From Rockford, Illinois, USA:
My nine year old son was diagnosed with typeá1 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'.
Original posting 25 May 2001
Posted to Daily Care
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Last Updated: Tuesday April 06, 2010 15:09:22
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