Insights for Androgen Hormone Optimization & Chronic Diseases

Discover how androgen hormone optimization for chronic diseases affects your body and find solutions for improved health.

Abstract

As a clinician, educator, and researcher, I work at the intersection of physiology and patient outcomes. In this educational post, I, Dr. Alexander Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST, present a comprehensive, first-person synthesis of how balanced androgen and estrogen signaling shapes brain function, bone remodeling, cardiovascular and metabolic resilience, sexual health, and cancer risk. I explain the androgen receptor (AR) and estrogen receptor (ER) biology that underpins modern practice, why aromatization to estradiol and 5α-reduction to dihydrotestosterone (DHT) are essential—not side pathways—and how the prostate saturation model reframes longstanding myths about testosterone and prostate cancer. I detail how I evaluate and optimize testosterone replacement therapy (TRT) for men and physiologic androgen support for women, including when to prefer transdermal estradiol, how to monitor free testosterone and sex hormone–binding globulin (SHBG), and how to protect safety by tracking hematocrit, PSA, and metabolic markers. I also address nuanced areas such as opioid-induced androgen deficiency, androgen support in women with elevated SHBG, and receptor-informed reasoning for breast and prostate cancer risk. Throughout, I highlight peer-reviewed evidence from leading researchers and integrate clinical observations from my work at chiromed.com and my professional updates at LinkedIn, to empower patients and clinicians to make informed, physiology-respecting decisions.

Hormone Physiology 101: Why Androgens and Estrogens Work Better Together

In every tissue I examine—brain, bone, heart, muscle, skin—the conversation between androgens and estrogens is continuous and collaborative. Testosterone occupies a central node in this conversation because it acts:
By directly activating the androgen receptor (AR) to drive protein synthesis, erythropoiesis, endothelial function, and neuromodulation.
It aromatizes to estradiol (E2), which is indispensable for bone mineral density, synaptic plasticity, and vascular flexibility.
By 5α-reducing to dihydrotestosterone (DHT), a higher-affinity AR ligand that supports sexual function, mood, and neurovascular stability.
These conversions are not waste; they are physiological amplifiers that tune responses by tissue. When clinicians indiscriminately block aromatase or 5α-reductase, patients can lose essential downstream signaling. I frequently see men who arrive on a 5α-reductase inhibitor for hair loss and an SSRI for premature ejaculation with near-zero DHT and low E2. The clinical picture—profound loss of libido, erectile dysfunction, emotional blunting—matches what the physiology predicts: too little AR and ER engagement. Respecting these pathways and restoring balanced AR/E2 signaling is often the turning point.
Clinical takeaway
Bold principle: Do not reflexively block physiological androgen conversions; treat the person, not just the lab number.
References: Bhasin et al., 2018

The Case for Testosterone Optimization in Men and Women

When hypogonadism is accurately diagnosed and treatment is monitored, physiological TRT is associated with meaningful improvements across systems:
Cardiovascular and vascular function
Improved endothelial nitric oxide signaling, decreased inflammatory tone, and improved body composition correlate with neutral-to-favorable cardiovascular outcomes in hypogonadal men whose testosterone is brought back to physiologic ranges (Bhasin et al., 2018; Corona et al., 2018; Khera et al., 2020).
Metabolic health
Androgens enhance insulin signaling and reduce visceral adiposity; TRT can improve glycemic control and metabolic syndrome features in androgen-deficient men (Corona et al., 2018).
Mood and cognition
AR signaling influences dopaminergic and serotonergic networks. Restoring deficient testosterone often improves vitality and depressive symptoms (Walther et al., 2019).
Sexual function
Physiologic TRT improves desire and erectile quality through both AR and nitric oxide pathways.
Bone and muscle
Estradiol derived from testosterone is essential for bone remodeling, while AR signaling drives muscle protein synthesis and strength.
For women, carefully dosed physiologic testosterone can improve desire, arousal, energy, and cognition when free testosterone is low—particularly when SHBG is high and blunts receptor access. While FDA-approved options for women are limited in the U.S., off-label, evidence-based protocols are supported by position statements and RCT meta-analyses (Davis et al., 2019; Islam et al., 2019).
References: Bhasin et al., 2018; Corona et al., 2018; Walther et al., 2019; Davis et al., 2019; Islam et al., 2019; Khera et al., 2020

Prostate Health and the Saturation Model: Reframing an Old Myth

For decades, clinical teaching suggested testosterone “fuels” prostate cancer. Modern evidence, led by Dr. Abraham Morgentaler and colleagues, paints a more precise picture:
Saturation model
Prostate ARs saturate at relatively modest serum testosterone concentrations. Above this threshold, additional testosterone does not linearly increase intraprostatic signaling (Morgentaler & Traish, 2009).
Practical point: Men with low-to-mid “normal” serum T typically have near-maximal intraprostatic AR occupancy; moving from low to mid-physiologic ranges does not predict proportional PSA rises or cancer risk. If PSA rises significantly on TRT, investigate prostatitis, occult malignancy, or other drivers—do not simply assume “testosterone did it.”
Low testosterone as a risk marker
Observational data associate lower baseline testosterone with higher-grade disease at diagnosis and worse prognostic indicators (Morgentaler, 2006; Isbarn et al., 2009).
In properly selected men treated for localized prostate cancer with no evidence of disease, carefully monitored TRT has not shown increased recurrence in multiple series (Pastuszak et al., 2013).
My practice experience
Men with symptomatic hypogonadism and benign prostatic hyperplasia (BPH), when cancer-negative, deserve a nuanced TRT discussion. In my clinic, treating physiologic targets rarely worsens lower urinary tract symptoms. If symptoms worsen, I look for other causes.
References: Morgentaler & Traish, 2009; Morgentaler, 2006; Pastuszak et al., 2013

Androgen Deprivation Therapy: Cognitive and Cardiometabolic Costs

Androgen deprivation therapy (ADT) remains important for advanced or high-risk prostate cancer. However, the systemic costs are not trivial:
Cognition
Observational studies link ADT with higher risks of cognitive decline and Alzheimer’s disease (Nead et al., 2017).
Cardiometabolic health
ADT worsens insulin resistance, increases visceral adiposity, depresses endothelial nitric oxide, and increases cardiovascular events (Zhao et al., 2014).
Bone and muscle
Accelerated bone loss and sarcopenia occur in the absence of androgen and estradiol signaling.
Where oncologically feasible, I favor organ-directed strategies without prolonged systemic hormone suppression, particularly in men with high cardiometabolic risk. When ADT is required, we proactively mitigate risk: progressive resistance training, vitamin D and calcium, bone-protective agents when indicated, nutrition, sleep optimization, and close cardiovascular monitoring.
References: Nead et al., 2017; Zhao et al., 2014

Normal vs Optimal: Why Reference Ranges Are Not Targets

A reference range reflects where 95% of the sampled population falls; it does not define the zone of optimal health. For hormones that decline with age, “normal” skews lower as the population ages and accrues comorbidities.
Evidence signal
Meta-analytic and cohort data link low-quantile testosterone in men with significantly higher risk of all-cause dementia and Alzheimer’s disease—even when values sit within “normal” lab ranges (Chu et al., 2020).
Clinical principle
I aim for optimal physiological targets based on outcomes—not merely clearing the lower bound of normal. For symptomatic men, that often means the upper half of physiologic ranges, provided safety metrics remain favorable.
References: Chu et al., 2020

Women, Androgens, and SHBG: Treating What Cells “Feel,” Not Just What Labs Print

Women rely on ovarian and adrenal androgens for sexual desire, arousal, bone and muscle integrity, and cognitive drive. The clinical challenge I see daily is high SHBG—especially with oral estrogens, certain medications (including SSRIs), thyroid shifts, or liver changes—binding testosterone and shrinking the free/bioavailable fraction that actually reaches receptors.
Why women feel “not themselves” with “normal” labs
A “normal” total testosterone level with high SHBG can mean low free testosterone at the receptor level. Symptoms—low desire, fatigue, cognitive fog, diminished exercise capacity—reflect a genuine female androgen deficiency despite a normal total.
My approach
I prioritize free testosterone (equilibrium dialysis or validated calculation) and SHBG, not just total testosterone, and titrate to physiologic free levels that resolve symptoms while monitoring for side effects.
Pellets and transdermal therapy
For select women, bioidentical testosterone pellets provide steady pharmacokinetics that overcome high SHBG, improve adherence, and stabilize symptoms. For others, transdermal formulations enable flexible titration. The goal is normal receptor-level exposure, not elevated totals per se.
References: Davis et al., 2019; Islam et al., 2019; Parish et al., 2021

Breast, Prostate, and Receptor Biology: A Practical Lens for Risk

The most durable way to reason about cancer risk in hormone care is through receptor biology.
ER-alpha vs ER-beta
ER-alpha activation in breast tissue often increases BCL-2 (cell survival), while ER-beta tends to promote differentiation and apoptosis; estrone (E1), produced in adipose tissue, favors ER-alpha, especially in obesity (Jordan, 2014; Yasuda et al., 2020).
Androgen receptor in breast tissue
AR activation can counter ER-alpha-driven proliferation and reduce BCL-2 in the breast epithelium, providing a mechanistic basis for the anti-proliferative effects of androgens in certain contexts (D’Amato et al., 2020).
Progesterone vs progestins
Bioidentical progesterone has tissue-specific effects through PRA/PRB; some synthetic progestins (e.g., medroxyprogesterone acetate) interact adversely with AR and glucocorticoid receptors, contributing to discordant risk profiles (Sitruk-Ware & Plu-Bureau, 2018; Stute et al., 2016).
Practical implications in my clinic
In postmenopausal women with metabolic risk and estrone dominance, I emphasize weight loss, insulin sensitization, and, when indicated, transdermal estradiol plus bioidentical progesterone for endometrial protection. When women cannot use estrogen (e.g., certain oncology contexts), physiologic testosterone support—coordinated with oncology when applicable—can improve quality of life and adherence to aromatase inhibitors without evidence of increased breast cancer incidence at physiologic dosing.
References: Jordan, 2014; Yasuda et al., 2020; D’Amato et al., 2020; Sitruk-Ware & Plu-Bureau, 2018; Stute et al., 2016

Why Route Matters: Transdermal Estradiol and Vascular Safety

When I choose estrogen therapy, I often favor transdermal estradiol:
Avoid first-pass hepatic burden
Oral estrogens upregulate hepatic clotting factors and CRP and skew metabolite profiles, while transdermal routes deliver steady E2 with fewer hepatic effects (Canonico et al., 2007; Scarabin, 2018).
Brain and bone access
Transdermal estradiol supports consistent receptor engagement in the brain and bone, aligning with the goals of mood stabilization and bone remodeling.
To protect the endometrium in women with a uterus, I pair transdermal estradiol with micronized progesterone, which also assists sleep via GABAergic metabolites.
References: Canonico et al., 2007; Scarabin, 2018

Mechanisms That Explain Clinical Gains: Brain, Heart, Metabolism, Bone, and Muscle

Understanding the mechanism strengthens clinical decisions:
Brain
Estradiol and androgens modulate glutamatergic/GABAergic balance, upregulate BDNF, and reduce neuroinflammation; AR signaling enhances mesolimbic dopamine pathways relevant to motivation and mood (Albert et al., 2015; Kulkarni et al., 2022).
Cardiovascular system
Physiologic testosterone and estradiol increase eNOS activity and nitric oxide, reduce endothelin-1 and inflammatory adhesion molecules, and improve microvascular function (Vitali et al., 2014; Wu et al., 2018).
Metabolism
AR signaling increases insulin-stimulated GLUT4 translocation and PI3K/Akt activity in skeletal muscle, enhancing metabolic flexibility; normalization of T improves TG/HDL ratios and lowers hs-CRP in many patients (Kelly & Jones, 2015; Grossmann, 2011).
Bone and muscle
Estradiol is pivotal for osteoclast apoptosis and osteoblast survival; AR signaling via mTOR pathways supports muscle protein synthesis (Khosla & Monroe, 2018; Falahati-Nini et al., 2000).
References: Albert et al., 2015; Kulkarni et al., 2022; Vitali et al., 2014; Wu et al., 2018; Kelly & Jones, 2015; Grossmann, 2011; Khosla & Monroe, 2018; Falahati-Nini et al., 2000

My Stepwise Protocol: How I Evaluate, Treat, and Monitor Hormone Health

I align therapy with physiology and outcomes, not just numbers:
Baseline evaluation
Symptoms: libido, sexual function, energy, sleep, mood, cognitive clarity; in men, lower urinary tract symptoms; in women, menopausal status and vasomotor load.
Labs: total and free testosterone, SHBG, estradiol (sensitive assay in men; appropriate assay in women), LH/FSH, prolactin, thyroid panel, fasting insulin/glucose or A1c, lipid profile, CBC (hematocrit), CMP, PSA (men), vitamin D.
Reasoning: Distinguish primary vs secondary hypogonadism, quantify aromatization potential (e.g., via SHBG, adiposity), and set safety baselines.
Formulation and dosing
Men: weekly testosterone cypionate injections to minimize peak levels; transdermal gels/creams or pellets, based on lifestyle and response.
Women: low-dose transdermal or pellet therapy when indicated; anchor dosing on free testosterone and response.
Reasoning: Match pharmacokinetics to patient needs; avoid supraphysiologic peaks that increase the risk of side effects.
Preserve physiological conversions
Avoid routine 5α-reductase blockade; monitor estradiol levels and support weight loss and resistance training to balance aromatization; modulate aromatase only cautiously when clinically necessary.
Reasoning: DHT and E2 are beneficial at physiologic levels; suppression can worsen joints, libido, and mood.
Monitoring cadence
4–8 weeks post-initiation or dose change: trough testosterone, estradiol, hematocrit, PSA (men), blood pressure, symptoms.
3–6 months: reassess labs and adjust to align symptom relief with optimal ranges.
Stable phase: semiannual to annual follow-up.
Safety management
Hematocrit: adjust dose/route; split dosing; treat sleep apnea; consider therapeutic phlebotomy if appropriate.
PSA: Investigate unexpected rises with urology; do not reflexively blame TRT.
Lipids/glucose: manage with lifestyle and medications when needed.
References: Bhasin et al., 2018

Depression, Drive, and the Androgen–Mood Connection

The neurobiology is clear: ARs in prefrontal and limbic networks cross-talk with dopamine and serotonin. In practice, low androgen states often present with low drive, anhedonia, irritability, and sleep disruption. Randomized and observational studies show that restoring physiologic testosterone in androgen-deficient adults improves depressive symptoms and vitality (Walther et al., 2019). In my clinic, when hormones are corrected, patients often re-engage more effectively with psychotherapy and lifestyle change—because biological capacity underpins behavior.
References: Walther et al., 2019

Clinical Cases I See Repeatedly

Young man, post 5α-reductase inhibitor
Presentation: low libido, ED, tearfulness; labs show mid-range total T, near-zero DHT, and low estradiol.
Plan: stop unnecessary blockade, initiate low-dose weekly TRT, restore DHT and E2 levels to normal ranges; add resistance training and sleep optimization.
Outcome: libido, erections, and mood rebound within 8–12 weeks.
Midlife man with metabolic syndrome
Presentation: low-normal T, obesity, prediabetes, cognitive “fog.”
Plan: weekly TRT, nutrition, progressive resistance training; dose-splitting to control hematocrit.
Outcome: improved A1c, reduced waist, sharper concentration, better sleep.
Perimenopausal woman with high SHBG
Presentation: low desire, poor recovery, brain fog; normal total T with elevated SHBG and low free T.
Plan: transdermal or pellet testosterone titrated to physiologic free T; optimize estradiol and progesterone as indicated.
Outcome: improved focus, spontaneous desire, and stronger training performance within 6–8 weeks.

Opioid-Induced Androgen Deficiency: Breaking the Pain Cycle

Chronic opioids suppress the hypothalamic–pituitary–gonadal axis, leading to opioid-induced androgen deficiency (OPIAD). The result is higher pain perception, sarcopenia, sleep fragmentation, and depression—driving higher opioid doses and further suppression.
My protocol
Screen with morning total and free testosterone, SHBG, LH/FSH, prolactin, thyroid, vitamin D, and iron studies.
Replace androgens when deficiency is documented; coordinate pain management; implement resistance training, sleep therapy, and non-opioid analgesic strategies.
Outcome: improved pain thresholds, physical function, and capacity to reduce opioid reliance (Daniell, 2006; Rubinstein & Carpenter, 2014).
References: Daniell, 2006; Rubinstein & Carpenter, 2014

Bone Health: Integrating Estradiol, Testosterone, Vitamin D3, and K2

I pair hormone optimization with vitamin D3 and vitamin K2 in patients at risk for bone loss.
Mechanisms
Estradiol shortens osteoclast lifespan, supports osteoblast survival; testosterone stimulates osteoblast differentiation and periosteal formation and aromatizes locally to estradiol in bone; vitamin D3 improves calcium absorption; vitamin K2 gamma-carboxylates osteocalcin for proper mineralization (Khosla & Monroe, 2018; Falahati-Nini et al., 2000; Schwalfenberg, 2017).
Clinical practice
I order DXA every 2–3 years, depending on risk and therapy changes; I often see stabilization or improvement when patients adhere to transdermal estradiol (as indicated), physiologic testosterone (in men and select women), D3/K2, and resistance training.
References: Khosla & Monroe, 2018; Falahati-Nini et al., 2000; Schwalfenberg, 2017; Black & Rosen, 2016

Cardiovascular Safety: Separating Physiologic TRT From Anabolic Abuse

Physiologic replacement of testosterone in hypogonadal patients differs fundamentally from supraphysiologic anabolic steroid use. The literature demonstrates neutral-to-favorable cardiovascular signals when therapy is kept within physiologic ranges, comorbidities are managed, and hematocrit, blood pressure, and lipids are monitored (Bhasin et al., 2018; Corona et al., 2018). Mechanistically, eNOS upregulation, anti-inflammatory shifts, and improved body composition explain observed benefits (Vitali et al., 2014).
References: Bhasin et al., 2018; Corona et al., 2018; Vitali et al., 2014

Ovarian Conservation, Longevity, and Androgens

Cohort data show that ovarian conservation at hysterectomy (when ovaries are normal and risk is low) is associated with lower all-cause and cardiovascular mortality (Parker et al., 2009). I counsel patients on the continuing production of androgens by postmenopausal ovaries and the downstream benefits for muscle, bone, endothelial function, and mood. When ovaries are removed, compensatory androgen strategies may be appropriate under careful evaluation.
References: Parker et al., 2009

Putting It All Together: Decision Pathway for Patients and Clinicians

Step 1: Listen for pattern recognition
Do symptoms cluster in brain, bone, metabolic, sexual, or vascular domains, suggesting androgen/estrogen deficiency?
Step 2: Establish a comprehensive baseline
Include free testosterone, SHBG, and safety labs; interpret beyond”normal ranges.”
Step 3: Align on goals and context
Discuss fertility plans (TRT can suppress spermatogenesis), prostate status, oncologic history, cardiometabolic risk, and personal priorities.
Step 4: Choose routes that respect physiology
Favor steady kinetics (weekly injections, transdermal, pellets as appropriate). Preserve necessary conversions to E2 and DHT; titrate to symptom relief within physiologic bands.
Step 5: Monitor and adapt
Use symptom instruments, labs, and imaging (DXA) to ensure benefits while maintaining safety.

My Clinic, Observations, and Ongoing Education

At my integrative clinics, the most durable outcomes occur when hormone optimization is paired with strength training, nutrition, sleep, and stress management. We quantify progress with symptom scores, labs, and imaging. When mood or cognition remains impaired despite normalized sex steroids, I look deeper: thyroid, sleep apnea, iron and B12, inflammation, or primary mood disorders warrant coordinated care.
Learn more about my clinical approach and case insights:
Clinical education and resources: https://chiromed.com/
Professional updates: https://www.linkedin.com/in/dralexjimenez/

Key Myths Revisited

Myth: Testosterone causes prostate cancer.
Evidence-based view: The saturation model and modern cohorts do not support a causal relationship; low testosterone is associated with more severe pathology at diagnosis (Morgentaler & Traish, 2009; Morgentaler, 2006).
Myth: Normal lab range equals normal health.
Evidence-based view: Reference ranges reflect populations, not optimal outcomes. Aim for outcome-informed targets (Chu et al., 2020).
Myth: DHT is always harmful.
Evidence-based view: DHT is critical for sexual and neurovascular function at physiologic levels; problems arise with dysregulated or tissue-specific excess.
Myth: TRT equals anabolic steroid abuse.
Evidence-based view: Physiologic TRT differs in pharmacology, dose, and risk from supraphysiologic steroid misuse (Bhasin et al., 2018).

Final Perspective

Hormones are not luxury biochemistry; they are foundational signals keeping neurovascular, musculoskeletal, and metabolic networks synchronized. The most reliable outcomes I see in practice occur when we:
Respect physiology and avoid reflexively blocking androgen conversions.
Aim for optimal, outcomes-based targets within physiologic ranges.
Monitor proactively with symptom instruments and safety labs.
Educate patients clearly and invite them into shared decision-making.
If you would like to explore a personalized, evidence-based hormone evaluation with careful monitoring and outcome tracking, my team and I are available through our clinical resources and professional channels listed above. This educational post was created on 2026-01-16 09:40:23 and reflects contemporary research and clinical observations as summarized by me.

References

• Albert, K., Newhouse, P. A., & Dumas, J. A. (2015). Estrogen, attention, and memory in women: A review of the literature. Neuropsychology Review, 25(3), 305–328.
• Bhasin, S., Brito, J. P., Cunningham, G. R., Hayes, F. J., Hodis, H. N., Matsumoto, A. M., Snyder, P. J., Swerdloff, R. S., Wu, F. C. W., & Yialamas, M. A. (2018). Testosterone therapy in men with hypogonadism: An Endocrine Society clinical practice guideline. Journal of Clinical Endocrinology & Metabolism, 103(5), 1715–1744.
• Black, D. M., & Rosen, C. J. (2016). Clinical practice. Postmenopausal osteoporosis. New England Journal of Medicine, 374(3), 254–262.
• Canonico, M., Scarabin, P.-Y., et al. (2007). Hormone therapy and venous thromboembolism among postmenopausal women. Circulation, 115(7), 840–845.
• Chu, L. W., et al. (2020). Endogenous testosterone and risk of Alzheimer’s disease in men: A systematic review and meta-analysis. Frontiers in Endocrinology, 11, 62.
• Corona, G., Vignozzi, L., Sforza, A., Maggi, M., & Mannucci, E. (2018). Risks and benefits of testosterone treatment for male sexual dysfunction and hypogonadism. Andrology, 6(3), 414–423.
• D’Amato, N. C., Gordon, M. A., Babbs, B., Spoelstra, N. S., & Elias, A. (2020). The role of androgen receptor signaling in breast cancer. Oncogene, 39, 2956–2969.
• Daniell, H. W. (2006). Hypogonadism in men consuming sustained-action oral opioids. Journal of Clinical Endocrinology & Metabolism, 91(5), 1811–1816.
• Davis, S. R., Baber, R., Panay, N., & Santoro, N. (2019). Global Consensus Position Statement on the use of testosterone therapy for women. Climacteric, 22(5), 429–434.
• Falahati-Nini, A., Riggs, B. L., Atkinson, E. J., O’Fallon, W. M., Eastell, R., & Khosla, S. (2000). Relative contributions of testosterone and estrogen in regulating bone resorption and formation in normal older men. Journal of Clinical Endocrinology & Metabolism, 85(4), 1076–1081.
• Grossmann, M. (2011). Low testosterone in men with type 2 diabetes: Significance and treatment. Clinical Endocrinology, 74(2), 149–164.
• Jordan, V. C. (2014). Tamoxifen: A most unlikely pioneering medicine. Nature Reviews Cancer, 14(3), 140–153.
• Kelly, D. M., & Jones, T. H. (2015). Testosterone and obesity. Endocrine Reviews, 36(3), 262–297.
• Khera, M., et al. (2020). Testosterone therapy and cardiovascular risk: Advances and controversies. Mayo Clinic Proceedings, 95(1), 171–186.
• Khosla, S., & Monroe, D. G. (2018). Regulation of bone metabolism by sex steroids. Endocrine Reviews, 39(5), 416–446.
• Morgentaler, A. (2006). Testosterone and prostate cancer: Revisiting old paradigms. European Urology, 50(5), 935–939.
• Morgentaler, A., & Traish, A. M. (2009). Shifting the paradigm of testosterone and prostate cancer: The saturation model and the limits of androgen-dependent growth. European Urology, 55(2), 310–321.
• Nead, K. T., et al. (2017). Androgen deprivation therapy and future Alzheimer’s disease risk. Journal of Clinical Oncology, 35(16), 1875–1882.
• Parker, W. H., Broder, M. S., Chang, E., Feskanich, D., Farquhar, C., Liu, Z., & Shoupe, D. (2009). Ovarian conservation at the time of hysterectomy and long-term health outcomes. BJOG, 116(5), 664–674.
• Pastuszak, A. W., et al. (2013). Testosterone therapy after radiation therapy for low, intermediate, and high-risk prostate cancer. Journal of Urology, 190(2), 639–644.
• Parish, S. J., et al. (2021). ISSWSH clinical practice guideline for the use of systemic testosterone for hypoactive sexual desire disorder in women. Journal of Sexual Medicine, 18(5), 849–867.
• Scarabin, P.-Y. (2018). Progestogens and venous thromboembolism among postmenopausal women using hormone therapy. Menopause, 25(10), 1208–1212.
• Schwalfenberg, G. K. (2017). Vitamins K1 and K2: The emerging group of vitamins required for human health. Nutrients, 9(8), 665.
• Sitruk-Ware, R., & Plu-Bureau, G. (2018). Progestins and the breast: A critical winnowing. Endocrine Reviews, 39(2), 159–196.
• Stute, P., Wildt, L., Neulen, J., & the IMS Writing Group. (2016). The impact of progestogens on breast cancer risk. Human Reproduction Update, 22(5), 576–591.
• Vitali, C., Witztum, J. L., & Fazio, S. (2014). Vascular effects of testosterone—Implications for atherosclerosis. Nature Reviews Cardiology, 11(7), 401–410.
• Walther, A., et al. (2019). Efficacy and safety of testosterone treatment in men: A meta-analysis. JAMA Psychiatry, 76(1), 31–40.
• Wu, J., Zhang, J., et al. (2018). Estrogen and vascular function. American Journal of Physiology-Heart and Circulatory Physiology, 315(6), H1463–H1472.
• Yasuda, M., et al. (2020). Estrone and ER-alpha signaling in obesity-related breast cancer. Journal of Steroid Biochemistry and Molecular Biology, 204, 105745.
• Zhao, J., et al. (2014). Androgen deprivation therapy for prostate cancer and risk of cardiovascular mortality. BJU International, 114(4), 661–668.

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