Popular magazine Psychology Today has reviewed my book Childhood Obesity in America: Biography of an Epidemic in their “This is America” blog. The reviewer, Glenn C. Altschuler, Professor of American Studies at Cornell University, describes the book as “a fascinating survey of popular perceptions and changing attitudes toward diagnosis and treatment” and “filled with thought-provoking insights about changing attitudes toward causes and cures”.” You can read the full review here. Or, you can buy a copy of the book and see for yourself what all the fuss is about…
In 1963, doctors and nurses from the National Centre for Health Statistics set out around the country in specially fitted out Winnebagoes. They were going to take a tape measure to American children’s health. That study—the National Health and Nutrition Examination Survey—is still going today. The survey shows that childhood obesity has steadily risen, more than tripling in the fifty years since those doctors in the 1960s first hit the road with rulers and scales. The increases were even bigger in African American and Hispanic children. But last week researchers from the Centre and from the Public Health Service reported a new development: for the first time since the study began, rates of obesity had dropped in 2- to 5-year-olds. In young children, obesity is still more common than it was back in the 1960s, but is about 40% lower than its peak in the early 2000s. In older children, the inexorable rise over the past fifty years seems to have plateaued and hovers at around 17%. This is cause for cautious—very cautious—optimism.
It has been true for a long time that American kids are big, and have been getting bigger. In 1877, a Boston physician named Henry Bowditch carried out the first significant study of American children’s heights and weights. He had teachers in Boston schools measure their pupils’ heights and weights. With no calculators or computers in the nineteenth century, Bowditch got Beantown’s accountants to crunch the numbers. Even then, American children were larger—taller and especially heavier—than children in Europe. At a time when undernourishment was the major childhood nutritional problem, the fact that American children were big was something to be proud of. Bowditch didn’t consider that there could be “too big”. Tall and heavy, American children were strapping specimens compared with their spindly European peers. The American way of life with its opportunities, its egalitarianism, its freedoms, was being written onto children’s bodies.
Over the next century, American kids kept getting bigger. By the time the National Health and Nutrition Examination Survey was launched, an eleven-year-old boy was about 4 inches taller and 16.5 pounds heavier than a boy of the same age in Bowditch’s time. This process is called “secular change” and is generally attributed to better nutrition and better health and housing allowing children to achieve their genetic potential for growth. The increase in children’s size up to about the 1960s was thought to be a sign of good things. But after about 1970, with children still getting bigger and especially getting heavier more than they were getting than taller, there was a growing sense that a tipping point had been passed. Children were becoming “too big” and bulk brought potential health problems.
The big increase in childhood obesity since the 1960s is also a sign of how the American way of life is still shaping children’s bodies, but in ways that we no longer think are desirable. The childhood obesity epidemic has been implicated with aspects of modern life—car driving, computers, television, working families, unsafe neighborhoods, and cheap, calorie-dense food pushed by massive marketing campaigns. Ironically, some of the major culprits fuelling obesity in adults and children are things that we enjoy and have worked hard to achieve. It’s not that children have changed in any essential way to cause the increases in obesity that the National Health and Nutrition Examination Survey has found, but the American way of life has become steadily more “obesogenic”.
Exactly why in recent years the rate of obesity should have dropped in young children is not entirely clear. But, because the drop has happened in young children, it seems likely that this change is due to families changing their habits. Good job Mom and Dad. This, of course, is much easier to do when children are young. It gets harder once children start school and go out into the world. Spending more time out of the house, kids have to deal with the environment they find there, and that environment seductively encourages obesity. The federal government’s program to address childhood obesity, Let’s Move, has put a lot of emphasis on arming children against this environment. First Lady Michelle Obama is routinely photographed doing yoga with grade-schoolers, or picking beans in the White House vegetable patch. She heads up the charge to get children to resist the lures of their environment and adopt healthy habits from the get go.
Let’s Move is heavy on “encouraging”, “educating” and “empowering” children to take responsibility for their eating and exercise habits. It’s a tough ask. Adults struggle to make good choices in their eating and exercise. All too often convenience, price, and advertising favor bad choices. Asking a kid to deal with all that is even harder. So it’s no surprise that the NCHS data show that obesity has not dropped in older children in the thick of this obesogenic mayhem. Programs like Let’s Move may have helped halt the rise of obesity in older children, but have yet to make inroads on current levels. Actions to tackle the obesogenic environment have been politically harder to implement, but there have been some notable efforts such as selling healthier beverages in school canteens.
With luck, the decline in obesity in 2- to 5-year-olds will stick. If this cohort maintains these lower levels of obesity as they get older, rates of childhood obesity will drop across the board. Let’s Move will have achieved its aim of “solving the challenge of childhood obesity within a generation”. But a generation is a while to wait, and is little use to children now in that 6-19 age bracket, for whom about 1 in 5 are obese. There is more that can be done to make healthy choices the convenient, cheap choices. Children shouldn’t have to be always on the defensive and they shouldn’t have to be tender experts on diet and exercise. These latest results may be the beginnings of change, but the childhood obesity epidemic isn’t history yet.
Interested? Want more? Check out my new book Childhood Obesity In America: Biography of an Epidemic, available from Harvard University Press and Amazon
Aloha, people. The Doctor is in.
An interesting study just published in PLOS Medicine (Public Library of Science) has thrown some intriguing light on the old, old, oooollllllddd question of whether obesity is due to nature – what we would think of today as your genes – or nurture – your environment and how you behave in it.
The vast group of researchers who worked on this research were interested in a particular gene, called the FTO gene. In 2007, a different group of researchers found that there is one allele for this gene (ie. a genetic variant) that about 16% of the population has, and, if you have that particular version of the FTO gene, then you are about 20% more likely to be obese than a person who has a different version of the gene.
That was big news in itself. Ever since the human genome was mapped, medical researchers have been trying to find specific genes that cause all kinds of health problems, obesity included. The first gene that was identified for obesity (the ob gene) was discovered in 1991 from studying an extremely fat breed of mouse – the poor things look like furry softballs with legs – which, because of its genetic make-up was unable to tell when it was full and so just kept eating constantly. Rather like Dr Then’s pet spaniel. [Whoo-hooo! Shout out for Bertie the spaniel!]
Now the ob gene, and the ten others like it which have been found to cause obesity are rare as rare as rare in the general population. Super rare. For example, there are only about five (human) families in the world who have been found to have the ob gene. And they’re weirdly inbred. No kidding. Dr Then likes an inbreeding joke as well as the next person, but in this case those ob families really are inbred. Cousins have been marrying cousins for a good few generations. They’ve probably only got one tooth between them.
So the point is – of those 11 genes that have been found to cause obesity, most are so rare that you’d never ever see them. Not so the FTO allele. That’s COMMON. 16% of the population. That’s like, of the 60 people who have looked at this blog to date, about 9 of them would have the FTO allele putting them at higher risk for obesity than the rest of you guys.
Well, here we are: as at 2007, we’d found the first commonly occurring gene for obesity. But wait on a second. The FTO allele doesn’t CAUSE obesity. It only increases risk of obesity. And what does ‘risk’ mean here? It means that if you got together a really big group of people with the FTO allele and another really big group of people without it, you’d find that about 32% of the people without the gene were obese compared with 38% of the people with the gene. (Big groups of Americans, that is. Other countries would have other (lower) figures, because their population rate of obesity is lower. I’m making life easy for me here with the calculations. Sue me.)
Amazing conclusion No 1:
You are not (necessarily) doomed by your genes. Since we’ve entered the genomic era (post the identification of DNA in 1953), we’ve developed the popular habit of thinking that
genes = FATE
Ok, so that’s true in some cases. (If, for example, you inherit a particular mutation of your Huntingtin gene, you are definitely getting Huntington’s disease. No doubt about it.) But for HEAPS and HEAPS of conditions, just having a gene or a particular version of a gene isn’t enough. Nearly 60 years of genetic research has shown that genetic disorders don’t all have the same ‘penetrance‘ (that’s the technical term, folks.) Some alleles, like the mutation of Huntingtin are completely penetrating (meaning, if you’ve got the allele, you’re getting the disease), while other alleles have a very low penetrance (meaning, you might have the allele, but it’s unlikely you’ll develop any symptoms.)
Why is this the case? We’re getting a bit off point here, people, but expect to be hearing a lot more about gene expression and epigenetics and multiple gene interactions in the next 60 years of gene research.
Anyhooo, to get back to the obesity bit, this common FTO variation has only middling penetrance. You might be genetically more susceptible to obesity if you have the variation, but you’re not doomed to fatness. Your genes may not fit, but your jeans will still fit.
And that latest study of the FTO variation found something even more interesting: people who had the obesity-associated FTO variation and who exercised lowered the risk of being obese. Exercise modified the effect of the gene.
Amazing conclusion No 2:
Behavior modifies gene effects.
Not only do genes not equal fate, but specific actions on your part can affect your susceptibility. Genes, environment and behavior all matter in causing obesity, as they do in so many instances of health.
Good stuff, huh? Well, I’m feeling nicely empowered for a Monday morning. I think I will chose to go and make a cup of tea now. And feed my spaniel.
Till next time, stay well,
Interested? Want more?
Here’s the orginal paper on the FTO gene’s affect on body weight:
Frayling T. M., Timpson N. J., et al. 2007, ‘A Common Variant in the FTO Gene Is Associated with Body Mass Index and Predisposes to Childhood and Adult Obesity’, Science, 316, 889-894. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2646098/
On the ob mouse and the ob gene:
Friedman J. M., Leibel R. L., et al. 1991, ‘Molecular Mapping of the Mouse Ob Mutation’, Genomics, 11, 1054-1062.
Castracane V. D. and Henson M. C. 2006, ‘The Obese (Ob/Ob) Mouse and the Discovery of Leptin’, in Castracane V. D. (ed) Leptin, New York: Springer.
On the latest reckoning of obesity-associated genes:
Rankinen T., Zuberi A., et al. 2006, ‘The Human Obesity Gene Map: The 2005 Update’, Obesity, 14, 529-644.
One of the earliest rigorous studies testing the respective contributions of nature and nurture to obesity:
Garn S. M., Bailey S. M., et al. 1976, ‘Similarities between Parents and Their Adopted Children’, American Journal of Physical Anthropology, 45, 539-543.
The Doctor is in.
Soooo-ho-ho, President Barack Obama is in Australia at the moment (in Canberra, in fact, where the physical manifestation of Dr Then resides) and while the cat’s away, let’s see what the mice are playing at back in the US.
This latest from Congress: a joint House-Senate panel has ruled that a slice of pizza constitutes a vegetable. What the hey? And huh?
Here’s the background: the US Department of Agriculture is responsible for setting rules about what can go in subsidised school meals – the meals that poorer children get for free or heavily subsidised cost at school canteens. And one of those rules is that the meals should meet government dietary recommendations. You remember the food pyramid with its food groups? (NB people, as of this year, it’s not a pyramid any more – it’s a plate, with a name and all: ‘MyPlate’. As opposed to the old ‘MyPyramid’. Who comes up with these? And how creatively stunted are they?? But triangle or circle, it’s the same idea – an icon that encapsulates dietary advice.) Any school lunch that the government pays for has to meet the dietary recommendations that MyPlate illustrates.
Now the USDA is more precise than just telling schools to make lunches that work with the MyPlate picture. The department tells schools how many cups of different food groups and should go into meals. Up until recently, the USDA has only specified amounts of fruit, cereals, meat, and milk that have to go into school lunches but now the department has started to set amounts of vegetables as well.
Here is where the fun begins: what constitutes a ‘vegetable’?
This is where pizza comes in.
The USDA would like to set a rule that one slice of pizza containing about two tablespoons of pizza sauce (ingredients: mainly water, with tomato paste, flavours, thickener (415), and vegetable oil) does NOT constitute a serving of vegetables. The American Frozen Food Institute – an industry lobby group for producers of such things as frozen pizza – disagrees. And has successfully persuaded congress-men and -women on the House Appropriations Committee to stop the USDA making the pizza-is-not-a-vegetable ruling.
The Appropriations Committee’s reasoning (or at the least its Republican members’) was that the rule would impose too harsh regulations on schools, increase costs of the school lunch program, ‘tell children what to eat’ (apparently a Bad Thing), and limit school districts’ ‘flexibility’ in ‘improving nutritional quality’. (Huh? How’d they get that last one?)
It, of course, sounds considerably more like the Committee is unwilling to do anything that would possibly lessen food producers’ markets or, ironically, ask producers to make healthier food. And, since the Democrats have a party policy to act against childhood obesity (publicised by Michelle Obama’s ‘Let’s Move’ activities), this move against improving school lunch nutritional levels is also the Republicans biffing the Democrats. Good times.
Sigh. Dr Then shakes her head.
This would not be the first time that American officialdom, influenced by manufacturers, has decided that children’s health was less important than adults’ money. (This latest is, however, particularly egregious because the school lunch program is directed at the poorest of American children, and they have the worse nutrition and the highest rates of childhood obesity.) Here’s just a little timeline of how child health gets a pretty raw deal:
1978-1979 “Kid-Vid” Hearings by the Federal Trade Commission
Following an application by children’s rights groups, the FTC held hearings into whether advertising on television to children, especially of foods like candy, fast food, and sugared cereals, should be restricted for health reasons. Under pressure from advertising agencies and food producers, Congress voted to end the FTC’s investigation. Even more, Congress then changed the FTC’s mandate so that it was no longer allowed to decide whether any advertising to children was ‘unfair’ or not. (Before it ended its investigation, the FTC had reviewed research into children and advertising. This research had shown that children were unable to understand that ads were trying to persuade them to buy something. Children either didn’t know that the ads were not part of the program or else understood them as simply giving them handy information as to what was out there. Since children are developmentally unable to understand advertisements’ persuasive intent, the implication would be that ANY advertising to children would be inherently unfair, let alone the sophistication of Madison Avenue’s messages of eat-this-food-and-you’ll-be-popular or buy-this-candy-and-have-heaps-of-fun!) So the FTC can’t rule on whether advertising to children is unfair, and food producers and fast food restaurants are allowed generous access to advertise to children.
2001 Lorrilard Tobacco v. Reilly case
Massachusetts passed a law prohibiting outdoor advertisements for smoking within 1000 feet of schools and children’s playgrounds to try to reduce child smoking. Tobacco companies, supported by the ACLU, argued that this law infringed companies’ first amendment right to advertise. (Yup, apparently it’s in there. “Congress shall make no law … abridging the freedom of speech..” Right there. See it? Companies’ right to advertise cigarettes to children.) The Supreme Court (Republican dominated) concurred and overturned the statute.
So, you see, there has been a historical tendency in the US to sacrifice children’s health in favor of making money (and often, irony of ironies, making money from children themselves.) I know – harsh words, hey? But what a country of contradictions! Family values are highly esteemed by both major political parties, but industry lobbying gussied up with the banner of the first amendment often gets the better deal.
The Appropriations Committee’s report is now going to go to Congress for the final decision. So come on Congress! Be bold on childhood obesity and improving children’s health! Sure, history doesn’t bode well for you doing the right thing on this one, but make a break with the past! I’m pretty sure we can all get together on the idea that pizza is not a vegetable.
Till next time, stay well,
Interested in more? Further reading:
Nestle M. 2002, Food Politics, Berkeley: University of California Press.
Hello people. The Doctor is in.
This is a new blog devoted to the history of medicine. That’s a small subfield of history (or a small subfield of medicine, if you look at it that way) which looks at things like…what options for healthcare were available in the past?…how did people understand illness and disease and how did they go about treating it or dealing with it?…what was it like to be sick 50 years ago…100 years ago…500 years ago? In my blog, I’ll be mainly looking at the historical background to current events and developments in medicine. There’s not often a lot of space in news announcements for much history, and there’s certainly not much space in scientific journal articles that announce researchers’ findings to comment on them and evaluate how they might fit in as part of a bigger–and especially LONGER, that is 4-dimensional–picture. So that’s where this blog comes in: medicine in 4-D.
So, welcome to Dr Then’s medical history blog. (Not Dr Now..er No…no, Now. Not now. Then.)
And who is what I’d like to think of as the intelligence behind Dr Then? I am, in fact a Dr, but in the sense of PhD rather than MD. (But my name’s not Then – that’s a funny, folks.) If you’ve wandered onto this blog looking for health tips, hit that BACK button, because that’s not what’s going on here. If you ask me for health advice, I might prescribe bleeding, rhubarb, and a grain or two of arsenic – all good stuff, taken at the right historical moment (which isn’t now. No? Not now, Then. Oh dear, we’re back to that again.)
Anyhoo, as I was saying, I have a PhD in the History of Medicine from Harvard, and I graduated last year. I am a shiny, newly minted, clean-about-the-ears, fresh-as-a-daisy historian of modern medicine. I wrote my thesis on the history of childhood obesity in America, starting at about 1870 (who knew it had that long a history?) and coming up to the present day. (Hint: expect a fair few posts on that topic! What else did you think that dissertation was going to be used for? Mulching the vege patch?) I’m working on turning that thesis into a book – so TOPICAL! So NOW! So INTERESTING! – and hopefully pretty soon a publisher will agree that all those zippy adjectives apply and pick it up. Don’t worry about missing it at your local bookshop — I’ll be sure to let you know when it’s out.
So that’s a little taster of what you can expect when you drop into Dr Then’s clinic.