The Sweet Sickness: A Brief History of Diabetes Mellitus

Diabetes Mellitus is a chronic metabolic disorder that has shadowed human civilization for millennia. At its core, it is a condition defined by high levels of blood glucose, or sugar, a state known as hyperglycemia. This occurs when the body can no longer produce or effectively use Insulin, a crucial hormone synthesized by the Pancreas. Insulin acts like a key, unlocking the body's cells to allow glucose from food to enter and be used for energy. Without this key, or if the lock is broken, glucose builds up in the bloodstream, starving the cells of fuel while simultaneously poisoning the body with its excess. This sweet poison gives the disease its name: diabetes from the Greek for “siphon,” describing the excessive urination it causes, and mellitus, Latin for “honey-sweet,” an ancient and tragically literal diagnostic observation. It is not a single entity but a spectrum, most commonly appearing as Type 1, an autoimmune condition where the body destroys its own insulin-producing cells, and Type 2, where the body either resists insulin's effects or doesn't produce enough to maintain normal glucose levels. From a mysterious wasting curse to a manageable chronic illness and now a global pandemic, the story of diabetes is a profound reflection of humanity's ever-evolving journey of scientific discovery, technological innovation, and our complex relationship with the very sustenance that gives us life.

Long before the gleaming laboratories and the precise language of modern medicine, humanity knew diabetes. It was not understood, but it was known as a terrifying and inescapable presence, a curse that caused the body to waste away from the inside out, its life force seemingly draining away in a constant, sweet stream. It was an ancient shadow, its contours first traced not in scientific journals, but in the fragile papyri of pharaohs and the sacred texts of sages.

The earliest known description of what we now recognize as diabetic symptoms appears in the ancient Egyptian medical text, the Ebers Papyrus, dated to around 1550 BCE. Buried with a mummy and rediscovered in the 19th century, this remarkable scroll of remedies and observations describes a condition of “too great emptying of the urine.” While the Egyptians lacked a name for the disease, they saw its devastating effect: a rapid, inexplicable decline into emaciation and death. Their treatments, a mixture of potions made from grains, fruits, and earth, were born of magical thinking rather than physiological understanding, a desperate attempt to staunch a flow they could not comprehend. Half a world away, in ancient India around the 6th century BCE, the physician Sushruta offered a far more insightful diagnosis in his treatise, the Sushruta Samhita. He named the condition “Madhumeha,” a strikingly descriptive term meaning “honey urine.” Sushruta observed that this particular type of urine was sticky to the touch and, most revealingly, that it attracted ants and flies. This simple, yet profound, observation—the “ant test”—was the world's first clinical test for diabetes. He noted that the disease afflicted the “rich and gluttonous,” who indulged in rice, flour, and sweets, an astonishingly prescient link between diet, lifestyle, and a specific form of the illness that would not be fully appreciated for another two and a half millennia. He saw the affliction as a harbinger of painful complications, including boils and abscesses, a grimly accurate portrait of uncontrolled diabetes.

The thread of understanding was picked up in the Roman Empire. It was the Greek physician Aretaeus of Cappadocia, practicing in the 2nd century CE, who gave the disease the name by which we know its first half: diabetes. Drawing from the Greek word for “siphon” or “to pass through,” he painted a harrowing and unforgettable picture of the condition's primary symptom. He wrote, “Diabetes is a wonderful affection… being a melting down of the flesh and limbs into urine.” To Aretaeus, the body of a diabetic was like a leaky vessel, incapable of holding onto its fluids. “The patients never stop making water,” he wrote, “but the flow is incessant, as if from the opening of aqueducts.” He saw it as a rare and dreadful disease, and like his predecessors, he could offer no effective treatment. The patients he described were caught in a cruel paradox: tormented by an unquenchable thirst, they drank copiously, only to have the fluid rush straight through them, carrying their very substance with it into the chamber pot. The “sweetness” of the urine, so keenly observed in India, was lost to European medicine for over a thousand years, and with it, the most important clue to the disease's nature.

With the fragmentation of the Roman Empire, much of the medical knowledge of the classical world was lost or scattered. The intricate observations of Aretaeus and the diagnostic wisdom of Sushruta faded into obscurity in the West. Diabetes once again became a murky, undifferentiated wasting sickness among many others. Physicians could see the symptoms—the thirst, the urination, the weight loss—but the unifying thread, the sweet, sticky signature of the disease, remained hidden. It was an era of medical stagnation where superstition and dogma often eclipsed clinical observation. The shadow of the sweet sickness persisted, but its face was veiled.

The veil began to lift in the 17th century, an age of scientific awakening in Europe. The English physician Thomas Willis, a founding member of the Royal Society, revived a diagnostic technique that was both revolutionary and viscerally primal: he tasted his patients' urine. In his 1674 work Pharmaceutice Rationalis, he wrote of his discovery that the urine of those afflicted with the “pissing evil” was “wonderfully sweet as if it were imbued with honey or sugar.” This courageous, if unsavory, act of clinical investigation was a monumental turning point. It re-established the core pathological fact of the disease. Willis was the first to add the Latin qualifier mellitus (from honey) to the ancient name, officially christening the condition Diabetes Mellitus. His work did more than just confirm an old observation; it created a crucial distinction. He noted that in some patients with excessive urination, the urine was tasteless. This, he correctly identified as a separate condition, which would later be named Diabetes Insipidus. For the first time, the “sweet sickness” was taxonomically separated from other diseases that caused similar symptoms. The “water tasters,” or uroscopists of his era, had finally given the ancient shadow a proper name and a distinct identity, setting the stage for a true scientific inquiry into its cause.

The 18th and 19th centuries witnessed a seismic shift in medicine. The focus moved from a catalog of symptoms to a search for underlying causes, from the patient's bedside to the laboratory bench. Armed with new tools and a philosophy of experimental science, researchers began to dissect the human body and its chemistry in a quest to understand the machinery of life and disease. For diabetes, this meant a journey deep inside the body, to a humble organ nestled behind the stomach, which held the secret to the sweet sickness.

For centuries, the Pancreas was an organ of mystery. While known to anatomists, its function was poorly understood, believed primarily to be involved in digestion. The first clue to its deeper role in metabolism came from a gruesome but illuminating experiment in 1889. In Strasbourg, Germany, two physicians, Oskar Minkowski and Joseph von Mering, were studying the pancreas's role in fat digestion. To do so, they surgically removed the entire organ from a healthy dog. Soon after, a lab assistant noticed something strange: swarms of flies were gathering on the dog's urine. The alert assistant reported this to Minkowski, who, remembering the ancient link between sweetness and diabetes, tested the urine for sugar. It was loaded with it. The dog had developed a severe, raging case of diabetes. It drank insatiably, urinated constantly, and wasted away. They had, for the first time, artificially induced diabetes in an animal. The conclusion was inescapable: the Pancreas was not just a digestive organ. It produced a substance that was essential for regulating blood sugar. The source of the ancient shadow was located.

The next piece of the puzzle came not from a physiologist, but from a young medical student peering through a Microscope. In 1869, Paul Langerhans, a German pathology student, was meticulously examining the cellular structure of the Pancreas. He noticed that scattered among the well-known cells that produce digestive juices were strange, previously undescribed clusters of cells, like little islands in a sea of tissue. Not knowing their function, he simply documented them, and they came to be known as the islets of Langerhans. For decades, these “islands” remained a biological curiosity. But after Minkowski and von Mering's discovery, a French physician named Édouard Laguesse had a flash of insight. In the 1890s, he hypothesized that it was these very islets, not the digestive cells, that produced the mysterious blood-sugar-regulating substance. The hunt was now on not just for a pancreatic secretion, but for a secretion from these specific, microscopic islands. Many tried to isolate it, but their efforts failed. The powerful digestive enzymes produced by the rest of the pancreas would destroy the delicate, unknown substance before it could be extracted. The key was tantalizingly close, yet seemingly impossible to grasp.

While the scientists hunted for the cause, clinicians had to face the reality of the disease. Before the 20th century, a diagnosis of what we now call Type 1 diabetes, particularly in a child, was a death sentence. The wasting described by Aretaeus was a certainty. In the early 1900s, pioneering physicians like Frederick Allen and Elliott Joslin developed the only treatment that offered any hope: starvation diets. By severely restricting carbohydrates and calories, they could lower blood sugar and prolong life. Children were put on diets of as little as 400 calories a day, becoming skeletal figures haunted by constant, gnawing hunger. This grim therapy was a trade-off: it could stave off the immediate death from diabetic ketoacidosis, but it ultimately led to a slow death from starvation. It extended life from weeks to perhaps a year or two, but it was a life of profound suffering. The photographs from this era are heartbreaking, showing emaciated children waiting for a cure that did not exist. The world was desperate for a miracle.

The miracle arrived not in a grand European institute, but in a stuffy, under-equipped laboratory in Toronto during the sweltering summer of 1921. The story of the discovery of Insulin is one of the most dramatic and inspiring in the annals of medicine, a tale of unlikely heroes, desperate ambition, and a breakthrough that would transform a fatal disease into a manageable condition.

The protagonist was Frederick Banting, a young, struggling orthopedic surgeon with a fledgling practice and a deep-seated desire to make his mark. He was not a trained researcher. But after reading an article about the pancreas, an idea seized him. He theorized that if he surgically tied off the pancreatic ducts of a dog, the digestive-juice-producing parts of the organ would wither away, leaving the islets of Langerhans intact. This would allow one to create an extract of the islets' secretion without it being destroyed by the digestive enzymes. He took his idea to John J.R. Macleod, a respected professor of physiology at the University of Toronto. Macleod was skeptical of the young surgeon's crude plan but reluctantly granted him lab space for the summer, ten dogs for experimentation, and the assistance of a bright medical student named Charles Best. While Macleod went on holiday to his native Scotland, Banting and Best began their grueling work. Through trial and error, in the intense summer heat, they operated on dogs, tied off ducts, and prepared their pancreatic extract.

Their breakthrough came with a diabetic dog, Marjorie (often identified by a lab number, like 92), who was near death. They injected her with their crude extract, which they initially called “isletin.” Her blood sugar plummeted. When they stopped the injections, it soared back up. When they resumed, it fell again. It was proof of concept. They had found it. However, their extract was impure, causing painful abscesses. Macleod, returning from his holiday and realizing the magnitude of their discovery, dedicated his entire lab to the project and brought in a brilliant biochemist, James Collip, to purify the substance. Collip developed a method using alcohol precipitation that could produce a purer, more reliable extract suitable for human use. On January 11, 1922, their purified extract was administered to Leonard Thompson, a 14-year-old boy dying of diabetes at Toronto General Hospital. He was emaciated, weighing only 65 pounds, and drifting in and out of a diabetic coma. The first injection caused an allergic reaction due to remaining impurities. But after 12 days of frantic work by Collip to further refine the extract, a second dose was given. The effect was miraculous. Leonard's blood sugar dropped to near-normal levels. He became alert and strong. The news spread like wildfire. The shadow had been tamed. For children in diabetic wards across the world, who had been subsisting on starvation diets, it was a literal resurrection.

The discovery was hailed globally. In 1923, the Nobel Prize in Medicine was awarded to Banting and Macleod. Banting, furious that Best was not included, immediately announced he would share his prize money with Best. Macleod, in turn, shared his with Collip. The four men, driven by a profound sense of purpose, sold the patent for Insulin to the University of Toronto for a symbolic one dollar each. They did not want to profit from their discovery; they wanted it to be available to everyone who needed it. It was an act of scientific altruism that saved millions of lives and set the stage for the next chapter in the story of diabetes: the age of management.

The discovery of Insulin was not a cure, but a treatment. It did not banish diabetes, but it transformed it from a swift executioner into a lifelong companion. The 20th century became an era defined by the challenge of living with the sweet sickness, a period marked by constant refinement of therapies, the empowerment of patients through technology, and a deepening understanding of the disease's complex nature.

The immediate challenge after 1922 was production. The task of turning a laboratory extract into a mass-produced medicine fell to pharmaceutical companies like Eli Lilly. They rapidly scaled up the process of extracting Insulin from the pancreases of cattle and pigs. The early insulins were fast-acting and had to be injected multiple times a day, requiring a rigid schedule of meals and shots managed with a reusable glass Syringe. Scientists soon began working to create longer-lasting formulations. In the 1930s and 40s, researchers like Hans Christian Hagedorn found that adding proteins could slow down insulin's absorption, leading to the development of NPH (Neutral Protamine Hagedorn) insulin. This began to free patients from the relentless cycle of frequent injections. The next great leap came in the 1980s with the advent of recombinant DNA technology, which allowed for the production of synthetic “human” insulin, eliminating reliance on animal sources and reducing allergic reactions.

For the first fifty years of the insulin era, patients lived in a state of relative blindness. They could not know what their blood sugar was at any given moment. Management was based on symptoms and clumsy, infrequent urine tests that only showed what glucose levels had been hours earlier. This changed forever in the 1970s with the invention of the first personal Glucose Meter. This revolutionary device allowed patients, for the first time, to test a single drop of blood and get a real-time reading of their glucose levels. This technology sparked a fundamental shift in diabetes care, moving from a passive model of following doctor's orders to one of active self-management. Patients could now make informed decisions about their insulin doses, food, and exercise. This empowerment was further enhanced by the development of the HbA1c test in the 1970s, a blood test that provides an average blood sugar level over the preceding three months, giving both doctors and patients a crucial long-term view of their control.

As more people lived longer with diabetes, a new picture began to emerge. It became clear that not all diabetes was the same. Researchers had noticed that while some patients—typically young and thin—were completely dependent on insulin, others—often older and overweight—still produced some of their own insulin but their bodies seemed resistant to its effects. As early as the 1930s, Sir Harold Himsworth had published work differentiating between “insulin-sensitive” and “insulin-insensitive” patients. This understanding was slowly formalized over the decades, leading to the modern classification system we use today:

• Type 1 Diabetes: An autoimmune disease where the body's immune system mistakenly attacks and destroys the insulin-producing beta cells in the islets of Langerhans. It typically appears in childhood or young adulthood and requires insulin for survival.
• Type 2 Diabetes: A condition characterized by insulin resistance, where the body's cells do not respond properly to insulin, coupled with a relative insulin deficiency. It is strongly linked to genetics, lifestyle factors like obesity and inactivity, and accounts for around 90% of all diabetes cases worldwide.

This “Great Schism” was a critical intellectual breakthrough. It explained why some people responded dramatically to insulin while others benefited more from diet, exercise, and oral medications. It also foreshadowed the enormous public health challenge that was about to unfold.

In the late 20th and early 21st centuries, the story of diabetes took another dramatic turn. The ancient shadow, once a rare and terrifying specter, began to swell into a global pandemic. But as the scale of the crisis grew, so too did the ingenuity of science and technology, pushing towards a future that moves beyond mere management and dares to seek a definitive end to the sweet sickness.

The modern world, with its abundance of processed, high-calorie foods and increasingly sedentary lifestyles, created the perfect storm for Type 2 diabetes. What Sushruta had observed in a few “rich and gluttonous” individuals thousands of years ago became a worldwide phenomenon. The disease, once primarily an affliction of old age, began appearing in younger adults and even children. The numbers are staggering: according to the World Health Organization, the number of people with diabetes rose from 108 million in 1980 to over 420 million today, with the vast majority being Type 2. This tsunami has brought with it immense human and economic costs. Diabetes is a leading cause of blindness, kidney failure, heart attacks, stroke, and lower limb amputation. It has transformed from a primarily medical issue into a profound sociological, cultural, and economic crisis that strains healthcare systems and impacts societies across the globe.

In the face of this challenge, technology has offered powerful new tools. The evolution of care has been breathtakingly rapid:

• Insulin Pumps: Small, computerized devices that deliver a continuous, customizable flow of insulin through a small tube inserted under the skin, mimicking the function of a healthy pancreas more closely than injections.
• Continuous Glucose Monitors (CGMs): Wearable sensors that measure glucose levels in the interstitial fluid every few minutes, 24 hours a day, sending the data to a smartphone or receiver and alerting users to high or low blood sugar.

The convergence of these two technologies has led to the dawn of the “artificial Pancreas” or closed-loop system. These systems use an algorithm to interpret CGM data and automatically adjust the insulin delivery from the pump, significantly reducing the burden of moment-to-moment management for people with Type 1 diabetes. This is not a cure, but it is a life-changing step towards automating control and restoring a degree of freedom lost to the disease.

The ultimate goal remains a true biological cure—to banish the shadow for good. The frontiers of research are buzzing with possibilities. For Type 1 diabetes, scientists are exploring:

• Immunotherapies: Treatments that could re-educate the immune system to stop it from attacking the beta cells, potentially halting the disease in its earliest stages.
• Cell Replacement: Transplanting healthy islet cells from donors or, more promisingly, using stem cells to grow brand-new, insulin-producing beta cells in the lab that could be implanted in patients.

For Type 2 diabetes, research focuses on new medications that tackle insulin resistance, protect the pancreas, and promote weight loss, alongside a crucial public health emphasis on prevention through lifestyle changes. From an ant-covered puddle of urine in ancient India to a sophisticated algorithm managing a closed-loop system, the history of diabetes mellitus is a powerful saga of human suffering, intellectual curiosity, and relentless ingenuity. It is the story of a disease that has evolved with us, its prevalence a dark reflection of our own societal changes. The journey is far from over, but for the first time in the long, shared history between humanity and its sweet sickness, the prospect of a final victory, a world without the shadow, feels closer than ever before.