Very Depressing

Today in the comments section of my previous post, the Inflexively Flixable Flux Guy pointed out some research by Robert J. McCarter et al.. Below are some of the more salient sentences from their paper:

Blood glucose levels are clearly a major determinant of HbA1c levels. Population studies in patients with diabetes have shown that HbA1c is highly correlated with preceding MBG [Mean Blood Glucose]. However, evaluation of the relationship between HbA1c and MBG among individuals within a population shows that there is considerable variation in HbA1c [for] any given MBG value. This variation is often treated as random, but there is considerable evidence that much of it is due to nonrandom, patterned variation of biological origin. Thus, some individuals at the same MBG value have consistently higher HbA1c levels [like me!] and others consistently lower HbA1c levels [not like me!] than that expected under the hypothesis that HbA1c is solely determined by MBG.

In a previous study, we developed a hemoglobin glycation index (HGI) based on the relationship between observed and predicted HbA1c levels. ...HGI quantifies the magnitude and direction of individual differences in observed HbA1c from that predicted by the population regression equation while accounting for the influence of MBG. The accumulated evidence... strongly suggests that an individual’s HbA1c levels are determined by two major components: 1) MBG and 2) other individual factors responsible for biological variation in HbA1c.

Data were available to evaluate the relationship between HGI and risk of retinopathy and nephropathy for up to 7 years. Risk for development or progression of retinopathy with MBG held constant was significantly different (P < 0.0001) among patients in the low-, moderate-, and high-HGI groups (Fig. 2A). After 7 years, patients in the high-HGI group had three times greater risk of retinopathy (30%) compared with those in the low-HGI group (9%). Risk for development or progression of nephropathy was also significantly different (P < 0.0001) in the low-, moderate-, and high-HGI groups (Fig. 2B). After 7 years, patients in the high-HGI group had six times greater risk of nephropathy (6%) compared with those in the low-HGI group (1%).

The important novel finding of this study is that biological variation in HbA1c is an important predictor for the development and progression of diabetes complications. This suggests that there are two important components of risk for the microvascular complications of diabetes. The first is the well-recognized effect of chronically elevated blood glucose. The second component is the less-recognized and poorly understood effect of factors other than glucose that are responsible for biological variation in HbA1c.


Robert J. McCarter, SCD, James M. Hempe, PHD, Ricardo Gomez, MD, and Stuart A. Chalew, MD. 2004. "Biological Variation in HbA1c Predicts Risk of Retinopathy and Nephropathy in Type 1 Diabetes" Diabetes Care 27:1259:1265.

This shit scares me (a lot). Even so, and in all seriousness, thanks for passing this on, Dr. Fluxtable.

Sincerely

I hope you don't take any offense to my having fun with your nom de internets. If so, I apologize in advance.

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While it scares me sometimes, knowledge is power. And if I have to work harder, than so be it. That's what I'll have to do (though this analysis implies that even that might not be sufficient).

On top of this/that "well, what'd ya know, I learned something new" feeling today, I had a hell of a roller-coaster day blood-sugar-wise.

Hold on to your hats folks! You might lose your cookies on this one!
(Note also, that this graph doesn't show the string of readings in the low 50s at around 3am the previous evening).


"Oh shit, that was fun!"
"Yeah! Wanna go again?"
(Um, no thanks (and besides, I don't even know who those sick characters having that conversation were). I hate roller-coasters (both literally and figuratively).).