I received my copy of the quarterly TCOYD newsletter a few days ago, and was intrigued to find an article explaining oxidative stress. I’d been hearing that term associated with diabetes complications for quite a while now and wondering what the heck the connection was.
The OnTarget blog offers a great core explanation:
“Oxidative stress (OS) occurs when the available supply of the body’s antioxidants is insufficient to handle and neutralize free radicals of different types. The result is massive cell damage that can result in cellular mutations, tissue breakdown and immune compromise.”
Lucky for us, Dr. Irl Hirsch and Dr. Michael Brownlee, Director of the JDRF Center for Diabetic Complications Research, have been studying the causes of diabetic complications for a number of years. The landmark DCCT study provided the first solid empirical evidence that high glucose levels have a direct impact on the development of complications. But how exactly does high blood sugar do its damage? Researchers have identified four biological pathways, all of which may be triggered by oxidative stress, according to Hirsch and Brownlee.
“To make high glucose inside a cell, these four pathways have to be turned on. But the question was, is there a black box in there controlling the whole process? We discovered there is. It’s an overproduction of reactive oxygen species or free radicals, generated because high blood glucose, which is normally burned off in sub-organ of the cell called mitochondria,” Dr. Brownlee explained to me in a recent telephone interview. (plus a lot more scary science-speak, wha?)
“When you have high glucose in the blood, most tissues can ‘close the gate’ and keep the internal glucose levels normal, but certain cells cannot do that, so they get high blood glucose inside the cell, causing damage. These happen to be mostly nerve cells… We’re focusing on focus on intra-cellular oxidative stress, due to the lack of the ability to ‘close the gate’ to glucose.”
Ah, got that. From my layman’s viewpoint, the discovery of a “black box” or “unifying mechanism” that causes complications sounds promising. The first step to curing anything is identifying the exact pathways by which the damage occurs.
So we should all be taking anti-oxidants like vitamin E, vitamin C and beta carotene, right? WRONG. According to Dr. Hirsch’s TCOYD article, human trials have shown no benefit for loading up on these, and doing so may even increase risk for heart attack and stroke.
Instead, current thinking centers on — you guessed it — reducing glycemic variability (our nemesis). “There is currently a huge controversy about how glucose variability and reducing the after-meal spikes may improve oxidative stress,” Dr. Hirsch writes. Some research apparently suggests that reducing high spikes “can provide a better defense against oxidative stress.”
So what does the good doctor suggest for us patient-types? “Using the tools we have at hand!” to reduce BG spikes.
For Type 2s, that would include the drugs Prandin, Starlix, Precose, Glyset, Januvia, and Byetta. For Type 1s, think Humalog, Novalog, Apidra and Symlin. CGM systems can help all diabetics improve their BG control, of course.
Nothing entirely new there — except for perhaps better motivation than ever to keep our post-meal BG levels in check. Yeeeooow.