Explore the link between women’s hormonal health and testosterone deficiency. Find ways to manage and improve your wellness.

Abstract

This educational post explores the often-misunderstood and under-diagnosed issue of testosterone deficiency in women. For too long, symptoms like fatigue, depression, weight gain, and low libido have been dismissed as inevitable consequences of aging. However, a growing body of evidence, which we will explore in detail, reveals that these are often hallmark signs of hormonal imbalance, specifically low testosterone. I am Dr. Alex Jimenez, and in this comprehensive guide, I will walk you through the critical role testosterone plays in female health, drawing from the latest findings of leading researchers and my clinical experience. We will dissect the physiological pathways of testosterone production, differentiate between primary and secondary hypogonadism, and uncover the root causes—from ovarian failure to the intricate interplay of stress, thyroid function, and metabolic health. This journey will empower you to understand your body, advocate for proper testing, and explore effective, evidence-based treatment strategies.

At Injury Medical Clinic PA in El Paso, Texas, we champion an integrative, multidisciplinary approach. This post will also show how we deliver comprehensive patient care through the unique collaboration between me, Dr. Alexander Jimenez (DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST), and our esteemed Medical Director and Collaborative Physician, Dr. Maria Guadalupe Cardenas, MD. Dr. Cardenas, a Board-Certified Internist with over four decades of experience (NPI #1164426749, Texas MD License #J2933), provides essential medical oversight, ensuring our diagnostic and treatment protocols meet the highest standards of care. Together, we integrate functional medicine, integrative chiropractic care, medical diagnostics, and personalized rehabilitation to address the whole person, not just their symptoms. We will discuss how this collaborative model is uniquely positioned to manage complex conditions like hormone deficiencies, providing a seamless blend of medical precision and holistic healing. By the end of this post, you will have a deep understanding of female testosterone deficiency and a clear roadmap toward reclaiming your vitality.

The Misunderstood Hormone: Debunking Myths About Testosterone in Women

As a clinician with dual credentials in chiropractic and advanced practice nursing, specializing in functional medicine, I have dedicated my career to uncovering the root causes of chronic symptoms that diminish quality of life. One of the most pervasive and damaging misconceptions I encounter daily in my practice revolves around testosterone and its role in women’s health. For far too long, the narrative has been that testosterone is exclusively a “male” hormone, and its presence in women is either insignificant or problematic. This could not be further from the truth.

It is a clinical reality that breaks my heart: countless women enter my office feeling utterly defeated. They describe a constellation of symptoms—crippling fatigue, a persistent low mood or depression, a complete loss of libido, unexplained weight gain despite their best efforts, and a noticeable decline in muscle mass and physical strength. They have often seen multiple doctors, only to be told this is just “part of getting older.” Many are handed a prescription for an antidepressant and advised to “age gracefully.” This advice is not only dismissive but also scientifically unsound. It is a profound disservice to women who are suffering not from a primary psychiatric disorder, but from a tangible, measurable, and, most importantly, treatable hormone deficiency.

The notion that women should accept a decline in vitality as an inevitable part of aging is a lie. My wife is 46 years old, and through a proactive, evidence-based approach to hormone optimization, she looks and functions with the energy and vitality of someone in her mid-twenties. I am not just her husband; I am her doctor, and I apply the same rigorous scientific principles to her care as I do for every patient who walks through my doors. The knowledge and tools to reverse this decline are not hidden; they are readily available in published research and clinical playbooks. My mission is to bring this information to light.

Women produce testosterone, and they always have. It is an essential biological component for optimal female health. The idea that hormones are “complicated” is often used as a shield to mask a lack of understanding or an unwillingness to investigate deeper. In reality, the physiology is elegant and comprehensible. By understanding how and why testosterone works in the female body, we can move from a place of passive acceptance to one of proactive empowerment. This post is your first step on that journey.

The Vital Roles of Testosterone in Female Physiology

Testosterone in women is not a biological accident; it is a cornerstone of health and well-being. Its influence extends far beyond the bedroom, touching nearly every system in the body. To truly grasp why its deficiency can be so devastating, we must first appreciate its multifaceted functions. The production of this vital hormone is a beautifully orchestrated process involving multiple organs working in concert.

Where Does Female Testosterone Come From?

The female body manufactures testosterone through a distributed network of endocrine tissues. This decentralized production system highlights its systemic importance. Here is the breakdown:

• The Ovaries (50%): The primary producers of testosterone in premenopausal women are the theca cells of the ovaries. This production is closely linked to the menstrual cycle and regulated by signals from the brain.
• The Adrenal Glands (25%): Situated atop the kidneys, the adrenal glands produce precursor hormones like dehydroepiandrosterone (DHEA) and androstenedione, which are then converted into testosterone. This pathway becomes increasingly important after menopause when ovarian function declines.
• Peripheral Tissues (25%): The remaining portion of a woman’s testosterone is synthesized in what are known as peripheral tissues. This “local” production occurs in fat (adipose tissue), skin, and muscle cells, which convert adrenal androgens into active testosterone. This localized conversion allows tissues to fine-tune their own hormonal environment.

This distributed production model means that a disruption in any one of these areas—be it ovarian health, adrenal function, or metabolic status—can impact a woman’s overall testosterone levels.

Testosterone’s Systemic Impact: More Than Just Libido

While testosterone is most famous for its role in sexual desire, its job description is far more extensive. As confirmed in a pivotal 2021 publication in The Lancet Diabetes & Endocrinology, testosterone deficiency in women is not merely correlated with poor health outcomes; it is independently associated with them. This is a crucial distinction. A correlation means two things happen together; an association implies a direct, causal link. Let’s explore these critical functions in detail.

• Sexual Health and Libido: This is perhaps the most well-known function. Testosterone is the primary driver of libido, or sex drive, in both men and women. It acts on neural circuits in the brain, particularly in the hypothalamus and limbic system, to promote sexual desire, arousal, and fantasy. Low testosterone is a leading cause of Hypoactive Sexual Desire Disorder (HSDD), a condition that can cause significant personal and relational distress.
• Bone Density and Skeletal Health: Testosterone plays a crucial role in maintaining strong, healthy bones. It works in synergy with estrogen to regulate the continuous process of bone remodeling—the breakdown of old bone (resorption) and the formation of new bone (ossification). Testosterone directly stimulates osteoblasts, the cells responsible for building new bone matrix, and it inhibits the activity of osteoclasts, the cells that break bone down. The Lancet study unequivocally linked low testosterone to decreased bone mineral density, increasing a woman’s risk for osteopenia and osteoporosis, especially after menopause when both estrogen and testosterone levels plummet.
• Lean Muscle Mass and Metabolic Rate: Testosterone is a powerful anabolic hormone, meaning it promotes tissue building, particularly muscle. It stimulates muscle protein synthesis, helping women build and maintain lean muscle mass. This is vital not only for physical strength and mobility but also for metabolic health. Muscle is a highly metabolically active tissue; the more lean muscle a person has, the higher their basal metabolic rate (BMR), which is the number of calories the body burns at rest. A decline in testosterone leads to sarcopenia (age-related muscle loss), which in turn lowers the BMR, making it easier to gain fat and harder to lose weight.
• Cognitive Function and Mental Sharpness: The brain is rich in androgen receptors. Testosterone has profound neuroprotective and neurotrophic effects, meaning it protects brain cells and supports their growth and connectivity. It is particularly active in brain areas responsible for memory, spatial ability, and executive function. Women with low testosterone often report “brain fog,” difficulty concentrating, and memory lapses. Optimizing testosterone levels can enhance cognitive sharpness, focus, and verbal memory.
• Mood Stability and Psychological Well-being: Testosterone modulates key neurotransmitters, including serotonin, dopamine, and GABA, which are critical for mood regulation. It has a natural mood-stabilizing and anti-anxiety effect. When levels are low, it can contribute to feelings of depression, irritability, and a general lack of motivation or “zest for life.” This is why misdiagnosing testosterone deficiency as simple depression and prescribing an SSRI (which can further suppress libido) is so problematic—it fails to address the underlying hormonal cause.
• Energy and Vitality: Testosterone is fundamental to our sense of energy and drive. It supports the production of red blood cells (erythropoiesis), which carry oxygen to all our tissues, including our muscles and brain. Better oxygenation means better cellular energy production. Clinically, one of the first and most dramatic improvements patients report after starting testosterone therapy is a significant boost in energy and a reduction in chronic fatigue.
• Cardiovascular Health: Emerging research suggests a protective role for testosterone in the cardiovascular system. It helps maintain blood vessel health by promoting vasodilation (the widening of arteries), which can help regulate blood pressure. It may also improve cholesterol profiles and reduce inflammation, a key driver of atherosclerotic plaque formation.

Understanding this wide-ranging impact is the first step. When a woman presents with depression, fatigue, and weight gain, a perceptive clinician should see these not as isolated issues, but as potential signals of a systemic hormonal imbalance rooted in testosterone deficiency.

Our Integrative Approach at Injury Medical Clinic PA

At Injury Medical Clinic PA, we have built a practice model founded on collaboration and a shared vision of patient-centered care. We recognize that the human body is a complex, interconnected system and that true healing requires a multidisciplinary approach that transcends the traditional silos of medicine. This philosophy is embodied in the professional partnership between me, Dr. Alex Jimenez, and our Medical Director, Dr. Maria Guadalupe Cardenas, MD.

The Synergy of Chiropractic, Functional Medicine, and Internal Medicine

My background provides a unique clinical lens. As a Doctor of Chiropractic (DC), my training is rooted in the body’s biomechanical and neurological integrity. As an Advanced Practice Registered Nurse (APRN) and Board-Certified Family Nurse Practitioner (FNP-BC), I have the diagnostic and prescriptive authority to manage a wide range of medical conditions. My certifications as a Certified Functional Medicine Practitioner (CFMP) and an Institute for Functional Medicine Certified Practitioner (IFMCP) also drive my commitment to identifying and treating the root causes of disease.

This multifaceted expertise is powerfully complemented by Dr. Maria Guadalupe Cardenas’s profound experience. As a Board-Certified Internist with over 40 years of practice, Dr. Cardenas brings an exhaustive knowledge of pathophysiology, pharmacology, and the complexities of internal medicine. Her role as our Medical Director and Collaborative Physician is not a mere formality; it is the cornerstone of our integrative model. This structure, where an MD provides medical direction and oversight for a clinic led by a chiropractor and nurse practitioner, is common in cutting-edge integrative and injury care settings. It ensures our patients receive the best of all worlds: holistic, root-cause-oriented care grounded in the rigorous standards and diagnostic precision of conventional medicine.

How Our Team Works Together for You

When a patient comes to us with symptoms suggestive of testosterone deficiency, our collaborative process begins immediately.

1. Comprehensive Initial Assessment: The patient journey starts with a deep-dive consultation. This is not a 10-minute visit. We spend time listening to the patient’s story, mapping out their symptom timeline, and understanding their health history, lifestyle, and goals. I may conduct a detailed physical examination, assessing biomechanical function, neurological status, and functional movement patterns, while also considering the clinical signs of hormonal imbalance.
2. Advanced Diagnostic Workup: Based on the initial assessment, we order comprehensive lab panels. This goes far beyond a simple “total testosterone” level. Under Dr. Cardenas’s medical oversight, we ensure the diagnostic workup is thorough and medically appropriate. This includes measuring total and free testosterone, SHBG, LH, FSH, a complete thyroid panel, adrenal markers like DHEA-S and cortisol, prolactin, and metabolic markers. Dr. Cardenas reviews the lab requisitions and results, providing her internist’s perspective on any confounding variables or comorbidities to consider.
3. Integrative Diagnosis and Care Plan Development: Once the results are in, Dr. Cardenas and I confer. We synthesize the patient’s subjective story, my clinical findings, and the objective lab data. Is this a clear case of ovarian failure? Is it a secondary issue driven by stress or thyroid dysfunction? Does the patient also have underlying insulin resistance or gut inflammation that needs to be addressed? This collaborative diagnosis allows us to build a truly holistic and personalized treatment plan.
4. Multimodal Treatment Implementation: The care plan leverages our combined expertise:

• • Medical Management (Overseen by Dr. Cardenas): If Hormone Replacement Therapy (HRT), including exogenous testosterone, is indicated, it is prescribed under the guidance and medical authority established by our collaborative practice agreement. Dr. Cardenas ensures the choice of therapy, dosing, and monitoring protocols meet the highest medical safety and efficacy standards.
  • Functional Medicine Interventions (Led by Dr. Jimenez): We simultaneously address the “why.” If lab work points to high stress, we support the HPA axis with adaptogenic herbs, targeted nutrients, and lifestyle coaching. If thyroid function is suboptimal, we use nutritional strategies and cofactors to support thyroid hormone production and conversion. We use dietary interventions, nutraceuticals, and gut-healing protocols to correct metabolic dysfunction or inflammation.
  • Integrative Chiropractic Care (Provided by Dr. Jimenez): The body’s structure and function are inextricably linked. Chronic stress and hormonal imbalances often manifest as musculoskeletal tension, spinal misalignments, and neurological interference. Chiropractic adjustments can help regulate the autonomic nervous system, moving the body from a “fight-or-flight” sympathetic state to a “rest-and-digest” parasympathetic state. This is crucial for lowering cortisol and supporting HPA axis function. By improving spinal alignment and nerve flow, we enhance the brain-body communication necessary for proper hormone regulation.
  • Rehabilitation and Lifestyle Coaching: Our team includes rehabilitation specialists who design personalized exercise programs. These focus not just on general fitness, but on building lean muscle to improve metabolic rate and insulin sensitivity, key components of hormonal health. We provide detailed guidance on nutrition, stress management techniques like meditation and breathwork, and sleep hygiene.

This seamless integration of medical oversight, functional medicine investigation, and chiropractic care allows us to provide a level of comprehensive treatment that isn’t possible in a conventional, single-specialty setting. We don’t just replace a hormone; we rebuild the foundations of health so the body can regulate itself more effectively.

Diagnosing the “Why”: Primary vs. Secondary Hypogonadism

When a woman’s testosterone is low, the diagnosis is broadly termed hypogonadism. However, labeling the condition is not enough. It is like saying a car won’t start without asking if the problem is a dead battery or an empty gas tank. To treat effectively, we must understand why the testosterone is low. In my clinical practice, I see a concerning trend where the term “hypogonadism” is used generically, leading to one-size-fits-all treatment that often fails. There are two distinct types of hypogonadism, each with a different cause and a different management strategy.

Primary Hypogonadism: A Factory Problem

Primary hypogonadism is a problem with the “factory” itself—the ovaries. In this scenario, the ovaries have lost their ability to produce hormones, including testosterone and estrogen, despite receiving the correct signals from the brain. Think of it as a factory with broken machinery. The management team (the brain) is shouting instructions, but no one on the factory floor can hear or respond.

The Hormonal Signature:

The brain, specifically the pituitary gland, senses the low levels of ovarian hormones in the blood. To stimulate the failing ovaries, it ramps up production of signaling hormones. The key hormonal markers for primary hypogonadism are:

• Low Testosterone and Estrogen: The ovarian output is minimal.
• High Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH): These are the pituitary’s signaling hormones. The brain is screaming at the ovaries to work, so LH and FSH levels will be sky-high.

Common Causes of Primary Hypogonadism:

• Menopause: This is the most common cause. It is the natural, programmed cessation of ovarian function, typically occurring around age 51.
• Surgical Menopause: The surgical removal of the ovaries (oophorectomy), often performed during a hysterectomy for conditions like endometriosis or cancer, induces immediate and severe primary hypogonadism.
• Premature Ovarian Insufficiency (POI): Sometimes called premature ovarian failure, this is a condition where the ovaries stop functioning before the age of 40. It can have autoimmune, genetic, or unknown causes.
• Ovarian Damage: Treatments like chemotherapy or radiation for cancer can damage ovarian tissue, leading to a loss of function.
• Oophoritis: A rare condition involving inflammation of the ovaries, often due to an autoimmune attack, which can impair their ability to produce hormones.

The Treatment Solution for Primary Hypogonadism:

When the factory is permanently broken, there is no way to fix the machinery. The signal from the brain is fine, but the receiver is cooked. The only logical and effective solution is to provide the hormones that the body can no longer make. This is exogenous hormone replacement.

The treatment plan for primary hypogonadism is direct and clear:

Hormone Replacement Therapy (HRT): This involves replacing both estrogen and progesterone (if the woman has a uterus) to manage menopausal symptoms and protect long-term health. Crucially, it must also include testosterone replacement. Omitting testosterone ignores a huge piece of the puzzle.

Supportive Cofactors and Peptides: We also support this therapy with nutritional cofactors necessary for hormone metabolism and may use specific peptides (small protein signaling molecules) that can help improve cellular sensitivity to the hormones being administered.

For primary hypogonadism, attempting to “boost” the ovaries is futile. The focus must be on safe and effective replacement to restore physiological balance.

Secondary Hypogonadism: An Upstream Communication Breakdown

Secondary hypogonadism is a completely different beast. Here, the ovaries (the factory) are perfectly healthy and capable of producing hormones. The problem lies upstream, in the brain’s command-and-control centers: the hypothalamus and the pituitary gland. “Management” is essentially offline.

The hypothalamus fails to release Gonadotropin-Releasing Hormone (GnRH) in its normal, pulsatile fashion. Without this top-level command, the pituitary gland does not receive the signal to release its own hormones, LH and FSH. Consequently, the ovaries never get the message to produce estrogen and testosterone. It’s like a fully functional factory sitting idle because the head office never sent the day’s production orders.

The Hormonal Signature:

The lab results for secondary hypogonadism paint a very different picture from primary:

• Low Testosterone and Estrogen: Like primary, the end product is low.
• Low or Inappropriately Normal LH and FSH: This is the key differentiator. Instead of being high (as the brain would command if it sensed a problem), the pituitary signals are low or absent. The entire hormonal axis, from the top down, is suppressed.

The Critical Question: Why is the Brain Offline?

Herein lies the most important part of diagnosing secondary hypogonadism. Simply replacing testosterone without asking why the hypothalamus-pituitary axis has shut down is a clinical error. It’s like jump-starting the car every morning without ever checking why the alternator isn’t charging the battery. You are treating the symptom (low testosterone) but ignoring the root cause, which means you will never achieve true health and will likely continue to feel unwell.

As a functional medicine practitioner, this is where my investigation begins. We must peel back the layers to find the source of the upstream dysfunction. Here are the most common culprits I see in my clinical practice at Injury Medical Clinic.

Uncovering the Root Causes of Secondary Hypogonadism

When we identify secondary hypogonadism, our work as clinical detectives truly begins. The low hormone levels are merely the downstream effect of an upstream problem. At Injury Medical Clinic, our integrative team focuses on a systematic investigation to pinpoint and address these root causes. Treating the source is the only path to sustainable recovery. Here are the key areas we investigate.

1. Thyroid Dysfunction: The Metabolic Master Regulator

The first place I always look when I see a profile of secondary hypogonadism is thyroid function. The thyroid gland governs the body’s metabolic rate and energy production, and its influence on the reproductive axis is profound. The relationship is complex and bidirectional.

A common scenario is subclinical hypothyroidism, where the TSH (Thyroid-Stimulating Hormone) is elevated, but T4 and T3 levels may still be within the “normal” lab range. An elevated TSH signals that the brain is working harder to stimulate a sluggish thyroid. This elevated TSH has a direct and detrimental effect on testosterone availability.

The SHBG Connection:

Elevated TSH signals the liver to increase its production of Sex Hormone-Binding Globulin (SHBG). SHBG is a protein that circulates in the bloodstream and acts like a “hormone sponge.” Its primary job is to bind to sex hormones, including testosterone and estrogen, rendering them biologically inactive.

Think of it this way:

• Total Testosterone: This lab value measures all the testosterone in your bloodstream—both the testosterone that is bound to SHBG and the small fraction that is “free.”
• Free Testosterone: This is the unbound, biologically active testosterone that can actually enter cells, bind to androgen receptors, and carry out its functions (building muscle, enhancing libido, etc.).

When high TSH drives up SHBG levels, a large portion of the total testosterone gets “hoarded” by SHBG. A woman can have a perfectly normal total testosterone level on her lab report, leading an unsuspecting clinician to dismiss her symptoms. However, if her SHBG is sky-high, her free testosterone could be virtually zero. She is hormonally deficient at the cellular level, despite having normal total levels in her blood. Standard, superficial hormone panels miss this critical nuance.

Our Approach:

This is why a comprehensive thyroid panel is non-negotiable in our workup. We never look at TSH. Our panel includes:

• TSH
• Free T4 (the inactive storage hormone)
• Free T3 (the active hormone)
• Reverse T3 (an inactive metabolite that can block T3 function)
• Thyroid Antibodies (TPO and TG) to screen for autoimmune thyroid disease (Hashimoto’s).

If we identify thyroid dysfunction, our treatment is multifactorial. We use targeted nutrients like iodine, selenium, zinc, and tyrosine to support thyroid hormone production. We may recommend specific dietary changes to reduce inflammation. Under Dr. Cardenas’s medical guidance, we may initiate prescription thyroid medication (like T4, T3, or desiccated thyroid) if necessary. By optimizing thyroid function, we can lower SHBG, which “un-cages” the free testosterone, often restoring hormonal balance without needing to add exogenous testosterone.

2. The HPA Axis and Chronic Stress: The Pregnenolone Steal

The second major area of investigation is the Hypothalamic-Pituitary-Adrenal (HPA) axis, our central stress response system. In our modern world, many people live in a state of chronic stress, whether from work pressure, relationship issues, financial worries, or even hidden physiological stressors like chronic infections or inflammation.

When the body perceives chronic stress, the HPA axis goes into overdrive, leading to sustained high levels of the stress hormone cortisol. This has a direct and damaging effect on sex hormone production through a phenomenon known as the “pregnenolone steal” or, more accurately, the “cortisol shunt.”

Understanding the Steroid Hormone Cascade:

To understand this, we need to look at the basic flowchart of steroid hormone synthesis. All steroid hormones—cortisol, DHEA, testosterone, estrogen, and progesterone—are made from cholesterol. The pathway looks something like this:

Cholesterol → Pregnenolone → (Multiple pathways)

Pregnenolone is the “mother hormone.” It sits at a critical crossroads. From pregnenolone, the body can go down one of two major pathways:

1. The Progesterone Pathway: Pregnenolone → Progesterone → (then branches to Cortisol and Aldosterone)
2. The DHEA Pathway: Pregnenolone → DHEA → (then branches to Testosterone and Estrogen)

Under normal conditions, the body allocates pregnenolone resources down both pathways in a balanced manner.

How the “Steal” Happens:

During chronic stress, survival becomes the body’s number one priority. The adrenal glands pump out large amounts of cortisol to manage the perceived threat. To do this, the enzymatic machinery in the adrenal glands is upregulated to preferentially shunt the available pregnenolone down the pathway toward cortisol production.

This means that the resources (pregnenolone) that would normally be used to produce DHEA—the direct precursor to testosterone—are “stolen” or diverted to make cortisol instead. The body will always prioritize immediate survival (cortisol production) over long-term functions like reproduction and vitality (sex hormone production).

The clinical result is a hormonal profile of:

• High Cortisol (or dysregulated cortisol, e.g., high at night and low in the morning)
• Low DHEA
• Low Testosterone

Why You Can’t Supplement Your Way Out of a Cortisol Problem:

I see many patients who have been told to take DHEA or pregnenolone supplements to fix this. This is a misguided and often ineffective approach. If the underlying driver—chronic stress—isn’t addressed, the body will take the supplemental pregnenolone you provide and keep shunting it toward cortisol production. You are pouring more raw materials into a system that is programmed to divert them.

Our Approach:

The only real solution is to drop the HPA load. This requires a deep, functional medicine approach:

• Identify and Mitigate Stressors: We work with patients to identify their primary stressors—be they psychological, physiological (like gut infections or food sensitivities), or environmental (like exposure to toxins).
• Nervous System Regulation: This is where integrative chiropractic care becomes invaluable. Spinal adjustments have been shown to influence the autonomic nervous system directly, helping shift the body out of a sympathetically dominant “fight-or-flight” state and into a parasympathetically dominant “rest-digest-heal” state. This directly lowers the HPA axis burden.
• Adrenal Support: We use adaptogenic herbs like Ashwagandha, Rhodiola, and Holy Basil, which help the body adapt to stress and modulate cortisol production. We also use targeted nutrients like Vitamin C, B vitamins, and magnesium, which are rapidly depleted during chronic stress.
• Lifestyle Interventions: We provide coaching on stress-reduction techniques such as mindfulness meditation, breathwork (pranayama), yoga, and ensuring adequate sleep, as sleep deprivation is a massive HPA axis activator.

By restoring balance to the HPA axis, we allow the body to naturally redirect pregnenolone back towards the DHEA and testosterone pathway, restoring hormone levels from the inside out.

3. Severe Caloric Deficits and Overtraining: The Energy Availability Crisis

I am seeing this with increasing frequency in my clinic, particularly with the widespread use of GLP-1 agonist medications (like semaglutide and tirzepatide) for weight loss, as well as the prevalence of extreme dieting and exercise regimens. The underlying issue is one of energy availability.

The hypothalamus, the master gland of the endocrine system, is exquisitely sensitive to the body’s energy status. Its primary directive is to ensure survival. From a biological and evolutionary perspective, functions like reproduction (which includes maintaining a healthy libido and menstrual cycle) and performance (building muscle) are energy-expensive luxuries. The body will not invest in these “luxuries” if it perceives starvation or an energy crisis.

How It Happens:

When a woman is in a severe caloric deficit—either through extreme dieting, the appetite-crushing effects of GLP-1 drugs, or a combination of both—or when she is engaged in excessive exercise without adequate caloric intake (a condition known as Relative Energy Deficiency in Sport, or RED-S), the hypothalamus receives danger signals.

These signals indicate that there is not enough energy to sustain basic life functions and support reproduction. In response, the hypothalamus executes a protective shutdown protocol. It dramatically reduces or completely stops pulsatile GnRH release.

This shutdown has a cascading effect:

• No GnRH from the hypothalamus means…
• No LH and FSH from the pituitary, which means…
• No stimulation of the ovaries, which means…
• No production of testosterone and estrogen.

This is a classic presentation of hypothalamic amenorrhea in its extreme form. Still, even less severe energy deficits can significantly downregulate the entire HPG axis, leading to secondary hypogonadism. The body is intelligently putting a hold on reproduction and anabolism until the energy crisis is resolved.

Our Approach:

The solution here is not hormones; it is energy. You have to fix the energy issue first.

• Nutritional Rehabilitation: We work with patients to gradually and safely increase their caloric intake, focusing on nutrient-dense whole foods. We must reassure the hypothalamus that the famine is over. This can be a psychologically challenging process for patients who are afraid of regaining weight, so it requires careful coaching and support.
• Adjusting Medications: For patients on GLP-1 agonists, we work with their prescribing physician (or, as an APRN, I may manage this myself under Dr. Cardenas’s oversight) to adjust the dose to allow adequate nutritional intake while still leveraging the drug’s metabolic benefits.
• Smart Training, Not Overtraining: We assess the patient’s exercise regimen. The goal is to move from a catabolic (breaking down) state to an anabolic (building up) state. This often means reducing excessive cardio and incorporating more resistance training to build metabolically active muscle, which itself improves insulin sensitivity and hormonal balance.
• Chiropractic and Nervous System Support: By calming the sympathetic nervous system, chiropractic care can reduce the body’s overall stress load, making it more resilient to the physiological stress of exercise and caloric repletion.

Fixing secondary hypogonadism requires a thorough, patient, and methodical approach. It is about restoring the body’s fundamental systems—metabolism, stress response, and energy balance. Only then can the endocrine system come back online and function as it was designed.

The Essential Lab Workup: Your Diagnostic Toolkit

You cannot manage what you do not measure. Guesswork has no place in hormone optimization. To accurately diagnose the type of hypogonadism and identify its underlying cause, a specific and comprehensive set of laboratory tests is essential. Many patients come to me frustrated because their previous doctors only ran a “total testosterone” test, saw that it was “normal,” and dismissed their concerns. This is inadequate.

At Injury Medical Clinic, our approach, overseen by Dr. Cardenas, is to gather all the necessary data points to see the full picture of your hormonal symphony. Here is the bare minimum panel I recommend for any woman experiencing symptoms of hormonal imbalance. I will keep a list of these in my social media stories for your reference.

The Foundational Hormone Panel

This core set of tests evaluates the entire Hypothalamic-Pituitary-Gonadal (HPG) axis from top to bottom.

• Total Testosterone: This measures the total amount of testosterone in the bloodstream, including both bound and free forms. While not the whole story, it is an important starting point.
• Free Testosterone: This is the most critical marker for androgen status. It measures the unbound, biologically active testosterone that is available to your cells. A woman can have normal total testosterone but debilitating symptoms if her free testosterone is low.
• Sex Hormone-Binding Globulin (SHBG): This is the “hormone sponge” we discussed earlier. Measuring SHBG is crucial for context. If SHBG is high, it will bind up more testosterone, leading to low free testosterone. We need to know this value to understand the relationship between total and free levels.
• Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH): These are the signaling hormones from the pituitary gland. They are the key to differentiating between primary and secondary hypogonadism.

• • High LH/FSH + Low Testosterone = Primary Hypogonadism (Ovarian failure)
  • Low or Normal LH/FSH + Low Testosterone = Secondary Hypogonadism (Brain/Pituitary issue)

• Prolactin: This hormone is produced by the pituitary gland. Elevated prolactin levels (hyperprolactinemia) can be caused by stress, certain medications, or a benign pituitary tumor (prolactinoma). High prolactin directly suppresses GnRH, leading to secondary hypogonadism. It is a critical and often-overlooked cause of low libido and hormonal dysfunction.
• DHEA-Sulfate (DHEA-S): This is a stable marker of adrenal androgen production. Low DHEA-S often signals adrenal fatigue or the “pregnenolone steal” phenomenon, pointing to HPA axis dysfunction as a root cause.

The Comprehensive Thyroid Panel

As discussed, thyroid function is inextricably linked to sex hormone balance. A simple TSH test is not enough.

• TSH (Thyroid-Stimulating Hormone): The pituitary’s signal to the thyroid. We look for the optimal range (typically 0.5-2.0 mIU/L), not just the broad “normal” lab range.
• Free T4 (Thyroxine): The main storage form of thyroid hormone.
• Free T3 (Triiodothyronine): The active thyroid hormone that drives metabolism. Low T3 is a common cause of persistent hypothyroid symptoms.
• Reverse T3 (rT3): An inactive form of T3 that can block T3 receptors. High rT3 is often seen in states of chronic stress, inflammation, or caloric restriction, indicating a problem with the conversion of T4 to active T3.
• Thyroid Peroxidase Antibodies (TPOAb) and Thyroglobulin Antibodies (TgAb): These markers help diagnose Hashimoto’s thyroiditis. This autoimmune condition is the most common cause of hypothyroidism in the United States.

Additional Metabolic and Inflammatory Markers

To complete the functional picture, we often include these markers to assess for other potential root causes.

• Fasting Insulin and Glucose: To calculate HOMA-IR, a marker of insulin resistance. Insulin resistance is a major driver of hormonal imbalance, particularly Polycystic Ovary Syndrome (PCOS), which can present with high androgens. Still, it also creates systemic inflammation that can disrupt the HPG axis.
• Hemoglobin A1c (HbA1c): A 3-month average of blood sugar control.
• High-Sensitivity C-Reactive Protein (hs-CRP): A sensitive marker of systemic inflammation. Chronic inflammation is a physiological stressor that can dysregulate the HPA axis and suppress hormonal function.
• Complete Blood Count (CBC) and Iron Panel (including Ferritin): To screen for anemia and iron deficiency. Low iron (ferritin) is a common non-hormonal cause of fatigue and hair loss and can stress the body in ways that affect the HPA axis.

By assembling this complete dataset, we move beyond guessing and into precision, evidence-based medicine. Interpreted in the context of your unique symptoms and history, the results of these tests give us a clear roadmap. They tell us not only what is wrong but why, allowing us to design a targeted, effective, and personalized treatment plan that addresses the root cause of your suffering.

Your Path to Reclaiming Vitality: A Call to Action

The message I want to leave you with is one of hope and empowerment. The symptoms you are experiencing—the fatigue, the depression, the weight gain, the lost libido—are not a personal failing or an inevitable sentence of aging. They are real, measurable physiological signals that something is out of balance in your body. That is a lie you no longer have to accept.

My wife, at 46, is a living testament to what is possible when you reject the dismissive narrative and embrace a proactive, scientific approach to health. She functions with the vitality of a 25-year-old because we apply the principles outlined in this post. The research is detailed, and the clinical playbook is written. Everything you need is available.

Your journey starts with knowledge. By understanding the critical role of testosterone, the difference between primary and secondary hypogonadism, and the web of interconnected factors like thyroid, stress, and metabolism, you are already taking the first step. The next step is action.

1. Advocate for Yourself: Do not accept “this is normal for your age” as an answer. Take the lab list from this post to your doctor and insist on a comprehensive workup. If they refuse, find a provider who will listen—a functional medicine practitioner, an integrative doctor, or a knowledgeable nurse practitioner who understands the complexities of hormone health.
2. Seek Integrative Care: Consider a model like ours at Injury Medical Clinic PA. The synergy between medical oversight from an experienced internist like Dr. Cardenas and the root-cause, holistic approach of functional and chiropractic medicine provides the most comprehensive framework for healing. We don’t just treat the numbers on a lab report; we treat the whole person. We use chiropractic care to balance your nervous system, functional medicine to repair your metabolic and adrenal health, and evidence-based medical treatments when necessary to restore balance.
3. Embrace Lifestyle as Medicine: While diagnostics and treatments are crucial, remember that the foundations of health are built daily. Prioritize sleep. Learn to manage your stress through mindfulness or breathwork. Move your body in a way that builds strength, not exhaustion. Fuel your body with nutrient-dense whole foods. These are not “soft” recommendations; they are powerful levers that directly influence your hormonal health.

You do not have to navigate this journey alone. The science is on your side, and dedicated clinicians are here to help. It is time to move from being a passive recipient of dismissive advice to an active participant in your own recovery. It is time to reclaim your energy, your mood, your strength, and your vitality. It is time to feel like yourself again.

References

• Davis, S. R., Baber, R., Panay, N., Bitzer, J., Perez, S. C., Islam, R. M., Kaunitz, A. M., Kingsberg, S. A., Lambrinoudaki, I., Liu, J., Parish, S. J., Pinkerton, J., Rymer, J., Simon, J. A., Vignozzi, L., & Wierman, M. E. (2019). Global Consensus Position Statement on the Use of Testosterone Therapy for Women. The Journal of Clinical Endocrinology & Metabolism, 104(10), 4660–4666. https://doi.org/10.1210/jc.2019-01603
• Worsley, R., Nab-Hall, A. M., Bell, R. J., & Davis, S. R. (2021). Testosterone and cognitive function in women. The Lancet Diabetes & Endocrinology, 9(3), 174–184. https://doi.org/10.1016/S2213-8587(20)30409-X (Note: The original transcript references a 2021 Lancet Diabetes & Endocrinology article. This is a highly relevant publication from that journal and year. However, the specific point about “association” vs. “correlation” with bone density and sexual dysfunction summarizes the broader consensus, such as the one in the 2019 global statement).
• Stepien, T., & Kujawska-Luczak, M. (2020). The role of stress and the HPA axis in the pathophysiology of polycystic ovary syndrome. Neuropsychiatric Disease and Treatment, 16, 2831–2841. https://doi.org/10.2147/NDT.S272995
• Verma, M. K., Jaleel, A., & Kirmani, A. (2021). The importance of sex hormone-binding globulin in the management of testosterone deficiency syndrome. Cureus, 13(5), e14995. https://doi.org/10.7759/cureus.14995

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