High Insulin in Hypothalamic Amenorrhea Recovery, and Why It Can Present Similarly to PCOS
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.
Why HA Can Temporarily Look Like PCOS in Lab Work
After periods of restriction, low energy availability, or disordered eating, many women recovering from hypothalamic amenorrhea (HA) notice unexpected shifts in their metabolism and hormones. Blood tests may reveal higher insulin and androgen levels, prompting some clinicians to question whether polycystic ovary syndrome (PCOS) is involved. While this can happen, in most HA recovery cases, these findings reflect a temporary, adaptive phase rather than true PCOS.
Why Insulin Rises During Recovery
In research examining endocrine and metabolic changes during refeeding in eating disorder recovery (especially anorexia nervosa), (1) scientists often describe a temporary state sometimes referred to as transient rebound hyperinsulinemia; however, this term is more commonly used in neonatal medicine and typically refers to a state of postnatal hyperinsulinemic hypoglycemia. Although most data regarding transient states of elevated insulin come from anorexia studies, the physiological mechanisms likely apply to HA recovery, since both conditions involve prolonged energy deficiency, suppressed insulin secretion, and adaptive metabolic downregulation. (1)
Given that there is little to no direct research on transient rebound hyperinsulinemia in adults recovering from functional hypothalamic amenorrhea, and considering the medical definition of the term, it is perhaps more accurate to describe this as a temporary phase of adaptive hyperinsulinemia—a physiological adjustment that occurs as the body transitions from a catabolic (energy-conserving) to an anabolic (energy-storing) state. (3) During this time, insulin levels rise disproportionately to glucose intake as the pancreas readjusts to higher carbohydrate availability (2,3) and as hepatic and peripheral tissues regain normal insulin sensitivity. This adaptive response is not pathological; rather, it reflects the body’s effort to restore glycogen stores, rebuild lean mass, and reestablish metabolic flexibility after a period of suppression. This doesn’t happen in everyone; it depends on the severity and duration of energy restriction, pre-recovery weight, and the individual’s metabolic state.
The Mechanisms Behind Transient Rebound Hyperinsulinemia
During energy deficiency, insulin levels fall because carbohydrate intake is low and the body prioritizes glucose conservation. When feeding resumes, especially with increased carbohydrate intake, the body must suddenly switch from conservation to storage mode. (1,4) Glycogen stores in the liver and muscle have been depleted, and key enzymes for glycogen synthesis and glucose uptake (such as glycogen synthase and GLUT4 transporters) have been downregulated. (5)
As glucose availability rises again, the pancreas produces an exaggerated insulin response to help shuttle glucose into storage. (1,6) This temporary “overshoot” can appear as hyperinsulinemia and mild insulin resistance, as the body readjusts to fed metabolism. Physiologically, this makes sense—during recovery, the body prioritizes energy storage and restoration rather than maintaining optimal insulin sensitivity.
Visceral Fat and the Liver’s Role
In early weight restoration, fat often redistributes unevenly. The body tends to deposit fat viscerally (around abdominal organs) before it redistributes peripherally. 7 This visceral fat accumulation is an adaptive, temporary phase seen in refeeding and recovery. (1,7)
Visceral fat is metabolically active and releases pro-inflammatory cytokines (such as IL-6 and TNF-α) and non-esterified fatty acids, which can impair insulin receptor signaling in muscle tissue and the liver. (1,2) These factors also alter adipokine secretion—leptin rises with fat restoration, but adiponectin (which improves insulin sensitivity) tends to lag behind. (8)
The liver plays a central role here. As insulin rises, hepatic glucose uptake and glycogen synthesis resume, but temporarily elevated insulin can suppress sex hormone–binding globulin (SHBG) production in the liver. This reduction in SHBG allows more free androgens to circulate—contributing to a PCOS-like hormonal profile even without the presence of true PCOS. (9)
SHBG, Androgens, and the PCOS-Like Pattern
During these early stages of recovery, this transient elevation in insulin can lead to a temporary reduction in hepatic sex hormone–binding globulin (SHBG) synthesis, increasing the proportion of bioavailable androgens in circulation. (10) Concurrently, as gonadotropin- releasing hormone (GnRH) pulsatility resumes, luteinizing hormone (LH) secretion can have a rebound effect. Elevated insulin further amplifies LH-stimulated androgen production by acting synergistically at the ovarian theca cells. (11) This combination of reduced SHBG and enhanced ovarian androgen synthesis can produce a biochemical profile that resembles polycystic ovary syndrome (PCOS)—characterized by higher insulin levels, lower SHBG, increased free androgens, and an elevated LH-to-FSH ratio. However, in the context of HA recovery, these changes are typically adaptive and transient, resolving as metabolic homeostasis, fat distribution, and ovulatory cycles are restored. (14)
The Takeaway
Transient rises in insulin and temporary reductions in insulin sensitivity may occur as the body shifts from a starvation to an anabolic state in HA recovery. This adaptive hyperinsulinemia accompanies glycogen repletion, increased hepatic de novo lipogenesis (allows the body to store excess energy from carbohydrates for later use), and initial visceral fat deposition — processes that help restore energy stores and support reproductive recovery, but that can also lower hepatic SHBG and raise free androgens. Studies of weight restoration and refeeding in eating-disorder cohorts show altered glucose–insulin dynamics after renourishment (12,13) , and clinical reviews describe SHBG falling with weight gain and hormones rebalancing over weeks to months (14,15) , supporting the interpretation that these changes are usually time-limited and reversible with continued adequate nourishment, carbohydrate intake, rest, and restoration of ovulation.
Thus, in the context of early HA recovery, transient hyperinsulinemia should be interpreted as a physiological sign of metabolic readaptation rather than a marker of chronic insulin resistance or PCOS pathology. Clinicians should therefore consider this adaptive pattern when evaluating PCOS-like labs in early HA recovery, while still ruling out chronic metabolic disease when clinically indicated.
IMPORTANT:
This is not medical advice. If you’re unsure whether your symptoms reflect recovery or another condition, seek care from a clinician who understands female endocrine and metabolic health—particularly HA, RED-S, and eating disorder recovery. And, if you have any suspicion that you may have type 2 diabetes or PCOS, it is important to consult a qualified healthcare professional or endocrinologist for appropriate evaluation and testing.
Understanding Your Labs in Recovery
If you’re currently working to restore your missing period and hormones or if you’re a practitioner wanting to better understand these nuanced patterns The HA Society is here to help.
Our 1:1 and group coaching programs guide you through fueling your body, balancing your hormones, and rebuilding trust with food and exercise. With science-backed education, compassionate coaching, and a community that gets it, you don’t have to do this alone.
And if you’re passionate about helping others navigate this same healing journey, check out our Holistic HA Practitioner Certification (HHAP) program. You’ll learn how to interpret labs, support recovery physiology, and help women restore both fertility and confidence, just like our students inside HHAP who are now changing lives with this knowledge.
FREE Lab Guide
When it comes to HA, context matters. Most lab ranges were developed for women who are cycling regularly, so interpreting results through that lens can lead to misdiagnosis or unnecessary worry. That’s why we created our FREE Lab Guide to help you decode what your values really mean. Inside, you’ll find the key labs and optimal ranges for HA, PCOS, and POI side by side, so you can see how your results fit into the bigger picture of recovery.
Want to explore more on the difference between HA and PCOS? Check out my YouTube.
Keep Reading:
What is Hypothalamic Amenorrhea?
Understanding Insulin and Blood Sugar in Functional Hypothalamic Amenorrhea (HA)
What Labs to Request if You Suspect Functional Hypothalamic Amenorrhea (HA)
References:
1. Kim, Y., Hildebrandt, T., & Mayer, L. E. S. (2019). Differential glucose metabolism in weight restored women with anorexia nervosa. Psychoneuroendocrinology, 110, 104404. https://doi.org/10.1016/j.psyneuen.2019.104404
2. Prioletta, A., Muscogiuri, G., Sorice, G. P., Lassandro, A. P., Mezza, T., Policola, C., Salomone, E., Cipolla, C., Della Casa, S., Pontecorvi, A., & Giaccari, A. (2011). In anorexia nervosa, even a small increase in abdominal fat is responsible for the appearance of insulin resistance. Clinical endocrinology, 75(2), 202–206. https://doi.org/10.1111/j.1365-2265.2011.04046.x
3. Levy-Shraga, Y., Ron, I., Enoch-Levy, A., Hemi, R., Kanety, H., Wolf, I., Stein, D., Tirosh, A., Rubinek, T., & Modan-Moses, D. (2025). Catabolic to anabolic transition during nutritional rehabilitation of female adolescents with anorexia nervosa. American journal of physiology. Endocrinology and metabolism, 328(6), E845–E855. https://doi.org/10.1152/ajpendo.00523.2024
4. Charlton, B. T., Forsyth, S., & Clarke, D. C. (2022). Low Energy Availability and Relative Energy Deficiency in Sport: What Coaches Should Know. International Journal of Sports Science & Coaching, 17(2), 445-460. https://doi.org/10.1177/17479541211054458 (Original work published 2022)
5. Rosen, E., Bakshi, N., Watters, A., Rosen, H. R., & Mehler, P. S. (2017). Hepatic Complications of Anorexia Nervosa. Digestive diseases and sciences, 62(11), 2977–2981. https://doi.org/10.1007/s10620-017-4766-9
6. René Klinkby Støving, MECHANISMS IN ENDOCRINOLOGY: Anorexia nervosa and endocrinology: a clinical update, European Journal of Endocrinology, Volume 180, Issue 1, Jan 2019, Pages R9–R27, https://doi.org/10.1530/EJE-18-0596
7. El Ghoch, M., Calugi, S., Lamburghini, S., & Dalle Grave, R. (2014). Anorexia nervosa and body fat distribution: a systematic review. Nutrients, 6(9), 3895–3912. https://doi.org/10.3390/nu6093895
8. Stern, J. H., Rutkowski, J. M., & Scherer, P. E. (2016). Adiponectin, Leptin, and Fatty Acids in the Maintenance of Metabolic Homeostasis through Adipose Tissue Crosstalk. Cell metabolism, 23(5), 770–784. https://doi.org/10.1016/j.cmet.2016.04.011
9. Balogh, Z., Csehely, S., Orosz, M., Bhattoa, H. P., Krasznai, Z. T., Deli, T., & Jakab, A. (2025). Relations of Insulin Resistance, Body Weight, Vitamin D Deficiency, SHBG and Androgen Levels in PCOS Patients. Biomedicines, 13(8), 1803. https://doi.org/10.3390/biomedicines13081803
10. Dinakaran, A., Ar, S., Rajagambeeram, R., Nanda, S. K., & Daniel, M. (2024). SHBG and Insulin resistance - Nexus revisited. Bioinformation, 20(8), 816–821. https://doi.org/10.6026/973206300200816
11. Ding, H., Zhang, J., Zhang, F., Zhang, S., Chen, X., Liang, W., & Xie, Q. (2021). Resistance to the Insulin and Elevated Level of Androgen: A Major Cause of Polycystic Ovary Syndrome. Frontiers in endocrinology, 12, 741764. https://doi.org/10.3389/fendo.2021.741764
12. Hussain, M., Lee, S., & Klibanski, A. (2021). Endocrine changes in anorexia nervosa: Mechanisms and implications for recovery. Frontiers in Endocrinology, 12, 683203. https://doi.org/10.3389/fendo.2021.683203
13. Misra, M., & Klibanski, A. (2014). Endocrine consequences of anorexia nervosa. The Lancet Diabetes & Endocrinology, 2(7), 581–592. https://doi.org/10.1016/S2213-8587(13)70180-3
14. Strokosch, G. R., Friedman, A. J., Wu, S. C., & Kamin, M. (2006). Effects of an oral contraceptive on bone mineral density in adolescent females with anorexia nervosa: A randomized trial. Journal of Adolescent Health, 39(6), 819–827. https://doi.org/10.1016/j.jadohealth.2006.06.013
15. Russell, J. D., Mitchell, A. J., & Wistow, G. (2009). Changes in sex hormone binding globulin and gonadal steroid concentrations during recovery from anorexia nervosa. Clinical Endocrinology, 71(5), 651–658. https://doi.org/10.1111/j.1365-2265.2009.03543.x
