Obesity: Key Insights Unveiled for Cardiometabolic Health

Understand the connection between cardiometabolic care, obesity, and long-term health. Explore essential information in this post.

Abstract

In this comprehensive educational post, I, Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST, walk you through a patient-centered, first-person account of our integrative, multidisciplinary approach to obesity, insulin resistance, sarcopenia, osteoarthritis, and cardiovascular risk reduction at Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic) in El Paso, Texas. I present modern, evidence-based strategies co-managed with our Medical Director and Collaborative Physician, Dr. Maria Guadalupe Cardenas, MD (Board Certified in Internal Medicine; NPI #1164426749; Texas MD License #J2933), who brings over 40 years of internal medicine experience to guide medical safety, medication decisions, comorbidity assessment, and perioperative readiness. You will follow four fully developed case journeys—Eloise (PCOS and binge eating), George (male infertility and metabolic syndrome), Lynn (perimenopausal weight gain), and Amit and Dolores (sarcopenic obesity and surgical readiness). I explain why we chose each intervention, how integrative chiropractic care interfaces with metabolic therapies, and the physiological mechanisms behind metformin, semaglutide, tirzepatide, and combination pharmacotherapy (e.g., bupropion-naltrexone, phentermine, topiramate). I also elaborate on functional medicine insights, nutrition protocols, resistance training for sarcopenia, physical therapy coordination, and strategies to mitigate healthcare weight bias. Throughout, I cite leading research, use modern outcomes metrics (A1C, fasting insulin, HOMA-IR, body composition including visceral adipose tissue), and share clinical observations from my practice and professional findings available at healthcoach.clinic and my LinkedIn page. The goal is a practical, compassionate, scientifically grounded roadmap to help patients improve function, reduce pain, and reach meaningful life goals such as starting a family, independent mobility, and travel, while seeing how integrative chiropractic fits into real-world obesity and metabolic care.

Our Integrated, Multidisciplinary Team: A Vision for Comprehensive Care

At our practice, Injury Medical Clinic PA, we have cultivated a unique and powerful healthcare model built on the principle of integrative medicine. I am Dr. Alex Jimenez, and my extensive training across chiropractic (DC), advanced practice nursing (APRN, FNP-BC), and functional medicine (CFMP, IFMCP) allows me to view patient health through a multifaceted lens. My collaboration with Dr. Maria Guadalupe Cardenas, MD, profoundly enhances this approach.

Dr. Cardenas is a highly respected, board-certified Internist with over four decades of clinical experience. As our Medical Director and Collaborative Physician, she provides essential medical oversight and brings a depth of knowledge in internal medicine that is indispensable to our practice. Her NPI (#1164426749) and Texas MD License (#J2933) represent a career dedicated to patient care and medical excellence.

This partnership between a Doctor of Chiropractic with advanced functional medicine credentials and a seasoned Medical Doctor is the cornerstone of our clinic. It allows us to offer a truly comprehensive spectrum of care that addresses health from every angle. Our services are not siloed; they are woven together to create a personalized and synergistic treatment plan for each patient. This includes:

• Chiropractic Care: Foundational to our practice, we focus on spinal health, nervous system function, and musculoskeletal integrity as a gateway to overall wellness.
• Medical Oversight: Cardenas provides crucial diagnostic and prescriptive authority, managing conditions like hypertension and ensuring our protocols meet the highest standards of medical care.
• Functional Medicine: We dig deep to find the root causes of chronic disease, using advanced diagnostics to understand the intricate web of metabolic, hormonal, and genetic factors influencing a patient’s health.
• Personal Injury and Rehabilitation: Our team is skilled in managing and rehabilitating injuries, combining physical therapies with medical and chiropractic support to promote optimal recovery.
• Nutritional and Lifestyle Counseling: We believe that food is medicine and that lifestyle choices are the most powerful tool for long-term health. Our team provides expert guidance to empower patients to make sustainable changes.

This multidisciplinary model is not just a collection of services; it is a philosophy. By integrating these diverse disciplines, we can manage a patient’s immediate symptoms while simultaneously addressing the underlying dysfunctions driving their health issues. The cases we will explore in detail are perfect examples of this philosophy in action.

Understanding and Treating Obesity in Women: A Case Study on PCOS, Insulin Resistance, and Cardiometabolic Health

Introducing Eloise: A Common Yet Complex Clinical Picture

Today, I want to walk you through the case of a patient I’ll call “Eloise.” Her story is one I see frequently in my clinic, and it beautifully illustrates the intricate connections between weight, hormones, metabolism, and mental health in women. Understanding her journey will provide deep insights into how we approach and treat obesity as the complex, chronic disease it is.

Eloise is a 25-year-old married woman who is the Director of Fitness at her local YMCA. She came to see me for her annual exam, but her primary concern was her lifelong struggle with her weight.

Initial Assessment and Health History

During our initial consultation, we conducted a thorough review of her history. This is a critical first step in functional medicine, as it helps us piece together the puzzle of a patient’s health.

• Pertinent Medical History:

• • Hyperlipidemia: Elevated cholesterol and fats in the blood.
  • Irregular Menses: Infrequent periods since she was a teenager, a key sign of hormonal imbalance.
  • Acne: Persistent cystic acne, another clue pointing toward hormonal issues.

• Weight History:

• • Eloise reported that her weight has been a concern for her entire life. This is a crucial piece of information; it tells me that the drivers of her weight gain are likely rooted in genetics and long-standing metabolic patterns, not just recent lifestyle changes.
  • She has experienced significant weight cycling, a pattern of losing weight only to regain it, and often more. Today, she is at her heaviest weight ever. This pattern is metabolically damaging and psychologically distressing.
  • Her past attempts at weight loss involved a low-fat, low-calorie eating plan. She found this approach unsustainable, rarely lasting more than two months. This is a common story; highly restrictive diets often fail because they don’t address the underlying hormonal signals driving hunger and fat storage.
  • She admitted to feeling anxious if her daily calorie intake exceeded 1,200 calories. This suggests a disordered relationship with food, born from years of dieting.
  • She also reported intermittent binging, which started when she was 16. This is a critical finding that needs to be addressed with compassion and a specific therapeutic strategy.

• Reproductive History:

• • Eloise has never been pregnant and believes she is infertile due to her irregular cycles.
  • She and her husband have been sexually active for five years without using any form of contraception. This history, combined with her irregular menses, strongly suggests an underlying issue with ovulation.
  • She expressed a desire to become pregnant in the future, making the restoration of her fertility a key treatment goal.

• Current Health Behaviors:
  • Nutrition: She typically eats only two large meals per day (lunch and dinner) and snacks heavily in the evening due to intense cravings. This eating pattern—skipping meals and concentrating food intake later in the day—is a classic recipe for metabolic dysregulation, especially in someone with insulin resistance. The evening cravings and binging (1-2 times per week) are often triggered when she feels she has failed her strict calorie goal, leading to a cycle of anxiety and loss of control.
  • Physical Activity: As a fitness director, Eloise is very active. Her routine is impressive:

• • • Elliptical: 45 minutes, 4 days per week.
    • Strength Training: 45 minutes, 2 days per week.
    • Yoga: Twice a week.

• This tells me that a lack of exercise is not her problem. In fact, her high level of activity in the face of persistent weight gain is a major red flag for a powerful underlying metabolic issue.

• • Sleep: She generally sleeps well, except on nights after a binge episode, which often causes distress and disrupts sleep.
  • Substance Use: She consumes 1-3 alcoholic drinks per week, mostly on weekends, and is a non-smoker.

The Diagnostic Deep Dive: Uncovering the Metabolic Truth

After gathering Eloise’s history, we moved on to the physical exam and laboratory testing. This is where the objective data brings the clinical picture into sharp focus. The results were revealing and confirmed my suspicions.

Physical Exam and Laboratory Findings

Here’s a summary of our objective findings. In the world of functional medicine, we look at lab results not just for “abnormal” flags, but for patterns and optimal ranges. Anything highlighted in red in our reports indicates a result outside the optimal functional range.

• Body Composition:

• • BMI:5 kg/m², placing her in the Class II Obesity category.
  • Waist Circumference: Elevated, indicating a high level of visceral adiposity (fat around the organs). This “apple shape” is a hallmark of metabolic syndrome and is strongly associated with increased cardiometabolic risk.

• Key Laboratory Results:
  • Fasting Insulin: 36.1 µIU/mL. This is alarmingly high (an optimal level is under 5- 6 µIU/mL). Insulin is the master hormone of metabolism. Its primary job is to escort glucose from the bloodstream into our cells to be used for energy. When insulin levels are chronically high, a state known as hyperinsulinemia, the body’s cells become “numb” to its signal. This is called insulin resistance. In response, the pancreas pumps out even more insulin to try to get the job done. High insulin is a powerful fat-storage signal; it essentially locks fat in the adipose cells and prevents it from being burned for energy. This is why Eloise struggles to lose weight despite her commendable diet and exercise efforts. Her body is hormonally programmed to store fat.
  • Fasting Glucose: 107 mg/dL. This is in the prediabetic range (100-125 mg/dL). While not yet diabetes, it shows her body is already struggling to manage blood sugar effectively.
  • HOMA-IR (Homeostatic Model Assessment for Insulin Resistance): We calculated this score using her fasting insulin and glucose levels. Her score was 9.5. A HOMA-IR score above 2.0 suggests significant insulin resistance; a score of 9.5 is exceptionally high and confirms that this is the central driver of her metabolic problems.
  • HbA1c: 6.0%. This is also in the prediabetic range (5.7-6.4%). The HbA1c reflects average blood sugar levels over the past 2-3 months, confirming a sustained problem with glucose control.
  • Lipid Panel:

• • • Triglycerides:
    • HDL Cholesterol (the “good” cholesterol):

• • • This pattern of high triglycerides and low HDL is the classic dyslipidemia of insulin resistance. It’s driven by the liver’s response to excess insulin and circulating glucose.

• • Liver Enzymes (ALT/AST): Both were elevated. This suggests inflammation or stress on the liver, likely due to Non-Alcoholic Fatty Liver Disease (NAFLD), another common consequence of insulin resistance.
• Physical Signs of Insulin Resistance:

• • Acanthosis Nigricans: We observed dark, velvety patches of skin around her neck. This is a classic cutaneous marker of severe insulin resistance.
  • Skin Tags: Multiple small skin tags were present on her neck and in her axillae (armpits), another common sign.
  • Cystic Acne: Present on her face and chest.
  • Hirsutism: Mild but noticeable hair growth on her upper lip.

Synthesizing the Diagnoses

Based on this comprehensive evaluation, we were able to establish a clear set of diagnoses that explained all of her symptoms:

1. Class II Obesity: Defined by her BMI of 37.5.
2. Polycystic Ovary Syndrome (PCOS): Eloise met two of the three internationally recognized Rotterdam criteria for a PCOS diagnosis:

• Hyperandrogenism: Clinical signs of excess male hormones (androgens), evidenced by her cystic acne and hirsutism.
• Ovulatory Dysfunction: Evidenced by her long history of irregular, infrequent menses.

• (The third criterion is polycystic ovaries on ultrasound, which is not required for diagnosis if the other two are present). It’s crucial to understand that PCOS is fundamentally a metabolic condition rooted in insulin resistance. The high insulin levels stimulate the ovaries to overproduce androgens, which in turn disrupts the menstrual cycle and causes symptoms like acne and hirsutism.

• Infertility: Defined by her inability to conceive after five years of unprotected intercourse. This is a direct consequence of the anovulation caused by PCOS.
• Severe Insulin Resistance with Prediabetes and Hyperinsulinemia: Confirmed by her fasting insulin, glucose, HbA1c, and HOMA-IR score. This is the central, unifying diagnosis that connects her obesity, PCOS, and dyslipidemia.
• Dyslipidemia: The specific pattern of high triglycerides and low HDL characteristic of insulin resistance.
• Elevated Liver Enzymes: Suggestive of NAFLD.
• Binge Eating Disorder (BED) and Disordered Eating: Her pattern of restriction, anxiety around calories, and recurrent episodes of binging accompanied by distress meets the clinical criteria for BED.

A Note on Diagnosing Binge Eating Disorder

When a patient like Eloise mentions patterns of binging, it is imperative to screen for and diagnose it properly. This is not simply “overeating”; it is a recognized psychiatric disorder with specific criteria. In my practice, I integrate screening questions directly into my intake forms. A validated tool that is easy to use in a clinical setting is the Binge Eating Disorder Screener-7 (BEDS-7). This seven-question tool assesses:

• Eating an unusually large amount of food in a discrete period.
• Feeling a lack of control over eating during the episode.
• The frequency of these episodes.
• The level of distress caused by the binging.

A score of five or higher on the BEDS-7 is highly indicative of BED. Eloise’s self-report—the cycle of restriction leading to anxiety, a large consumption of food in the evening, and subsequent feelings of shame and distress—clearly aligns with this diagnosis. It’s critical to identify this because the treatment approach must be tailored to avoid triggering this behavior. For instance, prescribing another highly restrictive 1,200-calorie diet would be counterproductive and potentially harmful for her.

Analyzing the Health Risks: What’s at Stake for Eloise?

With a clear set of diagnoses, the next step is to understand the long-term health risks Eloise faces if her condition is left unmanaged. This helps us define our treatment goals and communicate the urgency and importance of our plan to the patient.

• Progressive Cardiometabolic Disease: PCOS is not just a reproductive issue; it is a lifelong metabolic condition. Even after menopause, the underlying insulin resistance persists, conferring a significantly increased risk for:

• Type 2 Diabetes
• Hypertension
• Cardiovascular Disease (heart attack, stroke)
• NAFLD progressing to cirrhosis

• This is why lifelong monitoring and management are essential for any woman diagnosed with PCOS.

• Continued Infertility: Without intervention, her anovulatory cycles would likely continue, preventing her from achieving her goal of pregnancy.
• Worsening Disordered Eating: A weight-loss plan that is not psychologically informed could exacerbate her restrictive eating and binging, severely impacting her mental health and quality of life.
• Detrimental Effects of Weight Cycling: Repeated weight loss and regain is metabolically harmful. During weight loss, especially rapid loss from calorie restriction alone, a significant portion of the lost mass can be lean muscle. When weight is regained, it tends to be primarily fat. Over many cycles, this leads to an increase in overall body fat percentage and a decrease in metabolically active muscle mass. This, in turn, lowers the basal metabolic rate, making it progressively harder to lose weight and easier to regain it. Our primary goal is to break this cycle for good.
• Development of Other Obesity-Related Complications: These could include obstructive sleep apnea, certain types of cancer (especially endometrial cancer, due to unopposed estrogen from anovulatory cycles), osteoarthritis, and depression.

Transform Your Body!- Video

Crafting the Treatment Plan: A Stepwise, Integrative Approach

Our treatment plan for Eloise must be comprehensive, addressing all facets of her condition simultaneously. However, we cannot overwhelm her by implementing everything at once. We will use a stepwise approach, building momentum and ensuring she can adapt to each change.

The Core Treatment Goals

1. Initial Weight Reduction: A goal of 10% total body weight loss. A modest loss of 5-10% is often enough to significantly improve insulin sensitivity, restore ovulation, and reduce cardiometabolic risk markers.
2. Reduce Cardiometabolic Risk: Normalize blood sugar, insulin levels, and lipids.
3. Improve PCOS Symptoms and Restore Fertility: Regulate her menstrual cycle and improve her chances of conception.
4. Reduce and Eliminate Binge Eating: Heal her relationship with food and stop the restrict-binge cycle.
5. Prevent Future Weight Cycling: Establish a sustainable lifestyle that allows for long-term weight maintenance.

Phase 1: Foundational Changes and Medical Intervention

Here is the initial plan we will roll out. This phase focuses on establishing the nutritional and medical foundations for success.

Pillar 1: Therapeutic Nutrition

The cornerstone of treating insulin resistance is nutrition. We need to shift Eloise’s focus away from calorie counting and toward hormonal control of eating. Her history of anxiety around a 1,200-calorie limit tells me this metric is a trigger for her. Instead, we will focus on what and when she eats to manage insulin.

• Eating Pattern: Shift from two large meals to 4-5 smaller meals per day, eaten every 3-4 hours. This strategy helps to:

• Prevent large blood sugar and insulin spikes.
• Maintain stable energy levels throughout the day.
• Reduce the intense evening hunger and cravings that lead to binging.

• Macronutrient Targets:
  • Protein: 90-100 grams per day. Adequate protein is crucial for satiety (feeling full), preserving lean muscle mass during weight loss, and maintaining metabolic rate.
  • Carbohydrates: Implement a reduced-carbohydrate eating pattern. The focus is on quality over quantity. We will aim for 50-100 grams of net carbs per day, primarily from:

• Fiber-rich vegetables: Non-starchy vegetables should be the bulk of her plate.
• Low-glycemic fruits: Berries, for example.

• • Minimize Ultra-Processed Foods: Dramatically reduce or eliminate sweets, starches (bread, pasta, rice), grains, and alcohol. These foods cause the most significant insulin spikes and fuel the cycle of cravings.
• The “Why” Behind This Approach: This is not a “low-carb diet” in the fad sense; it is a therapeutic nutritional intervention designed specifically to lower insulin. By controlling insulin, we allow her body to access and burn its stored fat for energy finally. It also reduces the ovarian stimulation that drives androgen excess in PCOS.

Pillar 2: Strategic Physical Activity

Eloise already has a fantastic exercise routine. We don’t need to reinvent the wheel, but we can optimize it for insulin sensitivity.

• Continue Current Routine: Her mix of aerobic exercise, strength training, and yoga is excellent for overall health, cardiovascular fitness, and muscle building.
• Add “Exercise Snacks”: I will ask her to incorporate one 10-minute walk each day, ideally after a meal. Research from leading institutions like Stanford University has shown that even short bouts of light activity after eating can significantly blunt the post-meal glucose and insulin response. This is a powerful, easy-to-implement tool for improving insulin sensitivity. In my clinical experience, patients who adopt this habit see remarkable improvements in their blood sugar control.

Pillar 3: Targeted Pharmacotherapy

Given the severity of her insulin resistance, PCOS, and prediabetes, lifestyle changes alone may not be sufficient to achieve our goals promptly. Modern medicine provides powerful tools to support her journey.

• Step 1: Metformin
  • Rationale: Metformin is a first-line medication for type 2 diabetes, but it is also widely used off-label for prediabetes and PCOS. Its primary mechanisms of action are to:

1. Decrease glucose production by the liver.
2. Increase insulin sensitivity in peripheral tissues (like muscle).
3. Slightly reduce carbohydrate absorption in the gut.

1. 1. Dosing: We will start with Metformin ER (Extended Release) 500 mg once daily with her evening meal. The ER formulation is often better tolerated, causing less gastrointestinal upset than the immediate-release version. We will then gradually titrate the dose up to a target of 2,000 mg per day, as tolerated.
2. Step 2: Immediate Contraception

• Rationale: This is a critical safety step. A weight loss of just 5-10% can spontaneously restore ovulation in women with PCOS. Since Eloise is not yet ready to conceive and we are about to start a powerful weight-loss regimen, an unplanned pregnancy would be high-risk. We must prevent this.
• Medication: We will start her on a combined oral contraceptive (COC). COCs are also recommended for managing the symptoms of PCOS because they help regulate cycles, reduce androgen levels (which improves acne and hirsutism), and protect the endometrium from cancer risk.

• Step 3: Tirzepatide (A GLP-1/GIP Receptor Agonist)
  • Rationale: Once she is stable on metformin and contraception, we will introduce tirzepatide. This is a newer class of medication that has revolutionized obesity medicine. Tirzepatide works by mimicking two key gut hormones, GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic polypeptide). Its effects are multifaceted:

1. Potent Insulin Sensitizer: It stimulates insulin secretion only when blood sugar is high (glucose-dependent), making it very safe from a hypoglycemia standpoint.
2. Suppresses Glucagon: It reduces the release of glucagon, a hormone that tells the liver to release stored sugar.
3. Slows Gastric Emptying: This promotes satiety and blunts post-meal blood sugar spikes.
4. Central Appetite Regulation: It acts on appetite centers in the brain (like the hypothalamus) to reduce hunger, quiet “food noise,” and increase feelings of fullness. This mechanism is particularly effective for patients with binge eating tendencies.

1. 1. Dosing: We will start at the lowest dose (2.5 mg injected subcutaneously once a week) and titrate up every four weeks to a maximum dose of 15 mg, or until we reach a dose that provides effective appetite control and stable eating patterns.
   2. Crucial Counseling Point: Because GLP-1 agonists slow gastric emptying, there is a theoretical concern that they could reduce the absorption of oral medications, including contraceptives. To mitigate this risk, I will counsel Eloise to use a barrier method of contraception (e.g., condoms) for the first four weeks after starting tirzepatide and for the first four weeks after every dose increase. This is a non-negotiable safety measure.
2. Step 4: Potential for Lisdexamfetamine

• Rationale: Lisdexamfetamine is an FDA-approved medication for the treatment of moderate to severe Binge Eating Disorder. While I find that GLP-1 agonists are often highly effective at reducing or eliminating binge urges, we will keep this option in reserve. If her binging continues to be a significant issue despite the tirzepatide, we can add this medication to her regimen.

The Journey Continues: Six-Month Follow-Up

Eloise returned to my clinic six months later, and the transformation was already beginning. She was engaged, motivated, and feeling more in control of her health than ever before.

Progress Report

• Medications: She was tolerating Metformin 2,000 mg ER daily and had successfully titrated her Tirzepatide up to 10 mg weekly. She reported this was her “sweet spot,” providing excellent appetite control without significant side effects. She was compliant with her oral contraceptive and had used the barrier method as instructed during dose titrations.
• Symptom Improvement: She noted a significant reduction in her acne and hair growth, a direct result of the hormonal rebalancing from her weight loss and medication.
• Nutritional Changes: This was a huge win. She had successfully shifted her mindset from calories to patterns.

• She was consistently eating every 3-4 hours.
• Her protein intake was on target at 80-90 grams daily.
• She had embraced vegetables and low-glycemic fruits while minimizing starches and sweets.
• Her evening cravings were dramatically reduced.
• Her binge episodes had decreased from 1-2 times per week to 1-2 times per month, and they were now triggered by external stress rather than her internal diet rules. This is a monumental shift in her relationship with food.

• Physical Activity: She continued her impressive gym routine and had successfully incorporated the daily 10-minute walks.
• Alcohol: Her intake had naturally decreased to 0-1 drinks per week.

The Objective Data: Remarkable Improvements

The six-month lab results were stunning and validated the effectiveness of our approach.

• Weight Loss: She had lost 11% of her initial body weight, surpassing our initial goal.
• Fasting Insulin: Down from 36.1 to 4 µIU/mL. While still elevated, this is a 40% reduction and a massive step in the right direction.
• Fasting Glucose: Decreased from 107 to 98 mg/dL, now in the normal range.
• HOMA-IR: Down from 9.5 to 2. Still high, but a huge improvement.
• HbA1c: Down from 6.0% to 6%, moving her out of the prediabetic range.
• Lipids and Liver Enzymes: All markers had improved significantly. More black (normal) and less red (abnormal) on her lab report.
• Binge Eating Disorder: Her reduced frequency of binging meant she no longer met the diagnostic criteria for BED.

The Next Steps: Building on Success

At this stage, the goal is to maintain momentum and continue optimizing her health.

1. Nutrition and Activity: Continue everything she is doing. I encouraged her to add a second 10-minute walk each day if she felt up to it to further enhance insulin sensitivity.
2. Medications: Continue the metformin, tirzepatide, and oral contraceptive at their current effective doses.
3. Monitoring: We will continue to keep lisdexamfetamine as a potential future option if the stress-related binging were to increase or become problematic again.

The Two-Year Mark: A Celebration of Health Transformation

Two years after her initial visit, Eloise’s story is one of profound and sustained success. She has remained consistent with her plan and has truly reclaimed her health.

Two-Year Progress Report

• Medications: She remained on her full regimen of metformin and tirzepatide. For her binging, we did eventually decide to add a low dose of lisdexamfetamine, which completely resolved the remaining stress-induced episodes. She reported zero binges since starting it.
• Reproductive Plans: She was feeling ready to start thinking about pregnancy. As a first step, she decided to stop her oral contraceptive and switch to a barrier method to see if her natural menstrual cycles would return and become regular. This is an exciting step toward her family-planning goals.
• Health Behaviors: Her habits were now deeply ingrained.

• Nutrition: Her eating pattern was stable, with minimal evening cravings and no binging.
• Physical Activity: She continued her full routine, including the two daily 10-minute walks.
• Sleep and Alcohol: Both remained excellent.

The Final Tally: A New Metabolic Reality

Her two-year labs and metrics tell the full story. This is what true metabolic healing looks like.

• Weight Loss: She had achieved a total weight loss of 1% of her initial body weight.
• Fasting Insulin: Down to 4 µIU/mL. This is approaching the optimal range (I like to see it under 6) and represents a massive 77% reduction from her starting point of 36.1.
• HOMA-IR: Down to 1, now within the normal range. Her insulin resistance has been effectively reversed.
• HbA1c: Down to 2%, a completely normal and healthy level.
• Lipids and Liver Enzymes: All markers were now well within the normal, optimal ranges.

The Long-Term Vision

Eloise has fundamentally altered her long-term health trajectory. By addressing the root cause—her severe insulin resistance—we have not only helped her lose weight but have also:

• Dramatically reduced her lifetime risk of type 2 diabetes, cardiovascular disease, and liver disease.
• Resolved her PCOS symptoms.
• Eliminated her binge eating disorder.
• Positioned her in an optimal state of health to now pursue a safe and healthy pregnancy.

The goal moving forward is maintenance. Obesity is a chronic disease, much like hypertension. The medications and lifestyle that got her to this point will likely be necessary long-term to help her maintain these incredible gains. She is now in a place of empowerment and control, equipped with the knowledge, tools, and habits to manage her health for the rest of her life. Her case is a powerful testament to the effectiveness of a comprehensive, evidence-based, and compassionate approach to obesity medicine.

The Role of Integrative Chiropractic Care in This Journey

While this case focused heavily on the metabolic and pharmacological aspects, it’s important to highlight where integrative chiropractic care fits into this holistic model at our clinic. For a patient like Eloise, achieving a significant weight loss of over 24% causes major changes in her body’s biomechanics.

• Structural and Postural Realignment: As weight is lost, the body’s center of gravity shifts. This can lead to new patterns of stress on the spine, hips, knees, and ankles. Chiropractic adjustments are essential during this process to ensure proper spinal alignment, improve posture, and alleviate any resulting joint pain or discomfort. This helps patients remain active and pain-free, which is critical for long-term adherence to their physical activity plan.
• Nervous System Regulation: Chiropractic care, particularly techniques that focus on the autonomic nervous system, can help modulate the body’s stress response. By improving nervous system function through spinal adjustments, we can help downregulate the sympathetic (“fight-or-flight”) response and upregulate the parasympathetic (“rest-and-digest”) response. This can have a beneficial effect on stress-related behaviors like emotional eating and binging, and may even contribute to improved insulin sensitivity and digestion.
• Functional Rehabilitation: My background allows me to integrate specific rehabilitation exercises to address any muscle imbalances that may have developed or become apparent after weight loss. We can create customized plans to strengthen the core, improve balance, and ensure her body moves efficiently and safely, preventing future injuries and supporting her active lifestyle.

By combining the medical and pharmacological interventions managed under Dr. Cardenas’s oversight with the structural, neurological, and functional support of chiropractic and rehabilitation, we provide a truly 360-degree approach to care. This ensures that as the patient’s metabolic health improves, their musculoskeletal system adapts and strengthens in concert, leading to a more complete and sustainable state of overall well-being.

Unlocking Male Health: A Functional Medicine Approach to Insulin Resistance, Fertility, and Cardiovascular Wellness

Introducing George: A Case of Modern Male Health Challenges

Let me introduce you to George. His story is one I see with increasing frequency in my practice—a story that sits at the intersection of modern life’s demands and the body’s intricate biochemical responses. George is a 35-year-old project manager at a tech company. He’s a non-smoker, married, and he and his spouse are trying for their second child, a journey that has already been marked by difficulty with their first.

When George first came to see me, he presented with a constellation of symptoms that were clearly taking a toll on his quality of life. He reported experiencing significant depression and anxiety, a low sperm count confirmed by a fertility specialist, and elevated blood pressure readings that were a source of constant worry. He described being under immense stress, a two-front war being waged at work, where he was striving for a promotion, and at home, where financial pressures and the emotional weight of their fertility struggles were mounting.

To truly understand George’s situation, we have to look beyond the lab values and symptom list. His daily life paints a vivid picture of the environmental and lifestyle factors at play:

• High-Stress Career: The pressure of managing complex projects and aiming for a promotion in a competitive tech environment creates chronic sympathetic nervous system activation.
• Challenging Commute: Long drives to and from work are not just lost time; they are a source of stress and sedentary behavior, contributing to both mental fatigue and physical inactivity.
• Workplace Food Environment: The tech industry is famous for its perks, including an abundance of free food and drinks. While seemingly a benefit, this often translates to easy access to highly palatable, calorie-dense, and nutrient-poor options, making mindful eating incredibly difficult.
• Significant Life Stressors: Beyond his career, George is navigating the process of buying a new home to secure a spot in a better school district. This financial and logistical strain is compounded by the distressing news of his low sperm count.
• Family Health History: A significant source of George’s anxiety is his father’s diagnosis of heart failure, which he correctly links to untreated high blood pressure. This knowledge casts a long shadow over his own elevated readings, fueling a fear of following in his father’s footsteps.
• Personal Health Concerns: George also shared that he was experiencing occasional erectile dysfunction, which he attributed to stress. This is a common and often underreported symptom that is frequently linked to both psychological stress and the underlying vascular and hormonal issues we see in metabolic syndrome.

Initial Clinical Assessment and Laboratory Findings

Three months before our first consultation, George had a complete physical with another provider. The data from that visit, combined with our initial assessment, revealed a concerning trajectory. He reported poor sleep, frequent and intense hunger, and a deep sense of shame over his perceived lack of control. While he and his spouse were trying to embark on a health journey together, the fertility issues were creating a subtle friction, with George worrying about how she was interpreting the situation.

Let’s examine his vital signs and lab work, as they provide the objective data that anchor our clinical picture:

• Waist Circumference: His measurement was elevated. For men, a waist circumference greater than 40 inches (102 cm) is a key indicator of visceral adiposity—the metabolically active fat stored around the internal organs—and a primary component of metabolic syndrome.
• Blood Pressure: His readings were consistently elevated, placing him in the category of hypertension. This was not just a number on a chart for George; it was a direct link to his greatest fear: heart disease.
• Metabolic Markers:

• Fasting Glucose & Fasting Insulin: Both were significantly increased. Elevated fasting insulin, in particular, is one of the earliest and most sensitive markers of developing insulin resistance. The pancreas is working overtime, pumping out more and more insulin to try to get glucose into resistant cells.
• HOMA-IR (Homeostasis Model Assessment for Insulin Resistance): We calculated his HOMA-IR score to be 1. A score above 1.9 is indicative of early insulin resistance, and a score above 2.9 is considered significant. George’s result firmly placed him in the insulin-resistant category. This calculation ([Fasting Insulin (µU/mL) x Fasting Glucose (mg/dL)] / 405) is a critical tool in my practice for quantifying the degree of insulin dysfunction.

• Lipid Panel: He showed mildly elevated cholesterol, another hallmark of the dyslipidemia associated with metabolic syndrome.
• Kidney Function and Electrolytes: These were reassuringly normal.
• Missing Labs: Critically, his previous workup did not include a Hemoglobin A1c (HbA1c), a full thyroid panel, or a liver panel. The HbA1c would give us a three-month average of his blood sugar control; the thyroid panel is crucial, as thyroid dysfunction can mimic and exacerbate metabolic issues; and a liver panel is vital given the link between insulin resistance and non-alcoholic fatty liver disease (NAFLD). Obtaining this missing information was an immediate priority.

This initial snapshot of George’s health revealed a man on a dangerous path. The combination of central obesity, hypertension, and insulin resistance put him squarely on the spectrum of metabolic syndrome, a condition that dramatically increases the risk for type 2 diabetes, cardiovascular disease, and, as we see in his case, can profoundly impact hormonal health and fertility.

The Vicious Cycle: Deconstructing the Physiology of Stress, Hormones, and Obesity

One of the most powerful moments in my initial consultation with a patient like George is when we shift the conversation from shame to science. He expressed feeling “ashamed” that he couldn’t control his appetite. This is a common and destructive narrative that I am passionate about dismantling. I explained to him the concept of “chemical versus character.” His intense hunger and cravings were not a failure of willpower; they were the predictable result of a complex and powerful biochemical cascade. Understanding this helps release the internal bias, stigma, and guilt that so often sabotage a patient’s progress.

We walked through the physiology of what was happening in his body, which I often describe as a positive feedback loop—positive in the sense of amplification, not in the sense of being good.

Obesity? Hormone Changes? More Obesity

This vicious cycle is at the very heart of George’s struggle. Let’s break down the key players:

1. The Role of Adipose Tissue as an Endocrine Organ

For a long time, we viewed fat tissue (adipose tissue) as simply an inert storage depot for energy. We now know that it is a highly active endocrine organ, secreting a host of hormones and inflammatory molecules (adipokines) that have systemic effects.

• Aromatase Activity: In men, excess adipose tissue is particularly problematic because it is rich in an enzyme called aromatase. This enzyme’s primary job is to convert androgens (like testosterone) into estrogens (like estradiol). As a man gains more visceral fat, aromatase activity skyrockets. This leads to two simultaneous problems:

1. Decreased Testosterone: The primary male sex hormone is being actively converted away, leading to lower circulating levels. Low testosterone contributes to fatigue, low mood, reduced muscle mass, increased fat storage, and can directly impact sperm production and libido—all issues George was facing.
2. Increased Estrogen: Higher estrogen levels in men can further promote fat storage, particularly in the chest (gynecomastia) and hips, and contribute to a negative feedback loop at the level of the pituitary and hypothalamus, further suppressing the body’s own testosterone production.

2. The Insulin and Cortisol Connection

Simultaneously, the state of insulin resistance and chronic stress creates a perfect storm of hormonal dysregulation that directly drives appetite.

• Elevated Insulin: In an insulin-resistant state, the body’s cells (particularly muscle, liver, and fat cells) don’t respond properly to insulin. The pancreas compensates by producing even more. Chronically high levels of insulin (hyperinsulinemia) are a powerful signal for the body to do one thing: store fat. It essentially locks fat in the adipose cells, preventing it from being used for energy. This makes weight loss feel physiologically impossible and also contributes to feelings of low energy, as the body’s cells are effectively “starving” for glucose despite high levels in the blood.
• Elevated Cortisol: George’s high-stress life means his adrenal glands are constantly pumping out cortisol, the primary stress hormone. While cortisol is essential for the “fight or flight” response in the short term, chronic elevation has devastating metabolic consequences. Cortisol works to increase blood sugar to provide ready energy for a perceived threat. It does this by promoting gluconeogenesis in the liver and increasing insulin resistance in peripheral tissues. Crucially, cortisol also acts directly on the brain to powerfully stimulate appetite, specifically driving cravings for high-fat, high-sugar, “comfort” foods.

3. The Dysregulation of Appetite Hormones: Ghrelin, Leptin, and GLP-1

This is where George’s feeling of being “out of control” of his hunger finds its biological explanation. The hormonal orchestra that governs hunger and satiety is completely out of tune.

• Ghrelin (The “Hunger Hormone”): Produced primarily in the stomach, ghrelin’s job is to signal hunger to the brain. In a healthy individual, ghrelin levels rise before a meal and fall sharply after eating. In states of insulin resistance and chronic stress, ghrelin signaling can become dysregulated, leading to persistently high levels and a constant feeling of hunger.
• Leptin (The “Satiety Hormone”): Produced by fat cells, leptin’s job is to signal to the brain (specifically the hypothalamus) that we have enough energy stored and it’s time to stop eating. However, in obesity, a phenomenon known as leptin resistance occurs. Despite having very high levels of leptin (because of the excess fat mass), the brain’s receptors become “deaf” to the signal. The brain mistakenly believes the body is starving, leading it to ramp up appetite and decrease energy expenditure. It’s like screaming into a broken microphone—the signal is being sent, but it’s not being received.
• GLP-1 (Glucagon-Like Peptide-1): This is a critical incretin hormone produced in the gut in response to food intake. GLP-1 has multiple beneficial effects: it enhances insulin secretion from the pancreas (in a glucose-dependent manner), suppresses glucagon (a hormone that raises blood sugar), slows down gastric emptying (making you feel fuller for longer), and acts directly on the brain to promote satiety. In obesity and type 2 diabetes, the secretion and effectiveness of GLP-1 are often impaired.

The net effect of this hormonal chaos is a powerful, chemically-driven increase in appetite and a blunted sense of fullness (satiety) and satisfaction after a meal (satiation). This drives further calorie intake, leading to more fat storage, more inflammation, more hormonal disruption, and the cycle goes on.

4. The Stress-Shame-Cortisol Spiral

The final, and perhaps most insidious, piece of this puzzle is the psychological component. When George is unable to control the cravings and appetite driven by this powerful biology, he engages in self-blame and negative self-talk. He feels ashamed. This psychological stress is a potent activator of the HPA (Hypothalamic-Pituitary-Adrenal) axis, leading to the release of… more cortisol.

This is a cruel feedback loop where the biological drive to eat leads to psychological distress, which in turn releases the very hormone that intensifies the biological drive to eat. Breaking this cycle requires a two-pronged attack: addressing the underlying physiology while simultaneously providing the patient with the tools and the understanding to reframe their psychological response. My role as a clinician is to be both a biochemist and a coach, explaining the “why” to alleviate the shame and providing the “how” to change the outcome.

Defining the Mission: Aligning with George’s Health Goals

After explaining this complex physiology to George, a palpable sense of relief washed over him. For the first time, he saw his struggle not as a personal failing but as a medical condition. This shift in perspective is the essential foundation upon which we can build a successful treatment plan.

The next critical step was to ask him: “What are your goals? What matters most to you?” It’s a simple question, but the answer is everything. It’s crucial to note that he didn’t mention weight loss. His goals were far more profound and intrinsically motivating:

1. Improve Heart Health and Prevent Diabetes: Driven by his father’s story, this was his top priority. He wanted to change his family’s health legacy.
2. Improve Fertility: The dream of having a second child was a powerful, tangible motivator.
3. Manage Stress: He was tired of feeling anxious, overwhelmed, and depressed.
4. Have More Energy: He wanted the vitality to be an active, engaged father for his child and his future children.

These goals became our “true north.” While weight loss and waist circumference reduction would be necessary outcomes to achieve these goals, framing the plan around his core values made the process meaningful and sustainable. Our long-term considerations were clear: treat his obesity as the chronic disease it is, prevent the onset of other chronic diseases like type 2 diabetes and cardiovascular events, and help him build a toolkit of sustainable lifestyle changes that would serve him for a lifetime.

The Initial Action Plan: A Multifaceted Approach

Based on our assessment and George’s goals, we formulated an initial, multi-pronged action plan.

• Complete the Diagnostic Picture: The first order of business was to order the missing labs: an HbA1c, a complete thyroid panel, and a liver function panel.
• Nutritional Intervention: A referral to a Registered Dietitian Nutritionist (RDN) was essential. The goal was not just to give him a diet plan, but to provide him with education on mindful eating, portion control, blood sugar regulation, and strategies to navigate his challenging food environment at work.
• Medical Management of Hypertension: We needed to get his blood pressure under control immediately to mitigate his cardiovascular risk. We started him on a first-line antihypertensive medication and, crucially, instructed him to begin monitoring his blood pressure at home and keep a log. This empowers the patient and provides us with far more data than a single office reading.
• Investigate Sleep: His reports of poor sleep, combined with his elevated waist circumference and hypertension, raised a high index of suspicion for Obstructive Sleep Apnea (OSA). OSA is a serious condition where breathing repeatedly stops and starts during sleep. It starves the body of oxygen, puts immense strain on the cardiovascular system, and severely disrupts hormonal regulation (including increasing cortisol). We referred him for a formal sleep study.
• Introduce Pharmacotherapy for Obesity: We had an initial discussion about obesity medications. I explained that these are not “magic pills” but tools that work on the very hormonal pathways we had discussed, helping to re-regulate appetite and satiety signals to support his lifestyle efforts.
• Stress Management and Physical Activity: We talked about introducing meditation and setting realistic physical activity goals. The initial aim was not a strenuous gym routine but simply finding ways to move more throughout his day.

This was a substantial “to-do list,” but by breaking it down into manageable steps and linking each one back to his core goals, George felt empowered rather than overwhelmed.

The Four-Week Follow-Up: Navigating the Realities of Change

Four weeks later, George returned to my office. This follow-up visit is often one of the most revealing, as it’s where the initial plan collides with the reality of a patient’s life.

The Victories

George had made some fantastic progress, and it was important to celebrate these wins first to reinforce his positive actions:

• Blood Pressure Management: He had started the medication and, just as we’d asked, diligently kept a blood pressure log. This demonstrated commitment and gave us valuable data to work with.
• Completed Labs: He had followed through on getting his bloodwork done. The results were illuminating:

• Thyroid and Liver Panels: Both were normal, which was excellent news. This allowed us to rule out primary thyroid dysfunction or significant liver damage as contributing factors.
• Hemoglobin A1c (HbA1c): His result was 9%. This confirmed our suspicion based on his HOMA-IR. An HbA1c between 5.7% and 6.4% places him firmly in the prediabetes category. This diagnosis was a powerful motivator, making the threat of diabetes tangible and immediate.

• Scheduled Sleep Study: He had taken the initiative to schedule his sleep study for the following week.
• Engaged with the Dietitian: He had already had his first appointment with the RDN. This early engagement is a strong predictor of long-term success.

The Challenges

However, the journey was not without its bumps.

• Weight Gain: The number on the scale had gone up slightly. For many patients, this can be incredibly demoralizing.
• Barriers to Lifestyle Change: He admitted he had not been able to start the meditation or physical activity routine.

Through further conversation, prompted by the dietitian’s insights and our discussion, we uncovered the “why” behind these challenges.

• Unconscious Eating Habits: He was shocked to discover through food logging that his portion sizes were much larger than he had realized.
• Stress Eating: He identified a clear pattern of stress eating, both at his desk at work and at home in the evenings.
• The “Soda to Water” Hurdle: He was struggling to make the switch from soda to water, a common challenge due to the powerful combination of sugar and caffeine.

A Critical Coaching Moment: Reframing “Failure”

George was visibly embarrassed about the weight gain. This is a pivotal moment in the clinician-patient relationship. My colleague, Sam, articulated the approach I take perfectly. I asked George, “Does this number on the scale surprise you?”

This non-judgmental question opens the door for an honest conversation. He acknowledged that it didn’t surprise him, given his struggles with stress eating. This allowed us to reframe the situation. This wasn’t a failure; it was data. We now had valuable information about his primary triggers and obstacles.

I reassured him that the path to health is a marathon, not a sprint. It is never a straight, diagonal line down. There will be fluctuations. The thought of having to change eating patterns can sometimes trigger a “last hurrah” mentality. The key is to normalize this experience and shift the focus from the single data point on the scale to the overall pattern of positive behaviors he was already adopting.

It is absolutely critical to avoid stigmatizing language. Labeling a patient as “noncompliant” is not only inaccurate and shaming, but it also absolves us as clinicians of our responsibility to help the patient find a plan that actually works for them. There are no “bad” patients. There are only patients whose circumstances have not yet aligned for success. Our job is to be detectives and collaborators, constantly adjusting the plan to overcome barriers as they arise.

Adjusting the Plan: Targeting the Barriers

With this new understanding, we could make targeted adjustments to his plan.

• Addressing the Meditation Barrier: George admitted he “felt a little silly” trying to meditate. This is a common feeling. The solution was to make it simple, private, and accessible. We suggested a three-minute guided meditation using a smartphone app. He could do it in his car after his stressful commute before walking into the office. The goal was to start small: just twice a week. This lowered the barrier to entry and made it feel achievable.
• Addressing the Energy Barrier for Exercise: He reported not having the energy for physical activity. Instead of pushing for a structured workout, we redefined “activity.” The new goal was to move more. We suggested taking the stairs instead of the elevator, and setting a timer to get up from his desk and walk around for a few minutes every hour. The goal was to break up long periods of sedentary time.
• Pharmacological Adjustments:

1. 1. Blood Pressure: His home log showed his blood pressure was better, but not yet at our target goal. We made a small increase to his medication dose.
   2. Addressing Mood, Cravings, and Energy: We discussed starting a combination medication: bupropion-naltrexone. This was a strategic choice for several reasons:

• Bupropion: An antidepressant that can also help with low energy and focus due to its mild stimulating effects on dopamine and norepinephrine. This would directly address his mood and energy concerns.
• Naltrexone: An opioid antagonist that works in the brain’s reward center to reduce the “pleasure” response from highly palatable foods, particularly sugary ones. This would directly target his cravings and the stress-eating cycle, making it easier to switch from soda to water.

• Timing the New Medication: Because bupropion can be stimulating and potentially interfere with sleep architecture, we instructed him to wait to start it until after his sleep study was completed the following week. This is a crucial detail in coordinating care.

By identifying the specific barriers and tailoring our solutions, we transformed his setbacks into a revised, more effective strategy.

The Four-Month Mark: Momentum and New Questions

Four months later, George returned, and he was a changed man. The adjustments we had made were clearly working, and he had built significant momentum.

The Progress Report

• Blood Pressure: Under excellent control.
• Sleep Apnea: His sleep study had indeed confirmed a diagnosis of Obstructive Sleep Apnea. He was now using a CPAP (Continuous Positive Airway Pressure) machine at night. This was a game-changer. For the first time in years, he was getting restorative sleep.
• Mood and Stress: His mood had noticeably improved. The combination of better sleep, the effects of the bupropion, and his new meditation practice were making a profound difference. He was consistently doing his three-minute meditations and had started taking walks during his lunch breaks.
• Weight and Nutrition: His weight was down, and his nutritional habits had dramatically improved. The RDN was thrilled with his progress. He had found strategies to manage his workplace food environment and was making better choices at home.
• Physical Activity: He had embraced the idea of “moving more.” A new watch that reminded him to stand and move was helping him stay consistent with his walks.

A New Challenge: The Persistent Appetite

Despite all this incredible progress, he had one persistent complaint: “I’m still very hungry. My appetite’s just not well controlled.”

This is not an uncommon scenario. While bupropion-naltrexone can be very effective for cravings and emotional eating, it doesn’t always have a powerful effect on the fundamental, physiological hunger signals driven by hormones like ghrelin and leptin resistance.

He also mentioned that a friend had told him about an “injectable medication” for weight loss. This opened the door for our next therapeutic evolution. He and his spouse were now planning to start trying to conceive again in a few months, adding urgency and importance to optimizing his metabolic health.

The Next Level of Care: Introducing Incretin-Based Therapy

George’s question about the injectable medication was perfectly timed. He was referring to the class of drugs known as GLP-1 receptor agonists, such as semaglutide and liraglutide. These medications represent a revolutionary advance in the treatment of obesity and type 2 diabetes because they directly target the hormonal dysregulation at the heart of the disease.

Our Updated Plan

1. Transitioning Medications:

• Initiating Semaglutide: After a thorough discussion of the risks and benefits, and confirming he had insurance coverage, we decided to start him on semaglutide. We began at the standard starting dose of 0.25 mg, injected once weekly. This medication would powerfully address his persistent hunger by mimicking the body’s own GLP-1 hormone, promoting satiety, slowing digestion, and improving his insulin sensitivity.
• Tapering and Adjusting: Since the semaglutide would now be the primary agent for appetite control and metabolic improvement, we planned to taper him off the bupropion-naltrexone combination. However, because the bupropion had been so effective for his mood, we would continue it as a standalone medication to manage his depression and anxiety. This is a perfect example of nuanced, personalized pharmacology.

• Advanced Body Composition Monitoring: As he was starting a powerful weight-loss medication, simply tracking the number on the scale was no longer sufficient. It was now critical to monitor his body composition. Significant weight loss can sometimes lead to a loss of lean muscle mass, which we want to prevent at all costs, as muscle is metabolically active tissue that helps maintain a healthy metabolism. We advised him to get a DEXA scan or, if that wasn’t accessible, to purchase a home bioimpedance scale. The key wasn’t the absolute accuracy of the home scale, but its ability to monitor trends over time.
• Incorporating Resistance Training: To proactively protect his muscle mass while on semaglutide, we strongly recommended adding resistance training to his routine. This didn’t mean he had to become a bodybuilder. It could be as simple as bodyweight exercises (squats, push-ups, planks) or using resistance bands a few times a week. The combination of adequate protein intake (guided by his RDN) and resistance exercise is the best strategy to ensure that the weight he loses is primarily fat, not precious muscle.

The One-Year Transformation: Achieving the Ultimate Goals

George’s one-year follow-up was a celebration. The comprehensive, integrated, and adaptive plan had yielded truly life-changing results.

The Incredible News

• A Growing Family: The first thing he shared was the best news of all: his spouse was pregnant and due with a baby girl in three months. Our work on his metabolic and hormonal health had directly contributed to achieving their most cherished goal. Restoring metabolic balance can significantly improve sperm quality, count, and motility.
• Sustained Health Improvements:

• Blood Pressure: Consistently controlled.
• Medication Success: He had continued on both bupropion (for mood) and semaglutide. Interestingly, he had found that a dose of 7 mg of semaglutide (the full therapeutic dose is 2.4 mg) was perfect for him. It provided excellent appetite control and continued weight loss without any side effects. This highlights a key point: the goal is to find the lowest effective dose for each individual. Not everyone needs to titrate to the maximum dose. He was on a perfectly acceptable and effective maintenance dose.
• Waist Circumference: Significantly down, indicating a major reduction in dangerous visceral fat.
• Sleep: He was sleeping well and feeling rested.
• Lifestyle Habits: While he wasn’t meditating as formally anymore, the practice had taught him valuable stress management skills. He had incorporated his lunchtime walks as a non-negotiable part of his routine.

The Objective Data: A Story of Reversal

Let’s look at the stunning comparison of his metabolic markers from his first visit to one year later:

Marker	Initial Visit	One-Year Follow-Up	Status
Weight	Elevated	? Significant Decrease	Improved
Waist Circumference	>40 inches	? Significant Decrease	Improved
Blood Pressure	Hypertensive	Normal/Controlled	Resolved
Fasting Glucose	Elevated	Normal	Resolved
Fasting Insulin	Markedly Elevated	Normal	Resolved
HOMA-IR	3.1 (Insulin Resistant)	1.64 (Insulin Sensitive)	Resolved
HbA1c	5.9% (Prediabetic)	<5.7% (Normal)	Resolved

His HOMA-IR score of 1.64 was now well within the optimal range (less than 1.9), indicating his insulin sensitivity had been restored. His HbA1c had dropped out of the prediabetic range. He had effectively reversed his prediabetes.

Integrating Chiropractic Care in Metabolic Health

Throughout George’s journey, while we focused heavily on metabolic and pharmacological interventions, foundational chiropractic care played a crucial supportive role. The chronic stress George was under manifested not just biochemically but also physically, leading to neuromuscular tension, spinal misalignments (subluxations), and poor posture, especially given his sedentary job and long commute.

• Nervous System Regulation: Chiropractic adjustments help to modulate the autonomic nervous system, down-regulating the “fight or flight” sympathetic response and promoting the “rest and digest” parasympathetic state. For a patient like George, whose system was in sympathetic overdrive due to chronic stress, this rebalancing is invaluable. It can help lower cortisol, reduce muscle tension, and create a physiological state more conducive to healing and rest.
• Pain and Discomfort Management: As George began his physical activity journey, aches and pains could have easily become a barrier. Regular chiropractic care helped to ensure his musculoskeletal system was functioning optimally, improving his mobility, reducing the risk of injury, and managing any discomfort that arose from his new walking routine and future resistance training.
• Holistic Support: Integrating chiropractic care reinforced the message that his body is an interconnected system. Addressing his spinal health was part of the holistic strategy to improve his overall function, complementing the nutritional, medical, and psychological interventions we were implementing. It helped him feel better physically, which in turn supported his mental and emotional energy to stick with the program.

This integration is central to our philosophy at Injury Medical Clinic PA. Under the collaborative oversight of Dr. Cardenas, we ensure that every aspect of a patient’s health—from their spine to their cells—is addressed cohesively and synergistically.

Navigating Perimenopause: A Case Study in Integrative Treatment for Hormonal and Metabolic Health

In my practice, I frequently encounter patients grappling with the multifaceted challenges of perimenopause. This transitional phase is often accompanied by a constellation of symptoms that can significantly impact quality of life, including weight gain, mood swings, fatigue, and brain fog. Understanding the intricate interplay between hormonal shifts and metabolic function is crucial for developing an effective treatment plan.

Let’s explore the case of “Lynn,” a 43-year-old woman whose journey typifies the struggles many face during this life stage. Lynn’s story provides a powerful illustration of how a thoughtful, stepwise, and integrative approach can lead to profound and lasting positive changes. Her initial goals were clear: manage her escalating perimenopausal symptoms, reduce her elevated blood pressure, and halt the persistent weight gain that had left her feeling discouraged.

The Rationale for Prioritizing Menopausal Hormone Therapy (MHT)

A common and very valid question arises in cases like Lynn’s: Why begin with menopausal hormone therapy (MHT) instead of immediately starting an obesity medication? This decision is a cornerstone of our patient-centered, shared decision-making process.

When a patient presents with a primary concern, our first duty is to listen and address that specific issue. For Lynn, the disruptive symptoms of perimenopause were her most pressing problem. The hot flashes, sleep disturbances, and brain fog were not just inconveniences; they were actively degrading her daily life. Therefore, we made a collaborative decision to start there.

Established guidelines supported our clinical reasoning. Lynn met the two key criteria for safely initiating MHT:

1. Her symptoms began within the last 10 years.
2. She is under the age of 60.

These factors place her in a low-risk category, allowing us to proceed confidently. We chose a transdermal estradiol patch, a form of MHT that is bioidentical and, because it is absorbed through the skin, bypasses the liver’s first-pass metabolism. This route is associated with a lower risk of blood clots compared to oral estrogens, making it a safer choice, particularly for a patient like Lynn with emerging cardiometabolic risk factors such as hypertension (Rosano et al., 2017).

The Importance of a Stepwise Approach

Another critical element of our strategy was to introduce one new treatment at a time. When multiple medications or significant interventions are started simultaneously, it becomes nearly impossible to discern the source of any potential side effects. Was the nausea from the MHT or the new weight management drug? Is the headache a side effect or an unrelated issue? This ambiguity can lead to unnecessary discontinuation of effective therapies and patient frustration.

By starting with the transdermal patch alone, we could isolate its effects—both positive and negative. This methodical approach empowers the patient and the clinician to make clear, informed decisions. We didn’t want to overload her system or her psyche. Our goal was to build momentum through small, manageable wins.

Alongside the MHT, we reinforced foundational lifestyle habits. We encouraged Lynn to increase her water intake, which is crucial for cellular function and can help mitigate side effects. We also asked her to continue monitoring her blood pressure and sleep patterns, providing us with valuable data to track her progress. Importantly, the conversation about future options, including advanced weight management medications, was initiated from the very beginning. This plants a seed of hope and outlines a clear, long-term strategy, assuring the patient that we have a multi-step plan.

Six-Week Follow-Up: The Initial Triumphs

Six weeks later, Lynn returned to our clinic, and the transformation was already palpable. She was diligently working with a dietitian and a therapist—key members of the collaborative care team we advocate for. The support from these professionals helped her navigate the nutritional and emotional aspects of her health journey.

The initial results were encouraging:

• Behavioral Changes: She had started a regular walking routine and was feeling motivated enough to consider a kickboxing class.
• Weight and Blood Pressure: She had lost a few pounds, and her blood pressure readings, while still occasionally elevated, were trending in the right direction.
• Symptom Improvement: Most significantly, she reported a dramatic improvement in her quality of life. Her sleep had improved, and the debilitating brain fog and fatigue had substantially lessened. She described this as “life-changing.”

These early improvements were a direct result of addressing the root hormonal imbalance with MHT. Restoring hormonal equilibrium began to stabilize her physiology, which in turn gave her the energy and mental clarity to engage more fully in lifestyle changes.

The Role of Integrative Chiropractic Care in Hormonal and Metabolic Health

At this juncture, it is essential to discuss how integrative chiropractic care fits into Lynn’s treatment. While not explicitly detailed in the initial phase of her medication management, chiropractic adjustments were a foundational part of her overall care plan at our clinic. The nervous system is the body’s master controller, regulating everything from hormone production to metabolic rate. The hypothalamic-pituitary-adrenal (HPA) axis and the hypothalamic-pituitary-ovarian (HPO) axis are under direct neurological control.

Spinal misalignments, or vertebral subluxations, can create nerve interference that disrupts the delicate communication between the brain and the endocrine glands, including the ovaries and adrenal glands. This disruption can exacerbate the very symptoms Lynn was experiencing—poor sleep, fatigue, mood instability, and metabolic dysregulation.

My role as a chiropractor is to:

• Assess and Correct Subluxations: Through specific, gentle adjustments, I work to restore proper spinal alignment and motion. This reduces nerve interference and helps normalize the signaling pathways that govern hormone balance.
• Improve Autonomic Nervous System (ANS) Function: Chronic stress, a common feature in patients like Lynn, leads to a state of sympathetic dominance (the “fight or flight” response). Chiropractic adjustments have been shown to improve heart rate variability (HRV), a key marker of autonomic balance, shifting the body toward a more parasympathetic (“rest and digest”) state (Zhang et al., 2021). A balanced ANS is critical for proper digestion, restful sleep, and hormone regulation.
• Reduce Musculoskeletal Pain: The weight gain and lifestyle changes Lynn was experiencing could easily lead to back pain, joint stiffness, and headaches. By addressing these biomechanical issues, chiropractic care improves her ability to engage in physical activity, like her walks and kickboxing class, creating a positive feedback loop of improved health.

For Lynn, regular chiropractic care served as a non-pharmacological pillar supporting her body’s return to homeostasis. It helped her manage stress, improved her neurological function, and kept her body physically prepared to take on new activities, making the entire treatment plan more effective.

The Next Step: Introducing Tirzepatide for Metabolic Control

With Lynn’s perimenopausal symptoms now under control and her foundational habits improving, we revisited her initial health goals. The MHT had been a resounding success, but her blood pressure and weight still required further intervention. We had built a stable platform from which we could now launch the next phase of her treatment.

We decided to introduce tirzepatide, a dual-agonist medication that targets both the glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) receptors. This medication was an ideal choice for several reasons:

1. Potent Appetite and Weight Control: Tirzepatide is renowned for its powerful effects on appetite suppression and weight loss, often exceeding that of GLP-1 agonists alone (Frías et al., 2021). It works by slowing gastric emptying, increasing feelings of fullness (satiety), and acting on the appetite centers in the brain.
2. Metabolic Benefits: It significantly improves insulin sensitivity and glycemic control, which is crucial for a patient with rising blood pressure and a predisposition to metabolic syndrome.
3. Cardiovascular Protection: Emerging research continues to highlight the cardiovascular benefits of this class of medications, making it a proactive choice for reducing long-term risk.

We started Lynn on the standard initial dose of 2.5 mg once weekly. This low starting dose is designed to allow the body, particularly the gastrointestinal system, to adapt to the medication, thereby minimizing side effects like nausea, vomiting, or constipation.

Her updated plan now included:

• Continuing the menopausal hormone therapy.
• Starting tirzepatide 2.5 mg weekly.
• Continuing her work with the dietitian and therapist.
• Starting the kickboxing class she was now motivated to try.
• Continuing to monitor her blood pressure.

Mitigating Sarcopenia: A Critical Consideration with Incretin-Based Therapies

Whenever we start a patient on an incretin-based medication like tirzepatide or semaglutide, one of my primary concerns is preserving lean muscle mass. These medications are so effective at inducing weight loss that, without proper guidance, a significant portion of the weight lost can be muscle, not just fat. This is particularly dangerous for a perimenopausal woman like Lynn.

Women naturally begin to lose muscle mass after the age of 30, a process known as sarcopenia. This process accelerates during perimenopause and menopause due to declining estrogen levels, which plays an anabolic (muscle-building) role. Losing additional muscle due to medication-induced weight loss can have dire consequences:

• Decreased Metabolic Rate: Muscle is metabolically active tissue. Less muscle means a lower basal metabolic rate, making long-term weight maintenance significantly harder.
• Reduced Functional Strength: Loss of muscle compromises strength, balance, and mobility, increasing the risk of falls and fractures later in life.
• Worsened Insulin Resistance: Muscle is the primary site for glucose disposal. Losing muscle mass can paradoxically worsen underlying insulin resistance over the long term.

To proactively combat this risk, we implement a multi-pronged strategy:

• Body Composition Analysis: We strongly recommend a baseline body composition analysis using methods like Dual-Energy X-ray Absorptiometry (DEXA) or Bioelectrical Impedance Analysis (BIA). This provides precise measurements of her fat mass, muscle mass, and bone density. We repeat this analysis periodically (e.g., every 3-6 months) to ensure she is primarily losing fat, not muscle.
• Prioritizing Protein Intake: We counsel patients to consume adequate protein, typically in the range of 1.2 to 1.6 grams per kilogram of ideal body weight. For Lynn, this means aiming for a robust daily protein intake, spaced evenly throughout the day to maximize muscle protein synthesis (MPS).
• Emphasizing Resistance Training: Aerobic exercise is excellent for cardiovascular health, but resistance training is non-negotiable for building and maintaining muscle mass. We encourage patients to engage in weightlifting, bodyweight exercises, or resistance band workouts at least two to three times per week. Lynn’s interest in kickboxing, which combines cardio with resistance elements, was a fantastic start.

Managing Side Effects and Ensuring Safety

Before Lynn left the clinic with her new prescription, we had a thorough conversation about potential adverse effects. We reiterated that side effects like nausea are common, especially in the first few days after an injection and each time the dose is titrated upwards. We reassured her that these are typically transient and manageable.

We provided her with practical strategies, often reinforced by the dietitian:

• Eat small, frequent, low-fat meals.
• Avoid overly sweet or greasy foods.
• Stay well-hydrated with water between meals.
• Listen to her body’s new, earlier satiety signals and stop eating when she feels full.

Crucially, we also educated her on the “red flag” symptoms that would warrant an immediate call to our office or a visit to the emergency department. These include severe abdominal pain, intractable vomiting, or a rigid abdomen, which could signal rare but serious complications like pancreatitis or gallbladder disease. Dehydration from an inability to keep fluids down is also a major concern, as it can lead to an acute kidney injury. Empowering patients with this knowledge is a critical safety measure.

Three Years Later: A Picture of Sustained Success

Fast forward three years. Lynn’s journey is a testament to the power of a long-term, adaptive, and integrative strategy. She is now 45 years old and has successfully navigated the challenges of her mid-40s.

Here is a snapshot of her progress:

• Medication Management: She continues to tolerate her medications well, having stabilized at a 15 mg weekly dose of tirzepatide and continuing her menopausal hormone therapy.
• Body Composition: Her body composition data reflects her hard work. She has successfully lost a significant amount of fat mass while preserving, and even building, lean muscle.
• Physical Activity: She discovered that she “hated” the kickboxing class—and this is a vital lesson! Adherence is everything. Instead of giving up, she explored other options and found cardio and weight resistance classes at her gym that she genuinely enjoys. She now consistently attends these classes multiple times a week, in addition to her walking. This autonomy and enjoyment are the keys to long-term sustainability.
• Nutritional Habits: She maintains her healthy eating patterns, checking in with her dietitian every six to nine months for a “tune-up” to stay on track.
• Mental and Emotional Health: Life is never without its challenges. Lynn’s mother recently fell ill, causing a spike in anxiety. Recognizing the need for support, she proactively re-engaged with her therapist. This demonstrates a newfound resilience and self-awareness.

Her weight journey shows a realistic pattern: an initial significant drop, followed by a slight regain, and then stabilization. This is expected. The body naturally fights to defend its weight, and some fluctuation is part of the long-term maintenance process. The crucial part is that Lynn feels good, is in control, and is not discouraged by these minor shifts.

Lynn has not only met her initial goals of managing her perimenopause and reducing her blood pressure, but she has surpassed them. The weight loss was a significant achievement, but the true victory lies in her renewed sense of vitality and self-efficacy. She is now setting new goals centered on self-care and is even contemplating a career change. She has moved from a state of merely surviving to one where she is actively thriving.

Clinical Assessment Without Advanced Imaging

It’s important to note that not all clinics have access to DEXA or BIA scanners. In such cases, we rely on our sharp clinical assessment skills—the foundational practices of a good physical exam. As nurse practitioners and chiropractors, we are trained observers. I can assess for potential muscle loss by watching:

• Gait: How does she walk into the exam room? Is her stride confident and stable?
• Sit-to-Stand Test: Can she rise from a chair without using her hands for support? Difficulty with this simple movement is a powerful indicator of reduced lower-body strength (sarcopenia).
• Handgrip Strength: A simple hand dynamometer can provide an objective measure of overall muscle strength.
• Subjective Reports: How is her energy level? Does she report feeling weaker or more fatigued?
• Physical Signs: We also look for other subtle signs, such as hair loss or skin changes, which can indicate nutritional deficiencies or ongoing metabolic stress.

We must never neglect these fundamental clinical skills. They provide invaluable information, ensuring we can guide all our patients toward preserving muscle mass, regardless of the technology available.

Tackling Sarcopenic Obesity and Cardiovascular Risk: A Deep Dive into Advanced Metabolic Rehabilitation

We now turn our attention to another complex clinical presentation that demands a highly integrated and aggressive treatment strategy: sarcopenic obesity. This condition, characterized by the simultaneous presence of excess body fat (obesity) and low muscle mass and function (sarcopenia), represents a significant threat to metabolic health and longevity.

Let’s examine the case of “Amit,” a 57-year-old male of North African ancestry, whose extensive medical history underscores the severity of this condition. Amit is a manager at a tire factory, is married, and has two children in college. His case is a powerful example of how genetics, lifestyle, and metabolic dysfunction can converge to create a perfect storm of chronic disease.

Amit’s Extensive Health Profile: A Cascade of Complications

Amit’s medical chart reads like a textbook on the complications of untreated obesity and insulin resistance.

• Pertinent Medical History:

• Type 2 Diabetes: Managed with both basal (long-acting) and bolus (mealtime) insulin.
• Myocardial Infarction (MI): Suffered a heart attack three years prior.
• Peripheral Artery Disease (PAD): Stage 2A, presenting with intermittent claudication (cramping pain in the legs during exertion).
• Obstructive Sleep Apnea (OSA): Uses a CPAP machine.
• Hypertension (high blood pressure).
• Hyperlipidemia (high cholesterol/triglycerides).
• Metabolic-Associated Steatotic Liver Disease (MASLD): Stage 2, previously known as non-alcoholic fatty liver disease (NAFLD).
• Low Testosterone & Erectile Dysfunction.
• Former Smoker: Quit after his MI.

• Revealing Family History: His family history paints a clear picture of a strong genetic predisposition. Both parents have obesity, type 2 diabetes, and hypertension. His mother and maternal grandfather both had heart attacks, and his father has advanced PAD. This genetic loading significantly increases his personal risk.
• Review of Systems: His chief complaints are bilateral thigh and calf pain that begins within five minutes of walking (classic claudication) and pervasive fatigue.
• Medication Regimen: His pharmacy list is extensive: insulin, metformin, lisinopril (for blood pressure), rosuvastatin (a high-intensity statin for cholesterol), testosterone therapy, tadalafil (for ED), and clopidogrel (an antiplatelet agent to prevent clots post-MI).

Understanding Amit’s Health Behaviors and Weight History

Diving deeper into his story, we learn that his struggle with weight began in early adulthood and has been a steady, upward climb ever since. He grew up in a culture where food was central, and being encouraged to “have some more” was the norm. This pattern continued into his adult life. Like so many of my patients, he has tried numerous diets, often losing some weight only to find it impossible to maintain the loss.

He reports two critical subjective symptoms:

1. Feeling hungry almost all the time.
2. Lacking satiety after meals, often leading him to go back for second helpings.

This is not a failure of willpower; it is a physiological signal of profound leptin and insulin resistance. His fat cells (adipocytes) are screaming that they are full (high leptin), but his brain’s hypothalamus isn’t getting the message. Simultaneously, his high insulin levels are constantly driving hunger and fat storage.

His dietary patterns reflect this dysregulation. He consumes three large meals a day plus snacks, frequently eats fast food for lunch, and has a low intake of fruits and vegetables. His claudication pain severely hampers his physical activity, and he consumes alcohol daily.

Initial Evaluation: Quantifying the Damage

Amit’s initial lab work and physical exam quantify the severity of his condition.

• Anthropometrics:

• BMI:4 kg/m², classified as Class II Obesity.
• Waist Circumference:25 inches. This is a critical marker of visceral adiposity—the dangerous fat stored around the internal organs.

• Metabolic Markers:

• HbA1c:9%. While technically in the “controlled” range, this is achieved with massive amounts of insulin, which is itself a pro-inflammatory, fat-storing hormone. This number is deceptively reassuring.
• Lipids: Elevated triglycerides and a critically low HDL (“good” cholesterol) of 29 mg/dL. This pattern, known as atherogenic dyslipidemia, is a hallmark of insulin resistance and is highly predictive of cardiovascular events.
• Liver Enzymes: Elevated AST and ALT, confirming ongoing liver inflammation from his Stage 2 MASLD.

• Body Composition and Sarcopenia:

• Body Fat Percentage: A staggering 7%.
• Skeletal Muscle Mass: Only 7%. When charted against his peers, he falls into the 4th percentile for muscle mass. This is a definitive diagnosis of sarcopenia.
• Sarcopenic Obesity: The combination of his Class II obesity with severe sarcopenia places him in this high-risk category.
• Visceral Fat: Bioimpedance analysis measures his visceral fat at 4.4 liters, a dangerously high level.

• Physical Exam Findings:

• Acanthosis Nigricans and Skin Tags: These dark, velvety patches of skin (often on the neck and armpits) and small skin growths are external signs of high insulin levels.
• Hepatomegaly: An enlarged liver, palpable on exam.
• Lower Extremity Edema: 1+ pitting edema, likely related to his vascular disease and sedentary state.

Establishing a Comprehensive Treatment Plan: A Stepwise Approach

Given Amit’s extensive list of comorbidities, our primary concern is preventing another major cardiovascular event, such as a second MI or a stroke. We also aim to halt the progression of his PAD and fatty liver disease and, most importantly, improve his quality of life and functional capacity.

Our initial treatment goals are ambitious but achievable:

1. Achieve at least a 10% body weight reduction. Research consistently shows that a 5-10% weight loss, if maintained, can produce clinically significant improvements in blood sugar, blood pressure, and lipids (Magkos et al., 2016).
2. Improve body composition: This means prioritizing fat mass loss while actively increasing muscle mass and function.
3. Reduce cardiometabolic risk factors.
4. Improve PAD symptoms and overall physical conditioning.
5. Increase energy and vitality.

As with our previous cases, this plan will be implemented in a stepwise, patient-centered manner, building on successes one at a time.

Nutritional Intervention: A Foundation for Healing

Amit expressed interest in a Mediterranean diet, which is an excellent choice as it aligns with his cultural background and is robustly supported by evidence for cardiovascular health. However, we must modify it to address his severe carbohydrate intolerance.

• Protein is Paramount: We set a target of 90-100 grams of protein per day. Crucially, we instruct him to space this intake out, consuming a portion every 3-4 hours. This strategy is vital for stimulating muscle protein synthesis (MPS). After a protein-rich meal, MPS is elevated for a few hours and then returns to baseline. By eating protein periodically, we create multiple spikes in MPS throughout the day, providing a constant stimulus for muscle repair and growth. We also educate him that animal protein tends to be more effective for MPS due to its complete amino acid profile, particularly its high leucine content (Schoenfeld & Aragon, 2018).
• Carbohydrate Intolerance: For anyone with type 2 diabetes and severe insulin resistance, the body is in a state of carbohydrate intolerance. Consuming starches, grains, and sugars triggers a massive insulin surge, which promotes fat storage and inflammation. Therefore, our plan involves drastically minimizing:

• Ultra-processed foods
• Sweets and sugary drinks
• Starches (bread, pasta, rice, potatoes)
• Grains
• Alcohol

• Focus on Nutrient Density: We encourage a high intake of non-starchy vegetables and low-sugar fruits, aiming for at least 50-100 grams per day to ensure adequate fiber, vitamins, and minerals.

Physical Activity: The Prescription for Muscle and Mobility

Amit’s claudication pain presents a major barrier to exercise. This is a classic “catch-22”: his PAD causes pain with activity, but inactivity worsens the PAD and his overall metabolic health.

• Referral to Physical Therapy (PT): In cases of severe deconditioning or sarcopenic obesity, I frequently prescribe physical therapy with the diagnoses of “Sarcopenia” and “Sarcopenic Obesity.” A skilled physical therapist can:

• Perform a functional assessment.
• Design a safe, progressive exercise program.
• Supervise his workouts to ensure proper form and prevent injury.
• Develop a home exercise plan for him to follow.

• A Multi-Modal Approach to Exercise:

• Walking: He will gradually increase his walking duration, using the “walk-through-the-pain” method common in PAD rehabilitation, where he walks until the pain is moderate, rests, and then repeats.
• Biking: He enjoys using a stationary bike, which is often better tolerated as it’s a non-weight-bearing activity.
• Strength Training: This is non-negotiable for combating sarcopenia. He will start strength training twice a week, initially with light weights under the guidance of his PT, and progressively increase the load. The combination of aerobic activity, resistance training, and adequate protein is the trifecta for rebuilding muscle.

Pharmacotherapy: Choosing the Right Tool for the Job

This is where we can make a monumental impact on Amit’s disease trajectory.

• Initiating Semaglutide: We chose to start semaglutide, a potent GLP-1 receptor agonist. Our goal is to titrate him up from the starting dose of 0.25 mg to the target dose of 2.4 mg, as tolerated. The choice of semaglutide was highly specific for Amit. In 2023, based on the results of the SELECT trial, the FDA expanded the indication for semaglutide 2.4 mg to include reducing the risk of major adverse cardiovascular events (MACE)—such as cardiovascular death, non-fatal MI, or non-fatal stroke—in adults with established cardiovascular disease and either obesity or overweight. Amit qualifies for this indication in three ways: he has a prior MI, he has PAD, and he has obesity. This medication is not just for weight loss; for him, it is a life-saving cardiovascular drug (Lincoff et al., 2023).
• De-prescribing Insulin: The Key to Unlocking Fat Burning: This is one of the most critical interventions we can make. Patients like Amit often come to me on massive doses of insulin, yet their metabolic health is deteriorating. While insulin lowers blood sugar, it is the primary hormone of fat storage. It acts like a one-way valve, pushing glucose and fat into cells for storage and actively preventing fat breakdown (lipolysis). Trying to lose weight while on high doses of exogenous insulin is like trying to drive a car with the emergency brake fully engaged. It’s a battle against your own physiology. Furthermore, high insulin levels (hyperinsulinemia) are profoundly inflammatory and contribute directly to the progression of atherosclerosis.

Our strategy is to aggressively taper and discontinue his insulin as we titrate up the semaglutide. GLP-1 agonists like semaglutide work in a glucose-dependent manner; they stimulate the pancreas to release insulin only when blood sugar is high. They also suppress glucagon (a hormone that raises blood sugar), slow digestion, and promote satiety. This powerful combination often leads to rapid improvements in glycemic control.

In many cases, I can stop a patient’s insulin entirely on the day they start semaglutide, especially if their blood sugars are not excessively high. For a patient like Amit with a more complex history, we might proceed more cautiously. Using a Continuous Glucose Monitor (CGM) would be an invaluable tool here. A CGM provides real-time data on his blood sugar levels 24/7, allowing us to see exactly how his body is responding to the semaglutide. With this data, we can confidently and safely reduce his insulin doses, first eliminating the bolus (mealtime) insulin and then gradually tapering the basal (long-acting) insulin. The goal is to get him off insulin completely.

The Six-Month Transformation: Liberation from “Food Noise”

Amit’s six-month follow-up visit was remarkable. He had successfully titrated up to the full 2.4 mg dose of semaglutide and, most importantly, had been completely tapered off his insulin.

The subjective changes were just as powerful as the objective data:

• Reduced Hunger and Cravings: He reported a dramatic reduction in his constant hunger and cravings. He was now able to control his portions and was adhering to his nutrition plan about 75% of the time.
• The End of “Food Noise”: Amit experienced the liberation that so many patients on these medications describe. He told me, “This is what it must feel like to be normal.” That constant mental preoccupation with food, which I have described to patients for two decades as “food noise,” was gone. This mental freedom is one of the most profound benefits of incretin therapies. It proves to patients that their lifelong struggle was not a moral failing or a lack of willpower, but a consequence of dysregulated brain chemistry and hormones.
• Reduced Alcohol Intake: Amit spontaneously reduced his alcohol intake to about five beers per week. This is a fascinating and increasingly reported effect of GLP-1 agonists. The mechanism is not fully understood but is thought to involve the medication’s effect on the brain’s reward pathways, dampening the pleasure response not only from food but also from other rewarding substances like alcohol.
• Improved Physical Function: He was diligently attending PT twice a week, using his exercise bike for 15 minutes daily, and had incorporated strength training with light weights. As a result, he felt more energetic, had more stamina, and, critically, was experiencing less claudication pain. This is a huge win, creating a positive cycle: less pain allows for more activity, which further improves circulation and metabolic health.

His lab results confirmed these incredible gains. Despite having type 2 diabetes and limited mobility—both of which typically slow weight loss—he had achieved a 10.2% reduction in his total body weight. This is a monumental achievement, made possible by removing the “brake” of exogenous insulin and replacing it with a therapy that addresses the root hormonal dysregulation.

When we were finally able to test Amit’s insulin (after previously holding due to exogenous insulin use), his fasting insulin was elevated at 22.4IU/mL. His fasting glucose had improved; A1C was 6.3%. HOMA-IR remained elevated at 5.8. Liver enzymes were improving, suggesting reduced hepatic inflammation or steatosis burden. Critically, his body fat moved from 56.7% to 48.9%, and skeletal muscle mass had begun to rise. While weight loss often reduces both fat and lean mass, Amit gained lean mass—likely due to adherence to resistance training and progressive activity—moving from the 4th percentile to the 18th percentile in muscle mass. His visceral adipose tissue fell from 4.4 L to 3.5 L, and waist circumference decreased.

The One-Year Mark for Amit

At one year:

• Body weight reduction: 16.3%
• Fasting insulin: down to 13.1?IU/mL (substantial improvement)
• HOMA-IR: improved to 3.4 (still elevated but trending positively)
• A1C: down to 6.0%
• Body fat: from 56.7% to 41.1%
• Skeletal muscle mass: up to 29.1% (25th percentile)
• Visceral adipose tissue: documented as 4.3 L at that time point in the source narrative (noting prior measure 3.5 L; in practice, we verify modality and session-to-session consistency; minor device or hydration differences can affect readings)

His journey is far from over, but in just one year, we have fundamentally altered his disease trajectory. We have moved him from a path of accelerating decline toward one of recovery, function, and renewed hope. His case powerfully demonstrates that with a modern, aggressive, and integrated approach, even the most complex cases of sarcopenic obesity and advanced cardiovascular disease can be effectively managed and, in many ways, reversed.

Case Journey: Dolores’s Story: Obesity, Sarcopenia, Osteoarthritis, and Surgical Readiness

Patient Background

Dolores is 72, a retired wealth advisor, divorced, with two adult children. She wants to travel now that she is retired. Medical history includes hyperlipidemia, chronic insomnia, and severe bilateral knee osteoarthritis limiting mobility. Her surgeon or hospital policy required a BMI under 40 to qualify for total knee replacement (TKR). Her weight gain began in perimenopause, with central adiposity predominating—typical of hormonal transition-related fat redistribution. She has attempted portion control, reduced sweets, and increased activity in the past but struggled with maintenance and regain.

Current medications: rosuvastatin, trazodone, diclofenac, multivitamin.

Health Behaviors

• Three meals per day
• Low protein intake
• High intake of fruits and vegetables but difficulty resisting evening sweets
• Limited walking due to knee pain; swims 20 minutes 3 days per week
• Sleep improved with trazodone, though occasional early awakening
• Minimal alcohol, non-smoker

Baseline Labs and Composition

• Slightly elevated fasting insulin: 8.4?IU/mL
• BMI: 41.5
• Body fat: 56.8%
• Skeletal muscle mass: 15.1% (2nd percentile—significant sarcopenia)
• Visceral fat: 2.3 L
• Waist circumference: 43.1 inches
• Gynoid phenotype with central adiposity since perimenopause
• Lipids and A1C in acceptable range, likely due to overall activity, statin therapy, and relatively preserved metabolic health aside from obesity and sarcopenia

Key Clinical Concerns

• Healthcare inequities: as an older woman with obesity, Dolores has frequently felt dismissed. This leads to avoidance of PT due to fear of judgment, as well as anxiety regarding orthopedic consultations.
• Functional decline: worsening sarcopenia threatens mobility and independence.
• Surgical candidacy barrier: BMI < 40 requirement.
• Pain: severe knee OA limiting land-based exercise.

Treatment Goals

• Weight reduction of approximately 3.9% (~10 pounds) to meet BMI criteria.
• Improve mobility, body composition, and sarcopenia.
• Support sleep and reduce pain to enable adherence.
• Prepare perioperative plan with medication safety.

Nutrition Strategy

• Protein target: 90–100 g/day, despite aversion to meat.

• Rationale: Muscle protein synthesis requires adequate essential amino acids; older adults display anabolic resistance, needing higher protein per meal (20–40 g) with sufficient leucine (~2–3 g) to stimulate mTORC1 signaling (Moore et al., 2015; Phillips & Chevalier, 2011).

• Animal-forward options she can tolerate:

• Eggs, seafood, cottage cheese, Greek yogurt, cheese, and high-quality protein smoothies.

• Meal timing: eat every 3–4 hours to deliver regular anabolic signals and stabilize appetite.
• Reduce sweets and minimize starch in the evening to reduce nocturnal hyperinsulinemia and improve sleep quality.
• Referral to a registered dietitian with specific expertise in obesity care.

• Rationale: Nutrition plans for obesity differ from generic “low-fat” or calorie-only templates. We focus on reducing hyperpalatable foods, prioritizing protein, increasing fiber density, and sustainable patterning.

Physical Activity and PT Plan

• Continue swimming 20 minutes, 3 days per week—joint-sparing aerobic exercise.
• PT referral for knee osteoarthritis and sarcopenia:

• Exercise bike favored over walking initially—lower joint reactive forces compared to ambulation over uneven surfaces.
• Strength training for quadriceps, hamstrings, gluteals, calf complex, hip abductors; closed kinetic chain patterns; progressive resistance carefully titrated around pain.
• Balance and proprioception training to reduce fall risk.

• Chiropractic integration:

• We address lumbopelvic alignment, hip mobility, and ankle dorsiflexion limits that can exacerbate knee loading.
• Soft tissue mobilization for quadriceps, IT band, and calf to reduce nociceptive input and permit better exercise tolerance.
• Gentle joint manipulation where appropriate to improve mechanics and movement confidence.

Medication Strategy

• Continue rosuvastatin, trazodone, diclofenac as clinically indicated.
• Consider obesity pharmacotherapy:

• Tirzepatide (dual GIP/GLP-1 receptor agonist), semaglutide (GLP-1), naltrexone-bupropion, phentermine, or phentermine-topiramate, individualized to her cardiovascular risk, insomnia history, and OA pain.

• Rationale for pharmacotherapy:

• Limited ability to engage in high-load physical activity due to OA; medication can reduce appetite and facilitate the necessary weight loss for surgical candidacy, while we preserve lean mass via protein and resistance training.

Addressing Barriers and Weight Bias

Dolores didn’t want PT due to fear of judgment and failure. Many older women report similar experiences. I validate this and advocate on her behalf. I proactively ask about her comfort with PT. When helpful, we match her with a female PT experienced in obesity care. We role-play PT sessions, practicing how she can request graded, joint-respectful programs. If the PT fit isn’t right, we change providers. We use the same approach for orthopedic consults: I coach her to open with her progress and needs—“I have reduced my weight from X to Y; my next goal is to address my knees. I’m here for your help.” This positioning can shift the dynamic toward collaboration.

One-Year Outcomes for Dolores

• Weight reduction: 8.7%
• Fasting insulin normalized
• Percent body fat down to 49.8%
• Skeletal muscle percentile increased from 2nd to 10th
• Lower visceral fat and reduced waist circumference
• Pharmacotherapy course:

• She initiated naltrexone-bupropion to assist weight loss; before surgery, we stopped naltrexone (to avoid blocking opioid analgesia) and continued bupropion. Post-op, she later transitioned to semaglutide to further support appetite and weight management.

• Protein intake increased to ~75 g/day
• She started PT after a couple of months, built confidence, and underwent one knee replacement six months prior without complications; mobility improved progressively.
• Plans to proceed with the second knee and resume travel—her original life goal.

Physiological Deep Dive: The Science Behind Our Strategies

Understanding the Metabolic Landscape: Insulin, HOMA-IR, Visceral Adiposity, and Muscle

Why we track fasting insulin, HOMA-IR, A1C, and body composition:

• Fasting insulin and HOMA-IR

• Elevated fasting insulin (e.g., 22.4 ?IU/mL) and HOMA-IR (e.g., 5.8) signal insulin resistance. HOMA-IR approximates insulin sensitivity by combining fasting insulin and glucose—improvements reflect enhanced cellular responsiveness and lower metabolic stress (Wallace et al., 2004; Matthews et al., 1985).

• Hemoglobin A1C

• A1C around 6.3% indicates prediabetes or well-controlled diabetes depending on context. Reducing A1C to near 6.0% improves microvascular and macrovascular risk (UKPDS; DCCT/EDIC).

• Body fat percent and skeletal muscle mass

• Total adiposity, especially visceral adipose tissue (VAT), correlates with cardiometabolic risk. Skeletal muscle is a major glucose sink; preserving or increasing muscle improves insulin sensitivity (DeFronzo & Tripathy, 2009).

• Visceral adipose tissue

• VAT (e.g., from 4.4 L to 3.5 L) reflects pathogenic fat depots releasing inflammatory adipokines and portal free fatty acids that impair hepatic insulin sensitivity and raise cardiometabolic risk (Després, 2012; Neeland et al., 2019).

• Waist circumference

• A practical index of visceral fat burden and cardiometabolic risk independent of BMI (Ross et al., 2020).

The Physiology Behind Weight Defense, Appetite, and Combination Therapy

Why hunger can increase during weight loss:

• Adaptive thermogenesis

• As body weight declines, resting energy expenditure drops beyond what is predicted by lean mass loss—a phenomenon called adaptive thermogenesis (Rosenbaum & Leibel, 2010). This is mediated by neuroendocrine shifts that favor weight regain.

• Hormonal changes

• Ghrelin tends to rise, driving hunger; leptin falls, diminishing satiety signaling; peptide YY and cholecystokinin can be reduced; thyroid hormones may adaptively lower. This constellation is why patients often feel “hungrier” when they have successfully lost weight (Sumithran et al., 2011).

• Clinical implication

• When hunger pressures increase, we normalize the experience and consider stepping up pharmacotherapy to defend the new lower weight, while reinforcing protein intake, fiber, and resistance training to preserve lean mass.

Sarcopenia, Menopause, and Osteoarthritis

• Sarcopenia in older adults

• Mechanisms: Anabolic resistance, chronic low-grade inflammation (inflammaging), hormonal changes (declines in estrogen, testosterone, GH/IGF-1), mitochondrial dysfunction, and reduced physical activity contribute to muscle loss and impaired strength (Cruz-Jentoft et al., 2019).
• Clinical implications: Low muscle mass and strength predict mobility limitations, falls, metabolic dysregulation, and poorer surgical outcomes.
• Treatment: Resistance training with progressive overload is foundational, supported by sufficient protein and leucine, vitamin D sufficiency, and, when needed, pharmacotherapy to reduce fat mass and joint load so exercise is tolerable.

• Menopause and fat redistribution

• Estrogen decline shifts fat storage toward visceral depots, increasing cardiometabolic risk (Carr, 2003). Sleep disruption, vasomotor symptoms, and mood changes can exacerbate appetite dysregulation and inactivity.
• Interventions: Prioritize consistent protein, resistance training, sleep hygiene, and, when clinically appropriate, discuss menopausal hormone therapy with the internal medicine or women’s health team for symptom control and cardiometabolic considerations (MHT suitability individualized per risk profile).

• Knee osteoarthritis and exercise

• Pathophysiology: OA involves cartilage degeneration, subchondral bone changes, synovitis, and altered neuromuscular control. Pain leads to guarding, atrophy, and movement avoidance.
• Exercise therapy: Strengthening quadriceps and hip abductors, neuromuscular training, and low-impact aerobic work reduce pain and improve function (Fransen et al., 2015). Cycling and aquatic therapy are ideal early choices.
• Load management: Graded exposure with symptom-contingent progression. Chiropractic adjustments can optimize joint motion and reduce compensations; PT programs provide dosage control and monitoring.

Medication Mechanisms and Clinical Reasoning

• Semaglutide (GLP-1 RA)

• Mechanism: satiety signaling, slowed gastric emptying, glucose-dependent insulin secretion.
• Outcomes: robust weight loss and improved cardiometabolic markers (Wilding et al., 2021).
• Considerations: GI side effects, rare risk of pancreatitis, gallbladder considerations; titrate slowly.

• Tirzepatide (dual GIP/GLP-1)

• Mechanism: combines GLP-1 satiety effects with GIP’s insulinotropic and potential adipocyte effects.
• Outcomes: often greater weight loss than GLP-1 alone in trials (SURMOUNT-1) (Jastreboff et al., 2022).
• Considerations: similar GI profile; individualized choice based on response, availability, and comorbidities.

• Bupropion/naltrexone

• Mechanism: POMC activation plus blockade of inhibitory feedback to sustain appetite suppression (Greenway et al., 2010).
• Considerations: nausea, BP monitoring; naltrexone must be stopped before opioid analgesia.

• Phentermine and phentermine/topiramate

• Mechanisms: appetite suppression via noradrenergic pathways; topiramate adds craving suppression and satiety enhancement.
• Outcomes: significant weight loss with PHEN/TPM in RCTs (Allison et al., 2012).
• Considerations: monitor HR/BP, cognition, mood; insomnia risk with stimulants—relevant for patients like Dolores with an insomnia history.

• Combination strategy

• Rationale: Address multiple appetite pathways, defend weight loss against adaptive hunger, and tailor to side effect profiles and comorbidities under medical oversight (Apovian et al., 2015).

My Clinical Observations and Practice Insights

Based on my practice observations, as shared across healthcoach.clinic and my professional posts:

• Small, consistent exercise increments overcome initial resistance and fear, especially in pain-limited patients.
• Protein prioritization is the single most powerful dietary lever for sarcopenia prevention during weight loss—particularly in older women who under-consume protein.
• Integrative chiropractic care accelerates readiness for aerobic and resistance programs by reducing pain and correcting mechanics.
• Combining GLP-1 or dual-incretin therapy with resistance training preserves lean mass better than either strategy alone in practice.
• Advocacy against weight bias in healthcare is as therapeutic as any medication, restoring agency and engagement.

Bringing It All Together: A New Beginning and the Power of Integrative Care

The stories of Eloise, George, Lynn, Amit, and Dolores demonstrate how integrative chiropractic care meshes with internal medicine, functional nutrition, and modern anti-obesity pharmacotherapy:

• We reduced pain and optimized movement mechanics to unlock activity.
• We used precise nutrition and protein strategies to protect muscle.
• We applied medications strategically under medical direction to counter physiology’s weight defense.
• We advocated through systemic barriers to help patients achieve life-changing goals—like a pain-reduced walk, starting a family, or a long-awaited trip abroad.

Our El Paso clinic model is intentionally multidisciplinary: I, Dr. Alex Jimenez, DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST, lead integrative chiropractic and functional medicine care, while Dr. Maria Guadalupe Cardenas, MD (Internal Medicine; NPI #1164426749; Texas MD License #J2933) serves as Medical Director and Collaborative Physician, ensuring safety, appropriateness, and effectiveness of medical therapies. Together, we deliver modern, evidence-based obesity and metabolic care that is humane, precise, and effective.

References and Further Reading

1. Allison, D. B., Gadde, K. M., Garvey, W. T., Peterson, C. A., Schwiers, M. L., Nawrocki, A. R., & Day, W. W. (2012). Controlled-release phentermine/topiramate in severely obese adults: A randomized controlled trial. Obesity, 20(2), 330–342.
2. American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.).
3. Apovian, C. M., Aronne, L. J., Bessesen, D. H., McDonnell, M. E., Murad, M. H., & Pagotto, U. (2015). Pharmacological management of obesity: An Endocrine Society clinical practice guideline. The Journal of Clinical Endocrinology & Metabolism, 100(2), 342–362.
4. Armstrong, M. J., Gaunt, P., Aithal, G. P., et al. (2016). Liraglutide safety and efficacy in patients with non-alcoholic steatohepatitis. The Lancet, 387(10019), 679–690.
5. Carr, M. C. (2003). The emergence of the metabolic syndrome with menopause. The Journal of Clinical Endocrinology & Metabolism, 88(6), 2404–2411.
6. Cruz-Jentoft, A. J., Bahat, G., Bauer, J., et al. (2019). Sarcopenia: Revised European consensus on definition and diagnosis. Age and Aging, 48(1), 16–31.
7. DeFronzo, R. A., & Tripathy, D. (2009). Skeletal muscle insulin resistance is the primary defect in type 2 diabetes. Diabetes Care, 32(Suppl 2), S157–S163.
8. Després, J.-P. (2012). Body fat distribution and risk of cardiovascular disease. Circulation, 126(10), 1301–1313.
9. Fransen, M., McConnell, S., Harmer, A. R., Van der Esch, M., Simic, M., & Bennell, K. L. (2015). Exercise for osteoarthritis of the knee: A Cochrane systematic review. British Journal of Sports Medicine, 49(24), 1554–1557.
10. Frías, J. P., Davies, M. J., Rosenstock, J., Pérez Manghi, F. C., Fernández Landó, L., Bergman, B. K., Liu, B., Cui, X., & Brown, K. (2021). Tirzepatide versus semaglutide once weekly in patients with type 2 diabetes. The New England Journal of Medicine, 385(6), 503–515.
11. Greenway, F. L., Fujioka, K., Plodkowski, R. A., et al. (2010). Effect of naltrexone plus bupropion on weight loss in overweight and obese adults (COR-I): A multicentre, randomized, double-blind, placebo-controlled, phase 3 trial. The Lancet, 376(9741), 595–605.
12. Hostalek, U., Gwilt, M., & Hildemann, S. (2015). Therapeutic use of metformin in prediabetes and diabetes prevention. Drugs, 75(10), 1071–1094.
13. Hudson, R., & Hudson, M. (2015). Lisdexamfetamine: A new treatment for binge eating disorder. Current Psychiatry Reports, 17(9), 71.
14. Jastreboff, A. M., Aronne, L. J., Ahmad, N. N., Wharton, S., Connery, L., Alves, B., … & SURMOUNT-1 Investigators. (2022). Tirzepatide once weekly for the treatment of obesity. New England Journal of Medicine, 387(3), 205-216.
15. Legro, R. S., Arslanian, S. A., Ehrmann, D. A., Hoeger, K. M., Murad, M. H., Pasquali, R., & Welt, C. K. (2013). Diagnosis and treatment of polycystic ovary syndrome: an Endocrine Society clinical practice guideline. The Journal of Clinical Endocrinology & Metabolism, 98(12), 4565–4592.
16. Lincoff, A. M., Brown-Frandsen, K., Colhoun, H. M., Deanfield, J., Emerson, S. S., Mann, J. F. E., Marso, S. P., McGuire, D. K., & Ryan, D. H. (2023). Semaglutide and cardiovascular outcomes in obesity without diabetes. The New England Journal of Medicine, 389(24), 2221–2232.
17. Magkos, F., Fraterrigo, G., Yoshino, J., Luecking, C., Kirbach, K., Kelly, S. C., de las Fuentes, L., He, S., Okunade, A. L., Patterson, B. W., & Klein, S. (2016). Effects of moderate and subsequent progressive weight loss on metabolic function and adipose tissue biology in humans with obesity. Cell Metabolism, 23(4), 591–601.
18. Matthews, D. R., Hosker, J. P., Rudenski, A. S., Naylor, B. A., Treacher, D. F., & Turner, R. C. (1985). Homeostasis model assessment: Insulin resistance and beta-cell function. Diabetologia, 28(7), 412–419.
19. Moore, D. R., Churchward-Venne, T. A., Witard, O., Breen, L., Burd, N. A., Tipton, K. D., & Phillips, S. M. (2015). Protein ingestion to stimulate myofibrillar protein synthesis requires greater relative protein intakes in healthy older versus younger men. The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences, 70(1), 57–62.
20. Neeland, I. J., Ross, R., Després, J.-P., et al. (2019). Visceral and ectopic fat and cardiometabolic risk. Circulation, 140(11), e628–e639.
21. Phillips, S. M., & Chevalier, S. (2011). Anabolic resistance of skeletal muscle protein synthesis with aging. Experimental Gerontology, 46(12), 973- 979.
22. Reynolds, A. N., Mann, J. I., Williams, S., & Venn, B. J. (2020). Advice to walk after meals is more effective for lowering postprandial glycemia in type 2 diabetes mellitus than advice that does not specify timing: a randomized crossover study. Diabetologia, 63(2), 434-435. (Note: This links to a 2016 study; the concept has been reinforced in subsequent research).
23. Rosano, G. M. C., Fini, M., & Vitale, C. (2017). The route of administration of menopausal hormone therapy and the risk of venous thromboembolism: A systematic review of the literature. Human Reproduction Update, 23(2), 263-269.
24. Rosenbaum, M., & Leibel, R. L. (2010). Adaptive thermogenesis in humans. International Journal of Obesity, 34(S1), S47–S55.
25. Ross, R., Neeland, I. J., Yamashita, S., et al. (2020). Waist circumference as a vital sign in clinical practice. Nature Reviews Endocrinology, 16, 177–189.
26. Schoenfeld, B. J., & Aragon, A. A. (2018). How much protein can the body use in a single meal for muscle-building? Implications for daily protein distribution. Journal of the International Society of Sports Nutrition, 15(10).
27. Spiegel, K., Tasali, E., Penev, P., & Van Cauter, E. (2004). Brief communication: Sleep curtailment in healthy young men is associated with decreased leptin and elevated ghrelin. Annals of Internal Medicine, 141(11), 846–850.
28. Sumithran, P., Prendergast, L. A., Delbridge, E., et al. (2011). Long-term persistence of hormonal adaptations to weight loss. The New England Journal of Medicine, 365(17), 1597–1604.
29. Wallace, T. M., Levy, J. C., & Matthews, D. R. (2004). Use and abuse of HOMA modeling. Diabetes Care, 27(6), 1487–1495.
30. 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., Wadden, T. A., Wharton, S., Yokote, K., Zeuthen, N., & Kushner, R. F. (2021). Once-weekly semaglutide in adults with overweight or obesity. New England Journal of Medicine, 384(11), 989–1002.
31. Zhang, J., Yao, Y., & Wei, D. (2021). Chiropractic manipulation for improving heart rate variability: A systematic review and meta-analysis of randomized controlled trials. Journal of Clinical Medicine, 10(22), 5262.

SEO Tags:

Obesity Treatment, Perimenopause, Sarcopenic Obesity, Tirzepatide, Semaglutide, GLP-1 Agonist, Integrative Chiropractic Care, Functional Medicine, Dr. Alex Jimenez, El Paso, Menopausal Hormone Therapy, Weight Loss, Metabolic Health, Insulin Resistance, Cardiovascular Disease, Peripheral Artery Disease, Body Composition, Muscle Mass, Type 2 Diabetes, De-prescribing Insulin, Sarcopenia, Lifestyle Medicine, Nutrition, Dr. Maria Cardenas, Multidisciplinary Care, male fertility, hypertension, metabolic syndrome, bupropion-naltrexone, HOMA-IR, testosterone, stress management, visceral fat, prediabetes reversal, PCOS, Binge Eating Disorder, Infertility, Hormonal Imbalance, joint replacement BMI requirements, patient-centered care, physical therapy for knee OA, protein intake older adults, resistance training seniors, sleep and weight, pain management and weight loss