Manganese might be thought of as rather an unusual element to be important in human nutrition but it has vital importance for our bone health. It is a micronutrient needed for the biosynthesis of the mucopolysaccharides involved in bone matrix formation and is a co-factor for several enzymes in bone tissue. Too much, and it is toxic so biochemical systems exist for its regulation.
Good sources of manganese include avocados, spinach, raisins, pineapple, broccoli, egg yolks and green leafy vegetables. Tree saps, especially birch sap also contain significant quantities of this element.
Despite the integral part manganese is predicted to play in bone metabolism throughout our stages in life, studies investigating this micronutrient alone are very rare. There are however studies in manganese deficient animals that have indicated alterations in insulin-like growth factor (IGF) metabolism, linear growth and bone metabolism (Clegg et al., 1998). Young male rats subjected to a dietary manganese (Mn) deficiency generally responded by reductions in growth rate. The growth hormone (GH)/insulin-like growth factor (IGF) axis is critical for linear growth as this system is highly sensitive to the nutritional state of the animal. Clegg et al. (1998) examined circulating GH, IGF-1, and insulin levels in Mn-deficient (0.5 µg Mn/g of diet) and Mn-replete (45 µg Mn/g of diet) male rats. Mn-deficient animals displayed lower circulating concentrations of IGF-1 (66% of control levels) and insulin (60% of control levels) despite exhibiting significant elevations in circulating GH levels relative to Mn-replete animals (140% of control levels). Therefore, it was demonstrated that in young male rats, Mn deficiency is associated with alterations in IGF metabolism and these alterations may contribute to the growth and bone abnormalities observed in Mn-deficient animals.
Manganese deficiency has not been documented in humans eating natural diets; therefore the AI was based on average dietary intakes of manganese in healthy individuals; however, levels higher than AI (1.8 mg/day in women and 2.3 mg/day in men) have been associated with gains in BMD (5 mg/day) (Strause et al., 1994). Indeed, manganese supplementation, along with copper, calcium and zinc, resulted in an increased bone mineral density (BMD) compared to calcium supplementation alone in post-menopausal women supplemented over a 2 year period (Strause et al., 1994). However, the effect on BMD cannot be attributed to manganese alone in this case, and other limitations of this study included small sample size and a single sex study cohort. Additionally, Odabasi et al. (2008) reported no difference between osteoporotic patients and control groups in either plasma or red blood concentrations of manganese in an epidemiological study of 77 post-menopausal osteoporotic women and 61 post-menopausal controls. In contrast, it has been documented that women with osteoporosis actually have decreased plasma levels of manganese and also an enhanced plasma response to an oral dose of manganese. This suggests that osteoporotic women may have lower manganese status than women without osteoporosis (Freeland-Graves and Llanes, 1994).
Manganese intake can vary greatly with food choices, water composition, and supplement use. Thus, individuals consuming Western diets consume from less than 1 to over 10 mg Mn/day depending on source. The levels of manganese intake associated with adverse effects in terms of both deficiency and toxicity are questionable. Moreover, many of the symptoms of manganese deficiency such as growth retardation, changes in circulating high-density lipoprotein (HDL) cholesterol and glucose levels, reproductive failure and manganese toxicity associated with growth reduction and anaemia are non-specific, and the bone deformities observed in manganese-deficient animals are permanent (Greger, 1999). It simply illustrates the need for further study into adequate levels of supplementation for an efficacious and safe dosage for use as a nutraceutical.
EFSA opinion/claims submitted to date
To date, just one claim has been put forward regarding manganese and bone health and received a positive opinion. Additionally, claims regarding antioxidant activity and energy metabolism also gained positive opinions. However, claims regarding mental state and performance gained a negative opinion and those regarding fatigue and tiredness are still under review.
Clegg, M.S., Donovan, S.M., Monaco, M.H., Baly, D.L., Ensunsa, J.L., Keen, C.L. (1998) The influence of manganese deficiency on serum IGF-1 and IGF binding proteins in the male rat. Proc. Soc. Exp. Biol. Med. 219(1) pp. 41-7.
Freeland-Graves, J., Llanes, C. (1994) Models to study manganese deficiency. In: Klimis-Tavantzis, D.L., ed. Manganese in health and disease. Boca Raton: CRC Press, Inc.
Greger, J.L. (1999) Nutrition versus toxicology of manganese in humans: evaluation of potential biomarkers. Neurotoxicology. 20(2-3) pp. 205-12. Review
Odabasi, E., Turan, M., Aydin, A., Akay, C., Kutlu, M. (2008) Magnesium, Zinc, Copper, Manganese, and Selenium Levels in Postmenopausal Women with Osteoporosis. Can Magnesium Play a Key Role in Osteoporosis? Ann. Acad. Med. Singapore 37 pp. 564-7
Strause, L., Saltman, P., Smith, K.T., Bracker, M., and Andon, M.B. (1994). Spinal bone loss in postmenopausal women supplemented with calcium and trace minerals. J. Nutr., 124 pp. 1060–1064