Skip to main content Accessibility help

We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.

Close cookie message
×
Hostname: page-component-cd9895bd7-mkpzs Total loading time: 0 Render date: 2024-12-28T22:12:45.479Z Has data issue: false hasContentIssue false

Chapter 19 - Aging, Menopause, and Bone Health in Women with Epilepsy

Published online by Cambridge University Press:  19 December 2024

By
Alison M. Pack  and
Stephanie Shatzman
Edited by
Esther Bui  and
P. Emanuela Voinescu
Esther Bui
Affiliation:
Toronto Western Hospital
P. Emanuela Voinescu
Affiliation:
Brigham & Women's Hospital, Boston, MA
Get access

Summary

Menopause is a time of transition for women. It occurs when the ovarian follicles are depleted, therefore women who bear children tend to have later menopause due to the ovulation-sparing months of pregnancy. This transition occurs gradually over several years and is a normal aging process. It marks the end of the reproductive years and usually occurs during the late 40s or early 50s. The median age at menopause is 51 years and is influenced by various factors including but not limited to genetic and environmental factors such as family history and socioeconomic status, tobacco use, parity, and oral contraception use [1, 2].

Type
Chapter
Information
Women with Epilepsy
A Practical Management Handbook
 , pp. 306 - 321
Publisher: Cambridge University Press
Print publication year: 2025

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

Nelson, HD. Menopause. Lancet. 2008;371(9614):760–70. https://doi.org/10.1016/S0140-6736(08)60346-3.CrossRefGoogle ScholarPubMed
McNeil, MA, Merriam, SB. Menopause. Annals of Internal Medicine. 2021;174(7):97–112. https://doi.org/10.7326/AITC202107200.CrossRefGoogle ScholarPubMed
Prior, JC. The endocrinology of perimenopause need for a paradigm shift. Frontiers in Bioscience. 2011;S3(2):474–86. https://doi.org/10.2741/s166.CrossRefGoogle Scholar
Burger, HG. Hormonal changes in the menopause transition. Recent Progress in Hormone Research. 2002;57(1):257–75. https://doi.org/10.1210/rp.57.1.257.CrossRefGoogle ScholarPubMed
Reddy, DS, Gould, J, Gangisetty, O. A mouse kindling model of perimenstrual catamenial epilepsy. Journal of Pharmacology and Experimental Therapeutics. 2012;341(3):784–93. https://doi.org/10.1124/jpet.112.192377.CrossRefGoogle ScholarPubMed
Majewska, MD, et al. Steroid hormone metabolites are barbiturate-like modulators of the GABA receptor. Science. 1986;232(4753):1004–7. https://doi.org/10.1126/science.2422758.CrossRefGoogle ScholarPubMed
Pack, AM, Reddy, DS, et al. Neuroendocrinological aspects of epilepsy: Important issues and trends in future research. Epilepsy & Behavior. 2011;22(1):94–102. https://doi.org/10.1016/j.yebeh.2011.02.009.CrossRefGoogle ScholarPubMed
Younus, I, Reddy, DS. Seizure facilitating activity of the oral contraceptive ethinyl estradiol. Epilepsy Research. 2016;121:29–32. https://doi.org/10.1016/j.eplepsyres.2016.01.007.CrossRefGoogle ScholarPubMed
Velíšková, J. Estrogens and epilepsy: Why are we so excited? Neuroscientist. 2007;13(1):77–88. https://doi.org/10.1177/1073858406295827.CrossRefGoogle ScholarPubMed
Sazgar, M. Treatment of women with epilepsy. Continuum. 2019;25(2):408–30.Google ScholarPubMed
Frye, CA. Effects and mechanisms of progestogens and androgens in ictal activity: Progestogens, androgens, and epilepsy. Epilepsia. 2010;51:135–40. https://doi.org/10.1111/j.1528-1167.2010.02628.x.CrossRefGoogle Scholar
Smith, SS, et al. Neurosteroid regulation of GABAA receptors: Focus on the Α4 and δ subunits. Pharmacology & Therapeutics. 2008;116(1):58–76. https://doi.org/10.1016/j.pharmthera.2007.03.008.CrossRefGoogle Scholar
Gulinello, M, et al. Short-term exposure to a neuroactive steroid increases Α4 GABAA receptor subunit levels in association with increased anxiety in the female rat. Brain Research. 2001;910(1–2):55–66. https://doi.org/10.1016/S0006-8993(01)02565-3.CrossRefGoogle ScholarPubMed
Klein, P, et al. Premature ovarian failure in women with epilepsy. Epilepsia. 2001;42(12):1584–89. https://doi.org/10.1046/j.1528-1157.2001.13701 r.x.CrossRefGoogle ScholarPubMed
Harden, CL, et al. Seizure frequency is associated with age at menopause in women with epilepsy. Neurology. 2003;61(4):451–5. https://doi.org/10.1212/01.WNL.0000081228.48016.44.CrossRefGoogle ScholarPubMed
Kotsopoulos, IAW, et al. Systematic review and meta-analysis of incidence studies of epilepsy and unprovoked seizures. Epilepsia. 2002;43(11):1402–9. https://doi.org/10.1046/j.1528-1157.2002.t01-1-26901.x.CrossRefGoogle ScholarPubMed
Harden, CL, Pulver, MC, et al. The effect of menopause and perimenopause on the course of epilepsy. Epilepsia. 1999;40(10):1402–7. https://doi.org/10.1111/j.1528-1157.1999.tb02012.x.CrossRefGoogle ScholarPubMed
Koppel, BS, Harden, CL. Gender issues in the neurobiology of epilepsy: A clinical perspective. Neurobiology of Disease. 2014;72:193–7. https://doi.org/10.1016/j.nbd.2014.08.033.CrossRefGoogle ScholarPubMed
Roste, LS, et al. Does menopause affect the epilepsy? Seizure. 2008;17(2):172–5. https://doi.org/10.1016/j.seizure.2007.11.019.CrossRefGoogle ScholarPubMed
Harden, CL, et al. Hormone replacement therapy in women with epilepsy: A randomized, double-blind, placebo-controlled study. Epilepsia. 2008;47(9):1447–51. https://doi.org/10.1111/j.1528-1167.2006.00507.x.Google Scholar
Erel, T, Guralp, O. Epilepsy and menopause. Archives of Gynecology and Obstetrics. 2011;284(3):749–55. https://doi.org/10.1007/s00404-011-1936-4.CrossRefGoogle ScholarPubMed
Sveinsson, O, Tomson, T. Epilepsy and menopause: Potential implications for pharmacotherapy. Drugs & Aging. 2014;31(9):671–5. https://doi.org/10.1007/s40266-014-0201-5.CrossRefGoogle ScholarPubMed
Cardozo, L. Meta-analysis of estrogen therapy in the management of urogenital atrophy in postmenopausal women: Second report of the Hormones and Urogenital Therapy Committee*1. Obstetrics & Gynecology. 1998;92(4):722–7. https://doi.org/10.1016/S0029-7844(98)00175-6.Google Scholar
O’Neal, MA, editor. Neurology and psychiatry of women: A guide to gender-based issues in evaluation, diagnosis, and treatment. 1st ed. Cham: Springer International; 2019. https://doi.org/10.1007/978-3-030-04245-5.CrossRefGoogle Scholar
Adis Medical Writers. Be aware of the potential effects of menopause on epilepsy and its treatment. Drugs & Therapy Perspectives. 2015;31(5):161–3. https://doi.org/10.1007/s40267-015-0192-2.Google Scholar
Verrotti, A, Coppola, G, Parisi, P, et al. Bone and calcium metabolism and antiepileptic drugs. Clinical Neurology and Neurosurgery. 2010;112(1):1–10. https://doi.org/10.1016/j.clineuro.2009.10.011.CrossRefGoogle ScholarPubMed
Pack, AM, et al. Bone health in young women with epilepsy after one year of antiepileptic drug monotherapy. Neurology. 2008;70(18):1586–93. https://doi.org/10.1212/01.wnl.0000310981.44676.de.CrossRefGoogle Scholar
Karsenty, G. The central regulation of bone mass: Genetic evidence and molecular bases. In Bone regulators and osteoporosis therapy. Vol. 262. Stern, PH, ed. Cham: Springer International; 2020, pp. 309–23. https://doi.org/10.1007/164_2020_378.CrossRefGoogle Scholar
Qin, W, et al. Evolving concepts in neurogenic osteoporosis. Current Osteoporosis Reports. 2010;8(4):212–18. https://doi.org/10.1007/s11914-010-0029-9.CrossRefGoogle ScholarPubMed
Nicks, KM, et al. Reproductive hormones and bone. Current Osteoporosis Reports. 2010;8(2):60–7. https://doi.org/10.1007/s11914-010-0014-3.CrossRefGoogle ScholarPubMed
Wongdee, K, et al. Prolactin alters the MRNA expression of osteoblast-derived osteoclastogenic factors in osteoblast-like UMR106 cells. Molecular and Cellular Biochemistry. 2011;349(1–2):195–204. https://doi.org/10.1007/s11010-010-0674-4.CrossRefGoogle ScholarPubMed
Elefteriou, F. Regulation of bone remodeling by the central and peripheral nervous system. Archives of Biochemistry and Biophysics. 2008;473(2):231–6. https://doi.org/10.1016/j.abb.2008.03.016.CrossRefGoogle ScholarPubMed
Karsenty, G. The central regulation of bone mass: Genetic evidence and molecular bases. In Bone regulators and osteoporosis therapy. Vol. 262. Stern, PH, ed. Cham: Springer International; 2020, pp. 309–23. https://doi.org/10.1007/164_2020_378.CrossRefGoogle Scholar
Ducy, P, Amling, M, Takeda, S, et al. Leptin inhibits bone formation through a hypothalamic relay: A central control of bone mass. Cell 100(2):197–207.CrossRefGoogle Scholar
Elefteriou, F, et al. Serum leptin level is a regulator of bone mass. Proceedings of the National Academy of Sciences. 2004;101(9):3258–63. https://doi.org/10.1073/pnas.0308744101.CrossRefGoogle ScholarPubMed
Yadav, VK, Ryu, JH, et al. Lrp5 controls bone formation by inhibiting serotonin synthesis in the duodenum. Cell. 2008;135(5):825–37. https://doi.org/10.1016/j.cell.2008.09.059.CrossRefGoogle ScholarPubMed
Yadav, VK, Oury, F, et al. A serotonin-dependent mechanism explains the leptin regulation of bone mass, appetite, and energy expenditure. Cell. 2009;138(5):976–89. https://doi.org/10.1016/j.cell.2009.06.051.CrossRefGoogle ScholarPubMed
Zhao, B, Ivashkiv, LB. Negative regulation of osteoclastogenesis and bone resorption by cytokines and transcriptional repressors. Arthritis Research & Therapy. 2011;13(4):234. https://doi.org/10.1186/ar3379.CrossRefGoogle ScholarPubMed
Reid, IR. Menopause. In Primer on the metabolic bone diseases and disorders of mineral metabolism. Rosen, CJ, ed. Hoboken, NJ: Wiley; 2013, pp. 165–70. https://doi.org/10.1002/9781118453926.ch21.Google Scholar
Ross, FP. Osteoclast biology and bone resorption. In Primer on the metabolic bone diseases and disorders of mineral metabolism. Rosen, CJ, ed. Hoboken, NJ: Wiley, 2013, pp. 25–33. https://doi.org/10.1002/9781118453926.ch3.CrossRefGoogle Scholar
Pack, AM. Treatment of epilepsy to optimize bone health. Current Treatment Options in Neurology. 2011;13(4):346–54. https://doi.org/10.1007/s11940-011-0133-x.CrossRefGoogle ScholarPubMed
Pascussi, JM, et al. Possible involvement of pregnane X receptor–enhanced CYP24 expression in drug-induced osteomalacia. Journal of Clinical Investigation. 2005;115(1):177–86. https://doi.org/10.1172/JCI21867.CrossRefGoogle ScholarPubMed
Zhou, C. Steroid and xenobiotic receptor and vitamin D receptor crosstalk mediates CYP24 expression and drug-induced osteomalacia. Journal of Clinical Investigation. 2006;116(6):1703–12. https://doi.org/10.1172/JCI27793.CrossRefGoogle ScholarPubMed
Cerveny, L, et al. Valproic acid induces CYP3A4 and MDR1 gene expression by activation of constitutive androstane receptor and pregnane X receptor pathways. Drug Metabolism and Disposition. 2007;35(7):1032–41. https://doi.org/10.1124/dmd.106.014456.CrossRefGoogle ScholarPubMed
Vrzal, R, et al. Valproic acid augments vitamin D receptor-mediated induction of CYP24 by vitamin D3: A possible cause of valproic acid–induced osteomalacia? Toxicology Letters. 2011;200(3):146–53. https://doi.org/10.1016/j.toxlet.2010.11.008.CrossRefGoogle ScholarPubMed
Sheth, RD, et al. Effect of carbamazepine and valproate on bone mineral density. Journal of Pediatrics. 1995;127(2):7.CrossRefGoogle ScholarPubMed
Pack, AM, Morrell, MJ, et al. Bone mass and turnover in women with epilepsy on antiepileptic drug monotherapy: Bone metabolism and turnover. Annals of Neurology. 2005;57(2):252–7. https://doi.org/10.1002/ana.20378.CrossRefGoogle ScholarPubMed
Kafali, G, et al. Effect of antiepileptic drugs on bone mineral density in children between ages 6 and 2 years. Clinical Pediatrics. 1999;38(2):93–8. https://doi.org/10.1177/000992289903800205.CrossRefGoogle Scholar
Verrotti, A, Agostinelli, S, et al. A 12-month longitudinal study of calcium metabolism and bone turnover during valproate monotherapy: Increased bone turnover with valproate therapy. European Journal of Neurology. 2010;17(2):232–7. https://doi.org/10.1111/j.1468-1331.2009.02773.x.CrossRefGoogle Scholar
Verrotti, A, Greco, R, Latini, G, et al. Increased bone turnover in prepubertal, pubertal, and postpubertal patients receiving carbamazepine. Epilepsia. 2002;43(12):1488–92. https://doi.org/10.1046/j.1528-1157.2002.13002.x.CrossRefGoogle ScholarPubMed
Pack, AM, Walczak, TS. Bone health in women with epilepsy. International Review of Neurobiology. 2008;83:305–28. https://doi.org/10.1016/S0074-7742(08)00018-4.CrossRefGoogle ScholarPubMed
Souverein, PC, et al. Incidence of fractures among epilepsy patients: A population-based retrospective cohort study in the General Practice Research Database. Epilepsia. 2005;46(2):304–10. https://doi.org/10.1111/j.0013-9580.2005.23804.x.CrossRefGoogle ScholarPubMed
Stephen, LJ, et al. Bone density and antiepileptic drugs: A case-controlled study. Seizure. 1999;8(6):339–42. https://doi.org/10.1053/seiz.1999.0301.CrossRefGoogle ScholarPubMed
Cummings, SR, et al. Risk factors for hip fracture in white women. New England Journal of Medicine. 1995;332(12):767–73. https://doi.org/10.1056/NEJM199503233321202.CrossRefGoogle ScholarPubMed
Ensrud, KE, et al. Antiepileptic drug use increases rates of bone loss in older women: A prospective study. Neurology. 2004;62(11):2051–7. https://doi.org/10.1212/01.WNL.0000125185.74276.D2.CrossRefGoogle ScholarPubMed
Tsiropoulos, I, et al. Exposure to antiepileptic drugs and the risk of hip fracture: A case-control study. Epilepsia. 2008;49(12):2092–9. https://doi.org/10.1111/j.1528-1167.2008.01640.x.CrossRefGoogle ScholarPubMed
Vestergaard, P, et al. Fracture risk associated with use of antiepileptic drugs. Epilepsia. 2004;45(11):1330–7. https://doi.org/10.1111/j.0013-9580.2004.18804.x.CrossRefGoogle ScholarPubMed
Ensrud, KE, et al. Central nervous system: Active medications and risk for falls in older women. Journal of the American Geriatrics Society. 2002;50(10):1629–37. https://doi.org/10.1046/j.1532-5415.2002.50453.x.CrossRefGoogle ScholarPubMed
Petty, SJ, et al. Balance impairment in chronic antiepileptic drug users: A twin and sibling study. Epilepsia. 2010;51(2):280–8. https://doi.org/10.1111/j.1528-1167.2009.02254.x.CrossRefGoogle ScholarPubMed
Souverein, PC, et al. Use of antiepileptic drugs and risk of fractures: Case-control study among patients with epilepsy. Neurology. 2006;66(9):1318–24. https://doi.org/10.1212/01.wnl.0000210503.89488.88.CrossRefGoogle ScholarPubMed
Persson, HBI, et al. Risk of extremity fractures in adult outpatients with epilepsy. Epilepsia. 2002;43(7):768–72. https://doi.org/10.1046/j.1528-1157.2002.15801.x.CrossRefGoogle ScholarPubMed
Annegers, JF, et al. Risk of age-related fractures in patients with unprovoked seizures. Epilepsia. 1989;30(3):348–55. https://doi.org/10.1111/j.1528-1157.1989.tb05308.x.CrossRefGoogle ScholarPubMed
Teagarden, DL, et al. Low vitamin D levels are common in patients with epilepsy. Epilepsy Research. 2014;108(8):1352–6. https://doi.org/10.1016/j.eplepsyres.2014.06.008.CrossRefGoogle ScholarPubMed
Camacho, PM, et al. American Association of Clinical Endocrinologists and American College of Endocrinology clinical practice guidelines for the diagnosis and treatment of postmenopausal osteoporosis: 2016. Endocrine Practice. 2016;22:1–42. https://doi.org/10.4158/EP161435.GL.CrossRefGoogle Scholar
Elliott, JO, et al. Homocysteine and bone loss in epilepsy. Seizure. 2007;16(1):22–34. https://doi.org/10.1016/j.seizure.2006.10.001.CrossRefGoogle ScholarPubMed
Mikati, MA, Dib, L, Yamout, B, et al. Two randomized vitamin D trials in ambulatory patients on anticonvulsants: Impact on bone. Neurology 2006;67(11):2005–14. https://doi.org/10.1212/01.wnl.0000247107.54562.0e.CrossRefGoogle ScholarPubMed
DeGiorgio, CM, et al. Safety and tolerability of vitamin D3 5000 IU/day in epilepsy. Epilepsy & Behavior. 2019;94:195–7. https://doi.org/10.1016/j.yebeh.2019.03.001.Google ScholarPubMed
Pottoo, FH, et al. Raloxifene protects against seizures and neurodegeneration in a mouse model mimicking epilepsy in postmenopausal women. European Journal of Pharmaceutical Sciences. 2014;65:167–73. https://doi.org/10.1016/j.ejps.2014.09.002.CrossRefGoogle Scholar
Jetté, N, et al. Association of antiepileptic drugs with nontraumatic fractures: A population-based analysis. Archives of Neurology. 2011;68(1). https://doi.org/10.1001/archneurol.2010.341.CrossRefGoogle ScholarPubMed
Kumandas, S, et al. Effect of carbamazepine and valproic acid on bone mineral density, IGF-I and IGFBP-3. Journal of Pediatric Endocrinology & Metabolism. 2006;19(4):529–34CrossRefGoogle Scholar
Kim, SH, et al. A 6-month longitudinal study of bone mineral density with antiepileptic drug monotherapy. Epilepsy & Behavior. 2007;10(2):291–5. https://doi.org/10.1016/j.yebeh.2006.11.007.CrossRefGoogle ScholarPubMed
Hoikka, V, et al. Carbamazepine and bone mineral metabolism. Acta Neurologica Scandinavica. 2009;70(2):77–80. https://doi.org/10.1111/j.1600-0404.1984.tb00806.x.CrossRefGoogle Scholar
Andress, DL. Antiepileptic drug–induced bone loss in young male patients who have seizures. Archives of Neurology. 2002;59(5):781. https://doi.org/10.1001/archneur.59.5.781.CrossRefGoogle Scholar
el-Hajj Fuleihan, G, et al. Predictors of bone density in ambulatory patients on antiepileptic drugs. Bone. 2008;43(1):149–55. https://doi.org/10.1016/j.bone.2008.03.002.CrossRefGoogle ScholarPubMed
Vestergaard, P, et al. Anxiolytics, sedatives, antidepressants, neuroleptics and the risk of fracture. Osteoporosis International. 2006;17(6):807–16. https://doi.org/10.1007/s00198-005-0065-y.CrossRefGoogle ScholarPubMed
Guo, CY, et al. Long-term valproate and lamotrigine treatment may be a marker for reduced growth and bone mass in children with epilepsy. Epilepsia. 2002;42(9):1141–7. https://doi.org/10.1046/j.1528-1157.2001.416800.x.Google Scholar
Nissen-Meyer, LSH, et al. Levetiracetam, phenytoin, and valproate act differently on rat bone mass, structure, and metabolism. Epilepsia. 2007;48(10):1850–60. https://doi.org/10.1111/j.1528-1167.2007.01176.x.CrossRefGoogle ScholarPubMed
el-Haggar, SM, et al. Levetiracetam and lamotrigine effects as mono- and polytherapy on bone mineral density in epileptic patients. Arquivos de Neuro-Psiquiatria. 2018;76(7):452–8. https://doi.org/10.1590/0004-282x20180068.CrossRefGoogle Scholar
Babayigit, A, et al. Adverse effects of antiepileptic drugs on bone mineral density. Pediatric Neurology. 2006;35(3):177–81. https://doi.org/10.1016/j.pediatrneurol.2006.03.004.CrossRefGoogle ScholarPubMed
Cansu, A, et al. Evaluation of bone turnover in epileptic children using oxcarbazepine. Pediatric Neurology. 2008;39(4):266–71. https://doi.org/10.1016/j.pediatrneurol.2008.07.001.CrossRefGoogle ScholarPubMed
Çetinkaya, Y, et al. The effect of oxcarbazepine on bone metabolism. Acta Neurologica Scandinavica. 2009;120(3):170–5. https://doi.org/10.1111/j.1600-0404.2008.01148.x.CrossRefGoogle ScholarPubMed
Lado, F, et al. Value of routine screening for bone demineralization in an urban population of patients with epilepsy. Epilepsy Research. 2008;78(2–3):155–60. https://doi.org/10.1016/j.eplepsyres.2007.11.003.CrossRefGoogle Scholar
Cheng, HH, et al. Anti-epileptic drugs associated with fractures in the elderly: A preliminary population-based study. Current Medical Research and Opinion. 2019;35(5):903–7. https://doi.org/10.1080/03007995.2018.1541447.CrossRefGoogle ScholarPubMed
Heo, K, et al. The effect of topiramate monotherapy on bone mineral density and markers of bone and mineral metabolism in premenopausal women with epilepsy: Effect of topiramate on bone. Epilepsia. 2011;52(10):pp. 1884–9. https://doi.org/10.1111/j.1528-1167.2011.03131.x.CrossRefGoogle Scholar
Koo, DL, Nam, H. Effects of zonisamide monotherapy on bone health in drug‐naive epileptic patients. Epilepsia. 2020:61(10):2142–9. https://doi.org/10.1111/epi.16678.CrossRefGoogle Scholar
Takahashi, A, et al. Effects of chronic administration of aonisamide, an antiepileptic drug, on bone mineral density and their prevention with alfacalcidol in growing rats. Journal of Pharmacological Sciences. 2003;91(4):313–18. https://doi.org/10.1254/jphs.91.313.CrossRefGoogle Scholar
Kotloski, RJ, et al. Epilepsy and aging. In Handbook of clinical neurology. Vol. 167. Elsevier; 2019, pp. 455–75. https://doi.org/10.1016/B978-0-12-804766-8.00025-X.Google Scholar
Breuer, LEM, et al. Cognitive deterioration in adult epilepsy: Clinical characteristics of “accelerated cognitive ageing.” Acta Neurologica Scandinavica. 2017;136(1):47–53. https://doi.org/10.1111/ane.12700.CrossRefGoogle ScholarPubMed
Vestergaard, P. Epilepsy, osteoporosis and fracture risk: A meta-analysis. Acta Neurologica Scandinavica. 112(5):277–86. https://doi.org/10.1111/j.1600-0404.2005.00474.x.CrossRefGoogle Scholar
Unnanuntana, A, Gladnick, BP, Donnelly, E, Lane, JM. The assessment of fracture risk. Journal of Bone and Joint Surgery. American Volume. 2010;92(3):743–53. https://doi.org/10.2106/JBJS.I.00919.Google ScholarPubMed

Save book to Kindle

To save this book to your Kindle, first ensure [email protected] is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.

Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

Available formats
×

Save book to Dropbox

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.

Available formats
×

Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

Available formats
×