Hormone Therapy Explained for Vasomotor Symptoms & Cardiometabolic Risk

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Abstract

Menopause brings profound whole-body changes that can affect sleep, mood, metabolism, cardiovascular health, musculoskeletal comfort, and especially vasomotor symptoms (VMS) such as hot flashes and night sweats. In this educational post, I share a first-person, clinically grounded journey through the physiology of VMS, why symptoms occur, and the modern, evidence-based treatments that help. I am Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST. In our El Paso practice, Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic), I collaborate with Dr. Maria Guadalupe Cardenas, MD (Board Certified in Internal Medicine) (NPI #1164426749, Texas MD License #J2933), who serves as our Medical Director and Collaborative Physician. Together, we deliver multidisciplinary care that integrates chiropractic, internal medicine oversight, functional medicine, personal injury care, rehabilitation, and supportive therapies. You will learn how hypothalamic thermoregulation shifts with estrogen decline, how KNDy neurons drive hot flashes, and how hormone therapy, nonhormonal pharmacologic options (including fezolinetant), lifestyle, and spine-neuroendocrine-informed chiropractic strategies combine to provide relief. I include clinical observations from my work and from the HealthCoach platform. Clinic and LinkedIn to illustrate how patient-centered, stepwise care restores sleep, function, and confidence (Freedman, 2014; Harlow et al., 2012; North American Menopause Society, 2022; Prague & Dhillo, 2023).

My Role, Our Team, and Why Vasomotor Symptoms Matter

I am Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST. At Injury Medical Clinic PA, also known as Mission Plaza Injury Medical Clinic in El Paso, Texas, I partner with Dr. Maria Guadalupe Cardenas, MD, Board Certified in Internal Medicine (NPI #1164426749, Texas MD License #J2933). With over 40 years of experience in internal medicine, Dr. Cardenas serves as our Medical Director and Collaborative Physician. This multidisciplinary model is common to integrative and injury care clinics, where an MD provides medical direction alongside a chiropractor to create coordinated, safe, and comprehensive care.

Why focus on vasomotor symptoms (VMS)? Because hot flashes and night sweats derail sleep, cognition, mood, work performance, and relationships. I routinely see patients like the composite case of “Miss Jenny,” a 52-year-old postmenopausal researcher whose daytime hot flashes and nocturnal sweats escalated over two years, now impairing quality of life. Many patients previously felt ignored or rushed. Our mission is to listen, explain physiology clearly, and provide individualized, evidence-based care that respects preferences and risk profiles.

Menopause Definitions, Timelines, and Staging: The Clinical Grounding

• Menopause is clinically defined as the final menstrual period followed by 12 months of amenorrhea in the absence of other causes.
• The menopausal transition often begins between ages 45–55; the median age of natural menopause in the United States is approximately 52.5 years (Taylor, 2023; Santoro & Randolph, 2016).
• Terminology:

• • Early menopause: before age 45
  • Premature menopause: before age 40
  • Postmenopause: begins after 12 months of amenorrhea

• Multiple systems are affected: cardiovascular, skeletal, genitourinary, neuroendocrine, and central nervous system—a whole-body transition (Taylor, 2023; Santoro & Randolph, 2016).

Staging frameworks like STRAW+10 clarify expected patterns across late reproductive, transition, early postmenopause, and late postmenopause stages (Harlow et al., 2012):

• Late reproductive:

• • Subtle cycle changes; FSH variability; inhibin declines

• Menopausal transition (perimenopause):

• • Early: cycle length difference increases by ? 7 days
  • Late: intervals ? 60 days; intermittent amenorrhea; FSH rises; estradiol fluctuates; VMS increases

• Early postmenopause:

• • VMS often peaks; FSH stabilizes high; estradiol remains low

• Late postmenopause:

• • VMS may resolve, but up to 50% experience symptoms >7 years, with duration varying by ethnicity (Avis et al., 2015)

Clinical takeaway: For women at a typical menopausal age, diagnosis is primarily clinical; routine FSH/E2 testing is usually unnecessary due to variability and limited diagnostic utility (Harlow et al., 2012; Santoro & Randolph, 2016). Testing is reserved for atypical scenarios or when it aids shared decision-making.

Hormonal Physiology: What Drives Vasomotor Symptoms

Understanding hormone changes clarifies why treatments work.

• Inhibin decline:

• • Ovarian inhibin normally suppresses FSH. With follicular depletion, inhibin levels fall, FSH levels rise, and cyclicity becomes destabilized (Santoro & Randolph, 2016).

• Estradiol (E2) vs. estrone (E1):

• • E2 falls sharply after menopause. E1, derived from adrenal and adipose sources, becomes relatively predominant, but overall estrogenic tone is low. Reduced E2 influences hypothalamic thermoregulation and neurotransmission (Santoro & Randolph, 2016).

• Progesterone:

• • Declines due to anovulation during the transition; contributes to sleep fragmentation and cycle changes (Baker et al., 2017).

• Androgens and DHEAS:

• • Testosterone may decrease but often remains within the reference range. DHEAS declines with age rather than directly due to menopause (Davison et al., 2005).

• FSH and LH:

• • FSH rises with reduced ovarian feedback. LH pulsatility is closely associated with hot flashes, reflecting hypothalamic KNDy neuronal dynamics (Mostari et al., 2014).

Neuroendocrine Thermoregulation: Why Hot Flashes Happen

Hot flashes are measurable neurophysiologic events, not “just in the head.”

• Narrowed thermoneutral zone:

• • With decreased estrogen, the hypothalamus becomes hyperresponsive to small changes in core temperature. Heat-loss responses—vasodilation and sweating—trigger rapidly and are felt as a flash followed by chills (Freedman, 2014).

• KNDy neurons:

• • Hypothalamic neurons co-express kisspeptin, neurokinin B (NKB), and dynorphin. Estrogen dampens NKB. Low estrogen disinhibits NKB activity, increasing KNDy firing, narrowing the thermoneutral zone, and precipitating flashes (Rance et al., 2013; Prague & Dhillo, 2023).

Clinical implications:

• Therapies that restore estrogen signaling or modulate NKB/KNDy pathways reduce VMS frequency and intensity.
• This is the rationale for menopausal hormone therapy (HT) and NK3R antagonists like fezolinetant.

Clinical Presentation and Health Impacts

• Symptoms:

• • Sudden upper-body warmth, facial flushing, intense sweating lasting seconds to minutes, followed by chills; often worse at night, disrupting sleep (Freedman, 2014).

• Duration:

• • VMS can persist beyond 7 years for ~50% of women; duration varies by ethnicity, with African American women often experiencing longer symptoms (Avis et al., 2015).

• Associated risks:

• • Severe, prolonged VMS correlates with higher cardiovascular risk markers, including adverse endothelial function and blood pressure variability. Sleep fragmentation worsens insulin resistance, appetite regulation, and pain sensitivity (El Khoudary & Thurston, 2018).

Our Multidisciplinary Model: Medical Oversight Meets Integrative Chiropractic

At Injury Medical Clinic PA, our coordinated structure improves safety, speed, and personalization.

• Medical direction and safety (Dr. Cardenas):

• • Confirms diagnosis; evaluates contraindications; orders labs or imaging when indicated; guides pharmacotherapy choices (HT, SSRIs/SNRIs, fezolinetant); and coordinates with cardiology or oncology.

• Integrative chiropractic care (Dr. Jimenez):

• • Addresses musculoskeletal contributors to autonomic dysregulation: upper thoracic fascial tension, ribcage mobility, cervical sympathetic chain irritation, diaphragm mechanics. We use targeted spinal adjustments, myofascial release, rib mobilization, and breathing retraining to reduce sympathetic overdrive and improve vagal tone, supporting sleep and autonomic balance.

• Functional medicine:

• • Identifies cardiometabolic risks (insulin resistance, dyslipidemia, hypertension), nutrient insufficiencies, gut-liver detoxification issues, and inflammation that amplify VMS severity.

• Rehabilitation:

• • Customized strength, mobility, and aerobic prescriptions improve endothelial function, thermoregulation, and mood; physical therapy and corrective exercise reinforce structural and autonomic resilience.

• Personal injury care and related services:

• • For patients with concurrent injuries, coordinated rehab and pain modulation reduce central sensitization and promote restorative sleep.

Patient-Centered Workflow and Decision-Making

• History and exam:

• • Menstrual timeline; symptom triggers (heat, stress, alcohol, spicy food); sleep quality; mood changes; genitourinary symptoms; bone health; migraine history; VTE risks; oncologic history.

• Targeted testing when indicated:

• • Cardiometabolic panel (lipids, A1c, fasting glucose/insulin), thyroid screening, ferritin, vitamin D, and selected hormones if atypical. We do not rely on FSH/E2 for routine diagnosis, but use labs to personalize risk reduction.

• Shared decision-making:

• • We align options with patient values, reviewing efficacy, safety, and logistics. For “Miss Jenny,” prioritizing night sweats and sleep loss made VMS-targeted therapy

Evidence-Based Treatments: Hormonal and Nonhormonal Choices

Menopausal Hormone Therapy (HT)

• Indications:

• • Moderate to severe VMS in women within 10 years of menopause onset and under age 60, without contraindications (North American Menopause Society, 2022).

• Rationale:

• • Restores estrogen’s modulation of KNDy neurons and widens the thermoneutral zone; reduces VMS frequency/intensity; improves sleep; supports urogenital tissue health (Freedman, 2014; Prague & Dhillo, 2023).

• Choices:

• • Estrogen-only for those without a uterus.
  • Combined estrogen-progestin for those with an intact uterus to protect the endometrium; micronized progesterone is often favored for endometrial protection and potential sleep benefits (Baker et al., 2017).

• Formulations:

• • Transdermal estradiol is preferred for minimizing thrombotic risk; oral estradiol is appropriate for select patients. Combination patches or separate progesterone can be used based on tolerability.

• Risk management:

• • We review cardiovascular risk, breast health risk, migraine with aura, VTE history, and liver disease; route/dose adjusted accordingly (American College of Obstetricians and Gynecologists, 2023).

• Monitoring:

• • Symptom relief; blood pressure; weight; breast and pelvic exams; mammography per guidelines; periodic reassessment to taper or continue based on benefit-risk balance.

Clinical nuance: Following WHI-era concerns, modern practice often favors transdermal estradiol and micronized progesterone, which appear to offer more favorable VTE and, potentially, breast cancer risk profiles compared with older oral conjugated estrogens and certain synthetic progestins (Rossouw et al., 2002; L’hermite, 2017).

Nonhormonal Pharmacologic Options

• Neurokinin 3 receptor antagonist:

• • Fezolinetant directly targets NKB signaling in KNDy neurons, reducing hot flashes without estrogen exposure—ideal for women with contraindications to HT or preference for nonhormonal therapy (Prague & Dhillo, 2023).

• SSRIs/SNRIs:

• • Paroxetine, venlafaxine, escitalopram reduce VMS via central serotonergic/noradrenergic modulation of hypothalamic thermoregulation (North American Menopause Society, 2022).

• Gabapentin:

• • Useful for nocturnal VMS; enhances sleep continuity; mechanisms involve central calcium channel modulation and hypothalamic pathway stabilization.

• Clonidine:

• • Modest efficacy; alpha-2 agonist that can reduce sympathetic tone; considered when others are unsuitable.

Genitourinary Syndrome of Menopause (GSM)

• Local vaginal estrogen:

• • Restores epithelial integrity, pH, and microbiome with minimal systemic absorption; meaningful for dyspareunia and urinary symptoms (North American Menopause Society, 2020).

• Alternatives:

• • DHEA (prasterone) or ospemifene for specific scenarios.

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Aligned & Empowered: Chiropractic Conversations on Women’s Health- Video

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Lifestyle, Functional Medicine, and Rehabilitation: Building Physiological Resilience

• Sleep hygiene:

• • Cool bedroom; breathable fabrics; pre-sleep relaxation; optimize fluid timing; consistent wake times.

• Metabolic support:

• • Mediterranean-style nutrition with adequate protein; omega-3s, magnesium, vitamin D; alcohol moderation; caffeine timing to reduce nocturnal triggers (Estruch et al., 2018).

• Exercise:

• • Aerobic training improves thermoregulatory stability and endothelial function; resistance training preserves bone and muscle mass; mind-body practices (yoga, paced breathing) reduce sympathetic arousal (American College of Sports Medicine, 2021).

• Trigger management:

• • Identify and reduce hot, spicy foods, hot beverages, and acute stressors; leverage cooling strategies and paced respiration.

• Chiropractic and manual therapy:

• • Targeted upper thoracic and cervical adjustments reduce nociceptive input to autonomic centers, thereby mitigating sympathetic tone; rib cage mobilization and diaphragm release improve ventilation and heat dissipation efficiency.

• Stress and mood:

• • Cognitive behavioral therapy and integrative psychotherapeutic support; adaptogens considered under medical supervision when appropriate, acknowledging evidence variability.

Reasoning: These nonpharmacologic strategies rarely suffice on their own for severe VMS, but they add meaningful benefit when layered onto HT or nonhormonal pharmacologic therapy, thereby improving autonomic balance, sleep, and adherence.

Why Integrative Chiropractic Care Fits Into VMS Treatment

Hormonal transitions intersect with the autonomic nervous system and spine mechanics.

• Autonomic modulation:

• • Upper thoracic and cervical dysfunction can amplify sympathetic output. Gentle adjustments and soft-tissue work reduce sympathetic drive and facilitate parasympathetic balance, raising the body’s temperature-change threshold.

• Respiratory mechanics:

• • Rib mobility and diaphragmatic efficiency enhance heat loss by improving ventilation and peripheral circulation, thereby complementing medical therapies that widen the thermoneutral zone.

• Pain and sleep synergy:

• • Reducing neck/upper back pain decreases nocturnal arousals and improves sleep architecture, stabilizing hypothalamic responsiveness.

• Functional assessment:

• • Postural analysis and corrective exercises reduce upper-crossed patterns and thoracic kyphosis, which impede chest wall heat dissipation.

My clinical observations from HealthCoach.Clinic and LinkedIn data show that patients who combine chiropractic, breathing retraining, sleep optimization, and medical therapy report fewer, shorter, and less intense night sweats, with improved daytime performance.

Dr. Cardenas’ Medical Oversight: Safety, Coordination, and Precision

With over 40 years of internal medicine experience, Dr. Cardenas ensures:

• Rigorous screening for HT suitability: breast cancer history, coronary artery disease, stroke/TIA, liver disease, and VTE risk.
• Selection of transdermal vs. oral routes based on cardiometabolic profile.
• Coordination with cardiology, oncology, neurology, and primary care when needed.
• Monitoring of blood pressure, lipids, A1c, weight, and sleep
• Pharmacovigilance for SSRI/SNRI or fezolinetant side effects and interactions.

Medical leadership stabilizes risk and enables integrative modalities to do their work.

Case Journey: Miss Jenny’s Plan

For a 52-year-old postmenopausal patient with 15 months of amenorrhea and severe nocturnal VMS:

• Step 1: Explain physiology in plain language

• • Decreased estradiol narrows the thermoneutral zone; KNDy neurons become hyperresponsive; small temperature shifts trigger heat-loss responses and awakenings.

• Step 2: Shared decision on therapy

• • If no contraindications, low-dose transdermal estradiol with micronized progesterone for endometrial protection.
  • If HT is declined or contraindicated, consider fezolinetant or an SSRI/SNRI; gabapentin for nocturnal predominance.

• Step 3: Integrative supports

• • Chiropractic care focusing on upper thoracic mobility, cervical balance, ribcage mechanics, diaphragm release; breathing retraining with paced expiration; reinforce sleep hygiene.
  • Nutrition emphasizing anti-inflammatory, cardiometabolic support; limit alcohol and caffeine near bedtime.

• Step 4: Track outcomes

• • VMS frequency/intensity diaries; sleep quality indices; blood pressure and weight trends; mood and cognitive function.

• Step 5: Reassess and adjust

• • Titrate dosing, switch agents if needed, and progressively reduce triggers via structured rehab and stress management.

Patients often report rapid improvements—sleeping through the night and fewer hot flashes—which validate the plan and motivate sustained lifestyle change.

Physiological Rationale for Each Intervention

• Estrogen therapy:

• • Widens the thermoneutral zone via restored hypothalamic estrogen feedback; stabilizes KNDy activity; reduces flash triggers and nocturnal surges (Freedman, 2014; North American Menopause Society, 2022).

• Progesterone (micronized):

• • Improves sleep onset and continuity; protects the endometrium; may modulate GABAergic tone (Baker et al., 2017).

• Fezolinetant:

• • Direct modulation of the NKB pathway reduces KNDy-driven thermoregulatory hypersensitivity without estrogen exposure (Prague & Dhillo, 2023).

• SSRIs/SNRIs:

• • Central serotonergic/noradrenergic balancing reduces hypothalamic heat-loss hypersensitivity; supports mood/anxiety comorbidities (North American Menopause Society, 2022).

• Gabapentin:

• • Attenuates nocturnal hypothalamic hyperexcitability; improves sleep architecture and reduces awakenings.

• Chiropractic and manual therapy:

• • Decrease nociceptive afferents to autonomic centers; improve ribcage/diaphragm biomechanics for heat dispersion; enhance vagal tone through pain reduction and mechanoreceptor input.

• Exercise:

• • Improves endothelial function and thermoregulatory stability; reduces central adiposity and systemic inflammation; increases stress resilience (American College of Sports Medicine, 2021).

• Nutrition:

• • Stabilizes glucose/insulin dynamics; provides substrates for neurotransmitter synthesis and detoxification; reduces vasodilatory triggers linked to alcohol/spicy foods (Estruch et al., 2018).

Individualizing Care: Risk-Benefit, Preferences, and Diversity

• Ethnic and racial differences in VMS duration and severity inform expectations and care planning (Avis et al., 2015).
• Cardiometabolic profiles guide the choice of HT route and dose, with an emphasis on exercise and nutrition.
• Personal values—desire to avoid hormones, prioritize sleep, or prefer rapid relief—shape the choice among fezolinetant, SSRIs/SNRIs, or HT.
• Comorbid pain and injury contexts underscore the value of chiropractic and rehab in reducing sympathetic arousal and improving restorative sleep.

Shared decision-making ensures the plan aligns with each patient’s goals and risk tolerance.

Annual and Follow-Up Care: Monitoring, Safety, and Adjustments

We schedule early follow-ups (e.g., 6 weeks) and annual evaluations to optimize safety and efficacy:

• Symptom trajectory: VMS, sleep, mood, cognition, GSM, musculoskeletal pain, activity tolerance.
• Side effects: Spotting, breast tenderness, bloating, headaches, fluid retention; adjust dose/route if needed.
• Breast health: Clinical breast exam and mammography per guidelines; risk discussions for continuous use beyond 3–5 years (US Preventive Services Task Force, 2024).
• Pelvic health: Pelvic exam and Pap smear as indicated; evaluate any postmenopausal bleeding.
• Bone health: DXA for at-risk patients; review calcium, vitamin D, resistance training, impact-loading.
• Cardiometabolic status: Lipids, blood pressure, glucose/insulin markers.
• Comorbidities: Hypertension, liver function, migraines, thrombotic history; prefer transdermal routes in higher-risk profiles.

This vigilance prevents late detection of adverse effects and maintains benefit-risk balance over time (American College of Obstetricians and Gynecologists, 2023; American College of Cardiology, 2020).

Addressing Misconceptions, Contraindications, and Cautions

• Breast issues or estrogen-sensitive issues:

• • Coordinate with oncology; avoid systemic estrogen; consider localized vaginal estrogen for severe GSM with specialist input due to minimal systemic absorption (North American Menopause Society, 2020).

• Unexplained postmenopausal bleeding:

• • Suspend therapy; pelvic ultrasound to assess endometrial thickness; endometrial biopsy as indicated.

• Arterial thrombotic disease:

• • Avoid oral estrogen; consider transdermal routes in select cases with specialist input after stabilization.

• Untreated hypertension:

• • Control blood pressure before initiation.

• Active liver disease:

• • Avoid conjugated oral estrogens; consider non-oral pathways and non-estrogen strategies.

• Cerebrovascular or cardiovascular disease:

• • Stabilize disease states before hormone considerations; route decisions individualized with team oversight.

These cautions reflect estrogen’s impacts on coagulation, lipid metabolism, vascular tone, and endometrial proliferation; team-based oversight minimizes serious events (American College of Obstetricians and Gynecologists, 2023; American College of Cardiology, 2020).

Clinical Observations and Practical Insights

From daily practice and reflections shared at HealthCoach.Clinic and LinkedIn:

• Patients on transdermal estradiol with micronized progesterone report steadier sleep, fewer hot flashes, and improved mood stability compared with similar oral regimens in comparable risk categories.
• Coordinated chiropractic sessions reduce neck and upper back pain exacerbated by nocturnal awakenings, thereby enabling better exercise adherence and faster functional gains.
• Combining localized vaginal estrogen with pelvic floor strategies significantly reduces urinary urgency and nocturia, restoring comfort and confidence.
• Structured follow-up—six weeks, three months, then semiannual—enables early adjustments that prevent discontinuation due to manageable side effects.

Action Plan: Step-by-Step Implementation

• Initial assessment:

• • Comprehensive history, risk stratification, and symptom profiling.
  • Baseline labs and imaging as indicated (lipids, glucose/insulin, LFTs, DXA, mammogram).

• Therapy selection:

• • Prefer transdermal estradiol for VMS.
  • Add nightly micronized progesterone for endometrial protection if a uterus is present.
  • Consider localized vaginal estrogen for GSM and urinary symptoms.

• Integrative supports:

• • Chiropractic adjustments and myofascial work for autonomic balance.
  • Functional medicine protocols for sleep, stress, insulin sensitivity, and bone health.
  • Rehabilitation and graded exercise tailored to tolerance.

• Monitoring:

• • Six-week follow-up for tolerability and efficacy.
  • Dose/route adjustments if side effects arise.
  • Annual exams with breast and pelvic evaluations; mammography per guidelines.
  • Ongoing cardiometabolic monitoring and DXA as indicated.

• Duration and reevaluation:

• • Reassess benefits and risks at 3–5 years; consider tapering if symptoms permit; continue vigilant screening.

Closing Perspective: From Physiology to Relief

Vasomotor symptoms reflect hypothalamic thermoregulatory changes driven by estrogen decline and hyperactivity of KNDy neurons. By combining targeted medical therapies with autonomic-calming chiropractic care, functional medicine supports, and rehabilitative strategies, patients regain sleep, confidence, and daily performance. If you are experiencing hot flashes or night sweats, our El Paso team—guided by Dr. Cardenas’ medical oversight and my integrative chiropractic approach—will help you safely and effectively navigate evidence-based options.

Explore more of my clinical observations:

• Health Coach Clinic: healthcoach.clinic/
• LinkedIn: www.linkedin.com/in/dralexjimenez/

References

• Menopausal hot flashes: Mechanisms, endocrinology, and therapy (Freedman, 2014)
• STRAW+10: Addressing the challenges of staging reproductive aging (Harlow et al., 2012)
• Duration of menopausal vasomotor symptoms over the menopause transition (Avis et al., 2015)
• Reproductive aging, menopause, and health outcomes (Santoro & Randolph, 2016)
• Menstrual and menopausal sleep disturbances (Baker et al., 2017)
• Androgen levels in women across lifespan (Davison et al., 2005)
• Relationships between LH pulsatility and hot flashes (Mostari et al., 2014)
• Neurokinin B and menopausal hot flushes: Translating KNDy science to therapy (Prague & Dhillo, 2023)
• VMS and cardiovascular risk: Current evidence (El Khoudary & Thurston, 2018)
• Mediterranean diet and cardiometabolic protection (Estruch et al., 2018)
• Exercise guidelines for adults (American College of Sports Medicine, 2021)
• Management of menopausal symptoms (American College of Obstetricians and Gynecologists, 2023)
• Hormone therapy for menopause: Position statement (North American Menopause Society, 2022)
• USPSTF Breast Cancer Screening Recommendations (US Preventive Services Task Force, 2024)
• Cardiovascular disease and menopause: Timing and route (American College of Cardiology, 2020)
• Risks and benefits of estrogen plus progestin in healthy postmenopausal women: WHI (Rossouw et al., 2002)
• HRT optimization with transdermal estradiol and micronized progesterone (L’hermite, 2017)
• Genitourinary Syndrome of Menopause: Practice Pearl (North American Menopause Society, 2020)
• Clinical gynecologic endocrinology and infertility (Taylor, 2023)

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