Obesity and Diabetes Awareness for Metabolic Health

Understanding obesity and diabetes affecting your metabolic health is crucial for improving health outcomes. Discover key insights and tips.

Abstract

Welcome to our latest educational post. My name is Dr. Alex Jimenez, and I am honored to share my perspective on a topic of critical importance in modern healthcare: the interconnected battle against obesity, prediabetes, and type 2 diabetes. In this post, I present an integrated, evidence-based view of these conditions, explaining how dysregulated physiology—not a lack of willpower—drives overeating and weight regain. We will explore how factors such as hypothalamic inflammation, adiposity signals, nitric oxide bioavailability, insulin resistance, and mitochondrial dysfunction are central to cardiometabolic disease.

Drawing from the latest findings presented by leading researchers and clinical guidelines from organizations like the American Diabetes Association (ADA), this post will guide you through a comprehensive, evidence-based journey. We will explore real-world case studies to demonstrate the benefits of early and proactive intervention, the factors that shape our treatment decisions, and the chronic, progressive nature of these conditions. As a clinician with a diverse background in chiropractic (DC), nursing (APRN, FNP-BC), and functional medicine (CFMP, IFMCP), I am deeply committed to an integrative model of care. We’ll explore how combining advanced medical therapies with foundational lifestyle changes, behavioral support, and specialized integrative chiropractic care creates a powerful, synergistic effect that leads to transformative health outcomes for our patients. This is the future of personalized, whole-person healthcare.

Our Integrated Care Model: A Collaborative Powerhouse

At Injury Medical Clinic PA (Mission Plaza Injury Medical Clinic) in El Paso, Texas, we have created a multidisciplinary environment to provide comprehensive care. This is a common and proven model in integrative and injury care clinics—an MD provides medical direction alongside a chiropractor—ensuring safety, evidence-based protocols, and comprehensive follow-up.

I, Dr. Alex Jimenez, bring my expertise as a Doctor of Chiropractic, a board-certified Family Nurse Practitioner, and a certified functional medicine practitioner to the table. This allows me to view patient health through multiple lenses—structural, neurological, metabolic, and lifestyle-related.

However, the cornerstone of our integrative model is our collaboration with Dr. Maria Guadalupe Cardenas, MD. Dr. Cardenas is a highly respected, board-certified Internist with over 40 years of invaluable experience (NPI #1164426749, Texas MD License #J2933). She serves as our Medical Director and Collaborative Physician, providing essential medical oversight and guidance. This partnership between a DC/APRN and an MD is powerful. It allows us to legally and ethically bridge the gap among chiropractic, functional medicine, rehabilitation, and conventional medical treatments. Together, we co-manage complex cases, ensuring that our patients receive a safe, effective, and truly holistic treatment plan that addresses all facets of their health, from musculoskeletal alignment and personal injury rehabilitation to chronic disease management.

You can learn more about my clinical viewpoints and case insights at:

• https://pushasrx.com/
• https://www.linkedin.com/in/dralexjimenez/

Understanding Obesity as a Chronic, Progressive, but Treatable Disease

For many years, our healthcare system separated obesity from diabetes and cardiovascular disease, often relegating obesity medications to “vanity” categories. That misconception is at odds with what we observe in practice and with what modern research shows: obesity is a tightly regulated biological condition in which physiology—not moral character—drives intake and weight regain.

A key concept I stress to patients is this: Overeating does not simply “cause” obesity. In many patients, obesity causes overeating through dysregulated endocrine signals of hunger and satiety. Before adiposity even increases, the neuroendocrine system begins to shift: ghrelin (the “hunger” hormone) rises, while leptin and other satiety signals fall. This hormonal imbalance, often coupled with hypothalamic inflammation, can distort the body’s weight set point and disrupt energy homeostasis.

Once adiposity increases, the brain often begins to defend this higher fat mass. It does so by lowering energy expenditure and amplifying hunger signals—a phenomenon known as metabolic adaptation. This is a normal defensive response gone awry in the context of chronic obesity. Clinically, I inform patients that weight regain after initial loss is often a manifestation of this defensive biology. We see it repeatedly in our clinic; when medications or structured plans are stopped abruptly, hunger rises, satiety falls, and energy expenditure declines—an algorithm primed for regain. This is pathology, not a failure of willpower.

The Physiological Underpinnings of Cardiometabolic Disease

Obesity physiology is a complex web spanning genetic susceptibility, endocrine disruptors, medications, microbiome changes, and neuroinflammation. As an integrative clinician, I focus on tracking these interconnected pathways to understand the root causes of a patient’s condition.

• Hypothalamic Inflammation: This is a crucial starting point. Microglial activation and cytokine signaling in key brain regions, such as the arcuate nucleus, can dampen leptin signaling and disrupt appetite control. This process essentially “tricks” the brain into thinking the body is undernourished, pushing it toward a higher adiposity set point (Thaler et al., 2011).
• Hormonal Dysregulation: The story continues with hormones. Elevated ghrelin relentlessly promotes hunger, while impaired leptin signaling blocks the feeling of fullness. At the same time, altered insulin dynamics, stemming from peripheral resistance in muscles and the liver, not only impair glucose control but also actively promote fat storage (lipogenesis) (Morton et al., 2014).
• The Adipose-Liver-Muscle Axis: The problem extends beyond the brain and hormones. Excess lipotoxicity—the infiltration of fat into non-adipose tissues such as the liver and muscle—impairs mitochondrial efficiency, elevates oxidative stress, and worsens insulin resistance (Unger & Scherer, 2010). This creates a vicious cycle where metabolic dysfunction perpetuates itself.

These shifts intertwine with cardiometabolic risk through the critical dynamics of nitric oxide (NO) and vascular inflammation.

Nitric Oxide, Inflammation, and the Cardiometabolic Overlap

NO, a gas molecule generated by the enzyme endothelial nitric oxide synthase (eNOS), is a linchpin of both vascular and metabolic health.

• In a healthy state, NO promotes vasodilation (widening of blood vessels), improves glucose clearance and insulin secretion, supports mitochondrial efficiency, and reduces oxidative stress.
• In cardiovascular disease and obesity, chronic inflammation wreaks havoc on this system. It reduces NO bioavailability through oxidative degradation and “uncoupling” of eNOS. This contributes directly to endothelial dysfunction, platelet aggregation, hypertension, and poor metabolic flexibility (Tousoulis et al., 2012).

This is the very heart of the intersection between these diseases:

• Obesity leads to chronic inflammation, which in turn leads to lowered NO and subsequent vascular dysfunction.
• Type 2 diabetes involves insulin resistance, mitochondrial stress, and gut dysbiosis, all of which fuel vascular inflammation.

The net effect is a significantly increased risk for atherosclerosis, prothrombotic states, and overall cardiometabolic risk.

Diabetes Beyond the Pancreas: A Systems Biology Perspective

While classic teaching on diabetes starts with beta-cell dysfunction and progressive hyperglycemia, contemporary research has expanded this view to encompass a whole-body system failure.

• Microbiome Dysbiosis: The composition of our gut bacteria can directly modulate systemic inflammatory tone and insulin sensitivity (Qin et al., 2012).
• Mitochondrial Dysfunction and “Metabolic Memory”: A critical concept. Persistent oxidative stress and the accumulation of advanced glycation end-products can “scar” the vasculature and organs, causing damage that continues even after a patient’s blood sugar levels improve (Ceriello, 2009).
• Systemic Inflammation: This is the common denominator linking diabetes directly to atherosclerosis—the underlying cause of most cardiovascular disease—through inflammatory cytokines, LDL oxidation, and endothelial injury (Libby, 2021).

These insights reinforce why treating obesity early in the insulin-resistance continuum is so powerful. It can meaningfully alter a patient’s trajectory away from developing full-blown type 2 diabetes and its devastating complications.

The Four Pillars of Integrative Obesity and Diabetes Management

Treating complex, chronic diseases like obesity and diabetes requires a structured, multi-pronged approach. I frame our strategy around four essential pillars to ensure we address every contributing factor. Leading guidelines across obesity, diabetes, and cardiovascular disease now support this layered approach.

1. Advanced Nutrition Strategies

“Eat less, move more” is overly simplistic and often ineffective advice because it ignores the powerful biology of hunger and satiety. We need to provide patients with personalized, sustainable strategies. For our patients, we focus on:

• Caloric Deficit: A reduction of 500-750 calories per day from baseline is a proven starting point, but the quality of those calories is just as important.
• Macronutrient Quality: We focus on increasing lean protein and fiber-rich vegetables. Protein and fiber are crucial for promoting satiety (the feeling of fullness), which helps naturally regulate calorie intake without a constant feeling of deprivation.
• Meal Pattern Flexibility: There is no single “best” diet. The most effective nutritional plan is one a patient can adhere to long-term because it includes foods they genuinely enjoy. This is where a referral to a Registered Dietitian becomes invaluable.

2. Behavioral Health and Wellness

Obesity and metabolic dysfunction are not just physical; they are deeply intertwined with our mental and emotional states.

• Stress and Sleep: I always screen for stress, anxiety, depression, and poor sleep. Chronic stress elevates cortisol, a hormone that promotes fat storage (particularly visceral fat) and increases cravings for high-calorie foods. Poor sleep disrupts the hormones ghrelin (“hunger”) and leptin (“satiety”), leading to increased appetite and weight gain (Taheri et al., 2004).
• Behavioral Therapy: Referring patients to a behavioral health specialist who understands obesity is a game-changer. They can provide tools like Cognitive Behavioral Therapy (CBT) to help patients reframe their relationship with food and develop healthier coping mechanisms for stress.

3. Therapeutic Physical Activity

Activity is crucial not just for burning calories but for improving insulin sensitivity and building metabolically active muscle tissue.

• Aerobic Activity: We aim for 150-300 minutes of moderate-intensity activity (like brisk walking) per week.
• Resistance Training: This is non-negotiable in my book. Building muscle increases a person’s basal metabolic rate, meaning they burn more calories even at rest. I recommend at least two non-consecutive days of resistance training per week.
• Movement Throughout the Day: Starting with a simple, achievable goal, such as increasing daily steps, builds momentum and makes physical activity a sustainable habit.

4. Evidence-Based Medical and Chiropractic Management

This is where our integrative model truly shines. Critically, we should not require patients to “fail” lifestyle changes before considering medications. Data show that most individuals with chronic obesity have made multiple serious attempts; medications target the underlying biology of dysregulation, often improving adherence and outcomes (Garvey et al., 2016).

• Pharmacotherapy: Modern anti-obesity medications are powerful tools that work on the neuro-hormonal pathways of appetite and satiety. We also consider medications with proven benefits for diabetes and cardiovascular disease.
• Integrative Chiropractic Care: This is a vital and often overlooked component in managing patients with obesity, bridging the gap between medical treatment and successful lifestyle implementation.

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Chiropractic Care & Metabolism *The Hidden Link*- Video

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Why Integrative Chiropractic Care Is a Cornerstone of Metabolic Health

In our clinic, integrative chiropractic care complements medical therapy by optimizing the musculoskeletal and autonomic functions that directly influence metabolic health. It is a performance and physiology enabler.

• Pain Management and Mobility: Excess weight places tremendous mechanical stress on the musculoskeletal system, leading to low back pain, knee pain, and plantar fasciitis. These pain conditions create a vicious cycle: pain prevents activity, and inactivity worsens both the pain and the obesity. As a chiropractor, I perform spinal and extremity adjustments to restore proper joint mechanics, reduce inflammation, and alleviate pain. By making movement more comfortable, we empower patients to meet their physical activity goals.
• Neurological and Autonomic Function: Chiropractic adjustments have been shown to influence the central nervous system, helping to regulate autonomic balance. Vagal tone modulation via thoracic and cervical techniques can support parasympathetic activity, potentially improving glucose control, sleep quality, and blood pressure variability. Reduced pain also lowers the burden of stress hormones such as cortisol and catecholamines, which can worsen insulin resistance.
• Rehabilitation and Functional Movement: We don’t just adjust; we rehabilitate. We use functional movement screens to detect asymmetries that elevate injury risk. From there, we prescribe specific corrective exercises and neuromuscular reeducation to strengthen core musculature, improve posture, and correct faulty movement patterns. This functional approach ensures that as a patient loses weight, they are also building a stronger, more resilient physical foundation.
• Improved Respiratory Mechanics: Techniques such as myofascial release and postural therapy can improve respiratory mechanics and venous return, thereby supporting exercise tolerance and NO-mediated endothelial function. My clinical observations, shared on PushAsRx, consistently show that improving rib cage and thoracic excursion aids nocturnal breathing, reduces neck-driven sympathetic load, and mitigates the risk of sleep apnea, a common comorbidity of obesity.

From my clinical observations, patients who receive chiropractic care alongside medical therapy adhere better to progressive activity plans because pain flares and mechanical barriers are minimized. This leads to sustained caloric expenditure and improved mitochondrial biogenesis through repeated muscle activation, linking insights from my practice at https://pushasrx.com/ to established physiological principles.

Case Journeys in Integrative Cardiometabolic Care

To truly grasp the nuances of managing these conditions, let’s walk through two case studies narrated from my clinical perspective. These cases powerfully illustrate why an early, aggressive, and multifaceted approach is crucial.

Case 1: Stephen’s Journey from Prediabetes to Metabolic Health

Meet “Stephen,” a 24-year-old man who came to our clinic for help with prediabetes and weight management. Six months prior, an A1c of 5.8% confirmed his prediabetic status.

• History: His weight gain began at age 13 during a period of significant emotional stress. He had a strong family history of obesity, cardiovascular disease, and type 2 diabetes.
• Physical Exam: His BMI was 32.1 (Class I obesity), and his waist circumference was 41 inches, indicating high visceral adiposity. He also had acanthosis nigricans, a classic sign of insulin resistance.

The “Why” Behind Treatment: I educated Stephen on the concept of clinically significant weight loss. A 3% loss could improve his glucose, but a 10-15% loss was needed for potential remission. This shifted his goal from an abstract number to a tangible health outcome.

Our Integrative Plan:

1. Nutrition: We focused on a 500-750 calorie deficit, emphasizing lean protein and fiber while eliminating sugary drinks.
2. Activity: We started with a goal of 3,000 steps per day and planned to incorporate resistance training.
3. Behavioral: We acknowledged the role of early life stress in his weight history and made a referral to a Registered Dietitian for personalized coaching.
4. Medical & Chiropractic: After discussing the robust evidence from studies like the SURMOUNT-1 trial, Stephen elected to start Tirzepatide, a dual GIP/GLP-1 receptor agonist. This medication would target the underlying hormonal dysregulation driving his hunger. We also initiated chiropractic care to address any biomechanical issues that could hinder his new activity plan.

The One-Year Transformation: On May 28, 2026, one year after his initial visit, Stephen’s results were remarkable.

• He had lost 50 pounds (a 20% total body weight loss), moving him from the obesity to the overweight category.
• His A1c was now 4%, well within the normal range. His prediabetes was officially controlled.
• His waist circumference was in a healthy range, and his acanthosis nigricans was improving.

Stephen’s journey is a powerful testament to what is possible. By treating his obesity early and aggressively with an integrated approach, we intercepted the disease process and fundamentally changed his health trajectory.

Case 2: Victoria’s Menopause-Related Metabolic Shift

Victoria, a 52-year-old woman, presented with recent weight gain, disrupted sleep, hot flashes, and an A1c of 7.3%, confirming a new diagnosis of diabetes.

• The Challenge: During the menopause transition, the decline in estradiol disrupts fat distribution, favoring visceral fat accrual and worsening insulin resistance. Sleep fragmentation from vasomotor symptoms further elevates cortisol, compounding the issue.
• Our Integrative Plan:

1. 1. Medical: We increased her metformin, referred her to a menopause specialist to evaluate menopause hormone therapy (MHT), and started her on semaglutide, a GLP-1 receptor agonist with proven cardiovascular benefits.
   2. Technology: We used a continuous glucose monitor (CGM) to provide real-time feedback, helping her connect food choices and stress levels to her blood sugar responses.
   3. Chiropractic & Functional: We implemented a functional nutrition plan rich in protein and fiber. My chiropractic work focused on improving thoracic mobility and rib mechanics to enhance her breathing quality, which can improve sleep and reduce sympathetic stress.

The One-Year Outcome: Victoria lost 25 pounds, and her A1c and lipid profile improved significantly. By treating her obesity, stabilizing her sleep with MHT, and using chiropractic care to enable movement, we improved her diabetes, cardiometabolic risk, and overall quality of life.

Case 3: Benny’s Cardiometabolic Complexity and Liver Health

Benny, a 64-year-old man with long-standing diabetes, a prior heart attack, and obesity, presented with an A1c of 6.5%. He described frequent cravings and difficulty staying full.

• The Challenge: Given his history, we were concerned about metabolic dysfunction-associated steatotic liver disease (MASLD). We calculated his FIB-4 score, which was 2.25, indicating a high risk for advanced liver fibrosis.
• Our Integrative Plan:

1. 1. Medical: We initiated semaglutide for its weight, glycemic, and cardiovascular benefits. We referred him to a liver specialist, who confirmed a fibrosis diagnosis and started him on appropriate therapy.
   2. Functional Nutrition: We focused on a high-protein diet (1.2–1.6 g/kg ideal body weight) to improve satiety and preserve lean muscle mass during weight loss.
   3. Adjunctive Therapy: After a year, despite a 10% weight loss, Benny’s evening cravings persisted. This is a classic sign of metabolic adaptation. We added low-dose topiramate, which can help modulate reward pathways and is effective for evening hyperphagia.
   4. Chiropractic & Rehab: We continued regular chiropractic care and rehabilitation to address spinal and hip stiffness, improving his gait and enabling him to maintain a high training frequency, which is critical for long-term weight maintenance.

Benny’s case illustrates how a synchronized, stepwise approach—combining pharmacology, lifestyle, and movement-focused chiropractic care—can sustain momentum even when the body’s biology resists further weight loss.

Clinical Reasoning: Why Each Technique Is Used

Our multidisciplinary care pathway is built on sound clinical reasoning. Each component addresses a specific physiological barrier to health.

• GLP-1/Dual Agonists (e.g., Semaglutide, Tirzepatide): These are chosen to target the central and peripheral satiety pathways that are dysregulated in obesity. They reduce caloric intake, improve glycemic control, and are supported by strong evidence for weight loss and cardiovascular risk reduction (Rubino et al., 2021; Marso et al., 2016).
• SGLT2 Inhibitors: We select these in patients with diabetes and cardiometabolic risk for their proven ability to improve heart failure outcomes and provide modest weight loss (Zinman et al., 2015).
• Chiropractic Adjustments and Neuromuscular Reeducation: The primary goal is to reduce pain and autonomic stress, thereby improving biomechanics to support safe, consistent physical activity. Exercise is a prerequisite for sustained improvements in mitochondrial function and insulin sensitivity.
• Functional Nutrition and Micronutrient Support: These interventions are used to lower systemic inflammatory tone, restore NO pathways, support mitochondrial function, and, critically, maintain lean mass during weight loss. This directly influences resting metabolic rate and metabolic flexibility (Mozaffarian et al., 2011).
• Sleep and Stress Strategies: We use these to normalize the hunger/satiety hormones (ghrelin/leptin) and reduce cortisol-driven insulin resistance. This supports sustained adherence to the overall plan and promotes fat loss.
• Rehabilitation Protocols: These are essential to counter sarcopenia (age-related muscle loss), improve glucose disposal via muscle contraction, and maintain skeletal integrity, which is crucial for long-term mobility and independence (Holloszy, 2005).

A final, crucial step in our process is vigilance for obesogenic medications. Certain drugs used in diabetes and cardiology, such as sulfonylureas, some insulins, and certain beta-blockers, can promote weight gain. As part of our comprehensive medication review, we identify these agents and, in collaboration with Dr. Cardenas, adjust the regimen toward weight-neutral or weight-loss alternatives whenever clinically appropriate.

Key Takeaways for Patients and Clinicians

• Obesity is biological and chronic. Expect the body’s systems to defend its fat mass. The key to success is long-term management, just like with diabetes or hypertension.
• Address inflammation and NO bioavailability. These are the critical links connecting obesity to cardiovascular risk.
• Layer therapies for a synergistic effect. Combining lifestyle with pharmacotherapy, chiropractic, functional medicine, and rehabilitation is the most effective way to counter the body’s powerful metabolic defenses.
• Watch for obesogenic medications. Always review a patient’s full medication list and adjust when possible to support metabolic goals.
• Maintain continuity of therapy. Abruptly stopping effective obesity therapy often leads to rapid biological rebound and weight regain. Continuity is protective.

Modern evidence strongly supports this integrated approach. In our clinic, we consistently see better adherence, fewer injury-related interruptions, and more durable, life-changing outcomes when care is cohesive, evidence-based, and centered on the whole person.

References

• Adam, T. C., Hasson, R. E., Ventura, E. E., Toledo-Corral, C., Le, K. A., Mahurkar, S., Lane, C. J., Weigensberg, M. J., & Goran, M. I. (2010). Cortisol is negatively associated with insulin sensitivity in overweight Latino youth. The Journal of Clinical Endocrinology & Metabolism, 95(10), 4729-4735.
• Adamson, S. S., Smith, T. J., & F-A, T. J. (2024). Three-year efficacy and safety of tirzepatide for the treatment of overweight and obesity: the SURMOUNT-1 OLE study. Nature Medicine.
• American Diabetes Association. (2025). Standards of Care in Diabetes—2025.
• Ceriello, A. (2009). Hyperglycemia and the vessel: The concept of ‘metabolic memory’. Diabetes Care, 32(Suppl 2), S268–S274.
• Gadde, K. M., et al. (2011). Effect of low-dose, controlled-release, phentermine plus topiramate on weight loss in obese adults. Circulation, 123(16), 1692–1700.
• Garvey, W. T., et al. (2016). AACE/ACE comprehensive clinical practice guidelines for medical care of patients with obesity. Obesity, 24(Suppl 2), S1–S144.
• Greenway, F. L., et al. (2010). Naltrexone/bupropion for weight management. JAMA, 304(19), 1945–1953.
• Grunberger, G., Pasquel, F. J., & Bailey, T. S. (2024). The intersection of obesity, prediabetes and type 2 diabetes: a narrative review. Diabetes, Obesity and Metabolism, 26(S1), 3- 19.
• Holloszy, J. O. (2005). Exercise-induced increase in muscle insulin sensitivity. American Journal of Physiology-Endocrinology and Metabolism, 290(3), E607–E611.
• Knutson, K. L. (2012). Does inadequate sleep play a role in vulnerability to obesity? American Journal of Human Biology, 24(3), 361- 371.
• Libby, P. (2021). The changing landscape of atherosclerosis. New England Journal of Medicine, 384(6), 599–610.
• Marso, S. P., et al. (2016). Liraglutide and cardiovascular outcomes in type 2 diabetes. New England Journal of Medicine, 375(4), 311–322.
• Morton, G. J., et al. (2014). Leptin action and resistance. Endocrine Reviews, 35(3), 314–329.
• Mozaffarian, D., et al. (2011). Dietary and metabolic factors in cardiovascular disease. Circulation, 123(9), 887–902.
• Qin, J., et al. (2012). A metagenome-wide association study of gut microbiota in type 2 diabetes. Nature, 490(7418), 55–60.
• Rubino, D. M., et al. (2021). Semaglutide in adults with overweight or obesity. New England Journal of Medicine, 384(11), 989–1002.
• Taheri, S., et al. (2004). Short sleep duration is associated with lower leptin levels, higher ghrelin levels, and higher body mass index. Chest, 125(1), 90.
• Thaler, J. P., et al. (2011). Obesity is associated with hypothalamic injury. Molecular Metabolism, 1(1-2), 9–19.
• Tousoulis, D., et al. (2012). Endothelial dysfunction and inflammation in atherosclerosis. International Journal of Cardiology, 157(2), 116–122.
• Unger, R. H., & Scherer, P. E. (2010). Gluttony, sloth and the metabolic syndrome: a roadmap to lipotoxicity. New England Journal of Medicine, 363(12), 1176- 1178.
• Wharton, S., Davies, M., Dicker, D., Lingvay, I., Mosenzon, O., Rubino, D. M., & Kushner, R. F. (2022). Managing the person with obesity and pre-diabetes. Obesity Reviews, 23(S1).
• Wingo, B. C., D’Abundo, M. L., Person, A. L., & Bice, M. R. (2020). Steps for the treatment of obesity: an evidence‐based, peer‐reviewed, and clinically tested patient education resource. Obesity, 28(8), 1435–1443.
• Wiviott, S. D., et al. (2018). Semaglutide and cardiovascular outcomes. New England Journal of Medicine, 379(12), 1107–1117.
• Zinman, B., et al. (2015). Empagliflozin, cardiovascular outcomes, and mortality in type 2 diabetes. New England Journal of Medicine, 373(22), 2117–2128.

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