Hormone Health and Cardiovascular Risk: What You Need to Know

When people think about hormones, they often think about energy, mood, sleep, libido, body composition, or the menopause transition.

Cardiovascular health is rarely the first association—but it should be part of the conversation.

Estrogen, testosterone, thyroid hormones, insulin, and the body’s stress-response systems all interact with the heart, blood vessels, metabolism, and body composition. They can influence cholesterol, blood pressure, glucose regulation, vascular function, heart rhythm, inflammation, and where the body stores fat.

That does not mean every cardiovascular problem is caused by a hormone imbalance—or that adjusting a hormone level will necessarily reduce cardiovascular risk. Hormones may be a cause, a contributor, a consequence, or simply a marker of a larger metabolic process.

The distinction matters.

A laboratory value should never replace a comprehensive risk assessment. It should help make that assessment more complete.

This guide explains how hormone health and cardiovascular risk intersect, what current research does and does not establish, how hormone therapy fits into the picture, and what a rigorous, physician-led evaluation should consider.

The Central Principle: Hormones Influence Cardiovascular Risk, but They Do Not Define It

Cardiovascular disease develops through the interaction of many factors over time. These include blood pressure, cholesterol and other atherogenic particles, blood glucose, insulin resistance, smoking, kidney function, inflammation, sleep, physical activity, body composition, family history, age, and genetics.

Hormonal changes can affect several of these pathways simultaneously. The menopause transition, for example, may coincide with changes in LDL cholesterol, visceral fat, insulin sensitivity, and vascular function. Thyroid dysfunction can alter cholesterol and heart rhythm. Testosterone deficiency may coexist with obesity and metabolic disease.

The mistake is to reduce this complexity to a single number.

The more useful question is not: “Is this hormone high or low?”

It is: “What does this result mean within the context of this person’s symptoms, physiology, cardiovascular risk, and long-term health?”

That is the foundation of evidence-based hormone optimization—and of the Metriq Health approach.

How Hormones Influence Cardiovascular Health

Estrogen and the Menopause Transition

Estrogen has important effects throughout the body, including effects on blood-vessel function, lipid metabolism, glucose regulation, and the distribution of body fat.

During the menopause transition, declining ovarian function is accompanied by changes that may include:

• Rising LDL cholesterol
• Increased visceral or abdominal fat
• Greater insulin resistance
• Changes in blood pressure
• Loss of lean mass
• Vascular remodeling
• Changes in sleep and physical activity that may further affect risk

These changes are not identical for every woman, and they cannot all be attributed to estrogen alone. Aging, genetics, lifestyle, medications, and existing health conditions also matter. However, the American Heart Association identifies the menopause transition as an important period of cardiometabolic vulnerability and an opportunity for earlier prevention.[1]

The timing of menopause also provides useful clinical information. Premature menopause and earlier-than-average menopause are associated with greater subsequent cardiovascular risk. A woman’s reproductive history—including premature menopause, pregnancy-related hypertension, preeclampsia, and gestational diabetes—therefore belongs in a complete cardiovascular history.[1,13]

Menopause should not be viewed as a disease. It should be recognized as a biologically important transition during which cardiovascular risk factors may change—and should be reassessed rather than assumed to be unchanged.

Testosterone in Men

Testosterone is connected to muscle mass, fat distribution, sexual function, bone health, red-blood-cell production, and aspects of glucose metabolism.

Low testosterone is frequently found alongside obesity, type 2 diabetes, sleep apnea, chronic illness, and metabolic syndrome. The relationship can be bidirectional: metabolic dysfunction and excess visceral fat may suppress testosterone, while clinically significant testosterone deficiency may contribute to unfavorable changes in body composition and physical function.

However, an association between low testosterone and cardiovascular disease does not prove that low testosterone directly caused the cardiovascular risk—or that testosterone therapy will prevent a heart attack.

That distinction is essential.

The TRAVERSE trial evaluated more than 5,000 men with symptoms of hypogonadism, two testosterone measurements below 300 ng/dL, and established or elevated cardiovascular risk. Testosterone therapy was not inferior to placebo for the trial’s primary composite of cardiovascular death, nonfatal heart attack, or nonfatal stroke. However, atrial fibrillation, acute kidney injury, and pulmonary embolism occurred more often in the testosterone group.[5]

The responsible conclusion is not that testosterone is universally dangerous—or universally protective.

It is that testosterone therapy may be reasonable for appropriately selected men with confirmed, symptomatic testosterone deficiency, but it should not be prescribed as a cardiovascular-prevention strategy. Diagnosis, dosing, contraindications, cardiovascular risk, fertility goals, hematocrit, symptoms, treatment response, and adverse effects must all be considered and monitored.[5,12]

Thyroid Hormones

Thyroid hormones have direct and indirect effects on the cardiovascular system.

An underactive thyroid may contribute to:

• Higher LDL cholesterol
• Higher triglycerides
• Increased vascular resistance
• Changes in diastolic blood pressure
• Fatigue and reduced exercise tolerance
• A slower heart rate in more pronounced cases

An overactive thyroid may contribute to:

• A rapid heart rate
• Palpitations
• Atrial fibrillation or other rhythm disturbances
• Increased cardiac workload
• Changes in blood pressure
• Unexplained weight loss or exercise intolerance

Subclinical thyroid abnormalities are more nuanced. A laboratory result only slightly outside the reference range does not automatically require treatment, and the risks and benefits of intervention may differ by age, symptoms, cardiovascular history, and degree of abnormality.

The goal is not merely to normalize a thyroid marker. It is to determine whether thyroid dysfunction is clinically meaningful and whether it may be affecting cardiovascular or metabolic health.[6]

Insulin and Metabolic Health

Insulin is a hormone, and insulin resistance is one of the most consequential links between hormonal, metabolic, and cardiovascular health.

When tissues become less responsive to insulin, the body often compensates by producing more of it. Over time, insulin resistance may coexist with:

• Elevated glucose
• Type 2 diabetes
• High triglycerides
• Low HDL cholesterol
• Increased visceral fat
• Elevated blood pressure
• Fatty liver disease
• Chronic kidney disease
• A more atherogenic cardiovascular-risk profile

This is why cardiometabolic evaluation should extend beyond whether fasting glucose falls inside a laboratory reference range.

Fasting glucose, hemoglobin A1c, blood pressure, lipids, waist circumference or body composition, kidney function, family history, and—when clinically useful—additional metabolic markers can reveal risk that a single measurement may miss.

Patients with diabetes benefit substantially from comprehensive management of cardiovascular risk factors rather than focusing on glucose alone.[7]

Cortisol, Chronic Stress, and the Cardiovascular System

The body’s stress response involves cortisol, the autonomic nervous system, immune signaling, blood pressure, and vascular function. Chronic or recurring psychological stress has been associated with greater cardiovascular risk, although the pathways are complex and individual responses vary.[8]

True disorders of cortisol excess, such as Cushing syndrome, can contribute to hypertension, insulin resistance, diabetes, visceral fat accumulation, and cardiovascular disease.

That is different from everyday psychological stress.

A single random cortisol level—or an unvalidated commercial “adrenal” panel—does not reliably measure a person’s chronic stress burden. Cortisol testing should be ordered when the history and clinical findings raise a legitimate endocrine question, not simply because someone feels tired or overwhelmed. Random serum cortisol is not an appropriate screening test for Cushing syndrome.[14]

Stress still deserves attention. It can affect sleep, nutrition, blood pressure, alcohol use, physical activity, medication adherence, and other health behaviors. But stress management should not be reduced to chasing a cortisol number.

Menopause Hormone Therapy and Cardiovascular Risk: Why the Details Matter

Few areas of medicine have generated more confusion than the relationship between menopausal hormone therapy and cardiovascular health.

The evidence does not support a simple declaration that hormone therapy is either “good for the heart” or “bad for the heart.”

The more accurate questions are:

• Why is hormone therapy being considered?
• How old is the patient?
• How long has it been since menopause began?
• What is her cardiovascular and thrombotic risk?
• Which hormone is being used?
• At what dose?
• Through which route?
• Is endometrial protection required?
• What other medical conditions are present?

What Menopausal Hormone Therapy Is Proven to Do

Systemic menopausal hormone therapy remains the most effective treatment for bothersome vasomotor symptoms such as hot flashes and night sweats. It can also help prevent bone loss and fractures while treatment continues.[2]

Local vaginal estrogen is used primarily for genitourinary symptoms such as vaginal dryness, discomfort, painful intercourse, and certain urinary symptoms, with substantially lower systemic exposure than systemic therapy.[2]

For women who have a uterus, adequate progestogen is generally required with systemic estrogen to protect the endometrium.

The benefits and risks differ according to the type, dose, route, duration, timing of initiation, and whether a progestogen is used.[2]

What Hormone Therapy Is Not

Menopausal hormone therapy should not be prescribed solely to prevent cardiovascular disease.

For a healthy, symptomatic woman who is younger than 60 or within approximately 10 years of menopause onset—and who does not have a contraindication—the overall benefit-risk profile is often more favorable than it is for a woman initiating systemic therapy at an older age or much later after menopause.[2]

That does not mean early hormone therapy has been proven to prevent heart attacks. It means that absolute cardiovascular and thrombotic risks are generally lower in younger, recently menopausal women than in older women with more established vascular disease.[2]

What the “Timing Hypothesis” Actually Means

The timing hypothesis proposes that the cardiovascular effects of estrogen may differ depending on the condition of the vascular system when therapy begins.

In the ELITE randomized trial, oral estradiol was associated with slower progression of carotid-artery intima-media thickness among women who began treatment within six years of menopause, but not among women who were at least 10 years beyond menopause. Coronary CT measures did not significantly differ between treatment and placebo groups.[3]

The study supports the biological plausibility that timing matters. It does not establish hormone therapy as a treatment to prevent clinical cardiovascular events.

Route and Formulation Matter

Oral and transdermal estrogen are not metabolically identical.

Oral estrogen undergoes first-pass processing through the liver and can affect coagulation proteins, triglycerides, and inflammatory markers differently from estrogen delivered through the skin. Observational evidence suggests that transdermal estrogen may be associated with a lower risk of venous thromboembolism than oral estrogen, although definitive head-to-head randomized outcome data remain limited.[2]

The type of progestogen may also influence metabolic and vascular effects. However, claims that one formulation is universally “safe” or “natural” should be avoided. Every medication has potential benefits, limitations, and risks.

“Bioidentical” describes a molecule’s chemical structure; it does not establish the quality or safety of a product. FDA-approved estradiol and micronized progesterone are bioidentical hormones manufactured under regulated quality standards. Custom-compounded hormone products generally lack the same level of testing for potency, purity, safety, and clinical outcomes.[2]

The FDA’s 2026 Menopausal Hormone-Therapy Labeling Update

In February 2026, the FDA approved labeling changes for an initial six menopausal hormone-therapy products. Risk statements concerning cardiovascular disease, breast cancer, and probable dementia were removed from the boxed warning for those products to provide more specific and contemporary risk communication.[4]

This did not mean that every risk disappeared or that hormone therapy became appropriate for everyone. Relevant cardiovascular and breast-risk information continues to be addressed elsewhere in systemic-product labeling, and treatment decisions still require individualized clinical assessment.[4]

The labeling changes are best understood as a move away from applying the same generalized warning to every woman, every age, every formulation, and every route of therapy—not as permission to prescribe without careful evaluation.

A Whole-Person, Evidence-Based Lens

Hormonal, metabolic, cardiovascular, and behavioral health are interconnected.

Evaluating them together can reveal patterns that would remain hidden if each marker were considered separately.

But a whole-person approach should increase scientific discipline—not lower the evidence bar.

At Metriq Health, our objective is not to diagnose every symptom as hormonal or to order the largest possible laboratory panel. It is to ask better questions:

• Which symptoms are most specific and clinically meaningful?
• Which risk factors are modifiable?
• Is a hormonal abnormality a cause, consequence, or marker?
• Are there alternative explanations?
• What testing will change the clinical decision?
• What intervention has credible evidence of benefit?
• How will effectiveness and safety be monitored?

The goal is not to optimize every number.

It is to optimize the quality of the decision.

What a Comprehensive Hormone and Cardiovascular Evaluation Considers

The appropriate evaluation varies by patient, but it may include the following:

Medical and Reproductive History

• Personal and family history of cardiovascular disease
• Age at menopause
• Premature or early menopause
• Pregnancy-related hypertension or preeclampsia
• Gestational diabetes
• Prior blood clots, stroke, or heart disease
• Smoking and alcohol use
• Sleep quality and possible sleep apnea
• Physical activity and exercise capacity
• Nutrition and weight history
• Current medications and supplements
• Cancer history
• Symptoms and goals
• Fertility considerations where relevant

Core Cardiovascular and Metabolic Assessment

• Blood pressure
• Standard lipid profile
• Fasting glucose and hemoglobin A1c
• Kidney and liver function
• Body weight, waist circumference, or body-composition assessment
• Evaluation of smoking, sleep, movement, and nutrition
• A validated cardiovascular-risk estimate when applicable

Additional Risk Markers When Clinically Appropriate

Depending on age, history, and the clinical question, additional evaluation may include:

• Lipoprotein(a), or Lp(a): A largely inherited cardiovascular-risk factor that the 2026 ACC/AHA dyslipidemia guideline recommends measuring at least once in adulthood
• Apolipoprotein B, or ApoB: A measure of the number of atherogenic lipoprotein particles, which may add useful information in diabetes, high triglycerides, obesity, or cardiometabolic disease
• High-sensitivity C-reactive protein: A nonspecific marker that may assist risk assessment in selected cases but should not be interpreted as a stand-alone diagnosis
• Urine albumin-to-creatinine ratio: An important marker of kidney and vascular risk in appropriate patients
• Coronary artery calcium scoring: A low-radiation CT study that may help refine risk when a preventive-treatment decision remains uncertain

The 2026 multisociety dyslipidemia guideline emphasizes a more individualized approach to atherogenic lipoproteins, including selective ApoB testing, at least one lifetime Lp(a) measurement, and broader use of coronary calcium scoring when it can meaningfully change management.[9]

Hormonal Testing Guided by a Clinical Question

Hormonal evaluation may include thyroid testing and, depending on age, sex, symptoms, menstrual status, medical history, and treatment, selected sex-hormone measurements.

Not every person needs every hormone tested.

For example:

• Menopause and perimenopause are often clinical diagnoses; fluctuating FSH or estradiol measurements may not provide a definitive answer during the transition.
• Testosterone deficiency in men should be diagnosed using compatible symptoms and consistently low, properly timed measurements—not one isolated result.[12]
• Thyroid testing is useful when symptoms, medications, history, or cardiovascular findings suggest thyroid dysfunction.
• Cortisol testing should be reserved for patients whose history and clinical findings raise a legitimate concern about a disorder of cortisol production. Random serum cortisol should not be used as a general screening test.[14]

Testing is most valuable when the result will change what happens next.

Five Actions That Support Hormonal and Cardiovascular Health Together

1. Know the Cardiovascular Numbers That Matter

Do not allow an extensive hormone panel to distract from blood pressure, atherogenic cholesterol, glucose regulation, kidney function, smoking status, and family history.

Ask whether Lp(a), ApoB, or coronary calcium scoring would add useful information in your particular case.[9]

2. Treat Midlife as a Prevention Window

The menopause transition and age-related changes in men are opportunities to reassess risk before disease becomes symptomatic.

A meaningful change in weight, waist circumference, blood pressure, lipids, glucose, exercise capacity, sleep, or sexual function deserves thoughtful evaluation—not automatic attribution to aging.

3. Use Hormone Therapy for a Clear Indication

Hormone therapy should have a defined clinical purpose, such as treating significant menopausal symptoms or confirmed, symptomatic testosterone deficiency.[2,12]

It should not substitute for established treatment of hypertension, dyslipidemia, diabetes, sleep apnea, smoking, or known cardiovascular disease. Menopausal hormone therapy and testosterone therapy should not be prescribed solely as strategies to prevent cardiovascular disease.[2,5,12]

4. Build the Physiological Foundation

Depending on the individual’s health and physical abilities, this generally means:

• Regular aerobic activity
• Resistance training to preserve strength and lean mass
• A dietary pattern rich in vegetables, fruit, legumes, whole grains, nuts, healthy fats, and appropriate protein
• Adequate sleep and evaluation of possible sleep apnea
• Avoidance of tobacco
• Thoughtful alcohol intake
• Management of blood pressure, lipids, diabetes, and obesity when present
• Strategies that reduce chronic psychological stress and improve recovery

These are not generic add-ons to hormone care. They are among the most powerful tools available for improving cardiovascular and metabolic health.[10,11]

5. Monitor Outcomes—Not Just Laboratory Targets

After beginning hormone therapy, follow-up should consider:

• Whether the original symptoms improved
• Whether the dose remains appropriate
• Blood pressure and relevant metabolic markers
• Hematocrit in men receiving testosterone
• Bleeding patterns in women receiving menopausal hormone therapy
• Medication side effects
• New cardiovascular or thrombotic symptoms
• Whether the treatment remains necessary and aligned with the patient’s goals

Monitoring should be individualized according to the therapy, dose, symptoms, treatment response, medical history, risk profile, adverse effects, and the patient’s goals.[2,12]

A laboratory number can confirm exposure. It cannot, by itself, prove clinical benefit.

When Symptoms Should Not Be Assumed to Be Hormonal

Fatigue, palpitations, shortness of breath, reduced exercise tolerance, sweating, anxiety, sleep disruption, dizziness, and chest discomfort can sometimes occur during hormonal transitions.

They can also signal cardiovascular, pulmonary, hematologic, or other medical conditions.

New chest pressure, fainting, significant shortness of breath, sustained palpitations, sudden neurologic symptoms, or symptoms suggestive of a blood clot require prompt medical evaluation—not an assumption that hormones are responsible.

Frequently Asked Questions

Can Hormones Affect Heart Health?

Yes. Estrogen, testosterone, thyroid hormones, insulin, and the physiological stress response can influence cardiovascular factors such as lipids, blood pressure, glucose regulation, body composition, vascular function, and heart rhythm.

However, identifying an abnormal hormone level does not automatically identify the cause of a cardiovascular problem. Results must be interpreted within the broader clinical picture.

Does Menopause Increase Cardiovascular Risk?

Cardiovascular risk factors often change during the menopause transition. LDL cholesterol, visceral fat, insulin resistance, and blood pressure may increase, while lean mass and vascular function may change.[1]

Menopause is therefore an important time to reassess cardiovascular and metabolic health. Earlier-than-average menopause may also indicate higher long-term cardiovascular risk.[1]

Is Menopausal Hormone Therapy Safe for the Heart?

For many healthy women with bothersome symptoms who begin therapy before age 60 or within approximately 10 years of menopause onset, the overall benefit-risk profile may be favorable.[2]

The decision still depends on individual history, cardiovascular and thrombotic risk, cancer history, age, symptoms, route, dose, and formulation. Hormone therapy is not appropriate for every woman and should not be prescribed solely to prevent heart disease.

Is a Patch Safer Than Oral Estrogen?

Transdermal estrogen avoids first-pass liver metabolism and may have a more favorable effect on certain clotting and metabolic factors. Observational evidence suggests it may carry a lower venous-thromboembolism risk than oral estrogen.[2]

“Lower risk,” however, does not mean “no risk.” The best route depends on the patient’s symptoms, health history, preferences, and treatment goals.

Does Testosterone Therapy Increase Heart-Attack Risk?

In the TRAVERSE trial, testosterone therapy did not increase the primary composite rate of cardiovascular death, nonfatal heart attack, or nonfatal stroke compared with placebo among men with confirmed hypogonadism and preexisting or elevated cardiovascular risk.[5]

The testosterone group experienced more atrial fibrillation, acute kidney injury, and pulmonary embolism, however. Testosterone should therefore be used for an appropriate clinical indication following confirmation of symptomatic testosterone deficiency, with individualized assessment and ongoing monitoring—not as a general cardiovascular-prevention treatment.[5,12]

Should Cortisol Be Tested Because I Am Under Chronic Stress?

Usually not on that basis alone.

A random cortisol result does not reliably quantify everyday stress and should not be used to screen generally for Cushing syndrome. Cortisol testing is most useful when symptoms and clinical findings raise a legitimate concern about a disorder of cortisol production.[14]

Chronic stress still deserves attention because of its effects on sleep, blood pressure, behavior, and metabolic health, but it should not automatically lead to endocrine testing.

What Testing Evaluates Hormone and Cardiovascular Health Together?

A comprehensive assessment may include blood pressure, lipids, glucose and hemoglobin A1c, kidney function, body composition, thyroid testing, and selected sex-hormone measurements when clinically indicated.

Depending on the patient, ApoB, Lp(a), urine albumin, inflammatory markers, or coronary artery calcium scoring may add useful information.[9] The appropriate evaluation is individualized rather than based on a universal panel.

Hormone and Cardiovascular Evaluation in Los Angeles and the Conejo Valley

For patients throughout the greater Los Angeles and Conejo Valley region—including Thousand Oaks, Westlake Village, Agoura Hills, Calabasas, Oak Park, Newbury Park, and surrounding communities—Metriq Health provides physician-led evaluation of hormonal, metabolic, and cardiovascular health.

We combine advanced diagnostics with careful clinical interpretation. We do not treat hormones as isolated numbers or assume that every symptom has a hormonal solution.

We evaluate how your symptoms, physiology, body composition, metabolic health, cardiovascular risk, medical history, and goals fit together—then build an individualized plan grounded in evidence.

Because the goal is not simply to live longer. It is to protect the health that makes those years worth living.

Visit metriq.health to schedule a consultation.

By Eileen M. Higham, PhD
Medically reviewed by Thomas R. Anderson, MD

References

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2. The 2022 Hormone Therapy Position Statement of The North American Menopause Society Advisory Panel. The 2022 Hormone Therapy Position Statement of The North American Menopause Society. Menopause. 2022;29(7):767–794. doi:10.1097/GME.0000000000002028.
3. Hodis HN, Mack WJ, Henderson VW, et al. Vascular Effects of Early versus Late Postmenopausal Treatment with Estradiol. New England Journal of Medicine. 2016;374:1221–1231. doi:10.1056/NEJMoa1505241.
4. U.S. Food and Drug Administration. FDA Approves Labeling Changes to Menopausal Hormone Therapy Products. February 12, 2026.
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10. Lichtenstein AH, Appel LJ, Vadiveloo M, et al. 2021 Dietary Guidance to Improve Cardiovascular Health: A Scientific Statement From the American Heart Association. Circulation. 2021;144:e472–e487. doi:10.1161/CIR.0000000000001031.
11. Paluch AE, Boyer WR, Franklin BA, et al. Resistance Exercise Training in Individuals With and Without Cardiovascular Disease: 2023 Update. Circulation. 2024;149:e217–e231. doi:10.1161/CIR.0000000000001189.
12. Bhasin S, Brito JP, Cunningham GR, et al. Testosterone Therapy in Men With Hypogonadism: An Endocrine Society Clinical Practice Guideline. Journal of Clinical Endocrinology & Metabolism. 2018;103(5):1715–1744. doi:10.1210/jc.2018-00229.
13. Parikh NI, Gonzalez JM, Anderson CAM, et al. Adverse Pregnancy Outcomes and Cardiovascular Disease Risk: Unique Opportunities for Cardiovascular Disease Prevention in Women: A Scientific Statement From the American Heart Association. Circulation. 2021;143(18):e902–e916. doi:10.1161/CIR.0000000000000961.
14. Nieman LK, Biller BMK, Findling JW, et al. The Diagnosis of Cushing’s Syndrome: An Endocrine Society Clinical Practice Guideline. Journal of Clinical Endocrinology & Metabolism. 2008;93(5):1526–1540. doi:10.1210/jc.2008-0125.

Educational content only. This article is not a substitute for individualized medical advice, cardiovascular assessment, diagnosis, or treatment. Hormone evaluation and treatment decisions should be made between a patient and a qualified physician based on symptoms, medical history, examination findings, accurate laboratory testing, cardiovascular and thrombotic risk, potential benefits and harms, and individual preferences. Results and treatment responses vary.