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Why a form of autoimmune diabetes recognized nearly 50 years ago is receiving renewed attention—and what scientists are discovering about insulin resistance, endothelial health, inflammation, and cellular function.

You’ve probably heard of Type 2 diabetes, and perhaps you’re familiar with Type 1 diabetes. But did you know that some researchers have referred to Alzheimer’s disease as Type 3 diabetes because of its connections to insulin resistance and impaired insulin signaling in the brain? Although Type 3 diabetes isn’t an officially recognized medical diagnosis, the connection is certainly worth understanding.

And now, there’s another term getting attention: Type 1.5 diabetes.

I agree. It’s beginning to sound a little confusing.

And perhaps even more intriguing is this question: How is it possible that, in 2026, we’re still discovering what appear to be new types of diabetes?

What’s going on?

Well, there’s a lot going on. And the more scientists uncover about diabetes, the more we realize that elevated blood sugar doesn’t always tell the whole story.

That’s precisely why I believe it’s in our best interest to stay informed, ask questions, and become our own greatest health advocates.

So, let’s approach this with an open mind. What you’re about to learn may change how you think about diabetes.

A Diabetes Diagnosis That Doesn’t Tell the Whole Story

Imagine being 52 years old and visiting your doctor for a routine examination.

Your blood work reveals elevated glucose levels. Your physician tells you that you have Type 2 diabetes.

You’re advised to improve your diet, increase physical activity, and perhaps begin taking medication.

You follow the recommendations.

Initially, your blood sugar improves. But over the next several months or years, something unexpected happens. Your blood glucose becomes increasingly difficult to control, and your pancreas appears to be producing less insulin.

What if the problem isn’t simply insulin resistance?

What if your immune system is gradually destroying the very cells responsible for producing insulin?

Welcome to the often-overlooked world of Latent Autoimmune Diabetes in Adults (LADA), commonly called Type 1.5 diabetes.

Although some people describe LADA as a new form of diabetes, researchers have studied it for nearly 50 years.

An international expert consensus estimates that LADA accounts for approximately 2%–12% of adult-onset diabetes cases, depending on the population studied and diagnostic methods used (Buzzetti et al., 2020).

That raises an important question: How many people diagnosed with Type 2 diabetes actually have an autoimmune condition?

What Exactly Is Type 1.5 Diabetes?

To understand LADA, we first need to understand insulin.

Your pancreas contains specialized cells called beta cells. These cells produce insulin, a hormone that helps regulate blood glucose.

When you consume carbohydrates, your digestive system breaks many of them down into glucose, which enters your bloodstream. Insulin helps muscle and fat cells absorb glucose for energy or storage. It also signals your liver to store glucose as glycogen and reduce the amount of glucose it releases into your bloodstream. Together, these processes help maintain healthy blood sugar levels.

In LADA, the immune system mistakenly targets insulin-producing beta cells.

Over time, this autoimmune attack reduces the pancreas’s ability to produce insulin.

Unlike classic Type 1 diabetes, which can progress rapidly, LADA generally develops more gradually.

Some individuals continue producing enough insulin to avoid injections for months or years after diagnosis.

This explains why LADA can initially resemble Type 2 diabetes.

However, there’s an important distinction.

LADA isn’t officially classified as a separate type of diabetes halfway between Type 1 and Type 2. The American Diabetes Association (ADA) generally classifies it as slowly progressive autoimmune Type 1 diabetes (American Diabetes Association Professional Practice Committee, 2026).

The term Type 1.5 is an informal description.

The History of LADA: Nearly 50 Years of Scientific Discovery

One of the most surprising aspects of LADA is how long researchers have known about it.

In 1977, Dr. William Irvine and colleagues published research identifying pancreatic islet-cell antibodies in adults receiving oral medications for diabetes.

Their findings suggested that some individuals who appeared to have Type 2 diabetes were actually experiencing an autoimmune process (Irvine et al., 1977).

In 1986, Dr. Leif Groop and colleagues demonstrated that islet-cell antibodies could help identify slowly progressing autoimmune diabetes in adults (Groop et al., 1986).

Then came an influential 1993 study.

Dr. Tiinamaija Tuomi and colleagues examined 102 adults whose diabetes initially did not require insulin.

Among 33 participants classified as insulin-deficient, 25 tested positive for antibodies against glutamic acid decarboxylase (GAD), an enzyme associated with pancreatic beta cells.

Among 69 participants who were not insulin-deficient, eight tested positive.

These findings helped establish LADA as an important clinical condition (Tuomi et al., 1993).

In 1997, the United Kingdom Prospective Diabetes Study (UKPDS) demonstrated that diabetes-related autoantibodies could help predict which adults initially diagnosed with Type 2 diabetes would eventually require insulin (Turner et al., 1997).

By 2020, an international expert panel had published recommendations for identifying and managing LADA.

Think about this: Scientists have recognized adult-onset autoimmune diabetes for nearly five decades, yet many people have never heard of it.

Is Type 1.5 Diabetes Becoming More Common?

LADA appears to be receiving greater scientific attention, but that doesn’t necessarily mean more people are developing the disease.

There’s an important difference between a disease becoming more common and doctors becoming better at recognizing a disease that has been there all along.

Think about it this way: If thousands of people have a condition but very few are tested for it, how would we know how common it really is?

This is one of the challenges researchers face with LADA.

A 2026 American Diabetes Association (ADA) conference abstract examined healthcare records involving more than eight million adults over age 30 with newly recorded diabetes diagnoses.

The researchers reported that approximately 0.54% had recorded testing for glutamic acid decarboxylase (GAD) antibodies, while approximately 0.71% had recorded C-peptide testing (American Diabetes Association, 2026).

To put those numbers into perspective, that’s approximately 5 out of every 1,000 adults receiving GAD antibody testing and 7 out of every 1,000 receiving C-peptide testing.

Why does this matter?

GAD antibody testing helps doctors determine whether the immune system may be attacking the insulin-producing cells of the pancreas.

C-peptide testing provides different but equally valuable information. When your pancreas produces insulin, it also releases a substance called C-peptide. By measuring C-peptide, doctors can estimate how much insulin your pancreas is still producing naturally.

Here’s the important distinction: GAD antibody testing helps identify an autoimmune process, while C-peptide testing helps evaluate how well the pancreas is still producing insulin.

Neither test tells the complete story by itself, but together with other clinical findings, they can help doctors distinguish LADA from Type 2 diabetes.

Now consider someone who has been diagnosed with Type 2 diabetes but is actually experiencing the gradual autoimmune destruction of pancreatic beta cells. Without appropriate testing, that person could continue receiving treatment for Type 2 diabetes without anyone recognizing the underlying autoimmune condition.

These findings suggest that testing for autoimmune diabetes remains uncommon among adults. However, the reported percentages represent testing rates, not the percentage of people who actually have LADA. The research was also presented as a conference abstract, so the findings should be considered preliminary.

We also don’t have sufficient long-term population data to confidently conclude that LADA itself is becoming more common.

What we can say is that greater awareness and more appropriate testing could help identify people whose autoimmune diabetes has gone unrecognized.

And that brings us back to an important principle: Identifying elevated blood glucose is only the beginning. Understanding why it’s elevated can make all the difference.

Type 1, Type 2, and Type 1.5: What’s the Difference?

Although all three conditions can cause elevated blood glucose, their underlying mechanisms differ.

Characteristic	Type 1	Type 2	Type 1.5 (LADA)
Primary problem	Autoimmune beta-cell destruction	Insulin resistance and beta-cell dysfunction	Slowly progressing autoimmune beta-cell destruction
Typical onset	Any age	More common in adults	Adulthood
Insulin production	Often declines rapidly	Variable	Usually declines gradually
Autoantibodies	Usually present	Usually absent	Usually present
Insulin treatment	Required	Sometimes required	Often eventually required

One particularly important distinction is that insulin resistance and autoimmune diabetes can occur simultaneously.

Someone with LADA may experience both declining insulin production and reduced insulin sensitivity.

That combination can make blood glucose increasingly difficult to manage.

What Actually Causes LADA?

Scientists understand the underlying autoimmune process, but they don’t fully understand why it begins.

Several factors may influence susceptibility and disease development.

Genetics: Certain human leukocyte antigen (HLA) gene variants increase susceptibility to autoimmune diabetes. These genes help regulate how the immune system recognizes proteins.

Immune-system dysfunction: T lymphocytes participate in the destruction of pancreatic beta cells. Antibodies against proteins such as GAD65 help identify autoimmune diabetes, although the antibodies themselves are not necessarily responsible for the destruction.

Environmental and metabolic influences: Researchers are investigating smoking, excess body fat, insulin resistance, dietary patterns, infections, and other exposures.

Some factors are associated with LADA risk, but their precise causal roles remain uncertain (Carlsson et al., 2022).

Why Would the Immune System Attack the Pancreas After Decades of Normal Function?

Imagine someone reaching age 55 without diabetes.

Their pancreas has produced insulin throughout their life.

Then they develop an autoimmune condition that gradually destroys their insulin-producing cells.

Why now?

One explanation is that autoimmune activity may begin long before symptoms appear.

A person can experience gradual beta-cell damage while still producing enough insulin to maintain relatively normal glucose levels.

Eventually, the remaining cells cannot meet the body’s needs.

At that point, diabetes becomes clinically apparent.

Genetic susceptibility may exist throughout life, while environmental and metabolic influences could affect when the disease develops.

But scientists have not identified a single trigger that explains every case.

The Connection Between Insulin Resistance and LADA

Here’s where metabolic health becomes particularly interesting.

Insulin resistance means the body’s tissues respond less effectively to insulin.

As a result, the pancreas may need to produce more insulin to maintain normal blood glucose.

Now imagine someone whose immune system is already damaging pancreatic beta cells.

If that person also develops insulin resistance, the remaining beta cells face greater demands.

The pancreas may struggle to produce enough insulin—not only because cells are being destroyed, but because the body requires more insulin than before.

Research has associated excess body weight and obesity with LADA risk. Genetic epidemiology studies also suggest that adiposity may contribute to disease susceptibility (Carlsson et al., 2022).

However, improving insulin sensitivity has not been proven to stop autoimmune beta-cell destruction.

Supporting metabolic health and treating the underlying autoimmune disease are related—but different—goals.

The Overlooked Connection: Endothelial Cells, Inflammation, and LADA

When discussing diabetes, most people focus on blood glucose, insulin, and the pancreas.

But there’s another important player: the endothelium.

The endothelium is the thin layer of specialized endothelial cells lining the inside of blood vessels.

These cells help regulate blood flow, blood vessel relaxation, inflammatory signaling, and the movement of immune cells into surrounding tissues.

They also produce nitric oxide, a molecule that helps blood vessels relax.

Why does this matter to the pancreas?

The pancreas contains clusters of insulin-producing cells called pancreatic islets.

These islets are surrounded by an extensive network of tiny blood vessels.

Endothelial cells help support this environment by regulating circulation and communication between the bloodstream and pancreatic tissue.

During inflammation, endothelial cells can express adhesion molecules, including intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1).

These molecules help immune cells attach to blood vessel walls and migrate into tissues.

Researchers studying autoimmune Type 1 diabetes have investigated how endothelial activation and immune-cell trafficking contribute to inflammation within pancreatic islets.

Because LADA is a slowly progressing form of autoimmune diabetes, these mechanisms are biologically relevant.

However, there is not enough clinical evidence to conclude that endothelial dysfunction causes LADA or that restoring endothelial health can stop its autoimmune progression.

The connection to insulin resistance

The relationship between insulin resistance and endothelial dysfunction is better established.

Insulin normally participates in signaling pathways that stimulate nitric oxide production.

When insulin resistance develops, these pathways may become impaired.

Chronic hyperglycemia, oxidative stress, and metabolic disturbances can further compromise vascular function.

For someone living with LADA, protecting endothelial health is particularly important because diabetes increases the risk of cardiovascular disease, kidney damage, and other vascular complications.

The takeaway: Endothelial cells may participate in the inflammatory environment surrounding pancreatic beta cells, while maintaining endothelial health is already an established priority in diabetes care.

Environmental Factors, Smoking, and Nutrition

Researchers have investigated several potentially modifiable factors associated with LADA.

Smoking has emerged as a possible risk factor, particularly among genetically susceptible individuals.

Excess adiposity may contribute through insulin resistance and increased metabolic demands.

Dietary research has examined sugar-sweetened beverages, processed meats, fish consumption, and omega-3 fatty acids.

Some observational studies suggest associations between these exposures and LADA risk.

But association does not establish causation.

We cannot conclude that a particular food causes LADA or that a specific dietary pattern prevents autoimmune diabetes.

Nevertheless, maintaining metabolic health, avoiding smoking, and following a nutritionally balanced eating pattern remain valuable.

Omega-3 Fatty Acids, Cell Membranes, and Immune Regulation

One particularly interesting area of research involves fatty acids, cell membranes, and immune function.

Every cell in your body is surrounded by a membrane composed primarily of lipids and proteins.

These membranes help regulate cellular communication, nutrient transport, and signaling.

Two important long-chain omega-3 fatty acids are eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).

Both can become incorporated into cellular membranes and participate in pathways involved in inflammatory signaling.

DHA also contributes to membrane structure.

Why does cell membrane fluidity matter?

Cell membrane fluidity describes how freely lipids and certain proteins move within a membrane.

This characteristic can influence cellular signaling and receptor activity.

Because immune and endothelial cells depend on membrane-associated signaling, researchers are interested in how fatty acid composition influences their function.

Some observational research has associated omega-3 intake with lower LADA risk (Carlsson et al., 2022).

However, omega-3 supplementation has not been proven to prevent LADA or reverse autoimmune beta-cell destruction.

What about omega-6 to omega-3 balance?

Omega-6 and omega-3 fatty acids participate in numerous biological processes.

Arachidonic acid (AA), an omega-6 fatty acid, contributes to pathways involved in inflammation and its resolution.

EPA and DHA also participate in inflammatory regulation, including pathways involved in producing specialized pro-resolving mediators.

Blood testing can measure fatty acid status.

For example, the Omega-3 Index measures EPA and DHA as a percentage of total red blood cell membrane fatty acids.

An omega-6 to omega-3 ratio provides another perspective on fatty acid composition.

These measurements can offer nutritional information, but neither has been validated to diagnose LADA, predict its progression, or determine whether autoimmune beta-cell destruction has stopped.

Understanding cellular fatty acid composition may help inform broader nutritional decisions without replacing established diabetes testing.

 

Warning Signs You Shouldn’t Ignore

LADA symptoms can resemble those of Type 1 or Type 2 diabetes.

Common warning signs include:

• • Increased thirst and frequent urination.
  • Persistent fatigue.
  • Unexplained weight loss.
  • Blurred vision.
  • Increased hunger.
  • Blood glucose that becomes increasingly difficult to control.

An important clue is an unexpected decline in glucose control despite appropriate treatment for presumed Type 2 diabetes.

A personal or family history of autoimmune disease may also increase suspicion.

However, symptoms alone cannot confirm LADA.

As insulin deficiency progresses, some individuals may develop diabetic ketoacidosis (DKA), a potentially life-threatening complication.

Vomiting, abdominal pain, deep or rapid breathing, confusion, and severe dehydration require emergency medical evaluation.

The Blood Tests That Can Reveal Type 1.5 Diabetes

Standard fasting glucose and hemoglobin A1c (HbA1c) tests help diagnose diabetes, but they cannot reliably determine its underlying type.

When LADA is suspected, additional testing may be appropriate.

GAD65 antibodies: Often the most useful initial autoimmune marker for identifying LADA.

Islet antigen-2 (IA-2) antibodies: Can provide additional evidence of autoimmune diabetes.

Zinc transporter 8 (ZnT8) antibodies: May help identify autoimmune diabetes when other antibody results are inconclusive.

C-peptide: Helps assess how much insulin the pancreas is still producing.

C-peptide is particularly important because LADA often involves progressively declining insulin production.

Results must be interpreted alongside blood glucose, kidney function, medications, and clinical findings.

A low C-peptide level can indicate reduced insulin secretion, but it does not independently establish an autoimmune cause.

Together, autoantibody testing, C-peptide measurements, and clinical evaluation can help distinguish LADA from Type 2 diabetes.

Why the Correct Diagnosis Changes Treatment

A person with Type 2 diabetes may primarily need treatment addressing insulin resistance and glucose regulation.

A person with LADA is experiencing progressive autoimmune beta-cell loss.

Eventually, many individuals with LADA require insulin therapy.

The 2020 international consensus proposed treatment recommendations based partly on C-peptide levels (Buzzetti et al., 2020).

C-peptide level	General treatment consideration
Below 0.3 nmol/L	Multiple-insulin regimen generally recommended
0.3–0.7 nmol/L	Individualized treatment, with insulin considered
Above 0.7 nmol/L	Modified Type 2 approach may be appropriate, with continued monitoring

These are expert consensus recommendations, not universal treatment rules.

For someone with LADA, requiring insulin is not a personal failure. It reflects the biological reality that the pancreas may no longer produce enough of an essential hormone.

Delaying necessary insulin treatment can lead to serious complications.

Can Nutrition and Lifestyle Make a Difference?

Absolutely—but with an important limitation.

Nutrition, physical activity, adequate sleep, and other lifestyle factors can support insulin sensitivity, glucose management, and cardiovascular health.

Resistance training and aerobic exercise can improve insulin sensitivity.

Balanced meals containing adequate protein, fiber-rich carbohydrates, vegetables, and unsaturated fats can support metabolic health.

Managing blood pressure, cholesterol, kidney function, and other cardiovascular risk factors is also essential.

However, improving metabolic health does not necessarily stop autoimmune beta-cell destruction.

Someone with LADA may benefit substantially from lifestyle improvements while still requiring insulin treatment.

Care should be individualized, particularly when exercise or dietary changes affect insulin requirements and hypoglycemia risk.

Can Type 1.5 Diabetes Be Prevented or Reversed?

Currently, there is no established cure for LADA.

Researchers are investigating immune-modifying therapies, genetic susceptibility, and environmental influences.

Some immune therapies have demonstrated benefits in specific populations with presymptomatic Type 1 diabetes, but those findings cannot automatically be applied to established LADA.

Likewise, no dietary supplement has been proven to reverse LADA.

This highlights the difference between mechanistic and clinical evidence.

Mechanistic evidence helps explain how a biological process might work.

Clinical evidence evaluates whether an intervention produces meaningful outcomes in people.

A nutrient may influence immune signaling in laboratory experiments without demonstrating that it prevents autoimmune diabetes in clinical trials.

Both types of evidence are valuable, but they answer different questions.

Questions Worth Asking Your Healthcare Provider

If you’ve been diagnosed with Type 2 diabetes but your clinical course seems unusual, consider discussing these questions:

• • Could I have LADA rather than Type 2 diabetes?
  • Would GAD65 or other diabetes-related antibody testing be appropriate?
  • Should my C-peptide level be measured?
  • Is my insulin production declining?
  • Could insulin resistance also be contributing?
  • How can I better protect my cardiovascular and endothelial health?

Not everyone diagnosed with Type 2 diabetes requires autoimmune testing. The decision should reflect clinical findings and professional judgment.

Final Thoughts: Understanding the Disease Behind the Diagnosis

Type 1.5 diabetes isn’t new.

Scientists have recognized adult-onset autoimmune diabetes for nearly five decades.

What’s changing is our understanding of how autoimmune diabetes can develop gradually and why some adults may initially receive a Type 2 diagnosis.

We know that LADA involves autoimmune destruction of insulin-producing beta cells.

We know that genetics influences susceptibility.

Emerging research suggests that insulin resistance, excess adiposity, smoking, and other environmental factors may also play roles.

Scientists are also investigating how immune-cell movement, endothelial signaling, and the pancreatic microenvironment interact during autoimmune diabetes.

What we don’t fully understand is why autoimmune diabetes develops in one person but not another—or why it sometimes appears after decades of apparently normal pancreatic function.

The most important message is this:

Identifying elevated blood glucose is only the beginning. Understanding WHY blood glucose is elevated can change the entire treatment strategy.

For someone with insulin resistance, improving insulin sensitivity may be a central goal.

For someone with autoimmune beta-cell destruction, recognizing declining insulin production and providing insulin when necessary can be lifesaving.

And for someone experiencing both, comprehensive care must address both conditions.

Because when it comes to diabetes, understanding the disease behind the diagnosis is just as important as understanding the numbers on your laboratory report.

Take the Next Step Toward Understanding Your Cellular Health

Whether you’re living with diabetes, concerned about insulin resistance, or focused on long-term health, understanding your body helps you make informed decisions.

One area to explore is your cell membranes’ fatty acid composition.

That’s why I encourage you to learn more about the At-Home Cellular Health Test.

This convenient finger-prick blood test measures important markers of fatty acid status, including your omega-6 to omega-3 balance and Omega-3 Index.

These results give insight into fatty acid status and can guide discussions about nutrition and cellular health.

Important: This test does not diagnose Type 1.5 diabetes, measure pancreatic autoimmunity, or replace glucose, C-peptide, or diabetes-related antibody testing.

But understanding your cellular fatty acid status can be another useful part of a comprehensive approach to better health.

Interested in the At-Home Cellular Health Test? Have questions about this article? Want to learn more about our many nutrition, metabolic health, weight management, and wellness programs? I’d love to hear from you. Email me directly at robert@dietfreelife.com.

Whether your goal is to better understand your health, improve your nutrition, or find a program that fits your needs, we’re here to help you take the next step.

Better health begins with better information. Test. Don’t Guess.

Scientific References

1. 1. American Diabetes Association Professional Practice Committee. (2026). 2. Diagnosis and classification of diabetes: Standards of Care in Diabetes—2026. Diabetes Care. https://doi.org/10.2337/dc26-s002
   2. Buzzetti, R., Tuomi, T., Mauricio, D., Pietropaolo, M., Zhou, Z., Pozzilli, P., & Leslie, R. D. (2020). Management of latent autoimmune diabetes in adults: A consensus statement from an international expert panel. Diabetes, 69(10), 2037–2047. https://doi.org/10.2337/dbi20-0017
   3. Groop, L. C., Bottazzo, G. F., & Doniach, D. (1986). Islet cell antibodies identify latent type I diabetes in patients aged 35–75 years at diagnosis. Diabetes, 35(2), 237–241. https://pubmed.ncbi.nlm.nih.gov/?term=Islet+cell+antibodies+identify+latent+type+I+diabetes
   4. Irvine, W. J., McCallum, C. J., Gray, R. S., & Duncan, L. J. P. (1977). Clinical and pathogenic significance of pancreatic-islet-cell antibodies in diabetics treated with oral hypoglycaemic agents. The Lancet, 309(8020), 1025–1027. https://doi.org/10.1016/S0140-6736(77)91258-2
   5. Tuomi, T., Groop, L. C., Zimmet, P. Z., Rowley, M. J., Knowles, W., & Mackay, I. R. (1993). Antibodies to glutamic acid decarboxylase reveal latent autoimmune diabetes mellitus in adults with a non-insulin-dependent onset of disease. Diabetes, 42(2), 359–362. https://doi.org/10.2337/diab.42.2.359
   6. Turner, R., Stratton, I., Horton, V., et al. (1997). UKPDS 25: Autoantibodies to islet-cell cytoplasm and glutamic acid decarboxylase for prediction of insulin requirement in type 2 diabetes. The Lancet, 350, 1288–1293. https://pubmed.ncbi.nlm.nih.gov/?term=UKPDS+25+autoantibodies
   7. Carlsson, S., et al. (2022). Lifestyle or environmental influences and their interaction with genetic susceptibility on the risk of LADA. Frontiers in Endocrinology, 13, Article 917850. https://doi.org/10.3389/fendo.2022.917850
   8. American Diabetes Association. (2026). Testing for autoimmune diabetes among adults with newly diagnosed diabetes mellitus in a nationwide U.S. cohort [Conference abstract 2204-P]. Diabetes, 75(Supplement 1). https://diabetesjournals.org/diabetes/article/75/Supplement_1/2204-P/168305/2204-P-Testing-for-Autoimmune-Diabetes-among

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Robert Ferguson is a California- and Florida-based single father of two daughters, clinical nutritionist, Omega Balancing Coach™, researcher, best-selling author, speaker, podcast and television host, health advisor, NAACP Image Award Nominee, creator of the Diet Free Life methodology, and Chief Nutrition Officer for iCoura Health. He also serves on the Presidential Task Force on Obesity for the National Medical Association and the Health and Product Advisory Board for Zinzino, Inc.

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