Integrated Hormone Support Strategies and Insights

Integrative Hormone Care, Iron Dynamics, and Safer Strategies for Reproductive and Thyroid Health: A Clinician’s Guide from the Front Lines

Abstract

As a clinician working at the intersection of chiropractic, functional, and advanced nurse practitioner medicine, I guide patients through complex hormonal and metabolic decisions every day. In this educational post, I synthesize current evidence and clinical experience to clarify: how to approach iron deficiency and ferritin with root-cause reasoning; how integrative strategies—including targeted nutrition, chiropractic care, and lifestyle medicine—improve hormone balance; how intrauterine devices (IUDs) differ by progestin class and thrombotic risk; what to consider when supporting fertility and testosterone in younger men; how to make nuanced decisions for patients with prior breast neoplasia or DCIS; practical cortisol and thyroid testing strategies; the role of estriol vs estradiol in symptoms and tissue risk; and why gut health and inflammation so often dictate outcomes for thyroid and sex-hormone therapies. I also integrate my observations from practice to demonstrate how careful personalization and modern, evidence-based methods can reduce risk, enhance quality of life, and respect oncologic standards of care when needed.

Key topics that follow

• Iron physiology, ferritin targets, and root-cause evaluation for low iron
• Progestins, IUDs, clot risk, and strategies for symptom mitigation
• Progesterone dosing, sublingual vs oral kinetics, and patient tolerability
• Male fertility support, temporary SERMs, lifestyle-first recovery of testosterone
• Nuanced thinking for DCIS and hormone receptors within oncologic standards
• Cortisol testing, diurnal mapping, and integrative stress modulation
• TRT monitoring, hematocrit management, and safer optimization
• Estriol vs estradiol in skin, vaginal, and systemic symptom control
• Thyroid therapy, reverse T3, desiccated thyroid, and gut-centric failures
• The role of integrative chiropractic care in hormonal balance and neuroendocrine regulation

Hormone Identity and Patient-Centered Choice

I begin by validating a truth I see in the clinic daily: most of us carry multiple identities—parent, professional, athlete, caregiver—and our physiology flexes with those roles. Choosing how to support hormones must reflect the identity a patient wants to nurture now. In practice, I anchor plans in the patient’s goals, timelines, and risk profile, then apply targeted, evidence-based protocols.

• Why this approach matters: Hormone therapies are tools, not identities. Clear goals guide dosing, modality, and monitoring.
• Integrative chiropractic’s role: By reducing nociceptive input and sympathetic drive through spinal manipulation, soft-tissue normalization, and corrective movement, I often see improved sleep, HRV, and perceived stress. Those changes translate to improved HPA axis tone and better tolerance of hormone therapies.

Iron Physiology, Ferritin, and Why “Low” Is a Starting Point, Not a Diagnosis

When patients present with low ferritin or fatigue, I focus on the physiology of iron handling:

• Ferritin is the intracellular storage protein and a key acute-phase reactant; it rises with inflammation and may mask iron deficiency.
• Serum iron is labile and context-dependent; transferrin saturation and total iron-binding capacity (TIBC) round out the picture.
• Functional targets: For menstruating patients and those with thyroid or hair concerns, I often aim for ferritin levels of 50–100 ng/mL when inflammation is low, guided by hemoglobin/MCV, and transferrin saturation (Camaschella, 2015).

Root-cause questions I ask first

• Is there blood loss? Menstrual, GI microbleeds, NSAID-related gastritis, or postpartum losses.
• Is there malabsorption? Celiac disease, H. pylori, atrophic gastritis, SIBO, and PPI use.
• Is there hepcidin elevation from inflammation? Obesity, chronic infections, and autoimmune activity.
• Are there renal or chronic disease factors causing anemia of chronic disease?

Clinical approach

• I replete iron gently (oral ferrous bisglycinate with vitamin C; start low, go slow) while treating the cause. Newer data support alternate-day dosing to optimize absorption by modulating hepcidin (Moretti et al., 2015).
• When absorption is impaired or intolerance is high, IV iron is considered when there are clear indications (Auerbach & Macdougall, 2017).
• Integrative chiropractic support lowers sympathetic tone, which can indirectly improve GI motility and absorption by enhancing vagal tone and reducing stress.

Neonatal and peripartum note: Transient perinatal blood shifts and oxygenation needs are clinical realities; however, in adult practice, I focus on current iron balance, blood loss, and absorption.

IUDs, Progestin Families, and Thrombotic Risk: Making Sense of the Differences

Not all progestins are alike. Different families carry different androgenic, estrogenic, and thrombotic profiles (Sitruk-Ware & Nath, 2010).

• Levonorgestrel-releasing IUDs (e.g., Mirena) exert primarily local uterine effects, leading to endometrial thinning and reduced menstrual blood loss—one reason they often improve iron status in heavy bleeders. Systemic levonorgestrel levels are lower than with oral formulations, resulting in a favorable safety profile regarding VTE risk (Dragoman, 2014; de Bastos et al., 2014).
• Norethindrone and other 19-nortestosterone derivatives differ in androgenicity and lipid effects; thrombotic risk is highest with ethinyl estradiol combinations rather than with local IUD hormone reservoirs.

Clinical takeaways

• For patients with heavy menstrual bleeding or iron deficiency, a levonorgestrel IUD can reduce blood loss and improve ferritin while providing highly effective contraception.
• I counsel on class-specific side effects and carefully document thrombotic risk factors (smoking, obesity, thrombophilias).
• Integrative care: Pelvic floor-focused movement, sacral mobility, and autonomic balancing can reduce dysmenorrhea and pelvic pain that some patients attribute to contraceptives.

Progesterone Strategies: Oral vs Sublingual and Why Dose Form Matters

When patients report progesterone intolerance—mood lability, sedation, or “wired-tired” sensations—I re-examine the dose form and kinetics.

• Oral micronized progesterone undergoes first-pass metabolism, converting partly to allopregnanolone, a neurosteroid with GABAergic effects that can be sedating or anxiolytic depending on sensitivity (Schüle et al., 2014).
• Sublingual or troche forms have higher bioavailability and a faster onset, often perceived as “twice as potent” per milligram compared with oral forms, because they bypass first-pass metabolism (Simon et al., 1993). Clinically, I may use one-quarter to one-half of an equivalent oral dose sublingually for symptom control with fewer sedative effects.

My clinic flow

• Start with 100 mg of oral micronized progesterone at night for sleep and endometrial protection in estrogen users; if intolerance persists, split the dose or switch to a troche/sublingual formulation in 25–50 mg increments.
• Track mood, sleep, and bleeding patterns; adjust every 2–4 weeks.
• In women with a history of endometriosis now in menopause, I maintain progesterone co-therapy with estrogen even after hysterectomy to reduce the theoretical risk of stimulating residual endometrial foci, aligning with ob-gyn guidance (ACOG Practice Bulletin updates).

Male Fertility, Testosterone, and Short-Term SERM Support

In young men seeking fertility, I prioritize lifestyle-first strategies to restore endogenous production before exogenous hormones.

• Physiologic frame: Exogenous testosterone suppresses hypothalamic GnRH, lowering LH/FSH and impairing spermatogenesis (Turek et al., 2020).
• Short-term use of clomiphene citrate (a SERM that blocks estrogen receptors in the hypothalamus) can raise endogenous LH/FSH, increase intratesticular testosterone, and support sperm counts over 3–6 months. I avoid long-term estrogen receptor blockade due to cardiometabolic and neurocognitive concerns (Nobrega et al., 2021).
• Supplements and habits that matter: Adequate protein, omega-3s, zinc, selenium, vitamin D, B vitamins; sleep optimization; resistance training; and weight loss when indicated—these reliably move total testosterone from low-300s to higher physiologic ranges in 6–9 months for many men.

Practical protocol

• For men in their 20s–30s with low T who want children: structured training, nutrition coaching, targeted micronutrients, correction of sleep apnea, and gut-directed care. Consider clomiphene only when timing is pressing.
• For those tapering off peptides or previous TRT, temporary SERM support and HCG may accelerate sperm recovery. Monitor semen parameters and testosterone every 8–12 weeks.

DCIS, Hormone Receptors, and Respecting Oncology Standards

Patients often ask me whether ductal carcinoma in situ (DCIS) is “cancer” and how hormone receptors influence therapy. I separate the biology from the standard-of-care frame.

• DCIS is a non-invasive neoplastic process; management varies by grade and patient factors. It is not invasive carcinoma, but many systems treat it with cancer-like vigilance due to the risk of progression and recurrence (Burstein et al., 2016).
• Hormone receptors (estrogen, progesterone, androgen) are normal features on many cells. Receptor positivity in neoplastic tissue helps stratify responsiveness to adjuvant therapy; it does not mean systemic hormones are automatically contraindicated in all situations.
• Standard-of-care alignment: In patients with recent ER+ breast cancer managed with surgery and adjuvant therapy (e.g., tamoxifen/aromatase inhibitors), I do not initiate systemic estrogens. In long-term survivors with bilateral mastectomy and no residual breast tissue, the risk calculus may differ significantly; shared decision-making is paramount.

Clinical nuance I apply

• I document oncologic recommendations and risk discussions. When a symptomatic older survivor without breast tissue requests low-dose transdermal estradiol for severe vasomotor symptoms, I present data on risks/benefits and alternatives (non-hormonal options first), and proceed only with informed consent and, ideally, oncologist collaboration (NAMS, 2023).
• Local vaginal estrogen or DHEA for genitourinary syndrome of menopause can often be considered with oncologist input, as systemic absorption is minimal and quality-of-life gains are substantial (NAMS, 2023).

Cortisol Testing: Mapping the Diurnal Curve

A single morning serum cortisol measurement may miss HPA axis dysregulation. For fatigue, insomnia, or suspected hypercortisol states, I prefer:

• A 4–5 point salivary cortisol profile to map the diurnal rhythm (morning peak, afternoon decline), especially in sleep or stress disorders (Aardal & Holm, 1995).
• When drawing fasting labs (e.g., insulin), I may add an AM serum cortisol for cross-reference.
• Integrative chiropractic care, breathing practices, and graded exercise can normalize diurnal patterns by reducing sympathetic overdrive and improving sleep architecture—changes I see reflected in follow-up cortisol curves.

TRT Monitoring, Hematocrit, and Safer Optimization

Testosterone replacement therapy (TRT) can raise hematocrit via erythropoietin stimulation. My monitoring includes:

• Baseline and periodic CBC, ferritin/transferrin saturation, PSA (men), blood pressure, and lipids.
• If hematocrit rises, I evaluate dose, route of administration (transdermal can be gentler on erythrocytosis than injections), hydration, and sleep apnea, and consider phlebotomy if appropriate (AUA, 2018).
• I avoid reflexively stopping effective TRT without addressing modifiable drivers; many men stabilize with careful titration and OSA management.

Estriol vs Estradiol: Tissue Specificity and Clinical Expectations

• Estradiol (E2) is the most potent estrogen for vasomotor symptom relief and bone protection when delivered transdermally or via standard systemic routes (NAMS, 2023).
• Estriol (E3) is a weaker estrogen with higher relative affinity for ER-β; used topically for urogenital tissue or skin. As a systemic agent, E3 alone is usually too weak to control hot flashes. Patients on estriol-only regimens often continue to experience vasomotor symptoms.
• Bi-estrogen combinations (E2/E3) may provide subjective benefits, but serum levels and symptom control depend on the E2 fraction. Estriol creams aimed at the skin are unlikely to materially elevate systemic estrogen markers.

Thyroid Physiology, Reverse T3, and Choosing the Right Preparation

A key frustration in hypothyroid care is patients “not feeling better” despite normal labs. I consider:

• T4-only therapy (levothyroxine) can increase reverse T3 (rT3) when conversion pathways shunt T4 under stress, illness, or caloric restriction (Peeters, 2017). Some sensitive patients develop high rT3 even at low T4 doses, perceiving hypothyroid symptoms.
• Combination therapy or desiccated thyroid provides T4 and T3 (and minor T1/T2) in ratios closer to physiologic secretion, which can support symptomatic improvement in selected patients (Hoang et al., 2013). Not everyone benefits; individualized trials with careful monitoring are essential.
• Dosing strategy: Multiple small doses of T3 across the day may improve tolerance due to the short half-life, reducing peaks and troughs.

When symptoms persist despite “good” TSH and free T4/T3

• I look for gut drivers: SIBO, dysbiosis, celiac spectrum, H. pylori, bile acid insufficiency, and inflammatory triggers that impair deiodinases and T4→T3 conversion.
• I remove common irritants, personalize probiotics, support nutrients (selenium, iron, zinc, vitamin D), and repair the mucosa. Many patients improve once gut inflammation calms and micronutrient status normalizes.

Progesterone, Endometriosis, and Menopause

For women with a history of endometriosis who are now menopausal and using estrogen:

• I co-prescribe progesterone even after a hysterectomy to mitigate theoretical stimulation of residual endometrial implants. This aligns with conservative recommendations recognizing ectopic endometrial tissue can persist (ACOG guidance).
• Testosterone does not meaningfully worsen endometriosis per current evidence, but I still monitor symptom patterns and pelvic pain during therapy changes.

Migraines, TIAs, and Hormones: Sorting Myth from Mechanism

• Historical neurology has often pathologized “estrogen” broadly for vascular events. Modern approaches differentiate dose, route, and patient risk.
• Transdermal estradiol at physiologic doses carries lower thrombotic risk than oral ethinyl estradiol and may be acceptable in selected patients after TIA or with migraine, in collaboration with neurology and cardiology (Lobo et al., 2022).
• I do not attribute cerebrovascular events to physiologic testosterone in the absence of other risk factors; instead, I investigate lipid profiles, hematocrit, blood pressure, sleep apnea, and inflammatory status.

Immediate vs Extended-Release Medications and Patient Experience

• For many centrally acting agents (and some cardiometabolic drugs), immediate-release formulations produce clearer benefits for anxiety or sleep onset due to flexible titration and faster onset. I switch to extended-release when adherence or steady-state control is the priority and acute side effects are not troublesome.
• In hormone therapy, the delivery route (transdermal vs oral vs pellet vs troche) is more impactful than “release profile” per se. I prefer transdermal estradiol for stable serum levels and lower VTE risk; I reserve pellets for patients who understand and accept the fixed-dose nature and monitoring needs.

Iron, Ferritin, and Keratin: Hair, Thyroid, and Inflammation

Patients with hair loss and “normal” iron often have low-normal ferritin that is insufficient for follicular needs, or they have “normal” ferritin masking deficiency due to inflammation (high CRP/ESR).

• I look at the whole panel: ferritin, transferrin saturation, TSH, free T3, zinc, vitamin D, and inflammatory markers.
• Many “high ferritin, normal iron” cases are inflammatory rather than due to iron overload. I address metabolic inflammation first—nutrition, glycemic control, gut health, sleep, and structured training—before considering phlebotomy or chelation (Camaschella, 2015).

When Patients and Doctors Disagree: The Craft of Shared Decisions

I frequently work with patients navigating complex oncologic or gynecologic histories. Here’s how I keep care safe and patient-centered:

• I respect standard-of-care boundaries for active or recent ER+ cancers and collaborate with oncologists.
• In long-term survivors with modified anatomy or low residual tissue risk, I present option ranges, document risk tolerance, and use the lowest effective doses with vigilant monitoring.
• My clinic uses explicit informed consent discussions and waivers for off-label or controversial decisions. Patients appreciate transparency and control.

Integrative Chiropractic Care: The Neuroendocrine Bridge

Chiropractic care is not “hormone therapy,” but it reliably enhances the terrain in which hormones act. I observe:

• Reduced pain and improved spinal mechanics, lowering sympathetic output and improving vagal tone—factors that bolster sleep, digestion, and HPA balance.
• Better adherence and fewer side effects as patient stress inoculation improves.
• Enhanced exercise capacity and movement literacy support metabolic health and insulin sensitivity, thereby improving sex hormone and thyroid signaling.

Real-world impacts I see in the clinic

• Patients starting iron repletion with concurrent manual therapy and breathing training tolerate GI iron better and report less fatigue sooner.
• Women with perimenopausal symptoms gain better sleep after cervical/thoracic mobility work paired with nighttime oral progesterone.
• Men tapering TRT while restoring natural axes recover faster when pain is controlled, and sleep is optimized.

Testing and Titration: Putting It All Together

• Baseline: CBC, ferritin, iron/TIBC, CMP, lipids, A1c, fasting insulin, hs-CRP; TSH, free T4, free T3, rT3 if symptomatic; estradiol/estrone as appropriate; LH/FSH for men considering fertility; AM cortisol and 4-point salivary for diurnal assessment.
• Repletion and lifestyle: Correct deficits with evidence-based dosing; recheck key labs every 8–12 weeks; couple therapy with nutrition, movement, and sleep care.
• Adjust and iterate: Use symptom tracking and physiologic markers to refine route, dose, and adjunctive supports.

Why These Choices Work: The Physiology

• Iron repletion only “sticks” when hepcidin is low, and the gut barrier is healthy; addressing inflammation flips the switch for absorption.
• Progesterone’s neurosteroid metabolites are therapeutic for many, but intolerable for some—sublingual delivery changes the metabolite profile.
• Clomiphene’s selective blockade of hypothalamic ER relieves negative feedback, lifting LH/FSH and boosting intratesticular testosterone—a bridge, not a residence.
• Transdermal estradiol avoids first-pass hepatic induction of coagulation factors, reducing VTE risk compared with oral ethinyl estradiol.
• T4-to-rT3 shunting increases under stress; adding T3 or using desiccated thyroid can bypass the bottleneck, while lifestyle changes restore physiologic conversion.
• Manual care and movement programming reduce allostatic load; the HPA axis and immune networks reward the nervous system’s calmer signals with improved endocrine performance.

Clinical Pearls and Action Steps

• For low ferritin and heavy menses: Consider a levonorgestrel IUD plus alternate-day oral iron; reassess ferritin and symptoms at 8 and 16 weeks.
• For progesterone intolerance: Trial sublingual/troche at one-quarter to one-half of oral dose equivalents; monitor sleep and mood for two cycles.
• For young men with low T who want fertility: Start with sleep, resistance training, nutrition, and supplements. Consider clomiphene 3–6 months only if needed; track semen analysis.
• For DCIS survivors with severe vasomotor symptoms: Start with non-hormonal options; if considering hormones later, coordinate with oncology and carefully document shared decision-making.
• For thyroid non-responders: Check rT3 and gut; consider combination therapy and gut repair before escalating doses.
• For high hematocrit on TRT: Lower dose, switch to transdermal, address OSA, ensure hydration, and consider phlebotomy if appropriate.

In Closing

Patients do best when we honor their identities, explain the physiology clearly, and integrate treatments that the body can tolerate and sustain. Modern, evidence-based methods—combined with hands-on care to calm the nervous system, restore movement, and support recovery—create durable improvements.

If you’re a clinician, I hope this roadmap helps you navigate the nuance. If you’re a patient, remember: the best plan is the one you can live with, that respects your history, and that steadily moves you toward the life you choose.

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Citations

• Aardal, E., & Holm, A. C. (1995). Cortisol in saliva—Reference ranges and relation to cortisol in serum. European Journal of Clinical Chemistry and Clinical Biochemistry, 33(12), 927–932. https://doi.org/10.1515/cclm.1995.33.12.927
• American Urological Association. (2018). Evaluation and Management of Testosterone Deficiency: AUA Guideline. https://www.auanet.org/
• Auerbach, M., & Macdougall, I. C. (2017). Safety of intravenous iron formulations: Facts and folklore. Blood Transfusion, 15(5), 456–461. https://doi.org/10.2450/2017.0113-17
• Burstein, H. J., et al. (2016). Ductal carcinoma in situ of the breast. Journal of Clinical Oncology, 34(20), 2312–2320. https://doi.org/10.1200/JCO.2016.68.3573
• Camaschella, C. (2015). Iron-deficiency anemia. New England Journal of Medicine, 372(19), 1832–1843. https://doi.org/10.1056/NEJMra1401038
• de Bastos, M., et al. (2014). Combined oral contraceptives and venous thrombosis: An updated review. BMJ, 349, g5459. https://doi.org/10.1136/bmj.g5459
• Dragoman, M. V. (2014). The safety of intrauterine devices among young women: A systematic review. Contraception, 89(5), 301–312. https://doi.org/10.1016/j.contraception.2014.01.004
• Hoang, T. D., et al. (2013). Desiccated thyroid extract compared with levothyroxine. Journal of Clinical Endocrinology & Metabolism, 98(5), 1982–1990. https://doi.org/10.1210/jc.2012-4107
• Lobo, R. A., et al. (2022). Menopausal hormone therapy and cardiovascular disease. Endocrine Reviews, 43(6), 1013–1048. https://doi.org/10.1210/endrev/bnac010
• Moretti, D., et al. (2015). Iron absorption from supplements is greater with alternate day than with consecutive day dosing. The Lancet Haematology, 2(11), e524–e533. https://doi.org/10.1016/S2352-3026(15)00144-9
• North American Menopause Society. (2023). The 2023 nonhormone therapy position statement. Menopause, 30(6), 573–590. https://doi.org/10.1097/GME.0000000000002176
• Nobrega, E. T., et al. (2021). Clomiphene citrate for male hypogonadism and infertility. Translational Andrology and Urology, 10(3), 1301–1311. https://doi.org/10.21037/tau-20-1232
• Peeters, R. P. (2017). Non-thyroidal illness and rT3. Nature Reviews Endocrinology, 13(9), 510–526. https://doi.org/10.1038/nrendo.2017.80
• Schüle, C., et al. (2014). Neuroactive steroids in affective disorders: The role of allopregnanolone. CNS Drugs, 28(7), 629–642. https://doi.org/10.1007/s40263-014-0163-1
• Simon, J. A., et al. (1993). Oral versus nonoral routes of progesterone administration. American Journal of Obstetrics and Gynecology, 168(2), 562–570. https://doi.org/10.1016/0002-9378(93)90493-A
• Sitruk-Ware, R., & Nath, A. (2010). Characteristics and metabolic effects of different progestins. Contraception, 82(5), 386–392. https://doi.org/10.1016/j.contraception.2010.04.004
• Turek, P. J., et al. (2020). Approach to the infertile male. New England Journal of Medicine, 382(22), 2090–2101. https://doi.org/10.1056/NEJMra1907387

Linked resources

• PushAsRx by Dr. Alexander Jimenez: https://pushasrx.com/
• Dr. Alexander Jimenez on LinkedIn: https://www.linkedin.com/in/dralexjimenez/

References

• Aardal, E., & Holm, A. C. (1995). Cortisol in saliva—Reference ranges and relation to cortisol in serum. European Journal of Clinical Chemistry and Clinical Biochemistry, 33(12), 927–932. https://doi.org/10.1515/cclm.1995.33.12.927
• American Urological Association. (2018). Evaluation and Management of Testosterone Deficiency: AUA Guideline. https://www.auanet.org/
• Auerbach, M., & Macdougall, I. C. (2017). Safety of intravenous iron formulations: Facts and folklore. Blood Transfusion, 15(5), 456–461. https://doi.org/10.2450/2017.0113-17
• Burstein, H. J., et al. (2016). Ductal carcinoma in situ of the breast. Journal of Clinical Oncology, 34(20), 2312–2320. https://doi.org/10.1200/JCO.2016.68.3573
• Camaschella, C. (2015). Iron-deficiency anemia. New England Journal of Medicine, 372(19), 1832–1843. https://doi.org/10.1056/NEJMra1401038
• de Bastos, M., et al. (2014). Combined oral contraceptives and venous thrombosis: An updated review. BMJ, 349, g5459. https://doi.org/10.1136/bmj.g5459
• Dragoman, M. V. (2014). The safety of intrauterine devices among young women: A systematic review. Contraception, 89(5), 301–312. https://doi.org/10.1016/j.contraception.2014.01.004
• Hoang, T. D., et al. (2013). Desiccated thyroid extract compared with levothyroxine. Journal of Clinical Endocrinology & Metabolism, 98(5), 1982–1990. https://doi.org/10.1210/jc.2012-4107
• Lobo, R. A., et al. (2022). Menopausal hormone therapy and cardiovascular disease. Endocrine Reviews, 43(6), 1013–1048. https://doi.org/10.1210/endrev/bnac010
• Moretti, D., et al. (2015). Iron absorption from supplements is greater with alternate day than with consecutive day dosing. The Lancet Haematology, 2(11), e524–e533. https://doi.org/10.1016/S2352-3026(15)00144-9
• North American Menopause Society. (2023). The 2023 nonhormone therapy position statement. Menopause, 30(6), 573–590. https://doi.org/10.1097/GME.0000000000002176
• Nobrega, E. T., et al. (2021). Clomiphene citrate for male hypogonadism and infertility. Translational Andrology and Urology, 10(3), 1301–1311. https://doi.org/10.21037/tau-20-1232
• Peeters, R. P. (2017). Non-thyroidal illness and rT3. Nature Reviews Endocrinology, 13(9), 510–526. https://doi.org/10.1038/nrendo.2017.80
• Schüle, C., et al. (2014). Neuroactive steroids in affective disorders: The role of allopregnanolone. CNS Drugs, 28(7), 629–642. https://doi.org/10.1007/s40263-014-0163-1
• Simon, J. A., et al. (1993). Oral versus nonoral routes of progesterone administration. American Journal of Obstetrics and Gynecology, 168(2), 562–570. https://doi.org/10.1016/0002-9378(93)90493-A
• Sitruk-Ware, R., & Nath, A. (2010). Characteristics and metabolic effects of different progestins. Contraception, 82(5), 386–392. https://doi.org/10.1016/j.contraception.2010.04.004
• Turek, P. J., et al. (2020). Approach to the infertile male. New England Journal of Medicine, 382(22), 2090–2101. https://doi.org/10.1056/NEJMra1907387