Articles

Interview with Dr. John Higgins, M.D., and Steve Freed, Publisher of www.diabetesincontrol.com. John Higgins, MD, Associate Professor, Department of Systems Biology, Harvard Medical School, Department of Pathology, Massachusetts General Hospital.

Job insecurity found to prompt 19% increase in diabetes, myocardial infarction or coronary death risk.

Study focuses on differences in clinical outcomes between initiating glucagon-like peptide-1 receptor agonist (GLP-1 RAs) vs. insulin treatment in patients with type 2 treated with oral glucose-lowering medications (OGLM).

Study finds clinicians less likely to counsel less educated, and younger and older patients.

Device automatically monitors blood glucose levels and delivers insulin when appropriate for people age 14 years and older who have type 1 diabetes.

Semaglutide reduced major cardiovascular events by 26% in adults with type 2 at high cardiovascular risk.

Patients treated for cholesterol lowering appear to have extra benefits.

Research reveals important gaps in care.

For those healthcare providers who treat diabetes with any kind of regularity, it has become increasingly obvious that several of our patients fall outside the current diabetes classification system. With individualization of patient care being the new focus, it can be challenging to accomplish this, when certain diabetic individuals don’t “conform” to the current definitions.

I am a neuroendocrinologist by training, having received my Bachelor’s degree in biochemistry and molecular biology from the University of California, Santa Barbara and Master’s and Doctorate degrees from Louisiana State University (LSU) in physiology under the mentorship of Dr. Albert H. Meier. It was at LSU that my interest in the biological clock system and its role in the regulation of metabolic physiology was sparked by the revolutionary discoveries and elucidations made by Dr. Meier’s lab concerning biological clock mechanisms regulating physiology. He and his group in the early 1960s were the very first to demonstrate the existence in any organism of circadian rhythms of physiological responses to neuroendocrine factors. At LSU, I began investigating the possibility that modern human pathology of the metabolic syndrome (and several other progressive pathologies) was not a result of any “genetic defect” but of an environmentally induced (e.g., diet, stress, sleep-wake architecture) alteration of circadian neuroendocrine information presented to the clock system that then responded to direct the body to the obese/insulin resistant state as a survival response to such information.