Hypoglycemic Brain Damage

Abstract

Before the discovery of insulin, sources of insulin exogenous to the body were not available and hypoglycemic brain damage occurred only in the context of endogenous tumors of the islets of Langerhans of the pancreas (Auer 1986). Human consumption of food had reached the point where diabetes was becoming more common, but it was then only treatable through starvation. Indeed, diabetes can metabolically be considered “starvation in the midst of plenty” due to the inability of glucose to enter cells, in the face of high blood glucose levels. Once insulin was discovered, it was tested in diabetes and was found to allow improved survival over the unpalatable treatment option of starvation: the latter could reduce glucose loss through the urine but only slowed the diabetic process and could not stave off eventual death.

When insulin was discovered in 1921, islet cell adenoma was joined by diabetic insulin treatment in reports of hypoglycemic brain damage (Bodechtel 1933; Baker 1938). Suicide or homicide with insulin also occurred regularly, and together with medication error, provided a steady source of material with hypoglycemic brain damage. Tumors secreting insulin or congener molecules were later recognized to cause hypoglycemia (Le Roith 1999).