BJSM however, not in all studies98 as this strategy may fail to address many underlying dietary and psychological factors. While developing a strategy to implement a diet of known and appropriate EA may be logical, it is usually impractical due to the challenges of measuring EA in the field. Therefore, a practical treatment approach to address low EA is to implement an eating plan that increases current EI by ∼300–600 kcal/day (1.2–2.4 MJ/day) and addresses suboptimal practices related to energy spread over the day and around exercise sessions, dietary composition and foodrelated stress. Treatment strategies for low EA-associated menstrual dysfunction In collegiate athletes, weight gain is the strongest predictor of recovery of normal menstrual function.99–101 Adequate protein and carbohydrate intake is recommended to restore liver glycogen to facilitate LH pulsatility.31,102 The time frame for the resumption of menses varies according to the severity of the energy deficiency and the duration of the menstrual dysfunction.100 Although oral contraceptives (OCs) may be considered for athletes requiring contraception,103 these may mask the low EA, menstrual dysfunction and perpetuate bone loss. Injectable depot medroxyprogesterone, another form of contraception, can cause amenorrhoea and hence prolonged use can adversely affect BMD,104 bone mass accrual,105 on discontinuation.106 and adolescent which is reversible to a certain extent Many physicians prescribe low-dose OCs as hormone replacement in the amenorrheic athlete, however, this intervention does not correct the aetiological cause of relative energy deficiency and may compromise the attainment of peak bone density.107 Treatment options to restore fertility may include increasing EA. Pharmacological agents may be necessary to stimulate ovulation in luteal phase deficiency.27 Attention must be paid to infertility treatments identified in the WADA Prohibited List.58 Treatment strategies to optimise bone health Strategies to reverse bone loss in women with FHA parallel those used for amenorrheic women with anorexia.108 In the latter population, weight gain with or without the subsequent resumption of menses restores the coupling of bone formation and resporption109,110 and improves BMD.109 with anorexia.110,112 However, full recovery may not be feasible, as bone microarchitecture is also impaired.111 EI alone increases bone mass by 1–10% in women It is essential to restore the energy and 20 Sport & Geneeskunde | september 2014 | nummer 4 oestrogen-dependent mechanisms of bone loss in order to improve mineralisation of trabecular bone and growth of cortical bone.41 to positively affect BMD113,114 Mechanical loading and high-impact sports are known as well as bone geometry.115,116 Programmes of high-impact loading and resistance training should be implemented at least 2–3 days/week for athletes in non-weight bearing sports and/or those with decreased BMD.6 The athlete diet should include 1500 mg/day of calcium through dietary sources with supplementation if required.117 The Endocrine Society Guideline (2011) recommends maintaining vitamin D [25(OH)D] blood levels above 32–50 ng/ mL, with 1500–2000 IU/day of vitamin D.118,119 Vitamin D deficiency is common in northern latitudes, especially during winter when there are fewer hours of sunlight and among athletes who train indoors.120,121 Other factors include dark pigmented skin, and the use of sunscreen. A recent meta-analysis of vitamin D supplementation found a positive effect in femoral and hip BMD, with no effect in the spine.122 Transdermal oestradiol (given with cyclic progesterone) has shown some success in increasing BMD in patients with anorexia.123 In some studies, combination OCs containing 20–35 mg of oestradiol have maintained or improved BMD in amenorrheic athletes.124,125 However, use of the OCP in athletes with FHA have been reported to have a detrimental effect on BMD through the suppression of androgen secretion and cause premature closure of the epiphyses compromising growth of the long bones in adolescents.126 Bisphosphonates, which inhibit the resorption of bone, are not recommended for women of reproductive age, as they are stored in bone for prolonged amounts of time and have been shown to be teratogenic.127,128 Other therapies including raloxifene (a selective oestrogen receptor modulator or SERM), parathyroid hormone peptides, teriperatide and calcitonin, are also not approved for use in premenopausal women. Some novel potential therapies are being developed, but clinical trials are lacking.129,130 lin-derived growth factor (a bone anabolic agent)131,132 These include insuand leptin which can be used to stimulate appetite, thus effecting resumption of menses and subsequent improvement in BMD.133–135 In men, detection and correction of any underlying pathology is essential, including testosterone therapy with hypogonadism and osteoporosis. Bisphosphonates may be used as monotherapy, as consolidative therapy after a course of teriperatide administration or in combination with hormonal replacement.136 Denusomab and strontium ranelate also increase BMD in men with osteoporosis.137 Pagina 19

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