MountjoyM, etal. Br J Sports Med 2018;52:687–697. doi:10.1136/bjsports-2018-099193
IOC consensus statement on relative energy
deﬁciency in sport (RED-S): 2018update
Margo Mountjoy,1 Jorunn Kaiander Sundgot-Borgen,2 Louise M Burke,3,4
Kathryn E Ackerman,5,6 Cheri Blauwet,7 Naama Constantini,8 Constance Lebrun,9
Bronwen Lundy,3 Anna Katarina Melin,10 Nanna L Meyer,11 Roberta T Sherman,12
Adam S Tenforde,13 Monica Klungland Torstveit,14 Richard Budgett15
To cite: MountjoyM,
Br J Sports Med
For numbered afﬁliations see
end of article.
Dr Margo Mountjoy,
Department of Family Medicine,
Michael G. DeGroote School of
Medicine, McMaster University,
Hamilton, ON N2G 1C5,
mmsportdoc@ mcmaster. ca
This article has been
copublished in the International
Journal of Sport Nutrition
and Exercise Metabolism; doi:
Accepted 17 April 2018
In 2014, the IOC published a consensus statement
entitled ‘Beyond the Female Athlete Triad: Rela-
tive Energy Deficiency in Sport (RED-S)’. The
syndrome of RED-S refers to ‘impaired physiolog-
ical functioning caused by relative energy deficiency
and includes, but is not limited to, impairments of
metabolic rate, menstrual function, bone health,
immunity, protein synthesis and cardiovascular
health’. The aetiological factor of this syndrome is
low energy availability (LEA).1
The publication of the RED-S consensus state-
ment stimulated activity in the field of Female
Athlete Triad science, including some initial contro-
versy2 3 followed by numerous scientific publica-
1. The health parameters identified in the RED-S
conceptual model (figure 1).1 4
2. Relative energy deficiency in male athletes.
3. The measurement of LEA.
4. The performance parameters identified in the
RED-S conceptual model (figure 2).1 4
The IOC RED-S consensus authors have recon-
vened to provide an update summary of the interim
scientific progress in the field of relative energy
deficiency with the ultimate goal of stimulating
advances in RED-S awareness, clinical application
and scientific research to address current gaps in
Low energy availability
LEA, which underpins the concept of RED-S, is a
mismatch between an athlete’s energy intake (diet)
and the energy expended in exercise, leaving inade-
quate energy to support the functions required by the
body to maintain optimal health and performance.
Operationally, energy availability (EA) is defined as:
Energy Availability (EA)
= Energy Intake (EI) (kcal)
−Exercise Energy Expenditure (EEE) (kcal)/
Fat Free Mass (FFM) (kg)
where exercise energy expenditure (EEE) is
calculated as the additional energy expended above
that of daily living during the exercise bout, and
the overall result is expressed relative to fat-free
mass (FFM), reflecting the body’s most metaboli-
cally active tissues.5 6 Rigorously controlled labo-
ratory trials in women have shown that optimal
EA for healthy physiological function is typically
achieved at an EA of 45 kcal/kg FFM/day (188 kJ/
kg FFM/day).7 8 Meanwhile, although some caveats
are noted in relation to differential responses of
various body systems,9 many of these systems are
substantially perturbed at an EA <30 kcal/kg FFM/
day (125 kJ/kg FFM/day), making it historically
a targeted threshold for LEA. However, recent
evidence suggests that this cut-off does not predict
amenorrhoea in all women.10 11 In addition, and
not withstanding differences across body sizes and
pubertal age, it is noted that an EA of 30 kcal/kg/
FFM roughly equates to the average resting meta-
bolic rate (RMR).5 Because LEA has proven robust
in explaining markers of suboptimal health and
function in both laboratory7 8 and field settings,12 13
it seems logical that an EA assessment could serve as
a diagnostic tool in the prevention or management
Measurement of EA
Despite the primary importance of determining
whether an athlete has adequate EA, several barriers
prohibit the direct measurement of EA from being a
practical and reliable option. First, there is no stan-
dardised or reference protocol for undertaking an
EA assessment (eg, the number of collection days,
methodologies for assessing energy intake, exer-
cise energy expenditure or FFM). Furthermore,
there are significant concerns over the reliability
and validity of each of these metrics. The greatest
challenge is to gain an accurate record of usual
energy intake from self-reported sources.9 14 Other
challenges include the measuring of exercise energy
expenditure during many of the training/competi-
tion activities performed by athletes and accounting
for their additional recreational/lifestyle activity.9 15
These problems may partially explain why many
field studies report considerable discrepancies
between EA calculations and symptoms associated
with LEA.9 14 16–18 However, other explanations for
these observations include: (1) the temporal dissoci-
ation between the period of mismatched eating and
exercise behaviour that created the LEA problems
and the occasion on which the EA assessment was
undertaken and (2) the interaction of other dietary
characteristics that often co-exist with LEA and may
exacerbate its effects (eg, high intake of fibre, stim-
ulants and artificial sweeteners; low energy density
foods; high dietary restraint and poor spread of
energy within a day).19–23 Even if these problems
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688 MountjoyM, etal. Br J Sports Med 2018;52:687–697. doi:10.1136/bjsports-2018-099193
could be solved, EA calculations would likely involve specialised
equipment and expertise (eg, dual energy X-ray absorptiom-
etry measurement of body composition), good motivation and
compliance of the athlete (eg, keeping a food record or compre-
hensive activity diary) and considerable time and expertise to
process the information. Additionally, LEA states may develop at
different stages of training and competition due to varying phys-
iological demands. An EA assessment may achieve some valu-
able outcomes, such as strengthening the interaction between
the practitioner and athlete, which can create rapport, trust and
an appreciation of EA needs. However, the considerable effort
needed to assess EA and its frailties as a stand-alone diagnostic
tool prevent expert bodies from instituting it as a universally
Low energy availability in male athletes
Similar to female athletes, there is growing evidence that males
may experience LEA in situations when there is a mismatch
between energy intake and the exercise energy expenditure
of training or competition. Populations of male athletes at
increased risk for LEA and resulting health consequences of
RED-S include cyclists, rowers, runners, jockeys and athletes
in weight class combat sports.24–30 Factors that contribute to
LEA in male athletes are varied and often unique to the sport.
They include the cyclical changes in body mass and composition
(‘making weight’), prolonged inadequate energy intake to meet
high exercise energy expenditure of endurance sport, punctuated
changes in training volume/intensity and participation in stren-
uous endurance events without accompanied changes in nutri-
tion.26 Inadequate food availability, including food insecurity
from cultural practices or lack of financial resources may also
contribute risk for LEA in some male athletes, even among high
calibre athletes, as it undoubtedly also does in female athletes.26
While RED-S may occur in both sexes, there are likely differ-
ences in biological responses to LEA in male athletes compared
with their female counterparts. The prevalence of LEA has been
suggested to be higher in females than in males, although precise
differences are unknown.31 The threshold and duration of the
LEA state required to induce RED-S in men is unknown. Reduc-
tion in the sex hormone testosterone is likely to be of greater
health concern in male athletes.28 32 33
Low energy availability in para-athletes
The prevalence of LEA in para-athletes is incompletely char-
acterised.34 When extrapolating from trends noted in general
populations of individuals with disability, it can be assumed that
athletes who use a wheelchair for daily mobility are likely to
have reduced baseline energy needs.35 36 Despite this, male and
female athletes with spinal cord injury (SCI) may monitor or
restrict body weight for sport and are at risk for nutrient defi-
ciencies.37 38 Athletes with central neurological injury, such as
cerebral palsy, who demonstrate aberrant movement patterns
that include dyskinesis or athetosis, may have higher energy
expenditures than similar athletes without such non-purposeful
movements.39 Additionally, the presence of central neurolog-
ical injury may result in alterations of the hypothalamic–pitu-
itary axis and baseline menstrual function, regardless of energy
status.40–42 Amputee athletes may have higher energy needs in
the setting of prosthetic use and resultant gait asymmetry.43
Para-athletes are at high risk for impaired bone health and
bone-related injury secondary to many factors, including altered
skeletal loading. For example, in unilateral amputees, the affected
limb may exhibit reduced bone mineral density (BMD).44 Athletes
with SCI have disuse osteopenia/osteoporosis affecting the lower
extremities; however, positive adaptive changes in upper body
BMD values have been reported in wheelchair basketball players
compared with non-athletes (greater radial BMD and trend
towards increased lumbar BMD).45Characterising effects of
Figure 1 Health consequences of Relative Energy Deﬁciency in Sport
(RED-S) showing an expanded concept of the Female Athlete Triad to
acknowledge a wider range of outcomes and the application to male
athletes (*Psychological consequences can either precede RED-S or be
the result of RED-S).1 4
Figure 2 Potential Performance consequences of Relative Energy
Deﬁciency in Sport (*Aerobic and anerobic performance).1 4
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LEA on bone in para-athletes requires consideration of baseline
effects of each individual’s underlying disability. More work is
needed in this area.
Given rising participation in para sport from grass roots to
elite levels, further research is needed to investigate the impact
of LEA in athletes with a disability. The para-athlete population
requires screening for LEA to reduce complications of RED-S,
including low BMD.
Race and low energy availability
Whether race plays a role in the incidence and underlying aeti-
ology of RED-S remains speculative. Research shows a lower risk
of disordered eating (DE) in African-American, but not Latino
female high-school athletes compared with Caucasians.46 47
It is currently unknown whether the prevalence of menstrual
disorders differs among racially diverse athletic groups. Stress
fractures in African-American military recruits are lower than
in Caucasian recruits.48 Meanwhile, male Kenyan runners have
been observed to have greater BMD at weight-bearing sites (eg,
proximal femur) than healthy controls, but not at the lumbar
spine, where Z scores were reported to be below −2.0 in 40% of
study subjects.49 Such runners may have LEA resulting from low
energy intake and high exercise energy expenditure associated
with heavy training loads,49 as has been previously shown.50 51 In
another study of young Kenyan female athletes, middle-distance
and long-distance runners were found to exhibit one or more
subclinical and/or clinical components of the RED-S, including a
greater risk for LEA and menstrual dysfunction than controls.52
A study of sport nutrition knowledge, behaviours and beliefs
across sex, race/ethnicity and socioeconomic status in high school
soccer players identified that general sports nutrition knowledge
is lower in adolescent soccer players compared with prior reports
in adolescent athletes and that specifically females and Latinos
may benefit from sport nutrition education.53 Published research
is greatly lacking on RED-S in African-American, Hispanic and
Asian athletes, with a few exceptions.54 55 Thus, there is a need
to include more diverse athlete populations in RED-S research
and to integrate race/ethnicity in the prevention and treatment
HEALTH EFFECTS OF LOW ENERGY AVAILABILITY
Effects of LEA on the endocrine system have been described
predominantly in female athletes and only recently in male
athletes. Findings in some female athletes in LEA states
(measured EA and/or athletes with amenorrhoea) include disrup-
tion of the hypothalamic–pituitary–gonadal axis, alterations in
thyroid function, changes in appetite-regulating hormones (eg,
decreased leptin and oxytocin, increased ghrelin, peptide YY and
adiponectin), decreases in insulin and insulin-like growth factor
1 (IGF-1), increased growth hormone (GH) resistance and eleva-
tions in cortisol.8 56–59 Many of these hormonal changes likely
occur to conserve energy for more important bodily functions or
to use the body’s energy reserves for vital processes.60 61
Specific changes in men are not completely understood;
however, reduced leutinizing hormone (LH) pulsatility and
amplitude have been described in a case series of male mara-
thon runners, a population at high risk for LEA.62 Other studies,
primarily in endurance male athlete populations, have shown
reductions in testosterone and inconsistent findings in differ-
ences in basal LH parameters.63 64 Koehler et al assessed the
effects of short-term EA manipulation through diet and exercise
on various hormonal parameters in six male habitual exercisers.65
Each male experienced four separate 4-day conditions: LEA (15
kcal/kg FFM/day with and without exercise) and adequate EA
(40 kcal/kg FFM/day with and without exercise). Following both
LEA conditions, regardless of exercise, leptin and insulin were
reduced compared with baseline (−53% to −56% and −34%
to −38%, respectively). LEA did not significantly affect ghrelin,
triiodothyronine (T3), testosterone or IGF-1 levels. Thus, the
LEA state, often in combination with disruptions to endocrine
function in women and possibly men, may contribute to multiple
physiological disease states described by RED-S. However, the
relationship is likely to be subject to a large degree of within-par-
ticipant and between-participant variability; more research is
needed, particularly in men.11 66 67
The effects of LEA on reproductive hormones and menstrual
function in female athletes have been well described,8 68 69
although the complex hormonal signalling pathways underpin-
ning these effects are still being fully elucidated. Current evidence
supports a LEA-associated disruption of gonadotropin releasing
hormone (GnRH) pulsatility at the hypothalamus, followed by
alterations of LH and follicle stimulating hormone release from
the pituitary and decreased oestradiol and progesterone levels;
this is considered a form of functional hypothalamic amenor-
rhoea (FHA).68 70 The duration and severity of LEA needed to
create such disturbances are also unclear, reflecting both the
complex nature of the problem and discrepancies associated
with the different methodologies used to study it. For example,
Loucks and Thuma studied previously sedentary women in a
laboratory setting and identified that well-controlled interven-
tions reducing EA below 30 kcal/kg FFM/day via the short-
term (5 day) manipulation of exercise energy expenditure and
energy intake were associated with a dose–response decrease
in LH pulsatility.8 More recently, Williams et al reduced EA via
manipulation of energy intake and exercise energy expenditure
over several menstrual cycles in untrained, previously eumenor-
rhoeic subjects.11 The researchers found that the frequency of
menstrual disturbances (including luteal phase defects, anovu-
lation and oligomenorrhoea) was affected by the magnitude of
energy deficit compared with baseline needs,11 but a specific
threshold of EA below which menstrual disturbances occurred
was not identified.10
Meanwhile, Reed et al performed a cross-sectional analysis of
EA (measured using 3-day diet logs to determine energy intake
and a combination of exercise logs and heart rate monitoring to
measure estimated exercise energy expenditure) in female athletes
with eumenorrhoea and various menstrual disturbances.71 These
investigators reported mean EA was >30.0 kcal/kg FFM/day
in all the groups (amenorrhoeic, oligomenorrhoeic, ovulatory
eumenorrhoeic, inconsistent subclinical menstrual dysfunction
eumenorrhoeic and anovulatory eumenorrhoeic athletes) and EA
did not discriminate subclinical forms of menstrual disturbance;
however, EA was lower in amenorrhoeic athletes compared with
eumenorrhoeic athletes (mean 30.9 vs 36.9 kcal/kg FFM/day).71
Thus, severe energy deficiency is known to lead to amenor-
rhoea, but more work is needed to better understand the inter-
play of change in short-term and long-term EA and more subtle
It is established that LEA contributes to impaired bone health in
athletes, particularly women. Cross-sectional studies of physi-
cally active female athletes with oligomenorrhoea/amenorrhoea
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or measured LEA have demonstrated decreased BMD, altered
bone microarchitecture and bone turnover markers, decreased
estimates of bone strength and increased risk for bone stress inju-
ries compared with eumenorrhoeic athletes and those who are
energy replete.66 69 72–74 Short-term LEA (via diet and exercise)
has prospectively been shown to negatively affect bone turnover
markers in women and some men.57 67 Specific female and male
sport populations are at increased risk for lower BMD, including
jockeys, runners, swimmers and cyclists.24 29 30 75–83 Anatomical
sites with less bone loading and/or greater trabecular versus
cortical bone content (lumbar spine and radius vs total hip) are
at greater risk for low BMD and impaired microarchitecture in
populations susceptible to LEA.72 73 77 78 84
Low body mass index (BMI) is an imperfect surrogate
marker for LEA. However, BMI ≤17.5 kg/m2, <85% expected
body weight for adolescents or ≥10% weight loss in 1 month
are proposed indicators of LEA,85 and indeed both BMI and
expected body weight cut-offs are associated with increased risk
for low BMD in both sexes.24 82 86 LEA may be accompanied
by DE/eating disorders (EDs), menstrual dysfunction and low
BMD, and the combination of factors places athletes at higher
risk for bone stress injury.87–89
LEA has been correlated with decreased RMR in female endur-
ance athletes.90 Prospectively, increasing training load while
maintaining constant EI over 4 weeks in male and female elite
rowers led to a significant reduction in RMR.91 In normal weight
women with induced energy deficits via exercise and dietary
manipulation, measured weight loss over 3 months was less than
predicted.92 Subjects who were moderately energy deficient had
a significant decrease in RMR, and those who were severely
energy deficient demonstrated significant decreases in leptin, T3,
IGF-1 and an increase in ghrelin.92
Iron is essential for haematopoiesis and subsequent oxygen
carrying capacity. Iron deficiency, often seen in female athletes,
can contribute directly and indirectly to energy deficiency. This
is due to a potential reduction in appetite, decreased metabolic
fuel availability and impaired metabolic efficiency, leading to an
increase in energy expenditure during exercise and rest.93 Iron
deficiency may also interact with bone health via dysregulation
of the GH/IGF-1 axis, hypoxia and hypothyroidism, in addition
to playing an important role in thyroid function, fertility and
even psychological well-being.93 Thus, LEA may be partially
induced by, and may contribute to, iron deficiency.93 Surrogates
for LEA have been correlated with haematological dysfunction,
including low ferritin and iron deficiency anaemia, in adolescent
and young adult female athletes.94
Growth and development
Linear growth retardation has been reported in various studies of
male and female adolescents with severe anorexia nervosa, with
studies demonstrating partial, but not always complete, catch-up
growth after recovery.95–97 Decreases in IGF-1, increases in GH
and increased GH resistance are consistently noted in those
with anorexia nervosa.98 Studies in amenorrhoeic athletes have
demonstrated disorderly GH secretory patterns, decreased
GH and IGF-1 secretory response to exercise accompanied by
increased interpulse GH levels and decreased IGF-1/IGFBP-1
ratios, with more research needed to understand training and
growth implications.99 100
Early atherosclerosis may be associated with hypoestrogenism
and FHA in young athletes.101 Endothelial dysfunction and
unfavourable lipid profiles have been reported in amenorrhoeic
athletes,102 with resumption of menses leading to improvements
in vascular endothelial function.103 In one study, amenorrhoeic
athletes demonstrated lower heart rates and systolic blood
pressure compared with eumenorrhoeic athletes, in addition
to disruptions of the normal renin–angiotensin–aldosterone
response to an orthostatic challenge.104 In the more severe LEA
state of anorexia nervosa, significant cardiovascular changes can
occur, including valve abnormalities, pericardial effusion, severe
bradycardia, hypotension and arrhythmias.105
In the severe LEA state of AN, negative health influences on
the full gastrointestinal tract such as altered sphincter function,
delayed gastric emptying, constipation and increased intestinal
transit time, have been described.106 Melin et al measured EA
and developed the Low Energy Availability among Female
Athletes Questionnaire (LEAF-Q), both of which found a nega-
tive correlation with EA and gastrointestinal symptoms in elite
Swedish and Danish athletes.12 These findings were supported in
a survey of adolescent American female athletes with surrogate
markers of LEA, who also reported a higher incidence of stool
leakage and constipation than those considered to have adequate
The immune system may be altered by LEA. A study of 21 Japa-
nese elite, collegiate runners reported more upper respiratory
symptoms and lower immunoglobulin A secretion rates in the
amenorrhoeic versus eumenorrhoeic athletes.107 Meanwhile,
in observational studies of elite Australian athletes in prepara-
tion for the 2016 Rio Olympic Games, LEA, as measured by
the LEAF-Q in female athletes, was associated with increased
likelihood of illnesses (including those of the upper respiratory
tract and gastrointestinal tract), bodily aches and head-related
symptoms in the previous month.108 109
Psychological problems can precede or be caused by LEA.1 LEA
in athletes has been shown to have negative correlates with
various aspects of psychological well-being. Higher drive for
thinness may be a proxy for LEA, as higher drive for thinness
scores on the Eating Disorder Inventory have been associated
with reduced resting energy expenditure, lower T3 levels, and
higher ghrelin levels in female athletes.110 Athletes who scored
higher on DT also scored higher in domains of ineffective-
ness, cognitive restraint, and bulimic tendencies.110 Adolescent
females with FHA have been found to have a higher incidence of
mild depressive traits, psychosomatic disorders, and a decreased
ability to manage stress.111 112 A separate study found overlap in
adolescents with anorexia nervosa and those with FHA: both
groups demonstrated increased depression, social insecurity and
introversion and fears of weight gain compared with healthy
controls.113 More profound psychological disturbances were seen
in the presumably more restricted EA (anorexia nervosa) group
versus the FHA group.113 Results from a study with male athletes
indicated that dietary restraint and muscle building behaviours
were associated with bulimic symptomatology.114 Additionally,
studies of male body builders indicate that a prolonged EA of
approximately 20–25 kcal/kg FFM/day, as seen in the final stage
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of contest diets, might be pathological and have negative psycho-
logical effects for males.27 The restrictive diet patterns observed
resulted in a reduction in muscle mass and a loss of strength,
with reports of endocrine dysfunction and mood disturbances in
those athletes with body composition measurements of approxi-
mately 4% total body fat.27
Disordered eating and eating disorders
Disordered eating and eating disorders are more prevalent
among female and male athletes in weight-sensitive sports in
comparison to athletes representing sports in which leanness
is a less important performance variable.115–119 In a Norwegian
study of adolescent elite male and female athletes, a higher prev-
alence of disordered eating in non-athletes as compared with
athletes was found when using questionnaires,120 but when
using a clinical interview, the prevalence of eating disorders
was higher in athletes versus controls.121 These findings suggest
the need for personal interviews to diagnose eating disorders in
athletes.117 121 122 It should be noted that the revised diagnostic
criteria for eating disorders (Diagnostic and Statistical Manual,
fifth edition) may influence the prevalence of the different diag-
noses among athletes.123 124
The pathogenesis of eating disorders is multifactorial with
cultural, familial, individual and genetic/biochemical factors
playing roles.125 Weight pressure and unique eating disorder
risk and trigger factors have been reported and include perfor-
mance pressure, sudden increase in training volume, injury,
teammate modelling of eating disorder behaviours and team
weigh-ins.126–128 A desire to be leaner to enhance performance
seems to predict later disordered eating127 and the risk of eating
pathology increases when the coach–athlete relationship is char-
acterised by high conflict and low support.129 Disordered eating
seems to be influenced by perfectionism, competitiveness, pain
tolerance and the perceived performance advantage of weight
loss.130 These suggested risk factors need to be validated to
demonstrate a causal relationship. However, these findings serve
as a call to action for enhanced screening for eating disorder
risk among athletes who experience weight pressure, are injured,
or who have teammates with known disordered eating/eating
Performance consequences of low energy availability
Associations between various surrogates of LEA (eg, hormonal
aberrations, oligomenorrhoea/amenorrhoea, leanness sport
participation and increased scores on ED/DE/LEA screening
tools) and factors negatively influencing performance (eg, illness,
injury, iron deficiency, impaired cognition and mood) have been
reported.87 93 94 131–137 Intervention studies on long-term energy
restriction and sport performance are lacking.138 However, it has
been postulated that persistent LEA could impair sport perfor-
mance through a variety of different indirect mechanisms (eg,
impaired recovery leading to premature reduction in physical,
psychological and mental capacity and impairment of optimal
muscle mass and function).139 Indeed, LEA could be expected
to impair performance or interfere with optimal performance
gains via acute impairment of key processes such as glycogen
storage140 or protein synthesis,141 or by preventing consistent
and high quality training due to the increased risk of injury and
Despite the importance of these associations, it is only recently
that studies have tried to measure the direct impact of LEA on
sports performance. For example, Silva and Paiva reported
that athletic performance, measured as competition ranking,
negatively correlated with EA in elite rhythmic gymnasts.142
Furthermore, Tornberg et al found no difference in aerobic
capacity (VO2, O2 (mL/min/kg)) between elite eumenorrhoeic
endurance athletes and elite endurance athletes with secondary
FHA, despite lower body weight and fat mass in the athletes
with FHA.143 However, subjects with FHA had decreased neuro-
muscular performance (measured as knee muscular strength
and endurance) and reaction time compared with the eumen-
orrhoeic athletes.143 Overall, lower neuromuscular performance
was associated with higher cortisol levels, and lower blood
glucose, T3, oestrogen and FFM in the tested leg.143 Although
striving for a greater power to mass ratio is commonly regarded
as important for running performance, this study suggests that
achieving an idealised body weight or body composition through
severe and persistent energy restriction is likely to negatively
affect performance and health.143 This finding is supported in
a study of East African runners.144 Woods et al followed male
and female national team rowers through a 4-week intensified
training period, which was accompanied by a lack of increase in
energy intake despite a 21% increase in training load.91 It was
concluded that inadequate EA likely negatively affected training
recovery, at least partially explaining the alterations in 5 km time
trial pacing strategy and reduced performance.91
Considering the reported high prevalence of menstrual
dysfunction caused by energy deficiency,145 surprisingly, only
one study has investigated the direct impact of LEA on sport
performance. Vanheest et al reported a 10% decline in swim-
ming velocity over a 400 m time trial (after 12 weeks of
training) among young elite swimmers with ovarian suppression
secondary to energy deficiency compared with an 8% improve-
ment in their eumenorrhoeic teammates.13 Clearly, more investi-
gations, including robust protocols involving random allocation
of athletes to intervention groups, are needed to provide further
evidence and explanation of the effects of LEA on training adap-
tations and sport performance.
PREVENTION OF RELATIVE ENERGY DEFICIENCY IN SPORT
The prevention of RED-S requires increased awareness among
athletes and their entourage. Current evidence suggests that
there is much work to be done. Surveys have reported that
less than 50% of physicians, coaches, physiotherapists and
athletic trainers could identify the triad components (LEA with
or without an eating disorder, menstrual dysfunction and low
BMD),70 146–152 and only 19% of 370 US high school nurses
could identify all three triad components.153 In a survey of 931
multispecialty physicians, only 37% were aware of the triad, and
only one-half of these were comfortable treating or referring a
patient.70 In a group of exercising Australian women, one-third
believed irregular periods were ‘normal’ for active females, and
approximately half reported knowing that menstrual dysfunc-
tion was a risk factor for poor bone health.154 Educational
programmes typically identify their target audiences as health
professionals, coaches, athletic trainers, teachers, school admin-
istrators, athletes and parents.155 However, a survey of Inter-
national Sport Federations (IFs) identified that only 2 of 28
Olympic IFs had programmes on RED-S, indicating the need to
also involve a top-down approach.156 Peer-based eating disorder/
body image/triad education and cognitive-dissonance based
programmes have shown promise,157–160 and similar RED-S
peer-led programmes should be developed.
Effective eating disorder prevention programmes should be
multimodal, interactive and target athletes and coaching staff.161
One successful intervention is a peer-led educational programme
692 MountjoyM, etal. Br J Sports Med 2018;52:687–697. doi:10.1136/bjsports-2018-099193
for female athletes that resulted in improved bulimic pathology
1 year postintervention.162 A Norwegian school-based controlled
intervention programme, including elite male and female
athletes163 and coaches,164 resulted in no new cases of eating
disorders among females in the intervention schools as opposed
to eight (13%) in females at the control schools.163 There
was only one new eating disorder case in a male at a control
school and none in males from the intervention schools.163
These results suggest that effective disordered eating and eating
disorder prevention should target individuals beyond athletes
and coaches, be gender specific, involve significant others and
include changes to sport regulations, policy measures and the
SCREENING FOR RELATIVE ENERGY DEFICIENCY IN SPORT
Early detection of athletes at risk for energy deficiency is crit-
ical to prevent long-term health sequelae.1 69 85 There are several
disordered eating/eating disorder screening tools intended for
general population.166–169 Some tools have been developed to
target athletes, although none are validated for Diagnostic
and Statistical Manual of Mental Disorders, Fifth Edition
criteria.170–172 Additionally, due to stigma associated with eating
disorders, athletes may be motivated to hide their illness. An
elevated Eating Disorder Inventory—drive for thinness score168
has been reported to indicate energy deficiency in exercising
women,173 and amenorrhoeic athletes seem more likely to have an
elevated drive for thinness score compared with eumenorrhoeic
athletes.173 In order to diagnose an eating disorder, additional
in-depth personal interviews must be performed.117 121 122 166
However, the prevalence of energy deficiency is reported to be
high in some athletes even without the presence of disordered
eating/eating disorders.90 145
Although coaches are in an ideal situation to identify athletes
with disordered eating/eating disorders, they sometimes have
difficulty distinguishing between athletes whose appearance or
body composition metrics meets their sport-type expectations
(eg, thin) from those with an eating disorder, especially if the
athlete’s performance is good.174 Even if disordered eating is
identified, coaches may have difficulty convincing athletes to
The Periodic Health Examination176 and the Preparticipation
Physical Evaluation177 include relevant questions that may be
helpful for early detection. Recently, the LEAF-Q was devel-
oped12 as a brief questionnaire on physiological symptoms linked
to energy deficiency, and the Low Energy Availability in Males
Questionnaire is in development. Expanded testing of these
questionnaires in various athletic populations is needed. There is
limited evidence for the efficacy of self-reported questionnaires,
and additional individual evaluation is recommended.1 85 The
RED-S Clinical Assessment Tool (RED-S CAT) can assist clini-
cians in screening for RED-S and the management of return to
play decisions,178 although validation is needed.
TREATMENT OF RELATIVE ENERGY DEFICIENCY IN SPORT
If LEA is due to unintentional under eating, then simple nutri-
tional education may suffice. Regardless of the severity of the
eating pathology, early involvement of an accredited or appro-
priately trained expert (eg, sports dietitian) is recommended
to enhance the athlete’s nutritional practices. Optimising
EA can improve function of the hypothalamic–pituitary–
gonadal axis, as well as other systems negatively affected by
LEA in females.15 179–181 Energy deficits should be addressed
via modification of exercise and nutrition practices68 182 in
both female and male athletes and energy needs may be even
higher in growing adolescents. Treatment is typically based on
increased food intake but may also require changes in food
choices, energy spread and other dietary characteristics; these
changes must be individualised and periodised according to
the athlete’s energy expenditure and exercise goals. A reduc-
tion or cessation of exercise may be necessary, depending on
the severity of the energy deficit, symptoms and compliance
Adequate bone-building nutrients are critical; for example,
serum 25-hydroxy vitamin D levels <30 ng/mL are associated
with increased incidence of bone stress injury.183 184 Vitamin D
intake of 600–800 IU daily is recommended by USDA dietary
guidelines,185 but greater intake may be needed temporarily
to reach goal serum 25-hydroxy vitamin D levels of >30 ng/
mL.186–188 Improving 25-hydroxy vitamin D levels may also
reduce healing time and facilitate earlier return to play for bone
stress injury.189 Additionally, adequate consumption of calcium
may help decrease the incidence of bone stress injury.190 191 The
current recommendation for daily calcium intake is 1000 mg/day
of calcium for men and women aged 19–50 years, and 1300 mg/
day for children and adolescents aged 9–18 years.192
Cognitive behavioural therapy is another non-pharmacolog-
ical treatment for RED-S that has been shown to contribute
to the resumption of menses in some women with FHA.193 194
Initial non-pharmacological management of RED-S may restore
menstrual function over months,181 195 while improvements in
bone health take longer and may never reach optimal levels.15
Non-compliance with therapy may require removal of the athlete
from training/competition. Examples of treatment contracts and
clearance categories for return to play can be found in other
publications.1 85 196 Current recommendations need further vali-
dation and may lead to the eventual inclusion of other progress
parameters, such as RMR and blood biomarkers.
The use of combined oral contraceptives for the intention of
regaining menses or improving BMD in those with RED-S is
not recommended. Data regarding the effects of combined oral
contraceptives on BMD and fracture risk are inconsistent.68 197–200
If using combined oral contraceptives for contraception, the
athlete should understand that combined oral contraceptives
may mask the return of spontaneous menses, and bone loss may
continue if the energy deficit is not corrected. If menstrual cycles
do not return after a reasonable trial of nutritional, psycholog-
ical and/or modified exercise interventions, transdermal oestra-
diol (E2) therapy with cyclic oral progestin can be considered for
short-term use.68 Notably, transdermal E2 is not a reliable form
of hormonal contraception and an athlete should be counselled
to avoid unintended pregnancy if she receives transdermal E2
for bone health. Transdermal oestrogen does not affect IGF-1
secretion, a bone-trophic hormone that combined oral contra-
ceptives downregulate, and has been shown to improve BMD
in anorexia nervosa201 and BMD and bone microarchitecture
in oligo-amenorrhoeic athletes.202 Recombinant parathyroid
hormone 1–34 (rPTH) has been shown to improve BMD in
AN203 and rare, short-term use may be considered in adults with
LEA, FHA or RED-S in the setting of delayed fracture healing or
very low BMD.68 Transdermal oestrogen or rPTH should only
be prescribed in conjunction with a metabolic bone expert and it
is important to note that rPTH is contraindicated in adolescents
and young adults with open growth plates.68
MountjoyM, etal. Br J Sports Med 2018;52:687–697. doi:10.1136/bjsports-2018-099193
Treatment strategies for disordered eating/eating disorders
Apparent disordered eating/eating disorders should be treated
with a multidisciplinary team including medical, dietary and
mental health support. Inpatient treatment should be consid-
ered for patients with severe bradycardia, hypotension, ortho-
stasis and/or electrolyte imbalance.85 196 204 Athletes’ resistance to
treatment usually increases with the severity of the problem.205
Because many patients with eating disorders see their disorders
as purposeful and necessary,206 motivation to recover is a crit-
ical factor in treatment. With sport participation as leverage for
athletes, the desire to be healthy enough to return to sport most
often facilitates recovery for athletes with eating disorders.207
As higher levels of depression and anxiety are observed in
athletes with eating pathology,208 there is a need to treat these
pathologies in athletes with disordered eating/eating disor-
ders. Additionally, comorbid disorders of depression, anxiety
and substance abuse complicate eating disorder treatment and
require treatment modifications.165 209 Ideally, treatment should
be provided by a mental health professional experienced in
treating eating problems in athletes.205 For athletes, meeting
the diagnostic criteria for severe eating disorders (eg, anorexia
nervosa and bulimia nervosa), participation in competition is not
Since the original publication of the IOC consensus statement
on RED-S in 2014, there have been many scientific advances
to improve our understanding of the health and performance
effects of LEA in both female and male athletes. To address
remaining gaps, the IOC RED-S consensus authors encourage
scientific activity in the following domains:
1. Identification of athletes at risk for RED-S: it is evident
that there is no practical tool for the measurement of EA;
therefore, there is a recognised need to develop a methodology
to screen and identify athletes at risk for RED-S that is both
scientifically validated and relevant and applicable in clinical
2. Prevention of RED-S: improved awareness of RED-S is
required through educational initiatives for athletes, coaches,
members of the entourage and sport organisations. The
development of scientifically validated prevention interven-
tions is encouraged.
3. Male athletes: despite the improvement in the knowledge
base of RED-S in male athletes, there remains a gap in our
understanding of RED-S in specific sports with differing
energy demands, performance criteria, ethnicities and
4. Health and performance consequences of RED-S: there is
still much to be learned about the psychological and physi-
ological health risks and long-term consequences of RED-S
in all athletes, particularly male athletes, para-athletes and
athletes of various races. To best engage the attention of
athletes and coaches, it is imperative to further increase our
understanding of the performance effects of RED-S.
5. Treatment and ‘return to play’: practical guidelines for the
treatment and safe return to play for athletes with RED-S
need to be further developed to improve athletes’ health and
1Department of Family Medicine, Michael G DeGroote School of Medicine, McMaster
University, Hamilton, Ontario, Canada
2Department of Sports Medicine, The Norwegian School of Sport Sciences, Oslo,
3Sports Nutrition, Australian Institute of Sport, Beclonnen, Australia
4Centre for Exercise and Nutrition, Mary MacKillop Institute for Health Research,
Melbourne, Victoria, Australia
5Divisions of Sports Medicine and Endocrinology, Boston Children’s Hospital, Boston,
6Neuroendocrine Unit, Massachuetts General Hospital, Harvard Medical School,
Boston, Massachusetts, USA
7Department of Physical Medicine and Rehabilitation, Harvard Medical School,
Spaulding Rehabilitation Hospital/Brigham and Women’s Hospital, Boston,
8Heidi Rothberg Sport Medicine Center, Shaare Zedek Medical Center, Hebrew
University, Jerusalem, Israel
9Department of Family Medicine, Faculty of Medicine and Dentistry, Glen Sather
Sports Medicine Clinic, University of Alberta, Edmonton, Alberta, Canada
10Department of Nutrition, Exercise and Sport, University of Copenhagen,
11Health Sciences Department Colorado Springs, University of Colorado, Denver,
12Independent researcher, USA
13Department of Physical Medicine and Rehabilitation, Harvard Medical School,
Spaulding Rehabilitation Hospital, Charlestown, Massachusetts, USA
14Faculty of Health and Sport Sciences, University of Agder, Kristiansand, Norway
15IOC Medical and Scientiﬁc Department, Lausanne, Switzerland
Acknowledgements The authors would like to gratefully acknowledge the work
of Barbara Drinkwater in the ﬁeld of the Female Athlete Triad and for her ongoing
support of the advancement of science in this domain. A special thanks to Allyson L
Parziale and Bryan Holtzman for their logistical and editorial assistance.
Contributors MM, JKS-B, LMB substantially contributed to the conception and
design and are the co-coordinators of IOC Expert Group. MM, JKS-B, LMB and
KEA substantially contributed to drafting and revising the manuscript. CB, NC, CL,
BL, AKM, NLM, RTS, AST, MKT and RB are the members of IOC Expert Group and
substantially contributed to drafting the manuscript. RB is the Director IOC Medical
and Scientiﬁc Department and contributed to revising the manuscript. All authors
conﬁrmed the ﬁnal version to be published.
Funding The authors have not declared a speciﬁc grant for this research from any
funding agency in the public, commercial or not-for-proﬁt sectors.
Competing interests None declared.
Patient consent Not required.
Provenance and peer review Not commissioned; externally peer reviewed.
Data sharing statement There is no unpublished data.
© Article author(s) (or their employer(s) unless otherwise stated in the text of the
article) 2018. All rights reserved. No commercial use is permitted unless otherwise
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