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Diabetes stands as one of humanity’s oldest documented diseases, with a rich and complex history spanning thousands of years. From ancient physicians puzzling over mysterious symptoms to modern scientists unlocking genetic codes, the journey of diabetes research represents one of medicine’s most remarkable stories of persistence, innovation, and scientific breakthrough. Understanding this history not only illuminates how far we’ve come but also provides crucial context for the challenges and opportunities that lie ahead in diabetes care and treatment.
Ancient Observations: The Dawn of Diabetes Recognition
The story of diabetes begins in the ancient world, where physicians first documented the puzzling symptoms of a disease they could observe but not fully comprehend. The very name “diabetes” derives from the Greek word “diabainein,” meaning “to pass through” or “siphon,” a vivid description of the excessive urination that characterizes the condition. This naming reflects the acute observational skills of ancient healers who recognized the distinctive pattern of symptoms even without understanding their underlying cause.
The earliest known medical reference to diabetes appears in the Ebers Papyrus, an Egyptian medical text dating to approximately 1550 BCE. This ancient document describes a condition involving frequent urination and unexplained weight loss, symptoms we now recognize as hallmarks of untreated diabetes. The Egyptian physicians recommended a treatment mixture of bones, wheat, grain, grit, green lead, and earth, which, while ineffective by modern standards, demonstrates early attempts at therapeutic intervention.
Ancient Indian physicians made equally significant observations around the same period. The Sushruta Samhita and Charaka Samhita, foundational texts of Ayurvedic medicine written between 400-500 CE but containing knowledge from much earlier periods, described a condition called “madhumeha” or “honey urine.” Indian healers noted that the urine of affected individuals attracted ants and flies due to its sweet taste, an observation that would prove remarkably prescient in identifying the glucose content of diabetic urine.
Greek and Roman physicians further refined clinical descriptions of diabetes. Hippocrates, often called the father of medicine, made references to the condition between 460-370 BCE, though his descriptions were relatively brief. More detailed was the work of Aretaeus of Cappadocia in the first century CE, who provided one of the most comprehensive early clinical descriptions of diabetes. He characterized it as “a melting down of the flesh and limbs into urine,” noting the excessive thirst, constant urination, and progressive wasting that accompanied the disease. Aretaeus also observed that the condition was relatively rare but invariably fatal, a grim prognosis that would remain accurate for centuries.
Medieval Understanding: Stagnation and Gradual Progress
The Middle Ages brought relatively little advancement in diabetes understanding, as medical knowledge in Europe largely stagnated during this period. The prevailing medical theory centered on the concept of humoral imbalance, inherited from ancient Greek medicine. Physicians believed that diabetes resulted from an excess or deficiency of one of the four bodily humors: blood, phlegm, yellow bile, and black bile. This framework, while ultimately incorrect, represented an attempt to systematize medical knowledge within the intellectual constraints of the era.
Medieval medical texts often used the terms “diabetes” and “poliuria” interchangeably, sometimes conflating diabetes with other conditions causing excessive urination. The lack of diagnostic tools meant that physicians relied entirely on symptom observation and patient history, making precise diagnosis challenging. Treatment approaches during this period were largely ineffective, ranging from dietary modifications to bloodletting and herbal remedies, none of which addressed the underlying metabolic dysfunction.
However, the Islamic Golden Age, spanning roughly from the 8th to 14th centuries, saw continued medical scholarship that preserved and expanded upon ancient knowledge. Persian and Arab physicians made careful observations about diabetes, with some noting the connection between the disease and dietary factors. Avicenna, the renowned Persian polymath, described diabetes in his medical encyclopedia “The Canon of Medicine,” distinguishing between primary diabetes and secondary forms resulting from other diseases.
The Renaissance period brought renewed interest in systematic observation and documentation. Physicians began recording symptoms with greater precision, noting variations in disease presentation and progression. Paracelsus, the Swiss physician and alchemist, conducted experiments on diabetic urine in the 16th century, evaporating it to examine the residue. Though he incorrectly concluded that the residue was salt rather than sugar, his experimental approach represented an important methodological shift toward empirical investigation.
The Scientific Revolution: Chemistry Meets Medicine
The 17th and 18th centuries witnessed the gradual emergence of modern scientific methods, which would eventually transform diabetes research. In 1674, Thomas Willis, an English physician, made a crucial observation that would prove foundational to diabetes understanding. He noted that the urine of diabetic patients tasted “wonderfully sweet as if it were imbued with honey or sugar.” This observation, made through the rather unpleasant practice of tasting patient urine, provided the first clear European documentation of glucose in diabetic urine.
Building on Willis’s observation, Matthew Dobson, a British physician, conducted more systematic experiments in 1776. He demonstrated that the sweet taste of diabetic urine was indeed due to sugar, and he further showed that diabetic blood also contained excess sugar. Dobson’s work established diabetes as a systemic metabolic disorder rather than simply a kidney problem, a conceptual breakthrough that redirected research efforts toward understanding the body’s sugar metabolism.
The term “diabetes mellitus” was coined to distinguish this sweet-urine form of diabetes from “diabetes insipidus,” a different condition also characterized by excessive urination but without glucose in the urine. “Mellitus” comes from the Latin word for honey, directly referencing the sweet quality that had become the disease’s defining characteristic in medical understanding.
The 19th Century: Unlocking Metabolic Mysteries
The 19th century marked a watershed period in diabetes research, as advances in chemistry, physiology, and experimental medicine converged to dramatically expand understanding of the disease. This era saw the transformation of diabetes from a mysterious wasting disease into a recognized metabolic disorder with identifiable physiological mechanisms.
In 1815, French chemist Michel Eugène Chevreul proved that the sugar in diabetic urine was glucose, providing precise chemical identification of the substance that had been observed for centuries. This discovery enabled more accurate diagnosis and opened new avenues for research into how the body processes glucose. The development of chemical tests for urinary glucose soon followed, giving physicians their first objective diagnostic tool for diabetes.
The role of the pancreas in diabetes began to emerge through a series of crucial experiments. In 1848, while the exact discovery is sometimes attributed to various researchers, the presence of sugar in diabetic urine became more systematically studied through improved chemical analysis methods. More significantly, in 1869, German medical student Paul Langerhans made a discovery that would prove pivotal to understanding diabetes, though its importance wouldn’t be recognized for decades. While examining pancreatic tissue under a microscope, Langerhans identified previously unknown clusters of cells scattered throughout the organ. These cell clusters, later named the “islets of Langerhans” in his honor, would eventually be identified as the source of insulin production.
The connection between the pancreas and diabetes became clearer through animal experimentation. In 1889, German physiologists Joseph von Mering and Oskar Minkowski made a landmark discovery while investigating the pancreas’s role in digestion. They surgically removed the pancreas from dogs and observed that the animals subsequently developed severe diabetes, with symptoms including excessive thirst, frequent urination, and glucose in the urine. This experiment definitively established that the pancreas played a crucial role in regulating blood sugar, though the specific mechanism remained unknown.
Throughout the late 19th century, researchers attempted to treat diabetes by administering pancreatic extracts to diabetic patients, but these early efforts largely failed. The extracts were either inactive or caused severe toxic reactions, as researchers had not yet learned how to isolate and purify the active substance. Despite these setbacks, the groundwork was being laid for the breakthrough that would come in the early 20th century.
Dietary management emerged as the primary treatment approach during this period. Physicians experimented with various dietary restrictions, with some advocating for high-fat diets, others for carbohydrate restriction, and still others for near-starvation regimens. The “Allen starvation treatment,” developed by Frederick Allen in the early 1900s, became widely used despite its harsh nature. This approach severely restricted caloric intake, sometimes to as little as 400-500 calories per day, in an attempt to minimize the body’s glucose load. While this treatment could extend life somewhat, patients often died from starvation or succumbed to infections due to their weakened state.
The Insulin Revolution: A Medical Miracle
The discovery of insulin in 1921 stands as one of the most dramatic breakthroughs in medical history, transforming diabetes from a death sentence into a manageable chronic condition virtually overnight. This achievement resulted from the work of Frederick Banting, a young Canadian surgeon, and Charles Best, a medical student, working in the laboratory of Professor John Macleod at the University of Toronto.
Banting conceived the idea of isolating the pancreas’s internal secretion by ligating the pancreatic ducts, causing the digestive enzyme-producing cells to atrophy while preserving the islets of Langerhans. Working through the summer of 1921, Banting and Best extracted a substance from the pancreases of dogs and demonstrated that it could lower blood sugar in diabetic dogs. They initially called their extract “isletin,” though it would soon be renamed insulin, from the Latin “insula” meaning island, referencing the islets of Langerhans.
The first human trial of insulin occurred on January 11, 1922, when 14-year-old Leonard Thompson, dying from diabetes at Toronto General Hospital, received an injection of the extract. The initial preparation was impure and caused an allergic reaction, but biochemist James Collip worked to refine the purification process. On January 23, Thompson received a second injection of the improved extract, and the results were remarkable. His blood sugar dropped to near-normal levels, his symptoms improved dramatically, and he went on to live another 13 years with insulin treatment.
News of insulin’s success spread rapidly through the medical community and popular press. Pharmaceutical companies, particularly Eli Lilly in the United States, worked to scale up production to meet the enormous demand. By 1923, insulin was widely available, and thousands of patients who would have died were given new life. The discovery was recognized with extraordinary speed: Banting and Macleod were awarded the Nobel Prize in Physiology or Medicine in 1923, just two years after the initial breakthrough. Banting shared his prize money with Best, and Macleod shared his with Collip, acknowledging the collaborative nature of the achievement.
The early years of insulin therapy presented significant challenges. The insulin was derived from animal pancreases (primarily from cattle and pigs), and its potency varied between batches. Patients had to inject themselves multiple times daily with large needles, and determining the correct dosage was often a matter of trial and error. Hypoglycemia, or dangerously low blood sugar, emerged as a new risk, sometimes with fatal consequences. Despite these difficulties, insulin represented an unprecedented triumph, and researchers immediately began working to refine and improve the treatment.
Refining Insulin and Understanding Diabetes Types
The decades following insulin’s discovery saw continuous improvements in both the hormone’s formulation and the broader understanding of diabetes as a disease. Researchers recognized that diabetes was not a single uniform condition but rather encompassed different forms with distinct characteristics and causes.
In the 1930s, clinicians began to clearly distinguish between two major types of diabetes. Type 1 diabetes, typically appearing in childhood or adolescence, was characterized by absolute insulin deficiency and rapid onset of severe symptoms. Type 2 diabetes, usually developing in adults, involved insulin resistance and relative insulin deficiency, with a more gradual onset. This classification, though refined over the years, remains fundamental to diabetes care today.
Insulin formulations evolved significantly during this period. In 1936, researchers developed protamine zinc insulin, a long-acting formulation that reduced the number of daily injections required. NPH (Neutral Protamine Hagedorn) insulin, introduced in the 1950s, provided intermediate-acting coverage and became a mainstay of diabetes treatment for decades. These extended-release formulations allowed patients to achieve better blood sugar control with fewer injections, significantly improving quality of life.
The 1950s and 1960s brought another major advancement: oral medications for diabetes. In 1955, the first sulfonylurea drugs were introduced, offering a non-injectable treatment option for some patients with Type 2 diabetes. These medications worked by stimulating the pancreas to produce more insulin, an approach that was effective for patients whose pancreases retained some insulin-producing capacity. The development of oral agents expanded treatment options and made diabetes management more accessible for many patients.
Research during this era also began to illuminate the long-term complications of diabetes. Physicians observed that even patients successfully treated with insulin often developed serious complications over time, including kidney disease, vision loss, nerve damage, and cardiovascular problems. These observations raised important questions about the relationship between blood sugar control and complication development, questions that would drive research for decades to come.
The Molecular Era: Understanding Diabetes at the Cellular Level
The latter half of the 20th century witnessed revolutionary advances in molecular biology and biochemistry that transformed understanding of diabetes at the cellular and molecular levels. These insights opened new therapeutic avenues and explained mechanisms that had puzzled researchers for generations.
In 1955, Frederick Sanger determined the complete amino acid sequence of insulin, a groundbreaking achievement that earned him the first of his two Nobel Prizes. This work not only revealed insulin’s molecular structure but also demonstrated that proteins had specific, determinable sequences, a finding with profound implications for all of biochemistry. Sanger’s work laid the foundation for eventually producing synthetic human insulin through genetic engineering.
The 1960s and 1970s brought deeper understanding of how insulin works at the cellular level. Researchers discovered insulin receptors on cell surfaces and began to elucidate the complex signaling cascades that insulin triggers. This work revealed that Type 2 diabetes often involves defects in insulin signaling pathways, not just insulin deficiency, explaining why some patients produce insulin but still have elevated blood sugar.
A landmark study launched in 1983, the Diabetes Control and Complications Trial (DCCT), provided definitive evidence that intensive blood sugar control could prevent or delay diabetes complications. This large-scale clinical trial followed over 1,400 patients with Type 1 diabetes for an average of 6.5 years, comparing conventional treatment with intensive insulin therapy aimed at maintaining near-normal blood glucose levels. The results, published in 1993, showed that intensive control reduced the risk of eye disease by 76%, kidney disease by 50%, and nerve disease by 60%. These findings fundamentally changed diabetes care, establishing tight glycemic control as the standard of care.
The advent of recombinant DNA technology in the 1970s revolutionized insulin production. In 1978, scientists successfully inserted the human insulin gene into bacteria, enabling them to produce human insulin. By 1982, the first biosynthetic human insulin, marketed as Humulin, became available. This development eliminated reliance on animal pancreases, ensured consistent quality and potency, and reduced allergic reactions. It also demonstrated the therapeutic potential of genetic engineering, paving the way for numerous other biotechnology-derived medications.
Technology Transforms Diabetes Management
The late 20th and early 21st centuries have seen technology emerge as a transformative force in diabetes care, providing tools that enable unprecedented precision in monitoring and treatment. These innovations have dramatically improved patients’ ability to manage their condition and have significantly enhanced quality of life.
The development of portable blood glucose meters in the 1970s and 1980s represented a quantum leap in diabetes management. Prior to these devices, patients had limited ability to monitor their blood sugar, relying primarily on urine testing, which was imprecise and provided only delayed information. The first home glucose meters were large and cumbersome, requiring large blood samples and taking several minutes to produce results. However, successive generations of meters became smaller, faster, and more accurate, with modern devices requiring only a tiny drop of blood and providing results in seconds.
Self-monitoring of blood glucose revolutionized diabetes care by enabling patients to make real-time treatment decisions. Patients could adjust their insulin doses based on current blood sugar readings, dietary intake, and planned activities, achieving much better control than was possible with fixed dosing schedules. This empowerment of patients to actively manage their condition represented a fundamental shift in the patient-provider relationship and in the philosophy of chronic disease management.
Insulin delivery technology also advanced significantly. Insulin pens, introduced in the 1980s, offered a more convenient and discreet alternative to traditional syringes and vials. Insulin pumps, which deliver insulin continuously through a small catheter placed under the skin, became increasingly sophisticated and user-friendly. Modern pumps can deliver precise doses, store dosing histories, and calculate insulin requirements based on carbohydrate intake and current blood sugar levels.
Continuous glucose monitoring (CGM) systems, emerging in the early 2000s and rapidly improving since, have transformed diabetes management even more profoundly than blood glucose meters. These devices use a small sensor inserted under the skin to measure glucose levels in interstitial fluid continuously, providing readings every few minutes. CGM systems can alert users to dangerous highs or lows, show glucose trends and rates of change, and provide a comprehensive picture of glucose patterns over time. This wealth of data enables much more nuanced treatment adjustments than was possible with periodic fingerstick measurements.
The integration of insulin pumps with CGM systems has created “closed-loop” or “artificial pancreas” systems that automatically adjust insulin delivery based on real-time glucose readings. These systems, approved for clinical use beginning in 2016, represent the closest approximation yet to normal pancreatic function. While not perfect—they still require user input for meals and don’t respond as rapidly as a healthy pancreas—they significantly reduce the burden of diabetes management and improve glycemic control while reducing hypoglycemia risk.
Expanding the Therapeutic Arsenal
While insulin remains essential for Type 1 diabetes and many cases of Type 2 diabetes, the past few decades have seen an explosion of new medication classes for diabetes treatment, particularly for Type 2 diabetes. These drugs target different aspects of glucose metabolism, offering personalized treatment approaches based on individual patient characteristics.
Metformin, though discovered in the 1920s, became a cornerstone of Type 2 diabetes treatment in the late 20th century. It works primarily by reducing glucose production in the liver and improving insulin sensitivity in peripheral tissues. Metformin’s effectiveness, safety profile, and low cost have made it the first-line medication for most patients with Type 2 diabetes.
The 1990s and 2000s brought several new drug classes. Thiazolidinediones improve insulin sensitivity, though concerns about side effects have limited their use. Alpha-glucosidase inhibitors slow carbohydrate absorption in the intestine. DPP-4 inhibitors enhance the body’s natural incretin hormones, which stimulate insulin release in response to meals.
More recently, GLP-1 receptor agonists and SGLT2 inhibitors have emerged as particularly important additions to the therapeutic arsenal. GLP-1 agonists mimic a natural hormone that stimulates insulin secretion, suppresses glucagon, slows gastric emptying, and reduces appetite, often leading to significant weight loss. SGLT2 inhibitors work by causing the kidneys to excrete excess glucose in urine. Importantly, both drug classes have demonstrated cardiovascular and kidney protective effects beyond their glucose-lowering properties, leading to their use even in some patients without diabetes who have heart or kidney disease.
Insulin analogs, developed through genetic engineering, have also greatly improved treatment. Rapid-acting analogs begin working within minutes and are cleared quickly, better mimicking the natural insulin response to meals. Long-acting analogs provide steady background insulin for 24 hours or more with minimal peaks, reducing hypoglycemia risk. These analogs offer greater flexibility and better glycemic control than older insulin formulations.
Genetics, Immunology, and the Search for Root Causes
Modern diabetes research increasingly focuses on understanding the fundamental causes of diabetes at the genetic and immunological levels, with the ultimate goal of preventing or even curing the disease rather than simply managing it.
Genetic research has revealed that diabetes has strong hereditary components, though the genetic architecture differs between Type 1 and Type 2. Type 1 diabetes involves complex interactions between multiple genes, primarily in the immune system, that increase susceptibility to autoimmune destruction of insulin-producing beta cells. The HLA region on chromosome 6 plays a particularly important role, with certain HLA variants substantially increasing Type 1 diabetes risk.
Type 2 diabetes genetics are even more complex, involving hundreds of genetic variants, each contributing small effects. These variants affect diverse processes including insulin secretion, insulin action, glucose metabolism, and body fat distribution. Understanding these genetic factors helps explain why some people develop Type 2 diabetes while others with similar lifestyles do not, and may eventually enable personalized prevention and treatment strategies.
Immunological research has illuminated the autoimmune process underlying Type 1 diabetes. Scientists have identified the specific immune cells and antibodies that attack beta cells, and have traced the development of this autoimmune response, which often begins years before clinical symptoms appear. This understanding has enabled the development of screening tests that can identify individuals at high risk for Type 1 diabetes before they develop symptoms.
Efforts to prevent or reverse Type 1 diabetes through immune modulation have shown promising results. In 2022, the FDA approved teplizumab, the first drug that can delay the onset of clinical Type 1 diabetes in high-risk individuals. This monoclonal antibody modifies immune cell function, slowing the destruction of beta cells. While it doesn’t prevent Type 1 diabetes entirely, delaying onset by even a few years can significantly improve quality of life and reduce complication risk.
Research into beta cell biology has also advanced significantly. Scientists have learned how to generate insulin-producing cells from stem cells in the laboratory, raising the possibility of cell replacement therapy for Type 1 diabetes. Clinical trials of encapsulated beta cell transplants, which protect the transplanted cells from immune attack without requiring immunosuppressive drugs, are underway and showing encouraging early results.
The Modern Diabetes Epidemic and Prevention Efforts
While Type 1 diabetes incidence has remained relatively stable, Type 2 diabetes has reached epidemic proportions globally, driven by rising obesity rates, sedentary lifestyles, and aging populations. According to the World Health Organization, the number of people with diabetes has risen from 108 million in 1980 to 422 million in 2014, with prevalence continuing to climb. This dramatic increase has focused attention on prevention strategies and the social determinants of diabetes risk.
Landmark prevention trials have demonstrated that Type 2 diabetes can be prevented or delayed through lifestyle interventions. The Diabetes Prevention Program, a major U.S. study published in 2002, showed that intensive lifestyle modification—including weight loss, dietary changes, and increased physical activity—reduced diabetes incidence by 58% in high-risk individuals. This reduction was even greater than that achieved with metformin medication, highlighting the powerful role of lifestyle factors.
These findings have spurred public health initiatives aimed at diabetes prevention, including programs to promote healthy eating, increase physical activity, and reduce obesity. However, implementing effective prevention at a population level has proven challenging, as it requires addressing complex social, economic, and environmental factors that influence health behaviors.
Research has also revealed important health disparities in diabetes prevalence and outcomes. Certain ethnic and racial groups, including African Americans, Hispanic/Latino Americans, Native Americans, and Pacific Islanders, have substantially higher rates of Type 2 diabetes and experience worse outcomes. These disparities reflect complex interactions between genetic susceptibility, socioeconomic factors, access to healthcare, and environmental influences. Addressing these inequities has become a major focus of diabetes research and public health policy.
Current Frontiers and Future Directions
Contemporary diabetes research spans an enormous range of approaches, from basic molecular biology to large-scale population studies, all aimed at improving prevention, treatment, and ultimately achieving cures for different forms of diabetes.
Artificial intelligence and machine learning are increasingly being applied to diabetes care. Algorithms can analyze CGM data to predict future glucose levels and recommend treatment adjustments, potentially improving upon current automated insulin delivery systems. AI is also being used to identify patterns in large datasets that might reveal new insights about diabetes risk factors, disease progression, and treatment responses.
Research into the gut microbiome has revealed unexpected connections between intestinal bacteria and diabetes risk. Studies suggest that the composition of gut bacteria influences metabolism, inflammation, and insulin sensitivity, and that modifying the microbiome through diet, probiotics, or other interventions might help prevent or treat Type 2 diabetes. While this research is still in early stages, it represents a potentially important new therapeutic avenue.
Gene therapy and gene editing technologies like CRISPR offer tantalizing possibilities for diabetes treatment. Researchers are exploring whether these tools could be used to protect beta cells from autoimmune attack, enhance insulin production, or correct genetic defects that contribute to diabetes. While significant technical and safety challenges remain, these approaches could potentially provide long-lasting or even permanent solutions.
Efforts to develop a functional cure for Type 1 diabetes continue to advance on multiple fronts. Beyond beta cell replacement, researchers are investigating whether immune tolerance can be restored, allowing the body to accept its own beta cells without attacking them. Combination approaches that both replace beta cells and modulate the immune system may ultimately prove most effective.
For Type 2 diabetes, research increasingly recognizes the disease’s heterogeneity, with different patients having different underlying causes. This has led to efforts to develop more personalized treatment approaches, selecting medications and interventions based on individual patient characteristics, including genetic profiles, metabolic parameters, and disease stage. Precision medicine approaches may enable more effective treatment with fewer side effects.
The role of social determinants of health in diabetes is receiving growing attention. Researchers are investigating how factors like food insecurity, housing instability, education, and neighborhood environments influence diabetes risk and outcomes. This work is leading to interventions that address these social factors alongside medical treatment, recognizing that optimal diabetes care requires attention to the full context of patients’ lives.
Lessons from History, Hope for the Future
The history of diabetes research is a testament to human ingenuity, persistence, and the power of scientific inquiry. From ancient physicians who could only observe and describe, to modern researchers manipulating genes and cells, each generation has built upon the discoveries of those who came before. The journey from diabetes as an invariably fatal disease to a manageable chronic condition represents one of medicine’s greatest triumphs.
Yet significant challenges remain. Despite remarkable therapeutic advances, diabetes continues to cause substantial morbidity and mortality worldwide. Complications including heart disease, kidney failure, blindness, and amputations remain common, particularly among those with inadequate access to care or resources for optimal management. The rising global prevalence of Type 2 diabetes threatens to overwhelm healthcare systems and reverse gains in life expectancy in some populations.
The path forward requires continued investment in research across the full spectrum from basic science to clinical trials to implementation science. It requires developing not just new technologies and medications, but also ensuring these advances reach all who need them, regardless of geography or economic status. It requires addressing the social and environmental factors that drive the diabetes epidemic, not just treating the disease after it develops.
The accelerating pace of discovery in recent decades provides reason for optimism. Technologies that seemed like science fiction a generation ago—continuous glucose monitoring, automated insulin delivery, stem cell therapies—are now realities or near-realities. The tools of modern molecular biology, genetics, and data science are revealing diabetes’s secrets at an unprecedented rate. While we cannot predict exactly what breakthroughs the coming decades will bring, history suggests that continued progress is not just possible but likely.
For the millions of people living with diabetes today, and the millions more at risk, this history offers both perspective and hope. Perspective on how far we’ve come from the days when diabetes meant certain death, often within months of diagnosis. And hope that the same scientific enterprise that has already achieved so much will continue to deliver better treatments, better prevention strategies, and ultimately, cures for this ancient disease that continues to challenge humanity.