Why GI Distress Happens in Hypothalamic Amenorrhea Recovery (And Why It’s Temporary)
Before we dive in, we want to give credit to the author. This was written by Cat, a graduate of our Holistic HA Practitioner (HHAP) Certification Program. Cat brings a deep understanding of the root causes of HA and is passionate about supporting women on the path to recovery through education, empowerment, and holistic strategies.
If you’re recovering from hypothalamic amenorrhea (HA) or working to restore healthy cycles and fertility, you may notice uncomfortable digestive symptoms along the way—painful bloating, constipation, cramping, nausea, excess gas, or a general sense of fullness and sluggishness. These sensations can feel confusing or even triggering, and they often mimic irritable bowel syndrome (IBS). It’s important to know that these symptoms are common, temporary, and physiologically explainable in the context of HA and renourishing (1,6). While uncomfortable, they are signs that your body is recalibrating after a period of metabolic and hormonal downregulation. Think of it like restarting a car engine after months of inactivity—it sputters, shakes, and needs time to run smoothly again. Your digestive system is no different. Understanding what’s happening inside your body can make the discomfort more manageable and help you support your gut as it heals.
Water Retention and Early-Stage Bloating
One of the first, most temporary causes of bloating during recovery is water retention. As your energy intake increases, your body replenishes glycogen, the stored form of glucose in muscle and liver tissue. For every gram of glycogen stored, approximately three grams of water are held with it.(2,3) This process restores cellular hydration and energy reserves but can leave you feeling puffy or distended. As potassium and sodium levels change with the introduction of different nutrients, the fluid balance in your gut begins to shift, further contributing to bloating.(4)
During energy restriction and heightened stress, the gut’s mucosal lining and blood supply can become diminished as cardiac output and nutrients are diverted toward essential organs.(5,7) With refueling and consistent nutrition, energy is available to rebuild the mucosal lining of the gut and expand plasma volume, improving blood flow but also increasing the amount of fluid in the body. Even though these processes are healthy and necessary, they temporarily increase water content in the abdominal area. This is transient; as your body recalibrates, bloating naturally subsides.(8)
Enzyme and Bile Insufficiency
Digestive enzymes and bile acids are essential for breaking down and absorbing nutrients. (9) During HA, low energy availability causes the hypothalamus to suppress nonessential processes to conserve fuel. (10,12) This can include signals to the pancreas, liver, and stomach, reducing enzyme output, bile release, and gastric acid secretion. (10) When you start eating more, your gut is suddenly faced with larger, more varied meals, but its secretory capacity and motility haven’t yet caught up. This mismatch can cause bloating, reflux, cramping, or gas. With consistent, balanced nutrition, pancreatic enzymes, bile production, and gastric secretions gradually return to normal—a process that strengthens with nourishment, much like retraining a dormant muscle.
Microbiome Adaptation: The “Rebloom Effect”
Your gut microbiome—the trillions of bacteria inhabiting your intestines—depends on adequate energy and dietary diversity to thrive. (11,13) During periods of low energy intake, stress, or disordered eating, microbial diversity often declines, especially species that ferment carbohydrates and maintain mucosal integrity. (10,17) A reduction in these microbes can thin the protective mucus layer, increasing gut permeability and low-grade inflammation (14,22) contributing to a wide range of gut discomfort. Additionally, when you reintroduce a wider range of foods—particularly carbohydrates and fiber—the microbiome begins to rebloom. This resurgence is healthy but can temporarily increase gas production, mainly hydrogen and methane, as microbial fermentation restarts. (15,16) Over weeks to months, microbial diversity and short-chain fatty acid production (provide energy for colon cells, contribute to immune health, and strengthen the gut barrier) improve with adequate nutrition and hormonal balance, supporting energy for gut cells and improving digestion. (16,17)
The Vagus Nerve, Cortisol, and the Stress Response
The vagus nerve is the main communication pathway between your brain and gut, orchestrating digestion through the parasympathetic “rest-and-digest” response. (18) It regulates stomach acid secretion, intestinal contractions, enzyme release, and inflammation. During HA, chronic stress and energy deficiency elevate cortisol and activate the sympathetic (“fight-or-flight”) system, which suppresses vagal tone. (7,19)
Low vagal activity contributes to slowed gastric emptying, weakened peristalsis, and decreased digestive secretions, all of which contribute to nausea, bloating, and early fullness. (20,21)
Supporting vagal tone through deep breathing, relaxed meal time environments, light post-meal movement, and slower eating can help activate the parasympathetic system and improve digestion. (18,19)
The Enteric Nervous System: Your “Second Brain”
The enteric nervous system (ENS) regulates digestion through millions of neurons along the GI tract. (20) These neurons release neurotransmitters such as serotonin, acetylcholine, dopamine, and nitric oxide, which coordinate smooth muscle contractions, digestive secretions, and communication with the brain via the vagus nerve. (21)
In HA, reduced nutrient availability, low vagal tone, and decreased energy supply likely slow ENS activity and neurotransmitter production, especially serotonin and acetylcholine. This, along with a lack of mechanical stretch from smaller meals contributes to sluggish peristalsis (20,21) and thus feelings of bloating, fullness, and sometimes constipation.
During refeeding, these pathways gradually reactivate, often producing alternating constipation and loose stools as the ENS recalibrates. (22)
Hormonal Suppression and Sluggish Gut Motility
Hormonal suppression is a hallmark of HA and strongly affects digestion. Normally, estrogen enhances smooth muscle tone, serotonin production, and bile secretion (23,24), while progesterone helps soothe inflammation, coordinate contractions, and supports mucosal repair. (24) Thyroid hormones (T3 and T4) also play an important role as they act as metabolic pacemakers of digestion. In HA, we know that reduced TRH and TSH decrease T3/T4. Suppression of these hormones can slow gut motility, decrease bile flow, and increase gut sensistivity to different foods. Given that hormonal regulation may take a whiole to normalize, the lack thereof, along with the many other contributing factors, contributes to gut discomfort and irregular bowel patterns both during HA and in the early phases of recover. (25- 28)
In Summary
Ironically, it’s when we begin eating enough that digestive symptoms often flare most intensely. As systems suppressed during HA reactivate, they face stimuli they haven’t managed for a while. Like a sore, undertrained muscle, your digestive system must be retrained through consistent nourishment. Discomfort is temporary—it signals that your gut, hormones, and nervous system are relearning how to function in balance.
With restored energy intake, your body gradually rebuilds the mechanisms that support smooth digestion—hormonal signaling, vagal tone, gut motility, and digestive secretions.
Over time, symptoms subside and digestion becomes more rhythmic and reliable. GI distress in HA recovery is a sign of restoration!
The only way to resolve symptoms is to continue doing the thing that triggers them: eating enough, consistently. Each meal signals safety and abundance, retraining your digestive tract to function efficiently. With patience and nourishment, your digestion and overall vitality recover stronger than before.
How to Support Your Gut During Recovery
Eat regularly and consistently – Predictable meals retrain the ENS and vagus nerve to signal digestive enzyme release and peristalsis.
Support vagal activation – Deep breathing, light post-meal walks, meditation, journaling, and quite, calm eating environment can help stimulate parasympathetic tone.
Eat in a calm environment – Avoid stressful or multitasking meals; high cortisol directly impairs motility and digestion.
Reintroduce fiber and variety gradually – Slowly increase dietary diversity to prevent excess gas as your microbiome rebalances.
Be patient and compassionate – GI distress in recovery is a sign of healing. Your body is restoring balance one meal at a time.
Wondering if GI distress is a sign you’re doing something wrong in recovery?
If bloating, constipation, nausea, or digestive discomfort are making you question whether you’re fueling correctly, or tempting you to pull back on food, you’re not alone. GI symptoms are one of the most confusing and emotionally challenging parts of hypothalamic amenorrhea (HA) recovery, especially when hormones, nervous system regulation, and digestion are all recalibrating at once.
That’s why our 1:1 coaching and group coaching programs are designed to help you navigate HA recovery with clarity and confidence, so you’re not guessing, restricting, or trying to “fix” symptoms that are actually part of healing. At The HA Society, we combine science-backed education, individualized support, and a compassionate community to help you restore your cycle while supporting digestion, metabolism, and nervous system health along the way.
And if you’re a practitioner, or hope to become one, who wants to truly understand the physiology behind GI distress in HA recovery, our Holistic Hypothalamic Amenorrhea Practitioner (HHAP) Certification Program dives deep into the gut–brain–hormone connection. You’ll learn how to confidently support clients through digestive symptoms, renourishment, and cycle restoration using evidence-based, whole-person care.
Resources:
Parrish, C. R. (2022, August). The overlap between eating disorders and gastrointestinal disorders. Practical Gastroenterology, 32(224).
Nolte, J., Kirmse, M., de Marées, M., & Platen, P. (2025). Effects of short-term low energy availability on metabolism and performance-related parameters in physically active adults. Nutrients, 17(2), 278. https://doi.org/10.3390/nu17020278
Murray, B., & Rosenbloom, C. (2018). Fundamentals of glycogen metabolism for coaches and athletes. Nutrition Reviews, 76(4), 243–259. https://doi.org/10.1093/nutrit/nuy001
Macafee, D. A., Allison, S. P., & Lobo, D. N. (2005). Some interactions between gastrointestinal function and fluid and electrolyte homeostasis. Current Opinion in Clinical Nutrition and Metabolic Care, 8(2), 197–203. https://doi.org/10.1097/00075197-200503000-00015
Ma, Y., Yang, X., Chatterjee, V., Wu, M. H., & Yuan, S. Y. (2021). The gut–lung axis in systemic inflammation: Role of mesenteric lymph as a conduit. American Journal of Respiratory Cell and Molecular Biology, 64(1), 19–28. https://doi.org/10.1165/rcmb.2020-0196TR
Eating Disorders Charity. (n.d.). The effects of under-eating. https://eating-disorders.org.uk/information/the-effects-of-under-eating/
Granger, D. N., Holm, L., & Kvietys, P. (2015). The gastrointestinal circulation: Physiology and pathophysiology. Comprehensive Physiology, 5(3), 1541–1583. https://doi.org/10.1002/cphy.c150007
Lacy, B. E., Gabbard, S. L., & Crowell, M. D. (2011). Pathophysiology, evaluation, and treatment of bloating: Hope, hype, or hot air? Gastroenterology & Hepatology, 7(11), 729–739.
National Institute of Diabetes and Digestive and Kidney Diseases. (n.d.). Your digestive system & how it works.https://www.niddk.nih.gov/health-information/digestive-diseases/digestive-system-how-it-works
Dhopatkar, N., Keeler, J. L., Mutwalli, H., Whelan, K., Treasure, J., & Himmerich, H. (2023). Gastrointestinal symptoms, gut microbiome, probiotics and prebiotics in anorexia nervosa: A review of mechanistic rationale and clinical evidence. Psychoneuroendocrinology, 147, 105959. https://doi.org/10.1016/j.psyneuen.2022.105959
Rowland, I., Gibson, G., Heinken, A., Scott, K., Swann, J., Thiele, I., & Tuohy, K. (2018). Gut microbiota functions: Metabolism of nutrients and other food components. European Journal of Nutrition, 57(1), 1–24. https://doi.org/10.1007/s00394-017-1445-8
Hackney, A. C., Moore, S. R., & Smith-Ryan, A. (2025). Low energy availability, carbohydrate intake, and relative energy deficiency in sport: The low triiodothyronine hypothesis. International Journal of Sports Physiology and Performance. Advance online publication. https://doi.org/10.1123/ijspp.2025-0073
Randeni, N., Bordiga, M., & Xu, B. (2024). A comprehensive review of the triangular relationship among diet-gut microbiota-inflammation. International Journal of Molecular Sciences, 25(17), 9366. https://doi.org/10.3390/ijms25179366
Mutuyemungu, E., Singh, M., Liu, S., & Rose, D. J. (n.d.). Intestinal gas production by the gut microbiota: A review. Department of Food Science and Technology, University of Nebraska, Lincoln, NE, USA.
Crucillà, S., Caldart, F., Michelon, M., Marasco, G., & Costantino, A. (2024). Functional abdominal bloating and gut microbiota: An update. Microorganisms, 12(8), 1669. https://doi.org/10.3390/microorganisms12081669
Fusco, W., Lorenzo, M. B., Cintoni, M., Porcari, S., Rinninella, E., Kaitsas, F., Lener, E., Mele, M. C., Gasbarrini, A., Collado, M. C., Cammarota, G., & Ianiro, G. (2023). Short-chain fatty-acid-producing bacteria: Key components of the human gut microbiota. Nutrients, 15(9), 2211. https://doi.org/10.3390/nu15092211
Notaristefano, G., Ponziani, F. R., Ranalli, M., Diterlizzi, A., Policriti, M. A., Stella, L., Del Zompo, F., Fianchi, F., Picca, A., Petito, V., Del Chierico, F., Scanu, M., Toto, F., Putignani, L., Marzetti, E., Ferrarese, D., Mele, M. C., Merola, A., Tropea, A., Gasbarrini, A., … Apa, R. (2024). Functional hypothalamic amenorrhea: Gut microbiota composition and the effects of exogenous estrogen administration. American Journal of Physiology-Endocrinology and Metabolism, 326(2), E166–E177. https://doi.org/10.1152/ajpendo.00281.2023
Ma, L., Wang, H. B., & Hashimoto, K. (2025). The vagus nerve: An old but new player in brain-body communication. Brain, Behavior, and Immunity, 124, 28–39. https://doi.org/10.1016/j.bbi.2024.11.023
Mass General Hospital. (n.d.). Vagus nerve and stress regulation. https://www.massgeneral.org/news/article/vagus-nerve
Fleming, M. A., 2nd, Ehsan, L., Moore, S. R., & Levin, D. E. (2020). The enteric nervous system and its emerging role as a therapeutic target. Gastroenterology Research and Practice, 2020, 8024171. https://doi.org/10.1155/2020/8024171
Schneider, K. M., Blank, N., Alvarez, Y., Thum, K., Lundgren, P., Litichevskiy, L., Sleeman, M., Bahnsen, K., Kim, J., Kardo, S., Patel, S., Dohnalová, L., Uhr, G. T., Descamps, H. C., Kircher, S., McSween, A. M., Ardabili, A. R., Nemec, K. M., Jimenez, M. T., Glotfelty, L. G., … Thaiss, C. A. (2023). The enteric nervous system relays psychological stress to intestinal inflammation. Cell, 186(13), 2823–2838.e20. https://doi.org/10.1016/j.cell.2023.05.001
Tarasiuk-Zawadzka, A., & Fichna, J. (2025). Interaction between nutritional factors and the enteric nervous system in inflammatory bowel diseases. The Journal of Nutritional Biochemistry, 144, 109959. https://doi.org/10.1016/j.jnutbio.2025.109959
Nie, X., Xie, R., & Tuo, B. (2018). Effects of estrogen on the gastrointestinal tract. Digestive Diseases and Sciences, 63(3), 583–596. https://doi.org/10.1007/s10620-018-4939-1
Coquoz, A., Regli, D., & Stute, P. (2022). Impact of progesterone on the gastrointestinal tract: A comprehensive literature review. Climacteric, 25(4), 337–361. https://doi.org/10.1080/13697137.2022.2033203
Nachtigall, L. E., & Nachtigall, L. (2019). Menopause and the gastrointestinal system: Our gut feelings. Menopause, 26(5), 459–460. https://doi.org/10.1097/GME.0000000000001316
Ley, D., & Saha, S. (2025). Menopause and gastrointestinal health and disease. Nature Reviews Gastroenterology & Hepatology, 22(8), 556–569. https://doi.org/10.1038/s41575-025-01075-7
Yaylali, O., Kirac, S., Yilmaz, M., Akin, F., Yuksel, D., Demirkan, N., & Akdag, B. (2009). Does hypothyroidism affect gastrointestinal motility? Gastroenterology Research and Practice, 2009, 529802. https://doi.org/10.1155/2009/529802
Xu, G. M., Hu, M. X., Li, S. Y., Ran, X., Zhang, H., & Ding, X. F. (2024). Thyroid disorders and gastrointestinal dysmotility: An old association. Frontiers in Physiology, 15, 1389113. https://doi.org/10.3389/fphys.2024.1389113