In the not too distant past, patients with type 1 diabetes occupied their side of the diagnosis and management aisle, and those with type 2 diabetes occupied theirs. Patients with type 1 diabetes were generally thin and usually young — some still in diapers, others barely out of high school. Blood drawn from these patients would turn up antibodies that tried, and failed, to keep the body’s immune system from destroying its insulin-creating process.

As for patients with type 2 diabetes, who were virtually all adults in the prime of life, they would test with A1c levels above the norm.

For patients with type 2 diabetes, keeping their insulin resistance in check, generally with metformin at first, would be a lifelong battle. For those with type 1 diabetes, the fight to stay alive would start and stay with insulin.

Type 1 diabetes’ prevalence and incidence stayed the same until the mid-1950s. Since then, the incidence of type 1 diabetes has maintained a consistent upturn, at an average annual rate of 2%-5%. Edwin A.M. Gale in 2002 wrote: “The disease process underlying type 1 diabetes has changed over time and continues to evolve.”

The aisle separating these once presentation-distinct diseases has narrowed. Today, at least 13% of patients with type 1 diabetes also have insulin resistance, which means they are likely being diagnosed with type 2 diabetes upon presentation — as so many patients with type 1 diabetes also show dangerous metabolic syndrome numbers, especially obesity. For patients with type 1 diabetes, metformin isn’t effective in treating insulin resistance as it’s designed to reduce the amount of glucose the liver releases into the bloodstream.

So what happened to blur the phenotypes? Was a susceptibility factor gradually introduced into the environment, or was a protective factor removed, which made targeting the genetically vulnerable to type 1 diabetes easier to do? (A 2022 study looked at type 1 diabetes from a geographic perspective; the disease in patients in Japan, of Caucasian descent, and in Brazil developed from different genetic variations of the same gene complex, called human leukocyte antigen.)

Perhaps the following isn’t scientifically kosher as it lacks evidence-based trial data, (and because this type 1 diabetes surge might involve other factors), but the timing is too exquisite to ignore. In the 1960s, the obesity epidemic began. Since then, the BMIs of those diagnosed with type 1 diabetes have climbed as has the age of onset: at least 50% of those diagnosed with type 1 diabetes today are adults.

“The presence of excess weight is no longer a distinguishing feature between patients with type 1 diabetes and those with type 2 diabetes,” according to a study published in October in the journal Obesity.

“We see the same amount of obesity as in the general population,” said Irl B. Hirsch, MD, medical director, Diabetes Care Center, University of Washington Medical Center, Seattle, and co-author of the study.

A significant factor here, he said, is that “adulthood onset [of type 1] is different, immunity is more benign.” Most patients are misdiagnosed because type 2 is so common. “It’s not on [the physician’s] radar that it could be type 1,” Hirsch said.

Differentiating from type 1 diabetes adult onset and type 2 diabetes as quickly as possible is vital, said Hirsch, because “we are losing precious time to preserve beta cells.” One report from the early 2000s said that at the time of diagnosis, these patients have “considerable remaining beta cell mass.”

These are points that Hirsch wants stressed with primary care physicians (PCPs) because 50% of patients with type 1 diabetes present in adulthood — and overall, 50% of all adults are cared for by PCPs.

“The wait list to see [an endocrinologist] is 6 months. If you live in a large city, you might find [an appointment] quicker…if you live in southwestern Missouri, [for example] you will have to drive hours to see an endocrinologist.”

The recognition of latent autoimmune diabetes in adults also dubbed double diabetes, the term Hirsch prefers, is prominent in the new American Diabetes Association (ADA)’s diabetes guidance expected in early 2026, he said.

“PCPs need to know about treatments, and mitigating obesity is part of this,” he said.

Few Numbers to Consider

In 2001, type 1 diabetes prevalence (per 1000 youths) for those 19 years or younger was 1.48. By 2017, that figure was 2.15.

An October 2025 study of 388 patients in Portugal with type 1 diabetes showed nearly half had overweight or obese. Overall, these patients, compared with those with normal weight, had higher: waist circumferences, systolic and diastolic blood pressure, and triglyceride levels. The higher the waist circumference, the worse the metabolic syndrome numbers. The higher the BMI, the higher the A1c.

A significant percentage of adult patients with type 1 diabetes take anti-glycemic medications; a significant percentage of teens and young adults with the disease show signs of at least one comorbidity.

In type 1 diabetes, weight gain increases insulin need because weight gain increases insulin resistance. A 2024 study of 1969 adults with a A1c baseline of < 8.0% and who gained at least 20 lb in 5 years were taking at least 49 units more of daily insulin than at baseline.

Those with double diabetes will be insulin dependent within 3-5 years.

Diagnosis and Treatment

It isn’t easy to diagnose double diabetes.

According to Type 1 Trial Disease Net, getting autoantibody test results to determine if a patient has type 1 diabetes can take at least a month. And the results are not always reliable as at least 10% of patients with type 1 diabetes will be negative for antibodies.

“If the result is borderline positive, it won’t get you to a type 1 diagnosis,” Hirsch said.

But it will be another month of waiting for results, another month before determining appropriate treatment. The tests normally taken are glutamic acid decarboxylase (GAD), insulinoma-associated antigen 2, and zinc transporter 8. They are all markers indicating an autoimmune attack on pancreatic beta cells. In the Obesity study, the authors wrote that insulin is appropriate for any patient with uncontrolled glycemic levels and a positive GAD test.

One test that is fairly reliable is the C-peptide test. The level of C-peptide found in the blood [or urine] is related to the amount of insulin released by the pancreas. The more C-peptide found, odds are the patient has type 2 diabetes.

Hirsch stresses taking a thorough family history, including interviewing the family members. He looks for autoimmune thyroid diseases as well as Addison and celiac disease. He asks if vitiligo is in the family. “It all goes with type 1.”

And meeting the family can indicate if overweight and obesity run in the family. A referred patient “can come in with [diagnosed] type 2, who has responded to metformin, maybe is on sulfonylureas,” Hirsch said. The patient’s antibodies “are typed, and the antibodies are through the roof.”

Other comparisons to make: complications. In a 2017 study looking at patients with type 1 and type 2 diabetes diagnosed before adulthood, the four biggest standouts were diabetic kidney disease, arterial stiffness, hypertension, and peripheral neuropathy. Those with type 2 diabetes were at least twice more than their type 1 diabetes counterparts to have these comorbidities.

Coming up with a treatment plan isn’t easy either. Compared with type 2 diabetes, type 1 diabetes has very few approved medications: injectable or inhaled insulin and pramlintide, which is an analogue of the hormone amylin. GLP-1s for patients with type 1 diabetes are in clinical trials.

So the question becomes whether type 2 diabetes medications are friend or foe to those with double diabetes.

Two on the better-think-twice side are metformin and SGLT2 inhibitors.

Yes, metformin reduces weight and the daily insulin dosage but raises the risk for hypoglycemia. Jessica Bartfield, MD, clinical associate professor, Weight Management Center, Wake Forest University School of Medicine, Winston-Salem, North Carolina, cautioned against the SGLT2 inhibitors if there is high suspicion for type 1 diabetes.

“Overall, the benefits of obesity treatment with these medications is limited and I would try to utilize other medications first.” The SGLT-2 inhibitors increase the risk for diabetic ketoacidosis; The ADA says diabetic ketoacidosis is rare in those with type 2 diabetes.

Then there is the weight issue. Establishing a diet for someone with type 1 diabetes invites possible glycemic control problems. Patients with type 1 diabetes need counseling in this regard.

And counseling is warranted for those with type 2 diabetes. Bartfield, a co-author of the Obesity study, said the “very strong genetic component to obesity and type 2 diabetes” makes it critical to “counsel patients about this etiology to help them understand why they may be more susceptible to weight gain — patients too frequently view obesity as a lack of willpower.”

Patients with type 2 diabetes who take insulin or oral hypoglycemics “face higher risk of hypoglycemia and need to decrease their insulin dose and stop oral hypoglycemics when starting obesity treatment/active weight loss,” she said.

Patients with type 1 diabetes will likely need greater specificity and attention to insulin requirements, signs/symptoms of hypoglycemia, and macronutrient intake.

But, she said, regardless of whether a patient has type 1 diabetes, type 2 diabetes, or both, if they also have overweight/obesity the nutrition plan needs to “provide an energy deficit of about 500-700 calories per day for weight loss.”

Hirsch reported research with Tandem, Dexcom, and Mannkind and a consulting role with Abbott, Roche, and Hagar. Bartfield reported no disclosures.