Diabetes Diagnosis of the Future: 11 Types?

Written by Sari Harrar

Commentary by Stanley S. Schwartz, MD, an emeritus associate professor of medicine at the University of Pennsylvania and George Grunberger, MD, FACP, FACE, chairman of the Grunberger Diabetes Institute, clinical professor of internal medicine and molecular medicine & genetics at Wayne State University School of Medicine and president of the American Association of Clinical Endocrinologists.

Diabetes isn’t as simple as doctors and researchers once believed. “There’s lots of overlap between type 1 and type 2 – people can have features of both yet their doctors don’t always treat them with that in mind,” says endocrinologist Stanley S. Schwartz, MD, an emeritus associate professor of medicine at the University of Pennsylvania. "Treatment algorithms and insurance rules get in the way too often.”

Fed up and looking for a constructive solution, Dr. Schwartz and his colleagues have published an article in the February issue of the journal Diabetes Care, proposing a new way to classify this increasingly common high blood sugar problem – based on factors that threaten insulin-producing beta cells in the pancreas.

 “If beta cells can’t secrete enough insulin to control blood glucose, you have high blood sugar and diabetes,” he says. “We’re saying that you have to look more closely at why that’s happening. Everything from auto-immune reactions to insulin resistance to gut bacteria can play a role. We are suggesting that doctors look for these factors and develop treatment plans that target each person’s unique, beta cell-centric profile.”

Dr. Schwartz acknowledges that a new diabetes-diagnosis system wouldn’t happen overnight. “We’re calling on major diabetes and endocrinology organizations in the United States and Europe to support research,” he told EndocrineWeb. “In a meeting recently in Florida with diabetes leaders, I described this beta cell-centric approach. They voiced objections at first, but then came around to saying it made a lot of sense.”           

Under Assault

The list of known bad actors capable of killing, harming or overwhelming beta cells is still growing, Dr. Schwartz says. The team identified what he calls the “egregious 11” —six factors that in turn fuel five more processes that drive blood sugar up. The 11 are:

Genetics: Beta cells with certain DNA variations may self-destruct or quit functioning.

Changes in the “incretin effect”: Normally, the act of eating and digesting food stimulates the release of insulin. This is muted in some people with diabetes.

Faulty alpha cells: Also found in the pancreas, alpha cells balance blood-sugar levels by releasing glucagon. But too much can boost sugar levels too high.

Gut bugs gone bad: Some beneficial bacteria in the intestines seem to help control blood sugar – in part by encouraging the release of glucose-controlling hormones. People with different bacteria may have a higher risk for diabetes.

Immune-system troubles: An autoimmune reaction can destroy beta cells. Immune-system problems can also fire up inflammation, which harms beta cells.   

Digestive dysfunction: For some people with diabetes, blood sugar levels rise extra-fast after eating due to quick stomach emptying.   

A hungry brain: Shifts in levels of hormones that control appetite can lead to overeating and higher blood sugar and others increase insulin resistance

Kidney woes: As they filter wastes and sugar out of the blood, your kidneys can increase re-absorption of sugar back into the bloodstream.   

Insulin resistance in muscles: Muscle cells that don’t obey insulin’s commands contribute to rising blood sugar levels. Obesity and a lack of exercise contribute to this problem.

Insulin resistance in fat cells: This can dump more fats into the bloodstream, leading to more insulin resistance in muscle cells and higher blood sugar levels.  

 Insulin resistance in the liver: Liver cells that don’t listen to insulin may dump more glucose than usual into the blood.

"We have diabetes medications already that address all of these issues,” Dr. Schwartz says. “But a patient’s insurance plan may not cover the cost of a drug for insulin resistance – normally seen in type 2s – if the diagnosis is type 1 diabetes, where the major problem is immune-system destruction of beta cells. The best thing doctors and patients can do for now is to use all the lifestyle and treatment options they can, but we should have the option of using other medicines if they fit the cause and mechanism of hyperglycemia in that individual”

The idea is “provocative,” says George Grunberger, MD, FACP, FACE, chairman of the Grunberger Diabetes Institute, clinical professor of internal medicine and molecular medicine & genetics at Wayne State University School of Medicine and President of the American Association of Clinical Endocrinologists. “Dr. Schwartz’s point is that we’re not treating people according to exactly what’s wrong with them. I see people with type 1 diabetes who are also obese and have insulin resistance frequently in my practice. And we see people with type 2, who are supposed to just have insulin resistance, who in fact have antibodies that could destroy their beta cells over time—a feature that is supposed to happen only in type 1 diabetes.”

Finding underlying factors, Dr. Grunberger says, “sounds wonderful, but our diagnostic tools aren’t that good yet. Getting there would take a great deal of research.”









1. Schwartz SS, Epstein S, Corkey BE, Grant SF, Gavin JR 3rd, Aguilar RB. The Time Is Right for a New Classification System for Diabetes: Rationale and Implications of the β-Cell-Centric Classification Schema. D iabetes Care. 2016 Feb;39(2):179-86. Accessed February 8, 2016.

2. Everard A, Belzer C, Geurts L et al. Cross-talk between Akkermansia muciniphila and intestinal epithelium controls diet-induced obesity. Proc Natl Acad Sci U S A. 2013 May 28;110(22):9066-71. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3670398/. Accessed February 8, 2016.

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