Second great discovery in diabetes history
In 1936 a medical scientist named H. P. Himsworth proposed that type 1 and type 2 diabetes have different causes. He hypothesized that type 1 diabetes is due to a lack of insulin; while type 2 diabetes is due, not to a lack of insulin, but to an insensitivity or resistance to insulin. He was right., but his theory was largely ignored.
Another investigator, I. Arthur Mirsky, proposed a similar hypothesis in 1952. He proposed that adult-onset diabetes, type 2, might not be due to a deficiency of insulin secretion, as Himsworth had proposed in the first part of his theory, but rather to abnormally rapid degradation of insulin by an insulin enzyme in the liver. This part of Mirsky’s theory was wrong, but his hypothesis led to a radical change in the treatment of type 2 diabetes. How was 1952 different from 1936?
A Nobel Prize-winning breakthrough
In order to prove that type 2 diabetics produce insulin, it is necessary to show that insulin exists in the blood of type 2 diabetics. Insulin is a very small molecule; the technology to detect such small substances in the blood did not exist in 1936. It did not exist in 1952 either. However, two medical scientists, Solomon Berson and Rosalyn Yalow, set out to test Mirsky’s hypothesis. In the process they discovered a way to measure insulin in the blood. They named the technique radioimmunoassay. It enabled scientists to measure very small substances in the blood, such as insulin, and could be extended to measuring other very small substances as well, such as vitamins. The technique was such a significant breakthrough for medical research in general, not just for research on insulin, that Rosalyn Yalow received a Nobel prize for the discovery. (Berson had died prematurely and was not eligible since Nobels are not awarded posthumously.) With this new technique Berson and Yalow were able to perform an experiment to test Mirsky’s hypothesis.
They measured insulin in both type 1 and type 2 diabetics as well as in normal non-diabetic subjects. The measurements clearly showed that individuals with juvenile, or type 1, diabetes produced no insulin at all, as expected. But individuals with adult-onset diabetes, or type 2, did have insulin in their blood. This finding confirmed the first part of Mirsky’s theory – the pancreas of type 2 diabetics did indeed produce insulin.
Two types of diabetes, two different treatments
However, another finding contradicted the second part of Mirsky’s hypothesis – that insulin in the blood of type 2 diabetics is quickly destroyed after it is produced. The researchers found that type 2 diabetics had higher insulin levels after a meal than normal non-diabetic subjects did. So insulin did not disappear more rapidly from the blood of type 2 diabetics, but lingered for a longer time than normal. An even more unexpected finding was that type 2 diabetics frequently released more insulin than normal subjects did. Paradoxically, type 2 diabetics had high blood sugar levels, and they also had high insulin levels. In other words, while type 1 diabetics have high blood sugar levels because they have little or no insulin, most type 2 diabetics have high blood sugar levels despite the secretion of excessive amounts of insulin. Somehow, type 2 diabetics are resistant to the action of their own insulin. Thus H. P. Himsworth’s theory was vindicated.
Berson and Yalow’s findings led to the realization that the usual treatment for type 2 diabetes, daily injections of insulin, could have been doing more harm than good because a lack of insulin was not the problem. And excess insulin can have adverse effects, such as high blood pressure, high cholesterol levels, increased risk of heart disease, and weight gain. Another adverse effect recently discovered is increased risk of colon cancer: long-term insulin use by patients with type 2 diabetes is associated with an increased risk of colon cancer, according to research reported in the medical journal, Gastroenterology, October 2004, by Dr. Yu-Xiao Yang and colleagues.
The discoveries of Berson and Yalow provided the rationale for different treatments for the two types of diabetes. For type 1 diabetes, insulin therapy and diet. For type 2 diabetes, diet and exercise, alone ideally, and when diet and exercise are not enough, the addition of new types of non-insulin, oral anti-diabetic drugs that were developed after World War II.
How do you know if you have type 1 or type 2 diabetes? Are the symptoms the same? Are they different? If so, in what way? And what happens in the body that causes these symptoms? These questions will be answered in next month’s column.
Mary Lou Williams, M. Ed., is a lecturer and writer in the field of nutrition. She welcomes inquiries. She can be reached at 267-6480.