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Osteoporosis: The Role of Metabolic Health and Therapeutic Carbohydrate RestrictionThe Role of Metabolic Health and Therapeutic Carbohydrate Restriction

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Osteoporosis: The Role Of Metabolic Health And Therapeutic Carbohydrate Restrictionthe

Sarah Rice BSc. (Hons), MCOptom (UK), MHP, NNP

Import

Osteoporosis occurs when bone mineral density (BMD) and bone mass decrease or when structural changes occur that lead to weakness. Bone tissue is constantly remodeled through the action of osteoclasts and osteoblasts (bone resorption and formation) and osteocytes (regulation of bone remodeling by sensing mechanical forces) (1). When imbalances occur in these pathways and resorption exceeds formation, bone loss and osteoporosis can occur (1). Metabolic health plays an important role in the pathogenesis of osteoporosis, with increasing evidence linking metabolic syndrome, obesity, and diabetes to increased bone fragility and fracture risk (2–4).

Historically, the use of ketogenic interventions for children with epilepsy has raised questions about bone health. These concerns are characteristic of the complex interactions between medications, physical activity, metabolic disorders, and the strict macronutrient control required to maintain ketones at therapeutic levels in this population. This population cannot be generalized to adults with metabolic disorders due to differences in physiology and the fact that some epilepsy drugs interfere with bone metabolism. Even with these challenges, ketogenic diets have been successfully administered without harming bone health in these populations (5, 6). Ensuring nutritional adequacy in this population is important. TCR and ketogenic interventions for metabolic conditions are more relaxed and no adverse effects on bone health have been reported so far, although specific studies are limited (7-9).

Metabolic syndrome, hyperinsulinemia and type 2 diabetes

The metabolic syndrome, characterized by central obesity, hyperglycemia, hypertension, and dyslipidemia, exerts complex and sometimes contradictory effects on bone. While higher body mass index (BMI) may yield higher bone mineral density (BMD) scores, bone quality and fracture risk may be compromised, particularly where there is increased visceral obesity and insulin resistance (2, 4, 10). propensity for osteocyte apoptosis (2). Patients with metabolic disorders (ie, insulin resistance), which include type 2 diabetes and cardiovascular disease, have lower levels of osteocalcin and bone remodeling, along with increased fracture rates (2). In this phenotype, BMD may be normal or even elevated (2). Hyperglycemia increases advanced glycation end product formation in bone collagen, and improved glycemic control has been associated with improved bone metabolism in diabetic populations (2, 11). In addition, a recent study examined the effect of carbohydrate intake on BMD through a Mendelian randomization analysis and concluded that carbohydrates may specifically affect the metabolic pathway of of carbohydrates in (12).

Therapeutic carbohydrate restriction

TCR has been shown to improve markers of metabolic health and glycemic control in patients with metabolic syndrome and type 2 diabetes without affecting bone health (7). In 2019, Athin et al. reported two-year results using nutritional ketosis to manage patients with type 2 diabetes. They found that spine BMD in the intervention group remained unchanged compared to the usual care group, while glycemic control showed improvement (7). A 12-month study comparing a low-carb diet with a low-fat diet found that, despite increased weight loss in the low-carb group, BMD was better maintained (8). These findings are encouraging, as weight loss is typically accompanied by some loss of BMD (17). A two-year study by Foster et al. (2010) also found no harm to bone health when comparing a low-fat diet with a low-carbohydrate diet. In addition, the low-carb group had improved markers of cardiovascular disease risk (9).

Ensuring adequate protein intake is an important component of a well-designed low-carb or ketogenic diet. A recent meta-analysis found that higher protein intake (> 0.8 g/kg) reduced fracture risk in older populations and protected against BMD loss (16). For adults undergoing weight loss, a protein goal of 1.2 to 2.0 g/kg of reference weight (usually between ~80–150 g/day) is recommended (17). This helps maintain fat-free mass (FFM) during a weight loss phase (17).

Menopause

During menopause, decreased estrogen levels affect bone and muscle metabolism, increasing the risk of osteoporosis. An estimated 200 million women worldwide experience this condition (13). This demographic may also experience an increase in insulin resistance, which exacerbates the problem. TCR in postmenopausal women has been shown to improve metabolic health and is protective for bone health (14, 15).

Conclusion

Overall, optimizing metabolic health through weight management, glycemic control, and reduced visceral adiposity is important for preventing osteoporosis and reducing fracture risk. TCR is a safe and effective intervention for metabolic disorders, and a well-formulated ketogenic diet has been associated with neutral or positive markers of bone health in this population, although studies measuring bone metrics are limited. Further research on bone health and TCR in different populations is needed to better understand different nutritional needs and establish optimal protein intake. As with any intervention, an individualized approach that assesses nutritional needs and uses appropriate monitoring is recommended.

References

  1. Florencio-Silva, R. et al. (2017) ‘Osteoporosis and autophagy: What’s the connection?’, Revista da Associação Médica Brasileira63, pp. 173–179. Available in: https://doi.org/10.1590/1806-9282.63.02.173.
  2. Cooper, ID, Brookler, KH and Crofts, CAP (2021) ‘Revisiting fragility fractures in type 2 diabetes: The link between hyperinsulinemia and fragility’, Biomedical9(9), p. 1165. Available at: https://doi.org/10.3390/biomedicines9091165.
  3. Zuo, M. et al. (2023) ‘Association of insulin resistance with bone mineral density in a national health surveillance population in China’, Bonepp. 116703. Available at: https://doi.org/10.1016/j.bone.2023.116703.
  4. Krivelli, M. et al. (2020) ‘Association of visceral and subcutaneous fat with bone mineral density and vertebral fractures in severely obese women’, Journal of Clinical Densitometry [Preprint]. Available in: https://doi.org/10.1016/j.jocd.2020.10.005.
  5. De Amicis, R. et al. (2023) ‘Long-term follow-up of nutritional status in children with GLUT1 deficiency syndrome treated with a classical ketogenic diet: a 5-year prospective study’, Frontiers in Nutrition10, pp. 1148960. Available at: https://doi.org/10.3389/fnut.2023.1148960.
  6. Bertoli, S. et al. (2014) “Long-term effects of a ketogenic diet on body composition and bone mineral mineralization in GLUT-1 deficiency syndrome: a case series”. Nutrition (Burbank, Los Angeles County, California)30(6), pp. 726–728. Available in: https://doi.org/10.1016/j.nut.2014.01.005.
  7. Athinarayanan, SJ et al. (2019) ‘Long-term outcomes of a novel telecare continuum intervention including nutritional ketosis for the management of type 2 diabetes: a 2-year non-randomised clinical trial’. Frontiers in Endocrinology10. Available at: https://doi.org/10.3389/fendo.2019.00348.
  8. Hu, T., Yao, L. and Bazzano, L. (2016) ‘Effects of a 12-month low-carbohydrate versus a low-fat diet on bone mineral density: A randomized controlled trial’. The FASEB magazine30(S1), pp. 678.12-678.12. Available in: https://doi.org/10.1096/fasebj.30.1_supplement.678.12.
  9. Foster, GD et al. (2010) ‘Weight and metabolic outcomes after 2 years on a low-carbohydrate versus low-fat diet’. Annals of Internal Medicine153(3), pp. 147–157. Available in: https://doi.org/10.7326/0003-4819-153-3-201008030-00005.
  10. Tonks, KT et al. (2017) “Bone turnover is suppressed in insulin resistance, independent of adiposity”. The Journal of Clinical Endocrinology & Metabolism102(4), pp. 1112–1121. Available in: https://doi.org/10.1210/jc.2016-3282.
  11. Karadeniz, B. et al. (2021) “The relationship between glycemic control and osteocalcin, collagen type 1 C-terminal telopeptide, bone-specific alkaline phosphatase, and the effects of antidiabetic regimens on circulating markers of bone turnover in newly diagnosed diabetic patients: Bone Health in Diabetics,” Clinical Nephrology [Preprint]. Available in: https://doi.org/10.5414/CN110394.
  12. Zhao, X. and Chen, K. (2025) ‘Plasma metabolites mediate the causative effect of carbohydrate intake on bone mineral density’, Medicine104(31), pp. e43608. Available in: https://doi.org/10.1097/MD.0000000000043608.
  13. Wright, VJ et al. (2024) ‘The musculoskeletal syndrome of menopause’, Climacteric27(5), pp. 466–472. Available in: https://doi.org/10.1080/13697137.2024.2380363.
  14. Islamoglu, AH et al. (2020) “The effects of dietary changes on bone markers in postmenopausal vertebral osteopenia”, Clinical Nutrition0(0). Available in: https://doi.org/10.1016/j.clnu.2020.04.001.
  15. Pala, B. et al. (2024) ‘Very-low-calorie ketogenic diet reduces central blood pressure and cardiometabolic risk in postmenopausal women with essential hypertension and obesity: a single-centre, prospective, open-label, clinical study’, Nutrition, metabolism and cardiovascular disease: NMCDpp. 103838. Available at: https://doi.org/10.1016/j.numecd.2024.103838.
  16. Groenendijk, I. et al. (2019) ‘High versus low dietary protein intake and bone health in older adults: a systematic review and meta-analysis’. Computational and Structural Biotechnology Journal17, pp. 1101–1112. Available in: https://doi.org/10.1016/j.csbj.2019.07.005.

Volek, JS, Kackley, ML and Buga, A. (2024) ‘Nutritional considerations during major weight loss treatment: a focus on optimal protein and a low-carbohydrate dietary pattern’. Current Nutrition Reports [Preprint]. Available in: https://doi.org/10.1007/s13668-024-00548-6.

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