Emma Hitt, PhD

May 08, 2012

May 8, 2012 (Atlanta, Georgia) — Diabetes mellitus and a transition from impaired fasting glucose (IFG) to diabetes were associated with decreased brain volume, assessed with magnetic resonance imaging (MRI) over a 2-year period in community-dwelling elderly patients.

Katherine Samaras, MBBS, associate professor of medicine at the University of New South Wales and an endocrinologist at St. Vincent's Hospital in Sydney, Australia, presented the findings in an oral session here at the Joint 15th International Congress of Endocrinology and 14th European Congress of Endocrinology.

"In the elderly, the presence of diabetes, or its development over a 2-year period, was associated with a reduction in total brain volume and frontal lobe volume," Dr. Samaras told Medscape Medical News. "These findings were independent of important factors, such as original brain volume, age, sex, blood pressure, and lipid-lowering therapy," she said.

According to Dr. Samaras and colleagues, longstanding type 2 diabetes is associated with brain atrophy. In their prospective study, the researchers examined the impact of glycemic status on total brain volume in an elderly cohort.

The 2-year study involved 312 of the 542 participants (aged 70 to 90 years) in the Sydney Memory and Aging Study for whom prospective metabolic data and a baseline MRI were available.

Participants were categorized in 4 groups on the basis of glucose status at baseline and at 2 years: stable normoglycemia (normal glucose at both time points, n = 102); stable IFG (at both time points, n = 120); progression of glucose status (from normal glucose to IFG or diabetes or from IFG to diabetes, n = 57); and diagnosed diabetes at baseline (n = 33).

Total brain volume decrease was 1.4-fold greater in patients with stable IFG over the 2 years than in those whose glucose remained normal, and 2.3-fold greater in patients who either progressed in glucose impairment status or who had diabetes at baseline and at year 2 (< .05 for both).

Glucose status at 2 years remained predictive of a decline in volume (P < .01) after adjustment for covariates, including age, sex, trabecular bone volume at baseline, history of hypertension, history of hyperlipidemia, and use of lipid-lowering drugs.

According to the researchers, about three quarters of the total variance in brain volume was linked to baseline brain volume; however, 16% of the residual variance was explained by glucose status at follow-up, they found.

"We know diabetes is a risk factor for dementia," Dr. Samaras said. "We need to consider the complexity of diabetes management, education, and self-care in the elderly, and tailor-make these according to the specific needs of our patients, which, in the elderly, may include progressive cognitive changes due to the organic effects of diabetes on the brain."

Unanswered questions include whether it is possible to halt the effect of diabetes on brain volume, and if so, how, she said. Also, "it will be important to determine the mechanisms by which diabetes causes a decline in brain volume."

Session moderator Valdis Pirags, MD, professor of medicine at the University of Latvia, in Riga, noted that clinicians working with elderly patients with type 2 diabetes might not be surprised by these findings.

For many years, clinical researchers have debated whether so-called diabetic encephalopathy is something that can be objectively measured, he told Medscape Medical News.

According to Dr. Pirags, these findings "strongly support the importance of good glycemic control, even in elderly type 2 diabetes patients, to slow down the cognitive decline."

"It is extremely important that the study authors were able to show that hyperglycemia was an independent risk factor, beside already known risk factors for cognitive dysfunction," such as hypertension and hyperlipidemia, he said.

However, the relevance of brain MRI for diagnosing diabetic encephalopathy will require "further validation in broader clinical setting."

The study was not commercially funded. Dr. Samaras and Dr. Pirags have disclosed no relevant financial relationships.

Joint 15th International Congress of Endocrinology (ICE) and 14th European Congress of Endocrinology (ECE): Abstract OC3.6. Presented May 7, 2012.