Type 1.5 Diabetes

Type 1.5 diabetes, as the name implies, falls between type 1 and type 2 diabetes. It manifests some of the symptoms of both types, and it is important because it affects about 15% of those diagnosed with diabetes.

Type 1 diabetes is characterized by the presence of autoantibodies against insulin or against certain components of the insulin-producing system such as glutamic acid decarboxylase (GAD), tyrosine phosphatase or the islet cells themselves. These autoantibodies cause the patient's own immune system to kill the beta cells of the pancreas, making the patient unable to produce any endogenous insulin.

Type 2 diabetes is characterized by insulin resistance and diminished production of insulin by the pancreas. If a patient is well-managed, this kind of diabetes can be controlled for many years by diet, excercise and oral medication.

Type 1.5 diabetes has characteristics of type 1 and type 2. Like type 2, its onset is in adulthood, and the pancreas is able to produce insulin for several years. Like type 1, it often occurs in thin people, and it often involves autoantibodies to GAD or islet cells. Unlike type 1, in type 1.5 diabetes, the autoantibodies work much more more slowly. However, their destruction of beta cells is relentless, and within 5-10 years of diagnosis, patients with type 1.5 diabetes will require insulin.


Type 1.5 diabetes is sometimes called Mature Onset Diabetes of the Young (MODY), Latent Autoimmune Diabetes in Adults (LADA), slow onset type 1 diabetes, or double diabetes. As might be expected, each of these terms involves specific criteria and there is disagreement about who falls into which category. Leaving the questions about specific terminology aside, why should it matter that about 15% of the diabetic population is neither type 1 nor type 2?

It matters because type 1.5 diabetics are often misdiagnosed as type 2 diabetics. It matters because type 1.5 diabetics will initially respond to dietary modifications and oral medication, but because their condition stems from the death of beta cells rather than insulin resistance, eventually they will not. Physicians who are not familiar with type 1.5 diabetes may not understand why a misdiagnosed type 1.5 diabetic has stopped responding to standard treatments and may assume that the patient is no longer complying with their instructions. (This happens often enough that physicians have good reason to suspect noncompliance as an explanation for poor diabetic control.) If the patient knows that he or she is following the doctor's guidelines, it might be a good idea to ask for autoantibody tests to see if destruction of the pancreatic beta cells is taking place. As in every other aspect of health care, it becomes important for the patient to become an active participant in the monitoring and management of his condition.

Type 2 Diabetes

Type 2 diabetes is a condition affecting slightly more than 7% of Americans. It used to be called adult-onset diabetes, but we now know it can occur in children as well as in adults. Another term for it was non-insulin-dependent diabetes mellitus (NIDDM), but about 30% of type 2 diabetics are treated with insulin.

Type 1 diabetes begins with death of insulin-producing beta cells in the pancreas. Typically this happens over a period of weeks or months and is not reversible. Type 2 diabetes may begin with a diminished production of insulin by the pancreas. Several risk alleles have been identified and have been found to have an additive effect, resulting in decreased glucose sensitivity in the pancreas of people who have not yet developed overt diabetes. This condition may go undetected for years, only becoming evident when the patient starts to experience insulin resistance. Often this happens during pregnancy, when the mother's body becomes less responsive to insulin during the third trimester. Gestational diabetes is a temporary condition, but can be an early indicator of a predisposition to type 2 diabetes. More often, as a person ages and becomes overweight, his or her muscles, liver and pancreas gradually develop increasing resistance to the action of insulin, and the symptoms of hyperglycemia start to appear. Insulin resistance in the liver may lead to overproduction of glucose by the liver, causing even more hyperglycemia. Hyperglycemia, in turn, may initiate a process called apoptosis (programmed cell death) in the pancreas, resulting in a pancreas that is significantly smaller and less able to produce insulin than the pancreas of a person who does not suffer from type 2 diabetes.

Unlike type 1 diabetes, the progression to type 2 diabetes usually occurs over several years. It does not typically result in the death of all the beta cells of the pancreas, but the ability of the pancreas to regulate blood glucose is significantly compromised. The presence of a genetic component is even more significant than it is in type 1 diabetes. In fact, if a person has a relative with type 2 diabetes, chances are 80% that the person will develop type 2 diabetes in his or her lifetime. With that in mind, it is a good idea to monitor fasting and postprandial glucose levels to see if blood sugars are starting to trend outside the normal range. If symptoms are detected early and the condition is managed appropriately, the progression to fullblown type 2 diabetes can be slowed or perhaps prevented altogether.

If you would like to do some more reading on the progression to type 2 diabetes, here are some links:

Metabolic Syndrome

Reactive Hypoglycemia

Reversing Insulin Resistance

(For those who are interested, the picture at the top is a Texas snowman.)

Type 1 Diabetes

The pancreas is a multifunctional organ that sits below and behind the stomach. As an exocrine organ, it empties digestive enzymes into the gut at the level of the duodenum. The pancreas is also an endocrine organ, synthesizing insulin in its beta cells and glucagon in its alpha cells, and secreting those hormones into the blood.

Normally the pancreas performs its functions silently and efficiently. However in some cases the beta cells of the pancreas are vulnerable to an attack by the body's own immune system. For about three million Americans, the pancreatic beta cells are no longer functional, resulting in a condition called type 1 diabetes.

The cause of type 1 diabetes is not entirely clear. The peak age of diagnosis is 14 years, but type 1 diabetes can develop at any age. There is a genetic contribution--twenty percent of patients have a relative who also has the disease. The presence of other autoimmune disorders is a predisposing factor, and childhood viral infections such as rubella, cytomegalovirus and coxsackie B may trigger the condition. In any case, in these patients the body's immune system targets the beta cells of the pancreas and renders them unable to produce insulin.

Before Drs. Banting and Best discovered insulin in 1921, the diagnosis of type 1 diabetes was a death sentence. Victims had continuous thirst and voracious appetites, but without endogenous insulin to control their blood sugar, they wasted away because they could not properly utilize the food they ate. A very low carbohydrate diet could forestall the inevitable for several years, but most died before the age of 30.

With the advent of exogenous insulin therapy, a new set of problems arose for type 1 diabetics. Blood glucose could be controlled, but if it was poorly controlled, it would eventually result in eye, kidney and nerve diseases. If too much insulin was injected, it could result in severe hypoglycemia and even death. Dr. Richard K. Bernstein is a physician who developed type 1 diabetes in 1946 at the age of 12. He tells a fascinating story, showing how difficult it was in those days to match insulin dose to blood glucose level. The advent of the glucometer enabled patients to monitor their blood glucose much more accurately, but it also led to the temptation to eat large amounts of carbohydrates and then "cover" the carbs with injected insulin.


Today the American Diabetes Association recommends that diabetics eat 25-35% of calories from fat, 15-20% from protein and 45-55% from carbohydrates. By contrast, Dr. Bernstein proposes that eating a large number of calories as carbohydrates produces a large variability in blood glucose and a high level of difficulty in controlling blood sugar. To counteract this, he suggests something called the Laws of Small Numbers, which entails eating only small amounts of slow-acting carbohydrate, and no fast-acting carbohydrate at all.

Which approach is correct? No definitive scientific comparison is available, but this review notes that when the ACCORD study attempted tight glycemic control in type 2 diabetics through drug therapy, the study had to be terminated because of high mortality. By contrast, the reviewers cite a long list of references that indicate that dietary control of hyperglycemia is able to improve many of the long-term consequences of diabetes. Type 1 diabetics are unable to completely avoid the use of exogenous insulin, but the strategy of eating very small amounts of carbohydrate that require only small amounts of insulin, appears to be worth serious consideration.