A Three Year Case Study with a Multidisciplinary Treatment of Relative Energy Deficiency and Anorexia in a Female Tennis Player
- 1. Department of Health Sciences, Division of Physiotherapy, Lund University, Sweden
- 2. Karolinska Institutet, Institute of Environmental Medicine and Sophiahemmet University, Stockolm, Sweden
- 3. The Norwegian Olympic and Paralympic Committee and Confederation of Sport, Norway
Abstract
Tennis is an all-year racket sport requiring qualities such as speed, agility, flexibility, and endurance, as competitions may last up to five hours.
Elite players have an estimated daily need of carbohydrate (CHO) between 6-10 g/kg to sustain high amounts of training and frequent competitions. Low energy availability (LEA), over time, may impair both health and performance. LEA may cause metabolic suppression and altered hormone levels via hypothalamic–pituitary– gonadal axis (HPG). Female athletes with LEA have an increased risk of developing menstrual dysfunction, low bone mineral density (BMD), disordered eating behavior (DE) and an eating disorder (ED). This article provides a case-study of an internationally ranked female tennis player, with a recent performance-driven weight loss of 11 kg. She was diagnosed with functional hypothalamic primary amenorrhea (FHA) and anorexia nervosa (AN). The predetermined goal was to return to play and the treatment was based on the guidelines for relative Energy Deficiency in Sport (REDS-CAT). After three years of multidisciplinary interventions, the athlete safely returned to play. Her weight and body composition improved, her menstrual cycle was normalized and the diagnostically scores of AN indicated non-clinical significance. The multidisciplinary treatment enabled the athlete to return to play despite several years of LEA and AN.
Keywords
Elite athlete , Bone health , Carbohydrates , Relative energy deficiency in sport , Eating disorder , Body composition , Tennis, Anorexia nervosa
Citation
Lundström P, Edlund K, Garthe I (2020) A Three Year Case Study with a Multidisciplinary Treatment of Relative Energy Deficiency and Anorexia in a Female Tennis Player. Ann Sports Med Res 7(4): 1159.
ABBREVIATIONS
AN: Anorexia Nervosa; BIA: Bioimpedance Analysis; CBT-E: Congnitive Behavior Therapy – Enhanced; CHO: Carbohydrates; CO2 : Carbon Dioxide CV: Coefficients of Variability; BMD: Bone Mineral Density DRI: Daily Recommended Intake; DXA: DualEnergy X-Ray Absorptiometry; EA: Energy Availability; ED: Eating Disorders; EDE: Electrodermal Activity; EDE-Q: Eating Disorders Examination- Questionnaire; FM: Fat Mass; FFM: Fat-Free Mass; FAT: Female Athlete Triad; FHA: Functional Hypothalamic Amenorrhea: FSH: Follicle Stimulating Hormone; HPG: Hypothalamic–Pituitary–Gonadal Axis; LEA: Low Energy Availability; LH: Luteinizing Hormone; MADRS-S: Montgomery Asberg Depression Rating Scale – Selfreport; O2 : Oxygen Production; RED-S: Relative Energy Deficiency in Sports; RMR: Resting Metabolic Rate; SWA: Sensewear Armband; T3 : Triiodothyronine; TSH: Thyroid Stimulating Hormone; T4 : Thyroxin; VO2 : Oxygen Production; VCO2 : Carbon Dioxide Production.
INTRODUCTION
Tennis is defined as an intermittent, non-cyclical sport with brief periods of maximal work, followed by longer periods of moderate to low intensity work, emphasizing the evenly importance of anaerobic and aerobic metabolism, Physiological performance-variables such as speed, power, strength, agility, flexibility, and endurance are essential to succeed at an elite level. Further, tennis has an all-year and worldwide competition schedule demanding a stable physical and psychological level of performance [1].
The sport specific characteristics indicate a substrate use that is highly dependent on glycogen, thus, fatigue may be related to glycogen availability. Indeed, studies have reported an association between impaired performance capacity and duration of the match [2,3], which indicate that nutrition may have an important role in Tennis.
Nutrition regulate and influence several physiological processes such as training quality, training adaptations, recovery and risk of injury and illness [4-7]. Elite players in general, have an estimated daily need of carbohydrate (CHO) between 6-10 g/ kg to ensure adequate glycogen stores [6]. Elite players have an estimated daily need of carbohydrate (CHO) between 6-10 g/kg to ensure adequate glycogen stores.
Low CHO availability combined with high-intensity intermittent exercise may compromise performance due to suboptimal glycogen stores, reduced cognitive function, impaired recovery, and training adaptation [8].
Few studies have investigated the nutritional intake in tennis players [9,10], however, Juzwiak et al., observed a self-reported calorie deficit greater that 10 % of energy expenditure in 32 % adolescent tennis players, while protein and lipid intakes were above recommended values [11]. Although there are well-known methodological errors of underreporting, low CHO intake often reflects energy availability (EA), defined by the relative balance between dietary energy intake and energy expenditure required for health and activities of daily living [12].
EA is the key variable in “The Female Athlete Triad” (FAT) [13], as well as “Relative Energy Deficiency in Sports” (RED-S) [8], presenting two similar models of defining LEA. According to the literature, RED-S is considered to be a sports specific syndrome, with a slightly broader term than FAT, including metabolic rate, menstrual function, bone health, immunity, protein synthesis and cardiovascular health [14].
EA appears to be an important variable, as studies report that reproductive function [15], and bone formation [16], are impaired, indicating that prolonged periods with LEA will likely have negative implications for both health and performance [8]. LEA may occur in: 1) athletes who abruptly increase training load and energy expenditure without regulating energy intake, 2) athletes with a restricted energy intake, whether inadvertent or by intent or 3) athletes that have a disordered eating pattern or an ED [17].
One of the challenging physiological responses of LEA over time is metabolic suppression through neuroendocrine alterations via hypothalamic–pituitary–gonadal axis (HPG) [18,19]. This causes hormonal disturbances, followed by various local and systemic effects (15), exemplified by thyroid hormones (triiodothyronine, T3 ), shown to reflect resting metabolic rate (RMR), indicating a directly relation to RED-S [17]. Tennis players at elite level are facing several challenges, which may affect EA: year-around competition and frequent travelling may lead to lack of time, and possibilities to prepare a varied diet with sufficient energy in combination with high training loads [9]. Considering that the extensive travel schedule often starts at the age of 12, it is important that parents and coaches facilitate and establish good nutritional routines, until the athlete is prepared to take ownership and responsibility of important variables outside the training arena. Further, early specialization in sport and a history of injuries have shown to be related to an increased risk of developing eating disorders (ED) [8]. It’s common for athletes to engage in behaviors that may be regarded as functional and necessary by the athlete, coaches and team as part of the sport context. Although EDs are more prevalent in weight-dependent and leanness sports, onset of ED pathology may not only be a result of a preoccupation with weight and shape but performancedriven [17,20,21]. Due to the potentially irreversible health risks of LEA over time, FAT and RED-S guidelines suggest a multidisciplinary, systematic approach with associated treatment tools for practitioners. In the current article, we provide a case study of a female elite tennis player, internationally ranked at the age of fifteen. Going into the twenties, her position at the international ranking list was promising for the future. At the time of referral, she had a history of injuries and had been diagnosed with functional hypothalamic primary amenorrhea (FHA) with a self-reported ED triggered by restrictive eating behavior focusing on reduced CHO-intake. Although she had major symptoms reflecting LEA, she was convinced that this diet would reduce her body weight, followed by improved performance.
CASE PRESENTATION
The athlete was a 21-year-old elite tennis player referred for nutritional counselling. At the time she had recently lost 11.3 kg of body weight, suffering from frequent upper respiratory infections, self-reported gastro-intestinal dysfunction, FHA, multiple stress injuries in collum and sternum. In her previous attempt to seek treatment for the primary amenorrhea, she was advised to use oral contraceptives, which she ceased after 8 months. She was also diagnosed with iron deficiency and was recommended to use iron supplementation as well as including iron-rich foods in the regular diet to prevent larger drops and anemia over time. She reported core behaviors of ED (anorexia nervosa), such as weight phobia, restrictive eating behaviors and significant anxiety driven avoidance behaviors related to specific foods (“feared foods”). She clearly expressed her worries of not being able to continue her tennis career and more importantly, reduced fertility over time. She claimed that lack of nutritional knowledge was the main reason for the insufficient energy intake, and that her self-diagnosed ED was triggered by her restrictive CHO intake, caused by her intention of losing weight.
She tried to maintain her regular training routine (3-4 hr/ day 5-6 days/week) but reported an increased fatigue and was mentally depressed by her inability to meet the overwhelming demands of being an athlete. She was diagnosed with anorexia nervosa (AN), restrictive type, atypical (307:171; DSM 5, APA, 2013) and with a weight of 57.8 kg, body fat 8.9 %, and body fat (kg) 5.2 kg.
METHODS
The athlete has given her written informed consent for publication. Data collection was performed on several occasions during a period a total of 3 years 2015-2018, including retrospective data based on medical chart (referred to as previous assessment). Dietary intake was registered on regularly basis in agreement with the psychologist and evaluated in a nutrient analysis program, Dietist Net (Kost och Näringsdata AB, Bromma, Sweden).
Nutritional assessment
The athlete has given her written informed consent for publication of her case. Data collection was performed on several occasions during a period a total of 3 years 2015-, including retrospective data based on medical chart (referred to as previous assessment). Dietary intake was registered on regularly basis in agreement with the psychologist and evaluated in a nutrient analysis program, Dietist Net (Kost och Näringsdata AB, Bromma, Sweden).
Blood parameters
All blood samples were handled and analyzed according to Karolinska university hospital instructions. The biochemical markers and reproductive and regulatory hormones were assessed and analyzed at different occasions. At the previous assessment the following blood parameters were analyzed: luteinizing hormone (LH), follicle stimulating hormone (FSH), thyroid stimulating hormone (TSH); triiodothyronine (T3 ), thyroxin (T4 ), estradiol, progesterone, prolactin, androstenedione, cortisol, and insulin growth factor-1, in addition to Iron, ferritin, and hemoglobin. The second year, following blood parameters were included: LH, FSH, TSH, T3 , T4 estradiol, progesterone, prolactin, and androstenedione, whereas the third year the assessments included: (T3 ), estradiol, glucose, and haemoglobin (Table 1). In addition, following biochemical markers were assessed: glucose, triglycerides, cholesterol, iron, ferritin, haemoglobin, cobalamin, folate, zinc, magnesium, and vitamin D.
Resting metabolic rate
All measurements were standardized following a 12-hrs fast and 24-hrs without exercise and caffeine, completed between 7:00 and 8:30 am, using a ventilated open hood system (Oxycon Pro 4, Jeager, Germany). The system was automatically calibrated between tests, and on weekly basis, by an alcohol burning test with coefficients of variability (CV) of 0.7% for O2 , 1.1% for CO2 , 0.8 % for the respiratory exchange ratio, and 2% for energy expenditure (22). After voiding, the athlete rested in a horizontal position for 15 min before measuring oxygen consumption (VO2 ) and carbon dioxide production (VCO2 ), within the time frame of 35 minutes. Resting metabolic rate (RMR) was calculated from mean VO2 and VCO2 during the last 20 min of the measurement [23]: 3.94 (VO2) + 1.1 (VCO2) × 1.44. The ratio between measured RMR and predicted RMR was calculated using Cunningham’s equation (1991) which relay on fat-free mass (FFM) [24]. Indirect calorimetry is a noninvasive, widely used method for predicting respiratory exchanged ratio, mirroring energy expenditure and fuel utilization. As with all methods, indirect calorimetry has its uncertainties related to gas concentration (O2 , VO2 ), and volume measurements (e.g. leak and calculation errors). Other factors that influence the results are infections or illness and macronutrient composition of food [25].
Table 1: Regulatory and reproductive hormones and biochemical markers.
| Variables | Previous assessment | Year 1 | Year 2 | Year 3 | Normal range provided by the analytic laboratory |
| LH(I/L) | 1.4 | 7.2 | 9.0 | follicular phase 8-12, ovary phase 7.6 89, luteal phase 0.6-14 | |
| FSH (I/L) | 7.7 | 9.0 | 7.2 | follicular phase 3-12, ovary phase 9-23, luteal phase 1-12 | |
| S-TSH (mIE/L) | 1.2 | 1.3 | 0.4-3.5 | ||
| S-T4 | 9 | 12 | 8-14 | ||
| T3 3,6-6,3 (pmol/L) | 3 | 6.1 | 3,6-6,3 | ||
| Estradiol (pmol/L) | 61.0 | 61.0 | 123 | > 150 | |
| S-Progesterone (nmol/L) | 2.4 | follicular phase 1723, luteal phase <3.0 | |||
| S-Prolactin (mIE/L) | 60.9 | 264 | 102-496 | ||
| S-Androstenedione (mmol/L) | 4.8 | 4.8 | 1,0 - 11,5 | ||
| IGF-1 (µg/L) | 343 | 106-427 | |||
| Cortisol | 469 | 747 | 133 – 537 (6.00-10.00 AM) | ||
| Biochemical markers | |||||
| Glucose | 4.9 | 5.0 | 4.0-6.0 | ||
| fS-Triglycerides(nmol/L) | 0.9 | 0.45-26 | |||
| S-Cholesterol(nmol/L) | 4.6 | 2.9-61 | |||
| P-Iron (µmol/L) | 7 | 14 | 9-34 | ||
| S-Ferritin (µg/L) | 15 | 35 | 15-150 | ||
| Haemoglobin (g/L) | 130 | 112 | 121 | 117-153 | |
| Cobalamin (pmol/L) | 380 | 150-650 | |||
| S-Folate(mmol/L) | 11 | 7.0-40 | |||
| S-Zink (µmol/L) | 10 | 9-15 | |||
| P-Magnesium (mmol/L) | 12.95 | 0.70-0.95 | |||
| Vitamin D (nmol/L) | 109 | 75-120 | |||
| Abbreviations: Data are presented at previous measurements, at baseline and after 3 y of treatment. LH: Luteinizing Hormone; FSH: Follicle Stimulating Hormone; TSH: Thyroid Stimulating Hormone; T3 : triiodothyronine. | |||||
Table 2: Anthropometric measurements including Bone Mineral Density and Resting Metabolic Rate
| Variables | Previous assessment | Year 1 | Year 3 | Normal Range |
| Age (y) | 18 | 21 | 24 | |
| Height (cm) | 1.79 | 1.79 | 1.79 | |
| Weight (kg) | 68 | 57.8 | 67.0 | |
| BMI (kg/m2 ) | 21.2 | 17.8 | 21.0 | 18.5-24.9 |
| Average training h/week | 24± 2.0 | 20 ± 2.0 | 24 ± 2.0 | |
| Body Composition (BIA) | ||||
| Body fat (%) | 8.9 | 10.2 | ||
| Fat mass (kg) | 5.2 | 6.9 | ||
| FFM (kg) | 52.6 | 60.1 | ||
| Skeletal muscle mass (kg) | 29.5 | 33.7 | ||
| Body Composition (DXA) | ||||
| Weight (kg)(DXA | 67 | 58.7 | ||
| Fat mass (kg) | 6.9 | |||
| Lean mass(kg) | 49.1 | |||
| FFM (kg) | 51.9 | |||
| Body fat (%) | 24.2 | 12.3 | ||
| Bone Mineral Density | ||||
| BMD whole body (g/cm2 ) | 1.178 | 1.181 | ||
| BMD whole body (Z-score) | 0.7 | 1.3 | ||
| L1-l4 BMD (g/cm2) | 1.240 | |||
| BMD L1L4 (Z-score) | 0.6 | |||
| Metabolic characteristics | ||||
| RMR measured (kcal) | 1100 | 1398 | -1657 | |
| RMR (kcal/kg FFM) | 20.9 | 23.3 | 30 | |
| RMR (ratio) | 0.67 | 0.77 | 1.1 | |
| Abbreviations: Data are presented at previous measurements, at baseline and after 3 y of treatment. BMI, body mass index; BIA, bio impedance analysis; DXA, Dual-energy X-ray absorptiometry; RMR, resting metabolic rate; FFM, fat free mass | ||||
Body composition
Body composition was measured by two non-invasive methods: Dual-energy X-ray absorptiometry (DXA) (Lunar Prodigy Advance, GE Healthcare, Sweden), and Bio Impedance (BIA), InBody 720 (Table 2). All measurements were standardized following a 12-hrs fast and 24-hrs without exercise, completed between 7:00 and 8:30 am by a trained technician. DXA is widely accepted as a reference method, especially as a diagnostic tool for osteopenia and osteoporosis, as it provides both regional and whole body assessments including estimates of FM and lean body mass with a low radiation exposure (~0.5μSv) [26,27]. As a consequence of DXA being an expensive and inaccessible method, the athlete was only measured pre (2012), and post (2015), intervention, while using Bioimpedance (InBody 720), measurements more frequently to track changes in body weight and composition. The method is based on calculation of electrical resistance in various tissues based on water content, making it vulnerable in various conditions such as hydration status, temperature, and physical condition [28]. Although commonly used for estimating body composition, the software equations are built on assumptions that may not be accurate for athletes with a sports specific body shape and composition (e.g. small female gymnastics vs. heavy-weight wrestler). However, when acknowledging the methodological limitations and using specific protocols to minimize errors, BIA may be a safe and accessible tool for estimating changes over time [29]. With that in mind, both DXA and BIA are influenced by hydration status, as many body composition methods, and should always be assessed in standardized conditions.
Energy expenditure and sleep pattern
BodyMedia®SenseWear® Professional 8.0 software (Version 8.0.0.2903), was used to estimate total energy expenditure, sleeping pattern and quality. SenseWear armband (SWA) is a non-invasive device attached to the upper arm that measures heat flux, skin temperature, near-body ambient temperature, and galvanic skin response [30]. The components measure total daily energy expenditure, including exercise, and amount and quality of sleep. SWA has been demonstrated to produce accurate evaluation in the general population [30], however validation studies in athletic populations show a trend of underestimation high-intensity exercise (>10 METs), indicating a methodological limitation related to the pre-set algorithms [31]. Other factors that influence the accuracy are different types of training such as: running vs. bicycling, or resistance training [31], and fluctuations in body weight or composition may influence accuracy at an individual level [32]. The SWA has been demonstrated to be useful to capture sleep quantity and quality in athletic populations [33] The assessment is based on electrodermal activity (EDA), and is frequently used in psychophysiology, as it measures activity in the sympathetic nervous system. High levels of EDA are more common during slow wave sleep, while lower EDA levels reflects rapid eye movement sleep [34], suggesting that the normal pattern of EDA is a reliable indicator of sleep quantity and quality [34,35]. Used cautiously, it may be a useful tool in combination with the athlete’s subjective sleep report.
Psychological assessments
Eating Disorders Examination Questionnaire (EDE-Q): The EDE-Q 6.0 is a 28–item measure (© 2008 by Christopher G. Fairburn and Sarah Beglin), derived from the Eating Disorder Examination (EDE; [36]. The EDE-Q is a self-report measure with a 7-point Likert-type scale (0–6). There is a cut-off score indicative of a clinical eating disorder of > 4. Although a score < 1 has been an indication of non-ED, a score of > 4 has been critiqued for being too high of a cut-off score for clinical ED. EDE-Q consist of four subscales, restrained, eating concern, shape concern and weight concern) addressing core dimensions of eating disorders. The subscales and the total score have reported adequate psychometric properties. Internal consistency for the total EDE-Q (global score), with Cronbach’s alpha coefficients ranging from .70 to .83 in a clinical sample and from .78 to .93 in a sample from the general population [37,38]. A recent systematic review of the psychometric properties of the EDE-Q subscales, internal consistency was acceptable with the following range of alpha coefficients: restraint (70–.85), eating concern (73–.86), shape concern (.83–.93), and weight concern (72–.89) (39).
Montgomery Asberg Depression Rating Scale- Self report (MADRS-S): The Montgomery-Åsberg Depression Rating ScaleSelf-rated (MADRS-S) is a 9-item self-report scale that measures depressive symptoms. A cut-off score of 20 has been suggested to indicate clinical levels of depression. The scale assesses symptom severity on a scale ranging from 0 to 6, resulting in a total score ranging from 0 to 54. A higher score indicates a higher level of depressive symptoms. Satisfactory internal consistency has been reported which a Cronbach alpha of .84 [40]. The MADRS-S is a self-rated version of the original clinician-rated MADRS, which was especially designed to be sensitive to change in symptom levels [41].
Overview of nutritional and psychological interventions
A professional clinical sports nutritionist was responsible for the nutritional intervention, which was divided into different focus periods based on earlier assessments (Table 3). The predetermined goal was to initiate a gradual weight gain by an increased energy and carbohydrate intake, and the main goal with the intervention was to return to play. The intervention included approximately 40 individual sessions, lasting for 30-60 minutes. It was a multidisciplinary approach, including combined sessions with the coach, physician, and psychologist depending on the actual treatment goals (Figure 2). As the athlete’s health gradually improved the intervention shifted towards a performance-based perspective, focusing on nutritional need for training and competition (Figure 1).
The nutritional intervention was based on recommended guidelines from RED-S and FAT for healthy adult athletes [7,12,21,42], whereas the main assignment was to balance the macronutrient composition and gradually increase energy intake to achieve the goal of weight gain. Since she was diagnosed with iron deficiency and zinc below recommended values, she was recommended to use a daily iron and zinc supplement according an individual supplement-protocol. The dietary calcium intake was sufficient and vitamin D levels were within the optimal range.
Exercise
The athlete was instructed to refrain from training during the first 3 weeks. She gradually increased training load, started with 3 hours/week increasing to 5 hours/week after 2 months. The training load was adjusted based on her physiological response. As the psychological and nutritional treatment progressed, the training load increased in amount and intensity. Her training schedule were strictly followed until the end of the second year. At this point, she was stabilized and cleared to train up to 10 hours/ week. At the third year, she was cleared to gradually increase her training load to initial levels, given that her treatment proceeded as planned.
Results of nutritional intervention
The gradual increased energy intake, focused on adequate CHO, was followed by an increase in body weight, FFM and FM (Figure 1 and Table 2), At the end of the three-year intervention, her eating pattern was normalized, all hormones, except for estradiol, and biochemical markers had returned within normal range (Table 3), and the sleep pattern indicated a high sleep quality, without disruptions during the night. Although the results should be interpreted with caution, they were in accordance with her self-reported sleep. Further, her menstruation cycle normalized (confirmed by a gynecologist), and she reported an improved gastrointestinal function.
Bone mineral density
Results of total and lumbar BMD were above normal range despite the long period of LEA combined with heavy training load and FHA.
Resting metabolic rate
RMR was substantially lower year one than predicted with a ratio 0.66. At the end of the three-year intervention period, RMR increased to a ratio of 0.76, slightly above recommended ratio (0.70).
Psychological treatment: The transdiagnostic protocol Cognitive Behavior Therapy- enhanced (CBT-E) was provided by a senior clinical psychologist specialized in eating disorders (over a three year-period (2015-2018). There were 27 individual sessions, including all four stages of CBT-E supplementing with a few specific adaptations for elite sport, including interventions from Acceptance and Commitment Therapy (43) and Mindfulness Based Cognitive Therapy [44], the latter with a primary goal of performance-enhancement. CBT-E in summary [45].:
Stage one: Engage patient in treatment and initiate behavior change starting with self-observation of eating behaviors and
Table 3: Intake of energy, macro- and micronutrients fibres, and vitamin D
| Variables | Year 1 | Year 3 |
| Total Energy Expenditure | 2595(1900-3612) | 2782 (2133-3022) |
| Energy intake (kcal/day) | 1945 | 2957 |
| Energy deficiency(kcal/day) | -650 | 175 |
| EA (kcal/kg FFM) | 36.9 | 49.2 |
| CHO (g/kg) | 3.7 | 6.5 |
| Protein (g/kg) | 1.8 | 1.7 |
| Fat (g/kg) | 1.9 | 1.1 |
| Fibres(g/day) | 28 | 39.3 |
| Calcium intake (mg/day) | 1002 | 1054 |
| Iron (mg/day | 18.3 | 20.5 |
| Vitamin D (ug/day) | 1.9 | 5.0 |
| Abbreviations: EA: Energy availability; CHO: Carbohydrates | ||
Table 4: Eating Disorders (EDE-Q)* and Depression (MADRS-S)** scores over a three-year-period treatment period.
| Year 2015 | Year 2017 | Year 2018 | |
| Restrictive – Eating* | 3.8 | 1.0 | 1.0 |
| Concerns – Eating* | 1.4 | 1.2 | 1.2 |
| Concerns – Shape* | 2.3 | 1.8 | 0.5 |
| Concerns – Weight* | 2.2 | 2.0 | 0.4 |
| Global Eating Disorder* | 2.4 | 1.5 | 0.8 |
| Depression** | 28 | 8 | 10 |
food choices, as well as thoughts and behaviors related to her eating disorder. Treatment included Psychoeducation related to weight regulation and cognitive interventions, to self-explore the ineffectiveness of her strategies to regulate and control weight and shape. She was also introduced to weekly weighing, regular meal pattern with “normal” foods and involving significant others to facilitate treatment if appropriate.
Stage two: A transitional stage where the progress is jointly reviewed, identifying barriers to change and planning for Stage Three.
Stage three: Address key mechanisms maintaining the patient’s eating disorder. The following core features were addressed: over-evaluation of shape and weight, interventions targeting unhelpful body checking and avoidance, relabeling unhelpful thoughts and feelings such as “feeling fat”, developing previously marginalized domains of self-evaluation. Her dietary rigidity was challenged into more flexible guidelines, introduction of previously avoided food, event-triggered changes related to eating, with the aim of developing problem-solving skills, as well as skills to accept and modulate intense deviation in mood-states. Stage Four: Ensure that progress made in treatment is maintained and minimize the risk of relapse by providing education focused on realistic expectations, in addition to develop a short-term plan and a long-term plan to prevent relapse over time.
Results of Psychological assessments (EDE-Q)
The result of the EDE-Q showed that levels of ED (global score) decreased over the three-year treatment period. A score < 1.0 has been indicative of non-ED – indicating all results except, by margin “Concerns about eating”, being of non-clinical significance at the termination of treatment. The scores for depression (MADRS-S), decreased from clinical levels of depression to normal levels.
DISCUSSION
While recognizing the amount of resources required, the outcome of present case study, show that a multidisciplinary approach may be successfully implemented in similar cases. The treatment protocol focused initially on refeeding and exposure therapy, whereas the latter consisted of a long list of CHO-rich foods defined as “feared foods” by the athlete. Educational information related to foods in general and CHO-rich foods in particular, enabled the athlete to establish a balanced and healthy diet with an increased EA.
The athlete started manipulating her body weight at an early age and was diagnosed with FHA at the age of 18. LEA affects the HPG, which is essential for the reproductive function as well as a regulator of several biological processes. It is reasonable to assume that the athlete`s FHA was caused by chronical LEA, which she managed to turn around during the three-year treatment period. The regulatory hormones and biochemical markers were all returned within the normal range, except for estrogen. Although her estrogen-level increased considerably during the treatment period, it failed to reach recommended levels. However, she considered herself as healthy and robust and decided to continue the process by herself, independent on frequent support from the treatment-team.
Figure 1: Body Composition History.
Figure 2: A flow chart with contribution from various disciplines during a 3-year treatment plan.
The athlete was 18 years when diagnosed with FHA, LEA and ED, indicating an increased risk of potentially irreversible impaired health variables, in particular bone health. Although she had unprovoked collum- and sternum fractures, her total and lumbar BMD was above normal range throughout the three-year intervention period. The literature shows that heavy loads of exercise stimuli may protect loss of muscle mass and BMD, even in a negative energy balance, indicating that exercise stimuli may override the catabolic effects of LEA and hormonal changes [46]. Further, Schipilow et al., found that impact loading was positively associated with bone quality in elite athletes. Though tennis is a high impact sport with explosive twisting and turning [3], the athlete’s BMD was probably a result of systematic training stimuli over time, protecting BMD from the adverse effects of long-term LEA. Measurements of density does not always show the entire picture, as the micro-architecture within the bones is a strong determent of bone strength and are often used to predict fractional risk in osteoporotic patients [47]. Unfortunately, the measurements did not include analysis of the micro-architecture, which could give more information related to eventual changes over time.
The balance between energy intake and the energy expenditure is tightly linked and are influenced by hormonal status. Both T3 and RMR increased at the end of the intervention and it is reasonable to assume that the higher CHO and energy intake resulted in normal levels of T3 with positive consequences on the metabolic rate demonstrated in several measurements of RMR and restored menstrual cycle. The gradual increased weight consisted of both fat and fat-free mass, reaching a healthy level for a female elite tennis player [48].
Mental health issues such as ED may either precede or be caused by LEA [21]. Risk factors related to development of an ED such as drive for thinness and restrictive eating behavior and dieting may be a precursor for LEA [49]. Further, adolescents diagnosed with FHA have been reported to have higher incidence of low mood and lower skills of stress management [50,51].
At baseline, the athlete was diagnosed with LEA, ED, and health problems over several years, indicating an increased risk of potentially irreversible impaired health. However, the results show that a long-term intensive treatment program enabled the athlete to return to play despite chronic LEA and ED for several years. The treatment team consisted of a clinical sport nutritionist, clinical psychologist specialized in ED in athletes, a physician well experienced with ED in athletes, a gynecologist, and the coach. The multidisciplinary teamwork presented the opportunity to integrate concepts, theories, methods, and experience with the aim of increasing and advancing the knowledge from different disciplines [52].
CONCLUSION
Our case-study presents the possibility to return to play despite years of serious medical and psychological conditions, although the treatment protocol is time consuming, expensive and requires a multidisciplinary team. This model may be an option for elite athletes, with a clear ambition and motivation to return to elite sport. For many athletes ED is associated with shame, contempt, and fear of being disclosed from the team or club and therefore it is difficult to obtain adequate treatment at an early stage. There is no doubt of the necessity of an early identification for LEA and ED for a less time consuming and adequate treatment for better outcomes. Prevention and education are necessary to avoid the risk of losing a promising athlete.
ACKNOWLEDGEMENTS
The authors would like to thank the athlete for her consent to share her data.
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