Image by Magnus D

If you’ve enjoyed this post, please sign up for future updates on similar topics to be delivered to your email inbox or RSS reader.

[Update: For the clinical perspective on today's topic, check out the accompanying article on Dr Yoni Freedhoff's blog Weighty Matters]

I had an interesting experience at my last physical exam, and I thought it would be worth sharing here on the blog.  Before the physical a nurse put me through an eye test, then took my blood pressure, height and weight.  She then calculated my BMI, and told me that I was in the “normal range” (it was around 24.5).  But, she continued, I was pretty close to the overweight cut-off of 25.0, so I should “watch my weight” moving forward.

I said “un-huh” and sort of laughed inside my head, given that I’m an obesity researcher and we have written the odd post about BMI here on Obesity Panacea.  But the more I talked about the episode with other people, the more ridiculous it seemed.  Here’s why.

BMI is only one aspect of health

As we have said before, weight ≠ health. BMI is moderately useful at estimating body fat, and therefore health risk (especially at the population level).  However, as Peter and I have argued many times, your behaviour matters as much (or more) than your weight when it comes to health.  If you are physically active and eat a healthy diet, you’re likely to be relatively healthy whether your BMI is 22 or 32.  It’s not that weight doesn’t matter at all, but it’s far from the only thing that matters.

(For more on the relationship between BMI and health, I suggest this excellent post by Peter while Obesity Panacea was hosted on Scienceblogs.  Or, for a review paper on the health-benefits of exercise regardless of body weight, click here.)

Context matters

My weight has been stable for several years.  I am (extremely) physically active. I try to limit the amount of time I spend sitting.  And thanks to my wife’s positive influence, I eat a reasonably healthy diet (mostly homemade vegetarian food for breakfast and supper, with leftovers and/or pizza for lunch).  My metabolic health is also fine although, ironically, I had to specifically ask before I was be told my HDL and triglyceride levels.

Why would you counsel a weight stable person with a BMI in the healthy range about their weight (as opposed to their behaviour) anyway?  I’m certainly not the only person to have this experience – here’s what colleague Atif Kukaswadia had to say on twitter:

My BMI is around 24.9. My doc told me to “not gain any more weight” for the same reason.

Yet, as our science blogging friend DrugMonkey pointed out on twitter, none of that means that we’re going to be weight stable forever. I’m in my late 20′s, cutting back on my participation in competitive sports, recently married, and nearing the end of grad school.  It wouldn’t be at all surprising if someone in my position were to begin putting on a few pounds over the next few years. In that context, the nurse’s advice seems to make perfect sense.

Except for one (very big) oversight.

How do you “watch your weight”, anyway?

This is really the crux of the problem.  Weight is an outcome, not a behaviour. When someone tells you to watch your weight, what do they really mean?

Obviously one would assume that the nurse meant that I should be physically active and eat a healthy diet.  Except she didn’t say anything about either of those things.  She didn’t ask about my level of activity or my diet (although it had been recorded during an earlier visit), nor did she give me any counseling on what a healthy diet should look like.

What if someone in my position were to take the nurse’s advice and begin dieting to reduce their weight or prevent weight gain (despite being weight stable and already healthy)?  As our colleague Dr Arya Sharma has argued, trying to lose weight is actually a pretty good way to gain weight over the long term.

as I have said before, all weight loss attempts should be medically indicated and anyone attempting to lose weight needs to be warned that they may in fact be increasing their long term risk of becoming (even more) overweight or obese.

I don’t want to be too harsh on the nurse because she clearly meant well.  But a clinical strategy that focuses exclusively on body weight, with no information or counselling related to healthy behaviours, and completely ignoring all context, is almost certainly going to fail (and possibly make things worse than they were at the beginning).

As always, I’m curious to hear what others think.  Has anyone had a similar experience? Have a different perspective on the nurse’s advice?  I’d love to hear about it in the comments section.  And don’t forget to check out Dr Freedhoff’s thoughts on the issue over at Weighty Matters.

If you’ve enjoyed this post, please sign up for future updates on similar topics to be delivered to your email inbox or RSS reader.

Travis

The article was written by our colleague Ash Routen, and here is his take-home message:

…it appears for most children that increased time spent engaged in screen-based SB may lead to lower cardiorespiratory fitness (CRF), regardless of how much PA they engage in. However the negative associations reported were not stable across the CRF distribution. That is, there appeared to be no significant relation at the lower end (10th percentile) in boys and girls, and at the upper end (90th percentile) in boys.

The authors speculated that genetic predisposition may account for this non-uniform association, with some individuals at the lower end of the CRF distribution displaying a resistance to age and SB driven changes in CRF.

You can find the full article (as well as the world’s largest database of sedentary-behaviour related research) on the Sedentary Behaviour Research Network website.

Travis

I hope you don’t mind my straying off topic.

When Travis and I started blogging back in 2008, we were sharing a small office at Queen’s university; Travis was just finishing up his Master’s and I was midway through my PhD.

Since that time much has changed for both of us.

For instance, our old office no longer exists; the building which housed it now stands vacant.

Travis finished his master’s, moved to Ottawa, and is now happily married.

Even our blog has had three homes since inception (at www.obesitypanacea.com, at ScienceBlogs, and now on PLoS blogs).

Our long-time readers may also remember that back in April of 2010, I defended my PhD. A couple of weeks later, my partner, Marina, also defended hers.

Since my defense I have been a bit more absent on the blog, leaving Travis to do much of the heavy lifting in terms of content (Thank you buddy!) As some of you have been wondering what I have been up during this time, I’ll briefly explain.

You see, near the end of our respective degrees, some 10 years deep into post-secondary education, Marina and I had realized that we had allowed our work to overshadow our lives. We had let hobbies, friendships, and even our relationship become secondary in importance to filling our respective CVs with more publications, presentations and other tokens of academic success.

Thus, around the time we were finishing up our theses, we made a pact to remedy this imbalance.

Not surprisingly, within 3 days of Marina’s defense, the two of us were on a one-way flight to Ecuador.

For the first time in our lives we didn’t have the next step planned out.

And it was exhilarating.

Not to mention frightening.

Since then, we haven’t really stopped moving. Over the past year and a half, Marina and I have lived in four cities in 3 different countries, have traveled to over a dozen other countries, and have finally checked off a few items off of our bucket lists.

I’m actually writing these words from our current temporary home in Auckland, New Zealand.

When we first set off for South America, I hastily started a blog to document our travels and named it PhD Nomads.

At the time I had no idea how accurate this moniker would soon become.

Nevertheless, here we are, as our tagline suggests: “an over-educated couple on an extended ‘workation’.”

If I haven’t bored you yet, and you’d like to learn all the juicy details behind our currently nomadic lifestyle, please click here.

Also, if you would like to follow our adventure you can sign up for updates via email or RSS reader – just as you do with Obesity Panacea.

Finally, if you have any questions pertaining to any of the travel we have done, please feel free to contact me.

In the meantime, as we temporarily reside in New Zealand, I’ll do my best to write about our adventures in Southeast Asia over the past 4 months, as well as provide new content for Obesity Panacea.

Peter

Image created using photos from goldberg and Bengt Neyman (Flickr)

I recently came across a very interesting study published in Circulation in 2001.  In it, authors Darren McGuire and colleagues perform the 30-year follow-up on a group of 5 men who had taken part in the Dallas Bed Rest and Training Study (DBRTS).  The DBRTS took place in 1966, when all 5 men were healthy 20 year-olds.  They were assessed extensively at baseline, following 3 weeks months of bed rest, and following 8 weeks of physical training. In 1996 these same 5 men were re-assessed, allowing the researchers to compare the influence of 3 weeks of bed rest and 30 years of aging on markers of fitness.

As you’d expect, there was a significant increase in both body weight and body fat percentage over the 30 year period.  But what I find more interesting is what happened to aerobic fitness.  Below are the results of the VO2 max tests at baseline, post bed rest, and after 30 years of aging (error bars represent standard deviation)

It looks as though 3 weeks of bed rest resulted in a substantial reduction in fitness in the group as a whole, a reduction which was even larger than the one seen after 30 years of aging.  Given that there are only 5 participants, it is not surprising that the above changes were not statistically significant.  But when you look at the values for each individual participant (below), the results are even more striking.

The above figure would seem to suggest that 3 weeks of bed rest resulted in a consistent and rather substantial reduction in aerobic fitness in all 5 participants, while the impact of aging seems less consistent.  Again, there is no statistical significance, but it’s an interesting figure nonetheless.

Even moreso than with most papers, this study has a number of obvious limitations.  There were only 5 participants, the above results weren’t statistically significant, and the results were not controlled for other important factors.  So why post it here?  Frankly, because it’s kinda neat!  I love studies with rigorous design, but opportunistic studies like this can go a long way to filling in gaps in the narrative where more rigorous studies end off.  Not to mention that this was one of the first papers to suggest that sedentary time could have a strong influence on health.  Interestingly, the authors conclude that it is the lack of physical activity – as opposed to sedentary behaviour – which resulted in the apparent reduction in fitness following 3 weeks of bed rest.  Personally, I’m inclined to think that sedentary behaviour itself may have an independent impact on health, as I’ve discussed previously, but that’s a discussion for another day.

I know I’m reading more into this than the data itself might suggest.  So what do you think – is bed rest likely to be as bad or worse for fitness as 30 years of aging, or is this nothing more than over-interpretation of a null result?  I’d love to hear your thoughts.

Travis

McGuire DK, Levine BD, Williamson JW, Snell PG, Blomqvist CG, Saltin B, & Mitchell JH (2001). A 30-year follow-up of the Dallas Bedrest and Training Study: I. Effect of age on the cardiovascular response to exercise. Circulation, 104 (12), 1350-7 PMID: 11560849

This past weekend, my partner, Marina, showed me a under 10-min video created by Dr. Mike Evans from the Health Design Lab at the University of Toronto that absolutely blew my mind.

In asking the simple question: “Can you limit your sitting and sleeping to just 23.5 hrs per day?”, this video nails the importance of physical activity in a manner that can appeal to everyone. Please watch it, show it to your friends and colleagues, and forward it to anyone who you think would benefit from the message. The last time I was this excited about a video was when we posted the “Piano Stairs Experiment” some time ago.

Enjoy!

Peter

Note to our email subscribers: Please log onto Obesity Panacea to view the video.

Today’s guest post comes courtesy of a good friend of mine, and physiotherapist, Matt Sanchez. Matt and I have been friends since high-school, and also completed our undergraduate degrees together at the University of Western Ontario. Matt is currently the Director of Rehab & Technology at Aim2Walk Rehabilitation Center. Recently, I asked Matt to discuss some of the common musculoskeletal issues that overweight and obese people encounter and he graciously agreed.

So without further ado, here’s Matt!

Peter

——–

If there’s one thing my five years of experience as a Physical Therapist in the community has taught me, it’s that people don’t like pain.  I know, my 6 years in University and 30 years of life should’ve taught me that.  But seriously, the number one orthopaedic complaint I treat involves pain.

But making a Physical Therapy appointment for obesity? That is VERY rare.  In fact, I cannot recall a single case where a client stated the reason for the appointment was obesity.  The reason is almost always pain.  Approximately 1 in 4 people that walk/limp/roll through our clinic’s doors have a body mass index (BMI) of 30 kg/m² or more.  Their injuries range from low back pain to spinal cord injuries – same as the non-obese population – and there is almost always a complaint of pain.

Nevertheless, some injuries present themselves more than others in the obese population (1).  Let’s take a look at the 5 most common pain-causing injuries in the obese population seen in a physical therapy clinic:

1) Sprains and Strains

These two terms are commonly used interchangeably, but they actually refer to different musculoskeletal injuries.  You strain a muscle or tendon and sprain a ligament.  Now you can correct your friends.

This is a very broad category which is likely why it tops the list.  Muscle, tendon and ligament injuries are quite common and I suspect that many of you have had an injury of this sort in the past.  Sprains/strains can be acute or chronic and can have a plethora of possible causes.  These are very common injuries for weekend-warriors, or people that are not active and attempt moderately strenuous activities using their de-conditioned musculature.

2) Osteoarthritis and joint replacement

Obesity is a known risk factor for osteoarthritis (2) and joint pain has a strong association with body weight. You need not go any further than this blog entry by Peter discussing the effects of excess weight on predicting a younger age for needing a hip or knee replacement.  As Peter mentions though, we can’t jump to the conclusion of arthritis occurring purely due to increased joint load, as there is also a correlation between obesity and hand osteoarthritis (3).

3) Disc Herniation

Disc herniation is another injury associated with obesity, but not necessarily caused by the increased load on the discs between our vertebrae.  Obesity is closely linked with other disc herniation risk factors, such as inactivity, weak abdominal musculature and issues with circulation. Specifically, reduced blood flow through the descending aorta artery means reduced blood flow to the discs making them more likely to be injured.

4) Carpal Tunnel Syndrome

This refers to symptoms created by pressure in the wrist on the median nerve, which supplies feeling and movement to parts of the hand.  Approximately 10% of the general population will be diagnosed with carpal tunnel syndrome, whereas 25% of people classified as obese will get this condition.

5) Rotator Cuff Tendonitis

Pain with overhead movements and lifting using an outstretched arm may indicate rotator cuff pathology.  This injury can be associated with obesity in relation to reduced activity levels, weak supporting musculature, and poor postures adopted during prolonged sitting activities.

If experiencing one of the five injuries reviewed above, or any other pain causing injury, it is best to consult your physiotherapist.  Physiotherapists are specially trained to diagnose, treat and help prevent musculoskeletal injuries and neurological conditions.  You do not require a doctor’s note to see a physiotherapist, and you can find one near you by clicking here.

Matt Sanchez
Email: matt@aim2walk.ca
Blog: www.neurochangers.com
Website:  www.aim2walk.ca
Twitter: @aim2walkPT

References:

(1) Matter, K., Sinclair, S., Hostetler S., Xiang, H. (2007) A Comparison of the Characteristics of Injuries Between Obese and Non-obese Inpatients. Obesity.15: 2384-2390 doi: 10.1038

(2) Felson DT, Chaisson CE: Understanding the relationship between body weight and osteoarthritis.Baillieres Clinical Rheumatology 1997;11:671-681.

(3) Cicuttini FM, Baker JR, Spector TD: The association of obesity with osteoarthritis of the hand and knee in women: a twin study. J.Rheumatol. 1996;23:1221-1226.

Happy New Year!

For anyone living in the Fredericton area with an interest in the health impact of sedentary behaviour: I will be giving a guest lecture at the University of New Brunswick Fredericton campus January 5th (tomorrow) from 2:30 to 3:50.  The talk will be in Dr Gabriela Tymowski’s “Coaching Healthy Behaviours” course, and she has generously opened up the lecture to anyone who would like to attend.  The talk will focus on many of the topics that were covered in my series on sedentary physiology, so if you enjoyed that series then this talk may be of interest.

The talk will be in Room 139 in Carleton Hall, which is the bottom end of the Tilley – Singer complex, just below the Harriet irving library. I’m having trouble embedding the google map, so I’ve included a static picture of the map below, and anyone looking for the google map itself can click here.

We’re hoping to record the talk, so with any luck I’ll have it up on the blog and/or podcast in the coming weeks.

Hope to see some of you tomorrow!

Travis

Image Courtesy of the Canadian Obesity Network Image Gallery

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.

Palatable Food

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.

Vitamin D

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

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.

Stress

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.

That’s it!

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!

Travis

Saunders, T. (2011). Potential Contributors to the Canadian Pediatric Obesity Epidemic ISRN Pediatrics, 2011, 1-10 DOI: 10.5402/2011/917684

Image Courtesy of the Canadian Obesity Network Image Gallery

Welcome to Part 4 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.

Throughout the week we will examine the following potential contributors to the pediatric obesity epidemic:

• Reduced sleep
• Reduced physical activity
• Increased total energy intake
• Increased fat intake
• Increased sedentary time
• Exposure to endocrine-disrupting chemicals
• Increased consumption of sugar-sweetened beverages
• Inadequate calcium intake
• Increased maternal age
• Reduced breastfeeding
• Increased adult obesity rate

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. Today we look at the evidence (or lack thereof) linking adult obesity with the pediatric obesity epidemic, then examine the relative contributions of all of the risk factors we’ve discussed so far.

Adult Obesity

Available evidence suggests that both parental obesity and gestational weight gain are risk factors for childhood obesity [75, 110, 111]. For example, Reilly and colleagues examined the relationship between parental and childhood obesity in a prospective study of nearly 9,000 British children [75]. In comparison to children born to two nonobese parents, they report that children were 2.5 times more likely to be obese when they had an obese father, and 4.3 more likely to be obese if they had an obese mother. Further, children born to two obese parents were more than 10 times more likely to develop obesity by age 7 than those born to two non-obese parents [75]. It has been reported that gestational weight gain is also a predictor of childhood obesity, and that this impact is stronger in women who were obese prior to becoming pregnant [111]. Finally, recent reports suggest that surgical weight loss prior to pregnancy dramatically reduces the risk of childhood obesity in babies born to obese women [112]. These relationships suggest that any putative cause of the increasing prevalence of adult obesity [113] including those that are unlikely to play a direct role in the epidemic of childhood obesity (e.g., iatrogenic weight gain [25]) may nonetheless play important indirect roles.

The relationship between parental and childhood obesity is likely to be linked via numerous mechanisms. For example, genetic factors are reported to account for roughly 25% of the variance in fat mass [114], which is likely to mediate some of the relationship in body composition between parent and child. Further, learned behavioural characteristics such as food choices, PA, and sedentary behaviours are also likely to mediate the transmission of intergenerational obesity [75, 115]. Finally, studies of animal models suggest that obesity or excessive weight gain during pregnancy is likely to predispose childhood obesity through deleterious changes in the central regulation of energy balance [116]. For example, lambs born to overfed ewes are less sensitive to signals of excess nutrient supply or fat mass than lambs born to control animals [116]. Taken together, the strong association between parental and childhood obesity and the numerous plausible mechanisms underlying these associations suggest that one of the most important drivers of the childhood obesity epidemic may in fact be adult obesity.

Relative Contributions to Childhood Obesity

As has been noted by others, there is currently insufficient information to make a truly objective ranking of the putative causes of an issue as complex as the current obesity epidemic [25]. However, the evidence presented above does allow some general conclusions to be made. This review has identified 4 factors—reduced sleep, increased sedentary time, increased consumption of sugar-sweetened beverages, and secular increases in adult obesity—which are likely to have made an important contribution to Canada’s childhood obesity epidemic. Each of these factors has shown strong and consistent associations with childhood weight gain, has increased in prevalence during the obesity epidemic, and results in either biological or behavioural changes that are likely to promote positive energy balance. Of these, adult obesity appears to have the most powerful impact on childhood obesity levels, while reducing the consumption of sugar-sweetened beverages may be among the simplest ways to prevent future weight gain in individuals of all ages.

Available evidence provides only moderate support for the role of either total EI or PA in the etiology of childhood obesity. This is likely due to methodological limitations of self-reported intake and expenditure, as both of these factors are biologically plausible and have been shown to have impressive effects on adiposity in experimental studies. It is possible that methodological limitations may also explain the inconsistent relationships seen between obesity and dietary fat intake. Future studies employing more objective methods of measurement are important to determine the true role of these factors in the etiology of the childhood obesity epidemic.

Finally, although each has been linked in some way with childhood obesity, there is currently weak evidence supporting the role of maternal age, breastfeeding, exposure to endocrine disrupters, or calcium insufficiency in the etiology of the childhood obesity epidemic. Of these, maternal age, breastfeeding, and endocrine disruptors appear worthy of future study, while there is sufficient evidence to conclude that calcium intake plays little role in pediatric obesity rates at the population level.

Coming Soon

Tomorrow (now available here) we will take a brief look at some potential contributors that didn’t make it into the review – poverty, fast food intake, increased food palatability, and stress.  If there are any others that you’d like covered, feel free to add them in the comments below and I will do my best!

Travis

Saunders, T. (2011). Potential Contributors to the Canadian Pediatric Obesity Epidemic ISRN Pediatrics, 2011, 1-10 DOI: 10.5402/2011/917684

108. A. Yngve and M. Sjöström, “Breastfeeding in countries of the European Union and EFTA: current and proposed recommendations, rationale, prevalence, duration and trends,” Public Health Nutrition, vol. 4, no. 2, pp. 631–645, 2001.

109. A. S. Ryan, Z. Wenjun, and A. Acosta, “Breastfeeding continues to increase into the new millennium,” Pediatrics, vol. 110, no. 6, pp. 1103–1109, 2002.E.

110. Oken, E. M. Taveras, K. P. Kleinman, J. W. Rich-Edwards, and M. W. Gillman, “Gestational weight gain and child adiposity at age 3 years,” American Journal of Obstetrics and Gynecology, vol. 196, no. 4, pp. 322.e1–322.e8, 2007.

111. C. M. Olson, M. S. Strawderman, and B. A. Dennison, “Maternal weight gain during pregnancy and child weight at age 3 years,” Maternal and Child Health Journal, vol. 13, no. 6, pp. 839–846, 2009.

112. J. G. Kral, S. Biron, S. Simard et al., “Large maternal weight loss from obesity surgery prevents transmission of obesity to children who were followed for 2 to 18 years,” Pediatrics, vol. 118, no. 6, pp. e1644–e1649, 2006.

113. M. Shields, M. S. Tremblay, M. Laviolette, C. L. Craig, I. Janssen, and S. C. Gorber, “Fitness of Canadian adults: results from the 2007–2009 Canadian Health Measures Survey,” Health Reports, vol. 21, no. 1, pp. 21–35, 2010.

114. C. Bouchard, “Current understanding of the etiology of obesity: genetic and nongenetic factors,” American Journal of Clinical Nutrition, vol. 53, no. 6, pp. 1561S–1565S, 1991.

115. L. A. Francis, Y. Lee, and L. L. Birch, “Parental weight status and girls’ television viewing, snacking, and body mass indexes,” Obesity Research, vol. 11, no. 1, pp. 143–151, 2003.

116. I. C. McMillen, L. Rattanatray, J. A. Duffield et al., “The early origins of later obesity: pathways and mechanisms,” Advances in Experimental Medicine and Biology, vol. 646, pp. 71–81, 2009.

Image Courtesy of the Canadian Obesity Network Image Gallery

Welcome to Part 3 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.

Throughout the week we will examine the following potential contributors to the pediatric obesity epidemic:

• Reduced sleep
• Reduced physical activity
• Increased total energy intake
• Increased fat intake
• Increased sedentary time
• Exposure to endocrine-disrupting chemicals
• Increased consumption of sugar-sweetened beverages
• Inadequate calcium intake
• Increased maternal age
• Reduced breastfeeding
• Increased adult obesity rate

In Part 1 we examined the impact of changes in physical activity and sedentary behaviour, and in Part 2 we looked at changes in food intake.   Today we look at the evidence (or lack thereof) linking sleep, pollution, maternal age and breastfeeding with the pediatric obesity epidemic. To skip to Part 4, which looks at the relative contributions of all the risk factors discussed in this series, click here.

Sleep

Available evidence suggests that short-sleep duration may be another important risk factor for childhood overweight and obesity. A recent systematic review and meta-analysis by Cappuccio and colleagues reports that children who sleep less than 10 hours per night are at 89% greater risk than their peers who sleep more than 10 hours/night [73]. Using this same data, it has been estimated that 5 to 13% of all childhood obesity could be due to short-sleep duration [74]. Although the vast majority of the research to date has been cross-sectional [73], there is evidence of sleep as a predictor of weight gain in prospective studies as well. For example, Reilly and colleagues report that toddlers who slept less than 11 hours per night at age 2.5 years were 35–45% more likely to be obese at age 7 than toddlers who averaged more than 12 hours of sleep [75], with similar findings reported by Bell and Zimmerman [76].

Secular trends in sleep duration also support the putative role of sleep duration in the childhood obesity epidemic. Since the 1970’s, the average sleep duration of children has decreased significantly among industrialized nations. Between 1974 and 1986, the average sleep time of 2-year olds in the Zurich Longitudinal Studies decreased by 45 minutes [77], while Dollman and colleagues report a 30-minute decrease from 1985 to 2004 among South Australian teenagers [78]. Similarly, the prevalence of sleep-onset difficulties has also increased dramatically in recent years [79].

Finally, a putative role for shortened sleep in the etiology of the obesity epidemic is also supported by plausible mechanisms which are thought to influence both EE and EI [80, 81]. For example, it has been reported that sleep restriction in adults results in significant increases in hormones which promote EI including cortisol and ghrelin, along with decreases in anorectic hormones such as leptin and PYY [80,82–84]. Not surprisingly, short-sleep duration has also been shown to result in increased hunger and appetite, both of which were strongly associated with the changes in ghrelin and leptin mentioned earlier [84]. Given that leptin and ghrelin are thought to, respectively, promote and inhibit physical activity, it has been suggested that sleep debt could potentially result in reductions in EE as well [81, 85]. However, recent experimental evidence in young men suggests that acute sleep restriction results in relatively little change in EE [86]. Thus, at present it appears very likely that sleep deprivation results in increased EI, while there is little direct evidence that it results in reduced EE. When these biological mechanisms are considered alongside the consistent relationship between shortened sleep and obesity in prospective studies, and secular trends in sleep duration, there is currently strong evidence that shortened sleep plays a role in the childhood obesity epidemic.

Endocrine Disrupting Chemicals

Endocrine-disrupting chemicals (EDCs) are any “compound, either natural or synthetic, which alters the hormonal and homeostatic systems that enable the organism to communicate with and respond to its environment” [87], several of which (known as obesogens) may influence body weight [88]. Limited evidence suggests that EDCs may exert a negative influence on aspects of EE. For example, it has been reported that mothers who have high levels of polychlorinated biphenyls (PCBs) in their breast milk also have low levels of plasma triiodothyronine, a thyroid hormone which is known to stimulate basal metabolism [89]. Similarly, interventions in adults which increase plasma organochlorine concentrations result in significant decreases in both triiodothyronine and resting metabolic rate [90] and may also reduce skeletal muscle oxidative capacity [91]. However, despite this limited biological evidence linking EDCs and EE, at present it is unclear whether prenatal exposure to EDCs predisposes to future weight gain [92]. For example, while some reports suggest that the concentration of PCBs in cord blood is positively associated with BMI in early childhood [92], other reports suggest no relationship [93], or even a negative relationship [94] between prenatal PCB exposure and prospective weight gain. Similar inconsistencies have also been observed for other EDCs such as DDE [92]. Thus, while being an interesting area for future research, at present there is very little evidence that EDCs play a causal role in the childhood obesity epidemic.

Increased Maternal Age

The average age of first pregnancy has increased dramatically in recent decades in both Canada [95–97] and around the world [98–100], and several plausible mechanisms have been suggested, which could link maternal age with increased risk of childhood obesity. For example, older mothers are known to give birth to smaller infants, which is itself a risk factor for the development of obesity [96, 101]. Similarly, older women are also likely to have both higher plasma concentrations of EDCs and higher BMIs, both of which may also predispose their children to future weight gain, as discussed elsewhere in this review [102–104]. Finally, research in sheep suggests that older maternal age may result in increased fat deposition [105], which may be related to accelerated reductions of proteins responsible for thermogenesis-related energy expenditure [25], although it is not immediately clear how or if this relates to humans.

Although the mechanisms described above are all at least somewhat plausible, the relationship between maternal age and childhood obesity in observational studies is inconsistent. For example, while Patterson and colleagues report that the odds of obesity in a cohort of American girls increased by 14% for every 5-year increase in maternal age [106], a more recent study of 8234 British children found no relationship between maternal age and risk of obesity at age 7 [75]. Given this conflicting evidence, there is currently only weak evidence that maternal age plays a role in the childhood obesity epidemic, and future prospective studies are needed to clarify this relationship.

Reduced Breastfeeding

Duration of breastfeeding has been strongly and consistently linked with reduced risk of childhood overweight and obesity [107]. For example, Harder and colleagues performed a meta-analysis which examined the association between duration of breastfeeding and the risk of childhood overweight in 17 independent observational studies [107]. In comparison to children who were breastfed for less than 1 month, they report that children who were breastfed for 1–3 months had 19% reduced risk of overweight. The risk of being overweight continued to decrease as the duration of breastfeeding increased—risk was reduced by 24% among those breastfed for 4–6 months, 33% among those breastfed for 7–9 months, and by 50% for those breastfed for more than 9 months. On average, each additional month of breastfeeding reduced the risk of being overweight by 4%.

Despite consistent reports of the relationship between breast feeding and reduced risk of overweight and obesity, the mechanisms underpinning this relationship remain unclear. It has been suggested that it may be due to alterations in the neuroendocrine control of appetite, although this has yet to be verified in human participants [107]. Thus, it is not possible at present to determine the precise mechanisms linking the duration of breastfeeding to body weight in childhood.

While breastfeeding appears to have a strong relationship with the risk of excess weight gain in childhood, trends in the prevalence of breastfeeding suggest that it is not a major contributor to secular increases in childhood obesity rates during the 20th century. Since the 1970’s, the prevalence of breastfeeding has remained constant or increased among most western nations for which data is available [108, 109]. For example, in the early 1970’s roughly 20% of American women exclusively breastfed while in the hospital, but this increased to 45% by the year 2000 [109]. Given that obesity rates continued to increase steadily throughout this period despite increases in the prevalence of breastfeeding, there is currently weak evidence that breastfeeding plays a primary role in the childhood obesity epidemic.

Coming Soon

Come back tomorrow (now available here) when we look at a counter-intuitive contributor to the pediatric obesity epidemic: the adult obesity epidemic.  We will also compare the relative contributions of all the risk factors we’ve discussed so far.  See you then!

Travis

Saunders, T. (2011). Potential Contributors to the Canadian Pediatric Obesity Epidemic ISRN Pediatrics, 2011, 1-10 DOI: 10.5402/2011/917684

73. F. P. Cappuccio, F. M. Taggart, N. B. Kandala et al., “Meta-analysis of short sleep duration and obesity in children and adults,” Sleep, vol. 31, no. 5, pp. 619–626, 2008.

74. T. Young, “Increasing sleep duration for a healthier (and less obese?) population tomorrow,”Sleep, vol. 31, no. 5, pp. 593–594, 2008.

75.  J. J. Reilly, J. Armstrong, A. R. Dorosty et al., “Early life risk factors for obesity in childhood: cohort study,” British Medical Journal, vol. 330, no. 7504, pp. 1357–1359, 2005.

76. J. F. Bell and F. J. Zimmerman, “Shortened nighttime sleep duration in early life and subsequent childhood obesity,” Archives of Pediatrics and Adolescent Medicine, vol. 164, no. 9, pp. 840–845, 2010.

77. I. Iglowstein, O. G. Jenni, L. Molinari, and R. H. Largo, “Sleep duration from infancy to adolescence: reference values and generational trends,” Pediatrics, vol. 111, no. 2, pp. 302–307, 2003.

78. J. Dollman, K. Ridley, T. Olds, and E. Lowe, “Trends in the duration of school-day sleep among 10- to 15-year-old South Australians between 1985 and 2004,” Acta Paediatrica, vol. 96, no. 7, pp. 1011–1014, 2007.

79. S. Pallesen, J. Hetland, B. Sivertsen, O. Samdal, T. Torsheim, and H. I. Nordhus, “Time trends in sleep-onset difficulties among Norwegian adolescents: 1983–2005,” Scandinavian Journal of Public Health, vol. 36, no. 8, pp. 889–895, 2008.

80. C. A. Magee, X. F. Huang, D. C. Iverson, and P. Caputi, “Examining the pathways linking chronic sleep restriction to obesity,” Journal of Obesity, vol. 2010, Article ID 821710, 8 pages, 2010.

81. K. L. Knutson, K. Spiegel, P. Penev, and E. van Cauter, “The metabolic consequences of sleep deprivation,” Sleep Medicine Reviews, vol. 11, no. 3, pp. 163–178, 2007.

82. K. Spiegel, R. Leproult, M. L’Hermite-Balériaux, G. Copinschi, P. D. Penev, and E. van Cauter, “Leptin levels are dependent on sleep duration: relationships with sympathovagal balance, carbohydrate regulation, cortisol, and thyrotropin,” Journal of Clinical Endocrinology and Metabolism, vol. 89, no. 11, pp. 5762–5771, 2004.

83. K. Spiegel, R. Leproult, and E. van Cauter, “Impact of sleep debt on metabolic and endocrine function,” The Lancet, vol. 354, no. 9188, pp. 1435–1439, 1999.

84. K. Spiegel, E. Tasali, P. Penev, and E. van Cauter, “Brief communication: sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite,” Annals of Internal Medicine, vol. 141, no. 11, pp. 846–850, 2004.

85. C. M. Novak and J. A. Levine, “Central neural and endocrine mechanisms of non-exercise activity thermogenesis and their potential impact on obesity,” Journal of Neuroendocrinology, vol. 19, no. 12, pp. 923–940, 2007.

86. L. Brondel, M. A. Romer, P. M. Nougues, P. Touyarou, and D. Davenne, “Acute partial sleep deprivation increases food intake in healthy men,” American Journal of Clinical Nutrition, vol. 91, no. 6, pp. 1550–1559, 2010.

87. E. Diamanti-Kandarakis, J. P. Bourguignon, L. C. Giudice et al., “Endocrine-disrupting chemicals: an endocrine society scientific statement,” Endocrine Reviews, vol. 30, no. 4, pp. 293–342, 2009.

88. F. Grün and B. Blumberg, “Environmental obesogens: organotins and endocrine disruption via nuclear receptor signaling,” Endocrinology, vol. 147, no. 6, pp. S50–S55, 2006.

89. C. Koopman-Esseboom, D. C. Morse, N. Weisglas-Kuperus et al., “Effects of dioxins and polychlorinated biphenyls on thyroid hormone status of pregnant women and their infants,”Pediatric Research, vol. 36, no. 4, pp. 468–473, 1994.

90. C. Pelletier, E. Doucet, P. Imbeault, and A. Tremblay, “Association between weight loss-induced changes in plasma organochlorine concentrations, serum T(3) concentration, and resting metabolic rate,” Toxicological Sciences, vol. 67, no. 1, pp. 46–51, 2002.

91. P. Imbeault, A. Tremblay, J. A. Simoneau, and D. R. Joanisse, “Weight loss-induced rise in plasma pollutant is associated with reduced skeletal muscle oxidative capacity,” American Journal of Physiology—Endocrinology and Metabolism, vol. 282, no. 3, pp. E574–E579, 2002.

92. E. E. Hatch, J. W. Nelson, R. W. Stahlhut, and T. F. Webster, “Association of endocrine disruptors and obesity: perspectives from epidemiological studies,” International Journal of Andrology, vol. 33, no. 2, pp. 324–331, 2010.

93. W. Karmaus, J. R. Osuch, I. Eneli et al., “Maternal levels of dichlorodiphenyl-dichloroethylene (DDE) may increase weight and body mass index in adult female offspring,” Occupational and Environmental Medicine, vol. 66, no. 3, pp. 143–149, 2009.

94. H. M. Blanck, M. Marcus, C. Rubin et al., “Growth in girls exposed in utero and postnatally to polybrominated biphenyls and polychlorinated biphenyls,” Epidemiology, vol. 13, no. 2, pp. 205–210, 2002.

95. S. Loh and B. Ram, “Delayed childbearing in Canada: trends and factors,” Genus, vol. 46, no. 1-2, pp. 147–161, 1990.

96. S. C. Tough, C. Newburn-Cook, D. W. Johnston, L. W. Svenson, S. Rose, and J. Belik, “Delayed childbearing and its impact on population rate changes in lower birth weight, multiple birth, and preterm delivery,” Pediatrics, vol. 109, no. 3, pp. 399–403, 2002.

97. S. Wadhera, “Trends in birth and fertility rates, Canada, 1921–1987,” Health Reports, vol. 1, no. 2, pp. 211–223, 1989.

98. S. J. Ventura, “First births to older mothers, 1970–86,” American Journal of Public Health, vol. 79, no. 12, pp. 1675–1677, 1989.

99. G. Breart, “Delayed childbearing,” European Journal of Obstetrics Gynecology and Reproductive Biology, vol. 75, no. 1, pp. 71–73, 1997.

100. U. Kalberer, D. Baud, A. Fontanet, P. Hohlfeld, and D. de Ziegler, “Birth records from Swiss married couples analyzed over the past 35 years reveal an aging of first-time mothers by 5.1 years while the interpregnancy interval has shortened,” Fertility and Sterility, vol. 92, no. 6, pp. 2072–2073, 2009.

101. K. K. L. Ong, M. L. Ahmed, P. M. Emmett, M. A. Preece, and D. B. Dunger, “Association between postnatal catch-up growth and obesity in childhood: prospective cohort study,” British Medical Journal, vol. 320, no. 7240, pp. 967–971, 2000.

102. O. Hue, J. Marcotte, F. Berrigan et al., “Plasma concentration of organochlorine compounds is associated with age and not obesity,” Chemosphere, vol. 67, no. 7, pp. 1463–1467, 2007.

103. J. L. Kuk, T. J. Saunders, L. E. Davidson, and R. Ross, “Age-related changes in total and regional fat distribution,” Ageing Research Reviews, vol. 8, no. 4, pp. 339–348, 2009.

104. A. Smink, N. Ribas-Fito, R. Garcia et al., “Exposure to hexachlorobenzene during pregnancy increases the risk of overweight in children aged 6 years,” Acta Paediatrica, vol. 97, no. 10, pp. 1465–1469, 2008.

105. M. E. Symonds, S. Pearce, J. Bispham, D. S. Gardner, and T. Stephenson, “Timing of nutrient restriction and programming of fetal adipose tissue development,” Proceedings of the Nutrition Society, vol. 63, no. 3, pp. 397–403, 2004.

106. M. L. Patterson, S. Stern, P. B. Crawford et al., “Sociodemographic factors and obesity in preadolescent black and white girls: NHLBI’s Growth and Health Study,” Journal of the National Medical Association, vol. 89, no. 9, pp. 594–600, 1997.

107. T. Harder, R. Bergmann, G. Kallischnigg, and A. Plagemann, “Duration of breastfeeding and risk of overweight: a meta-analysis,” American Journal of Epidemiology, vol. 162, no. 5, pp. 397–403, 2005.

108. A. Yngve and M. Sjöström, “Breastfeeding in countries of the European Union and EFTA: current and proposed recommendations, rationale, prevalence, duration and trends,” Public Health Nutrition, vol. 4, no. 2, pp. 631–645, 2001.