What is Latent Autoimmune Diabetes in Adults (LADA, Type 1.5)?

LADA, sometimes called type 1.5 diabetes, is an adult-onset autoimmune diabetes that overlaps features of type 1 and type 2.

Diabetes

Latent Autoimmune Diabetes in Adults (LADA, Type 1.5)

2025-09-14

Intro

Latent Autoimmune Diabetes in Adults (LADA) — sometimes called “type 1.5 diabetes” — is a form of autoimmune diabetes that appears in adulthood.
It looks like type 2 at first, but behaves more like type 1 over time. Recognizing it matters: the wrong diagnosis can delay proper treatment and increase complications.

Key Points

Autoimmune diabetes that develops in adults, usually >30 years.
Often misdiagnosed as type 2, leading to treatment delays.
Autoantibodies (especially GAD) confirm diagnosis.
Progression is slower than type 1, but most eventually need insulin.
Early insulin therapy may help preserve pancreatic function; sulfonylureas can speed up decline.

Background

Historically, type 1 diabetes was called “juvenile diabetes,” because it was usually recognized in children and teenagers.
We now know type 1 can start at any age — even in people in their 60s. The “juvenile vs. adult” labels are outdated.

LADA emerged as a concept in the 1990s to describe adults with autoimmune diabetes that didn’t fit neatly into type 1 or type 2.
The Immunology of Diabetes Society defines it as:

Adult onset (usually >30 years)
At least one positive islet autoantibody
No insulin needed for the first 6 months after diagnosis【NCBI†source】

Causes or Mechanisms

Immune attack: The body’s immune system targets insulin-producing beta cells.
Slower progression: Compared with type 1, the autoimmune attack is less aggressive, giving the illusion of “type 2” for a time.
Overlap: Some patients also show features of insulin resistance, blurring lines further.

Diagnosis

Tests used:

Autoantibodies: The most common in LADA are GAD antibodies.
GAD stands for Glutamic Acid Decarboxylase, an enzyme found in pancreatic beta cells.
When the immune system produces antibodies against GAD, it signals autoimmune diabetes.
Other useful markers include IA-2, ZnT8, and insulin autoantibodies.
C-peptide: Measures insulin production; often intermediate at diagnosis, declining gradually.
Clinical clues: Normal or low BMI, family/personal history of autoimmune disease, poor or short-lived response to oral diabetes drugs.

Key Difference in Diagnosis

Type 1 diabetes (classic): Usually antibody positive, rapid onset, low/absent C-peptide. Often diagnosed clinically without waiting for antibody tests.

LADA (Type 1.5): Antibody positive, slower progression, adult onset. Antibody testing is critical to avoid mislabeling as type 2.

Type 2 diabetes: No autoimmune antibodies. Driven by insulin resistance. If antibodies are present, it’s not true type 2.

🔑 Rule of thumb: Antibodies = autoimmune diabetes (type 1 or LADA). No antibodies = type 2.

Differences at a Glance

Feature	Type 1	Type 2	LADA (“Type 1.5”)
Typical onset	Childhood/teens (but any age possible)	>40 years	30–50 years, but variable
Cause	Autoimmune	Insulin resistance ± beta-cell decline	Autoimmune, slower pace
Autoantibodies	Present	Absent	Present (esp. GAD)
C-peptide	Very low at diagnosis	Normal/high	Intermediate; declines
Body type	Often lean	Often overweight	Often lean/normal
Insulin need	Immediate	Years (or never)	Usually within years
Oral meds response	None	Often effective	Poor; sulfonylureas hasten decline
Other autoimmune disease	Common	Rare	Common

Honeymoon Phase vs. LADA

Honeymoon phase (type 1):

Short remission after diagnosis when some insulin is still made.
Lasts months to a few years.
Always temporary.

LADA:

Not a temporary phase but an entire disease course.
The autoimmune attack is slower, so people may manage for years without insulin.
Eventually, insulin is required — but later than in classic type 1.

Treatment / Options

Insulin: Evidence suggests early insulin can protect remaining beta cells and improve control【ADA†source】.
Sulfonylureas: Not recommended; they accelerate beta-cell decline.
Other agents: DPP-4 inhibitors, GLP-1 receptor agonists, or thiazolidinediones show promise in small studies, often alongside insulin.
Lifestyle: As with type 2, diet, exercise, and cardiovascular risk management are essential.

Myth Buster: “Does insulin make the pancreas stop working?”

No. In LADA, beta cells fail because the immune system is attacking them, not because insulin “makes them lazy.”
In fact, insulin can reduce stress on surviving cells and may preserve their function longer【Cochrane†source】.

Risks / Prognosis

Most patients require insulin within a few years of diagnosis.
Risks of complications (heart, eyes, kidneys, nerves) are similar to type 1 and type 2.
Delayed recognition increases the risk of poor blood sugar control and earlier complications.

FAQ

Q: How is LADA different from type 1 diabetes?
A: Both are autoimmune, but LADA develops later and progresses more slowly.

Q: How is it different from type 2?
A: Unlike type 2, LADA involves autoimmune destruction of beta cells, confirmed by antibodies.

Q: Is it just the honeymoon phase of type 1?
A: No. The honeymoon phase is temporary; LADA is a long-term, slower-progressing autoimmune disease.

Q: Won’t taking insulin make the pancreas stop working faster?
A: No. Insulin doesn’t shut down the pancreas — the immune system does. Early insulin may actually preserve function.

Q: Who should be tested?
A: Adults with “type 2 diabetes” who are not overweight, respond poorly to oral drugs, or have other autoimmune conditions.