Osteoporosis and Bone Health in EDS & HSD: Can Nutrition Make a Difference?
When we think about nutrition for bone health, Calcium and Vitamin D are usually the first nutrients that come to mind, with good reason.
But for people living with Hypermobility Spectrum Disorder (HSD), Ehlers-Danlos Syndromes (EDS), and commonly co-occurring conditions like Mast Cell Activation Syndrome (MCAS), there are other factors which have to be considered.
Osteoporosis and osteopenia are growing health concerns, especially for women and people assigned female at birth who face increased bone loss post-menopause. But in connective tissue disorders like HSD & EDS, there are unique nutritional challenges and considerations which add complexity to the bone health conversation.
This blog will explore key nutritional considerations for bone health in HSD & EDS.
Do connective tissue changes from HSD & EDS affect bone health?
Collagen is a key component of bone, acting as a scaffold that provides structure, flexibility, and strength. As a connective tissue protein, it plays a crucial role in maintaining bone integrity by supporting the mineral framework that gives bones their hardness.
In the context of Hypermobility Spectrum Disorders (HSD) and Ehlers-Danlos Syndromes (EDS), changes in collagen current research on EDS & HSD suggest that hEDS is associated with somewhat lower bone mineral density, and rather that only a few of the rarer and genetically identifiable types of EDS (like kEDS, clEDS, aEDS, spEDS) carry a significantly increased risk of bone disease and fracture (Basalom & Rauch, 2020). Another connective tissue disorder, Osteogenesis Imperfecta is characterised by altered Collagen I and often is associated with severe osteoporosis and fracture.
There is still more research needed to understand specifically how bone health is affected in HSD & EDS and via what mechanisms.
Bone Health: Factors To Consider
These are a few of the factors we consider when a client expresses concern over bone health, or has been identified as having osteoporosis or osteopenia.
Mast cell activation syndrome and chronic inflammation
Mast cells are immune cells found in connective tissue throughout the body, including bone marrow, playing a large role in bone homeostasis. In the context of MCAS, mast cells degranulate and release mediators and cytokines (e.g. histamine, TNF, IL-6) throughout bone tissue. The overload of inflammatory mediators and cytokines promotes osteoclast activity (cells that remove bone tissue), while often suppressing osteoblasts (cells that promote bone growth). Studies have shown that patients with low bone density, often have increased numbers of mast cells present, indicating that increased mast cell activity is associated with accelerated bone turnover.
What this means in practice, is that MCAS management (e.g. antihistamines, mast cell stabilisers, nutrition etc.) is key in preventing bone loss.
Malnutrition, and protein/energy intake
Malnutrition refers to a mild-severe deficit in energy (calorie) and micronutrient intake. Sadly this is a common occurrence in HSD and EDS, often related to:
Dietary restrictions from food allergies, sensitivities and sensory preferences
Nutrient malabsorption due to gastrointestinal symptoms
Symptoms such as nausea, vomiting, pain and loss of appetite, limiting oral intake
Eating disorders, including ARFID, often co-occurring in neurodivergent populations
When the body is not receiving enough energy, it undergoes metabolic adaptations to prioritise vital organs for survival - and bones are not prioritised! In fact, the body can downregulate or even shut off ‘non-essential’ systems, such as the reproductive system, to conserve energy. This can lower crucial hormones like oestrogen, testosterone, and IGF-1, which increases osteoclast activity, and bone loss. Women in perimenopause and menopause are therefore at further risk of bone loss due to the decline in oestrogen, which is a protective factor for bone health.
Malnutrition also leads to loss of muscle mass, as muscles are broken down and converted to energy to fuel essential organs. Reduced muscle mass exerts less force on bones, further reducing the mechanical load needed for bone growth and density. This is partly why protein needs are slightly higher in HSD and EDS, to support collagen, muscle strength and healing.
If malnutrition is a factor for you, working alongside a dietitian to optimise your intake and find suitable food alternatives is key to supporting bone health.
3. Key nutrients for bone health
Vitamin D
Vitamin D and calcium are key nutrients for bone health. Vitamin D is a fat-soluble vitamin that plays a critical role in helping the body absorb calcium from the gut. While small amounts are obtained from foods, most vitamin D is synthesised in the skin through sunlight exposure. Once absorbed, vitamin D plays a key regulatory role in maintaining blood calcium levels, which are essential for muscle contraction, nerve signalling and heart rhythm.
The body tightly regulates blood calcium levels and will prioritise maintaining them, even at the expense of bone health. When serum calcium drops, parathyroid hormone (PTH) is released, increasing the conversion of vitamin D to its active form and stimulating calcium and phosphorus release from bone to restore circulating levels. Over time, vitamin D deficiency can result in secondary hyperparathyroidism, accelerating bone turnover and mineral loss. Given that around one-third of Australians are vitamin D deficient, and higher vitamin D targets are recommended in HSD and EDS (>90 nmol/L), supplementation is often needed, even with appropriate sun exposure. Serum vitamin D testing is covered under Medicare if you meet the criteria (which most people with HSD and EDS do!). While small amounts of Vitamin D is found in foods such as oily fish and egg yolks, food alone is rarely sufficient to support optimal levels.
Calcium
Calcium provides the structural framework of bone, with 99% stored in bones and teeth and 1% circulating in blood and soft tissues. Adequate intake supports osteoblast-driven bone formation, while insufficient calcium or impaired vitamin D absorption can lower serum calcium and further stimulate bone resorption via PTH. For individuals who cannot tolerate dairy due to MCAS or gastrointestinal symptoms, calcium-fortified plant milks, tofu, canned fish with bones, nuts, seeds, and leafy greens are important alternatives. When supplementation is required, calcium citrate is often better tolerated and absorbed.
Vitamin K2
Vitamin K2 supports bone mineralisation by activating proteins that help direct calcium into bone and away from blood vessels, preventing vascular calcification. For people who also have high cholesterol, or who are at risk of heart diseases, K2 provides additional cardioprotective benefits. While Vitamin K2 is found in a range of foods, such as leafy greens, it is often added to Vitamin D and calcium supplements to further improve bone formation.
Sodium
While not often talked about in relation to bone health, it is important to note that high intakes of sodium lead to increased urinary calcium excretion. Many people with HSD and EDS also have dysautonomias, such as POTS, which require sodium intakes up to >10g per day. Studies indicate that those with HSD and EDS typically have lower bone mineral densities (BMD); however, given the multisystemic causes of low BMD, it is unknown to what extent this is influenced by high sodium intakes. Given the significant benefits of high sodium intakes on POTS, it is generally still considered safe to consume high levels of sodium; however, working with a dietitian to mitigate the risks is essential.
Key takeaways
People with HSD and EDS are at increased risk of low BMD and developing osteoporosis. To improve bone health, people with HSD and EDS should consider:
MCAS management
Optimising energy, protein and micronutrient intake (and absorption)
Working with a dietitian or health professional to test serum micronutrients and supplement as needed.
Asking your GP for a bone mineral density scan - this provides valuable insight into your current bone health, and can be repeated over time to assess risk.
I hope this blog has provided further insight into the value of nutrition in optimising bone health in HSD and EDS. If you have any questions, or if you are seeking support with MCAS, Hypermobility, POTS or complex gastrointestinal concerns, please don't hesitate to reach out.
References:
https://pmc.ncbi.nlm.nih.gov/articles/PMC7025484/
https://pmc.ncbi.nlm.nih.gov/articles/PMC4355339
Advanced Nutrition and Human Metabolism 7th Ed.
