Follow me on

Intergenerational Transmission of Obesity and Diabetes



Regular readers should by now be quite familiar with the accumulating data suggesting that your risk for future development of obesity, diabetes, and possibly other metabolic diseases, may begin in the womb.

This topic is nicely reviewed in a paper by Marie-Claude Battista and colleagues from the University of Sherbrooke, Quebec, published in Experimental Diabetes Research.

In this paper, the authors not only discuss the relationship between maternal obesity and pregnancy risk (for both mother and child) but also discuss the complex factors that link excess weight to gestational diabetes.

They then extensively review the animal data that shows how intra-uterine epigenetic modifications can lead to a (permanent) metabolic adaptation that substantially increases the risk for obesity and diabetes in the offspring.

Finally, they critically discuss the emerging human data demonstrating the impact of lifestyle and bariatric surgery on both maternal and fetal health and the ability of these interventions to possibly break the vicious circle that perpetuates the transmission of obesity and metabolic conditions to the next generations

As the authors conclude:

“Fetal programming of metabolic function induced by obesity and GDM may have intergenerational effect and thus, perpetuate the burden of such conditions. Mechanisms by which reprogramming of fetal function might occur is directly through maternal metabolic and hormonal effects, epigenetic alterations or impaired placental function. Periconceptional weight loss interventions have demonstrated their ability to reverse the impacts of maternal obesity and GDM on the child and are of great importance for the prevention of future cardiometabolic risks in the offspring, and may thus be the best approach to break the vicious circle of intergenerational propagation of obesity and diabetes.”

They, however also caution that:

“…the nature and the timing of intervention should be carefully considered because it could also by itself induce organ reprogramming and potential long-term effect on the offspring.”

Not an easy topic (and certainly not an easy read) given the complexity of the emerging molecular, metabolic and genetic animal and human data on this issue.

However, certainly a topic that cannot be ignored in any discussion about finding solutions to the obesity epidemic.

AMS
Leipzig, Germany

Battista MC, Hivert MF, Duval K, & Baillargeon JP (2011). Intergenerational cycle of obesity and diabetes: how can we reduce the burdens of these conditions on the health of future generations? Experimental diabetes research, 2011 PMID: 22110473

2 Comments

  1. Did they control for genetic factors? Being fat is up to 70% genetic, just like height, and one’s risk for type 2 diabetes is increased if one has direct relatives who also have type 2 diabetes. If those factors weren’t controlled for in this study, their conclusions are suspect, at best.

    Post a Reply
  2. I agree with Vesta. Everyone seems determined to blame the existence of fat people on someone’s behaviour. Mothers are the go-to people for blame in our society.

    In reality, if fat mothers tend to have fat children, then it’s more likely in the DNA, and if behaviour has an impact, then it’s probably dieting during pregnancy that creates children who are predisposed to be fat. Look at the Dutch hunger winter research.

    Personally, I have a normal-sized mom who keeps herself thinner than she would be naturally by restricting her eating. My parents are divorced, and my mom raised me. If I restrict my eating like she does, my BMI is slightly over 30. If I don’t, I’m 30 pounds heavier.

    People in mom’s family are thin to slightly fat. Young people are never fat on that side of the family, and only the yo-yo dieters get to be big enough to have shop in plus-sized or big and tall stores. My dad’s side of the family tends to be much heavier, and he and his sisters were fat as children. It’s pretty clear that I inherited my build from Dad, not Mom. Therefore, in my case it was DNA, not a big, bad momma. Sorry.

    And actually this whole trope really annoys me.

    So here I am, with a BMI around 35. Let’s say I want to get pregnant. The doctor tells me to lose weight first. I start eating 1500 calories a day, and in a year my BMI is under 30. When I lose these 40 or 50 pounds, I lose both muscle and fat. My heart, which is a muscle, shrinks.

    Then, I get pregnant. Now, I have two choices. I can eat normally or I can continue to diet while pregnant.

    If I eat normally, I’ll rapidly gain back all the weight plus some. My heart, which has shrunk, will have to get stronger fast to handle the weight returning and the simultaneous pregnancy. My muscle mass, which has decreased, will not be sufficient to haul around my body, which will suddenly be much heavier and have a different center of gravity. If I followed the doctor’s weight loss advice, then this option would be better for the baby. However, it would make the pregnancy extremely hard on my body. Does this sound like a good idea to you? No?

    Well, the alternative is to continue to diet while pregnant. That would raise all kinds of risks for the baby. It would be difficult to get proper nutrition. I would be ravenously hungry all the time. And the baby would likely be predisposed to be fat as an adult, because the dieting would mimic the effects of the Dutch hunger winter. Does that sound like a good idea to you? No?

    What if I just started paying more attention to nutrition and regular exercise for the six months before getting pregnant? This wouldn’t make me lose much, if any, weight. However, it would give me a strong, healthy body that would be equipped to take on a pregnancy. Does any doctor give that advice to a woman my size? I doubt it. Instead, I’d get blamed for the horrible sin of being fat while pregnant if tragedy struck (/sarcasm) and my kid came out looking like me.

    Post a Reply

Submit a Comment

Your email address will not be published. Required fields are marked *