Diabetic encephalopathy is a condition many have not heard of, but it is a silent threat to those with diabetes.
Diabetic encephalopathy refers to brain damage caused by diabetes (both type 1 and type 2). The term was coined in 1950 to describe cognitive issues resulting from diabetes.
Encephalopathy is a broad term for brain damage due to various diseases. In a study published in the Journal of Alzheimer’s Disease (2005), the dysregulation of insulin and insulin-like growth factor (IGF) leading to dementia, such as Alzheimer’s disease, was first proposed as “type 3 diabetes”.
Many times, diabetic encephalopathy leading to the precipitation of Alzheimer’s is often loosely termed as type 3 diabetes.
The development and causes of type 1 and type 2 diabetes-related encephalopathy are different. In long-standing type 2 diabetes, Alzheimer’s disease is often linked to insulin resistance, where there is too much insulin (hyperinsulinemia) and sugar in the blood (hyperglycemia).
This is often accompanied by other health issues like high cholesterol levels (hypercholesterolemia), which can harm your heart. Type 2 diabetes-related encephalopathy is often associated with high blood pressure (hypertension) and obesity.
Conversely, type 1 diabetic encephalopathy can affect learning abilities, hinder intellectual development, and make it difficult for one to remember things. These challenges can significantly affect performance at school and work.
The blood-brain barrier (BBB) serves as a protective shield of tiny blood vessels lined with endothelial cells. It keeps harmful substances in the blood away from the brain while allowing essential nutrients from the bloodstream to pass through. However, uncontrolled diabetes can weaken BBB over time, making it easier for harmful substances to enter the brain. Clinical studies have confirmed this by showing that people with diabetes may experience issues with blood vessels in their brains.
Though the precise mechanism of disease manifestation is mainly unknown, on a molecular level, studies have established enlarged gaps in specialized structures of BBB known as “tight junctions” in diabetes encephalopathy with tandem loss of tight junction proteins such as ZO-1 and occludin. These tight junctions are like security guards that keep bad stuff out of the brain.
Oxidative and nitrosative stress, harmful molecules that damage cells and tissues, play a significant role in causing diabetic brain problems (diabetic encephalopathy). Malfunctioning brain astrocyte cells in the brain and spinal cord contribute to weakening the brain’s protective barrier, potentially leading to brain swelling in uncontrolled diabetes.
Lactate is a chemical that our bodies make when we digest food. When there’s an excess of lactate, it can be linked to diabetes.
Astrocytes produce lactate and it can accumulate in the brain, especially when insulin isn’t functioning properly. This may happen when the body has trouble using insulin, which is linked to diabetes. So, all these things together can make brain problems worse in diabetics.
Diabetic encephalopathy causes cognitive impairments and involves issues with blood-brain barrier, tight junctions, oxidative stress, and brain astrocyte cells. For those with long-standing type 2 diabetes, insulin resistance and high blood sugar levels are common culprits, often accompanied by related health concerns like high cholesterol, hypertension, and obesity.
Type 1 diabetic encephalopathy can affect learning, intellectual development, and memory, affecting daily life. Understanding the importance of controlling diabetes, adopting a healthy lifestyle, and managing blood sugar levels is crucial in preventing or delaying the onset of diabetic encephalopathy. Recent studies suggest that omega 3 and 6 polyunsaturated fatty acids (PUFA) supplementation may hold promise in ameliorating diabetic encephalopathy.
While diabetic encephalopathy is a silent threat, knowledge and proactive measures can empower individuals to protect their brain health in the face of diabetes.
(The writer is a US-based medical scientist)
