Gestational Diabetes: The Numbers Game

by KMom

Copyright 1998 KMom@Vireday.Com. All rights reserved.

DISCLAIMER: The information on this website is not intended and should not be construed as medical advice. Consult your health provider. This particular web section is designed to present more than one view of a controversial subject, pro and con. It should be re-emphasized that nothing herein should be considered medical advice.



Why All The Confusion?

One thing that is especially confusing in gd is the various numbers that are tossed around all the time. It is very common to get confused! For example, 140 mg/dl is a number you see a lot, but it means different things in different contexts. It is the cutoff for the one-hour glucose challenge test in pregnancy, it used to be the number for diagnosing 'true' diabetes outside of pregnancy, and it is the cutoff for desirable blood glucose levels one hour after a meal in many programs. When the levels for diagnosing diabetes outside pregnancy were recently revised to lower levels (126 mg/dl), it confused many pregnant women, who wondered if the cutoff for the one-hour test in pregnancy was also going to be lowered or if their target bG for one hour after eating was going to be lowered too. The answer is that one has nothing to do with the others. They all refer to different measurements; it is just coincidence that they use the same number as a cutoff.

But even among those who have studied the basics of gd, the various reference numbers commonly used in gd discussions can be very confusing. Kmom knows from experience that when gd comes up for discussion on mailing lists, people often mix up their references, compare numbers incorrectly, and generally make the discussion even more confusing. This websection is an attempt to clarify this very confusing issue and discuss the various guidelines that gd women are often given.

Many newcomers to gd issues will find it too confusing at first and may need multiple readings in order to really keep straight all of the various recommended numbers. If you find it confusing at first, take heart; many people do! Even experienced gd laypeople make errors because they don't completely understand the big picture, so always take great care when reading any discussions or making any posts about the issue.


Special Note: As if things weren't confusing enough already, remember that the USA uses different standards of measurement than the rest of the world. This FAQ mostly uses the USA measurement of mg/dl for convenience, but readers from outside the US will probably need to convert these readings. US readers that review the actual medical studies listed will often need to convert measurements as well, since most use the measurement of mmol/L instead.

To convert between mg/dl and mmol/L, use a factor of 18----in other words, to go from mmol/L to mg/dl, multiply by 18; to go from mg/dl to mmol/L, divide by 18. For example, the usual cutoff for the one-hour glucose challenge test is 140 mg/dl, but many medical references will use the worldwide standard of 7.8 mmol/L instead. These refer to the same standard, just expressed differently. (A further discussion of the conversion issue and the reasons for using primarily mg/dl in this FAQ can be found in the section on Glucose Testing.)


ADDITIONAL REMINDER: Choice of provider is a HUGE decision when you have gd, and one of the most important points of this FAQ is to point out that gd care is extremely variable at times. Don't feel that the position of your provider is the only advice you would get; there are many others who will offer different advice. This doesn't mean your provider is right or wrong, just that standards can differ a great deal. It's very difficult to know which protocols and numbers to go by. This section of the FAQ is to give you an idea about some of the commonly-recommended blood sugar goals and the pros and cons of each, as well as familiarity with issues surrounding bG protocols. The purpose of this section is NOT to advocate one treatment philosophy over any other, but to give readers more background on the issue and an idea of the variance of care possible and the reasons behind it. A more thorough treatment of the debate will be found in the section on GD: Controversies.



A Brief Overview of Treatment Numbers

Some people find all the different number references so confusing that they just basically want the summary version of this issue. This part is therefore just a brief listing of the numbers most commonly used by the majority of gd providers and some of the thinking behind them; a more complete discussion will be found below, as well as variations on the most common recommendations. Remember that if YOUR provider's recommendations differ from the ones listed below, it simply represents a difference in opinion and protocol. It doesn't mean that the numbers below are incorrect or that your provider is incorrect. It simply means that there is a divergence of opinion among even the experts, something very common in gd!

Basically, the crux of the matter is that a woman with gd needs to keep her blood sugar levels equivalent to those found in non-diabetic women. The usual target range is between 60-120 mg/dl. The exact numbers depend on the philosophy of your provider (how strict of control he/she insists on) and the exact requirements of when the measurement is done and what kind of measurement it is (fasting vs. post-meal). You must be extremely careful to understand EXACTLY what your provider requires and why. Be sure to ask lots of questions so that you understand it thoroughly.

Fasting Numbers (the first measurement upon waking, before eating)

The most-preferred fasting number is usually below 95, with most providers starting insulin at levels of 105 and others starting insulin right at 95. A few providers will even start insulin at readings >90, but this is more unusual. The explanation is that although they prefer that your numbers be below 95, there is usually more leeway among many providers before actually *requiring* that you go on insulin, since there is a tradeoff of risks and treatment burden at borderline levels. The official recommendation from the American College of Obstetricians and Gynecologists for requiring insulin is 105 fasting; it notes that lower numbers may be preferable but that this is not proven yet. Lower levels may prevent more macrosomia (large babies) but this comes at the price of much more intervention, cost, and some possible risk. At what level the purported reduction of macrosomia etc. justifies the increased level of intervention, risk, and cost is one of the most hotly debated issues of gd. Also at issue is the safety (for both mother and baby) of more aggressive use of insulin.

Basically, any fasting numbers between 90-105 are in a very gray area; some providers will deem them too high and in need of insulin, and some will deem them acceptable in view of the tradeoff of risks. It's safe to say that it is MOST optimal to aim for fastings under 95 and preferably under 90, but whether readings of 90+ justify the assignment of insulin is highly debatable. (See below and the sections on What If I Need Insulin?, and GD: Controversies for further perspectives on this issue.) At this time the issue is not proven, one way or the other.

If you are in need of insulin treatment, generally speaking the treatment goal numbers are lower. Most providers want fasting levels below 90 mg/dl if you are on insulin already. Some providers demand even lower numbers, but generally <90 is standard.

Post-Meal Numbers (the reading taken a set amount of time after a meal [post-prandial])

The most-preferred post-meal number is usually <120 two hours after a meal, or <140 one hour after a meal. A great deal depends on how they time the post-prandial (pp) measurement. Some providers prefer measuring one hour after meals, others two hours after meals. Another important question is whether the measurement is timed from the beginning of the meal or the end of the meal---recommendations vary. With the two-hour measurement, it is usually measured as two hours from the beginning of the meal. With the one-hour measurement, it is usually measured as one hour after the end of the meal, but this is not always standard. And some providers demand even stricter numbers than noted above, especially if you are on insulin treatment. Again, ask your provider THEIR requirements.


Important Distinctions to Make

These are the most basic requirements you'll come across in your gd treatment process. If you are easily confused, stop here. If you want to understand the issues further, be sure to read and understand this section especially well. You may want to refer back to it at later points as well; it can be very confusing at times.

When you run across any reference numbers used in the process of dealing with gd or 'regular' diabetes, it is important that you make critical distinctions about exactly what the numbers refer to. Many numbers are similar, but mean different things in different contexts. For example, as noted above, the number 140 mg/dl is used in a number of contexts:

So you see that any one number can mean different things in different contexts. This can quickly become extremely confusing! It is especially important to pay attention to WHAT the number refers to. Consider a reading of 105. This could be a bit worrisome, alarming news, or excellent news, all depending on the situation it occurs in.

So you MUST pay close attention to the CONTEXT of the number. The critical quesitons are who is being tested (are they pregnant or not), what type of test is it (fasting, post-meal, glucose challenge, glucose tolerance test, capillary test, venous plasma test), what the purpose of the test is (screening, diagnosis or treatment), and what is the timing of the test (how long since eating/testing). Another important question is whether this a universally accepted protocol or whether recommendations vary from one provider to the next.

Here is a summary of the important questions to ask and why:

  1. Is it for use in pregnancy or outside of pregnancy? Because there is a fetus involved, the control required in pregnancy is MUCH stricter than for people who are not pregnant.
  2. Are the numbers for the purpose of diagnosis or for the purpose of a treatment plan? - The numbers for diagnosing gd on a test will be different than those used as treatment goals. Also, the numbers used to diagnose the need for insulin in gd will be higher than the treatment goals that your provider will want you to aim for once you start using insulin.
  3. Do the numbers refer to gestational diabetes or to 'regular' diabetes? - For example, target numbers for treatment of type I pregnant diabetics may be lower than the initial numbers given as treatment goals to diet-controlled gestational diabetics, though this will vary between providers.
  4. Are the numbers for insulin-dependent people or those treated by diet alone? - The treatment goals for gestational diabetics who need insulin may be somewhat stricter than for those who do not use insulin, though again this depends a lot on provider philosophy.
  5. What do the terms mean? Do the numbers refer to fasting readings or post-prandial readings and how exactly does your provider measure these? Fasting numbers refer to the first morning reading before eating, while post-prandial results are measured after eating. The exact protocol for taking each measurement, too, will vary between providers---some want fastings only after 12 hours, while others want them after only 8-9 hours. Post-prandial protocols also vary quite markedly; see above for more detail.
  6. How are the readings being measured? What was being tested? Home monitoring uses capillary whole blood. Lab tests usually use plasma. On rare occasions, venous whole blood might be used on a home monitor. Plasma readings tend to be higher by about 15% as a general rule, but not always. References for diagnostic and screening tests refer to PLASMA levels, not capillary levels.
  7. Are the numbers standard to all providers or are they the recommendation of your own provider, based on his/her personal philosophy of treatment? Some providers require much more stringent control and will put you on insulin at much lower levels than other providers because of a difference in treatment philosophy. Just because one provider requires certain levels of adherence does not mean that all will. In gd, there is significant variance in treatment requirements between providers.


Examples of Common Causes of Confusion

Here are some sample situations that tend to confuse people. If you find these confusing, go back and review the key issues listed above, but don't get upset---many people find these pretty confusing!

Example One: Diagnosing diabetes. The cutoff for diagnosing diabetes in non-pregnant people used to be 140 mg/dl, fasting. This diagnosis level has since been lowered to 126 mg/dl. However, a pregnant woman, due to safety issues for the fetus, is diagnosed with gd if her fasting levels exceed 105 mg/dl, and some providers diagnose at levels of 95 mg/dl or so because they personally feel that stricter goals lead to better outcomes (this is still being debated).

Example Two: Changing Treatment Goals. Treatment goals may get more strict once you are on insulin. A woman newly diagnosed with gd (but not using insulin yet) may be told to keep her fasting levels under 105 mg/dl, but if she exceeds that and needs insulin, she may be told to aim for a target fasting range of <90 mg/dl, or even less in certain very stringent protocols. Some providers demand the same numbers before or after needing insulin, but in practice, they are often a bit different. Be sure to ask your provider their recommendations for each situation.

Example Three: Differing Protocols Between Providers. Scenario: Several women with gd are chatting online. The first mother has been told that she will be put on insulin if her fasting numbers exceed 105, the second mother was put on insulin when her fastings went over 95, and the third was put on insulin at fastings over 90. (Some women have even been put on insulin at fastings of 80). The women are puzzled and concerned. The mother who has been permitted to have higher fasting readings without insulin wonders if she is endangering her baby by not being assigned to insulin; the women who have been subjected to stricter protocols are distressed at the realization that if they had the first mother's doctor, they would not now be required to inject with insulin several times a day and face higher-risk protocols. They wonder which is the 'right' answer here. The truth is that nobody knows for sure but every provider has his/her own preferences. Some providers want women with gd to have extremely low numbers, feeling that this minimizes macrosomia (big baby) and provides better results. Others are much more liberal with their numbers, feeling that aggressive insulin use entails its own risks and not enough research has been done on its safety. The numbers that YOUR provider tells you to aim for can differ markely from the numbers a different provider might give you; there is no 'correct', universally accepted protocol here.

Example Four: Differing Number Contexts and Differing Protocols Between Providers. A gd mom may be told to keep her post-meal levels under 120, two hours after testing. She may talk online to another woman who has been told to keep her post-meal levels to <140 after one hour. They may be joined online by another woman whose provider has even stricter protocols and wants levels of <120 one hour after eating. They may get completely puzzled if one declares to all that 120 is the 'correct' standard. They forget that they are measuring post-meals at different times, and that required readings differ markedly sometimes between providers. By and large, treatment protocols are NOT standardized for gd and it is difficult to compare treatment requirements with others unless you thoroughly understand the context and meaning of the readings.

Example Five: Pregnant vs. Non-Pregnant Standards. Scenario: Several pregnant moms with gd chat online about their post-meal treatment goals but are joined by a woman married to a diabetic. Confusion arises when she states that he needs to keep his levels after eating under 150, while they have been told to keep their post-meal levels under 120. (The difference is that he is not pregnant.) The treatment goals of a non-pregnant diabetic are much less strict than the treatment goals of a pregnant woman with gd; goals must be stricter when a baby is involved. How strict, of course, is the big debate.

Example Six: GD vs. Other Types of Diabetic Pregnancy. Some providers feel that treatment numbers for all types of diabetic pregnancies should be exactly the same, but in practice, the standards can diverge. Sometimes the requirements for type one and type two pregnancies are stricter than for diet-controlled gd pregnancies, though once insulin is needed in gd, the requirements tend to be similar. However, sometimes low enough control is simply not achievable for type one pregnancies, and some providers will accept slightly higher numbers in treatment. The lesson here is not to compare apples and oranges. Type one and two pregnancies have their own concerns and requirements and these may or may not be applicable to gd pregnancies. Just how comparable they are is another subject of academic debate.

Example Seven: Pregnant vs. Non-Pregnant Standards. Scenario: A woman who is not pregnant but plans to start trying soon gets her fasting blood sugar tested. It is 110. Under the old non-pregnant guidelines, diabetes was not diagnosed unless readings hit 140, and a borderline condition called 'Impaired Glucose Tolerance' was diagnosed at readings of 115. Her reading of 110 under the old guidelines is considered a bit high but still normal. Under the new non-pregnant guidelines for diabetes, however, the cutoff for diabetes is 126 and the cutoff of Impaired Glucose Tolerance is 110, right where she is. She is right at the borderline of abnormal, but not strongly enough to start treatment under most protocols. However, she is planning to get pregnant and a fasting reading of 110 is significantly above the pregnant fasting cutoffs of 95-105, so she may actually need to start insulin before she even becomes pregnant even though she is not diabetic, although the course of action will depend on the doctor involved. Certainly, a woman diagnosed as having Impaired Glucose Intolerance before pregnancy will almost certainly get 'gestational diabetes' during pregnancy when hormones decrease insulin sensitivity anyway. So although this woman's readings outside pregnancy are borderline normal, she may need to take other steps before planning a pregnancy. She should consult carefully with a specialist before starting to try to conceive.

Example Eight: Plasma vs. Capillary Whole Blood. A woman who already owns a home monitor from her first pregnancy takes it along with her during her gd screen in her next pregnancy. She measures her blood sugar on her home monitor at the same time they measure it at the lab. She is upset when her lab readings come back much higher than the readings she got on her glucometer. However, she made the mistake of trying to compare capillary blood readings with venous plasma readings. Plasma readings, on the whole, tend to be higher, some say by about 15% on average. However, women do occasionally find that their home meter is close to the lab readings or even over it, although this is unusual. The lesson here is that it's difficult to compare home readings with official lab results. Some new glucometers and testing strips report that they are more 'lab-equivalent' these days, but some are not. Also, labs have been known to make mistakes. So you never can say for sure if your home results will be close to those from the lab. Remember also that home monitors have an error range of plus or minus 10 mg/dl, so a reading of 87 fasting could easily be within the range of 77-97 mg/dl. For non-pregnant diabetics, this error range is not a big deal, but in pregnancy it IS a big deal! A reading of 77 fasting would be considered excellent control, while a reading of 97 fasting would be considered borderline and might get you placed on insulin. So if you have any doubts about your home monitor readings, be sure to get an official lab test and compare the results.



The general rule of thumb is that any pregnant woman should keep her blood sugars between 60 and 120 mg/dl, as noted above. These are the levels that pregnant women with normal glycemic response usually have, so this is what pregnant diabetics of ANY type are supposed to aim for too . This is supposed to provide the best outcome. In practice, this is usually followed but with variations as to exact recommendations.

When diagnosing GD, the first test is the 1-hour Challenge test, which is simply a screen to find a subgroup of people who need further testing. Its cutoff is 140 mg/dl, though this level will miss up to 10% of gd cases. Therefore some providers order further testing for results in the 130s, especially in higher-risk groups with more risk factors. The 3-hour Glucose Tolerance Test typically has 4 results, one fasting (before the sugar drink) and 3 other after the drink at one hour intervals. There are different scales used to diagnose, but the most common one (National Diabetes Data Group, or NDDG) seems to be fasting=105, one hour=190, two hour=165, and three hour=145. Sometimes tests at 15 or 30 minutes are added to the test regimen, and sometimes urinary tests (on ketones or urinary sugar) may be added as well. GD is diagnosed if the fasting number is elevated OR if any two numbers are elevated. Any number over 200 basically also qualifies as gd and may indicate either pre-existing 'true' Diabetes or Impaired Glucose Tolerance (a borderline state) before the pregnancy.

There are a number of variations of this protocol, however. Some doctors diagnose gd with ONE abnormal result on the GTT, since these women do seem to be at some extra risk for larger babies. Other doctors feel strongly that the fasting cutoff should be 95 or 96 in order to diagnose gd (and to need insulin). Other doctors use not only a lower fasting but also other lower cutoffs as well. They contend that the standard recommendations used above were based on faulty conversion of data and a more accurate conversion is fasting=95, one hour=180, two hour=155, and three hour=140 (Carpenter and Coustan, 1982). This is the set of cutoffs now recommended for use by the 4th International Conference on GD, although this group is known for its conservative approach to gd. Other providers have come up with slightly different diagnostic scales as well, but these are the two most commonly used. Sacks et al., 1989, did another analysis and conversion and came up with a scale of fasting=96, one hour=172, two hour=152, and three hour=131. This scale also has some support, but most providers use either the NDDG scale or the Carpenter and Coustan scale.

It should be further noted that all of these numbers are subject to change in the next 10 years since the standard recommendations were based on work that looked at long-term maternal development of diabetes, not on what levels promoted the most optimal fetal outcome. Lowering the diagnostic levels may strongly improve fetal outcome, or it may simply vastly overtreat a huge number of pregnant women, creating a false epidemic of cases and a new industry for diabetes doctors, depending on your point of view. (The real answer probably lies somewhere between these two views.) See the Testing section and Controversies section of this FAQ for further details, and remember that there is a great deal of disparity between providers' practices. Furthermore, ALWAYS ask for your exact numbers and the scale/cutoffs used to diagnose you.

Note: Readers outside the USA will probably use one 75g test instead of the 50g screening and 100g diagnostic test. The diagnostic cutoffs for this test is strongly debated at this time; consult your provider for exact recommendations. The World Health Organization's Recommendations are noticeably looser; the 4th International Conference on GD has called for a 2-hour cutoff of 155 for diagnosing gd on the 75g test.

Recommended fasting numbers in GD treatment vary from provider to provider but the most commonly used recommendation is to absolutely stay below 105 mg/dl. When fastings rose above 110, higher levels of significant problems were found in studies, so 105 is deemed to be the cutoff. At 105, a woman is diagnosed as needing insulin, although some providers give a little lee-way. A number of providers believe that the best results occur if fastings stay at or below 90 or 95 and will start insulin above these numbers. Some will ask you to aim for fastings below 90-95 but not actually start insulin until levels around 105. A few providers have even instituted insulin at fastings around 80, though this is unusually strict. The point here is that there is a great deal of variability on exact fasting requirements short of the cutoff of 105, and it may or may not be justified to use lower goals. The question is whether the supposed benefits of using insulin at lower levels justify the higher-risk label and aggressive delivery protocols that generally come with being on insulin, and whether the insulin itself poses any risks to mother or baby. These questions have not been satisfactorily answered at this time.

It should be emphasized that most OBs use 105 as the cutoff for needing insulin, and this is currently the level recommended by ACOG (American College of Obstetricians and Gynecologists), though it does note that the optimum fasting number has yet to be established and lower levels may improve macrosomia risk. A high fasting number is considered a very clear indication of gd and the need for insulin. It is probably best to aim for fastings <90-95 in treatment, but exactly when the tradeoff in risk occurs of instituting insulin versus allowing occasional fastings in the 90s is highly debatable.

Once you are on insulin, however, the fasting number recommendations tend to get lower. This reflects the perception that if you needed insulin, you are at a strongly increased risk of macrosomia and therefore more stringent treatment may be desirable. The exact recommendations vary depending on which book you read or the provider you consult, but usually these fall between 60-85 or so. It is considered most optimal to fall between 70-85, but readings up to close to 90 are acceptable. However, if your readings are over 90 or consistently around 90, your provider will probably adjust your insulin dosage (usually your bedtime insulin dose) in order to lower your morning numbers to what they consider your optimum range.

So, in other words, a gd mother not already on insulin may be told to keep her fastings below 95-105, preferably below 90, but may not be put on insulin for a few borderline readings because of the tradeoff of risks. However, if she comes to need insulin, she may be given a target range of 60-85 or so instead----for fastings.

Recommended post-prandial numbers in GD also vary from provider to provider, but there seems to be slightly less confusion on this point. The most common standard is below 120 mg/dl, two hours after the start of a meal. Others recommend 140, one hour after a meal, though providers differ on whether this is timed from the beginning of the meal or the end of it. Occasionally you will find providers who want a measurement of less than 130 or even 120 one hour after a meal (especially for those on insulin), but the most commonly seen recommendation is 120 mg/dl for a 2-hour post-meal measurement or 130-140 for a 1-hour measurement.

On the other hand, the recommendation of 120 post-meals has been liberalized by a few providers, who contend that post-prandial numbers are less important than fasting numbers. One mainstream OB Kmom spoke to indicated that if fastings were fine, she would not prescribe insulin until the post-prandials were in the vicinity of 150-180! Anecdotally, some Canadian women have reported that their providers recently raised their accepted levels for post-meal measurements (though Kmom is still seeking official confirmation of this). Kmom's midwife in her second pregnancy indicated that she would not worry about occasional 2-hour pp elevations of 120-140 or so unless sugar was also being spilled in urine or there were elevated fastings, and that this was based on the very latest research and agreed upon by her back-up OBs. However, Kmom has yet to see the exact research these new guidelines were based on, though the fact that the back-up OB practice (a very mainstream practice) also agreed signifies that some alternate research must be present somewhere.

In contrast, more conservative diabetic providers feel that elevated postprandial levels are one of the strongest indicators of macrosomia risk, and are very strict about these. They would be horrified by the very thought that some providers have looser postprandial standards, and many want to tighten postprandial recommendations even further, to 120 one hour after meals or even less. In fact, this view represents the mainstream of research at this time--most providers will not be more liberal with postprandial numbers. At one time, some providers only required gd moms to measure their pre-meal levels (and keep them under 100); postprandial measurements were considered more optional. However, some research has shown that women who kept control of postprandial levels improved macrosomia and outcomes over women who kept control only of pre-prandial and fasting levels. Thus, the majority of researchers now place a great deal of emphasis on very strict fasting numbers and postprandial numbers----but not all do.

To demonstrate the variations that can be seen, Kmom has spoken to women on the internet whose providers insisted on post-meal levels of 107 mg/dl or less, while others permitted levels up near 150 without objection. So while some factions are tightening the post-prandial numbers, others are liberalizing it. Obviously, there is some controversy in this area as well, though there is a bit more widespread acceptance of the standard recommendations than in the fasting area. It seems most sensible to stay below 140 one hour after a meal or below 120 two hours afterwards, but consult your provider.


What If My Provider Recommends Radically Different Standards?

Sometimes providers recommend an approach totally different from the usual standard of care, either more liberal or more conservative. Some providers disregard gd as a concern at all or treat it lightly. Sometimes providers treat gd as a concern but don't emphasize it much or order nearly as many tests as some mothers would prefer. Conversely, some providers treat gd as an extremely high-risk situation, especially if the mother has other considerations like obesity or previous c-section, yet the mother doubts whether such a highly interventive approach is really necessary. Some providers order protocols that seem extreme to the mother, demanding extremely low numbers, prophylactic insulin, early induction of labor, elective c-section, etc. Each type of provider obviously feels that they are providing the mother and baby with the most optimal treatment and least amount of risk, yet their recommendations differ so strongly! What's a gd mom to do?

It can be very disconcerting to have a provider whose protocols differ markedly from the usual standard of care. And of course, the standard of care DOES alter over time, and who's to say if this provider is actually visionary or reactionary in these differing protocols? It's very difficult emotionally to question your care, and some mothers can never bring themselves to do it, despite misgivings about their provider's approach. Yet because there is SUCH a diversity of care in this issue, it is vital that mothers become aware of gd issues and rationales so that they can choose consciously and wisely.

Please note that the current ACOG standards (American College of Obstetricians and Gynecologists) are for a level of 120 two hours post-prandial and 105 fasting. In Kmom's non-expert opinion, these seem to be the most sensible guidelines to go by, although there is room for debate for a slightly lower fasting number. Some providers will deviate from this standard ACOG protocol; if your provider does, you will need to ask some hard questions as to why they do and what research they base their recommendations on. Be sure to consider more than one opinion and read from sources that have different recommendations just to be sure to get a well-rounded picture from which to decide.

You may find your provider's arguments convincing and agree to a recommendation differing from the current ACOG standard, which is fine if you understand the issues and make an educated choice. However, if your provider does not answer your concerns satisfactorily, you may want to consider getting a second opinion or switching care providers. It is not necessarily a good idea to go 'shopping' for a provider who will give you the most lenient or most strict guidelines around; you have to look into the matter and decide what seems prudent and reasonable and backed up by research. It is an extremely difficult issue to face, and a very emotionally draining matter to switch providers. However, sometimes, in some cases, some women need to switch. Kmom has heard from women who preferred to switch care to more aggressive protocols, and from women who switched to avoid aggressive protocols. Either position can be justified if done with careful thought and consideration. (For more information about considering switching providers, see the discussion in the section on GD Providers: Who to See?)


The Debate About Stricter Treatment Protocols: A Brief Overview

The debate over which protocol regimen to use is a very hot and controversial topic of research these days. Some research supports instituting more stringent protocols ('prophylactic insulin') and some does not. Furthermore, the methodological design of many gd studies has come under fire and the 3rd International Workshop-Conference on Gestational Diabetes called for more definitive studies with impeccable design in order to try and clear up the matter. A few of these studies are currently under way, but no permanent results are available yet, and there are many factors to consider. This section is intended to give a brief overview of some of the arguments; the GD: Controversies section will cover this more thoroughly and with even more research references than here. Readers are strongly encouraged to pursue their own research in this area.

Proponents of Prophylactic Insulin

There are two types of treatment sometimes referred to as "prophylactic insulin" use. The first approach is to institute insulin use at levels lower than current official recommendations; for example, the move to use insulin at fastings of >95 instead of the official recommendation of >105. This may or may not be considered true 'prophylactic' use of insulin, but since a fair number of sources use the term that way, we will also.

The second approach to 'prophylactic' use of insulin is to use insulin aggressively with ALL gd women or those in subgroups identified as being particularly high-risk for macrosomia. This approach was popular in the 70s and early 80s but its use for ALL gd women is generally not done anymore. However, there is a resurgence of some researchers now who are promoting extremely aggressive use of insulin in subgroups (such as obese gd women or women with prior macrosomic babies), regardless of normal numbers through dietary treatment alone.

Researchers who defend these approaches (use of insulin at even lower numbers, or aggressive treatment for subgroups like the obese) contend that it reduces macrosomia (thus hopefully preventing birth trauma), normalizes the metabolic intrauterine environment of the fetus (thus theoretically preventing a host of future metabolic problems like obesity and diabetes), and will therefore lessen the amount of metabolic aberrations a gd newborn might experience (like hypoglycemia, jaundice, polycythemia, and hypocalcemia). They contend that the gd pregnancy represents an intrauterine environment where the maternal fuel substrates levels (hyperglycemia and others) are so abnormal that they imprint a harmful pattern of growth and pancreatic development. They feel that children of diabetic pregnancies are more at risk for obesity, hypertension, impaired glucose tolerance at very young ages, and perhaps even motor, neurological, or learning difficulties. They feel that the uterine environment of gd moms is so unbalanced that it produces a child likely to be at high risk of health problems, and at earlier and earlier ages. They see their mission as one of prevention of diabetes and a host of other metabolic difficulties for a future generation by 'normalizing' the uterine environment through aggressive use of insulin. Basically, they feel that the ends justify the means. Though little research exists yet to address whether aggressive insulin use actually accomplishes these goals, they feel that what research there is supports this position.

To support their point of view they point to research that shows that more aggressive insulin use does indeed tend to lower levels of macrosomia, and in a few cases, even the c-section rate. They note that macrosomic babies of diabetic pregnancies tend to have high rates of shoulder dystocia (where the head is delivered but the shoulders get stuck) which can result in higher rates of birth trauma injuries such as brachial plexus injury or clavicular fracture, or even very very rarely, fetal death. They feel justified in promoting aggressive protocols for insulin and elective delivery in order to hopefully prevent these rare but possibly serious consequences of difficult birth.

They furthermore point to new studies that seem to show that babies of gd pregnancies tend to be more obese and more hypertensive as they grow up, and to get diabetes or impaired glucose tolerance at much younger ages. Little long-term follow-up has been done till now on the mothers and babies of gd pregnancies treated aggressively, but of the little study that has been done, some of it has seemed to show that mothers treated prophylactically with insulin may progress to diabetes less slowly, and that their babies may tend to be less obese after a couple of years. However, this research is still extremely sparse, it has methodological problems, and its followup has been minimal; little can be concluded from it at this point. But proponents feel so strongly about its possible benefits that they question the ethics of letting a generation of babies go untreated or 'undertreated' when it may be possible to lessen the coming epidemic of diabetes and its consequences.

Proponents also further point out that the current cutoffs for diagnosing 'gd' were arbitrarily chosen decades ago, but they were chosen for their ability to predict future diabetes in the mother, not for their ability to prevent complications to the fetus. Because of this, proponents feel that the mediocre results of gd treatment thus far have not resulted from a failure of gd treatment itself but because the treatment has not been aggressive enough, and not based on numbers that reflect improved fetal outcome instead of numbers that reflect the mother's future prognosis for getting diabetes. This is an excellent point; the cutoffs were originally derived for analysis of the mother's future risk, not the baby's risk. However, in fairness it's important to point out that conclusive research tied to fetal outcome does not exist at this time, either to support or refute the hypothesis that lower cutoffs will normalize outcome. Much research remains to be done, but proponents feel that it is only a matter of time before it is proven and that not treating aggressively in the meantime discriminates against a whole generation that could benefit from the intervention.

It is safe to say that the majority of the major researchers and organizations that study gd tend to fall under the umbrella of the more aggressive approach at this point, though some are more aggressive in treatment than others. However, all along there has been a very vocal minority challenging the assumptions and conclusions of the aggressive-protocol researchers. They tend to be proponents of "evidence-based medicine" and point out the weaknesses and gaps in the arguments of the aggressive treatment advocates. They mostly feel that care must be taken to carefully prove that aggressive protocols not only help significantly but also "do no harm"; at this time the majority of critics do not feel that the case for aggressive protocols is proven by any means.

Critics of Prophylactic Insulin

Critics of aggressive or prophylactic insulin use point out that the research supporting aggressive insulin use has been extremely mixed, much more than proponents want to admit. While some results have seemed to indicate its benefits, other research shows a totally different picture. Some research has shown that aggressive use of insulin did not lower macrosomia at all, nor improve outcome in any way. Other research shows that while aggressive insulin did lower macrosomia rates, it did not in turn lower the c-section rate or the rate of complications in the newborn at all. In fact, some research shows that the using insulin aggressively actually RAISED the c-section rate, despite having lowered the size of the babies. Reducing the rate of macrosomia should have lowered the c-section rate, but in most studies it did not, and sometimes it raised the rate instead. This is a very serious problem. Proponents like to point to the few studies where both the macrosomia rate and the c-section rate were diminished, but in reality, most research has not borne out this trend, and has often even shown the opposite effect.

Part of the problem lies in the fact that once a gd mother is put on insulin (generally called class A2), she is considered even more high-risk and subject to ever-more interventive protocols, experiencing far more prenatal testing, early induction, and aggressive management protocols. The c-section rate for some insulin-dependent gd moms in some studies exceeds 40%, a HUGE rate. Critics question whether using an aggressive insulin protocol is a quick way to buy a one-way ticket to a c-section for a significant number of gd moms. Proponents of prophylactic insulin insist that the gains in lowering risk by lowering baby size outstretch the rise in risks that come from an increased number of interventions. However, studies of this question have either not been done or have been methodologically flawed. The point of reducing rates of macrosomia is to reduce the high accompanying rate of c-section of macrosomic babies, yet aggressive insulin use seems to either not affect or actually increase the c-section rate instead, negating this part of its very purpose. Whether aggressive insulin use is actually beneficial or detrimental to the c-section rate (and is therefore justified or not) is a burning question in the field of gd.

Furthermore, although the rate of macrosomia was lowered in a number of studies, the amount that it was lowered was not terribly significant. Several studies managed to lower the average birthweight of their children, but the average difference in size amounted only to a few ounces. It is questionable whether this is of any real benefit to the children, and whether it is clinically significant in terms of preventing difficult births or problems. Again, studies have showed a variety of responses; some showed significant reductions in size of more than a pound, most showed the reduction of only a few ounces, and some showed no difference in birth weight between groups.

Proponents counter, however, that though the overall average birthweight was not reduced by a great deal, the percentage of babies falling in the range of 'Large-for-Gestational-Age' and "Macrosomic' did decrease, and that this is meaningful. Critics would respond by noting that the cutoffs for LGA and macrosomia are artificial constructs and that most of the babies must have fallen very close to this border for a fairly small overall reduction to have reduced the number of LGA and macrosomic babies so much. Just because some of them now fall a few ounces below the arbitrary cutoff, is the clinical difference in risk really that great from a few ounces? Do a few ounces really translate into a measurable difference in mode of delivery or birth injury or other outcome? Or is it simply a measurable difference in the physician's perception of risk and therefore their treatment? Some studies show improvement in shoulder dystocia and birth injuries when birth weights were reduced, but many do not. If aggressive insulin use is designed to lower the c-section rate and to lower the rate of birth trauma, more studies where macrosomia was reduced should be showing that result, but results are decidedly mixed on this count. Some studies actually show an increase in the c-section rate and NO reduction in shoulder dystocia or birth trauma.

Another criticism of the macrosomia/shoulder dystocia concern is that the labor and delivery protocols of providers can strongly influence the amount and severity of shoulder dystocia or other problems; that the restrictive way these women are forced to labor due to gd and macrosomia protocols tends to cause more problems, which then get blamed on the gd. These iatrogenic (doctor-caused) problems include forcing early induction, using forceps or vacuum to 'speed' up births, restricting mobility and positions, and forcing the woman to push in ways that may exacerbate a more snug fit (semi-reclined, stirrups, etc.). Many critics contend that the main problem with macrosomia (increased c-section rates and other birth trauma) simply means that physicians have lost the knowledge on how to best handle the births of macrosomic babies and how to resolve shoulder dystocia in low-tech ways that tend to reduce the number of complications and injuries. It is clear that diabetic women DO have a higher rate of shoulder dystocia and that some of this is intrinsic, so caution IS definitely justified. However, the restrictions and interventions commonly used in these women and the lack of skills on the part of doctors in handling macrosomic babies well probably has inflated the mathematical risk scenarios for suspected macrosomia/shoulder dystocia and because of this, it is very difficult to know at what point concern is truly justified and intervention necessary.

Proponents would also claim that there is futher reason to aggressively lower macrosomia rate, besides simply trying to prevent c-sections and birth trauam. They contend that by lowering the rate of macrosomia, they have probably prevented a whole host of problems for the child as it grows. This is possible, but in reality, there is no way to know if that claim is true yet. There are no studies showing this conclusively; in fact, there is VERY little long-term follow-up of gd children at all, let alone comparing the long-term outcome between modes of treatment. This raises one of the most troubling questions of all: what is the long-term effect on the children given this extremely aggressive insulin treatment? Most of the time, researchers simply note that the babies turned out smaller, congratulate themselves, and pat themselves on the back in the journals. But is this REALLY better for the babies? Are there any consequences to using large amounts of exogenous insulin during pregnancy, even when the numbers do not seem to require it? Is it proven to be SAFE to use such aggressive treatment?

Another troubling question is whether it is healthy to try to alter a baby's birth weight. Henci Goer, a strong critic of traditional gd treatment protocols, says "The price of reducing macrosomia is the manipulation of the primary growth mechanism of infants, roughly 80% of whom would not be LGA if they were left alone. And this, like GD itself, presumes without evidence that this physiologic variation in birth weight is pathological." In other words, artificially reducing the natural birth weight of a baby may be dangerous. Nine pound babies may just be a variation of normal, not necessarily an indication of abnormality, disease, or macrosomia caused by excessive blood sugar and hyperinsulinemia. Genetics may play a role as well for some babies, and what will using unneeded insulin do to babies that nature intended to be larger anyhow?

Numerous studies have shown that low-birthweight babies are at especially high risk for diabetes, heart problems, and other health difficulties later in life. Other studies have shown that *extremely* tight protocols have caused an increase in the number of SGA [Small-for-Gestational-Age] babies. What if extreme treatment to bring a normally 9 lb. baby down to an 'acceptable' level of 7.5 lbs. actually exposes him to this same type of risk? In essence, a baby who is genetically supposed to be 9 lbs. but whose birthweight is reduced through aggressive treatment is being born 'underweight'. Is that baby's health going to be improved or vastly put at risk? Do these aggressive protocols to reduce the size of 'macrosomic' babies really improve the baby's health in the long run by preventing a 'misprogramming' of its metabolism, or does it skew its metabolism by trying to alter its primary growth rate? These are very troubling and confusing questions, but the most troubling problem of all is that THESE QUESTIONS ARE NOT EVEN BEING ASKED BY RESEARCHERS.

Furthermore, as Henci Goer pointed out, not all babies of gd pregnancies are macrosomic; in fact the majority are not. Since macrosomia of whichever type only occurs in 20-30% of gd pregnancies anyhow on average, treating all gd patients aggressively assures that 70-80% of gd patients receive treatment to reduce birth size that wouldn't be a problem anyhow. We know that this aggressive treatment is often likely to lead to more c-sections, but what are the effects of aggressive treatment on babies not likely to be macrosomic? Are any babies being harmed long-term by this? No one knows, because no one is asking the question. Researchers are, however, beginning to recognize that not all gd babies need aggressive treatment, and are starting to recommend targeting the more aggressive therapy instead to those statistically more likely to have macrosomic babies.

However, even this presents problems. Obese women, who do have more macrosomic babies as a group, do not all have macrosomic babies as individuals by any means. Even women who have had macrosomic babies previously do not all have macrosomic babies subsequently; in fact, the majority do not! Targeting even just these groups for aggressive intervention means that a number of babies that would not have been macrosomic will be receiving extremely aggressive treatment. What effect will this have on those babies, and can they assure these mothers that it will be benign? And how many more unnecessary c-sections will be performed on these women because they are in the 'aggressive' treatment category?

As for those babies who will be macrosomic, a further good point is that not all macrosomia is created equal. It is QUITE clear that 'pathological' macrosomia (where baby clearly grows asymmetrically and has an extra-large trunk and organomegaly) is something that ABSOLUTELY needs to be prevented and that this DOES happen in some babies of diabetic pregnancies, but it is unclear at this stage whether every or even most babies of diabetic pregnancies over 9 lbs. are really 'pathologically' macrosomic or whether some so-called macrosomia is just another variation of normal. This may be especially true for obese women who may just genetically tend to have larger babies (just as tall people tend to have longer babies). At this time, few researchers distinguish between 'pathological' macrosomia (clearly problematic) and 'constitutional'/genetic macrosomia that may simply be a variation of normal and not necessarily problematic. Are all large babies from gd pregnancies really a result of 'failed' control, treatment goals that are not strict enough, or failure to use aggressive-enough intervention? Or do genetics play an additional role?

A related point that is absolutely critical is whether insulin is more effective on obese women or not. In a few studies, prophylactic insulin has appeared to nearly normalize macrosomia rates and improve outcome, even in obese women. In many other studies, however, it has apparently much less effect on obese women and their babies, or little effect at all. Even the most stringent of treatment plans has not really been able to reduce the number of large babies from obese mothers down to desired levels, raising the question of whether this is really possible. Is expecting the same rate of fetal size from obese women as from average-sized women really a realistic treatment goal? If so, how aggressive a protocol is justified to try to achieve this goal? Is it really safe or even desirable for the babies? And are they even asking these questions?

In large women, is the high rate of macrosomic babies due to abnormal metabolic factors, simple genetics, or a combination of the two? How can we distinguish between these? If the contribution to fetal size is metabolic and truly shown to be harmful, then aggressive therapy is probably justified and may help prevent a host of future problems. However, if the contribution of size is simply an example of normal genetic variance, then tinkering with a baby's natural size could have very serious consequences indeed. If both genetic size and metabolic abnormalities contribute to the generally greater size of babies born to larger women, then how do we define how much reduction in birthweight is appropriate and possible, and how much aggressive correction might be harmful? Researchers always seem to assume that with larger-than-average people, smaller is always better. But do they know this for sure? And how much is too much?

The extreme emphasis placed on reducing the larger birthweights of babies of obese mothers (no matter what) in research is particularly troubling philosophically, because it smacks of putting a baby on a diet before it is even born. This all-out emphasis on reducing the birthweights of babies that are larger-than-average, especially those of obese women, has very troubling implications. Is an entire generation of children of large women being 'saved', or are they being put at risk by the very treatment that is supposed to 'save' them? Or is the answer somewhere between these two extremes?

Much more definitive study needs to be done on these questions. DOES aggressive insulin use really benefit obese women more, or does it have less effect on them instead? How much of the overall larger size of babies of heavy women is due to genetics vs. 'abnormal maternal milieu'? How safe are aggressive efforts to reduce infant size? What are the long-term effects of aggressive treatment? Only time and more research can answer this, but unfortunately, at present, most researchers are ASSUMING that it will be helpful and targeting ever more aggressive treatment to the obese gd mother. Some researchers have advocated giving ALL obese gd mothers insulin, even when they have had good control with diet alone. There have even been credible anecdotal reports of obese mothers WITHOUT gd being pressured into using insulin if they've previously had large babies, even when their gd tests are not even close to borderline positive. This raises a lot of troubling ethical questions.

Other researchers have also been troubled by the ethics of some of the most aggressive insulin protocols. Enkin et al. in their book, A Guide to Effective Care in Pregnancy and Childbirth, make the following very strong statement:

Trials comparing the use of insulin plus diet with diet alone show a decrease in macrosomia, but no significant effect on other outcomes such as use of caesarean section, the incidence of shoulder dystocia...perinatal mortality...[or] neonatal jaundice or hypoglycaemia...The available data provide no evidence to support the wide recommendation that all pregnant women should be screened for 'gestational diabetes', let alone that they should be treated with insulin. Until the risks of minor elevations of glucose during pregnancy have been established in appropriately conducted trials, therapy based on this diagnosis must be critically reviewed. The use of injectable therapy on the basis of the available data is highly contentious, and in many other fields of medical practice such aggressive therapy without proven benefit would be considered unethical.

Critics feel that much more research needs to be done to clarify the issue of prophylactic insulin use and its effectiveness, especially in groups at higher risk for macrosomic babies. Furthermore, it's not enough to simply reduce the baby's birthweights; it has to be shown to be beneficial to the child in both the short-term and the long-term. And few have addressed the most important question of all: what are the tradeoff risks in prescribing extreme protocols such as hypocaloric diets or prophylactic insulin? Has the long-term effect on the baby really been studied? Critics believe that the purported 'benefits' of aggressive treatment have not been proven at this point, nor has its lack of harm. Therefore, they strongly question the appropriateness and safety of aggressive therapies like prophylactic insulin.


Past studies on whether aggressive prophylactic insulin treatment successfully reduces macrosomia and related problems have had mixed results. Some studies clearly showed improvement, while others did not. Even when the macrosomia rate was decreased, c-section rates did not usually decrease with it, though it should have. A few studies showed drops in the c-section rate, but most did not, and some even showed strong increases. Furthermore, the drops in birthweight were sometimes not very clinically significant, and critics question whether baby was really better off after all that aggressive treatment. They also point to the many methodological flaws of the studies promoting stringent protocols.

Proponents of more aggressive treatment basically point to a few studies that have shown stellar results (including lower c-section rates) and charge that the mediocre results of other studies have been because the treatment hasn't been aggressive enough, and that high rates of c-sections even when macrosomia is reduced may be due to anticipatory treatment on the part of physicians (who may have a lower c-section 'threshold' for gd patients than for non-gd patients). Some also hold gd patients to be so high-risk they probably could not achieve 'normal' c-section rates anyhow, and they question whether it is realistic to expect any treatment to reduce the c-section rate to completely normal levels in gd mothers. (Critics note that this certainly provides a convenient excuse not to try!)

Not treating gd patients at all does tend to raise the amount of macrosomia present, and the cases of true 'pathological' macrosomia would not receive treatment, something that could be potentially very harmful. So dietary treatment and insulin at previously identified levels seems a reasonable choice to many (though not all). However, whether such treatment should be extended into use of insulin at even lower levels, or use of insulin prophylactically in so-called 'higher-risk' groups even when all bG numbers remain normal is very controversial. Proponents of 'evidence-based medicine' or the 'minimum school of management' feel that until prophylactic insulin use has been proven unequivocably to be beneficial and also shown to be not harmful in the long term or short-term, aggressive insulin protocols should not be adopted. Proponents of prophylactic insulin (the 'maximum school of management') feel that they are preventing EXCESS size in babies, possible birth trauma, and a whole host of future health problems, and that preventing the worst possible outcome justifies more intervention.

Carr and Gabbe (Clinical Diabetes, 1998) take a middle course in their excellent summary of current treatment standards for gestational diabetes. They note that "the ACOG criteria for initiating insulin therapy include a fasting plasma glucose level of >105 mg/dl and 2-hour plasma postprandial levels >120 mg/dl. It is important to recognize data suggesting that insulin therapy may achieve lower rates of macrosomia if initiated when fasting blood glucose is >95 mg/dl. However, prophylactic insulin treatment in patients whose fasting and postprandial values remain within the recommended range is not advised." In other words, they believe there may be merit in the argument to initiate insulin treatment at lower fasting values than previously used, but they do not suggest aggressive treatment with insulin for patients whose readings are all normal with dietary treatment. There are certainly experts who disagree with this opinion, but this article is from leading experts in the field and appears in a journal designed to guide physicians in their treatment choices in diabetes. It probably represents the most common view of the issue at this time (bearing in mind that there is not a great deal of consensus on gd!).

All this simply reinforces once again that choice of provider and guidelines is one of the most difficult decisions you will make with gd. Many women abdicate their responsibility to be informed and let their providers decide for them, though they might have gotten exactly the opposite advice had they happened to choose a different provider! Other women will research for themselves, interview providers to see what their beliefs are and why, and then choose. It is a very difficult position to be in, either way. The medical community should be urged to work strenuously to resolve these issues more clearly.


Kmom's Opinion (insert medical caveats here!): Kmom is generally reluctant to offer her own opinion on such controversial issues, lest people take it as medical advice. It is not. However, with all the confusing and contradictory information available, it can be informative to read about someone else's experiences and opinions after reviewing the research. That does NOT mean that Kmom is an expert or that her opinion is correct; it is simply a sharing of her thought processes and reasonings. It is NOT medical advice! Please feel free to disagree or choose another course of action.

In Kmom's non-expert, non-medical opinion, all the various protocols actually have some distinct arguments to be made for them AND potential risks associated with them; at this time it is very difficult to judge which is the best protocol to follow. However, if forced to take a position, she would probably not choose prophylactic insulin for herself at this time. In particular, Kmom is troubled by the proposal to treat all obese gd moms with insulin universally, by the lack of credence for the idea that genetics may have some influence on fetal size, by the opinon that all macromia must be 'pathological', and by the lack of long-term follow-up to determine the safety of aggressive treatment. Specifically, Kmom would not accept prophylactic insulin based simply on her size or her children's birthweights, especially since there was no real difference in size between the child of her gd pregnancy and the child of her non-gd pregnancy, probably indicating a genetic component. As far as using lower fasting values for starting insulin, Kmom would decline absolute judgments and consider the circumstances first. If she had only a very occasional fasting over 95, she would not consent to insulin treatment, since home monitors do have error ranges of +/- 10 points and illness and stress can affect readings abnormally too. However, if she had fastings consistently around 100 on a regular basis, she probably would strongly consider it. Situations between these two scenarios would have to be considered on an individual basis.

These are the choices Kmom would make for herself at this time, based on her understanding of the issues. She would also carefully consult her provider before making these choices, since recommendations can change over time or there may be other issues pertinent to the choice. Remember that Kmom does NOT offer medical advice or suggest courses of action for other people, and she does not pretend to be a medical expert. However, neither does she believe that laypeople should never offer their own opinions on medical controversies or share their experiences and choices. These are simply Kmom's opinions, clearly marked as such, and readers should not see them as medical advice or expert opinion. Other mothers might well choose different courses of action on this issue, which is also fine. There are arguments to be made for both sides!


Non-GD Numbers


What blood sugar readings do you find in people who are normoglycemic (have no problems with blood sugar)? It depends on the source that you read and how strict of a definition researchers use. Below are some typical references seen, but be aware that you might see different numbers listed elsewhere.

For non-pregnant people, a normal fasting number is about 70-110. 100-110 are definitely on the high side of normal, since 110 and above is considered 'Impaired Glucose Tolerance' (IGT), a sort of borderline state to diabetes. 70-100 is considered most normal and optimal. A normal post-meal number for normoglycemic people is under 140 one hour after a meal, under 120 two hours after a meal (look familiar?). Impaired Glucose Tolerance is between 140-200 postprandial.

Once a normoglycemic woman becomes pregnant, she often experiences a drop in her fasting numbers but a rise in her post-prandial levels during pregnancy, according to some sources. The placental hormones tend to increase insulin resistance so that more glucose and energy is available to the baby for growth. This is normal and an important part of the process of regular pregnancy. The difference between normoglycemic and gd moms is that normoglycemic women are able to produce enough insulin to make up for the increased resistance and therefore keep their blood sugars in a normal range. Gd moms, either due to too much insulin resistance or because they are predisposed to a pancreatic beta cell defect (and thus have trouble making enough insulin), cannot produce enough insulin to counteract the effect of the placental hormones, so their blood sugars begin to go too high. All pregnant women experience some degree of carbohydrate intolerance, but basically normoglycemic women are able to compensate enough to stay in the normal range and gd moms cannot.


How Do People with Normoglycemia Progress to Diabetes?

Later in life, people who have a lot of insensitivity to their own insulin tend to develop type II diabetes because their pancreases become fatigued by having to produce so much insulin over time in an effort to keep up. When their pancreases cannot keep up, they develop type II diabetes. This is very common in overweight people, since weight gain tends to increase insulin resistance, as does being sedentary.

For people who are simply insulin-resistant, regular daily exercise seems to be pretty effective in preventing or delaying diabetes. This improves their body's insulin sensitivity and increases glucose uptake by the muscles, even after the exercise has ceased. If their bodies use their insulin more effectively, then they need to produce less of it and it is less stressful on the pancreas. Not gaining any extra weight is also important, since gaining may decrease insulin sensitivity. A small weight loss of 15-20 pounds may also help improve insulin sensitivity, but a person's weight history must be taken into account here. If the weight has tended to yo-yo a great deal, a small loss could trigger a bigger gain in the long run, which is absolutely to be avoided. There is also some evidence that weight cycling tends to increase a tendency towards diabetes, but other evidence does not show the same effect, so conclusions on this are limited. For some people, a small weight loss might be a good idea in conjunction with changes in diet and exercise; for others, a focus on changes in diet and much more exercise might be more appropriate instead of an emphasis on weight loss. Extreme hypocaloric or diet fads should definitely be avoided. Each person must consider her own history and consult with her provider in order to decide what's best for her.

Other people get diabetes because they have a beta cell defect in their pancreas and cannot produce enough insulin to keep up, in addition to whatever insulin resistance they have. These people are highly predisposed to diabetes and it's difficult to prevent the continuation on to the disease. If they are highly insulin-resistant on top of having trouble producing insulin, they tend to get diabetes at very early ages. There is no way to tell if you have a beta cell defect, but relatively high readings at an early age may indicate a tendency towards this problem.

Generally speaking, women of average size who get gd are generally thought to have a beta cell defect, which is why their gd cases often tend to be more severe. Women who are heavy and get gd are generally thought to have insulin resistance instead, and with proper diet and especially exercise, may have milder cases, since insulin resistance is more amenable to intervention. However, there is also a subset of heavy women who have BOTH the severe insulin resistance and the beta cell defect; these women will tend to get Type II Diabetes at very early ages, often already in their 30s, and tend to have the most severe cases of gd. They often also have other related metabolic disorders, such as Polycystic Ovarian Syndrome. In fact, some studies of gestationally diabetic women have found a very large subset actually also have PCO, which may be the source of their metabolic problems.

There are a few cases of 'gd' which are actually undiscovered cases of type I diabetes. In type I diabetes, the pancreas produces little or no insulin, and type I diabetics must have exogenous (outside) sources of insulin or they will die. Sometimes this occurs early in childhood (why it used to be called 'juvenile' diabetes) and sometimes not until early adulthood, but whenever it happens it is truly life-threatening. Occasionally, a woman becomes pregnant during this process, and her diabetes is only discovered during her pregnancy. Although this is still called 'gd', it tends to carry more risk since the problem likely existed to some extent beforehand, and these women tend to either continue their diabetes after pregnancy, or to have it recur within a short time. Northern European populations tend to have a higher frequency of this than other ethnic populations, but in any population it is true that a few cases of 'gd' are actually undiscovered type I diabetes. However, the majority of gd cases do not fall into this category.

Type II Diabetes most commonly tends to occur after 45 or so, especially in women, although it can occur earlier, as noted above. In your 40s, it may be related to the hormonal changes of menopause; certainly many gd moms tend to progress to diabetes at about that point. In normoglycemic women, the hormonal changes of aging are compensated for by the pancreas, and blood sugars are able to remain normal. In women with a lot of insulin resistance or a relative weakness in producing insulin, it tends to trigger a progression to true diabetes; it tends to be the 'straw that breaks the camel's back', as it were.

These are the most common mechanisms by which normoglycemic people are thought to progress to overt diabetes, as Kmom understands it. There are other mechanisms too; disease causes some cases of diabetes, as does simple aging and fatigue of the pancreas. However, a great deal is still unknown about the disease itself and the process. It is certainly possible that some of this information will be proved wrong in the future or that new discoveries will lead to radical new understanding of and treatment for diabetes. It's also important to note that the gestational diabetes to diabetes progression is not a 100% correlation; some women who had gd never progress to true diabetes. However, since at least 50% most likely will become diabetic within 10-20 years, it is important to understand the process and what you can do to help prevent or delay it. More information on this subject can be found in the websection on GD: Future Risk of Diabetes.


'Regular' Diabetes Reference Numbers

Women who were diabetic before pregnancy often have different numbers recommended for them. Theoretically, many providers feel that 'all diabetic pregnancies' (type I, II, or gd) should be treated alike and have the same goals, but in reality different recommendations are seen at times. From some providers, these numbers tend to be even lower for pre-gestational diabetics, since long-term diabetics have greater risks of eye, heart, kidney, and nerve damage to themselves and birth defects and stillbirth for their babies. [For example, The Diabetic Woman by Jovanovic et al. lists fasting goals of 55-70, much lower than the usual gd goals, even with insulin.Other sources do not list such strict numbers, giving 60-90 as fasting goals instead.]

However, since good control tends to be harder for long-term diabetics, you will occasionally find providers who will accept higher numbers, even though lower numbers tend to provide better outcomes. It is not within the scope of this FAQ to discuss the number recommendations of type 1 or 2 pregnant diabetics, but it is important to note that their recommendations may or may not be exactly the same as those for gestational diabetics. In theory they should be, but in practice they are not always the same.

Non-pregnant diabetics are a totally different case, and their numbers should NOT be confused with those for pregnancy. When diagnosing diabetes in a non-pregnant person, the cutoff used to be a fasting level of 140 mg/dl. This has recently been lowered to 126, though not every provider has switched yet. The new lower cutoff for overt diabetes reflects research that shows long-term damage from even moderately high blood sugars, so the authorities decided to lower the diagnostic numbers in hopes that treatment at lower levels will prevent more complications.

Those are the diagnostic numbers for diabetes now. Treatment numbers, of course, are lower. Fasting goals for the non-pregnant diabetic are considerably more lenient than in pregnant women, since there is no fetus to consider. Recommendations will vary depending on the philosophy of the provider, but anywhere from 70-115 fasting is common. Some will accept slightly higher fastings, but < or = 100 fasting is considered more optimal.

Post-prandial numbers vary some from provider to provider. Under 180 used to be the most common goal, but now it is thought that better long-term outcomes may occur at lower levels. Therefore, most providers prefer goals of <150 after meals. As in gd, the timing of the post-prandial measurement varies, so each diabetic must consult his/her own provider for exact requirements.

At levels below the official diagnosis of diabetes is an intermediate class between normoglycemia and overt diabetes. This gray borderline area is called "Impaired Glucose Tolerance" (IGT), as noted before. People with IGT have a high rate of progressing to overt diabetes, but do not always do so. Sometimes they remain in the IGT category and never progress, and sometimes they even return to normoglycemia. However, because of the high rate of progression to overt diabetes, people with IGT should be watched extremely carefully, and there are some programs to try treating even people with IGT to see if it can help prevent them from developing diabetes or lessen complications if they do. A fasting level between 110-125 or a post-75g GTT level of 140-200 is now considered Impaired Glucose Tolerance and at risk for developing diabetes. Treatment goals for people with IGT are to keep the blood sugars as normal as possible, preferably <100 fasting and <140 post-prandial.

Diabetes standards, like many medical standards, evolve over time, and are always subject to differences in philosophy. Therefore it is certainly quite possible that you might find references that list different diagnostic or treatment goals than those given here. Some providers prefer extremely strict treatment goals in hopes of preventing complications, but this has risks of its own as well. Other providers are more flexible in their goals, but may not prevent as many long-term complications. Research on this issue is ongoing and will surely lead to reconsideration and revision of these commonly-found goals. Be sure to do your own research into these considerations, since they may well change over time and between providers.




American Diabetes Association Position Statement: Gestational Diabetes Mellitus. Diabetes Care. Volume 21: Supplement 1, 1998.

Official 1998 position statement on the definition, detection, diagnosis, and therapeutic strategies for gd. However, "Currently there is a committee considering a major revision of this position statement based on the 4th International Workshop on Gestational Diabetes Mellitus."

Carr, DB and Gabbe, S. Gestational Diabetes: Detection, Management, and Implications. Clinical Diabetes. 16(1):4-24, 1998 Jan-Feb.

Outstanding article summarizing gd testing, management, and even some of the controversies involved in gd, though from a traditional medical approach. Excellent overview, but may be too technical for beginners unfamiliar with some of the terminology and issues in gd. Those more familiar with gd terms and issues will find it invaluable, and beginners will want to return to it when their understanding increases.

Stephenson, M.J. Gestational Diabetes Mellitus. Canadian Family Physician. 39:745-8, April 1993.

A must-read article for those serious about understanding gd treatment options. Covers fairly both philosophies of treatment, both the maximum and minimum schools of management. An excellent overview of the controversies. This should be one of the first articles read about gd.

Diabetes and Pregnancy, ACOG Technical Bulletin (An Educational Aid to Obstetrician-Gynecologists), #200--Decemeber 1994.

The definitive summary from the American College of Obstetricians and Gynecologists; it covers pre-existing diabetes in pregnancy as well as gestational diabetes. Technical but still readable. This is the 'bible' many doctors rely on for advice, and represents the current standard of care in the field. A must-read for those seriously interested in the subject.

Garner, P et al. A Randomized Controlled Trial of Strict Glycemic Control and Tertiary Level Obstetric Care Versus Routine Obstetric Care in the Management of Gestational Diabetes: A Pilot Study. American Journal of Obstetrics and Gynecology 177(1):190-5, 1997.

One of the largest and best-designed studies of the effectiveness of gd care; is a pilot study designed to be followed up with a multicenter trial of sufficient sample size to confirm their findings. Criticizes the inadequacies of other clinical trials to date and points to the need for further prospective randomized controlled trials of larger size. Its preliminary findings based on the pilot study is that intensive treatment of gd may have little effect on birth weight, birth trauma, operative delivery, or neonatal metabolic disorders, but emphasizes that the sample size (though the largest of its kind so far) is insufficient to allow any recommendations on the effect of treatment vs. no treatment in gd. A must-read for anyone serious about researching gd.

Jovanovic-Peterson, Lois, M.D. with Morton B. Stone. Managing Your Gestational Diabetes. Minneapolis: Chronimed Publishing, 1994. To order, write P.O. Box 59032, Minneapolis, MN 55459-9686, or call 1-800-848-2793.

A good introduction to gd issues by one of the leading researchers in the field, who also happens to be diabetic (Type I) and a mother herself. Be aware her treatment guidelines in this book are quite conservative and not all providers use the same guidelines. Her writings also contain some patronizing and fat-phobic statements (fat people "live to eat rather than eat to live"). But she is an excellent introduction to the conservative approach to gd. She happens to be a very prolific writer in the field, so she tends to dominate the available published material on gd. Many more articles and books are available under her name.

Gestational Diabetes: What to Expect, The American Diabetes Association, Inc. Alexandria, Virginia: American Diabetes Association, 1992. To order, write to the ADA, 1970 Chain Bridge Road, McLean, VA 22109-0592, or call 1-800-232-3472.

The standard intro to the subject, written by the leading authorities on diabetes. A good, easy-to-read summary for those not desiring a great deal of detail. It is, of course, the standard medical approach to gd and does not contain any discussion of the controversies involved in gd. Definitely read this text as one of your first introductions to gd, while also keeping in mind that alternative views do exist.

Goer, Henci. Obstetric Myths vs. Research Realities. Westport, Connecticut: Bergin and Garvey, 1995. Can be ordered online from

This excellent book reviews common obstetrical practices and analyzes which practices are truly justified by medical research. One chapter in the book is devoted to Gestational Diabetes, where she examines the history of its discovery, treatment, and variations in protocols. She extensively reviews the medical research available on gd and concludes that many common gd protocols are questionable because they do not sufficiently alter outcome but did increase the incidence of cesarean sections and resulting complications. She is one of the strongest voices critical of the assumptions of the traditional medical view of gd and backs up her opinions with research citations. She sometimes engages in rhetoric and should be less dismissive of research that shows some success with gd intervention, and she does exhibit some size prejudice in her writings. Still, Kmom would highly recommend reading her analysis of the research available to get one alternative view of gd, remembering this is just another viewpoint to consider and weigh, and being aware of her assumptions about size and weight loss. A must-read.

Walkinshaw S.A. Dietary Regulation for 'Gestational Diabetes'. In: Neilson JP, Crowther CA, Hodnett ED, Hofmeyr GJ (eds.) Pregnancy and Childbirth Module of The Cochrane Database of Systematic Reviews, [updated 01 September 1997]. Available in The Cochrane Library [database on disk and CDROM]. The Cochrane Collaboration; Issue 4. Oxford: Update Software; 1997. Updated quarterly.

A review of the efficacy and methodological design of previous studies that examined dietary treatment vs. no treatment. Concludes that studies do not support the value of primary dietary treatment for gd, but cites a number of methodological problems with previous studies and notes the need for further research with better research design. Hard-to-find article but well worth the search.

Blank A., Grave G.D., Metzger B.E. Effects of Gestational Diabetes on Perinatal Morbidity Reassessed. Report of the International Workshop on Adverse Perinatal Outcomes of Gestational Diabetes Mellitus, December 3-4, 1992. Diabetes Care. 18(1):127-9, January 1995.

Another must-read article, a report of some of the findings from the Third International Workshop on GDM. (The Fourth took place in 1997.) A quick summary of some of the perinatal morbidities associated with gd and the serious concerns they may present; notable for acknowledging some of the research controversies such as possible alternative causes for some of the problems, the problems with reproducibility of gd testing, the lack of cost-effectiveness of aggressively trying to reduce macrosomia on a wide scale, and the problems with research design and data of previous studies. Strongly promotes the need for further well-designed research done on a multi-center, multi-ethnic, and multi-national long-term scale.

Langer, O. et al. Glycemic Control in Gestational Diabetes Mellitus--How Tight is Tight Enough: Small for Gestational Age versus Large for Gestational Age? American Journal of Obstetrics and Gynecology. 161(3):646-53. September 1989.

334 gd mothers (and 334 controls) were studied to find out the relationship between optimal levels of glycemic control and perinatal outcome. Extremely tight control (mean blood glucose values <87 mg/dl) increased the number of small-for-gestational-age babies significantly, while high blood glucose values (mean > 104 mg/dl) had significantly more large-for-gestational-age babies. The middle group (mean blood glucose between 87-104 mg/dl) was similar to the control group. Critics have used this study to point out that excessively low bG goals may introduce risk and may lead to more SGA infants.

Javanovic-Peterson, Lois, M.D. The Diagnosis and Management of Gestational Diabetes Mellitus. Clinical Diabetes. pp32-39, March/April 1995.

A very technical journal article covering the basic information in great detail, including lots of information on hormonal influences. Very conservative guidelines are used for deciding when to start a mother on insulin, and 'morbidly obese' patients are recommended to only receive 12 kcal/kg in their diabetic food plan, a level less than half that of average-sized women and which would result in low caloric intakes for pregnancy, which is controversial. Very dense reading, with lots of technical detail, but good for those strongly interested in further detail.

Weller, KA. Diagnosis and Management of Gestational Diabetes. American Family Physician. 53(6):2053-7, 2061-2. May 1, 1996.

A review of gd treatment regimens, though it tends to be much less intervention-oriented than many treatment regimens found in endocrinology and obstetrics literature.

Hod, M et al. Gestational Diabetes: Is It a Clinical Entity? Diabetes Reviews. 3(4):602-613, 1995.

A review of the debate over whether gd is really a problem, with a strongly affirmative conclusion about the dangers of gd and the effectiveness of treatment. Advocates lowering treatment thresholds even further. Has the most astounding list of newborn treatment test protocols Kmom has ever seen listed, and some of the most extensive prenatal treatment protocols for the mother, too. Definitely worth reading for a representation of an extremely traditional view of gd and gd treatment.

Naylor, CD et al. Cesarean Delivery in Relation to Birth Weight and Gestational Glucose Tolerance: Pathophysiology or Practice Style? Journal of the American Medical Association. April 17, 1996. 275(15):1165-70.

One of the few studies to adequately address the issue of physician style and perception on the treatment of gd patients. Macrosomia is usually used as the excuse for higher c-section rates in gd moms, but even when macrosomia rates are reduced through treatment, most (not all) studies have found a higher c/s rate anyhow, raising the question of the benefits vs. risks of treatment. This study found that treatment lowered macrosomia rates to the level found in normoglycemic populations, but that treated patients had more risk of a c/s anyhow. Only 10.5 % of gd women had macrosomic babies in this study, yet there was a 33% c/s rate. Furthermore, the study examined the outcome of 115 women who had gd by the stricter criteria of Carpenter and Coustan but did not qualify as gd by official NDDG standards and were not treated. The rate of macrosomia in these women was 28.7%, compared with 13.7% for normoglycemic women and 10.5% for 'official' gd moms. Shoulder dystocia, which should have been higher in the 'untreated' group, was not. Their overall c/s rate was higher, though---29.6%, compared to 20.2% for normoglycemic women. However, the c/s rate for non-macrosomic infants in this 'untreated' gd group was similar to that of the controls, but the c/s rate for the macrosomic babies in the 'untreated gd' group was a huge 45.5%! This could reflect the labor problems encountered due to untreated macrosomia, or it could reflect simply the tremendous bias of providers about delivery of macrosomic infants, diabetic or not---or it could be both. Among women with 'official' gd who had had a previous c/s, the VBAC rate was an atrocious 18%. Among normoglycemic controls, the rate was 31%; among those with 'untreated' gd, it was 40%. [VBAC success rates are usually about 70%, putting an overall rate of VBACs around 30-40%.] An especially strong indication of the predisposition towards c/s that the simple label of 'gd' may give is shown in the rates of primary (first) c/s among women who'd had babies before. Among multiparous gd women, the primary c/s rate was strongly increased (23%) compared to 6% for women who were normoglycemic and 6% for women with 'untreated' gd. The authors concluded that "while detection and treatment of GDM normalized birth weights, rates of cesarean delivery remained inexplicably high. Recogniation of GDM may lead to a lower threshold for surgical delivery that mitigates the potential benefits of treatment."

Goldman, M et al. Obstetric Complications with GDM: Effects of Maternal Weight. Diabetes. December 1991. 40 (Suppl. 2):79-82.

Retrospectively assessed 150 women with gd for obstetric complications with special attention to the influence of the mother's weight (305 normoglycemic controls were used for comparison, matched for size etc.). Found that hypertension and pre-eclampsia were more common in gdm, but it was not totally attributable to being overweight. Unlike in most studies, abnormalities of labor, shoulder dystocia, birth trauma, and macrosomia were not more common with gd. However, despite macrosomia not being more common with gd, there were more c-sections in gd patients (35% c/s with gd; 22% without gd). This clearly points out that c/s are more common with the 'gd' label, even when macrosomia (the usual 'cause' given to justify more c/s) is not present. However, the most interesting result was the comparison of the number of elective c/s without labor---there were twice as many in the gdm group (17% vs. 8%). The authors state that "the increase is due to more repeat cesarean sections and more operations performed due to anticipations of macrosomia." When the data was stratified by pre-pregnancy weight, the descrepancy in elective c-sections was even more pronounced. The rate of elective c/s in overweight and obese gd moms was 32.5% overall, 12% for overweight and obese controls overall, vs. 13.7% in 'ideal weight' gd moms and 6.3% in ideal weight controls. In other words, a fat gd mom had 2.4x the risk of being assigned an elective c/s that an ideal weight gd mom had. This shows the bias of the providers----they are less willing to 'allow' a trial of labor and quicker to resort to surgical intervention in women of size, probably because of their presumptions and fears of macrosomia, and the label of 'gd' strongly reinforces that tendency. Fully 1/3 of large gd moms in this study were not given a trial of labor.

Cohen, B et al. Sonographic Prediction of Shoulder Dystocia in Infants of Diabetic Mothers. Obstetrics and Gynecology. July 1996. 88(1):10-13.

Predicting shoulder dystocia is very tricky, even in macrosomic infants of diabetic mothers. This study retrospectively looks at a specific technique of ultrasound examination (comparing the difference between the abdominal diameter and biparietal diameter, or "AD-BPD difference") to see if it is better at predicting shoulder dystocia in this group, since these infants sometimes experience preferential growth in the truncal area as opposed to the head. Eligibility requirements included diabetic pregnancy, ultrasound with the above measurements within 2 weeks of delivery, estimated fetal weight of 3800-4200g, and vaginal delivery. Found 31 patients who fit this criteria; 6 had shoulder dystocia (rate of 19%). Rate of injury and conditions of laboring (position, stirrups, etc.) not noted. The mean AD-BPD difference for the shoulder dystocia group was 3.1, whereas the mean for the non-shoulder dystocia group was 2.6. Therefore, the trunks of those babies who experienced shoulder dystocia were asymmetrically larger. Shoulder dystocia occurred in 6 of 20 patients (30%) with a AD-BPD difference of at least 2.6, but not in any of the 11 patients where it was <2.6. Therefore the authors propose using this test and this cutoff to identify "those fetuses at high risk for birth injury." This sounds promising, but it's also important to note that if 2.6 were used as the cutoff for doing an elective c-section, only 30% of those c-sections would have been necessary to prevent shoulder dystocia; 70% would have been unnecessary! And not all of those infants with shoulder dystocia have injuries; how many more c-sections would have been unnecessary by the criteria of actually preventing injury?

Davis, R et al. The Role of Previous Birthweight on Risk for Macrosomia in a Subsequent Birth. Epidemiology. November 1995. 6(6):607-11.

Assessed the risk for delivery of a macrosomic infant after delivery of a previous macrosomic infant (doesn't specify diabetic vs. nondiabetic cases). Used a population-based cohort study, studying 1793 infants weighing >4500g in Washington State between 1984-90 that were linked to a subsequent birth, and comparing them with 3596 randomly selected infants >4500g also linked to a subsequent livebirth. "The overall prevalence of macrosomic infants subsequent to a previous macrosomic birth was 22%, a proportion that did not vary notably with parity, or when paternity changed between successive births." The authors then conclude that women with one macrosomic infant are a markedly increased risk for repeat macrosomic births, an interesting conclusion when 78% did NOT go on to have another macrosomic child. Since the overall population risk of having an infant >4500g is very low, 22% recurrence is an increased risk, but still 3/4 of them did not go on to have another similarly sized baby. If early inductions or elective c-sections were routinely done for women who had previously had a large baby, then 78% of those inductions and c-sections would have been unnecessary, based on size alone. If shoulder dystocia or birth injury were the outcome considered instead, the rates of unnecessary inductions and unnecessary c-sections would be even higher.

Prophylactic Insulin References

Coustan DR and Lewis SB. Insulin therapy for gestational diabetes. Obstetrics and Gynecology. 1978. 51:306-10.

Small but randomized study that found that instituting daily insulin therapy reduced the incidence of macrosomia. However, according to other sources, no differences in rates of operative delivery or birth trauma could be demonstrated.

Coustan DR and Imarah J. Prophylactic insulin treatment of gestational diabetes reduces the incidence of macrosomia, operative delivery and birth trauma. American Journal of Obstetrics and Gynecology. 1984. 150:836-42.

The classic, must-read study that really intensified the prophylactic insulin movement. Retrospectively examined 445 charts of gd women delivered over a 5 year period. Examined the rate of macrosomic infants (>4000g), the rate of operative delivery (forceps, vacuum, c-section), and birth trauma (shoulder dystocia, injury) in the gd women, stratified by treatment modes (no treatment, diet alone, diet plus insulin). Found that insulin treatment significantly lowered the rates of macrosomia, operative delivery, and birth trauma. One of the few studies that found that lowering the macrosomia rate also lowered the c/s rate. The rates for macrosomia among gd women with no treatment, diet-only treatment, and diet+insulin treatment was 17.8%, 18.5%, and 7%. The rates for operative delivery for each group respectively were 28.5%, 30.4%, and 16.3%. The rates for birth trauma for each group respectively were 20.4%, 13.4%, 4.8%. Note that this was a retrospective study, not randomized. Still, one of the best results from prophylactic insulin use on the books yet. Critics note that using insulin reduced the birthweight on average, a total of 6 ounces (170g) and question whether that is clinically significant, but the percentage of very large babies *was* reduced significantly. Authors were fair enough to note at the end that it was appropriate to question the safety of prophylactic insulin use, but they only addressed a couple of areas of maternal safety and did not at all address fetal safety. Finally the authors note, "It would thus seem appropriate to offer prophylactic insulin therapy as a possible means of lessening the likelihood of a difficult delivery or cesarean section. The gestational diabetic woman should not be made to feel that this is a life-or-death issue for her fetus but rather a quality-of-delivery issue."

Thompson DJ et al. Prophylactic insulin in the management of gestational diabetes. Obstetrics and Gynecology. 1990. 75:960-4.

Randomized gestational diabetics into diet alone or diet plus insulin groups, with equal numbers of obese and average-weight women in each treatment group. Babies were delivered between 40-42 weeks, generally. Among 68 women successfully treated for a minimum of 6 weeks, the mean birth weight, macrosomia rate, and ponderal index were reduced significantly in the insulin group. Unlike in some studies, insulin significantly reduced the size of the babies of obese women, by an average level of about a pound and a half (very significant). However, the birth weights of the babies born to obese mothers on insulin were still heavier than those of non-obese women. Despite the big reduction in birth weight in the insulin group in both average-sized and obese mothers, their overall c/s rate was actually higher. The diet alone group had a c/s rate of 35% while the insulin group had a c/s rate of 41% (overall c/s rate for both groups was 38%, very high). Nor was morbidity reduced, raising the question of the value of treatment. No shoulder dystocia occurred in any patient, including the obese patients with macrosomic babies. Study advocates more aggressive insulin use in obese women based on the yet-unproven speculation that a decrease in macrosomia at birth may lead to less obesity and early diabetes among the offspring. Contains a good review of other prophylactic insulin studies.

Persson B, Stangenberg M, Hansson U, Nordlander E. Gestational Diabetes: Comparative Evaluation of Two Treatment Regimens, Diet Versus Diet and Insulin. Diabetes. 1985. 34:101-5.

Randomized 202 pregnant women with gd into diet-only and diet+insulin treatment groups. "The two treatment regimens disclosed no differences regarding achieved degree of maternal blood glucose control, hemoglobin A1c at delivery, obstetric or neonatal complications, infant's size at birth including skin-fold thickness, or C-peptide concentration in cord serum. Routine treatment of pregnant women with mild carbohydrate intolerance with insulin seems unnecessary."

Santini, DL and Ales, KL. The Impact of Universal Screening for Gestational Glucose Intolerance on Outcome of Pregnancy. Surgery, Gynecology and Obstetrics. May 1990. 170: 427-436.

Looked at the debate over universal screening and its impact on treatment and pregnancy outcome. Retrospectively studied 1307 pregnancies at Cornell University Medical Center over 5 months, where some providers did universal screening and some did not screen at all. Compared the screened population vs. the unscreened population to see if screening and treatment helped reduce the number of large infants, and how treatment and outcome differed. "The process of screening not only failed to decrease the rate of large infants, but also failed to improve otherwise pregnancy outcomes and was associated with more intensive surveillance during pregnancy and a significantly higher rate of primary cesarean delivery." The c/s rate for those unscreened for gd was 21%; the c/s rate for those screened for gd was 27.6%, and the c/s rate for those screened and treated was 32.5%. The c/s rate for those screened and treated with diet alone was 30%; the c/s rate for those screened and then treated with diet plus insulin was 38.5%. "The process of screening is itself linked with more intensive surveillance during pregnancy...even in the absence of the diagnosis, labeling or treatment of gestational glucose intolerance." Furthermore, only about half of the women labeled as having gd actually met the criteria for having it. The rate of large infants was not significantly different between the screened and unscreened groups. No difference was found, either, in the rate of metabolic complications in newborns. A few explanations could be made; physician style probably impacted the difference in c/s rates some, and the unscreened population tended to be less obese, so perhaps that is why they had less large babies than expected. However, the unscreened population was more likely to be parous and to be older (factors which generally make for bigger babies) and to have private doctors (a factor which would tend to increase the c/s rate, not decrease it). C/S was also more common in women with larger infants in either group (31.5% vs. 23.9%), raising the question of how much is due to actual physical problems of having a larger baby and how much is due to physician bias and interventions for larger babies. Examines the difficulty in setting up a randomized, controlled trial with enough power to determine the value of universal screening and gd treatment to reduce infant size---it would have to have a very large amount of participants. Notes that up to now, screening and treatment both were assumed to have no significant adverse effects, but that this needs to be strongly questioned.

Langer, O. et al. Glycemic Control in Gestational Diabetes Mellitus--How Tight is Tight Enough: Small for Gestational Age versus Large for Gestational Age? American Journal of Obstetrics and Gynecology. 161(3):646-53. September 1989.

334 gd mothers (and 334 controls) were studied to find out the relationship between optimal levels of glycemic control and perinatal outcome. Extremely tight control (mean blood glucose values <87 mg/dl) increased the number of small-for-gestational-age babies significantly, while high blood glucose values (mean > 104 mg/dl) had significantly more large-for-gestational-age babies. The middle group (mean blood glucose between 87-104 mg/dl) was similar to the control group. Critics have used this study to point out that excessively low bG goals may introduce risk and may lead to more SGA infants.

Garcia-Patterson, A et al. In Pregnancies with Gestational Diabetes Mellitus and Intensive Therapy, Perinatal Outcome is Worse in Small-For-Gestational-Age Newborns. American Journal of Obstetrics and Gynecology. August 1998. 179(2):481-5.

821 pregnancies of gd moms receiving intensive metabolic therapy were examined for the relationship between perinatal outcome and birth weight. 7% were Small-For-Gestational-Age (SGA), 85% were Appropriate-for-Gestational-Age (AGA), and 8% were Large-For-Gestational-Age. After adjustment for preterm delivery, rates of adverse fetal outcome were about 3x as likely in SGA babies than in AGA or LGA babies. "Among women with gestational diabetes mellitus who are receiving intensive therapy, perinatal outcome is worse for small for gestational age neonates than for appropriate and large for gestational age neonates." Critics have used this study as well to point out that excessively low bG goals may introduce risk and may lead to more SGA infants.

Kitzmiller, JL. Sweet Success with Diabetes: The Development of Insulin Therapy and Glycemic Control for Pregnancy. Diabetes Care. December 1993. 16(3):107-21.

Mostly a very technical history of the treatment of type I diabetic pregnancies, it does contain a few notes of interest here. It traces the modification of Pederson's Hypothesis (about maternal hyperglycemia increasing fetal insulin levels, causing macrosomia); it is now thought that other maternal substrates, notably Free Fatty Acids and Beta-Hydroxybutyrate, may be responsible for some of fetal macrosomia. Notes that higher doses of insulin may decrease macrosomia by decreasing these levels. Also examines the controversy of whether ketones impair IQ or cause learning problems, and notes that insulin requirements often decrease in the last few weeks in type I pregnancies. Finally, notes the potential dangers of adding excess insulin to the mother and the lack of research on its safety. "An important that hyperinsulinemia is produced by clinical methods of insulin treatment of diabetic women...There has been little investigation of the effects of this iatrogenic hyperinsulinemia on placental physiology, blood vessels, or the tendencies toward hypertension in pregnant diabetic women."

Langer, O. Maternal Glycemic Criteria for Insulin Therapy in Gestational Diabetes Mellitus. Diabetes Care. August 1998. 21(Supplement 2). Available for viewing at

Supports a very aggressive approach to insulin therapy, especially in obese women. Contends that many women qualifying for insulin are actually receiving too-small doses, and highlights the need for studies to compare optimal insulin dosage. Recounts a study showing that the majority of specialists studied were not instituting insulin at even the ACOG target range (105 fasting/120 post-prandial)--it's doubtful whether this is really true of all OBs. Blames the use of too-liberal insulin standards and the under-dosage of insulin for the lack of improvement of macrosomia rates in many gd studies. Advocates insulin use if fastings are >95, treatment goals of <95 fasting/<115 postprandial/<95 pre-meal, and mean blood glucose readings of 90-100 mg/dl. Also strongly advocates use of self-monitoring by patients and contends it is being vastly underused (questionable, but promotion of self-monitoring is a reasonable position). Theorizes that the rate of insulin use will be about 50-60% in this regimen but that providers should not shy away from this percentage--that normoglycemia is more important than avoiding insulin. Fails to address the issue of higher c/s rates in groups given insulin, or the issue of safety of aggressive insulin use. Makes a reasonable case for study of insulin dosage (are the doses being used too low?), and a decent argument for lowering the fasting requirement to 95, though the point is still debatable. However, he concludes that "patients with fasting plasma glucose on the OGTT of <96 mg/dl (and ideally nonobese) be assigned to diet therapy. Obese women or those with fasting plasma glucose >95 mg/dl on the OGTT should be referred to insulin therapy in order to minimize exposure of the fetus to a hyperglycemic environment." This seems to be saying that ALL obese women should be placed on insulin, regardless of favorable bG results on the OGTT or dietary treatment. If the results are <95, then by his definition they are not 'hyperglycemic', yet they would still be assigned to insulin. Does not make a case to justify the use of insulin for successfully treated obese moms, just makes the sweeping recommendation for it.

Garner, P et al. A Randomized Controlled Trial of Strict Glycemic Control and Tertiary Level Obstetric Care Versus Routine Obstetric Care in the Management of Gestational Diabetes: A Pilot Study. American Journal of Obstetrics and Gynecology 177(1):190-5, 1997.

One of the largest and best-designed studies of the effectiveness of gd care; is a pilot study designed to be followed up with a multicenter trial of sufficient sample size to confirm their findings. Criticizes the inadequacies of other clinical trials to date and points to the need for further prospective randomized controlled trials of larger size. Its preliminary findings based on the pilot study is that intensive treatment of gd (insulin started at fastings of 80!) may have little effect on birth weight, birth trauma, operative delivery, or neonatal metabolic disorders, but emphasizes that the sample size (though the largest of its kind so far) is insufficient to allow any recommendations on the effect of treatment vs. no treatment in gd. A must-read for anyone serious about researching gd.

Simmons, D and Robertson, S. Influence of Maternal Insulin Treatment on the Infants of Women with Gestational Diabetes. Diabet Med. September 1997. 14(9):762-5.

Examined the long-term impact of insulin therapy on the adiposity of the offspring. Looked at the degree of fatness at about age 2.5 of babies of moms treated for gd. Babies of insulin-treated women had less subscapular fat and less biceps fat than diet-treated moms, despite insulin-treated moms being more obese, older, and more hyperglycemic. "Insulin therapy in gestational diabetes may reduce the incidence of obesity in the offspring of women with gestational diabetes and this should now be tested by a larger, randomized controlled trial." Note that sample size was extremely small, significantly limiting the power of this finding, and that children were only examined at the age of about 2.5 (difficult to make long-term generalizations from). Also, it is unclear if this is meaningful at all, i.e. will having less subscapular and biceps fat translate into less or more diabetes later in life? Still, it is an interesting finding and one of the few studies to study the results of insulin on the child. Its call for further studies with adequate methodology is very important.

O'Sullivan, JB and Mahan, CM. Insulin Treatment and High Risk Groups. Diabetes Care. May-June, 1980. 3(3):482-5.

Follow-up study of 615 gd mothers by the author whose classic works were most instrumental in early gd research. Followed these mothers over 16 years. Half of the group were randomly assigned to insulin therapy originally, half were not. Evaluated whether initial treatment with prophylactic insulin potentially reduced the rate of subsequent diabetes in mothers; it did not. However, a sub-analysis found that among women who bore a baby of large birthweight or who had a family history of diabetes, "subsequent decompensated diabetes was found to be significantly reduced" among those who had been treated prophylactically with insulin. "This finding suggests the possibility of long-term preventive benefits from insulin treatment in high risk subsets of women with gestational diabetes." However, it's important to note that O'Sullivan's original study groups were notable for having multiple risk factors that muddy his original analyses; it is difficult to know the significance of these early findings. Still, it's an interesting study.

Sacks, DA. Fetal Macrosomia and Gestational Diabetes: What's the Problem? Obstetrics and Gynecology. May 1993. 81(5, part 1):775-81.

A truly outstanding, well-balanced review of the issue of macrosomia and gd pregnancies. Reviewed 79 articles through 1993 relevant to the subject, then summarizes the difficulties in drawing conclusions from them and suggests strategies for further investigation. For example, found that some studies clearly found a relationship between maternal glucose levels and fetal macrosomia, while others did not. Notes all the confounding variables possible, and the differences in study design and observational content---"because of these differences, meaningful comparison of data between studies is exceedingly difficult." Notes the problems even defining what macrosomia is, but treats seriously the potential for shoulder dystocia and injury. However, it still notes that this concern should be "placed in clinical perspective. Only a small proportion of LGA infants of diabetic mothers will develop shoulder dystocia. Brachial plexus palsy...usually resolves during the neonatal period. Physical and sonographic estimates of excessive fetal weight carry substantial margins of error. Furthermore, cesarean delivery introduces a significant risk of maternal morbidity." Regarding prophylactic insulin, the study has multiple observations. "Despite insulin treatment, obese women had a higher incidence of macrosomic neonates, even when the data were stratified by maternal glucose levels...[other] data suggest a potential benefit of routine insulin administration to certain gestational diabetic women. However...the lack of uniformity in reporting and control of variables that may influence birth weight makes it exceedingly difficult to draw definitive conclusions."

Carr, DB and Gabbe, S. Gestational Diabetes: Detection, Management, and Implications. Clinical Diabetes. 16(1):4-24, 1998 Jan-Feb.

Outstanding article summarizing gd testing, management, and even some of the controversies involved in gd, though from a traditional medical approach. Excellent overview, but may be too technical for beginners unfamiliar with some of the terminology and issues in gd. Those more familiar with gd terms and issues will find it invaluable, and beginners will want to return to it when their understanding increases. Re: prophylactic insulin, it says, "It is important to recognize the data suggesting that insulin therapy may achieve lower rates of macrosomia if initiated when fasting blood glucose is >95 mg/dl. However, prophylactic insulin treatment in patients whose fasting and postprandial values remain within the recommended range is not advised."

Ratner, RE. Clinical Review 47. Gestational Diabetes Mellitus: After Three International Workshops Do We Know How to Diagnose and Manage It Yet? Journal of Clinical Endocrinology and Metabolism. July 1993. 77(1):1-4.

An excellent if conservative review of gd and many of its controversies. Notes that more than just glucose levels are implicated in the possible morbidities associated with gd. Discusses many of the treatment issues of gd, and notes the need to balance aggressive glycemic control with possible risks to the mother and fetus from overly aggressive treatment. Does favor moderate caloric restriction for obese women, though it notes that this is "one of the most contentious issues in the literature" and that "long-term effects, however, remain unknown and require additional investigation." Regarding prophylactic insulin, it states that "controlled trials comparing diet plus insulin to diet alone in GDM reveal mixed results...preliminary data may support revision of these [traditional] goals to initiation of insulin when fasting plasma glucose levels exceed 95 mg/dL but prophylactic insulin treatment is not convincingly beneficial."

Metzger, BE. Treatment of Mild Gestational Diabetes: Is It Time for a Controlled Clinical Trial? Editorial in Diabetes Care. 11(10):813-16. Nov/Dec 1988.

Reviews a number of studies where intensive insulin therapy has been used and finds that "insulin therapy has not always been more successful than dietary treatment, and corresponding improvements in obstetrical outcomes and reductions in neonatal morbidities have not been found to be consistent." In some studies, intensive insulin use reduced the c-section rate, while in others it either had no effect or actually increased the c-section rate. Calls for a large-scale, multicenter controlled clinical trial with a large number of subjects and rigidly defined protocols.

Enkin, Murray et al. A Guide to Effective Care in Pregnancy and Childbirth. Second Edition. Oxford: Oxford University Press (Oxford Medical Publications), 1995.

Based on the conclusions and research from the Cochrane Database of Systematic Reviews, which examined the research of 60 key journals. Careful attention was paid to the methodology of the research design, with an emphasis on the 'gold standard' of research, randomized controlled studies. "Evidence-Based Medicine" at its best. Found significant reason to question the current aggressive approach to gd. "There is no convincing evidence that treatment of women with an abnormal glucose tolerance test will reduce perinatal mortality or morbidity. Trials of dietary regulation... do not demonstrate a significant effect on any outcome, including macrosomia. Trials comparing the use of insulin plus diet with diet alone show a decrease in macrosomia, but no significant effect on other outcomes such as use of caesarean section, the incidence of shoulder dystocia...perinatal mortality...[or] neonatal jaundice or hypoglycaemia." They further go on to make the very strong statement that "The available data provide no evidence to support the wide recommendation that all pregnant women should be screened for 'gestational diabetes', let alone that they should be treated with insulin. Until the risks of minor elevations of glucose during pregnancy have been established in appropriately conducted trials, therapy based on this diagnosis must be critically reviewed. The use of injectable therapy on the basis of the available data is highly contentious, and in many other fields of medical practice such aggressive therapy without proven benefit would be considered unethical."






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