Your shoes are the first point of contact between your body and the ground. When soles compress, heels tilt, or tread wears unevenly, walking mechanics can change. For tech workers, Amazon associates, data-center employees, parents, and adults who alternate between sitting and long hours on hard floors, those changes may influence loading at the knees, hips, and back. This article explains what worn shoes can reveal and when strengthening, chiropractic care, or custom foot orthotics may help.
Most people do not think about their shoes until something hurts. A sneaker may look fine from above, but the heel may be compressed, the tread smooth on one side, and the midsole flat. Then a long shift or hours on concrete can leave the feet tired and the knees, hips, or back stiff.
That doesn’t mean every backache starts in the feet. Pain can come from joints, muscles, tendons, nerves, workload, sleep, injuries, or medical conditions. Still, footwear is one practical piece of the movement puzzle.
Look at an old pair of work shoes from behind and underneath. You may notice one heel worn more than the other, the outer edge rounded down, forefoot tread disappearing, or the shoe leaning inward. These patterns are clues about repeated loading, not diagnoses.
Signs include:
One heel wearing faster than the other.
A midsole that feels flattened or creased.
Uneven tread under the forefoot.
Shoes that tilt inward or outward on a flat surface.
New foot, knee, hip, or back discomfort that improves in a different pair.
Research on worn running shoes shows that people may alter ankle and trunk movement as cushioning degrades, even when outside forces remain similar (Kong et al., 2009). That finding does not prove an old shoe causes pain, but it shows the body can adapt when footwear changes.
Pronation Is Normal—Until It Becomes Part of the Problem
Pronation is the natural inward rolling and flattening that helps the foot absorb load after ground contact. Everyone pronates. The question is not, “Do you pronate?” It is whether the amount, timing, control, or side-to-side difference fits your symptoms and activities.
Systematic reviews suggest foot posture can be associated with changes in lower-limb movement, but effects are often small and inconsistent (Buldt et al., 2013). That is why a good examination looks beyond arch height.
A clinician may assess ankle mobility, big-toe motion, calf flexibility, foot strength, knee tracking, hip control, balance, stride, and the movements that reproduce symptoms.
The Kinetic Chain: How the Foot Can Influence the Rest of You
Think of the body as a linked system, not isolated parts. When the foot meets the floor, motion and force travel through the ankle, knee, hip, pelvis, and trunk. A change at one link may influence another, especially when repeated thousands of times.
For example, a flexible flat foot may show more rearfoot motion during walking. A meta-analysis found that foot orthoses can change rearfoot, ankle, and some knee mechanics in adults with flexible flat feet (Jafarnezhadgero et al., 2024). That does not mean changing foot motion automatically fixes knee, hip, or back pain. It means the foot can be one modifiable factor when the examination shows a meaningful connection.
The reverse matters too. Weak hip muscles, limited ankle motion, reduced trunk endurance, or poor load tolerance can change what happens at the foot. Treatment should follow the person, not a simple “feet cause back pain” story.
Why Concrete Floors and Long Standing Matter
Data centers, warehouses, hospitals, and industrial settings may require long periods of standing or walking on hard surfaces. Tech workers may alternate between desk time and long walks through facilities.
Prolonged occupational standing is associated with more low-back and lower-extremity symptoms, although individual responses vary (Coenen et al., 2018). A newer systematic review found that footwear characteristics can influence comfort during prolonged standing, and that cushioning and support need to be balanced for the task (Kang et al., 2026).
The softest shoe is not automatically the best shoe. Standing and walking may require different balances of fit, stability, cushioning, and support.
When Shoes May Be Contributing to Your Symptoms
Consider footwear when discomfort appears after changing shoes, improves in another pair, or follows a clear increase in standing and walking. Also pay attention when an older pair has obvious asymmetrical wear.
A shoe check is especially reasonable if you notice:
Heel, arch, or forefoot fatigue late in the day.
Knee discomfort after long walking routes.
Hip tightness that builds during standing.
Back fatigue after prolonged time on concrete.
One shoe collapsing faster than the other.
Repeated blisters, calluses, or pressure points.
These signs still need context. Numbness, progressive weakness, major swelling, redness, severe night pain, a recent injury, or symptoms that don’t respond to simple changes warrant medical evaluation rather than a shoe purchase alone.
What a Chiropractic and Functional Movement Assessment Can Include
At ChiroMed, we don’t look at your shoes and declare them guilty. A useful assessment connects symptoms with movement, work demands, health history, and examination findings.
Depending on the complaint, evaluation may include posture, spinal and pelvic motion, foot and ankle mobility, gait, balance, squat or step mechanics, muscle strength, neurological testing, and inspection of the shoes you wear most often.
Chiropractic care may help address painful or restricted joints when appropriate, while rehabilitation builds strength and control. Foot and ankle exercises, calf work, hip strengthening, balance drills, walking progression, and load management can improve capacity instead of simply telling a patient to rest.
This supports beneficence: treatment should provide a clear functional benefit. It also supports non-maleficence by favoring conservative, non-invasive options before escalating to medication, injections, or surgery when those are not necessary.
When Custom Foot Orthotics May Make Sense
Custom foot orthotics are not required for everyone with flat feet, pronation, or back pain. Evidence for orthotics in adults with flat feet remains mixed, and prescription should be based on symptoms, examination findings, and response to simpler options (Herchenröder et al., 2021).
They may be reasonable for persistent symptoms linked to foot mechanics, significant asymmetry, pressure-redistribution needs, or support that standard footwear cannot provide. Foot-focused interventions may also help selected people with chronic low-back pain and pronated feet, but research remains limited (Alam et al., 2025).
A practical progression may include:
Replace shoes that are clearly broken down or unstable.
Improve fit and choose footwear that matches the job.
Restore ankle and foot mobility when it is limited.
Strengthen the foot, calf, hip, and trunk.
Reassess gait and symptoms.
Consider prefabricated or custom orthotics when the examination supports them.
The goal is not to lock the foot into a “perfect” position. The goal is to improve comfort, load distribution, and tolerance for movement.
Your Shoes Are Data, Not Destiny
One simple step is to bring your most-worn shoes to an appointment. They can show patterns that are easy to miss during a short exam. A clinician can compare those clues with gait, mobility, strength, and symptoms.
Patient autonomy matters. You should understand why a recommendation is being made, what alternatives exist, and how success will be measured. If you already work with a primary-care physician, podiatrist, orthopedist, or physical therapist, care should coordinate rather than compete.
At Injury Medical Clinic PA, Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, bridges chiropractic and medical evaluation, while Dr. Maria Guadalupe Cardenas, MD, provides internal medicine oversight for complex concerns. Use advanced testing, acupuncture, electroacupuncture, or medical treatment only when the history and examination justify them—not simply because you wear footwear.
Take the Next Step From the Ground Up
If your feet feel exhausted, your knees ache after long shifts, or your hips and back feel worse in old shoes, check the whole picture. Sometimes replacing footwear helps. Sometimes mobility, strength, gait, workload, or an underlying condition needs attention.
A coordinated chiropractic, rehabilitation, and medical team can help identify the most important factors, explain your options, and build a conservative plan around your goals. Care connects daily demands, examination findings, and your preferences instead of chasing one perfect shoe. Better movement starts with good information—not with blaming one body part for everything.
Abstract: Monday stiffness can feel puzzling: you rested longer, yet your neck, back, or hips may feel less ready. Extra sleep does not mean you damaged your spine. Different sleep timing, longer stillness, weekend driving or chores, and a fast return to work can change how your body feels. Gentle movement, consistent habits, and individualized chiropractic care can support comfortable motion.
The Monday-Morning Surprise
Picture a familiar weekend. Friday ends late. Saturday starts slowly. You sleep in, sit over coffee, run errands, tackle chores, and relax Sunday evening. Then Monday arrives.
You stand up, and your hips feel tight. Your low back needs a few minutes to “warm up.” Your neck feels less willing to turn toward the mirror on the drive to work.
Sleeping late did not injure your spine.
Sleep timing and consistency can influence health, and research favors regular sleep schedules. At the same time, weekend catch-up sleep isn’t automatically harmful and may help in some situations (Chaput et al., 2020). The practical explanation for Monday stiffness is often a change in routine: different sleep timing, longer periods without movement, different weekend activities, and then a fast transition back into work.
Longer Rest Can Mean Longer Stillness
Sleep is essential recovery time. The issue is not “too much sleep” in a simple sense. Sleeping longer can also mean spending more continuous time in a relatively limited range of positions.
Joints, muscles, and connective tissues often feel better after they begin moving again. Anyone who has sat through a long movie, driven several hours, or worked through a marathon coding session knows that feeling. Research on office workers suggests prolonged sitting can increase discomfort, while active breaks and position changes may reduce it (Waongenngarm et al., 2018).
Weekend Sleep Timing Changes the Rhythm
Many people keep one schedule Monday through Friday and another on Saturday and Sunday. Researchers sometimes describe this mismatch as “social jet lag.” It does not mean your weekend is unhealthy. It means your internal timing and social schedule aren’t perfectly aligned.
That matters because Monday can combine several transitions at once:
You wake earlier than you did on Sunday.
You move quickly instead of easing into the morning.
You sit in traffic or return to a workstation.
You return to lifting, standing, climbing, or repetitive tasks.
You may have less time to walk, stretch, or eat breakfast.
Stiffness may therefore reflect a schedule change rather than structural damage.
Weekend Activity Counts Too
Maybe Saturday included a long drive to visit family. Maybe you cleaned the garage, carried groceries, worked in the yard, sat through a child’s tournament, or spent several hours gaming. Sunday may have involved meal preparation, home projects, or more screen time than usual.
A Gentle Monday Reset
You do not need an aggressive stretching routine to “fix” normal morning stiffness. Start by letting your body move.
Try this simple sequence:
Walk around your home for three to five minutes.
Take several slow breaths while gently moving your shoulders.
Rotate your upper body comfortably from side to side.
Perform a few easy sit-to-stands from a chair.
Move each hip through a comfortable range.
Take a brief walk before settling into a long commute or computer session.
Regular movement supports long-term health; Monday’s goal is gradual motion, not forcing range (Centers for Disease Control and Prevention, 2025).
When Chiropractic Care May Help
If stiffness repeatedly limits your ability to turn, bend, walk, lift, or work comfortably, an examination can help determine what is contributing.
Chiropractic care should not assume that sleeping late “put something out.” A thoughtful evaluation may assess joint motion, muscle tenderness, posture, movement control, work demands, prior injuries, and neurological signs. For low-back pain, evidence-based guidelines support nonpharmacologic approaches, including exercise, education, manual therapy, and spinal manipulation when appropriate (George et al., 2021; Qaseem et al., 2017).
At ChiroMed, the practical goal is better function: easier morning movement, greater mobility, less pain, improved work tolerance, and confidence using your body.
Care may combine chiropractic treatment with mobility work, progressive rehabilitation, and home strategies. Clinically, acupuncture or electroacupuncture may be considered for selected patients with persistent musculoskeletal pain, but not as a replacement for diagnosis, movement, or rehabilitation.
Build a More Consistent Weekend
You do not need to make Saturday look exactly like Tuesday. Family life needs flexibility. A few anchors, however, can make Monday feel smoother.
Try keeping your weekend wake time reasonably close to your weekday schedule. Get daylight and some movement after waking. Break up long drives or screen sessions when practical. Stay active enough so Sunday doesn’t become an all-day sitting marathon. If you do heavy chores, treat them like physical work: pace yourself and change tasks.
Know When Stiffness Deserves More Attention
Seek medical evaluation when stiffness or pain is accompanied by new weakness, spreading numbness, loss of bowel or bladder control, fever, unexplained weight loss, major trauma, severe night pain, or other significant changes. Persistent symptoms also deserve assessment rather than endless self-treatment.
Sleep and pain can influence each other, particularly in chronic musculoskeletal conditions (Runge et al., 2024). That is another reason to look at the whole pattern instead of blaming one night of extra sleep.
Monday Should Feel Like a Restart, Not a Warning
Your weekend did not fail because you slept in. Monday stiffness often signals your body needs a transition.
A steadier sleep rhythm, regular movement, thoughtful pacing, and a few minutes of gentle mobility may be enough for many people. If stiffness keeps returning or interferes with work and family life, coordinated care can help identify the cause.
Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, works within an integrated model that connects chiropractic care, medical diagnostics, rehabilitation, and functional health strategies. Dr. Maria Guadalupe Cardenas, MD, provides internal medicine oversight and collaborative medical direction when broader evaluation is needed.
That multidisciplinary approach supports beneficence by matching care to your actual needs, non-maleficence by prioritizing conservative, non-invasive options when appropriate, and autonomy by keeping you informed and involved in every decision. Your existing medical team can remain part of that conversation.
If Monday mornings keep starting with pain or restricted movement, schedule an evaluation with the ChiroMed team. The goal is not to fear sleep or avoid weekends. It is to help your neck, back, and hips move comfortably enough for the workweek, family life, and activities you enjoy.
Chaput, J.-P., Dutil, C., Featherstone, R., Ross, R., Giangregorio, L., Saunders, T. J., Janssen, I., Poitras, V. J., Kho, M. E., Ross-White, A., Zankar, S., & Carrier, J. (2020). Sleep timing, sleep consistency, and health in adults: A systematic review. Applied Physiology, Nutrition, and Metabolism, 45(10 Suppl. 2), S232-S247. doi:10.1139/apnm-2020-0032
George, S. Z., Fritz, J. M., Silfies, S. P., Schneider, M. J., Beneciuk, J. M., Lentz, T. A., Gilliam, J. R., Hendren, S., & Norman, K. S. (2021). Interventions for the management of acute and chronic low back pain: Revision 2021. Journal of Orthopaedic & Sports Physical Therapy, 51(11), CPG1-CPG60. doi:10.2519/jospt.2021.0304
Abstract: A full day at a desk can leave your hips stiff or tired even when you barely moved. This article explains how prolonged sitting reduces movement variety, changes hip position, and can make walking, parenting, exercise, or commuting feel harder. Workstation changes, movement breaks, chiropractic care, mobility work, and strengthening can help restore comfort and function.
At 5:15 p.m., you close the laptop, stand up, and expect your body to feel rested. Instead, your hips feel stiff. Your first few steps are short. Your lower back may feel tight, and your hips may feel tired.
It feels confusing because you mostly sat.
The body is built to change positions. Sitting is not automatically harmful, but staying in one position for hours creates a different kind of workload. The problem is often how little your joints and muscles varied.
In a laboratory study, two hours of computer sitting increased discomfort in the hip, thigh, and buttock region, even though researchers did not find clear electrical signs of fatigue in several measured muscles (Baker et al., 2018). Feeling “tired” does not always mean a muscle was worked like it was during exercise. It may reflect stiffness, sustained positioning, altered pressure, reduced movement, or a need for a change.
Your Hips Were Still Working
When you sit, the hips stay flexed. Your pelvis rests against the chair, your trunk must stay organized over that base, and your muscles make small adjustments as you type, reach, turn toward another screen, or shift your weight.
Those demands are light, but repetitive.
A remote worker may sit through a video meeting, then move into focused project work, eat lunch at the desk, and drive for errands or school pickup. By evening, the hips have spent much of the day in similar angles.
A cross-sectional study found an association between prolonged sitting, lower physical activity, and reduced passive hip extension. It could not prove that sitting caused the limitation, but it suggests movement habits may influence hip motion over time (Boukabache et al., 2021).
That helps explain why standing after a long work block can feel awkward. Your hips move from a familiar flexed position toward extension while your trunk and legs suddenly support full body weight.
Movement Variety Beats Perfect Posture
People often search for the one “correct” sitting posture. A better goal is usually a comfortable setup plus regular movement.
Your body can tolerate many reasonable positions when it can move among them. Problems may build when one posture becomes the only posture for long periods.
A systematic review found that occupational sitting and musculoskeletal symptoms are complexly related, but reducing prolonged workplace sitting was associated with reductions in some musculoskeletal discomfort and pain outcomes (Dzakpasu et al., 2021). More recent evidence suggests short activity breaks may help some sedentary workers, although no single break schedule fits everyone (Zeng et al., 2026).
Try adding variety:
Stand for a phone call or short meeting.
Walk to refill water instead of keeping everything nearby.
Take several easy hip-extension steps after a long work block.
Alternate desk work with small household tasks when working remotely.
Change sitting positions rather than forcing one “perfect” posture.
The goal is not constant fidgeting. Avoid making stillness your only strategy.
Gluteal Endurance Matters
The gluteal muscles help extend and stabilize the hips during walking, stair climbing, lifting, and rising from a chair. They work with the abdominal wall, spinal muscles, pelvis, and legs.
If most of the day involves sitting and little purposeful loading, the issue may not be that your glutes have “turned off.” That phrase oversimplifies the problem. A more useful explanation is that the hips and trunk may not have enough endurance for what comes next.
You may notice that standing to cook becomes uncomfortable quickly, stairs feel harder than expected, playing with children on the floor feels less natural, or a workout feels difficult even though your job was physically quiet.
The answer is rarely to squeeze the glutes all day. Instead, gradually rebuild capacity with movements your body tolerates.
Chair Height Changes the Experience
A chair that is too low can place the hips in deeper flexion and make standing more demanding. A chair that is too high may leave the feet unsupported, increasing pressure under the thighs or encouraging you to slide forward.
Adjust the seat so your feet are supported, and your hips and knees feel comfortable. Position the keyboard and screen so you do not have to reach excessively. NIOSH recommends office setups that reduce awkward postures, unnecessary reaching, and prolonged static positions, and suggests short breaks to reduce computer-related discomfort (National Institute for Occupational Safety and Health [NIOSH], 2026).
No chair replaces movement. Even an expensive ergonomic setup becomes static if you stay there long enough.
Do Not Forget the Commute
For many workers, the workday ends with more sitting.
A programmer may leave an office and drive forty minutes. A parent working remotely may finish at the computer and immediately drive for pickup, groceries, or activities. Your hips don’t care whether the sitting happened at a desk or behind a steering wheel; the overall pattern matters.
Before a long commute, try two or three minutes of easy walking. After arriving home, take another short movement break before dropping onto the couch.
A Simple After-Work Hip Reset
You do not need an intense workout to restore movement. Start with a short sequence that feels comfortable:
Walk for three to five minutes.
Perform five to ten controlled sit-to-stands.
Try gentle standing hip extension without forcing the low back.
Add a comfortable supported split-stance stretch.
Finish with slow bodyweight squats or step-ups.
If an exercise causes sharp pain, spreading numbness, significant weakness, or worsening symptoms, stop and seek an appropriate evaluation.
For long-term improvement, gradually add resistance. Bridges, step-ups, split squats, carries, and controlled hinging can build hip and trunk capacity. A 2026 systematic review found that workplace programs combining exercise, ergonomics, and education produced some of the most consistent improvements for chronic musculoskeletal problems (Skamagki et al., 2026).
How Chiropractic Care Can Help
When tired or stiff hips keep returning, chiropractic care can look beyond the place that hurts. An examination may assess hip motion, lumbar and pelvic mechanics, gait, muscle endurance, movement control, and whether the hip, low back, or another structure reproduces symptoms.
Appropriate chiropractic care may use manual treatment to improve comfortable motion while rehabilitation builds the strength and endurance needed to keep that motion useful. The patient benefit is not simply “better alignment.” The larger goal is easier walking, smoother sitting-to-standing transitions, better exercise tolerance, and greater comfort during work and family life.
At an integrated clinic, we can also coordinate persistent symptoms medically when needed. Dr. Alex Jimenez, DC, APRN, FNP-BC, bridges chiropractic examination, rehabilitation, and medical diagnostics, while Dr. Maria Guadalupe Cardenas, MD, provides internal medicine oversight for complex conditions. This model supports beneficence by matching care to findings, non-maleficence by prioritizing conservative options when appropriate, and autonomy by helping patients understand choices and coordinate with their existing medical team.
Occasional stiffness after a long day may improve with movement. Evaluation becomes more important when symptoms persist, worsen, or affect normal function.
Seek prompt care for significant weakness, inability to bear weight, major trauma, fever with severe pain, unexplained swelling, loss of bowel or bladder control, or numbness in the saddle region. Also seek assessment for recurring symptoms that repeatedly limit walking, sleep, exercise, work, or family activities.
Build a Body That Handles the Day
Your hips don’t need a perfect chair or a heroic stretching routine. They need options each day.
Change positions. Walk regularly. Adjust the workstation. Strengthen gradually. Treat discomfort as information, not proof that your body is damaged.
If your hips feel tired every evening, the goal is not simply to survive another workday. The goal is to restore enough mobility, strength, and endurance so sitting, standing, commuting, parenting, exercise, and everyday life feel easier.
Multidisciplinary CTA
If hip stiffness or fatigue keeps returning, schedule a comprehensive evaluation with the ChiroMed team. We can coordinate chiropractic assessment, rehabilitation, medical evaluation, and supportive therapies around your findings, goals, and preferences. You remain the informed decision-maker, and we can integrate care with your current physicians when needed.
Improve your thyroid health through a functional medicine approach, emphasizing personalized and holistic care for better results.
Abstract
Welcome to our educational post on thyroid health from a functional and integrative medicine perspective. My name is Dr. Alex Jimenez, and I hold certifications as a Doctor of Chiropractic (DC), Advanced Practice Registered Nurse (APRN), Family Nurse Practitioner (FNP-BC), Certified Functional Medicine Practitioner (CFMP, IFMCP), and further specializations in Anti-aging, Regenerative & Functional Medicine (ATN) and Chiropractic Cranial Spinal Techniques (CCST). This post will take you on a journey to understand the intricate workings of your thyroid, moving beyond the simplistic view of just prescribing medication. We will explore the case of “Jennifer,” a 41-year-old woman who, despite being on multiple thyroid medications, continued to suffer from debilitating symptoms. Her story illustrates a common problem: addressing symptoms without understanding the root cause. We will explore the four primary physiological mechanisms that account for over 90% of thyroid dysfunction, none of which medication alone can resolve. These mechanisms include systemic inflammation, liver congestion, gut dysbiosis, and HPA axis dysregulation (chronic stress). We will dissect how these issues disrupt the critical conversion of the inactive thyroid hormone (T4) into the active hormone (T3), effectively leaving you metabolically “running on empty.” Throughout this discussion, I will explain the underlying physiology in detail, highlighting the roles of enzymes like deiodinases, the impact of inflammatory cytokines, and the critical functions of the liver and gut. I will also explain how our unique, multidisciplinary practice at Injury Medical Clinic PA in El Paso, Texas, integrates chiropractic care, functional medicine, and conventional medical oversight to create a comprehensive, personalized treatment plan. Our approach, which I lead alongside our esteemed Medical Director, Dr. Maria Guadalupe Cardenas, MD, an internist with over 40 years of experience, is designed to restore function, not just mask symptoms. This is modern, evidence-based healthcare, focused on you as a whole person.
Our Integrative and Collaborative Practice: A New Model of Care
Before we dive into the complexities of thyroid physiology, I believe it is essential to provide some context about our clinical philosophy and practice structure here at Injury Medical Clinic PA. I am Dr. Alex Jimenez, and my journey in healthcare has been driven by a passion for understanding the interconnectedness of the human body. My extensive training across multiple disciplines—from chiropractic (DC) and advanced practice nursing (APN, FNP-BC) to the deep, systems-based approach of functional medicine (CFMP, IFMCP)—has given me a unique perspective on health and healing.
This multidisciplinary foundation is the bedrock of our practice. We believe the most effective patient care comes not from a single viewpoint but from collaboration among different experts. This is why I am honored to work alongside Dr. Maria Guadalupe Cardenas, MD. Dr. Cardenas is a board-certified internist with a remarkable career spanning over four decades. Her profound experience in internal medicine provides an invaluable layer of medical oversight and diagnostic acumen to our team. As our Medical Director and Collaborative Physician (NPI #1164426749, Texas MD License #J2933), she plays a crucial role in our multidisciplinary model.
This setup, where a Doctor of Chiropractic like myself works in close collaboration with a Medical Doctor, is a hallmark of modern integrative and injury care clinics. It allows us to offer the best of both worlds. We can harness the power of chiropractic adjustments to restore nervous system function and structural integrity, utilize functional medicine to uncover the biochemical root causes of chronic disease, and rely on Dr. Cardenas’s medical expertise for comprehensive diagnostics, conventional treatment options when necessary, and overall medical direction. Our services extend to personal injury care, rehabilitation, nutritional counseling, and more, all under one roof. This integrated team approach ensures that our patients receive a truly holistic and robust plan of care, tailored precisely to their individual needs. This collaborative spirit allows us to successfully manage complex cases like the one we are about to explore.
A Patient’s Cry for Help: The Story of Jennifer
Let me introduce you to Jennifer. Her story is one I’ve seen repeated countless times over my 30 years in practice, and it perfectly encapsulates why a new approach to thyroid care is so desperately needed. Jennifer is 41 years old. She first reached out by sending me a video message. In the video, she was in tears, a raw and honest portrait of desperation and fatigue. Her story was heartbreaking. For seven long years, she had been trapped in a body that felt like it was betraying her.
Despite being under the care of five different doctors and being prescribed both Synthroid® (levothyroxine sodium) and a generic form of levothyroxine, her health was deteriorating. She was gaining weight no matter how little she ate or how much she exercised. A profound, unshakeable depression had settled over her, casting a gray shadow on every aspect of her life. Her hands and feet were perpetually cold, a classic sign of a sluggish metabolism. A thick brain fog clouded her thoughts, making it difficult to concentrate, remember things, or even engage in simple conversation. She described her daily existence as “dragging herself through life.” The vibrant, energetic woman she once was had become a distant memory.
Jennifer’s doctors had followed the standard protocol. They saw that her TSH (Thyroid-Stimulating Hormone) was elevated, diagnosed her with hypothyroidism, and wrote a prescription. When her symptoms didn’t improve, they adjusted the dose. When that didn’t work, they tried another brand or combination. Yet, with each new prescription and each passing year, she only felt worse.
Her story is a tragic but common example of a fundamental flaw in the conventional approach to thyroid disease. It focuses almost exclusively on the thyroid gland itself and the medication designed to supplement its hormone production, while ignoring the vast and complex biological landscape where these hormones must actually do their work. Jennifer didn’t need more medication; she needed someone to ask why her body wasn’t using the hormones it was being given. This is where our journey into functional medicine begins.
Thyroid Biology 101: Beyond the Gland
To understand why Jennifer’s treatment was failing, we need to take a step back and revisit some fundamental biology. It’s crucial to move past the overly simplistic idea that the thyroid gland is the sole player in metabolic health.
The Manufacturing Plant: The Thyroid Gland and T4
Think of your thyroid gland, that small, butterfly-shaped organ in your neck, as a specialized manufacturing plant. Its primary job, and really its only job, is to produce thyroid hormones. It accomplishes this by taking iodine from your diet and combining it with the amino acid tyrosine. The main product it cranks out is a hormone called thyroxine, or T4. The “4” refers to the four iodine atoms attached to its molecular structure.
T4 is largely a prohormone, meaning it is biologically inactive. It’s a stable, well-packaged product ready for shipment, but it can’t actually do much on its own. It can’t bind effectively to the nuclear receptors inside your cells to turn on your metabolic machinery. T4 is simply the raw material, the precursor to what your body truly needs. The conventional medical model often stops here, assuming that if you provide enough T4 (in the form of medications like Synthroid® or levothyroxine), the body will take care of the rest. As Jennifer’s case shows, this assumption is often tragically wrong.
The Conversion Engines: Where the Real Magic Happens
The real metabolic magic doesn’t happen in the thyroid gland; it happens in your body’s peripheral tissues. These tissues act as powerful conversion engines. They take the inactive T4 and convert it into the powerhouse hormone: triiodothyronine, or T3. The “3” signifies that one iodine atom has been removed, a seemingly small change that has monumental biological consequences.
This conversion is the single most critical step in thyroid physiology, and a family of enzymes called deiodinases carries it out. T3 is the biologically active hormone. It’s what binds to receptors in the nucleus of nearly every cell in your body—from your brain to your muscles to your fat cells—and tells them to rev up their engines. T3 is what dictates your basal metabolic rate, controls your body temperature, supports your mood and cognitive function, and regulates your energy levels.
Where are these crucial conversion engines located?
The Liver: This is the undisputed champion of T4-to-T3 conversion. Approximately 60-80% of your active T3 is generated within the liver’s cells, known as hepatocytes. The primary enzyme at work here is Deiodinase Type 1 (D1).
The Gut: The gastrointestinal tract is another significant player, contributing up to 20% of T3 conversion. This process is heavily dependent on a healthy population of gut bacteria and an enzyme called intestinal sulfatase.
Other Tissues: The remaining conversion occurs in various other tissues, including the kidneys, skeletal muscle, and even the brain. The brain, in particular, relies on a different enzyme, Deiodinase Type 2 (D2), to ensure it has a steady, locally controlled supply of T3, which is vital for neurotransmitter function and cognitive clarity.
If this peripheral conversion system is broken, you are effectively running on an empty metabolic tank. It doesn’t matter how much T4 you have circulating in your bloodstream, whether it comes from your own thyroid gland or from a bottle of Synthroid®. If your body cannot convert that T4 into active T3, you will experience all the debilitating symptoms of hypothyroidism: fatigue, weight gain, depression, cold intolerance, and brain fog.
This is precisely what was happening to Jennifer. Her doctors were pouring more and more T4 into her system, but her conversion engines were offline. Her body wasn’t just failing to make active T3; it was actively shunting the excess T4 down a defensive pathway, making things progressively worse. All her biology was doing was converting those medications into something called reverse T3 (rT3), a competitive inhibitor that blocks T3 receptors, further deepening her hypothyroid state. This is a crucial concept we will explore in detail next.
The Four Horsemen of Thyroid Dysfunction
Over my three decades of clinical practice and deep immersion in functional medicine research, I have consistently found that over 90% of thyroid problems trace back to four primary physiological mechanisms. The beauty of this framework is that none of them inherently require medication. Instead, they require a deep, investigative approach to identify and correct the underlying imbalance. Let’s break them down one by one, because understanding them is key to unlocking true thyroid healing.
1. Systemic Inflammation: The Biological Grenade
The first and perhaps most pervasive disruptor of thyroid function is systemic inflammation. Think of inflammation as your body’s internal fire alarm. A short-term, localized fire (like from a cut or an infection) is healthy and necessary for healing. But chronic, low-grade, body-wide inflammation is like a fire alarm that is blaring 24/7. This constant state of alert wreaks havoc on your delicate hormonal signaling pathways.
The Source of the Fire
This chronic inflammation can stem from many sources, and identifying the specific trigger is a cornerstone of the functional medicine approach. Common culprits include:
Chronic Infections: Latent or reactivated viral infections, such as Epstein-Barr Virus (EBV), Cytomegalovirus (CMV), or Herpes Simplex Virus (HSV), can keep the immune system in a constant state of high alert.
Gut-Derived Inflammation: A condition known as “leaky gut,” or increased intestinal permeability, allows bacterial components like Lipopolysaccharides (LPS) to leak from the intestines into the bloodstream, triggering a massive inflammatory response. We’ll discuss this in more detail later.
Obesity: Adipose tissue (body fat) is not just an inert storage depot for calories. It is a highly active endocrine organ that produces and secretes many pro-inflammatory signaling molecules.
Autoimmunity: Conditions like Hashimoto’s Thyroiditis, where the immune system mistakenly attacks the thyroid gland, are fundamentally driven by an underlying inflammatory process.
Poor Diet: A diet high in processed foods, refined sugars, and industrial seed oils is inherently pro-inflammatory.
Environmental Toxins: Exposure to heavy metals, pesticides, and plastics can also fuel chronic inflammation.
The Molecular Mayhem: Cytokines and NF-kappaB
Regardless of the source, the biological result is the same: your immune cells dump massive quantities of inflammatory messengers called cytokines into your circulation. Molecules like Tumor Necrosis Factor-alpha (TNF-α), Interleukin-6 (IL-6), and Interleukin-1 (IL-1) are the primary agents of this inflammatory cascade.
I often describe these cytokines to my patients as biological grenades. They are designed for short-range combat, but when they flood the entire system, they cause widespread collateral damage. One of their primary targets is a master switch for inflammation inside your cells called Nuclear Factor-kappa B (NF-κB).
When cytokines activate NF-κB, it initiates a powerful genetic program that has devastating consequences for thyroid hormone conversion:
It shuts down D1 and D2 deiodinase: NF-κB activation directly suppresses the genes that code for Deiodinase Type 1 (D1) and Deiodinase Type 2 (D2). These two enzymes convert inactive T4 into active T3 in the liver, brain, and other tissues. The conversion engines are effectively turned off.
It cranks up D3 deiodinase: Simultaneously, NF-κB powerfully upregulates the gene for another enzyme, Deiodinase Type 3 (D3). D3’s sole job is to convert T4 into reverse T3 (rT3).
This is a disastrous one-two punch. Your body not only stops making the active hormone (T3) but also starts actively converting your precious T4 supply into a useless imposter (rT3).
Reverse T3: The Metabolic Brake
Reverse T3 (rT3) is the competitive inhibitor I mentioned earlier. Its molecular structure is a mirror image of T3, which allows it to fit perfectly into the T3 receptors on your cells. However, itdoesn’tt activate the receptor. It just sits there, blocking it. It’s like putting the wrong key into a lock; it gets stuck and prevents the right key from getting in.
From a physiological perspective, this is a brilliant survival mechanism. If the body is under severe stress (like a life-threatening infection, a major source of inflammation), it makes sense to slow metabolism to conserve energy. The body intentionally hits the metabolic brakes by producing rT3. The problem arises when this “emergency brake” gets stuck in the “on” position due to chronic, low-grade inflammation.
This is why simply giving a patient like Jennifer more levothyroxine (T4) can be so counterproductive. In an inflamed body, that extra T4 becomes more fuel for the D3 enzyme to produce more rT3. The patient’s TSH might look better on a lab report, but they feel worse because their cells are being starved of active T3 at an even greater rate. Their metabolic brakes are being slammed harder and harder.
Chiropractic Care’s Role: From a structural and neurological standpoint, chronic inflammation is often linked with physical stress and nervous system dysregulation. A subluxation, or misalignment in the spine, can create nerve interference that disrupts the body’s ability to regulate its immune and inflammatory responses properly. Chiropractic adjustments help restore proper neurological function, which can downregulate the sympathetic “fight-or-flight” response that often fuels inflammation. By improving nervous system communication, we can help the body better manage its inflammatory state, creating a more favorable environment for thyroid hormone conversion.
2. Liver Congestion: The Clogged Conversion Engine
As we established, the liver is the primary site of T4-to-T3 conversion, accounting for up to 80% of your body’s active thyroid hormone. If the liver isn’t healthy, your thyroid function will inevitably suffer, regardless of how well your thyroid gland is working. I often refer to this as a congested liver, a state where the liver’s ability to perform its myriad metabolic tasks is impaired.
The Fatigued Hepatocyte: NAFLD and ER Stress
The main conversion enzyme in the liver is D1 deiodinase, and its activity is highly sensitive to the health of the liver cells, or hepatocytes. In our modern world, one of the most common assaults on the liver is Non-Alcoholic Fatty Liver Disease (NAFLD). Driven by diets high in sugar, refined carbohydrates, and unhealthy fats, this condition causes hepatocytes to accumulate tiny lipid droplets.
This fat accumulation does more than take up space. It triggers cellular stress, particularly within an organelle called the endoplasmic reticulum (ER). The ER is like a cellular factory floor where proteins are folded and assembled. When it becomes overwhelmed with misfolded proteins and metabolic stress (a condition known as ER stress), it sends out alarm signals that shut down non-essential processes to conserve resources. Unfortunately, from the cell’s perspective, D1 deiodinase activity is considered “non-essential” during a crisis.
Research, such as the study by Wajner et al. (2011), has shown that conditions inducing ER stress significantly decrease D1 deiodinase expression and activity. So, in a person with a fatty, congested liver, the very machinery needed to convert T4 to T3 is systematically dismantled at the cellular level.
The Bile Backlog: Stalled Hormone Clearance
It gets even worse. The liver’s role in thyroid health extends beyond simple conversion. It’s also responsible for conjugating thyroid hormones and preparing them for elimination or recycling. This process involves attaching molecules like glucuronic acid or sulfate to the hormone, making it water-soluble so it can be excreted in the bile.
A portion of this conjugated hormone travels with the bile into the intestines. In a healthy gut, some is deconjugated by bacterial enzymes and reabsorbed into the bloodstream for reuse. This elegant recycling system is known as the enterohepatic circulation.
However, in a congested liver—often the same liver suffering from NAFLD—bile production and flow are compromised. The bile becomes thick and sludgy, a condition known as cholestasis. When bile flow stalls, this entire enterohepatic loop grinds to a halt. Thyroid hormones, both active and inactive, are not properly cleared or recycled. They can back up in the system, creating a “hormone traffic jam” that further disrupts the delicate feedback loops controlling thyroid function. This impaired clearance can contribute to the very inflammation and ER stress that initiated the problem, creating a vicious, self-perpetuating cycle of liver dysfunction and thyroid resistance.
Our Integrative Approach: Here, the collaboration between functional medicine and our medical director, Dr. Cardenas, is key. Dr. Cardenas can order and interpret liver function tests (LFTs) and imaging, such as an ultrasound, to formally diagnose conditions like NAFLD. From a functional medicine perspective, we then go deeper, using specialized testing to look at markers of inflammation and oxidative stress. Our treatment plan would include a comprehensive nutritional protocol to reverse fatty liver—eliminating sugars and refined carbs and incorporating liver-supportive foods and nutrients like milk thistle, N-acetylcysteine (NAC), and phosphatidylcholine. This multifaceted approach addresses both the medical diagnosis and the underlying metabolic dysfunction.
3. Gut Dysbiosis and Leaky Gut: The Broken Gateway
While the liver does the heavy lifting, the gut contributes a crucial 20% of the body’s active T3. This may sound modest, but the gut’s influence extends far beyond its direct conversion capabilities. The health of your gastrointestinal system can, in many ways, determine whether your liver is even capable of functioning as an efficient conversion organ.
The Role of the Microbiome in T3 Recycling
As mentioned, a significant amount of conjugated T3 and T4 enters the intestines via bile. The fate of these hormones then falls to your gut bacteria, or microbiome. A healthy, diverse microbiome produces an enzyme called intestinal sulfatase. This enzyme acts like a pair of scissors, cleaving the sulfate or glucuronic acid molecule off the conjugated thyroid hormone. This process, called deconjugation, effectively reactivates the hormone and allows it to be reabsorbed through the intestinal wall back into the portal circulation, where it returns to the liver and the rest of the body.
This is a vital part of the body’s T3 economy. However, in a state of dysbiosis—an imbalance in the gut microbiome where beneficial bacteria are diminished, and pathogenic or opportunistic organisms overgrow—this system breaks down. When the healthy bacteria that produce sulfatase are gone, the body can’t recycle conjugated T3d. Instead, it remains bound and is flushed right down the toilet in your stool. You are literally pooping out your precious active thyroid hormone. This loss of 20% of your T3 supply is a massive metabolic blow.
Leaky Gut and the LPS Firestorm
The consequences of dysbiosis often don’t stop there. An unhealthy microbiome frequently leads to increased intestinal permeability, or leaky gut. The single-cell layer lining your intestines is meant to be a tightly controlled barrier. In leaky gut, the junctions between these cells become loose, allowing substances that should remain in the gut to “leak” into the bloodstream.
One of the most damaging substances to leak through is Lipopolysaccharide (LPS). LPS is a component of the outer membrane of Gram-negative bacteria and a potent endotoxin. When LPS enters the circulation, the immune system sees it as a major invasion and mounts a massive inflammatory response.
This brings us full circle back to our first mechanism. The flood of LPS into the bloodstream is one of the most powerful triggers for releasing inflammatory cytokines like TNF-α and IL-6. As we discussed, these cytokines activate NF-κB, which in turn annihilates D1 deiodinase activity in the liver.
So, a sick gut delivers a devastating double blow to your thyroid:
It prevents the recycling of active T3, causing you to lose it in your stool.
It floods your body with inflammatory LPS, shutting down T3 conversion in your liver.
This is how a problem that starts in your gut can manifest as classic hypothyroid symptoms throughout your entire body.
The Functional Medicine and Chiropractic Connection: In our clinic, addressing the gut is paramount. We utilize advanced stool testing to analyze the microbiome, check for pathogens, and assess markers of inflammation and leaky gut. Our treatment protocols—often referred to as the “5R Program” (Remove, Replace, Reinoculate, Repair, Rebalance)—are designed to heal the gut systematically. At the same time, chiropractic care plays a supportive role. The autonomic nervous system extensively innervates the gut. Spinal misalignments, particularly in the thoracic and lumbar regions, can impair the nerve signals that control gut motility, secretion, and immune function. By performing targeted adjustments, we can help restore proper nerve flow to the digestive organs, complementing our functional medicine protocols and helping the gut heal and function optimally.
4. HPA Axis Dysregulation: The Stress-Famine Connection
The final, and critically important, mechanism is the dysregulation of the Hypothalamic-Pituitary-Adrenal (HPA) axis. This is our central stress response system. Biology, in its ancient wisdom, cannot tell the difference between being chased by a predator, the chronic psychological stress of a modern lifestyle (financial worries, relationship problems, traffic), or the physiological stress of a prolonged caloric deficit. To the HPA axis, they all look identical.
Cortisol: The Conversion Crusher
When the HPA axis is activated, the adrenal glands release the stress hormone cortisol. In short bursts, cortisol is essential for survival. It mobilizes energy, heightens focus, and suppresses non-essential functions. However, when stress becomes chronic, cortisol levels become chronically elevated, and this has a direct and devastating effect on thyroid conversion.
Just like the inflammatory cytokine NF-κB, high levels of cortisol directly crush D1 deiodinase activity in the liver. This is another one of the body’s innate survival mechanisms. If the body perceives it is in a state of chronic danger or famine, the last thing it wants is to run a fast, energy-expensive metabolism. So, it puts the brakes on T4-to-T3 conversion to conserve resources. This is why individuals under immense, prolonged stress often develop hypothyroid symptoms, even if their thyroid gland is perfectly healthy.
The “Dieting” Trap: A Self-Imposed Famine
Here is where so many well-intentioned people, including many of my patients when they first come to see me, go terribly wrong. A person feels tired, notices they’ve gained weight, and correctly identifies that their metabolism is sluggish. Their logical next step is to “fix” their metabolism by going on a strict diet. So they start fasting, drop into a huge caloric deficit, and dramatically cut their carbohydrate intake. They have great commitment, but absolutely lousy timing.
Let’s break down why this is so catastrophic for thyroid function.
Hepatic Glycogen Depletion: The conversion of T4 to T3 in the liver is not a “free” process. It is insulin- and glycogen-dependent. Your liver needs a stored supply of glucose (in the form of glycogen) to fuel the deiodinase enzymes. Low-carb diets and heavy caloric restriction rapidly deplete these crucial hepatic glycogen stores. The factory runs out of power.
Crashing Leptin and Insulin: Heavy caloric restriction and low carbohydrate intake also cause circulating levels of two key metabolic hormones, insulin and leptin, to crash. Leptin is the hormone that tells your brain you have enough energy stored in your fat cells.
The liver is exquisitely sensitive to these signals. From the liver’s perspective, low glycogen, low insulin, and low leptin can mean only one thing: famine. The body believes it is starving. In response, it does what any intelligent organism would do during a famine: it enters survival mode. It immediately and dramatically shuts down D1 deiodinase activity to conserve every possible calorie. The metabolic rate plummets.
This is a cruel irony. Trying to “fix” a slow metabolism through aggressive dieting is what slows it down even further. The body fights back against perceived starvation, leading to a frustrating plateau, followed by rebound weight gain as soon as normal eating patterns resume.
What is Thyroid Dysfunction?- Video
The Common Denominator: A Path to Healing
Do you know what these four cases—inflammation, a congested liver, a leaky gut, and HPA axis dysregulation—all share?
They are all detectable through a combination of standard and functional laboratory testing.
Well-established principles of physiology and biochemistry all easily explain them.
They are all addressable without writing a single prescription.
Everything we need to diagnose and treat these conditions is in the research playbook. We can measure inflammatory markers like hs-CRP and cytokines. We can use advanced stool analysis to assess the gut. We can run a DUTCH test to map out cortisol patterns. We can look at liver enzymes and blood sugar markers. The answers are there if you know where to look.
Jennifer’s case was a classic combination of all four. Years of chronic stress had dysregulated her HPA axis. A poor diet had led to a congested liver and gut dysbiosis. This combination created a firestorm of systemic inflammation that completely shut down her ability to use the thyroid hormone medication her doctors were prescribing. Our job was not to give her a different pill, but to put out the fires, decongest her liver, heal her gut, and teach her body that it was safe to run a healthy metabolism again.
This is the power of integrative and functional medicine. It’s about being a biological detective, asking “why,” and respecting the profound interconnectedness of the body’s systems. It’s about providing the body with what it needs to heal itself. And it is a path to lasting wellness that has brought hope and health back to countless patients just like Jennifer. The specific labs we ran for her case will be available for viewing in my stories. You are welcome.
References
Wajner, S. M., & Maia, A. L. (2011). New insights into the physiology of deiodinases. Arquivos Brasileiros de Endocrinologia & Metabologia, 55(8), 647-654. https://doi.org/10.1590/S0004-27302011000800008
Gereben, B., Zavacki, A. M., Ribich, S., Kim, B. W., Salvatore, D., Harney, J. W., & Larsen, P. R. (2008). Cellular and molecular basis of deiodinase-regulated thyroid hormone signaling. Endocrine Reviews, 29(7), 898–938. https://doi.org/10.1210/er.2008-0019
Kneifel, U., & Staudinger, R. (2015). The role of the gut microbiome in the regulation of thyroid hormones. Clinical Nutrition ESPEN, 10(5), e213. https://doi.org/10.1016/j.clnesp.2015.07.037
Mancini, A., Di Segni, C., Raimondo, S., Olivieri, G., Silvestrini, A., Meucci, E., & Currò, D. (2016). Thyroid hormone, oxidative stress, and inflammation. Mediators of Inflammation, 2016, 6757154. https://doi.org/10.1155/2016/6757154
van der Spek, A. H., Fliers, E., & Boelen, A. (2017). The classic pathway of thyroid hormone metabolism and its role in the regulation of developmental and adult physiology. Journal of Endocrinology, 232(2), R67-R81. https://doi.org/10.1530/JOE-16-0498
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Find out how integrative OUD care combined with chiropractic rehabilitation can enhance health outcomes and support recovery journeys.
Abstract: Navigating Opioid Use Disorder in Special Populations: An Integrative Approach
Hello, I’m Dr. Alex Jimenez. Welcome to our educational series where we explore complex health challenges through the lens of integrative and functional medicine. My extensive background as a Doctor of Chiropractic (DC), Advanced Practice Registered Nurse (APRN), board-certified Family Nurse Practitioner (FNP-BC), and a dual-certified practitioner in Functional Medicine (CFMP, IFMCP), alongside my work in advanced topics in nutrigenomics (ATN) and chiropractic spinal trauma (CCST), has shaped my comprehensive approach to patient care. At Injury Medical Clinic, we are deeply committed to a multidisciplinary model. This is made possible through our collaborative partnership with Dr. Maria Guadalupe Cardenas, MD. Dr. Cardenas is a highly respected, board-certified Internist with over four decades of experience and serves as our Medical Director and Collaborative Physician. Together, our team provides a unique fusion of medical oversight, advanced chiropractic care, functional medicine, rehabilitation, and personal injury services, ensuring our patients in El Paso, Texas, receive the most thorough and personalized care possible. In this comprehensive post, we will delve into the multifaceted challenges of treating Opioid Use Disorder (OUD), particularly within special populations. Our journey will cover the intricate relationship between OUD and co-occurring mental health conditions like depression, anxiety, and PTSD. We will analyze evidence-based treatment strategies, including pharmacotherapy and trauma-informed care, and discuss how to integrate these with our foundational chiropractic and functional medicine principles. We will then navigate the complexities of managing OUD during pregnancy, emphasizing the safety and efficacy of Medications for Opioid Use Disorder (MOUD) for both mother and child. Following this, we will explore the alarming rise of OUD among adolescents, highlighting key risk factors, screening tools, and age-appropriate interventions. We will also address the unique considerations for treating older adults with OUD and, finally, tackle the clinical challenge of managing patients who use Central Nervous System (CNS) depressants, such as benzodiazepines, concurrently with MOUD. Throughout this discussion, I will share clinical insights from our practice, showing how an integrative team that combines medical expertise with chiropractic and functional wellness can create a powerful synergy for healing and recovery. This post is based on the latest findings from leading researchers and aims to provide a clear, evidence-based roadmap for understanding and addressing this critical public health issue.
Our Collaborative and Integrative Care Model at Injury Medical Clinic
At the heart of Injury Medical Clinic is a philosophy of integrative care, where different healthcare disciplines converge to provide a holistic and patient-centered treatment experience. The close collaboration between me, Dr. Alex Jimenez, and our esteemed Medical Director, Dr. Maria Guadalupe Cardenas, exemplifies this model. Dr. Cardenas, a board-certified Internist with an impressive career spanning over 40 years, provides the essential medical oversight for our practice. Her NPI number is 1164426749, and she holds Texas MD License #J2933. Her extensive experience in internal medicine brings a depth of knowledge in diagnostics, pharmacology, and the management of complex systemic diseases that is invaluable to our patients, especially those dealing with multifaceted conditions like OUD co-occurring with chronic pain or mental health disorders. As our collaborative physician, Dr. Cardenas reviews complex cases, provides medical direction, and ensures all our treatment protocols meet the highest standards of medical safety and efficacy. This is a common and highly effective setup in multidisciplinary clinics focused on integrative or injury care, where the expertise of a medical doctor and a chiropractor are combined to optimize patient outcomes. My role is to integrate this medical foundation with advanced chiropractic care and functional medicine. As a Doctor of Chiropractic, I focus on the biomechanical and neurological aspects of health. Many patients with OUD have a history of chronic pain, often stemming from musculoskeletal injuries like degenerative disc disease or trauma from an accident. My expertise in chiropractic spinal trauma (CCST) allows me to address these root physical issues. Through precise spinal adjustments, mobilization techniques, and targeted rehabilitation exercises, we can often reduce a patient’s reliance on pain medication by improving function, alleviating nerve compression, and restoring structural integrity. This is a crucial component of a non-pharmacological approach to pain management, which is essential in the context of OUD. Furthermore, my certifications as a Functional Medicine Practitioner (CFMP, IFMCP) and Advanced Practice Registered Nurse (APRN) allow me to bridge conventional and holistic care. Functional medicine seeks to understand the “why” behind disease by examining genetic, environmental, and lifestyle factors that influence long-term health. For a patient with OUD and depression, for example, we might use advanced lab testing to investigate neurotransmitter imbalances, nutrient deficiencies (like B vitamins or magnesium), gut dysbiosis, or inflammatory markers that could be contributing to both their mood and their substance use patterns. This allows us to create highly personalized interventions, including targeted nutritional supplementation, dietary changes, and stress management strategies that support brain health and reduce cravings. Our combined approach means a patient at Injury Medical Clinic benefits from the best of both worlds:
Medical Oversight (Dr. Cardenas): Ensuring the safe prescription and management of medications like MOUD or antidepressants, monitoring for drug interactions (e.g., QTc prolongation), and managing co-existing medical conditions.
Chiropractic and Rehabilitative Care (Dr. Jimenez): Addressing the underlying physical pain generators through non-invasive techniques, improving mobility, and empowering patients with physical strategies to manage their pain.
Functional Medicine (Dr. Jimenez): Investigating and correcting the biochemical and physiological imbalances that contribute to addiction, mental health issues, and chronic disease.
Team-Based Strategy: Regular case conferences between Dr. Cardenas and me ensure that every aspect of the patient’s health is considered, and the treatment plan is synergistic, cohesive, and continuously optimized.
This integrated framework is not just about offering multiple services under one roof; it’s about creating a unified treatment plan where each modality supports and enhances the others. For a patient with OUD, this means we are not just managing their addiction; we are rebuilding their health from the ground up—physically, biochemically, and emotionally.
Understanding OUD and Co-Occurring Mental Health Conditions
One of the most critical aspects of treating Opioid Use Disorder (OUD) is recognizing that it rarely exists in a vacuum. More often than not, it is deeply intertwined with other mental health challenges. From my clinical experience, addressing the substance use without simultaneously addressing the underlying psychological distress is like trying to fix a leaking roof by only mopping the floor. To achieve lasting recovery, we must treat the whole person, and that begins with understanding the profound connection between OUD and conditions like depression, anxiety, and PTSD.
The Overwhelming Statistics
The data paints a stark picture of this co-occurrence. According to the 2022 National Survey on Drug Use and Health from the Substance Abuse and Mental Health Services Administration (SAMHSA), an estimated 21.5 million adults in the United States are living with a co-occurring disorder, meaning they have both a mental health condition and a substance use disorder (SAMHSA, 2023). The treatment gap is deeply concerning:
Approximately 60% of these individuals received treatment for either their substance use or their mental health issue, but not necessarily both.
A staggering 40% received no treatment at all for either condition.
Of those who did receive care, the majority were treated for their mental health disorder, with the substance use disorder often going unaddressed.
When we focus specifically on OUD, the prevalence of co-occurring mental health conditions is exceptionally high. The research consistently shows:
Major Depressive Disorder (MDD): Can be found in up to 50% of individuals with a substance use disorder. This is a staggering statistic that highlights the deep symbiotic relationship between mood and substance use.
Anxiety Disorders: Affect approximately 30% of this population. Often, opioids are initially used to self-medicate the overwhelming feelings of worry and panic associated with anxiety.
Post-Traumatic Stress Disorder (PTSD): Is present in nearly 20% of individuals with OUD. The link between trauma and substance use is powerful and undeniable.
Furthermore, these co-occurring conditions are more likely to affect females and significantly increase the risk of both overdose and suicide attempts (Davis et al., 2021). This is a life-or-death issue that demands a comprehensive and integrated screening and treatment approach.
Essential Screening Tools in Clinical Practice
In our practice, we believe proactive and universal screening is the cornerstone of effective care. We cannot treat what we do not identify. For this reason, we routinely integrate standardized screening tools into patient intake and follow-up. It’s not enough to ask, “How are you feeling?” We need objective measures to quantify symptoms and track progress over time.
PHQ-9 (Patient Health Questionnaire-9): This is our go-to tool for screening for depression. It’s a simple, nine-question survey that aligns with the diagnostic criteria for major depressive disorder. Patients rate the frequency of symptoms like anhedonia (loss of pleasure), sleep disturbances, and feelings of worthlessness over the past two weeks. The score helps us gauge the severity—mild, moderate, or severe—and guides our treatment decisions.
GAD-7 (Generalized Anxiety Disorder-7): This seven-item questionnaire is highly effective for screening for anxiety. It assesses how often a patient has been bothered by symptoms like uncontrollable worrying, restlessness, and irritability. Like the PHQ-9, the GAD-7 provides a severity score that helps us tailor our therapeutic approach.
PCL-5 (Post-Traumatic Stress Disorder Checklist for DSM-5): While depression and anxiety are often screened for in primary care, PTSD can be overlooked, despite its high prevalence in the OUD population. The PCL-5 is a 20-question self-report measure that assesses the 20 DSM-5 symptoms of PTSD. It asks about symptoms experienced in the past month, such as nightmares, flashbacks, avoidance behaviors, and hypervigilance.
Scoring and Interpretation: A score between 31 and 33 is generally considered a clinical cutoff, suggesting that treatment for PTSD is warranted.
Monitoring Progress: One of the great benefits of the PCL-5 is its utility in tracking treatment efficacy. A reduction of 10 points or more strongly indicates that our interventions are working and the patient’s symptoms are meaningfully improving.
By consistently using these tools, we move from subjective impressions to objective data, allowing us to have more informed conversations with our patients and make evidence-based decisions about their care.
The Imperative of Trauma-Informed Care
Given the high prevalence of PTSD and the fact that many individuals with OUD have a history of trauma (whether physical, emotional, or psychological), adopting a trauma-informed care approach is not just best practice—it is an ethical necessity. This is more than a buzzword; it’s a fundamental shift in perspective, moving from asking “What’s wrong with you?” to “What happened to you?” It involves recognizing that a patient’s behaviors, including substance use, may be adaptive responses to traumatic experiences. At Injury Medical Clinic, we embed the six core principles of trauma-informed care into every patient interaction:
Safety: We strive to create an environment that is both physically and emotionally safe. This means everything from the layout of our clinic to the tone of our voice. For a patient who has experienced trauma, a predictable and calm environment can be profoundly healing. From a chiropractic perspective, this also means ensuring physical treatments are performed with the utmost care and explaining every step of an adjustment or procedure. This helps the patient feel in control and not re-traumatized by unexpected physical contact.
Trustworthiness and Transparency: Building trust is paramount, especially with individuals who healthcare systems may have let down in the past. We are committed to being open, honest, and respectful. This means no surprises. If we need to conduct a urine drug screen, we explain why. If we are recommending a new therapy, we discuss the rationale, benefits, and potential side effects. Transparency builds the therapeutic alliance that underpins all healing.
Peer Support: We strongly encourage and facilitate connections to peer support networks. Hearing from others with lived experience can be incredibly powerful. It helps to build trust, establish a sense of safety, and combat the isolation that so often accompanies addiction and mental illness. Peers can offer a type of hope and understanding that we, as clinicians, cannot.
Collaboration and Mutuality: We reject the old, paternalistic model of healthcare where the doctor dictates and the patient complies. Instead, we view our relationship with patients as a partnership. We work with them to develop a treatment plan that aligns with their goals and values. The patient is the expert on their own life, and we provide our expertise to help them achieve their vision of health.
Empowerment, Voice, and Choice: Recovery is about reclaiming one’s agency. We empower our patients by consistently offering choices. This can be as simple as asking, “Which of these two exercises would you like to start with today?” or as significant as discussing different medication options. By ensuring the patient drives their care, we help them build self-efficacy and confidence.
Cultural, Historical, and Gender Issues: We recognize that each patient comes with a unique set of experiences shaped by their culture, history, and gender identity. Our lived experiences as providers are not universal. We must remain humble, curious, and committed to understanding the social and historical contexts that may be influencing our patients’ health, perceptions, and interactions with the healthcare system.
Evidence-Based Therapy and Pharmacotherapy
A truly integrative approach combines psychosocial support with appropriate medical interventions. Therapy is a cornerstone of treating co-occurring OUD and mental health disorders.
Therapeutic Modalities: While many forms of therapy can be beneficial, we emphasize evidence-based practices.
For Depression and Anxiety, Cognitive Behavioral Therapy (CBT) is a well-established and highly effective approach. CBT helps patients identify and challenge negative thought patterns and behaviors that contribute to their distress.
For PTSD, more specialized therapies are often required. These include Prolonged Exposure (PE), which helps patients gradually confront trauma-related memories and situations; Cognitive Processing Therapy (CPT), which focuses on changing unhelpful beliefs related to the trauma; and Eye Movement Desensitization and Reprocessing (EMDR), a unique therapy that uses bilateral stimulation to help the brain process traumatic memories.
We maintain a strong referral network of therapists skilled in these modalities, ensuring our patients receive the specialized care they need.
Pharmacotherapy: SSRIs and SNRIs: For moderate to severe MDD, GAD, and PTSD, Selective Serotonin Reuptake Inhibitors (SSRIs) and Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs) are considered first-line medications. These medications work by increasing the levels of key neurotransmitters in the brain, which can help regulate mood and anxiety.
Here is a breakdown of some commonly used medications and their clinical considerations:
Medication
Class
FDA Indications (for these conditions)
Key Clinical Notes
Paroxetine
SSRI
MDD, GAD, PTSD
Indicated for all three, but has a notoriously high rate of sexual dysfunction, which is a common reason for non-adherence. It’s a critical point to discuss with patients.
Sertraline
SSRI
MDD, PTSD
Often associated with gastrointestinal (GI) side effects like nausea or diarrhea, particularly when starting. These are usually transient but can be bothersome initially.
Fluoxetine
SSRI
MDD
Has a very long half-life, which can be forgiving for patients who occasionally forget a dose. However, this also means it can be dangerous in an overdose attempt, requiring careful patient selection.
Escitalopram
SSRI
MDD, GAD
Generally one of the best-tolerated SSRIs, but can be associated with weight gain, which should be monitored.
Duloxetine
SNRI
MDD, GAD
Tends to have less sexual dysfunction than many SSRIs. It also has an indication for neuropathic pain, which can be a significant benefit for our patients with co-occurring chronic pain syndromes.
Venlafaxine
SNRI
MDD, GAD
Also known for GI side effects and potential weight gain. It can also increase blood pressure, so monitoring is required.
Integrating MOUD with Psychiatric Medications: A Balancing Act
This is where our collaborative model with Dr. Cardenas is absolutely crucial. Managing a patient on both Medications for Opioid Use Disorder (MOUD) and psychiatric medications requires a deep understanding of pharmacology and potential drug-drug interactions.
Buprenorphine and Serotonin Syndrome:Buprenorphine (a key component of Suboxone) is a partial opioid agonist, but it also has some serotonergic properties. When combined with an SSRI or SNRI, there is a theoretical, albeit low, risk of serotonin syndrome. However, the clinical evidence is overwhelmingly clear: the benefits of treating both OUD and depression/anxiety concurrently far outweigh this small risk. Research has consistently found that treating the underlying mental health condition significantly increases retention in OUD treatment (Schuman-Olivier et al., 2014). We discuss this risk-benefit profile openly with our patients to make a shared, informed decision.
Methadone and QTc Prolongation:Methadone is a highly effective medication for OUD, but it carries a known risk of prolonging the QTc interval on an electrocardiogram (ECG). A prolonged QTc interval can increase the risk of a life-threatening cardiac arrhythmia called Torsades de Pointes. Many other medications, including some SSRIs, can also prolong the QTc interval.
Citalopram is a particular concern, especially at doses above 40 mg per day (or 20 mg in adults over 60).
Venlafaxine also has a slightly higher risk profile for QTc prolongation compared to other antidepressants.
Our Protocol: For any patient on methadone, especially if we are adding another QTc-prolonging agent, our protocol, overseen by Dr. Cardenas, is strict:
Obtain a baseline ECG before starting the new medication.
Monitor for symptoms like palpitations, dizziness, lightheadedness, or syncope (fainting).
Obtain a follow-up ECG after the new medication has reached a steady state (typically after five half-lives).
Perform annual ECGs thereafter.
We pay close attention to QTc values, especially if they exceed 450 milliseconds for men or 460 milliseconds for women, as these are the thresholds where risk begins to increase significantly.
Naltrexone and Depression:Naltrexone is an opioid antagonist used for both OUD and alcohol use disorder. It’s important to be aware that naltrexone itself carries a warning that it can increase or cause depression and suicidality. This doesn’t mean it’s contraindicated for a patient with depression, but it demands a crucial conversation. Again, we must weigh the risks and benefits. Often, the patient was using opioids or alcohol to self-medicate their depression, and those substances carry a far higher risk of overdose and death by suicide. The key is to initiate naltrexone concurrently with robust mental health support and vigilant monitoring.
Recognizing Serotonin Syndrome
All clinicians and patients on serotonergic medications should be aware of the signs and symptoms of serotonin syndrome. It’s a rare but potentially fatal condition. The mnemonic SHIVERS can be a helpful way to remember the key features:
S – Shivering: A very characteristic early sign.
H – Hyperreflexia and Myoclonus: Exaggerated reflexes and sudden muscle twitching or jerking.
I – Increased Temperature: Fever indicates increasing severity.
V – Vital Sign Instability: Tachycardia (fast heart rate) and hypertension (high blood pressure) are common.
E – Encephalopathy: Mental status changes, such as confusion, agitation, or delirium.
R – Restlessness: A feeling of inner turmoil and inability to stay still.
S – Sweating: Diaphoresis, often profuse and unrelated to the ambient temperature.
If these symptoms emerge, it is a medical emergency requiring immediate attention.
Case Study: Integrating Care for Depression and OUD
Let’s apply these concepts to a real-world scenario, representative of many patients we see at our clinic.
Patient Profile: A 32-year-old divorced female, mother of two, working part-time in retail.
History: She has chronic low back pain from degenerative disc disease, which led to opioid misuse following an injury. She is currently stable on buprenorphine-naloxone 8mg three times a day for severe OUD. Her father has a history of alcohol use disorder, and her mother has depression, highlighting a potential genetic predisposition. She lives with her mother and children, has a limited support network, but does attend peer recovery groups. She has a history of intimate partner violence, a significant traumatic experience.
Presentation: At her follow-up, she denies any return to non-prescribed opioid use. However, she reports debilitating symptoms of depression and anxiety. She feels “exhausted,” is unable to enjoy time with her children (anhedonia), and is “overwhelmed by worry.” She emphatically states, “I am staying away from pills, but I feel like I am drowning most days.” She denies any suicidal ideation.
Our Assessment:
Screenings: We administer our standard panel. Her PHQ-9 score is 18 (moderately severe depression), and her GAD-7 is 15 (severe anxiety). Her PCL-5 is 10, which does not indicate active PTSD, but her history of intimate partner violence remains a crucial part of her story.
Urine Drug Screen (UDS): Her UDS is positive for buprenorphine (as expected) and negative for all other substances. This confirms her adherence to her MOUD.
Our Integrated Treatment Plan:
Continue MOUD: We will continue her buprenorphine-naloxone. It is working effectively to manage her OUD, and stability is key.
Initiate Antidepressant: We need to treat her MDD and GAD. After a thorough discussion with her about options, side effect profiles, and the small risk of serotonin syndrome, we decide to start a well-tolerated SSRI like escitalopram. Dr. Cardenas will manage the prescription and titration.
Referral for Therapy: We refer her to a therapist in our network who specializes in Cognitive Behavioral Therapy (CBT) to equip her with coping skills for both depression and anxiety.
Chiropractic and Functional Medicine: I will work with her to address the root cause of her chronic back pain. This will involve gentle chiropractic adjustments to improve spinal mechanics, core strengthening exercises to provide better support for her degenerative discs, and anti-inflammatory nutritional guidance to reduce systemic inflammation that can exacerbate both pain and depression. This addresses the original trigger for her opioid use.
Safety Planning: We prescribe naloxone (Narcan) for her and her family to have on hand as a universal precaution. We also provide her with the 988 National Suicide & Crisis Lifeline number and clear instructions to go to the nearest emergency room if she ever feels she is in crisis.
Follow-Up: We schedule a close follow-up appointment in two weeks to monitor her response to the new medication and provide ongoing support.
This case perfectly illustrates our multidisciplinary approach. Dr. Cardenas manages the pharmacology, I address the biomechanical and functional root causes, we refer for specialized therapy, and the entire team works together to create a safety net of support around the patient.
Navigating Opioid Use Disorder and Pregnancy
The intersection of opioid use disorder and pregnancy presents one of the most complex and emotionally charged challenges in healthcare. The statistics are alarming and reflect a growing crisis that demands a compassionate, evidence-based, and non-judgmental approach.
A Sobering Trend
The increase in OUD during pregnancy has been dramatic and devastating:
From 1999 to 2014, the incidence of OUD in pregnancy quadrupled (Haight et al., 2018).
Between 2010 and 2017 alone, OUD documented at the time of delivery increased by 131% (Admon et al., 2021).
This has had a direct and tragic impact on newborns. Neonatal Opioid Withdrawal Syndrome (NOWS), a condition affecting babies exposed to opioids in utero, increased fivefold from 2002 to 2009. It then rose another 82% between 2010 and 2017 (Winkelman et al., 2018).
Current data from 2021 indicates that a baby is born experiencing opioid withdrawal approximately every 24 minutes in the United States.
Research also suggests that rates are often higher in rural areas, where access to specialized care may be limited.
The Pervasive Barrier of Stigma
Beyond the physiological challenges, pregnant individuals with OUD face a crushing weight of stigma. They are often subjected to harmful stereotypes—labeled as “unfit mothers,” “drug seekers,” or “criminals.” Tragically, this poor treatment often comes from the very healthcare professionals they turn to for help. The literature is filled with reports of patients experiencing judgmental verbal and non-verbal interactions that leave them feeling shamed and alienated (Stone, 2015). This stigma is not just hurtful; it is dangerous. It creates a massive barrier to care, causing pregnant individuals to avoid prenatal appointments, hide their substance use, and disengage from treatment. This is counterproductive to recovery and can directly lead to a return to use and an increased risk of overdose. At our clinic, we are fiercely committed to creating a sanctuary free from judgment, where pregnant patients feel safe, respected, and supported.
Universal Screening: A Non-Negotiable Standard
Because of the high prevalence and the dangers of stigma, universal screening for substance use in all pregnant patients is the only ethical and effective approach. We cannot and should not “pick and choose” who we think might be at risk. This avoids bias and normalizes the conversation about substance use as a standard part of comprehensive healthcare. Several validated screening tools are available:
The 4 P’s: This is a simple and quick tool. An affirmative answer to any of these questions triggers a more in-depth assessment.
Parents: Did any of your parents have a problem with alcohol or other drugs?
Partner: Does your partner have a problem with alcohol or drugs?
Past: In the past, have you had difficulties in your life because of alcohol or other drugs?
Present: In the present, have you drunk any alcohol or used any drugs?
NIDA Quick Screen: This tool asks about substance use in the past year, with specific questions for women about drinking more than four drinks in a day and any use of tobacco or other drugs.
CRAFFT: This tool is validated for individuals under 27 and is excellent for screening adolescents and young adults. The acronym stands for:
Car: Have you ever ridden in a car driven by someone (including yourself) who was high or had been using?
Relax: Do you ever use alcohol or drugs to relax or feel better about yourself?
Alone: Do you ever use alcohol or drugs while you are alone?
Forget: Do you ever forget things you did while using?
Family/Friends: Do your family or friends ever tell you to cut down?
Trouble: Have you ever gotten into trouble while you were using?
Two or more “yes” answers indicate a high risk and the need for a comprehensive assessment.
The Risks of Untreated OUD in Pregnancy
It is crucial to understand that the greatest danger to both mother and fetus comes from untreated opioid use disorder. The cyclical nature of using illicit substances—going from intoxication to withdrawal—creates a state of profound physiological instability. This cycle, combined with the inconsistent prenatal care that often results from stigma and fear, leads to a host of severe complications:
Placental abruption: The premature separation of the placenta from the uterine wall, a life-threatening emergency.
Problems with fetal growth: Including fetal growth restriction.
Preterm birth: Delivery before 37 weeks of gestation.
Stillbirth: Fetal death.
Maternal overdose: The risk of which is tragically high.
It is vital to use precise and non-stigmatizing language when discussing the effects of in-utero opioid exposure on a newborn. The term Neonatal Abstinence Syndrome (NAS) has largely been replaced by Neonatal Opioid Withdrawal Syndrome (NOWS) to be more specific. A critical point of education for patients and even other healthcare providers is this: babies cannot be born “addicted.” According to the DSM-5, a substance use disorder is diagnosed based on a pattern of maladaptive behaviors. A newborn cannot exhibit these behaviors. What the baby is experiencing is physiological dependence and subsequent withdrawal after being exposed to opioids in the womb. Symptoms of NOWS we watch for in newborns include:
Shaking and tremors
Poor feeding or an uncoordinated suck
High-pitched, incessant crying
Fever and sweating
Diarrhea and vomiting
Sleep problems
There are formal assessment tools to quantify the severity of NOWS:
Eat, Sleep, Console (ESC): A newer, simplified, function-based approach that is gaining popularity. It focuses on three key questions:
Can the baby eat at least one ounce per feeding?
Can the baby sleep for at least one hour uninterrupted?
Can a caregiver console the baby within ten minutes?
This approach prioritizes non-pharmacological care and keeping the mother and baby together.
Finnegan Neonatal Abstinence Scoring System (FNASS): This older, more complex system includes 21 items scored to assess everything from the pitch of the baby’s cry to the intensity of their reflexes, respiratory rate, and yawning. While comprehensive, it can be cumbersome, which is why many institutions are shifting to the ESC model.
The withdrawal period can last from days to weeks, depending on the substance and its half-life. The most important message of reassurance we can give to an expecting mother is that there are no known long-term physical or intellectual problems associated with NOWS itself if the baby is properly cared for (Jansson et al., 2017). The baby should be roomed-in with the mother, and non-pharmacological interventions like swaddling, skin-to-skin contact, and a low-stimulation environment should be the first line of treatment. In some cases, pharmacological intervention is necessary. Morphine is typically the first-line medication used to taper the baby slowly. It is critical to note that naloxone (Narcan) should never be given to a newborn in withdrawal, as it can precipitate a sudden, severe, and potentially fatal withdrawal.
Breastfeeding: A Powerful Tool for Healing
We strongly encourage breastfeeding for mothers with OUD who are stable in treatment, as the benefits are immense for both mother and child.
Neonatal Benefits: Decreased risk of asthma, obesity, SIDS, ear infections, diabetes, and more.
Maternal Benefits: Decreased risk of breast and ovarian cancer, postpartum depression, and diabetes. It also promotes a faster recovery from childbirth and, most importantly, strengthens the maternal-infant bond. This bonding can be a powerful protective factor against maternal neglect and a cornerstone of the mother’s own recovery journey.
It is a common misconception that breastfeeding is unsafe. It is absolutely safe for mothers to breastfeed while on stable doses of buprenorphine or methadone. The amount of medication that passes into the breast milk is minimal and can actually help to ease the baby’s withdrawal symptoms slightly. Breastfeeding would only be contraindicated if the mother returns to using non-prescribed or illicit substances, has HIV, or is on other specific medications that are not safe for lactation.
Enhancing Health Together: Embracing Multidisciplinary Evaluation and Treatment- Video
The Gold Standard: MOUD in Pregnancy
The message from every major medical organization, including the American College of Obstetricians and Gynecologists (ACOG), SAMHSA, and the World Health Organization (WHO), is unanimous and unequivocal: Medications for Opioid Use Disorder (MOUD), specifically buprenorphine and methadone, are the first-line, gold-standard treatment for OUD in pregnancy.
Why MOUD is Safer: MOUD eliminates the dangerous cycle of use and withdrawal. It provides a stable level of the medication in the mother’s system, which in turn creates a stable environment for the developing fetus. This dramatically improves both maternal and neonatal outcomes, increasing the likelihood of a full-term birth and normal birth weight.
Not All Babies Experience Withdrawal: Even with MOUD, not all babies will experience clinically significant NOWS. They do need to be observed in the hospital for about 3-4 days after birth to monitor for withdrawal symptoms, as the half-life of methadone and buprenorphine is long.
No Evidence of Birth Defects: There is no evidence that buprenorphine or methadone cause congenital disabilities.
Medically Supervised Withdrawal is NOT Recommended: Attempting to detox or taper a pregnant patient completely off opioids (“medically assisted withdrawal”) is strongly discouraged. This practice is associated with an extremely high rate of return to use. A return to use after a period of abstinence is incredibly dangerous, as the mother’s tolerance is lowered, placing her at a very high risk of a fatal overdose.
Naltrexone is not considered a first-line treatment during pregnancy, but it is not strictly contraindicated. This would require a careful, detailed conversation with the patient about the limited data and potential risks.
Case Study: A Hopeful Path Forward in Pregnancy
Let’s consider another common scenario that illustrates our approach.
Patient Profile: A 28-year-old female, pregnant for the second time (G2P1), at 18 weeks gestation. She has a history of mild asthma and generalized anxiety disorder.
History: She lives with a supportive partner and works part-time. She reports daily misuse of prescription oxycodone, taking about 60mg per day.
Presentation: She comes to our clinic expressing a strong desire to stop using opioids, aware of the risks to her pregnancy. She is terrified of withdrawal and cravings. She says, “I want to be healthy for my baby and myself. I’ve tried quitting on my own, but I can’t.” This statement is a powerful cry for help, filled with motivation.
Our Assessment:
UDS: Positive for opioids, negative for other substances.
Labs: We order a comprehensive panel including a CBC, CMP, HIV test, hepatitis panel, and STI screening, all of which come back within normal limits.
Our Integrated Treatment Plan:
Initiate MOUD: We explain the benefits and safety of MOUD in pregnancy. Buprenorphine is often preferred in pregnancy as it is associated with less severe NOWS compared to methadone (Jones et al., 2010). We would start her on buprenorphine about 24 hours after her last dose of oxycodone to ensure she is in mild withdrawal, preventing precipitated withdrawal. We would titrate the dose up from an initial 2-4 mg to a therapeutic level, which could be up to 24 mg, that eliminates her cravings and withdrawal symptoms. This is managed under the direct supervision of Dr. Cardenas.
Harm Reduction: We prescribe naloxone and educate both her and her partner on how to use it.
Collaborative Care: We immediately refer her to, and collaborate with, a high-risk OB/GYN for prenatal care. Communication between our clinic and her obstetrician is key.
Psychosocial and Biomechanical Support: We recommend psychosocial support, such as therapy or support groups, to address her anxiety and the emotional aspects of her recovery. As a chiropractor, I would also offer gentle, pregnancy-safe chiropractic care. Many pregnant women experience back pain, sciatica, and pelvic pain. By addressing these biomechanical issues, we can improve her comfort, reduce her stress levels, and reinforce the principle of managing physical discomfort without resorting to opioids.
Postpartum Planning: We begin the conversation early about her postpartum plan. We encourage breastfeeding if no contraindications arise and discuss continuing her MOUD after delivery to support her long-term recovery.
This comprehensive, supportive, and non-judgmental approach gives this mother and her baby the best possible chance for a healthy future.
Addressing the Adolescent Opioid Crisis
The landscape of opioid use among young people has shifted dramatically and terrifyingly in recent years. While overall substance use among teenagers has shown some decline, the lethality of the available drug supply has led to a catastrophic increase in overdose deaths. This is a public health emergency that requires a unique approach tailored to adolescents’ developmental, social, and psychological needs.
A Frightening New Era
The statistics are a wake-up call:
From 2019 to 2020, overdose deaths among 14- to 18-year-olds increased by 94%.
From 2020 to 2021, they rose another 20% (Friedman et al., 2022).
The key driver of this tragedy is not an increase in use, but a devastating increase in the potency of the drugs. The illicit drug market is flooded with Illicitly Manufactured Fentanyl (IMF) and its analogs.
Deaths involving IMFs in this age group surged by 182%. Teenagers who believe they are experimenting with a counterfeit prescription pill (like Percocet or Xanax) are often unknowingly ingesting a fatal dose of fentanyl.
Looking at the profiles of the young people we have lost:
40% had a known history of mental health conditions.
35% had a prior history of opioid use.
But only 5% had ever received treatment for OUD. This is a monumental failure of our systems to identify and engage these vulnerable youth in care.
Understanding Risk and Protective Factors
In our work with adolescents, we focus on bolstering protective factors while mitigating risks. This framework guides our screening and counseling efforts. Protective Factors:
Family Engagement and Guardian Disapproval: A strong, supportive family environment where substance use is openly discouraged is a powerful protective shield.
School Connectedness: Feeling connected to school—to teachers, activities, and peers—gives adolescents a sense of purpose and belonging.
Self-Efficacy: A young person’s belief in their own ability to handle challenges and make good decisions is crucial for resisting peer pressure and navigating stress.
Risk Factors:
Social Determinants of Health: Factors like poverty, community violence, and lack of opportunity create a backdrop of stress and hopelessness that can drive substance use.
Other Substance Use: Early use of substances like alcohol or marijuana is a strong predictor of later, more dangerous drug use.
Early Age of Onset: The younger a person starts using substances, the higher their risk of developing a substance use disorder.
History of Impulsivity or Risk-Taking Behavior: Some adolescents are wired for higher sensation-seeking, which can increase their vulnerability.
Co-occurring Psychiatric Disorders: Conditions like ADHD, depression, and anxiety are significant risk factors.
Maltreatment: A history of physical, emotional, or sexual abuse is a profound trauma that dramatically increases the risk of substance use as a coping mechanism.
Family History of Substance Use Disorder: Genetics and the family environment both play a role.
Screening Adolescents: The Importance of Confidentiality
Effective screening in this population hinges on one critical element: confidentiality. Before asking a single question, we must have a clear, transparent conversation with the adolescent about the limits of confidentiality. We explain what we can keep between us and the circumstances that would legally or ethically require us to disclose information to their parents or guardians (e.g., imminent risk of harm to self or others). Building this trust is essential. If a teen does not feel safe, they will not be honest. We always aim to have some one-on-one time with the adolescent patient, without a parent in the room. This private space can be invaluable for providing education, harm reduction counseling, and building a therapeutic rapport. Recommended screening tools for adolescents include:
S2BI (Screening to Brief Intervention): This tool asks about the frequency of use (from never to weekly) for various substances over the past year.
BSTAD (Brief Screener for Tobacco, Alcohol, and other Drugs): This screener asks for the number of days a substance was used in the past year and gets very specific, listing street drugs, inhalants, and a wide range of prescription medications.
CRAFFT: As mentioned earlier, this tool is specifically designed for youth and screens for the negative consequences and behaviors associated with substance use.
Treatment Recommendations for Adolescents with OUD
Treating an adolescent with OUD requires a multi-pronged approach that involves the youth, their family, and a team of healthcare professionals.
Naloxone, Naloxone, Naloxone: This is non-negotiable. The adolescent, their family, and even their friends should have naloxone and know how to use it. Many schools are now stocking naloxone, but we need to ensure it’s in the hands of the people closest to the at-risk youth. We have direct conversations about high-risk scenarios (e.g., using alone, using after a period of abstinence) and develop a safety plan.
Behavioral Health Services: Therapy is essential. This can take many forms, including individual, group, and family therapy. Multi-systemic therapy that involves the school, family, and community can be particularly effective.
Medications for Opioid Use Disorder (MOUD):
Buprenorphine: Is FDA-approved for adolescents aged 16 and older. For a 16- or 17-year-old with moderate to severe OUD, buprenorphine is a life-saving intervention and should be strongly considered.
Methadone and Naltrexone are not FDA-approved until age 18. While off-label use may be considered in severe cases, buprenorphine is typically the preferred and more accessible option for 16- and 17-year-olds.
We are eagerly awaiting updated guidelines from the American Society of Addiction Medicine (ASAM) for this “transition-age youth” population, which are anticipated in 2026.
Case Study: A Teenager’s Path from Injury to Addiction
This case reflects a tragically common pathway to OUD in young people.
Patient Profile: A 16-year-old female in 11th grade. She was formerly a competitive soccer player, but her grades and school attendance are now declining.
History: At age 15, she suffered an ankle fracture that required surgery. She was prescribed oxycodone for postoperative pain. Her father has alcohol use disorder in remission, and her mother has depression. She lives with her mother and younger brother. After her injury, she drifted away from her athletic peer group and began associating with older friends who misuse opioids.
Presentation: Her mother brings her to the emergency department after finding her extremely drowsy and nauseated. She admits to snorting heroin daily for the past six months. She explains the progression perfectly: “At first, I needed the pills for pain, but then I needed them to feel okay. When I couldn’t get them anymore, heroin was the only thing around.” This story—from a legitimate prescription for an injury, to misuse for emotional coping, to transitioning to illicit substances—is one we hear far too often.
Our Assessment:
UDS: Positive for heroin, but importantly, negative for fentanyl. This is critical information for harm reduction counseling. We would have a frank conversation with her about the high likelihood of fentanyl being present in the heroin supply and that she may not be so lucky next time.
Our Integrated Treatment Plan:
Initiate Buprenorphine: As she is 16 years old and has a severe OUD, she is a clear candidate for buprenorphine. We would start it 12-24 hours after her last heroin use and titrate it to a dose that controls her cravings.
Prescribe Naloxone: We provide naloxone to her and her mother with comprehensive training.
Comprehensive Support: We would facilitate a referral to an adolescent-specific substance use treatment program that includes family therapy. Involving the mother is crucial for creating a supportive home environment.
Address Root Causes: Part of her therapy would involve processing the loss of her identity as an athlete and developing new, healthy coping mechanisms for stress and emotional pain. From a chiropractic and functional medicine perspective, we would also ensure her ankle has fully healed and that she has no residual biomechanical issues causing chronic pain. We would explore nutritional support for mood and brain health, which can be particularly beneficial for the developing adolescent brain.
With a comprehensive, compassionate, evidence-based plan, we can help this young woman reclaim her future.
Other Special Populations and Considerations
The principles of treating OUD must be adapted to meet the unique physiological and social needs of different populations. Beyond the groups already discussed, older adults and individuals using other CNS depressants require special attention.
Opioid Use Disorder in Older Adults
The opioid crisis is often perceived as a problem of the young, but it is increasingly affecting older adults, a demographic with unique vulnerabilities.
Rising Rates: Since 2013, OUD has increased threefold among adults aged 65-69. The increase is particularly pronounced in patients covered by both Medicare and Medicaid, who often have more complex health and socioeconomic challenges.
Racial and Ethnic Disparities: Data show an increased vulnerability among Black Americans, Native Americans, and Alaska Natives, highlighting systemic inequities in pain management and addiction care.
Key Considerations for MOUD in Older Adults: Treating OUD in this population requires a cautious, “start low, go slow” approach, but we must not let caution become a barrier to life-saving treatment. The risk of an older adult overdosing on street fentanyl is far greater than the risks associated with properly managed MOUD.
Lack of Data: A major challenge is that most pivotal clinical trials for MOUD did not include enough participants over age 65. This leaves us with less specific guidance.
Physiological Changes of Aging:
Renal and Hepatic Function: Always consider age-related declines in kidney and liver function, which affect how drugs are metabolized and cleared.
Methadone: If a patient’s creatinine clearance (a measure of kidney function) is less than 10 mL/min, a 50-75% dose reduction may be necessary. We also need to be hypervigilant about QTc prolongation, as older adults are more likely to be on other QTc-prolonging medications and have underlying cardiac issues.
Buprenorphine: Buprenorphine is generally safer in renal impairment, as it does not require a dose reduction. However, in cases of severe hepatic impairment, a dose reduction should be considered. The long-acting subcutaneous buprenorphine injections are not recommended for individuals with moderate to severe liver impairment.
Respiratory Depression: Older adults may be more sensitive to the respiratory depressant effects of opioids. Methadone, as a full agonist, carries a higher risk than the partial agonist buprenorphine. We must monitor these patients closely, especially during initiation and dose titration.
The Challenge of Co-Prescribed CNS Depressants
One of the most common clinical dilemmas we face is managing a patient with OUD who is also taking other Central Nervous System (CNS) depressants, most notably benzodiazepines (e.g., Xanax, Klonopin, Ativan). For years, many providers were hesitant or outright refused to prescribe MOUD to patients taking benzodiazepines, fearing the combined risk of respiratory depression. However, this practice is dangerous and deadly. In 2017, the FDA issued a crucial safety announcement clarifying its position. The agency urged caution but explicitly stated that the immense benefits of treating OUD with MOUD outweigh the risks of co-prescribing with benzodiazepines. Our Guiding Principles:
The Greater Risk: The risk of an individual combining a benzodiazepine with MOUD (like buprenorphine) pales in comparison to the risk of them combining that same benzodiazepine with illicit fentanyl or heroin. The latter combination is far more likely to be fatal. Therefore, withholding MOUD is the more dangerous option.
Not a Contraindication: The presence of a benzodiazepine or other CNS depressant is not an absolute contraindication for starting or continuing MOUD.
No Arbitrary Dose Reductions: We do not arbitrarily reduce a patient’s buprenorphine or methadone dose simply because they are on a benzodiazepine. Under-dosing MOUD leads to cravings, withdrawal, and a return to illicit use, which defeats the entire purpose of treatment.
Education is Key: The cornerstone of our approach is patient education. We have a frank, non-judgmental conversation with the patient about the increased risk. We explain that the combination does increase the risk of respiratory depression and overdose, and we provide extensive harm reduction counseling (e.g., never using alone, having naloxone readily available).
Tapering as the Goal: The ideal long-term strategy is to slowly and safely taper the patient off the benzodiazepine, if possible. Benzodiazepines are not considered a first-line long-term treatment for anxiety, and we would work with the patient to transition them to a safer alternative like an SSRI and evidence-based therapy.
The FDA’s statement also mentioned other CNS depressants to be aware of, including:
With all these medications, the principle remains the same: weigh the risks and benefits, prioritize treating the OUD, educate the patient, and create a collaborative plan to reduce polypharmacy whenever it is safe and clinically appropriate.
Conclusion: An Integrated Path to Recovery
The journey through the complexities of opioid use disorder in special populations underscores a fundamental truth: effective treatment must be comprehensive, compassionate, and individualized. From the intricate dance of co-occurring mental health conditions to the delicate care required during pregnancy and the unique challenges of treating adolescents and older adults, a one-size-fits-all approach is doomed to fail. As we have explored:
Co-occurring disorders like depression, anxiety, and PTSD are the rule, not the exception. They must be proactively screened for and treated concurrently with OUD using evidence-based practices like therapy and appropriate pharmacotherapy.
For pregnant individuals with OUD, Medications for Opioid Use Disorder (MOUD) are the life-saving, gold-standard of care, protecting both mother and child from the devastating consequences of untreated addiction.
The alarming rise in adolescent overdose deaths demands a focus on harm reduction, family involvement, and age-appropriate MOUD, recognizing the lethal potency of the current drug supply.
Treating older adults and those on other CNS depressants requires a careful risk-benefit analysis, where the profound benefit of MOUD in preventing fatal overdose almost always outweighs the risks of co-prescribed medications.
At Injury Medical Clinic, our collaborative model, uniting the medical direction of Dr. Maria Cardenas with my expertise in chiropractic and functional medicine, allows us to embody this integrated approach. We don’t just manage symptoms; we seek to heal the whole person. We address the biochemical imbalances with functional medicine, correct the structural pain generators with chiropractic care, support the psychological wounds with therapy referrals, and stabilize the addiction with evidence-based medical treatment. This journey is not easy, but with a dedicated, multidisciplinary team and a commitment to trauma-informed, patient-centered care, we can offer our patients a real and lasting path to recovery. Thank you for joining me in this vital discussion. Please do not hesitate to reach out with any questions.
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Abstract: A Modern, Integrative Approach to Obesity Management
Obesity is a chronic, relapsing, and multifactorial disease that affects a staggering number of individuals worldwide. This educational post delves into the complexities of obesity, moving beyond outdated notions of willpower to explore its deep-seated neurobehavioral, metabolic, and genetic roots. We will examine the latest findings on the pharmacology of weight management, exploring how modern, evidence-based medications such as GLP-1 receptor agonists, GIP/GLP-1 therapies, naltrexone-bupropion, and others can serve as powerful tools in a comprehensive treatment plan. This discussion will highlight the critical need to combat weight bias in healthcare, which significantly hinders patient outcomes. Furthermore, we will explore how an integrative care model that combines advanced chiropractic techniques with internal medicine, functional medicine, and personalized rehabilitation provides a holistic and effective pathway for patients on their journey toward sustainable health. At our clinic, this collaborative approach is championed by Mr. Maria Guadalupe Cardenas, MD, and me, ensuring our patients receive comprehensive, multidisciplinary care.
Our Collaborative and Integrative Care Model in El Paso
At Injury Medical Clinic PA, also known as Mission Plaza Injury Medical Clinic, in El Paso, Texas, we have cultivated a unique and powerful multidisciplinary environment designed to address complex health issues, such as obesity, from multiple angles. I am Dr. Alex Jimenez, and my expertise in chiropractic care, functional medicine, and Family Nurse Practitioner practice is complemented by the invaluable medical oversight of Dr. Maria Guadalupe Cardenas, MD. Dr. Cardenas is Board Certified in Internal Medicine and serves as our Medical Director and Collaborative Physician. With over 40 years of experience as an internist (NPI #1164426749, Texas MD License #J2933), she provides the essential medical framework for our integrative protocols.
This collaborative setup allows us to blend different disciplines for a truly holistic patient experience seamlessly:
Medical Oversight (Dr. Cardenas): Dr. Cardenas provides crucial medical direction, overseeing diagnoses and medication management, and ensuring that all treatments align with established medical safety and efficacy standards. Her role is vital, especially when considering pharmacotherapy for obesity and its related comorbidities such as hypertension, type 2 diabetes, and cardiovascular risk.
Chiropractic and Functional Medicine (Dr. Jimenez): My role involves focusing on the biomechanical and functional aspects of health. Through advanced chiropractic adjustments, we address musculoskeletal issues such as osteoarthritis, which is often exacerbated by excess weight. Using a functional medicine lens, we investigate the root causes of metabolic dysfunction, from gut health to hormonal imbalances, creating personalized nutritional and lifestyle strategies.
Integrated Services: Our team works cohesively to offer a spectrum of care that includes personal injury rehabilitation, physical therapy, and nutritional counseling. This allows us to create a unified treatment plan in which a patient can receive a chiropractic adjustment to alleviate back pain, consult with a provider on evidence-based weight-management medications under medical supervision, and receive a personalized nutrition plan, all within one coordinated system.
This team-based approach ensures that we treat the whole person, not just the symptoms, embodying the principles of modern, patient-centered integrative care. Patients are not isolated body parts; a patient with obesity, diabetes, back pain, and depression needs a coordinated strategy that respects the whole person.
Deconstructing Obesity: A Chronic and Complex Disease
We must begin by framing obesity correctly. It is not a simple matter of choice or a lack of discipline. Obesity is a chronic, progressive, relapsing, and treatable disease. This perspective is fundamental to how we approach patient care. When patients stop their anti-obesity medications, the weight often returns. This is no different than when a patient stops their antihypertensive medication, and their blood pressure rises, or when they stop chemotherapy and a malignancy returns. The condition relapses because it is chronic and deeply embedded in our physiology.
Obesity is profoundly multifactorial. It involves intricate neurobehavioral, neuroendocrine, and metabolic components. The accumulation of excess body fat promotes adipose tissue dysfunction, which is a key driver of the chronic inflammation and metabolic chaos associated with the disease. Obesity affects the body through several overlapping mechanisms:
Insulin resistance
Chronic low-grade inflammation
Leptin resistance
Altered appetite regulation
Reward pathway dysregulation
Mitochondrial dysfunction
Reduced skeletal muscle metabolic flexibility
Gut-brain signaling changes
Sleep disruption and cortisol imbalance
Mechanical overload on the spine, hips, knees, and feet
The consequences are far-reaching, impacting every system of the body:
Metabolic: Type 2 diabetes, dyslipidemia, hypertension.
Biomechanical: Osteoarthritis, back pain, incontinence.
Psychosocial: Depression, anxiety, social stigma, and discrimination.
In the United States, the statistics are sobering. 41.9% of the adult population meets the criteria for obesity (BMI ≥ 30), and a startling 9.2% have severe obesity (BMI ≥ 40). These numbers underscore the urgency of developing effective, accessible, and compassionate treatment strategies.
The Social and Environmental Drivers of Obesity
When we consider the roots of this epidemic, we must look beyond the individual to the broader environment. I often refer to the “social determinants of obesity” because factors like socioeconomic status, education, and environment play such a powerful role.
Economic Instability: For centuries, poverty was associated with being underweight. Today, the opposite is often true. In many impoverished areas, access to fresh, nutrient-dense food is limited, while calorie-dense, processed foods are cheap and abundant. This creates an environment where metabolic disease can thrive.
Neighborhood and Built Environment: If a person lives in a neighborhood where it is unsafe to walk outside, opportunities for regular physical activity are severely limited. The lack of green spaces, sidewalks, and recreational facilities contributes directly to a sedentary lifestyle.
Genetic and Hormonal Factors: We are identifying an ever-growing list of genetic and hormonal players that regulate appetite and metabolism, including ghrelin (the “hunger hormone”), GLP-1 (a satiety hormone), and leptin (which signals fullness). Research into the gut microbiota is also revealing how the balance of our intestinal flora can profoundly influence weight.
The Modern Environment: The rise of technology has engineered physical activity out of our daily lives. From desk jobs to digital entertainment, we are more sedentary than any previous generation.
Over the last decade, virtually every major medical organization, including the American Medical Association, has officially recognized obesity as a disease. This recognition is a critical step, as it validates the patient’s struggle and opens the door for proper diagnosis, treatment, and insurance coverage.
The Overwhelming Complexity of Appetite Regulation
The regulation of our appetite is an incredibly complex symphony conducted by the brain and a host of hormones. When you look at the intricate network of signals involved, it’s easy to see how a disruption in even one pathway can lead to dysfunction. Hormones like leptin, cortisol, ghrelin, and GLP-1 are in constant communication with the brain’s appetite centers, like the hypothalamus.
For many individuals with obesity, these signaling pathways are dysregulated. They may have leptin resistance, in which the brain doesn’t receive the “I’m full” signal, or ghrelin imbalances that drive persistent hunger. It becomes incredibly difficult for someone to “overpower” these potent neuroendocrine signals through willpower alone. This physiological reality is often overlooked, leading to significant clinical inertia.
Consider this shocking statistic: of the 100 million people with obesity in the United States, less than 1% receive a prescription for an anti-obesity medication. Less than 300,000 undergo bariatric surgery, despite 9.2% of the population having severe obesity. Why is there such a massive gap between the need for treatment and the care being provided? A large part of the answer lies in bias.
Binge Eating Disorder and the Physiology of Loss of Control Eating
A key concept in obesity care is recognizing binge eating disorder (BED). Binge eating disorder is not simply eating too much. It involves eating, within a discrete period of time, an amount of food larger than most people would eat under similar circumstances, combined with a sense of loss of control during the episode.
Clinically, binge eating episodes are often associated with several features:
Eating much more rapidly than normal
Eating until uncomfortably full
Eating large amounts when not physically hungry
Eating alone because of embarrassment
Feeling disgusted, depressed, guilty, or ashamed afterward
Marked distress about binge eating
Episodes occurring at least once weekly for at least three months
Absence of compensatory behaviors, such as purging, that would suggest bulimia nervosa
In practice, patients may describe getting up at night to eat while family members are asleep, hiding food, eating in the car, or waking up the next morning feeling shame and physical discomfort. I approach these disclosures with compassion because shame worsens the cycle. Patients need an evidence-based treatment plan, not judgment.
The physiology behind binge eating disorder involves dysregulation of:
Dopamine reward pathways
Impulse control circuits
Stress-related cortisol signaling
Serotonin and norepinephrine pathways
Prefrontal cortex regulation
Gut-brain satiety signaling
Emotional regulation networks
From a clinical standpoint, binge eating disorder can drive weight gain, worsen insulin resistance, aggravate depression and anxiety, and contribute to musculoskeletal pain because additional body mass increases mechanical load across the spine and joints.
Confronting Weight Bias: The Last Socially Acceptable Discrimination
Weight bias and stigma are perhaps the greatest barriers to effective obesity care. There is a pervasive, often unconscious, belief in our society—and even within the medical community—that obesity is a character flaw, a result of laziness or a lack of willpower. This prejudice is not only hurtful but also dangerous.
Research has shown that patients who experience weight bias have increased complications and mortality, independent of their BMI. The bias itself, through the stress it causes and the lack of care it fosters, becomes a risk factor. What drives this?
Lack of Reimbursement: Historically, treatments for obesity, especially medications, have not been well-covered by insurance, discouraging providers from offering them.
Time Constraints: Meaningful lifestyle counseling takes time, a luxury many providers in a fee-for-service model do not have.
Cultural Stigma: The belief that “people should just try harder” prevents us from treating obesity with the same seriousness as other chronic diseases.
This bias manifests in shocking ways. Imagine if we told patients with schizophrenia to “just stop listening to the voices.” It sounds absurd, yet we often tell patients with obesity to “just eat less and move more,” ignoring the powerful physiological drivers of their condition. We require extensive psychological screening for bariatric surgery patients—a practice not required for equally life-altering procedures like coronary artery bypass grafts—based on the biased assumption that overeating is purely a behavioral problem.
In a landmark Harvard study on implicit bias, weight bias was the only form found to increase over time. As providers, we must be the ones to break this cycle.
Shifting the Conversation: How to Engage Patients Effectively
The first step in combating bias is to change the way we talk to our patients. We need to approach the conversation with empathy, respect, and a genuine desire to help. The 5 A’s model provides a great framework:
Ask: “Is it okay if we talk about your weight and its potential effects on your health?” This simple question asks for permission and shows respect for the patient’s autonomy.
Assess: Take a detailed history. Understand their weight journey, family history, what they’ve tried in the past, and their understanding of how weight impacts health.
Advise: Provide clear, non-judgmental advice. Explain that even a modest weight loss of 3-5% can lead to significant improvements in blood pressure, blood sugar, and cholesterol.
Agree: Work with the patient to set realistic, achievable goals. What is a goal weight they feel is sustainable?
Arrange/Assist: Connect them with the resources they need. This could be a referral to a dietitian, an exercise program, or a discussion about pharmacotherapy or surgical options.
This approach transforms the conversation from one of judgment to one of partnership. Shared decision-making improves adherence because the patient becomes an active participant rather than a passive recipient.
A Framework for Treatment: Lifestyle, Medication, and Surgery
Our treatment approach is tiered and personalized, based on BMI and the presence of comorbidities (obesity-related health conditions). Current research strongly supports the idea that obesity should be treated as a chronic disease requiring ongoing monitoring, not as a temporary problem solved by short-term dieting. The Endocrine Society, American Gastroenterological Association, and American Diabetes Association emphasize that structured lifestyle therapy, medication when appropriate, and long-term follow-up are essential for improving outcomes (Apovian et al., 2015; American Diabetes Association Professional Practice Committee, 2026; Grunvald et al., 2022).
Lifestyle Interventions (BMI ≥ 25 with comorbidities, or ≥ 30): This is the foundation for everyone. It includes healthy eating, regular physical activity, and behavioral therapy. As a chiropractor and functional medicine practitioner, I often begin here, helping patients build a sustainable foundation. We focus on anti-inflammatory food plans, stress management techniques, and personalized exercise regimens that account for any musculoskeletal limitations.
Pharmacotherapy (BMI ≥ 27 with comorbidities, or ≥ 30): Medications should be considered for patients who have not reached their goals with lifestyle changes alone. These are not “magic pills” but powerful tools to aid the biological processes of appetite and metabolism.
Bariatric Surgery (BMI ≥ 35 with comorbidities, or ≥ 40): For individuals with severe obesity, surgery remains the most effective long-term treatment for significant weight loss and remission of comorbidities. It is a vital option that is tragically underutilized. A shocking 71% of providers never discuss surgical options with eligible patients.
Our goal is typically a 5-10% reduction in total body weight over six months. This level of weight loss is clinically significant and can dramatically reduce health risks.
Why “First, Do No Harm” Matters in Obesity Treatment
One of the most important principles I use in integrative obesity care is “first, do no harm.” Before adding a new medication or supplement, I want to understand whether the patient is already taking medications that may be contributing to weight gain. Common obesogenic medications may include:
Antidepressants and Antipsychotics: (e.g., some SSRIs, mirtazapine, olanzapine)
Shockingly, patients with obesity are often prescribed these medications more frequently. If a patient is on one of these drugs and struggling with their weight, we collaborate with their prescribing physician to see if a weight-neutral or weight-loss-promoting alternative exists. For instance, a patient with diabetes on a sulfonylurea like glyburide might be a candidate for a GLP-1 receptor agonist or an SGLT2 inhibitor, which can aid in weight loss. This is a perfect example of how the collaboration between Dr. Cardenas and me benefits the patient, ensuring patient safety and optimized outcomes.
Modern Pharmacotherapy for Weight Management
The good news is that we now have a growing arsenal of safe and effective long-term medications for obesity. All approved medications are more effective than placebo. A 12-week trial is often sufficient to determine whether a medication is working for a patient. If a patient does not achieve at least a 5% reduction in body weight after approximately 3 months at a therapeutic dose, we reassess the plan.
Here is an overview of some key long-term options:
Phentermine/Topiramate (Qsymia): This combination drug pairs a well-known appetite suppressant (phentermine) with an anticonvulsant (topiramate) that also reduces appetite and may lower leptin levels. Because phentermine can stimulate the sympathetic nervous system, increasing heart rate and blood pressure, it requires careful dose titration and monitoring, especially in patients with cardiovascular concerns.
Naltrexone/Bupropion (Contrave): This combination works on the brain’s reward and appetite-control centers. Bupropion stimulates the POMC system to reduce appetite, while naltrexone blocks an inhibitory feedback loop, allowing the appetite-suppressing effect to persist. This may be particularly useful for patients with co-occurring depression or reward-driven eating patterns.
Orlistat: This medication works by inhibiting gastrointestinal lipases, thereby reducing the absorption of dietary fat. It is a non-stimulant option but can cause gastrointestinal side effects and may interfere with the absorption of fat-soluble vitamins (A, D, E, K), requiring monitoring.
Liraglutide (Saxenda): A daily injectable GLP-1 receptor agonist. GLP-1 is a natural gut hormone that slows stomach emptying, promotes feelings of fullness (satiety), and acts on the brain’s appetite centers. It is started at a low dose and titrated up to 3.0 mg daily to manage potential GI side effects like nausea.
Semaglutide (Wegovy): A weekly injectable GLP-1 receptor agonist. It works similarly to liraglutide but has a longer half-life, allowing for once-weekly dosing. It has demonstrated even greater weight loss in clinical trials, with an average loss of approximately 15% of body weight (Blundell et al., 2017; Wilding et al., 2021). It is important to note that semaglutide is sold as Ozempic for type 2 diabetes and Wegovy for chronic weight management; they are the same molecule but have different indications and dosing.
Tirzepatide (Zepbound): A novel weekly injectable that is a dual GIP/GLP-1 receptor agonist. By targeting two different incretin hormone pathways, it produces a powerful synergistic effect on appetite suppression and glucose control. Clinical trials have shown unprecedented levels of weight loss, with some participants achieving more than a 20% reduction in body weight (Jastreboff et al., 2022). This potent therapy may be particularly appropriate for patients with severe obesity.
Lisdexamfetamine (Vyvanse): While not approved for general obesity, this medication is FDA-approved for moderate to severe binge eating disorder (BED). Since BED is a common co-occurring condition in patients with obesity, identifying and treating it can be a critical part of the overall weight management strategy. It works on dopamine and norepinephrine pathways to improve impulse control (McElroy et al., 2015).
Emerging Obesity Medications and Future Directions
The obesity medicine pipeline is advancing quickly. Researchers are studying therapies that may produce even more substantial weight loss while improving metabolic markers. Emerging therapies include:
Retatrutide: A triple agonist targeting GLP-1, GIP, and glucagon receptors, which has shown very large weight reduction percentages in trials (Jastreboff et al., 2023).
Oral GLP-1 agonists: Medications like orforglipron and danuglipron are being developed to provide an oral alternative to injections.
Combination therapies:CagriSema, a combination of cagrilintide and semaglutide, is being studied for its synergistic effects on appetite and metabolism.
Discovering the Benefits of Chiropractic Care- Video
The Role of Integrative Chiropractic Care in Weight Management
So, where does integrative chiropractic care fit into this modern, medical approach? It is a crucial component of our holistic model, addressing the biomechanical consequences of excess weight and enhancing the body’s ability to heal and adapt.
Addressing Biomechanical Pain: Excess weight places tremendous stress on the musculoskeletal system, leading to conditions like osteoarthritis, degenerative disc disease, and chronic back and joint pain. In my clinical observations, I frequently see patients whose weight-related concerns overlap with low back pain, sciatica, and knee pain. This pain creates a vicious cycle: it hurts to move, so the person becomes more sedentary, which can lead to further weight gain. Through precise chiropractic adjustments, spinal decompression, and soft tissue therapies, we can alleviate pain, improve joint function, and restore mobility. This enables patients to engage in the physical activity essential for weight loss.
Improving Neurological Function: The spine houses the central nervous system, which is the master controller of all bodily functions, including metabolism and hormonal regulation. By correcting spinal misalignments (subluxations), we can reduce interference in the nervous system, potentially improving the body’s ability to self-regulate and heal.
Functional Medicine and Lifestyle Coaching: As a practitioner certified in functional medicine, I look beyond the symptoms to find the underlying root causes of dysfunction. We may use advanced testing to assess gut health, hormonal imbalances, or nutrient deficiencies that contribute to weight gain. Based on these findings, we develop highly personalized nutrition plans, stress-reduction protocols, and targeted supplement recommendations to optimize metabolic function from the inside out.
Rehabilitation and Muscle Preservation: A major concern with weight loss, particularly rapid loss, is the loss of lean muscle mass. Muscle is critical for resting metabolic rate, glucose disposal, and long-term weight maintenance. My clinical approach, as reflected on my professional platforms like ChiroMed and my LinkedIn profile, emphasizes a rehabilitation-focused plan that includes progressive resistance training, core stabilization, and balance work to preserve this metabolically active tissue. Movement is metabolic medicine.
By integrating these approaches under the medical direction of Dr. Cardenas, we ensure that the patient is supported on every level—structurally, neurologically, metabolically, and medically.
Final Clinical Takeaway
If there is one concept I want patients and clinicians to remember from this post, it is this: obesity care must be individualized, medically safe, and integrated. Before adding a medication, we must ask whether current medications are worsening weight gain. Before recommending exercise, we must ask whether pain, injury, or joint dysfunction is limiting movement. Before assuming noncompliance, we must ask whether binge eating disorder, depression, anxiety, or sleep apnea are present.
With the collaborative oversight of Dr. Maria Guadalupe Cardenas, MD, and the integrative chiropractic, functional medicine, and rehabilitation services I provide, our El Paso practice model is designed to evaluate the whole patient. Modern obesity medicine is no longer about simply telling people to eat less and move more. It is about understanding physiology, reducing harm, improving function, supporting the nervous and musculoskeletal systems, and applying evidence-based tools with compassion and precision. This is the future of effective and compassionate obesity care.
Jastreboff, A. M., Aronne, L. J., Ahmad, N. N., Wharton, S., Connery, L., Alves, B., Kiyosue, A., Zhang, S., Liu, B., Bunck, M. C., & Stefanski, A. (2022). Tirzepatide once weekly for the treatment of obesity. The New England Journal of Medicine, 387(3), 205–216.
Wilding, J. P. H., Batterham, R. L., Calanna, S., Davies, M., Van Gaal, L. F., Lingvay, I., McGowan, B. M., Rosenstock, J., Tran, M. T. D., Wadden, T. A., Wharton, S., Yokote, K., Zeuthen, N., Kushner, R. F., & STEP 1 Study Group. (2021). Once-weekly semaglutide in adults with overweight or obesity. The New England Journal of Medicine, 384(11), 989–1002.
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Find out about GLP-1 receptor therapy on cardiometabolic health and its revolutionary role in modern medicine and patient care.
Abstract
Hello, I’m Dr. Alex Jimenez, and I am honored to share transformative insights into managing cardiovascular and metabolic conditions, such as type 2 diabetes. This educational post explores a significant shift in our medical understanding, moving from a purely glucose-centric model to a comprehensive, risk-reduction strategy. Here, we will journey through the latest findings from leading researchers, backed by robust, evidence-based studies, to understand this new paradigm. We’ll delve into the mechanisms of two groundbreaking classes of medications—SGLT2 inhibitors and GLP-1 receptor agonists—and their profound benefits for cardiovascular and renal health, often independent of their glucose-lowering effects. We will also discuss how our multidisciplinary team at Injury Medical Clinic PA, including the invaluable medical direction of Dr. Maria Guadalupe Cardenas, MD, integrates these advancements with integrative chiropractic care, functional medicine, and rehabilitation to provide a truly holistic treatment plan for our patients in El Paso, Texas. This post aims to illuminate the interconnectedness of cardiac, metabolic, and kidney health and present a collaborative path forward for optimal patient outcomes.
Our Collaborative and Integrative Practice at Injury Medical Clinic PA
Before we delve into the clinical science, I want to take a moment to explain our unique approach to patient care here in El Paso, Texas. At Injury Medical Clinic PA, also known as Mission Plaza Injury Medical Clinic, we have built a truly multidisciplinary practice. I am Dr. Alex Jimenez, and my credentials include DC, APRN, FNP-BC, CFMP, IFMCP, ATN, and CCST. My passion lies in functional medicine and chiropractic care, focusing on the body’s innate ability to heal and the musculoskeletal system’s foundational role in overall health. A cornerstone of this model is my collaboration with Dr. Maria Guadalupe Cardenas, MD. With over 40 years of experience as a board-certified internist, Dr. Cardenas serves as our Medical Director and Collaborative Physician (NPI #1164426749, Texas MD License #J2933). Her extensive expertise in internal medicine provides essential medical oversight and direction, allowing us to seamlessly merge advanced medical protocols with chiropractic, functional medicine, rehabilitation, and personal injury care. Our model is built on the synergy between different disciplines:
Medical Oversight (Dr. Cardenas): Provides diagnoses, prescribes medications like the advanced therapies we will discuss today, and oversees the overall medical treatment plan, ensuring patient safety and efficacy.
Chiropractic and Functional Medicine (Dr. Jimenez): I focus on identifying and addressing the root causes of dysfunction. Through chiropractic adjustments, we restore proper nerve function and biomechanics. With functional medicine, we analyze a patient’s genetics, lifestyle, and environment to correct underlying imbalances in metabolism, inflammation, and gut health.
Integrated Services: Together, we manage personal injury cases, rehabilitation, nutritional counseling, and chronic disease management. This team-based approach ensures that a patient with diabetes, for example, not only receives the latest medications but also benefits from dietary overhauls, targeted supplementation, and structural care to improve insulin sensitivity and reduce systemic inflammation. This is the essence of integrative medicine—uniting the best of multiple worlds for superior patient outcomes.
The Critical Link Between Diabetes and Cardiovascular Disease
For a long time, the primary focus in managing type 2 diabetes was on lowering blood glucose. While important, this approach was incomplete. We now have an overwhelming body of evidence showing that people with diabetes face a significantly elevated risk for Atherosclerotic Cardiovascular Disease (ASCVD), which includes coronary heart disease, stroke, and peripheral arterial disease. In fact, ASCVD is the leading cause of death for individuals with diabetes.
Consider this startling fact: over 70% of individuals with diabetes over the age of 65 will likely succumb to heart disease or a stroke.
Following a heart attack (myocardial infarction or MI), people with diabetes have a much higher mortality risk and a poorer long-term prognosis.
These grim outcomes persist even when blood sugar levels are well-controlled, and they affect individuals with both type 1 and type 2 diabetes.
This reality has forced a paradigm shift in how we manage these interconnected conditions. The focus has expanded from aggressive glucose reduction to a holistic strategy to reduce overall cardiovascular and renal risk. This involves managing not just blood sugar, but also blood pressure, cholesterol levels, weight, physical activity, and smoking cessation. For the first time in my career, all the major guideline-issuing bodies—including the American College of Cardiology (ACC), the American Heart Association (AHA), the American Diabetes Association (ADA), and the Kidney Disease: Improving Global Outcomes (KDIGO)—are in complete agreement on this new, integrated approach to care. This consensus marks a monumental step forward, allowing us to view and treat our patients through a unified, comprehensive lens.
Rethinking Treatment Algorithms: A Risk-Based Approach
This new paradigm is reflected in the latest treatment algorithms from the American Diabetes Association. The guidelines now emphasize a risk-stratified approach. For any patient with type 2 diabetes who has established ASCVD, heart failure, chronic kidney disease (CKD), or is at high risk for developing these conditions, the recommendation is to concurrently address all risk factors and prioritize specific classes of medications. The algorithm directs us to move beyond traditional first-line agents like metformin alone and immediately consider two powerful classes of drugs:
SGLT2 (Sodium-Glucose Cotransporter-2) Inhibitors
GLP-1 (Glucagon-Like Peptide-1) Receptor Agonists
These medications are now recommended as foundational therapies for high-risk patients precisely because they have demonstrated proven cardiovascular (CV) benefits in large-scale clinical trials. The choice between them, or the decision to use them in combination, depends on patient-specific factors, comorbidities, and preferences. This marks a significant departure from simply trying to lower the A1C; it’s about proactively protecting the heart and kidneys.
The History and Evolution of Diabetes Medication Trials
How did we arrive at this pivotal moment? The story begins around 2008, when the U.S. Food and Drug Administration (FDA) issued mandatory guidance for all new antidiabetic medications. The FDA required pharmaceutical companies to conduct long-term Cardiovascular Outcomes Trials (CVOTs). The primary goal was to ensure that these new drugs did not increase the risk of Major Adverse Cardiovascular Events (MACE)—a composite of non-fatal heart attack, non-fatal stroke, and cardiovascular death. This mandate was a direct response to past experiences where certain drugs, such as rosiglitazone (Avandia) and others like Vioxx, were later found to cause cardiovascular harm. Earlier studies were often too short, underpowered, or poorly designed to detect these risks. The FDA’s new requirement forced the industry to conduct large, well-designed, placebo-controlled trials that were robust enough to demonstrate safety or non-inferiority. What happened next was truly surprising. As the results of these CVOTs began to be published, starting with the EMPA-REG OUTCOME trial for empagliflozin (Jardiance) in 2015, researchers discovered something extraordinary. These new drugs weren’t just safe—some of them were actively protective.
Empagliflozin (Jardiance), an SGLT2 inhibitor, was the first to show a significant reduction in MACE, CV death, and hospitalization for heart failure.
Liraglutide (Victoza), a GLP-1 receptor agonist, followed in 2016 with the LEADER trial, also demonstrating significant cardiovascular benefits.
These unexpected findings of superiority, not just safety, were game-changers. They provided the evidence needed to completely overhaul the clinical guidelines and place these drug classes at the forefront of managing patients with cardiovascular, metabolic, and renal disease.
A Deeper Dive into SGLT2 Inhibitors
Let’s explore the SGLT2 inhibitor class more closely. These medications work by blocking glucose reabsorption in the kidney, causing excess sugar to be excreted in the urine. While this helps lower blood glucose, their profound cardiovascular and renal benefits appear to stem from multiple other mechanisms.
Landmark Cardiovascular Outcomes Trials for SGLT2 Inhibitors
Several major CVOTs have established the benefits of this class:
EMPA-REG OUTCOME (empagliflozin/Jardiance): This trial was a watershed moment. It showed a highly statistically significant reduction in MACE, CV death, and hospitalization for heart failure.
CANVAS Program (canagliflozin/Invokana): Demonstrated significant reductions in MACE and hospitalization for heart failure.
DECLARE-TIMI 58 (dapagliflozin/Farxiga): While it didn’t show a significant reduction in MACE, it showed a substantial and statistically significant reduction in the risk of hospitalization for heart failure.
VERTIS-CV (ertugliflozin/Steglatro): Also showed a significant reduction in hospitalization for heart failure risk (a 30% relative risk reduction).
The consistent and powerful effect on reducing hospitalizations for heart failure across the class is particularly noteworthy and has led to their widespread adoption in cardiology.
The Multifaceted Mechanisms of SGLT2 Inhibitors
What makes these drugs so effective? The benefits go far beyond simple glucose lowering. Some of the proposed mechanisms that contribute to their cardioprotective and renoprotective effects:
Hemodynamic Effects: SGLT2 inhibitors have a mild diuretic effect, which helps reduce blood pressure by about 3-5 mmHg systolic. This is achieved through natriuresis, or the excretion of sodium and water, which reduces fluid volume and preload on the heart.
Reduced Glomerular Pressure: In the kidneys, these drugs reduce pressure within the glomerulus (the kidney’s filtering unit). This is a key theorized mechanism for their nephroprotective (kidney-protecting) effects, slowing the progression of diabetic kidney disease.
Metabolic Shifts: SGLT2 inhibitors promote a slight shift towards ketosis. The heart is a unique metabolic organ that can efficiently use ketones as a fuel source. This “super fuel” improves myocardial efficiency and function, especially in a stressed or failing heart.
Systemic Benefits: They also contribute to a modest weight loss (around 5-7 pounds), reduce inflammation, decrease oxidative stress, and may improve endothelial function and stabilize atherosclerotic plaques.
Improved Myocardial Energetics: By reducing the workload on the heart (via lower blood pressure and volume) and providing a more efficient fuel source (ketones), these drugs improve the overall energy balance and function of the heart muscle.
SGLT2 Inhibitors in Heart Failure and Kidney Disease
The benefits of SGLT2 inhibitors have been so profound that their use has expanded to patients without diabetes.
Heart Failure Trials
DAPA-HF and EMPEROR-Reduced: These trials studied dapagliflozin and empagliflozin, respectively, in patients with heart failure with reduced ejection fraction (HFrEF). Both showed a remarkable 25-26% relative risk reduction in the composite outcome of cardiovascular death or hospitalization for heart failure, regardless of whether the patients had diabetes.
EMPEROR-Preserved: This was the first trial to show a meaningful benefit in patients with heart failure with preserved ejection fraction (HFpEF), a very common and difficult-to-treat type of heart failure, particularly in older adults, women, and those with obesity. Empagliflozin reduced the primary composite endpoint by 21%.
Kidney Disease Trials
The evidence for kidney protection is just as compelling:
DAPA-CKD (dapagliflozin): This trial was stopped early due to overwhelming efficacy. It showed a 39% reduction in the risk of progression of kidney disease.
EMPA-KIDNEY (empagliflozin): Also demonstrated a significant 28% reduction in the risk of kidney disease progression or cardiovascular death.
CREDENCE (canagliflozin): Showcased a 30% reduction in the risk of kidney failure and cardiovascular events in patients with type 2 diabetes and kidney disease.
These trials have firmly established SGLT2 inhibitors as a cornerstone therapy for chronic kidney disease, even in patients without diabetes.
Understanding the Incretin Effect: TheBody’ss Natural Glucose Response System
For years, the management of type 2 diabetes centered on a few key strategies. However, a fascinating discovery completely shifted our understanding and opened the door to a new class of powerful therapies. Researchers observed a peculiar phenomenon: when people consumed glucose orally (by drinking it), their bodies produced a much more robust insulin response to lower blood sugar than when the same amount of glucose was administered intravenously (IV). This observation led them to a logical conclusion: there must be something happening in the gut when food is ingested that signals the pancreas to ramp up insulin production. This phenomenon was termed the “incretin effect.” The “somethings” responsible were identified as gut hormones called incretins, primarily glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP).
The Process: When you eat, food travels to your stomach and intestines. Specialized cells in your gut (L-cells) detect the presence of nutrients and release GLP-1 and GIP into your bloodstream.
The Signal: These hormones then travel to the pancreas, where they act as messengers. They bind to receptors on pancreatic beta cells, stimulating the cells to release insulin.
The Result: This insulin release helps your body’s cells take up glucose, effectively lowering your blood sugar levels after a meal.
Crucially, this entire process is glucose-dependent. This means the incretins only stimulate insulin release when blood sugar levels are high, as they are after a meal. This built-in safety mechanism significantly reduces the risk of hypoglycemia (dangerously low blood sugar) when these pathways are targeted with medication, especially compared to older diabetes drugs.
The Blunted Incretin Effect in Type 2 Diabetes
One of the key physiological defects we see in patients with type 2 diabetes is a blunted or even absent incretin effect. Their bodies produce insufficient amounts of native GLP-1 in response to food. This deficiency contributes significantly to the hallmarks of the disease:
Poor Post-Meal Glucose Control: Without a strong incretin signal, the pancreas doesn’t release sufficient insulin after eating, resulting in prolonged periods of high blood sugar.
Dysregulated Appetite: Native GLP-1 also plays a critical role in promoting satiety, or the feeling of fullness. Low levels of this hormone can lead to a state of poor satiety, contributing to overeating and the obesity that is so often a comorbid condition with type 2 diabetes.
Excess Glucagon Secretion: GLP-1 normally helps suppress the release of another hormone called glucagon. Glucagon tells the liver to produce and release more sugar into the bloodstream (gluconeogenesis). In type 2 diabetes, this suppression is impaired, so the liver continues to release glucose even when blood glucose is already high.
Understanding this hormonal defect was the key that unlocked the development of GLP-1 receptor agonists—medications designed to mimic the action of our natural GLP-1 and restore these vital functions.
The Silent Threat: Hyperhomocysteinemia and its Impact on Your Health- Video
How GLP-1 Receptor Agonists Revolutionize Treatment
GLP-1 receptor agonists are a class of medications that bind to and activate GLP-1 receptors throughout the body, just as our native GLP-1 would, but they are engineered to last much longer. Their multifaceted mechanism of action addresses several core issues in type 2 diabetes and obesity simultaneously.
Stimulates Insulin Secretion: By activating pancreatic receptors, they prompt a glucose-dependent release of insulin, directly lowering blood sugar.
Inhibits Glucagon Secretion: They effectively tell the liver to stop producing excess sugar, which is a major contributor to high fasting and post-meal glucose levels.
Slows Gastric Emptying: This is a key mechanism for both glucose control and weight loss. By slowing down the rate at which food leaves the stomach, they prevent rapid spikes in blood sugar after meals. This delay also contributes to a prolonged feeling of fullness, which naturally leads to a decrease in overall food intake. This effect is often responsible for the common initial side effects like nausea, but it is also a primary driver of the medication’s success.
Increases Satiety: GLP-1 receptor agonists act directly on appetite centers in the brain, enhancing the feeling of fullness and reducing food cravings. This neurobiological effect is fundamental to the significant weight loss seen with these therapies.
Collectively, these actions lead to profound improvements in A1c, blood glucose, and body weight, tackling the metabolic dysfunction of type 2 diabetes at its source.
The Challenge of Over-Basalization: A Case Study
To truly understand the paradigm shift in diabetes care,let’ss consider a typical patient I might see in our clinic, whom we’ll call Tony. He represents a common challenge where adding a GLP-1 agonist is the superior strategy.
Patient Profile: Tony
Age: 62 years
Diagnosis: Type 2 Diabetes (11 years), Hyperlipidemia, Hypertension
Recent A1c: 8.2% (well above the target of <7.0%)
Kidney Health: Proteinuria (protein in the urine), an early sign of kidney damage.
Tony’s case highlights a critical issue we call over-basalization. We’ve pushed his basal (long-acting) insulin dose to a high level, yet his A1c and post-meal sugars remain dangerously elevated. Research in pharmacokinetics reveals that once you exceed a certain dose of basal insulin, typically around 0.5 units per kilogram of body weight per day, you get diminishing returns. For Tony, who weighs 100 kg (220 lbs), this threshold is about 50 units. He is already on 65 units, pushing him past the point of modest glycemic effect and into the territory of significant side effects, primarily weight gain and a higher risk of hypoglycemia. For a patient like Tony, the conventional next step might have been to add prandial (mealtime) insulin. While this can control post-meal spikes, it comes with a heavy price: a near-certainty of further weight gain and a significantly increased risk of hypoglycemia. Given his BMI of 32.5, adding more weight would only worsen his insulin resistance, creating a vicious cycle. This is where the 2024 guidelines from the American Diabetes Association (ADA) strongly recommend adding a GLP-1 receptor agonist. It addresses multiple problems at once, moving beyond simple glucose lowering, weight loss, and cardiovascular protection, which are crucial for a high-risk patient like Tony.
Beyond Blood Sugar: The Cardiovascular and Renal Benefits of GLP-1s
Perhaps the most exciting development in the story of GLP-1 agonists is the overwhelming evidence of their protective effects on the heart and kidneys. Several landmark trials have established these powerful benefits:
The LEADER Trial (Liraglutide): This trial studied patients with type 2 diabetes and high cardiovascular risk. It showed a significant reduction in the risk of major adverse cardiovascular events (MACE), including cardiovascular death, non-fatal heart attack, and non-fatal stroke.
The SUSTAIN-6 and PIONEER 6 Trials (Semaglutide): Both the injectable (SUSTAIN-6) and oral (PIONEER 6) forms of semaglutide were studied in patients with high cardiovascular risk. Both trials demonstrated a robust reduction in MACE, confirming the class effect.
The REWIND Trial (Dulaglutide): What made this trial unique was its focus on a broader population, including many patients who had risk factors for cardiovascular disease but had not yet had an event. It demonstrated that dulaglutide can be used for primary prevention, reducing the risk of a first cardiovascular event.
Tirzepatide (Mounjaro®, Zepbound™): This is a newer, highly potent dual GIP/GLP-1 receptor agonist. While its final CVOTs are still pending as of June 15, 2026, preliminary data suggest powerful cardiovascular benefits are likely.
More recently, the FLOW trial for semaglutide was stopped early because of overwhelmingly positive results showing a significant reduction in the risk of kidney disease progression (nephropathy). These findings are game-changers, solidifying the role of GLP-1 agonists as essential therapies for patients with or at high risk for heart and kidney disease.
Navigating Side Effects and Safety Considerations of GLP-1 Agonists
As with any potent medication, GLP-1 agonists are not without side effects. As clinicians, our job is to help patients navigate these challenges.
Gastrointestinal (GI) Issues: Nausea, vomiting, and diarrhea are common and caused by delayed gastric emptying. My clinical advice is always to “start low and go slow,” beginning with the lowest dose and titrating upwards gradually.
Dehydration and Acute Kidney Injury (AKI): Patients on these medications must drink plenty of water to prevent dehydration due to GI side effects.
Gallbladder Disease: Rapid weight loss, regardless of the method, is associated with an increased risk of gallstone formation.
Pancreatitis: Recent large-scale studies as of early 2025 have been reassuring, finding no statistically significant increase in the risk of pancreatitis and even suggesting a potential long-term risk reduction by improving metabolic health.
Thyroid C-Cell Tumors: These medications carry a black box warning due to an increased risk of thyroid C-cell tumors in rodents. They are contraindicated in patients with a personal or family history of medullary thyroid carcinoma (MTC) or Multiple Endocrine Neoplasia syndrome type 2 (MEN 2).
Muscle and Bone Loss: This is a feature of significant weight loss in general, not something specific to these drugs. This is where our integrative care becomes critical.
An Integrative Chiropractic Perspective on Metabolic Health
As a Doctor of Chiropractic with advanced training in functional medicine, I view the body as an integrated system. When I see a patient, I don’t just see a person with diabetes and heart disease. I see a complex interplay of systemic inflammation, metabolic dysfunction, and biomechanical stress. This is where our unique approach at Injury Medical Clinic PA provides immense value. The side effects and physiological changes associated with modern diabetes therapies are whole-body issues we can address. Here’s how integrative chiropractic care fits into this new paradigm:
Addressing Systemic Inflammation: Chronic inflammation is a root cause of both ASCVD and insulin resistance. Chiropractic adjustments have been shown to modulate the nervous system and can have a downstream effect on inflammatory pathways. By reducing spinal misalignments (subluxations), we can help normalize nerve function, which in turn influences the body’s inflammatory response.
Promoting Physical Activity and Combating Muscle Loss: Exercise is a critical component of managing diabetes. However, many patients are limited by musculoskeletal pain. As chiropractors, our primary role is to improve biomechanical function, reduce pain, and restore mobility. Furthermore, with the rapid weight loss induced by GLP-1s, there is a risk of sarcopenia (muscle loss). We implement targeted strength training and rehabilitation protocols to preserve and build lean muscle mass. By treating underlying musculoskeletal issues, we empower patients to engage in the physical activity necessary for their metabolic health.
Functional Medicine and Nutritional Counseling: My training as a Certified Functional Medicine Practitioner (CFMP) allows us to go deeper. We create personalized nutrition plans and recommend targeted supplementation to reduce inflammation, improve insulin sensitivity, and support cardiovascular health. To combat muscle loss, we ensure patients consume adequate protein to support muscle synthesis. This complements the work of medications by addressing the foundational lifestyle factors that drive disease.
Stress Management and Autonomic Balance: The autonomic nervous system plays a huge role in regulating blood pressure, heart rate, and metabolic function. Chronic stress leads to a state of sympathetic (“fight-or-flight”) dominance, which can worsen hypertension and insulin resistance. Chiropractic care, along with techniques like breathwork and meditation, helps promote a parasympathetic (“rest-and-digest”) state, supporting better cardiovascular and metabolic regulation.
In our clinic, a patient would receive a comprehensive plan. Under the medical direction of Dr. Cardenas, they might be started on an SGLT2 inhibitor or a GLP-1 agonist. Simultaneously, my team would work with them on a personalized plan including chiropractic adjustments to improve mobility, an anti-inflammatory diet, and a progressive exercise program they can perform without pain. This integrated approach addresses the disease from multiple angles, leading to far better and more sustainable outcomes. This is the future of chronic disease management—a holistic, patient-centered, and team-based model of care.
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Understand the effects of obesity and diabetes on overall wellness and take steps towards improvement in your metabolic health.
Abstract
Hello, I’m Dr. Alex Jimenez. In this educational post, we will embark on a comprehensive journey to understand the intricate and often overlapping physiological pathways of obesity, type 2 diabetes, and cardiovascular disease. I will present a patient-centered, first-person narrative describing how I approach these conditions through an integrative lens that blends chiropractic care, functional medicine, medical oversight, and rehabilitation. Drawing on the latest evidence-based research from leading experts, we will explore why treating obesity is not a matter of willpower but of addressing deep-seated biological dysregulation. We will delve into how inflammation, insulin resistance, and hormonal imbalances form a common pathological foundation for these chronic conditions. This discussion will highlight how modern pharmacotherapy targets these underlying mechanisms and why a chronic disease management model is essential for long-term success. Furthermore, I will explain how our unique multidisciplinary practice at Injury Medical Clinic PA integrates my chiropractic and functional medicine care with medical direction from our collaborative physician to provide a holistic and powerful treatment strategy for patients grappling with these complex cardiometabolic issues. We will break down the science, examine treatment guidelines, and illustrate how a synergistic approach, through real-world patient scenarios, can lead to profound improvements in health and quality of life.
Our Integrative Team: A Multidisciplinary Powerhouse
At Injury Medical Clinic PA, also known as Mission Plaza Injury Medical Clinic, in El Paso, Texas, our philosophy is rooted in collaboration and integration. We believe that the most effective patient care comes from combining the strengths of different medical disciplines. I am Dr. Alexander Jimenez, and my credentials as a Doctor of Chiropractic (DC), Advanced Practice Registered Nurse (APRN), board-certified Family Nurse Practitioner (FNP-BC), and advanced certifications in Functional Medicine (CFMP, IFMCP, ATN, CCST) allow me to view patient health through a multifaceted lens. My focus is on the structural, neurological, and functional aspects of wellness.
A cornerstone of our practice is our collaboration with Dr. Maria Guadalupe Cardenas, MD. Dr. Cardenas is Board Certified in Internal Medicine with an impressive 40 years of experience (NPI #1164426749, Texas MD License #J2933). She serves as our Medical Director and Collaborative Physician, providing invaluable medical oversight, ensuring our protocols are evidence-based, and offering a deep understanding of internal medicine. This partnership between a chiropractor and an internist allows us to create a truly comprehensive care model, which is a standard and effective setup in integrative and injury care clinics.
Our team works in synergy to address the full spectrum of a patient’s needs. Here’s how our services fit together:
Medical Oversight (Dr. Cardenas, MD): Dr. Cardenas guides our medical protocols, confirms diagnoses, manages complex internal medicine conditions, reviews contraindications, and provides the necessary supervision for prescription therapies and advanced medical interventions. Her extensive experience is crucial for diagnosing and treating systemic diseases that often accompany musculoskeletal issues, such as diabetes and cardiovascular disease.
Chiropractic & Functional Medicine (Dr. Jimenez, DC, APRN, FNP-BC): I focus on restoring the body’s natural function. Through chiropractic adjustments, we can improve nervous system function, reduce pain, and enhance mobility. This is particularly important for patients with obesity, as pain can be a major barrier to physical activity. Through functional medicine, we dive deep to identify the root causes of dysfunction—be it gut dysbiosis, hormonal imbalances, or nutrient deficiencies—and create personalized plans involving nutrition, supplementation, and lifestyle changes to restore health from the inside out.
Rehabilitation & Personal Injury Care: Our team also includes specialists in physical rehabilitation who help patients recover from injuries and improve their functional capacity. This is a critical component of managing obesity, as structured exercise programs are essential for building muscle, improving metabolism, and supporting weight loss.
By integrating these disciplines, we don’t just treat symptoms; we treat the whole person. We address the structural, biochemical, and medical aspects of health simultaneously, providing a level of care far more effective than any single approach could be.
Understanding the Roots of Cardiometabolic Disease
In my clinical practice, we frequently manage conditions like dyslipidemia (abnormal blood fats), hypertension (high blood pressure), and various metabolic disorders. For decades, we have had a wide array of medications to manage the symptoms of these diseases. However, a crucial understanding has emerged from modern research: in many cases, obesity is the underlying root cause of these interconnected health problems.
Imagine a tree. The branches and leaves—the visible parts—are the diseases we commonly treat, such as heart disease, diabetes, and high blood pressure. But the roots, hidden beneath the surface, represent the foundational issue of obesity. These are the obesity-related complications and comorbidities that drive the majority of chronic diseases we face today.
The Misconception of Willpower: Obesity Causes Overeating
The human body possesses remarkably resilient, tightly regulated systems. If you become dehydrated, your kidneys conserve water, and you feel thirsty, prompting you to drink. In the same way, body weight is meant to be tightly regulated. However, in obesity, this regulatory system becomes dysfunctional. A groundbreaking shift in our understanding is this: Overeating doesn’t cause obesity; obesity causes overeating. Before a noticeable increase in fat mass (adiposity) occurs, a dysregulation of the endocrine system is already underway.
The First Hit: Hormonal Dysregulation
The process begins when something—be it genetics, environmental factors, or obesogenic medications—triggers the “on” switch for obesity. Once activated, the body’s production of hunger hormones (like ghrelin) increases, while the production of satiety hormones (like leptin and GLP-1) decreases. This creates a powerful biological drive for increased hunger and food intake.
The Second Hit: The Brain Defends a Higher Weight
The second, and perhaps more insidious, part of this pathology is that the brain begins to defend this new, higher body weight as its “normal.” This is the biological reality behind the frustrating cycle of weight regain. We now know it’s a consequence of dysregulated biology. The leading hypothesis is that this defense mechanism arises from inflammation in the hypothalamus, the brain’s control center for appetite and energy expenditure.
Obesity is an incredibly multifactorial disease, influenced by over 200 genes, endocrine-disrupting chemicals, poor sleep, and chronic stress.
The Pathophysiological Overlap of Diabetes and Heart Disease
To truly appreciate the interconnected nature of these conditions, let’s look at the underlying biology of each.
The Progression of Type 2 Diabetes
The pathophysiology of type 2 diabetes unfolds over years, beginning with insulin resistance, where cells become less responsive to insulin. To compensate, the pancreatic beta cells work overtime, producing more insulin. Eventually, these cells become exhausted, leading to impaired insulin secretion and elevated blood sugar (hyperglycemia), a condition known as prediabetes. As function declines further, type 2 diabetes is diagnosed. Beyond the pancreas, diabetes involves chronic inflammation, gut dysbiosis, and mitochondrial dysfunction, which contribute to “metabolic memory,” perpetuating the disease.
The Inflammatory Core of Cardiovascular Disease
Cardiovascular disease shares a similar common denominator: atherosclerosis, the buildup of plaque in the arteries, which is fundamentally driven by inflammation. A key player is nitric oxide (NO), a critical molecule that promotes vasodilation (widening of blood vessels) and reduces inflammation. In cardiovascular disease, nitric oxide availability decreases, leading to increased blood clotting, rampant inflammation, and endothelial dysfunction (damage to blood vessel linings). Metabolically, this leads to decreased glucose tolerance, elevated triglycerides, and increased oxidative stress.
The Unifying Theory: Inflammation, Lipotoxicity, and Mitochondrial Dysfunction
A clear picture emerges when we put it all together. The journey often begins with obesity, which fosters chronic inflammation and lipotoxicity (cellular damage from excess fats). This environment leads to mitochondrial dysfunction, impairing cellular energy production. This trifecta—inflammation, lipotoxicity, and mitochondrial dysfunction—creates a vicious cycle, driving the progression of obesity, insulin resistance, type 2 diabetes, and ultimately, cardiovascular disease.
Patient Journey: Stephen’s Case and Early Intervention for Prediabetes
To illustrate these concepts, let’s look at a patient I’ll call Stephen. His journey highlights how we apply this integrative model in practice.
Case Introduction and Risk Profile
Stephen is a 24-year-old male who sees me for follow-up regarding prediabetes and weight management. His A1C is 5.8%. He has a history of progressive weight gain, reaching a current weight of 250 lb with a BMI of 32.1 (class I obesity). His family history is significant for obesity, cardiovascular disease, and type 2 diabetes. His exam reveals central adiposity with a waist circumference of 41 inches, acanthosis nigricans, and skin tags, all signs of chronic hyperinsulinemia and insulin resistance.
From a physiological standpoint, Stephen exhibits a classic metabolic phenotype driven by:
Visceral adiposity: Central fat secretes pro-inflammatory adipokines and reduces adiponectin, impairing insulin sensitivity.
Hepatic insulin resistance: Increased liver glucose production and dyslipidemia, increasing his risk of metabolic dysfunction-associated steatotic liver disease (MASLD).
Endocrine signals: Altered leptin signaling and dysregulated GLP-1/GIP pathways that reduce satiety.
Biomechanics: Excess abdominal load increases lumbar lordosis and knee strain, areas where chiropractic integrative care can provide structural relief.
Evidence-Based Weight Loss Targets: Why Percentages Matter
I explained to Stephen that targeted weight-loss thresholds can dramatically change his health trajectory:
3% weight loss: Measurable improvements in prediabetes and insulin sensitivity.
10% weight loss: Robust changes in glucose control, lipids, and blood pressure.
15%+ weight loss: Meaningful impact on type 2 diabetes, dyslipidemia, hypertension, sleep apnea, and MASLD.
Reducing adipose tissue lowers inflammatory cytokines, restores hormonal balance, and improves insulin signaling. These targets guide our decision on whether to use lifestyle changes alone or incorporate anti-obesity pharmacotherapy.
Patient Journey: Victoria – The Intersection of Menopause, Weight Gain, and Diabetes
Now, let’s explore a case representative of what many women experience during menopause.
Initial Presentation and History
Victoria, a 52-year-old woman, came to my clinic for a follow-up on her prediabetes and recent weight gain. She had recently entered menopause and gained 15 pounds in the past year. Her job is largely sedentary, her activity level has decreased, and she suffers from poor sleep due to night sweats.
Key Clinical Details:
BMI: 31.8 (class 1 obesity)
Fat Distribution: Central adiposity, with a neck circumference of 16 inches, a risk factor for sleep apnea.
Symptoms: Hot flashes, snoring, and high stress.
The Menopausal Transition and Metabolic Disruption
Victoria’s case is a classic example of the metabolic storm that accompanies menopause. The decline in estradiol leads to a rise in LDL cholesterol, decreased insulin sensitivity, a shift toward increased body fat, and endothelial dysfunction. These changes amplify cardiovascular risk. Fortunately, menopause hormone therapy (MHT) can mitigate many of these risks.
Laboratory Findings and Diagnosis
Victoria’s lab work confirmed our concerns. Her HbA1c had risen to 7.3%, diagnosing her with type 2 diabetes. Her HOMA-IR score, a measure of insulin resistance, was 4.7, indicating significant dysfunction.
Crafting a Patient-Centered Treatment Plan
Using a shared decision-making model, I asked Victoria, “What area would you like to target first?” She chose to try a higher dose of metformin and was intrigued by the idea of using a Continuous Glucose Monitor (CGM). The CGM provides invaluable real-time feedback that drives positive behavior changes. We also referred her to a menopause specialist.
When Victoria returned, her CGM data was eye-opening. Her average glucose was 173 mg/dL, and she was spending 34% of her time in hyperglycemia. Armed with this new insight, she committed to increasing her metformin, boosting protein intake, and eliminating sugar-sweetened beverages. A month later, after starting MHT, her sleep and hot flashes improved, but her weight loss was slow. At this point, I introduced semaglutide, a GLP-1 receptor agonist. One year later, she had lost 25 pounds, her BMI dropped from 31.8 to 27.5, and her metabolic markers improved dramatically. By treating her obesity, we achieved remission of her diabetes.
Patient Journey: Banny – Addressing Long-Standing Diabetes and Cardiovascular Risk
Our next case involves Banny, a 64-year-old man with a long and complex medical history, including type 2 diabetes for 25 years, hypertension, and a previous heart attack. His weight was 230 lbs (BMI of 36), and he struggled with food cravings and uncontrolled blood pressure.
The “5 C’s” of Obesity Treatment
When evaluating Banny, I used my “5 C’s” framework: Criteria, Contraindications, Combine, Cues/Causes, and Cost/Coverage. His history of cardiovascular disease made him a prime candidate for a GLP-1 receptor agonist like semaglutide, which has been shown to reduce the risk of major adverse cardiovascular events. I framed it as a way to not only manage his diabetes and weight but also reduce his risk for a second heart attack. He was immediately on board.
Uncovering Hidden Liver Disease
Banny’s labs showed a slightly elevated liver enzyme (ALT), prompting me to calculate his FIB-4 score, a non-invasive screen for liver fibrosis. His score of 2.25 placed him at high risk. This is critical, as up to 65% of people with type 2 diabetes have Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD). I referred him to a gastroenterologist for further evaluation.
One year later, Banny had lost 23 pounds, and his HbA1c improved to 5.9%. He was diagnosed with liver fibrosis and started on a new medication. However, his weight loss had plateaued, and he struggled with intense food cravings. To address this, we added a low dose of topiramate at night to help control cravings, demonstrating a multi-pronged approach to modern obesity management.
Chiropractic Care & Metabolism *The Hidden Link*- Video
A Unified Approach to Treatment: Beyond “Eat Less, Move More”
The treatment guidelines for obesity, diabetes, and cardiovascular disease share a common foundation: a healthy eating plan, increased physical activity, and behavioral interventions. For diabetes and heart disease, we readily use medications, yet for obesity, there’s a misguided notion that patients must first “fail” lifestyle changes. This ignores the biological reality of the disease, where metabolic adaptation fiercely defends a higher body weight. Medications for obesity directly counteract the pathological hormonal and neurological changes driving the disease.
For patients like Stephen, we design a sustainable, enjoyable nutrition plan. This includes:
Caloric reduction: A deficit of 500- 750 kcal daily.
Carbohydrate management: Moderating refined carbs to improve insulin signaling.
Protein prioritization: To support satiety, thermogenesis, and muscle retention.
Fiber and non-starchy vegetables: To improve glycemic control and gut microbiome diversity.
Behavioral Health Strategy: Sleep, Stress, and Mood
Chronic stress and poor sleep worsen insulin resistance and weight gain by increasing cortisol and altering ghrelin and leptin levels. We screen for and address stress, mood, and sleep disorders, such as sleep apnea.
Physical Activity: Graded Movement and Functional Capacity
I provide evidence-based recommendations, such as 150-300 minutes/week of moderate-intensity activity and resistance training at least two days a week. For patients with pain, we incorporate referrals to physical and occupational therapy.
The Role of Modern Medications
The advent of GLP-1 receptor agonists (like liraglutide and semaglutide) and dual GIP/GLP-1 agonists (like tirzepatide) has been a game-changer. These medications mimic the body’s natural satiety hormones, helping patients achieve an average weight loss of 15-20% or more. Excitingly, many of these newer drugs, along with SGLT-2 inhibitors, have demonstrated significant cardiovascular benefits.
Recent multi-year research on tirzepatide has shown it can sustain a diabetes-free status in adults with prediabetes and deliver high-magnitude weight loss. For Stephen, after reviewing his options, we selected tirzepatide, starting at 2.5 mg weekly and titrating up. Two weeks later, he had lost 3 lbs. At one year, after reaching a 15 mg weekly dose, he had lost 50 lbs, his A1C was 5.4%, and his BMI dropped to 25.7.
An important part of my job is also avoiding obesogenic medications—drugs like certain sulfonylureas, insulins, and beta-blockers that can cause weight gain.
Chiropractic Integration: How Structural Care Supports Metabolic Therapy
While pharmacological and lifestyle interventions are central, integrative chiropractic care is a foundational element of our holistic approach.
Stress Reduction and Nervous System Regulation: Chronic stress is a major driver of metabolic dysfunction. My clinical observations show that patients with central obesity often develop thoracolumbar junction stiffness. Chiropractic adjustments can influence the autonomic nervous system, helping to shift the body from a “fight-or-flight” (sympathetic) state to a “rest-and-digest” (parasympathetic) state. This modulation can lower physiological stress, supporting better glycemic control (Jimenez, n.d.-a).
Improving Mobility and Reducing Pain: For patients like Stephen, Victoria, and Banny, joint pain and stiffness can be significant barriers to physical activity. By performing spinal and extremity adjustments, we can improve joint function, reduce pain, and make it easier for patients to engage in regular exercise. This facilitates adherence to activity prescriptions.
Optimizing Biomechanics: Correcting thoracolumbar junction dysfunction and sacroiliac joint mechanics can improve gait efficiency and reduce the energy cost of movement, making it easier for patients to increase their daily steps (Jimenez, n.d.-b).
Enhancing Sleep Quality: Alleviating neck and upper back tension can support airway mechanics and reduce nocturnal discomfort, which, in my clinical experience, can improve morning glucose stability.
The Chronic Disease Model: Why Treatment Must Be Long-Term
I want to end by reinforcing the most crucial concept: obesity is a chronic, relapsing disease that requires long-term management. The pathology of weight regain is a biological certainty, not a personal failing. When a person with obesity loses weight, the brain initiates a powerful counter-response: metabolism slows down, hunger hormones surge, and satiety hormones decrease. This creates an overwhelming drive to regain weight.
The STEP 1 trial extension starkly illustrates this: when participants stopped taking semaglutide, they began regaining weight, and their blood pressure and A1C levels started to creep back up (Wilding et al., 2022). We must apply the same chronic care model to obesity that we use for hypertension or diabetes. The goal is sustainable, long-term management to control the disease and prevent its devastating complications.
At Injury Medical Clinic, this philosophy guides us. By integrating chiropractic care to restore function, functional medicine to address root causes, and medical oversight from Dr. Cardenas to leverage the best of modern pharmacotherapy, we provide our patients with the comprehensive, long-term support they need to conquer these interconnected diseases and reclaim their health.
SEO Tags: Obesity Treatment, Type 2 Diabetes, Prediabetes Management, Cardiovascular Disease, Integrative Care, Chiropractic, Functional Medicine, Tirzepatide, GLP-1 GIP Agonists, Dr. Alex Jimenez, Dr. Maria Cardenas, El Paso Clinic, Injury Medical Clinic PA, Mission Plaza Injury Medical Clinic, Inflammation, Insulin Resistance, Metabolic Adaptation, Weight Regain, Cardiometabolic Health, Chronic Disease Management, Atherosclerosis, Nitric Oxide, Pharmacotherapy, Menopause and Weight Gain, Continuous Glucose Monitor, Semaglutide
How Dysbiosis Starts, How to Rebalance, and How Integrative Care Supports Recovery
Your gut holds trillions of microbes that help break down food, protect your gut lining, train your immune system, and even influence mood and energy. When helpful and harmful microbes fall out of balance—too many “unhelpful” species and not enough “helpful” ones—you get dysbiosis. Dysbiosis can look like gas, bloating, irregular stools, food sensitivities, skin changes, fatigue, or brain fog. The important part: your daily choices and your care plan can push the gut back toward balance. (Penn State Health, 2018; Cleveland Clinic, 2022). (Penn State Health News)
This article keeps things simple and actionable. You’ll learn how and why dysbiosis starts, how specific habits can fix it, and how an integrative chiro-medical team can connect gut health with musculoskeletal recovery, stress care, and, when needed, imaging and documentation.
Dysbiosis in Plain Language
Dysbiosis means the gut ecosystem is out of balance. That can be too many of certain microbes, not enough of others, or lower overall diversity. Diets high in sugar and ultra-processed foods, repeated antibiotics, alcohol and toxins, stress, and short sleep can all nudge the gut in the wrong direction. (Cleveland Clinic, 2024; Better Health Channel, 2023; USDA ARS, 2025). (Cleveland Clinic)
Think of the gut like a garden. Fiber-rich plants feed “good” bacteria, helping them grow and produce protective compounds. Ultra-processed foods are like empty soil—little to no fiber—and may include additives that disturb the gut barrier. Antibiotics (essential when needed) can clear infections but also sweep away helpful species, opening space for invasive strains until balance is restored. Stress and sleep loss tilt the brain–gut axis toward poor motility and inflammation. (Healthline, n.d.; Cleveland Clinic, 2023; Cleveland Clinic, 2024). (Healthline)
SIBO: A Special Case of Dysbiosis
Small Intestinal Bacterial Overgrowth (SIBO) happens when bacteria overgrow in the small intestine—a place that normally carries far fewer microbes. SIBO can cause bloating, fullness after meals, diarrhea, weight loss, and nutrient problems. The usual care includes treating the root cause (like slow motility, adhesions, or structural loops), correcting nutrition gaps, and using targeted antibiotics when appropriate. (Mayo Clinic, 2024a; Mayo Clinic, 2024b). (Mayo Clinic)
SIBO often recurs if the underlying driver isn’t addressed. That’s why an organized plan (nutrition + motility support + follow-ups) matters. Breath testing can help, but it has limits; clinicians weigh test results with symptoms and history. (Mayo Clinic Professionals, 2024). (Mayo Clinic)
How “Bad” Bacteria Gain Ground
Unhealthy bacteria flourish when the environment favors them. Three common patterns:
Fiber-poor, ultra-processed diets Helpful microbes eat plant fibers and resistant starches from beans, whole grains, fruits, and vegetables. When meals lack fiber and rely on refined flours, added sugars, and certain additives, beneficial species starve while opportunistic ones thrive. (Cleveland Clinic, 2023; Nova, 2022). (Cleveland Clinic)
Antibiotics and antimicrobial exposure Antibiotics can be lifesaving. They also reduce helpful species. During recovery, “unhelpful” species can take over unless you rebuild the ecosystem with food-based fiber and, in some cases, probiotics. (Cleveland Clinic, 2024). (Cleveland Clinic)
Stress and sleep loss Chronic stress and short sleep change motility, increase gut permeability, and alter immune signals, pushing the biome toward imbalance. (Cleveland Clinic, 2022; Better Health Channel, 2023). (Cleveland Clinic)
What the Science Says (Quick Tour)
Diet is powerful. Changes in what you eat can shift the microbiome’s makeup and activity—sometimes within days. Diverse plants and resistant starches support short-chain fatty acids (SCFAs) like butyrate, which help protect your gut lining. (Singh et al., 2017; Nova, 2022; Washington Post, 2025). (PMC)
Fermented foods help many people. Yogurt with live cultures, kefir, kimchi, and sauerkraut can increase microbial diversity. Not all fermented foods contain live microbes (e.g., some breads and beers), so check labels for “live and active cultures.” (Cleveland Clinic Magazine, 2023; Health.com, 2025). (magazine.clevelandclinic.org)
Small steps add up. Simple upgrades—more plants, fewer ultra-processed foods, steady sleep—can move digestion and comfort in the right direction. (Penn State Health, 2018). (Penn State Health News)
A Chiromed-Style Gut-Reset You Can Start This Week
Goal: build a friendlier environment for helpful microbes and a calmer gut-brain axis. Keep it simple and repeatable.
1) Plant-Forward, Not Perfect
Aim for 4–6 cups of colorful vegetables and fruit most days.
Include beans or lentils at least 4 days/week.
Choose whole grains like oats, barley, quinoa, and brown rice. These foods feed microbes that make SCFAs, which help calm inflammation and seal the gut lining. (Nova, 2022; Washington Post, 2025). (PMC)
2) Fermented Food “Starter Pack”
Daily yogurt or kefir with live cultures.
Kimchi or sauerkraut as a spoonful on bowls, tacos, or salads.
Optional kombucha (watch added sugar). Look for “live and active cultures.” (Cleveland Clinic Magazine, 2023; Health.com, 2025). (magazine.clevelandclinic.org)
3) Swap the Usual Suspects
Replace sugary drinks with water or unsweetened tea.
Swap white bread/treats for whole-grain options.
Keep ultra-processed snacks for rare treats, not daily habits. These swaps support diversity and reduce the additives and refined sugars that disadvantage helpful microbes. (Cleveland Clinic, 2023). (Cleveland Clinic)
4) Stress & Sleep—The Hidden Drivers
Walk 20–30 minutes most days; add 2 short strength sessions weekly.
Breathe: 4–6 slow breaths/min for 5 minutes, especially before bed.
Sleep: target 7–9 hours with a consistent wind-down. Stress and sleep shape motility and the gut barrier, which are key to lasting results. (Cleveland Clinic, 2022; Better Health Channel, 2023). (Cleveland Clinic)
5) Medications—Partner With Your Clinician
If you need antibiotics or other meds that affect the gut, do not stop them on your own. Ask about food-first strategies (fiber, fermented foods) and whether a probiotic is reasonable in your case. (Cleveland Clinic, 2024). (Cleveland Clinic)
6) Hygiene Basics Still Matter
Wash hands, rinse produce, and avoid cross-contamination in the kitchen to lower exposure to harmful bacteria. (Better Health Channel, 2023). (Better Health Channel)
What If You Suspect SIBO?
Talk with your clinician if you have persistent bloating, abdominal pain, diarrhea, unintended weight loss, or symptoms that wake you from sleep. Testing and treatment are individualized. If SIBO is confirmed, nutrition is often phased: address overgrowth and root causes first, then gradually re-expand fiber and fermented foods under guidance to support a resilient microbiome. (Mayo Clinic, 2024a; 2024b). (Mayo Clinic)
Where Chiropractic and Medical Care Fit (The Chiro-Med Advantage)
Many Chiromed readers also deal with neck or back pain, sports strains, work injuries, or motor-vehicle accidents (MVAs). Pain, poor sleep, and high stress can worsen gut symptoms through the brain–gut axis. A coordinated chiro-medical model can address both fronts at the same time.
1) Dual-Scope Assessment and Imaging (When Indicated)
A combined clinical exam can separate joint, nerve, and soft-tissue drivers of pain. When needed, X-ray or MRI helps confirm the picture so your plan is safe and specific. (Jimenez Clinic Site; A4M profile). (El Paso, TX Doctor Of Chiropractic)
2) Conservative Therapies That Calm the System
Spinal adjustments to improve joint motion and ease nerve irritation.
Targeted exercise therapy to restore mobility and strength.
Massage therapy for soft-tissue pain, circulation, and relaxation.
Acupuncture (when available) for pain relief and stress reduction. These approaches can reduce pain and nervous-system “overdrive,” which often helps gut comfort too. (Sciatica.clinic articles, 2025). (sciatica.clinic)
3) Nutrition & Lifestyle Coaching Built Into Care
An integrated team can translate gut-friendly science into your reality—food swaps, stress skills, and sleep routines that fit busy schedules. The focus is on small wins that add up. (Penn State Health, 2018; Cleveland Clinic, 2022). (Penn State Health News)
4) Injury Documentation and Care Coordination
For work injuries or MVAs, you may need clear medical records, imaging reports, and functional assessments. An integrated clinic can coordinate your care and provide the documentation insurers and legal teams request, while keeping your recovery plan unified. (Jimenez Clinic Site; Scheduler). (El Paso, TX Doctor Of Chiropractic)
Clinical observation (Jimenez): Patients with spine pain and poor sleep often report IBS-like flares. When we combine adjustments or mobilization with gradual activity, breath work, and a simple plant-forward plan (plus one fermented food daily), reports of bloating and meal-related discomfort tend to drop—especially as sleep improves. (Jimenez Clinic Site). (El Paso, TX Doctor Of Chiropractic)
Sample 2-Week “Ease-In” Plan
Week 1: Foundations
Breakfast: Oats with yogurt or kefir, berries, and nuts.
Lunch: Grain bowl (quinoa or barley) + beans + mixed veggies; add a spoon of sauerkraut/kimchi.
Dinner: Chili or lentil curry + salad with olive oil.
Daily: 20–30 min walk, 5-minute breathing before bed, lights-out window set.
Limit: one ultra-processed snack per day, max.
Week 2: Build
Add beans/lentils 5 days/week.
Add a second fermented food for two days.
Replace one sweet drink with water or tea each day.
Add two short strength sessions (15–20 minutes).
Keep a simple symptom log (bloating, energy, stools, sleep).
Small steps, big difference over time. (Penn State Health, 2018). (Penn State Health News)
When to Seek Care Promptly
Unintended weight loss, blood in stool, fever, severe or night-time symptoms, or a history of GI surgery.
Persistent pain and gut complaints despite steady changes. Talk with your clinician; ask about testing, SIBO evaluation, and tailored treatment. (Mayo Clinic, 2024a). (Mayo Clinic)
Key Takeaways for Chiromed Readers
Dysbiosis is common and usually fixable with realistic habit changes.
A plant-forward pattern, along with live-culture foods, stress management skills, and better sleep, can steady the gut and the nervous system.
When injuries, pain, or SIBO are part of the picture, a coordinated chiro-medical team can blend diagnostics, hands-on care, lifestyle coaching, and documentation—so your gut and your musculoskeletal system improve together. (Cleveland Clinic, 2022; Jimenez Clinic Site). (Cleveland Clinic)
Peripheral neuropathy refers to the irritation or damage of nerves outside the brain and spinal cord. Common signs include tingling, burning pain, numbness, sensitivity to cold or heat, weakness, cramping, and balance issues. Causes vary: diabetes and prediabetes, spine or joint compression (pinched nerves), vitamin deficiencies, medication effects (including some chemo drugs), autoimmune conditions, infections, alcohol overuse, and trauma from work, sports, or car crashes.
Why this matters: Two people can both have “neuropathy,” but they need very different treatment plans. The first step is a careful assessment to identify likely drivers and eliminate potential red flags.
Can chiropractic care cure neuropathy?
No. Most cases of neuropathy are not “curable.” However, when combined with active rehabilitation and smart medical co-management, chiropractic care can often reduce symptoms, improve mobility, enhance balance, and support daily functioning. The goal is to alleviate mechanical irritation, enhance joint mobility, and promote safer patterns—while medical teams address glucose control, medication issues, wound care, and other systemic factors.
How a ChiroMed-style program helps
A modern chiropractic program doesn’t rely on one tool. It blends gentle hands-on care with progressive exercise and lifestyle support:
Low-force spinal and extremity adjustments to restore motion and reduce local nerve stress.
Soft-tissue therapy (myofascial techniques, instrument-assisted work) to ease guarding and improve circulation.
Nerve mobility drills (nerve glides) to reduce sensitivity where appropriate.
Traction/decompression for select patients with disc or foraminal narrowing.
Balance, gait, and strength training to lower fall risk and protect joints.
Lifestyle coaching on sleep, stress, ergonomics, and foot care; nutrition support coordinated with your medical team.
Acupuncture or electro-acupuncture in clinics that offer it, to modulate pain and sensitivity.
Safety first (and always)
Chiropractic care is generally low-risk when delivered after a thorough interview and physical examination. Your clinician should screen for red flags, adapt techniques to account for bone density and age, adjust for diabetes or chemotherapy history, and co-manage with your primary-care clinician, neurologist, endocrinologist, podiatrist, or pain specialist when necessary.
Call your medical team or urgent care first if you develop:
sudden severe weakness or paralysis
bowel or bladder changes, groin numbness
rapidly worsening numbness with foot wounds or infection
unexplained fever, night pain, or weight loss
cancer history with new bone pain
How chiropractic integrates with traditional medicine
Think team sport.
Diabetic neuropathy: medical teams focus on glucose control, wound/foot care, and medication choices; chiropractic care adds mobility, balance exercises, and joint care to protect walking and daily activities.
Spine-related neuropathy (radiculopathy): chiropractors address motion, posture, and stability, while physicians guide imaging, medications if needed, and surgical opinions for non-responders or those with red flags.
Post-injury neuropathy (work/sport/MVA): Coordinated plans address soft-tissue strain, scar, and joint mechanics; objective testing and documentation support a safe return to work or sport.
What results should I expect?
Results depend on cause, severity, and time. Some people feel better in weeks; others progress slowly over months. Programs that combine hands-on care, progressive exercise, balance training, and lifestyle steps tend to produce the best long-term function and comfort. Expect regular re-checks with objective measures (sensation, strength, balance, gait, daily tasks).
A sample 12-week roadmap (personalized to your exam)
Weeks 1–4 | Calm & Protect
Low-force adjustments and gentle soft-tissue work
Basic nerve-glide and mobility drills, tolerance-based
Foot-care education and home safety for fall prevention
Short walking intervals; sleep and stress routines
Weeks 5–8 | Rebuild
Posture, hip/core strength, ankle/foot stability
Balance and gait training; ergonomic coaching
Consider traction/decompression or acupuncture where indicated
Nutrition tweaks (with your medical team) for inflammation and glucose control
1) Will I still need medications? Maybe. Chiropractic is complementary. As movement and sleep improve, some people need fewer pain meds—decisions are made with your prescribing clinician.
2) Are adjustments painful? Most patients tolerate them well. We can start with very gentle, low-force methods and progress as you gain confidence.
3) How often are visits? Usually more frequent early on, then fewer as you learn self-care. Re-testing guides when to taper.
4) What about imaging or nerve tests? If your exam suggests it—or if progress stalls—your team may order X-rays/MRIs, EMGs/NCVs, labs, or vascular studies.
5) What can I start at home? Daily foot checks, short walks, simple balance drills by a counter, gentle mobility, and a regular sleep routine. For diabetic cases: medical-guided glucose control and protective footwear.
6) Is this safe if I’m older or osteoporotic? Yes, with proper screening and adapted techniques (instrument-assisted, mobilization, or position-based methods).
7) Does this help after a car crash or work injury? Yes. Plans target alignment, soft tissue, and movement patterns; clinicians also document objective findings to support authorizations and return-to-work decisions.
What to look for in a clinic
Clear explanation of findings and plan, in plain language
Customized techniques (not one-size-fits-all)
Built-in active rehab (balance, gait, strength)
Coordination with your medical team
Regular outcome measurements and progress notes
Education on home care and prevention
The take-home message
Not a cure—but helpful. Modern chiropractic care, combined with active rehabilitation, can help reduce neuropathic pain, improve mobility, and support a safer daily life.
Safety and teamwork matter. Screening, personalization, and medical co-management make care smarter and safer.
Movement is medicine. Gentle hands-on care plus progressive exercise and healthy habits protect gains and prevent setbacks.
