Future Diabetes Diagnosis Could Be Based on 11 Factors

Written by Sari Harrar

Reviewed 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

It doesn’t look like much. In fact, it’s hard to find. But inside your pancreas—an organ shaped like a squished banana that’s tucked behind your stomach—tiny little beta cells rule your blood sugar. Healthy ones pump out plenty of insulin. Dysfunctional or dead ones don’t.

Now, a team of diabetes experts says the health of beta cells should be at the center of any diabetes diagnosis and therapy. “Six different factors affect beta cells resulting in 5 downstream effects of abnormal beta cell function. That adds up to 11 mechanisms of hyperglycemia that can define patient-centered therapy,” says endocrinologist Stanley S. Schwartz, MD, an emeritus associate professor of medicine at the University of Pennsylvania. “A diagnosis focused on what’s threatening a person’s beta cells would let doctors treat the real problems that cause that person’s diabetes, rather than getting locked into treatments based on a simplistic diagnosis of type 1 or type 2.”

Dr. Schwartz and his colleagues have published an article in the February issue of the journal Diabetes Care proposing a new way to classify diabetes based on these 11 factors. He points out that plenty of people with diabetes have overlapping beta-cell problems. “The definition of type 1 diabetes is that an autoimmune reaction has destroyed beta cells. And the definition of type 2 is that you have insulin resistance and your muscle cells aren’t absorbing blood sugar, but your beta cells can’t produce enough insulin to force the blood sugar inside. But it’s not that simple. Some people with type 1 may have insulin resistance, too. And some people with type 2 may have some of the antibodies that kill beta cells.” 

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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 DiabeticLifestyle. “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.” 

The Egregious Eleven

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 a different mix of 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 diagnosed with type 2 diabetes, who are supposed to just have insulin resistance, who in fact have antibodies—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.”

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