The nature of Long COVID and of many adverse events being reported are uniquely in line with the metabolic landscape of starvation.  

Starvation increases gluconeogenesis and proteolysis while metabolic substrates including vitamins and intracellular. electrolytes are depleted.[7][8] Sudden initiation of nutritional replenishment following extended periods of starvation results in rising glucose levels in the bloodstream.

With rising glucose levels, the body produces a countermeasure that increases insulin levels which then drive phosphorus and potassium intracellularly; causing a decrease in the amount of available extracellular potassium or hypokalemia. This occurs in part due to the need for phosphorylation of glucose in glycolysis but also through direct stimulation of the sodium-potassium ATP pump. This increase in insulin and the effects on electrolyte migration (intracellular vs extracellular) are compounded by nutritional electrolyte deficiencies.

Hypokalemia may lead to cardiac arrhythmias or weakness, fatigue, paralysis, hypoventilation and respiratory distress, and metabolic alkalosis. Low levels of phosphorous are linked to decreased cardiac contractility and arrhythmias, which could be fatal. A depletion of phosphorous can also decrease the production of 2,3 diphosphoglycerate (2,3 DPG) which causes a leftward shift in the oxygen-hemoglobin dissociation curve; increasing hemoglobin’s affinity for oxygen and decreasing oxygen release to the tissues; ultimately, starving metabolically active tissues of oxygen and worsening prognosis through secondary organ failure.[12] Lastly, phosphorous is implicated in preserving respiratory muscle function, and in severe cases, hypophosphatemia can = acute respiratory failure.