Welcome to Part 5 in a series on potential contributors to the pediatric obesity epidemic. This series is based on a recent paper in the journal ISRN Pediatrics, which is available for free here. Big thanks to the University of Ottawa Author Fund for covering the Open Access publication costs.
In Part 1 we examined the impact of changes in physical activity and sedentary behaviour, in Part 2 we looked at changes in food intake, and in Part 3 we looked at sleep, breastfeeding, maternal age and pollution. In Part 4 we looked the the impact of adult obesity, as well as the relative contributions of all the risk factors that we’ve discussed throughout the week.
Today we will look at other potential contributors to the pediatric obesity epidemic which I didn’t include in my paper. There are a few reasons for that – some risk factors are ones that I just felt didn’t have much evidence behind them, others were similar to ones that were included, and some just didn’t fit within the space constraints (since this paper was originally written for my comprehensive exams, it was limited to 15 pages).
A quick word of warning: some of the risk factors that I will be discussing today (e.g. Vitamin D) are ones that I have not had time to research thoroughly, and so my answers are going to be a combination of research and guesswork based on what I know of the literature. If you disagree with any of my conclusions, and especially if you can point to studies suggesting otherwise, then please share your (constructive) thoughts in the comments.
This topic was suggested in a comment by Margaret Leich, who said that:
How about the explosion of availability of palatable food- not just higher fat, but higher sugar- which is directly marketed to children? Foods that are resistant to sensory specific satiety, and foods that exploit endogenous opioids?
Children can’t really stop themselves from liking and wanting these foods. Food companies, in their need to achieve financial targets, exploit this natural predilection. Bewildered parents stand very little chance to controlling food intake of children, 100% of the time, and these preferences are twigged almost immediately.
I think that’s an excellent point. Unfortunately I’m not aware of any research into changes in food palatability – e.g. were foods in the 1940’s objectively less palatable than foods today? My guess though is that as the proportion of fat and refined carbohydrates in our diet has increased, so has the palatability – why else would companies put those things in refined foods? So I would tend to lump this topic together with the sections looking at the contributions of fat and sugar sweetened beverages, and suggest that this is likely to have played a role in the epidemic.
More Refined Foods
blu-k had a similar question about the impact of more refined foods:
This is just a thought – but as a mum of a toddler I’m seeing more baby food that comes in tubes/packs to be sucked down, rather than jars to be spooned out. I’ve read that people consume more calories when they drink something rather than eat it, so I do wonder if kids sucking down these tubes are consuming more calories than if they had to chew.
I’m not a parent so I haven’t seen these tube-based baby foods, but I would agree with blu-k’s reasoning. In general, liquids are less filling than solids, which means that people will consume more calories before getting full. It has also been suggested that softer foods may require less energy to digest than harder foods.
However, since these tubes are just emerging I would say that they are unlikely to have caused the obesity epidemic, although they may add to it.
Reduced Home Cooking/Increased Fast Food
This is a topic that is frequently suggested, and I think that increasing the public’s ability and inclination to cook at home is a very good step in tackling the obesity epidemic. However (this is a bit of a cop-out), I would say that the reason that fast food is bad is because it’s so high in calories (especially from fat and sugar). So fat and sugar remain the problem, while these are the mechanisms that may explain the problem and provide a way to fix it.
Yesterday Kevin Gelling asked if I would look at vitamin D, and linked to this study suggesting that low vitamin D levels are associated with increased risk of obesity. I did some quick searching, and I’ve found several studies like this one suggesting that vitamin D may increase the health benefits of weight loss (e.g. greater reductions in LDL cholesterol for a given amount of weight loss), but I haven’t come across any suggesting that vitamin D causes more weight to be lost. I’m also not aware of any evidence suggesting that vitamin D levels in the population are lower than they were 50-60 years ago, although I may just not be looking in the right places.
Those are my thoughts on vitamin D, but since this one is well outside of my area of study feel free to jump in with links to articles that either support or refute my opinions on the matter.
Poverty was suggested to me over twitter, and it’s a good suggestion. Although I didn’t include it in my paper, it was a topic that was discussed at the oral defense of my paper. I chose not to include poverty or other measures of socio-economic status for one reason: while body weight is associated with income, that association differs greatly from decade to decade, and from country to country.
In developed countries like Canada and the USA, obesity is negatively associated with income (e.g. rich people are less likely to be obese than poor people). However, in developing nations like much of sub-Saharan Africa, obesity is positively associated with income (e.g. rich people are more likely to be obese). Similarly, 100 years ago in North America, obesity was seen as a status symbol of the rich. Poverty is also a bit of a moving target, given that a poor person in 2010 could be relatively richer than a poor person in 1910.
I should mention that there is some evidence that countries with higher levels of income inequality (e.g. the USA) also have higher levels of obesity than countries with less inequality (e.g. Scandinavia). However, my sketchy knowledge of American history would suggest that the obesity epidemic in the USA started shortly after the New Deal, when I’m assuming equality was on a downward trend? This is not my area, so economics buffs feel free to correct me here.
My fogginess on the history of inequality notwithstanding, I found the relationship between poverty and obesity to be too contradictory to conclude that it is a cause of the obesity epidemic. That being said, I believe strongly that barriers related to poverty and inequality predispose people to obesity in current North American society, and are likely fueling increases in obesity in certain segments of the population. I just don’t think they can explain the obesity epidemic as a whole, going back 50-60 years.
One topic that I personally feel that many of the factors in this series share is that they are all linked to stress. Lack of sleep and physical activity can increase stress, which can in turn result in increased food intake, and more likelihood of eating fast food and refined foods. Whether stress has gone up or down in the past 50 years is debatable though, and I’m sure it would vary greatly from country to country. This is a topic that I wanted to include in the review, but just couldn’t find a clear enough picture to fit it in.
We have now reached the end of this series on the childhood obesity epidemic. I would be remiss if I didn’t mention that some people disagree with the term “obesity epidemic” as a whole, and you can see my discussion with faithful commenter WRG on a previous post here.
Thanks to everyone who has read or commented on the series, or who has gone to download the paper itself (which is available for free). This may be our last post before the holiday season kicks in, in which case I’d like to wish everyone a very Merry Christmas, Happy Hanukkah, a Happy Festivus, and an especially Happy New Year.
See you in 2012!
Saunders, T. (2011). Potential Contributors to the Canadian Pediatric Obesity Epidemic ISRN Pediatrics, 2011, 1-10 DOI: 10.5402/2011/917684