The accepted knowledge is that Diabetes destroys gradually over years. Ketosis Prone Type 2 diabetes is an acute form of type 2. This type 2 can reach fasting blood sugars of 300 or higher in months. This blog brings together all the documentation that I could find in the world and my speculation of what it means for KPD’s in specific and diabetics in general. I ask you to leave your stories about what happened to you so that we can all gain a better understanding of what we are dealing with.

Wednesday, March 10, 2010

G6PD - something else you haven't heard of

What is G6PD and why should a KPD care? Well, it's another one of your problems and it may be the reason  why KPD's should be wary of carbohydrates.

G6PD is an enzyme that helps in the breakdown of carbohydrates. If it isn't present then certain pathways that deal with glucose metabolism aren't activated. There's a lot more to it but the short form is that glucose is a bad actor and this helps keep it contained. You more than likely are deficient here. This shouldn't be a great surprise since this is the most common deficiency in humans.

G6PD deficiency: its role in the high prevalence of hypertension and diabetes mellitus

Currently, there are 200 million people worldwide with red cell x-linked chromosome defects who, with the persistent ingestion of refined carbohydrates, are at greater risk of developing hypertension or diabetes mellitus... 

What has been found is that KPD's are far more likely to have G6PD deficiency than other diabetics. You could view it as a marker for KPD.

High Prevalence of Glucose-6-Phosphate Dehydrogenase Deficiency without Gene Mutation Suggests a Novel Genetic Mechanism Predisposing to Ketosis-Prone Diabetes 

The prevalence of G6PD deficiency was higher in KPD than in T2DM and controls (42.3%; 16.9%; 16.4%; P = 0.01). In KPD, but not in T2DM, insulin deficiency was proportional to the decreased G6PD activity (r = 0.33; P = 0.04).

42% to 17% that's big. What I find interesting is that insulin deficiency was proportionate to decreased G6PD activity. The other really important part is that, for the most part, there was NO gene mutations beyond regular type 2's controls. So we are looking at a difference of about 20% that comes from some where but it isn't genetic.This, however, was done on a West African population so it could be a bit skewed.

If you took the time to read this post, you really should read this other post which puts it all in context for this type of diabetes. Here

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