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Glass Shards of Diabetes

When I heard Dr. Oz talk about what diabetes does to the body (synopsis below), it finally sank in what was happening (diabetes-wise) to my body as I ate and ate and ate some more, giving me my ponderous belly (“Buddha belly”) and I could visualize the internal damage I was surely causing myself when I ignored the disease that has killed several members of my family.

Gestational and regular Diabetes Mellitus (GDM/DM) have been an on-going discussion on my Navelgazing Midwife Facebook Page for the last few days. The conversation began with the vaginal, pain-med-free birth of this 13 pound, 11 ounce baby boy in England. When there are babies this huge in the news, I typically comment about undiagnosed GDM and then the rebuttals ensue. “I had an 11 pound baby and I didn’t have GDM!” or “Not everyone with a big baby has GDM.” And I end up explaining diabetes, over and over again, so I thought it was darn tootin’ time to explain myself here, offering a place to refer to because the discussion will continue coming up as our privileged cultures get fatter and fatter, and more and more women will be diagnosed with GDM/DM and our families, with DM, too.

Also, when this topic comes up, I get comments like this one:

“I have a huge family history of Type II DM, and I've had two 9+ babies. I'm a healthy weight, active, and eat a decent diet... but I feel like I'm just a ticking time bomb for DM!”

The last thing I want to do is scare the bejeezus out of anyone! What I do want to do is 1. Make my Self grasp the gravity of my own situation and 2. Encourage women (people) at risk to pay attention, not freak out.

So, as I said, Dr. Oz explained why diabetes is so devastating in a way, for the first time, that made so much sense. He had an animation that (in its most simplistic form) showed how a carbohydrate changes into a glucose molecule after we eat it and how the glucose (sugars) flow through our bodies, literally feeding our brains and muscles so they are able to function. He also showed how the pancreas sends out insulin receptors, scattering them throughout the body so they can metabolize the glucose for the brain and muscles to absorb, explaining they act almost like vacuums, the glucose zooming towards the insulin. However, when we eat more carbs/sugars than our bodies need, the pancreas can’t keep up with sending out enough insulin receptors and the glucose then zips around the body, causing damage and the extra calories make fat, especially fat around the middle of the body. This inability to keep up is the Insulin Resistance (IR) we’re hearing more and more about. The newest term is Impaired Glucose Tolerance (IGT), a description often called Prediabetes. Other forms of IR are Polycystic Ovary Syndrome (PCOS) and Metabolic Syndrome (MS). All of these are often used interchangeably, but do have nuances of differences that are better explained by the experts, not in this basic piece.

What is a part of this piece is that when I say “GDM,” I am lumping in all the different IR, PCOS, MS, etc. issues because they all go hand in hand, merely located on different parts of the same spectrum of pancreatic metabolic pregnancy disorders.

I know this part is boring as crap, but bear with me, the good stuff’s coming.

So, when we left the glucose, it was floating around looking for some insulin to metabolize it. Dr. Oz brilliantly describes the glucose (crystals) as glass shards that course through the body, slicing things as it wanders hither and yon. In our arteries, the shards make cuts and the artery then “bleeds”, forming a clot and then a scar when it heals. Over and over again, the shards cut, “bleed,” then scar, building up on each other. Sometimes the shard slices off a section of the scar tissue, making an even bigger spot that eventually scars and the part sliced off “floats” downstream, mashing up against another group of scars. Eventually, over time, the scar tissue... and other cholesterol thingies... have built up so much, it completely closes off the artery; arteriosclerosis, one of the major risks of diabetes.

This shard analogy explains a lot of the damage diabetes causes, from slicing the kidneys into eventual failure to causing eye damage, blinding the diabetic. However, I cannot, for the life of me, find why GDM causes stillbirths. As a midwife and as someone who discusses this topic so often, it frustrates me terribly not to know the exact biochemical/physical mechanisms between diabetes and babies being born still. All over everywhere, we can find that stillbirth is a potential complication of GDM, but I’ve scoured .org and medical journals looking for the specific piece of information I’m looking for. If someone out there can help, I would very much appreciate it –and I know others would, too.

This brings me to a point, actually, that we hear such and such is a risk of <fill in the blank> (stillbirth from diabetes, as an example), yet it isn’t explained why. I believe if we knew why complications happened, women would be more compliant; I know I would be.

Audit on Stillbirths in Women with Pregestational Type 1 Diabetes, found in Diabetes Care, written in 2003, is one of very few articles/studies I found that explains what happens to the fetus in utero and why he or she eventually dies:

Early as well as late suboptimal glycemic control may predispose to fetal distress, due to fetal hyperinsulinemia, acidosis, and hyperlacticemia, as maternal hyperglycemia and elevated HbA1c are risk factors for fetal asphyxia, possibly leading to intrauterine death.

And while this speaks about Type 1 diabetes, it does, absolutely, have a great deal to say about Type 2 during pregnancy; mainly, the better the glycemic control, the safer the baby.

(As an aside, I learned a new term: “neglectors.” In the same study, explaining the stillbirths goes this way:

The lack of fetal surveillance together with the lacking improvement in glycemic control during pregnancy, the high rate of smokers, and the low social status indicate that this group has limited compliance, corresponding to the term “neglectors” introduced by Mølsted-Pedersen and Pedersen in 1967.

I suspect today’s term is closer to “non-compliant.”)


Large-for-Gestational-Age vs. Macrosomic

During these endless Net conversations (which I thoroughly enjoy, by the way), big-babies-as-a-genetic-factor butts up against the big-baby-because-of-undiagnosed-GDM. What is the difference and who gets to say which is which (or who is who)?

In the olden days, a large for gestational age (LGA) baby was different than a macrosomic baby, but in the literature now, I see the terms being used interchangeably; odd. This makes the distinction between the genetically large and macrosomic babies nearly impossible. But, I did find these two definitions, what I have been familiar with for many years.

Large for Gestational Age:

“Gestational age is a measure of the growth and development of the fetus in the uterus and the infant after birth. LGA refers to a fetus or infant who is larger than expected for the age and gender or with a birth weight above the 90th percentile. The measurement is based on the estimated gestational age of the fetus or infant, compared with what is considered normal height, weight, head size, and developmental level for a fetus or infant of the same age and gender.”


“One of the most important factors about macrosomia is the differential rate of growth of the fetal head, chest, and trunk as gestation proceeds, both in the babies of diabetic and of nondiabetic mothers. Until 36-38 weeks, the fetal head generally remains larger than the trunk. Between 36 and 40 weeks, however, the relative growth of the abdomen, chest, and shoulders begins to exceed that of the fetal head. This is especially the case in babies of diabetic mothers where glucose substrate levels are higher in both the mother and fetus. Thus both in prolonged gestation and in babies of diabetic mothers the size of a baby's trunk is likely to increase, increasing its chances of shoulder dystocia.”

I do agree there can be ten pound babies of six feet tall moms and that is likely enough to not be a macrosomic baby, but ten pound babies of  5’4” 200+ pound moms are a different story.

The basic point of this whole post is to say that just because a woman tests negative for GDM does not mean there aren’t other insulin-related issues at play… issues that can make for abnormally-sized babies and include the complications that come along with such babes. For those with IGT/Prediabetes, most will develop Type 2 Diabetes within ten years. I’ve also read there are ten to fifteen years before the Type 2 Diabetes diagnosis where pre-diabetes is taking a toll; one that, too often, includes pregnancy.

I met a woman just today whose first baby weighed eleven pounds and she’s post-dates with her second. When I mentioned glucose issues, she defensively told me she didn’t have GDM, but how can someone not be convinced there is some glucose/insulin issue at play? What are doctors and midwives not saying that lead moms to believe nothing is wrong? Do these women have to finally develop diabetes in order to retrospectively acknowledge their child’s size was, indeed, a giant wake-up call about their future health? That is exactly what I had to do after bragging about not being diabetic with a 10 pound 6 ounce baby; I might not have tested positive, but I positively had something glucose-related going on.

Why are there so few of us talking about this in the midwifery/natural birth community? I believe this is something we all need to work with. Don’t we want our mamas and babies to stay safe? Sweeping this issue under the rug is going to do nothing but cause more stillbirths, more shoulder dystocias and more diabetes for everyone. Let me tell you, first hand… diabetes SUCKS.