ABSTRACT
Because of the availability of pantothenic acid in the food supply, human deficiency has been diagnosed only in severely malnourished patients.7,8 The abundance in nature results, in part, from its structural role in CoA. From 1930 to 1950, various animal species were studied under conditions that induced pantothenic acid deficiency.9−17 The deficiency in humans was difficult to characterize because of inconsistencies in chemical and clinical symptoms induced by diets devoid of pantothenic acid or the use of pantothenic acid antagonists.18−24 Inducement of the deficiency in humans produced variable symptoms indicative of other vitamin deficiencies or possible interrelationships with other nutritional deficiencies. Because of the lack of a clear biological marker, human status indicators are difficult to interpret. General symptoms, common to many nutritional deficiencies noted in the earlier cited studies on humans included irritability and restlessness, fatigue, apathy, malaise, sleep disturbances, nausea, vomiting, abdominal cramps, neurological symptoms (numbness, abnormal sensations in the hands and feet, muscle cramps, staggering gait), hyperglycemia, and increased sensitivity to insulin.25
