Bone Resorption:

Nutritional, Endocrine and Environmental Considerations

Julia Malkowski, ND, DC | April 7, 2021

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.


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Wellness Wednesday Webinar

Neurotransmitter Primer

Lylen Ferris, ND

April 7, 2021 at 9:30 AM and 12 PM Pacific

Each session is approximately 60 minutes in length with Q&A

Review the anatomy and physiology of neurotransmitter (NT) secretion and function

Exam the role of individual NTs and how imbalances present clinically

Learn to incorporate NT evaluation and treatment in your hormone balancing practice

Obtain treatment considerations for addressing neurotransmitter imbalances, without prescription medications

Beyond Adrenal Fatigue: Reframing our Understanding of Stress and the HPA Axis

Tom Guilliams PhD

April 21, 2021 | 12-1 PM Pacific

For too long, complex stress-related changes to HPA axis function have been labeled as "adrenal fatigue." This outdated and incorrect nomenclature has often prevented clinicians from properly understanding how the HPA axis adapts to stressors and why simplistic solutions (i.e., adrenal support) are inadequate for most patients. Our knowledge of the stress response system, HPA axis maladaptation, and the factors that influence glucocorticoid signaling have greatly advanced in just the past decade, though much of this knowledge is not well leveraged in most clinical practices. This webinar will reframe our orientation of stress in a way that focuses on the brain (rather than the adrenal gland), and shows that the stress response is not as linear as it is often perceived. While navigating through one of the premier resources to help clinicians understand the functional medicine approach to stress and the HPA axis, this lecture will also help re-frame the stress response within the larger (non-stress) functions performed by the HPA axis


Disclaimer: All information given about health conditions, treatment, products, and dosages are for educational purposes only and do not constitute medical advice.



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