February 2, 2016
Experts Calling for New Diabetes Classification System
While this is research, six experts have a convincing argument for a change in the diabetes classification system. Type 1, type 2, and LADA do not provide clear guidance for diagnosis and treatment of patients with diabetes. The experts in the American Association of Clinical Endocrinologists (AACE) claim that their algorithm is sufficient, but not that accurate.
The new method would make β-cell centric classification of diabetes a single common denominator for all types. At present, the classification identifies only four types of diabetes mellitus. These are type 1, type 2, 'other specific types' (which include genetic defects of beta-cell function, genetic defects in insulin action, diseases of exocrine pancreas and more) and gestational diabetes.
Since the first distinction between presentations of the disease from back in January 1936, the categorization of diabetes has been through numerous changes in order to keep up with new research and findings on the best way to help patients combating the disease. However, the inherent setback with the currently established system lays in the fact that it is inadequate with the present understanding of the phenotypes associated with diabetes. In addition, this and
the limited research and information present at the time of formulating the current system, the designations related with the different types of diabetes are vague and inaccurate. Due to this fact and current evidence-based practice, there is a call to revise the current classification of diabetes mellitus and focus on a β-cell centric classification schema, according to a new article published online in Diabetes Care Jan. 21, 2016.
Based on new research performed by Stanley Schwartz and affiliates, there is a new proposition for using a β-cell centered model for diabetes, which supports the notion that all diabetes originates from an abnormal pancreatic β-cell. Type 1 diabetes has been thought of as an ailment of low insulin production, while type 2 has usually been of insulin resistance. This discrepancy is not clear or helpful. Schwartz and colleagues suppose all diabetes is a product of impairment to beta cells (which produce insulin) and according to this theory, insulin resistance just reveals the rudimentary deficiency in insulin production.
Presently, only about one-third of individuals with insulin resistance will go on to develop diabetes. The basis of the new classification system is treatment of patients as individuals though currently most prescribers will initiate treatment based on a diagnosis instead of the person.
Schwartz believes that diabetes is rooted to β-cell and because of this, classification of diabetes types should be based on causes of that damage so physicians will know how to go about treatment. This “β-cell centric” criterion recognizes that β-cell damage can be caused by inflammation, immune actions, gut biome, high fatty acids, high glucose levels, genetics and other causes; categorization founded on these sources can help cultivate an improved treatment strategy, as opposed to simply knocking down an individual’s glucose level.
Defining key markers and the processes of care in using them will allot appropriate patient-centric approaches with either currently established medications or an up-and-coming drug.
This proposed model acknowledges a total of 11 interconnecting pathways that contribute to hyperglycemia, which are prompted by the transformation of genetic predispositions to insulin resistance. These pathways of hyperglycemia contribute to β-cell dysfunction within the liver, adipose, brain, colon, immune dysregulation and muscle. The “damage caused results in downstream hyperglycemia arising from increased glucagon secretion, as well as a reduction in insulin production, incretin effect and amylin levels.” For any one patient, the routes for hyperglycemia vary and more than likely involve numerous pathways. It is significant to note that these arbitrating pathways of hyperglycemia are common across prediabetes, type 1 diabetes, type 2 diabetes and other outlined forms of the disease state.
The most ideal management model presented was the impression that treatment should comprise the use of the least amount of agents to help in targeting the greatest number of these particular mediating pathways of hyperglycemia in any given patient. The research also noted that any treatment option that would potentially be detrimental to the long-term integrity of the β-cells–specifically including sulfonylureas and glinides–should be avoided because any potential benefits of the medications are severely outweighed by the risks associated with their use. It will be very interesting if the ADA will even consider this as important, but it should be very important.