What Infants Teach Us About Preventing Obesity.

Public health has been telling you for years: you are fat because you move too little and eat too much. And yes, it's your fault if you don't break a sweat every day to keep your waist line in check. But research says, that's not the entire truth. In fact, public health might have taken the easy way out, and here is how it could finally make amends. [tweet this].

If an alien scientist came to earth to study us in the same way in which we study lab rats, he would come to the same simple conclusion as we do: give those animals more than enough food, take away the need to move around, and what you'll get is a population of mostly overweight individuals. I say "mostly" because there are always the odd ones who fall away from the norm. What fascinates me most in this image is the fact that, while mice and rats probably do not communicate among each other the benefits of staying slim, we humans do so and still, the result is the same. What our alien researcher sees is biology trumping consciousness. For a good reason. Neither rats nor humans would survive in their natural habitat without the ability to store excess calories as fat, which then sees them through the inevitable lean periods. It gave our ancestors a good shot at survival, with no or little chance to become overweight. At least not then.

Today, obesity is the new normal. I won't bore you with the percentages. You hear and read about them in the media almost daily, with one or the other pundit citing the ever increasing number of people who are overweight or outright fat (the politically correct term being "obese"). Not that any of those pundits offers any solution or view of things other than that too little exercise and too much food are the cause. Those platitudes are typically topped off with denouncing people's weakness to do something about it, such as exercising more and eating less. When you look at the effectiveness of public health calls for exercising more and eating less, you'll find that overweight and obesity have increased nicely alongside those calls. Which simply means one thing: we need to do something differently. 

Now, remember, I said there are always some odd individuals who seem to escape the fate of the majority of our experimental animals, be that rats in the lab or humans in free living conditions. It is here where we ought to look at what makes them so different. And whether this difference is in their genetic program or in their mental ability to override this program.  

The funny thing is, the answer to this question has been relatively clear for years, but hardly anybody seems to draw the right conclusions from it. Just about a week ago, another wonderful study has emerged on this subject. 

  

Britt Eriksson and her colleagues investigated the correlation between body composition development and energy expenditure through physical activity in 1.5 year old infants [1]. That's not a first, but the way they did it is. When you look at energy expenditure of any individual it is necessary to know how much of this energy expenditure comes from basal metabolic rate (BMR). This BMR tells us how much energy an organism needs to maintain life under resting conditions. There are large differences in these rates between individuals, such that two persons who share the same body weight, height and composition and who do the same type of exercise may burn substantially different amounts of calories, simply because one person has a higher basal metabolic rate than the other. So, If you want to know exactly how much of an individual's total energy expenditure is coming from physical activity, you better have accurate knowledge about his basal metabolic rate because you need to subtract it from total energy he or she burns.  In previous studies of infants, physical activity levels (PAL) had been estimated based on predicted BMR rather than on actually measured BMR. Obviously, if your BMR prediction is incorrect so will be your conclusions about PAL. That's why Eriksson and her colleagues objectively measured basal metabolic rates. They did so by analyzing carbon dioxide production and oxygen consumption while infants slept under a ventilated hood system. Add to this the researchers' way of measuring total energy expenditure with the gold standard doubly labeled water method, and what you get is the most accurate differentiation between BMR and PAL possible in living humans.

Our researchers did all those measurements on 44 children aged 1.5 years. All of them had participated in a body composition study when they were 1 and 12 weeks old. Body composition was again measured in the current study. Before we look at the correlation between body fatness and PAL in those 1.5 year old children, let's recall what is normal in human development during infancy. 

Healthy infants typically gain body fat, expressed as a percentage of bodyweight, during the first 6 months of life, after which the total body fat percentage (TBF%) slowly decreases. By the way, that was the case in only about 20% of the infants in this study. The majority increased their body fat percentage but with large differences between individuals. At age 1.5 years TBF% varied between 21% and 35%. And these changes in body fat correlated with the physical activity levels of the infants, such that those with a higher PAL had decreased their body fat percentage more than those with a lower PAL. The beauty of investigating these associations in infants is that you don't need to worry about your study subjects' volitional exercise habits, such as treadmill running, mountain biking or kicking ass instead of writing anonymous comments to blog posts. All their physical activity is non-exercise activity. I'll get to this important distinction in a moment. The point here is: genetic influences show up relatively unmasked.  If there are such large inter-individual differences in body fat development already being evident in the earliest years of life, we have every reason to assume that there is a phenotype and a genotype which is better protected against fat gain than others. We also know that body fat percentage in the youngest years tracks into adolescence and on into adulthood. 

Which of course also means that we should see such differences in adults, too. In fact we have been seeing them for more than 10 years, but somehow these observations don't make it into the media where the doom and gloom prophets of obesity have our ears and eyes but no solutions to offer.

Back to those studies: Levine and colleagues put 16 non-obese young adults, aged 25-36, on an 8-weeks supervised diet which provided a daily excess of 1000 Kcal over what each individual needed for weight maintenance [2]. The participants had to maintain their usual level of exercise throughout the experiment. Physical activity and body composition were measured with the same gold standard methods, which the Eriksson group used on their infants. As a group, the participants of the overfeeding experiment stored 44% of the excess kcal as fat, and dissipated 53% through increased energy expenditure. 

But those average values over a group of people don't interest us here. What we want to know is how much difference was there between participants. Well, fat gain varied more than 10-fold from a minimal increase of 360 Grams to a whopping 4.23 kg. Think about this for a moment: you let 16 people gorge themselves on a daily excess of 1000 kcal for 8 weeks and what you get is one whose weight remains virtually the same, while another gains more than 9 pounds, and all the other 14 show up anywhere in between those two.

The laws of physics tell us that energy cannot be lost or created, it can only be converted from one form to another. What this means to our weight gain experiment is that those who didn't store the energy as fat must have burned it somehow through physical activity. But how could that have happened if all participants kept their exercise on an even keel throughout the experiment? Had an enormous increase of BMR protected them against weight gain? Our researchers didn't think so, because experiments on BMR response to over- and underfeeding have been fairly consistent, showing only small changes in the range of 5%. Levine's participants were no exception to that rule. So, what happened? 

The answer is in the details of what constitutes physical activity. There are two components, one of which you certainly know: exercise. Then there is the other, which I just mentioned a few lines earlier. It's called NEAT, which is short for non-exercises activity thermogenesis. In a less convoluted way it means the energy you burn through acitivities of daily living, fidgeting, spontaneous muscle contractions and maintaining or adjusting posture while not lying down. In other words, the energy you burn through physical activity which is not volitional exercise.  

NEAT accounted for over 70% of the increase in daily energy expenditure, with an average increase of 336kcal/day. Mind you, this was the average over the entire group. Far more interesting, again, is the range, which spanned from a decrease of 98 kcal/day to an increase of 692 kcal/day. It's the same picture we saw in the fat weight development. And yes, the larger a participant's increase in NEAT the smaller his weight gain. The fellow with the 692 kcal/ increase subconsciously moved around more often. He had increased his strolling-equivalent activity by an average of 15 minutes per waking hour! Interestingly, the 4 female participants in this study had the smallest changes in NEAT. While this study is certainly underpowered to tell us anything about gender differences, its observations fits neatly with an another observation: The age-dependent increase of obesity risk is steeper for women than for men. 

Now, back to the study results. If NEAT is NON-VOLUNTARY activity energy expenditure, then conscious rationally driven behavior has nothing to do with it. It's purely physiology talking. It's our genes' handwriting. And if this handwriting reveals such a substantial effect on weight development, shouldn't we look at means to increase NEAT, rather than keeping our current tunnel vision on exercise, which we already know is so difficult to adopt for most people? Let's put some effort into designing "obligatory" NEAT into our life. Or rather, designing NEAT killers (such as remote controls) out of it. 

To our alien researcher, this might just be the next experiment, as it is for his human peers who are already experimenting with running wheels and wheel locks in their lab rats' cages. After all, a 332 kcal/day deficit translates into almost 14 kg of fat over a year. That's certainly something which public health ought to be interested in. 

  

1. Eriksson B, Henriksson H, Löf M, Hannestad U, Forsum E: Body-composition development during early childhood and energy expenditure in response to physical activity in 1.5-y-old children. The American Journal of Clinical Nutrition 2012.

2. Levine JA, Eberhardt NL, Jensen MD: Role of Nonexercise Activity Thermogenesis in Resistance to Fat Gain in Humans. Science 1999, 283(5399):212-214.

Eriksson B, Henriksson H, Löf M, Hannestad U, & Forsum E (2012). Body-composition development during early childhood and energy expenditure in response to physical activity in 1.5-y-old children. The American journal of clinical nutrition PMID: 22836033

Levine JA, Eberhardt NL, & Jensen MD (1999). Role of nonexercise activity thermogenesis in resistance to fat gain in humans. Science (New York, N.Y.), 283 (5399), 212-4 PMID: 9880251

PrintPDF