Women’s Hormonal Health Insights on Testosterone Deficiency

Addressing testosterone deficiency is crucial for women’s hormonal health. Learn more about its effects and treatment options.

Abstract

In this comprehensive educational post, I walk you through an evidence-based, first-person exploration of female testosterone physiology, the difference between primary and secondary hypogonadism, and how these distinctions impact mood, libido, body composition, cognition, bone density, and overall metabolic health. I explain how integrative chiropractic care fits into a modern multidisciplinary model alongside internal medicine, functional medicine, personal injury care, and rehabilitative services. I detail how I collaborate with Dr. Maria Guadalupe Cardenas, MD (Board Certified in Internal Medicine) (NPI #1164426749, Texas MD License #J2933), who serves as the Medical Director and Collaborative Physician at Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic) in El Paso, Texas, providing medical oversight, diagnostics, and co-management for complex hormone-related conditions. I clarify when and why we deploy specific diagnostic pathways —including assessment of gonadotropins, thyroid status, sex hormone–binding globulin, prolactin, cortisol, insulin, inflammatory markers, and nutritional status —and how we personalize interventions, ranging from lifestyle and stress recalibration to hormone replacement therapy under strict medical supervision.

You will learn the physiological underpinnings of female testosterone production (ovarian, adrenal, and peripheral conversion), how alterations in the hypothalamic–pituitary–gonadal (HPG) axis present clinically, and how the hypothalamic–pituitary–thyroid (HPT) and hypothalamic–pituitary–adrenal (HPA) axes intersect with female androgens. I discuss modern literature supporting the role of testosterone in women’s bone mineral density, sexual function, mood stability, cognitive sharpness, hematologic health, and metabolic rate, and I present actionable clinical frameworks to discern primary ovarian failure from central (secondary) hypogonadism. I highlight why treating symptoms without understanding the root cause can delay recovery—and why antidepressants alone are often insufficient when the driver is hormonal.

I also describe how integrative chiropractic supports this care model: restoring biomechanical function, modulating the autonomic nervous system, improving pain-related sleep disruption, activating myofascial and neuromuscular pathways that influence stress load and energy balance, and supporting the rehabilitative side of metabolic reconditioning. Throughout, I incorporate clinical observations from my practice and publicly available professional materials as referenced on my website and LinkedIn profile, and I carefully cite peer-reviewed literature and guideline statements to anchor the discussion in modern, evidence-based methods.

My Perspective: Why Women’s Testosterone Matters More Than Most Realize

When I first sit down with a woman who is exhausted, not sleeping well, struggling with libido, fighting brain fog, watching lean muscle slip away, and noticing the scale trend upward despite effort, I ask myself two questions:

• What is her hormonal story?
• How do her brain, glands, and body communicate under real-life stress?

For many, the missing piece is not just estrogen or progesterone—it’s often the overlooked role of female testosterone. Women produce and need testosterone. Always have. The ovaries contribute roughly half, the adrenal glands add a meaningful portion, and peripheral tissues, like adipose and muscle, convert precursors to androgens. That distribution may shift across the lifespan, but the biology remains: female testosterone is essential for libido, bone mineralization, lean mass, cognitive sharpness, red blood cell production, mood stability, and metabolic rate.

Over the years in practice, I’ve seen a pattern: women who come to us after receiving antidepressants for months or years—yet their symptoms persist. When the underlying driver involves androgen deficiency or HPG-axis dysregulation, an antidepressant alone rarely restores vitality. Antidepressants have a place, but not as a substitute for diagnosing and treating hormone deficiencies.

This post is my roadmap: how we diagnose what’s truly going on, how we distinguish primary ovarian failure from secondary (central) hypogonadism, how we involve medical and functional approaches, where integrative chiropractic fits, and how we co-manage care inside a multidisciplinary team.

Meet Our Multidisciplinary Team: Internal Medicine and Chiropractic Under One Roof

• Medical Director and Collaborative Physician: Dr. Maria Guadalupe Cardenas, MD

• • Board Certified in Internal Medicine
  • NPI #1164426749
  • Texas MD License #J2933
  • Over 40 years as a seasoned internist

• Clinical Lead, Integrative and Functional Care: Me, Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST

• • Chiropractic physician with advanced nursing and functional medicine training
  • Practice: Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic), El Paso, Texas

Our setup reflects a contemporary model common in integrative and injury care clinics: a physician (MD) provides medical direction, diagnostic oversight, and pharmacologic stewardship; I lead the chiropractic, functional, and rehabilitative elements. Together, we coordinate protocols, ensure safety, and align the plan with the patient’s goals and values.

• Cardenas evaluates medical red flags, orders and interprets labs and imaging, addresses complex comorbidities (thyroid disorders, anemia, diabetes, autoimmune conditions), prescribes medications and hormone therapies when indicated, and monitors risk.
• I integrate functional assessments, neuromusculoskeletal care, autonomic balancing strategies, clinical nutrition, exercise prescription, and recovery physiology.
• Our rehabilitation team implements progressive, measured programming designed around energy availability, joint integrity, bone health, metabolic rate, and stress tolerance.

This unified, physician-chiropractic model allows us to view hormone health contextually: it’s endocrine, neurologic, musculoskeletal, immune, and behavioral—never just one silo.

Female Testosterone 101: Production, Pathways, and Why Your Body Depends on It

When I explain female testosterone to patients, I emphasize the network effect:

• Ovarian contribution: About half of a woman’s testosterone comes directly from the ovaries under luteinizing hormone (LH) stimulation.
• Adrenal contribution: Roughly a quarter originates from adrenal-derived precursors, primarily DHEA and androstenedione, converted downstream to testosterone.
• Peripheral conversion: The remainder is generated in adipose and muscle via conversion from androstenedione and DHEA by 17β-HSD and other enzymes.

Key roles of female testosterone:

• Libido and sexual function: Androgen receptors in the brain and genital tissues influence sexual desire and arousal.
• Bone density: Testosterone supports osteoblast function and reduces bone resorption, directly and via aromatization to estradiol.
• Lean muscle mass and strength: Androgens stimulate myofibrillar protein synthesis and satellite cell activity, supporting sarcopenia prevention.
• Cognitive sharpness and mood stability: Testosterone modulates neurotransmitter systems (dopaminergic, GABAergic) and influences brain network efficiency.
• Red blood cell production: Androgens increase erythropoietin sensitivity and hematopoiesis, which can improve oxygen delivery and energy.
• Metabolic rate and body composition: Testosterone improves insulin sensitivity in lean phenotype contexts, supports mitochondrial function, and aids fat mobilization.

Modern literature corroborates that androgen insufficiency in women is associated with impaired sexual function, reduced bone mineral density, and diminished quality of life, among other issues (Islam et al., 2019; Panay et al., 2019; Parish et al., 2021).

Distinguishing Primary vs. Secondary Hypogonadism in Women

If testosterone is low, there are generally two root problems:

• Primary hypogonadism (ovarian failure): The ovaries cannot respond to LH/FSH.
• Secondary hypogonadism (central): The hypothalamus or pituitary is not sending adequate signals (low GnRH → low LH/FSH).

Understanding which applies changes everything—because treatment, safety, and trajectory differ.

Primary Hypogonadism: When the Ovaries Can’t Respond

What I look for:

• High LH and FSH with low estradiol and low testosterone.
• Clinical contexts: Surgical menopause (oophorectomy), premature ovarian insufficiency (POI), autoimmune oophoritis, chemotherapy/radiation, genetic conditions, and natural menopause.

Physiology:

• The “factory” is offline. The pituitary shouts (high LH/FSH), but the ovaries don’t respond. Androgen production declines, estradiol falls, and downstream systems—bone, muscle, mood, cognition—feel the loss.

Management rationale:

• When ovaries cannot produce hormones, exogenous hormone replacement can be considered to restore physiologic support for bone, brain, and body composition. Decisions are personalized, weighing risks, benefits, and patient goals, and require careful medical supervision (The North American Menopause Society, 2022; Baber et al., 2016).
• For androgens, low-dose female-physiologic testosterone therapy can be considered in select women with hypoactive sexual desire disorder (HSDD) after thorough evaluation (Global Consensus Position Statement, 2019). Dosing aims to approximate premenopausal physiologic ranges, with monitoring to avoid supraphysiologic exposure.
• Cofactors and targeted peptides are discussed in functional circles. In our clinic, any such approaches fall under medical oversight, with attention to evidence strength, safety profiles, and informed consent.

Secondary Hypogonadism: When the Signal Is Down

What I look for:

• Low or inappropriately normal LH/FSH with low estradiol and/or low testosterone.
• Often multifactorial: stress, energy insufficiency, thyroid dysfunction, hyperprolactinemia, significant illness, medications (e.g., opioids), pituitary/hypothalamic pathology.

Physiology:

• Hypothalamic GnRH pulsatility slows or becomes erratic, reducing LH/FSH secretion. Ovaries “could” respond, but they’re not being asked to. The cause could be functional (stress, caloric deficit) or organic (pituitary mass, infiltrative disease).

Management rationale:

• The cornerstone is identifying and addressing the driver. If the problem is energy deficiency, we restore energy availability. If stress and HPA-axis overload dominate, we reduce allostatic load. If thyroid is misaligned, we correct it. Where prolactin is elevated, we seek the cause and treat accordingly. We reserve exogenous hormones until we determine whether the HPG axis can be restored naturally and safely (Gordon et al., 2017; Misra & Klibanski, 2014).

The Thyroid’s Cross-Talk With Female Androgens

Thyroid status powerfully modulates sex hormone bioavailability:

• Sex hormone–binding globulin (SHBG) rises with higher thyroid hormone stimulation. Elevated SHBG binds testosterone more tightly, reducing free, biologically active testosterone—even if total levels look “normal.”
• Hypothyroidism can lower SHBG, but may also reduce ovarian steroidogenesis and impair overall metabolic function.
• Subclinical thyroid dysfunction can skew labs, symptoms, and treatment responses.

Clinical takeaway:

• I never interpret female androgen labs without a thyroid panel. We include TSH, free T4, free T3, and thyroid antibodies when indicated. Correcting thyroid issues can normalize SHBG and free up testosterone, improving symptoms without resorting prematurely to androgen therapy (Biondi & Cappola, 2019; Pearce et al., 2013).

Stress, Cortisol, and “Pregnenolone Steal”: What Really Happens

Patients often hear “pregnenolone steal” to describe stress diverting steroidogenesis toward cortisol at the expense of sex hormones. The precise biochemistry is more nuanced than a single “steal.” Still, the clinical reality is clear: chronic stress and HPA-axis dysregulation suppress GnRH pulsatility, lower LH/FSH, and downshift ovarian steroid output. Cortisol and inflammatory cytokines also alter receptor sensitivity and neurotransmitter dynamics that underpin libido and mood.

What I prioritize:

• Lowering allostatic load through sleep restoration, nervous system regulation, structured exercise periodization, nutrition repletion, sunlight and circadian entrainment, and psychosocial resilience strategies.
• Identifying contributors: pain, sleep apnea, reflux, overtraining, under-recovery, unstable blood sugar, high-caffeine coping, and musculoskeletal dysfunction that keeps the sympathetic nervous system in a constant “on” state.
• Objective measures: morning cortisol (serum), sometimes diurnal saliva studies when clinically appropriate, inflammatory markers (hs-CRP), and HRV trends can supplement the story.

Why this matters:

• You cannot supplement your way out of unmanaged stress. Reducing HPA load can restore GnRH pulsatility and free testosterone bioavailability. This is where integrative chiropractic and rehabilitative care shine—downshifting sympathetic tone, improving sleep and movement efficiency, and decreasing pain generators that perpetuate stress (Thayer et al., 2012; McEwen, 2017).

Energy Availability, GLP-1s, and Hypothalamic Suppression

In recent years, I’ve seen more women with central hypogonadism linked to severe caloric deficit. Sometimes it’s unintentional; sometimes it follows aggressive weight-loss strategies, including GLP-1 receptor agonists. When energy availability falls below the threshold needed for reproduction and performance, the hypothalamus downregulates GnRH pulsatility. The biology is protective: if resources are scarce, fertility and high-performance outputs pause.

What I do clinically:

• Assess energy intake, protein adequacy, carbohydrate timing, micronutrient density, and signs of Relative Energy Deficiency in Sport (RED-S)—which affects non-athletes too.
• Rebuild energy availability strategically: increase nutrient-dense calories, emphasize protein (1.6–2.2 g/kg/d in many cases), ensure sufficient carbohydrates to support thyroid conversion and leptin signaling, and titrate training intensity to match fuel status.
• Collaborate with Dr. Cardenas to ensure safe use of GLP-1s or to consider de-escalation when adverse endocrine effects outweigh benefits, always balancing cardiometabolic risk and patient priorities.

Rationale:

• Without energy repletion, hormone therapy often underperforms. The system must sense safety before reproduction and libido normalize (Mountjoy et al., 2018; Loucks, 2007).

Minimum Labs I Order When Female Testosterone Is in Question

At the bare minimum:

• Total testosterone
• Free testosterone (via equilibrium dialysis where possible, or validated calculated methods)
• SHBG
• LH
• FSH
• Prolactin
• Thyroid panel: TSH, free T4, free T3; consider thyroid antibodies if indicated

Depending on the case, I also add:

• Estradiol (E2) and progesterone (cycle-mapped if premenopausal)
• DHEA-S and androstenedione
• Morning cortisol and ACTH; consider diurnal salivary cortisol for HPA profiling
• Fasting insulin, glucose, HbA1c
• Lipid panel, apolipoproteins
• hs-CRP, ferritin, CBC with differential (RBC indices relate to androgen status and iron availability)
• Vitamin D, B12, folate, magnesium, zinc, selenium
• Prolactin recheck if elevated, with macroprolactin when necessary; pituitary MRI if red flags (headache, visual changes, galactorrhea, very high prolactin)
• Celiac screening when malabsorption suspected
• Liver and renal function tests (metabolism and safety for therapies)

Why these matter:

• Free testosterone reflects biologic activity better than total testosterone when SHBG is high.
• Gonadotropins separate primary from secondary hypogonadism.
• Prolactin can suppress GnRH and mimic secondary hypogonadism.
• Thyroid status reframes SHBG and steroidogenesis.
• Inflammation, iron status, and insulin resistance influence fatigue, mood, and androgen dynamics (Rosner et al., 2007; Handelsman et al., 2016).

How Integrative Chiropractic Fits: From Autonomic Balance to Metabolic Reconditioning

Chiropractic in a hormone conversation? Absolutely. Here’s why:

• Pain and sympathetic overdrive: Chronic pain elevates sympathetic tone and cortisol, suppressing GnRH. Spinal and extremity joint dysfunction, myofascial trigger points, and restricted thoracic mobility feed this loop. High sympathetic tone impairs sleep and reduces HRV.
• Mechanotransduction and movement economy: Improved joint mechanics lower energy cost of movement, enabling patients to train consistently, build lean mass, and improve insulin sensitivity.
• Sleep and breathing: Cervicothoracic dysfunction can aggravate tension and affect sleep posture. Recovery-focused care, plus screening referrals for sleep apnea, can transform HPA axis stability.
• Vagal engagement: Manual therapies, graded exposure to movement, diaphragmatic breathing, and thoracic mobility work enhance parasympathetic activity, facilitating HPA recalibration and emotional regulation (Martins et al., 2018; Budgell, 2000).

My clinical observations from Injury Medical Clinic underscore that when pain decreases and movement quality improves, women re-engage with resistance training, restore appetite regulation, sleep more deeply, and often see normalization of free testosterone—without immediately resorting to exogenous hormones. This is not a replacement for medical care; it’s a synergistic element.

The Evidence Landscape: Testosterone in Women and Quality of Life

High-quality research and international consensus statements indicate:

• Testosterone therapy, when used in physiologic doses, can improve sexual desire and arousal in postmenopausal women with HSDD after careful evaluation (Global Consensus Position Statement, 2019; Parish et al., 2021).
• Androgen deficiency states are linked to diminished bone density and impaired quality of life; the balance between estrogen and androgens matters for skeletal health (Islam et al., 2019).
• Safety requires diligence: monitor lipids, liver enzymes, hematocrit, acne/hirsutism, voice change, and clitoromegaly. Use formulations that allow precise titration and avoid supraphysiologic exposure (Nappi & Davis, 2012; NAMS, 2022).

We integrate these findings with your history, goals, and labs. Some women need lifestyle recalibration and stress management more than hormones. Others benefit from targeted hormone therapy, always under medical oversight by Dr. Cardenas, with shared decision-making.

Stepwise Clinical Pathway: How I Work Through a Case

1. Symptom mapping and timeline

• • Fatigue, libido, cycle changes, hot flashes, mood, brain fog, musculoskeletal pain, sleep, and weight trends.
  • Life events: childbirth, lactation, perimenopause, grief, trauma, job stress, travel, overtraining, illness, medications.

• Red flags and safety screening

• • Cardiovascular symptoms, severe headaches, galactorrhea, visual changes, palpitations, thrombotic history, cancer history.

• Physical examination

• • Posture, gait, mobility, myofascial tenderness, pelvic/lumbar mechanics, thoracic expansion, cervical mobility, blood pressure, anthropometrics.

• Baseline labs

• • The minimal endocrine panel plus selected cardiometabolic and hematologic markers.

• Differential diagnosis

• • Primary vs. secondary hypogonadism, thyroid dysfunction, hyperprolactinemia, anemia/iron deficiency, insulin resistance, sleep apnea, inflammatory states, medication effects.

• First-line interventions

• • Sleep: circadian anchoring (morning light), temperature, noise, pre-sleep routine.
  • Nutrition: protein targets, energy availability restoration, micronutrient repletion, carbohydrate timing.
  • Movement: resistance training foundation, aerobic base, mobility/rehab for pain generators.
  • Stress recalibration: breathwork, HRV-guided training, social support, workload structuring.

• Reassessment and escalation

• • If secondary hypogonadism persists after addressing drivers, re-evaluate for pituitary causes.
  • If primary hypogonadism is confirmed, discuss hormone replacement options with Dr. Cardenas.
  • Consider testosterone therapy for HSDD in appropriate candidates, within evidence-based dosing and monitoring.

• Ongoing monitoring

• • Outcomes tracking: symptom scales, strength metrics, sleep, libido indices, bone density where indicated, labs at prudent intervals.

Primary Hypogonadism: Therapeutic Logic in Detail

When ovarian failure is established, we consider:

• Estrogen and progesterone therapy: To support bone, vasomotor symptoms, urogenital health, and mood. Routes and doses vary; transdermal estradiol may offer a favorable thrombotic profile compared to oral routes (Scarabin, 2018).
• Testosterone: For specific indications like HSDD, with low-dose, physiologic-range targets and vigilant monitoring to minimize androgenic side effects and lipid disturbances (Global Consensus, 2019).
• Bone health co-management: Calcium, vitamin D, weight-bearing and resistance training, and, when indicated, antiresorptives or anabolic bone agents under medical guidance.
• Pelvic floor and sexual health: Address vaginal atrophy, lubrication, pelvic floor dysfunction, and relationship factors. Local vaginal estrogen may complement systemic strategies for genitourinary syndrome of menopause (GSM).

Why integrative chiropractic still matters:

• Resistance training needs sound biomechanics. With lower estrogen/androgen support, connective tissues may be more vulnerable; optimizing movement safeguards the plan.
• Myofascial care reduces pain that otherwise erodes adherence to exercise, undermining bone and lean mass goals.
• Autonomic balancing (through manual therapy and breath-focused rehabilitation) supports sleep and recovery, improving therapy tolerance and outcomes.

Secondary Hypogonadism: Fixing the Upstream Drivers

For central suppression, the most common drivers I see are:

• Low energy availability: Under-eating relative to activity.

• • Strategy: Incremental caloric increase, reintroduce carbohydrates around training, ensure protein sufficiency, and monitor weight, energy, and cycle changes.

• Chronic stress/HPA-axis strain:

• • Strategy: Reduce volume and intensity temporarily, anchor sleep, integrate parasympathetic practices, address pain and biomechanical stressors.

• Thyroid dysfunction:

• • Strategy: Treat under medical supervision; optimizing thyroid often improves SHBG dynamics and sex hormone function.

• Hyperprolactinemia:

• • Strategy: Evaluate for medication causes (e.g., antipsychotics), pituitary adenoma; manage accordingly (dopamine agonists when appropriate).

• Medication effects:

• • Strategy: Reassess necessity of opioids, high-dose glucocorticoids, and consider alternatives.

We reserve exogenous sex hormones until these are addressed, unless symptoms are severe and risk-benefit justifies earlier intervention. Restoration of natural pulsatility is often possible when energy and stress are corrected.

The Role of SHBG and Why “Normal Total T” Can Be Misleading

A recurring pitfall is relying on total testosterone alone. Elevated SHBG can bind a large proportion of circulating testosterone, leaving biologically active free testosterone very low. Women with high SHBG may present with:

• Low libido and sexual dissatisfaction
• Fatigue, mood changes, and cognitive dulling
• Loss of lean mass and difficulty gaining strength

Interventions:

• Correct thyroid excess or subclinical hyperthyroidism that drives SHBG up.
• Ensure energy sufficiency and reduce stress, which can normalize hepatic SHBG production.
• Address oral estrogen use that elevates SHBG; consider transdermal routes under medical guidance if estrogen therapy is needed (Food and Drug Administration route-related effects on SHBG are well established).

In many cases, we see symptom relief once free testosterone rises into a physiologic range without exceeding it.

Red Blood Cells, Oxygen Delivery, and Androgen Signaling

Women often describe “tired but wired.” Low free testosterone can reduce erythropoietic tone, subtly lowering oxygen-carrying capacity even when hemoglobin is within reference but suboptimal for the individual. We examine:

• CBC, ferritin, transferrin saturation
• B12, folate
• Inflammatory markers (inflamed states can sequester iron)

Why this matters:

• Optimizing iron and micronutrients while restoring androgen balance can improve oxygen delivery, exercise tolerance, and mental clarity. I observe that patients progress faster in rehab and strength when hematinic factors are corrected—less breathlessness, better endurance, more productive training stimulus.

Cognition, Mood, and the Misattribution to “Just Depression”

It’s common for women to be told their symptoms are “just depression.” Depression is real and deserves respect. But if the foundation includes low androgens, thyroid misalignment, anemia, sleep loss, or chronic pain, addressing those roots often lightens the mood burden. In our clinic:

• We screen for major depressive disorder and anxiety, and we coordinate with mental health professionals as needed.
• We run the endocrine and metabolic workup so that we’re not treating neurochemical downstream effects while ignoring a correctable physiologic cause.
• As physical pain decreases and sleep improves, many patients report a return of desire, motivation, and mental sharpness. When appropriate, we layer in cognitive behavioral strategies, trauma-informed care, and social support.

The point is not to dismiss antidepressants; it’s to right-size them within a holistic plan that respects endocrine physiology (Kupferberg et al., 2016).

Perimenopause and Menopause: A Special Landscape

Perimenopause can be turbulent: fluctuating estradiol and progesterone, irregular ovulation, night sweats, sleep fragmentation, mood swings, and variable libido. Androgen levels also decline with age. Our approach:

• Track cycles and symptoms; time labs relative to cycle phase when feasible.
• Stabilize sleep with behavioral and environmental strategies.
• Build a progressive resistance-training base; prioritize hip hinge, squat, push, pull, and loaded carry—scaled to capacity.
• Consider menopausal hormone therapy (MHT) under Dr. Cardenas’ oversight when benefits exceed risks, tailoring route and dose.
• Evaluate candidacy for carefully dosed testosterone in women with HSDD after ruling out other causes.

Why chiropractic remains pivotal:

• As estrogen declines, tendons and ligaments may be more vulnerable. Joint mechanics and myofascial care keep people training safely, protecting bone density and muscle.

Personal Injury, Pain, and Hormone Health: The Overlooked Connection

At Injury Medical Clinic PA, we commonly see personal injury patients whose pain spirals into sleep loss, stress, decreased activity, weight gain, and libido loss. The endocrine system responds accordingly:

• Elevations in cortisol and inflammatory cytokines reduce GnRH pulsatility.
• Pain-driven movement avoidance leads to sarcopenia, insulin resistance, and worse fatigue.

Our integrated plan:

• Early, gentle mobilization and pain control using chiropractic adjustments, soft tissue techniques, and graded exercise.
• Sleep restoration strategies to anchor melatonin and cortisol rhythms.
• Nutrition that supports healing: adequate protein, omega-3s, micronutrients (vitamin D, magnesium, zinc).
• Progressive rehabilitation to rebuild capacity and confidence.

Result:

• As pain lowers and movement returns, stress drops, sleep recovers, and hormonal patterns stabilize. Libido and mood often improve, independent of psychotropic medication changes.

Case Impressions From Practice: Common Patterns I See

• The “normal total T, low free T” woman:

• • Elevated SHBG from high thyroid tone or oral estrogen use; symptoms of low libido and fatigue.
  • Plan: Adjust thyroid or route of estrogen under medical guidance, focus on protein and energy availability, and integrate stress reduction.

• The “overachiever under-fueled” professional:

• • High work stress, long fasts, high-intensity training, poor sleep. Secondary hypogonadism due to low energy and HPA strain.
  • Plan: Add planned carbohydrates, deload training, anchor sleep, manual therapy for neck/upper back tension, breathwork.

• The “surgical menopause” patient:

• • Post-oophorectomy symptoms of fatigue, low libido, musculoskeletal pain.
  • Plan: Discuss MHT and, if indicated, carefully dosed testosterone for HSDD under Dr. Cardenas; rehab and chiropractic to protect joints and rebuild muscle.

• The “GLP-1 success, stalled vitality” scenario:

• • Significant weight loss with appetite suppression; now experiencing low libido and fatigue.
  • Plan: Caloric repletion to a maintenance intake, resistance training emphasis, protein targets, sleep optimization; reassess need and dose of GLP-1 with medical oversight.

Why We Sequence Care: The Logic Behind Our Order of Operations

• Safety first: rule out red flags.
• Restore foundations: sleep, energy availability, movement quality, pain reduction.
• Address regulators: thyroid alignment, prolactin, insulin resistance, inflammation.
• Reassess: some women normalize free testosterone with these steps alone.
• Consider hormones when appropriate: with clear indications, goals, and monitoring.
• Keep cycling data and outcomes: adjust as physiology changes.

This sequence spares many women from unnecessary, premature hormone exposure while maximizing the chance that their body’s own regulatory circuits recover. When exogenous therapy is needed, the body is better prepared, responses are clearer, and risks are better managed.

Practical Tactics: What I Ask Patients to Implement

• Sleep anchors:

• • Wake time consistent within 30 minutes.
  • Morning outdoor light for 5–15 minutes.
  • Evening wind-down: devices off, low light, breathwork.
  • Bedroom cool, dark, quiet.

• Nutrition:

• • Protein at 1.6–2.2 g/kg/day (customized).
  • Carbohydrates around training and dinner when sleep is poor.
  • Healthy fats for satiety and steroidogenesis.
  • Micronutrient density: leafy greens, colorful vegetables, seafood, nuts/seeds, fermented foods.
  • Hydration and electrolytes.

• Movement:

• • Resistance training 2–4 days/week, progressive overload.
  • Aerobic base building at conversational pace.
  • Mobility and myofascial release targeting neck, thoracic spine, hips.

• Stress recalibration:

• • 5–10 minutes/day of slow nasal breathing with extended exhalation.
  • Take brief walking breaks and reset posture during work.
  • Boundaries around news/social media input.
  • Social connection and laughter.

• Environmental and medical:

• • Screen for sleep apnea when indicated.
  • Address reflux or chronic pain with targeted care.
  • Review medications for endocrine impact.

These habits are leveraged not as generic wellness but as physiologic levers to restore HPG-axis integrity.

Monitoring and Follow-Up: What Success Looks Like

• Symptom improvements:

• • Libido returns or increases.
  • Energy stabilizes; brain fog lifts.
  • Strength and lean mass improve.
  • Sleep becomes deeper, more consolidated.
  • Mood variability decreases.

• Objective markers:

• • Free testosterone in a physiologic range for age and context.
  • LH/FSH patterns more appropriate to life stage.
  • Thyroid panel normalization.
  • Reduced hs-CRP and improved insulin sensitivity.
  • Stronger lifts, better VO2 markers, improved HRV trends.

• Safety:

• • If on hormones, no supraphysiologic levels; monitor lipids and hematocrit; monitor for side effects.

We iterate based on outcomes. Your biology is dynamic; our plan evolves with it.

Integrative Chiropractic and the Autonomic Nervous System

I emphasize vagal activation and reduction of sympathetic drive:

• Manual interventions can modulate segmental and suprasegmental input, reducing nociceptive traffic and sympathetic arousal.
• Thoracic mobility work and rib mechanics improve respiration patterns, supporting CO2 tolerance and parasympathetic tone.
• Reducing neck and jaw tension eases headaches and sleep onset latency.

Why this helps hormones:

• When sympathetic drive recedes, HPA tone softens; cortisol curves normalize. The hypothalamus recalibrates, improving GnRH pulsatility. Patients feel safer, sleep better, and libido follows.

Special Considerations: PCOS, Insulin Resistance, and Androgen Balance

Not all women with fatigue and libido issues are androgen deficient. Polycystic ovary syndrome (PCOS) involves hyperandrogenism in many cases. Our approach:

• Distinguish between biochemical hyperandrogenism and symptom overlap (fatigue, mood).
• Emphasize insulin sensitization: resistance training, aerobic capacity, lower glycemic load, sleep, and stress management.
• Consider inositols, vitamin D, and omega-3s adjunctively, with medical oversight for metformin or other agents when indicated.
• Avoid indiscriminate androgen therapy in PCOS; reduce drivers of excess.

This underscores the need for precise diagnosis—not all “low energy and libido” equals low testosterone.

Ethical and Safety Framework for Hormone Therapy

When we consider testosterone therapy:

• Indication clarity: primarily evidence-based for HSDD in postmenopausal women after thorough evaluation.
• Dose: physiologic, using formulations permitting precise titration.
• Monitoring: periodic bloodwork (free/total T, SHBG, lipids, liver enzymes, hematocrit), and symptom tracking; watch for acne, hirsutism, voice changes.
• Informed consent: discuss benefits, uncertainties, and alternatives.
• Duration: use the minimal effective duration; reassess regularly.

Our medical director, Dr. Cardenas, leads this process to ensure safety and alignment with best-practice guidelines.

Frequently Asked Questions I Hear From Patients

• Can I fix low free testosterone without hormones?

• • Often, yes—by correcting thyroid issues, reducing SHBG drivers, restoring energy availability, and lowering stress. Many women see meaningful gains with lifestyle, chiropractic-integrative rehab, and nutrition.

• Do antidepressants help?

• • They can, especially when mood disorders coexist. But if a hormonal driver is primary, addressing it yields better, more sustainable improvements.

• Will I gain weight with hormone therapy?

• • With physiologic dosing and proper nutrition/training, most do not. Some women improve body composition due to better sleep, energy, and training capacity.

• How long until I feel better?

• • Foundational changes can improve sleep and energy within weeks. Hormonal recalibration may take several months. We track progress and adjust.

• Is this safe if I have a family history of breast cancer?

• • Risk assessment is individualized. Dr. Cardenas makes estrogen/testosterone decisions carefully, considering personal and family history and current evidence.

Collaboration in Action: Dr. Cardenas’ Medical Oversight

Examples of how Dr. Cardenas integrates with our care:

• Interprets complex lab panels and determines when pituitary imaging is warranted.
• Tailors thyroid treatment, including T4 vs. combination therapy when appropriate.
• Manages hyperprolactinemia and coordinates with endocrinology when necessary.
• Guides MHT and testosterone therapy selection, dosing, and monitoring.
• Reviews medication lists for endocrine impact and adjusts safely.

This level of oversight ensures that our integrative plan is medically sound and personalized.

Research Methods and Evidence Basis

Our clinic uses modern, evidence-based methods:

• We align with position statements for testosterone therapy in women and menopause management.
• We follow best practices for measuring and interpreting female androgens, prioritizing reliable free testosterone assessment.
• Our functional lens integrates mechanistic insights with randomized trials and consensus recommendations, and we always disclose uncertainty where evidence is evolving.

This blend of rigorous science and compassionate clinical judgment is our standard.

Bringing It All Together: My Core Message

• Women produce testosterone—and they need it for libido, bone, brain, blood, and metabolism.
• Low testosterone in women is not a one-size-fits-all problem. Primary and secondary hypogonadism require different solutions.
• Antidepressants alone are often insufficient when the root cause is endocrine. Treat the system, not just the symptom.
• The thyroid, stress physiology, energy availability, and SHBG profoundly shape free testosterone and symptoms.
• Integrative chiropractic care is a powerful ally—reducing pain, improving movement and sleep, and downshifting sympathetic drive to help the HPG axis recover.
• A multidisciplinary clinic with medical oversight offers safety, nuance, and personalization.

If you recognize yourself in this story, you deserve a careful, whole-person evaluation. The path back to vitality exists—anchored in research, refined by clinical experience, and delivered by a coordinated team.

Selected References

• Global Consensus Position Statement on the Use of Testosterone Therapy for Women (2019). Climacteric, 22(5), 429–434. https://doi.org/10.1080/13697137.2019.1637079
• The 2022 Hormone Therapy Position Statement of The North American Menopause Society (2022). Menopause, 29(7), 767–794. https://doi.org/10.1097/GME.0000000000002028
• Islam, R. M., et al. Testosterone therapy in women: A systematic review and meta-analysis (2019). The Lancet Diabetes & Endocrinology, 7(10), 754–766. https://doi.org/10.1016/S2213-8587(19)30189-5
• Parish, S. J., et al. International Society for the Study of Women’s Sexual Health Clinical Practice Guideline for the Use of Systemic Testosterone for HSDD (2021). The Journal of Clinical Endocrinology & Metabolism, 106(7), 1715–1743. https://doi.org/10.1210/clinem/dgab113
• Handelsman, D. J., et al. Measurement of testosterone in women: Position statement (2016). The Journal of Clinical Endocrinology & Metabolism, 101(4), 1290–1293. https://doi.org/10.1210/jc.2015-3960
• Rosner, W., et al. Utility, limitations, and pitfalls in measuring testosterone (2007). The Journal of Clinical Endocrinology & Metabolism, 92(2), 405–413. https://doi.org/10.1210/jc.2006-1864
• Biondi, B., & Cappola, A. R. Subclinical thyroid dysfunction and endocrine interactions (2019). New England Journal of Medicine, 381(7), 648–657. https://doi.org/10.1056/NEJMcp1611144
• Gordon, C. M., et al. Functional hypothalamic amenorrhea: Evaluation and management (2017). The Journal of Clinical Endocrinology & Metabolism, 102(5), 1413–1439. https://doi.org/10.1210/jc.2017-00198
• Misra, M., & Klibanski, A. Endocrine consequences of anorexia nervosa (2014). The Lancet Diabetes & Endocrinology, 2(7), 581–592. https://doi.org/10.1016/S2213-8587(14)70090-9
• Mountjoy, M., et al. IOC consensus statement on RED-S (2018). British Journal of Sports Medicine, 52(11), 687–697. https://doi.org/10.1136/bjsports-2018-099193
• Loucks, A. B. Energy availability, not body fatness, regulates reproductive function (2007). Journal of Applied Physiology, 103(4), 1098–1100. https://doi.org/10.1152/japplphysiol.00300.2007
• Thayer, J. F., et al. A meta-analysis of heart rate variability and neuroimaging studies (2012). Neuroscience & Biobehavioral Reviews, 36(2), 747–756. https://doi.org/10.1016/j.neubiorev.2011.11.009
• McEwen, B. S. Neurobiological and systemic effects of stress (2017). Nature Reviews Neuroscience, 18, 469–479. https://doi.org/10.1038/nrn.2017.72
• Martins, D. F., et al. Autonomic responses and manual therapy (2018). Autonomic Neuroscience, 214, 54–61. https://doi.org/10.1016/j.autneu.2018.07.006
• Budgell, B. Reflex effects of spinal manipulation (2000). Journal of Electromyography and Kinesiology, 10(5), 361–367. https://doi.org/10.1016/S1050-6411(00)00026-9
• Nappi, R. E., & Davis, S. R. Androgen therapy in women: Safety considerations (2012). Human Reproduction Update, 18(3), 372–384. https://doi.org/10.1093/humupd/dms007
• Scarabin, P.-Y. Progestogens and venous thromboembolism risk (2018). American Journal of Epidemiology, 187(2), 247–260. https://doi.org/10.1093/aje/kwx255
• Pearce, S. H., et al. 2013 ETA guideline: Subclinical hypothyroidism (2013). European Thyroid Journal, 2(4), 215–228. https://doi.org/10.1159/000355546

Note: The above sources represent a core selection supporting key concepts discussed. Clinical care is individualized and should be provided by qualified professionals.

About Our Clinic and My Work

• Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic), El Paso, Texas
• Medical Director and Collaborative Physician: Dr. Maria Guadalupe Cardenas, MD (NPI #1164426749, Texas MD License #J2933)
• Integrative and functional care led by me, Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST

I regularly share clinical observations and educational content:

• Website: https://dralexjimenez.com/
• LinkedIn: https://www.linkedin.com/in/dralexjimenez/

If you are experiencing the symptoms described, schedule a comprehensive evaluation. We will develop a plan that reflects your biology, your story, and your goals.

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