Potassium Magnesium Citrate Is Superior to Potassium Chloride in Reversing Metabolic Side Effects of Chlorthalidone.
Level 2 - randomized trial
Double-blind randomized controlled trial
PubMed 37846572 · doi:10.1161/HYPERTENSIONAHA.123.21932
What was done
A double-blind randomized controlled trial evaluated 60 non-diabetic hypertensive participants (mean age 59±11 years, 30% Black) undergoing chlorthalidone treatment. Each participant received chlorthalidone alone for a 3-week run-in period before being randomized to 16 weeks of potassium chloride (KCl) or potassium magnesium citrate (KMgCit) supplementation. The primary endpoint was the change in fasting plasma glucose from the chlorthalidone monotherapy baseline; liver fat was measured using magnetic resonance imaging.
What was found
Chlorthalidone monotherapy led to a significant increase in fasting plasma glucose and significant decreases in serum potassium, serum magnesium, and 24-hour urinary citrate excretion (all P < 0.05). Supplementation with KMgCit attenuated the rise in fasting plasma glucose by 7.9 mg/dL compared with KCl (P < 0.05). No significant difference in liver fat was observed between the two groups.
Why it matters
Thiazide-induced hyperglycemia is a common adverse metabolic effect often attributed to potassium loss, but concomitant magnesium depletion is rarely addressed. This demonstrates that KMgCit is superior to conventional KCl in counteracting glucose elevations caused by chlorthalidone.
Limits
The trial had a small sample size (n = 60) and a relatively short 16-week intervention period. It excluded patients with preexisting diabetes, and the abstract omits specific supplement dosages, exact baseline glucose values, and absolute electrolyte concentrations.
Cited by
- supports Thiazide and loop diuretic medications for high blood pressure deplete the body of potassium and block magnesium.