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Thread: Article: Gestational Diabetes by Henci Goer

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    Default Article: Gestational Diabetes by Henci Goer

    Gestational Diabetes: The Emperor Has No Clothes
    by Henci Goer

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

    * The condition has to pose a health risk;
    * Diagnosis must accurately distinguish between those who have the disease and those who don't;
    * Treatment should be effective; and
    * The benefits of diagnosis and treatment should outweigh the risks.

    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.

    To begin with, GD doesn't fit the definition of a disease. GD as a concept began in 1964 when O'Sullivan and Mahan performed a 100g 3- hour oral glucose tolerance test (OGTT) on 752 pregnant women and tracked all women with at least two values above two standard deviations beyond the mean to see if hyperglycemic women were predisposed to develop diabetes down the road (O'Sullivan 1964). They were, leading the two researchers to conclude that the metabolic stress of pregnancy revealed a woman's "pre-diabetic status." This should not surprise anyone since overweight women are more likely to have hyperglycemia in pregnancy and to develop diabetes later in life.



    Since insulin-dependent diabetes was known to threaten the fetus, researchers extrapolated that sub-diabetic glucose elevations might also do harm. This leap in logic was faulty on its face because GD does not share the risk factors of either type of true diabetes. In Type I diabetes, extremes of low and high blood glucose early in pregnancy can cause congenital anomalies or kill the forming embryo. Gestationally diabetic women make normal or above-normal amounts of insulin and have normal blood sugar metabolism in the first trimester. With either Types I or II, diabetes of long standing may damage maternal blood vessels and kidneys, causing hypertension or kidney complications. These may in turn jeopardize the fetus. Gestational diabetics do not have long- standing diabetes. The one problem GD shares with both types is that chronic hyperglycemia can overfeed the fetus, resulting in macrosomia (generally defined as birth weight greater than 4000 g) or large-for- gestational-age (LGA) (greater than the 90th percentile) babies.

    Logic notwithstanding, these concerns launched a series of studies into the risks of mild glucose elevations. Unfortunately, they were badly flawed.

    Studies selected women for glucose testing based on such factors as prior still birth or hypertension in the current pregnancy and then compared outcomes with the general population. Hunter and Keirse observe that according to Sutherland and Stowers' 1975 edition of CARBOHYDRATE METABOLISM IN PREGNANCY AND THE NEWBORN, the rate of fetal loss increases eightfold as the number of indications for glucose tolerance testing increasing from one to four. Glucose intolerance does not add to this risk (Hunter and Keirse 1989).

    Studies included women who were known diabetics prior to pregnancy.
    Studies failed to account for confounding factors such as that glucose intolerance associates with increasing maternal weight and age, which themselves are strong independent predictors of macrosomia and maternal hypertension.
    Studies used management protocols that increased risks such as starvation diets, early elective induction, and withholding nourishment from the newborn.
    In addition, glucose level turned out to be a poor predictor of macrosomia. Other factors such as race, age, parity, sex, and especially maternal weight, far outweighed glucose intolerance in determining birth weight. Hunter and Keirse observed that GD mothers had a 3-fold risk of giving birth to a baby weighing over 4500 g compared with normoglycemic women. However, a woman weighing over 90 kg had a 26-fold risk of having a baby this heavy compared with normal weight women (Hunter and Keirse 1989). Oats and colleagues could not find a significant association between glucose levels and birth weight until birth weight exceeded the 90th percentile. Even then, 77 percent of women had normal glucose tolerance (Oats et al. 1980).

    Nonetheless, researchers concluded that mildly deviant glucose values in pregnancy constituted a new form of diabetes that required diagnosis, surveillance, and treatment. Researchers have gone on adding rooms and stories to the GD edifice, never noticing that they have built a house on sand.

    Secondly, the OGTT, the standard diagnostic test, has many problems. A diagnostic test should be reproducible, its thresholds should be values at which morbidity either first appears or incidence greatly increases, and normal ranges should apply to the population undergoing testing. The OGTT is none of the above.

    Obstetricians adopted O'Sullivan and Mahan's curve as the normative curve for all pregnant women, but it is not representative. For one thing, O'Sullivan and Mahan tested women without regard to length of gestation, whereas today, women are typically tested at the beginning of the third trimester. Glucose values rise linearly throughout pregnancy, but no corrections have been made for this. For another thing, O'Sullivan and Mahan studied a population that was 60 percent white and 40 percent black. Hispanics, Native Americans, and Asian women average higher blood sugars than black or white women. Since diagnostic thresholds are set at two standard deviations beyond the mean, values for O'Sullivan and Mahan's population have arbitrarily been established as the norms for all women. This means that some women are being identified as diseased simply because of race.

    Worse yet, studies show that when pregnant women undergo two OGTTs a week or so apart, test results disagree 22 percent to 24 percent of the time (Catalano et al. 1993) (Harlass et al. 1991). An individual's blood sugar values after ingesting glucose (or food) vary widely depending on many factors. For this reason, the OGTT has been abandoned as a diagnostic test for true diabetes in favor of excessive fasting glucose values, which show much greater consistency, or postprandial values of 200 mg.dl or more, which are rare. Moreover, pregnancy compounds problems with reproducibility. Because glucose levels rise linearly throughout pregnancy, a woman could "pass" a test in gestational week 24 and "fail" it in week 28. These same problems hold true for the glucose screening test that precedes the OGTT (Sacks et al. 1989) (Watson 1989).

    More importantly, no threshold has ever been demonstrated for onset or marked increase in fetal complications below levels diagnostic of true diabetes. O'Sullivan and Mahan chose their cutoffs for convenience in follow-up, but all studies since then have used their criteria or some modification thereof as a threshold for pathology in the current pregnancy. Numerous studies since have documented that birth weights and other outcomes fail to correlate with O'Sullivan's or anybody else's thresholds.

    A test with arbitrary diagnostic thresholds is akin to claiming that all people over six feet tall have a growth abnormality or all people with a cough and a fever have pneumonia. The authors of A GUIDE TO EFFECTIVE CARE IN PREGNANCY AND CHILDBIRTH relegate "screening for gestational diabetes" to "Forms of Care Unlikely to be Beneficial" (Enkin 1995).

    The original intent of treating GD was preventing excess perinatal mortality and congenital anomalies. Whatever the cause of increased deaths, it wasn't hyperglycemia. O'Sullivan and colleagues randomly assigned gestational diabetics to treatment with diet and insulin and compared outcomes among treated diabetics, untreated diabetics, and a normoglycemic control population. They found more perinatal deaths in the GD population, treated or not (O'Sullivan et al. 1966). Perinatal mortality statistics among non-insulin dependent diabetics remained unchanged between 1946 and 1972 in a Copenhagen study despite aggressive treatment throughout the timespan (Pedersen, JL et al. 1974) (Pedersen J 1977). Conversely, a Swedish study showed a marked reduction in perinatal mortality rates between 1961 and 1971, also while treating vigorously (Karlsson et al. 1972).

    As for congenital anomalies, GD cannot cause congenital anomalies because glucose metabolism is normal in the first trimester. Even if it did, testing isn't done until the third trimester.

    The main rationale for current GD management is to reduce the incidence of birth injuries and cesarean section by reducing the incidence of macrosomia. The goal of reducing birth weight raises philosophical problems. As with glucose values, doctors are defining deviation beyond an arbitrary point as inherently pathological. Moreover, can we justify manipulating the growth mechanism of a group of babies roughly 75 percent to 80 percent of whom will fall below the 90th percentile for weight if left alone?

    Philosophical considerations aside, we have little evidence that GD management succeeds. As mentioned above, macrosomia associates with maternal weight, age, race, parity, and male fetus. Maternal overweight cannot be rectified during pregnancy; the rest cannot be altered at all. According to M.J. Stephenson, there have been only four randomized trials of diet or diet and insulin. All were flawed and taken together achieved a reduction in birth weight of 87 g, a benefit "of questionable clinical significance" (Stephenson 1993). A GUIDE TO EFFECTIVE CARE IN PREGNANCY AND CHILDBIRTH also lists insulin and diet therapy for GD under "Forms of Care Unlikely to be Beneficial."

    Santini and Ales report results from a national trial that occurred in the early 1980's when some doctors at Cornell University Medical Center screened women for GD routinely and others did not. No differences in perinatal mortality, morbidity, LGA or macrosomia rates were found between screened and unscreened populations, but women in the screened population were more likely to have primary cesarean sections (19 percent versus 12 percent), more clinic visits, more fetal surveillance tests, and more prenatal hospitalization (Santini et al. 1990).

    Non-randomized trials show that diet modification rarely works without severely limiting calories or the liberal or universal use of insulin. Even where it does work, only two studies of GD management reduced operative delivery or cesarean rates to reasonable levels, the main point of preventing macrosomia (Langer et al. 1994) (Coustan et al. 1984). In both studies, doctors knew which women were treated and which were controls. If they believed their therapy prevented macrosomia, which other work shows they did, this belief could well have influenced management decisions. A third study also reported similar cesarean rates in GD women and the total hospital population, but these were 27 percent and 25 percent respectively (Thompson et al. 1994).

    As Santini and Ales' study suggests, not only does GD management offer little benefit, it confers risks, the gravest being a marked increase in cesarean section. The cesarean rate in a population of gestational diabetics cared for by midwives was 9 percent to 11 percent including women transferred to obstetric management, or about half the primary cesarean rate reported in populations managed by obstetricians in the same or an earlier time period (O'Brien et al. 1987). Goldman and colleagues reported that gestational diabetics had one-third more cesareans compared with a matched population with normal glucose tolerance, although birth weights were similar (Goldman et al. 1991). In another study, gestational diabetics were randomly assigned to insulin or standard treatment in the third trimester in an effort to minimize macrosomia. Insulin reduced LGA rates to 13 percent compared with LGA rates of 45 percent in the diet group and 38 percent in the group that refused randomization. Despite this, cesarean rates were 14 percent and 21 percent in the diet-treated groups versus 43 percent in the insulin-treated group, a difference attributed to transferring women on insulin to the high-risk service (Buchanan 1994).

    Many doctors view high cesarean rates as a reasonable trade-off for preventing shoulder dystocia. This ignores that many shoulder dystocias occur in non-macrosomic infants (Keller 1991) and that the increase in cesarean rate for infants weighing over 4000 g has not improved outcomes (Boyd et al. 1983); not to mention the role typical obstetric management plays in causing shoulder dystocia.

    Increased likelihood of cesarean is not the only risk of GD management. Insulin increases the risk of small-for-gestational-age babies and causes symptomatic hypoglycemic episodes (Langer et al. 1994) (Buchanan et al. 1994). Reducing calories by more than one-third in overweight gestational diabetics causes ketosis (Knopp et al. 1991). Finally, the poor predictability of the fetal weight estimates and surveillance tests doctors feel obliged to order, even the belief that GD is a high-risk condition, undoubtedly lead to countless unnecessary inductions and operative deliveries.

    Few have noticed that the diagnosis and treatment of GD is a spectacular failure. A review article analyzes the OGTT, finds it worthless, and recommends continuing to use it to diagnose GD (Nelson 1988). After showing that current cutoffs fail to discriminate a group of women at high risk for macrosomia, obstetricians conclude in defiance of logic that they should lower the values or that insulin should be given to more women or that cutoffs should be chosen by fiat (Sacks et al. 1995) (Neiger et al. 1991) (Weiner 1988) (Tallarigo et al. 1986). Researchers take note that sonography to estimate fetal weight did no better than a coin toss at predicting macrosomia and recommended it anyway (Combs et al. 1993). Doctors find that rigid glycemic control did not improve infant outcomes and assume that means they should try harder (Hod et al. 1980). Goldman and colleagues, with similar birth weights but one-third more cesareans in the GD group, congratulated themselves on the success of their management (Goldman et al. 1991). The gestational diabetes literature reads more like ALICE IN WONDERLAND than science.

    Still, midwives can winnow some grain from the chaff. Maternal weight has the strongest correlation with macrosomia rate; it makes sense to advise heavily overweight women to lose weight before becoming pregnant. Pregnancy makes extra demands on insulin production; to minimize the pressure, pregnant women should eat a diet low in simple sugars, high in complex carbohydrates and fiber, and moderate in fat. Moderate, regular exercise also improves glucose tolerance. Within the GD population lurk a few women who were either undiagnosed pregestational diabetics or who were tipped into true diabetes by the metabolic stress of pregnancy; a fasting glucose to screen for them might be prudent. And, of course, midwives already use strategies that help women minimize the likelihood of operative delivery or birth injury. Finally, to reduce the chance of neonatal hypoglycemia, the baby should be put to breast soon after the birth, especially if the baby is big, small, or the labor has been difficult.



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    Henci [sic] Goer is an ASPO-educator and doula. Over the past ten years , she has written numerous pamphlets and articles for childbirth professionals and expectant couples. In 1993 she received the National Association of Childbearing Centers Media Award, and in 1995 ASPO/Lamaze presented her with its President's Award in recognition of her book, OBSTETRIC MYTHS VERSUS RESEARCH REALITIES: A GUIDE TO THE MEDICAL LITERATURE. She also serves on CHILDBIRTH INSTRUCTOR MAGAZINE's Advisory Board.

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    Bibliography
    Goer, H. OBSTETRIC MYTHS VERSUS RESEARCH REALITIES: A GUIDE TO THE MEDICAL LITERATURE. Westport: Bergin and Garvey, 1995.
    "Gestational diabetes," INTERNATIONAL JOURNAL OF CHILDBIRTH EDUCATION. 1991;6(4):1991.
    "Gestational diabetes: It's Not What It Seems," CHILDBIRTH INSTRUCTOR. In press

    O'Sullivan JB. and Mahan CM. Criteria for the oral glucose tolerance test in pregnancy. DIABETES 1964;13:278-285. [Ed. - No Abstract Available]
    Hunter JS. and Keirse MJNC. GESTATIONAL DIABETES. In EFFECTIVE CARE IN PREGNANCY AND CHILDBIRTH, Enkin M. Keirse MJNC, and Chalmers, eds. Oxford: Oxford University Press, 1989.
    Oats JN. et al. Maternal glucose tolerance during pregnancy with excessive size infants. OBSTET GYNECOL 1980;55:184-186.
    Catalano PM, et al. Reproducibility of the oral glucose tolerance test in pregnant women. AM J OBSTET GYNECOL 1993;169(4):874-881.
    Harlass FE. Brady K. Read JA. Reproducibility of the oral glucose tolerance test in pregnancy. AM J OBSTET GYNECOL 1991;164(2):564-568.
    Sacks DA. et al. How reliable is the fifty-gram, one-hour glucose screening test? AM J OBSTET GYNECOL 1989;161(3):642-645.
    Watson WJ. Serial changes in the 50-g oral glucose test in pregnancy: implications for screening. OBSTET GYNECOL 1989;74(1):40-43.
    Enkin M. et al. A GUIDE TO EFFECTIVE CARE IN PREGNANCY AND CHILDBIRTH, 2nd ed. Oxford: Oxford University Press, 1995.
    O'Sullivan et al. The potential diabetic and her treatment in pregnancy. OBSTET GYNECOL 1966;27:683-689. [Ed. - No Abstract Available]
    Pedersen JL. Molsted-Pedersen, and Andersen B. Assessors of fetal perinatal mortality in diabetic pregnancy: analysis of 1,322 pregnancies in the Copenhagen series 1946-1972. DIABETES 1974;23:302-305. [Ed. - No Abstract Available]
    Pedersen J. "White Class-A-mild diabetes in pregnancy" and "Management of diabetic pregnancy and the newborn infant," in THE PREGNANT DIABETIC AND HER NEWBORN, 2nd ed. Baltimore: the Williams and Wilkins Co., 1977.
    Karlsson K. and Kjellmer I. The outcome of diabetic pregnancies in relation to the mother's blood sugar level. AM J OBSTET GYNECOL 1972;112:213-220. [Ed. - No Abstract Available]
    Stephenson MJ. Screening for gestational diabetes mellitus: a critical review. J FAM PRACT 1993;37(3):27-283.
    Santini DL. and Ales KL. The impact of universal screening for gestational glucose intolerance on outcome of pregnancy. SURG GYNECOL OBSTET 1990;170(5):427-436.
    Langer O. et al. Intensified versus conventional management of gestational diabetes. AM J OBSTET GYNECOL 1994;170(4):1036-1047.
    Coustan DR. and Imarah J. Prophylactic insulin treatment of gestational diabetes reduces the incidence of macrosomia, operative delivery, and birth trauma. AM J OBSTET GYNECOL 1984;150(7):836-842.
    Thompson DM. et al. Tight glucose control results in normal perinatal outcome in 150 patients with gestational diabetes. OBSTET GYNECOL 1994;83(3):362-365.
    O'Brien ME. and Gilson G. Detection and management of gestational diabetes in an out-of-hospital birth center. J NURSE-MIDWIFERY 1987 Mar/Apr;32(2):79-84. [Ed. - No Abstract Available]
    Goldman M. et al. Obstetric complications with GDM. Effects of maternal weight. DIABETES 1991;40(Suppl 2):79-82.
    Buchanan TA. et al. Use of fetal ultrasound to select metabolic therapy for pregnancies complicated by mild gestational diabetes. DIABETES CARE 1994;17(4):275-283.
    Keller JD. et al. Shoulder dystocia and birth trauma in gestational diabetes: a five-year experience. AM J OBSTET GYNECOL 1991;165(4 Pt 1)928-930.
    Boyd ME, Usher RH, and McLean FH. Fetal macrosomia: prediction, risks, proposed management. OBSTET GYNECOL 1983;61(6):715-722.
    Knopp RH. et al. Metabolic effects of hypocaloric diets in management of gestational diabetes. DIABETES 1991;40(Suppl 2):165-171.
    Nelson RL. Oral glucose tolerance test: indications and limitations. MAYO CLIN PROC 1988;63(3):263-269.
    Sacks DA. et al. Toward universal criteria for gestational diabetes: the 75-gram glucose tolerance test in pregnancy. AM J OBSTET GYNECOL 1995;172:607-614.
    Neiger R and Coustan DR. Are the current ACOG glucose tolerance test criteria sensitive enough? OBSTET GYNECOL 1991;78(6):1117-1120.
    Weiner CP. Effect of varying degrees of "normal" glucose metabolism on maternal and perinatal outcome. AM J OBSTET GYNECOL 1988;159(4):862- 870.
    Tallarigo L et al. Relation of glucose intolerance to complications of pregnancy in nondiabetic women. NEW ENGL J MED 1986;315(16):989-992.
    Combs CA. Singh NB, and Khoury JC. Elective induction versus spontaneous labor after sonographic diagnosis of fetal macrosomia. OBSTET GYNECOL 1993;81(4):492-496.
    Hod M. et al. Gestational diabetes mellitus: a survey of perinatal complications in the 1980's. DIABETES 1991;40(Suppl 2):74-78.
    Last edited by BellyBelly; August 3rd, 2006 at 03:13 PM.
    Kelly xx

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    Author of Want To Be A Doula? Everything You Need To Know
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    Hmmm, interesting reading - thanks Kelly. I was wondering about the "history" of GD

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    I am sorry but this article is very short sighted and misinformed. It totally ignores the symptomatic effects of any level of hyperglycaemia to the mother and the subsequent physical effects on bodily functioning. Regardless of what is happening to the baby here, there is also a mother involved who I am sure would like to maintain normal organ and metabolic functioning for the rest of her pregnancy and beyond. I will come back and post more when I have calmed down...this article has made me very angry!!

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    well, I only read the first halfish last night, before having to run... And didn't get to where, as Mel points out (or might have been elsewhere to me), that doing nothing, whilst probably causes not much of change of anything to the baby, having high BSL's in the mother can make someone who already feels sore and uncomfy due to the pregnancy, feel like absolute crap due to the high BSL

    Jen calls me "narky boy" when my levels are high - so I take some extra insulin to bring my levels back down. She also was diagnosed with GD earlier this year - both her Ob and the Endo we saw gave what I call incorrect info in treatment - one said low-gi, the other low-carb - neither mentioned the other... when in fact, a low of both was better.

    After 33+years of type 1 diabetes, I can tell you there is a remarkable difference in the way one feels when they have a say 10+ BSL to say 7. The BSL management of the mother very much does need to be taken into account, something that is not touched on at all in that article and is what Mel is quite, and rightfully so, upset/angry about

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    Very interesting.
    The last point you highlighted in particular. When my daughter was born I couldn't believe they wanted to take her away from me for "observation" - when she was breathing normally and had apgars of 8 and 9.... they said they had to make sure her BSL's were normal and didn't plummet.
    I already knew that the best thing for stabilising her BSL's was breastfeeds so I said they couldn't take her until she'd been fed. I fed her and they took her to nursery afterwards. But still cheesed me off that she "had" to go anyway, we were separated for two days and not once did she have an abnormal reading the whole time she was in special care.

    As for the testing protocol - I have had about 6 OGTT's in my time and I've long suspected they're not an exact science.

    With my daughter I tested 7.9 on my OGTT which failed me by the most minute amount (at that time 7.8 or lower was a "pass"). I was constantly monitored, ended up on insulin, pushed into inducing when my water broke and was separated from DD when she was born for no good reason I can see.

    This time I passed my OGTT with a 7.2 and that's it. No intervention, no further testing, they're off my case. But I bet if I took another OGTT today I might be 7.8 again....they wouldn't know. When I monitor at home the reading will vary depending on the finger I test with. There is no way this is an exact science.
    Last edited by Tobily; August 4th, 2006 at 11:44 AM.

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    It is far from an exact science Flea....especially for us type ones who produce no insulin of all to back us up. I agree that there shouls be a eries of tests done to confirm GD as you correctly point out fluctuations are normal and can just tip youover the edge. I also don't agree with unecessary interventions such as induction ceaserean etc. I agree that bubs should be monitored for a time but the changing trend is for them to monitor the baby whilst in your care..that scenario is more a hospital protocol thing and as with most things re-education takes time to filter through. What I don't like about this article is that it totaly ignores the mother and the effect that high sugars have short and long term on physiological systems. It appears to be advocating no treatment because the treatment doesn't affect outcomes...for the baby maybe, but definitely not for the mother. Even one trimester of hyperglycaemia will cause permanent damage to organs. It mentions a low carb diet as causing ketosis...true maybe in some cases but extended hyperglycaemia will lead to ketoacidosis which could kill both mother and baby in a matter of hours...which is worse? It also doesnt mention that hyperglycaemia can cause placental breakdown and spontaneous fetal death in utero. I couild go on but wont.

    I reiterate that I agree that intervention is an old school tool that needs revamping and in most larger hospitals this is happening...it again depends on the education of obs and hospital policies. But I am angry because I feel that this article, which is no more than a very biased literature review could lead to people who have less knowledge about hyperglycaemia getting the wrong idea that it is okay not to treat it....It is not okay to ignore high blood sugars at any time pregnant or not.......at the very least they make you **** like a puppy, drink like a fish, feel like crap, have blurry vision, no energy...Hang on I'm just describing pregnancy...hehe......at the worst they can lead to kidney damage, circulation problems, permanent eye damage, cardiac issues and nerve damage......I just want people to be aware there is more to this issue than that article presents....*end rant* *off soapbox*

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    Melanie, this article is about Gestational Diabetes and not your standard Diabetes. As a very well respected and awarded midwife said:

    "The best way for those who disagree is to find the definitive studies that address all of Henci’s points. If is such an important issue, those studies would be available for us all to read. There is harm being done to mothers and babies by the definition of Gestational diabetes."

    And another midwife:

    "There seems to be a real misconception even amongst obstetricians that gestational diabetes has the same risks as pre-existing diabetes. A couple of years ago I did a bit of research on it for my masters and could find no evidence that this was so. And according to cochrane (independant study review database) the OGT test is not reproducible 50-70% of the time."

    Those with that knowledge choose not to have the OGTT in pregnancy because there are no proven improved outcomes for mums or babies with diagnosed and 'treated' GD.

    Henci writes amazing stuff, she is a scholar and very well educated, choosing to cover topics effecting birth and as you can see, she has all her references which can be checked below her article. She is very well researched and writes some GREAT, highly successful books, for example, Obstetric Myths vs Research Realities.
    Last edited by BellyBelly; August 5th, 2006 at 09:32 AM.
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    From the The Cochrane Database of Systematic Reviews 2006 Issue 3 :

    Background
    “Gestational diabetes and impaired glucose tolerance (IGT) in pregnancy affects between 3 and 6% of all pregnancies and both have been associated with pregnancy complications. A lack of conclusive evidence has led clinicians to equate the risk of adverse perinatal outcome with pre-existing diabetes. Consequently, women are often intensively managed with increased obstetric monitoring, dietary regulation, and in some cases insulin therapy. However, there has been no sound evidence base to support intensive treatment. The key issue for clinicians and consumers is whether treatment of gestational diabetes and IGT will improve perinatal outcome.”

    Main results

    Three studies with a total of 223 women were included. All three included studies involved women with IGT. No trials reporting treatments for gestational diabetes met the criteria. There are insufficient data for any reliable conclusions about the effect of treatments for IGT on perinatal outcome. The difference in abdominal operative delivery rates is not statistically significant (relative risk (RR) 0.86, 95% confidence interval 0.51 to 1.45) and the effect on special care baby unit admission is also not significant (RR 0.49, 95% confidence interval (CI) 0.19 to 1.24). Reduction in birthweight greater than 90th centile (RR 0.55, 95% CI 0.19 to 1.61) was not found to be significant. This review suggests that an interventionist policy of treatment may be associated with a reduced risk of neonatal hypoglycaemia (RR 0.25, 95% CI 0.07 to 0.86). No other statistically significant differences were detected. A number of outcomes are only reported by one study resulting in a small sample and wide confidence intervals.

    Authors' conclusions
    There are insufficient data for any reliable conclusions about the effects of treatments for impaired glucose tolerance on perinatal outcome.
    Kelly xx

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    Again you focus on the perinatal outcome and not the symptomatic outcomes during the period of hyperglycaemia for the mother. I totally agree that perinatal outcomes may not be affected but what I disagree with is the fact that this article and yourself appear to be advocating no treatment for hyperglycaemia which can be a very dangerous condition if left untreated. Note I use the term hypoglycaemia..you are right the term diabetes is bandied about and causes confusion......there is even debate as to whether type 1 and type 2 diabetes should even have the same name they are so different in many respects. It concerns me that people who have no extensive knowledge of this condition are making assumptions based on reading a few articles not and are not comprehensively educated about the condition. It would be like me taking the stance that why bother treating mild asthma as it wont affect the outcome for the baby but the mother is sure as hell gonna feel a lot better not wheezing, coughing and having no energy all the time.
    I don't know enough about the mechanics of asthma to make that judgement and neither do you or Henci or anyone who has not suffered the condition of hyperglycaemia or has not undergone extensive training into what is an incredibly complex metabolic function, have the right to advocate for no treament of this condition. The article is dangerous, people who don't know any better will read this and think cool I can just ignore these high sugars. It only becomes an article of value and insight when it is coupled with all the other facts and ramifications of this condition - perinatal outcome is only a small percent of what GD,D,asthma or any condition for that matter is about. should we ignore all medical conditions that don't affect perinatal outcome...I don't think so. How would you feel if soomeone who is less educated abut hyperglycaemia and GD reads this article and then decides that they don't have to treat their GD and then ends up in a coma from ketoacidosis? I know I would never forgive myself. I am all for articles like this that prompt you to think and question but they need to be presented along all the other relevant information so as not to unwittingly steer people down the wrong path for the right reasons. Perhaps articles on what hyperglycaemia is and how it can be treated, articles on the GI diet which is excellent for EVERYONE in all walks of life not just people with GD (even elite athletes use its principles to maximise performance), things like that will show a balanced approach to this issue.

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    No it doesn't really just mean the perinatal outcome for the baby. Because of the nature of the inaccurate testing, you could be unfortunately be told that you have GD, then as a result, be deemed high-risk, have to follow proceedures and protocols, which mean induction, exclusion from birth centres and we all know inductions often result in pain relief then assisted birth or even caesarean. So these are things that are not about the baby.

    I am currently supporting a woman who has pressure on her from doctors despite her blood sugar levels being fine but they want to get an induction date in. Baby on the 50th percentile and their concern is that the placenta will deteriorate quicker if she goes past term. Mum is perfectly fine. So mum is fine, baby is fine, yet she is faced with all this pressure, and the threat of being thrown out of the birth centre if she doesn't agree to the induction by a certain date. Placenta function scans can be done, so she is going to see if she can negotiate to have them.

    You seem very angry about this article - I am not one to tell people what to do and I think it would be very biased for people to hear the one side they hear from the Obs - what if no-one said anything about cigarettes causing cancer and that was kept a secret? People would be angry. People were angry. So where are the studies opposing the findings that Henci has made? As the midwife said, we'd know about it, but it's not been done. Why hasn't it been done? Do they know this is right?

    Of course if you had symptoms and things were obviously wrong, you would do something about it. But these days there is so much interference even when nothing is going wrong... and not all of us want that. Some might, but not all. If you were already a diabetic I am sure this would be different. They are talking about Gestational Diabetes only here - not where you already have diabetes - as the Cochrane Review says:

    "However, there has been no sound evidence base to support intensive treatment."

    This doesn't mean don't treat it at all and I would think only treat it IF necessary. I haven't just picked the Cochrane Review because it agrees with the article, but because it is a huge medical database which independently reviews studies, excluding them or including them dependant on them meeting certain criteria. Anyways, we could go on about this forever probably but that's all from me.
    Kelly xx

    Creator of BellyBelly.com.au, doula, writer and mother of three amazing children
    Author of Want To Be A Doula? Everything You Need To Know
    Follow me in 2015 as I go Around The World + Kids!
    Forever grateful to my incredible Mod Team and many wonderful members who have been so supportive since 2003.

  11. #11

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    I'm the mum that Kelly mentioned above: my perspective is that the diagnosis of gestational diabetes has been very stressful and I'm yet to see any real benefit from it. Others may find that the diagnosis does not greatly affect them and they are happy to go along with induction etc. However you feel about these interventions, I think it's important to read articles like the one by Henci Goer in order to be informed about the research findings, because often doctors/midwives/diabetes educators don't or can't give you all the facts (they may not know themselves or there isn't always time in the space of a consultation). Shouldn't we all try to be well-informed in order to take some responsibility for our own (and our baby's) health?

    melbel, you seem really upset that the article doesn't discuss hyperglycemia and organ damage, but I think this is shooting the messenger. Henci Goer's article doesn't mention it for the simple reason that obstetricians themselves don't focus on it, and she is talking about the standard obstetric approach. The Australian Guidelines for the treatment of gestational diabetes do not mention risk of organ damage at all. The risks that they are concerned about are macrosomia (having a big baby), shoulder dystocia (where the baby gets "stuck" on the way out), and the baby having hypoglycemia after birth.

    If treating gestational diabetes were only about controlling blood glucose levels, that would be one thing, but it is associated with high rates of other interventions (inductions, caesareans, taking babies away from their mothers at birth), so it's reasonable to question whether the benefits genuinely outweigh the risks.

  12. #12

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    You are absolutely right Nic and I hope you get the birth you are fighting for. I too am vehemently against intervention unless there is a genuine medical need for it....macrosomia is so uncommon now that there really should be an update of the guidelines...high risk obs that deal with this more often seem to be coming around but there a still a lot who need a good kick up the pants. Do you have and endocrinologist looking after you....if so they can often be helpful in pushing for non-intervention. As for taking babies away at birth...I'm gonna sit on the fence as I have seen neo natal hypoglycaemia first hand many times and its not pretty but having said that I know that it is not always an outcome so it is hard to make a judgement call. My suggestion there is to push to put bubs to the breast a soon as possible after delivery ( this has been shown to have a huge impact on the outcomes) and also to try expressing in the days before birth and storing this. At Frances Perry House they will often feed the bub if necessary using a little spoon and their little finger to stimulate bubs sucking mechanism rather than an n/g tube or bottle. This way nipple confusion can be avoided and breast feeding better established.
    I sincerely wish you all the luck in the world in your quest for justice for you and your bub.....

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    It's also important to remember that the elevated BSL's involved in GD are usually nowhere near as high as in regular diabetes. You're usually looking at levels around the 8/9 mark in GD which are highish but not high enough for long enough to be of any real danger to the mother in terms of organ damage or ketoacidosis etc.

  14. #14
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    Flea, it's the usually that is the problem

    I know Mel has come in pretty strong, but I too feel the original article pretty much says for zero intervention full stop - for everyone.

    My thoughts are that there needs to be a rethink on when to kick in the intervention. Saying to everyone don't worry about is not the way to go. Even if its one in 10000 where intervention really is needed is enough for that article to be rethought, at least in my thoughts

    I agree, majority of those "diagnosed with GD" will probably have levels of 8-9, and probably with diet alone, can regain normal BSL's, but there will be a couple where a handful of units of insulin can bring those double digit BSL's down to single digits etc

    Ketoacidosis can get dangerous very quickly, as Mel said earlier, in a matter of hours. I do know of a number of T1's who have been hospitalised due to it, some critically.


    And the fact that treatment of GD doesn't cover the full range of things that GD can do, is a full on fault with the treatment, and something that Henri does not discuss either

  15. #15

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    The comments below is from a midwife who has read the conversation, because clearly there still is confusion here and I don't want anyone thinking I am advocating for no treatment. I believe in offering two sides of the story, often one side gets presented by those posting on my site, I like to offer another alternative because I am sure there are some out there that are interested in it, knowing there is more than one option for them. I also think that any sensible person would take this information to their carer for discussion rather than be completely dismissive of a carer's comments based on what I have written, hence the disclaimer on BellyBelly. Also as Nic mentioned to me based on her experience with doctors, different doctors have their own 'thresholds' as to what levels they deem acceptable and what not - so again, not an exact science.

    "She has Type 1 diabetes and hyperosmolar ketoacidosis is very serious to them pregnant or not. It is not a common feature of Type 2 unless you have a serious infection going on or have a huge electrolyte imbalance.

    Now with pregnancy most mothers who develop GDM are purely pregnant who have developed diabetes, they are not pre-existing Type 1 or 2. The main feature with GDM is insulin resistance and placental hormonal influences. Hence the reason most women's baseline BGL in the morning is high as other hormones of repair such as cortisol have increased production overnight when the woman is asleep. Progesterone and oestrogen add to the insulin resistance of the blood vessels. women have circulating insulin often at high levels but the insulin cannot get through to the cell to be used. BGL's rise as a result. Some require extra insulin to keep BGL's within a normal range. If the woman has an added infection that can be cause of concern.

    Some of the comments made from the women seem like they are being based around their own Type 1 diabetes. I have found these women usually do not listen to what you say, same as women who develop GDM who have family members who are non-compliant with their Type 2 diabetes. Their family member is the one who usually says "oh 8.9 mmol/l is pretty good'' simply because they do not understand the high BGL does to the infant with switching on its insulin production.

    I know a person with T2 diabetes from a pituarity problem. Her endocrinologist has reassured her when her levels were elevated between 10-14 mmol/l it would require at least 6 months to cause long-term damage to ones circulation to feet, eyes and other organs. this person is now on 3 types of oral medication to control the diabetes to between 3.3-8 mmol/l. She recognises when the levels are elevated with extra fatigue and hunger.

    It's important to see a good diabetes counsellor and an educator to remove gross fear and terror of normal physiological processes. Like anything in medical science one treatment is not perfect but to give opinions about GDM based on T1 experiences is not accurate."
    Kelly xx

    Creator of BellyBelly.com.au, doula, writer and mother of three amazing children
    Author of Want To Be A Doula? Everything You Need To Know
    Follow me in 2015 as I go Around The World + Kids!
    Forever grateful to my incredible Mod Team and many wonderful members who have been so supportive since 2003.

  16. #16
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    Again, from I'd say both mine and Mel's reading of the Henri's article is that there is no need for any anything to be done, just go with the flow.

    And again, you have stated reasons for possible problems to kick in... As soon as a single reason for problems to kick in can be identified, then the "no need for any anything to be done" goes straight out the window

    Giving educated opinions based on personal experience I believe is extremely accurate. We know what can happen in the dare I say worst case scenarios that someone with GD can stray into... this is what I at least am trying to get through... Most people posting here (in this thread) seem to agree with Henri's overall opinion, yet keep identifying reasons where that opinion should be not be taken as the holy grail. Yes, Kelly has finally stated that yes it is an opinion, and use it in conjunction with what the Ob and possibly an Endo will tell you

    We don't want to stray into those scenarios, but just be aware, dismissing treatment of GD can be dangerous, and that also the original article really only covers one of the two people involved in the pregnancy - anyway, I'm off to bed

  17. #17

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    Okay, I was prepared to leave this thread alone, but now feel like I have come under personal attack re: my control and fears of D.

    FYI, I have been a diabetic for close on 30 years, hBa1c is averaging approx 6.0 for the last few years, and I have no fears or terror of normal physiological processes.

    And hows that for a generalisation "I have found these women usually do not listen to what you say". I thought this was a support site where differing views were put forward, again let me say I too am vehemently against intervention unless there is a genuine medical need for it.

    Night

  18. #18

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    hehehe I often feel like I am often under attack too, no matter if they are my opinions or opinions of those trained in these things! I can't win either

    I have posted a range of responses from several midwives, a scholar, an independant review database etc and I haven't made my own personal comment on the matter because I am still learning. I find it all very interesting, and form my own opinions as a result to reading / hearing a range of views and information. Not just one. So I will keep reading and form my opinion on this. I hope others find it interesting reading too and I promise not to reply again LOL.
    Last edited by BellyBelly; August 6th, 2006 at 08:55 PM.
    Kelly xx

    Creator of BellyBelly.com.au, doula, writer and mother of three amazing children
    Author of Want To Be A Doula? Everything You Need To Know
    Follow me in 2015 as I go Around The World + Kids!
    Forever grateful to my incredible Mod Team and many wonderful members who have been so supportive since 2003.

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