The clinical team at Doctor's Data is often asked whether it’s “worth testing hormones” when a patient is using hormonal birth control. The most accurate answer is: it depends on the clinical questions being asked. Hormone testing can offer valuable insight into ovarian suppression, androgen availability, adrenal physiology and overall hormone metabolism, but is less informative if the goal is to establish baseline endocrine function.
What Hormone Testing Reflects on Hormonal Contraception
Whether via saliva or urine, hormone testing in patients using hormonal contraception reflects the physiologic effects of the medication rather than baseline ovarian function. Results capture the downstream physiologic effects of exogenous hormones: suppression of endogenous production, alterations in binding proteins, and shifts in hormone metabolism and clearance. Importantly, neither saliva nor urine testing methodologies can quantify synthetic hormones such as ethinyl estradiol and progestins. Instead, these methods provide insight into free hormone availability, metabolite patterns, and hypothalamic–pituitary–adrenal (HPA) axis signaling.
Methods with Predictable Effects on Ovarian Hormone Production
There are two categories of birth control methods that reliably suppress ovulation by blocking the LH surge, subsequently suppressing ovarian production of estradiol and progesterone, effectively eliminating the mid-luteal progesterone peak::
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Ethinyl estradiol (EE)–containing methods (combined oral contraceptives, vaginal ring, transdermal patch)
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Progestin-only long-acting methods (etonogestrel subdermal arm implant, and depot medroxyprogesterone acetate injections)
With these methods, progesterone suppression is expected and the absence of a mid-luteal progesterone rise should be anticipated when interpreting results.
Progestin-Only Pills: Variable Ovulation Suppression
By contrast, progestin-only pills (POPs) demonstrate variable ovulation suppression depending on the formulation. Drospirenone suppresses ovulation more consistently, whereas norethindrone and norgestrel often allow ovulation to occur. When ovulation is not reliably suppressed, contraceptive efficacy is driven primarily by cervical mucus thickening and endometrial thinning, rather than pituitary or ovarian suppression. As a result, many patients using these formulations will continue to show cyclic estradiol and progesterone production at attenuated levels.
Methods That Preserve Ovulation
Methods that do not suppress ovulation, such as the levonorgestrel (LNG) intrauterine device and the copper IUD, generally preserve endogenous cycling. In these cases, hormone results may be interpreted in a near-physiologic context, although appropriate cycle timing of collections can be difficult to determine if the patient doesn’t have a monthly bleed.
Androgen Binding and Cortisol Physiology
While ovarian suppression by hormonal contraceptives is well established, their impact on androgens is less appreciated. In combined contraceptive methods, the ethinyl estradiol (EE) component increases hepatic production of sex hormone–binding globulin (SHBG), which can reduce free testosterone by as much as 60%. While this androgen-lowering effect may be beneficial for hyperandrogenic phenotypes such as PCOS, it can be problematic in individuals who already have low androgen reserves.
The effects of hormonal contraception on androgen binding and cortisol physiology are often under-recognized. Ethinyl estradiol (EE) –containing methods increase hepatic production of sex hormone–binding globulin (SHBG), which lowers free testosterone by increasing the protein-bound fraction, often without a corresponding change in total testosterone. Because standard total testosterone assays measure both bound and unbound hormone, this shift in binding can mask a clinically meaningful reduction in bioavailable testosterone.
Cortisol regulation is also altered by ethinyl estradiol (EE), though through a different binding-protein mechanism than testosterone. EE induces an increase in cortisol-binding globulin (CBG), which raises total serum cortisol by expanding the protein-bound pool without increasing free cortisol. At the same time, EE acts centrally on estrogen receptors within the hypothalamus and pituitary, modulating CRH signaling and reducing ACTH pulse amplitude, which can blunt HPA-axis reactivity to stress while baseline free cortisol output is typically preserved. In this context, salivary testing reflects free cortisol at a given moment, whereas urinary cortisol and cortisone patterns provide insight into total adrenal output, metabolism, diurnal rhythm, and stress reactivity across the day.
Clinical Takeaway
Understanding each contraceptive method’s mechanism of action allows clinicians to anticipate findings and determine when hormone testing -whether focused on sex hormones, adrenal hormones, or metabolic patterns - is likely to be clinically actionable.
