What follows is a real clinical case of a female athlete who lost her menstrual period after several years of intense exercise and caloric restriction, and who then regained normal menses after enacting corrective measures. I have taken care to remove details which might make it possible to identify the patient. However, the patient did grant me permission to share this case with any detail that I thought might provide benefit to the reader, including her actual lab values and clinical history. Her hope, and mine, is that the presentation of this case might help add context for anyone going through a similar process. Please understand that this article is not medical advice and that this patient’s case may not be applicable to your own. See the bottom of the page for a full disclaimer.
A 27 year old female presented to me in 2019 with three years of progressive symptoms which began with the loss of her menstrual period. This was followed by gradually worsening generalized fatigue, fragmented and restless sleep, and decreased exercise motivation and tolerance. Several other signs and symptoms appeared intermittently: headaches, light-headedness, palpitations, dry skin, and muscle aches and cramps.
Past Medical History: At the time of presentation, the patient was otherwise in excellent health. She had no significant past medical history, was not on any medications, and had a history of only several minor orthopedic surgeries.
Athletic History: The patient competed in collegiate level sports. After college, she engaged in consistent resistance and endurance training, as well as several years of recreational Crossfit.
Diet: The patient’s diet consisted of a whole food diet with an attention to carbohydrate restriction. She often consumed less than 100 grams of carbohydrate per day, even on days with a high training volume. Additionally, she often intentionally maintained an energy deficit, consuming fewer calories than she expended.
Stress: The patient reported several stressors including career uncertainty, relationship uncertainty, “health anxiety,” and a compulsion to maintain a high level of fitness and a lean physique.
Menarche (first menses) occurred at age 14, after which the patient had regular menstrual periods even during her participation in collegiate sports. Her weight at the time was roughly 70 kg (154 lbs). After graduating from college, she began a more restrictive diet with carbohydrate and overall caloric restriction. Simultaneously, she maintained a rigorous training regimen, often enduring one or more workouts daily.
After one or two years, her menstrual period ceased, which prompted her to consult a gynecologist in May of 2018. At this time, her weight was 67.6 kg (149 lbs). She underwent laboratory studies and pelvic ultrasonography.
Laboratory Evaluation – May, 2018
|Free T3||2.1||Low Normal|
Pelvic Ultrasonography – May, 2018
Normal ovaries without polycystic morphology.
The patient was diagnosed with secondary amenorrhea and given a prescription for ethinyl estradiol and desogestrel, a combination of estrogen and progestin which is typically used as a contraceptive. She reported to me that the combination contraceptive did induce bleeding. However, she chose to stop using the medication after one or two menstrual periods due to mood lability. Subsequently, her menses once again ceased.
For the next 18 months, the patient proceeded to participate in Crossfit on a near daily basis, and to eat a diet restricted in carbohydrates and overall energy (caloric restriction).
In December of 2019, the patient consulted me for help with her symptoms, which now included worsening generalized fatigue, restless sleep, and now decreased exercise motivation and tolerance. She described feeling sluggish and heavy when trying to perform her workouts. She was concerned that all of the symptoms were connected to the loss of her menstrual period, and furthermore, that the absence of her menses could be detrimental to her long-term reproductive and overall health.
My evaluation included a full medical history, record review, nutrition analysis, body composition evaluation, and physical examination.
The results of this examination were as follows:
The pertinent medical history was: menarche at age 14, no history of pregnancy or gynecological procedures, but amenorrhea beginning three years prior to presentation and remitting only in response to combination oral contraceptive. There was no abdominal pain, pelvic pain, headache, vision abnormality, nausea, or vomiting.
Resting heart rate was 50 beats per minute, blood pressure 110/60 mm Hg, respiratory rate 10 breaths per minute. Weight was 142 lbs (64.4 kg) and height 5’7’’ (170 cm).
Nutrition analysis revealed a daily carbohydrate intake sometimes less than 100 grams, and a total calorie intake often less than 2000 calories. By comparison, energy expenditure on an average day was often greater than 2500 calories (by indirect calorimetry), leaving a daily energy deficiency sometimes upwards of 500 calories.
Dual-energy X-ray absorptiometry (DXA or DEXA) scan revealed 17% body-fat and bone mineral density (BMD) T-score of 2.1, with a spine BMD of 1.1 g/cm^2.
Physical exam demonstrated a well appearing female with a lean body habitus. Examination of the head and neck revealed intact and symmetric extraocular movements, an absence of scleral icterus, a clear and symmetric oropharynx, healthy dentition, and a soft and mobile thyroid without nodules. No palpable lymphadenopathy of the head or neck was found. Auscultation of the thorax revealed normal heart sounds and clear lungs. Pulse examination confirmed symmetric upper and lower extremity distal pulses. Abdominal exam revealed a flat non-tender abdomen without hepatosplenomegaly. Genital exam was deferred to the patient’s gynecologist. Examination of the hair, skin, and nails revealed clear, well-hydrated skin without brittle hair or nails. Neurologic testing revealed intact strength and sensation.
Laboratory Evaluation – December, 2019
|Free T3||2.1||Low Normal|
|TC||Trigs||HDL-C||VLDL-C Calc||LDL-C Calc|
Differential diagnosis is the process whereby a physician attempts to differentiate the correct diagnosis from other possible diagnoses. The process is based on the law of non-contradiction, and the corollary methods of difference and agreement. The first step in conducting a differential diagnosis is to identify a “chief complaint.” The physician typically chooses the most essential and/or prominent sign or symptom of illness – often referred to as a “chief complaint.” This serves as a starting point to generate a list of possible diagnoses. For instance, a chief complaint might be chest pain. The differential diagnosis for this chief complaint might include the following conditions: heart attack, acid reflux, and pneumonia. The list is then narrowed down as more data are acquired. Each data point either supports or detracts from each possible diagnosis. For the patient with chest pain, the physician might ask if the patient has a productive cough. If the answer is “no,” the possibility of pneumonia drops to the bottom of the list. The physician iterates through the process, obtaining more data as necessary, until eventually, and hopefully, a definitive or most-probable diagnosis is discovered.
In this particular case, the primary sign, or chief complaint was amenorrhea, which is defined as the absence of a menstrual period for at least three consecutive months. The possible causes of amenorrhea are myriad, because the system that supports regular menstruation is comprised of many parts, and is modulated by many outside factors. It is worthwhile to understand this system a little bit before attempting to discover the cause of a particular case of amenorrhea.
Menstruation is regulated by the body’s endocrine system. The endocrine system is a system of glands that secrete hormones (signalling molecules) into the blood stream. Once secreted, hormones travel to a target organ or tissue, and bind to a receptor. The binding of a hormone to its target receptor causes further downstream action.
The regulator of the endocrine system is an area of the brain called the hypothalamus. It carries this name because it sits below (hypo-) the thalamus (another area of the brain). The hypothalamus receives inputs from other areas of the brain, as well as several organs and tissues of the body. You can think of these signals as read-outs from sensors that provide information about various conditions to the hypothalamus.
For example, there are several tissues in the body capable of storing energy (e.g. liver, muscle, fat cells). These tissues secrete hormones (e.g. leptin) that tell the hypothalamus how much energy, or fuel, exists in storage. You can think of this as a sort of fuel tank gauge. Similarly, the hypothalamus receives information about core body temperature. You can think of this as a thermometer.
The hypothalamus isn’t just a dashboard of gauges, though. It uses these signals to allocate resources, and to make adjustments to the system. If energy intake and storage is high, the hypothalamus can increase metabolic rate and allocate resources towards growth and reproduction. If temperature is high, the hypothalamus can decrease metabolic rate, and thus decrease heat production. If energy is scarce, the hypothalamus can decrease metabolic rate, decrease growth, and decrease reproductive function – all to save energy. So, the hypothalamus is a sort of processing unit which is responsible for allocating metabolic resources based on external conditions (e.g. temperature, energy availability, stress) and internal needs (e.g. growth, heating/cooling, reproduction).
The hypothalamus carries out its functions, in part, by communicating with a gland that sits just below it – the pituitary gland. The pituitary gland is capable of sending signals to other glands and organs which causes them to carry out various functions. For example, if the hypothalamus senses a need to increase metabolic rate, it can stimulate the release of TSH (thyroid stimulating hormone) from the pituitary gland, which then causes the thyroid gland to release thyroid hormone. Thyroid hormone then directly affects cells in various tissues to increase metabolic rate.
In the case of reproduction, under favorable conditions, the hypothalamus releases GnRH (gonadotropin releasing hormone), which causes the pituitary to release LH (luteinizing hormone) and FSH (follicle stimulating hormone). LH and FSH cause the ovary to release an ovum (an egg), and to secrete estradiol and progesterone, which cause the uterus to build up its lining to prepare for implantation and pregnancy. If this process does not occur, the uterine lining is shed, resulting in menstrual bleeding.
If anything is wrong with this system – functionally or structurally, normal menstruation can be disrupted.
Sometimes, women are born with problems with the system, and do not have a menstrual period by age fifteen. This is called primary amenorrhea.
The distinction between primary and secondary amenorrhea is important, because women with secondary amenorrhea by definition have had normal menses at one time or another. They have proven that they possessed (at least at some time, if not still) the biochemical and anatomical potential for menstruation. Women with primary amenorrhea have never had a menstrual period, and therefore it is in question as to whether there is an absence of a biochemical or anatomical element necessary for menstruation.
It’s important to realize that many of the causes of secondary amenorrhea could also cause primary amenorrhea. Take for example a case of functional hypothalamic amenorrhea, which can be caused by inadequate nutrition. An individual might have all of the normal anatomy and physiology required for menstruation, but they do not have enough nutrition during their adolescent years to induce menstruation. This is an extrinsic cause of amenorrhea, but the case will be defined as primary amenorrhea, simply because the patient did not have her first menstrual period by age fifteen.
Thus, I think it may be more useful to think of amenorrhea as either intrinsic or extrinsic. That is, due to an inborn (intrinsic) cause versus an acquired (extrinsic) cause. An example of an intrinsic cause is an enzyme deficiency like congenital adrenal hyperplasia. In this group of conditions, there is an enzyme deficiency that causes an abnormal hormone profile often leading to primary amenorrhea in females.
An example of an extrinsic cause of amenorrhea is Asherman’s Syndrome in which scarring of the uterus, usually from a surgical procedure, can prevent menstruation from occurring.
Another way to categorize causes of amenorrhea would be to divide it into the following categories:
- External – caused by external factors such as starvation, exercise, or stress.
- Central – caused by damage or dysfunction of the central controllers – the hypothalamus or pituitary, such as a tumor of the pituitary gland.
- Peripheral – caused by a problem with the peripheral glands or tissues like the thyroid, adrenal glands, or pancreas – such as hypothyroidism or congenital adrenal hyperplasia.
- Gonadal – caused by a problem with the ovaries such as polycystic ovary syndrome or hyperandrogenism[mfn]:A. Javed, R. Kashyap, and A. N. Lteif, “Hyperandrogenism in female athletes with functional hypothalamic amenorrhea: A distinct phenotype,” Int J Womens Health, vol. 7, pp. 103–111, Jan. 2015, doi: 10.2147/IJWH.S73011[/mfn].
- Genital – caused by a problem with the genital tract such as scarring of the uterus or an obstruction of the outflow tract.
Any classification system has its benefits and detriments, so its useful to understand the system as a whole and to be able to think of it in different ways.
With all of this said, it is overwhelmingly likely in a patient who has previously had regular menses for years, that all of the anatomy is normal and that there are no inborn abnormalities that would prevent normal menstruation. This means that one of two things has happened:
The previously normal anatomy has become abnormal (e.g. through injury, infection, tumor growth, or infarct – tissue death).
The biochemical signaling has been disrupted by an external cause.
In the current case, the differential diagnosis included causes from both categories:
- Functional Hypothalamic Amenorrhea
- Polycystic Ovarian Syndrome
- Pituitary lesion, such as a tumor
- Non-classical congenital adrenal hyperplasia
- Asherman’s Syndrome
- Thyroid Abnormalities
In this case, I noted the presence of normal menarche at age 14. At age 24, amenorrhea coincided with an increase in exercise and stress and a decrease in sleep and caloric intake.
In order to narrow down the list of diagnoses above, I obtained a pelvic ultrasound, and measured the hormone levels from the endocrine glands that could contribute towards a disruption of the system. Pelvic ultrasound verified normal ovaries and uterus, and laboratory tests revealed normal levels of cortisol, prolactin, androgens, thyroid hormones, 17-OH progesterone, and insulin. However, LH, estradiol, and progesterone all registered either below normal or at the absolute bottom of the reference range. Furthermore, the hormone levels as a group were not compatible with any stage of a normal menstrual cycle.
The normal pelvic ultrasound as well as normal androgens (testosterone and free testosterone), made PCOS and hypernadrogenism very unlikely. Normal prolactin level made a pituitary tumor very unlikely. Normal thyroid studies ruled out hyper and hypothyroidism. Normal fasting insulin and hgbA1c made hyperinsulinemia an unlikely contributing factor. There was no history of cervical or uterine instrumentation, and no endometrial abnormality on pelvic ultrasound, so Asherman’s Syndrome was unlikely. A normal 17-OH progesterone level made non-classical CAH unlikely as well.
Source: Gordon et al. 2017
Therefore, these normal results, along with the abnormally low LH and estradiol, combined with the clinical history, suggested that there was some factor or factors causing a disruption in the hypothalamus or pituitary signalling. Some circumstances caused a low secretion of LH and FSH, leading to insufficient stimulation of the ovary, and therefore an absence of menses. This condition is called functional hypothalamic amenorrhea (FHA). Let’s break this term down:
- Functional – functional as opposed to physical or structural. In other words, the anatomy, the cells, the enzymes, glands, etc. are all capable of functioning normally, but currently they are not.
- Hypothalamic – this word refers to the hypothalamus – an area of the brain which receives inputs from many parts of the brain and body and acts to regulate many metabolic and reproductive functions.
- Amenorrhea – this word means the absence of menses.
If FHA is a functional rather than a structural condition, the next logical question is, what causes it?
Recall that certain conditions are required to stimulate GnRH release from the hypothalamus which has the downstream effects of generating a menstrual period. Chief among these conditions is adequate nutrition. The hypothalamus will shut down reproductive function if it senses insufficient energy intake. This makes sense from an evolutionary perspective. A woman would be unable to support a pregnancy and a newborn during a period of starvation. Similarly, a relative lack of stress is required for similar reasons. If a woman’s life or health was at risk for any variety of reasons – for instance, she is subjected to hostile conditions, it would be disadvantageous to become pregnant. On the contrary, if she were forced to fight for her life, it would be advantageous to have all physiologic resources dedicated to survival. Women who compete in sport and attempt to maintain a lean physique are often undergoing relative energy deficiency as well as putting themselves under consistent physiologic stress. These conditions decrease the hormonal signals that would typically trigger normal ovulation, and thus, fertility and menstruation fail to occur.
My patient was indeed putting herself through stress and maintained a consistent energy deficiency as described above. So, FHA was our initial working diagnosis. But, other diagnoses, however unlikely, were still possible. Given that the initial workup heavily favored the diagnosis of FHA, we sought to identify and correct the underlying circumstances that led to the hormonal disruption. Simultaneously, we surveiled for contradictory signs and symptoms that could indicate an alternate diagnosis.
FHA is usually caused by a disruption in the biochemical signals necessary to stimulate normal GnRH (gonadotropin releasing hormone) release from the hypothalamus. One function of the hypothalamus is to integrate signals from other parts of the body to induce fertility. In other words, when conditions are sufficient to carry a child, the hypothalamus will generate signals that ultimately result in ovulation and other changes that support pregnancy.
The conditions necessary for a successful pregnancy are: rest, safety (i.e. absence of significant threats, or perceived threats), and abundance of nutrients and energy. When these conditions are met, the hormonal milieu facilitates the allocation of resources towards reproduction.
With this knowledge, and that of my patient’s diet, exercise, sleep, and psychological stressors, we developed a plan.
Broadly, I recommended a whole-food (as opposed to processed-food) diet diverse in both animal and plant foods. I suggested eating based on hunger and satiety cues as opposed to counting calories. Using internal cues for guidance, we sought to achieve a caloric surplus. Tracking with Cronometer was utilized to monitor progress and ensure a nutritionally replete diet.
More specifically, we aimed to add roughly 2-4kg (approximately 4.5-9 lbs) of body fat over an eight to twelve week period. For my patient, this meant a daily base calorie count of 2250-2500 calories with an additional 100-200 calories for every thirty minutes of exercise.
In addition to the overall calorie count, we set macronutrient requirements. We decided to start with a minimum carbohydrate intake of 150 grams daily, with an additional 100-200 grams for each thirty minutes of exercise. Protein requirements were set at a minimum of 2 grams / kg of lean body mass which was roughly 100 grams daily. The balance of caloric intake was to be made up of either fat or carbohydrate if desired.
Specific food suggestions were based on the patient’s personal tastes and micronutrient requirements. These recommendations were: meat, fish, eggs, potato, rice, beets, carrots, dark green leaves, avocado, berries, nuts, olive oil, and a prenatal vitamin.
We agreed on a two week hiatus from all exercise except for walking. After that two week period, I recommended 30-90 minutes of zone one or zone two exercise 3-5 times per week. I recommended against resistance training and against any moderate or high intensity training until the return of menses, and perhaps for some time afterwards depending on the trajectory of the recovery. This prescription was based on the patient’s desire to regain menses at the expense of her fitness if need be. It may be possible, though not necessarily advisable, for some individuals to regain menses without a two week rest period, and while still maintaining some moderate or high-intensity exercise[mfn]:M. Warren and N. Perlroth, “The effects of intense exercise on the female reproductive system,” J. Endocrinol., vol. 170, no. 1, pp. 3–11, Jul. 2001, doi: 10.1677/joe.0.1700003[/mfn]. This aspect of treatment is controversial and variable on an individual basis. There is some evidence that intense exercise alone is not enough to induce amenorrhea, and that the more important factors are adequate energy intake and management of other physiologic and psychological stressors[mfn]:M. E. Sophie Gibson, N. Fleming, C. Zuijdwijk, and T. Dumont, “Where Have the Periods Gone? The Evaluation and Management of Functional Hypothalamic Amenorrhea,” J Clin Res Pediatr Endocrinol, vol. 12, no. Suppl 1, pp. 18–27, Jan. 2020, doi: 10.4274/jcrpe.galenos.2019.2019.S0178; :A. D. Genazzani, F. Ricchieri, C. Lanzoni, C. Strucchi, and V. M. Jasonni, “Diagnostic and therapeutic approach to hypothalamic amenorrhea,” Ann. N. Y. Acad. Sci., vol. 1092, pp. 103–113, 2006, doi: 10.1196/annals.1365.009[/mfn].
I suspected in this case that the patient’s fragmented sleep, early-awakenings, and long sleep-latency were secondary to stress and hormonal disturbance. I hypothesized that once energy intake was adequate and psychological stressors were addressed, that sleep would improve on its own. Nevertheless, we did seek to address sleep issues primarily, as sleep deprivation could play a primary role in contributing to stress and thus amenorrhea. To this end, I discussed a variety of sleep strategies with my patient. Briefly, we sought to i) avoid caffeine after 9am, ii) to aim for an 11pm in-bed time, and a 7am out-of-bed time, iii) to obtain morning sunlight, natural light in the late afternoon and evening, and iv) to read and/or meditate as part of a “wind-down routine.”
Psychological stressors are ubiquitous. Even if stressors are not a primary issue in a particular case of FHA, they could develop as part of a “recovery period” which necessarily involves changes to a patient’s routine.
In this case, there were numerous pre-existing stressors that likely contributed to the patient’s amenorrhea and also made the recovery more challenging. To mitigate these stressors, we maintained an open line of communication at all times. I spoke with the patient via phone, video, email, and text message often several times a week, especially for the first two months. The patient also sought counsel from a clinical psychologist on several occasions, which was highly encouraged. In addition, the patient also had an excellent support system of friends and family.
Despite these measures, additional sources of stress arose as a result of the recovery plan. The patient endured a change in daily exercise routine, decreased contact with her exercise community, and changes to her physique. All of these stressors proved to be by far the most challenging aspect of the recovery period.
December, 2019 – February, 2020
During the first two months, the plan was executed with variable success. Weight gain was minimal, at roughly 1 kg. However, physical activity was significantly decreased. Repeat labs demonstrated:
Laboratory Evaluation – February, 2020
|Lab||Feb, 2020||Dec, 2019||Unit|
You can see a significant increase in both LH and estradiol, whereas FSH is roughly the same. However, in order to interpret these changes, you first need to know three things:
- Reproductive hormone levels (e.g. LH, FSH, estradiol, and progesterone), all fluctuate on a daily-weekly basis in women with an active menstrual cycle.
- Each of the above hormones have their own pattern of fluctuation, with a surge of LH, FSH, and estradiol around the time of ovulation, and increase in progesterone the week of and after ovulation.
- Hormone levels vary from individual to individual.
With that in mind, realize that it’s difficult to interpret the chart above. Given that this patient was not having menstrual bleeding, it’s impossible to tell (without repeated daily or weekly measurements) whether this patient is having a normal fluctuating pattern of hormone levels or rather that her levels were persistently low and now returning to normal.
My interpretation, especially in retrospective review of this case, and in the context of the full recovery and subsequent lab checks (discussed in more detail below), that the higher LH and estradiol levels were indicative of a return of function of the endocrine system rather than an accident of the timing of measurement. For this patient, this was the first time estradiol was measured at a value over 20 in over three years.
February, 2020 – April, 2020
In April of 2020, four months after the initial consultation, the patient reported light cramping and the presence of cervical mucous, but still no menstrual bleeding. Body weight at this time was now up to 73 kg, nearly 10 kg (20 lbs) heavier than the starting weight. We were successful in adding body weight. However, fragmented sleep and psychological stressors remained a challenge. Labs were checked once again and revealed:
Laboratory Evaluation – April, 2020
|Lab||Apr, 2020||Feb, 2020||Dec, 2019||Unit|
You can see once again that LH, FSH, and estradiol all remain higher than the original baseline values.
April, 2020 – June, 2020
Over the next two months, we worked together to fine-tune all aspects of the recovery plan including improvements in nutrition, exercise, and sleep. Walks, light-jogging, and body-weight movements were reintroduced. We emphasized a whole-food diet, and eating to satiety.
In June of 2020, six months after the initiation of our interventions, the patient had her first episode of menstrual bleeding.
Here is a graph showing hormone levels plotted against weight over time starting in 2016 and extending through recovery of menses in June of 2020, with the most recent measurements in November, 2020. The green shaded area begins in January of 2020 and extends through April of 2020. This period of time accounts for nearly 20 lbs of weight gain, and a significant decrease in exercise, an increase in sleep, and attempts to address psychological stressors. You can see the gold and red lines increasing significantly during the period of weight gain. The gold line represents LH levels, the red line estradiol. Menses resumed approximately eight weeks after these increases (the pink shaded area).
If you’re looking at the chart above, it may be tempting to try to make some sense of the absolute hormone levels within the context of the shaded areas of the chart. For example, you might look at the red line, which represents estradiol levels, and conclude that once a person is menstruating regularly, estradiol will go up from the thirties or forties into the nineties. This is not necessarily true. Individuals may have different ranges and fluctuations for each of the hormone levels. For instance, estradiol levels can range from fifteen up into the several hundreds depending on the individual and the segment of the menstrual cycle in which the level is measured. To me, the most notable finding on this chart occurs in the green shaded area. Prior to this time period, the patient’s LH and estradiol levels were very low for a period of years regardless of when measurements were taken. Then, within several weeks of gaining weight and undertaking the other interventions discussed in this case report, LH went up nearly eight-fold, and estradiol doubled.
Applying this to yourself, or to a future patient might work by plotting out several random levels of LH and estradiol on a graph during a period of amenorrhea. Once interventions begin, a substantial rise in LH and estradiol might suggest recovery of the hypothalamic-pituitary-gonadal system. After that, levels should fluctuate daily and weekly as pulsatile release of LH is restored and hormones resume their usual monthly pattern. You can see the typical pattern of reproductive hormones throughout a menstrual cycle in this chart below (the chart represents one cycle, roughly 28 days).
My patient’s recovery of menstrual periods took approximately six months from day one of intervention. By the time I encountered this patient, she was already convinced that her lack of menstruation was a problem and that it tied in with many other symptoms she was experiencing. So, she was highly motivated to fix the problem. We were able to work closely together during this process and made small adjustments to nutrition and exercise along the way. There were also many discussions that took place to evaluate whether we were headed in the right direction or not, and to provide reassurance.
Six months is a long time to wait, and it can be difficult to tell at any point during the process if and when menses will resume. In some cases, menses might resume more quickly, and in others it might take much longer[mfn]:“No Period. Now What? A book about regaining missing periods.” Accessed: Jan. 07, 2021. [Online]. Available: https://www.noperiodnowwhat.com/[/mfn]. Even though some women gain weight, there can still be psychological stressors that prevent normal menstruation from resuming. Because of the complexity of treating FHA, professional societies recommend a multidisciplinary approach – physician, nutritionist, trainer, and psychologist – especially for competitive athletes[mfn]:C. M. Gordon et al., “Functional hypothalamic amenorrhea: An endocrine society clinical practice guideline,” J. Clin. Endocrinol. Metab., vol. 102, no. 5, pp. 1413–1439, May 2017, doi: 10.1210/jc.2017-00131[/mfn].
There is far more to say on this topic, but for now I’ll close out with a few questions that I’d like to answer in future articles:
- Is amenorrhea a problem in the context of an otherwise healthy athlete?
- Is there a corollary condition in men?
- Are medications useful and/or safe in the treatment of FHA?
- What other problems occur as a result of energy deficiency, especially in athletes?
If you read this far, thank you, and please feel free to send feedback or questions you’d like answered on this and similar topics.
References: A. Javed, R. Kashyap, and A. N. Lteif, “Hyperandrogenism in female athletes with functional hypothalamic amenorrhea: A distinct phenotype,” Int J Womens Health, vol. 7, pp. 103–111, Jan. 2015, doi: 10.2147/IJWH.S73011. : M. Warren and N. Perlroth, “The effects of intense exercise on the female reproductive system,” J. Endocrinol., vol. 170, no. 1, pp. 3–11, Jul. 2001, doi: 10.1677/joe.0.1700003. : M. E. Sophie Gibson, N. Fleming, C. Zuijdwijk, and T. Dumont, “Where Have the Periods Gone? The Evaluation and Management of Functional Hypothalamic Amenorrhea,” J Clin Res Pediatr Endocrinol, vol. 12, no. Suppl 1, pp. 18–27, Jan. 2020, doi: 10.4274/jcrpe.galenos.2019.2019.S0178. : A. D. Genazzani, F. Ricchieri, C. Lanzoni, C. Strucchi, and V. M. Jasonni, “Diagnostic and therapeutic approach to hypothalamic amenorrhea,” Ann. N. Y. Acad. Sci., vol. 1092, pp. 103–113, 2006, doi: 10.1196/annals.1365.009. : “No Period. Now What? A book about regaining missing periods.” Accessed: Jan. 07, 2021. [Online]. Available: https://www.noperiodnowwhat.com/. : C. M. Gordon et al., “Functional hypothalamic amenorrhea: An endocrine society clinical practice guideline,” J. Clin. Endocrinol. Metab., vol. 102, no. 5, pp. 1413–1439, May 2017, doi: 10.1210/jc.2017-00131.
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