Category Archives: Obesity

What “The Hardy Boys” taught me about childhood obesity

Frank, Joe and Chet (with big clue!)

Frank, Joe and Chet (with big clue!) 1927

When my son John was in third grade he briefly glommed on to my collection of old Hardy Boys story books. We’d read them together at bedtime as I tried to instill in John a love for the Boys, their pals (“chums,” to be precise) and their ancient (to him) adventures. Alas, Harry Potter soon distracted him and the Hardy Boys went back to gathering dust.

For those of you too young to remember (or too Nancy Drew-ish in your literary tastes to care), The Hardy Boys was a 58-book series that ran from 1927 to 1979, coinciding with the sweet spot of my 1950s and ’60s childhood. (The success of the books also spawned a black-and-white Disney TV serial in the ’50s, a Saturday morning cartoon from 1969-71, and the truly awful Hardy Boys/Nancy Drew Mysteries, which ran from 1977-79.)* Long story short, The Hardy Boys books described the sleuthing adventures of Frank and Joe Hardy, sons of the famous private investigator Fenton Hardy, in sometimes excruciating prose.

Frank and Joe evolved over the books and years from cynical, in-it-for-the-money 1920s teenagers to paragons of 1950s authority-respecting American youth. A Hardy sidekick, Chet Morton, evolved in somewhat different fashion, which brings me to today’s topic: Parents of overweight and obese kids are getting really bad at telling that their kids have a weight problem. 

Chet was the clumsy, jalopy-driving foil to Frank and Joe’s buff manliness. In the very first book, “The Tower Treasure,” Chet is described thusly: “He was a plump boy who loved to eat and was rarely without an apple or a pocket of cookies.”** This puzzled John, who looked at the accompanying drawing and said, “Why do they call him plump? He looks pretty skinny to me.” He had a point. As you can see, Chet may have had a roundish face and a bit of fullness to his arms, but his waistline and legs are as skinny as Frank and Joe’s. “I guess that was considered fat back in those days,” I explained to John with a shrug. Then I looked it up and found that only about 2% of children were obese in the 1930s. By the time we were reading this in ~ 1999, about 15% of children were obese. By 2012, 21% of American teens were obese. It was true: back in the 1930s, an artistic bit of a double chin or a pinch of chub at the belt line was all it took to portray a kid who liked to keep his pockets lined with cookies.

Chet Morton, aka

Chet Morton, aka “Chubby,” 1971

Chet’s evolution over time says a lot about how we perceive child obesity. As time went on and obesity rates rose, his Jazz Era chubbiness wasn’t enough. Chet got fleshier. By the time the late ’60s cartoon appeared, Chet (renamed “Chubby,” in case kids zoned out on Sugar Smacks didn’t get the point) had taken on a doughy, full-figured form that signaled to contemporary viewers that Chet was, well, chubby. Today, when more than 1/3 of adults are considered to be obese, it’s getting harder to send that signal: portrayals of characters as truly “fat” have kind of gone over the top, and they’re usually pretty cruel.

A new study in the journal Child Obesity shows how society’s idea of “normal” weight has changed since the Depression. In a survey of parents of 2-5 year-olds, 94.9% of parents whose child was in the “overweight” category, and 78.4% of those who were frankly obese said that their child’s weight was “just about right.” As our kids get heavier, our “parent goggles” simply adjust. In a strange corollary, I talk to parents all the time who worry that their average-build kids are too skinny.

The sorta-good news? Parents’ mis-perception of their overweight children actually improved somewhat from a similar study done 20 years earlier.

Given all that, I wonder how Mr. and Mrs. Morton viewed their cookie-pocketed boy who got steadily heavier over the years but, strangely, never aged? Alas, in 58 books, they never said a word…

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* Shaun Cassidy as Joe Hardy?? Spare me…

Joe Hardy? Looks more like Justin Bieber...

Joe Hardy? Looks more like Justin Bieber…

** Chet was also described at various times as “big boy,” fat, plump, chubby, stout, heavy-set, chunky, “the chubby one,” portly and round. (“Portly” was my favorite.)

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Cesareans and chronic childhood disease: Time for a public discussion

From the Ishinhō, Japanese medical text, 1860

From the Ishinhō, Japanese medical text, 1860

In an analysis published in the most recent edition of The BMJ, Drs. Jan Blustein and Jianming Liu examine the evidence that cesarean delivery is associated with an increased risk of chronic childhood diseases like asthma, type 1 diabetes, and obesity. Their conclusion: the bulk of the evidence suggests that the association is real.

The time has come, Blustein and Liu write, for maternity care providers to include the risk of chronic childhood disease in their discussions with women considering a “non-essential” cesarean, such as when the choice is between a VBAC or repeat cesarean, or in the case of a woman choosing a medically unneccessary cesarean in lieu of vaginal birth—the so-called “maternal request” cesarean.

This topic has intrigued me for some time now. As part of my recently completed MPH program at the University of Minnesota, I wrote a paper titled, “Do Cesarean Sections Increase the Risk of Child Asthma? A Systematic Literature Review.”

In writing the paper I read and analyzed every research study on the subject since 2001. Roughly two-thirds of those studies detected a small-to-moderate association between cesarean birth and childhood asthma. (In fact, 90% of the studies detected an association between the two, but not all were statistically significant.) Most of the studies that didn’t find the association were seriously flawed—too few subjects, for example, or ignoring possible confounders, like prematurity or a history of maternal asthma. Three meta-analyses (two in 2008, one in 2014) all reached similar conclusions: cesarean section is associated with about a 20% increase in the risk of child asthma.

My paper was limited to asthma, but as described in the BMJ analysis there’s evidence that cesareans increase the risk of other chronic childhood illnesses, too–type 1 diabetes and obesity. A 2015 study by Sevelsted et. al. analyzed a cohort of two million Danish children and found small-to-moderately increased risks of juvenile rheumatoid arthitis, connective tissue disorders, inflammatory bowel diseases, immune deficiencies, and even leukemia.

Given that body of evidence, you’d think that organizations like ACOG (the American Congress of Obstetricians and Gynecologists) and the U.K.’s National Institute for Health and Care Excellence would be pushing their members to share this information with their pregnant patients. But they’re not. According to Blustein and Liu,

“…knowledge about chronic disease risks could affect decision making in non-essential caesarean. The American College of Obstetrics and Gynecology and the UK’s National Institute for Health and Care Excellence recently issued consensus statements on caesarean delivery at maternal request. Based on evidence about maternal and perinatal outcomes, both groups concluded that a pregnant woman requesting caesarean should have that choice, if she still desires it after discussion of the risks and benefits of the procedure. Importantly, neither group acknowledged the long term risk of chronic disease. [Emphasis mine.]

Critics can (and do) point to the uneven quality and designs of the studies that support such links—it’s association versus causation all over again—but that’s not entirely fair. To prove beyond doubt that cesarean birth increases the risk of child asthma, you’d have to do trials where women are randomly assigned to cesarean or vaginal birth…which, as you can imagine, is a practical and ethical non-starter. That leaves us with observational studies, which can only point out that two things seem to be related, not that they definitely are.

Ah, but there has been a randomized study of the long-term effects of cesareans versus vaginal birth in term, breech deliveries, and at least one research team has made the case that randomized trials of mode of delivery aren’t really unethical. More on those topics soon.

Finally, just to re-re-reiterate: I’m not anti-cesarean. My wife and son are alive and well today thanks to a medically necessary cesarean. But the cesarean rate today is 6 times higher than it was when I was a junior in high school (1970, if you must know…). As Blustein and Liu point out in their analysis:

“We live in a world where caesarean rates cannot be explained by compelling medical indications.”

Perhaps increased awareness of the potentially negative impact of cesareans on child health will help reverse that decades-long trend.

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Filed under Asthma, Cesareans, Diabetes, Obesity, VBAC

Is it the cesarean, or the absence of labor?

Stem cells, pondering the future

Stem cells, pondering the future

I’ve written a fair amount about the association between cesarean birth and the increased risk of immune-related diseases like asthma, diabetes, celiac disease, and even obesity. Most of the research out there has focused on the newborn gut microbiota—the collection of bacteria that colonize a baby’s intestines at birth and play a key role in the development of the immune system. These bacteria are primarily acquired from the mother’s birth canal and rectum during a vaginal birth, but for cesarean-born babies those “pioneer” bacteria are often derived from the hospital environment. Such “wrong” bacteria in the bowel early on can lead to inflammation and, the theories go, to immune-related diseases later in life.

But is the cesarean per se at the root of all this? Or might the absence of labor (or an incomplete labor) have something to do with it? Childbirth is, after all, a fabulously complicated dance of maternal and fetal hormones, anti-oxidants, and other chemicals that are known to influence the immune system. What happens to the newborn’s immune system development when that dance is cut short, or never starts in the first place?

A study from Sweden’s Karolinska Institutet published in the current issue of the American Journal of Obstetrics and Gynecology has me wondering about the “absent-labor” scenario again. The study’s authors compared cord blood samples from babies born by elective cesarean section (ECS) with those who were vaginally born (VB). They looked specifically at hematopoietic stem cells—the precursor cells that go on to become, among other things, the white blood cells that play a critical role in the human immune system.

Here’s what they found: the DNA in stem cells from ECS babies was significantly different from that of the VB babies, particularly in an area devoted to production of antibodies. The study’s genetic analysis is way above my pay grade, but boiled down to the essentials, the differences are all about epigenetics, which is defined as:

 “…the study of changes in gene function that are mitotically and/or meiotically heritable and that do not entail a change in DNA sequence.”

Ouch!

Plain English version (mine): Epigenetics is the study of how genes are turned on and off, typically by the addition of methyl groups (ouch, again!) to genes. The timing of all this light-switch-like activity, and the potential for permanent change, has big-time implications for health throughout life.

The Swedish researchers found that stem cell DNA methylation (the addition of methyl groups to genes) increased steadily with the duration of labor. So one could conclude, couldn’t one, that normal labor plays an important role in preparing future white blood cells for their task, and, ergo, the absence of labor is why everyone’s so chubby these days? Sure, one could conclude that…but one would be jumping the gun, big time.

Hold that smokin' gun, pardner!

Hold that smokin’ gun, pardner!

Why? Because this was a small, observational study—the kind of study designed to make readers sit up and take notice (Hmm…that’s interesting!”) but that requires much more research before any guns start smoking. The small numbers of subjects in this study makes it easier for error to creep in, for example, and there were significant differences between the mothers as well—the ECS group was significantly older than the VB group, and their babies were born an average of a week and a half earlier, factors which might cause their own epigenetic effects.

It’s going to take much larger studies to see if these findings are in fact true, and if so to tease out how significant such cesarean-related epigenetic changes may be in the grand scheme of childhood immune system diseases. A lot of vaginally born kids end up asthma, after all. Including me.

But still, how fascinating! I’m looking forward to reading more about this.

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Photos courtesy Joseph Elsbernd, Jim Sher

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Filed under Asthma, Cesareans, Gut microbiota, Natural childbirth, Obesity

Starvation and the infant gut

Even worse for babies...

Even worse for babies…

The gut microbiota—the collection of trillions of bacteria that populate the bowel in humans—goes through somewhat predictable developmental stages in infancy and early childhood. Some types of bacteria dominate right after birth, while others increase in number as the diet changes from milk to solid foods over the course of the first two years of life. The final profile is largely set by about age 3—what you’ve got in your gut at that point is basically what you’ll have into adulthood.

Many factors can affect the final profile—I’ve written about cesarean birth, antibiotic use, and the typical high-calorie, high-fat western diet as likely culprits. As you might suspect, these are problems of affluence. We can debate the effects of too many cesareans, too much antibiotics, and too many calories, but in developing countries there’s another potent shaper of the developing gut microbiota in childhood: starvation.

A recent study performed by Washington University in St. Louis and the International Center for Diarrheal Disease Research in Dhaka, Bangladesh, showed that children with severe acute malnutrition (SAM) have immature gut microbiota profiles—the types of bacteria in the bowel didn’t change over time as would be expected in well-nourished infants and children.

The study followed Bangladeshi infants and toddlers with SAM over the course of acute treatment and for several months afterwards. The malnourished children did gain weight rapidly with very high-calorie diets, but they were unable to achieve or maintain a normal weight once the treatment ended and they switched to a more typical diet. Signficantly, their gut microbiota remained immature—the bacteria present in the gut both before and after treatment were woefully inefficient at extracting calories from food.

So now we have evidence that the gut microbiota plays an important role in two very different nutritional diseases: obesity and malnutrition. Future SAM research will be aimed at supplementing probiotic bacteria as well as calories in hopes of promoting healthy, long-lasting changes to the microbiota.

The sooner the better, given the terrible toll malnutrition takes on children in many parts of the world.

Photo courtesy of Chris Turner

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Michelle Obama and “Let’s Move!”

As anyone who watched her speech at the Democratic convention knows, Michelle Obama is an impressive woman. She’s quite sincere in her concern for children, too, as evidenced by her “Let’s Move!” initiative–an admirable, sensible approach to fighting childhood obesity. (If you haven’t visited the “Let’s Move!” website, here’s the link. It’s worth a look.)

“Let’s Move!” isn’t just a public relations stunt. Michelle Obama has had considerable success in changing the national conversation on childhood obesity, such as putting mega-food producers on notice. I’d like to see her be more aggressive on fast food industry shenanigans (marketing to kids and such), but for now she’s no doubt held in check a bit by her First Lady gig. It’s definitely a vast improvement over the efforts of past administrations, though.

It will be interesting to see what her future holds. I’m betting she gets the girls off to college (after a second White House term), then enters the political fray herself, with Barack tending the garden back home… Should be interesting, and good for children.

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Photo by Statsministerens kontor

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Food for thought: Teen brains and obesity

Teen brain + metabolic syndrome = Trouble

A worrisome new study in the journal Pediatrics has found that teens with metabolic syndrome (MetS)* have something in common with adults suffering from the same disease: They, too, can have brain deficiencies and cognitive difficulties.

When a group of 49 New York teens with MetS was compared with 64 normal-weight kids, the MetS teens had lower scores on tests of mental ability, arithmetic, and reading. In addition, MRIs showed that the typical MetS teen had a smaller hippocampus than his or her normal classmates–that’s the part of the brain that deals with memory formation and storage. Such changes in adults had been thought to be the result of long-term metabolic disease; the discovery of similar changes in teens was unexpected, and scary.

Are these changes permanent? Does the brain recover if a teen loses significant weight and reverses his or her metabolic syndrome? No one knows for certain as yet, but this study adds a bit more urgency to the fight against childhood obesity. As Dr. Antonio Convit writes in the study’s conclusion:

“Although obesity [alone] may not be enough to stir clinicians or even parents into action, these results in adolescents strongly argue for an early and comprehensive intervention. We propose that brain function be introduced among the parameters that need to be evaluated when considering early treatment of childhood obesity.”

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Metabolic syndrome is defined by the American Heart Association as the combination of high blood sugar, elevated blood triglycerides, reduced “good” cholesterol, abdominal obesity, and high blood pressure.

Photo by Dierk Schaefer

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Early antibiotics and obesity?

An English study of more than 11,000 children has turned up an association between early antibiotic use (that is, antibiotics given to babies less than 6 months of age) and later obesity.  Interestingly, the study did not find that antibiotics given to children between the ages of 6 and 14 months increased the risk of obesity, and the effect of antibiotics on children aged 15-23 months was inconsistent.

Why would the antibiotic-obesity association be found primarily in younger babies? The authors speculate that an altered gut microbiota may be the culprit.

The germs that make up the gut microbiota (GM) are acquired at birth and shortly afterwards. By a few months of age the “core” GM is more or less set for life. An altered GM has long been associated with obesity in older children and adults (see more extended discussions in my posts here and here)–it would make sense that antibiotics given in this sensitive period of GM development would have greater impact than later on, when the GM is more stable.

The added risk of obesity from early antibiotic administration is small for any individual baby,  the study’s authors stress, but even small increases spread over an entire population can have significant public health implications.

Still, sometimes babies need antibiotics. Studies like this one highlight the unintended (but real) consequences of the overuse of a sometimes life-saving tool.

***(Photo credit: Seattleye)

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Filed under Infectious diseases, Obesity