Gestational Diabetes

What is gestational diabetes?
Gestational diabetes (or “glucose intolerance of pregnancy”) is defined clinically as “a carbohydrate intolerance of variable severity that begins or is first recognized during pregnancy”.

What in the world does that mean???
Tough to understand, isn’t it? That’s a clinical definition…what you’ll probably read in most pregnancy books, or on medical sites on the web. But we’ll take it a step further. Our goal here is to help you understand the diagnosis of GD, including a bit of history, which is very important. Let’s start by understanding what is a NORMAL insulin response during pregnancy.

What’s normal during pregnancy?
There are several mechanisms involved…

  • Insulin: transports glucose (sugar) out of your bloodstream, and into your cells.
  • Insulin suppression: in normal pregnancy, certain hormones prevent insulin from doing it’s job.
  • Hyperglycemia: the result of insulin suppression is that there is more glucose circulating in your blood.

The extra glucose circulating in your bloodstream is specifically there for your baby: since he gets his nutrients from your blood supply, this glucose provides fuel for his growth.How does this affect you, the expectant mom?
Your insulin levels are most likely normal, or even above normal, however…

  • This insulin-suppresant effect increases as pregnancy advances, so you will naturally have higher levels of blood glucose (hyperglycemia) after eating than the average non-pregnant woman.
  • You will also have LOWER levels of blood glucose (hypoglycemia) after an overnight fast — that’s why you may feel a bit queasy or just extremely tired when you first wake up in the morning. (Based on Goer 1995. References: Goer 1991; Kuhl 1991; Forest et al. 1983)
  • In routine prental tests, you may be told there is some sugar in your urine. About half of all pregnant women will have some sugar in their urine at some point during pregnancy. (Eisenberg et al. 1991)

OK, so if this insulin suppression and hyperglycemia is normal, then what’s gestational diabetes?
Here’s where it becomes important to understand some history of the diagnosis of gestational diabetes. But first, a few FACTS to keep in mind:

  • FACT #1: Diabetes (the pre-existing sort, not gestational diabetes) is known to pose serious threats to the baby.
  • FACT #2: Diabetes is more common in women who are overweight and older, and is commonly preceded by a lifetime of sugar addiction, or high-glycemic eating.
  • FACT #3: Pregnant women with glucose levels at the upper end of the spectrum are more likely to develop diabetes later in life. (O’Sullivan and Mahan 1964) This makes sense, considering FACT #2 above. A woman who eats too much sugar would logically have higher blood glucose levels than one who eats a balanced, low glycemic diet.
  • FACT #4: Pregnant women with blood glucose values in approximately the upper 3% for pregnancy (1-2% of all pregnant women) are diagnosed with “gestational diabetes”.

With those facts in mind, we’re ready for a little history lesson.

When O’Sullivan and Mahan (1964) studied 752 pregnant women in Boston, they showed that pregnancy could reveal a woman’s “prediabetic” condition (i.e., her likelihood to develop true diabetes later in life), researchers assumed that glucose intolerance during pregnancy would be dangerous to the baby, in the same way as true diabetes poses risks.

So, in the 1960s and 1970s, “glucose intolerance” in pregnant women was studied — and sure enough, these studies showed higher rates of complications. However, a close review of those studies reveals many flaws (Goer 1991). In some cases, women were selected for the studies because they had a previous bad outcome or certain risk factors…some studies mixed in known prepregnant diabetics…generally, these studies completely confused the issues about glucose intolerance by serious errors in design. Furthermore, management of the condition probably contributed to the poorer outcomes these studies showed: starvation diets, early elective induction and withholding nourishment from the newborn, all of which we now know predispose both mother and baby to serious complications. In spite of the problems with study design, researchers were convinced that they were dealing with a serious problem which required further investigation.

The Conferences

International conferences began in 1979. At the first conference, one of the organizers opened with a metaphor which reduced pregnancy to a “tissue culture experiment” and pregnant women to “incubators” supplying a potentially faulty growth medium (Freinkel 1980; Goer 1995). Add to this the assumptions of the researchers based on faulty studies and you have the perfect recipe for rather biased results.

The next conference was in 1985. It was at this conference that “gestational diabetes” was officially established as a new disease. The name “gestational diabetes” was chosen by the conferees over “glucose intolerance of pregnancy” so that insurance companies would pay for treatment, and so women would take the condition seriously (Second International Workshop-Conference 1985). About 1-2% of pregnant women are now diagnosed as gestational diabetics, making it the most common complication of pregnancy.

The 1990 conference reaffirmed the screening procedures recommended by the 1985 conference, which included screening all pregnant women with the now-standard oral glucose tolerance test (OGTT). The American Diabetes Association concurred (American Diabetic Association 1987). The American College of Obstetricians and Gynecologists recommends only selected screening (i.e., screen only those with risk factors) for women under age 30 (ACOG 1986); however, many U.S. obstetricians screen everyone.

The screening and diagnostic blood glucose values recommended by the conference and endorsed by ADA and ACOG are based on the 1964 values set by O’Sullivan and Mahan. This study defined abnormality by the later appearance of diabetes during the women’s lives, not by any existing diabetes nor did it account for the outcomes of the pregnancies, good or bad. It should also be noted that O’Sullivan and Mahan chose their cutoffs for convenience. It is on this study that current diagnostic values are based. There has never been any research to determine when “gestational diabetes” actually begins, nor when fetal complications begin to arise. This lack of correlation with complications has led some researchers to suggest lowering diagnostic values, rather than reexamining the validity of GD testing. This would, of course, lead to more women being diagnosed as gestational diabetics. (Ed. Note)

So, you’re saying that the test for GD isn’t really all that accurate?
Yes. First of all, the range of “normal” blood sugar is no longer the same for pregnant and non-pregnant women. In 1979, the “normal” range for pregnant women was redefined as lower than the normal range for non-pregnant women. So more pregnant women will actually test positive for diabetic levels of glucose than non-pregnant women will. The typical screening test (though it may vary by location and care provider) is done at 24-28 weeks of pregnancy, and requires the pregnant woman to drink a 50 gram dose of “Glucola”, a glucose-containing drink, after a 12 hour fast. Her blood sugar level is tested before the drink, and one hour later. This screening test is performed without regard for what the woman has eaten in the days before the test, and there is no preliminary preparation. Note that this is an abnormal ingestion of glucose. Under normal circumstances, glucose is a by-product of foods you eat, which gets into your bloodstream after the breakdown of foods by your body. If you get more glucose than you need at a given time, your liver will convert it to glycogen and store it for fuel later on. If you haven’t eaten in a while, your body begins to draw on this stored glycogen. Conversely, if you need more glucose than usual (as you do in pregnancy) you will burn more glucose immediately, and save less glycogen for later. Now consider what happens when you take the OGTT. In the testing situation, you are ingesting 50 grams of plain glucose on an empty stomach. This is a highly concentrated glucose load! If you haven’t stored enough glycogen over the past few days (and most normal pregnant women store less, because they need more glucose circulating for the baby), then your body is going to react strongly to this huge dose of glucose. Worse yet, if you’ve had too many refined (simple) carbohydrates and processed foods in the days before the test, your glycogen reserves will

This is all fascinating….especially since I’m supposed to have my 1 hour screening test for GD tomorrow!! My doctor said it was important…but now I’m really confused. What should I do?
The first thing you need to do is evaluate your current diet.

Diabetes is known to be dangerous the the baby, but you’re saying it’s different from gestational diabetes. What is the difference?
Type I diabetes is where the insulin making cells in the pancreas have been destroyed. In this case, extremes of high and low blood sugar in early pregnancy can damage the baby while it’s being formed. But this is not your problem. You are producing plenty of insulin (Hadden 1980). Type II diabetes is similar to the situation in pregnancy. Found mainly in overweight and older women, Type II diabetes is a problem of insulin resistance not production. But there are still marked differences between you, the “gestational diabetic” and a pre-pregnant diabetic woman.

There are two risk factors in regular diabetes which differ from so-called gestational diabetes:

  1. Long standing diabetes may damage the mother’s blood vessels and kidneys, which may in turn put the baby at risk. But you don’t have long standing diabetes.
  2. Chronic hyperglycemia (too much sugar in your blood) can overfeed the baby in utero resulting in an unusually large (macrosomic) baby. However, other factors far outweigh glucose intolerance in determining baby’s weight (Keen 1991; Phillipou 1991, Green et al. 1991; Farmer et al. 1988).

Ed. note: Following my routine OGTT screening test in my first pregnancy (1994, age 27, no risk factors) I argued that I had no symptoms and no risk factors, so how could I have “failed” the screen? My doctors told me that the lab had recently lowered their diagnostic values for the 1-hour screening test. I stalled on the follow up 3-hour OGTT, which involved fasting and a larger dose of Glucola. However, my obstetrician finally told me that if I didn’t take the test, he’d have to have my baby tested and treated for hypoglycemia — blood tests and sugar water from a bottle — after birth. This was enough to scare me into having the test, which caused me considerable physical distress (nausea) and risk (I nearly lost conciousness while driving to get food after the test was over. I had been fasting for about 16 hours by that time. It would have been longer, if I’d taken the original appointment time they offered, which was noon. The protocol was nothing to eat for 12 hours before the test, but since I was not likely to eat a 11:45 p.m., I would have fasted from about 9:00 p.m. to noon, plus the three hours of the test itself when I’d have been running on Glucola. Fortunately I knew enough of Dr. Brewer’s work at the time to know that fasting was not healthy for me or my baby, and chose to put off the test until they could fit me in at the earliest possible appointment time.). I was told later that my obstetrician really had no right to make such a threat. It would have been up to my baby’s doctor (pediatrician) to make the call on the baby’s treatment.

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