Hormones and the Heart: A Foundational Perspective
February 28, 2022
In Recognition of National Heart Month
Updated Editorial Note (2026)
This article was originally written in 2022 and remains a strong educational overview of the relationship between hormonal balance and cardiovascular health. While research on hormone therapy continues to evolve, the foundational physiology discussed here remains clinically relevant. The content below has been lightly edited for clarity and flow while preserving the original scientific intent and referenced research.
Hormones: Essential Messengers for Whole-Body Health
Hormones act as chemical messengers that regulate nearly every system in the body — including blood pressure control, metabolism, immune function, stress response, cognitive performance, and cardiovascular health. From a holistic perspective, hormonal balance is essential for maintaining long-term vitality and optimal organ function, particularly as we age.
Hormones are released from one area of the body and communicate signals to tissues and organs elsewhere, functioning much like an orchestra. When this hormonal “orchestra” is in balance, the body operates in harmony. When hormones become depleted or imbalanced — due to aging, chronic stress, environmental exposures, or lifestyle factors — dysfunction can emerge across multiple systems.
While public discussion around hormones often centers on reproductive health, menopause, PMS, or andropause, many other organs are profoundly affected by hormonal balance. One of the most important — and frequently overlooked — is the heart.
The Heart and Hormonal Balance
Growing research continues to explore how inadequate or imbalanced hormone levels may negatively affect cardiovascular health, and how restoring balance may support heart function. Cardiovascular disease rises sharply after menopause and remains the leading cause of death in women, underscoring the importance of understanding the hormonal influences on vascular health.
Estrogens and the Cardiovascular System
Estrogens are commonly associated with female reproductive function, yet they play critical roles in non-reproductive tissues, including the brain and cardiovascular system. Estrogen receptors are present in blood vessels, where they support vascular reactivity, promote healthy vessel dilation, influence lipid metabolism, and exert antithrombotic (clot-preventing) effects.¹
Epidemiologic studies consistently demonstrate lower rates of cardiovascular disease in premenopausal women compared to age-matched men and postmenopausal women — an effect attributed, in part, to differences in estrogen levels.² As estrogen declines after menopause, cardiovascular risk increases significantly.³⁻⁴
Some large hormone replacement therapy (HRT) trials failed to show cardiovascular benefit in postmenopausal women; however, important distinctions exist. Many of these studies relied on orally administered estrogens and synthetic progestins, which can promote pro-coagulant effects and interfere with estrogen’s vascular benefits. In contrast, non-oral (transdermal or percutaneous) estrogen delivery and natural progesterone do not demonstrate these same adverse effects.⁵
Studies using naturally derived estradiol and progesterone delivered transdermally have shown neutral or favorable effects on blood pressure, lipid profiles, and clotting markers — even in women with mild to moderate hypertension.⁶
Progestins vs. Progesterone
Confusion between these two terms is common and clinically significant. Progesterone refers to naturally derived progesterone, whereas progestins are synthetic analogs. Although often grouped together in public discourse, their physiological effects differ markedly.
Research demonstrates that synthetic progestins can disrupt endothelial function, activate platelets, promote clot formation, and contribute to vascular inflammation.⁷⁻⁸ These detrimental effects are not observed with natural progesterone, which does not demonstrate the same impact on blood vessels.
Progesterone also plays an important role in inflammation regulation, serving as a precursor to cortisol — the body’s primary anti-inflammatory hormone. Chronic stress increases cortisol demand, drawing on progesterone reserves in a process commonly referred to as the “progesterone steal.” Over time, this can contribute to hormonal imbalance and increased inflammatory burden, a central driver of cardiovascular disease.⁹
Testosterone, Vitamin D, and Cardiovascular Health
Lower levels of testosterone are associated with increased cardiovascular mortality and are also linked to insulin resistance, metabolic syndrome, and type 2 diabetes — all major cardiovascular risk factors.¹⁰ In men with heart failure, testosterone deficiency is common, with estimates ranging from 26–37%.¹¹
Testosterone plays a vital role in maintaining muscle mass, metabolic efficiency, vascular tone, and anti-inflammatory balance. Heart failure represents a multisystem condition characterized by a shift toward catabolism (tissue breakdown), increased inflammatory cytokine production, loss of muscle mass, and impaired vasodilation. Clinical studies demonstrate that low-dose testosterone therapy can improve functional capacity and heart failure symptoms in men with moderate disease severity.¹²
Vitamin D status is closely linked to testosterone physiology and cardiovascular health. Research shows that vitamin D supplementation can increase total, free, and bioavailable testosterone levels, particularly in individuals with vitamin D insufficiency. Adequate vitamin D levels are also independently associated with improved cardiovascular outcomes, insulin sensitivity, and inflammatory regulation, further reinforcing its importance in heart health.²⁰
Testosterone therapy in women with chronic heart failure has also demonstrated improvements in functional capacity, muscular strength, and markers of insulin resistance without significant adverse effects.¹³
Measuring Hormone Levels and Stress Physiology
This article highlights only a portion of the complex relationship between hormones and cardiovascular health. Hormonal balance extends far beyond reproductive function and plays a central role in vascular integrity, inflammation control, metabolic regulation, and stress adaptation.
Assessing estrogen, progesterone, testosterone, and cortisol levels through salivary or blood spot testing can provide valuable baseline insight. Cortisol, the body’s primary stress hormone, is particularly relevant to cardiovascular health due to its influence on inflammation, blood pressure regulation, glucose metabolism, and vascular tone. Chronic stress and dysregulated cortisol patterns can contribute to hormonal imbalance and increased cardiovascular risk.
For a deeper educational discussion on hormone balance, metabolic health, and cardiovascular aging, readers may also explore additional hormone-focused resources available throughout VitalHealthPharmacist.com.
Susan’s Clinical Perspective — National Heart Month
In recognition of National Heart Month, it’s important to remember that cardiovascular health is never driven by a single hormone, supplement, or intervention. The heart reflects the integrated balance of hormones, inflammation, metabolic health, stress physiology, and lifestyle factors.
For many adults — particularly in midlife — understanding hormonal patterns can provide valuable insight into cardiovascular risk and resilience when approached thoughtfully and individualized appropriately. Education, careful assessment, and collaboration with qualified healthcare professionals remain essential.
Educational Disclaimer
This article is intended for educational purposes only and is not meant to diagnose, treat, or replace medical care. Hormone therapy and cardiovascular risk assessment should always be individualized and managed in collaboration with a qualified healthcare provider.
References
1. Billeci AM, Paciaroni M, Caso V, Agnelli G. Hormone replacement therapy and stroke. Curr Vasc Pharmacol. 2008 Apr;6(2):112-23.
2. Masood DE, Roach EC, Beauregard KG, Khalil RA. Impact of sex hormone metabolism on the vascular effects of menopausal hormone therapy in cardiovascular disease. Curr Drug Metab. 2010 Oct 1;11(8):693-714.
3. Schenck-Gustafsson K, Brincat M, Erel CT, et al. EMAS position statement: Managing the menopause in the context of coronary heart disease. Maturitas. 2011 Jan;68(1):94-7.
4. Ballard VL, Edelberg JM. Harnessing hormonal signaling for cardioprotection. Sci Aging Knowledge Environ. 2005 Dec 21;2005(51):re6.
5. Kuttenn F, Gerson M, de Lignères B. Effects of hormone replacement therapy in menopause on cardiovascular risk. Need for a European study. Presse Med. 2002 Mar 16;31(10):468-75.
6. Spritzer PM, Vitola D, Vilodre LC, Wender MC, Reis FM, Ruschel S, Castro I. One year follow-up of hormone replacement therapy with percutaneous estradiol and low-dose vaginal natural progesterone in women with mild to moderate hypertension. Exp Clin Endocrinol Diabetes. 2003 Aug;111(5):267-73.
7. Thomas T, Rhodin J, Clark L, Garces A. Progestins initiate adverse events of menopausal estrogen therapy. Climacteric. 2003 Dec;6(4):293-301.
8. Sitruk-Ware R. Progestins and cardiovascular risk markers. Steroids. 2000 Oct-Nov;65(10-11):651-8.
9. Bucova M, Bernadic M, Buckingham T. C-reactive protein, cytokines and inflammation in cardiovascular diseases. Bratisl Lek Listy. 2008;109(8):333-40.
10. Yeap BB. Curr Opin Endocrinol Diabetes Obes. 2010 Jun;17(3):269-76. Androgens and cardiovascular disease.
11. Naghi JJ, Philip KJ, Dilibero D, et al. Testosterone Therapy: Treatment of Metabolic Disturbances in Heart Failure. J Cardiovasc Pharmacol Ther. 2010 Nov 19.
12. Malkin CJ, Pugh PJ, West JN, et al. Testosterone therapy in men with moderate severity heart failure: a double-blind randomized placebo controlled trial. Eur Heart J. 2006 Jan;27(1):57-64.
13. Iellamo F, Volterrani M, Caminiti G, et al. Testosterone therapy in women with chronic heart failure: a pilot double-blind, randomized, placebo-controlled study. J Am Coll Cardiol. 2010 Oct 12;56(16):1310-6.
14. Wang C, Mäkelä T, Hase T, et al. Lignans and flavonoids inhibit aromatase enzyme in human preadipocytes. J Steroid Biochem Mol Biol. 1994 Aug;50(3-4):205-12.
15. Prager N, Bickett K, French N, et al. A randomized, double-blind, placebo-controlled trial to determine the effectiveness of botanically derived inhibitors of 5-alpha-reductase in the treatment of androgenetic alopecia. J Altern Complement Med. 2002 Apr;8(2):143-52.
16. Hiipakka RA. Structure-activity relationships for inhibition of human 5alpha-reductases by polyphenols. Biochem Pharmacol. 2002 Mar 15;63(6):1165-76.
17. Schottner M, Gansser D, Spiteller G, et al. Lignans from the roots of Urtica dioica and their metabolites bind to human sex hormone binding globulin (SHBG). Planta Med. 1997;63:529-32.
18. Ang HH, Cheang HS, Yusof AP. Effects of Eurycoma longifolia Jack (Tongkat Ali) on the initiation of sexual performance of inexperienced castrated male rats. Exp Anim. 2000;49:35-8.
19. Ang HH, Ikeda S, Gan EK. Evaluation of the potency activity of aphrodisiac in Eurycoma longifolia Jack. Phytother Res. 2001;15:435-6.
20. Pilz S, Frisch S, Koertke H, et al. Effect of Vitamin D supplementation on testosterone levels in men. Hormone and Metabolic Research. December 10, 2010.