What Is Diabetes? Causes, Types, and Symptoms

Diabetes is a group of metabolic diseases that share one defining feature: blood sugar (glucose) stays too high because the body either cannot make enough insulin, cannot use insulin properly, or both. An estimated 828 million adults worldwide had diabetes in 2022, up from roughly 108 million in 1980, making it one of the fastest-growing chronic conditions on the planet.¹ The word “diabetes” gets used as though it names a single disease, but the causes, progression, and treatment differ dramatically depending on the type.

What Insulin Does and Why It Matters

Every cell in your body needs glucose for energy, but glucose cannot simply walk through a cell’s outer membrane. Insulin, a hormone released by beta cells in the pancreas, acts like a key: it signals muscle and fat cells to move a glucose transporter called GLUT4 from storage compartments inside the cell up to the surface, where it can pull glucose in from the bloodstream.² When this process breaks down at any point, glucose piles up in the blood while cells go hungry. That mismatch is the core of every form of diabetes, though the reasons for the breakdown vary.

Type 1 Diabetes

In type 1 diabetes, the immune system’s own T cells attack and destroy the insulin-producing beta cells of the pancreas.³ Once enough beta cells are gone, the body produces little to no insulin. People with type 1 diabetes need external insulin, delivered by injection or pump, from diagnosis onward. There is no lifestyle change that prevents or reverses it.

Type 1 accounts for a relatively small share of all diabetes cases, but it tends to appear earlier in life, often in children and teenagers, though adults can develop it too. The triggers are still not fully understood. Genetic susceptibility plays a role, and researchers suspect that viral infections or other environmental exposures may set off the autoimmune process in people who are already predisposed.

When someone with type 1 diabetes goes without insulin, the situation can deteriorate fast. Without insulin, the body cannot use glucose for fuel and begins breaking down fat at a dangerous pace, producing acidic byproducts called ketones. This condition, diabetic ketoacidosis, often develops over just hours to a couple of days and starts with heavy urination and extreme thirst driven by the excess glucose pulling water out of the body. Left untreated, it progresses to dehydration, low blood pressure, rapid heart rate, and eventually a medical emergency.⁴

Type 2 Diabetes

Type 2 is by far the most common form, responsible for the vast majority of diabetes worldwide. It develops through a combination of two problems: the body’s cells become resistant to insulin’s signal, and the beta cells gradually lose the ability to keep up with the extra demand.⁵ These two processes feed each other, creating a vicious cycle that worsens over time.⁶

Genetics matter, but so does body composition. Visceral fat, the fat packed around internal organs rather than directly under the skin, has been shown through genetic analysis to be a causal risk factor for type 2 diabetes, not merely correlated with it. One large genome-wide study found that this causal link was especially strong in women, where the odds ratio for type 2 diabetes associated with visceral fat was roughly seven-fold, compared to about two-and-a-half-fold in men.⁷ This helps explain why some people who appear thin by standard measures can still develop type 2 diabetes if they carry excess internal fat, and why others with higher overall body weight but less visceral fat may be at lower risk.

Unlike type 1, type 2 diabetes often creeps in silently. Many people have elevated blood sugar for years before symptoms become obvious. When symptoms do appear, the classic ones overlap with those in type 1: frequent urination, increased thirst, blurred vision, fatigue, and slow-healing wounds. But because type 2 progresses gradually, a large number of cases are caught through routine blood work rather than through dramatic symptoms.

Type 2 diabetes has its own acute emergency, distinct from ketoacidosis. The hyperosmolar hyperglycemic state occurs when blood sugar climbs extremely high, sometimes above 600 mg/dL, causing severe dehydration and confusion. It is most common in older adults, and its mortality rate has been estimated as high as roughly 20%, about ten times the rate seen in ketoacidosis.⁸ It often strikes people who do not yet know they have diabetes or who have an illness that sends blood sugar soaring.

Gestational Diabetes

Pregnancy changes the way a woman’s body handles glucose. The placenta releases hormones that naturally reduce insulin sensitivity so that more glucose stays available for the growing fetus. In most pregnancies this is a manageable shift, but when the process goes too far, gestational diabetes develops.⁹ Recent research has implicated a protein called IGFBP1, produced in the placenta, as part of the story. Women whose placentas produce less of this protein tend to have greater insulin resistance during pregnancy and a higher chance of developing gestational diabetes.¹⁰

Gestational diabetes usually resolves after delivery, but it is not without consequences. It raises the risk of complications during pregnancy, including having a larger-than-average baby and the difficulties that come with that during labor. More concerning for the long term, both the mother and child carry a higher risk of developing type 2 diabetes and metabolic problems later in life.¹¹ For this reason, women who have had gestational diabetes are typically advised to get regular blood sugar screenings in the years that follow.

Less Common Forms

Not every case of diabetes fits neatly into the type 1, type 2, or gestational categories. There are several rarer forms worth knowing about, partly because they are frequently misdiagnosed.

Monogenic diabetes is caused by a mutation in a single gene. The two main subtypes are neonatal diabetes, which appears in the first six months of life, and maturity-onset diabetes of the young, known as MODY, which typically shows up in adolescence or early adulthood.¹² Because MODY often strikes young, relatively lean individuals, it can look like type 1 at first glance. But people with MODY frequently respond well to certain oral medications rather than needing insulin, making the correct diagnosis practically important.

Latent autoimmune diabetes in adults (LADA) sits somewhere between type 1 and type 2. Like type 1, it involves immune-system antibodies targeting the beta cells. But unlike typical type 1, the destruction is slow enough that many LADA patients do not need insulin for at least six months after diagnosis, and some go years without it. Among people initially diagnosed with type 2 diabetes, roughly a quarter of those under 35 and about one in ten of those over 35 actually have LADA.¹³ Getting this diagnosis right matters because these patients will eventually need insulin, and some evidence suggests that starting it earlier can help preserve remaining beta cell function.

Diabetes can also develop secondary to diseases of the pancreas itself. Chronic pancreatitis, pancreatic cancer, and cystic fibrosis can all damage or destroy enough of the pancreas to cause diabetes. This category, sometimes called diabetes of the exocrine pancreas, is considered separate from both autoimmune diabetes and type 2.¹⁴ It carries its own set of management challenges because the damaged pancreas may also fail to produce digestive enzymes, requiring enzyme replacement alongside glucose management.

Common Symptoms Across Types

Despite their different causes, the major types of diabetes share a core set of symptoms because the underlying problem is the same: too much glucose in the blood.

Frequent urination: The kidneys try to flush excess glucose by pulling more water into the urine, so you end up in the bathroom constantly.
Excessive thirst: The fluid loss from all that urination triggers intense thirst.
Unexplained weight loss: Especially in type 1, the body starts burning fat and muscle for energy because it cannot access glucose.
Fatigue: Cells are starved for fuel even though the blood is loaded with sugar.
Blurred vision: High blood sugar pulls fluid from the lens of the eye, temporarily distorting its shape.
Slow-healing cuts and infections: Elevated glucose impairs immune function and circulation, particularly in the extremities.

Type 1 symptoms tend to appear suddenly and severely, often over a matter of weeks. Type 2 symptoms build gradually and can be easy to dismiss as stress, aging, or being out of shape. That gradual onset is why type 2 diabetes is sometimes called a “silent” disease. A person can have it for years without realizing it, all while the elevated blood sugar is quietly damaging blood vessels and nerves.

How Diabetes Is Diagnosed

Doctors use a few standard blood tests. A fasting blood glucose test measures your blood sugar after you have not eaten for at least eight hours; a result of 126 mg/dL or higher on two separate occasions points to diabetes. An oral glucose tolerance test checks how your body handles a sugary drink over two hours. And the HbA1c test measures your average blood sugar over the past two to three months. Research on optimal HbA1c cutoffs for identifying type 2 diabetes has found that a threshold around 6.5% balances sensitivity and specificity reasonably well.¹⁵ An HbA1c between 5.7% and 6.4% generally indicates prediabetes, a state of elevated blood sugar that has not yet crossed the diabetes threshold.

Distinguishing between types sometimes requires additional tests. If a doctor suspects type 1 or LADA, they may check for specific autoantibodies targeting the beta cells. Genetic testing can confirm MODY. Getting the type right is more than academic: it determines whether you need insulin immediately, which oral medications will work, and how the disease is likely to progress.

Long-Term Complications

The reason diabetes demands management, even when you feel fine, is the damage that sustained high blood sugar does over years. The excess glucose and related metabolic changes fuel oxidative stress, damage blood vessel walls, and disrupt nerve function.¹⁶ These effects hit smallest blood vessels first, which is why the classic complications target the eyes (diabetic retinopathy, the leading cause of new blindness in working-age adults), the kidneys (diabetic nephropathy, a major cause of kidney failure), and the peripheral nerves (diabetic neuropathy, which causes numbness, tingling, and pain in the feet and hands).

Larger blood vessels are affected too. People with diabetes face roughly double the risk of heart disease and stroke compared to those without it. Foot problems deserve special mention: neuropathy means you may not feel a blister or cut, poor circulation means it heals slowly, and infection risk is elevated. This combination is the main reason diabetes is the leading cause of non-traumatic lower-limb amputations. Nearly all of these complications can be delayed or reduced with consistent blood sugar control, blood pressure management, and regular screening.

Can Type 2 Diabetes Be Prevented

For type 2, the answer is a qualified yes. The Diabetes Prevention Program, a landmark study of over 3,200 people with prediabetes, found that an intensive lifestyle intervention focusing on modest weight loss and regular physical activity cut the rate of developing type 2 diabetes by about 58% over roughly three years, compared to placebo. A medication-only arm using metformin achieved about a 31% reduction. Follow-up a decade later showed that the lifestyle group had delayed the onset of diabetes by approximately four years.¹⁷ The Finnish Diabetes Prevention Study produced a strikingly similar result, also finding a 58% reduction with lifestyle changes.¹⁷

A recent meta-analysis of fifteen studies confirmed that intensive lifestyle interventions reduce the risk of progressing from prediabetes to type 2 diabetes by about 22% over longer follow-up periods compared to general advice alone, though the protective effect appears to fade somewhat with time.¹⁸ The gap between the 58% short-term reduction and the 22% long-term figure tells an important story: the lifestyle changes work well while people maintain them, but adherence drifts over years. Prevention is real, but it requires sustained effort.

Prediabetes itself is worth understanding clearly. More than 100 million people in Europe alone meet the criteria, yet only about 5% to 10% of people with prediabetes actually develop type 2 diabetes in any given year, and roughly 10% revert to normal blood sugar without intervention.¹⁷ The label is useful as a warning sign, but it is not a sentence.

The Global Picture

The scale of diabetes has changed dramatically in a single generation. In 1980, roughly 108 million adults had diabetes worldwide. By 2014 that number had reached 422 million, and by 2022 it had nearly doubled again to an estimated 828 million.¹ About 40% of the earlier rise from 1980 to 2014 was attributable simply to population growth and aging, while the rest reflected a genuine increase in rates.¹⁹

The geography of diabetes has shifted. The fastest-growing prevalence between 1990 and 2022 occurred in low- and middle-income countries, particularly in southeast Asia, south Asia, the Middle East, north Africa, and parts of Latin America and the Caribbean. Meanwhile, a handful of high-income countries saw prevalence hold steady or even decline modestly in certain populations.¹ Type 2 diabetes, which drives the global numbers, is projected to keep rising. One analysis estimated that global prevalence would increase from about 6,059 cases per 100,000 people to over 7,000 per 100,000 by 2030.²⁰

The Gut Microbiome Connection

One of the more intriguing research threads in recent years is the relationship between gut bacteria and diabetes. A systematic review of the evidence found that people with diabetes consistently show altered gut microbial communities, a state called dysbiosis, which contributed to reduced insulin sensitivity and poorer blood sugar control.²¹ The proposed mechanism involves a “leaky gut” scenario: when the microbial balance shifts, the intestinal lining becomes more permeable, allowing bacterial fragments to enter the bloodstream and trigger low-grade inflammation that interferes with insulin signaling.

This does not mean probiotics or fermented foods will cure diabetes. The research is still working out which specific bacterial shifts matter, whether the changes cause diabetes or merely accompany it, and whether targeting the microbiome can meaningfully improve outcomes. But it has opened up a new front in understanding why some people develop type 2 diabetes and others with similar diets and body weight do not.

The Thrifty Gene Idea and Why It Persists

In 1962, geneticist James Neel proposed what became known as the “thrifty gene hypothesis.” The idea was straightforward: populations whose ancestors endured cycles of feast and famine would have evolved genes favoring efficient fat storage. Those genes would have been a survival advantage historically but become harmful in modern environments with constant food availability, leading to obesity and type 2 diabetes.²²

The hypothesis gained enormous influence, particularly in explanations of why certain Indigenous and minority populations have disproportionately high diabetes rates.²³ It sounds tidy, but it has not held up well under scrutiny. No specific “thrifty genes” have been conclusively identified despite decades of searching. Critics have pointed out that the hypothesis risks oversimplifying diabetes disparities as genetic destiny, diverting attention from the structural factors, like poverty, food access, and colonization-related disruption, that more clearly drive risk. The idea still shows up in textbooks and popular explanations, but researchers have largely moved on to more nuanced frameworks that account for the complex interplay of genetics, epigenetics, and social environment.

A Brief History of Insulin

Diabetes has been recognized for thousands of years. Descriptions appear in ancient Egyptian papyri, classical Indian medical texts, and Chinese writings. The Greek physician Aretaeus of Cappadocia gave the first detailed clinical description in the second century and coined the name “diabetes,” while Thomas Willis added “mellitus” (Latin for “honey-sweet”) in the seventeenth century after noting the sweet taste of patients’ urine.²⁴ For most of that history, a diagnosis of type 1 diabetes was effectively a death sentence.

The breakthrough came in 1921, when Frederick Banting and Charles Best isolated insulin from pancreatic tissue and demonstrated that injecting it could save the lives of people with severe diabetes. Their work built on an 1889 experiment in which Oskar Minkowski and Joseph von Mering removed a dog’s pancreas and observed that the animal quickly developed fatal diabetes.²⁴ Within months of the first human insulin injections, patients who had been near death began recovering. The discovery has been called one of the most important milestones in the history of medicine.²⁵ Insulin therapy has evolved dramatically since then, from crude animal-derived extracts to highly engineered human insulin analogs, but the fundamental principle remains the same: replace what the body can no longer make.

1
PubMed. Worldwide trends in diabetes prevalence and treatment from 1990 to 2022: a pooled analysis of 1108 population-representative studies with 141 million participants
2
PubMed Central. Molecular mechanisms for the regulation of insulin-stimulated glucose uptake by small guanosine triphosphatases in skeletal muscle and adipocytes
3
PubMed Central. T Cell-Mediated Beta Cell Destruction: Autoimmunity and Alloimmunity in the Context of Type 1 Diabetes
4
PubMed Central. Diabetic Ketoacidosis in Young Adults with Type 1 Diabetes: The Impact of the Ketogenic Diet—A Narrative Literature Review
5
PubMed Central. Pancreatic β-cell dysfunction in type 2 diabetes: Implications of inflammation and oxidative stress
6
PubMed Central. Beta cell dysfunction and insulin resistance
7
Nature Medicine. Contribution of genetics to visceral adiposity and its relation to cardiovascular and metabolic disease
8
Diabetes Care. Hyperosmolar Hyperglycemic State: A Historic Review of the Clinical Presentation, Diagnosis, and Treatment
9
PubMed Central. The Placental Role in Gestational Diabetes Mellitus: A Molecular Perspective
10
Nature Medicine. Placental IGFBP1 levels during early pregnancy and the risk of insulin resistance and gestational diabetes
11
PubMed. The fetal and maternal consequences of gestational diabetes mellitus
12
PubMed. Monogenic Diabetes: A Comprehensive Overview and Therapeutic Management of Subtypes of Mody
13
Diabetes. Latent Autoimmune Diabetes in Adults: Definition, Prevalence, β-Cell Function, and Treatment
14
Oxford Academic. DIAGNOSIS OF ENDOCRINE DISEASE: Diagnosing and classifying diabetes in diseases of the exocrine pancreas
15
PubMed Central. The Utility of HbA1c as a Diagnostic Criterion of Diabetes
16
PubMed. Vascular factors and metabolic interactions in the pathogenesis of diabetic neuropathy
17
PubMed Central. Lifestyle precision medicine: the next generation in type 2 diabetes prevention?
18
Diabetes Research and Clinical Practice. Long-term lifestyle intervention can reduce the development of type 2 diabetes mellitus in subjects with prediabetes: A systematic review and meta-analysis
19
The Lancet. Worldwide trends in diabetes since 1980: a pooled analysis of 751 population-based studies with 4·3 million participants
20
PubMed Central. Epidemiology of Type 2 Diabetes – Global Burden of Disease and Forecasted Trends
21
PubMed Central. Understanding the Role of the Gut Microbiome in Diabetes and Therapeutics Targeting Leaky Gut: A Systematic Review
22
PubMed. The thrifty genotype in type 2 diabetes: an unfinished symphony moving to its finale?
23
PubMed Central. Commentary: The Invention of Aboriginal Diabetes: The Role of the Thrifty Gene Hypothesis in Canadian Health Care Provision
24
PubMed Central. Milestones in the history of diabetes mellitus: The main contributors
25
PubMed Central. The Discovery of Insulin: An Important Milestone in the History of Medicine