How to treat gallstone disease?

Gallstone disease is closely related to mineral metabolism, and its basis often lies in the imbalance of calcium and magnesium.

Composition of stones. Stones in the gallbladder mostly consist of cholesterol (70–80%), less often of bilirubin or calcium salts.

But it is the calcium salts (carbonates, phosphates, calcium bilirubinates) that provide the "framework" for crystallization around which the stone forms.

Role of calcium. When there is too much calcium in the bile, it binds with bile acids or bilirubin and forms insoluble crystals.

Excess calcium can occur due to its disturbed metabolism, low stomach acidity (poor digestion of fats and calcium), and magnesium and vitamin D deficiency.

Role of magnesium. Magnesium is an antagonist of calcium: it prevents excessive crystallization of calcium salts and improves the solubility of bile.

Magnesium relaxes the smooth muscles of the gallbladder and ducts, improving bile flow and reducing its stagnation. Magnesium also participates in the activation of liver enzymes that regulate cholesterol metabolism.

What happens with magnesium deficiency:

• Calcium starts to "behave aggressively": more precipitates in soft tissues and bile, less goes to the bones.
• The function of bile acids is disrupted, and cholesterol precipitates, forming the basis for the stone.
• Spasm of the gallbladder increases, further hindering normal outflow.

Therapeutic significance of magnesium. Thus, increased intake of magnesium (through food or supplements) reduces the risk of stone formation. It helps normalize the function of the sphincter of Oddi and the motility of the gallbladder. Magnesium stabilizes calcium levels and reduces the formation of insoluble salts.

Therefore, gallstone disease can indeed be considered a consequence of a calcium-magnesium imbalance, where excess calcium with a deficiency of magnesium leads to crystallization and stone formation.