The Role of Natural Antioxidant Products That Optimize Redox Status in the Prevention and Management of Type 2 Diabetes.

The worldwide prevalence of type 2 diabetes (T2D) and prediabetes is rapidly increasing, particularly in children, adolescents, and young adults. Oxidative stress (OxS) has emerged as a likely initiating factor in T2D. Natural antioxidant products may act to slow or prevent T2D by multiple mechanisms, i.e., (1) reducing mitochondrial oxidative stress, (2) preventing the damaging effects of lipid peroxidation, and (3) acting as essential cofactors for antioxidant enzymes. Natural antioxidant products should also be evaluated in the context of the complex physiological processes that modulate T2D-OxS such as glycemic control, postprandial OxS, the polyol pathway, high-calorie, high-fat diets, exercise, and sleep. Minimizing processes that induce chronic damaging OxS and maximizing the intake of natural antioxidant products may provide a means of preventing or slowing T2D progression. This "optimal redox" (OptRedox) approach also provides a framework in which to discuss the potential benefits of natural antioxidant products such as vitamin E, vitamin C, beta-carotene, selenium, and manganese. Although there is a consensus that early effective intervention is critical for preventing or reversing T2D progression, most research has focused on adults. It is critical, therefore, that future research include pediatric populations.

Oxidative Stress in Type 2 Diabetes: The Case for Future Pediatric Redoxomics Studies.

Considerable evidence supports the role of oxidative stress in adult type 2 diabetes (T2D). Due to increasing rates of pediatric obesity, lack of physical activity, and consumption of excess food calories, it is projected that the number of children living with insulin resistance, prediabetes, and T2D will markedly increase with enormous worldwide economic costs. Understanding the factors contributing to oxidative stress and T2D risk may help develop optimal early intervention strategies. Evidence suggests that oxidative stress, triggered by excess dietary fat consumption, causes excess mitochondrial hydrogen peroxide emission in skeletal muscle, alters redox status, and promotes insulin resistance leading to T2D. The pathophysiological events arising from excess calorie-induced mitochondrial reactive oxygen species production are complex and not yet investigated in children. Systems medicine is an integrative approach leveraging conventional medical information and environmental factors with data obtained from "omics" technologies such as genomics, proteomics, and metabolomics. In adults with T2D, systems medicine shows promise in risk assessment and predicting drug response. Redoxomics is a branch of systems medicine focusing on "omics" data related to redox status. Systems medicine with a complementary emphasis on redoxomics can potentially optimize future healthcare strategies for adults and children with T2D.

Pediatric diabetic ketoacidosis presenting with Streptococcus intermedius brain abscess.

OBJECTIVES: Report a novel case of new-onset type 1 diabetes in a pediatric patient presenting with DKA and concurrent Streptococcus intermedius brain abscess. CASE PRESENTATION: The following case report is that of a previously healthy 12 year-old girl presenting with new-onset type 1 diabetes with mild diabetic ketoacidosis and subsequently found to have a brain abscess. Over the course of her hospital stay, she developed seizures and was found to have a 1.3 × 1.0 × 1.2 cm right frontal parasagittal mass culture-positive for S. intermedius. Neurologic symptoms were unmasked once insulin treatment was initiated and ketosis improved, supporting the relationship between therapeutic ketosis and the management of medication-refractory epilepsy. CONCLUSIONS: This case both supports the relationship between therapeutic ketosis and the management of medication-refractory epilepsy and highlights the need to carefully consider comorbid conditions in patients with DKA and new onset neurological symptoms.

Reliability of Trained Dogs to Alert to Hypoglycemia in Patients With Type 1 Diabetes.

BACKGROUND: We examined the reliability of trained dogs to alert to hypoglycemia in individuals with type 1 diabetes. METHODS: Patients with type 1 diabetes who currently used diabetes alert dogs participated in this exploratory study. Subjects reported satisfaction, perceived dog glucose sensing ability and reasons for obtaining a trained dog. Reliability of dog alerts was assessed using capillary blood glucose (CBG) and blinded continuous glucose monitoring (CGM) as comparators in 8 subjects (age 4-48). Hypoglycemia was defined as CBG or CGM <70 mg/dL. RESULTS: Dog users were very satisfied (8.9/10 on a Likert-type scale) and largely confident (7.9/10) in their dog's ability to detect hypoglycemia. Detection of hypoglycemia was the primary reason for obtaining a trained dog. During hypoglycemia, spontaneous dog alerts occurred at a rate 3.2 (2.0-5.2, 95% CI) times higher than during euglycemia (70-179 mg/dL). Dogs provided timely alerts in 36% (sensitivity) of all hypoglycemia events (n = 45). Due to inappropriate alerts, the PPV of a dog alert for hypoglycemia was 12%. When there was concurrence of a hypoglycemic event between the dog alert and CGM (n = 30), CGM would have alerted prior to the dog in 73% of events (median 22-minute difference). CONCLUSIONS: This is the first study evaluating reliability of trained dogs to alert to hypoglycemia under real-life conditions. Trained dogs often alert a human companion to otherwise unknown hypoglycemia; however due to high false-positive rate, a dog alert alone is unlikely to be helpful in differentiating hypo-/hyper-/euglycemia. CGM often detects hypoglycemia before a trained dog by a clinically significant margin.