Abstract
In this educational post, I will guide you through several complex but crucial aspects of hormonal health. We will begin by demystifying Sex Hormone Binding Globulin (SHBG), exploring why higher levels are often associated with positive clinical outcomes and why the goal isn't simply to lower SHBG. From there, we will transition to a detailed discussion of Polycystic Ovary Syndrome (PCOS), highlighting its varied presentations beyond the classic textbook symptoms and outlining a modern, integrative treatment approach that addresses root causes such as insulin resistance and gut dysbiosis. We will also examine the latest guidelines for prostate cancer screening, explaining how to interpret Prostate-Specific Antigen (PSA) levels, the significance of free PSA, and when advanced imaging, such as a prostate MRI, is warranted. Finally, we will delve into the vital role of Dehydroepiandrosterone (DHEA), its impact on brain health, libido, and overall vitality, and how to approach supplementation. Throughout this journey, I will integrate my clinical observations and explain how integrative chiropractic care and functional medicine principles provide a holistic framework for managing these conditions and optimizing patient health.
Understanding Sex Hormone Binding Globulin (SHBG)
Many practitioners, especially those new to hormone optimization, often ask, "How do I lower a patient's Sex Hormone Binding Globulin (SHBG)?" It's a common question, but it stems from a slight misunderstanding of SHBG's function. Let's clarify its role and why aiming to lower it might not be the best strategy.
SHBG is a protein produced by the liver that acts like a transport vehicle for your hormones, primarily androgens like testosterone and, to a lesser extent, estrogens. It circulates in your bloodstream, binding to these hormones and carrying them to various cells throughout your body. Once a hormone is bound to SHBG, it is inactive. The magic happens when SHBG reaches a cell's receptor, releasing the hormone, which then becomes active and performs its specific function inside the cell.
A key point to understand is that SHBG has a higher affinity for androgens. This means it will preferentially bind to testosterone over estrogen. This is clinically significant. For instance, a patient's lab work showed a total testosterone of 130 ng/dL, which is quite low. Despite having relatively high estrogen levels, they were experiencing classic symptoms of low testosterone. Why? Because a high level of SHBG was binding up most of their testosterone, leaving very little free testosterone—the bioavailable, active form—to do its job.
Why High SHBG Is Not the Enemy
The instinctive reaction is to find a way to lower SHBG to "free up" more testosterone. However, modern, evidence-based research tells us a different story. A high SHBG level is actually associated with positive clinical outcomes. Conversely, low SHBG levels are now understood to be a powerful predictive marker for significant health issues.
Cardiovascular and Metabolic Health: Studies have consistently linked low SHBG levels with an increased risk of cardiovascular disease, metabolic syndrome, and overall cardiovascular mortality (Ding et al., 2009). This makes physiological sense. Conditions that drive metabolic dysfunction, such as insulin resistance and high cortisol levels, also tend to suppress SHBG production.
Predictive Marker for Insulin Resistance: Low SHBG can be an early warning sign. We often see shifts in SHBG levels long before a patient's HbA1c (a marker for long-term blood sugar control) moves out of the optimal range. This makes SHBG a valuable tool for identifying metabolic dysfunction in its earliest stages, especially in overweight or obese individuals (Jayagopal et al., 2003).
So, the goal isn't to artificially lower SHBG. The only ways to do that would be to increase insulin or estrogen levels, both of which carry significant health risks. Instead, the strategy is to overcome high SHBG by ensuring sufficient total testosterone to saturate the binding sites on SHBG molecules. Whatever testosterone is "left over" becomes the free, active hormone that alleviates symptoms. This is where treatments that effectively and safely raise total testosterone levels become crucial. From my clinical experience, this approach allows us to achieve optimal patient outcomes without fighting the body's natural processes.
A Deeper Dive into Polycystic Ovary Syndrome (PCOS)
Polycystic Ovary Syndrome (PCOS) is one of the most common endocrine disorders in women of reproductive age, yet it is frequently misdiagnosed. The classic image of a PCOS patient—overweight, with acne, and hirsutism (excess male-pattern hair growth)—only represents a fraction of those affected. Many women with PCOS are fit, have no visible skin issues, and their primary complaint might be fertility struggles or irregular periods.
The primary defect underlying PCOS is often hyperinsulinemia (excess insulin), which frequently originates from gut dysbiosis and inflammation. This is a critical concept in functional medicine. The elevated insulin levels lead to a cascade of hormonal imbalances:
The liver produces less SHBG.
With lower SHBG, more testosterone remains in its free, active state.
This hyperandrogenism (high level of androgens) causes the symptoms associated with PCOS.
The Evolving Diagnostic Criteria for PCOS
Diagnosis can be complex because not all women with PCOS have cysts on their ovaries, and not all ovarian cysts indicate PCOS. The widely accepted Rotterdam criteria state that a diagnosis requires two of the following three conditions to be met:
Oligo- or anovulation: Infrequent or absent ovulation, often presenting as irregular or absent menstrual cycles.
Clinical or biochemical signs of hyperandrogenism: Physical signs like acne or hirsutism, or lab results showing high free testosterone.
Polycystic ovaries on ultrasound: The presence of multiple small follicles on the ovaries.
An elevated ratio of Luteinizing Hormone (LH) to Follicle-Stimulating Hormone (FSH), specifically a ratio greater than 2:1, can also be a strong diagnostic clue in premenopausal women.
I recently consulted with a 21-year-old patient, a five-foot-eleven, highly athletic volleyball player. Her primary complaint was severely painful and irregular periods. Based on her physical appearance, one would never suspect PCOS. However, her labs told a different story: her LH was nearly triple her FSH, her free testosterone was over 8.0 ng/dL (with a reference range top of about 4.5), and her DHEA levels were high. She exhibited no hirsutism, acne, or weight issues. This case perfectly illustrates that PCOS can present in many ways. Our treatment plan for her wasn't a cocktail of hormones but a foundational approach: we started by investigating her gut health with a GI-MAP test.
An Integrative and Functional Treatment for PCOS
Conventional treatment often relies on androgen-blocking medications like spironolactone or certain birth control pills. While these can manage symptoms such as acne and hirsutism by blocking androgen receptors, they do not address the root cause: underlying insulin resistance.
A comprehensive, integrative approach is far more effective for long-term resolution. My clinical observations have shown that when we address the foundational issues, the hormonal dysregulation and fertility challenges can be resolved.
Address Insulin Resistance: This is the cornerstone of treatment. Medications like metformin are historically used and can be effective, but often require high doses (up to 2000mg/day), which can cause significant gastrointestinal side effects. Newer GLP-1 receptor agonists (such as semaglutide) are game-changers because they directly address insulin resistance and promote weight loss. We can also use natural approaches. Supplements containing Akkermansia muciniphila, a beneficial gut bacterium, have been shown in multiple studies to naturally increase the body's own GLP-1 production, making them an excellent tool for these patients (Cani & de Vos, 2017).
Heal the Gut: An anti-inflammatory diet and intermittent fasting are non-negotiable. We must reduce the inflammation that drives insulin resistance. A solid gut-healing protocol is essential, even if it seems minimal at first.
Manage Symptoms: For hirsutism, spironolactone can be used, but it may take 6 months to a year to see significant improvement. Doses are typically around 100 mg daily. For menstrual regulation, cycling with progesterone can help restore a more normal rhythm.
Hormone Pellet Therapy in PCOS: If a PCOS patient is symptomatic for low testosterone (despite high free T, their total T can be low), pellet therapy can be an option, but it requires extreme caution. Due to their low SHBG, even a small dose of testosterone can cause their levels to spike, leading to side effects. The rule is to start low and go slow, beginning with 50-75 mg.
This comprehensive strategy works. I had a patient in her mid-30s who, after gaining weight and developing insulin resistance, was diagnosed with PCOS and struggled with secondary infertility for five years. After committing to a full integrative protocol—addressing her diet, gut health, thyroid, and insulin resistance—it took three years for her ovulatory cycles to normalize, but she successfully conceived at age 37. The process requires patience, but fixing the underlying physiology is what leads to lasting success.
Modern Guidelines for Prostate Health and PSA Screening
Navigating the recommendations for Prostate-Specific Antigen (PSA) screening has become a challenge for clinicians and patients alike. The guidelines have shifted over the years, leading to confusion about when to test and when to refer a patient to urology. A more nuanced approach that goes beyond the total PSA level alone is essential for accurate risk assessment.
The key is to use both total PSA and percent free PSA. While total PSA is an antigen specific to the prostate, it's not very sensitive for cancer. Many benign conditions, like benign prostatic hyperplasia (BPH) or prostatitis (inflammation of the prostate), can cause it to rise.
Percent free PSA, however, offers higher sensitivity. It measures the percentage of PSA that is not bound to proteins in the blood. There is an inverse relationship here: the lower the percent free PSA, the higher the risk for prostate cancer. Looking at both markers together gives us a much more accurate picture. Another crucial factor is PSA velocity, or the rate of change over time. A rapid increase, such as a jump of more than 2.0 ng/mL in a single year, is a red flag for aggressive cancer, even if the total number is still within the "normal" range.
Practical Guidelines for PSA Interpretation
Here is the protocol we use in our practice to guide decision-making, which helps us avoid unnecessary biopsies while not missing clinically significant cancers:
Reflex Testing: We have an arrangement with our labs to automatically run a percent free PSA test if a man's total PSA comes back greater than 4.0 ng/mL. This saves the patient a return visit for a second blood draw.
High Risk (Free PSA < 10%): If the free PSA is less than 10%, the likelihood of prostate cancer is over 50%. This patient needs a definitive workup.
Intermediate Risk (Free PSA 10-20%): In this range, we can consider treating for prostatitis if the patient is symptomatic, then retesting in 3 months.
Low Risk (Free PSA > 20%): A free PSA above 20% indicates a very low likelihood of cancer. We can comfortably monitor this patient and recheck in a few months to a year.
In our clinic, for a high-risk patient, our next step is often a 3-Tesla multi-parametric prostate MRI. This is the gold standard for detecting prostate lesions and is far less invasive than a biopsy. The MRI can not only identify suspicious tumors but also confirm the presence of prostatitis, giving me confidence in managing a patient with an elevated PSA due to inflammation rather than malignancy. This evidence-based approach prioritizes accurate diagnosis while enhancing patient comfort and safety.
The Overlooked Importance of DHEA
Dehydroepiandrosterone (DHEA) is a vital hormone produced by the adrenal glands and, in smaller amounts, by the brain itself, classifying it as a neurosteroid. Like other hormones, DHEA levels peak in our 20s and decline steadily with age. This decline has a profound effect on our well-being, cognitive function, and overall health.
I have seen countless patients in my practice who, despite having optimized testosterone levels, continue to complain of low libido, mood issues, and brain fog. More often than not, a check of their DHEA levels reveals they are suboptimal, often in the double digits. Why does this happen? Because DHEA has its own independent receptors in the brain. Low DHEA can cause these specific symptoms even when other hormones are balanced.
The physiological effects of DHEA are extensive, influencing everything from inflammation and bone density to sexual function and mood (Rutkowski et al., 2014). Low levels are particularly associated with conditions like Alzheimer's disease.
Dosing and Supplementing DHEA
When supplementing DHEA, the goal is to bring levels to the optimal range, typically the upper quartile of the lab's reference range for a young, healthy adult.
When to Treat: If a patient's DHEA is in the low triple digits, I often find that optimizing their thyroid and other hormones will naturally bring it up. However, if their level is in the double digits, I recommend treating it from the outset.
Prescription vs. Over-the-Counter: In the United States, DHEA is sold as an over-the-counter supplement. In most other countries, it is a prescription medication. This should tell you something about its potency and the importance of quality. The supplement industry is notoriously unregulated. For this reason, I almost exclusively use compounded, pharmaceutical-grade DHEA in my practice to ensure purity and efficacy.
Dosing: Typical starting doses are 5-10 mg for women and 10-25 mg for men. It's important to monitor levels and watch for potential side effects related to androgen conversion, such as acne or hair thinning, though these are rare with appropriate dosing. DHEA should not be given to PCOS patients, who typically have high levels already.
Restoring DHEA to youthful levels can be the missing piece of the puzzle for many patients, dramatically improving their libido, mood, and cognitive clarity. It is an essential component of a comprehensive anti-aging and wellness strategy.
The Role of Integrative Chiropractic Care
Throughout these complex hormonal scenarios, the principles of integrative chiropractic care provide a foundational support system. Chiropractic adjustments do more than address musculoskeletal pain; they optimize the function of the central nervous system. The nervous system is the master controller of the entire body, including the endocrine system, which governs hormone production and regulation.
By reducing physical stressors on the body through spinal adjustments, we help modulate the autonomic nervous system, decreasing the "fight-or-flight" sympathetic tone that contributes to high cortisol and insulin resistance. This creates a more favorable physiological environment for hormonal balance. Furthermore, as an integrative practitioner, I incorporate nutritional counseling, lifestyle modifications, and targeted supplementation into a holistic plan. This whole-body approach ensures that we are not just treating a single lab value but are supporting the body's innate ability to heal and self-regulate, leading to more profound and sustainable health outcomes.
References
Click to expand
Cani, P. D., & de Vos, W. M. (2017). Next-generation beneficial microbes: The case of Akkermansia muciniphila. Frontiers in Microbiology, 8, 1765. https://doi.org/10.3389/fmicb.2017.01765
Ding, E. L., Song, Y., Malik, V. S., & Liu, S. (2009). Sex hormone-binding globulin and risk of type 2 diabetes in women and men. The New England Journal of Medicine, 361(12), 1152–1163. https://doi.org/10.1056/NEJMoa0804381
Jayagopal, V., Kilpatrick, E. S., Jennings, P. E., Hepburn, D. A., & Atkin, S. L. (2003). The biological variation of sex hormone-binding globulin in type 2 diabetes: a case for using the homeostatic model assessment of insulin resistance in preference to fasting insulin. Diabetes Care, 26(11), 3147–3151. https://doi.org/10.2337/diacare.26.11.3147
Rutkowski, K., Sowa, P., Rutkowska-Talipska, J., Kuryliszyn-Moskal, A., & Rutkowski, R. (2014). Dehydroepiandrosterone (DHEA): Hypes and hopes. Drugs, 74(11), 1195–1207. https://doi.org/10.1007/s40265-014-0259-8
The information herein is not intended to replace a one-on-one relationship with a qualified healthcare 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. Our information scope is limited to chiropractic, musculoskeletal, and physical medicine, as well as wellness, sensitive health issues, and functional medicine articles, topics, and discussions. We provide and facilitate clinical collaboration with specialists across disciplines. Each specialist is governed by their professional scope of practice and the jurisdiction in which they are licensed. We utilize functional health and wellness protocols to treat and support care for musculoskeletal injuries or disorders. Our videos, posts, topics, subjects, and insights cover clinical matters and issues that directly or indirectly support our clinical scope of practice. Our office has made a reasonable effort to provide supportive citations and identify relevant research studies for our posts. We provide copies of supporting research studies upon request to regulatory boards and the public.
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Dr. Alex Jimenez, DC, MSACP, APRN, FNP-BC*, CCST, IFMCP, CFMP, ATN
email: coach@elpasofunctionalmedicine.com
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Dr. Alex Jimenez, DC, APRN, FNP-BC*, CFMP, IFMCP, ATN, CCST
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