Poor bone mineral density (BMD) may result from an imbalance between bone resorption and bone formation. Compromised BMD may limit mobility, increase risk of fractures and contribute to “endogenous” lead exposure. Dietary, endocrine and environmental factors contribute to net bone resorption and demineralization.

Primitive human diets consisted of organ meats, eggs and bioavailable sources of minerals, to support optimal BMD. Bioavailable sources of calcium and other minerals such as magnesium and potassium, are best derived from dark green leafy vegetables. The Standard American Diet (SAD) is characterized by excess fats, proteins and simple carbohydrates and uniquely recommends daily consumption of dairy. Populations that do not consume dairy have been shown to have lower incidence of osteoporosis. Those consuming a SAD are at risk of vitamin and mineral deficiencies contributing to bone demineralization. Calcium, vitamin D and parathyroid hormone work together to support optimal bone health. Red blood cell elements testing assesses important intracellular minerals such as magnesium and potassium that function in conjunction with calcium.

Thyroid status influences BMD. Thyroid hormones stimulate bone turnover via increased osteoclastic bone resorption, and T3 has been shown to exert catabolic effects contributing to bone loss. Although thyrotoxicosis is clinically rare, subclinical hyperthyroidism has been associated with an increase in bone turnover, decreased BMD and an increased risk of fracture. Furthermore, thyroid status at the upper end of the euthyroid reference range is associated with decreased BMD and an increased risk of fracture. Decreased TSH and higher fT4, still within normal limits, has been associated with up to 25% increased risk of hip fractures. Clinical considerations include those undergoing hypothyroid treatments, as these may inadvertently induce hyperthyroid conditions.

Excessive consumption of simple carbohydrates may compromise BMD. Glycosuria has been shown to increase urinary calcium excretion. Those diagnosed with type II diabetes mellitus (T2DM) display significantly increased cortical porosity and decreased BMD. Glycosylation suppresses bone formation and bone resorption. Advanced glycation end products (AGEs) are proteins or lipids that become glycated in the presence of sugars. AGEs lead to bone fragility via altering the properties of bone collagen. T2DM is associated with significant bone marrow changes as a result of inflammation induced oxidation combined with a hyperglycemic bone marrow environment, which inhibits the maturation of osteoblasts. This process shifts the mesenchymal stem cell differentiation from osteo-blastogenesis to adipogenesis.

Overall, environmental exposure to lead (Pb) has decreased over recent decades, yet with a 30-year half-life this is still a factor for those exposed earlier in life. Bone stores account for 90-95% of an adult’s current body burden of Pb. Pb in bone may contribute to increased bone turnover via a stimulation of osteoblast and osteoclast activity resulting in net resorption that is associated with decreased bone density. Aging, lack of regular physical activity, thyroid dysfunction, diabetes and hormonal changes, specifically menopause, contribute to bone demineralization and release of Pb. This re-exposure to Pb increases risk of Pb-related health outcomes. Persistent effects of exposure to Pb lead to hypertension, cancer and neurodegeneration.

Net bone resorption and demineralization are persistent factors influencing BMD. Addressing dietary choices, especially the SAD, as well as endocrine and environmental factors, such as Pb, may improve BMD. Normal physical activity such as walking and light weight bearing activities have been associated with improved BMD.


Author: Julia Malkowski, ND, DC | April 7, 2021
Goldman RH, White R, Kales SN, Hu H. Lead poisoning from mobilization of bone stores during thyrotoxicosis. Am J Ind Med. 1994 Mar;25(3):417-24. doi: 10.1002/ajim.4700250309. PMID: 8160659.
Maret W. The Bioinorganic Chemistry of Lead in the Context of Its Toxicity. Met Ions Life Sci. 2017;17:/books/9783110434330/9783110434330-001/9783110434330-001.xml. doi:10.1515/9783110434330-001
Murray CE, Coleman CM. Impact of Diabetes Mellitus on Bone Health. Int J Mol Sci. 2019;20(19):4873. Published 2019 Sep 30. doi:10.3390/ijms20194873
Stiles VH, Metcalf BS, Knapp KM, Rowlands AV. A small amount of precisely measured high-intensity habitual physical activity predicts bone health in pre- and post-menopausal women in UK Biobank. Int J Epidemiol. 2017;46(6):1847-1856. doi:10.1093/ije/dyx080
Opinder Sahota, Understanding vitamin D deficiency, Age and Ageing, Volume 43, Issue 5, September 2014, Pages 589–591, https://doi.org/10.1093/ageing/afu104
Palacios C, Gonzalez L. Is vitamin D deficiency a major global public health problem?. J Steroid Biochem Mol Biol. 2014;144 Pt A:138-145. doi:10.1016/j.jsbmb.2013.11.003
Theppeang K, Glass TA, Bandeen-Roche K, et al. Associations of bone mineral density and lead levels in blood, tibia, and patella in urban-dwelling women. Environ Health Perspect. 2008;116(6):784-790. doi:10.1289/ehp.10977
Williams GR, Bassett JHD. Thyroid diseases and bone health. J Endocrinol Invest. 2018;41(1):99-109. doi:10.1007/s40618-017-0753-4

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