I Eat Healthy… So Why Do I Have High Cholesterol and No Period?

Written By Dani Sheriff

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.

When most of us hear the word “cholesterol,” we immediately think of heart disease, clogged arteries, and warnings to cut back on foods—namely animal products. In the context of hypothalamic amenorrhea (HA), this couldn’t be more misleading. While the mechanisms involved in the regulation of cholesterol are extremely complex, it is clear that cholesterol is not your enemy—it is actually one of the most vital substances in your body, especially when it comes to hormone production and recovery from HA.

What Is Cholesterol and Why Do We Need It?

Cholesterol is a fat-like molecule known as a sterol. It has several critical roles in the body including but not limited to: (1,2)

  • Production of steroid hormones like estrogen, progesterone, and testosterone 

  • Synthesis of vitamin D

  • Building and maintaining the structure of cell membranes 

  • Producing bile acids, which are necessary in the digestion and absorption of fat-soluble vitamins A, D, E, and K 

We get cholesterol from two main sources: dietary intake and synthesis in the liver. Cholesterol is soluble in water, so it travels through your bloodstream in special transport vehicles called lipoproteins. There are two primary lipoproteins that carry cholesterol: (3) 

  • LDL (low-density lipoprotein) delivers cholesterol to your tissues. Too much circulating LDL can lead to buildup in arteries, which is why it’s often labeled as “bad” cholesterol.

  • HDL (high-density lipoprotein) collects excess cholesterol and returns it to the liver for recycling or disposal.3 This is known as your “good” cholesterol.

What Happens to Cholesterol in HA?

In HA, the body is in a state of chronic energy deficiency. Often, women with HA have low energy availability, low fat stores, high activity levels, and elevated stress. We know that all of these conditions disrupt hormone balance. (4) These adaptive hormonal shifts are what can cause cholesterol to rise. Studies show that individuals with HA frequently present with elevated LDL cholesterol and impaired lipid metabolism. (5) This isn’t due to dietary cholesterol intake—in fact, it’s the opposite. When the body is underfed, over-exercised, or both, it shifts into a conservation mode that disrupts key hormonal systems. The result of hormonal and metabolic adaptations to chronic low energy availability contribute to rises in cholesterol. (4,5)

Estrogen and Cholesterol Clearance

Estrogen—specifically estradiol (E2)—is a key regulator of cholesterol metabolism in the liver. Specifically, it upregulates hepatic LDL receptors, which bind LDL particles and remove them from circulation. (7) It also increases HDL levels by stimulating the production of apolipoprotein A-I (apoA-I), a major structural component of HDL particles. HDL then supports reverse cholesterol transport, carrying cholesterol away from arteries and tissues back to the liver for excretion. (7)

When estrogen is low, as in HA, the number of LDL receptors in the liver decreases, and HDL synthesis is impaired. This leads to higher circulating LDL cholesterol and lower HDL cholesterol. (1,6)

Thyroid Hormones and Cholesterol

T3, the active thyroid hormone, plays a complementary role in managing cholesterol metabolism. Like estrogen, it upregulates LDL receptor gene expression, increasing the liver’s ability to remove LDL from the bloodstream. (8) T3 also promotes cholesterol breakdown by stimulation of CYP7A1, the enzyme responsible for converting cholesterol into bile acids, a key route for cholesterol excretion. (8)

In HA, T3 levels are reduced as part of the body’s energy-conserving response (known as "euthyroid sick syndrome "). (11) This further impairs LDL clearance and contributes to elevated cholesterol levels.

Low Dietary Fat Intake and The Connection to HA

In individuals experiencing HA, dietary intake of cholesterol and fats is often significantly reduced.

This reduction can disrupt the body's cholesterol homeostasis. Specifically, when dietary cholesterol intake is low, the liver may compensate by increasing endogenous (internally produced) cholesterol synthesis to maintain necessary levels for vital functions, such as hormone production and cell membrane integrity. (12) This compensatory mechanism is regulated by feedback loops involving enzymes like HMG-CoA reductase, which become more active when dietary cholesterol is scarce. (12,13)

In turn, this may result in elevated endogenous cholesterol production. This, alongside suppressed hormone levels contribute to the unfavorable lipid profiles often seen in HA.

The Bigger Picture: Hormones, Not Fat Intake, Drive Dyslipidemia in HA

HA creates a perfect storm: low estrogen, low T3, high cortisol, and restricted dietary fat. Together, these hormonal shifts can reduce cholesterol clearance, increase LDL production and impair HDL synthesis.

Many females tend to respond to high cholesterol by cutting back even more on fat and cholesterol, but this only makes things worse. Why? Because dietary cholesterol and fats—especially saturated fat from whole foods—are raw materials your body needs to produce hormones like estrogen.

Why the Fear of Cholesterol and Saturated Fat Then? 

For decades, we were told to limit cholesterol and saturated fat in our diets to protect heart health. But newer research has challenged this simplistic view. Recent large-scale reviews and population studies have consistently shown that dietary cholesterol, on its own, is not strongly associated with heart disease in most people. (13-16) What is known however, is that there’s significant individual variation in how people respond to dietary cholesterol. (15) Some people (called “hyper-responders”) experience modest increases in LDL cholesterol when they eat more cholesterol-rich foods. However, most people see little to no change, thanks to the body’s built-in regulatory systems. (16,18)

And if you’re someone dealing with hypothalamic amenorrhea (HA) or low energy availability (LEA), the last thing you want to do is restrict the very foods that support your hormonal recovery.

Whole Foods, Real Recovery

Foods rich in cholesterol and saturated fat—like eggs, meat, full-fat dairy, and butter—are not your enemy. In fact, they’re packed with vital nutrients like fat-soluble vitamins (A, D, E, K), choline and B vitamins (17)—all of which are necessary for reproductive health and HA recovery! These foods do not directly lower LDL cholesterol, but they support the recovery of normal endocrine function, which in turn restores the body’s ability to regulate lipid metabolism effectively. (19) When you start nourishing your body properly again, hormonal signaling improves, and—surprisingly to many—cholesterol levels often normalize as a result.

Bottom Line

In HA, high cholesterol isn’t about dietary excess—it’s about a hormonal system in distress. The solution is not to restrict more, but to restore energy availability, eat nutrient-dense whole foods (including fat and cholesterol), and allow your hormonal and metabolic systems to reset.

It’s not about cutting cholesterol—it’s about healing your body so it can handle cholesterol the way it’s supposed to.

Are You Missing Your Period and Concerned About Your Missing Period?

If you’re navigating high cholesterol alongside a missing period, it’s easy to feel confused about what your body actually needs.

That’s why our 1:1 and group coaching programs are designed to help you interpret your labs in the context of HA recovery, so you’re not left guessing or worrying about results that may actually be part of your body’s adaptive response. At The HA Society, we combine science-based education with individualized guidance to help you restore your cycle while supporting metabolic and hormonal health.

And for practitioners (or aspiring practitioners), our HHAP Certification Program goes deeper into the physiology of HA—including how cholesterol, hormones, and metabolism are all connected—so you can support clients with confidence and clarity.

Keep Reading

References:

  1. Craig, M., Yarrarapu, S. N. S., & Dimri, M. (2023). Biochemistry, cholesterol. In StatPearls. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK513326/

  2. Hundt, M., Basit, H., & John, S. (2022). Physiology, bile secretion. In StatPearls. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK470209/

  3. Feingold, K. R. (2024). Introduction to lipids and lipoproteins. In K. R. Feingold, S. F. Ahmed, B. Anawalt, et al. (Eds.), Endotext. MDText.com, Inc. https://www.ncbi.nlm.nih.gov/books/NBK305896/

  4. Roberts, R. E., Farahani, L., Webber, L., & Jayasena, C. (2020). Current understanding of hypothalamic amenorrhoea. Therapeutic Advances in Endocrinology and Metabolism, 11, 2042018820945854. https://doi.org/10.1177/2042018820945854

  5. Grosman-Rimon, L., Wright, E., Freedman, D., Kachel, E., Hui, S., Epstein, I., Gutterman, D., & Eilat-Adar, S. (2019). Can improvement in hormonal and energy balance reverse cardiovascular risk factors in athletes with amenorrhea? American Journal of Physiology-Heart and Circulatory Physiology, 317(3), H487–H495. https://doi.org/10.1152/ajpheart.00242.2019

  6. Rickenlund, A., Eriksson, M. J., Schenck-Gustafsson, K., & Hirschberg, A. L. (2005). Amenorrhea in female athletes is associated with endothelial dysfunction and unfavorable lipid profile. The Journal of Clinical Endocrinology & Metabolism, 90(3), 1354–1359. https://doi.org/10.1210/jc.2004-1286

  7. Zimodro, J. M., Mucha, M., Berthold, H. K., & Gouni-Berthold, I. (2024). Lipoprotein metabolism, dyslipidemia, and lipid-lowering therapy in women: A comprehensive review. Pharmaceuticals, 17(7), 913. https://doi.org/10.3390/ph17070913

  8. Rizos, C. V., Elisaf, M. S., & Liberopoulos, E. N. (2011). Effects of thyroid dysfunction on lipid profile. The Open Cardiovascular Medicine Journal, 5, 76–84. https://doi.org/10.2174/1874192401105010076

  9. Cox, R. A., & García-Palmieri, M. R. (1990). Cholesterol, triglycerides, and associated lipoproteins. In H. K. Walker, W. D. Hall, & J. W. Hurst (Eds.), Clinical Methods: The History, Physical, and Laboratory Examinations(3rd ed., Chap. 31). Butterworths. https://www.ncbi.nlm.nih.gov/books/NBK351/

  10. Thau, L., Gandhi, J., & Sharma, S. (2023). Physiology, cortisol. In StatPearls. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK538239/

  11. Męczekalski, B., Niwczyk, O., Battipaglia, C., Troia, L., Kostrzak, A., Bala, G., Maciejewska-Jeske, M., Genazzani, A. D., & Luisi, S. (2024). Neuroendocrine disturbances in women with functional hypothalamic amenorrhea: An update and future directions. Endocrine, 84(3), 769–785. https://doi.org/10.1007/s12020-023-03619-w

  12. Goedeke, L., & Fernández-Hernando, C. (2012). Regulation of cholesterol homeostasis. Cellular and Molecular Life Sciences, 69(6), 915–930. https://doi.org/10.1007/s00018-011-0857-5

  13. Lecerf, J.-M., & de Lorgeril, M. (2011). Dietary cholesterol: From physiology to cardiovascular risk. British Journal of Nutrition, 106(1), 6–14. https://doi.org/10.1017/S0007114511000237

  14. Berger, S., Raman, G., Vishwanathan, R., Jacques, P. F., & Johnson, E. J. (2015). Dietary cholesterol and cardiovascular disease: A systematic review and meta-analysis. The American Journal of Clinical Nutrition, 102(2), 276–294. https://doi.org/10.3945/ajcn.114.100305

  15. Griffin, J. D., & Lichtenstein, A. H. (2013). Dietary cholesterol and plasma lipoprotein profiles: Randomized-controlled trials. Current Nutrition Reports, 2(4), 274–282. https://doi.org/10.1007/s13668-013-0064-0

  16. McNamara, D. J. (2013). Cholesterol: Sources, absorption, function, and metabolism. https://www.researchgate.net/publication/369044047_Cholesterol_Sources_absorption_function_and_metabolism

  17. Astrup, A., Magkos, F., Bier, D. M., Brenna, J. T., de Oliveira Otto, M. C., Hill, J. O., King, J. C., Mente, A., Ordovas, J. M., Volek, J. S., Yusuf, S., & Krauss, R. M. (2020). Saturated fats and health: A reassessment and proposal for food-based recommendations: JACC state-of-the-art review. Journal of the American College of Cardiology, 76(7), 844–857. https://doi.org/10.1016/j.jacc.2020.05.077

  18. Carson, J. A. S., Lichtenstein, A. H., Anderson, C. A. M., Appel, L. J., Kris-Etherton, P. M., Meyer, K. A., Petersen, K., Polonsky, T., & Van Horn, L. (2020). Dietary cholesterol and cardiovascular risk: A science advisory from the American Heart Association. Circulation, 141(3), e39–e53. https://doi.org/10.1161/CIR.0000000000000743

  19. Dobranowska, K., Plińska, S., & Dobosz, A. (2024). Dietary and lifestyle management of functional hypothalamic amenorrhea: A comprehensive review. Nutrients, 16(17), 2967. https://doi.org/10.3390/nu16172967

Dani Sheriff
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