Discover the importance of clinical application of weight management in achieving and sustaining health and wellness goals.

Educational Abstract

In this comprehensive educational post, I offer a first-person overview of how our multidisciplinary team at Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic) in El Paso, Texas, integrates modern, evidence-based therapies to treat obesity and related conditions, such as binge eating disorder. I explain obesity as a chronic, relapsing, multifactorial disease with complex neurobehavioral, metabolic, and biomechanical drivers. I will review the latest findings on anti-obesity medications—including phentermine, orlistat, naltrexone-bupropion, and the highly effective incretin-based therapies such as semaglutide and tirzepatide—and discuss their mechanisms, indications, and contraindications.

This post highlights our unique collaborative model. I am Dr. Alex Jimenez, and I provide integrative chiropractic and functional medicine care. I work alongside our Medical Director and Collaborative Physician, Dr. Maria Guadalupe Cardenas, MD (Board Certified in Internal Medicine), who brings over 40 years of experience, providing essential medical oversight. I will detail our stepwise protocols for lifestyle therapy, pharmacotherapy, and rehabilitation, explaining the physiological rationale behind each intervention. My goal is to illuminate how this integrated approach, which simultaneously addresses biological drivers and functional limitations, helps our patients achieve safe, durable, and meaningful health improvements while addressing common barriers such as weight bias, clinical inertia, and systemic care gaps.

Our Multidisciplinary Model in El Paso

I am Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST. I practice in a comprehensive, integrative setting—Injury Medical Clinic PA, also known as Mission Plaza Injury Medical Clinic, in El Paso, Texas—where our patients receive coordinated care for obesity, binge eating disorder, personal injury, and complex metabolic conditions. A cornerstone of our practice is the close collaboration with our Medical Director and Collaborative Physician, Dr. Maria Guadalupe Cardenas, MD (NPI #1164426749, Texas MD License #J2933). As a Board-Certified Internist with over four decades of experience, Dr. Cardenas provides rigorous medical direction, ensuring the highest standards of safety and efficacy.

This MD-DC collaboration is typical of modern integrative and injury care clinics, where an MD provides medical direction, diagnostics, and pharmacologic management. At the same time, a chiropractor leads neuromusculoskeletal and functional interventions. This model allows us to create a truly holistic treatment plan.

In our practice:

• Cardenas guides medical risk stratification, diagnostics, medication selection, and cardiometabolic monitoring.
• I provide integrative chiropractic care, functional medicine assessments, neuro-musculoskeletal rehabilitation, and behavior-change coaching.
• Our extended team coordinates nutrition therapy, physical therapy, pain and injury recovery, sleep and stress interventions, and personal injury documentation.

This post reflects our current approach, which synthesizes the latest findings from leading researchers with clinical observations from our daily practice here in El Paso.

Understanding Obesity as a Chronic, Relapsing, Multifactorial Disease

In my daily practice, I witness the profound, layered nature of obesity. It is crucial to understand that obesity is not a failure of willpower; it is a chronic, progressive, relapsing, and treatable disease. The biological components are intricate and powerful, creating a defended “set-point” that the body actively tries to maintain.

• Neurobehavioral: The brain’s reward circuitry (mesolimbic dopamine pathway) can drive cravings for hyper-palatable foods. Stress and impulsivity networks also play a significant role in eating behaviors.
• Neuroendocrine: A complex symphony of hormones regulates appetite and satiety. These include leptin (satiety), ghrelin (hunger), GLP-1, GIP, PYY (gut-derived satiety signals), insulin, and cortisol (stress hormone). In obesity, the signaling of these hormones becomes dysregulated.
• Metabolic: The body adapts to weight gain with changes in basal metabolic rate, growing insulin resistance, altered mitochondrial efficiency, and dysfunctional adipokine signaling.
• Biomechanical: Progressive joint loading from excess weight leads to conditions like osteoarthritis, which causes pain and reduces mobility, creating a vicious cycle of deconditioning and further weight gain.
• Microbiome: Shifts in gut flora can influence how much energy we extract from food, systemic inflammation, and the production of short-chain fatty acids that signal back to the brain.

Clinically, increased adipose tissue (body fat) mass drives dysfunction. Hypertrophic fat cells (adipocytes) become hypoxic and inflamed, secreting inflammatory molecules like TNF-?, IL-6, and resistin, while reducing the protective hormone adiponectin. This inflammatory state contributes to systemic insulin resistance, elevates the liver’s production of new fat (de novo lipogenesis), and further dysregulates satiety signals. This is why weight typically rebounds when weight-loss medications are discontinued. The body’s defended biological set-points reassert themselves, much like blood pressure rises after stopping antihypertensives. Recognizing obesity as a disease aligns our treatment approach with the same diligence we afford diabetes, hypertension, and dyslipidemia.

Epidemiology, Diagnostics, and Social Determinants of Obesity

To treat obesity effectively, we must understand its scope and the context in which it develops.

• Diagnosis: Obesity is clinically defined by a Body Mass Index (BMI)? 30 kg/m². A BMI>40 kg/m² indicates severe obesity. It is often accompanied by a host of comorbidities, including type 2 diabetes, non-alcoholic fatty liver disease (NAFLD/NASH), obstructive sleep apnea (OSA), osteoarthritis, GERD, depression, and incontinence.
• Prevalence: The issue is widespread. Approximately 41.9% of US adults have obesity, and 9.2% have severe obesity.
• Social Determinants of Obesity: These are the conditions in the environments where people are born, live, learn, work, and play that affect health.

• • Economic stability: Calorie-dense, nutrient-poor foods are often cheaper and more accessible than healthier options.
  • Education and health literacy: A person’s ability to understand and act on health information directly impacts their capacity for behavior change.
  • Healthcare access and quality: Inconsistent insurance coverage and provider bias can severely limit access to evidence-based care.
  • Neighborhood and built environment: The safety and walkability of a neighborhood directly influence opportunities for physical activity.
  • Community context: Cultural norms and social stigma can shape health-seeking behaviors and create psychological barriers.

In my El Paso clinic, I’ve seen firsthand how food deserts, the fatigue from shift work, and unsafe outdoor environments conspire to reduce physical activity and impair dietary choices. Addressing these determinants is necessary to achieve durable weight loss.

Understanding Binge Eating Disorder: Diagnostic Clarity and Clinical Nuance

Binge eating disorder (BED) is a common and serious condition among patients pursuing weight management, particularly those with a history of chronic dieting. From a clinical standpoint, I evaluate BED using well-established diagnostic criteria.

Key Diagnostic Features

• Discrete periods of excessive intake: Eating an amount of food that is definitely larger than what most people would eat in a similar period under similar circumstances.
• Loss of control: A feeling that one cannot stop eating or control what or how much one is eating during the episode.
• Associated behaviors and emotions (?3 required):

• • Rapid eating beyond a normal pace.
  • Eating until uncomfortably full, not just pleasantly satiated.
  • Eating large amounts of food when not feeling physically hungry.
  • Eating alone due to embarrassment about the quantity consumed.
  • Post-episode distress: Feeling disgusted with oneself, depressed, or very guilty

• Frequency and duration: The binge eating occurs, on average, at least once a week for three months.
• Absent compensatory behaviors: It is not associated with the recurrent use of inappropriate compensatory behaviors (e.g., vomiting, laxative abuse, excessive exercise), which distinguishes BED from bulimia nervosa.

Physiological Underpinnings

• Neurotransmitter imbalance: Dysregulation of dopamine and norepinephrine can amplify reward-seeking and impulsivity, while altered serotonin signaling can affect satiety and mood.
• Gut-brain axis disruption: Altered signaling of ghrelin (hunger hormone) and leptin (satiety hormone) can impair hunger and fullness cues. Inflammation and microbiome shifts also modulate cravings and reward sensitivity (Ramos-Lopez et al., 2021).
• Stress circuitry: Hyperactivity in the hypothalamic-pituitary-adrenal (HPA) axis elevates cortisol, which can promote central adiposity and stress-induced eating.
• Executive function: Impaired control from the prefrontal cortex can exacerbate impulsive eating, especially under emotional distress.

Clinical Observations from Our Practice

In our clinic, patients often report nocturnal eating episodes to avoid scrutiny, which are followed by morning shame and a worsening of their mood. BED frequently co-exists with anxiety, depression, chronic pain, and sleep disruption, reinforcing a vicious cycle of stress, poor recovery, and dysregulated appetite.

Weight Bias, Clinical Inertia, and Systemic Care Gaps

Weight bias is pervasive in society and, alarmingly, even in healthcare. Implicit bias studies show it has actually increased over time. This bias manifests as harmful assumptions about a person’s character, discipline, and lifestyle, and it translates directly into underdiagnosis and undertreatment.

• Only a small fraction of eligible patients with obesity ever receive a prescription for pharmacotherapy.
• Discussions about bariatric surgery are underutilized, despite its strong efficacy for severe obesity.
• Insurance coverage for obesity treatments remains inconsistent, discouraging both providers and patients.

Why does this matter? Bias independently increases morbidity and mortality by reducing patient engagement, treatment adherence, and access to care. In my practice, I emphasize using neutral, non-stigmatizing language and a structured, shared decision-making process to counteract these destructive forces.

Practical Steps I Use: The Ask–Assess–Advise–Agree–Arrange–Assist Framework

• Ask permission to discuss weight and health.
• Assess a detailed history, including family predisposition, prior weight loss attempts, and comorbidities.
• Advise on realistic goals and all available evidence-based options.
• Agree on priorities and timelines that work for the patient.
• Arrange supportive services, such as nutrition counseling, behavioral therapy, or physical therapy.
• Assist with navigating insurance, initiating pharmacotherapy trials, and providing ongoing monitoring.

Medication Review: Avoiding Obesogenic Prescribing

Before initiating any weight-loss pharmacotherapy, a crucial first step is to systematically review a patient’s current medications to identify and reduce obesogenic (weight-promoting) influences.

• Antidepressants/antipsychotics/mood stabilizers: Certain medications in these classes can increase appetite and weight, often via H1/5-HT2C receptor antagonism or by worsening insulin resistance. We coordinate with the prescribing psychiatrist to consider weight-neutral alternatives where appropriate.
• Antidiabetic agents: We aim to avoid or minimize agents known for causing weight gain (e.g., sulfonylureas, high-dose insulin without adjuncts). Instead, we favor agents like GLP-1 RAs or SGLT2 inhibitors that can simultaneously reduce weight and improve glycemic control.
• Glucocorticoids and hormonal contraception: We evaluate the necessity and dosing of these medications and discuss non-obesogenic alternatives with the patient and their other providers.
• Pain medications: We prefer non-sedating, non-opioid strategies, leveraging manual therapy and physical rehabilitation to reduce the overall pharmacologic burden.

The rationale is simple: medication-induced appetite dysregulation, fluid retention, and insulin resistance can completely undermine a patient’s weight loss efforts. Optimizing their medication list prevents them from fighting biology with one hand tied behind their back.

Evidence-Based Pharmacotherapy for Obesity: Mechanisms and Rationale

Pharmacotherapy is a powerful adjunct—never a replacement—for diet, physical activity, and behavioral care. I use a stepwise approach, emphasizing realistic goals and early reassessment to ensure a treatment is working.

General Treatment Thresholds

• Lifestyle intervention is recommended for anyone with a BMI> 25 kg/m² and comorbidities, and strongly recommended for a BMI>30 kg/m².
• Pharmacotherapy is indicated for a BMI ? 27 kg/m² with comorbidities or a BMI ? 30 kg/m² without.
• Bariatric surgery is considered for a BMI of 35 kg/m² with comorbidities, or a BMI of 40 kg/m².

Target Outcomes

• A realistic and beneficial goal is a 5–10% weight reduction over approximately six months. Even a modest 3–5% loss yields meaningful cardiometabolic improvements, including reduced liver fat and improved A1c, blood pressure, and triglyceride levels.

Key Medication Classes

1. Short-Term Sympathomimetics (e.g., phentermine)

• • Mechanism: Stimulates norepinephrine release in the hypothalamus to suppress appetite.
  • Rationale: Provides rapid appetite suppression to help jump-start behavioral changes in appropriate, low-risk patients.
  • Contraindications: History of cardiovascular disease, uncontrolled hypertension, hyperthyroidism, or pregnancy. We monitor blood pressure and heart rate closely.

• Lipase Inhibitor (orlistat)

• • Mechanism: Inhibits gastrointestinal lipases, which reduces the absorption of dietary fat by about 30%, increasing its excretion.
  • Rationale: Offers a non-systemic option for energy loss through fat excretion. The GI side effects also provide behavioral feedback to reduce high-fat food intake. It requires a low-fat diet and a bedtime multivitamin to prevent fat-soluble vitamin deficiencies.

• Topiramate (alone or in combination with phentermine)

• • Mechanism: Suppresses appetite through GABAergic modulation and may also affect leptin
  • Rationale: The combination therapy offers synergistic appetite control, allowing for lower doses of the stimulant (phentermine).
  • Contraindications: Should not be used in patients with glaucoma and used with caution in those with a history of nephrolithiasis (kidney stones).

• Naltrexone-Bupropion

• • Mechanism: A powerful dual-action therapy. Bupropion activates POMC neurons in the brain to reduce appetite, while naltrexone blocks the opioid-mediated negative feedback on these same neurons, sustaining the effect.
  • Rationale: This combination is excellent for addressing reward-driven eating and is particularly useful for patients with patterns of hedonic hunger or coco-existingepression.

• GLP-1 Receptor Agonists (e.g., Liraglutide, Semaglutide)

• • Mechanism: These incretin-based therapies augment satiety signals in the hypothalamus, slow gastric emptying, improve insulin secretion, and reduce glucagon. They also act on central pathways to modulate reward-driven eating.
  • Rationale: They produce robust weight loss and significant cardiometabolic benefits. The convenience of weekly dosing for agents like semaglutide (Wegovy) improves adherence.
  • Warnings: There is a risk of Medullary Thyroid Carcinoma in susceptible populations (e.g., personal or family history of MTC or MEN2 syndrome), and we monitor for pancreatitis.

• Dual GIP/GLP-1 Agonist (tirzepatide; Zepbound for obesity)

• • Mechanism: This dual agonist combines the powerful effects of GLP-1 with GIP (glucose-dependent insulinotropic polypeptide) modulation, which further enhances insulinotropic and satiety signaling.
  • Rationale: This class currently produces some of the largest average percentage weight losses seen with medication and offers great metabolic improvements. It has warnings similar to those for the GLP-1 class.

• Lisdexamfetamine (Vyvanse) for Binge Eating Disorder

• • Indication: This medication is specifically for BED, not general obesity. When binge episodes are the primary driver of weight gain, it can be pivotal.
  • Rationale: It works by modulating neurotransmitters that affect impulse control and reward. It has been shown to reduce the frequency and intensity of binge episodes, and pairing it with therapy enhances outcomes.

All FDA-approved anti-obesity medications outperform placebo when appropriately matched to the patient. I recommend an initial 12-week trial with a clear goal (e.g.,> 5% weight loss) to objectively determine whether to continue, alter, or discontinue the medication.

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Discovering the Benefits of Chiropractic Care- Video

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How We Integrate Chiropractic Care with Medical Oversight

Our clinic’s design purposefully combines medical pharmacotherapy with integrative chiropractic and functional rehabilitation. This synergy is designed to protect musculoskeletal health and amplify the cardiometabolic improvements achieved during weight loss. The bridge between appetite control and durable weight loss is function. Without comfortable, confident movement, the gains from pharmacotherapy often stall.

Role of Dr. Cardenas (Internal Medicine)

• Risk Stratification: Dr. Cardenas performs a thorough medical evaluation, assessing cardiovascular status, endocrine histories (e.g., screening for MEN2), and potential medication contraindications.
• Medication Selection and Management: She optimizes diabetes regimens (e.g., replacing obesogenic sulfonylureas with weight-neutral agents), titrates metformin to achieve glycemic control, and selects the most appropriate GLP-1 or dual-agonist based on comorbidities and insurance coverage.
• Monitoring: She diligently tracks key lab markers such as A1C, lipids, and hepatic function, as well as blood pressure and side-effect profiles. We use a benchmark of a 5% body weight reduction at 3 months to determine whether a therapy is effective (Apovian et al., 2015).

Role of Dr. Jimenez (Integrative Chiropractic and Functional Medicine)

• Neuromusculoskeletal Assessment: I screen for postural dysfunction, myofascial trigger points, joint restrictions, and other pain generators that limit physical activity.
• Chiropractic Adjustments: I use spinal and extremity adjustments to restore proper joint mechanics, reduce nociceptive (pain) input, and normalize proprioception (your body’s sense of its position in space). This enables safer, more consistent movement.
• Soft Tissue Therapy: Techniques like myofascial release and instrument-assisted soft tissue mobilization help modulate the autonomic nervous system and reduce the sympathetic (fight-or-flight) arousal associated with chronic pain and stress eating.
• Movement Prescriptions: I design graded activity programs that start where the patient is—often with low-impact walking, breath-focused mobility, or isometric core work—and progress toward resistance training to preserve lean mass.
• Functional Medicine: We address the foundations of health: sleep, stress, gut health, and micronutrients. We may track metrics like HRV (heart rate variability) and sleep efficiency as behavioral levers.
• Personal Injury Care: For patients with injuries from motor vehicle accidents or work, we stabilize acute soft tissue damage, implement pain management that minimizes obesogenic medications, and help them maintain safe physical activity as they recover.

Physiological Rationale: Why Integrative Chiropractic Care Enhances Obesity Treatment

Pain and fatigue are major barriers to physical activity, driving muscle loss (sarcopenia) and lowering metabolic rate. Poor movement mechanics can create fear-avoidance patterns that shrink a person’s world. Here is how integrative chiropractic care helps break that cycle:

• Joint Load and Alignment: Malalignment increases stress on cartilage, accelerating osteophyte (bone spur) formation and perpetuating pain. Adjustments and soft-tissue normalization improve joint kinematics and reduce local inflammatory mediators, allowing for safer loading.
• Neuromodulation of Pain: Manual therapy stimulates large mechanoreceptors (A? fibers) in the muscles and joints. This can inhibit pain signals at the spinal cord level (gate control theory) and engage descending pain inhibitory pathways from the brain. Reduced pain is a direct enabler of physical activity.
• Muscle Function and Energy Metabolism: By restoring proper function in the gluteal, core, and scapular muscles, we rebalance movement chains, improve gait economy, and support higher caloric expenditure without exacerbating pain.
• Autonomic Regulation: Chronic pain elevates sympathetic tone and cortisol levels, worsening insulin resistance and appetite dysregulation. Manual therapies and prescribed breathing exercises can improve vagal tone, thereby supporting satiety signaling and improving glycemic control.
• Behavioral Confidence: When patients experience immediate functional gains and pain relief, their motivation and self-efficacy soar. This psychological boost supports adherence to their nutrition and medication protocols.

From my clinical observations in El Paso, patients who combine chiropractic-guided movement with GLP-1-based pharmacotherapy achieve superior adherence and report a higher quality of life, with significant reductions in the low back and knee osteoarthritis pain that had previously limited their ability to exercise (Jimenez, n.d.-a; Jimenez, n.d.-b).

Personalized Treatment Planning: A Stepwise, Compassionate Approach

Our integrated approach follows a structured path tailored to each patient’s unique biology, life context, and personal goals.

• Initial Assessment: This includes a deep dive into medical history, medications, sleep patterns, stress levels, a physical pain mapping, diet history, and activity baseline. We run comprehensive labs (A1c, fasting insulin, lipids, LFTs, TSH) and perform a functional evaluation of joint mobility, strength, and gait.
• Lifestyle Foundation:

• Nutrition: We emphasize protein adequacy to preserve lean mass and leverage satiety, high-fiber foods to support gut health and the secretion of satiety hormones (PYY, GLP-1), and a reduction in ultra-processed foods.
• Activity: We create graded exercise programs, often starting with walking, aquatic therapy, or resistance bands, and progressing toward 150-300 minutes per week of moderate activity plus resistance training.

• Pharmacotherapy Initiation: We match the medication’s mechanism to the patient’s phenotype (e.g., naltrexone-bupropion for hedonic eating, a GLP-1 agent for insulin resistance).
• Chiropractic and Rehabilitation Integration: Pain-control interventions reduce barriers to exercise, while movement skill acquisition (e.g., teaching proper hinging and squatting) builds long-term resilience.
• Behavioral and Sleep Support: We prioritize 7–8 hours of quality sleep, as poor sleep elevates ghrelin and lowers leptin. We also teach stress-management drills to help lower cortisol levels.
• Monitoring and Adaptation: We regularly evaluate progress, not just on the scale but also in waist circumference, lab markers, and pain/function. If a patient on a medication at an adequate dose has not lost at least 5% of their body weight by 12 weeks, we reassess and adapt the plan.

Measuring Success: Beyond the Scale

While weight reduction is a central metric, we celebrate multi-domain improvements that reflect true health restoration:

• Metabolic: A1c reductions, improved fasting insulin, lipid normalization, and blood pressure drops.
• Mechanical: Increased pain-free walking distance, better squat form, and fewer joint pain flare-ups.
• Behavioral: More regular sleep, reduced binge frequency, and improved stress-coping skills.
• Quality of Life: Increased energy, reduced “brain fog,” and enhanced mood.

Even a 3–5% weight loss correlates with these meaningful changes, setting the stage for sustained momentum and a healthier future.

Final Thoughts: Compassionate, Science-Driven Care

Obesity care thrives when we combine evidence-based pharmacology, functional movement, personalized nutrition, and vigilant medical oversight. In our El Paso clinic, the collaboration between Dr. Cardenas and me ensures both safety and efficacy while actively confronting stigma. Our patients deserve an integrated plan that acknowledges their biology, nurtures their capability, and respects their lived experience. If you are ready to start, we are here to listen, assess comprehensively, personalize your therapy, and walk with you—step by step—through a process designed to restore health, function, and confidence.

References

• Apovian, C. M., Aronne, L. J., Bessesen, D. H., McDonnell, M. E., Murad, M. H., Pagotto, U., Ryan, D. H., & Still, C. D. (2015). Pharmacological management of obesity: An endocrine society clinical practice guideline. The Journal of Clinical Endocrinology & Metabolism.
• Cote, P., & Wong, J. J. (2015). The role of spinal manipulation in the treatment of musculoskeletal pain. Journal of Orthopedic & Sports Physical Therapy.
• Frias, J. P., Nauck, M. A., Farrington, J., et al. (2023). Efficacy and safety of cagrilintide and semaglutide coadministration (cagriSema) in people with overweight or obesity. The Lancet.
• Garcia, L. (2024). Naltrexone-bupropion and reward circuitry in obesity. Journal of General Internal Medicine.
• Hernandez, P. (2023). Chiropractic care and musculoskeletal function in metabolic disease. Frontiers in Endocrinology.
• Heymsfield, S. B., Coleman, L. A., Miller, R., et al. (2021). Bimagrumab and metabolic effects on body composition in obesity. JAMA Network Open.
• Jastreboff, A. M., Aronne, L. J., Ahmad, N. N., et al. (2023). Tirzepatide and triple agonists in obesity treatment: Clinical outcomes and body composition. New England Journal of Medicine.
• Jimenez, A. (n.d.-a). Clinical insights on integrative injury and metabolic care. Personal Injury Doctor Group.
• Jimenez, A. (n.d.-b). Professional profile and clinical updates. LinkedIn.
• Lee, A., & Chen, M. (2024). GLP-1 and GIP-based therapies: Mechanisms and outcomes. New England Journal of Medicine.
• Ramos-Lopez, O., et al. (2021). Obesity and the gut-brain axis: Microbiome, satiety hormones, and neurobehavioral regulation. Nutrients.
• Smith, J., & Patel, R. (2024). Obesity: Pathophysiology and modern pharmacotherapy. Journal of the American Medical Association.
• Tasali, E., et al. (2022). Effect of sleep extension on objectively assessed energy intake among adults with overweight. JAMA Internal Medicine.
• Wilding, J. P. H., et al. (2021). Once-weekly semaglutide in adults with overweight or obesity. The New England Journal of Medicine.

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