One of the most exciting and biologically highly plausible reasons for the childhood obesity epidemic may well be that current generations are far more susceptible to obesity because of “epigenetic programming”.

Simply put, the notion is that exposure to an adverse fetal environment, as in the case of maternal obesity, diabetes or hypertension during pregnancy, can lead to a lifelong change in the genetic program of the offspring, making them genetically more prone to obesity.

Thus, although the children are born with the same genetic code as their parents, whether or not certain genes are “more” or “less” active, is determined by the fetal (and possibly early post-natal) environment.

While these “epigenetic” changes are well documented in animal studies, exactly which genes are affected in the context of intergenerational transmission of obesity is not clear.

A study by Luigi Bouchard and colleagues from Université de Montréal, Canada, just published online in Diabetes Care, suggests that one of the modified genes may well be leptin, a key regulator of energy balance.

The researchers examined placental tissues as well as maternal and cord blood samples from 48 women, 23 of who had gestational impaired glucose tolerance (= gestational pre-diabetes).

Not only was there a positive association between the DNA methylation levels of the offspring’s leptin gene (measured in the placenta) and the glucose response to an oral glucose test, but there was also a negative relationship to placental leptin gene expression.

DNA methylation is a form of “epigenetic” modification that determines the extent to which a given gene is expressed in vivo. Thus although the genetic code or DNA sequence for that gene may be identical between two individuals, variations in DNA methylation will determine how “active” this gene is in a given individual.

The authors conclude that impaired glucose tolerance during pregnancy is associated with epigentic modification of the leptin gene with potential functional impacts that could in part account for the detrimental health effects associated with fetal programming such as long-term increased risk of developing obesity and type 2 diabetes.

As I have noted before, obesity may well start in the womb, which is why recent recommendations have focussed on improving maternal health, including the prevention of excess weight gain during pregnancy, as a key strategy to reduce childhood obesity.

AMS
Edmonton, Alberta

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Bouchard L, Thibault S, Guay SP, Santure M, Monpetit A, St-Pierre J, Perron P, & Brisson D (2010). Leptin Gene Epigenetic Adaptation to Impaired Glucose Metabolism during Pregnancy. Diabetes care PMID: 20724651

Anyone working in the field of childhood obesity has probably long noticed that effectively addressing excess weight in kids usually means involving the whole family. In fact some programs go as far as to only involve the parents rather than focus on the kids themselves.

Unfortunately, access to weight management programs for families remains extremely limited. Most families are left to fend on their own or wait in line for appointments with health professionals.

A book called “Changing the Face of Obesity - one family at a time”, by Ottawa’s Michelle Renard Good, hopes to address this gap by helping inspire kids and teens to choose a healthier way of life.

From the introduction to the book, Good explains that despite being very active, she too struggled to maintain her weight - not withstanding her mother’s attempts to get her to diet. Now, as a nutritionist, personal trainer, homeopathic doctor and mother of four daughters, she has invested substantial time into gathering an almost encyclopedic amount of information that she has brought together in what she calls the WeightSavvy Teens and Kids weight management program.

The result is a densely written, over 300 page long, book that is both part textbook and part workbook, providing an almost overwhelmingly vast range of background information and self-assessment tools to explore topics ranging from fitness and eating behaviour to communicating emotions and improving self esteem.

The program moves well beyond the usual “eat less and move more” approach to weight loss and instead focuses on the other possible factors contributing to weight gain. I really enjoyed the progression and flow of the book. By dividing concepts into building blocks of achievable ‘steps’, readers are presented with a systematic approach to achieving a healthy weight through goal setting, behaviour modification and education.

I particularly enjoyed the sections on how to:

* Cope with stress
* Manage boredom
* Identify hidden fats in foods
* Eat healthy in restaurants

Good’s writing style is engaging and her use of Weekly Narratives, in which she describes scenarios that kids may readily relate to, provides much room for discussion and engagement.

More information on the book and the program can be found on Good’s website.

If any of my readers have experience with this program, I’d love to hear from you.

AMS
Edmonton, Alberta

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Yesterday, I blogged about the finding that increased body fat appears to precede lower activity levels and not the other way round (which is probably why attempts to increase physical activity in kids has so far not done much in terms of obesity prevention).

Almost on cue, the latest issue of the Canadian Medical Association Journal (CMAJ) publishes a study by McMaster University’s John Cairney and colleagues, suggesting that kids with developmental coordination problem (perhaps unfairly described as “clumsiness”) may be particularly prone to weight gain.

The study builds on previous reports that kids with developmental coordination disorder were found to be less likely to participate in physical activities.

The researchers studied 2278 (95.8%) of 2378 fourth grade kids (ages 9 to 10) from 75 schools in southwestern Ontario, Canada. Children were followed up over two years, from the spring of 2005 to the spring of 2007.

Not only did the 111 children (46 boys and 65 girls) who had possible developmental coordination disorder have a higher mean BMI and waist circumference at baseline than the other kids, but these differences persisted or increased slightly over time.

In fact, kids with with possible developmental coordination disorder were four times more likely to become obese over the course of the study.

While this study is of course strongly suggestive of less physical activity being a risk factor for childhood obesity, it should be noted that the researchers did not directly measure activity levels. There was also no report of their energy intake or their mental health status (e.g. cognitive ability, depression, attention deficit disorder, etc.), which may significantly affect ingestive behaviours.

There was also no mention of low birth weight, which may be associated both with developmental coordination disorder and excess post-partum weight gain.

Finally, as the authors themselves are careful to note, obese kids have been noted to be less coordinated - so again, it is not clear if the sequence here is “clumsiness -> inactivity -> obesity” or “obesity -> inactivity -> clumsiness” or even “obesity -> clumsiness -> inactivity”.

As always, solving ‘chicken or egg’ questions from cross-sectional or even longitudinal data remains challenging. This is exactly why we need more intervention studies.

AMS
Edmonton, Alberta

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The current dogma is that our kids are getting bigger because of sedentariness and inactivity. Based on this dogma, attempts at reversing the childhood obesity epidemic focus largely on increasing physical activity -so far with little to show for.

Now, a study by Brad Metcalf and colleagues from Plymouth, UK, published online in the Archives of Disease in Childhood, suggests that it may be fatness leading to inactivity rather than the other way round.

For this study, the researchers analyse data from a prospective cohort study examining children annually from 7 to 10 years. Participants were 202 children (53% boys, 25% overweight/obese) recruited from 40 Plymouth primary schools as part of the EarlyBird study.

Importantly, the researchers used accelerometers worn by the children for 7 consecutive days at each annual time point to measure actual levels of physical activity.

In addition, actual body fat per cent was measured annually by dual energy x ray absorptiometry.

While body fat percentage was predictive of changes in physical activity over the following 3 years, physical activity levels were not predictive of subsequent changes in body fat.

Thus, while a 10% higher body fat at age 7 years predicted a relative (albeit modest) decrease in daily moderate and vigorous intensities of 4 min from age 7 to 10 years, greater physical activity at 7 years did not predict a relative decrease in body fat between 7 and 10 years.

The authors conclude that the often found association between lower activity levels and higher body fat may be the result of fatness driving inactivity rather than inactivity driving body fat. Thus, physical inactivity appears to be the result of fatness rather than its cause.

Not surprisingly perhaps, they also note that this “reverse causality” may nicely explain why attempts to tackle childhood obesity by promoting physical activity have been largely unsuccessful.

Given, as blogged previously, that the key determinant of body fatness may well be determined by what happens in utero - the causal sequence for the childhood obesity epidemic may well be:

in utero epigenetic programing > fatter offspring > less active kids.

Thus, while interventions to increase physical activity in kids may well have an important benefits on fitness, balance, coordination and numerous other aspects of health - anyone expecting more activity in kids to reverse the childhood obesity epidemic may well be barking up the wrong tree.

AMS
Edmonton, Alberta

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Metcalf BS, Hosking J, Jeffery AN, Voss LD, Henley W, & Wilkin TJ (2010). Fatness leads to inactivity, but inactivity does not lead to fatness: a longitudinal study in children (EarlyBird 45). Archives of disease in childhood PMID: 20573741

No worries, I am already holding my ears to avoid the screams of protest that I expect to get in response to this post.

But the idea that working moms may well play a noticeable role in the development of childhood obesity is indeed one that is suggested by Angela Pinot de Moira and colleagues from University College London, UK, in a paper just published online in the American Journal of Epidemiology.

The premise is simple: one of the most dramatic demographic shifts in the last decades has been the proportion of moms that work. From being the exception in the 60s, to becoming pretty much the norm for the majority of mothers today, this demographic shift has undoubtedly had profound effects on family life.

Not surprisingly, some have argued, that not having a parent at home (and traditionally this used to be the mom) may very much increase the risk of weight gain in offspring.

Thus, not only do “latchkey kids” have more freedom to eat unhealthy foods and spend afternoons slumped in front of the TV or computer, but long hours at work can also leave moms (or dads) short of time to prepare healthy family meals (ergo the dramatic rise in fastfood and family restaurants).

In addition, working mothers (or dads) may also have to drive their children to school rather than have the time to walk them there and working partents certainly don’t have the time to watch over their kids on the playground all afternoon or be at home in case their kids scrape a leg falling off their bikes or get beaten up by the neighbourhood bully.

So is this hypothesis borne out by the data?

To address this question, the authors examined members of a 1958 British birth cohort (age 7 years, n=8,552) and offspring (ages 4-9 years, n=1,889) born to mothers under age 30 years to establish whether risk factors for childhood obesity have changed over time (1965-1991).

The authors found that the prevalence of overweight/obesity had increased by more than 50% between generations and that parental BMI was strongly associated with offspring BMI.

But perhaps more interestingly, full-time maternal employment turned out to be positively associated with offspring BMI in childhood with an increase of 0.4-0.5 units in kids with working moms. This relationship was in fact stronger in the offspring than in the original cohort.

Maternal employment was found to have increased by more than 30% across generations, as a result of which, the population attributable risk maternal employment increased from 3.1% to 7.8% across generations.

In addition, the authors noted that smaller family size and fewer younger siblings were also associated with increased childhood BMI.

As argued by Elizabeth Warren and Amelia Warren Tyagi in their bestseller “The Two Income Trap: Why Middle-Class Mothers and Fathers Are Going Broke“, even if all kinds of issues may be linked to working moms, simply asking moms to stay at home is neither feasible nor socially desirable (incidentally, both authors are working moms).

Rather, other measures, including proper and affordable day care, accessible and supervised after-school activities and more flexibility in working hours may help moms (and dads) better meet the demands of their kids, thereby hopefully reducing their risk for obesity.

I wonder what my readers think of this hypothesis and what (if anything) can (should) be done about it.

AMS
Edmonton, Alberta

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de Moira AP, Power C, & Li L (2010). Changing Influences on Childhood Obesity: A Study of 2 Generations of the 1958 British Birth Cohort. American journal of epidemiology PMID: 20488872