New research presented at the Annual Meeting of the European Association for the Study of Diabetes sheds light on a concerning issue – the correlation between food insecurity and severe hypoglycaemia in adults with diabetes. As the cost of living continues to rise, the results of this study carry significant implications for public health and diabetes management.

Severe Hypoglycaemia: A Serious Concern: Severe hypoglycaemia is a critical condition characterized by dangerously low blood sugar levels, which can lead to loss of consciousness, seizures, coma, and even death. Typically, this condition is rare in individuals with diabetes, unless they are taking insulin or secretagogues, two commonly prescribed classes of diabetes medications.

The Alarming Connection: Data analysis from the United States has revealed a striking link between food insecurity and severe hypoglycaemia. Those who struggle to afford food were found to be 2.2 times more likely to experience severe hypoglycaemic events. While the impact of food insecurity on health has been recognized, this study provides valuable real-world insights into its effect on severe hypoglycaemia rates.

A Groundbreaking Study: Dr. Alexandria Ratzki-Leewing and her colleagues conducted a groundbreaking investigation using data from the iNPHORM study, a 12-month prospective panel survey of hypoglycaemia risk in the real world. Their analysis involved 1,001 adults with either type 1 or type 2 diabetes who had been treated with insulin and/or secretagogues for at least one year. The participants were diverse, with an average age of 51 years and a median diabetes duration of 12 years.

Key Findings: The study employed a screening question to identify individuals who had experienced food insecurity in the past year. Shockingly, approximately one in five participants reported food insecurity, with similar rates observed in both type 1 and type 2 diabetes patients. Among those who experienced food insecurity, over half had encountered at least one Level 3 hypoglycaemic event in the past year.

The Impact of Food Insecurity: Multivariable regression analysis, adjusting for potential confounders such as age, income, insurance coverage, living arrangements, and diabetes type, revealed a compelling result. Those who had faced food insecurity were found to have more than doubled the rate of severe hypoglycaemia events compared to those without food insecurity.

Recommendations and Implications: Dr. Ratzki-Leewing emphasized the importance of this study’s findings, calling for increased vigilance among clinicians when managing individuals with food insecurity who are prescribed insulin or secretagogues. Additionally, she stressed the need for public health strategies to address food insecurity, as it plays a pivotal role in preventing severe hypoglycaemia and its severe consequences.

The Short and Long-Term Impact: Severe hypoglycaemia can result in immediate dangers such as seizures and coma, as well as long-term complications including nerve and heart damage, and even premature mortality. The economic costs associated with these health effects are substantial. Thus, addressing food insecurity not only reduces the burden of diabetes-related severe hypoglycaemia but also improves overall health and economic well-being.

This groundbreaking study reveals the urgent need to address food insecurity among adults with diabetes taking insulin or secretagogues. By doing so, we can mitigate the risks of severe hypoglycaemia and its dire consequences, ultimately improving the health and well-being of individuals with diabetes. In a world where the cost of living is on the rise, these findings resonate not only in the United States but also globally.

Can not eating enough cause hypoglycemia? Yes, not eating enough can indeed cause hypoglycemia, especially in individuals with diabetes who are taking medications like insulin or secretagogues. When you skip meals or consume inadequate amounts of carbohydrates, your blood sugar levels can drop significantly, leading to hypoglycemia. This condition occurs when there isn’t enough glucose (sugar) in your bloodstream to provide energy to your body’s cells and organs.

What can happen with severe hypoglycemia? Severe hypoglycemia can have serious consequences. It can lead to symptoms such as confusion, dizziness, shakiness, irritability, and, in extreme cases, loss of consciousness, seizures, coma, and even death if left untreated. Severe hypoglycemia is a medical emergency and requires immediate intervention, typically in the form of consuming a fast-acting source of glucose, such as fruit juice or glucose gel, to raise blood sugar levels.

Why is diabetes associated with food insecurity? Diabetes is associated with food insecurity for several reasons. People with diabetes often require special diets that can be more expensive, and the cost of diabetes medications and supplies can be a financial burden. Additionally, managing diabetes may require regular meals and snacks, making it challenging for individuals who cannot afford an adequate and consistent food supply. Food insecurity can lead to irregular eating patterns and, as shown in the mentioned study, is associated with a higher risk of severe hypoglycemia in people with diabetes.

How does hypoglycemia lead to increased hunger and food cravings? Hypoglycemia can lead to increased hunger and food cravings as a natural response by the body to restore blood sugar levels to normal. When your blood sugar drops too low, your body perceives it as an energy crisis. In response, it releases hormones like adrenaline and glucagon to raise blood sugar levels. These hormones can trigger feelings of hunger and cravings for carbohydrate-rich foods because carbohydrates are a quick source of glucose. This phenomenon is the body’s way of trying to resolve the hypoglycemic state and ensure a steady supply of energy to the brain and body.

Researchers have unveiled a groundbreaking method to peer into the intricate world of lipoproteins in the central nervous system, shedding light on the genetic underpinnings of Alzheimer’s disease. This discovery promises to revolutionize our understanding of the brain’s inner workings.

In a remarkable revelation, scientists have discovered that the lipoproteins in our nervous system, akin to the well-known “good cholesterol” HDL particles in our bloodstream, are far more diverse than previously imagined. Over 300 different proteins, organized into at least 10 different families, have been detected on these particles. These lipoproteins are brimming with proteins that influence crucial processes like wound healing, immune responses, and the development of neurons vital for cognitive function.

At the forefront of these discoveries is apolipoprotein E, or APOE, which reigns as the most prevalent protein in these particles. Interestingly, APOE4, one of the three commonly studied forms of APOE, elevates the risk of Alzheimer’s disease. A single copy of the APOE4 gene increases the risk of dementia by fourfold while possessing two copies amplifies the vulnerability by a staggering twelvefold.

These remarkable findings, published in Science Advances on August 30, have been spearheaded by John Melchior, a protein biochemist at the Department of Energy’s Pacific Northwest National Laboratory. Melchior, a prominent figure in lipoprotein research, carries two copies of the APOE4 gene, adding a personal dimension to his quest to decipher the protein’s role in the nervous system.

The nervous system’s lipoproteins have long been shrouded in mystery, as they are less prevalent than their circulatory system counterparts. In the bloodstream, lipoproteins such as “good” HDL and “bad” LDL are abundant and easily detectable. However, their actions and presence in the nervous system have remained enigmatic.

Within the central nervous system, APOE serves as a linchpin, not only holding fats and proteins together but also facilitating the transport of nutrient-rich lipids and groups of molecular collaborators. These specialized proteins contribute to cell repair, gene regulation, and the processing of amyloid beta, a molecule linked to dementia development. While APOE plays a pivotal role, something goes awry in individuals with one or two copies of APOE4, leading to dementia. The precise mechanisms remain elusive.

Researchers speculate that APOE4 may also play a role in other neurological conditions, including Parkinson’s and Huntington’s diseases, multiple sclerosis, amyotrophic lateral sclerosis, and traumatic brain injury.

Detecting lipoproteins in the nervous system posed a unique challenge due to their scarcity. The research team devised a novel fluorescent technology to tag lipoproteins in spinal fluid, enabling the study of minute quantities of cerebrospinal fluid.

By analyzing just one-third of a milliliter of spinal fluid, researchers uncovered a staggering 303 different proteins across various particle families. Most of these proteins had never been observed on nervous system lipoproteins before.

The future holds immense promise, as this technology could be shared with clinicians to delve into conditions like Alzheimer’s, multiple sclerosis, and Parkinson’s disease. Profiling lipoproteins in these conditions may yield insights into disease pathology and potential treatment targets.

This groundbreaking study was made possible through collaborative efforts involving researchers from various institutions. It underscores the importance of interdisciplinary research in unraveling complex scientific mysteries.

As the quest to understand Alzheimer’s and other neurological diseases gains momentum, early support from the National Institutes of Health and innovative technologies may pave the way for transformative discoveries.

1. Which lipoprotein is associated with Alzheimer’s disease?
   • Apolipoprotein E (apoE), particularly the APOE4 gene variant, is closely linked to an increased risk of Alzheimer’s disease. Possessing one copy of APOE4 raises the risk fourfold while having two copies multiplies it by twelve.
2. What is the role of apoE in Alzheimer’s disease?
   • ApoE, a protein involved in lipid metabolism, plays a critical role in Alzheimer’s disease. The APOE4 gene variant impacts the brain’s lipid metabolism and contributes to the accumulation of harmful substances, increasing the risk of Alzheimer’s.
3. Is there a link between high cholesterol and Alzheimer’s?
   • While a direct link between high cholesterol and Alzheimer’s remains uncertain, disruptions in cholesterol metabolism in the brain may be associated with the disease. Abnormal cholesterol levels can affect brain function and potentially contribute to Alzheimer’s progression.
4. What is the Alzheimer’s causing protein?
   • The primary protein associated with Alzheimer’s disease is amyloid beta. This protein forms plaques in the brain, disrupting neuronal function, triggering inflammation, and contributing to cognitive decline in individuals with Alzheimer’s.

Understanding the complex interplay between lipoproteins, apoE, cholesterol, and amyloid beta is crucial for unraveling the mysteries of Alzheimer’s disease. This knowledge holds promise for future treatments and preventive strategies.