There was a little girl,
Who had a little curl,
Right in the middle of her forehead
When she was good
She was very good indeed
But when she was bad she was horrid.
So goes the familiar poem by Henry Wadsworth Longfellow, and so goes most of our low-carb diets I suspect. When we are in diet mode and are deeply committed, we are very good indeed, but when we break and hit the carbs (and this includes yours truly) we are horrid. A paper in this week’s JAMA presents data confirming what I’ve long suspected: carb bingeing now and then could actually cause worse free radical damage than regularly eating more carbs on an ongoing basis.
The paper titled Activation of Oxidative Stress by Acute Glucose Fluctuations Compared with Sustained Chronic Hyperglycemia in Patients With Type II Diabetes shows that patients with diabetes who have fluctuations in their blood sugars incur more free radical damage than those with high but not fluctuating blood sugar levels. Before we get into the nitty gritty of the paper, I will step back a little and go over some of the biochemistry involved so that the data will be more understandable to those who might not have a technical background.
First, let’s look at how blood sugar is measured. The standard way is to draw blood (usually after the patient has fasted for 12-14 hours) and test it for a blood sugar level. Although this is the way that diabetics were monitored for years, it’s not a particularly accurate means of managing patients with diabetes. The fasting blood sugar test itself is reliable, but it only tells what the blood sugar is at the precise moment the blood was drawn–not what it was the week before or the day before or even the hour before. The typical drill was that diabetic patients would come to the office, have their blood sugar levles checked, and based on the results, leave with their medications or insulin adjusted as necessary. Many diabetic patients who didn’t like getting lectured by their doctors on following the proper diet, exercising, etc., learned that if they were very good indeed for the few days before their office visit, their blood sugar levels would be close to normal. They would leave with the congratulations of their doctors ringing in their ears and head back to the trough until a few days before their next visit.
A while back a clever person figured a way to detect blood sugar levels not just at the precise moment the blood was drawn but in a way that measures the average blood sugar level for the previous month or two. The test, called a hemoglobin A1C (pronounced, logically enough, hemoglobin A one see), tells the doctor what the patient’s average blood sugars have been over the past couple of months. No more can patients be very good indeed for a day or two before their blood draw because a day or two of lower sugar levels won’t change the test values. As you might imagine, the advent of the Hgb A1C test allowed doctors to manage their diabetic patients much better.
Just for grins I’ll explain how the test works. If you’re not interested, skip on down to the next paragraph. If you take a glass of water and stir some protein into it along with some sugar, over time the sugar will react with the protein in an irreversible way. The sugar will actually attach itself to some to some of the protein chains. The process takes a fair amount of time, but the longer you leave the sugar in the water with the protein, the more of it will attach. If you measure the amount of the protein-sugar complex that forms, you will have a rough measure of how long the sugar and the protein were together. If you don’t find much of the protein-sugar compound, then you can figure that the two haven’t been together for long; or if you find a lot, then you know they’ve been mixing it up for a while. The same goes for the amount. If you stir the protein into the water and add a tiny bit of sugar, after a time you will find a small amount of the protein-sugar compound; if you add a lot of sugar, then after the same amount of time you will find more of the protein-sugar compound. By taking multiple samples over time and tabulating the results you will be able to come up with a scale that says if you find this much of the protein-sugar compound after a certain number of days, then you can determine how much sugar was added. This is precisely the way that the Hgb A1C measurement works. Sugar in the blood attaches to protein in the blood. By measuring one of those proteins-sugar compounds (Hgb A1C) you can tell what the average amount of sugar in the blood has been over the past couple of months.
The second test I want to discuss that is critical to an understanding of this paper is the urinary measurement of 8-iso prostaglandin F2 alpha (8-iso PGF). When free radicals attack fatty acids that are a part of the cell membrane the damaged products produced are called isoprostanes. Isoprostanes in general are indicators of free radical damage and oxidative stress. Researchers can perform various experimental procedures and measure the release of isoprostanes in the urine and determine how much oxidative stress and free radical damage their procedure caused. 8-iso PGF is simply a specific isoprostane commonly used experimentally to determine the degree of oxidative stress/free radical damage.
Now that you know what all the tests are and what they mean, the paper is a pretty straightforward affair. It is well known that elevated blood sugar levels cause oxidative stress and free radical damage, which is probably the primary reason diabetic patients have increased risk for atherosclerosis and accelerated aging. The authors of this paper wanted to see if a steadily elevated blood sugar caused the production of more 8-iso PGF, i.e., more free radical damage, than wildly erratic blood sugars that averaged out to about the same as the steady state ones. In other words would a blood sugar level that stayed at around 180 (definitely diabetic) most of the time cause the same, more, or less free radical damage than a blood sugar that fluctuated between 100 (upper end of normal) and 250 (pretty high), but averaged by Hgb AiC measurement at about 180?
The researchers recruited 21 subjects with diabetes and 21 age and sex matched non-diabetic controls. They monitored the diabetic patients on a round the clock basis to determine not just their average sugar levels but their fluctuations as well.
The data showed that the diabetic subjects had much higher urinary levels of 8-iso PGF than did the non-diabetic patients, which would be expected. But the data also showed that diabetic subjects who had large fluctuations in blood sugar levels had even greater 8-iso PGF formation than diabetic subjects with more stable, yet still high, blood sugar levels.
These data were in diabetic patients but I suspect the situation holds true in non-diabetic patients as well. And, unfortunately, especially in followers of the low-carb diet. Why so?
Following a low-carb diet makes one a little glucose intolerant, which is the reason that the instructions for a glucose tolerance test always include the admonition to eat plenty of carbs in the week before the test. Why? Because all the macronutrients–glucose, fat and protein–are broken down by enzymes during the metabolic process. And all the enzymes necessary for the metabolism of the various macronutrients are made on demand but not immediately. If you are on a high carbohydrate diet, then you will have plenty of enzymes on hand to deal with the carbohydrates you consume. If you switch to a low-carbohydrate diet, it takes a while to manufacture the enzymes in the quantities needed to deal with the extra fat and protein that your metabolic system hadn’t been exposed to. This deficiency of protein/fat metabolizing enzymes is the reason people starting a low-carb diet become so easily fatigued–they’ve got plenty of enzymes on hand to break down carbs, they just don’t have the carbs to metabolize. Once they produce the enzymes necessary to deal with the load of protein and fat, which takes a few days, they become low-carb adapted and no longer feel fatigued.
Once people become low-carb adapted–as I hope we all are–then the same thing happens if they go face down in the donuts. They don’t have the enzymes on board to deal with the sudden influx of glucose, and, as a consequence, their blood sugar spikes higher than it would on a person eating the same amount of carbohydrate who is already carb adapted.
This paper shows that these carb spikes are not benign. As the paper points out
Risk factors of atherosclerosis such as hypertension, regular smoking, hyperlipidemia, and obesity have been described as being associated with elevated urinary excretion rates of isoprostanes.
Since the best thing we can do for ourselves is limit free radical damage as much as possible, the obvious way to do so is to maintain a constant low level of blood sugar, for which the low-card diet is just the ticket. In view of these recent findings when we’re good, we should be very good indeed, but when we’re bad maybe we shouldn’t be quite so horrid.