In a small, early study, a vaccine for type 1 diabetes helped preserve the body's natural production of insulin, at least in a subset of newly diagnosed patients.
In patients with type 1 diabetes, the body's immune system attacks the beta cells in the pancreas that produce insulin, a hormone that's necessary for cells to absorb glucose from the bloodstream. These patients need lifelong insulin injections to stay alive.
And because so many hidden factors inside the body can affect how much insulin a person needs, people who are insulin-dependent often have high and low blood sugar. High blood sugar, or hyperglycemia, damages the organs over the long term, while low blood sugar, or hypoglycemia, can lead to seizures or death in the short term.
In the current study, the researchers wanted to test whether a vaccine might be able to stop or slow the destruction of these insulin-producing beta cells.
"Studies have shown that even an extremely small production of insulin in the body is highly beneficial for patient health," lead author Dr. Johnny Ludvigsson, a senior professor in the Department of Biomedical and Clinical Sciences at Linköping University in Sweden, said in a statement. "People with diabetes who produce a certain amount of insulin naturally do not develop low blood sugar levels, hypoglycemia, so easily."
Ludvigsson and his team developed a vaccine made from glutamic acid decarboxylase (GAD), a protein anchored to the surface of beta cells that many people with type 1 diabetes form antibodies against. (The treatment is called GAD-alum).
People with certain versions of immune system genes, known as human leukocyte antigen (HLA) genes, are at higher risk of developing type 1 diabetes. Several HLA types increase the risk of the autoimmune disorder, but one genetic variant, known as "HLA-DR3-DQ2," exposes a form of the GAD protein (GAD65) to the immune system on the surface of beta cells, according to the statement. This triggers the immune system to produce antibodies against the protein and target the beta cells for destruction.
The researchers wanted to see if a vaccine that exposed the body to more GAD would help the immune system better tolerate the body's natural GAD65 and thus stop attacking the insulin-producing cells.
For the phase 2 clinical study, the researchers recruited 109 patients between the ages of 12 and 24 who had been diagnosed with type 1 diabetes within the past six months. About half of the patients carried the HLA-DR3-DQ2 gene variant.
The researchers divided the participants into two groups: Half of the participants, assigned randomly, were given three shots of the vaccine into their lymph nodes, each one month apart, and the other half were given a placebo.
The researchers analyzed how much natural insulin the participants produced at the start of the study and after 15 months. They also analyzed changes to long-term blood sugar levels and how much supplementary insulin they needed to take daily.
As a whole, there was no difference in the treatment and placebo groups. But the subset of patients who had the HLA-DR3-DQ2 variant did not lose insulin production as quickly as other patients did.
"Treatment with GAD-alum seems to be a promising, simple and safe way to preserve insulin production in around half of patients with type 1 diabetes, the ones who have the right type of HLA," Ludvigsson said. "This is why we are looking forward to carrying out larger studies, and we hope these will lead to a drug that can change the progress of type 1 diabetes."
The study, published online May 21 in the journal Diabetes Care, was funded by the pharmaceutical company Diamyd Medical AB, which was also involved in planning and collecting data in the trial, the Swedish Child Diabetes Foundation and the Swedish Diabetes Foundation.
Originally published on Live Science.