Normal potassium range should be 3.6-5.2 mmol/l but many of us may feel more comfortable around 4.2-4.6 mmol/l It's important to remember that both hypo and hyper kalemia can be deadly, so regular monitoring is advised. symptoms for hypokalemia: Drug induced hypokalemia: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4357351/table/t2-ptj4003185/ I found another possible trigger: supplementation with B12 can compete with Potassium chloride for intestinal absorption. Sublingual B12 or injections may prevent this issue. Other triggers (follow the link if you wish a more complete list): "Increased potassium entry into cells This can occur by a number of mechanisms. Elevation in extracellular pH: metabolic or respiratory alkalosis can facilitate potassium entry into cells (hydrogen ions leave the cells and potassium enters into cells to maintain electroneutrality). Administration of sodium bicarbonate to treat metabolic acidosis can also cause this phenomenon. Increased beta-adrenergic activity: catecholamines promote potassium entry into the cells by increasing Na-K-ATPase activity.  .... Transient hypokalemia may also occur during stress-induced release of epinephrine and cortisol (e.g., during acute illness or coronary ischemia).  Increased availability of insulin: insulin promotes the entry of potassium into skeletal muscle and hepatic cells by increasing the activity of the Na-K-ATPase pump.  ... The plasma concentration of potassium may also be reduced by a large carbohydrate load. Increased blood cell production during anabolic states: increased potassium entry into cells may be caused by sharp increases in hematopoietic cell production that occurs with the use of granulocyte-macrophage colony-stimulating factor (GM-CSF) in neutropenia.  This may also occur after the administration of vitamin B12 or folic acid in megaloblastic anemia.  Chloroquine intoxication: hypokalemia is a common finding in acute chloroquine intoxication.  This is caused by potassium movement into cells and can be exacerbated by the use of epinephrine to help treat the intoxication. Hypothermia: there have been reports that hypothermia may result in a drive of potassium into cells associated with a plasma potassium concentration decrease to below 3.0 to 3.5 mEq/L.  This is reversible on rewarming. Supplementation of potassium during hypothermia can also cause a significant increase in serum potassium concentration on rewarming. Losses from the GI tract Loss of gastric or intestinal secretions from any cause (vomiting, diarrhea, laxatives, or tube drainage) can cause hypokalemia.  Increased loss of potassium in urine A wide variety of causes are associated with increased potassium loss in urine. Mineralocorticoid excess: urinary potassium wasting is also characteristic of any condition associated with primary hypersecretion of mineralocorticoids (primary aldosteronism) or hypersecretion of catecholamines via enhanced release of renin. Apparent mineralocorticoid excess, characterized by edema, hypertension, and hypokalemia, has been well documented as occurring in disorders with congenital deficiency, or lack of renal 11-beta-hydroxysteroid dehydrogenase type 2 or its inhibition by chronic licorice ingestion, acute alcoholism, chronic liver or renal disease, preeclampsia (hypocalcemia), ..... Presence of nonreabsorbable anions: a marked increase in potassium excretion by reabsorbing sodium in exchange for potassium can occur during vomiting or type 2 renal tubular acidosis, or beta-hydroxybutyrate in diabetic ketoacidosis, or it may be drug-induced.   In these conditions a decrease in distal chloride delivery and the enhanced secretion of aldosterone also promote potassium secretion.  Hypomagnesemia: this is present in up to 40% of patients with hypokalemia.  Hypomagnesemia can lead to increased urinary potassium loss via an uncertain mechanism, possibly involving an increase in the number of open potassium channels. The presence of hypocalcemia is often a clue to underlying hypomagnesemia. It is important to determine whether there is hypomagnesemia because hypokalemia often cannot be corrected until the magnesium deficit is corrected first. Polyuria: this is most likely to occur in primary (often psychogenic) polydipsia in which the urine output may be elevated over a prolonged period of time.  Polyuria can also occur in central diabetes insipidus, although patients typically seek medical care soon after the polyuria begins. Increased loss via sweating and skin Exercising in a hot climate can produce more than 10 L of sweat daily, leading to potassium depletion if losses are not replaced.  Urinary potassium excretion also may contribute, since aldosterone release is enhanced both by exercise (via catecholamine-induced renin secretion) and volume loss. Burns and other dermatologic conditions (i.e., eczema or psoriasis involving a large surface area of the skin, especially with the use of topical steroids) can cause increased loss of potassium through the skin. Miscellaneous Chronic alcoholism is a common cause of hypokalemia. Hypokalemia occurs for various reasons, such as poor oral intake, associated vomiting, and secondary hyperaldosteronism. Hypokalemia can be induced in some patients by maintenance dialysis. Potassium losses can reach up to 30 mEq/day in patients on chronic peritoneal dialysis. This may become clinically important if potassium intake is reduced or if there are concurrent GI losses.  Plasmapheresis removes potassium in the same concentration as it is present in plasma. Albumin use as a replacement fluid can cause transient dilutional hypokalemia. "