Magnesium

TRPM6 encodes a channel in the kidney and gut responsible for active magnesium reabsorption — the step that decides how much of the magnesium already filtered by the kidney actually gets kept rather than lost in urine. Rare, severe TRPM6 mutations cause a genetic disorder of magnesium wasting; the common variant here is a much smaller nudge on the same system.

A 2010 genome-wide association study of serum magnesium in 15,366 people, replicated in a further 8,463, found six loci meeting genome-wide significance — MUC1, ATP2B1, DCDC5, TRPM6, SHROOM3 and MDS1. Every one of the initially significant variants also showed at least nominal association with clinically defined low magnesium (hypomagnesemia), which is what makes this more than a laboratory curiosity — the genetics tracks a real clinical state.

What it is not is a reason to guess. No guideline sets a magnesium dose from genotype, and the much larger, more common causes of low magnesium — diuretics, proton-pump inhibitors, heavy alcohol use, chronic diarrhoea, poorly controlled diabetes — outweigh this locus by a wide margin. Magnesium status is measured directly and cheaply, and that measurement, not a genotype, is what a deficiency is diagnosed and treated on.