Diabetes blogger, Allie Beatty, wrote this week nearly screaming that type 1 diabetics should be lobbying the FDA to force insulin manufacturers to incorporate c-peptide into analog insulin products. Her stance is that people who do not have diabetes do not have complications because they have c-peptide. She cites a highly technical document in a 2007 issue of Diabetologia as her source and she seems to be almost dismissive of the role of higher than normal blood sugar as a cause of complications. Her blog includes specific instructions to contact the FDA if anyone is interested.
I had heard of the lack of c-peptide in analog insulin products prior to this blog. “Talking” it through with other diabetics, we realized that 1) humulin products do not have c-peptides either but that 2) beef and pork insulin probably did since it came from animals not a “dish in a lab.” I think we were assuming animals have c-peptide in their insulin. We did not go much further with the discussion and I had long forgotten about he subject.
However, after reading Allie’s blog, I started reading the article she had attached. It is quite technical, so I am sure I did not entirely understand it. However, there is a basic assumption that is clearly in English that gives me cause to disagree with the analysis, at least until they are comparing apples to apples. They say:
“The DCCT study demonstrated a decreased occurrence of complications in the group of type 1 diabetes patients that received intensive insulin therapy and achieved improved blood glucose control, in keeping with the view that hyperglycemia is a major culprit in the pathogenesis of microvascular complications. Even though blood glucose levels were close to normal in the group that received intensive treatment, a large proportion of these patients still developed complications: 40% presented with clinical neuropathy or grossly abnormal nerve conduction after 5 years , and a similar fraction had developed signs of nephropathy or retinopathy. This suggests that factors in addition to hyperglycemia may be involved in the development of microvascular complications in type 1 diabetes patients. In view of the data for C-peptide described above, we suggest that lack of C-peptide contributes to the pathogenesis of complications of type 1 diabetes.”
What they neglect to say is that the DCCT trial blood sugar targets were NOT even close to normalized, non-diabetic blood sugar numbers. Non-diabetic A1Cs are 4.2 – 4.6 and average blood sugar is in the 85 range. The DCCT trials started before most of us even thought of targeting A1Cs of 5.0 or even closer to blood sugar. Their study population therefore could never have achieved “close” to normal blood sugar.
In fact, according to a January 2008 article in Diabetes Self-Management, “In actuality they achieved a median HbA1c of 7.2%.” This “actuality” is nowhere close to “normal;” so it should be no big surprise that “a large proportion of these patients still developed complications.” An A1C of 7.2 is >50% higher than a (healthy, thin) non-diabetic A1C. How could that NOT cause complications?
So, that leaves me with two thoughts: 1) How can we judge whether the lack of c-peptide is very important if researchers are not comparing apples to apples? Why don’t they consider studying those of us who target and attain closer to normalized blood sugar? 2) Is it even possible to add c-peptide into humulin and/or analog insulin products? (I see no reference to this possibility. There is not much need to lobby the FDA without knowing this.) If it is possible to add c-peptide to insulin products, is it cost effective (to the insurer or the diabetic)? Does it have to be a separate, secondary injection, unit for unit? Again, at what cost?
Now, keep in mind, I am often on the FDA bashing bandwagon. However, this time, I think we best do some more homework and get back to the basic KNOWN cause of diabetes complications – non-normalized blood sugar – before we look for yet again, another, hugely expensive “complication alleviator.”
Doris J. Dickson