delerium tremens. In terms of medications, anything that inhibits reabsorption in the Loop of Henle is going to result in shedding of magnesium into the urine. The most common are:
- loop diuretics
- proton pump inhibitors
6. Too much is equally bad
Equally, too much is rarely good for you, and magnesium toxicity can happen even if the serum levels are normal, so knowing what to look out for in a clinical setting can be life-saving for the patient. Usually this is rare because your kidneys are seriously good at shifting it from the blood, so you don’t tend to get it from dietary overdose. Typically it’s your renally-impaired patient who’s on magnesium supplementation who sees their blood levels gradually climbing, and as expected, there is usually concurrent hyperkalaemia and hypocalcaemia, which generate most of the symptomatology:
Symptoms of hypermagnesaemia:
- respiratory depression
- hypo or areflexia
- dizziness and somnolence
Treatment of hypermagnesaemia is done by antagonising it with calcium. Calcium gluconate IV help to reduce the cardiac manifestations of hypermagnesaemia, while diuretics and dialysis can reduce the magnesium levels in the body to a more tolerable level.
So there you go, a brief intro into why you should care about magnesium. It’s a puppet-master, controlling potassium and calcium, and for the most part it’s your friend, as long as you don’t have too much of it!