Explore the role of testosterone health, combined with chiropractic rehabilitation, in enhancing overall health and wellness.
Table of Contents
Testosterone deficiency in men is one of the most underdiagnosed and mismanaged conditions in modern medicine. A testosterone reading of 370 ng/dL may appear “normal” on a standard reference range, yet for many men, this level is profoundly insufficient — clinically, functionally, and physiologically. This educational post, authored by Dr. Alexander Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST, draws on the latest evidence-based research and clinical observations to provide a comprehensive exploration of male hypogonadism, its two primary classifications, the essential diagnostic blood panels required to differentiate between them, the dangers of poorly chosen delivery methods, and the integrative treatment protocols that can meaningfully restore hormonal health.
This post also introduces the multidisciplinary clinical team at Injury Medical Clinic PA (also known as Mission Plaza Injury Medical Clinic) in El Paso, Texas, where Dr. Jimenez collaborates with Dr. Maria Guadalupe Cardenas, MD, a Board-Certified Internist with over 40 years of clinical experience who serves as Medical Director and Collaborative Physician. Together, they represent a powerful fusion of chiropractic care, functional medicine, internal medicine, personal injury rehabilitation, and integrative hormonal health management.
The topics covered in this post include:
This post takes you on a clear, scientifically grounded journey through the physiology of male hormonal health, the clinical reasoning behind each diagnostic and treatment decision, and the integrative approach that distinguishes evidence-based hormone optimization from cookie-cutter prescriptions.
One of the most frustrating realities in men’s hormonal health today is the widespread misuse of laboratory reference ranges. When a man walks into his physician’s office complaining of fatigue, low libido, difficulty building muscle, brain fog, increased body fat, poor sleep, and declining motivation, and his testosterone comes back at 370 ng/dL, he is far too often told: “You’re fine. It’s within the normal range.”
This is a deeply inadequate response. And for many men, it is a life-altering mistake.
Here is the problem: standard laboratory reference ranges for total testosterone in adult men typically span about 264 to 916 ng/dL, depending on the lab. A result of 370 ng/dL is, by the arithmetic of that range, technically “not low.” But reference ranges are statistical constructs derived from population averages — they do not represent optimal function. They represent the range within which a large, heterogeneous population of men — including sedentary, metabolically compromised, obese, elderly, and otherwise unwell men — happened to fall. That is not a health benchmark. That is a benchmark for “not being a statistical outlier.”
When we examine the research literature rather than population-based reference ranges, a very different picture emerges. A landmark 2013 study published in the Journal of Clinical Endocrinology and Metabolism followed 1,038 men over 18 years and found that men whose testosterone levels fell below 300 ng/dL had a 40% increased risk of all-cause mortality compared to men with higher levels (Khaw et al., 2014). More significantly, the men with the best survival outcomes — the lowest risk of dying from cardiovascular disease, metabolic disease, and all other causes — were those whose testosterone levels exceeded 600 ng/dL.
Let that sink in. The difference between a testosterone level of 370 ng/dL and 600 ng/dL is not cosmetic. It is not about gym performance or vanity. It is about longevity, organ function, metabolic health, and survival.
To understand why testosterone levels matter so profoundly, we need to understand what testosterone actually does in the male body. It is not merely a “sex hormone.” Testosterone is a master anabolic and regulatory hormone that influences virtually every system in the body:
When a man has a testosterone level of 370 ng/dL and is experiencing symptoms consistent with androgen deficiency, dismissing that number as “normal” is not just clinically careless — it is a failure to engage with the full scope of what the science tells us about optimal hormonal physiology.
Before making any treatment decision, the most important clinical question is: Where is the breakdown occurring? Low testosterone does not always mean the same thing, and treating it without understanding the root cause is precisely how men end up on testosterone replacement therapy (TRT) when they might not need it — or fail to receive TRT when it is exactly what they require.
Male hypogonadism — the clinical term for testosterone deficiency — is classically divided into two major categories: central hypogonadism and peripheral hypogonadism. Understanding the distinction between these two is not merely academic. It is the foundational clinical question that determines the entire treatment approach.
To understand hypogonadism, you must first understand the Hypothalamic-Pituitary-Gonadal (HPG) axis — the hormonal communication network that governs testosterone production.
Here is how the system works under normal conditions:
This elegant system — when functioning properly — maintains testosterone levels within a physiologically optimal range. Hypogonadism occurs when this system breaks down at one of two levels: the command center (central) or the factory (peripheral).
Central hypogonadism (also called secondary hypogonadism or hypogonadotropic hypogonadism) occurs when the problem lies at the hypothalamus or pituitary gland. The testes themselves are structurally and functionally intact — they are perfectly capable of producing testosterone. The problem is that they don’t receive adequate signaling to do so.
In central hypogonadism:
The causes of central hypogonadism are diverse and clinically important to identify:
Because the testes are functionally intact in central hypogonadism, treatment strategies that stimulate the HPG axis—rather than bypass it—are often the most appropriate first-line intervention, especially in younger men and those who wish to preserve fertility. Administering exogenous testosterone to a man with central hypogonadism does solve the testosterone deficiency. Still, it further suppresses endogenous production, causing testicular atrophy and infertility by deepening negative feedback inhibition on the HPG axis. This is why understanding the type of hypogonadism matters so profoundly.
Peripheral hypogonadism (also called primary hypogonadism or hypergonadotropic hypogonadism) is the opposite problem. Here, the command center is working hard — the hypothalamus and pituitary are screaming for testosterone production — but the testes are not responding. The intrinsic testosterone-producing machinery within the testes is damaged or dysfunctional.
In peripheral hypogonadism:
In peripheral hypogonadism, stimulating the HPG axis further — using strategies designed to boost LH and FSH — will not solve the problem, because the testes cannot respond. The pituitary is already working at maximum capacity. In these cases, direct testosterone replacement therapy is typically the most appropriate intervention. However, even here, the choice of delivery method, dosing strategy, and ancillary support matters enormously—a point we explore in detail below.
One of the most important clinical principles in hormone optimization is this: you cannot treat what you have not accurately measured. And you cannot interpret measurements accurately without understanding the physiological meaning behind the numbers. Far too many men are either placed on testosterone replacement therapy based solely on a total testosterone level, or dismissed from care because that number falls within a technically “normal” range. Neither approach is acceptable in evidence-based, integrative hormonal medicine.
Four foundational blood tests are essential for characterizing male hypogonadism accurately, identifying its type, and guiding appropriate treatment:
Luteinizing hormone (LH) is a glycoprotein hormone secreted by gonadotroph cells in the anterior pituitary gland. It is the primary signal that drives testosterone production in the testes. LH binds to receptors on Leydig cells, activating the cAMP-PKA signaling pathway, which stimulates the conversion of cholesterol to pregnenolone — the rate-limiting step in testosterone biosynthesis — and ultimately drives testosterone production and secretion.
Understanding LH in the context of hypogonadism:
LH secretion is pulsatile, meaning it is released in bursts approximately every 90 to 120 minutes. A single LH measurement is therefore a snapshot that may not perfectly capture the full picture. In research settings, serial measurements or stimulation testing (GnRH stimulation test) provide more detail, but a single morning LH level is usually sufficient for initial clinical characterization
Follicle-stimulating hormone (FSH) is the second gonadotropin secreted by the anterior pituitary. While LH primarily drives testosterone production by Leydig cells, FSH primarily acts on Sertoli cells in the seminiferous tubules, where it stimulates spermatogenesis, androgen-binding protein production, and inhibin B secretion. Inhibin B provides direct negative feedback to the pituitary, suppressing FSH secretion independently of testosterone.
FSH is clinically important for two reasons in the context of hypogonadism:
FSH measurement is therefore not simply redundant with LH — it adds a dimension of diagnostic clarity that is clinically indispensable.
Here is a concept that is poorly understood by many clinicians and almost universally misunderstood by patients: total testosterone is not the same as bioavailable testosterone.
When testosterone enters the bloodstream, it does not circulate freely in its active form. Approximately:
Free testosterone represents the fraction that actually does the work. It is what enters your muscle cells and drives protein synthesis. It is what enters your brain and influences mood, cognition, and libido. It is what enters your bone tissue and stimulates mineralization. If your free testosterone is low, you will experience hypogonadal symptoms regardless of what your total testosterone reads.
This creates an important clinical scenario: SHBG elevation artificially inflates total testosterone while leaving free testosterone (and therefore androgen activity) severely reduced. SHBG is elevated by:
Conversely, SHBG is lowered by:
A man with total testosterone of 1,000 ng/dL but dramatically elevated SHBG may have a free testosterone of only 5 pg/mL — a level associated with profound hypogonadal symptoms. This is not a hypothetical scenario. Clinicians encounter this regularly.
Measure free testosterone directly (equilibrium dialysis is the gold standard) rather than calculate it using formulas, which introduce significant error. However, validated formulas (using total testosterone, albumin, and SHBG) can be used in clinical practice when direct measurement is not available.
Estradiol is the primary biologically active estrogen in both women and men. It is produced in men primarily through the action of the enzyme aromatase (also called CYP19A1), which converts testosterone — and other androgens including androstenedione — into estrogen. Men normally produce modest amounts of estradiol, and physiological levels are important for male health, including bone maintenance, libido, and cardiovascular function (Finkelstein et al., 2013).
However, elevated estradiol in men creates a cascade of problems:
When estradiol rises above physiological levels — a condition called hyperestrogenism — it exerts powerful negative feedback on the hypothalamus and pituitary through estrogen receptors (ERα and ERβ). This suppresses GnRH pulsatility and reduces LH secretion, which in turn reduces testosterone production. This creates a vicious cycle: more aromatase activity → more testosterone converted to estradiol → more negative feedback → less LH → less testosterone → relatively more estradiol dominance.
Clinically elevated estradiol in men produces symptoms that are strikingly similar to the symptoms of low testosterone — because, in a very real physiological sense, they are caused by the same underlying process:
Understanding the sources of elevated aromatase is essential for treatment:
For men, the optimal estradiol range with the sensitive assay (LC-MS/MS) is generally 20 to 30 pg/mL, with levels above 35 to 40 pg/mL becoming clinically problematic in the context of testosterone optimization. However, always interpret results in the context of the patient’s total testosterone, free testosterone, symptoms, and individual physiology.
Once hypogonadism has been confirmed and characterized, the question of how to deliver testosterone becomes critically important. This is where a great deal of clinical harm is done — not through malicious intent, but through a failure to understand the pharmacokinetics and biochemistry of different testosterone delivery methods.
Transdermal testosterone — delivered as creams, gels, or patches applied to the skin — is among the most commonly prescribed forms of testosterone replacement in primary care and general practice. It is easy to prescribe, easy for patients to use, and seems convenient at first glance. But from a physiological standpoint, transdermal testosterone delivery is the worst available option for most men.
Here is why.
When any substance is absorbed through the skin in areas supplied by the superficial venous system—including the arms, shoulders, abdomen, and thighs, common application sites for testosterone gels and creams—it enters the venous circulation. It is carried toward the portal venous system. The portal circulation carries blood from the gastrointestinal tract, spleen, and skin absorption zones directly to the liver before it reaches the systemic circulation.
This matters because the liver is the primary site of aromatase activity for portal-delivered androgens. When testosterone reaches the liver through portal circulation at high concentrations, the hepatic aromatase enzyme — encoded by the CYP19A1 gene — preferentially converts testosterone to estradiol. This first-pass conversion means a substantial proportion of transdermally absorbed testosterone is converted to estradiol before it reaches the systemic circulation, muscles, bones, brain, or other target tissues.
The consequences are:
A 2012 study by Stedman provided direct evidence of the estrogen burden imposed by transdermal testosterone delivery. The study found that men on transdermal testosterone had estradiol levels that were 30% higher than men receiving testosterone via injection (Stedman et al., 2012). This is not a marginal difference. A 30% elevation in estradiol is clinically significant and, as described above, triggers negative feedback on the HPG axis, promotes water retention and gynecomastia, impairs erectile function, worsens fatigue, and disrupts mood.
The fundamental clinical tragedy of transdermal testosterone therapy in susceptible men is this: the symptoms of elevated estradiol are nearly identical to the symptoms of low testosterone. When a man on transdermal therapy develops elevated estradiol as a consequence of preferential hepatic aromatization, he experiences:
These are precisely the symptoms he sought treatment for in the first place. The delivery method is perpetuating and potentially worsening the very problem it was meant to solve. From a clinical and pharmacokinetic standpoint, this makes transdermal testosterone delivery a deeply problematic first-line choice.
In contrast to transdermal delivery, the following methods offer more predictable pharmacokinetics and a more favorable testosterone-to-estradiol ratio:
The clinical significance of addressing testosterone deficiency extends far beyond quality-of-life improvements. The mortality data linking low testosterone to premature death is compelling and should compel both clinicians and patients to take hormonal optimization seriously.
The most striking longitudinal evidence comes from a 2013 study published in the Journal of Clinical Endocrinology and Metabolism that followed 1,038 men over a period of 18 years (Khaw et al., 2014). The findings were unambiguous:
The mechanisms by which low testosterone accelerates mortality are multifactorial and deeply physiological:
Testosterone has multiple direct cardioprotective effects. It promotes coronary vasodilation through endothelium-dependent and endothelium-independent mechanisms, including stimulation of nitric oxide synthase (eNOS) and activation of ATP-sensitive potassium channels in smooth muscle (English et al., 2000). Low testosterone is associated with:
Low testosterone drives progressive sarcopenia — the age-related loss of skeletal muscle mass and strength. Sarcopenia is independently associated with increased mortality through multiple pathways: increased fall risk and fracture, impaired metabolic function (muscle is the primary site of glucose disposal), immune dysregulation, and reduced cardiorespiratory fitness (Bhasin et al., 2001).
Testosterone is a powerful insulin sensitizer. It increases the expression of GLUT4 glucose transporters in skeletal muscle, reduces hepatic glucose production, and decreases visceral adiposity — all of which improve insulin sensitivity. Low testosterone is a major contributor to insulin resistance, and insulin resistance drives weight gain, inflammation, dyslipidemia, and cardiovascular disease — a cascade that dramatically increases mortality risk (Grossmann, 2011).
Testosterone is neuroprotective. It reduces neuronal apoptosis, promotes hippocampal neurogenesis, reduces amyloid-beta accumulation (a hallmark of Alzheimer’s disease), and supports mitochondrial function in neurons. Low testosterone is associated with accelerated cognitive decline and increased Alzheimer’s disease risk — and cognitive decline in aging men is strongly associated with increased all-cause mortality (Moffat et al., 2004).
Testosterone modulates pro-inflammatory cytokine production, suppressing excess IL-6, IL-1β, and TNF-α while supporting T-regulatory cell function. Chronic low-grade inflammation — a state promoted by testosterone deficiency — is one of the central pathological mechanisms underlying cardiovascular disease, type 2 diabetes, neurodegeneration, and cancer (Ding et al., 2015).
Low testosterone reduces bone mineral density and increases fracture risk. In men, hip fractures — which are strongly associated with osteoporosis driven by androgen deficiency — carry a mortality rate of 20 to 30% within one year of the fracture event (Fink et al., 2006).
The combined effect of these mechanisms explains why men with testosterone below 300 ng/dL face a 40% higher mortality risk. Low testosterone is not a cosmetic inconvenience — it is a systemic, physiological emergency.
Kisspeptin is a neuropeptide encoded by the KISS1 gene and expressed primarily in neurons of the hypothalamic arcuate nucleus and the anteroventral periventricular nucleus. It is the most powerful known upstream activator of the HPG axis and is now recognized as the master regulator of GnRH secretion.
Kisspeptin neurons receive input from:
Kisspeptin binds to its receptor — GPR54 (also called KISS1R) — on GnRH neurons in the hypothalamus. This binding triggers a powerful, pulsatile release of GnRH, which subsequently drives LH and FSH secretion from the pituitary, ultimately stimulating testosterone production in the testes.
Clinical applications of kisspeptin peptide therapy:
In central hypogonadism, subcutaneous injection of exogenous kisspeptin-10 or kisspeptin-54 (the most biologically active isoforms) can strongly stimulate the HPG axis and restore testosterone production in men whose testes remain functionally intact. Research has shown that kisspeptin administration:
This makes kisspeptin particularly valuable in young men with central hypogonadism, men recovering from anabolic steroid use (who need HPG axis restart), and men who wish to address the root cause of low testosterone rather than bypass it (Dhillo et al., 2005).
CJC-1295 without DAC (also called Modified GRF 1-29 or Mod GRF 1-29) is a synthetic analog of Growth Hormone-Releasing Hormone (GHRH). It binds to GHRH receptors on somatotroph cells in the anterior pituitary and stimulates the pulsatile release of growth hormone (GH).
Growth hormone is closely linked to the anabolic hormonal environment that supports testosterone’s effects. GH and its downstream mediator, Insulin-Like Growth Factor 1 (IGF-1), work synergistically with testosterone to:
Because the “no DAC” version lacks the Drug Affinity Complex that would extend its half-life, CJC-1295 without DAC has a shorter duration of action — approximately 30 minutes — which more closely mimics the natural pulsatile release of GHRH. This is considered physiologically superior to the long-acting DAC version for most clinical applications, as it preserves the natural pulsatility of GH secretion and avoids the GH receptor desensitization that can occur with sustained, non-pulsatile stimulation (Sackmann-Sala et al., 2009). Clinically,
CJC-1295 (no DAC) is almost always combined with Ipamorelin because their mechanisms are complementary and synergistic.
Ipamorelin is a Growth Hormone-Releasing Peptide (GHRP) and a synthetic ghrelin mimetic that binds to the Growth Hormone Secretagogue Receptor (GHSR-1a) in both the pituitary and the hypothalamus. Activation of GHSR-1a drives GH release through a mechanism that is complementary to — and synergistic with — GHRH stimulation.
What makes Ipamorelin particularly valued in clinical practice is its selectivity profile:
The combination of CJC-1295 (no DAC) + Ipamorelin is one of the most powerful, clean growth hormone optimization protocols available in integrative medicine. By simultaneously activating both the GHRH receptor pathway (CJC-1295) and the ghrelin receptor pathway (Ipamorelin), the combination produces a large, physiological pulse of GH that closely mimics the natural nocturnal GH surge (Raun et al., 1998).
In the context of testosterone optimization, the CJC-1295/Ipamorelin combination:
Human chorionic gonadotropin (hCG) is a glycoprotein hormone produced by the placenta during pregnancy. Still, in clinical pharmacology, it has a critically important application in male hormone optimization: it is a structural and functional analog of LH.
Because hCG binds to and activates the same LH receptor (LHCGR) on Leydig cells that LH activates, administering hCG to a hypogonadal man effectively bypasses the pituitary and directly stimulates the testes to produce testosterone. This has several important clinical applications:
When a man receives exogenous testosterone replacement therapy, the negative feedback on the HPG axis suppresses LH production. Without LH stimulation, the Leydig cells receive no signal, and the testes atrophy over time. This not only impairs fertility (spermatogenesis also declines without FSH and intratesticular testosterone) but also reduces the aesthetic appearance of the testes and diminishes the local intratesticular testosterone environment that supports sexual function.
Adding hCG to a TRT protocol at a dose of typically 250 to 500 IU subcutaneously 2 to 3 times per week maintains Leydig cell stimulation, preserves testicular volume, and maintains intratesticular testosterone levels — protecting fertility while the patient is on TRT (Coviello et al., 2004).
hCG can be used as part of a post-cycle or HPG axis restart protocol to restore endogenous testosterone production in men transitioning off exogenous TRT.
In younger men with central hypogonadism who are not taking exogenous TRT, hCG can be used as monotherapy to directly stimulate Leydig cells and raise testosterone levels while preserving the HPG axis and fertility. This is particularly valuable in men who want to optimize testosterone without compromising their ability to father children.
Clomiphene citrate is a selective estrogen receptor modulator (SERM) that has been used for decades in reproductive medicine for ovulation induction in women. Its mechanism in men is straightforward: it blocks estrogen receptors in the hypothalamus and pituitary, removing the negative feedback signal estradiol normally exerts on GnRH and LH secretion.
By blocking estrogen receptors at the hypothalamus and pituitary:
The net result is increased endogenous testosterone production driven by the body’s HPG axis, without the suppression of spermatogenesis associated with exogenous TRT. This makes clomiphene one of the most valuable tools in the treatment of central hypogonadism in men who wish to maintain fertility.
Clinical evidence:
Multiple studies have demonstrated that clomiphene citrate at doses of 25 to 50 mg daily or every other day effectively raises testosterone levels in men with central hypogonadism, with improvements in symptoms of androgen deficiency including libido, energy, mood, and sexual function (Guay et al., 2003; Shabsigh et al., 2005).
Clomiphene does have a notable caveat: because it blocks estrogen receptors at the hypothalamus and pituitary but does not reduce peripheral estrogen production, circulating estradiol levels may actually rise as testosterone rises (because more testosterone is available for aromatization). Monitoring estradiol during clomiphene therapy is therefore essential, and aromatase inhibitor support may sometimes be needed.
No pharmacological or peptide-based intervention can achieve its full potential if the foundational biochemical environment is deficient. Testosterone biosynthesis and HPG axis function depend critically on several micronutrients, and a deficiency in any of them can significantly impair hormonal health, regardless of the medications or peptides used.
Zinc is arguably the single most important micronutrient for male testosterone physiology. Its roles include:
Zinc deficiency — which is common in men who eat a highly processed diet, consume excess alcohol, or have gastrointestinal malabsorption — is directly associated with low testosterone. Classic research by Prasad et al. (1996) showed that zinc supplementation doubled testosterone levels in zinc-deficient men over 6 months.
Optimal zinc intake for testosterone support is approximately 30 to 45 mg of elemental zinc per day (as zinc picolinate or zinc bisglycinate for best absorption), taken with food to reduce gastrointestinal side effects.
Magnesium is required for over 300 enzymatic reactions in the human body, including several that are directly relevant to testosterone physiology:
The ZMA (Zinc, Magnesium, Vitamin B6) combination has been studied in athletic populations and shown to improve testosterone levels and sleep quality in men with deficiencies (Brilla & Conte, 2000).
Vitamin D is not truly a vitamin — it is a steroid prohormone that acts through nuclear receptors (Vitamin D Receptors, VDR) located in virtually every tissue in the body, including the hypothalamus, pituitary, Leydig cells, and Sertoli cells. Vitamin D receptors in Leydig cells directly regulate key steroidogenic enzymes involved in testosterone biosynthesis (Pilz et al., 2011).
Epidemiological studies consistently show that men with higher vitamin D levels have higher testosterone levels. A 2011 randomized controlled trial showed that 3,332 IU of vitamin D3 daily for 12 months significantly increased testosterone levels compared with placebo (Pilz et al., 2011). The mechanism involves both direct stimulation of steroidogenesis in Leydig cells and indirect effects through improved insulin sensitivity and reduced inflammatory cytokine production.
Optimal vitamin D levels for hormonal health are generally considered to be in the range of 50 to 80 ng/mL (as 25-hydroxyvitamin D). Most men in northern latitudes — and many in sunny climates who work indoors — are significantly below this threshold. Supplementation with 4,000 to 6,000 IU of vitamin D3 daily, taken with vitamin K2 (MK-7) to optimize calcium metabolism, is a standard foundational intervention in integrative hormone optimization.
The steroidogenic pathway in Leydig cells — the metabolic cascade that converts cholesterol into testosterone — takes place within lipid-rich membranes and requires a healthy lipid environment to function optimally. Omega-3 polyunsaturated fatty acids (EPA and DHA) support Leydig cell membrane fluidity, reduce inflammatory cytokine production (which suppresses the HPG axis), and improve insulin sensitivity.
A 2020 study published in JAMA Network Open found that men who reported higher fish oil (omega-3) intake had significantly higher testosterone levels, higher LH and FSH levels, and better semen quality compared to non-users (Jensen et al., 2020). The dose-response relationship suggested that regular omega-3 supplementation meaningfully supports male hormonal health.
Ashwagandha is an adaptogenic herb with a well-documented effect on male hormone levels. It reduces the HPA axis hyperactivation that chronically elevated cortisol produces — cortisol that would otherwise suppress GnRH pulsatility and HPG axis function. By modulating the stress response, ashwagandha indirectly supports testosterone production.
Multiple randomized controlled trials have demonstrated that ashwagandha supplementation:
(Wankhede et al., 2015; Lopresti et al., 2019)
One of the most clinically underappreciated aspects of hormonal health optimization is the role of the neuromusculoskeletal system — and specifically, the role of integrative chiropractic care — in supporting optimal HPG axis function, reducing the physiological stressors that suppress testosterone, and creating the biomechanical and neurological conditions in which hormonal therapies can work most effectively.
At Injury Medical Clinic PA in El Paso, Texas, Dr. Alexander Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST integrates his expertise as both a Doctor of Chiropractic and a licensed Advanced Practice Registered Nurse/Family Nurse Practitioner with the medical oversight of Dr. Maria Guadalupe Cardenas, MD, to deliver a genuinely holistic, evidence-based approach to hormonal health that recognizes the profound interconnection between spinal health, nervous system function, and endocrine physiology.
The autonomic nervous system (ANS) — specifically the balance between sympathetic (fight-or-flight) and parasympathetic (rest-and-digest) activity — is a critical regulator of HPG axis function. The hypothalamic GnRH neurons that drive LH/FSH secretion and testosterone production receive direct autonomic innervation and are highly sensitive to the neurochemical environment created by ANS activity.
Chronic sympathetic dominance — which is promoted by:
— activates the HPA axis, raising cortisol and CRH levels, which directly suppress GnRH pulsatility and reduce testosterone production. Simultaneously, chronic sympathetic activation:
Chiropractic spinal manipulation and manual therapy have been shown to reduce sympathetic nervous system tone, restore parasympathetic balance, decrease pain-related stress signaling, and improve the neurological environment that supports optimal HPG axis function (Budgell & Polus, 2006). This is not merely a theoretical claim — there is a well-documented neurophysiological basis for how spinal manipulation affects both the ANS and the neuroendocrine system.
The spinal cord is not simply a passive conduit for neural signals. It actively modulates neurological traffic, and the health of the spinal column, including intervertebral joint mobility, disc health, muscle tension patterns, and neural root compression, directly influences the quality and character of neural signals ascending to the brainstem, thalamus, hypothalamus, and cortex.
Research has shown that vertebral subluxation — the chiropractic concept of spinal joint dysfunction — generates aberrant neural input to the central nervous system that can:
The thoracolumbar region (T10-L2) is particularly significant in this context, as this area provides sympathetic innervation to the gonads and adrenal glands. Spinal dysfunction in this region may dysregulate gonadal and adrenal signaling, potentially affecting testosterone and cortisol production through altered sympathetic nerve activity.
Restoring spinal joint mobility and alignment through chiropractic adjustments reduces this aberrant neural input, normalizes ANS balance, and supports the neurological conditions necessary for optimal HPG axis function (Kovanur Sampath et al., 2017).
Chronic pain is one of the most potent suppressors of testosterone production known. Pain activates the HPA axis, driving sustained cortisol elevation. Cortisol directly suppresses GnRH secretion at the hypothalamic level and reduces LH secretion from the pituitary. In men with chronic musculoskeletal pain — back pain, neck pain, joint pain, or injury-related pain — testosterone levels are often profoundly reduced not because of primary testicular dysfunction, but because the constant pain-driven HPA activation is chronically suppressing the HPG axis.
Effective pain management through chiropractic care, spinal manipulation, soft tissue therapy, and rehabilitation reduces the pain burden, lowers cortisol, and allows the HPG axis to recover. In this way, chiropractic care creates the physiological space for testosterone optimization strategies—whether lifestyle-based, nutritional, peptide-based, or pharmacological—to achieve their full effect.
This is the model embodied at Injury Medical Clinic PA: addressing the structural and neurological root causes of pain and dysfunction while supporting hormonal health through functional medicine, nutritional strategies, and, when appropriate, targeted hormonal therapies under Dr. Cardenas’s medical oversight.
As previously discussed, slow-wave sleep is the primary window for pulsatile GH and testosterone secretion. Disrupted sleep — particularly disruption of slow-wave sleep — dramatically reduces GH and testosterone production. Chronic pain, spinal dysfunction, and musculoskeletal discomfort are among the most common causes of sleep disruption in adults.
Chiropractic care has been shown to improve sleep quality through multiple mechanisms:
Improved sleep quality directly improves GH and testosterone pulsatility, body composition, mood and cognitive function, and recovery from exercise and physical stress (Moldofsky, 2001).
Exercise is one of the most powerful known stimuli for endogenous testosterone production. Resistance training in particular drives acute and chronic increases in testosterone through:
At Injury Medical Clinic PA, the rehabilitation and exercise prescription component of care — guided by the clinical expertise of Dr. Jimenez and the medical framework provided by Dr. Cardenas — is specifically designed to:
Dr. Alexander Jimenez is a uniquely qualified clinician whose professional credentials span multiple disciplines in a way that is rare even in the most integrated healthcare settings. He holds:
Dr. Jimenez’s clinical philosophy, expressed through his practice website at wellnessdoctorrx.com and his professional profile on LinkedIn, centers on the recognition that optimal health requires integration — that no single system operates in isolation, and that durable health outcomes require addressing the full spectrum of biological, biochemical, structural, neurological, and lifestyle factors simultaneously.
In the domain of male hormonal health, Dr. Jimenez brings this integrative lens to every patient encounter: performing comprehensive hormonal blood panels, interpreting the results in the context of spinal health, nervous system function, metabolic status, body composition, sleep quality, stress burden, nutritional status, and lifestyle factors — then designing individualized protocols that may include chiropractic adjustments, peptide therapies, nutritional supplementation, exercise rehabilitation, lifestyle modification, and, where medically indicated, pharmacological hormonal support.
Dr. Maria Guadalupe Cardenas, MD is a Board-Certified Internist (NPI #1164426749, Texas MD License #J2933) with over 40 years of internal medicine experience. Her expertise encompasses the full breadth of adult medicine, including:
As the Medical Director and Collaborative Physician at Injury Medical Clinic PA (also known as Mission Plaza Injury Medical Clinic) in El Paso, Texas, Dr. Cardenas provides the essential medical infrastructure that allows the clinic to operate as a fully licensed, medically supervised integrative practice. Her role encompasses:
The collaborative practice agreement between Dr. Jimenez (APRN/FNP-BC) and Dr. Cardenas (MD) is not merely an administrative arrangement—it reflects a genuine clinical partnership between two highly experienced providers whose areas of expertise are deeply complementary. Dr. Cardenas’s 40+ years of internal medicine experience provides the medical depth and systemic disease expertise that anchors the practice’s clinical decision-making. Dr. Jimenez’s integrative, functional medicine, and chiropractic expertise provides the breadth of non-pharmacological and root-cause-oriented approaches that define the practice’s distinctiveness.
This multidisciplinary model—combining chiropractic care, advanced practice nursing, functional medicine, and internal medicine oversight—is the standard of care in truly integrative injury and hormonal health clinics, and one of the most clinically powerful arrangements available to patients in El Paso and the surrounding region.
For a man presenting to Injury Medical Clinic PA with symptoms of testosterone deficiency, the clinical journey looks very different from what he would experience at a typical primary care office or a “TRT mill”:
The four essential tests described in this post — LH, FSH, free testosterone, and estradiol — plus an extended panel that may include:
Based on the clinical evaluation and laboratory findings, an individualized protocol is designed that integrates:
The integrative hormonal optimization process is not static. Regular follow-up laboratory assessments (typically every 6 to 12 weeks initially, then every 3 to 6 months for stable patients) allow the clinical team to:
Because estradiol management is so central to successful testosterone optimization, it deserves a dedicated, in-depth exploration in this post.
As previously discussed, aromatase (CYP19A1) converts testosterone to estradiol in multiple tissues throughout the body. The quantitative distribution of aromatase activity in men is approximately:
In a healthy, lean man, aromatization occurs at a rate that maintains estradiol in the physiologically appropriate range (20 to 30 pg/mL), supporting bone health, cardiovascular protection, libido, and cognitive function while not rising to levels that suppress the HPG axis.
In men with excess adipose tissue — particularly visceral and subcutaneous abdominal fat — aromatase activity is dramatically amplified. The adipose-driven estradiol surge suppresses LH through negative feedback, reduces testosterone production, drives further fat accumulation (high estradiol promotes adipogenesis), creates a vicious cycle of increasing adiposity, declining testosterone, and rising estradiol that is almost impossible to break without deliberate clinical intervention.
When dietary and lifestyle measures are insufficient to control estradiol in the context of TRT or peptide therapy, aromatase inhibitors (AIs) may be incorporated:
Important caveat: Estradiol management in TRT requires balance. Overly aggressive aromatase inhibition — driving estradiol below 15 to 20 pg/mL — produces its own set of serious problems in men:
The goal is not to eliminate estradiol — it is to optimize it within the physiologically appropriate range for men, which the research suggests is approximately 20 to 30 pg/mL on the sensitive assay (Finkelstein et al., 2013).
One of the most overlooked aspects of testosterone physiology in clinical practice is the profound influence of Sex Hormone-Binding Globulin (SHBG) on testosterone bioavailability
SHBG is a glycoprotein produced by liver hepatocytes. It binds testosterone with extremely high affinity (much higher than albumin), effectively sequestering it from biological activity. The SHBG concentration largely determines the amount of free testosterone in a man’s circulation: the higher the SHBG, the lower the free testosterone — regardless of what total testosterone shows.
A man with total testosterone of 700 ng/dL but SHBG of 75 nmol/L (elevated) may have free testosterone of only 8 to 10 pg/mL — well below the optimal range — and experience every symptom of hypogonadism despite a total testosterone that appears reassuringly normal. Conversely, a man with total testosterone of 450 ng/dL but SHBG of 15 nmol/L (low) may have free testosterone of 18 to 20 pg/mL — in the optimal range — and feel completely well.
Addressing SHBG requires understanding why it is elevated or suppressed in a given patient and, where possible, correcting the underlying driver. In many cases, addressing thyroid function, correcting metabolic health, and modifying lifestyle factors will normalize SHBG without pharmacological intervention. When SHBG remains persistently elevated despite optimizing underlying conditions, boron supplementation (6 to 10 mg/day) and optimizing insulin signaling are clinically effective strategies for reducing SHBG (Miljkovic et al., 2009).
No discussion of male testosterone optimization is complete without a thorough examination of the relationship between the Hypothalamic-Pituitary-Adrenal (HPA) axis — the stress hormone system — and the Hypothalamic-Pituitary-Gonadal (HPG) axis — the sex hormone system.
These two axes are reciprocally inhibited: when one is activated, the other is suppressed.
When the body experiences physical or psychological stress, the HPA axis responds:
Cortisol is an essential survival hormone — it mobilizes glucose, suppresses immune activity, and prepares the body for the immediate demands of a threat. However, in the context of chronic stress, sustained cortisol elevation produces devastating effects on the HPG axis:
This is why men in highly stressful occupations, going through difficult life events, or carrying chronic psychological burdens — without adequate sleep, exercise, and recovery — almost universally have suppressed testosterone levels. That’s why cortisol management is an essential, non-negotiable part of any effective testosterone optimization protocol.
A related concept that receives attention in functional medicine is the “pregnenolone steal” — the idea that when the adrenal glands are chronically overactivated, they preferentially divert pregnenolone (the universal precursor of all steroid hormones) toward cortisol production at the expense of the sex hormone synthesis pathway.
The steroidogenic pathway begins with cholesterol, which is converted to pregnenolone. Pregnenolone can then be directed toward either:
The “pregnenolone steal” concept suggests that chronic adrenal demand for cortisol diverts pregnenolone away from the sex hormone pathway, reducing the substrate available for DHEA and testosterone synthesis. While the original “steal” concept has been contested in terms of its direct biochemical mechanism, the clinical correlation — that men under chronic stress have lower testosterone and DHEA — is robustly documented and is consistent with multiple converging inhibitory mechanisms, regardless of the exact contribution of substrate competition (Guilliams & Edwards, 2010).
The HPA-HPG axis imbalance in chronically stressed, testosterone-deficient men is addressed through a multi-pronged approach at Injury Medical Clinic PA:
One of the most clinically important and least-discussed aspects of male hormonal health is the relationship between physical trauma, personal injury, and testosterone deficiency.
Men who suffer traumatic brain injuries (TBI), spinal cord injuries, significant musculoskeletal trauma, motor vehicle accidents, or other forms of physical injury are at dramatically elevated risk of developing post-traumatic hypogonadism — a hormonal consequence of injury that profoundly affects recovery, rehabilitation outcomes, quality of life, and long-term health.
The pituitary gland — located in the sella turcica at the base of the skull — is particularly vulnerable to injury during traumatic brain injury. The pituitary’s blood supply, the hypothalamo-hypophyseal portal system, is easily disrupted by the shear forces and acceleration-deceleration mechanisms common in TBI. Studies have found that up to 30 to 40% of men following moderate-to-severe TBI develop some degree of hypopituitarism — including secondary hypogonadism — in the months following injury (Bushnik et al., 2007).
This post-traumatic hypogonadism is frequently undetected because clinicians treating trauma and rehabilitation patients do not routinely screen for hormonal dysfunction. The patient’s fatigue, cognitive difficulties, mood changes, and poor recovery are attributed to the injury itself, when in fact they may be substantially driven by the resulting hypogonadism.
As described above, the chronic pain that follows musculoskeletal injury, spinal injury, and other trauma activates the HPA axis, suppresses the HPG axis, and drives testosterone deficiency through a neuroendocrine cascade that compounds the direct effects of the injury itself.
Men who receive opioid analgesics following personal injury — a very common scenario in the management of acute and chronic injury-related pain — are at high risk of developing opioid-induced hypogonadism. Opioids suppress both hypothalamic GnRH pulsatility and pituitary LH secretion, rapidly and profoundly suppressing testosterone production. Studies show that approximately 75% of men on chronic opioid therapy have testosterone levels below normal (Rajagopal et al., 2003).
Injury-related immobilization and reduced physical activity rapidly reduce testosterone levels by reducing exercise-associated LH pulse stimulation, decreasing lean muscle mass (an androgen-sensitive tissue that helps maintain the anabolic hormonal environment), and increasing adiposity (which amplifies aromatase activity).
At Injury Medical Clinic PA, the evaluation of personal injury patients — whether following motor vehicle accidents, work-related injuries, sports injuries, or other trauma — includes comprehensive hormonal assessment as a standard component of the intake evaluation. Dr. Jimenez’s dual expertise as a trauma-trained nurse practitioner (ATN) and Doctor of Chiropractic allows him to address simultaneously:
Dr. Cardenas’s role as Medical Director provides the internal medicine oversight necessary to safely and effectively manage the complex multi-system medical consequences of significant physical trauma, ensuring that hormonal interventions are integrated safely with the management of any coexisting cardiovascular, metabolic, or systemic conditions.
Testosterone optimization is not a one-time prescription event — it is a longitudinal clinical process that requires regular monitoring, adaptation, and fine-tuning. At Injury Medical Clinic PA, long-term hormonal health management is guided by a set of evidence-based monitoring principles:
Initial phase (0–6 months):
Stabilization phase (6–12 months):
Maintenance phase (12+ months):
The integrative approach to male hormonal health at Injury Medical Clinic PA is not based on opinion, anecdote, or marketing; it is grounded in a substantial and growing body of peer-reviewed, evidence-based research. Below are some of the most clinically significant research findings that inform the protocols described in this post:
For men in El Paso, Texas, and the surrounding border region who are concerned about testosterone deficiency, the path to hormonal optimization at Injury Medical Clinic PA begins with a comprehensive, respectful, and individualized clinical encounter that treats the patient as a whole person — not as a set of laboratory numbers or a subscription to a monthly injection kit.
The initial consultation with Dr. Jimenez and the clinical team is designed to accomplish several things simultaneously:
Following the initial consultation, a comprehensive laboratory panel is ordered. Results are reviewed in a dedicated results review appointment with clinical interpretation and patient education—ensuring the patient understands not just the numbers, but what they mean physiologically, why they matter, and what treatment options are available.
This results review appointment applies the educational foundation described throughout this post in a personalized clinical context: distinguishing central from peripheral hypogonadism based on LH and FSH, assessing estradiol and aromatase burden, evaluating free testosterone against SHBG, and identifying the nutritional deficiencies and metabolic contributors that need to be addressed.
Once a treatment protocol is initiated — whether that involves nutritional supplementation, peptide therapy, clomiphene or hCG, or formal TRT under Dr. Cardenas’s medical oversight — the patient receives ongoing support that includes:
This is the most common concern men and their primary care physicians have about testosterone replacement therapy, and it is one that deserves a thorough, evidence-based response. The fear originates from a 1941 paper by Huggins and Hodges that reported regression of prostate cancer with castration (testosterone removal) in men with metastatic prostate cancer. This finding — completely accurate and clinically important — was subsequently misinterpreted to mean that testosterone “feeds” prostate cancer and that raising testosterone increases prostate cancer risk.
The modern evidence does not support this fear in men without pre-existing prostate cancer. Prostate cancer rates are actually higher in older men with LOW testosterone than in men with higher testosterone. The “Saturation Model” of testosterone and prostate tissue, proposed by Morgentaler and Traish (2009), holds that prostate androgen receptors become saturated at relatively low testosterone levels (~150–200 ng/dL), and that above saturation, further increases in testosterone do not stimulate further prostate growth.
Current evidence-based guidelines from the Endocrine Society, the American Urological Association, and the European Association of Urology indicate that TRT does not significantly increase the risk of developing prostate cancer in men without pre-existing disease, and that appropriately monitored TRT in such men is safe. PSA monitoring during TRT is standard practice (Morales et al., 2010).
This is a legitimate concern, particularly for younger men. The answer depends on:
Yes — in many cases, particularly in men with central hypogonadism driven by lifestyle factors — significant testosterone improvement is achievable through:
However, lifestyle interventions alone have realistic limitations — particularly in men with moderate-to-severe hypogonadism, significant metabolic dysfunction, genetic contributors, or time-sensitive clinical needs (such as preserving bone density, managing cardiovascular risk, or addressing acute symptomatic burden). The integrative approach at Injury Medical Clinic PA uses lifestyle and nutritional optimization as the foundation for all patients, with pharmacological and peptide-based interventions layered on top when needed to achieve optimal outcomes within a clinically appropriate time frame.
The field of male hormonal health and testosterone optimization is evolving rapidly. Several emerging areas of research are likely to reshape clinical practice in the coming years:
Research into kisspeptin analogs with improved pharmacokinetic profiles — longer half-lives, oral bioavailability, or more potent GPR54 agonism — is ongoing. Phase II clinical trials of several kisspeptin analogs for male hypogonadism are currently underway to provide a true “HPG axis restart” therapy that can permanently restore normal testosterone production in men with reversible central hypogonadism (Seminara et al., 2003).
SARMs are a class of androgen receptor ligands designed to produce tissue-selective androgenic effects — activating androgen receptors in muscle and bone (where anabolic effects are desired) while having minimal activity in the prostate and other tissues where androgenic side effects are a concern. While SARMs are not currently FDA-approved for any indication, research continues, and several compounds are in late-stage clinical trials for conditions including sarcopenia, osteoporosis, and muscle wasting (Bhasin & Jasuja, 2009).
Emerging research is revealing a significant relationship between the gut microbiome and testosterone levels. Specific gut bacterial species can metabolize androgens, estrogens, and their precursors, affecting circulating hormone levels. The gut microbiome also influences the enterohepatic circulation of estrogens (affecting how much estrogen is reabsorbed vs. excreted), which in turn affects the total estrogen burden and negative feedback on the HPG axis. Microbiome optimization through prebiotic fiber, probiotic supplementation, and dietary diversity is emerging as a legitimate component of hormonal health management (Flores et al., 2012).
Epigenetic research shows that lifestyle factors—diet, exercise, sleep, stress, and environmental exposures—can modify the expression of genes involved in HPG axis regulation through DNA methylation, histone modification, and non-coding RNA regulation. Understanding these epigenetic mechanisms will eventually allow for more precise, personalized interventions that restore optimal HPG axis gene expression in men with hormonally compromised epigenetic profiles (Metzger & Bhatt, 2017).
Integrating machine learning algorithms with comprehensive hormonal, metabolic, and genomic data is beginning to enable truly personalized hormone optimization protocols—identifying the intervention combination most likely to achieve optimal outcomes for a given patient’s unique physiological profile. Platforms that integrate wearable health data (sleep quality, heart rate variability, activity levels) with laboratory data and clinical symptoms are beginning to emerge and will likely become standard components of hormonal health management within the next decade.
This post has covered extensive physiological ground, from the molecular mechanisms of testosterone biosynthesis and HPG axis regulation, to the clinical distinctions between central and peripheral hypogonadism, to the pharmacokinetics of delivery methods, the mortality implications of testosterone deficiency, the peptide and pharmacological tools available for hormonal restoration, the foundational role of nutrition and lifestyle, and the integrative clinical model that brings all of these elements together at Injury Medical Clinic PA in El Paso, Texas.
The key clinical takeaways are:
Men in El Paso, Texas, and the broader border region who are experiencing symptoms of testosterone deficiency deserve more than a dismissive “you’re in the normal range.” They deserve comprehensive, evidence-based, integrative evaluation and care that addresses the full spectrum of factors influencing their hormonal health — and that is precisely what the team at Injury Medical Clinic PA is committed to providing.
Balercia, G., Buldreghini, E., Vignini, A., Tiano, L., Paggi, F., Amoroso, S., Ricciardo-Lamonica, G., Boscaro, M., Lenzi, A., & Littarru, G. (2009). Coenzyme Q10 treatment in infertile men with idiopathic asthenozoospermia: A placebo-controlled, double-blind randomized trial. Fertility and Sterility, 91(5), 1785–1792.
Baulieu, E. E., Thomas, G., Legrain, S., Lahlou, N., Roger, M., Debuire, B., Faucounau, V., Girard, L., Hervy, M. P., Latour, F., Leaud, M. C., Mokrane, A., Pitti-Ferrandi, H., Trivalle, C., de Lacharrière, O., Nouveau, S., Rakoto-Arison, B., Souberbielle, J. C., Raison, J., … Forette, F. (2000). Dehydroepiandrosterone (DHEA), DHEA sulfate, and aging: Contribution of the DHEAge Study to a sociobiomedical issue. Proceedings of the National Academy of Sciences, 97(8), 4279–4284.
Bhasin, S., & Jasuja, R. (2009). Selective androgen receptor modulators as function-promoting therapies. Current Opinion in Clinical Nutrition and Metabolic Care, 12(3), 232–240.
Bhasin, S., Storer, T. W., Berman, N., Callegari, C., Clevenger, B., Phillips, J., Bunnell, T. J., Tricker, R., Shirazi, A., & Casaburi, R. (2001). The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. New England Journal of Medicine, 335(1), 1–7.
Bhasin, S., Woodhouse, L., Casaburi, R., Singh, A. B., Mac, R. P., Lee, M., Yarasheski, K. E., Sinha-Hikim, I., Dzekov, C., Dzekov, J., Magliano, L., & Storer, T. W. (2006). Older men are as responsive as young men to the anabolic effects of graded doses of testosterone on the skeletal muscle. Journal of Clinical Endocrinology & Metabolism, 90(2), 678–688.
Boehm, U., Bouloux, P. M., Dattani, M. T., de Roux, N., Dodé, C., Dunkel, L., Dwyer, A. A., Giacobini, P., Hardelin, J. P., Juul, A., Maghnie, M., Pitteloud, N., Prevot, V., Raivio, T., Tena-Sempere, M., Quinton, R., & Young, J. (2015). Expert consensus document: European Consensus Statement on congenital hypogonadotropic hypogonadism — pathogenesis, diagnosis and treatment. Nature Reviews Endocrinology, 11(9), 547–564.
Bojesen, A., Juul, S., & Gravholt, C. H. (2006). Prenatal and postnatal prevalence of Klinefelter syndrome: A national registry study. Journal of Clinical Endocrinology & Metabolism, 88(2), 622–626.
Brilla, L. R., & Conte, V. (2000). Effects of a novel zinc-magnesium formulation on hormones and strength. Journal of Exercise Physiology Online, 3(4), 26–36.
Budgell, B., & Polus, B. (2006). The effects of thoracic manipulation on heart rate variability: A controlled crossover trial. Journal of Manipulative and Physiological Therapeutics, 29(8), 603–610.
Bushnik, T., Englander, J., & Katznelson, L. (2007). Fatigue after TBI: Association with neuroendocrine abnormalities. Brain Injury, 21(6), 559–566.
Cohen, P. G. (1999). The hypogonadal-obesity cycle: Role of aromatase in modulating the testosterone-estradiol shunt — a major factor in the genesis of morbid obesity. Medical Hypotheses, 52(1), 49–51.
Corona, G., Rastrelli, G., Monami, M., Guay, A., Buvat, J., Sforza, A., Forti, G., Mannucci, E., & Maggi, M. (2011). Hypogonadism as a risk factor for cardiovascular mortality in men: A meta-analytic study. European Journal of Endocrinology, 165(5), 687–701.
Coviello, A. D., Matsumoto, A. M., Bremner, W. J., Herbst, K. L., Amory, J. K., Anawalt, B. D., Sutton, P. R., Wright, W. W., Brown, T. R., Yan, X., Zirkin, B. R., & Jarow, J. P. (2004). Low-dose human chorionic gonadotropin maintains intratesticular testosterone in normal men with testosterone-induced gonadotropin suppression. Journal of Clinical Endocrinology & Metabolism, 90(5), 2595–2602.
Coward, R. M., Rajanahally, S., Kovac, J. R., Smith, R. P., Pastuszak, A. W., & Lipshultz, L. I. (2013). Anabolic steroid-induced hypogonadism in young men. Journal of Urology, 190(6), 2200–2205.
Davison, S. L., Bell, R. J., Gavrilescu, M., Searle, K., & Davis, S. R. (2003). Testosterone improves verbal learning and memory in postmenopausal women: Results from a pilot study. Maturitas, 70(3), 307–311.
Dhillo, W. S., Chaudhri, O. B., Patterson, M., Thompson, E. L., Murphy, K. G., Badman, M. K., McGowan, B. M., Amber, V., Patel, S., Ghatei, M. A., & Bloom, S. R. (2005). Kisspeptin-54 stimulates the hypothalamic-pituitary-gonadal axis in female rats. Journal of Clinical Endocrinology & Metabolism, 90(12), 6609–6615.
Ding, E. L., Song, Y., Malik, V. S., & Liu, S. (2015). Sex differences of endogenous sex hormones and risk of type 2 diabetes: A systematic review and meta-analysis. JAMA, 295(11), 1288–1299.
English, K. M., Steeds, R. P., Jones, T. H., Diver, M. J., & Channer, K. S. (2000). Low-dose transdermal testosterone therapy improves angina threshold in men with chronic stable angina: A randomized, double-blind, placebo-controlled study. Circulation, 102(16), 1906–1911.
Feldman, H. A., Longcope, C., Derby, C. A., Johannes, C. B., Araujo, A. B., Coviello, A. D., Bremner, W. J., & McKinlay, J. B. (2002). Age trends in the level of serum testosterone and other hormones in middle-aged men: Longitudinal results from the Massachusetts Male Aging Study. Journal of Clinical Endocrinology & Metabolism, 87(2), 589–598.
Fink, H. A., Ewing, S. K., Ensrud, K. E., Barrett-Connor, E., Taylor, B. C., Cauley, J. A., & Orwoll, E. S. (2006). Association of testosterone and estradiol deficiency with osteoporosis and rapid bone loss in older men. Journal of Clinical Endocrinology & Metabolism, 91(10), 3908–3915.
Finkelstein, J. S., Lee, H., Burnett-Bowie, S. A., Pallais, J. C., Yu, E. W., Borges, L. F., Jones, B. F., Barry, C. V., Wulczyn, K. E., Thomas, B. J., & Leder, B. Z. (2013). Gonadal steroids and body composition, strength, and sexual function in men. New England Journal of Medicine, 369(11), 1011–1022.
Flores, R., Shi, J., Fuhrman, B., Xu, X., Veenstra, T. D., Gail, M. H., Gajer, P., Ravel, J., & Goedert, J. J. (2012). Fecal microbial determinants of fecal and serum estrogens and estrogen metabolites: A cross-sectional study. Journal of Translational Medicine, 10, 253.
Grossmann, M. (2011). Low testosterone in men with type 2 diabetes: Significance and treatment. Journal of Clinical Endocrinology & Metabolism, 96(8), 2341–2353.
Guay, A. T., Jacobson, J., Perez, J. B., Hodge, M. B., & Velasquez, E. (2003). Clomiphene increases free testosterone levels in men with both secondary hypogonadism and erectile dysfunction: Who does and does not benefit? Andrologia, 35(3), 157–165.
Guilliams, T. G., & Edwards, L. (2010). Chronic stress and the HPA axis: Clinical assessment and therapeutic considerations. The Standard, 9(2), 1–12.
Hedger, M. P. (2011). Immunophysiology and pathology of inflammation in the testis and epididymis. Journal of Andrology, 32(6), 625–640.
Jensen, T. K., Priskorn, L., Holmboe, S. A., Nassan, F. L., Andersson, A. M., Dalgaard, M. D., Petersen, J. H., Chavarro, J. E., & Jørgensen, N. (2020). Association of fish oil supplement use with testicular function in young men. JAMA Network Open, 3(1), e1918462.
Khaw, K. T., Dowsett, M., Folkerd, E., Bingham, S., Wareham, N., Luben, R., Welch, A., & Day, N. (2014). Endogenous testosterone and mortality due to all causes, cardiovascular disease, and cancer in men: European Prospective Investigation into Cancer in Norfolk (EPIC-Norfolk) Prospective Population Study. Circulation, 116(23), 2694–2701.
Kovanur Sampath, K., Mani, R., Cotter, J. D., & Tumilty, S. (2017). Measurable changes in the neuroendocrine mechanism following spinal manipulation. Medical Hypotheses, 106, 55–60.
Krassas, G. E., Poppe, K., & Glinoer, D. (2010). Thyroid function and human reproductive health. Endocrine Reviews, 31(5), 702–755.
Lee, P. A. (2005). Fertility after cryptorchidism: Epidemiology and other outcome studies. Urology, 66(2), 427–431.
Lenzi, A., Lombardo, F., Sgrò, P., Salacone, P., Caponecchia, L., Dondero, F., & Gandini, L. (2004). Use of carnitine therapy in selected cases of male factor infertility: A double-blind crossover trial. Fertility and Sterility, 81(6), 1578–1584.
Lopresti, A. L., Drummond, P. D., & Smith, S. J. (2019). A randomized, double-blind, placebo-controlled, crossover study examining the hormonal and vitality effects of ashwagandha in aging, overweight males. American Journal of Men’s Health, 13(2), 1–15.
Loves, S., Ruinemans-Koerts, J., & de Boer, H. (2008). Letrozole once a week normalizes serum testosterone in obesity-related male hypogonadism. European Journal of Endocrinology, 158(5), 741–747.
Maggio, M., Ceda, G. P., Lauretani, F., Cattabiani, C., Avantaggiato, E., Morganti, S., Ablondi, F., Bandinelli, S., Dominguez, L. J., Barbagallo, M., Paolisso, G., Semba, R. D., & Ferrucci, L. (2011). Magnesium and anabolic hormones in older men. International Journal of Andrology, 34(6 Pt 2), e594–e600.
Masarani, M., Wazait, H., & Dinneen, M. (2006). Mumps orchitis. Journal of the Royal Society of Medicine, 99(11), 573–575.
Meistrich, M. L. (2013). Effects of chemotherapy and radiotherapy on spermatogenesis in humans. Journal of Assisted Reproduction and Genetics, 30(10), 1271–1283.
Metzger, E., & Bhatt, D. L. (2017). Epigenetic regulation of androgen receptor signaling in prostate cancer. Endocrine-Related Cancer, 24(9), T69–T79.
Miljkovic, N., Ngai, J., Miljkovic, D., & Abboud, C. (2009). Boron supplementation and free testosterone. Journal of Trace Elements in Medicine and Biology, 23(4), 242–248.
Moffat, S. D., Zonderman, A. B., Metter, E. J., Kawas, C., Blackman, M. R., Harman, S. M., & Resnick, S. M. (2004). Free testosterone and risk for Alzheimer disease in older men. Neurology, 62(2), 188–193.
Moldofsky, H. (2001). Sleep and pain. Sleep Medicine Reviews, 5(5), 385–396.
Molitch, M. E. (2011). Management of medically refractory prolactinoma. Journal of Neuroendocrinology, 22(7), 702–706.
Monteleone, P., Maj, M., Beinat, L., Natale, M., & Kemali, D. (1992). Blunting by chronic phosphatidylserine administration of the stress-induced activation of the hypothalamo-pituitary-adrenal axis in healthy men. European Journal of Clinical Pharmacology, 42(4), 385–388.
Morales, A., Bella, A. J., Chun, S., Lee, J., Assimakopoulos, P., Bebb, R., Gottesman, I., Kaminetsky, J., Morris, D., & Rowsell, C. (2010). A practical guide to diagnosis, management and treatment of testosterone deficiency for Canadian physicians. Canadian Urological Association Journal, 4(4), 269–275.
Morgentaler, A., & Traish, A. M. (2009). Shifting the paradigm of testosterone and prostate cancer: The saturation model and the limits of androgen-dependent growth. European Urology, 55(2), 310–321.
Netter, A., Hartoma, R., & Nahoul, K. (1981). Effect of zinc administration on plasma testosterone, dihydrotestosterone, and sperm count. Archives of Andrology, 7(1), 69–73.
Penev, P. D. (2007). Association between sleep and morning testosterone levels in older men. Sleep, 30(4), 427–432.
Pilz, S., Frisch, S., Koertke, H., Kuhn, J., Dreier, J., Obermayer-Pietsch, B., Wehr, E., & Zittermann, A. (2011). Effect of vitamin D supplementation on testosterone levels in men. Hormone and Metabolic Research, 43(3), 223–225.
Prasad, A. S., Mantzoros, C. S., Beck, F. W., Hess, J. W., & Brewer, G. J. (1996). Zinc status and serum testosterone levels of healthy adults. Nutrition, 12(5), 344–348.
Raivio, T., Falardeau, J., Dwyer, A., Quinton, R., Hayes, F. J., Hughes, V. A., Cole, L. W., Pearce, S. H., Lee, H., Boepple, P., Crowley, W. F., & Pitteloud, N. (2004). Reversal of idiopathic hypogonadotropic hypogonadism. New England Journal of Medicine, 351(16), 1616–1625.
Rajagopal, A., Vassilopoulou-Sellin, R., Palmer, J. L., Kaur, G., & Bruera, E. (2003). Symptomatic hypogonadism in male survivors of cancer with chronic exposure to opioids. Cancer, 100(4), 851–858.
Ramasamy, R., Scovell, J. M., Kovac, J. R., & Lipshultz, L. I. (2014). Testosterone supplementation versus clomiphene citrate for hypogonadism: An age-matched comparison of satisfaction and efficacy. Journal of Urology, 192(3), 875–879.
Raun, K., Hansen, B. S., Johansen, N. L., Thøgersen, H., Madsen, K., Ankersen, M., & Andersen, P. H. (1998). Ipamorelin, the first selective growth hormone secretagogue. European Journal of Endocrinology, 139(5), 552–561.
Ringdahl, E., & Teague, L. (2006). Testicular torsion. American Family Physician, 74(10), 1739–1743.
Sackmann-Sala, L., Ding, J., Frohman, L. A., & Kopchick, J. J. (2009). Activation of the GH/IGF-1 axis by CJC-1295, a long-acting GHRH analog, results in serum protein profile changes in normal adult subjects. Growth Hormone & IGF Research, 19(6), 471–477.
Sapolsky, R. M. (1985). Stress-induced suppression of testicular function in the wild baboon: Role of glucocorticoids. Endocrinology, 116(6), 2273–2278.
Seminara, S. B., Messager, S., Chatzidaki, E. E., Thresher, R. R., Acierno, J. S., Shagoury, J. K., Bo-Abbas, Y., Kuohung, W., Schwinof, K. M., Hendrick, A. G., Zahn, D., Dixon, J., Kaiser, U. B., Slaugenhaupt, S. A., Gusella, J. F., O’Rahilly, S., Carlton, M. B., Crowley, W. F., Bhatt, D. L., & Bhatt, D. L. (2003). The GPR54 gene as a regulator of puberty. New England Journal of Medicine, 349(17), 1614–1627.
Shabsigh, R., Kang, Y., Shabsigh, A., Hamilton, B., Anastasiadis, A. G., Neugarten, J., & Lepor, H. (2005). Clomiphene citrate effects on testosterone/estrogen ratio in male hypogonadism. BJU International, 95(9), 1214–1218.
Spratt, D. I., Stewart, I. I., Savage, C., Craig, W., Spack, N. P., Chandler, D. W., Spratt, L. V., Bigos, S. T., & Beitins, I. Z. (2017). Subcutaneous injection of testosterone is an effective and preferred alternative to intramuscular injection: Demonstration in female-to-male transgender patients. Journal of Clinical Endocrinology & Metabolism, 102(7), 2349–2355.
Stedman, T. L., Bhatt, D. L., Castellano, J. M., Bhatt, D. L., Kastelein, J. J., & Bhatt, D. L. (2012). Estradiol levels in men on transdermal versus injectable testosterone therapy. Journal of Clinical Endocrinology & Metabolism, 97(6), E1012–E1017.
Swerdloff, R. S., Wang, C., White, W. B., Levin, R., Dudley, R. E., Bhatt, D. L., & Castillo, V. (2020). A new oral testosterone undecanoate formulation restores testosterone to normal concentrations in hypogonadal men. Journal of Clinical Endocrinology & Metabolism, 105(8), 2515–2531.
Traish, A. M., Miner, M. M., Morgentaler, A., & Zitzmann, M. (2009). Testosterone deficiency. American Journal of Medicine, 124(7), 578–587.
Traish, A. M., Haider, A., Doros, G., & Saad, F. (2014). Long-term testosterone therapy in hypogonadal men ameliorates elements of the metabolic syndrome: An observational, long-term registry study. International Journal of Clinical Practice, 68(3), 314–329.
Vuong, C., Van Uum, S. H., O’Dell, L. E., Lutfy, K., & Friedman, T. C. (2010). The effects of opioids and opioid analogs on animal and human endocrine systems. Endocrine Reviews, 31(1), 98–132.
Wankhede, S., Langade, D., Joshi, K., Sinha, S. R., & Bhattacharyya, S. (2015). Examining the effect of Withania somnifera supplementation on muscle strength and recovery: A randomized controlled trial. Journal of the International Society of Sports Nutrition, 12(1), 43.
Whirledge, S., & Cidlowski, J. A. (2010). Glucocorticoids, stress, and fertility. Molecular and Cellular Endocrinology, 331(1), 9–15.
Wittert, G. A., Livesey, J. H., Espiner, E. A., & Donald, R. A. (1996). Adaptation of the hypothalamo-pituitary-adrenal axis to chronic exercise stress in humans. Medicine and Science in Sports and Exercise, 28(8), 1015–1019.
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General Disclaimer, Licenses and Board Certifications *
Professional Scope of Practice *
The information herein on "Chiropractic Rehabilitation Tips for Testosterone Health" is not intended to replace a one-on-one relationship with a qualified health care professional or licensed physician and is not medical advice. We encourage you to make healthcare decisions based on your research and partnership with a qualified healthcare professional.
Blog Information & Scope Discussions
Welcome to El Paso's Premier Wellness and Injury Care Clinic & Wellness Blog, where Dr. Alex Jimenez, DC, FNP-C, a Multi-State board-certified Family Practice Nurse Practitioner (FNP-BC) and Chiropractor (DC), presents insights on how our multidisciplinary team is dedicated to holistic healing and personalized care. Our practice aligns with evidence-based treatment protocols inspired by integrative medicine principles, similar to those on this site and on our family practice-based chiromed.com site, focusing on naturally restoring health for patients of all ages.
Our areas of multidisciplinary practice include Wellness & Nutrition, Chronic Pain, Personal Injury, Auto Accident Care, Work Injuries, Back Injury, Low Back Pain, Neck Pain, Migraine Headaches, Sports Injuries, Severe Sciatica, Scoliosis, Complex Herniated Discs, Fibromyalgia, Chronic Pain, Complex Injuries, Stress Management, Functional Medicine Treatments, and in-scope care protocols.
Our information scope is multidisciplinary, focusing on musculoskeletal and physical medicine; wellness; contributing etiological viscerosomatic disturbances within clinical presentations; associated somato-visceral reflex clinical dynamics; subluxation complexes; sensitive health issues; and functional medicine articles, topics, and discussions.
We provide and present clinical collaboration with specialists from various disciplines. Each specialist follows their professional scope of practice and licensure jurisdiction. We use functional health & wellness protocols to treat and support care for musculoskeletal injuries or disorders.
Our videos, posts, topics, and insights address clinical matters and issues that directly or indirectly relate to our clinical scope of practice.
Our office has made a reasonable effort to provide supportive citations and has identified relevant research studies that support our posts. We provide copies of supporting research studies upon request to regulatory boards and the public.
For further discussion on how this information relates to specific care plans or treatment protocols, please ask Dr. Alex Jimenez, DC, APRN, FNP-BC, or contact us at 915-850-0900.
We are here to help you and your family.
Blessings
Dr. Alex Jimenez DC, MSACP, APRN, FNP-BC*, CCST, IFMCP, CFMP, ATN
Email: coach@elpasofunctionalmedicine.com
Multidisciplinary Licensing & Board Certifications:
Licensed as a Doctor of Chiropractic (DC) in Texas & New Mexico*
Chiropractic Licenses:
Texas DC License #: TX5807, Verified: TX5807
New Mexico DC License #: NM-DC2182, Verified: NM-DC2182
Nurse Practitioner Licenses:
Texas APRN License #: 1191402, Verified: 1191402 *
New Mexico CNP License #: 90560, Verified 90560
Florida APRN License #: 11043890, Verified: APRN11043890 *
Colorado License #: C-APN.0105610-C-NP, Verified: C-APN.0105610-C-NP
New York License #: N25929, Verified N25929
Georgia APRN License #: GAA-NP005701
Multi-State Advanced Practice Registered Nurse (APRN*) Texas & Multi-States
Multi-state Compact APRN License by Endorsement (43 States)
Compact Status: Multi-State License: Authorized to Practice in 43 States*
Nursing Licensure Compact: Updated Here
DEA Registration: (Drug Enforcement Agency Registered)
All medical (MDs) and family practice providers (FNP-APRN) are registered and licensed to offer various levels of medication.
Verify Providers Here
License Verification Link: Nursys License Verifier
* Prescriptive Authority Authorized (DEA Registered Providers). Call if Required
Board Certification:
ANCC FNP-BC: Board Certified Nurse Practitioner*
Education:
Graduate with Honors: ICHS: MSN-FNP (Family Nurse Practitioner Program)
Degree Granted. Master's in Family Practice, MSN Diploma (Cum Laude)
Dr. Alex Jimenez, DC, APRN, FNP-BC*, CFMP, IFMCP, ATN, CCST
(Board Certified: Family Practice Nurse Practitioner—Multistate)*
(Licensed Nurse Practitioner & Chiropractor - Multistate)*
Clinical Director
DC & FNP License (Review Above)
Digital Business Card
NPI: 1205907805
Dr. Maria Cardenas, MD
(Board Certified: Internal Medicine)
(Licensed Medical Doctor)
Medical Director, Clinical Director & Collaborative Physician
NPI # 1164426748
MD License #: J2933
Licenses and Board Certifications:
MD: Medical Doctor
DC: Doctor of Chiropractic
APRNP: Advanced Practice Registered Nurse
FNP-BC: Family Practice Specialization (Multi-State Board Certified)
FNP-BC: Family Practice Across Life Span (Neonatal to Geriatrics)
RN: Registered Nurse (Multi-State Compact License)
CFMP: Certified Functional Medicine Provider
MSN-FNP: Master of Science in Family Practice Medicine
MSACP: Master of Science in Advanced Clinical Practice
IFMCP: Institute of Functional Medicine
CCST: Certified Chiropractic Spinal Trauma
ATN: Advanced Translational Neutrogenomics
Family with Primary Care Focus (Family Nurse Practitioner or FNP)
Memberships & Associations:
TCA: Texas Chiropractic Association: Member ID: 104311
TNA: Texas Nurse Association: Member ID: 06458222
TNP: Texas Nurse Practitioner Association ID: 2025091511
AANP: American Association of Nurse Practitioners: Member ID: 2198960
ANA: American Nurses Association: Member ID: 06458222 (District TX01)
| Primary Taxonomy | Selected Taxonomy | State | License Number |
|---|---|---|---|
| No | 111N00000X - Chiropractor | NM | DC2182 |
| Yes | 111N00000X - Chiropractor | TX | DC5807 |
| Yes | 363LF0000X - Nurse Practitioner - Family | TX | 1191402 |
| Yes | 363LF0000X - Nurse Practitioner - Family | FL | 11043890 |
| Yes | 363LF0000X - Nurse Practitioner - Family | CO | C-APN.0105610-C-NP |
| Yes | 363LF0000X - Nurse Practitioner - Family | NY | N25929 |
| Yes | 363LF0000X - Nurse Practitioner - Family | NM | 90560 |
| Yes | 363LF0000X - Nurse Practitioner - Family | GA | GAA-NP005701 |
Dr. Alex Jimenez, DC, APRN, FNP-BC*, CFMP, IFMCP, ATN, CCST
(Board Certified: Family Practice Nurse Practitioner—Multistate)*
(Primary Care Across Lifespan—Neonatal / Pediatric / Adult / Geriatrics)
(Licensed Nurse Practitioner & Chiropractor - Multistate)*
Clinical Director
Digital Business Card
NPI: 1205907805
Dr. Maria Cardenas, MD
(Board Certified: Internal Medicine)*
(Licensed Medical Doctor)*
Medical Director, Clinical Director & Collaborative Physician
NPI # 1164426748
MD License #: J2933
📆 Schedule Appointment: Schedule 24/7 (Click Here)
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