Diabetic Eye Disease

Diabetes can affect many parts of the eye, not just one. The term diabetic eye disease refers to a group of eye conditions that are caused or made worse by diabetes. The most well-known is diabetic retinopathy—damage to the blood vessels in the back of the eye. But diabetes also raises the risk of other serious eye conditions, including diabetic macular edema (fluid buildup in the center of the retina), diabetes-related cataracts (clouding of the eye’s natural lens), and diabetes-related open-angle glaucoma (increased pressure that damages the optic nerve). Having diabetes makes a person two to five times more likely to develop cataracts—often at a younger age than people without diabetes—and nearly doubles the risk of developing glaucoma. Managing all of these conditions together is an important part of diabetes care.

Diabetic retinopathy (DR) is the most common form of diabetic eye disease and the leading cause of new blindness among working-age adults in the United States. It develops when high blood sugar levels damage the tiny blood vessels that supply the retina—the light-sensitive layer of tissue at the back of the eye that converts what we see into signals sent to the brain. When these vessels are damaged, they can leak fluid, swell, or grow in abnormal ways that progressively impair vision.

Approximately 9.6 million people in the United States currently live with diabetic retinopathy. Globally, an estimated 93 million people are affected. Those numbers are expected to grow significantly—U.S. projections estimate 16 million Americans will have the condition by 2050. The condition is progressive, meaning it worsens over time without treatment and management of the underlying diabetes. However, when detected early and treated appropriately, the risk of severe vision loss can be dramatically reduced. Regular eye exams are the most powerful tool available for protecting vision in people with diabetes.

Doctors classify diabetic eye disease by which part of the eye is affected and how far the damage has progressed. Diabetic retinopathy is divided into stages based on severity. Other diabetic eye conditions are distinct diagnoses but share the same underlying cause—chronic high blood sugar.

Nonproliferative diabetic retinopathy (NPDR) is the early stage of diabetic retinopathy. The word nonproliferative means that abnormal new blood vessels have not yet started to grow. In NPDR, the walls of the small blood vessels in the retina weaken and may develop tiny bulges called microaneurysms that can leak blood or fluid into the retina. NPDR is divided into three levels of severity:

• Mild NPDR: a small number of microaneurysms are present. Vision may be entirely normal at this stage. This is often the first sign of retinal damage detectable on examination.
• Moderate NPDR: More widespread changes appear, including blockages in retinal blood vessels, small hemorrhages (bleeding spots), and fatty deposits called hard exudates. Vision may still be minimally affected.
• Severe NPDR: a large area of the retina has lost its blood supply. The retina begins sending chemical signals to stimulate the growth of new blood vessels. This stage carries a high risk of progressing to proliferative disease within one year if untreated.

Proliferative diabetic retinopathy (PDR) is the advanced stage of diabetic retinopathy. In response to the loss of blood supply in the retina, the eye grows new, abnormal blood vessels—a process called neovascularization. These new vessels are fragile, grow in the wrong places (including on the surface of the retina and into the vitreous—the gel-like substance filling the eye), and bleed easily. PDR can lead to:

• Vitreous hemorrhage: Bleeding from fragile new blood vessels into the vitreous gel causes sudden floaters, dark streaks, or a complete loss of vision.
• Tractional retinal detachment: Scar tissue from abnormal blood vessels contracts and pulls the retina away from the back of the eye, causing severe, potentially permanent vision loss.
• Neovascular glaucoma: Abnormal new blood vessels grow on the iris (the colored part of the eye) and block fluid drainage, dramatically raising eye pressure and threatening the optic nerve.

Diabetic macular edema (DME) is a complication that can occur at any stage of diabetic retinopathy—including early NPDR. It develops when damaged blood vessels leak fluid into the macula, the central part of the retina responsible for sharp, detailed vision used for reading, driving, and recognizing faces. The buildup of fluid causes the macula to swell, blurring and distorting central vision. Over time, about 1 in 15 people with diabetes will develop DME. It is currently the most common cause of vision loss from diabetic retinopathy.

Cataracts—a clouding of the eye’s natural lens—develop earlier and more frequently in people with diabetes than in the general population. High blood sugar causes chemical changes in the lens proteins that accelerate clouding. Diabetes-related cataracts respond well to the same surgical treatment used for age-related cataracts.

People with diabetes are nearly twice as likely to develop open-angle glaucoma—a condition in which increased pressure inside the eye damages the optic nerve and causes peripheral vision loss over time. In advanced proliferative retinopathy, neovascular glaucoma (described above) can develop, which is more aggressive and harder to treat than typical open-angle glaucoma.

Diabetic eye disease is caused by persistently elevated blood sugar levels that damage the small blood vessels throughout the body, including those that supply the retina. The retina has one of the highest metabolic demands of any tissue in the body—it needs a rich, constant blood supply to function. When that supply is compromised by diabetes-related vascular damage, a cascade of changes begins that can progressively destroy vision.

The primary biological mechanism is microvascular damage—injury to the smallest blood vessels (capillaries) in the retina. High blood sugar causes these vessels to leak, swell, and eventually close off entirely. Several specific pathways contribute to this damage:

• Polyol pathway activation: Excess glucose is converted to sorbitol inside retinal cells, causing osmotic stress and cell damage.
• Advanced glycation end-products (AGEs): High glucose causes proteins and fats in vessel walls to become permanently modified by sugar molecules (glycation). AGEs make vessel walls stiffer, more permeable, and more prone to inflammation.
• Protein kinase C (PKC) activation: High glucose activates PKC, an enzyme that increases vascular permeability, promotes abnormal blood vessel growth, and impairs blood flow.
• Oxidative stress: An overproduction of unstable molecules, called reactive oxygen species, damages retinal cells and vessel walls directly.
• Vascular endothelial growth factor (VEGF) overproduction: When retinal blood vessels close off, the deprived tissue releases large amounts of VEGF, a protein that signals the body to grow new blood vessels. In the retina, these new vessels are abnormal, fragile, and prone to bleeding.
• Neurodegeneration: Recent research has identified that retinal nerve cells begin to degenerate in the early stages of diabetes, even before blood vessel changes are visible on examination. This may contribute to vision changes that precede clinically detectable retinopathy.

Every person with diabetes is at risk for diabetic eye disease. The longer a person has had diabetes and the less well their blood sugar is controlled, the higher their risk becomes. Several additional factors further increase the likelihood of developing retinopathy or accelerating its progression.

• Duration of diabetes: The length of time a person has had diabetes is the strongest predictor of diabetic retinopathy. After 20 years of diabetes, the majority of people with type 1 diabetes and a significant proportion of those with type 2 will have some degree of retinopathy.
• Poor blood sugar control: Chronically elevated hemoglobin A1c (a measure of average blood sugar over three months) is directly linked to faster development and progression of retinopathy. The landmark Diabetes Control and Complications Trial (DCCT) showed that tight blood sugar control reduces the risk of retinopathy by up to 76% in type 1 diabetes.

• Type 1 diabetes: People with type 1 diabetes have a high lifetime risk of retinopathy. Retinopathy rarely appears in the first five years after diagnosis but becomes increasingly common with disease duration.
• Type 2 diabetes: Retinopathy may already be present at the time of type 2 diabetes diagnosis because the condition often goes undetected for years. Type 2 diabetes is responsible for the majority of all diabetic retinopathy cases due to its much higher prevalence.
• Gestational diabetes: Pregnant women who develop diabetes during pregnancy face a risk of pregnancy-related retinopathy progression, particularly if they already had diabetes before becoming pregnant.

• High blood pressure (hypertension): Hypertension raises pressure in the retinal blood vessels and accelerates damage from diabetes. Managing blood pressure is one of the most effective ways to slow retinopathy progression alongside blood sugar control.
• High cholesterol and lipids: Elevated lipid levels increase the deposition of hard exudates (fatty deposits) in the retina and worsen macular edema.
• Kidney disease (diabetic nephropathy): The kidneys and retina are affected by diabetes through similar microvascular mechanisms. The presence of kidney disease is a strong indicator that retinopathy is also present or advancing.
• Anemia: Low red blood cell count reduces oxygen delivery to the retina, worsening the effect of reduced blood flow from damaged vessels.
• Sleep apnea: Intermittent drops in oxygen levels during sleep may worsen retinal ischemia (oxygen deprivation) in people with diabetes.

• Smoking: Cigarette smoking constricts blood vessels and compounds vascular damage from diabetes.
• Obesity: Associated with insulin resistance, poorer blood sugar control, and higher rates of hypertension and hyperlipidemia—all of which worsen retinopathy risk.
• Pregnancy: Women with pre-existing diabetes should have a dilated eye exam before or early in pregnancy, as diabetic retinopathy can worsen significantly during gestation.
• Ethnicity: Black, Hispanic, and Native American populations face higher rates of diabetic retinopathy compared to non-Hispanic white populations, reflecting both higher rates of diabetes and disparities in access to preventative care.

Diabetic retinopathy can cause significant retinal damage before a person notices any change in their vision. By the time symptoms appear, irreversible damage has often already occurred. Regular dilated eye exams are the cornerstone of screening and are recommended for all people with diabetes.

• Type 1 diabetes: The first dilated eye exam should occur within five years of diagnosis. After that, annual exams are recommended.
• Type 2 diabetes: A dilated eye exam should occur at or shortly after diagnosis, because retinopathy may already be present. Annual exams are then recommended.
• Gestational diabetes: Women who develop diabetes during pregnancy should have an eye exam as early in pregnancy as possible and follow their doctor’s guidance for follow-up based on findings.
• More frequent screening: People with known retinopathy, poorly controlled blood sugar or blood pressure, kidney disease, or those who are pregnant may need exams every three to six months rather than annually.

During a dilated eye exam, the doctor places drops in the eyes to widen the pupils and uses a special lens and light to examine the retina directly. Retinal photography—taking detailed photographs of the retina—allows changes to be documented and compared over time. Optical coherence tomography (OCT) is a noninvasive imaging scan that produces cross-sectional images of the retina and can detect fluid in the macula (the central retina) before it causes noticeable vision change. Fluorescein angiography—a test in which a dye is injected into the bloodstream and photographs are taken as it passes through the retinal vessels—can reveal leaking or closed vessels and guide laser or injection treatment decisions.

Artificial intelligence (AI)-based retinal imaging systems are now U.S. Food and Drug Administration (FDA)-authorized as screening tools. These systems analyze retinal photographs and can detect more-than-mild diabetic retinopathy without a specialist present. They are being used in primary care and endocrinology offices to reach patients who may have limited access to eye care specialists.

Diabetic eye disease cannot be fully prevented in people with diabetes, but the risk of developing it and the rate at which it progresses can be substantially reduced through consistent systemic management. The most important preventative measures are:

• Control blood sugar: Keeping hemoglobin A1c as close to target as possible (as determined by your diabetes care team) is the single most effective way to reduce retinopathy risk. Landmark clinical trials have demonstrated reductions in retinopathy risk of up to 76% with tight glucose control.
• Control blood pressure: A target blood pressure below 130/80 mmHg is recommended for most people with diabetes. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) have additional protective effects on retinal blood vessels beyond blood pressure lowering.
• Control cholesterol and lipids: Managing low-density lipoprotein (LDL) cholesterol and triglycerides reduces the deposition of hard exudates in the retina and protects retinal vessel health.
• Do not smoke: Quitting smoking reduces vascular damage and slows retinopathy progression.
• Maintain a healthy weight and exercise regularly: Physical activity improves insulin sensitivity and supports blood sugar control.
• Attend all scheduled eye exams: Early detection and treatment before vision is affected is the most powerful tool for preventing blindness from diabetic retinopathy.

One of the most important and often misunderstood features of diabetic retinopathy is that it typically causes no symptoms in its early stages. The retina can sustain considerable damage—including the development of microaneurysms, hemorrhages, and even moderate NPDR—without the person noticing any change in their vision. By the time vision symptoms appear, significant damage has usually already occurred. This is why annual dilated eye exams are essential, even when vision feels perfectly normal.

Most people with early diabetic retinopathy have no symptoms at all. When changes do begin to appear, they may be subtle and easy to dismiss:

• Slightly blurry vision: Objects may appear mildly unclear, similar to needing a new glasses prescription.
• Difficulty reading or seeing fine detail: Early macular changes may make close-up tasks harder than usual.
• Colors that appear less vivid: Some people notice that colors seem washed out or less sharp than before.
• Fluctuating vision: Vision may change from day to day or throughout the day, sometimes related to fluctuations in blood sugar levels.

As retinopathy advances, symptoms become more noticeable and more serious:

• Floaters: Spots, strings, webs, or dark shadows drifting through the field of vision are caused by blood leaking into the vitreous gel. Sudden onset of multiple new floaters is a warning sign that requires urgent evaluation.
• Dark streaks or shadows: A curtain-like shadow or a large dark area in the field of vision may indicate a vitreous hemorrhage (significant bleeding into the eye).
• Blurred or distorted central vision: Difficulty seeing clearly in the center of vision, making reading, driving, and recognizing faces progressively harder. This is the hallmark symptom of diabetic macular edema.
• Straight lines that appear wavy or bent: This is a sign of macular edema or retinal distortion.
• Blank or dark areas in central vision: Patches or gaps in the center of sight that indicate the macula is increasingly damaged.
• Sudden or rapid vision loss: This can occur with vitreous hemorrhage, tractional retinal detachment, or neovascular glaucoma. This is a medical emergency.
• Loss of peripheral (side) vision: This is more common when diabetic retinopathy is accompanied by glaucoma.
• Eye pain or pressure: Not typical in retinopathy alone, but can occur with neovascular glaucoma caused by advanced proliferative disease.

• In children and young adults with type 1 diabetes: Retinopathy is rare in the first five years after diagnosis and before puberty. After puberty and with increasing disease duration, risk rises significantly. Regular screening must begin no later than five years after diagnosis. Young people with type 1 diabetes should also be screened for glaucoma and cataracts.
• In working-age adults (30s to 60s): This age group bears the highest burden of vision-threatening diabetic retinopathy and accounts for the majority of diabetes-related blindness in the United States. Adults in this group often have type 2 diabetes that went undiagnosed for years, meaning retinopathy may already be at a moderate stage when diabetes is first identified.
• In older adults (65 and over): Older adults with diabetes face compounding risks—diabetic retinopathy, cataracts, and glaucoma frequently coexist. Age-related changes in the eye can make it harder to detect early retinopathy changes, and recovery after treatment may be slower. Comprehensive annual eye exams remain critically important in this age group.

An ophthalmologist (a medical doctor specializing in eye disease and surgery) or an optometrist (a licensed eye care provider) diagnoses diabetic eye disease. Diagnosis requires a dilated eye examination—the pupil must be fully widened with eye drops to allow the doctor to see the entire retina. A standard eye chart test alone is not sufficient to detect early diabetic retinopathy, because vision may be completely normal even when significant retinal damage is present. The following tests and tools are used:

• Visual acuity testing: A standard eye chart test that measures the sharpness of central vision. Results establish a baseline and track how vision changes over time. Normal visual acuity does not rule out retinopathy.
• Dilated fundus examination: The doctor places dilating drops in the eyes to widen the pupils and then uses a special lens and bright light to examine the retina, optic nerve, macula, and retinal blood vessels. This is the foundational diagnostic exam for all diabetic eye disease.
• Intraocular pressure measurement (tonometry): The doctor measures the pressure inside the eye to screen for glaucoma, which occurs at higher rates in people with diabetes.

• Fundus photography: Color photographs of the retina document the presence and location of microaneurysms, hemorrhages, hard exudates, and new blood vessels. Serial photographs allow comparison over time to track progression.
• Optical coherence tomography (OCT): A noninvasive scan that uses light waves to create detailed cross-sectional images of the retina’s layers. It is the primary test for diagnosing and monitoring diabetic macular edema, measuring the thickness of the retina, and detecting fluid accumulation with very high precision. It is fast, painless, and requires no injection.
• Wide-field retinal imaging: Advanced cameras capture a much wider view of the retina than standard photography, allowing detection of peripheral retinal changes that might otherwise be missed. Increasingly used for both screening and monitoring.
• Fluorescein angiography (FA): A yellow dye called fluorescein is injected into a vein in the arm. As the dye travels through the retinal blood vessels, a camera takes rapid-sequence photographs. The test reveals leaking vessels, areas of poor blood flow, and the location and extent of abnormal new blood vessel growth. It is particularly useful in planning laser treatment and evaluating treatment response.
• Optical coherence tomography angiography (OCTA): A newer, noninvasive version of fluorescein angiography that uses light rather than an injected dye to map retinal blood flow. It can detect early microvascular changes and abnormal vessel growth without the small risks associated with dye injection.

• Hemoglobin A1c: A blood test measuring average blood sugar control over the past two to three months. While not a test of the eye itself, A1c levels directly correlate with retinopathy risk and are essential for understanding the overall severity of a patient’s diabetes management.
• Blood pressure measurement: Hypertension is a major independent risk factor for retinopathy progression. Blood pressure is checked at every visit.
• Kidney function tests: The presence of diabetic kidney disease (nephropathy) is closely associated with diabetic retinopathy. Kidney function tests help identify patients who are at higher risk for advanced eye disease.

Diabetic eye disease cannot be cured, but its progression can be slowed or stabilized, and in many cases, vision can be significantly improved with treatment. The goals of treatment are to prevent further damage to retinal blood vessels, reduce fluid and bleeding in the retina, eliminate abnormal new blood vessel growth, and preserve as much vision as possible. Your doctor will tailor treatment to the type and severity of the condition—whether that is mild retinopathy requiring only close monitoring, macular edema requiring injections, or advanced proliferative disease requiring laser or surgery.

The most important treatment for diabetic eye disease is not an eye treatment at all—it is optimal control of the underlying diabetes and its associated risk factors. Studies have shown that improving blood sugar control, blood pressure, and cholesterol can slow the onset and progression of retinopathy significantly. Your primary care doctor or endocrinologist (a specialist in hormonal and metabolic conditions) is an essential partner in your eye care team.

• Blood sugar control: Keeping hemoglobin A1c at your personalized target reduces the risk of retinopathy developing and slows its progression once it has begun.
• Blood pressure management: Medications including ACE inhibitors (such as lisinopril) and angiotensin receptor blockers—ARBs (such as losartan) lower blood pressure and provide additional protection to the retinal blood vessels.
• Cholesterol management: Statin medications (such as atorvastatin) and fenofibrate (a lipid-lowering medicine that has been shown in clinical trials to reduce the need for laser treatment in diabetic retinopathy) are sometimes used.
• Smoking cessation: Stopping smoking reduces vascular damage and may slow progression.

Anti-VEGF medicines are currently the first-line treatment for diabetic macular edema and for certain stages of proliferative diabetic retinopathy. VEGF is the protein responsible for stimulating the growth of abnormal, leaky blood vessels in the diabetic retina. Anti-VEGF drugs block this protein, reducing fluid leakage, shrinking abnormal vessels, and, in many patients, actually improving vision.

These medicines are injected directly into the vitreous gel of the eye using a very fine needle. The procedure is performed in the doctor’s office under topical anesthesia (numbing eye drops). Most patients describe feeling pressure rather than pain. Injections are given on a regular schedule—typically monthly at first, then spaced out as the condition stabilizes. FDA-approved anti-VEGF agents used for diabetic eye disease include:

• Ranibizumab (Lucentis®): FDA-approved for DME and DR. A fragment of a monoclonal antibody that binds and blocks VEGF-A.
• Aflibercept (Eylea®): FDA-approved for DME and DR. A fusion protein that binds multiple forms of VEGF and a related factor called placental growth factor (PIGF), with a longer duration of action than ranibizumab. A higher-dose formulation (Eylea HD®) is also available.
• Faricimab (Vabysmo®): FDA-approved in 2022 for DME and wet age-related macular degeneration. A bispecific antibody that targets both VEGF-A and angiopoietin-2 (Ang-2), a second protein that destabilizes retinal blood vessels. It has the longest approved treatment interval of the currently available agents for some patients.
• Bevacizumab (Avastin®): An off-label anti-VEGF agent (approved for cancer but widely used in ophthalmology) that has shown similar efficacy to ranibizumab in large clinical trials and is substantially less expensive. It is commonly used when cost is a barrier to treatment.

Laser therapy has been a mainstay of diabetic retinopathy treatment for decades. While anti-VEGF injections have become first-line for DME, laser treatment remains important for proliferative retinopathy and as a secondary treatment when injections alone are insufficient.

• Panretinal photocoagulation (PRP): Also called scatter laser treatment, PRP is used for proliferative diabetic retinopathy. The laser creates hundreds to thousands of small burns across the peripheral retina, reducing the area of the retina that is oxygen-deprived and signaling the eye to stop producing VEGF. This causes abnormal blood vessels to shrink and prevents new ones from forming. PRP may cause some permanent reduction in peripheral and night vision, but is highly effective at preventing severe vision loss.
• Focal and grid laser photocoagulation: Used for diabetic macular edema, this treatment applies laser spots directly to leaking microaneurysms in the macula (focal) or in a grid pattern across the swollen area (grid). It reduces leakage and helps stabilize vision. It has largely been replaced by anti-VEGF injections as first-line therapy for DME but remains useful in select cases.

Corticosteroids (steroids) reduce inflammation and fluid leakage in the retina. They are used for DME in patients who have not responded adequately to anti-VEGF injections or in patients for whom injections are not suitable.

• Ozurdex® (dexamethasone intravitreal implant): A small, biodegradable (dissolving) implant injected into the vitreous releases dexamethasone (a steroid) slowly over several months. FDA-approved for DME. It requires less frequent dosing than anti-VEGF injections but carries a risk of elevated eye pressure and cataract formation with repeated use.
• Iluvien® (fluocinolone acetonide intravitreal implant 0.19 mg): A tiny, non-biodegradable implant is inserted into the vitreous that releases a very low dose of fluocinolone acetonide continuously for up to three years. FDA-approved for DME in patients who have previously been treated with a course of corticosteroids and did not have a significant rise in eye pressure. It is particularly useful for patients who struggle with the burden of frequent injections.

When diabetic retinopathy has advanced to the point where bleeding into the vitreous or retinal detachment has occurred, surgery is often necessary to restore or preserve vision.

• Vitrectomy: the most common surgical procedure for advanced diabetic retinopathy. The vitreous gel is removed from the eye and replaced with a clear saline solution or gas bubble. This clears blood that has leaked into the vitreous (vitreous hemorrhage), allows the surgeon to cut away scar tissue pulling on the retina (tractional membranes), and enables repair of a detached retina. Vitrectomy is performed under local or general anesthesia and requires careful post-operative positioning in some cases (face-down positioning when a gas bubble is used). Recovery takes weeks to months. Many patients regain useful vision after vitrectomy, though outcomes depend on how long the retina was detached and the degree of underlying damage.
• Vitrectomy with membrane peeling: When scar tissue (epiretinal membrane) has formed on the surface of the macula and is distorting central vision, the surgeon carefully removes this thin membrane during vitrectomy to allow the retina to relax back to its normal position.

When abnormal blood vessels grow on the iris and drainage structures of the eye (a complication of severe proliferative retinopathy), the resulting glaucoma is aggressive and can be difficult to control. Treatment typically combines anti-VEGF injections to shrink the abnormal vessels, panretinal laser to reduce the driving VEGF signal, and glaucoma medications or surgery to lower eye pressure. In some cases, a glaucoma drainage device (tube shunt) is implanted surgically to create a new drainage pathway.

When diabetes-related cataracts significantly impair vision, cataract surgery—the removal of the cloudy natural lens and replacement with an artificial intraocular lens (IOL)—is highly effective. People with diabetes who need cataract surgery should have their retinopathy optimally treated before the procedure when possible, and should be monitored closely afterward, as surgery can sometimes temporarily worsen diabetic macular edema.

A diagnosis of diabetic eye disease—even in its early stages—is a serious signal that diabetes is affecting the body’s blood vessels in ways that require prompt and sustained attention. For most people, it is also a powerful motivator to take better control of blood sugar, blood pressure, and other risk factors. The encouraging reality is that the vast majority of vision loss from diabetic retinopathy is preventable when the condition is caught early, treated appropriately, and the underlying diabetes is managed well. Many people live for decades with diabetic retinopathy and maintain useful, functional vision with regular monitoring and treatment. If you have already experienced some vision loss, your doctor can connect you with low-vision rehabilitation specialists and support services that can help you adapt and continue doing the things that matter to you. Staying engaged with your eye care team and your diabetes care team—and attending every scheduled appointment—is the single most important thing you can do for your long-term vision.

To further your understanding of your diagnosis and to contribute to cutting-edge research, consider participating in a clinical trial so clinicians and scientists can learn more about causes, symptoms, treatment, and prevention of diabetic eye disease and related disorders. Clinical research uses human volunteers to help researchers learn more about a disorder and perhaps find better ways to safely detect, treat, or prevent disease.

All types of volunteers are needed—those who are healthy or may have an illness or disease—of all different ages, sexes, races, and ethnicities to ensure that study results apply to as many people as possible, and that treatments will be safe and effective for everyone who will use them.

To learn more about clinical trials and find studies that may be right for you, visit National Institutes of Health (NIH) Clinical Research Trials and You to search active studies by condition, location, and age group.