Manganese deficiency in humans is uncommon but it has been reported in several laboratory-induced experiments.16 The first was by Doisey who inadvertently fed a low-manganese diet (0.34mg/day) for 3.5 months to a subject on a semi-purified vitamin K-deficient diet. Symptoms that were not ameliorated by restoration of vitamin K were reddening of a black beard and hair, diminished hair and nail growth, hypocholesterolemia and a scaly, transitory dermatitis.

The last two symptoms were observed also in a metabolic study by the author.19 Seven college men were fed a semi-purified diet containing 135 mg cholesterol and 2.59mg Mn/day for 3 weeks, which then decreased to 0.1 mg Mn. After 35 days, 5 of the 7 subjects developed Miliaria crystallina, a scaling dermatitis covering the upper torso, groin and lower legs.20 This dermatitis vanished with manganese repletion. It was theorized that manganese may have been insufficient for the activation of glycosyltransferases, enzymes that add sugars to protein in the formation of collagen. Total cholesterol also declined, presumably related to the requirement of manganese at sites in the biosynthesis of cholesterol.21 Finally, serum calcium (Ca), phosphorus and alkaline phos-phatase increased, suggesting that manganese was being mobilized from stores in bone. The loss of manganese from bone is not surprising as skeletal abnormalities have been observed in manganese deficiencies in chickens, swine and ruminants,18 and in one child on total parenteral nutrition (TPN) without manganese for 4 years.22

Poor manganese status has been implicated in a variety of disease states and metabolic disorders, including osteoporosis, congenital malformations, TPN, Perthes' disease (necrosis of femur head), senile cataracts, epilepsy, amyo-trophic lateral sclerosis (degenerative disease of motor neurons), acromegaly (pituitary disorder of excess growth of extremities and face), hip abnormalities, multiple sclerosis,23 phenylketonuria (congenital defect causing mental retardation) and maple syrup urine disease (neurodegenerative disease of amino acids in urine).8 One exacerbating factor is the iron intake and status of an individual, as both iron and manganese share a common transport protein in the blood (transferrin) and cell (divalent metal transporter: DMT1). In young women, a supplement of 60 mg Fe/day for 4 months decreased activity of leukocyte manganese.24 Also, manganese absorption was lowered in women with high ferritin, the iron storage protein.25

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