- Functional hypothalamic amenorrhea is common in both eating disorders and athletes.
- Consequences of FHA are reduced motivation to eat, increased anxiety, and depression.
- By increasing risk factors for an eating disorder, FHA makes an individual more vulnerable to developing an eating disorder.
- Not all eating disorders start with body shape and weight concerns.
We often think of eating disorders (EDs) as consequences of body dissatisfaction. The trope is that young women begin dieting to achieve an idealized body size and shape based on western culture preferences.
What's not discussed enough, though, is how reproductive dysfunctions, often brought on by intense athletic training, can increase ED susceptibility.
Relationships between intense athletic training, reproduction, and ED risk are important to consider because we often think of athletes as models of good health. Consequently, if an athlete isn't showing the typical signs of an ED (i.e., worrying about body shape) we might overlook signs that she is developing an ED.
Also, people who don’t meet clinical criteria for an ED diagnosis can still develop reproductive dysfunctions and, consequently, are at risk for developing an ED.
Functional Hypothalamic Amenorrhea
One reproductive disorder common in athletes is functional hypothalamic amenorrhea (FHA).
FHA is a condition where an individual capable of menstruation experiences consecutive missed menses due to dysfunction in her brain’s reproductive circuit, the hypothalamic-pituitary-ovarian axis, or HPOA.2
The diagnosis of FHA rules out other causes of missed menses—pregnancy, late puberty, disease, or anatomical abnormalities. Rather, common causes for FHA are stress, weight loss, nutritional deficits, and excessive exercise, all of which could be normalized in intense athletic training.
How Does Menstruation Happen?
To understand how FHA increases ED risk, we first need to understand how the female reproductive system works.
All people with a healthy ovarian cycle have an overseer of reproduction in their brains called the gonad-releasing hormone (GnRH) pulse generator.3 This overseer of reproduction makes sure that hormones get released in the right quantities at the right times for egg release.
While the exact nature of this pulse generator remains a mystery, scientists think that it might be made up of cells called kisspeptin neurons.
When it's time for egg release during the ovarian cycle, kisspeptin neurons release kisspeptin, a chemical that starts a chain of events leading to egg release.
Kisspeptin neurons are smart in that they won’t initiate egg release unless they know that the body has enough energy to support its reproductive needs.4 Consequently, a body low in available energy runs the risk of terminating egg release. This has an evolutionary component in that, if food were scarce, it wouldn't be wise for a woman to get pregnant.5
Leptin and Kisspeptin: Working Together
How do kisspeptin neurons sense that the body has enough energy to support reproductive functions? Scientists think that these neurons join forces with leptin, the body's satiety chemical.6
In addition to making people feel full, leptin has another job regulating puberty and reproduction by informing kisspeptin neurons when the body has enough energy to support egg release.7
Consequently, low leptin levels (low energy availability) means no egg release.8
Common behaviors in athletic training, such as food restriction and excessive exercise, decrease leptin levels. It's been demonstrated that elite athletes who are amenorrheic (missing their periods) have significantly lower leptin levels than athletes who menstruate.7
Following this logic would mean that if leptin regulates kisspeptin, then kisspeptin levels should also be low in elite athletes.
While this makes sense, we need more evidence, as few studies have looked at these relationships. What we do know is that, in people with anorexia, high levels of physical activity are associated with low levels of kisspeptin.1 In animal research it's been demonstrated that rodents who swim excessively have lower kisspeptin levels compared to non-swimming rodents.9
How Does FHA Increase Eating Disorder Risk?
Besides overseeing reproduction, kisspeptin also plays a role in regulating food intake. Specifically, low kisspeptin levels might make people less motivated to eat. This was demonstrated in a rodent model of anorexia, where an injection of kisspeptin increased food intake in rats who otherwise voluntarily neglected eating.10
How kisspeptin increases eating motivation isn't clear, though. One possibility is that it elevates neuropeptide Y, a brain chemical involved in eating motivation. Therefore, restoring reproductive function in people with FHA might increase their food intake via increases in kisspeptin.11
Regardless of the exact mechanism through which kisspeptin regulates feeding behavior, the takeaway is that energy deficiency, whether through food restriction or excessive exercise, decreases a person's desire to eat by preventing kisspeptin release through reproductive impairment.
There are additional ways that FHA increases an individual's vulnerability to developing an ED, such as emotion regulation.12
Though evidence is slightly mixed, it’s been demonstrated that high levels of kisspeptin reduce anxiety and improve mood. Similarly, low levels of kisspeptin are associated with anxiety and depression. Both anxiety13 and depression14 are common risk factors for ED development.
Therefore, excessive athletic training might increase an individual's susceptibility to developing an ED by making her more anxious or depressed, while reducing her motivation to eat. This, coupled with the stressful and competitive nature of athletics, might be enough to push someone towards an ED.
There are few, if any, definitive causes for an ED. Therefore, it's important to consider all possibilities that increase an individual's risk for developing one. While intense athletic training won't directly cause disordered eating, it can change an individual's biology in ways that elevate her vulnerability to developing one. Consequently, it's important to monitor athletes for ED risk beyond the obvious body shape concerns.
1) Hofmann, T., Elbelt, U., Hass, V., Ahnis, A., Klapp, B., Rose, M., & Stengel, A. (2017). Plasma kisspeptin and ghrelin levels are independently correlated with physical activity in patients with anorexia nervosa. Appetite, 108, 141-150.
2) Gibson, M., Fleming, N., Zuijdwijk, C., & Dumont, T. (2020). Where have the periods gone? The evaluation and management of functional hypothalamic amenorrhea. Journal of Clinical Research in Pediatric Endocrinology, 12, 18-17.
3) Herbison, A. (2018). The gonadotropin-releasing hormone pulse generator. Endocrinology, 159, 3723-3736.
4) Lambrou, G., & Flora, B. (2020). Kisspeptin and the “special relationship” between reproduction and metabolism: A computational approach. Medicinal Chemistry, 16, 796-811.
5) Fontana, R., & Torre, S. (2016). The deep correlation between energy metabolism and reproduction: A view on the effects of nutrition for women fertility. Nutrients, 8, 87.
6) Sanchez-Garrido, M., & Tena-Sempere, M. (2013). Metabolic control of puberty: Roles of leptin and kisspeptins. Hormones and Behavior, 64, 187-194.
7) Thong, F., McLean, C., & Graham, T. (2000). Plasma leptin in female athletes: Relationship with body fat, reproductive, nutritional, and endocrine factors. Journal of Applied Physiology, 88.
8) Chou, S., Chamberland, J., Liu, X., Matarese, G., Gao, C., Stefanakis, R.,…& Mantzoros, C. (2011). Leptin is an effective treatment for hypothalamic amenorrhea. Proceedings of the Natural Academy of the Sciences, 108.
9) Arisha, A., & Moustafa, A. (2019). Potential inhibitory effect of swimming exercise on the kisspeptin-GnRH signaling pathway in male rats. Theriogenology, 133, 87-96.
10) Skowron, K., Jasinski, K., Kurnik-Lucka, M., Stach, P., Kalita, K., Weglarz, W., & Gil, K. (2020). Hypothalamic and brain stem neurochemical profile in anorectic rats after peripheral administration of kisspeptin-10 using 1H-nmr spectroscopy in vivo. NMR in Biomedicine, 33, 1-10.
11) Fu, L., & van den Pol, A. (2010). Kisspeptin directly excites anorexigenic proopiopmelanocortin neurons but inhibits orexigenic neuropeptide Y cells by an indirect synaptic mechanism. The Journal of Neuroscience, 30, 10205-10219.
12) Comninos, A., & Dhillo, W. (2018). Emerging roles of kisspeptin in sexual and emotional brain processing. Neuroendocrinology, 106.
13) Forrest, L., Sarfan, L., Ortiz, S., Brown, T., & Smith, A. (2019). Bridging eating disorder symptoms and trait anxiety in patients with eating disorders: A network approach. International Journal of Eating Disorders, 52, 701-711.
14) Silberg, J., & Bulik, C. (2005). The developmental association between eating disorders symptoms and symptoms of depression and anxiety in juvenile twin girls. The Journal of Child Psychology and Psychiatry, 46, 1317-1326.