My nine year old son was diagnosed with type�1 diabetes about six months ago, and his endocrinologist says that he is still in the honeymoon phase. I have noticed a pattern in his blood glucose levels, and I am wondering if there is physiological data that supports my lay observations!

On three or four occasions in the past six months, I have noticed that after several weeks of good control, he has several days of unexplained lows. For example he usually runs 120-130 mg/dl [6.7-7.2 mmol/L] at lunch then has a week of readings 60-65 mg/dl [3.3- 3.6 mmol/L] as well as other lows throughout the day. By the time I establish a pattern, talk to my endocrinologist and adjust his insulin doses, he starts running to the other extreme (above 300 mg/dl [16.7 mmol/L]). During this phase, he almost seems insulin resistant. He finally levels off with usually a small adjustment upward to his previous insulin dose.

I have a feeling that this is related to the slow destruction of his pancreatic cells. Maybe, they hyper-secrete insulin in their final days. Is there a logical answer to this pattern? Is this reported by others?

I know of no specific analysis of a group of stories like this, but I think that there may indeed be a physiological explanation. To begin with, the normal pancreas has a substantial excess of insulin producing cells which is one reason why the process of autoimmune destruction is such a slow one. However, in the honeymoon phase, there is a mixture of beta cells that are no longer functioning with some that are essentially normal, and some that are still responding to rises in blood sugar; but abnormally.

At present it is not possible to evaluate these proportions and only indirectly possible to measure overall decay as serum C-peptide levels. It would fit in with other evidence though to suppose that at any given time some of the beta cells are showing what is called a delayed first phase insulin release which would mean that insulin would be secreted after the surge in blood glucose levels and so cause hypoglycemia. This might in turn lead to a compensatory decrease in insulin dose which, as autoimmune damage progressed, would in turn bring hyperglycemia and the need for a modest overall increase in insulin.

An armchair hypothesis I know, but a possible one, and one which could have been additionally moulded by changes in activity, stress and food intake. Logical, but not ‘additionally reported by others’.

DOB