Diabetes mellitus is a chronic metabolic disorder characterized by sustained high blood glucose levels (hyperglycemia). This occurs when the body either fails to produce enough insulin or cannot effectively use the insulin it produces. Insulin, produced by the pancreas, acts as a regulator to keep blood sugar within a normal range. The growing global prevalence of this condition presents a major public health challenge, with an estimated 537 million adults worldwide currently living with diabetes.
The Major Types of Diabetes
The disorder is broadly classified into three main types based on their underlying mechanisms. Type 1 diabetes is an autoimmune condition where the body’s immune system mistakenly attacks and destroys the insulin-producing beta cells in the pancreas. This destruction results in an absolute deficiency of insulin, meaning the body can no longer produce the hormone. This form of diabetes typically manifests in childhood or young adulthood, requiring lifelong insulin therapy from the time of diagnosis.
Type 2 diabetes, the most common form, accounts for over 90% of all cases. It involves a dual problem of insulin resistance and inadequate insulin secretion. Initially, the body’s cells become less responsive to insulin’s signal, a state called insulin resistance, causing the pancreas to produce more insulin to compensate. Over time, the pancreatic beta cells become exhausted and can no longer secrete enough insulin to overcome this resistance, leading to persistently high blood glucose.
A temporary form, Gestational Diabetes Mellitus (GDM), is first diagnosed during pregnancy, usually in the second or third trimester. This condition is primarily driven by pregnancy hormones, which induce a state of insulin resistance in the mother. If the mother’s pancreas cannot produce enough additional insulin to counteract these effects, GDM results, though it often resolves shortly after delivery.
Before a full diagnosis of Type 2 diabetes, an intermediate state called prediabetes exists. In prediabetes, blood glucose levels are above normal but not high enough to meet the criteria for a diabetes diagnosis. Prediabetes is an important warning sign, as it indicates an increased risk of eventually developing Type 2 diabetes and its associated complications.
Understanding the Underlying Causes
The factors that trigger diabetes vary significantly between types, involving a complex interplay of genetic susceptibility and external influences. In Type 1 diabetes, the genetic risk is high, with genes within the human leukocyte antigen (HLA) complex accounting for approximately 50% of the inherited predisposition. This genetic background primes the immune system for an autoimmune response against the beta cells.
Environmental factors then act as potential triggers that initiate this autoimmune attack in genetically susceptible individuals. Viral infections, particularly those caused by enteroviruses, are considered strong candidates for triggering the destructive immune response. Other proposed environmental influences include certain dietary factors and differences in the gut microbiome in early life, though the exact mechanism remains under investigation.
The etiology of Type 2 diabetes is linked to lifestyle and metabolic factors acting upon a genetic predisposition. The disease is polygenic, meaning multiple genes contribute to the overall risk, affecting functions like insulin secretion and cell sensitivity to insulin. However, the development of Type 2 diabetes is overwhelmingly accelerated by modifiable factors such as excess body weight and a sedentary lifestyle.
Abdominal obesity, in particular, promotes the pathological state of insulin resistance, where fat, liver, and muscle cells do not respond effectively to insulin. This chronic resistance forces the pancreas to work harder until its insulin-producing capacity eventually declines. While the genetic component is evident in familial clustering, the global rise in Type 2 diabetes correlates directly with increasing rates of physical inactivity and energy-dense diets.
The Long-Term Health Effects of Diabetes
The persistent presence of high glucose in the bloodstream causes progressive damage to blood vessels and nerves throughout the body. These long-term consequences are grouped into two categories: microvascular and macrovascular complications. Microvascular complications arise from damage to the body’s small blood vessels.
Diabetic retinopathy, damage to the blood vessels in the retina, is the leading cause of vision impairment in working-age adults. The damaged blood vessels can leak fluid, causing swelling, or close off completely. This can lead to retinal ischemia, which drives the formation of fragile new vessels that can bleed and cause vision loss.
Diabetic nephropathy involves damage to the specialized filtering units of the kidney, the glomeruli, leading to a progressive loss of function. This complication is a common cause of chronic kidney disease and can eventually require dialysis or a kidney transplant.
Diabetic neuropathy is nerve damage that results from chronic hyperglycemia, affecting up to 50% of people with diabetes. This can manifest as sensory loss, particularly in the feet and hands. Sensory loss increases the risk of undetected injuries and severe foot ulcers.
The damage also extends to large blood vessels, resulting in macrovascular complications driven by accelerated atherosclerosis, which is the hardening and narrowing of the arteries. This damage significantly increases the risk of cardiovascular events, including coronary artery disease, which can lead to a heart attack. The risk of cerebrovascular disease, such as stroke, is also higher due to the buildup of plaque in the arteries supplying the brain. Peripheral artery disease (PAD) occurs when large blood vessels in the limbs, often the legs, narrow, causing poor circulation, which can lead to pain during walking and increase the risk of amputation.