Metabolic Health: Understanding Risks With Obesity & Diabetes

Get informed on obesity and diabetes and how they affect your body as well as your metabolic health, plus tips for managing these challenges.

Abstract

In this educational post, I will explore the intricate, closely linked relationship among obesity, type 2 diabetes, and cardiovascular disease. We will delve into how these conditions converge through shared physiological pathways—chiefly chronic inflammation, insulin resistance, oxidative stress, and neuroendocrine dysregulation. I will clarify why obesity is a chronic, progressive, and treatable disease and summarize the evidence supporting comprehensive care that integrates lifestyle, pharmacotherapy, functional medicine, rehabilitation, and chiropractic interventions.

My goal is to guide you through real-world clinical scenarios to demonstrate the profound benefits of early, proactive intervention. We will discuss the crucial factors that influence our treatment decisions, from advanced pharmacotherapy, such as GLP-1 receptor agonists, to foundational lifestyle changes in nutrition, physical activity, and behavioral health. This discussion will also highlight the power of an integrative care model, where chiropractic, functional medicine, and conventional medical oversight converge to create a comprehensive, patient-centered treatment plan.

I will also highlight how our multidisciplinary team in El Paso, Texas—led by me and medically directed by Dr. Maria Guadalupe Cardenas, MD (Board Certified in Internal Medicine; NPI #1164426749; Texas MD License #J2933)—coordinates integrative care at Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic). You will learn practical, evidence-informed strategies for aligning obesity treatment with cardiometabolic risk reduction; why and how to pair anti-obesity medications with structured behavioral programs; and where integrative chiropractic fits into modern care plans, using a mechanistic, clinically relevant rationale.

Who We Are: A Multidisciplinary Model With Medical Direction in El Paso, Texas

I practice in a multidisciplinary, integrative clinic—Injury Medical Clinic PA (also known as Mission Plaza Injury Medical Clinic)—where internal medicine and chiropractic collaborate every day. Our Medical Director and Collaborative Physician, Dr. Maria Guadalupe Cardenas, MD, brings more than 40 years of internal medicine expertise. As our medical director, she provides essential medical oversight and works in tandem with our team. This synergy between chiropractic care, functional medicine, and internal medicine ensures that our patients receive a comprehensive and robust treatment plan. This blended structure—common in injury and integrative clinics—ensures that patients receive cohesive, medically supervised, whole-person care, in which each intervention is chosen to affect upstream mechanisms, not just downstream symptoms.

• Dr. Cardenas provides:

• • Medical oversight, risk stratification, and guideline-based pharmacotherapy.
  • Diagnostic stewardship (labs, imaging), medication safety, and chronic disease management.
  • Coordination for cardiology, endocrinology, and sleep medicine referrals when indicated.

• I provide:

• • Integrative chiropractic care for neuromusculoskeletal dysfunctions linked to metabolic and inflammatory stress.
  • Functional medicine assessment of lifestyle, nutrition, sleep, stress, and microbiome-influencing habits.
  • Rehabilitation programming, injury care, movement re-education, and ergonomic strategies.
  • Collaborative monitoring of body composition, metabolic markers, and recovery metrics.

Whether managing a personal injury, a complex chronic condition, or focusing on preventive wellness, our integrated approach allows us to address the full spectrum of a patient’s health needs, from spinal alignment and nervous system function to metabolic health and medical management.

The Intertwined Epidemics of Obesity and Cardiometabolic Disease

Greetings, and thank you for joining me. In my years of clinical practice, I have witnessed firsthand the devastating impact that obesity, type 2 diabetes, and cardiovascular disease have on individuals and families. These conditions are not separate issues; they are two sides of the same metabolic coin, sharing significant overlap in their underlying disease processes. The modern healthcare landscape is shifting, and we now have more effective tools than ever to combat them.

My purpose today is to walk you through a case study format that vividly illustrates three key principles:

1. The immense benefit of treating obesity early and aggressively.
2. The critical factors that guide our personalized treatment decisions.
3. The chronic, progressive nature of both diabetes and obesity, which necessitates long-term management.

Obesity Is a Regulated Biology Problem: Why It’s Treatable and Why “Try Harder” Fails

In tightly regulated systems—such as fluid balance or red blood cell production (hematopoiesis)—the body defends specific set points. Body fat mass is similar: the central nervous system, particularly the hypothalamus, maintains a set point for adiposity through hunger and satiety hormones and by adjusting energy expenditure. In obesity, these biological controls become dysregulated, often long before visible weight gain occurs.

• Key point: Overeating does not simply cause obesity; in many cases, the neuroendocrine state of obesity drives overeating through heightened hunger signaling and blunted satiety.
• Mechanism:

• • Elevated ghrelin (the “hunger hormone”) and reduced leptin sensitivity (the “satiety hormone”) and PYY/GLP-1 signaling drive an increased appetite.
  • Hypothalamic inflammation impairs the neuronal circuits that regulate energy balance, contributing to a defended higher fat-mass set point.
  • The “second hit” is metabolic adaptation: after weight loss, total energy expenditure declines more than expected for body size, hunger rises, and satiety signals diminish—a perfect storm promoting weight regain unless the underlying biology is therapeutically supported (Sumithran & Proietto, 2013).

This is why the common advice to “try harder” often fails. Anti-obesity medications (AOMs) are designed to address these dysregulated pathways. They are not “willpower substitutes”; they are physiology-corrective tools that reduce the biological drive to eat, improve satiety, and temper the metabolic adaptation that follows weight loss, all while patients work to build durable habits.

The Shared Roots: Chronic Inflammation, Lipotoxicity, and Oxidative Stress

Obesity, type 2 diabetes, and atherosclerotic cardiovascular disease all grow from the same soil: chronic low-grade inflammation, lipotoxicity, mitochondrial dysfunction, oxidative stress, and endothelial dysfunction (Hotamisligil, 2017; Zinöcker & Lindseth, 2018).

• As adipose tissue expands, hypertrophic fat cells become hypoxic (lacking oxygen) and inflamed. They recruit immune cells like macrophages and begin producing inflammatory cytokines (e.g., TNF-?, IL-6).
• This inflammation causes a spillover of fatty acids into the bloodstream, leading to ectopic fat deposition in organs like the liver, muscle, and pancreas. This is lipotoxicity, a primary driver of insulin resistance and impaired insulin secretion.
• Mitochondrial quality control falters, resulting in reduced ATP (energy) efficiency, increased reactive oxygen species (ROS) production, and impaired fatty acid oxidation. This vicious cycle exacerbates insulin resistance and contributes to fatigue.
• In the vasculature, inflammation reduces the bioavailability of nitric oxide (NO), a crucial molecule for blood vessel health. This promotes vasoconstriction, platelet aggregation, and endothelial dysfunction—all of which are central to the progression of atherosclerosis (Tousoulis et al., 2012).

When we address obesity intelligently, we are not just focused on weight. We are actively working to reduce inflammatory signaling, restore metabolic flexibility, and improve endothelial function. This is why even modest weight loss can produce outsized cardiometabolic benefits.

Nitric Oxide as a Bridge Between Metabolism and Vascular Health

NO is a critical metabolic-vascular nexus. Adequate levels of NO promote vasodilation, antiplatelet activity, endothelial health, and efficient glucose disposal. In cardiometabolic disease, NO bioavailability plummets due to oxidative stress, the accumulation of asymmetric dimethylarginine (an inhibitor of NO synthesis), and endothelial insulin resistance.

• Metabolically, NO enhances glucose uptake into cells and supports insulin secretion. It also helps improve mitochondrial efficiency and lower oxidative stress.
• Clinically, interventions that restore NO—such as exercise, a Mediterranean-style diet rich in nitrates, improved sleep, and a reduced inflammatory burden—translate into better blood pressure, enhanced exercise tolerance, and improved glycemic control (Lundberg et al., 2015).

Our team’s integrated plans focus on NO-friendly strategies: progressive aerobic exercise, resistance training, polyphenol-rich foods, sleep optimization, and targeted nutraceuticals, when appropriate, under medical oversight.

ADA-Aligned Goals: Treat Weight, Glycemia, and Cardiometabolic Risk

As a clinician, I align my care plans with the American Diabetes Association (ADA) standards: treat overweight/obesity, achieve glycemic targets, and reduce risks of cardiovascular, liver, and kidney disease. Treating obesity directly improves all of these outcomes by lowering insulin resistance, reducing lipotoxicity, improving blood pressure, shifting adipokine balance, and decreasing systemic inflammation (American Diabetes Association, 2025).

This is because:

• Excess visceral adiposity promotes hepatic and systemic insulin resistance via increased free fatty acid flux, ectopic lipid deposition, and pro-inflammatory cytokines, which impair insulin signaling in the liver and muscle (Kahn et al., 2006).
• Weight reduction improves insulin sensitivity, decreases hepatic glucose production, and lowers triglycerides and LDL, reducing the risk of both atherosclerotic and hepatic fibrosis progression (Lean et al., 2018).
• Addressing sleep, stress, and physical inactivity favorably modulates the HPA axis, circadian alignment, and autonomic balance—factors tightly linked to glycemic variability and cardiometabolic health (Depner et al., 2014; Thayer et al., 2010).

Our integrative care model ensures these physiological drivers are addressed simultaneously with medication and lifestyle therapies.

Case Study Part 1: Stephen’s Journey with Prediabetes and Obesity

To illustrate these principles in action, let’s begin this journey by meeting Stephen.

Stephen, a 24-year-old man, came to my clinic for a follow-up on prediabetes and for help with weight management. His opening words are ones I hear all too often: “I’ve been trying to lose weight, but it’s just not working.”

Six months prior, an A1c of 5.8% confirmed his prediabetes diagnosis. Despite his efforts to change his nutrition, the scale wouldn’t budge. His medical history was significant for a cholecystectomy (gallbladder removal), but more telling was his family history—obesity, cardiovascular disease, and type 2 diabetes were prevalent in both of his parents. Stephen worked a sedentary job, lived with his partner, and reported no history of tobacco, alcohol, or illicit drug use. His A1c today remained at 5.8%, a clear sign that his metabolic dysfunction was static, not improving.

Understanding the Weight History: The Story of a Lifetime

Because Stephen was a new patient, my first step was to take a detailed weight history. This is not just about numbers; it’s about understanding the narrative of a person’s life and how it has shaped their physiology.

• Childhood Onset: His weight gain began around age 13, coinciding with the stress of his parents’ divorce. This is a crucial observation, as it highlights the strong link among chronic stress, cortisol, and metabolic dysregulation, which often begin early in life.
• Life Transitions: He gained another 15 pounds in college, a common period for weight gain due to changes in routine, diet, and stress.
• Current State: His weight had continued to climb, with his current weight of 250 pounds being his highest ever. His lowest adult weight was 220 pounds at age 18.
• Past Interventions: He had never used any weight management medications and had no contraindications, such as a history of pancreatitis, seizure disorders, glaucoma, or a personal or family history of medullary thyroid cancer or Multiple Endocrine Neoplasia type 2 (MEN2).

At 250 pounds, Stephen’s Body Mass Index (BMI) was 32.1, placing him in the Class 1 Obesity category. His other vital signs were within normal limits.

An Integrative Assessment Reveals Metabolic Dysfunction

My approach to obesity is built on what I call the four pillars of treatment: nutrition, physical activity, behavioral health, and medical management. To build a truly effective plan, I needed to assess Stephen across all these domains.

• Nutrition: His 24-hour dietary recall revealed a high intake of processed foods and sugary beverages.
• Activity: His physical activity was minimal due to his sedentary job.
• Behavioral Health: We explored his sleep quality, stress levels, and overall mood—all of which profoundly affect hormones that regulate appetite and fat storage, such as cortisol, ghrelin, and leptin.
• Physical Examination: The physical exam revealed key metabolic markers:

• • Waist Circumference: 41 inches. A waist circumference over 40 inches in men is a strong indicator of visceral adiposity—the dangerous fat that surrounds internal organs and drives inflammation.
  • Neck Circumference: 17 inches. This is often associated with an increased risk of obstructive sleep apnea.
  • Acanthosis Nigricans: Dark, velvety patches of skin, particularly along his neckline. This is a classic cutaneous sign of insulin resistance.
  • Skin Tags: Small, benign growths also commonly associated with insulin resistance.
  • Central Adiposity: A pattern of weight gain concentrated around the abdomen, further confirming the presence of metabolically active visceral fat.

When I asked Stephen, “Would you be interested in a treatment that could prevent you from developing diabetes and help you lose weight?” he responded with an enthusiastic “Absolutely yes!” He was motivated and ready for change.

Chiropractic Care & Metabolism *The Hidden Link*- Video

What Lifestyle Alone Achieves—And Its Limits

To help Stephen understand the “why” behind our treatment goals, I shared a chart illustrating the amount of weight loss required to see meaningful improvements. For prediabetes, losing just 3- 5% of body weight can begin to improve glucose metabolism, while a 10- 15%+ loss is often needed to make an impact on conditions like type 2 diabetes, dyslipidemia, and Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD).

High-quality trials show lifestyle intervention produces meaningful, but often transient, benefits if biology is not supported:

• Weight loss: Approximately 5.2–8.6% at year 2; most is regained by year 5 without continued structured support (Look AHEAD Research Group, 2013).
• A1C reduction: About 0.15–0.3% with lifestyle alone; improvements grow as weight loss deepens (DPP Research Group, 2002).
• Blood pressure: Modest systolic improvements.

Why the regression? Metabolic adaptation, shifts in hunger hormones, and environmental drivers are powerful forces. Patients do not “fail” lifestyle; biology overwhelms behavior unless addressed with pharmacotherapy and integrative care.

Anti-Obesity Medications: Early Response and Cardiometabolic Payoffs

Modern AOMs, particularly GLP-1 receptor agonists and dual agonists, directly target the appetite centers in the brain, delay gastric emptying, enhance satiety, and reduce energy intake. They may also improve beta-cell function and inflammation markers.

• Typical outcomes:

• • GLP-1 RA (e.g., liraglutide, semaglutide): Often 8–15% weight loss over 1 year (Wilding et al., 2021).
  • Dual agonists (e.g., tirzepatide): Higher mean weight loss, with favorable changes in A1C, triglycerides, and blood pressure (Jastreboff et al., 2022).

• Cardiovascular outcomes:

• • Semaglutide and liraglutide have demonstrated reduced major adverse cardiovascular events in high-risk populations (Marso et al., 2016; SELECT Investigators, 2023).
  • SGLT2 inhibitors improve heart failure outcomes and reduce CKD progression—valuable in patients with obesity, diabetes, or both (McMurray et al., 2019).

A landmark study, the SURMOUNT-1 trial, provides a powerful example. This trial involved over 2,500 participants with a BMI of 27 or greater and prediabetes. The results were astounding:

• After 88 weeks, participants on the 15 mg dose of tirzepatide experienced an average weight reduction of nearly 5%.
• Crucially, nearly all participants on tirzepatide who had prediabetes at the start of the study had reverted to normal glucose levels by the end.

In our clinic, Dr. Cardenas guides the initiation and monitoring of these medications, while I structure the complementary behavioral, rehabilitative, and integrative plan that amplifies their benefits.

Translating Guidelines Into One Integrated Plan for Stephen

Our integrated protocol for Stephen combined all four pillars of care.

1. Comprehensive Assessment: We started with a full workup including body composition, metabolic markers, and a pain/function inventory.
2. Medical Direction and Pharmacotherapy: After discussing all options, considering contributing factors, and reviewing insurance coverage, Stephen elected to start Tirzepatide for his obesity and prediabetes. Dr. Cardenas oversaw the prescription and titration schedule, starting with 2.5 mg weekly for four weeks.
3. Nutrition and Behavior: We began with foundational changes: increasing his steps to 3,000 per day and limiting juice intake. We also placed a referral to a Registered Dietitian for medical nutrition therapy.
4. Chiropractic and Rehabilitation Plan: This is where integrative chiropractic care becomes a cornerstone. For many patients with obesity, musculoskeletal pain is a significant barrier to exercise. My role as a chiropractor is to:

• • Assess and Correct Biomechanical Imbalances: Through spinal adjustments and other manual therapies, I improve joint mobility, reduce pain, and restore proper function.
  • Improve Neurological Function: Adjustments help optimize the communication between the nervous system and the rest of the body, impacting physiological regulation.
  • Prescribe Therapeutic Exercises: I designed a safe, progressive exercise program to build strength and endurance without causing injury. By alleviating pain, chiropractic care enables engagement in the physical activity necessary for metabolic improvement.

Stephen’s Progress: A Remarkable Transformation

• Two-Week Follow-Up: Stephen was already down three pounds. We planned to titrate his Tirzepatide dose up to 5 mg and increase his daily step count to 4,000. He felt confident and motivated.
• One-Year Follow-Up: The results were a testament to his dedication and our comprehensive approach.

• • Weight: His weight dropped from 250 to 198 pounds, a total loss of 52 pounds (20.8% total body weight loss).
  • BMI: His BMI fell from 32.1 to 7, moving him from “obesity” to “overweight.”
  • Metabolic Health: His A1c was now 4% (normal range), and his lipid panel was normal. His prediabetes was effectively in remission.
  • Physical Exam: His waist and neck circumferences were now in the healthy range.

His ongoing plan involves continuing his medication and lifestyle habits, with regular three-month follow-ups. Obesity is a chronic disease, and long-term management is essential.

Case Study Part 2: Menopause, Diabetes, and MASLD Risk

Our model also adapts to more complex scenarios. I met Victoria, a 52-year-old Black woman in the menopause transition, for follow-up of weight gain and prediabetes. Over the prior year, her weight increased by 15 lb, and her A1C rose to 7.3%, indicating new-onset diabetes. She also suffered from hot flashes and poor sleep.

Menopause Physiology and Cardiometabolic Risk

During menopause, declining estradiol levels reduce endothelial function, worsen LDL cholesterol levels, increase visceral adiposity, and elevate insulin resistance. These shifts dramatically increase cardiovascular risk (El Khoudary et al., 2020).

A Multi-Modal Plan for Victoria

Our shared decisions included:

• Increasing her metformin and starting a trial of continuous glucose monitoring (CGM) for real-time nutritional feedback.
• A referral to a menopause specialist to evaluate menopause hormone therapy (MHT), which can improve vasomotor symptoms and support metabolic profiles (NAMS, 2023).
• Initiating semaglutide, a GLP-1 receptor agonist, to enhance satiety and glycemic control.
• At one year, her weight decreased by 25 pounds, her BMI moved into the normal range, and her A1C, lipids, and insulin resistance all improved.

Finally, consider Benny, a 64-year-old with a 25-year history of diabetes, a prior heart attack, and obesity. His labs indicated a high risk for advanced liver fibrosis, so I calculated his FIB-4 score. The result of 2.25 prompted a referral to a gastroenterologist for further testing, alongside initiation of semaglutide to address his weight, glycemia, and cardiovascular risk. His case illustrates the need to screen for MASLD, a common comorbidity, and integrate specialty care.

Integrative Chiropractic Care: Why It Belongs in Cardiometabolic Management

As a chiropractor and family nurse practitioner trained in functional medicine, I see daily how neuromusculoskeletal function intersects with metabolic health. Chronic pain, poor movement patterns, and low physical capacity feed a cycle of inactivity, sleep disruption, and stress—all of which worsen insulin resistance, inflammation, and weight gain.

Here is how integrative chiropractic care fits:

• Pain Modulation and Function Restoration:

• • Techniques: Diversified spinal manipulation, extremity adjustments, soft-tissue mobilization, and graded mobilizations.
  • Why: Restoring joint mechanics and reducing nociceptive (pain signal) input can downshift sympathetic overactivity, reduce cortisol load, and make movement more accessible. Improved mechanical efficiency lowers the energy cost of activity, expanding what patients can do without flaring symptoms.

• Anti-inflammatory Movement Prescription:

• • We build structured progressions: mobility? motor control? strength? work capacity.
  • Why: Resistance and aerobic training increase GLUT4-mediated glucose uptake, improve mitochondrial biogenesis, enhance NO bioavailability, and reduce visceral fat. Tailored, pain-informed progression is key for adherence and metabolic gain.

• Breathing and Autonomic Rehabilitation:

• • Techniques: Diaphragmatic breathing, rib/thoracic mobility drills, and paced respiration.
  • Why: Improving thoracic mechanics and vagal tone decreases sympathetic dominance, which can lower resting heart rate and blood pressure, and improve glycemic control through stress-axis recalibration.

• Posture, Gait, and Ergonomics:

• • We correct load distribution and energy-leak patterns, making everyday movement more efficient.
  • Why: Reduced mechanical strain mitigates inflammatory signaling from overloaded tissues and supports sustainable daily energy expenditure.

Clinical observation from my practice: when pain is managed and movement feels safe, adherence to nutrition, sleep, and medication plans improves dramatically. Over the years, my notes shared on my professional channels consistently show that restoring mechanical confidence is a turning point in weight and A1C trajectories (see clinical reflections at my sites: Chiropracticscientist.com and LinkedIn profile).

The Reality of Weight Regain: Understanding Metabolic Adaptation

Patients often say, “I can lose 20 pounds, but it finds five friends and comes back.” That is biology, not a personal failure. As mentioned, weight loss reduces resting energy expenditure, elevates ghrelin levels, and suppresses satiety hormones, thereby increasing the likelihood of weight regain if therapy is stopped. Studies show that discontinuing GLP-1 therapy leads to early regain and rising blood pressure and A1C—reinforcing that obesity requires long-term management (Rubino et al., 2021).

Our approach is to set expectations for chronic care, maintain pharmacotherapy when appropriate, and invest in durable lifestyle structures. Chiropractic-led movement and pain control make these structures livable.

When Insurers Lag Behind the Science

Some insurers still categorize obesity medications as “vanity,” ignoring robust data that obesity is a chronic, relapsing, neuroendocrine disease and a root cause of cardiometabolic morbidity. Denying coverage undermines diabetes and CVD control and escalates long-term costs. Our team documents clinical necessity, aligns with ADA/AHA/AACE recommendations, and presents data demonstrating improvements in A1C, blood pressure, and lipid profiles to advocate for patients.

Key Takeaways for Patients and Clinicians

• Obesity is a biologically defended condition, not a behavioral flaw.
• The same mechanisms that drive obesity also drive diabetes and cardiovascular disease—especially inflammation, insulin resistance, and endothelial dysfunction.
• Early, physiology-targeted therapy works best: pair lifestyle structure with medications that correct appetite and metabolic signaling.
• Integrative chiropractic care reduces pain and mechanical barriers, enabling the movement practice that amplifies metabolic benefits.
• Long-term management prevents regain: keep the biological supports in place while building habits that last.

Stephen’s journey powerfully illustrates that obesity and its related conditions are treatable, chronic diseases that respond best to a comprehensive, multifaceted, and long-term management strategy. By combining foundational lifestyle changes with targeted integrative chiropractic care to support movement and using modern medical therapies under the guidance of our collaborative medical team, we can achieve outcomes once thought impossible.

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