If asked to name the types of diabetes, most people would name gestational diabetes, type 1 diabetes, and type 2 diabetes. In the past, it seemed as if solid lines delineated these types. Gestational diabetes occurred during pregnancy. Type 1 diabetes, autoimmune in nature and usually occurring abruptly during the childhood/teen years, renders the pancreas incapable of producing insulin. Type 2 diabetes has a genetic component, occurs most often in adulthood, is influenced by environmental stressors, and characterized by inadquate insulin production and/or insulin resistance.
Over the past years, we’ve seen these solid lines of delineation become blurred with the discovery of what has been called type 1.5 diabetes or latent autoimmune diabetes of adults (LADA). Discovered in the 1970’s and more regularly discussed since the early 1990’s, many diabetes practitioners subscribe to its existence although there is not yet a classification for LADA.
Although it is most often diagnosed in adulthood as type 2 diabetes, after 3-12 years, it begins to present like type 1 diabetes. LADA has characteristics of both type 1 diabetes and type 2 diabetes.
A quick review of the differences between type 1, type 2, and LADA:
Type 1 diabetes is an autoimmune disease. A combination of genetic and environmental factors such as virus exposure or environmental toxins increases the risk of type 1 diabetes. An autoimmune response targets the destruction of the beta cells of the pancreas. In short order, the beta cells are rendered unable to produce life sustaining insulin. People with type 1 diabetes do not respond to oral medications for blood sugar regulation and require insulin (injections or infusion) for life.
Although type 1 diabetes was once called juvenile diabetes (the majority of new diagnoses abruptly occur in childhood/teen years), adults can also develop type 1 diabetes.
Type 2 diabetes most often occurs in adults; although, children are increasingly being diagnosed with what used to be called adult onset diabetes. Type 2 diabetes is progressive in nature and fasting blood glucose may take years to elevate to the point of diabetes diagnosis. There is a stage in the progression called prediabetes during which time it is possible to make lifestyle changes to prevent the progression to type 2 diabetes.
In type 2 diabetes, three metabolic situations may be underway: The body may produce ample insulin, but there is insulin resistance; the body may not produce enough insulin; or there may be a combination of insulin resistance and inadequate insulin production.
Many who develop type 2 diabetes are overweight at diagnosis, with fat stores evident around the middle. This increased belly fat along with elevated cholesterol, triglycerides appears to occur after years of “over production” of insulin.
Years of insulin over production and fat cell growth leads cells to become resistant to insulin. In fact, at this point, there may be high levels of insulin and high levels of glucose in the blood. Over time, the over worked pancreas fatigues and eventually produces less insulin. Eventually, those with type 2 diabetes have insulin resistance and inadequate insulin production. All the while, the pancreas still produces insulin.
Type 1.5 diabetes accounts for roughly 10 percent of people with diabetes. It is estimated that 20 percent of those initially diagnosed as having type 2 diabetes actually have LADA.There is still uncertainty over how to define LADA or how it develops and progresses. Often, a person with LADA may be lean or normal weight when diagnosed. Oral medications may initially work to decrease elevated blood sugar. Over time (in much shorter order than typical type 2s,) oral medications become ineffective. Blood sugar worsens and insulin must be prescribed. This process can take place over years as LADA progresses more gradually than the abrupt onset of type 1.
For anyone interested in reading more about the different diabetes classifications, they can read ADA’s Forecast magazine and the chart they developed here.
Some diabetes practitioners recommend that in adult patients who present as lean or normal weight and have no known family history of type 2 diabetes, antibody testing should be performed to differentiate between type 2 diabetes and LADA.
Why would it be beneficial to “know in advance” if a person has type 2 or LADA? Well, think of it this way, many oral medications work by forcing the pancreas to produce more insulin. Sulfonylureas are one class of diabetes drugs that cause the pancreas to work harder. By prescribing more and more insulin- provoking oral medications (to no avail), we would be speeding the demise of beta cells.
Also, if we keep a patient with LADA on a traditional diet for diabetes—calorie controlled/low fat—we are exposing the pancreas to an increased need to produce insulin caused by the high blood sugar rendered from the breakdown of 50-55% carb dieting. In the same way that some oral medications press the pancreas to produce more insulin, so, too, does the higher carbohydrate diet require more insulin production.
So, perhaps instead of it taking years for LADA to run its course and render the pancreas null and void, we can make lifestyle changes that can promote the health and wellness of this portion of the population.
In the years it takes to prove that oral medications are not working, the patient is subjected to higher than necessary A1cs. The faster blood sugar is normalized, the better the long term outcomes. If insulin use is inevitable and orals can actually stress a pancreas that has begun to degrade, why not remove that excess stress from the pancreas and the body of the person with LADA?
The case could be made to first diagnose or recognize a patient with LADA and then begin appropriate treatment. Here is a perspective regimen I would use for such patients:
•Use insulin as treatment immediately to prevent the pancreas from being over stressed by insulin provoking medications. I have seen great results using a long acting insulin like Lantus or Levimir at bedtime. This dose is titrated until the patient regularly awakens with “normal” blood sugar. The medical provider and patient set this wake up goal. For an example, let’s use a wake up blood sugar of 90-110mg/dl. The patient with LADA would test blood sugar pre meals and bedtime and can use rapid acting insulin (if needed) before meals to correct high blood sugar. On the diet plan I will next describe, there is a chance that rapid acting insulin will not be needed at each meal during Steps 1 and 2!
•Change the recommendation of the 50-55% carb diet to a balanced diet with low glycemic index and low glycemic load. Normoglycemia can be reached more easily when excess carbohydrates are eliminated from the dietary intake. (See the graph Diet Recommendations below.)
•Space carbohydrate grams throughout the day. When a person exceeds 5 hours without eating carbohydrates, the pancreas is forced to release glucagon to stimulate the liver to release glucagon. If carbohydrate grams are spread accordingly, there is a lesser need for glucagon.
•Ask these patients to exercise. It is a great way to build and retain muscle mass and consume excess blood sugar. With the help of regular, properly fueled physical activity, the pancreas need not produce as much insulin or glucagon. Optimal exercise is a minimum of 30 minutes of exercise 5 days a week over and above usual activity. Optimal time to exercise: 1 to 2 hours after any meal.
•Ingest adequate water. Those with LADA have a greater chance of forming ketones than a person with type 2 diabetes. The less insulin they produce, the greater the rise of ketones and the greater the ph imbalance in the blood. For those 5’3” and under a minimum of 48 ounces of water a day; For those over 5’3”, a minimum of 64 ounces of water a day.
•A multi-vitamin daily. Having diabetes increases the risk of inflammation and physical stress; vitamins act as insurance that daily nutritional needs are met.
By resting the pancreas and normalizing blood sugar, we may be able to extend the lifespan of the LADA pancreas—from 5 years to perhaps 10 years or more. It’s important to remember that those with type 1 diabetes do not produce insulin, amylin, and may produce inadequate amounts of glucagon. It would be advantageous to keep the beta cells of the pancreas functioning as long as is possible—and not unnecessarily speed up their demise.