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Solving the Childhood Obesity Puzzle, One Piece at a Time

Fighting Fat: SSW profs focus on roles of maternal employment, abuse

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In part three of a four-part series on the nation’s obesity epidemic, BU Today spotlights the innovative research taking place at BU to better understand and solve this health problem.

The statistics on childhood obesity are grim. In 1974, only about 5 percent of American children were obese. Today that number is 16.9 percent. If you include kids who are overweight as well, the number reaches 31 percent. Children who are overweight or obese often have a host of health problems, from type 2 diabetes and asthma to high blood pressure and depression. They are also more likely to be overweight as adults. But the scariest thing of all is that nobody knows what has caused the epidemic or how to reverse the trend.

Daniel Miller, a School of Social Work assistant professor, has spent his career trying to figure that out. There are plenty of places to point the finger: too many video games and television, not enough school recess, ads for sugary cereals that target kids, high-fructose corn syrup, and super-sized fries. But none of these things can be the sole culprit. Complex problems like childhood obesity have no easy cause and no easy solution. “I think that we get into trouble when we try to default into simple explanations about what’s causing a very complicated thing,” says Miller. “It’s a lot of stuff together.”

Miller, a policy analyst, pores over huge sets of data, looking at different pieces of the obesity puzzle and trying to get a sense of the whole picture. He doesn’t have any answers—yet. But his long-term goal is to construct what he calls the “social ecology” of child obesity, putting the whole puzzle together and helping to influence policies that can change it.

His first foray into obesity began during his doctoral research on working mothers and how their employment may affect their families’ health. (Fathers’ employment seems to have little effect on child obesity, by the way.) “We know obesity has increased over time. What else has increased over time? Maternal employment,” says Miller. Other studies had suggested that the two trends were connected. He decided to investigate.

To do so, he crunched data from the National Longitudinal Survey of Youth, which is run by the Bureau of Labor Statistics, examining data on working mothers. Miller’s results were intriguing, but not straightforward. He found that children were more likely to be overweight at ages 9 to 11 and 12 to 14 when their mothers worked. But mom working when the kids were younger—ages six to eight—led to a decreased risk for obesity. In another study, which Miller coauthored with Wen-Jui Han of New York University, he found that children whose mothers worked either a few years or many years at nonstandard shifts were more likely to be overweight or obese at age 13 to 14. What’s going on? Miller isn’t sure, but he suspects that when a mother is working, younger children are being closely monitored by someone. Older kids, however, are more likely to be home alone, munching chips in front of the TV.

Boston University BU, Daniel Miller research, childhood obesity, socioeconomic contributors obesity epidemic trend, Social Work, Boston Medical Center BMC

Miller pores over huge sets of data, looking at different pieces of the obesity puzzle and trying to get a sense of the whole picture. Photo by Michael Malyszko

Other factors are at play, Miller adds, and they probably come down to choice, especially when it comes to shift work. If a mother works odd hours so she can make breakfast and walk the children to school, that’s an advantage for the kids. But if a mother has to work a poorly paid, stressful, or exhausting night shift, she may not have the time or energy to cook healthy meals or take the kids to the park.

Miller is quick to point out that his work is not about blaming working mothers for childhood obesity. “It’s not that working moms say, ‘Okay, now I’ve finished up my work. I’m going to make all these unhealthy choices for my family,’” he says. “It’s just that the way that our society is structured, it doesn’t support the working activities of mothers.”

And, he adds, even today, the brunt of housework and child care still falls to mothers.

“We’re not exactly clear about the story of how maternal employment gets to child obesity,” Miller says, but “it’s pretty clear that it has something to do with what happens at home.” He points out that it’s usually—although not always—moms who set the rules at home when it comes to meals, screen time, and eating behavior. “We’re still stuck in this relic of older, familiar patterns,” he says. “It persists today.”

Miller’s latest work, conducted with Sunny Shin, another SSW assistant professor, moves away from working mothers to focus on another question: whether physical abuse, sexual abuse, or neglect may lead to childhood obesity.

Shin and Miller examined data from the National Longitudinal Study of Adolescent Health (AddHealth), which collected data from 8,471 children and parents at four points in their lives. They found that kids who were abused or neglected were more likely to have higher body mass indexes as adolescents. This wasn’t particularly surprising, but as Miller notes, the results could have easily pointed the other way. “If a child is abused or neglected, they could have an eating disorder, not be fed correctly, or be malnourished,” he says.

But not all the trends were clear. “There was one thing that surprised me a lot,” says Shin. “We looked at all different combinations of different types of abuse. We expected that kids who had experienced all three things—physical abuse, sexual abuse, and neglect—would develop obesity, but that was not the case.” In other words, the most abused and neglected kids were the least likely to be overweight.

One explanation, says Shin, is that the chronically abused, extremely high-risk children got a lot of attention from child protective services very early on, and this intervention helped save them from some of the long-term effects of abuse. “Maybe the system is working, in some way,” she says.

This research on abuse and neglect is leading Miller to think about how the body responds to stress, and whether that may play a role in obesity. “Kids that are maltreated are exposed to tremendous duress and stress,” he notes. “And there’s very clear findings from the literature that stress is awful for you…it can harm your body.” Miller suspects prolonged stress may lead to biological and behavioral changes that promote obesity. So far, he says, there’s little data to back up the idea, so the area is ripe for study.

Where will Miller’s work lead? Hopefully, he says, to comprehensive policies that can fight childhood obesity from multiple angles. In the end, any new policies to tackle obesity will have to be coordinated and comprehensive in order to succeed, he says, and will have to account for the way a child’s environment affects both biology and behavior. “That’s the way that has to be framed,” Miller says. “It’s not that you’re making bad choices. It’s just that your choices are constrained by an environment that doesn’t allow you to make good choices all the time.”

It’s not an easy answer. But in the end, it may be the only answer that works.

Next, in part three of our series, “The Cure for Obesity: Fat?” Read the entire series here.

Barbara Moran (COM’96) is a science writer in Brookline, Mass. She can be reached through her website, WrittenByBarbaraMoran.com.

6 Comments

6 Comments on Solving the Childhood Obesity Puzzle, One Piece at a Time

  • Vika Zafrin on 11.27.2012 at 9:42 am

    I’m surprised that there’s no mention of the economic factor. There is a correlation between shift work — especially in “nonstandard” shifts — and the ability to afford “healthier” (more balanced) foods. Both nonstandard shifts and obesity are common markers of poverty, or living close to poverty.

    Yeah, maternal employment has increased over time — in part because single-income households have become increasingly unsustainable. One of the tragedies of the current economic disparity is the direct effect of food prices, driven by subsidies and mass production, on deepening this disparity by adversely affecting the health of poor(er) people.

    I am certain that Miller and his fellow researchers are looking into this. (I mean… right?) I’m disappointed that the article doesn’t discuss it at all.

  • Pam Peeke, MD on 11.27.2012 at 6:08 pm

    There is actually a great deal of sound science on the role stress plays in obesity. Stress is a clinically proven cause of both weight gain and overeating. Worse, brand-new research shows direct evidence of lasting and fundamental injuries to a part of the brain that helps us regulate our food intake. Within three days of being placed on a high-fat diet, a rat’s hypothalamus shows increased inflammation; within a week, researchers see evidence of permanent scarring and neuron injury in an area of the brain crucial for weight control. Brain scans of obese men and women show this exact pattern as well.

    A mouse’s body mass, brain and lifespan are obviously different from a human’s but we can infer that it takes relatively little exposure to hyperpalatable foods to create an addiction.

    Feeding children processed foods sets them up for increased addiction (including video gaming) and disease risks. One study found that when 3-year-olds ate a high fat/high sugar diet of predominantly processed foods, their IQs were lower at age 8 — regardless of whether their diet had changed in the interim. Think about how much processed food we feed our kids — ketchup alone has 4 grams of sugar per teaspoon! Limiting time with media and sending the kids out to play not only gets them amping up those good dopamine neurotransmitters that aid in learning, memory, attention, motivation and reward, it gets them away from food and hungry enough to eat the whole foods they need.

  • Darliene Howell on 11.28.2012 at 12:07 am

    I would like to recommend the free NAAFA Child Advocacy ToolkitSM (CATK) to assist you looking at programs. The total health of our nation’s children is a serious responsibility.

    The NAAFA Child Advocacy Toolkit shows how Health At Every Size® takes the focus off weight and directs it to healthful eating and enjoyable movement. It addresses bullying, building positive self-image and eliminating stigmatization of large children. Additionally, the CATK lists resources available to parents and educators or caregivers for educational materials, curriculum and programming that is beneficial for all children. It can be found at:
    http://issuu.com/naafa/docs/naafa_childadvocacy2011combined_v04?viewMode=magazine&mode=embed

  • Anthony Priestas on 05.30.2013 at 1:27 pm

    “…nobody knows what has caused the epidemic or how to reverse the trend. But his long-term goal is to construct what he calls the “social ecology” of child obesity.”

    Obesity is a disorder of excess fat accumulation, driven by the hormonal state of one’s body. The hormone chiefly responsible for the regulation of fat tissue is insulin. The macronutrient that increases insulin to highest levels and longest duration is carbohydrate (especially refined sugar and flour). Since the normal blood sugar level of an adult is about 1 teaspoon for the entire blood volume, spikes in blood sugar level is met with an appropriate insulin response to bring it down (recall that chronically high blood sugar destroys tissue and organs – i.e., Type I diabetes). However, if insulin levels are always elevated due to continuous consumption of carbohydrate (250 – 350 g per day, or what the USDA calls “normal”) then over time, cells become resistant to the effects of insulin resulting in what was once thought as a paradox – chronically elevated sugar levels simultaneous with high insulin levels – i.e., Type II diabetes. The notion of calories in, calories out doesn’t address the issue of calories stored, which requires an understanding of biochemical pathways, and the relative roles of insulin and leptin. Just like starvation or semi-starvation will result in weight loss, it doesn’t address the root cause. This is a problem fundamentally rooted in biology, not environmental factors or “social ecology.”

    “In another study, which Miller coauthored with Wen-Jui Han of New York University, he found that children whose mothers worked either a few years or many years at nonstandard shifts were more likely to be overweight or obese at age 13 to 14. What’s going on? Miller isn’t sure, but he suspects that when a mother is working, younger children are being closely monitored by someone. Older kids, however, are more likely to be home alone, munching chips in front of the TV.”

    This is what is known in the scientific world as “confounders” which confuses associations with cause and effect. It is also the reason why epidemiological studies often lead to incorrect assumptions about cause and effect (red meat causes lower life expectancy), or contradictions between various studies.

    “Miller suspects prolonged stress may lead to biological and behavioral changes that promote obesity. So far, he says, there’s little data to back up the idea, so the area is ripe for study.”

    That’s a huge understatement.

    From the above comments:

    “I’m surprised that there’s no mention of the economic factor.”

    Same as above, the economic issue only confounds the fundamental – and biological – mechanisms driving obesity. This does, however, have some merit as to the ubiquitous availability of cheap foods, and they consist of mind-numbing quantities of carbohydrates, partially driven by agribusiness subsidies. But that only means people who are poorer are more likely to consume carb-rich foods (what college student doesn’t live off of pasta, ramen noodles, chips and soda, etc.). People would quickly make different food choices if they associated carbs with poor health, as the government and health agencies have done with fat.

    “One study found that when 3-year-olds ate a high fat/high sugar diet of predominantly processed foods, their IQs were lower at age 8.”

    This, again, is a confounder. Is it the sugar or the fat? 100 years ago, the average person consumed about 10 lbs of sugar per year. Today, that number is closer to 120+ lbs per person per year. Meanwhile, since the 1970’s, people have reduced their fat intake (spawning a market response by offering low-fat, but high carb foods) from 40% to ~34% of calories, serum cholesterol levels have fallen as a population, people are terrified of salt, there are more gyms than Starbucks, and overall people are generally more “health conscious” than ever before, yet obesity (and the related “diseases of modern civilization”) are greater than ever before. Yeah, the food pyramid, and the shotty science it’s based on, has done incalculable harm.

    Gary Taubes, in his book Good Calories, Bad Calories, summarizes his digging into 100 years worth of research as a list of “inescapable conclusions”:

    Taubes’s “inescapable” conclusions (p.454):

    1)Dietary fat, whether saturated or not, is not a cause of obesity, heart disease or any other chronic disease of civilization.

    2) The problem is the carbohydrates in the diet, their effect on insulin secretion, and thus the hormonal regulation of homeostasis—the entire harmonic ensemble of the human body. The more easily digestible and refined the carbohydrates, the greater the effect on your health, weight and well-being.

    3) Sugars—sucrose and high-fructose corn syrup specifically—are particularly harmful, probably because the combination of fructose and glucose simultaneously elevates insulin levels while overloading the liver with carbohydrates.

    4) Through their direct effect on insulin and blood sugar, refined carbohydrates, starches and sugars are the dietary cause of coronary heart disease and diabetes. They are most likely dietary causes of cancer, Alzheimer’s disease, and the other chronic diseases of civilization.

    5) Obesity is a disorder of excess fat accumulation, not overeating, and not sedentary behavior.

    6) Consuming excess calories does not cause us to grow fatter, any more than it causes a child to grow taller. Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger.

    7) Fattening and obesity are caused by an imbalance—a disequilibrium—in the hormonal regulation of adipose tissue and fat metabolism. Fat synthesis and storage exceed the mobilization of fat from the adipose tissue and its subsequent oxidation. We become leaner when the hormonal regulation of fat tissue reverses this balance.

    8) Insulin is the primary regulator of fat storage. When insulin levels are elevated—either chronically or after a meal—we accumulate fat in our fat tissue. When insulin levels fall, we release fat from our fat tissue and use it for fuel.

    9) By stimulating insulin secretion, carbohydrates make us fat and ultimately cause obesity. The fewer carbohydrates we consume, the leaner we will be.

    10) By driving fat accumulation, carbohydrates also increase hunger and decrease the amount of energy we expend in metabolism and physical activity.

  • Anthony Priestas on 05.30.2013 at 1:38 pm

    P.S.

    What A Degree In Dietetics DIDN’T Teach [this dietician] About Saturated Fat:
    http://www.dietriffic.com/2012/05/16/saturated-fat-good-or-bad/

  • sir john on 10.22.2013 at 3:08 am

    Very important issue you have talked about. I like your writing.

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