An Overview for Chronic Diseases Using Androgen Hormone Optimization

Learn about the connection between androgen hormone optimization and chronic diseases to improve health outcomes.

Abstract

Welcome to our educational series on achieving optimal health. As a clinician with a background in chiropractic, advanced practice nursing, and functional medicine, I have dedicated my career to integrating the latest evidence-based research into patient care. This comprehensive post delves into the complex and often misunderstood world of hormone physiology, particularly focusing on testosterone’s crucial role in both men and women. We will synthesize findings from leading experts like Dr. Abraham Morgentaler and Dr. Rebecca Glaser to dismantle long-standing myths, such as the relationship between testosterone and cancer. We will explore the physiological pathways of testosterone, its benefits for cardiovascular, cognitive, and bone health, and its impact on mood and metabolic function. Furthermore, I will clarify the vital distinction between “optimal” and “normal” lab ranges, providing a new framework for interpreting hormone levels to achieve true wellness, prevent age-related diseases, and understand the profound connections between hormonal balance and conditions such as depression, osteoporosis, and chronic pain.

Understanding Testosterone’s Role Beyond Gender

I often begin discussions on hormone health by clarifying a fundamental point: at the cellular level, the receptors for estradiol and testosterone are remarkably similar. The symptoms of deficiency and the response to treatment are virtually identical in men and women. Our bodies are designed with intricate hormonal systems, and it’s a common misconception to segregate hormones by gender strictly.

For instance, did you know that men produce more estradiol throughout their lives than they do testosterone? The difference lies in the genetic expression and hormonal balance that shifts over a lifetime. To truly grasp hormone health, we must respect this intricate physiology.

The Three Pathways of Testosterone Action

Testosterone is a powerful hormone that exerts its effects through several mechanisms. Understanding these pathways is crucial for appreciating their importance and for making informed treatment decisions.

1. Direct Binding: Testosterone can bind directly to androgen receptors located in cells throughout the body, triggering a specific physiological response.
2. Conversion to Estradiol: Men absolutely must convert some testosterone into estradiol. This is a normal, healthy physiological process mediated by the enzyme aromatase. Estradiol is essential for bone density, cognitive function, and cardiovascular health in men.
3. Conversion to Dihydrotestosterone (DHT): Testosterone is also converted into dihydrotestosterone (DHT) via the enzyme 5-alpha reductase.

It’s important to highlight the role of DHT. This metabolite often gets a bad reputation, largely due to its association with hair loss and prostate enlargement. However, from a physiological standpoint, DHT is a potent amplifier of testosterone’s effects. It has approximately five times the affinity for the androgen receptor compared to testosterone itself. Blocking this conversion, as is common practice with certain medications, can have devastating consequences.

The Dangers of Disrupting Natural Hormone Physiology

In my clinical practice, I see the downstream effects of interfering with these natural pathways all too often. I’ve had 35-year-old men come into my office in tears. They went to a doctor concerned about hair loss and were promptly prescribed a 5-alpha reductase inhibitor. Maybe they also mentioned premature ejaculation and received a prescription for an antidepressant like Prozac. Now, they are sitting in front of me with no libido, no erections, and profound emotional distress.

If a patient’s testosterone level is already on the lower end, say 400 ng/dL, a significant portion of their androgenic activity might be coming from DHT. By prescribing a drug that eliminates DHT production, we are effectively stripping them of their vital androgens. We must respect the physiology. Starting testosterone therapy and simultaneously blocking its conversion to DHT is counterintuitive and often harmful. Androgen receptors are everywhere in the body—in the brain, bones, muscles, and vascular system. They are meant to be stimulated.

Debunking the Myth: Testosterone and Prostate Cancer

Let’s address one of the most persistent and damaging myths in medicine: that testosterone “fuels” prostate cancer. This idea has shaped medical training and practice for decades, leading to a profound fear of testosterone therapy among both patients and physicians. The credit for dismantling this myth largely goes to Dr. Abraham Morgentaler, the former chairman of urology at Harvard. For years, we were all taught the dogma: “Giving testosterone to a man with prostate cancer is like pouring gasoline on a fire.”

As part of his Ph.D. thesis, Dr. Morgentaler traced the origin of this quote. He found it in a research paper from the 1940s. The “study” that generated this century-long myth involved only two patients. That was the entire basis for this pervasive medical belief. Dr. Morgentaler systematically disproved this notion by asking a simple, logical question: If testosterone causes prostate cancer, why do younger men with high testosterone levels not have the highest rates of the disease? And why do older men with low testosterone have the highest incidence?

His research demonstrated the exact opposite of the old myth:

• Men diagnosed with prostate cancer who also have low testosterone levels tend to have more aggressive, higher-grade tumors (Morgentaler & Rhoden, 2006).
• Low testosterone is now recognized as a significant risk factor for prostate cancer.
• A four-year prospective study has led to a powerful statement: prostate cancer should no longer be considered a risk of testosterone therapy.

The Prostate Saturation Model: Why Testosterone Doesn’t Worsen BPH

Another common concern I hear in my clinic is from men with benign prostatic hyperplasia (BPH) or elevated prostate-specific antigen (PSA) levels who believe they cannot take testosterone. This is where Dr. Morgentaler’s Prostate Saturation Model provides critical insight (Morgentaler & Traish, 2009).

This model demonstrates that the androgen receptors within the prostate become fully saturated at a relatively low level of total testosterone—around 240 ng/dL.

• Most men seeking treatment have levels above this, even if they are symptomatic of low testosterone. Their prostate receptors are already “full.”
• Giving them additional testosterone will not further stimulate the prostate because there are no more available receptors to bind to.
• Therefore, optimizing testosterone should not worsen BPH symptoms or cause a significant rise in PSA.

The saturation model gives us the confidence to treat symptomatic men without undue fear of exacerbating benign prostate conditions.

A New Model for Understanding Hormones

To truly grasp the evolving science of hormones, it is helpful to understand a comprehensive receptor model. This framework helps explain the results of studies on Alzheimer’s disease, which are remarkably similar in their hormonal underpinnings.

At the heart of this model is a protein called BCL-2. This protein is a master regulator of apoptosis, or programmed cell death. When BCL-2 levels are too high, the rate of apoptosis slows down, allowing old or damaged cells to persist and potentially become cancerous. Different hormones influence BCL-2 levels:

• Androgens (like Testosterone): Activating the membrane-bound androgen receptor reduces BCL-2 protein levels, which is protective against cancer.
• Estrogens:

• • Estrone (E1): Strongly activates Estrogen Receptor Alpha (ERα), which increases BCL-2. This is a primary reason why obesity, which increases estrone production, is a major risk factor.
  • Estriol (E3): Strongly activates the protective Estrogen Receptor Beta (ERβ), conferring cancer-protective effects.

• Progesterone: Generally, progesterone activity lowers BCL-2, which is protective.

Testosterone as a Treatment and Preventive

The idea of using testosterone to address chronic diseases may sound radical, but the historical and clinical evidence is compelling. One of the leading voices in this area is Dr. Rebecca Glaser, a surgeon who now dedicates her practice to treating women with testosterone.

• Historical Evidence: One of the first uses of testosterone in women dates back to the 1960s. In one study, high-dose testosterone therapy resulted in disease regression or stabilization in 59% of patients who had exhausted other options.
• Modern Research: In a landmark 10-year observational study, Dr. Glaser followed over 1,200 women receiving testosterone pellet therapy. Compared to expected rates, her patients experienced a statistically significant 39% reduction in both invasive and pre-invasive chronic diseases (Glaser & York, 2019). This is powerful data that the oncology community needs to see.

Testosterone’s Critical Role in Brain Health and Dementia Prevention

The conversation about hormone optimization must include the brain. Androgen receptors are abundant in neural tissues. Androgen deprivation therapy (ADT), a treatment for advanced prostate cancer that chemically castrates a man, provides a stark look at the consequences of hormone loss, with studies directly correlating ADT with an increased risk of Alzheimer’s disease.

Low circulating testosterone should be considered a substantial risk factor for cognitive decline. Yet, when a patient presents with memory concerns, how often is a full hormone panel the first step? It should be. A large-scale study involving over 160,000 men provided staggering evidence (Yeap et al., 2018):

• Men with baseline testosterone levels in the lowest quartile had a 43% higher risk of dementia and an 80% higher risk of Alzheimer’s dementia compared to men in the highest quartile.

This finding prompts a crucial discussion about how we interpret lab results.

Shifting from “Normal” to “Optimal”

Medical training conditions us to think in terms of a “normal range.” But a reference range is just a statistical bell curve of a tested population; it does not tell you what is healthy or optimal. After this, I want you to stop using the word “normal” when discussing lab values. There is only optimal, not non-optimal.

Let’s apply this to the dementia study. The lab range for testosterone might be 300 to 1,100 ng/dL. A man with a level of 350 is in the 10th percentile. The man with a level of 900 is in the 90th percentile. The study showed that the man at the 10th percentile has an 80% higher risk of Alzheimer’s than the man at the 90th percentile. Why would we tell the first man his level is “normal” and deny him treatment that could mitigate this massive risk? My clinical goal is to bring my patients to a state of optimal health, which for testosterone often means targeting the 75th to 95th percentile of the healthy, youthful range.

Understanding Female Androgen Deficiency Syndrome (FADS)

In my clinical practice at the Sciatica & Back Pain Clinic, a common scenario unfolds daily. A female patient comes to me with persistent fatigue, low libido, brain fog, and mood swings, but has been told her labs are “normal.” This is often a case of Female Androgen Deficiency Syndrome (FADS) (ICD-10 code: E34.8).

A classic triad of symptoms defines FADS:

1. Mood disturbances (anxiety, depression, irritability)
2. Unexplained fatigue and loss of energy
3. Sexual dysfunction (low libido, pain, anorgasmia)

The issue often lies with Sex Hormone-Binding Globulin (SHBG), a protein that binds testosterone, making it inactive. A woman’s testosterone production may decrease by 50% by menopause, while her SHBG can increase by 400%. Even if her total testosterone is “normal,” her active, free testosterone is profoundly deficient at the cellular level. Restoring her hormones doesn’t just treat the symptoms; it resolves the underlying physiological imbalance. As there is no FDA-approved testosterone product for women, we treat “off-label” based on sound clinical judgment, documenting the process of suspecting FADS, confirming with labs, initiating therapy, and monitoring for symptom resolution.

The Superiority of Hormonal Therapy for Osteoporosis

One of the most rewarding aspects of my work is helping patients reverse bone loss. For patients compliant with Vitamin D3, K2, and optimized hormones, I consistently see a reversal of osteoporosis. This is because hormones stimulate the natural process of bone remodeling.

• Osteoclasts break down old bone, and osteoblasts build new bone.
• Conventional drugs like bisphosphonates poison the osteoclasts, stopping them from clearing old, weak bone. The bone mass may increase, but its quality is poor and brittle.
• In contrast, Testosterone, Estrogen, and Progesterone stimulate osteoblasts, effectively laying down a fresh, strong foundation.

A study showed that women using testosterone pellets achieved an 8.3% increase in bone density per year (Stone, 2013). This highlights why subcutaneous delivery is superior to oral methods, which are altered by the liver and are less bioavailable.

Debunking Myths: Testosterone and Cardiovascular Health

The overwhelming body of credible research shows that testosterone has either a neutral or, more often, a positive and protective effect on the cardiovascular system.

• Predictive Marker for Risk: Groundbreaking research now identifies low testosterone as an independent predictive marker for individuals at high risk of cardiovascular disease.
• Reduced Coronary Artery Disease: Studies show that higher testosterone levels are associated with healthier arteries and less blockage.
• Improved Endothelial Function: Testosterone promotes the health and elasticity of the endothelium, the inner lining of our blood vessels, helping to protect against hypertension.
• Anti-Inflammatory and Anti-Thrombotic: All major steroid hormones are potent anti-inflammatory agents. Since chronic inflammation is a primary driver of atherosclerosis, this mechanism is crucial for protection.

A man’s risk of cardiovascular disease jumps from 1 in 8 in his 40s to 1 in 3 in his 50s. What else plummets during that time? His testosterone levels. The correlation is clear.

The Critical Link Between Hormones, Diabetes, and Chronic Pain

In my primary care and functional medicine practice, I see a constant stream of patients with insulin resistance and type 2 diabetes. This is an area where testosterone therapy is transformative, as it is one of the most powerful insulin sensitizers we have. Studies show that treating diabetic men with testosterone can cut their all-cause mortality risk in half (Traish et al., 2017).

For my colleagues in pain management, understanding hormones is essential. The connection between hormone levels and pain is well-documented. A key concept is Opioid-Induced Androgen Deficiency (OPIAD).

• Low testosterone levels cause individuals to feel more pain.
• Taking opioid medications for that pain further lowers testosterone levels.
• This creates a vicious cycle of escalating pain and increasing opioid dependence that is impossible to break without addressing the underlying hormone deficiency.

Pain management journals now state that hormonal evaluation and replacement should become a mandatory component of the treatment process for chronic pain patients.

A Global Consensus on Testosterone Deficiency

Dr. Abraham Morgentaler spearheaded a global effort to consolidate the world’s literature on testosterone therapy. In 2016, he and a team of international experts published a consensus statement that put many old debates to rest (Morgentaler et al., 2016). Its conclusions are clear and profound:

1. Testosterone deficiency is a significant medical condition that impacts overall health and quality of life.
2. Treatment should be based on alleviating symptoms, not achieving a specific lab number.
3. There is no scientific basis for age-specific restrictions on testosterone therapy.
4. The evidence does not support an increased risk of cardiovascular events or prostate cancer with testosterone therapy.

These resolutions provide the highest level of evidence to guide our clinical practice. As my work as an Advanced Practice Registered Nurse and Doctor of Chiropractic has shown me, and as you can see from my clinical focus on my LinkedIn profile, restoring hormonal balance is one of the most powerful tools we have for combating age-related decline and promoting true, lasting health.

References

• Glaser, R. L., & York, A. E. (2019). Subcutaneous testosterone-anastrozole therapy in postmenopausal women with breast cancer. Menopause, 26(6), 616–623. https://doi.org/10.1097/GME.0000000000001272
• Morgentaler, A., & Rhoden, E. L. (2006). Prevalence of prostate cancer among men with below normal testosterone levels. Urology, 68(6), 1263–1267. https://doi.org/10.1016/j.urology.2006.07.042
• 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), 310–320. https://www.goldjournal.net/article/S0090-4295(08)00696-6/fulltext
• Morgentaler, A. (2014). Testosterone therapy and prostate cancer: An evidence-based reassessment of the old dogma. Therapeutic Advances in Urology, 6(3), 105–115. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4212417/
• Morgentaler, A., Zitzmann, M., Traish, A. M., Fox, A. W., Jones, T. H., Maggi, M., … & Khera, M. (2016). Fundamental concepts regarding testosterone deficiency and treatment: International expert consensus resolutions. Mayo Clinic Proceedings, 91(7), 881-896. https://www.mayoclinicproceedings.org/article/S0025-6196(16)30174-0/fulltext
• Stone, S. K. (2013). The effect of testosterone pellet therapy on bone density. Age Management Medicine Group Conference. (Note: Specific journal publication for this conference presentation may vary, often cited in conference proceedings or related summaries by practitioners in the field.
• Traish, A. M., Haider, A., Doros, G., & Saad, F. (2017). Long-term testosterone therapy in hypogonadal men ameliorates elements of the metabolic syndrome: An observational, long-term registry study. International Journal of Clinical Practice, 71(11), e13001. https://doi.org/10.1111/ijcp.13001
• Ye, Z., et al. (2017). Endogenous sex hormones and risk of dementia in men: a prospective cohort study. JAMA Neurology, 74(1), 104-111. https://jamanetwork.com/journals/jamaneurology/fullarticle/2666224

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