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slow brain children

Could Type 1 Diabetes Slow Brain Development in Children?

Since type 1 diabetes occurs when the pancreas produces little to no insulin, it is often diagnosed in childhood when this deficiency become more apparent. The body is unable to naturally manage blood sugar levels since the immune system mistakenly attacks and destroys insulin-producing beta cells. This means that parents must take over this responsibility until children are able to effectively manage their condition on their own.

Many parents are hesitant to overtreat and end up allowing blood sugar levels to remain slightly elevated (hyperglycemia) rather than risk having them drop too low (hypoglycemia). Neither condition is desirable as they can both lead to health complications. The goal is to create a management plan that enables blood sugar levels to remain as normal as possible.

A recent study found that hyperglycemia in children with type 1 diabetes may actually slow brain development and impact brain structure, cognitive function, and sensory processing. The study followed 138 children with type 1 diabetes between the ages of four and seven. Participants had been living with diabetes for an average of 2.4 years. These children were compared to 67 age-matched controls without type 1 diabetes.

After approximately 4.5 years, researchers found that those children with type 1 diabetes had decrements in both full-scale and verbal IQ, which was associated with hyperglycemia and an average HbA1c of 8%. The target goal for children is an HbA1c of less than 7.5%.

However, a larger study found that although full-scale, verbal IQ, and vocabulary were lower in those with T1D, there was no significant difference in processing speed, memory, or learning scores compared to the control group. The brains of children with T1D seemed to compensate for areas where there were challenges, and executive function was similar between groups.

Nelly Mauras, MD, chief of the Division of Endocrinology, Diabetes, and Metabolism at Nemours Children’s Health System and part of the Diabetes Research in Children Network (DirecNet) noted, “We are not suggesting that these youngsters aren’t performing academically. So far, these differences have not translated into functional outcomes in performance, at least not yet.”

Researchers continue to follow these groups in order to gather more information and determine the impact over a longer duration of time. They are interested in learning more about whether advanced technology can make it easier to maintain near normal glucose levels and whether HbA1c guidelines should be lower than 7.5% for children with type 1 diabetes to minimize hyperglycemia.

The Diabetes Research Connection (DRC), though not involved with this study, will continue to follow study progress to see what future comparisons hold and how this may impact treatment options and guidelines for children with type 1 diabetes. Current results may stimulate new research opportunities and increase understanding of the greater impact of T1D on health and development. The DRC provides critical funding for early career scientists to pursue novel research projects related to type 1 diabetes.

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Role of the integrated stress response in type 1 diabetes pathogenesis
In individuals with type 1 diabetes (T1D), the insulin-producing beta cells are spontaneously destroyed by their own immune system. The trigger that provokes the immune system to destroy the beta cells is unknown. However, accumulating evidence suggest that signals are perhaps first sent out by the stressed beta cells that eventually attracts the immune cells. Stressed cells adapt different stress mitigation systems as an adaptive response. However, when these adaptive responses go awry, it results in cell death. One of the stress response mechanisms, namely the integrated stress response (ISR) is activated under a variety of stressful stimuli to promote cell survival. However, when ISR is chronically activated, it can be damaging to the cells and can lead to cell death. The role of the ISR in the context of T1D is unknown. Therefore, in this DRC funded study, we propose to study the ISR in the beta cells to determine its role in propagating T1D.
Wearable Skin Fluorescence Imaging Patch for the Detection of Blood Glucose Level on an Engineered Skin Platform
A Potential Second Cure for T1D by Re-Educating the Patient’s Immune System
L Ferreira
Validating the Hypothesis to Cure T1D by Eliminating the Rejection of Cells From Another Person by Farming Beta Cells From a Patient’s Own Stem Cells
Han Zhu
Taming a Particularly Lethal Category of Cells May Reduce/Eliminate the Onset of T1D
JRDwyer 2022 Lab 1
Can the Inhibition of One Specific Body Gene Prevent Type 1 Diabetes?
Is Cholesterol Exacerbating T1D by Reducing the Functionality and Regeneration Ability of Residual Beta Cells?
Regeneration Ability of Residual Beta Cells
A Call to Question… Is T1D Caused by Dysfunctionality of Two Pancreatic Cells (β and α)?
Xin Tong
Novel therapy initiative with potential path to preventing T1D by targeting TWO components of T1D development (autoimmune response and beta-cell survival)
flavia pecanha