Lord of the Fats —
“Save the fat kids!” has become the rallying cry of anti-obesity activists. Perhaps sensing that most full-grown adults with a functioning right parietal cortex get noticeably testy when others try to make decisions for them, advocates have decided that hyper-focusing on the fat kids is the way to go.
Aside from pointing at the fattest of the fat children, these well-meaning (if misguided) do-gooders will inevitably cite the rise of type 2 diabetes as proof that we have to intervene on their behalf.
Except there’s one problem: type 2 diabetes is hardly the greatest health threat facing children today, as just 12 in 100,000 children develop type 2 diabetes, while 2,700 in 100,000 suffer from an eating disorder.
But diabetes isn’t the only arrow in the concern troll’s quiver.
For years, headlines have warned us that girls are going through puberty at an earlier and earlier age, and the cause is clear.
Experts have no trouble explaining the link:
Speaking at the Cheltenham Science Festival this week, Professor Richard Sharpe, an expert in early puberty at the Medical Research Council, underlined the clear link between obesity and young girls reaching puberty as early as five years old.
When a child’s fat tissue level reaches a certain point, a hormone signal is sent to the brain instructing puberty to begin, Professor Sharpe explains to Huffpost Lifestyle.
And yet Dr. Sharpe, as well as experts quoted in the articles listed above, goes on to cite multiple contributors to the shift in early puberty onset:
Professor Sharpe adds: “The only point we’re trying to emphasise is that obesity is the one modifiable known factor that we can do something about.
Ah, so the reason they’ve been emphasizing obesity isn’t that obesity is the most important cause, but that it’s the one thing that Sharpe and his colleagues believe is controllable. Since families can prevent their kids from getting fat, they should also be able to prevent their kids from entering puberty sooner.
Then Sharpe goes on to cite other potential causes:
Professor Sharpe also suggested environmental factors and social factors, such as family breakdown, could also be ‘puberty accelerators’ — but their influence was far harder to determine.
“Social factors might trigger a stress response that could alter hormone levels in young girls. But you can’t investigate these delicate subjects with any great ease, so they’re difficult to tie down. “
The logic behind this boggles my mind. First off, obesity is emphasized because it’s “modifiable,” yet family breakdown is not? The message seems to be that families should do everything they can to keep their kids thin to prevent the early onset of puberty. But maintaining a cohesive family unit? Not possible.
But what’s even more intriguing is that stress is a significant cause of weight gain, which brings us to a gaping flaw in this argument. If stress is less modifiable than obesity, but stress contributes to obesity, then what is truly modifiable and what is a consequence of societal factors?
An ABC News article brings this confusing relationship into sharper relief:
The breakdown of the family unit may cause a domino effect in young girls, which can prompt overeating, obesity and potential early puberty, according to a scientific meeting intended to review a myriad of studies based on girls and puberty.
And yet, the study that launched this and a thousand other articles decrying obese puberty is hardly definitive. The ABC News segment attached to the article informs us that “The girls in this study are not representative of the general population. In some cases, were selected because they had existing risk factors for early puberty.”
But by all means, don’t let the preliminary nature of this study hold you back from railing against fat girls.
Interestingly, ABC actually cites two potential causes for early puberty. Dr. Joyce Lee, Pediatric Endocrinologist at the University of Michigan, told ABC, “We’ve done studies to show that heavier girls do have earlier onset of puberty, but the other issue that’s of growing concern is chemicals that are found in every day household products.”
Man-made chemicals have also been implicated in obesity, with endocrine disruptors being eyed as a contributor to childhood obesity rates. One of the primary endocrine disruptors said to contribute to obesity, phthalates, has also been implicated in early onset of puberty, according to the Mount Sinai School of Medicine.
And yet society largely ignores the effects of endocrine disruptors, according to a recent article by Nick Kristoff in the New York Times:
Last month, the Endocrine Society, the leading association of hormone experts, scolded the Food and Drug Administration for its failure to ban bisphenol-A, a common endocrine disruptor known as BPA, from food packaging. Last year, eight medical organizations representing genetics, gynecology, urology and other fields made a joint call in Science magazine for tighter regulation of endocrine disruptors.
Instead of taking a long, hard look at the environmental factors that contribute to this chemical soup that we’re all swimming in, most journalists prefer the “sexier” stories of how fatness is triggering early puberty in girls.
But when it comes to boys, the problem is the exact opposite, according to MSNBC:
Puberty for boys typically begins about age 10, but for those at the top of the body mass index charts, the earliest changes of puberty may not begin until age 11 and a half or later, according to the University of Michigan in Ann Arbor study of 401 boys. Researchers followed them from age 2 to 11 and a half.
If fat girls are cursed with early puberty, then fat boys are cursed with estrogen-induced late puberty, according to the headlines:
Momentarily setting aside the validity of the study itself, the headlines for boys and girls both include a dog whistle that crops up frequently in anti-obesity circles. In short, fat girls are at risk for being slutty and fat boys are at risk for being effeminate.
Returning to the validity of the underlying research, the authors admit that comparatively few studies have actually looked the relationship between obesity and boys, rather than girls. Even so, their results aren’t terribly alarming:
The report, just published in the Archives of Pediatrics and Adolescent Medicine, found about 14 percent of the heaviest boys studied showed no changes by age 11 and a half, compared to 8 percent of those who had the lowest BMI. By that age, most girls are well into puberty.
A vital bit of information has been left out, though. Boys who were average weight, halfway between the heaviest and lightest boys, included 13% who hadn’t gone through puberty by that age. But we can’t let a little thing like that stand in the way of a powerful headline narrative, can we? Especially when some of those previous studies contradict this one, according to MSNBC:
While the new study contradicts previous research on male adolescence, which suggested boys, like girls, are entering puberty earlier, scientists do agree that obesity seems to be affecting how youngsters are developing.
The culprit? The feminizing of fat boys:
Theories on what might cause late puberty in overweight boys center on hormones produced in fat cells. Obese males have higher levels of estradiol, a relative of estrogen that may interfere with the male hormone androgen.
And yet, for all the estrogen surging through our country’s fat boys, more recent studies have confirmed that boys, like girls, are going through puberty at a younger and younger age, according to CNN:
In the study, lead author Marcia Herman-Giddens from the University of North Carolina’s School of Public Health and her colleagues show that boys are starting to sexually develop six months to two years earlier than medical textbooks say is standard.
But this makes no sense. If puberty in girls is advancing due to hormonal changes caused by obesity, then puberty in boys should be delayed for the same reason, right?
Well… sort of:
“The changes are too fast,” Herman-Giddes said. “Genetics take maybe hundreds, thousands of years. You have to look at something in the environment. That would include everything from (a lack of) exercise to junk food to TV to chemicals.”
Once again, both obesity and chemicals are implicated in the phenomenon. You see, it may not be the fat tissue that is speeding up puberty in boys, but the gluttony and sloth of fat boys that is responsible.
And yet, studies have found that candy consumption is inversely associated with obesity, according to CBS News:
For the study, published in Food & Nutrition Research, researchers at Louisiana State University tracked the health of more than 11,000 youngsters between the ages of two and 18 from 1999 to 2004. They found that children who ate sweets were 22 percent less likely to be overweight or obese than kids who shunned sweets. Adolescents? Those who ate candy were 26 percent less likely to be overweight or obese than their non-candy-eating counterparts.
But… but… but… fat kids are stuffing their faces with candy! I seen it!
Hold your disbelief, there’s more:
And that wasn’t the only surprising finding. Researchers also found that the blood of candy-eating kids had lower levels of C-reactive protein. That’s a marker of inflammation in the body and a risk factor for cardiovascular disease and other chronic illnesses.
Interestingly, C-reactive protein (CRP) is also a marker for leptin (the hormone that tells your body when to stop eating). Many fat people are leptin resistant, so they aren’t able to register the signal that they got all the energy they needed, and may eat more than is biologically necessary. But research suggests that leptin resistance may be caused, at least in part, by CRP binding to leptin and preventing our bodies from recognizing that signal.
But what’s even more interesting (yeah, that’s right, this post is just a nonstop trip through Interestingville) is that sugar cravings may be related to developmental necessity, according to NPR:
A reason for this may be that a preference for sweet, caloric substances during rapid growth may have given children as an evolutionary advantage when calories were scarce. That notion is supported by the fact that sugar doesn’t just taste good to children — it actually makes them feel good, too.
The preference for sweet foods seems linked to physical growth:
What they found was that kids who were still growing preferred sweets. Those whose growth had already stopped — around age 15 or 16 — had taste preferences similar to adults.
The research team behind this study have presented a fascinating theory:
Exactly how this all works is still somewhat of a mystery, but Coldwell says that one important clue lies in the discovery that growing bones actually secrete hormones that can influence metabolism. Other well-known metabolic hormones like leptin and insulin have been shown to act on brain areas that control cravings and appetites, and even directly bind to the tongue, where they affect the preference for sweet tastes. Coldwell suspects that hormones from growing bones may be doing the same thing. In other words, it’s not your kid’s fault he raided the cookie jar – the hormones from his growing bones made him do it.
And yet the cliché of the candy-crazed fat kid lives on, in spite of the fact that research dating back to 1959 (PDF) has shown that fat kids actually eat fewer calories than thin kids and expend just as many calories playing (although obese kids have a slightly higher preference for sedentary activities).
And yet the myth of the gluttonous fat boy eating his way to type 2 diabetes and delayed puberty persists. Even though every article on the relationship between puberty and weight saves space at the bottom to identify additional contributors. What makes for sensational headlines is the out-of-control fatties and their insatiable appetite for self-destruction.
It’s because of this over-zealous, and unfounded, “Save the fat kids!” culture that we allow Strong4Life and other terrible childhood obesity efforts to thrive. Perhaps if we as a society took a step back and looked at the entire picture, we might not be so bold as to wage war on fat kids.