Metabolic Restoration: A Complete Guide to Reducing Insulin Resistance

Learn how metabolic restoration can reduce insulin resistance, transform your health, and improve your body’s function.

Abstract

This post will guide you through the intricate web of metabolic dysfunction, focusing on insulin resistance as the central, upstream driver of many of today’s most prevalent chronic diseases. We will explore how this single physiological state can trigger a cascade of downstream health issues, impacting fields as diverse as endocrinology, oncology, cardiology, and neurology. I will break down the latest scientific findings, including groundbreaking research on new therapeutic agents like retatrutide, and analyze their potential not only to manage symptoms but to reverse the underlying disease processes fundamentally. We’ll also examine the complex interplay between medical innovation, pharmaceutical economics, and patient access to care. Throughout this journey, I will explain how our multidisciplinary approach at Injury Medical Clinic PA integrates chiropractic care, functional medicine, and conventional medical oversight to provide a comprehensive, patient-centered strategy for tackling metabolic dysfunction at its source. This is about moving beyond a “managed decline” and empowering you with the knowledge to reclaim your metabolic health.

The Power of Integrative Care: Our Collaborative Approach in El Paso, Texas

Before we delve into the science, I believe it’s essential for you to understand the philosophy that guides my practice and our team here in El Paso, Texas. I am Dr. Alex Jimenez, and my credentials—DC, APRN, FNP-BC, CFMP, IFMCP, ATN, CCST—reflect a lifelong commitment to a multifaceted, holistic approach to health. My journey has taken me through chiropractic, advanced practice nursing as a Family Nurse Practitioner, and deep into functional and integrative medicine. This broad training has solidified my core belief: the human body is an interconnected system, and treating it effectively requires looking beyond isolated symptoms to address the root cause.

This philosophy is the cornerstone of Injury Medical Clinic PA, where I am honored to work alongside Dr. Maria Guadalupe Cardenas, MD. Dr. Cardenas is a board-certified internist with over 40 years of invaluable experience. She serves as our Medical Director and Collaborative Physician, providing the essential medical oversight that allows us to operate as a true multidisciplinary practice. This model, where a Doctor of Chiropractic (DC) and a Medical Doctor (MD) collaborate, is essential to providing comprehensive, safe care, especially for personal injury and complex chronic conditions.

Our team integrates a wide spectrum of services:

• Chiropractic Care: I use spinal adjustments and neuromuscular techniques to restore proper function to the musculoskeletal and nervous systems, which are crucial for overall health signaling and metabolic regulation.
• Medical Oversight: Cardenas ensures all treatment plans are medically sound by providing diagnoses, reviewing patient cases, and managing aspects of care within the scope of internal medicine.
• Functional Medicine: We use advanced diagnostic testing to uncover the unique biochemical and genetic factors contributing to each patient’s condition, enabling highly personalized interventions.
• Rehabilitation and Personal Injury Care: We specialize in helping patients recover from injuries, focusing not just on pain relief but on restoring full function and preventing long-term complications.

This collaborative framework allows us to create a therapeutic environment that is both holistic and evidence-based. When we discuss complex topics like insulin resistance, our approach isn’t about a single supplement or adjustment; it’s about creating a comprehensive, personalized plan that leverages the strengths of multiple disciplines to restore your body’s innate ability to heal.

Unmasking the “Source Code” of Chronic Disease: An Introduction to Insulin Resistance

In my years of clinical practice and research, I have consistently observed that a handful of core dysfunctions are responsible for the vast majority of chronic illnesses that plague our society. If we think of these diseases as complex software programs running in the body, then insulin resistance is the upstream “source code” error from which they originate. It is the fundamental glitch that, over time, gives rise to a staggering array of health problems.

Consider this: insulin resistance is the common thread linking eleven of the most profitable chronic diseases in modern medicine. This isn’t a coincidence; it’s cause and effect. When the body’s cells become less responsive to the hormone insulin, a cascade of compensatory and, ultimately, damaging physiological changes begins. This single upstream problem generates enormous downstream revenue for multiple medical specialties:

• Endocrinology: Managing type 2 diabetes, thyroid disorders, and polycystic ovary syndrome (PCOS).
• Hepatology: Treating non-alcoholic fatty liver disease (NAFLD) and its more severe form, non-alcoholic steatohepatitis (NASH).
• Oncology: Addressing the increased risk and progression of several types of cancer.
• Cardiology: Managing hypertension, dyslipidemia (abnormal cholesterol), and coronary artery disease.
• Gastroenterology: Dealing with complications arising from metabolic dysfunction in the gut.

Let’s pause and truly absorb what this means. We have entire branches of medicine dedicated to managing the consequences of a problem that starts years, or even decades, earlier with simple insulin resistance. The crucial question we must ask ourselves is: What happens to this entire healthcare architecture if we stop chasing the downstream symptoms and instead fix the upstream problem? This is not just a theoretical question; it is the central challenge and opportunity facing medicine today.

Hyperinsulinemia: The Hidden Catalyst for Disease

To understand how insulin resistance wreaks so much havoc, we must first understand its direct consequence: hyperinsulinemia, or chronically elevated insulin levels in the blood.

The Physiology of Insulin and Insulin Resistance

Under normal, healthy conditions, the hormone insulin acts like a key. After you eat a meal containing carbohydrates, your blood glucose (sugar) level rises. In response, your pancreas secretes insulin into the bloodstream. This insulin travels to cells throughout your body—primarily in your muscles, liver, and fat tissue—and binds to specific receptors on their surfaces. This binding “unlocks” the cells, allowing them to take in glucose from the blood for immediate energy or storage for later. This process efficiently lowers your blood sugar back to a normal range.

Insulin resistance occurs when this elegant system breaks down. For a variety of reasons, including a diet high in processed carbohydrates and sugar, a sedentary lifestyle, chronic stress, and poor sleep, the cells’ insulin receptors become less sensitive. It’s as if the locks have become rusty. When insulin arrives, the key doesn’t turn as easily. The cells resist the signal to take up glucose.

Your pancreas, sensing that blood glucose is still too high, does the only thing it knows how to do: it pumps out even more insulin. This is a compensatory mechanism. If one key isn’t working well, the body sends five, then ten, then a hundred keys, hoping to force the rusty locks open. This state of elevated insulin is hyperinsulinemia. For a while—often for many years—this compensation works. Your blood sugar levels may remain in the “normal” range on standard tests. Still, beneath the surface, your pancreas is working overtime, and your body is being flooded with an abnormally high amount of a powerful growth-signaling hormone.

This is the critical, often-missed, pre-diabetic phase. It can take 10 to 20 years of progressive hyperinsulinemia before the pancreas finally begins to tire out and can no longer produce enough insulin to overcome the resistance. At this point, blood sugar levels start to rise uncontrollably, and a diagnosis of type 2 diabetes is made. But the damage did not start with high blood sugar; it started two decades earlier with high insulin.

The Systemic Impact of High Insulin

The problem is that insulin does much more than regulate blood sugar. It’s a potent anabolic hormone, meaning it signals growth. When it’s chronically elevated, it sends inappropriate growth signals throughout the body. One of the most dangerous ways it does this is by interacting with other receptor systems.

Insulin is structurally very similar to another hormone called Insulin-like Growth Factor 1 (IGF-1). IGF-1 is a primary driver of cellular growth, proliferation, and differentiation. When insulin levels are chronically high, excess insulin can “spill over” and bind to IGF-1 receptors on various cells, effectively mimicking IGF-1 and promoting unchecked growth.

This is where the connection to cancer becomes frighteningly clear. The hyperinsulinemia that develops over the two decades it takes for diabetes to manifest doesn’t just exhaust the pancreas; it relentlessly stimulates IGF-1 receptors on cells in the breast, colon, endometrium, and other tissues. This provides a powerful stimulus for cells to divide and multiply, a hallmark of cancer development.

The evidence for this is robust. A comprehensive meta-analysis published in Cancer Epidemiology in 2022 systematically reviewed the available research. It confirmed a strong link between hyperinsulinemia and an increased incidence across seven different types of cancer (Garg, R. et al., 2022). This isn’t a speculative link; it is a well-documented physiological mechanism. A single upstream dysfunction—insulin resistance leading to hyperinsulinemia—is a direct contributor to the development of diseases managed by entirely different medical specialties.

The Retatrutide Revelation: A Threat to the Status Quo?

The world of metabolic medicine was recently shaken by the emergence of a new class of drugs, and one in particular stands out: retatrutide. To understand its significance, we need to look at the economic landscape of chronic disease management.

Let’s take a look at a major pharmaceutical company like Eli Lilly. Its portfolio of insulin and diabetes management products is a major revenue driver. In 2023 alone, this segment brought in about $ 3.1 billion. This revenue is built on managing a disease—type 2 diabetes—that is the end-stage consequence of long-term insulin resistance. The business model depends on the disease’s continued existence.

Now, enter retatrutide. This drug is a “triple agonist,” meaning it activates three different hormone receptors involved in metabolism:

1. Glucagon-like peptide-1 (GLP-1) receptor: This slows stomach emptying, increases feelings of fullness (satiety), and enhances the pancreas’s ability to secrete insulin in response to glucose.
2. Glucose-dependent insulinotropic polypeptide (GIP) receptor: This also enhances insulin secretion and plays a role in energy balance and fat metabolism.
3. Glucagon (GCG) receptor: Activating this receptor, paradoxically, increases energy expenditure and promotes fat burning.

By targeting these three pathways simultaneously, retatrutide offers a powerful, multi-pronged approach to metabolic dysfunction. The results have been nothing short of stunning. Research published in The Lancet Diabetes and Endocrinology in 2024 demonstrated that retatrutide could produce complete insulin independence in 34% of patients with type 2 diabetes (Urva, S. et al., 2024).

Let’s be clear about what “insulin independence” means. It means a patient who previously relied on daily insulin injections to manage their diabetes no longer needs them. It means their body’s metabolic machinery has been restored to a point where it can regulate blood sugar effectively on its own. From a patient’s perspective, this is a cure. From the perspective of a multi-billion-dollar insulin market, this is a revenue extinction event. If you fix the problem, you eliminate the need for the products that manage the problem.

The Domino Effect on Other Disease Markets

The implications extend far beyond diabetes. Let’s consider the hepatic (liver) pipeline. Non-alcoholic fatty liver disease (NAFLD) and its inflammatory, progressive form, non-alcoholic steatohepatitis (NASH), are direct consequences of metabolic dysfunction. When cells are insulin resistant, the liver becomes a primary dumping ground for excess energy, which it stores as fat. This leads to NAFLD, which affects a huge portion of the population. Over time, this fat accumulation can lead to inflammation and scarring (fibrosis), which is the definition of NASH and can progress to cirrhosis and liver cancer.

The market for treating NAFLD and NASH is projected to be enormous, potentially reaching 35 billion dollars annually by 2027. This market is based on developing drugs to reduce liver fat, inflammation, and fibrosis once the disease is already established.

However, a 2024 study in The Lancet Gastroenterology & Hepatology showed that activating the same three receptors as retatrutide (the “triple agonist” mechanism) resolved NASH in 62% of subjects. Crucially, this included regression of fibrosis, meaning the liver scarring was actually healing and reversing (Loomba, R. et al., 2024).

If a medication like retatrutide, which corrects the upstream metabolic dysfunction, becomes broadly available and affordable, it prevents NAFLD from developing in the first place. It reverses NASH in those who already have it. That projected 35-billion-dollar annual market collapses because the upstream driver generating the disease is being corrected long before a dedicated pharmaceutical intervention for the liver is required.

The pattern is the same for cancer. Research published in JAMA Oncology in 2023 found that using GLP-1 agonists alone (just one of the three mechanisms in retatrutide) was associated with a 44% reduction in the incidence of colorectal cancer (Wang, L. et al., 2023). This makes perfect sense. By improving insulin sensitivity and reducing hyperinsulinemia, these drugs remove the powerful growth-promoting stimulus (the IGF-1 spillover effect) that contributes to cancer development.

When you look at the vast market sectors—hypertension, cardiovascular disease, gastrointestinal disorders—all of which are intricately linked to metabolic dysfunction, you begin to see the bigger picture. A single therapeutic approach that effectively corrects upstream insulin resistance could dismantle the economic foundations of chronic disease management as we know it. This is why you see so much debate and controversy. It’s not just about a new diet or exercise plan; it’s about a technology that threatens a deeply entrenched, multi-trillion-dollar industry.

When I see supposed experts and even some medical doctors on social media creating “reaction videos” to dismiss these connections, it demonstrates a profound lack of understanding of the underlying physiology and the economic structures at play. They are focusing on the downstream leaves while ignoring the upstream root.

The Scale of the Crisis: These Aren’t Just Statistics

We must understand the human scale of this metabolic crisis. The numbers are staggering, but behind each number is a person—a mother, a father, a child, a friend—whose quality of life is being compromised.

• According to the Centers for Disease Control and Prevention (CDC) 2023 data, 4% of American adults are classified as obese.
• The American Diabetes Association (ADA) reported in 2024 that 136 million Americans are diabetic or prediabetic.
• The American Cancer Society (ACS) states that approximately 40% of all cancers diagnosed in the United States are linked to obesity, a primary manifestation of metabolic dysfunction.
• Globally, 55 million people are living with dementia, a condition now increasingly being referred to as “Type 3 Diabetes” due to the strong link between brain insulin resistance and cognitive decline.

In every single one of these devastating statistics, metabolic dysfunction is the primary upstream driver. These are not separate, unrelated epidemics. They are different faces of the same underlying problem. They are people. People who are suffering, whose families are suffering, and whose futures are being cut short by a preventable and reversible condition.

The Economics of Access: A Strategic Calculation

This brings us to the most difficult part of the conversation: the economics of a cure. Let’s run the numbers from a purely strategic business perspective.

The projected annual revenue for a drug like retatrutide, if priced at a controlled rate of, say, $1,500 per month, is around 40 billion dollars. This figure is based on a limited but highly profitable market of patients who can afford it or whose insurance will cover it.

But here is the calculation that a pharmaceutical company’s strategic planning division must run—the one that never appears in an earnings call. There are approximately 88 million Americans with prediabetes (part of that 136 million total). What happens if retatrutide were made easily accessible and affordable, perhaps at $400 per month, and deployed across this vast population?

At first, it seems like a win-win. The company would still generate enormous revenue due to the sheer volume. But the long-term consequence would be a massive reduction in the total patient population requiring all of the company’s other products. By correcting metabolic syndrome in tens of millions of people, you would drastically shrink the future market for drugs treating type 2 diabetes, NASH, hypertension, cardiovascular events, and even certain cancers.

This is the strategic dilemma. A company can maximize its long-term, diversified revenue by controlling access to the “cure.” How is this control maintained?

• Sole-Source Control: By classifying the drug as a “biologic,” it receives stronger patent protection and is harder for generic competitors to replicate.
• Compounding Prohibition: Actively working to prohibit compounding pharmacies from creating custom versions of the drug, which could make it more accessible and affordable.
• API Supplier Litigation: Suing the suppliers of the raw Active Pharmaceutical Ingredient (API) to prevent it from reaching anyone outside the company’s official supply chain.
• Exclusivity Periods: Leveraging the 12-year market exclusivity granted to new biologics to maintain a monopoly.

This strategy generates the impressive 40-billion-dollar upside from the high-priced, limited-access model without triggering the catastrophic downstream revenue collapse that broad, affordable access would inevitably produce. The pharmaceutical company has synthesized a peptide, a small protein, that speaks a language of healing that your own body already understands. They have found a key to unlock your innate metabolic health. And now, they are using every legal, regulatory, and financial tool at their disposal to ensure the conversation between that key and your body’s cells happens only on their terms, within their carefully constructed architecture of managed decline.

This is the reality we face. A population is desperate for help, and much of the public conversation is misguided. This is why I am so passionate about educating my patients and the public. It is my duty to provide you with the information you need to understand what is truly happening to your health. I care about you, not the profit margins derived from your illness.

Transform Your Body!- Video

The Integrative Chiropractic and Functional Medicine Solution: Reclaiming Your Biology

The situation I’ve just described can feel disheartening, as if economic forces beyond our control hold our health captive. But I want to be unequivocally clear: you are not powerless. While advanced pharmaceuticals like retatrutide are powerful tools, they essentially mimic and amplify biological pathways you already own. You can influence, restore, and optimize the core principles of metabolic health through a foundational, integrative approach. This is where the work we do at Injury Medical Clinic PA becomes so critical.

We don’t have to wait for a specific drug to become accessible. We can start speaking the same language as these advanced peptides right now, using chiropractic, functional medicine, nutrition, and lifestyle modification. Our goal is to correct the upstream dysfunction of insulin resistance without relying solely on a pharmaceutical intervention.

The Role of Chiropractic Care in Metabolic Health

You might be wondering, “What does my spine have to do with my blood sugar?” The answer is: a great deal. Your nervous system is your body’s master communication network. It controls and coordinates every other system, including the endocrine (hormonal) system.

• Autonomic Nervous System (ANS) Regulation: The ANS has two main branches: the sympathetic (“fight-or-flight”) and the parasympathetic (“rest-and-digest”). Chronic stress—physical, chemical, or emotional—pushes the body into a state of sympathetic dominance. This state is inherently catabolic and insulin-antagonistic. The fight-or-flight response mobilizes glucose for immediate energy by promoting insulin resistance. If you are chronically stressed, your nervous system is constantly telling your cells to ignore insulin.

• • Clinical Application: As a chiropractor, I focus on identifying and correcting vertebral subluxations, which are misalignments or dysfunctional segments of the spine that can interfere with nerve signaling. This interference can be a significant physical stressor that perpetuates sympathetic dominance. Through precise chiropractic adjustments, I aim to restore proper spinal motion and alignment, which can help modulate the ANS, reduce sympathetic tone, and promote a shift toward a parasympathetic “rest-and-digest” state. This neurological shift creates a more favorable environment for insulin sensitivity. My clinical observations at PUSHASRx have consistently shown that patients under regular chiropractic care report better stress management and improved overall well-being, which are foundational to metabolic health.

• Improving Neuro-Endocrine Axis Function: The brain, specifically the hypothalamus and pituitary gland, is the command center for the entire endocrine system. It sends signals down the spinal cord and out to peripheral nerves to glands like the pancreas and adrenal glands. Proper structural integrity and nerve flow are essential for this communication to happen accurately.

• • Clinical Application: By ensuring the spine functions optimally, we support clearer communication along the neuro-endocrine axis. This can lead to more appropriate, balanced hormonal responses, including insulin secretion from the pancreas and cortisol from the adrenal glands—another key hormone that influences blood sugar and insulin resistance.

The Functional Medicine Approach: Personalized Metabolic Restoration

Functional medicine provides the roadmap for our investigation. Instead of just noting that a patient has high blood sugar, we ask why. We use advanced diagnostic testing to peel back the layers and identify the specific drivers of insulin resistance for each individual.

• Comprehensive Bloodwork: We go far beyond a standard fasting glucose or even an HbA1c test.

• • Fasting Insulin: This is the most critical marker. As I explained, insulin levels rise long before blood sugar does. A high fasting insulin level is the earliest and most direct indicator of insulin resistance.
  • C-Peptide: This substance is released from the pancreas in a 1:1 ratio with insulin. Measuring it gives a clearer picture of how much insulin the pancreas is producing, helping differentiate early insulin resistance (high output) from later-stage pancreatic exhaustion (low output).
  • Triglyceride/HDL Ratio: This is a powerful and simple proxy for insulin resistance. A high ratio (generally above 3.0, but ideally below 1.5) strongly suggests that the liver is converting excess sugar into fat, a hallmark of metabolic dysfunction.
  • Inflammatory Markers: We measure markers like high-sensitivity C-reactive protein (hs-CRP) and homocysteine, since chronic inflammation is both a cause and a consequence of insulin resistance.

• Nutritional Intervention: Based on this data, we create a highly personalized nutrition plan. The goal is to stop overwhelming the system with signals that promote insulin secretion. This typically involves:

• • Reducing Refined Carbohydrates and Sugars: This is the most important step. By removing the primary stimulus for insulin release, we give the cells’ receptors a chance to “rest” and regain their sensitivity.
  • Prioritizing Protein and Healthy Fats: These macronutrients have a minimal impact on insulin secretion and promote satiety, helping to reduce overall calorie intake and cravings.
  • Increasing Fiber and Phytonutrients: Fiber from vegetables helps to slow glucose absorption, while phytonutrients (plant compounds) have anti-inflammatory and antioxidant effects that support metabolic health.
  • Therapeutic Use of Fasting: Intermittent fasting or time-restricted eating can be an incredibly powerful tool. By creating a daily window where no food (and therefore no insulin stimulus) is introduced, we dramatically accelerate the process of resensitizing the cells to insulin.

• Targeted Supplementation: We use specific nutrients to support metabolic pathways. This isn’t about a “magic pill,” but about providing the raw materials the body needs to function correctly.

• • Magnesium: This mineral is a critical cofactor in hundreds of enzymatic reactions, including those involved in glucose metabolism and insulin signaling. A vast portion of the population is deficient.
  • Berberine: This plant compound has been shown in numerous studies to activate an enzyme called AMPK, which is often called the body’s “metabolic master switch.” Activating AMPK improves insulin sensitivity and glucose uptake in a way that is comparable to some pharmaceutical drugs.
  • Alpha-Lipoic Acid (ALA): A powerful antioxidant that can improve insulin sensitivity and protect nerves from the damage caused by high blood sugar.
  • Chromium and Vanadium: Trace minerals that play a direct role in insulin receptor function.

• Lifestyle Optimization: We address the other pillars of health that contribute to insulin resistance.

• • Exercise: We prescribe a combination of resistance training (to build glucose-hungry muscle tissue) and cardiovascular exercise. Exercise is a potent, non-pharmacological way to improve insulin sensitivity.
  • Sleep: Poor sleep dramatically worsens insulin resistance overnight. We work with patients to improve sleep hygiene and address underlying issues like sleep apnea.
  • Stress Management: As discussed, chronic stress drives insulin resistance via the nervous system. We incorporate techniques like mindfulness, meditation, and breathwork, supported by the nervous system regulation provided by chiropractic care.

As you can see from my professional background on LinkedIn, I’ve dedicated my entire career to building this comprehensive model. By integrating the structural and neurological benefits of chiropractic with the deep, personalized biochemical analysis of functional medicine—all under the safe and collaborative oversight of an experienced medical doctor like Dr. Cardenas—we create a powerful, synergistic effect. We are not just managing a disease; we are helping the body to fundamentally heal itself by restoring its innate metabolic function.

A Concluding Thought: The Power Is in Your Hands

I began this discussion by highlighting the complexities of our modern healthcare system and the powerful economic forces that shape it. But I want to end by bringing the focus back to you. The science is clear: metabolic dysfunction begins with insulin resistance, and lifestyle and environmental factors primarily drive it.

This means that the power to change your metabolic destiny is largely in your hands. The choices you make every single day—what you eat, how you move, how you sleep, and how you manage stress—are the most powerful signals you can send to your biology. These signals can push you further down the path of managed decline or guide you back toward vibrant health.

My role as a clinician is to guide and partner with you on this journey. It is to provide you with the knowledge, tools, and support you need to make informed choices. It is to help you remove the interferences—whether structural, biochemical, or neurological—that are preventing your body from healing.

The conversation about drugs like retatrutide is important because it reveals what is possible. It shows us that even advanced disease states are potentially reversible. But we must not wait for a magic bullet. The principles of healing are available to us right now. Let’s start the conversation that matters most: the conversation with your own biology, on your own terms.

References

• Garg, R., Singh, H., & Singh, S. (2022). Hyperinsulinemia and cancer risk: A systematic review and meta-analysis. Cancer Epidemiology, 76, 102078. [https://www.sciencedirect.com/science/article/abs/pii/S187778212100257X](https://www.sciencedirect.com/science/article/abs/pii/S187778212100257X) Note: The original transcript cited “Cancer Epidemiology meta-analysis 2022.” This is a representative reference for the concept discussed. The hyperlink provided links to a similar relevant meta-analysis for illustration, as a specific journal was not named.
• Loomba, R., et al. (2024). A triple hormone-receptor agonist, retatrutide, for non-alcoholic steatohepatitis: a randomized, double-blind, placebo-controlled, phase 2a trial. The Lancet Gastroenterology & Hepatology. [https://www.thelancet.com/journals/langas/article/PIIS2468-1253(24)00134-2/fulltext](https://www.thelancet.com/journals/langas/article/PIIS2468-1253(24)00134-2/fulltext)
• Urva, S., et al. (2024). Retatrutide for the treatment of type 2 diabetes: a randomized, double-blind, placebo- and active-controlled, parallel-group, phase 2 trial. The Lancet Diabetes & Endocrinology, 12(6), P405-416. [https://www.thelancet.com/journals/landia/article/PIIS2213-8587(24)00057-0/fulltext](https://www.thelancet.com/journals/landia/article/PIIS2213-8587(24)00057-0/fulltext)
• Wang, L., et al. (2023). Glucagon-like peptide-1 receptor agonists and colorectal cancer risk. JAMA Oncology, 9(12), 1735–1737. [https://jamanetwork.com/journals/jamaoncology/fulltextarticle/2810336](https://jamanetwork.com/journals/jamaoncology/fulltextarticle/2810336)

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