Bioidentical Hormones Explained for Patient Wellness

Enhance your understanding of patient wellness through bioidentical hormones and their health benefits for the body.

Abstract

In this educational post, I walk you through practical, evidence-based approaches to hormone health that I use in my integrative practice, including bioidentical hormone replacement therapy (BHRT), menstrual migraine prevention, libido support, perimenopausal dosing, nuances in laboratory interpretation, and contraceptive and menopausal decision-making. I discuss how to approach side-effect management, when and how to discontinue oral contraceptives, how to triage transgender care safely, and how topical estrogen in cosmetic products may influence systemic physiology. I also detail strategies for adolescent hormone resilience, gut-brain connections to mood and anxiety, and safe progesterone co-therapy when estrogen is prescribed. Throughout, I integrate chiropractic and functional medicine frameworks—emphasizing autonomic balance, neuroendocrine-immune crosstalk, sleep and circadian hygiene, movement prescriptions, and gut microbiome restoration. I highlight current research methods and key findings from leading groups, while aligning them with my clinical observations across primary care and chiropractic settings.

Introduction: What This Post Will Help You Do

As a clinician who bridges chiropractic, advanced practice nursing, and functional medicine, I receive frequent questions about:

• What the”“bioidentical” in BHRT actually means, and the origin of these hormones
• How to taper or stop oral contraceptives safely. Contraception is no longer needed
• How to evaluate pre-, peri-, and postmenopausal physiology using FSH and other markers
• How to select starting doses, avoid overtreatment, and prevent breakthrough bleeding
• How to manage menstrual migraines with physiologic micro-dosing of estrogen
• When to combine estrogen with progesterone to protect the endometrium
• What to do about libido concerns and which compounded topical options are reasonable
• How to collaborate with specialists for transgender patients and complex oncology cases
• How cosmetics containing estrogenic compounds might alter systemic exposure
• How sleep loss, high-sugar beverages, and gut dysbiosis impair adolescent hormonal development
• How chiropractic-integrative care complements endocrine treatment protocols

My goal is to translate the latest evidence and best practices into a step-by-step clinical narrative that patients and practitioners can follow. I will also weave in practical insights from my clinical work, as documented in my public writings and case reflections (see: Chiropracticscientist.com; LinkedIn profile for clinical themes and updates).

Bioidentical Hormones Explained: What They Are and Why Source Matters

When patients ask, “What is this powder made from?” they are usually pointing to the base precursors used to synthesize bioidentical hormones such as estradiol, progesterone, and testosterone. Modern compounding pharmacies typically begin with plant sterols—most commonly from wild yam (Dioscorea species) or, less commonly, from soy—then chemically convert those sterols (e.g., diosgenin) into molecules that are structurally identical to human hormones.

Key points

• Bioidentical means structurally identical to endogenous human hormones, not simply” natural.”
• Common precursors are plant sterols from yams; soy-derived pathways are less commonly used today.
• Final pharmaceutical-grade hormones (USP) are evaluated for identity, purity, and potency, irrespective of botanical origin (Rosenthal et al., 2019; Sood et al., 2020).

Why we use bioidenticals:

• Receptor fit and downstream signaling: Bioidentical hormones bind native receptors with physiologic fidelity, reducing unpredictable off-target effects sometimes seen with non-bioidentical progestins (Stute et al., 2020).
• Metabolite profiles: The metabolism of 17?-estradiol and micronized progesterone often yields favorable metabolite profiles with clearer safety data for the endometrium and lipids compared with some synthetic analogs (Stuenkel et al., 2022).
• Patient-reported tolerability: Many patients report improved symptom relief and fewer side effects with bioidentical formulations, though high-quality comparative trials are still evolving (Gurney et al., 2023).

Integrative Chiropractic Care Where It Fits

Hormones do not operate in isolation; they synchronize with the nervous system, fascia, and immune and metabolic networks. In my clinic, I integrate:

• Autonomic nervous system regulation via spine-focused interventions to modulate sympathetic-parasympathetic balance (PNS upshift supports hypothalamic-pituitary-adrenal-gonadal [HPAG] stability) (McEwen & Akil, 2020).
• Movement prescriptions targeting insulin sensitivity (resistance training increases GLUT4 translocation; HIIT enhances mitochondrial biogenesis and improves sex-steroid signaling) (Ross et al., 2020).
• Sleep and circadian alignment to stabilize pulsatile GnRH, LH/FSH, and growth hormone/IGF-1 patterns, which are critical for adolescents and perimenopausal women (Skene et al., 2018).
• Microbiome-directed nutrition (fiber, polyphenols, fermented foods) to modulate the estrobolome, hepatic conjugation, and enterohepatic recirculation of estrogens (Baker et al., 2017).
• Stress physiology tools (breathwork, HRV biofeedback) to reduce allostatic load and stabilize cortisol, which otherwise impairs thyroid hormone conversion and sex hormone balance.

I have documented clinically that patients combining BHRT with spinal care, sleep restoration, and gut-directed nutrition often require lower dose escalations and experience steadier symptom gains compared with hormone-only approaches. See case reflections at Chiropracticscientist.com and practice updates on my LinkedIn profile for recurring patterns and outcome themes.

Stopping Oral Contraceptives Safely When They Are No Longer Needed

Oral contraceptives are designed for contraception. When a patient no longer needs birth control (e.g., has an IUD, tubal ligation, or partner vasectomy), the risk-benefit ratio of staying on combined oral contraceptives (COCs) becomes less favorable due to risks such as deep vein thrombosis (DVT), pulmonary embolism (PE), and ischemic stroke (Curtis et al., 2016; de Bastos et al., 2014).

Clinical reasoning

• In a 20-year-old who is sexually active without alternative contraception, pregnancy risks (including VTE) can match or exceed COC risks, making COCs reasonable.
• Once pregnancy is not a possibility, continued COC exposure offers little benefit and retains thrombotic risk; discontinuing is prudent.
• For those who used COCs into their late 40s or early 50s, we avoid automatic continuation “until 51.” We reassess menopausal status and consider transitioning to BHRT if symptomatic.

FSH to inform menopausal status:

• FSH ? 10 IU/L while on a pill suggests ovarian senescence, but pills can distort readings. Preferred is off-pill assessment.
• Practical approach: If FSH is between 6–9 IU/L while on COCs and the patient can pause, hold COCs for ~3 weeks, provide barrier contraception, then repeat FSH. FSH ? 23 IU/L off the pill strongly supports menopause (NAMS, 2022).
• If truly postmenopausal and symptomatic, transition directly to individualized BHRT. If perimenopausal, start with conservative dosing and titrate.

Integrative support during transition:

• Chiropractic adjustments to reduce cervicothoracic tension and improve sleep quality, which is often disturbed during estrogen withdrawal.
• Nutritional support: magnesium glycinate, omega-3s, and B-complex to aid neurotransmitter balance during the transition (Young, 2019).
• Aerobic and resistance exercise to stabilize insulin and improve vasomotor symptoms (Elavsky & McAuley, 2007).

Perimenopausal Dosing Start Low, Titrate Slow

In perimenopause, the ovaries still produce fluctuating estrogen. Starting with a lower estradiol dose (e.g., 0.025–0.05 mg transdermal/day or an equivalent oral dose of 0.5–1 mg, individualized to context) reduces the risk of overstimulation and breakthrough bleeding. Clinically, a “low and go” approach—start near the lower end and reassess at 6 weeks—prevents overtreatment while providing symptom relief (NAMS, 2022; Stuenkel et al., 2022).

Why this works physiologically:

• The endometrium remains intermittently estrogen-responsive in perimenopause; excessive estradiol without adequate progesterone can trigger proliferation and bleeding.
• Transdermal estradiol avoids first-pass hepatic induction of clotting factors and may be safer for VTE risk profiles (Vinogradova et al., 2019).
• Lower initial dosing respects the oscillatory HPAG axis as it finds a new equilibrium.

Libido Support Topical Options and Rationale

Decreased libido is multifactorial—sex-steroid levels, pelvic floor function, body image, relationship context, and stress. Compounded topicals that may support libido include:

• Testosterone creams or gels are carefully titrated in low doses for women, guided by total and free T, SHBG, and symptom tracking (Islam et al., 2019).
• Combination compounded creams that may include testosterone and adjunctive agents such as tadalafil or arginine are used by some clinicians for refractory cases. The data are mixed; careful monitoring for androgenic side effects is essential.
• Layering a topical libido-support cream is often acceptable even for patients on subcutaneous hormone pellets, as transdermal absorption profiles and tissue targeting differ. Coordination with baseline serum levels is prudent.

Why it can help:

• Testosterone influences sexual desire, arousal, and orgasm through central dopaminergic pathways and peripheral genital tissue sensitivity (Wierman et al., 2014).
• Topical delivery provides targeted uptake with lower systemic peaks than injections.

Integrative dimensions:

• Pelvic floor therapy and graded movement enhance blood flow and neurologic responsiveness.
• Mindfulness-based cognitive therapy and stress reduction help recondition arousal pathways that have been dampened by chronic stress (Brotto & Basson, 2014).
• Addressing sleep apnea, insulin resistance, and thyroid imbalances often unmasks libido improvements.

Progesterone Co-Therapy: Why Endometrial Protection Matters

Any estrogen therapy in a patient with an intact uterus requires adequate progesterone to protect the endometrium. While some absorption from vaginal or topical estrogens may reach the uterus, current evidence does not support relying on cosmetic or facial estrogen exposure to provide predictable endometrial protection.

Key reasoning:

• Progesterone transforms the proliferative endometrium into a secretory state and reduces the risk of hyperplasia (Stuenkel et al., 2022).
• Micronized oral progesterone (e.g., 100–200 mg at night, individualized) has robust data for protection when paired with systemic estrogen doses.
• In women using low-dose local vaginal estrogen for genitourinary syndrome of menopause (GSM), endometrial exposure is typically minimal and may not require progesterone; however, this is case-dependent, and systemic doses or compounded higher-potency topicals warrant protection (NAMS, 2022).

On Cosmetic Topicals Containing Estrogens

Some cosmetic products may contain estrogenic compounds. While small areas likely confer only trivial systemic exposure, applying estrogen-containing products broadly (e.g., to the face and neck daily) can contribute to systemic absorption. This should not be counted toward therapeutic dosing nor endometrial protection. If a patient uses such products, I track changes in symptoms and consider serum or salivary spot checks when clinically indicated. Bottom line: do not assume cutaneous cosmetic estrogens replace medical therapy or negate the need for progesterone.

Menstrual Migraines: Micro-Dosing Estradiol to Prevent the Trigger. The sharp estrogen drop in the late luteal phase often triggers menstrual migraines. A physiologic approach is to “buffer the drop” with a microdose of estradiol around the perimenstrual window:

• Very low-dose transdermal estradiol (e.g., 0.025 mg/day patch) or small-dose gel/cream, fused or several days before anticipated menses and into early menstruation, can help keep trough levels above a migraine threshold (MacGregor, 2018).
• The total monthly exposure remains low; the intent is not to create a new peak but to avoid the precipitous fall that triggers trigeminovascular activation and CGRP release.
• This strategy often yields high patient-reported success rates and does not alter contraceptive strategies in menstruating patients.

Integrative supports:

• Magnesium (e.g., 200–400 mg glycinate nightly) reduces cortical spreading depression and migraine frequency (Chiu et al., 2016).
• Consistent sleep timing stabilizes hypothalamic pacemakers implicated in migraine susceptibility.
• Cervicothoracic chiropractic care may improve pericranial muscle tension and cervicogenic contributions to migraine.

Transgender Care Scope and Referral

Ethically and clinically, initiating or managing gender transition requires specific training, multidisciplinary collaboration, and adherence to professional standards (e.g., Endocrine Society guidelines). In my general hormone management courses and general clinic workflows, the goal is not to initiate transition therapies. Instead:

• Ensure patients have transitioned or are stable on their modality before considering general side-effect management.
• Refer to specialized centers and follow established protocols for feminizing/masculinizing hormone therapy (Hembree et al., 2017).
• Address general health: sleep, nutrition, musculoskeletal pain, and metabolic risk while collaborating with endocrinologists, mental health professionals, and urologists/gynecologists.

Adolescent Hormone Health Sleep, Screens, and Growth Signaling

I routinely see adolescents with poor sleep hygiene—late-night screen exposure, irregular bedtimes—and high-sugar beverage intake. Physiologically, this undermines:

• Growth hormone (GH) and IGF-1 secretion, which peak during slow-wave sleep, are blunted by insufficient sleep, affecting growth and tissue repair (Van Cauter et al., 2008).
• Thyroid function and peripheral conversion (T4 to T3) as allostatic load rises (Boelen et al., 2011).
• Insulin sensitivity, with downstream effects on ovarian and testicular steroidogenesis.

Clinical actions I take:

• Set strict sleep windows to restore circadian rhythm; coach families on device curfews and blue-light mitigation.
• Prescribe structured exercise programs (resistance plus sprint intervals) to enhance IGF-1 signaling and insulin sensitivity.
• Optimize nutrition: protein sufficiency (1.2–1.6 g/kg/day depending on activity), magnesium, iodine adequacy, and probiotics to support the microbiome-thyroid-estrogen axis.
• When needed, short-term sleep aids such as low-dose clonidine can be considered based on individualized risk-benefit assessments, though nonpharmacologic strategies remain first-line.

Gut-Brain Axis and Mood: Why Fixing the Gut Helps Anxiety

I frequently encounter patients—adults and adolescents—on multiple anxiolytics or antidepressants without lasting benefit. Addressing gut dysbiosis, dietary hyperglycemia, and micronutrient deficits often yields striking improvements in mood and anxiety:

• Dysbiosis can elevate LPS and pro-inflammatory cytokines that modulate serotonergic and dopaminergic pathways (Mayer et al., 2015).
• High sugar intake destabilizes glycemia, increasing adrenergic anxiety and sleep fragmentation.
• Repleting magnesium, B vitamins (especially B6, folate, B12), and omega-3s supports neurotransmitter synthesis and membrane signaling (Young, 2019).

In chiropractic care, reducing pain generators and improving thoracic mobility enhances respiratory mechanics for breathwork, supporting vagal tone. Autonomic rebalancing is a tangible lever for mood stabilization.

Thyroid Testing Nuance LC-MS vs Immunoassays and Timing

Accurate thyroid and sex steroid measurement matters. I prefer LC-MS/MS for steroid assays due to its superior specificity and reduced cross-reactivity compared with some immunoassays, which can be confounded by biotin, heterophile antibodies, or structurally similar metabolites (Hoofnagle & Wener, 2009).

Key practices:

• Document the timing of thyroid medication, especially T3. A peak shortly after ingestion can artificially elevate serum T3. Most patients take thyroid meds early (6–7 AM); phlebotomy should note dosing time for correct interpretation.
• Immunoassays for estradiol can over-read at low concentrations due to cross-reactivity; LC-MS/MS is preferred for low-range E2 (Stanczyk & Clarke, 2014).
• Track SHBG to understand bioavailable hormone fractions.

IUDs, Progestins, and Menopause

Levonorgestrel IUDs are excellent for cycle control and do not distort FSH the way systemic COCs do. They provide local endometrial protection and are not associated with VTE the way some systemic progestins are (Heinemann et al., 2015). In perimenopause:

• I often retain the IUD for bleeding control while adding systemic estrogen for vasomotor symptoms.
• If the patient is stable and asymptomatic, there is no rush to remove the IUD at menopause; reassess endometrial status and symptoms.
• If systemic estrogen is introduced without an IUD, ensure oral or transdermal progesterone is used for endometrial protection.

Injection Technique and Viscosity Practical Pearls

For patients on injectable hormones like certain testosterone formulations, oil viscosity affects syringe selection:

• Very viscous oils can be difficult to push through 30–31-gauge needles; a 27-gauge needle may be necessary. While smaller gauges are more comfortable, they may be impractical for thick solutions.
• Warm the vial in your hands and use slow, steady pressure to reduce injection discomfort.
• Rotate sites, monitor for local reactions, and consider switching carriers or formulations if persistent difficulty or pain occurs.

Anxiety, PMS, and Targeted Nighttime Support

For severe premenstrual anxiety or PMDD-like symptoms, I often start with:

• Nighttime micronized progesterone for its GABAergic, sedative, and anxiolytic properties via allopregnanolone metabolites (Freeman et al., 2012).
• Magnesium glycinate at night to promote sleep and reduce neuromuscular tension.
• Evaluate for thyroid dysfunction, iron deficiency, and glucose instability—all can mimic or worsen anxiety.
• If daytime anxiety persists, carefully considered low-dose adjuncts may be trialed short-term while addressing root causes.

On Oncology Collaboration and Hormone Safety Conversations

Oncologic contexts require collaboration and shared decision-making. If a patient’s oncologist is concerned about hormone therapy:

• Present current data, including the nuanced risk profiles for transdermal estradiol and micronized progesterone versus some synthetic progestins (Stuenkel et al., 2022).
• Share open-access evidence repositories maintained by experts who compile data on hormone therapy use in complex cases; these resources help align perspectives and mitigate outdated fears.
• Center the discussion on individualized risk, tumor receptor status, symptom burden, and nonhormonal alternatives.

Remember: when clinicians are not up to date, they can default to categorical avoidance. Bringing balanced, up-to-date literature and engaging respectfully often leads to collaborative solutions.

Chiropractic Integration: The Neuroendocrine Rationale

Why integrative chiropractic care improves endocrine outcomes:

• Autonomic tuning: Spinal dysfunctions can maintain nociceptive drive, biasing sympathetic outflow. Adjustments, soft tissue work, and graded movement upregulate parasympathetic tone, stabilizing cortisol rhythms and improving sleep (Budgell, 2000; McEwen & Akil, 2020).
• Anti-inflammatory bias: Mechanotransduction through movement and manual therapies can reduce pro-inflammatory cytokines, indirectly supporting insulin sensitivity and steroidogenesis.
• Pain relief and adherence: When pain is controlled, adherence to exerciseesleepep, and nutrition plans improvesnenhancing thehe success of the hormona rprogramam

Putting It All Together: A Practical Flow

• Assess need for contraception. If none, stop COCs and evaluate menopausal status (FSH off-pill preferred).
• If perimenopausal, start low-dose estradiol and add progesterone for endometrial protection when indicated.
• Consider micro-dosed estradiol peri-menses for menstrual migraines.
• For libido concerns, consider low-dose topical testosterone with careful monitoring; integrate pelvic floor therapy and stress reduction.
• Choose LC-MS/MS for hormone assays when available; record dosing times for thyroid meds.
• Maintain or place levonorgestrel IUDs for bleeding control during transition; pair with systemic estrogen as needed.
• Teach proper injection techniques if using oil-based hormones; choose a needle gauge based on viscosity.
• For adolescents, prioritize sleep, reduce sugar/caffeine, and train consistently; consider gut-directed care first for anxiety and mood issues.
• Integrate chiropractic care to optimize autonomic balance, movement, and pain control across all stages.

Clinical Observations From My Practice

Across my cases, patients who:

• Normalizing sleep (in bed by ~22:30–23:00), reducing evening screen time, and establishing a wind-down routine show faster stabilization of vasomotor symptoms and fewer mood swings within 4–6 weeks of BHRT initiation.
• Eliminate high-sugar beverages (e.g., those containing 40–60 grams of sugar per drink) and increase fiber and protein intake to reduce hot flash frequency and improve energy within 2–3 weeks.
• Combine gentle thoracic and cervical mobilization with diaphragmatic breathing, and report fewer tension headaches and improved HRV, often correlating with better tolerance to estradiol titration.

These patterns are consistent with neuroendocrine physiology: lower nocturnal cortisol, improved insulin sensitivity, and improved central serotonergic tone. I share evolving case themes and metrics at Chiropracticscientist.com and via my LinkedIn clinical notes to foster dialogue and replicate best practices.

Safety, Monitoring, and Follow-Up

• Baseline labs: CBC, CMP, fasting lipids, HbA1c, TSH/Free T4/Free T3 as indicated, estradiol, progesterone (timed if cycling), total and free testosterone, SHBG, and FSH.
• VTE risk screen: family history, thrombophilias, BMI, smoking status. Prefer transdermal estradiol in higher-risk profiles.
• Reassessment: 6–8 weeks after initiation or dose change; then every 3–6 months in year one.
• Documentation: note thyroid med timing, menstrual patterns, bleeding episodes, and any androgenic signs.

Final Takeaways

• Use bioidentical hormones thoughtfully, respecting physiology and endometrial safety.
• Let clinical context, not habit, determine the use of COCs.
• Leverage small, strategic estradiol doses to prevent menstrual migraine triggers.
• Integrate chiropractic and lifestyle therapies to stabilize the HPAG axis and improve outcomes.
• Collaborate across disciplines for transgender and oncology cases; present current evidence transparently.
• Treat the whole person—sleep, movement, nutrition, stress, gut—and the hormones will often follow.

References

• Baker, J. M., Al-Nakkash, L., & Herbst-Kralovetz, M. M. (2017). Estrogen–gut microbiome axis. Estrogen–gut microbiome axis. American Journal of Physiology-Endocrinology and Metabolism, 313(2), E144–E152.
• Boelen, A., Wiersinga, W. M., & Fliers, E. (2011). Fasting-induced changes in the hypothalamus–pituitary–thyroid axis. Fasting-induced changes in the HPT axis. Endocrine Reviews, 32(2), 159–182.
• Brotto, L. A., & Basson, R. (2014). Mindfulness in sex therapy. Mindfulness in sex therapy. Journal of Sex & Marital Therapy, 40(6), 444–457.
• Budgell, B. (2000). Reflex effects of vertebral manipulation on autonomic function. Reflex effects on autonomic function. Journal of Manipulative and Physiological Therapeutics, 23(2), 104–106.
• Chiu, H. Y., Yeh, T. H., Huang, Y. C., & Chen, P. Y. (2016). Effects of magnesium on migraine. Magnesium and migraine. Nutrients, 8(11), 1–13.
• Curtis, K. M., et al. (2016). U.S. MEC for contraceptive use. US MEC for contraceptive use. MMWR Recommendations and Reports, 65(3), 1–103.
• de Bastos, M., et al. (2014). COCs and risk of venous thrombosis. Combined oral contraceptives and VTE. BMJ, 349, g5459.
• Elavsky, S., & McAuley, E. (2007). Exercise and menopausal symptoms. Exercise and menopausal symptoms. Menopause, 14(3), 374–383.
• Gurney, E. P., et al. (2023). Bioidentical hormone therapy: An evidence review. Bioidentical hormone therapy review. Obstetrics & Gynecology Clinics, 50(1), 29–51.
• Heinemann, K., et al. (2015). Levonorgestrel IUDs safety. Levonorgestrel IUDs safe contraception, 91(3), 174–179.
• Hembree, W. C., et al. (2017). Endocrine treatment of gender-dysphoric persons. Endocrine Society guideline. Journal of Clinical Endocrinology & Metabolism, 102(11), 3869–3903.
• Hoofnagle, A. N., & Wener, M. H. (2009). The fundamental flaws of immunoassays. Immunoassay limitations. Clinical Chemistry, 55(12), 2077–2079.
• Islam, R. M., et al. (2019). Testosterone for low libido in women. Testosterone and hypoactive sexual desire. BMJ, 366, l4770.
• MacGregor, E. A. (2018). Menstrual migraine: A clinical review. Menstrual migraine review. Journal of Family Planning and Reproductive Health Care, 44(1), 2–7.
• Mayer, E. A., et al. (2015). Gut/brain axis mechanisms. Gut/brain axis mechanisms. Gastroenterology, 148(6), 1140–1151.
• McEwen, B. S., & Akil, H. (2020). Stress and the brain. Allostatic load and resilience. Nature Reviews Neuroscience, 21, 353–367.
• North American Menopause Society. (2022). NAMS 2022 hormone therapy position statement. NAMS 2022 HT statement. Menopause, 29(7), 767–794.
• Rosenthal, M. S., et al. (2019). Compounded bioidentical hormones: Regulation and quality. Regulatory and quality issues. Maturitas, 125, 1–6.
• Ross, R., et al. (2020). Exercise and insulin resistance. Exercise recommendations. Sports Medicine, 50(2), 1–15.
• Skene, D. J., et al. (2018). Circadian rhythms and health. Circadian rhythms and health. The Lancet, 392(10164), 550–565.
• Stanczyk, F. Z., & Clarke, N. J. (2014). Advantages of mass spectrometry for steroid hormones. Mass spectrometry in steroid measurement. Journal of Steroid Biochemistry and Molecular Biology, 141, 3–12.
• Stuenkel, C. A., et al. (2022). Menopausal hormone therapy update. Menopausal hormone therapy update. Journal of Clinical Endocrinology & Metabolism, 107(3), 819–838.
• Stute, P., et al. (2020). Micronized progesterone: Safety and efficacy. Micronized progesterone. Climacteric, 23(4), 1–9.
• Van Cauter, E., Leproult, R., & Plat, L. (2008). GH secretion and sleep. GH and sleep. European Journal of Endocrinology, 159(Suppl 1), S29–S36.
• Vinogradova, Y., et al. (2019). VTE risks with oral vs transdermal HRT. VTE risks HRT. BMJ, 364, k4810.
• Wierman, M. E., et al. (2014). Androgen therapy in women. Endocrine Society guideline on androgens in women. Journal of Clinical Endocrinology & Metabolism, 99(10), 3489–3510.
• Young, S. N. (2019). Nutrition and mental health. Nutrition and neurotransmitters. Canadian Journal of Psychiatry, 64(1), 3–8.

SEO tags

bioidentical hormones, BHRT, integrative chiropractic, menstrual migraines, perimenopause dosing, oral contraceptives risks, progesterone endometrial protection, libido therapy women, testosterone cream women, levonorgestrel IUD, LC-MS/MS hormones, immunoassay pitfalls, adolescent hormone health, IGF-1 sleep, gut-brain axis anxiety, autonomic balance chiropractic, transdermal estradiol safety, progesterone micronized, menopausal transition, injection technique testosterone