Holly,
You won't find any research on this observation/opinion (at least I couldn't find any), but from what I know about magnesium deficiency's tendency to cause insulin resistance, I'll bet a GF cookie that the increase in your A1C level is due to an increase in your magnesium deficiency caused by the malabsorption problem associated with MC and other IBDs. The fact that you are gaining weight when there is no logical reason why you should be is further evidence that that my theory is correct.
Most people believe that increased adiposity increases the risk of insulin resistance, and that's generally true. But it's also true that the reverse can happen — increased insulin resistance (due to magnesium deficiency) can compromise the way that nutrients are transported to cells, and the increased insulin resistance would surely boost A1C levels.
IOW, I suspect that your A1C increase is due to increased insulin resistance because of a magnesium deficiency problem. Here's a quote from page 25 of my Pancreatic Cancer book (to be published in August, I hope). But note that this page number and this text may change before I finish the final edit.
But this leads us to the magnesium connection again.
As mentioned in the previous chapter, magnesium deficiency plays an important role in the development of insulin resistance and type 2 diabetes. Researchers have shown that both hypertension and type 2 diabetes involve low intracellular magnesium levels.24 In the research article cited, Takaya, Higashino, and Kobayashi (2004) concluded that because magnesium is necessary for the proper utilization of glucose, and it's also used for insulin signaling, an intracellular magnesium deficiency may alter glucose availability and contribute to the development of insulin resistance.
Magnesium and insulin are co-dependent.
One cannot function properly without the other. And this is a 2-way street in many regards. Not only does a magnesium deficiency cause insulin resistance in the cells of the body and reduced insulin production by the pancreas, but there is a reciprocal effect. Insulin is responsible for the transport of nutrients to locations where they can either be immediately utilized or stored for future use. When the availability and effectiveness of insulin is compromised, extra magnesium in the blood cannot be properly stored, so most of it may be wasted instead.25
This can dramatically increase the odds that diabetes patients may develop a magnesium deficiency. And of course as the magnesium deficiency becomes worse, insulin resistance may increase and insulin production by the pancreas may decline even further.
Here are references 24 and 25 from that quote:
24.Takaya, J., Higashino, H., & Kobayashi, Y. (2004). Intracellular magnesium and insulin resistance. Magnesium Research, 17(2), 126-136. Retrieved from
http://www.ncbi.nlm.nih.gov/pubmed/15319146
25.Sircus, M. (2009, December 8). The Insulin Magnesium Story [Web log message]. Retrieved from
http://drsircus.com/medicine/magnesium/ ... um-story-2
But fructose is the main problem associated with weight gain, because fructose is metabolized differently form other sugars and it skips the insulin-signaling step. I have highlighted in red why fructose causes weight gain. From pages 49–50 of the PC book:
Contrary to advertising claims made by certain industry interests, including their paid lobbyists in Washington, D.C., all sugars are not equal. The contention arises around the differences between the ways in which the body processes glucose fructose.
Sucrose, fructose, and glucose are all simple sugars. Sucrose (aka common table sugar) contains a 50–50 combination of glucose and fructose. By contrast, high fructose corn syrup (HFCS) contains a higher percentage of fructose, and the amount can vary over a wide range depending on the individual product specifications. When analyzed for their specific properties, they all provide the same amount of energy per unit of mass. But despite the fact that they contain equal amounts of energy (calories), the ways in which the body utilizes these sugars varies dramatically.
Glucose is the most important sugar (as far as energy production in the body is concerned) and it is also called blood sugar because it's the type primarily used by both the body and the brain as fuel. It can provide all the energy the body and the brain need (although when necessary, both the body and the brain can operate on the conversion of fat into energy).
It's important to note that glucose is the only sugar that triggers an insulin response.
Insulin is produced in response to an increase in the blood glucose level, but an increase in the blood fructose level does not cause an insulin response.54 This results in a completely different way of handling fructose metabolization.
Fructose can only be metabolized by the liver and the process requires the enzyme fructokinase. Insulin allows glucose to pass from the blood into the muscles where it can be immediately burned as fuel. But because fructose does not prompt the release of insulin, it will not have the opportunity to be burned as fuel, and because of that important difference, fructose digestion tends to result in the formation of more fat deposits.
Another important difference is the production of leptin.
Leptin is a hormone produced by fat cells and used by the body to regulate energy balance (read that "prevent overeating") by suppressing hunger whenever energy levels are already sufficient. Glucose stimulates the production of leptin, but fructose does not. Obviously the failure to promote the production of leptin creates an increased likelihood of overeating.
Here is reference 54 from that quote:
54. Ancira, K. (n.d.). What is the differene between sucrose, glucose & fructose? Healthy Eating [Web log message]. Retrieved from
http://healthyeating.sfgate.com/differe ... -8704.html
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