Starting on November 4th 2012, I began a 13 week experiment in changing my eating and exercise habits, for the best of all reasons: I didn’t want to die. I was chronically ill with stomach troubles, I was sleeping badly, and my average blood glucose was in the neighborhood of 150 mg/dL — well into the range of type II diabetes mellitus. For the experiment, I’ve cut my daily consumption of carbohydrates to a net of 30 grams a day and cut wheat out entirely, and I’ve added exercise following a Tabata Protocol, along with yoga, kettlebells, and (too rarely) weight lifting. I report my results here at PJ Media Lifestyle, and also on my 13 Weeks Facebook page.
If you’re been reading 13 Weeks since I started, you’ll remember that I had realized on about October 15 that I was 100 lbs or so overweight at 301.5; I was in chronic ill health with both gastric reflux disease and irritable bowel syndrome; and I had moved from pre-diabetic to flat-out diabetic in the span of about a year. At 57, I realized I was only 12 years younger than my father when he died, and only 20 years younger than my mother was when she died on January 11, 2012. Twenty years wasn’t enough, and twelve years was for damn sure not enough; something had to be done.
Now, after Week Nine, the effects of what I’ve done are starting to really show up. Here’s the chart I’ve been keeping to plot my progress. The plus signs are my weight in pounds, the x’s are my blood glucose as measured with a drugstore glucometer, and the lines are the linear best fit line to the data.
As you can see, the lines are headed down — which is the good direction. On Wednesday I went to the doctor, and got weight and my bloods done again. My weight’s down 30 lbs since October 19, 19 lbs since I started this November 4th. But I swore I wasn’t paying attention to the weight (gloat). Even if I lost a lot. (Gloat.) One of the blood tests I did was the glycosylated haemoglobin HbA1c test, which is a diabetes test. I’ll tell you my results below; before I do, however, I want to explain the test and why it’s important.
With diabetes, of course, we’re primarily concerned with the blood glucose level. When I was a kid, my “second mom” Julia Medina took care of us; Mrs. Medina was diabetic and dependent on insulin, but home glucometers weren’t available; the only real test diabetics had was to watch their urine for ketones using test strips, and the only real measure they had for control of diabetes was whether you tended to fall into a coma, either from low blood sugar, or from high. If your blood sugar stayed too high, you risked blindness, advancing neuropathy and pain, and kidney disease, hearth disease, or — worst of all from my point of view — creeping necrosis of the extremities. (Your fingers and toes die and become gangrenous; they’re amputated. The stumps become gangrenous; they’re amputated a little higher. Eventually you run out of pieces and you die. Don’t even google “diabetic necrosis”, you don’t want to look at those pictures.)
Luckily, Mrs. Medina was well-controlled; she lived a long life. A whole lot of diabetics didn’t. Three things, put together, improved the chances of a diabetic living a long life over the last 20-30 years. The first was inexpensive direct tests for blood glucose levels; the second was bio-engineered human insulin (before then, insulin extracted from the pancreases of hogs was used, but it doesn’t exactly match human insulin. It was better than nothing but still had problems.) The third was the wide availability of the glycosylated haemoglobin HbA1c test (which we’re going to just call the A1c from now on.) What the A1c let doctors do is infer what your average glucose had been over about the last three months.
Here’s how it works. Hemoglobin, the chemical component of the blood that carries oxygen and makes the blood red, can bind to glucose, forming glucose-bearing (or glycosylated) hemoglobin. The rate at which it binds is proportional to the concentration of glucose in the blood. It binds fairly slowly, so your hemoglobin doesn’t just suck up all the sugar right away. Instead, over the life of a red blood cell (an erythrocyte), which is about 100 days in the normal human, a fairly small percentage of the hemoglobin will glycosylate. At the end of the average 100-day lifespan of the red blood cell, it’s broken down by the body and it’s components recycled; part of that process separates iron from the hemoglobin, which also liberates the glucose.
Remember, though, that the rate at which the glucose binds is dependent on the concentration – the more glucose, the more it binds to the hemoglobin, and once bound it stays bound until the red blood cell dies. The result is that the percentage of cells with glycolated hemoglobin in the blood is proportional to the average blood glucose level for the last several weeks.
Still with me? We’re getting to the payoff. From my blood glucose readings, I’d known things were improving.
In October, A1c was 7.5 percent. You can compute the equivalent average blood glucose, which comes out to be about 170 mg/dL. An A1c of 6.5 percent or more is diabetes.
Yesterday, my A1c was 6.2 percent, or an average of around 130 mg/dL. An A1c of between 5.7 percent and 6.4 percent is considered enough for a diagnosis of pre-diabetes.
Or, in my case, post-diabetes. By blood sugar is controlled now, down to healthy levels — and I’m only about two-thirds of the way through the life span of red blood cells that were new when I started this; I can expect the A1c to go down. If it keeps declining at the rate it has been, it might be as low as 5.5 percent by the end of this 13 weeks.
That would be normal.
One more thing I want to mention. A dear young friend of mine has decided she wants to enter the military, but to do so she needs to lose ten pounds, and wants to get in better shape. As a result, she’s started a blog of her own, 14 Weeks for Freedom, where she’s making her own open commitment to some life changes.
I am extremely proud of her; please drop over to the blog and give her your support.