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.
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