Type 1 Diabetes Epidemiology Revisited - Who Gets Diabetes? - Diabetes

Type 1 Diabetes Epidemiology Revisited

Parents of children with newly diagnosed Type 1 diabetes invariably want to know whytheir children developed diabetes. On many occasions, several newly diagnosed patients actually live in the same neighborhoods, prompting families to wonder if there is something in the environment responsible for causing diabetes. At present the working theory is that Type 1 diabetes is caused by a combination of two factors. (1) A genetic predisposition or risk (low, moderate, high) for the possibility of the development of Type 1 diabetes that is located in HLA region of chromosome six and (2) a trigger that causes the killer T cells to attack the beta islet cells of the pancreas. We currently believe that infections (i.e. mumps, rubella, coxsackie b virus, and influenza) are one type of trigger based on extensive, evidence-based research.

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According to the authors, this pattern of occurrence is consistent with the involvement of exogenous agents, such as infection, that may demonstrate epidemicity. The control, influenza infection, was also noted to demonstrate temporal clustering at levels of months, quarters of a year, and flu seasons. Several referenced studies have reported “seasonality” in dates of diagnosis of pediatric Type 1 diabetes, noting peaks in October to January and valleys in June to August for Diabetes Centers in the Northern Hemisphere. 

More than twenty years of registration of type 1 diabetes in Sardinian children: temporal variations of incidence with age, period of diagnosis and year of birth

More than twenty years of registration of type 1 diabetes in Sardinian children: temporal variations of incidence with age, period of diagnosis and year of birth

In conclusion, incidence increased over time, the increase tended to level off in more recent years by calendar period but not by birth cohort, with some evidence of a stronger increase among girls than boys. Should the increase be attributable to the effects of some perinatal environmental factor, this would mean that such a factor has started affecting females before males.

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WEDNESDAY, June 26 (HealthDay News) -- A new type of vaccine may stop the autoimmune attack that occurs in people with type 1 diabetes, researchers report.

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Instead of increasing the immune system's activity like the polio or influenza vaccine does, the new vaccine turns off a portion of the immune response, acting as a reverse vaccine. The researchers were able to isolate a part of the immune response that only seems to be involved with type 1 diabetes, according to the study. That means the vaccine likely wouldn't have the risks that medications that suppress the immune system do.

"We were able to destroy the rogue cells that are attacking the insulin-producing cells without destroying any other part of the immune system, and that's truly exciting," said senior study author Dr. Lawrence Steinman, a professor of pediatrics and neurology and neurological sciences at Stanford University School of Medicine.

"Once the immune attack is stopped, I believe there's great potential for recovery in the beta cells," Steinman added.

Beta cells in the pancreas produce the hormone insulin. In people with type 1 diabetes, it's believed that the immune system mistakenly destroys the healthy beta cells, leaving the person with no or too little insulin.

Insulin is a crucial hormone because it's involved in the metabolism of the carbohydrates. It allows the glucose (sugar) from those carbohydrates to fuel the cells in the body and brain. Without enough insulin, a person will die. That's why people with type 1 diabetes must take multiple daily injections of insulin, or deliver insulin through a catheter inserted under the skin that's attached to an insulin pump.

The vaccine was designed by changing a piece of immune-system DNA so that it would shut down the immune system's response to signals in the body that have previously triggered the mistaken destruction of beta cells. These signals come from fragments of a protein (peptides) called proinsulin, which is found on the surface of beta cells. Proinsulin is a precursor to insulin.

"We just wanted to throw the off switch for the one cell being attacked," Steinman explained.

The researchers recruited 80 volunteers diagnosed with type 1 diabetes during the past five years. They were randomly placed in one of five groups. Four groups received various doses of the vaccine, and the fifth group received placebo injections. Shots were given weekly for 12 weeks.

No one in the study was able to stop using insulin. "That's a possible goal, but it's too early to start saying cure," Steinman noted.

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No serious adverse events occurred during the trial.

Dr. Richard Insel, chief scientific officer at JDRF (formerly the Juvenile Diabetes Research Foundation), said, "The encouraging results from this initial trial ... in established type 1 diabetes not only demonstrated safety, evidence during the vaccine dosing period showed preservation of beta cell function, a decrease in detectable immune cells [that likely attack the beta cells], and a relationship between the two."

He added that further clinical trials will be needed to figure out the optimal dose for vaccine efficacy and safety.

The study was funded by Bayhill Therapeutics, which helped to develop the vaccine. The JDRF provided funding for the trial, as did the Iacocca Family Foundation.

Steinman said it's too soon to know how the vaccine might work in the real world. It's not clear how often someone would need to be given the vaccine, and how well the body might recover its ability to produce insulin once the autoimmune attack has stopped. It's also not clear if the vaccine might be more effective in people who've recently developed the disease, or in people who have a high risk of developing type 1 diabetes.

Steinman said he hopes to have the next trial under way in a year or so.

The study appeared online June 26 in the journal Science Translational Medicine.

Dr. Joel Zonszein, director of the clinical diabetes center at Montefiore Medical Center in New York City, expressed more caution about the vaccine. "The immune response in type 1 diabetes is very complex, and we've been burned many times with the idea of a vaccine for type 1 diabetes," he noted.

"Because this is a new technology -- a DNA-based vaccine -- I think it would have to be approved for use in something like advanced cancer first, because it may do good things and bad things.," Zonszein said. "We don't know, so we don't want to give it to otherwise healthy people with type 1 diabetes until we know what the potential for harm is."

Still, he said that the new vaccine is an exciting discovery. "This is a welcome discovery. It helps us to understand the immune process better," he said.

SOURCES: Lawrence Steinman, M.D., professor, pediatrics, neurology and neurological sciences, Stanford University School of Medicine, California; Richard Insel, M.D., chief scientific officer, JDRF, New York City; Joel Zonszein, M.D., director, clinical diabetes center, Montefiore Medical Center, New York City; June 26, 2013, Science Translational Medicine

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Diabetes tipo 1 e as infeções respiratórias | ALERT® ONLINE - PT

Diabetes tipo 1 e as infeções respiratórias | ALERT® ONLINE - PT

As infeções respiratórias durante a infância podem ser um fator de risco para o desenvolvimento da diabetes tipo 1, sugere um estudo publicado no “JAMA Pediatrics”.

A incidência da diabetes tipo1 tem aumentado em todo o mundo. Apesar da etiologia desta doença ainda não ser bem conhecida, as infeções têm sido apontadas com fator ambiental importante.

Neste estudo, os investigadores do Institute of Diabetes Research, na Alemanha, propuseram- se a determinar se a exposição precoce de curta duração ou a exposição acumulada a episódios de infeção e febre durante os três primeiros anos de vida estavam associados com o início do desenvolvimento de anticorpos contra as células do pâncreas, em crianças com risco aumentado de diabetes tipo 1.

“Verificámos que as infeções na infância, especialmente no primeiro ano de vida, são um fator de risco para o desenvolvimento da diabetes tipo1. Foram também encontradas algumas evidências dos efeitos de curto prazo dos eventos infeciosos no desenvolvimento da autoimunidade, enquanto a exposição cumulativa por si só não parece ser a causa”, revelaram, em comunicado de imprensa, os autores do estudo.

Para o estudo os investigadores contaram com a participação de 148 crianças que apresentavam um elevado risco de diabetes tipo 1, as quais tinham sido alvo de 1.245 infeções documentadas durante os três primeiros anos de vida.

O estudo apurou que as infeções respiratórias ocorridas no primeiro de vida estavam associadas com um aumento da taxa de risco da seroconversão dos autoanticorpos produzidos contra as células do pâncreas.

Durante o segundo ano de vida, não foram detetadas associações significativas. Um maior número de infeções respiratórias nos seis meses anteriores à seroconversão dos autoanticorpos também foi associado a um aumento da taxa de risco.

“As estratégias de prevenção contra a diabetes tipo 1 deverão focar-se na vacinação contra agentes infeciosos específicos. Infelizmente, não foi possível identificar um único agente infecioso que poderá ser útil no desenvolvimento da diabetes tipo 1. Os nossos resultados sugerem um possível envolvimento das infeções do trato respiratório superior, especificamente da rinofaringite aguda”, concluem os investigadores.

ALERT Life Sciences Computing, S.A.