Study Of Deer Antlers Throws Light On Workings Of Osteoporosis

Research / March 1, 2012

More insights were had on the possible development of osteoporosis through a study of deer antlers by researchers at Research Institute of Hunting Resources (University of Castilla La Mancha), Spain. We have long been reading literature about how important Vitamin D and magnesium are to calcium metabolization. This new study shows another dietary mineral plays a vital role in the osteoporosis equation and that is manganese.

The study of deer antlers began when there was a marked increase in the reported breakage of deer antlers in 2005 in Spain. The study pointed out that it was not really the deficiency of dietary calcium that made antlers in deer weak, but low levels of dietary manganese caused the calcium to not ‘stick’ as it were causing poor quality antlers. In that particular year, due to an abnormally cold winter, the plants reduced their manganese concentration and deer on their diet lost antlers in large numbers. It is believed that as much as 20% of a deer’s skeletal calcium gets directed towards growing antlers. However, when their diets lacked or were deficient in manganese, the ‘glue’ that stuck calcium to antler bones went near absent. (1)

As per the one of the team’s researchers and sub-director of the IREC, Tomás Landete, “previous antler studies show that manganese is necessary for calcium absorption. Our hypothesis is that when the human body absorbs less manganese or when it is sent from the skeleton to other organs that require it, such as the brain, the calcium that is extracted at the same time is then not properly absorbed and is excreted in the urine. It is in this way that osteoporosis can slowly strike.” (2)

However, this is only a hypothesis and more tests need to be conducted to validate the findings. The theory was published in the January 2012 issue of Frontiers of BioScience journal. (3)

So what significance is this finding to humans? First of all it gives value to the idea that calcium loss could be a consequence of the disease and not the origin of osteoporosis. Secondly, because important organs in our body such as our brain draw out manganese from our bones when required, when manganese leaches out of our system (due to either poor dietary intake or age-related poor metabolization) our brain has no sources within the body to draw out the manganese from and conditions like Alzheimer’s diseases, osteoporosis and Parkinson’s disease set in.

In order to test this hypothesis the research team conducted a data analysis project at Hellín Hospital in Albacete, Spain between 2008 and 2009 on 113 patients with surgery prescribed either for osteoporosis or osteoarthritis. It was observed that 40% of the osteoporosis cases also exhibited some type and extent of cerebral dysfunction probably stemming from depletion of manganese reserves while this was not the case for the osteoarthritis patients.

Landete recalls that studies that linked onset of Parkinson’s disease to deficiencies of manganese had clearly demonstrated that cells called astrocytes which provide support to brain cells had in them enzymes that required manganese for optimal function. Apart from this studies have been conducted on rates for Alzheimer’s disease (brought on by aluminum intoxication) point that acuity of Alzheimer’s disease increases as manganese levels in the bones decreases.

More studies are required to validate the hypothesis into a scientifically established fact which will help address conditions such as osteoporosis with finality.


1. Deer Antlers Inspire a New Theory On Osteoporosis; Science Daily News; January 2012;
2. Deer antlers inspire a new theory on osteoporosis; Alpha Galileo Foundation; January 2012;
3. Alternative hypothesis for the origin of osteoporosis: The role of Mn; Frontiers In Bioscience; January 2012;

Lara Pizzorno

Very interesting! Another way in which manganese deficiency would promote bone loss is by disrupting the activity of a key antioxidant enzyme called superoxide dismutase. Manganese is a required cofactor for the form of the SOD enzyme that is found in the mitochondria (the energy production factories within our cells). Manganese deficiency would result in this enzyme (Mn-SOD) being unable to function, so the production of free radicals in cells throughout the body would greatly increase, causing inflammation — and inflammation increases both the production and activity of osteoclasts.

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