Gestational Diabetes: What Is GD?

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. Please be sure to read the introductory section of this FAQ first in order to understand completely the purpose and focus of this information.


Reminder: This GD FAQ is about the controversies surrounding gestational diabetes. It is intended to examine in detail the differing opinions about and treatments for gestational diabetes, give research references and avenues for further research, and give coping strategies for dealing with gd. Most material on gd for the layperson (traditional or alternative) does not discuss the controversies in research and treatment or look fairly at all sides. This is an attempt to do so in order for women to do further research on their own, question their providers more competently along the way, and participate more fully in their own care decisions. Kmom acknowledges that she is not a medical professional, just a layperson interested in the research, and has no pretentions to being an expert or offering medical advice. After presenting various sides of controversies, she has felt free to add her own opinions (hopefully clearly labeled), to share her experiences, opinions, choices, and reasoning. However, it is important to her that readers should NOT feel unduly influenced by her opinions and should feel free to disagree or pursue their own course. She cautions readers to consult their health providers, to carefully use critical thinking skills when reading any health information (especially from the internet) and reminds readers again that none of this is medical advice, just an attempt to look further into the issues surrounding gestational diabetes and the research literature on it.





What is Gestational Diabetes?

"Glucose intolerance that is first diagnosed during pregnancy is termed gestational diabetes mellitus. The definition is ambiguous, and the treatment controversial. Most important, the threshold at which glucose intolerance adversely affects the course of pregnancy and increases the risk of future diabetes in the mother and her child is not known....we think the optimal care for women with gestational diabetes remains to be defined." Editorial by Anne Dornhorst and Joanna C. Girling in The New England Journal of Medicine, November 9, 1995, Volume 333, Number 19.

"By some, even the slightest degree of glucose intolerance is suspected to be guilty until proven innocent. Others hold that the case against lesser degrees of glucose intolerance is weak and that its innocence should be presumed until its guilt is more clearly established...The use of the single NDDG [National Diabetes Data Group] diagnostic class of GDM gives only an estimate of average risk across the whole range, even though the lesser degrees of glucose intolerance might contribute little, if anything, to it. If the lesser degrees of glucose intolerance carry significant risk, then 3 or 4% of the pregnant population require identification and special clinical attention, an exercise in logistics and economics of major proportions. If the risk of lesser degrees of glucose intolerance is diminutive, nonexistent, or confined to a small subset, then many women could be submitted to the physical, emotional, social, and economic disadvantages of diagnosis and treatment for no good reason." Harry Keen, "Gestational Diabetes: Can Epidemiology Help?" Diabetes, December 1991. Vol. 40, Suppl. 2:3-7.


Gestational Diabetes is another name for carbohydrate intolerance of pregnancy. It occurs when the placenta manufactures hormones that interfere with the body's ability to use insulin effectively ("insulin resistance"). Insulin is like a key that unlocks the door of the cells, letting them access the blood glucose (bG) in the blood for energy. Insulin resistance causes this key to become 'warped', in essence, and reduces the amount of glucose that can get into the cell, letting the cells starve while the blood outside contains an excess of blood sugar.

According to the traditional view of gd, this causes several problems. The excess sugar in the blood (hyperglycemia) can cause a number of problems for mother and baby, while the starving cells must then access body fat (and other sources) for energy, causing an acid by-product called ketones, which are probably not good for the baby. Maternal blood sugars begin to swing from highs to lows and back again; the large swings may be a problem in addition to consistent hyperglycemia. The baby receives the high blood sugar from its mother, and then produces extra insulin in order to compensate (the"Pederson Hypothesis"), possibly causing it to grow 'too big' or in abnormal growth patterns and sometimes interfering in other ways.

More recent research has expanded upon the Pederson Hypothesis, finding that maternal hyperglycemia alone is probably not solely to blame for fetal 'overgrowth'. The Fourth International Workshop-Conference On Gestational Diabetes Mellitus noted that "other nutrients, such as amino acids and lipids, and specific growth factors may also be important determinants of fetal growth in diabetic and in normal pregnancy. There may also be variability in fetal response to a given nutrient environment." More research is just beginning in this area to further delineate the influence of other maternal substrates and is a fascinating area of inquiry.

It is the combination of maternal hyperglycemia, bG swings, ketone by-products, fetal hyperinsulinemia, and perhaps other excess maternal substrates that can cause the complications of gd, especially in more severe cases. A list of the potential risks of gd will be found in another section of this FAQ but some of the most common complications can include fetal hypoglycemia, macrosomia, jaundice, and possibly birth trauma for the baby, plus potentially increased rates of pre-eclampsia, polyhydramnios, pre-term labor, induction and especially high rates of c-sections for the mother. Just how common these complications are and to what degree they are caused by the actual gd versus being caused by unnecessarily stringent interventions by the doctor is a big but under-researched controversy. Some complications are quite probably caused by the gd, but it has been documented in several studies that even when other risk factors are accounted for, just the very label of 'gd' increases the rate of complications like c-sections. The strong interventions that have often accompanied gd pregnancies in the past probably need re-evaluation to determine what exactly is necessary and effective and what may add extraneous risk.

All pregnant women encounter some insulin resistance, but most women are able to produce enough insulin to overcome the interference of the placental hormones. Gestational diabetes occurs when a woman's pancreas cannot produce enough insulin to compensate for the increased resistance during pregnancy. This usually occurs around the 26th-28th week of pregnancy or so, when 4 of the 5 most potent diabetogenic hormones peak, so gd is usually tested for at about week 28 in most pregnancies. This allows enough time to identify most cases of gd while still allowing enough time to mediate the possible effects of hyperglycemia. However, in a few pregnancies gd will not develop until around week 32, when the 5th diabetogenic hormone (progesterone) peaks, so some providers may choose to retest women with previously borderline results or multiple strong risk factors at that time. It should also be noted that some women enter pregnancy with impaired glucose tolerance or previously undiscovered diabetes (usually type II but occasionally type I) but because the problem is first discovered during pregnancy, it is still labeled 'gd'. These women may actually have 'gd' occur earlier, within the first trimester. For women with very strong risk factors, it may be appropriate to test for gd in the first trimester as well, especially since early 'gd' can cause the most damage and tends to be the most severe.

Risk factors for gd include a family history of diabetes, age over 25 (and especially over 30), obesity, previous stillbirth or poor obstetric outcome, prevous baby over 9 lbs, polycystic ovarian syndrome, smoking, etc. Contrary to popular belief, obesity does not cause diabetes or gd, but it is associated with it. In order to get gd, one must have a genetic predisposition to it. Some extremely heavy people never get diabetes or gd, simply because they do not have the genes for it, and some thin people get it, simply because it is in their genes. However, lifestyle does have some impact. The great majority of people who get Type II Diabetes and gd do tend to be heavier on average, perhaps reflecting an underlying tendency towards metabolic problems and/or a tendency for abdominal obesity to worsen insulin resistance. An inactive or sedentary lifestyle can also potentiate a genetic tendency as well. Furthermore, an area that has received little attention in gd research is that many women with gd actually have an undiagnosed underlying metabolic problem called 'PolyCystic Ovarian Syndrome' (PCOS). [Any woman diagnosed with gd should ask her health provider to consider testing for PCOS postpartum, especially if she also has problems with irregular cycles, cystic acne, facial or abnormal body hair, infertility, obesity, or thinning hair on the head. More information on PCOS can be found in other sections of this website.]

Ethnicity is also a very strong predictor of the rate of gd, much as type II diabetes occurs more strongly in some populations than in others. Women of Hispanic, African, Native American, South or East Asian, Hindu, Pacific Islands, or Indigenous Australian ancestry are most at risk, especially if they reside in Westernized countries or in urban areas. One criticism of gd research is that a fair amount has occurred in very high-risk populations such as Hispanics and Native Americans where the onset of type II diabetes is much earlier, frequent, and severe, yet their risk is often generalized to apply to all populations. Ethnicity is an important factor in gd research and must be carefully considered, yet researchers must be careful not to overgeneralize conclusions across populations.

For most women, institution of dietary counseling and a light exercise program is enough to control the gd. For some women, however, dietary control does not keep the blood glucose levels within the levels currently deemed to be most safe. These women need to add daily insulin to their regime and need to be more closely monitored as a result. The American Diabetes Association reports that only 15% of women with gd need to use insulin during their pregnancy, but some research studies have found much higher rates of insulin use (sometimes as high as 50-80%). A great deal depends on the standards of the provider as to when insulin becomes necessary; some providers institute insulin use at much lower levels than others and some have advocated using it prophylactically in order to try to reduce the risk of macrosomia. Other factors include the willingness of the provider to try adjustments to the mother's gd food plan and utilize alternative therapies (such as exercise) before starting insulin. When insulin is truly needed and what levels of average blood glucose are most optimal remain an area of strong controversy.

Delivery guidelines and prenatal testing protocols differ significantly from one provider to the next and is a source of great controversy as well. Some providers begin stringent prenatal testing regimes at about 32-34 weeks while others do not begin testing until 38 or even 40 weeks. Complications such as the need for insulin, high blood pressure or previous stillbirth will also influence the decision on when to begin testing, but some providers insist on extremely early testing in gd women regardless of their degree of control and lack of complications. Although officially most well-controlled non-insulin-dependent mothers can continue their pregnancy to term or even beyond, many providers in the past have insisted on early induction (or elective c-section for suspected macrosomia) for the gd mother, fearing that placental function will deteriorate earlier (as it can in 'true' diabetic pregnancies), or that abnormal growth patterns may cause significant birth trauma. This high rate of early induction and elective sections is probably the reason why the c-section rate for gd mothers is so high (between 20-40% in most studies, averaging nearly 30%, but much higher in some studies). Some researchers are advocating easing off on this early delivery protocol, but others are advocating an even more stringent approach. Much depends on the philosophy of your personal provider.

In general, most insulin-dependent gd women are induced (or electively sectioned) at about 38-39 weeks, though some providers contend that going to term presents little extra risk. Most diet-controlled gd mothers are induced between 39-40 weeks, especially if the baby is thought to be 'big'; diet-controlled women with excellent control, reassuring tests, and babies estimated to be of 'average' size are usually delivered around 40-41 weeks. A few providers will wait until 42 weeks to induce labor if all other factors are favorable. However, it should be emphasized that the optimum timing and delivery protocols are extremely controversial and much contradictory research exists. The final determination of optimal delivery timing and method is still the subject of great debate and the 'general' standard of care listed above does not necessarily mean that it is the most optimal, only the most common.

GD offers no contraindication to breastfeeding. In fact, there is some preliminary research that suggests it may well be even more important for gd mothers and babies, although more research needs to be done on the topic to confirm and expand upon preliminary findings. But breastfeeding mothers tend to return to normoglycemia faster than formula-feeding mothers, and breastfeeding may help prevent or delay later overt diabetes in the mother. There is also some limited evidence that breastfeeding may cut the risk for diabetes later in life for the child, and other evidence that it may help prevent or minimize obesity in the child later in life. Clearly, the medical evidence shows that in the general population breastfeeding helps prevent or reduce many child health problems significantly; preliminary evidence now seems to show that it may offer additional benefits to children of gestational diabetes pregnancies. However, although nearly all sources pay lip service to the value of breastfeeding in gd mothers, many of the delivery practices commonly used with gd patients (early induction, high rate of c-section, routine supplementation of the newborn, admittance to the nursery for special observation, delayed contact with mother for nursing, etc.) interfere with the establishment of breastfeeding. Much more needs to be done to truly support gd patients' efforts to establish and maintain breastfeeding.

GD almost always goes away after delivery of the placenta, since this makes the interfering hormones go away. However, women who have had gd have a good chance of it recurring in a subsequent pregnancy, often earlier and more severely than in the first pregnancy. They are also at increased risk (about 50%) of developing Type II diabetes (NIDDM) later in life, usually within 10-20 years, some even sooner. There is also some preliminary research that babies of a gd pregnancy may be at a greater risk of impaired glucose tolerance, diabetes, and obesity as they grow, and at earlier ages than babies not from diabetic pregnancies, although it is difficult to differentiate the role of genetics versus the role of diabetes in pregnancy in this issue. This is a new hot area for research, since it gives doctors possible new justifications for treating gd aggressively, though it has not yet been proven that gd treatment alters the development of obesity or diabetes in the child in any significant way. Much more research remains to be done in this area, but if it is proven that babies of even borderline gd pregnancies are more at risk and that treatment improves their outcome significantly, then some gd interventions may indeed prove to be justified. However, at this time, there is not enough research to substantiate or refute this.



Testing Issues

"There is not universal agreement on how to diagnose gestational diabetes. The most widely used diagnostic criteria in the U.S. were validated by their predicitve value for subsequent diabetes in the mother, rather than by their ability to identify risk to the fetus and newborn. The best available evidence supports the notion that the relationship between carbohydrate intolerance in pregnancy and adverse perinatal outcomes is a continuous one, and no single cutoff can separate pregnant women into those with high risk and those with no risk at all." Coustan, D.R. and M.W. Carpenter, "The Diagnosis of Gestational Diabetes." Diabetes Care. Volume 21, Supplement 2. August 1998.


The majority of women who develop gd do not experience any symptoms different than those normal to pregnancy, such as fatigue, thirst, bladder infections, etc. However, some women do experience repeated bladder or vaginal infections, sudden strong bursts of hunger, a feeling of being constantly sick with colds and fatigue and such, and other similarly vague symptoms. These are rarely identified as being part of gd except in retrospect, since they are quite common in many pregnant women, even those without gd. However, with hindsight some gd moms can identify a general feeling of malaise, strong hunger alternating with nausea, and stubborn or recurrent infections; these tend to improve after treatment is initiated in many women. On the other hand, some gd women never notice any problems at all. Symptoms are not a reliable way to discern who needs gd testing or treatment.

Although many women who develop gd have certain risk factors such as age, parity (number of children), ethnicity, etc., many who are diagnosed with gd do not have any of these risk factors, which is why it has been recommended in the past that all pregnant women be screened for gd at 26-28 weeks. Currently, this universal screening is a hotly debated research topic. Since gd prevalence seems to mirror the diabetes rate found in various ethnic populations, 'universal' testing may make sense in some populations but not in others, or it might still be overall more effective to do extensive testing. Certainly, much research has been done on gd in populations at high risk of diabetes, and some of this shows some benefit to intervention. Research in populations with generally lower rates of diabetes have shown far less benefit to intervention. However, because few populations are completely homogenous and immigrants who have taken on Western lifestyle may be particularly susceptible to gd risks, proponents have generally felt that nearly universal screening is appropriate. Also, since the rate of diabetes is predicted to rise strongly in the world in the next few years, universal testing may become more important, even in lower-risk populations. At this time, the consensus between the American College of Obstetricians and Gynecologists (ACOG) and the American Diabetes Association (ADA) is that universal testing is not necessary, but the list of exclusions is so small (under 25, not obese, no family history of diabetes, of caucasian ethnicity, no other major risk factors such as smoking, etc.) that testing is still nearly universal.

Testing is usually done at 26-28 weeks because it is the most common time for gd to manifest, yet it still allows enough time to correct metabolic imbalances before the baby experiences any real negative effects. If blood sugar is kept under tight control for the rest of pregnancy, most gd pregnancies turn out fine with no real problems for baby or minor, transient problems that are easily remedied (such as minor jaundice or mild hypoglycemia); however, the rates of intervention for the mother are fairly high. This is why so many critics question whether the burdens of intervention justify the treatment.

Testing differs around the world. In the USA, a one-hour/50 gram screening glucola 'challenge' test is used to find those women who need further testing. About 85% of women who 'fail' the one-hour test pass the second (more stringent) test, but it should be noted that some research shows that women who 'fail' even the screening test are at some risk for macrosomia (big babies) and might benefit from some instruction in eating on a diabetic plan. The second test, used for diagnosing gd in the USA, is the three-hour/100g glucose tolerance test (GTT). Women who 'fail' this test by the set criteria are officially labeled as having gd and subjected to various treatment protocols. The cutoffs that should be used to diagnose gd is an area of very strong controversy in gd research, with many researchers advocating lowering the current standards for diagnosis, and also lowering the standards at which insulin is initiated. Much literature can be found on this debate, none of it conclusive yet. Another big issue is the reproducibility of the tests; many criticize the fact that the same test repeated later often produces a different result. Others criticize the validity of the tests themselves, since they do not reflect real-life scenarios well.

Further complicating the issue is the fact that most countries around the world do not use the US testing scheme of two separate tests. Most countries instead use only one, the two-hour/75g glucose tolerance test, which is the standard diabetes diagnostic test for non-pregnant people around the world. ACOG and the ADA contend that this test as done in the past permits too many women with questionable results to go undiagnosed, while the World Health Organization contends that it is sufficient and that the double-testing scheme of the USA is too cumbersome and expensive for use in most countries. While there is some consensus beginning to occur on appropriate cutoffs for using the 75g/two-hour test to diagnose gd, the differing tests used around the world make it difficult to compare international results of testing and treatment and add greatly to the confusion over gd protocols. Again, this issue of testing cutoffs, protocols, and validity is a very hot area of research debate.

Finally, one more benefit to univeral (or nearly universal testing) is that it identifies a group of women at high risk for developing overt diabetes later in life. A diagnosis of gd can serve as an 'early warning system' to alert the woman and her doctors to the need to test frequently after pregnancy for the development of gd. Since so much of the damage that diabetes does is done early and silently when the patient is unaware of the disease, frequent post-partum testing because of a previous diagnosis of gd may actually prove extremely useful for improving diabetic prognosis. Furthermore, a new area of research is whether lifestyle intervention programs instituted postpartum may prevent or delay onset of diagnosis of overt diabetes, a possibility that, if effective, could be very important. However, at this time, the efficacy (or even lack of harm) of this approach is not known and has only begun to be studied. Still, these possibilities, if they are effective, provide a strong argument for the benefits of aggressive screening.


Criticisms of GD Treatment

"Good medicine demands that diagnosis and treatment of any disease fulfill four criteria:

An entire medical industry has grown up around diagnosing and treating gestational diabetes (GD) in the belief that doing so prevents perinatal deaths, congenital anomalies, neonatal complications, macrosomic babies, and because of fetal macrosomia, birth injuries and excessive cesarean rates. However, diagnosis and treatment of gestational diabetes don't fulfill any of the above criteria." Henci Goer. "Gestational Diabetes: The Emperor Has No Clothes." Birth Gazette. Spring 1996: Volume 12, Number 2.

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


There are many criticisms of current gd thinking in the medical community, several of which have already been noted. A big problem in discovering the true nature of risk in gestational diabetes is the fact that currently, ANY diabetes that is first discovered during pregnancy is called 'gestational diabetes'. Remember that this includes women who had previously been undiscovered type I or II diabetics, and women who had borderline diabetes/Impaired Glucose Tolerance. It seems clear that these women would experience risks that are close to those experienced by 'true' type I and II pregnancies, which are quite significant (major birth defects, stillbirths, etc.). In contrast, women whose gd is mild, occurs later, and is mostly caused by the insulin resistance from placental hormones tend to have fewer complications and problems, though there is apparently some risk. However, much of the research done on gd does not adequately separate these risk categories, and women with mild, relatively lower-risk cases are often managed with similar degrees of strong intervention as women with higher-risk presentations, and these interventions may introduce more risk than they avert. This is one of the main criticisms of gd offered by critics.

It appears that GD presents a continuum of risk, but the treatment that many providers offer tends to be "one-size-fits-all" and assumes interventions based on the worst-possible scenario of risk. For these providers, prevention of the worst-possible outcome justifies any and all interventions and treatment tends to err on the cautious side; interventions are assumed to be beneficial with minimal side effects. This is known as the maximum school of treatment. For other providers, however, treatment is recognized as also carrying risks that may outweigh the risks of non-treatment or minimal treatment, and they tend to insist on treatment protocols that have clearly been proven to be of value without causing undesirable side-effects or complications. This is generally known as the minimum school of treatment ('evidence-based medicine'). The tension between these two approaches is a microcosm of the vast majority of gd controversies. Anyone desiring to truly investigate gd thoroughly should read the excellent article that delineates these approaches, written by Canadian M.J. Stephenson (Canadian Family Physician, 1993). It is one of the few fair and impartial overviews of the issue out there in the research literature.

Another criticism is whether the mild degree of problems found in borderline gd cases is really attributible to gd or to other factors. Henci Goer (Obstetric Myths vs. Research Realities) and others (as noted in Blank et al., Diabetes Care, 1995) contend that these problems (macrosomia, mild hypoglycemia, etc.) may be occurring because gd moms tend to be older, more obese, and have higher rates of other complications such as hypertension and PCO. The fact that these 'gd' problems have not responded well to gd treatment in many instances could be taken as an indication that the assumptions of treatment are based on fallacies or have a different cause (the critic's point of view), or that the treatment protocols are simply not strict enough and need to be lowered even more (the traditionalist's point of view). The debate over efficacy of treatment and the true cause of gd risks needs much more attention in the research literature.

One controversy absolutely central to the gd debate is the question of macrosomia ('big baby') and its risks. Modern obstetrics increasingly focuses its attention upon its perceived 'dangers' of macrosomia, including birth trauma for mother and baby and what are thought to be subsequent risks for obesity, high blood pressure, and earlier diabetes. Clearly, true diabetic pregnancies have produced true diabetic macrosomia, in which the child may develop asymmetrically (more trunk growth than head growth), have organomegaly, and show excess adipose tissue. This pattern of development clearly is abnormal and unhealthy for baby, these babies clearly have higher rates of shoulder dystocia (shoulders getting stuck at delivery) and birth trauma, and this macrosomia clearly responds well to tighter control and intervention. The question in milder cases of gd, however, is whether the somewhat higher rate of 'bigger babies' (usually 9-10 lbs.) is abnormal and unhealthy, what its real cause is, whether treatment satisfactorily lowers baby size, whether such treatment is safe, and the degree of clinical importance of reducing baby size.

Critics claim that the higher rate of bigger babies in mild gd is due more to other factors such as maternal obesity (which, as a group, is quite predictive of bigger baby size), older age, and higher parity (more children). If a higher percentage of mothers with mild gd are obese, perhaps it also makes sense that genetically, their children might also be bigger naturally. The question is whether this is these babies' natural size (a simple harmless variation of normal) or whether it results from an unnatural 'maternal milieu' of excessive nutrients, etc. If the babies' size is unnatural, as gd proponents believe, then aggressive treatment to 'normalize' the uterine environment may help prevent obesity, high blood pressure, and later diabetes in the child (although this is still a hypothesis at this time and has not been proven). However, if their size is natural and simply a minor variation of normal, then aggressive treatment to 'normalize' size is interfering with a baby's primary growth mechanism (a potentially very dangerous and worrisome thing) and, in essence, trying to put a baby on a diet before it is even born.

A key question is whether this type of mild macrosomia (babies somewhat bigger than average) is really comparable to the dangers of true diabetic macrosomia (where the babies clearly have abnormal growth and clinical problems), and whether the benefits of reducing baby size really justify the intensive and expensive treatment regimens required. The first question is largely unanswered because few in the gd research community have asked the question. No one really knows whether slightly bigger babies are really a big health concern or not. Bigger babies do have higher rates of birth trauma and shoulder dystocia, but again, is this due to their size or to the way doctors handle the deliveries of big babies? Midwives deliver big babies all the time with significantly less trauma and c-section rates. Is the proper treatment for big babies simply relearning better delivery skills and a less interventive style, or is it better to aggressively reduce the size of babies so the problem presumably doesn't arise in the first place?

Does the presumed benefits of reducing baby size really justify intensive and expensive treatment regimens? The first extensive set of trials of gd treatment found contradictory results. Some trials found that there were no significant differences between those treated and those not treated, in which case treatment regimens were clearly unnecessary. Some trials found that treatment lowered size to the statistical equivalent of the normoglycemic population, but while a few of these lowered the c-section rate, the majority of these actually increased the c-section rate, bringing into question whether the 'cure' was worse than the problem. Many other trials found that in spite of intensive treatment, 'macrosomia' levels were not reduced to the levels found in the normal populations; this seemed especially true in obese women, supporting the possibility of genetic size as the source of 'macrosomia' in many women instead of high blood sugar. Furthermore, the level of intervention remained very high in these women despite treatment, strongly questioning the efficacy and value of treating gd at all. For extensive gd treatment to be justified, it should significantly reduce risk for both mother and child, and improve both short-term and long-term outcome. At present, little research has been done on long-term outcome of treatment vs. no treatment; in the short term, some studies show benefit while others show increased morbidity. More study is needed.

GD critics contend that the majority of gd treatment has proceeded on the basis of questionable results. GD proponents have responded that the mediocre results have occurred because the treatment regimes were not intensive enough, and that more aggressive regimens will show more uniform and beneficial results. They have strongly lowered the targeted treatment levels and are using more and more 'prophylactic' insulin--especially for obese women, even those with normal blood sugar levels through diet alone. Other treatment has included strongly hypocaloric diets or exercise as a possible alternative or addition to aggressive insulin use. Some critics contend that this is overkill for what is probably simple biological diversity of size, and that the risks introduced by intensive treatment with insulin outweigh the dubious benefits of a smaller baby. Again, they stress that problem with large infants may lie more with the way doctors handle these labors than with the actual size of the babies.

Furthermore, the long-term safety (for the child) of extremely strict protocols has not been adequately studied, a concern which has hardly been addressed in the research literature at all. This is an issue of critical importance, and one that receives almost NO attention. One of the few articles to really mention it (Metzger, 1991, Diabetes) cautions that "because each of these [treatment] approaches may alter other aspects of maternal metabolism differently, questions remain about safety, efficacy, and impact on long-term development." Gd research must start addressing this more adequately instead of simply assuming that stringent protocols will result in better long-term outcome for the child.

Another criticism is that of the many trials and studies produced on gd, many do not manage to meet stringent research design models, calling into question their conclusions. Furthermore, results from various trials often contradict each other. Even Dr. Donald Coustan, one of the most prominent and conservative gd researchers, admits that "in this country and some other parts of the world, we've established a standard of care and widespread screening based on imperfect data...Rather than continue as we are, I think it's appropriate to stop and obtain more data." (Blank et al., Diabetes Care, 1995)

Every 5 years, a big conference on gestational diabetes is held, research reviewed, and policy debated. The most recent was held in 1997 (The Fourth International Workshop-Conference on Gestational Diabetes Mellitus) and it noted that "there is considerable controversy about the clinical importance of GDM and the magnitude of its impact on mother and offspring. Lack of uniformity in approach to detection and diagnosis of GDM has hampered efforts to resolve these issues." (Metzger and Coustan, Diabetes Care, 1998). However, the Conference's response to criticisms was very limited and mostly chose to ignore contradictory data. Other recent research seems to be continuing as before, with some studies showing great benefit to gd intervention and some showing no benefit at all or even harm from it. Since more definitive trials of more impeccable design are now being designed but are years away from completion, the debate is sure to continue. This is a fascinating area for further exploration.

Finally, critics question the ethics of gd treatment as commonly handled thus far, contending that few women are being given the opportunity for truly informed consent. Few women are ever told that there are variations of treatment (or alternatives to highly interventive protocols), and may never realize that if they had chosen a different health provider, they might well have been given a different care protocol. Many gd mothers are being prescribed extremely aggressive treatments without full disclosure of the possible benefits and risks involved. Those mothers who try to question the aggressiveness of treatment are often pressured into unquestioning acquiescence. Some critics feel that targeting such aggressive and interventive treatment without full disclosure may well be unethical.

It should be emphasized that both proponents and critics of aggressive gd treatment have good intentions; each fully believe that their point of view will lead to the best health for mothers and babies. Proponents of aggressive care see the opportunity to reduce birth size, birth trauma, and hopefully the higher c-section rates associated with bigger babies. They feel that such care will also lessen the newborn problems sometimes encountered by gd babies, such as hypoglycemia, jaundice, etc. They feel that by 'normalizing the maternal milieu' aggressively, the child may have a better chance later in life at avoiding obesity, high blood pressure, diabetes, and other health problems. They also feel that universal testing benefits the mother by identifying a group of women at high risk of diabetes later in life, enabling them to be tested regularly post-partum and possibly to have lifestyle intervention that may reduce their risk of developing diabetes later.

Critics point out that the studies these assumptions are based on were largely done with poor methodology, that proponents have jumped to conclusions and aggressive treatment without adequate proof, that the extreme rate of intervention in mild gd pregnancies may actually cause more harm than it averts, that mild degrees of glucose intolerance are of dubious significance, that there is little agreement on treatment protocols among providers so the treatment gd mothers face varies widely, that treatment is not very effective so far in trials, and that truly informed consent is not being practiced by most health providers so that mothers are being forced into treatments without adequate information and choices. They feel that the four criteria for diagnosis and treatment of disease noted at the beginning of this section (poses a real health risk, distinguishes adequately between those with the disease and those without it, existence of effective treatments, benefits of treatment outweigh the risks) are not supported by the data, and the aggressive screening and treatment programs currently practiced by many providers are not justified.




In summary, studies have shown that poorly-controlled, severe 'gd' (which some would call true diabetes or impaired glucose intolerance instead of 'gd') does indeed have very serious risks and needs intervention; what is less clear is whether the same degree of intervention is needed in cases where the gd is mild and well-controlled. Again, at this time, most research does not make adequate distinction between categories of risk in gd (according to the critics) so it is important to realize that the scary lists of possible complications of gd mostly tend to occur when diabetes pre-existed before pregnancy or developed extremely early in the pregnancy. That does not mean that gd is not a potentially serious condition or should not be treated cautiously. Even many of the strongest critics often agree on certain precautions and treatments, such as some dietary counseling and perhaps more frequent testing/monitoring. There is apparently some risk at lower levels, but just how much risk there is, what its cause is (how much is due to concommitant factors), how intensive (or not intensive) the treatment should be, and how effective this treatment is at improving outcome is of great concern and the subject of intense debate. There is much to recommend on both sides of the debate.

The main issues of controversy in gd are:

Further discussion of each of these controversies (with research citations) will be found in the websection on GD: The Controversies. This section is under construction currently and will be a while in coming in order to do it proper justice. In the meantime, the following references and resources can be used to do your own research into the controversies. Kmom's comments about the content of each reference have been added to give you quick help in deciding which resources to pursue, depending on your interest in specific issues and available time. Note that some references will be cited in nearly every websection, but that some will appear only in one or two sections. Be sure to read each reference section carefully. When available, some websites for certain articles or books are given, though it must be cautioned that websites change quickly and the URLs that are valid for these as Kmom writes this may not be available later. Also, some websites only provide a quick summary of an article or an abstract, which can sometimes be misleading. When in doubt, go to your local medical library and order the whole article. A lot of information can be left out in the on-line summaries or abstracts. Don't neglect the full written copy from the original journal in favor of quick web access information. The original often tells a more complete story.

Best wishes to all the gd moms out there, and good luck in your research. May you have a healthy pregnancy, a wonderful delivery, and a happy healthy baby. Happy gestating!





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.

Proceedings of the Fourth International Workshop-Conference on Gestational Diabetes Mellitus. Diabetes Care. August 1998. Volume 21 (Supplement 2).

The entire issue of this Diabetes Care journal is devoted to the recommendations and papers from the 4th International Conference on GD. Many important issues are discussed, from contraception for gd mothers, long-term effects on the child, screening issues, recommendations for insulin therapy, delivery protocols, etc. Contains many articles from leaders in the gd research field. Generally very conservative views but a must-read for those wishing to stay abreast of this field. Although it is extensive and lengthy reading, it is worth the time involved, but does tend to conveniently ignore the criticisms and studies that contradict their conclusions. One-sided but still valuable.

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.

Greene, Michael F. Screening for Gestational Diabetes Mellitus. (Editorial) New England Journal of Medicine. 337(22):1625-7, Nov. 27, 1997.

An editorial accompanying a research article about gestational diabetes testing. A good look at some of the controversies in gd testing.

Metzger, BE. 1990 Overview of GDM: Accomplishments of the Last Decade--Challenges for the Future. Diabetes. December 1991. 40(Supplement 2): 1-2.

Interesting account of some of the history of gd, starting with the first conference in 1979. Points out the explosion of gd research in the 80s, and gives a brief summary of some of the information from the Third International Conference, covered later in that journal edition. One of the few journal articles to note the importance of ascertaining the long-term safety and efficacy of treatment.

Dornhorst, Anne and Joanna C. Girling. Editorial in The New England Journal of Medicine. 333(19), November 9, 1995.

Another editorial accompanying research on gd; a valuable discussion of some controversies.

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 test 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, while also being aware of her assumptions about size and weight loss. A must-read.

Goer, Henci. "Gestational Diabetes: The Emperor Has No Clothes." Birth Gazette. Spring 1996: Volume 12, Number 2.

A shorter summary of the gd chapter from the above book. A must-read. Can be found at

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.

Stephenson, M.J. Screening for Gestational Diabetes Mellitus: A Critical Review. The Journal of Family Practice. 37(3):277-83, 1993.

A review critical of the practice of universal screening for gd and the research literature justifying it. Some of the criticisms are a bit picky, but flaws in methodological design are a real issue for gd research so far since so much research is contradictory. For those wanting a more in-depth look.

Napier, Kristine."Gestational Diabetes: Are You at Risk?" American Baby. pp. 60-64, August, 1994.

A good simplified summary of the cause, risks and treatments of gd. It is written from the traditional medical view. The author is a registered dietician and medical writer.

Hill-Blakely, Linda. Gestational Diabetes. CBE (Childbirth Educator?). Winter 1988/89, pp. 24-29.

An older summary of gestational diabetes; good overall view. However, it should be noted that since 1988, some changes in treatment protocols have occurred so the article, while excellent, is a bit outdated. Still worthwhile to read.

Franz, Marion J. Taking Care of Gestational Diabetes. International Diabetes Center, Park Nicollet Medical Foundation, Chronimed Publishing, 1992.

An extremely simple explanation of gd, presumably written for people with very low reading skills. Very patronizing and condescending, but the basic information is there. For those who want a very simple, clear explanation of the main issues and no discussion about any of the controversies, or who need a simple pamphlet to use with patients with very low reading or English skills.

Lucas, MJ et al. Class A1 Gestational Diabetes: A Meaningful Diagnosis? Obstetrics and Gynecology. August 1993. 82(2):260-265.

Compared pregnancy outcomes in 159 women with A1 gd (diet-controlled) vs. 151 women with normal GTT results. Found no significant differences in any neonatal outcome variable, including large-for-gestational-age babies. Obstetric interventions, dietary intervention, etc. were 'unlikely explanations' for the lack of differences in outcome. Noted in particular that unlike in other studies, women with one abnormal result on the GTT had a frequency of LGA infants similar to that of women with all normal GTT values. "The diagnosis of class A1 gestational diabetes is not significantly associated with obstetric and perinatal morbidities. A nondiscriminating diagnostic test undermines the validity of population screening for glucose intolerance."

Li, DF et al. Is Treatment Needed for Mild Impairment of Glucose Tolerance in Pregnancy? A Randomized, Controlled Trial. British Journal of Obstetrics and Gynaecology. September 1987. 94(9):851-854.

Study looked at 216 women diagnosed as gd by US standards (NDDG-National Diabetes Data Group) but normal glucose tolerance (NGT) or impaired glucose tolerance (IGT) by the World Health Organization (WHO) criteria of the past. Study tested whether treatment changed the perinatal outcome in the 111 women (51%) with NGT or the 98 women (45%) with IGT by WHO criteria (7 had frank diabetes and were excluded from randomization into control/treatment groups). "The perinatal outcome in these two groups was comparable whether the NGT and IGT groups were analysed together or separately except, that in those who were treated for IGT, smaller babies were born one week earlier than in the control group...this suggests that the WHO criteria [which were less stringent--kmom] can safely replace the 100g OGTT with substantial savings in manpower, money and patients' time...We have demonstrated that it is safe to replace the NDDG test with the WHO test. If this is so, more than half of the pregnant women will not be treated as abnormal, and much time, manpower and money can be saved. The women can be spared the unnecessary anxiety of being labelled as diabetic, and they need not suffer the inconvenience and discomfort of diet control, sugar profile and fetal surveillance."

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.

Diabetes A to Z: What You Need to Know About Diabetes, Simply Put, American Diabetes Association, Inc. Alexandria, Virginia: American Diabetes Association, 1996. To order, write to the ADA, 1970 Chain Bridge Road, McLean, VA 22109-0592, or call 1-800-232-3472.

A fairly simple but comprehensive look at diabetes and its basic issues.

Keen, Harry. Gestational Diabetes: Can Epidemiology Help? Diabetes. December 1991. Volume 40, Supplement 2: 3-7.

Examines some of the history of diabetes and gd diagnosis, with special attention to the problems of a borderline range between normal and clearly diabetic. Notes that severe gd clearly needs treatment but that "there is much less certainty about the hazards, if any, associated with the lesser degrees of glucose intolerance...Attention is drawn to the paucity of evidence linking lesser degrees of glucose intolerance with significant disturbance of pregnancy outcome when confounding variables such as maternal age, adiposity, and parity are allowed for. It is in the area of the detection and treatment of these lesser degrees of glucose intolerance in pregnancy that serious questions of the detriment-to-benefit ratio arise. A population-based multiethnic multicultural inquiry into diagnostic methodology and criteria in pregnancy is a controlled clinical trial of the effects of intervention." A fair and unbiased overview of the controversy, history, and implications of gd. Adequately represents both sides. HIGHLY recommended reading.

Nordlander, E et al. Factors Influencing Neonatal Morbidity in Gestational Diabetic Pregnancy. British Journal of Obstetrics and Gynecology. June 1989. 96(6):671-678.

The influence of obstetric factors vs. maternal blood glucose control on neonatal morbidity was examined in 261 women with gd (plus a control group of 218 women without gd). Although the gd group had more morbidity (23%) than the control group (13%), it was found to be mostly due to gestational age at delivery. After correction for this factor, pre-pregnancy maternal weight was the only factor with added significance. "The present study clearly illustrates that other factors besides blood glucose control are of importance for neonatal outcome in gestatational diabetic pregnancy."

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."

Pettitt, D.J. et al. Breastfeeding and Incidence of Non-Insulin-Dependent Diabetes Mellitus in Pima Indians. Lancet. July 19, 1997. 350(9072):166-168.

"Exclusive breastfeeding for the first 2 months of life is associated with a significantly lower rate of NIDDM in Pima Indians." The odds ratio for NIDDM in exclusively breastfed people, compared with those exclusively bottlefed, was .41 (less than half), even after adjusting for confounding factors. It should be noted that the effect of breastfeeding could be exaggerated in the study because the Pima Indians have the highest rates of diabetes in the world, or they might be under-represented because the study only examined the effect of 2 months of breastfeeding, whereas the current recommendation from the American Academy of Pediatrics is to breastfeed if possible for a full year or more. The study's effects need to be examined in other ethnic populations, with larger samples, and with longer periods of exclusive breastfeeding, but it is a striking finding nonetheless.

Cordero, L et al. Management of Infants of Diabetic Mothers. Arch Pediatr Adolesc Med. March 1998. 152(3):249-254.

Studied babies of gd and type I diabetic pregnancies, and the effect of 'routine care' instead of the more common intensive care and observation period usually used with babies of diabetic pregnancies. "Routine care feedings were more common among infants whose mother had advanced diabetes, but less frequent among breast-fed infants...Breastfeeding among women with GDM and IDDM should be encouraged."

Kjos, S.L. et al. The Effect of Lactation on Glucose and Lipid Metabolism in Women with Recent Gestational Diabetes. Obstetrics and Gynecology. September 1993. 82(3):451-5.

Examined the effects of 4-12 weeks of breastfeeding (or not breastfeeding) on the blood sugar and cholesterol levels of recent gd mothers. 50% of women breastfed, 50% did not. Those who breastfed had lower fasting levels, better glucose metabolism, and better HDL cholesterol levels. Those who did not breastfeed had twice the rate of developing overt diabetes in the immediate postpartum period. "Lactation, even for a short duration, has a beneficial effect on glucose and lipid metabolism in women with gestational diabetes. Breast-feeding may offer a practical, low-cost intervention that helps reduce or delay the risk of subsequent diabetes in women with prior gestational diabetes."


Copyright 1998 KMom@Vireday.Com. All rights reserved. No portion of this work may be sold, either by itself or as part of a larger work, without the express written permission of the author; this restriction covers all publication media, electrical, chemical, mechanical or other such as may arise over time.

[ Back to Kmom Area ]