Magnesium is an ‘intracellular cation’, it is magnesium within the cells that matters. Deficiency can arise from inadequate intake, excess loss or a shift from the intracellular to the extracellular space. There is no easy way to measure magnesium status, blood tests are of limited use. A low serum ionised Mg will indicate deficiency, but a normal result does not show sufficiency. Measuring Mg levels in erythrocytes (red blood cells) or lymphocytes (a type of white blood cell) can sometimes help but these tests are not definitive. The preferred option is a ‘magnesium loading test’: subjects are given oral magnesium and their clinical response or urinary Mg excretion assessed. Even this ‘gold standard’ test has limitations, if there is an intra to extra-cellular shift it will not show up.
Insufficient Dietary Intake
Sources of magnesium are whole grains, nuts and green vegetables including tomatoes (chlorophyll is a Mg based molecule). It makes sense to try supplementing, I use Mg Citrate, other forms are good but not Mg oxide or hydroxide which are poorly absorbed. It is safe to take oral magnesium but if you suffer from low blood pressure or kidney problems you must consult your doctor first. Supplementing should help but I suspect most IBS patients have other reasons for low magnesium status.
Bowel surgery can lead to malabsorption as can hyperthyroidism (an overactive thyroid).
Diarrhoea causes malabsorption and loss of electrolytes including Mg. I noticed when I had travellers’ diarrhoea a few years ago that after a couple of days, I started to suffer from abdominal bloating which resolved with magnesium supplementation. I believe this is a transient form of IBS. Magnesium salts are used as a treatment for constipation, e.g. Epson Salts (MgSO4) as they can cause osmotic diarrhoea. Paradoxically, my view is that diarrhoea should be treated with prudent doses of Mg, especially in cases of IBS with diarrhoea.
The likelihood of developing post infective functional bowel disease has been shown to depend upon the duration of diarrhoea rather than the severity of the infection. This is consistent with a process of gradual magnesium depletion. Thus, this variant of IBS may simply be a reversible consequence of diarrhoea. Whilst restoring magnesium levels will address the cause of the diarrhoea, we can anticipate a reduction in, or elimination of, IBS symptoms such as abdominal bloating and pain.
The kidneys help regulate magnesium levels in the blood. Kidney disease, uncontrolled diabetes, hyperthyroidism, hyperparathyroidism, hyperaldosteronism and use of loop or thiazide diuretics all cause loss of Mg. Caffeine and alcohol also increase renal loss and are known to trigger IBS attacks.
Low vitamin D causes malabsorption whereas high levels increase renal loss of vitamin D. It’s a long time ago (1998) but I found that taking twice the RDA amount of vitamin D was best for me, I don’t know what my vitamin D levels were at the time.
Hypothyroidism causes a shift from the intracellular to the extracellular space which increases blood Mg levels a bit and so increases renal loss leading to a net deficit. These low intracellular levels can’t be measured in practice. This was the cause of my IBS, as described in the Hypothyroidism section.
Stress (physical or emotional) acts on the adrenals releasing hormones that cause a shift from the intra to the extra-cellular space and promotes renal loss. Conversely magnesium deficit creates a state of hyper-susceptibility to stress. Thus, magnesium deficit and stress reinforce each other in a pathogenic vicious circle.
Personality Type A subjects are more sensitive to stress and produce more stress hormones than type B subjects; hence the magnesium loss originating from stress occurs mainly in type A subjects. We can therefore expect this form of magnesium deficiency to predominate in type A individuals, they will also exhibit enhanced stress responses because of their magnesium deficiency. This sort of enhanced stress response is seen in IBS patients.
A research project carried out by a team including IBS Network’s Christine Dancey showed that IBS symptoms worsened not just during, but to a greater extent two days after stressful events. This is consistent with the process of magnesium loss due to stress and is unlikely to be due to a direct psychological response. Another study shows a very strong link between IBS severity and long-term stress, consistent with gradual loss of magnesium due to stress.
The Cause of My IBS
My IBS came on gradually, intermittent at first and then regular. I carried out extensive research for many years, lots of ideas were wrong. Eventually I discovered the role of magnesium deficiency. I systematically excluded all the possible causes one by one, this included measuring hormones that affect magnesium status. Non-IBS symptoms like fatigue, constant yawning and poor working memory pointed to hypothyroidism but the very helpful endocrinologist I saw said I couldn’t be hypothyroid: ‘because the blood tests say so‘. I investigated further and found that patients do indeed become hypothyroid with ‘normal’ blood test results. I made an appointment with Dr Skinner and he told me he thought I might be hypothyroid, based on my clinical signs and symptoms. We trialled a small dose of levothyroxine and I started to respond. Note that my IBS came on long before my more severe signs and symptoms of hypothyroidism.
Within two weeks of initiating levothyroxine my IBS had completely resolved. I worked in computing and we used to carry out ‘stress tests’ on our systems. My IBS was always triggered by hot-cross buns from the local bakery. For two weeks I ate two or three every day – I could not trigger an IBS attack.
The origins of my hypothyroidism were complex, it took fifteen years to identify the ‘aetiology’, the underlying cause. This is detailed in the section ‘Acquired Resistance to Thyroid Hormone (ARTH)‘ under the Hypothyroidism tab.