Fat? Blame Mom

“Adverse factors encountered during fetal life have the dual effect of perturbing prenatal growth patterns and establishing a pre-susceptibility to major disease states in adult life”

Langley Evans: Proc Nutr Soc. 2001;60(4):505-13.

Jimmy Moore of Livin’ La Vida Low Carb wrote a great post recently entitled “When Does Being Fat Become Your Fault?”  In it he states that his weight is 295 pounds. I would guess that’s accurate.  I have had the pleasure of meeting Jimmy many times & he’s a big guy. From what I understand, so was Dr. Atkins of the Atkins Diet fame. So is my 18-year old son.

In the past, when people meet some of the vocal and active members of the low-carb community who don’t necessarily match expectations of what a socially-acceptable “healthy” weight would be, I’ve been asked if the whole low-carb thing is a farce. Maybe people feel comfortable posing this question to me because I’m not heavy (anymore). And I think I can say that my weight loss journey was probably a little easier for me than for others, but not because I have more willpower or I just don’t eat that much (I love food!!). It may be because my mother insisted that I eat an egg for breakfast every morning as a child. I wasn’t there to check this out, but I assume that’s how she ate when she was pregnant with me. We were a meat-at-every-meal family. Why am I telling you this? Because it matters.

Epigenetics is a new term that gets used a lot without people know just exactly what it means. Simply put, epigenetics is the study of how the environment (especially the prenatal environment) can effect gene expression, as opposed to changing the genetic material itself. This means that certain metabolic features that are controlled by our genetic material—for instance, hormones, enzymes, appetite regulation signaling factors—may be upregulated or downregulated due to influences from our environment.

The effect of prenatal environment—including diet—on how genes are expressed can then in turn effect how we end up interacting with our current environment. Some folks get a “triple whammy”—genes that code for obesity, a prenatal environment that affects the expression of those and other genes, and an obesogenic environment. Can we honestly say that these folks have some character flaw that makes being fat their fault?


There are many things beyond our control, especially intrauterine environment, which have a primary impact on how much we weight as adults–perhaps even more impact than our current dietary habits.  I know this personally because my son, who was born when I was in my most strict vegetarian phase, has had much more trouble with his weight than my son whose pregnancy was one in which the doctor insisted that I eat high quality protein–at every single meal (unheard of for me).  My “vegetarian phase” pregnancy was a difficult one. I was on bed rest or in the hospital most of my last trimester; my son was born 6 weeks early anyway. He was a skinny little kid, but as soon as adolescence kicked in (a hyperinsulinemic phase in general), he began gaining weight.

  • In terms of genetics, he got flat feet and a large build (his father’s side)
  • In terms of epigenetics, he got a vegetarian mother who ate little fat and protein while he was swimming about in utero.
  • In terms of environment, he got a vegetarian mother through his first 6 years of life; now he has a college dining hall to contend with.


His fasting insulin is higher than “normal,” (a likely result of my eating habits, not his), so he has an uphill battle even though he lifts weights, is active, and eats a low-carb diet.  He does pretty well, but imagine if he’d first spent years trying to control his weight with a high-carb, low-fat diet?

That’s just my n=1 perspective. But if what he experienced is a real effect, imagine the population-size effect. It might look a lot like the obesity and diabetes rates we are experiencing now. So what does the science tell us about that possibility? Here’s a brief glance, much of it courtesy of a lecture by Dr. Linda Adair in Fall 2009.

If the mother’s supply of nutrients does not meet the demands of the fetus, there are a few adaptive measures that take place:

  • The fetus will grow less, but maintain head & brain circumference at the expense of skeletal muscle and some other organs.
  • The fetus will become more metabolically efficient as endocrine function is altered to enhance survival.

From animal studies, scientists have seen that, even with normal nutrition after birth, adult offspring of prenatally malnourished mothers have:

  • Increased blood pressure
  • Abnormal glucose tolerance
  • Impaired inflammatory response
  • More body fat
  • Eat more
  • Move less

Hmmm. Should we assume that these mice have some sort of lack of willpower or other character flaw?


Vickers, M. H. et al. Am J Physiol Regul Integr Comp Physiol 285: R271-R273 2003;

From epidemiology studies, especially the Dutch Hunger Winter, we’ve seen that exposure to famine during pregnancy results in higher rates of markers of insulin resistance and higher rates of obesity in adults. Note the type of nutrients that were most restricted during the “Hunger Winter” were protein and fat.  In fact, the protein-to-carbohydrate ratio has been shown to be the most predictive marker with regards to some of the negative health outcomes in adulthood.


Calories derived from carbohydrate, protein, and fat in the official daily rations provided between April 1941 and April 1947.  

Follow-up studies for the Dutch Hunger Winter and other famine or near-famine situations show that babies conceived during nutrient-restricted periods grow up to have increased risk of impaired glucose tolerance, obesity, high blood pressure, and other negative health outcomes in adulthood.

Other population studies have shown a consistent association between low weight for length at birth (a possible sign that the body is selectively nourishing the brain rather than the body, see above) and impaired glucose tolerance, insulin resistance, and type 2 diabetes.


In the Nurses’ Health Study, smaller babies grew up to have an increased risk of type 2 diabetes.

Other factors, such as environmental toxins may pre-dispose kids to obesity, either as children or later in life.

People who may be affected by these epigenetic mechanisms may be metabolically—not psychologically—inclined to eat more and move less. It’s not a character flaw; it’s a biological imperative. It is what their bodies are telling them to do. At what point do we stop blaming these people (who may now make up a majority of our population) and start trying to figure out how to assist them with their efforts to be healthy?

I don’t want to go all mama grizzly on people, but my blood pressure goes through the roof when I hear my classmates make comments like:

“Well, any diet intervention is going to show an improvement in obese people. They’ve been stuffing their faces with tons of calories before this.”

and

“People are fat because they eat too much. Period.”

I think of all the wonderful people I met at the clinic. Of myself. Of Jimmy. And my son. I can count on one hand the number of overweight/obese people I’ve met whom I think actually fit these generalizations.

The thing about the low-carb approach is that it attracts people who have been unsuccessful any other way–for a good reason.  A highly dysregulated system needs a stronger intervention.  It isn’t going to turn someone with a dysregulated system into a model-thin person, but it will often allow them to lower insulin levels to the point where good health is an achievable goal, even if it doesn’t come with a socially-approved weight. Let me emphasize: I do not think low-carb is the only way to do this, but it certainly should be considered as an option.

Until we can move past our “calories-in, calories out,” preconceived notions about what constitutes “healthy” food and what makes people fat, we are doing much of the population a tremendous injustice. Our refusal to entertain any other theories besides the current high carb/low fat dietary regime (which is still, after all, a theory although it is treated as a fact) is possibly the worst failure in public health since the rejection of germ theory in the 19th century. My son is the funniest person I know, and he doesn’t hate me for my very-likely part in mucking up his metabolism. He deserves better.

References:

de Rooij SR, Painter RC, Holleman F, Bossuyt PM, Roseboom TJ. The metabolic syndrome in adults prenatally exposed to the Dutch famine. Am J Clin Nutr. 2007 Oct;86(4):1219-24.

Heijmans BT, Tobi EW, Stein AD, Putter H, Blauw GJ, Susser ES, Slagboom PE, Lumey LH.Persistent epigenetic differences associated with prenatal exposure to famine in humans. Proc Natl Acad Sci U S A. 2008 Nov 4;105(44):17046-9. Epub 2008 Oct 27

Langley-Evans SC. Fetal programming of cardiovascular function through exposure to maternal undernutrition. Proc Nutr Soc. 2001 Nov;60(4):505-13. Review

Painter RC, de Rooij SR, Bossuyt PM, de Groot E, Stok WJ, Osmond C, Barker DJ, Bleker OP, Roseboom TJ. Maternal nutrition during gestation and carotid arterial compliance in the adult offspring: the Dutch famine birth cohort. J Hypertens. 2007 Mar;25(3):533-40.

Rich-Edwards JW, Colditz GA, Stampfer MJ, Willett WC, Gillman MW, Hennekens CH, Speizer FE, Manson JE.Birthweight and the risk for type 2 diabetes mellitus in adult women. Ann Intern Med. 1999 Feb 16;130(4 Pt 1):278-84.

Vickers MH, Breier BH, McCarthy D, Gluckman PD. Sedentary behavior during postnatal life is determined by the prenatal environment and exacerbated by postnatal hypercaloric nutrition. Am J Physiol Regul Integr Comp Physiol. 2003 Jul;285(1):R271-3

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