Before we go any further, I want to make sure we are all defining obesity the same. Obesity is defined as an abnormal or excessive fat accumulation that may impair health. In pregnancy, we use the pre-pregnancy BMI estimate to assess overweight and obesity.
One of the things to understand when you read news articles is that obesity can be measured in several ways. You can use waist circumference or measure percentage of body fat, or you can ask people to report their height and weight and calculate a BMI.
Which do you think is the cheapest and easiest measure for researchers to use? The BMI – you don’t even have to talk to the patient because you can grab this from de-identified medical records. As it turns out, BMI isn’t as accurate at estimating obesity as the methods that actually measure obesity. Not only is it an estimate rather than a measurement of body compassion, it turns out people don’t always give accurate information about their height and weight on surveys. In a recent review of literature investigating the existence of the “obesity paradox”, the research team discovered that it was not actually an obesity paradox that was being reported, but an “overweight” paradox – and it ONLY existed in studies that used BMI to estimate overweight and obesity status.
Unfortunately the accurate methods don’t really work in pregnancy. So we use the pre-pregnancy BMI , which isn’t perfect, but all the research into obesity and pregnancy will use pre-pregnancy reported BMI, so we can make generalizations based on BMI and feel pretty confident about them.
Physiology of Obesity
I’m not going to get too deep into the biochemistry, because honestly I don’t even get all of it. But basically I want you to think of adipose tissue as an endocrine organ. If you are not sure what an endocrine organ is, it is a part of the body that makes and secretes hormones. Adipose tissue acutally makes and distributes a variety of biochemicals including cytokines, angiotensinogen and the hormones Leptin, Adiponectin and Resistin which are known as adipokines.
Excess adipose means the body has excess leptin, and just like too much estrogen messes up the hormonal regulation for reproduction, too much leptin disrupts the things that leptin regulates. So what does leptin do?
Leptin is the energy – balance regulating hormone, and it has a circadian rhythm with the highest levels between midnight and early morning – the lowest levels are in the early afternoon. Leptin levels do NOT change in response to meals. The hormones that regulate hunger and satiety by meals are different. In obese individuals, we see very high leptin levels – but these levels are proportional to their fat mass. Just as type II diabetics become resistant to insulin as the levels of insulin increase, obese individuals become resistant to leptin. A hormone that influences endocrine function and the immune system – and they become resistant to it.
Adiponectin is directly related to insulin sensitivity. In fact, it improves whole-body insulin sensitivity. It also is protective of the vascular system because it inhibits many steps in the inflammatory process and is involved in lipid oxidation. In muscle, it enhances glucose transport with insulin. Unfortunately, unlike leptin, circulating levels of adiponectin are negatively correlated with fat mass – so obese women have lower blood concentrations.
We understand the least about resistin. I can tell you the levels are increased in obesity – especial abdominal obesity, and it appears to play a role in insulin resistance.
An obese pregnant woman enters pregnancy with the physiological changes of obesity. She has an abnormally high amount of metabolically active adipose tissue. She has high leptin levels and low adipnectin levels and high resistin levels. She enters pregnancy at higher risk for diabetes and hypertension because of this.
But pregnancy adds another endocrine organ to the mix – the placenta. As far as we can tell, the placenta makes and secretes all the adipokines except adiponectin (the good one). We know the placenta secretes leptin, and maternal leptin levels increase during the first and second trimesters, and they decline drastically post-partum. This leads researchers to believe there is a functional importance to leptin during pregnancy.
We know leptin can modify insulin sensitivity and tissue metabolism. So we may speculate that the increased leptin level is working to increase nutrient transfer to the baby. We also know leptin plays a role in amino acid transport through the placenta. But leptin is also a primer for placental inflammation – and obesity leads to a placental environment that is associated with decreased angiogenesis and increased inflammation and oxidative stress. In other words, obesity contributes to placental dysfunction. Not only placental dysfunction, but obesity also affects placental proliferation. As BMI increases, the ability of the placenta to grow properly decreases. This has effects on the ability of the baby to grow. A dysfunctional placenta affects what the baby is able to get.
Tomorrow we will talk about how these physiological differences play out in pregnancy risk.
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