Men’s Health: Your Essential Guide in Hormone Therapy

Find out how hormone therapy for men’s health can optimize health and enhance quality of life for men facing hormonal changes.

Abstract

In this educational post, I walk you through the physiology, risk factors, diagnostic steps, and comprehensive treatment options for erectile dysfunction and testosterone deficiency, informed by contemporary research and my clinical experience at Injury Medical Clinic PA in El Paso, Texas. I explain how our multidisciplinary team integrates chiropractic care, internal medicine oversight, functional medicine, rehabilitation, and personal injury services to optimize vascular, neurological, endocrine, and musculoskeletal health. I highlight the molecular nitric oxide–cGMP pathway, lifestyle and pharmacologic interventions (PDE5 inhibitors, urethral alprostadil, intracavernosal therapy, vacuum devices, penile prosthesis), device-based modalities (low-intensity shockwave therapy), and emerging approaches (PRP, stem cells, hyperbaric oxygen, nutraceuticals). I also present how Dr. Maria Guadalupe Cardenas, MD, serves as our Medical Director and Collaborative Physician, ensuring medical safety and continuity in complex cases. This post provides practical guidance, clinical reasoning, and references to leading evidence to help you confidently navigate the spectrum of care.

About Our Multidisciplinary Team in El Paso, Texas

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), we practice integrated care that combines chiropractic, functional medicine, and internal medicine oversight. Our Medical Director and Collaborative Physician, Dr. Maria Guadalupe Cardenas, MD (Board Certified in Internal Medicine) (NPI #1164426749, Texas MD License #J2933), has over 40 years of experience as an internist. Together, we coordinate care across disciplines to address the interconnected vascular, neural, hormonal, and musculoskeletal components of men’s health. This collaborative model—common in integrative and injury care clinics—aligns chiropractic adjustments, rehabilitation, and functional nutrition with evidence-based medical management to improve patient outcomes.

I draw on my clinical observations and experience, including documented insights from WellnessDoctorRx and my professional LinkedIn profile, to structure personalized plans that respect the latest research findings while honoring each patient’s lived experience.

Integrative Men’s Health: Why a Systems Approach Matters

Men’s health concerns—especially erectile dysfunction (ED) and low testosterone—rarely occur in isolation. They reflect complex interactions among vascular integrity, neural signaling, endocrine balance, and biomechanical function. Our approach integrates:

• Internal medicine evaluation for cardiometabolic risk and medication safety.
• Chiropractic care to optimize autonomic tone, pelvic biomechanics, and musculoskeletal function.
• Functional medicine and nutrition to reduce inflammation, support endothelial health, and modulate insulin sensitivity.
• Rehabilitation to improve vascular fitness, pelvic floor coordination, and neuromuscular control.
• Personal injury care to address spinal, pelvic, and soft-tissue trauma that can impair autonomic and vascular responses.

Erectile Dysfunction: Definition, Prevalence, and Impact

• Definition: ED is the consistent or recurrent inability to achieve or maintain an erection sufficient for satisfactory sexual performance.
• Prevalence: Approximately 30 million men in the United States are affected. Age is a dominant factor; prevalence rises substantially after age 70.
• Care gap: Fewer than half of men with ED receive treatment, despite expanding access via online platforms. This gap underscores the need for de-stigmatized, evidence-based care pathways.

Physiology of Erection: Neural and Vascular Integration

A normal erection requires a healthy vascular system, intact neural pathways, and adequate hormonal support.

Key steps and molecules:

• Sensory and psychogenic arousal initiate parasympathetic activity via sacral spinal segments (S2–S4).
• Nitric oxide (NO), released by endothelial cells and nitrergic neurons, activates soluble guanylate cyclase, converting GTP to cyclic GMP (cGMP).
• cGMP drives smooth muscle relaxation in the corpus cavernosum, opening sinusoids for rapid blood inflow and trapping venous outflow via tunical compression.
• Phosphodiesterase type 5 (PDE5) degrades cGMP, terminating the erection. PDE5 inhibitors slow this degradation and sustain cavernosal smooth muscle relaxation.
• Additional pathways may be engaged: prostaglandin E1 (alprostadil) via adenylate cyclase/cAMP, and nonselective phosphodiesterase inhibition (papaverine) augment vasodilation.

Why this matters clinically:

• Conditions that diminish NO bioavailability (diabetes, hypertension, smoking, hyperlipidemia) impair endothelial responses.
• Autonomic dysfunction, neuropathy, and pelvic floor dysfunction can blunt neural stimulation and venocclusive mechanisms.
• Testosterone deficiency can lower libido and reduce NO synthase expression, compounding vascular limitations.

Risk Factors and Mechanisms

• Cardiometabolic: Age, hypertension, diabetes, obesity, dyslipidemia—each promotes endothelial dysfunction and arterial stiffness.
• Medications: SSRIs, certain diuretics, beta-blockers, and central agents can dampen libido, neurovascular tone, or penile blood flow.
• Neurogenic: MS, spinal cord injury, pelvic surgery can disrupt signaling.
• Substance use: Alcohol, nicotine, opioids, cocaine, and stimulants compromise vascular and neural function.
• Psychological: Performance anxiety, depression, and relational stress alter sympathetic-parasympathetic balance.

Assessment: History, Physical, and Validated Scales

• History: Sexual function, onset and context, nocturnal/morning erections, relationship factors, medications, comorbidities.
• Physical: Genitourinary exam, prostate assessment as indicated, cardiovascular risk screening, BMI/waist circumference, signs of hypogonadism.
• Scales: The International Index of Erectile Function (IIEF) and Sexual Health Inventory for Men (SHIM) provide quantifiable measures of severity that facilitate shared decision-making and track therapeutic response.
• Labs: Morning total testosterone, fasting glucose/A1c, lipid panel, thyroid studies, and PSA when clinically appropriate.

The Role of Integrative Chiropractic Care

Chiropractic care contributes to ED management by optimizing:

• Autonomic balance: Reducing sympathetic overdrive can lower vasoconstrictive tone; adjustments and vagal-supportive strategies may improve parasympathetic output to pelvic organs.
• Pelvic biomechanics: Lumbo-pelvic alignment influences pelvic floor function and pudendal nerve dynamics; tailored mobilization and soft-tissue work reduce myofascial restrictions and venous-leak tendencies.
• Pain reduction: Lower back, hip, and pelvic pain elevates stress hormones that antagonize NO-mediated vasodilation; decreasing pain improves arousal signaling.
• Exercise prescription: Coordinated programs enhance endothelial health, NO production, and insulin sensitivity.

Our internal medicine oversight ensures safety for patients with complex cardiac histories or polypharmacy, while functional medicine addresses root drivers—metabolic inflammation, oxidative stress, and hormonal insufficiencies.

Treatment Spectrum: Evidence-Based Modalities

Shared decision-making frames our approach. We align therapy with patient goals, comorbidities, and tolerance.

PDE5 inhibitors (sildenafil, tadalafil)

• Mechanism: Inhibit PDE5, raise cavernosal cGMP, and promote smooth muscle relaxation in response to arousal.
• Use: Taken on demand (about one hour before sexual activity). Tadalafil can be used daily or on demand. Sildenafil’s efficacy may decrease when taken with fatty meals—I advise taking it on an empty stomach.
• Considerations: Lower responsiveness occurs after radical prostatectomy or in severe diabetes. Contraindicated with nitrates and use with caution with nonselective alpha-blockers due to the risk of hypotension.
• Why: Address endothelial signaling deficits and venous trapping by prolonging NO-mediated pathways, often first-line due to safety and efficacy data (Goldstein et al., 1998).

Vacuum erection devices (VED)

• Mechanism: Negative pressure draws blood into the penis; a constriction ring retains venous blood.
• Pros: Useful when PDE5 response is partial or contraindicated; can be combined with oral agents.
• Cons: Cumbersome, may reduce spontaneity; can cause penile discomfort.
• Why: Offers a mechanical solution that bypasses endothelial limitations; beneficial where neuropathy or vasculopathy is prominent.

Urethral alprostadil (MUSE)

• Mechanism: Prostaglandin E1 increases cAMP, inducing smooth muscle relaxation independent of NO.
• Use: Inserted post-void; onset is rapid; in-clinic test dosing recommended.
• Cons: Cost, urethral burning, risk of hypotension; lower efficacy than intracavernosal injections.
• Why: Provides an alternative pathway when NO/cGMP modulation is insufficient or not tolerated.

Intracavernosal injections (alprostadil, bimix, trimix)

• Mechanism: Direct cavernosal vasodilation via PGE1 (alprostadil) and/or papaverine-phentolamine.
• Use: Start low, titrate cautiously; rotate sites; limit frequency to avoid priapism and fibrosis.
• Cons: Cost, refrigeration requirements (trimix), risk of priapism, scarring, and the need for training and adherence.
• Why: Bypasses systemic factors by delivering immediate vasoactive agents to cavernosal tissue, often second-line for PDE5 nonresponders, post-surgical ED, and severe vascular disease.

Penile prosthesis

• Mechanism: Inflatable systems mechanically create rigidity; a reservoir, pump, and cylinders replace physiological erectile function.
• Pros: High satisfaction (>90%), durability (typically 10–20 years), and restored reliability.
• Cons: Invasive surgery, loss of spontaneous erections, small risk of infection.
• Why: Definitive solution for refractory ED; appropriate for men whose quality of life is significantly impaired and who value predictability.

Low-intensity shockwave therapy (Li-ESWT)

• Mechanism: Non-invasive acoustic energy induces microtrauma and stimulates neovascularization and endothelial repair, potentially enhancing NO signaling and perfusion.
• Evidence: Best for mild to moderate ED; often used in patients with suboptimal response to PDE5 inhibitors. Still considered investigational in many settings and not covered by insurance (Clarus et al., 2017).
• Why: A restorative strategy aimed at improving tissue-level vascular health rather than temporarily boosting vasodilation.

Online Platforms and Compounded Medications

• Observations: Direct-to-consumer platforms offer convenience but may utilize compounded medications without FDA approval. Safety, ingredient consistency, and oversight of drug–drug interactions can vary.
• Why we emphasize oversight: Medical direction from an experienced MD ensures appropriate screening for cardiovascular risk, contraindications, and endocrine causes of ED.

Over-the-Counter ED Gel (Eroxon)

• Mechanism: Evaporative cooling and warming of the glans to stimulate sensory nerves and reflex vascular responses.
• Evidence: Reported trials in Europe and the US; user satisfaction varies. Contains alcohol and other inert ingredients; no prescription vasodilators.
• Why: May serve as an adjunct for psychogenic or mild cases seeking spontaneity; we counsel realistic expectations and monitor outcomes.

Emerging Therapies: PRP, Stem Cells, Hyperbaric Oxygen, Nutraceuticals

• PRP and stem cells: Injected into penile tissue to promote regeneration; not FDA-approved for ED; limited robust efficacy data; cost and standardization challenges.
• Hyperbaric oxygen: Enhances oxygen delivery and angiogenesis; theoretical and preliminary support for improved perfusion; protocols vary.
• Nutraceuticals:

• • L-arginine: NO precursor; may assist NO synthesis in endothelial cells.
  • L-citrulline: Converts to arginine; can improve NO availability more reliably than oral arginine due to first-pass metabolism constraints (Rizza et al., 2017).

• Why: These options target the root biology—angiogenesis, oxidative stress, and NO supply—yet evidence is mixed. We consider them selectively as adjuncts within supervised care plans.

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Signs of Hormonal Imbalances In Men *THIS IS WHY*- Video

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The Growing Concern of Low Testosterone

Many men I see in my practice want to recapture the vitality, energy, and physical appearance they had in their twenties and thirties. When they hear about the potential benefits of optimizing testosterone, they are naturally intrigued. The market for “Low T” treatments reflects this desire. Sales of testosterone products have quadrupled in a single decade, and the global market is projected to reach $2.2 billion by 2027.

However, there’s a concerning trend. Research indicates that one-third of men currently on testosterone therapy may not even meet the clinical criteria for deficiency, and a staggering 25% were prescribed treatment without ever having their levels tested. This highlights a “loosey-goosey” clinical practice that we aim to counteract with a rigorous, evidence-based approach.

Statistics show a clear age-related decline in testosterone. Studies report that:

• 13% of men in their 50s have low T.
• 19% of men in their 60s.
• 28% of men in their 70s.
• 49% of men in their 80s.

Let’s start by looking at a representative case to frame our discussion.

A Case Study in Low T and ED: Meet Mr. T

Consider “Mr. T,” a 66-year-old man who presents with a list of common complaints: fatigue, decreased physical performance, low libido, weight gain, and moderate erectile dysfunction (ED). His medical history includes hypertension, hyperlipidemia, obesity, and obstructive sleep apnea (OSA). His SHIM score is 8, indicating moderate ED, and he has a poor response to sildenafil. His primary care provider checked his testosterone, which came back at 150 ng/dL, but this test was conducted in the afternoon, which can skew the results. He has a CPAP machine for his sleep apnea but admits he is noncompliant with its use.

As we move through this discussion, keep Mr. T’s case in mind. We will revisit him to develop a comprehensive, integrative treatment plan.

What is Hypogonadism? Defining Testosterone Deficiency

Hypogonadism is the clinical syndrome that results from the failure of the testes to produce physiological concentrations of testosterone. Men frequently encounter low testosterone messaging and assume ED is solely hormonal. In reality, ED is predominantly vascular-neural, while testosterone modulates libido, mood, energy, muscle mass, and NO synthase expression. A formal diagnosis of testosterone deficiency requires two separate morning total testosterone measurements below 300 nanograms per deciliter (ng/dL), coupled with one or more of the following symptoms (Bhasin et al., 2018):

• Decreased libido (sex drive)
• Erectile dysfunction (ED)
• Fatigue and decreased energy levels
• Reduction in lean muscle mass
• Loss of beard and body hair
• Poor memory, concentration, and focus

In my clinical experience, the top four complaints that bring men into my office are low sex drive, fatigue, loss of muscle, and ED. It’s important to recognize that as men age, other health conditions can cause similar symptoms, making it a diagnostic challenge to determine if low testosterone is the primary culprit or if another comorbidity is at play. Low T may coexist with ED but is not always causal.

Primary vs. Secondary Causes of Testosterone Deficiency

Understanding the cause of low testosterone is crucial for effective treatment. We categorize the causes as either primary or secondary.

Primary Causes (Testicular Failure)

These involve direct damage or dysfunction of the testes.

• Aging: A natural, gradual decline of 1-2% per year.
• Damage to the testicles: From trauma, infection, or torsion.
• Chemotherapy or radiation: Can damage the testosterone-producing cells.
• Removal of a testicle (orchiectomy).
• Autoimmune conditions.
• Genetic disorders (e.g., Klinefelter syndrome).

Secondary Causes (Hypothalamic-Pituitary Axis Dysfunction)

These involve problems with hormonal signaling from the brain (the hypothalamus and pituitary gland) to the testes.

• Obesity: Fat cells contain the enzyme aromatase, which converts testosterone to estrogen, lowering testosterone levels.
• Type 2 Diabetes: Often linked with obesity and metabolic syndrome, which disrupts hormonal balance.
• Obstructive Sleep Apnea (OSA): Chronic oxygen deprivation during sleep disrupts the pituitary gland’s function, suppressing testosterone production.
• Medications: Opioids, steroids, and some other drugs can suppress the hormonal axis.
• Excessive alcohol consumption.

When a patient presents with conditions like obesity or OSA, my first step is to address these root causes. For instance, I insist that patients with OSA use their CPAP machine religiously for three months before we re-evaluate their testosterone levels. Often, simply treating the underlying condition can restore normal hormonal function.

The Diagnostic Pathway for Low Testosterone: A Step-by-Step Algorithm

Following the American Urological Association (AUA) guidelines, the diagnostic process is systematic and precise.

1. Initial Lab Work: Measure a morning total testosterone level. Testosterone levels are highest in the morning, so timing is critical.

• • If the level is above 300 ng/dL, we consider other causes for the patient’s symptoms.

• Confirmation and Further Testing: If the initial level is low, we repeat the morning total testosterone test to confirm the result. At this time, we also order additional labs:

• • Luteinizing Hormone (LH): Helps differentiate between primary and secondary hypogonadism.
  • Hematocrit: A baseline measure of red blood cell concentration, as testosterone can increase it.
  • Prostate-Specific Antigen (PSA): A baseline for prostate health monitoring.
  • Prolactin: Elevated levels could indicate a pituitary tumor.
  • Assess SHBG and free testosterone (via equilibrium dialysis or validated calculations) to get a full picture.

• Interpreting the Results:

• • Elevated Prolactin (>25 ng/mL): This warrants a referral to an endocrinologist and consideration for a pituitary MRI to rule out a prolactinoma.
  • High Hematocrit (>50%): We must investigate the cause before starting therapy.
  • Confirmed Low Testosterone with Unremarkable Labs: If two morning tests are low and other labs are normal, we can confirm testosterone deficiency and proceed to discuss treatment options.

An Important Note on Hematocrit: Testosterone stimulates erythropoietin production, a hormone that increases red blood cell production. This can lead to elevated Hematocrit and hemoglobin levels, a condition known as secondary polycythemia or erythrocytosis. This “thickens” the blood, increasing the risk of clots, stroke, or heart attack. Therefore, regular monitoring of Hematocrit is non-negotiable.

Testosterone Replacement Therapy (TRT): Formulations and Considerations

The cornerstone of treatment for confirmed testosterone deficiency is Testosterone Replacement Therapy (TRT), used in conjunction with lifestyle modifications. It’s crucial to emphasize that TRT is not a magic bullet. Patients must commit to a healthy diet, regular exercise, smoking cessation, and reduced alcohol consumption to achieve optimal results. TRT is a Schedule III controlled substance and comes in several formulations.

1. Intramuscular Injections

This is the most common and often most affordable formulation.

• Types: Testosterone cypionate (in cottonseed oil) and testosterone enanthate (in sesame seed oil) are most common.
• Dosing: Typically 75-100 mg weekly or 150-200 mg every two weeks.
• Pros: Cost-effective and covered by most insurance plans.
• Cons: Creates “peaks and valleys.” Patients often feel great right after the injection but may experience a return of symptoms as their levels trough before the next dose. Proper storage at room temperature and away from light is important.
• Aveed® (Testosterone Undecanoate): A long-acting injection given every 10 weeks after initial loading doses. It carries a black box warning for Pulmonary Oil Microembolism (POME), a serious lung reaction, so it is used less frequently.

2. Subdermal Pellets (Testopel®)

These are small, crystalline pellets implanted under the skin of the buttock.

• Procedure: A minor in-office procedure where pellets (each containing 75 mg of testosterone) are inserted into the subdermal fat.
• Dosing: The number of pellets varies, but a typical starting dose is six pellets (450 mg). They last for 3-4 months.
• Pros: Provides a steady, consistent release of testosterone, avoiding the peaks and valleys of injections.
• Cons: Requires a minor surgical procedure for implantation and removal.

3. Topical Gels (AndroGel®, Fortesta®)

This is the second most common formulation I prescribe.

• Application: Applied daily to the shoulders, upper arms, or thighs.
• Dosing: A typical starting dose is 50 mg daily.
• Pros: Provides stable, daily testosterone levels, which many patients prefer.
• Cons: The primary concern is transference. It carries a black box warning for secondary exposure, as the gel can be transferred to women or children through skin-to-skin contact, causing virilization. Patients must be meticulous about washing hands after application and covering the application site with clothing.

4. Oral and Nasal Formulations

These are less commonly used.

• Oral (Jatenzo®, Tlando®): These are expensive and often not covered by insurance. They are absorbed via the intestinal lymphatics, bypassing the liver’s first-pass metabolism. They carry a black box warning for increased risks of blood pressure elevation and cardiovascular events.
• Nasal (Natesto®): Not frequently used. It can cause nasal irritation, scabbing, and a distorted sense of smell. There is also a risk of transference.

Side Effects, Monitoring, and Contraindications of TRT

TRT is a powerful therapy that requires careful monitoring.

Common Adverse Effects:

• Slight increase in PSA
• Gynecomastia (breast tissue development)
• Mood swings
• Increased red blood cell count (elevated Hematocrit)
• Mild elevation in blood pressure

Monitoring Protocol:

• Testosterone and hematocrit levels should be checked within 9-12 weeks of starting therapy and then every 6-12 months.
• We monitor for secondary polycythemia. If the Hematocrit rises above 52-54%, we may need to lower the dose, change the formulation, or have the patient donate blood.
• The optimal on-therapy testosterone level is generally between 450-650 ng/dL.

Absolute Contraindications to TRT:

• Active prostate or breast cancer.
• Severe, untreated obstructive sleep apnea.
• Hematocrit > 54%.
• Severe lower urinary tract symptoms.
• Poorly controlled congestive heart failure (CHF).
• Recent heart attack (MI) or stroke (CVA).
• Active desire for fertility. TRT suppresses spermatogenesis by lowering Follicle-Stimulating Hormone (FSH), acting as a male contraceptive.

How Chiropractic and Functional Medicine Support Low T Care

From an integrative perspective, the health of the nervous system is paramount to the function of the endocrine (hormonal) system. The brain, specifically the hypothalamus and pituitary gland, is the master regulator of hormone production. Chiropractic adjustments work to remove interference in the nervous system by correcting spinal misalignments (subluxations).

• Improving Neuro-Endocrine Communication: Chronic pain and stress increase cortisol and inflammatory cytokines that suppress the hypothalamic-pituitary-gonadal axis. By optimizing nerve flow between the brain and the rest of the body, including the endocrine glands, chiropractic care, soft-tissue techniques, and stress-reducing care can help support the body’s innate ability to regulate hormone production and normalize neuroendocrine tone.
• Movement prescriptions: Resistance training robustly increases androgen receptor sensitivity and improves metabolic health, indirectly supporting testosterone function (Kraemer et al., 2012).
• Nutritional strategies: Adequate micronutrients (zinc, vitamin D), omega-3 fatty acids, and anti-inflammatory diets support endocrine health and vascular function.

By integrating chiropractic care, we are not just treating a number; we are supporting the entire physiological system responsible for health and vitality.

Revisiting Mr. T: An Integrative Treatment Plan

Now, let’s return to our 66-year-old patient, Mr. T. His case highlights a classic endothelial dysfunction profile with comorbidities of hypertension, diabetes, obesity, and hyperlipidemia. What is our next step?

1. Address the Root Causes: His untreated OSA is a major red flag.

• • CPAP Compliance: He must use his CPAP machine religiously for three months. This is non-negotiable.
  • Optimize Cardiometabolic Status: Under Dr. Cardenas’s oversight, we will intensify glycemic control, lipid and blood pressure management, and screen for medications that impair erectile function.

• Proper Diagnostic Workup: His afternoon testosterone level of 150 ng/dL is suggestive but not diagnostic.

• • We will order a baseline morning total testosterone level
  • After three months of consistent CPAP use, we will repeat the morning testosterone level. This will give us a true picture of his hormonal status once the confounding factor of OSA is managed.

• Symptom Management and ED Therapy:

• • We will switch therapy from sildenafil to tadalafil (up to 20 mg on demand), with counseling on timing and arousal requirements. Daily low-dose tadalafil can also improve endothelial function.
  • As an adjunct, we will consider Li-ESWT to encourage neovascularization and endothelial repair, or add a medical-grade VED to reinforce venous occlusion.
  • If oral therapy fails, we will offer intracavernosal injection options with careful training, which is appropriate for patients comfortable with injections (e.g., insulin-experienced diabetics).

• Integrative Support:

• • Lifestyle and Rehabilitation: We will prescribe structured exercise to improve VO2, endothelial NO production, and insulin sensitivity; introduce pelvic floor training to enhance venous trapping (Crisp et al., 2013); and perform chiropractic adjustments to reduce sympathetic tone and improve pelvic biomechanics.
  • A functional medicine evaluation to look for other imbalances, such as nutritional deficiencies or inflammation.

• Follow-up: We will reassess in about 3 months from May 7, 2026, using SHIM/IIEF scores, patient satisfaction, and partner feedback to refine the plan.

Only after this comprehensive workup would we consider TRT. If his testosterone remains low despite treating his OSA and improving his lifestyle, he would be a candidate for therapy under close supervision.

Beyond TRT: Other Strategies to Boost Testosterone

Clomiphene Citrate (Clomid)

For some men, particularly younger men who wish to preserve fertility, we can use clomiphene citrate (Clomid) off-label.

• Mechanism: Clomid is an estrogen receptor modulator. It blocks estrogen receptors in the brain, tricking the pituitary into thinking there isn’t enough estrogen (which is derived from testosterone). This stimulates the release of FSH and LH, which in turn trigger the testes to produce more testosterone and sperm.
• Dosing: Typically 25-50 mg three times a week (e.g., Monday, Wednesday, Friday).
• Candidates: Younger men desiring fertility or those averse to traditional TRT.

The Role of Nutrition and Supplements

While no food will magically double your testosterone, certain nutrients are essential for its production.

• Zinc: Found in oysters, red meat, and poultry. Zinc is a critical mineral for the function of the Leydig cells in the testes, which produce testosterone.
• Selenium: A mineral found in fish, nuts, and seeds, also thought to support testosterone production.

Many patients ask me about popular “testosterone boosters” like Nugenix. These products often contain ingredients like fenugreek extract, vitamins, and zinc. While the ingredients themselves may be beneficial, the formulations are often overpriced. A bottle of Nugenix can cost $70, whereas a high-quality men’s multivitamin with comparable or better ingredients, such as one from Nature Made, costs around $20. My recommendation is to skip the expensive, overhyped boosters. Instead, invest in a healthy, whole-foods diet and a good-quality men’s multivitamin that contains essential minerals like zinc.

Collaborative Safety: The Role of Dr. Maria Guadalupe Cardenas, MD

Dr. Cardenas ensures:

• Safe prescribing: Screening for cardiovascular contraindications, medication interactions, and oncologic considerations before ED or testosterone therapies.
• Continuity: Coordination of diagnostics and follow-up labs (testosterone, Hematocrit, PSA, lipids, A1c) and communication with patients’ primary care and specialists.
• Escalation pathways: Clear criteria for referral to urology or cardiology when complex anatomy, surgical history, or high-risk profiles require subspecialty input.

Practical Steps for Patients

• Start with validated questionnaires (SHIM, IIEF) to gauge severity and track progress.
• Obtain morning testosterone twice if symptoms suggest hypogonadism.
• Prioritize lifestyle change: smoking cessation, weight loss, structured exercise, and sleep optimization improve endothelial and endocrine health.
• Discuss pharmacologic options with medical oversight: PDE5 inhibitors, alprostadil (urethral or intracavernosal), and device therapy, considering risks and expectations.
• Consider restorative modalities: Li-ESWT in appropriate cases; use emerging therapies cautiously within supervised frameworks.
• Integrate chiropractic and rehabilitation to improve autonomic tone, pelvic floor function, and biomechanics, thereby supporting vascular and neural pathways.

Clinical Observations from My Practice

From my work chronicled on WellnessDoctorRx and my professional activities, I frequently observe:

• Men with persistent low back or pelvic instability exhibit heightened sympathetic tone and reduced erectile responsiveness; targeted mobilization and pelvic floor integration often enhance outcomes.
• Diabetic patients improve ED metrics when resistance training and glycemic control are combined with PDE5 inhibitors—consistent with improved endothelial NO and improved cavernosal compliance.
• Sleep optimization (especially treating sleep apnea) materially affects both ED and testosterone levels, reinforcing the need for multidisciplinary coordination.

Conclusion: Integrated Care Elevates Outcomes

ED and low testosterone demand more than a single medication—they require a coordinated plan that restores vascular function, optimizes neural signaling, and supports hormonal balance. At Injury Medical Clinic PA, our collaborative model with Dr. Cardenas allows us to provide this high level of care. We combine the best of conventional medicine, chiropractic, and functional medicine to create a treatment plan that is not only effective but also aligns with the body’s natural healing capacity. If you are experiencing symptoms of low testosterone or erectile dysfunction, I encourage you to seek a comprehensive evaluation from a provider who will look beyond the numbers and treat you as a whole person.

References

• American Urological Association (AUA). (2018). Evaluation and Management of Testosterone Deficiency: AUA Guideline.
• Bhasin, S., Brito, J. P., Cunningham, G. R., Hayes, F. J., Hodis, H. N., Matsumoto, A. M., Snyder, P. J., Swerdloff, R. S., Vigen, R., & Yalamanchi, S. (2018). Testosterone Therapy in Men With Hypogonadism: An Endocrine Society Clinical Practice Guideline. The Journal of Clinical Endocrinology & Metabolism, 103(5), 1715–1744.
• Burnett, A. L. (1997). Nitric oxide in the penis: physiology and pathology. Nature Medicine, 3(4), 450.
• Charan, S. (2022). Testosterone Therapy: A Comprehensive Guide.
• Clavijo, R. I., Hsiao, W., & Burnett, A. L. (2017). Low-intensity extracorporeal shockwave therapy for the treatment of erectile dysfunction: a systematic review and meta-analysis. BJU International, 119(2), 200–207.
• Crisp, C. B., Fellner, C., & Kim, E. D. (2013). The role of pelvic floor muscle training for male sexual dysfunction. The Journal of Sexual Medicine, 10(1), 7- 14.
• Global Market Assessment for Testosterone. (2021). Market Research Report.
• Goldstein, I., Lue, T. F., Padma-Nathan, H., Rosen, R. C., Steers, W. D., & Wicker, P. A. (1998). Oral Sildenafil in the Treatment of Erectile Dysfunction. The New England Journal of Medicine, 338(20), 1397–1404.
• Guay, A. T. (2007). ED2: erectile dysfunction = endothelial dysfunction. Circulation, 116(13), 1397- 1401.
• Khera, M. (2018). 2018 AUA guidelines on erectile dysfunction. The Journal of Clinical Endocrinology & Metabolism, 103(5), 1715–1744.
• Kraemer, W. J., Ratamess, N. A., Nindl, B. C., & Volek, J. S. (2012). The effects of resistance training on the endocrine system. Journal of Applied Physiology, 113(1), 162-171.
• Maiorino, M. I., Bellastella, G., & Esposito, K. (2004). Diabetes and sexual dysfunction: current perspectives. Diabetes Care, 27(7), 1686-1693.
• Nature Made. (n.d.). Men’s Health Supplements.
• (n.d.). Product Information.
• Rizza, S., Cardile, V., & Monti, L. (2017). L-Arginine and L-Citrulline supplementation in erectile dysfunction: A systematic review. Fertility and Sterility, 108(3), e22.

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