PLMI Blog

Hormones are the body’s master messengers, regulating metabolism, mood, fertility, sleep, and more. Their balance is deeply influenced by daily choices—nutrition, movement, sleep, and stress—that feed back into the endocrine system. These lifestyle factors shape hormonal harmony through interconnected pathways, including metabolism, inflammation, immunity, detoxification, and the gut-brain axis (1).

Nutrition

Nutrition is a robust modulator of hormonal health, providing the structural components and biochemical cofactors necessary for hormone synthesis, activation, signaling, and detoxification. Cholesterol serves as the precursor for all steroid hormones, while healthy fats and amino acids are essential for the formation of sex, thyroid, and peptide hormones, including insulin and growth hormone (2-4). Key micronutrients, including B vitamins, magnesium, zinc, and selenium, act as enzymatic cofactors throughout these processes.

Among macronutrients, dietary fats and proteins play notable roles. Adequate fat intake is critical for steroidogenesis and cell membrane integrity, which influence hormone signaling and receptor function (3). Insufficient dietary fat or extreme caloric restriction can suppress the hypothalamic-pituitary-thyroid (HPT) axis, reducing thyroid hormone (T3) levels and impeding reproductive health (5).

Protein supplies amino acids required for thyroid hormone and neurotransmitter synthesis, while also supporting hepatic detoxification of hormone metabolites and preserving lean body mass—key for hormonal balance. Moreover, protein intake stabilizes glycemic control, reducing insulin fluctuations that can disrupt ovulation, cortisol rhythms, and androgen balance—core mechanisms in PCOS, adrenal dysfunction, and metabolic syndrome (6).

Glycemic regulation is essential for endocrine stability. Diets high in refined carbohydrates and low in fiber promote insulin resistance and systemic inflammation, disrupting critical hormonal feedback loops. Proinflammatory cytokines impede thyroid receptor sensitivity and T4-to-T3 conversion, while also interfering with neurotransmitter signaling and sex hormone metabolism (5).

The gut microbiome is significantly influenced by diet and plays a critical role in modulating hormone metabolism, particularly through the estrobolome, a collection of microbes that regulate estrogen recycling. Dysbiosis can lead to estrogen reabsorption and hormonal excess, whereas a balanced microbiome supports healthy estrogen clearance and metabolic signaling.

Cruciferous vegetables (including broccoli, brussels sprouts, and cauliflower) contain glucosinolates, which are converted into sulforaphane—a potent inducer of the Keap1-Nrf2 pathway. This activation enhances hepatic detoxification, reduces systemic inflammation, and boosts antioxidant defenses (7–8). In postmenopausal women, higher intake of these vegetables has been associated with a more favorable estrogen metabolism profile, specifically an increased urinary ratio of 2-hydroxyestrone to 16α-hydroxyestrone (9).

Liver function is integral to hormone clearance, as it conjugates excess estrogens and thyroid hormones for excretion, a process dependent on adequate intake of amino acids, methyl donors (folate, choline), and antioxidant nutrients. Impaired hepatic detoxification—due to inflammation, toxicant exposure, or nutrient deficiencies—can lead to hormone metabolite accumulation, contributing to symptoms of estrogen dominance.

Nutrition influences hormone signaling through neural and mechanical pathways. Nutrient intake modulates the release of gut-derived hormones, including GLP-1 and GIP, which regulate insulin secretion, satiety, and neuroendocrine feedback (6).

Mitigating Stress

Stress management is pivotal in endocrine regulation, with chronic stress recognized as a significant disruptor of hormonal homeostasis. Central to this process is the hypothalamic–pituitary–adrenal (HPA) axis, which governs the body’s stress response. Under conditions of chronic stress, this system becomes dysregulated, leading to sustained elevations of corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and cortisol—the end-product of glucocorticoid hormone. Prolonged hypercortisolemia disrupts the function of the hypothalamic–pituitary–gonadal (HPG) and hypothalamic–pituitary–thyroid (HPT) axes, altering synthesis, secretion, and bioavailability of key sex and thyroid hormones (10-11).

Prolonged elevations of cortisol suppresses gonadotropin-releasing hormone (GnRH), reducing levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), impairing ovarian and testicular steroidogenesis (12-13). Cortisol disrupts the conversion of thyroxine (T4) to the active triiodothyronine (T3), diminishes thyroid receptor sensitivity, and contributes to autoimmune dysregulation within the thyroid gland—mechanisms that may exacerbate or trigger thyroid conditions (14). Elevated cortisol has also been correlated with reductions in testosterone and reduced libido (15).

Chronic activation of the HPA axis increases intestinal permeability and promotes gut dysbiosis, inducing a cycle of systemic inflammation that feeds back into hormonal disruption, underscoring the role of the gut in perpetuating HPA dysregulation and influencing sex and thyroid hormone metabolism.

Chronic stress activates the amygdala, which sends ongoing threat signals that sustain HPA axis activation. This persistent neurobiological stress response suppresses gonadotropin-releasing hormone (GnRH), reduces reproductive hormone output, and perpetuates adrenal hyperactivity (16). Addressing physiological and psychosocial aspects of stress, therefore, is important to hormonal balance.

Mind-Body Practices

Yoga, meditation, and breathwork have been shown to downregulate sympathetic activity, reduce circulating cortisol, and modulate inflammatory cytokines. These effects are mediated through enhanced parasympathetic tone, increased vagal activation, and improved circadian alignment of the HPA axis. A 2025 systematic review demonstrated that regular yoga practice improved markers of insulin sensitivity and led to favorable shifts in sex and thyroid hormones in populations experiencing PCOS, perimenopausal symptoms, and chronic stress. These outcomes are mediated by neuroendocrine pathways involving increased parasympathetic tone, enhanced vagal activity, and improved circadian alignment of the HPA axis (17).

Movement

Physical activity is a potent regulator of hormonal health, influencing insulin sensitivity, sex hormone balance, adrenal function, and sleep. Consistent, appropriate exercise improves insulin response, reduces inflammation, and boosts brain-derived neurotrophic factor (BDNF), supporting mood, cognition, and stress resilience (18).

Resistance and moderate aerobic training enhance the body’s production of anabolic hormones, including testosterone and growth hormone, supporting libido and metabolic function and promoting ovulatory health and progesterone balance (19–20). Exercise also aids hepatic estrogen metabolism and fecal excretion, helping to manage estrogen dominance.

Movement modulates the hypothalamic-pituitary-adrenal (HPA) axis, promoting adrenal resilience and lowering basal cortisol over time. However, overtraining without adequate nutrition or recovery can suppress GnRH and LH, disrupt sex hormone production, and elevate cortisol, especially in those with low energy reserves, perpetuating hormonal imbalance (21). Therefore, personalized and balanced protocols should be utilized.

Nature

Forest bathing has demonstrated profound effects on hormonal and autonomic regulation; lowering salivary and serum cortisol, urinary catecholamines, and inflammatory markers, supporting HPA axis downregulation, and increased parasympathetic activity for improved autonomic balance.

These shifts foster physiological states that promote rest, repair, and hormone balance. Forest therapy has also been linked to elevated levels of DHEA-S, an adrenal hormone with neuroprotective and immune-modulating effects, and adiponectin, supporting glucose regulation and lipid metabolism (22).

Nature immersion also enhances mood, reduces negative affect, and improves sleep quality—key for optimizing cortisol, growth, and sex hormone balance.

Sleep & Circadian Rhythm

Sleep is a central orchestrator of hormonal balance, while also governing nearly all of the body’s systems. During sleep, the body engages in critical endocrine activities: pulsatile growth hormone secretion peaks, testosterone synthesis increases, and cortisol follows its natural lowest point, before rising in anticipation of waking. The regulation of metabolic hormones, including insulin, leptin, and ghrelin are also recalibrated to maintain glucose homeostasis and appetite control.

Circadian misalignment and disruptions in sleep can dysregulate hormonal processes. Elevated evening cortisol, impaired glucose tolerance, suppressed thyroid function, and altered reproductive hormone secretion are all observed consequences of poor sleep and circadian disruption (23). The circadian clock, governed by the suprachiasmatic nucleus (SCN) in the hypothalamus, interacts intricately with peripheral clocks in organs, including the liver, gut, and adrenal glands. These molecular clocks modulate gene expression and hormonal rhythms over a 24-hour cycle, tightly coupling endocrine function to environmental cues, including light, food intake, and activity.

A recent cross-sectional study of over 250 women with poor sleep quality—measured via the Pittsburgh Sleep Quality Index—was strongly correlated with increased severity of premenstrual syndrome (PMS) symptoms, including emotional lability and fatigue (24). These findings underscore the relationship between restorative sleep and hormone balance.

Botanicals

While not a standalone solution for hormonal imbalance, botanicals exert notable effects on neuroendocrine pathways, with specific compounds modulating enzymatic activity and receptor signaling involved in endocrine regulation—especially when combined with nutrition and lifestyle interventions. A few notable examples include diindolylmethane from cruciferous vegetables, saffron, licorice root, and chromium picolinate.

Diindolylmethane (from cruciferous vegetables) supports Phase I estrogen metabolism by enhancing cytochrome P450-mediated 2-hydroxylation of estradiol, favoring the production of protective 2-hydroxy metabolites over potentially genotoxic forms, such as 4- and 16α-hydroxyestrone (25).

Saffron has demonstrated benefits for sexual function, stress, and mood modulation. Research shows that saffron supplementation enhances sexual arousal and significantly reduces anxiety and depressive symptoms in perimenopausal women. A 2021 meta-analysis of 23 trials further supports saffron’s efficacy in improving mood, via serotonergic, dopaminergic, and glutamatergic modulation, along with anti-inflammatory and antioxidant actions (26–27).

Licorice root extract inhibits 11β-HSD2, regulating cortisol activity and supporting adrenal function in cases of low output or HPA axis dysregulation (28). Licorice also contains phytoestrogenic isoflavonoids, supporting estrogen receptor activity in hypoestrogenic or transitional states such as perimenopause.

Chromium picolinate improves insulin receptor sensitivity and glycemic control, indirectly supporting androgen regulation. This is particularly beneficial in insulin-resistant conditions, including polycystic ovary syndrome (PCOS) and metabolic syndrome, where insulin dysregulation contributes to hormonal imbalance (29).

Toxins & Detoxification Pathways

Environmental toxins—especially xenoestrogens—play a significant role in hormonal disruption. These estrogen-mimicking compounds, found in plastics (BPA, phthalates), pesticides, industrial chemicals (PCBs, dioxins), and personal care products, bind estrogen receptors without adhering to the body’s regulatory feedback systems. Chronic exposure may promote estrogen dominance and increase the risk of hormone-sensitive cancers (30).

Hormonal balance depends not just on estrogen levels, but also on how these hormones are metabolized and cleared. Estrogen detoxification occurs primarily in the liver through two phases. In Phase I, cytochrome P450 enzymes (notably CYP1A1, CYP1A2, and CYP1B1) convert estrogens into metabolites—2-OH (protective), 4-OH, and 16α-OH (often associated with higher genotoxic risk). CYP1B1 overexpression or polymorphisms, often linked to inflammation or toxin exposure, can favor the 4-OH pathway, leading to reactive quinones and oxidative stress (31–32).

In Phase II, these metabolites undergo conjugation via methylation (COMT), glucuronidation, and sulfation, rendering them inactive and excretable. This phase is highly nutrient-dependent, requiring methyl donors (folate, B12, B6), magnesium, and antioxidants including glutathione and selenium. Deficiencies or genetic variants (MTHFR, COMT) can impede this process, reducing clearance and increasing symptom burden (33).

Gut health further influences detoxification. Elevated β-glucuronidase activity—common in dysbiosis—can reverse estrogen conjugation in the gut, leading to reabsorption and prolonged estrogenic exposure. Optimizing detoxification pathways through nutrition, lifestyle, and microbiome support is essential for hormonal balance and reducing long-term estrogenic risk.

Lifestyle Synergy for Hormonal Balance

Hormonal balance emerges from the synergy of daily habits that includes nutrition, movement, stress management, and restorative sleep – all working together to regulate the endocrine system through complex, interwoven pathways that shape overall health.

Join us for this webinar, Understanding Hormonal Imbalances in Women: Symptoms, Health Impacts, and Integrative Approaches, on June 24th from 5-7 PDT, with Jeffrey Bland, PhD, Felice Gersh, MD, and Malisa Carullo, ND, as they provide novel, valuable clinical insights into the key hormones driving women’s health and evidence-based strategies to restore hormonal balance.

References:

1. Pataky MW, Young WF, Nair KS. Hormonal and Metabolic Changes of Aging and the Influence of Lifestyle Modifications. Mayo Clin Proc. 2021 Mar;96(3):788-814. doi: 10.1016/j.mayocp.2020.07.033. PMID: 33673927; PMCID: PMC8020896.
2. Craig M, Yarrarapu SNS, Dimri M. Biochemistry, Cholesterol. [Updated 2023 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK513326/
3. Mumford SL, Chavarro JE, Zhang C, Perkins NJ, Sjaarda LA, Pollack AZ, Schliep KC, Michels KA, Zarek SM, Plowden TC, Radin RG, Messer LC, Frankel RA, Wactawski-Wende J. Dietary fat intake and reproductive hormone concentrations and ovulation in regularly menstruating women. Am J Clin Nutr. 2016 Mar;103(3):868-77. doi: 10.3945/ajcn.115.119321. Epub 2016 Feb 3. PMID: 26843151; PMCID: PMC4763493.
4. Sreekumaran Nair, Kevin R. Short,Hormonal and Signaling Role of Branched-Chain Amino Acids12,The Journal of Nutrition,Volume 135, Issue 6,2005, Pages 1547S-1552S,ISSN 0022-3166,

5. Pałkowska-Goździk E, Lachowicz K, Rosołowska-Huszcz D. Effects of Dietary Protein on Thyroid Axis Activity. 2017 Dec 22;10(1):5. doi: 10.3390/nu10010005. PMID: 29271877; PMCID: PMC5793233.
6. Marks V. How our food affects our hormones. Clin Biochem. 1985 Jun;18(3):149-53. doi: 10.1016/s0009-9120(85)80099-0. PMID: 3888442.
7. Sikorska-Zimny K, Beneduce L. The Metabolism of Glucosinolates by Gut Microbiota. 2021 Aug 10;13(8):2750. doi: 10.3390/nu13082750. PMID: 34444909; PMCID: PMC8401010.
8. Fahey JW, Raphaely M. The Impact of Sulforaphane on Sex-Specific Conditions and Hormone Balance: A Comprehensive Review. Applied Sciences. 2025; 15(2):522. https://doi.org/10.3390/app15020522
9. Fowke JH, Longcope C, Hebert JR. Brassica vegetable consumption shifts estrogen metabolism in healthy postmenopausal women. Cancer Epidemiol Biomarkers Prev. 2000 Aug;9(8):773-9. PMID: 10952093.
10. Herman JP, McKlveen JM, Ghosal S, Kopp B, Wulsin A, Makinson R, Scheimann J, Myers B. Regulation of the Hypothalamic-Pituitary-Adrenocortical Stress Response. Compr Physiol. 2016 Mar 15;6(2):603-21. doi: 10.1002/cphy.c150015. PMID: 27065163; PMCID: PMC4867107.
11. Thau L, Gandhi J, Sharma S. Physiology, Cortisol. [Updated 2023 Aug 28]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK538239/
12. Oakley AE, Breen KM, Clarke IJ, Karsch FJ, Wagenmaker ER, Tilbrook AJ. Cortisol reduces gonadotropin-releasing hormone pulse frequency in follicular phase ewes: influence of ovarian steroids. 2009 Jan;150(1):341-9. doi: 10.1210/en.2008-0587. Epub 2008 Sep 18. PMID: 18801903; PMCID: PMC2630911.
13. Hantsoo L, Jagodnik KM, Novick AM, Baweja R, di Scalea TL, Ozerdem A, McGlade EC, Simeonova DI, Dekel S, Kornfield SL, Nazareth M, Weiss SJ. The role of the hypothalamic-pituitary-adrenal axis in depression across the female reproductive lifecycle: current knowledge and future directions. Front Endocrinol (Lausanne). 2023 Dec 12;14:1295261. doi: 10.3389/fendo.2023.1295261. PMID: 38149098; PMCID: PMC10750128.
14. Fekete C, Lechan RM. Central regulation of hypothalamic-pituitary-thyroid axis under physiological and pathophysiological conditions. Endocr Rev. 2014 Apr;35(2):159-94. doi: 10.1210/er.2013-1087. Epub 2013 Dec 13. PMID: 24423980; PMCID: PMC3963261.
15. Rahardjo HE, Becker AJ, Märker V, Kuczyk MA, Ückert S. Is cortisol an endogenous mediator of erectile dysfunction in the adult male? Transl Androl Urol. 2023 May 31;12(5):684-689. doi: 10.21037/tau-22-566. Epub 2023 Apr 14. PMID: 37305638; PMCID: PMC10251093.
16. McCosh RB, O’Bryne KT, Karsch FJ, Breen KM. Regulation of the gonadotropin-releasing hormone neuron during stress. J Neuroendocrinol. 2022 May;34(5):e13098. doi: 10.1111/jne.13098. Epub 2022 Feb 6. PMID: 35128742; PMCID: PMC9232848.
17. Naragatti, S. (2025, January 29). The role of yoga in balancing hormones: A comprehensive research review. International Journal for Multidisciplinary Research, 7, 1–12.
18. Szuhany KL, Bugatti M, Otto MW. A meta-analytic review of the effects of exercise on brain-derived neurotrophic factor. J Psychiatr Res. 2015 Jan;60:56-64. doi: 10.1016/j.jpsychires.2014.10.003. Epub 2014 Oct 12. PMID: 25455510; PMCID: PMC4314337.
19. Jennifer L. Copeland, Leslie A. Consitt, Mark S. Tremblay, Hormonal Responses to Endurance and Resistance Exercise in Females Aged 19–69 Years, The Journals of Gerontology: Series A, Volume 57, Issue 4, 1 April 2002, Pages B158–B165, https://doi.org/10.1093/gerona/57.4.B158
20. Ennour-Idrissi K, Maunsell E, Diorio C. Effect of physical activity on sex hormones in women: a systematic review and meta-analysis of randomized controlled trials. Breast Cancer Res. 2015 Nov 5;17(1):139. doi: 10.1186/s13058-015-0647-3. PMID: 26541144; PMCID: PMC4635995.
21. Orio F, Muscogiuri G, Ascione A, Marciano F, Volpe A, La Sala G, Savastano S, Colao A, Palomba S. Effects of physical exercise on the female reproductive system. Minerva Endocrinol. 2013 Sep;38(3):305-19. PMID: 24126551.
22. Li Q. Effects of forest environment (Shinrin-yoku/Forest bathing) on health promotion and disease prevention -the Establishment of “Forest Medicine”. Environ Health Prev Med. 2022;27:43. doi: 10.1265/ehpm.22-00160. PMID: 36328581; PMCID: PMC9665958.
23. Gnocchi D, Bruscalupi G. Circadian Rhythms and Hormonal Homeostasis: Pathophysiological Implications. Biology (Basel). 2017 Feb 4;6(1):10. doi: 10.3390/biology6010010. PMID: 28165421; PMCID: PMC5372003.
24. Mighani, S., Taghizadeh Shivyari, F., Razzaghi, A. et al. Association between sleep quality and premenstrual syndrome in young women in a cross-sectional study. Sci Rep 15, 6260 (2025). https://doi.org/10.1038/s41598-025-90581-4
25. Godínez-Martínez E, Santillán R, Sámano R, Chico-Barba G, Tolentino MC, Hernández-Pineda J. Effectiveness of 3,3′-Diindolylmethane Supplements on Favoring the Benign Estrogen Metabolism Pathway and Decreasing Body Fat in Premenopausal Women. Nutr Cancer. 2023;75(2):510-519. doi: 10.1080/01635581.2022.2123535. Epub 2022 Sep 15. PMID: 36111381.
26. Goyal, Aman MBBSa; Raza, Fatima Ali MBBSc; Sulaiman, Samia Aziz MDf; Shahzad, Abeer MBBSd; Aaqil, Syeda Ilsa MBBSe; Iqbal, Mahrukh MBBSc; Javed, Binish MBBSb; Pokhrel, Prakriti MBBSg. Saffron extract as an emerging novel therapeutic option in reproduction and sexual health: recent advances and future prospectives. Annals of Medicine & Surgery 86(5):p 2856-2865, May 2024. | DOI: 10.1097/MS9.0000000000002013
27. Lopresti AL, Smith SJ. The Effects of a Saffron Extract (affron®) on Menopausal Symptoms in Women during Perimenopause: A Randomised, Double-Blind, Placebo-Controlled Study. J Menopausal Med. 2021 Aug;27(2):66-78. doi: 10.6118/jmm.21002. PMID: 34463070; PMCID: PMC8408316.
28. Whorwood CB, Sheppard MC, Stewart PM. Licorice inhibits 11 beta-hydroxysteroid dehydrogenase messenger ribonucleic acid levels and potentiates glucocorticoid hormone action. 1993 Jun;132(6):2287-92. doi: 10.1210/endo.132.6.8504732. PMID: 8504732.
29. Havel PJ. A scientific review: the role of chromium in insulin resistance. Diabetes Educ. 2004;Suppl:2-14. PMID: 15208835.
30. Diamanti-Kandarakis E, Bourguignon JP, Giudice LC, Hauser R, Prins GS, Soto AM, Zoeller RT, Gore AC. Endocrine-disrupting chemicals: an Endocrine Society scientific statement. Endocr Rev. 2009 Jun;30(4):293-342. doi: 10.1210/er.2009-0002. PMID: 19502515; PMCID: PMC2726844.
31. Hu S, Ding Q, Zhang W, Kang M, Ma J, Zhao L. Gut microbial beta-glucuronidase: a vital regulator in female estrogen metabolism. Gut Microbes. 2023 Jan-Dec;15(1):2236749. doi: 10.1080/19490976.2023.2236749. PMID: 37559394; PMCID: PMC10416750.
32. Miao S, Yang F, Wang Y, Shao C, Zava DT, Ding Q, Shi YE. 4-Hydroxy estrogen metabolite, causing genomic instability by attenuating the function of spindle-assembly checkpoint, can serve as a biomarker for breast cancer. Am J Transl Res. 2019 Aug 15;11(8):4992-5007. PMID: 31497216; PMCID: PMC6731443.
33. Lavigne JA, Goodman JE, Fonong T, Odwin S, He P, Roberts DW, Yager JD. The effects of catechol-O-methyltransferase inhibition on estrogen metabolite and oxidative DNA damage levels in estradiol-treated MCF-7 cells. Cancer Res. 2001 Oct 15;61(20):7488-94. PMID: 11606384.