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.”


“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.


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

Healthy Food? No Such Thing

A word about “healthy” food. I have no idea what that means. To be honest, I’d love for that term to disappear altogether. The World Health Organization describes health as “a state of complete physical, mental, and social well-being, and not merely the absence of disease or infirmity.” If “being healthy” is the equivalent of “being well,” then it is easy to see that the phrase “healthy food” makes little sense. It’s hard to be “well” and be “food” at the same time!

Think about it for a minute from your own perspective in the food chain. Becoming food is not a healthy thing to have happen to you. This is why the antelope runs away from the lion and why many plants, which can’t run away, have developed a number of biochemical toxins to defend themselves.

This looks like healthy kale:

This looks like yummy kale:

But this is not “healthy” kale; it’s dead kale. It might be delicious, and it might help make you a healthy person, but it definitely not “healthy” kale. It isn’t going to grow or propagate. It is—I hope–going to get eaten.

The term “healthy” is appropriately applied to things that live and grow: people, plants, animals, environments, communities, economies. Food—i.e. something about to be eaten—isn’t living and growing. The things we consume as food may or may not allow us to become healthy (well) people in a healthy community with a healthy economy and environment.

Why am I splitting hairs over an over-used term like “healthy food”? Why does it even matter whether or not we refer to food as “healthy” or not? And aren’t some foods always “healthy”—for everyone? Y’know, like spinach, and chocolate?

To answer the first two questions: How we speak reflects how we think. When we use the phrase “healthy foods” there is an underlying assumption that

1) we know and are in agreement about how to define “healthy” foods

2) there exists a specific set of foods that fit this definition, while the rest do not.

Which brings me to the last question, aren’t some foods always “healthy/unhealthy”? Hmm. For someone whose current health status requires a low-fiber diet, kale is not “healthy.” For a kid surviving on a subsistence diet who needs the calories and the 8 essential vitamins and minerals in a bowl of Lucky Charms (not to mention the marshmallow surprises!) cereal is “healthy” (not optimal, not perfect—but better than nothing).

Note that I am not saying “Everything in moderation.” I am saying “Everything in context.”

I can tell you what foods contain the nourishment that humans require; I can tell you what foods frequently create health problems for many people. I can look back on our recent history and tell you what has happened in our food system that has not worked to create a healthy environment, economy, or society. But I cannot determine what foods or what lifestyle will create a state of health or wellness for you right now and certainly not 30 years down the road—no one can but you, and you can really only do that through educated guesswork and listening to the expert within. Nutrition experts can (if properly trained) help you with both of those things, but they can’t if they’ve already determined that they “know” what “healthy” food—for you and everyone else—is.

Just what the world needs – another blog

My blog reflects my own efforts to begin to translate what I learn about science into meaningful information, policy input, and dinner. This is science put into practice, in the kitchen and in my advocacy work.

Here’s the problem as I see it, plain and simple:

Really, though, there’s nothing simple about it. As a student of epidemiology I must claim that this only shows an association, not cause-effect. Whether the Guidelines “caused” the rapid rise in obesity has yet to be determined, but it’s clear that they certainly did not prevent it. To me, what is more interesting is why nutrition epidemiologists aren’t all over this particular—and remarkably obvious– association trying to figure it out. Instead, I read study after study on the arcuate nucleus and the “built” environment and circadian rhythms and the health belief model and how these things contribute to obesity—and virtually no one says “Um, excuse me, but what about the one public policy piece that since 1980 has influenced every single aspect of our food environment from our cultural norms to how nutrition research gets funded and everything in between?  You know, the Dietary Guidelines?”

As Dr. Su from Carbohydrates Can Kill said, it is like there is an invisible electric fence when it comes to questioning our national dietary policy. Scientists just don’t go there.

So of course, I want to go there.

Although I love nothing more than a romantic evening for one at PubMed, don’t expect a lot of article-jousting here. Frequently those arguments (leptin insulin ghrelin, oh my!) boil down to a collection of snapshots from experimental data that may or may not create a physiologically significant or practically useful collage.  I spent a few years at the Duke Lifestyle Medicine Clinic working with patients who were overweight/obese and frequently struggling with diabetes. This experience has focused my interests on the interactions between biology, culture, and the individual and how these influences become manifest in individual differences and population-wide similarities with regards to nutritional needs, food choices, and consumption patterns (a framework borrowed from anthropology and applied to eating, hence the name of the blog).

In addition, my experiences so far in graduate school—including an interning stint at the American Dietetic Association’s Washington, DC office—have made it very clear that when it comes to the science of nutrition, the playing field is far from level. In fact, I’m not sure our current crisis can be solved by science, or certainly not by science alone. Since the advent of the Dietary Guidelines for Americans in 1980, all aspects of nutrition research have become warped by industry and politics. And–as any grad student can tell you—the most political industry of all is the scientific/academic one.

At the same time, I’m not here to wring my hands in anguish. I’m actively trying to figure out what to do about this mess we’re in. I’d love all the feedback and help and ideas I can get from anyone with enough time on their hands to wade through my musings. Let’s save the world & have fun doing it.