FEMALE ATHLETE TRIAD AND RED-S...So when I prepped for this original talk last year I started by...
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FEMALE ATHLETE TRIAD AND RED-S: Are You Missing It In Your Clinic? Kenzie Johnston, MD CAQSM
FEMALE ATHLETE TRIAD AND RED-S...So when I prepped for this original talk last year I started by googling female athlete since we are talking about the female \ൡthlete triad. This
FEMALE ATHLETE TRIAD AND RED-S: Are You Missing It In Your Clinic?
Kenzie Johnston, MD CAQSM
Objectives1. Define and discuss the evolving definition of the female athlete
triad and relative energy deficiency in sport2. Discuss screening and diagnosis 3. Discuss both nonpharmacologic and pharmacologic treatment 4. Discuss clearance and return to play for affected athletes
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So when I prepped for this original talk last year I started by googling female athlete since we are talking about the female athlete triad. This is what I got - Sexualized representation of the female athlete. Almost everyone is half naked. This is what is portrayed to young women and I think starting our talk today by showing you this helps to give you some context for the rest of the discussion.
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I will admit I then quickly googled male athlete and this is also what I got (still topless and sexualized to some extent)
Gender vs Sex
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Before we dive in I want to just clarify some language. Lets talk about the difference between female gender and female sex Sex differences include anatomical and physiological characteristics such as female organs, smaller bone structure, hormonal differences, and differing body compositions Gender relates to society’s norms and trends that affect individuals in social, cultural, and emotional ways Both are at play in the female athlete triad - sex difference can predispose female athletes to certain conditions, but as you saw on the previous slide, society’s representation of or an individual’s feeling about gender and what it means to be female also contributes to the development of the triad (Girls as young as 5 feel pressure to lose weight). I like to think of it as sex is an intrinsic risk factor and gender as an extrinsic risk factor for the triad.
1997: The Task Force on Women’s Issues of ACSM● Syndrome of 3 distinct but interrelated conditions
○ Disordered eating○ Amenorrhea○ Osteoporosis
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First identified in 1992, the ‘Female Athlete Triad’ was originally characterized by disordered eating, amenorrhea, and osteoporosis by ACSM. The organization noticed that these conditions were becoming increasingly prevalent amongst female athletes. In 1997 ACSM had put together a task force on the topic and they published a position statement on the triad. In studies conducted after the publication of the 1997 Triad position stand, investigators identified negative health consequences of the Triad associated with subclinical/less severe conditions than the aforementioned clinical endpoints. Reports of a high prevalence of subclinical menstrual disturbances, including luteal phase defects and anovulatory cycles, were observed in athletes and recreationally active women. Investigators have documented mild-to-moderate low BMD among athletes with oligomenorrhoea (infrequent menstraul periods) and subclinical menstrual disturbances (ie, anovulation and luteal phase defects - lining doesn’t properly grow which makes implantation and pregnancy unlikely). Other investigators have identified that a delay in menarche, a history of oligomenorrhoea and amenorrhoea and/or low BMD (not just osteoporosis) were significant risk factors for stress fractures and bone stress injury in athletes.
2007: Triad redefined by ACSM
3 interrelated components:● Energy availability● Menstrual function● Bone Health
EA = Dietary energy remaining after exercise, for all other physiological functions each day
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So with these findings in mind, in 2007, the Triad was redefined as a clinical entity that refers to the relationship between 3 interrelated components; EA, menstral function, and bone health. Overtime, an athlete moves along a continuous spectrum ranging from the health, optimized end to the opposite end. EA is defined as the amount of dietary energy remaining after exercise training for all other physiological functions each day. The new Triad model represented each of the conditions listed here as the pathological endpoint of one of the three inter-related spectrums ranging from a healthy endpoint to subclinical and clinical conditions. And the next slide does a good idea of illustrating that.
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At the ‘healthy’ end of the continuum, each Triad component is optimised, that is, EA meets total energy expenditure, reproductive and bone health needs; ovulatory menstrual cycles are maintained and bone mass is normal. At the ‘unhealthy’ end of the continuum, each Triad component presents the clinical endpoints of the syndrome, including low EA with or without DE, FHA and osteoporosis. So now FAT involves any one of the three components: 1) low energy availability (EA) with or without disordered eating (DE), 2) menstrual dysfunction, and 3) low bone mineral density (BMD) - not just the clinical endpoints Since then we’ve also come to understand that FAT extends past these domains and actually affects many other systems as well including endocrine, GI, renal, and neuropsych systems as well which we will discuss
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So we finally had a good definition of FAT but no guidelines for how to treat. Until ACSM’s 2007 position was further supplemented by the 2014 Female Athlete Triad Coalition Consensus Statement, which focused on treatment and return to play. While the actual prevalence of athletes who fall under the female athlete triad remains unknown, by the early definition (disordered eating, amenorrhea, and osteoporosis), studies showed 1–4% prevalence among female athletes. Prevalence is expected to be much higher now that the definition is more inclusive and is likely underestimated due to a variety of factors including, failure by professionals to recognize symptoms, a spectrum of clinical presentation, and lack of symptom reporting by athletes. In 2014, the International Olympic Committee (IOC) expert working group introduced a broader, more comprehensive term of ‘Relative Energy Deficiency in Sport’ (RED-S) for the condition previously known at ‘Female Athlete Triad.’ The term RED-S is meant to refer to the broad and various impaired physiologic functions that can be caused by relative energy deficiency and is meant to be inclusive of male athletes who may also be affected.
2014: Relative Energy Deficiency in Sport (RED-S)
“…syndrome resulting from relative energy deficiency that affects many aspects of physiological function including metabolic rate, menstrual function, bone health, immunity, protein synthesis, cardiovascular, and psychological health.”
And also affects men!
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Although the lit has focused on female athletes it has also been reported to occur in male athletes. Low EA appears to occur among the same at risk sports as for female athletes.
Why do we care?
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This is a graph of potential consqeuences of low EA Those with longterm EA are at risk for nutrition deficiencies like anemia Stress and depression can result in low EA but can also be a result of low EA Research shoes that muscle protein synthesis is reduced at EA of 30 Low EA causes unfavorable lipid profiles and endothelial dysfuction, resulting in increased CV risk Irregular menses can confound contraception leading to unexpected pregnancy and inaccurate dating Adverse consquences for bone (peak mass is 19 in women and 20.5 in men) – we will discuss this more In the shortterm – dehydration, electrolyte imbalance, GI issues
Why did I choose to talk about this here?
In a survey of 931 multispecialty docs, only 37% were even aware of the triad and only ½ of those were comfortable treating or even referring a patient!
Awareness, prevention, and diagnosis are key!
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Less than 50% of docs, coaches, Ats can identify all parts of the triad and only 19% of 370 US high school nurses can identify all 3 parts In a survey of 931 multispeclity docts, only 37% were even aware of the triad and only ½ of those were comfortable treating or even referring a patient
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Less than 50% of docs, coaches, Ats can identify all parts of the triad and only 19% of 370 US high school nurses can identify all 3 parts In a survey of 931 multispeclity docts, only 37% were even aware of the triad and only ½ of those were comfortable treating or even referring a patient Athlete Awareness is mixed. In a group of exercising Australian women – 1/3 thought that irregular periods were normal for active females Its become more mainstream in the running community recently – perhaps thanks to some big names. This is a recent cookbook from runners Shalane Flanagan (Olympian and winner of the 2017 NYC marathon) and Elyse Kopecky where they provide nutritious recipes for athletes - encouraging healthy fats, carbs, and real food. They also address the culture of undernutrition and weight in running. ** Consider reading a portion from the Run Fast, Cook Fast, Eat Slow Cook book discussing nutrition
This is Stephanie Bruce. She is a professional runner. She just put out this great article about menstrual cycles and being a professional runner. She has only had 6 months were she missed her periods (in college) and she discusses the importance of normal cycle. This is Jackie Merritt - also a BA ultra runner who I was lucky enough to interview over email. (We went to middle school together and played bball against each other in HS). 1)�As an elite ultra runner, how would you describe your overall approach to nutrition? to training? I�consider my approach to nutrition very non restrictive and filled with a wide variety of high nutrient dense foods that I love. I never really let myself feel deprived. Of course I treat food as “fuel” for my body in training but it’s also a very fun and enjoyable�aspect of my life. I�would consider my approach to training intentional and goal oriented. I usually focus on 2 races per year with a very long and deliberate build up to each. And of course, fun sometimes too :-) 3)�Do you use any apps/resources/websites to help you monitor your training load and energy expenditure? No.�In my personal experience and interactions with other athletes I have found that counting and monitoring calories often leads to an unhealthy relationship with food and it’s not sustainable. I believe that if you are mindful and aware, your body will tell you�when and how much to eat. Eating a wide variety of different plant-based food can give you everything you need in training and recovery..maybe an app could be helpful for some people who don’t know what nutrients are offered with different plant foods to monitor�that, but I think it’s pretty easy to do if you eat a variety of foods each week. 5)�Do you take any supplements? The�only supplement that I take specific to being vegan is B12. I started taking iron in high school years before being plant-based when I was anemic. I think my anemia has improved over the years but I take an iron supplement called Floradix, which I highly recommend�for female athletes with this issue. 6)�Do you see any particular nutrition/diet trends emerging within the competitive running scene? Sadly,�yes. Usually it’s some kind of ketogenic or low carb high fat diet. But in my experience, people who say they eat low carb high fat diets usually just cut the crackers and other processed carbs out of their diet and eat less junk food so they tend to feel better.� 7)�What advice would you give other endurance athletes when it comes to fueling? For�ultrarunners, learning to eat while you�run is critical for survival in a race. Also don’t deprive�yourself of good high quality carbohydrates like sweet potatoes, fruits and vegetables. They are essential for fueling good workouts. 8)�Have you dealt with any medical conditions as a result of your diet or training? No,�fortunately I have not had many serious injuries in the 10 years I’ve been running ultramarathons. My most serious injury was a stress reaction in my tibia that I had about 6-7 years ago. I believe it occurred as a result of training mistakes and probably underfueling�for too many miles. Fortunately I haven’t had any injury like that since. It was a mistake I made in training that I really learned from. 9)�What's the overall culture in the competitive running scene surrounding female athlete triad/relative energy deficiency aka do you think that most female runners find it normal to not have a regular menstrual cycle? I think most people know it’s not normal, but until recently I�think many women viewed it as a common thing that happened with runners and not a legitimate health concern. Over the past few years I have seen a shift in how female elite athletes are talking about this issue (mostly that they are talking about it as an issue)�and an increased awareness that seems to be occurring with younger high school aged women in sport. I truly believe that women can train and compete at the highest level in sport and be healthy with healthy functioning reproductive systems. I hope women today�and in the future also believe that and I love that more and more women are demonstrating that it is possible. A common misconception is that you need to stop running or dramatically reduce your running volume to have a normal regular menstrual cycle and it’s�just not the case. You just need to fuel adequately and take an appropriate amount of rest. After having normal regular cycles at my highest levels of training and competition myself, I was running 110 mile weeks last year when we conceived our baby and she�and I are both healthy and thriving now as she is 2 months old.
The Nitty Gritty of Defining and Evaluating the Triad
Energy Availability (EA)● Dietary energy level for bodily function after exercise expenditure● Low EA can lead to reduced energy for cellular maintenance,
thermoregulation, growth, and reproduction● EA less than 45 kcal/kg of FFM/day (in women)
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Like we discussed earlier, EA is the dietary energy left for bodily function after exercise expenditure. A particular index of daily EA is defined as energy intake (kcal) minus exercise energy expenditure (kcals) divided by kilograms of fat-free mass (FFM) or lean body mass. This index has been significantly associated with changes in reproductive and metabolic hormone concentrations and markers of bone formation and resorption that occur in controlled laboratory experiments where EA is manipulated using varying combinations of reductions in food intake and increases in exercise energy expenditure in women. From these short-term experiments, a threshold below which detrimental physiological changes in reproductive function, metabolism and bone occur has been identified as 30 kcal/kg of FFM/day but many sources use 45 as their cut off as this ensures adequate EA. In men the threshold for RED-S remains unknown – reduction in sex hormone testosterone is more likely more of a concern.
● BMI < 17.5 or <85% expected body weight ○ May have stable body weight
● Physiological signs of adaptation to chronic energy deficiency ○ Reduced resting metabolic rate (RMR)○ Low T3
What might you see?
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Signs of low EA are listed above. It is important to note that athletes can have stable body weight as a suppression of physiology functions but still have FAT (they have essentially shut off other systems).
2011 Compendium of Physical Activities
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You can try to calculate someone’s EA by hand but its very time consuming and likely not accurate. There are numerous web-based calculators of exercise energy expenditure; however, the Panel recommends that the 2011 Compendium of Physical Activities be used to calculate exercise energy expenditure, whereby kilocalories of energy expenditure= metabolic equivalent of task × weight in kilograms × duration of activity in hours. All methods of estimating energy expenditure have an error associated with them. The third component of the EA equation is kilograms of FFM, which is obtained from measurement of body weight in kilograms, and from an estimate of body fatness. Various methods can be used to estimate body fat.
EA calculator
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One can access the EA Calculator provided on the Female Athlete Triad Coalition website (http://www.femaleathletetriad.org/calculators/) to estimate EA. Ideally, physically active women should aim for at least 45 kcal/kg of FFM/day of energy intake to ensure adequate EA for all physiological functions
Who is at most risk for low EA?Those who:
- Restrict dietary intake- Exercise for long periods
of time- Vegetarians- Limit the types of foods
they eat
Also:
- Environmental and social factors
- Psychological predisposition- Low self esteem- Family issues- Abuse- Biological and genetics
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Low EA May be intentional or inadvertent. The continuum starts with appropriate easting and exercise behaviors including healthy dieting and occasional use of more extreme weight loss methods such as short term restrictive diets. It ends with clinical eating disorders. Risk factors for low EA include those listed above - those with restrictive diets, who exercise for extended periods of time, come from difficult backgrounds. There are many studies out there looking at the prevalence of eating disorders in various sporting populations - which does not capture the prevalence of low EA but likely underestimates it. The prevalence of disordered eating is 20% and 13% among adult and adolescent female elite athletes and 8% and 3% in adult male and adolescent elite athletes. When it comes to actual DSM5 eating disorders, One study found eating disorders in 31% of elite female athletes in “thin-build” sports Another study found 25% of female elite athletes in endurance sports, aesthetic sports, and weight-class sports had clinic eating disorders Male athletic populations at risk include cyclists, rowers, runners, jockeys, and weight class combat sports
FHA/Menstrual DysfunctionAmenorrhea: Absence of menstrual cycle for more than 3 months
- Primary: Delay of onset of menarche (recently reduced to 15 years)
- Secondary: Amenorrhea after onset of menarche
Not always apparent by loss of period,
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So what do we mean by functional hypothalamic amenorrhea? Amenorrhea is the Absence of menstrual cycle (can come in 2 flavors - primary or secondary) and FHA is when it is caused by hypogonadotropic hypogonadism. By that, we mean that FHA is presumed to be functional disruption of pulsatile hypothalamic gonadotropin-releasing hormone (GnRH) secretion. The abnormal GnRH secretion characteristic of FHA leads to decreased pulses of gonadotropins, absent midcycle surges in luteinizing hormone (LH) secretion, absence of normal follicular development, anovulation, and low serum estradiol (E2) concentrations. Variable neuroendocrine patterns of LH secretion can be seen. Serum concentrations of follicle-stimulating hormone (FSH) are low or normal, and they often exceed those of LH, similar to the pattern in prepubertal girls. This is caused by low EA or stress and other causes have been ruled out. Less than 1% of the general population experiences primary amenorrhea but more than 22% of athletes in cheerleading, diving, and gymnastics experience it. 2-5% of the general population experiences secondary amenorrhea but 65% of long distance runners experience it at some point. And then there are the harder to recognize or diagnose subclinical menstrual disorders which are defined by luteal deficiency or anovulation. Studies have shown that a whopping 78% of eumenorrheic recreational runners experience some type of subclinical disorder in at least one menstrual cycle out of three.
Low EA alters metabolic hormones like GH and IGF-1 and this is thought to disrupt GnRH pulsatility which in turn effects LH pulsatilityDisruption of LH pulsatility results in anovulation and luteal deficienciesLH pulsatility disrupted within 5 days when EA is reduced to <30kcal/kg
● If physical exam or history suggests:○ Total and free testosterone○ Estradiol○ DHEA/S○ Early morning 17-hydroxyprogesterone○ Pelvic US
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The diagnosis of FHA in athletes secondary to low EA is a diagnosis of exclusion. It is recommended to r/o pregnancies and endocrinopathies before arriving at this diagnosis. The most common causes of amenorrhoea are usually identified following a thorough medical history, physical examination, a pregnancy test, as well as evaluation of thyroid stimulating hormone, follicle stimulating hormone and prolactin, to assess for thyroid disease, primary ovarian insufficiency and hyperprolactinemia. A serum oestradiol and/or a progesterone challenge test (medroxyprogesterone acetate 10 mg for 10 days) may be useful to assess the degree of hypoestrogenism. In an estrogen-deficient state there will be no bleeding and an in estrogen-sufficient state there will be withdrawal bleeding. If there is physical evidence of androgen excess (ie, hirsutism, acne and androgenic alopecia), additional laboratory testing may include total and free testosterone, and dehydroepiandrosterone and its sulfate (DHEA/S). An early morning 17-hydroxyprogesterone may be obtained in those with hyperandrogenism to assess for non-classic 21-hydroxylase deficiency (the most common cause of congenital adrenal hyperplasia) on initial or follow-up testing. A pelvic ultrasound may be obtained in those with clinical or biochemical hyperandrogenism to confirm polycystic ovaries or to rule out virilising ovarian tumours.
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This is a proposed evaluation flow.
What about the men?
● Specific changes in male sex hormones are not completely understood and more research is needed
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Thought to maybe also have reduced LH pulsatility and magnitude
Low BMD/osteoporosis
In our population, comes from decreased accrual of bone
Increased risk of stress fractures
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The third part of the triad is low bone mineral density with the end point being osteoporosis. Interestingly, in the young athlete population low BMD is more likely from decreased accrural of bone rather than increased loss of bone like what we see in the aging population. Estrogen increases uptake of calcium into blood and deposition into bone while progesterone facilitates action of estrogen Even subclinical estrogen/progesterone imbalance may produce negative changes in bone In male athletes – low T levels have been associated with low BMD Changes in bone structure lead to increased risk for stress fracture
Low BMD
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So how do you actually define low bone mineral density and its clinical endpoint of osteoporosis? There are 2 different definitions which are dependent on the age of the athlete (5-19) vs older than 19. In children and adolescents osteoporosis is diagnosed when there is both a clinically significant fracture (which is described in this slide) and a low bone mineral content or low BMD. Instead of T scores that we use in the order population, for this population Z scores are used to compare to age and sex controls. In the population of premenopausal women osteoporosis should be diagnosed only when low BMD is present with secondary clinical risk factors that reflect an elevated short-term risk of bone mineral loss and fracture. Secondary risk factors include –chronic malnutrition – eating disorders – hypogonadism – glucocorticoid exposure – previous fractures . Of note, the term osteopenia should not used.
Who should have a DXA? >= 1 ‘High risk’ triad factors
a. History of DSM-V dx eating disorder
b. BMI < 17.5, < 85%ile estimated weight, or recent weight loss > 10% in 1 month
c. Menarche >= 16d. Current or history of <6 menses
over 1 yeare. 2 prior stress reactions/fractures,
1 high risk stress reaction/fracture, or low energy non traumatic fracture
f Prior Z score < 2 0
>= 2 ‘Moderate risk’ triad factors
a. Current of history of DE for 6 months or greater
b. BMI between 17.5 and 18.5, < 90% estimated weight, or recent weight loss 5-10% in 1 month
c. Menarche between 15 and 16d. Current or history of 6-8 menses
over 1 yeare. One prior stress
reaction/fracturef. Prior Z score between -1.0 and -2.0
(after at least 1 year interval from baseline DXA)
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So, based on the previous slide, you need a DEXA then to diagnose osteoporosis and/or low BMD. Well, who should get a DEXA? Those with 1 or more high risk triad factor or those with 2 or more moderate risk triad factors. Also, any athlete with history of >=1 non-peripheral or >= 2 peripheral long bone traumatic fractures if there any of the above risk factors. You can consider getting a DXA for athletes on medications for 6 months or greater than may impact bone (Depo-Provera)
How to use DXA● Z scores, not T scores
○ Adult women age >= 20■ Weight bearing sites (PA spine, total hip, femoral neck)■ Radius if weight bearing sites cannot be assessed
○ Children, adolescents, women < 20■ PA lumbar spine bone mineral content and areal BMD■ Whole body less head if possible BMC and areal BMD■ Adjust for growth delay or maturational delay■ Use peds reference data with height adjusted Z scores
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This slide goes over how to use/read a DXA in this population which we won’t spend much time on today because of limited time. Areal meaning g/square cm instead of volumetric which is g/cubic cm
Screening for the Triad
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So, we now know how to define and evaluate for low EA, FHA and menstrual dysfunction, and low BMD/osteoporosis but who should we screen for these conditions and how should we screen them? The goal of screening is not only to identify those with the conditions but really to aid in early detection of athletes at risk, and therefore to prevent the triad. Early detection is crucial. Screening should be part of the PPE but likely most of us and most primary care providers out there are not thinking about female athlete triad when doing PPEs Various screening instruments exist but they have no been validated The good news is that the current standard PPE form includes 9 questions related to triad but the bad news that these questions are heavily geared towards women and are not ethnically diverse Screening should start at High school level, not at college because you reach 90% peak bone mass by age 18 and any positive question on screening should prompt further investigation.
What to look for on your physical exam
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So you know what screening questions to ask but what should you also be looking for on physical exam as another tool for screening? You want to look for things like Low BMI, weight loss, orthostatic hypotension, lanugo (wispy hair which is the body’s attempt at insulation when fat layers are diminished), hypercarotenemia, parotid gland swelling, and Russell’s sign (which are cuts on MCPs related to attempts to induce vomiting) Why do you get hypercarotenemia? Investigations have suggested that a metabolic deficit that occurs in the setting of dieting prevents the normal metabolism of carotene, a precursor of vitamin A. This yellow substance is deposited in the subcutaneous layer of the skin and is seen in patients with hypothalamic amenorrhea related to dieting.
TreatmentNonpharmacologic
1. Inadvertent undereating - referral for nutritional education
2. Intentional weight loss without Disordered eating - nutritional education
3. Disordered eating - physician and nutritional counseling
4. Clinical ED - physician, nutritional education, referral to mental health provider
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Ok so you’ve screened, identified, and evaluated an athlete with female athlete triad. What do you do now? How do you treat it? You must address the underlying cause of the Triad, that is, low EA. Energy status must be normalised -primarily through modifications of diet and exercise training if necessary, with the goal of increasing EA. Restoration or normalisation of body weight is the best strategy for successful resumption of menses and improved bone health. The amount of weight gain needed to resume menses is variable but usually in the 5-10% range. Usually this is fat mass but not always. When thinking through how you are going to get your athlete to increase their energy availability by changing their diet you will likely have to evaluate if there is disordered eating or even a clinical eating disorder. Disordered eating is irregular eating behaviors that do not warrant the diagnosis of a particular eating disorder (binge, anorexia, bulimia). More resources are usually recommended for those with disordered eating or a clinic eating disorder.
Treatment targetsMay include one or more of the following:● Reversal of recent weight loss● Return to body weight associated with normal menses● Weight gain to achieve BMI > 18.5 or >= 90% of predicted weight● Energy intake minimum of 2000 kcal/day
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You may want to set specific targets with your athletes and all of these are recommended as potential targets - should be personalized based on your patient. For example, if your patient is on contraception and wants to remain on it it would be hard to have a goal of return to body weight associated with normal menses so you may need to pick another target that helps you know if you are meeting your overall goal of increasing EA. Diet changes should be gradual, beginning with approx 10-20% increase in caloric intake which would result in a gain of 0.5 kg every week
Stepwise approach1. Perform assessment of baseline energy needs2. Using appropriate target for EA, develop meal plans
a. Macronutrients and micronutrients - in particular: Ca, Vit D, Iron, Zinc, and Vit K.
i. Calcium 1000-1300 mg/dayii. Vitamin D optimized between 32-50
b. Increase real foods vs dietary or meal supplementsc. Consider small and frequent meals if history of GI discomfort
3. Perform standardized period monitoring of body weight, consider weekly
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When coming up with a plan for specific diet changes - diet quality, diet variety, food preferences and practical aspects of food availability should be considered. Goals would include achieving an adequate balance of macronutrients and appropriate intake of micronutrients, particularly calcium, vitamin D, iron, zinc and vitamin K. Nutrition can speak on this more. Whenever possible, the recommendation should be to increase intake of real foods versus dietary or meal supplements. Dietary recommendations should include incorporation of energy and nutrient-dense foods such as fortified milk drinks and essential fatty acids in the form of fish, healthy oils, nuts avocados and dried fruit. If there is a possibility of gastrointestinal discomfort with high caloric loads, small and frequent meals should be consumed throughout the day, with timing dependent on practice and competition. Particular attention should be paid to identifying times across the day where dietary energy intake may be particularly low. Adjustments in dietary strategies for increasing EA should also take into account changes across the season in accordance with competition schedules.
Special consideration for ED
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For those with ED, consider CBT as it may help with compliance to prescription for increased energy intake and associated weight gain
Special considerations in those with low BMD● Amenorrhoeic women will lose 2-3% of bone mass per year if
remains untreated
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There are special treatment considerations depending on what triad conditions your athlete has. The etiology of bone loss in amenorrheic women is energy and estrogen deficiency. Thus goal should be weight gain and resumption of menses to prevent further loss of bone mass. Weight gain alone has been shown to have a positive effect on BMD but normalization of BMD is not likely to occur without resumption of menses (indicating an increased estrogen state). We routinely recommend weight bearing exercises and loading activities to improve bone health. However, it is important to note that prospective studies are lacking on resistance training and high magnitude loading and their effect on bone health in amenorrheic athletes. Estrogen may be permissive for the positive effects.
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Bone Mineral density is one of the last things to recover and can take years as this slide illustrates.
Nonpharmacologic treatment should be the mainstay but you may want to consider pharmacologic treatment for comorbidities (like clinical EDs). Consider SSRIs in treatment of bulimia nervosa and consider other medications to treat comorbid anxiety, depression, or OCD. In men, consider treating with testosterone is there is hypogonadism and osteoporosis
What about OCPs? Won’t they fix it?COCs or non-oral routes of contraceptive therapy DO NOT restore spontaneous menses COCs are not associated with improved BMD
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What about medications for menstrual dysfunction? It has been common practice and often still is common practice to just put an athlete with abnormal periods on OCPs and call it fixed. But should we be doing that?! Contraceptive therapy DOES NOT restore spontaneous menses; indeed, contraceptive therapy simply creates an exogenous ovarian steroid environment that often provides a false sense of security when induced withdrawal bleeding occurs. In fact, combined oral contraceptive (COC) therapy is not consistently associated with improved BMD in amenorrhoeic athletes and may in fact further compromise bone health given first-pass effects on hepatic production of insulin-like growth factor-1 (IGF-1), an important bone trophic hormone. Therefore, treatment with OCPs to with the goal of restoring menses is not recommended!
Whom to consider for pharmacologic treatment1. BMD Z scores <= -2.0, clinically significant fx history, and lack of response to 1
year of non-pharm treatment2. BMD Z scores between -1.0 and -2.0, significant fx history, and >=2 additional
Triad risk factors, and lack of response to 1 year of non-pharm treatment
Transdermal estrogen therapy with cyclic progesterone may be considered in ages 16-21 with FHA to prevent further bone loss during this time if they have:
1. BMD Z scores <= -2.0 without significant fx history and at least 1 Triad risk factor and lack of response to 1 year of non-pharm treatment
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So when should you consider pharmacologic therapy for the triad and what should you actually consider? The big takeaway here is that everyone should have tried one year of non pharmacologic treatment.
What do use: Estrogen replacement (women)Transdermal estradiol 100 microgram twice weekly along with cyclic progesterone (2.5 mg daily for 10 days of the month) increased BMD
May work to maintain BMD but may not help bone accrual exceed controls
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Transdermal does not suppress IGF-1 (unlikely oral OCPs). It needs to be partnered with progesterone to avoid the effects of unopposed estrogen. Of note, it has shown maintenance of BMD in those with anorexia but not gain (and in our patients we really need gain). It is also unproven for contraception. Vaginal estrogen also does not suppress (there are combo rings) so they may be safer than OCPs but unclear if they would help bone maintenance because of their low dose.
What about bisphosphonates?Pharmacologic therapy for osteoporosis is recommended in postmenopausal women but we are lacking data in our age group.
Bisphosphonates are not approved by FDA for increasing BMD or fracture reduction in young or adult athletes. They may not be as effective in our population because they work by preventing resorption (which is happening at a much lower rate in our population - our issue is lack of accrual).
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Pharmacologic therapy for osteoporosis is recommended in postmenopausal women but we are lacking data in our age group. Bisphosphonates are not approved by FDA for increasing BMD or fracture reduction in young or adult athletes. They may not be as effective in our population because they work by preventing resorption (which is happening at a much lower rate in our population - our issue is lack of accrual). Can consider in male athletes. There are very rare circumstances for offering additional therapy (aka bisphosphonates) - must have osteoporosis, failed conservative therapy and one of the following Contraindications to estrogen Lack of response to estrogen after 18 months Eumenorrheic Multiple debilitating fractures The last 2 should have a metabolic and genetic workup done as well. There are also concerns about risk of teratogenicity of bisphosphonates (although the data to date is reassuring) so it is recommended that any use of bisphosphonate therapy in young women with the Triad should only be executed by or in consultation with a board-certified endocrinologist or specialist in metabolic bone diseases.
Return to play
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And lastly, how do you decide when its safe for your athlete to return to sport? The panel did put together tools to help with this decision by helping you risk stratify your athletes.
Figure 5
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Provisional clearance would be full training and competition with understanding that they will be compliant with recommendations. Limited clearance includes limitations within training and competition. They may be able to progress activity if meeting goals. If an athlete is High risk it is recommended that their participation be restricted until they can reach health goals but if they don’t you could consider disqualification for the season. Of note, this suggested return to play decision model has yet to be studied to see if it results in improved outcomes for female athletes with triad disorders.
Other Risk FactorsImportant to consider age, eating disorder status
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In the evaluation of health risk and participation risk, an important consideration is also the age of the athlete. The preadolescent and adolescent athlete has more vulnerability to physeal and other skeletal injuries, especially during periods of rapid growth. Adolescence is a period of rapid bone mineral acquisition. Inadequate EA and menstrual dysfunction may result in a delay of bone mineralisation that lags behind bone linear growth. The mechanical stresses from repetitive loading in this population may increase susceptibility to fracture in an already vulnerable area of bone, which may have potentially catastrophic consequences. Similar scrutiny should be directed towards athletes meeting DSM-V criteria for an ED. While the presence of an ED is considered a high-risk attribute in the Cumulative Risk Factor Assessment, it should be noted that patients with EDs have a higher risk of premature mortality when compared with individuals with other psychiatric diagnoses, and that is especially true for those with anorexia nervosa. It is the recommendation of the Consensus Panel that athletes diagnosed with anorexia nervosa who have a BMI <16 kg/m2 or with moderate-to-severe bulimia nervosa (purging >4 times/week should be categorically restricted from training and competition. Future participation is dependent on treatment of their ED, including ascertainment of BMI >18.5 kg/m2, cessation of bingeing and purging and close interval follow-up with the multidisciplinary team.
Contracts
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Athletes in moderate risk and high risk categories should receive a written contract Specify criteria for ongoing or future clearance and return to play Include frequency and expectations of visits with each team member
Multidisciplinary team
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Overall, it should be a team decision on when and how to return an athlete with the triad to sport. This team may include - Physician, sports dietician, mental health professional, family, coach, and athlete.
“An ounce of
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A study of sport nutrition knowledge, behaviors, and beliefs across sex, race/ethnicity, and SE status in HS soccer players identified that general sports nutrition knowledge is lower in adolescent soccer players than previously found and that specifically females and Latinos may benefit the most. Norwegian studies have shown that school based programs which go beyond athletics may be successful
References
Mountjoy, Margo, et al. “IOC Consensus Statement on Relative Energy Deficiency in Sport (RED-S): 2018 Update.” British Journal of Sports Medicine, vol. 52, no. 11, 2018, pp. 687–697., doi: May 28, 2019.
Mountjoy, Margo, et al. “The IOC Consensus Statement: beyond the Female Athlete Triad—Relative Energy Deficiency in Sport (RED-S).” British Journal of Sports Medicine, vol. 48, no. 7, 2014, pp. 491–497., doi: May 28, 2019.
Souza, Mary Jane De, et al. “2014 Female Athlete Triad Coalition Consensus Statement on Treatment and Return to Play of the Female Athlete Triad.” Clinical Journal of Sport Medicine, 2014, p. 1., doi: March 13, 2019.
