Childhood Obesity Walks on Big Feet

Feet are remarkably complex structures exquisitely designed to buffer and carry the weight of our bodies. Whether standing, running, jumping, hopping, skipping - the feet do it all. Not surprisingly, painful feet affect the whole organism.

Interestingly, not much is known about the impact of increased body weight on foot architecture in kids. This knowledge is of course of great importance for orthopaedic and paediatric physicians with regard to prevention, clinical treatment and management of foot problems but also of obesity.

Now, Marlene Mauch and colleagues from the University of Tuebingen, Germany, studied the foot morphology of normal, underweight and overweight children in 1450 boys and 1437 girls aged 2-14 years (Int J Obesity). Foot morphology was measured using a three-dimensional (3D) foot scanner (Pedus, Human Solutions Inc., Germany) in a bipedal upright position. Twelve relevant 3D foot measures were recorded, as well as the children's age, gender, height and mass.

Five foot types were identified: flat, robust, slender, short and long feet. While normal weight children displayed an almost equal distribution of all foot types throughout childhood, overweight and obese children were more likely to have flat and robust feet, whereas underweight children tended to have slender and long feet.

The authors not only conclude that excess weight may have a significant effect on foot morphology but may also increase the risk for foot discomfort as a result of various musculoskeletal disorders. This in turn may keep the overweight children from being active thereby further promoting weight gain.

Clearly, the role of foot morphology and the maintenance of foot health in overweight and obese kids deserves more attention and further study.

I would add that careful analysis of foot morphology and recommendation of proper footwear, orthotics and exercises should be part of every assessment of an overweight kid - damage to feet resulting from well-meant but ill-advised physical activity at an early age could precipitate lifelong foot problems and prove a major obstacle to long-term weight management.

AMS
Edmonton, Alberta

Walk and Work

Two days ago I reminded readers that not too long ago, people were actually paid to be physically active. Today, choosing to be physically active actually costs money (not to mention time).

So the big challenge is, how do we reintroduce activity into the work place so that people can actually be physically active at work again (allowing them to lounge around the couch in front of the TV when they get home).

Well, one obvious solution is to create a workspace where someone can get a workout in while on the computer. That is exactly the idea behind the "Walk Station" a desk that comes matched with a treadmill instead of a chair.

The device, the science (and the hype) behind it are described in an article from the Edmonton Journal from which I quote:

The device allows people to work on their computers while walking on a treadmill at a slow speed of up to three kilometres per hour, enabling small amounts of movement that supporters say have the potential to reap big health benefits.

The product, made by Details, a unit of Michigan-based office furniture maker Steelcase, is selling 30 to 40 units per week, according to company president Bud Klipa.

The Walkstation was unveiled last year based on research from James Levine, a researcher at the Mayo Clinic, who contends that fitness can be improved through small, modest movements for people who are otherwise sedentary.

Levine's research indicates that people who use the Walkstation can increase energy expenditure by 100 calories per hour when walking at a 1.6 kilometres (one mile) per hour, helping weight loss.

The treadmill, which costs around $4,500 for a base model, never exceeds a speed of three kilometres per hour, which, according to the manufacturer, allows most people to use it for a few hours each day.

So here are my questions:

Where is the evidence that this device will actually promote weight loss?

What will prevent this device from going down the same path as previous workplace health initiatives - embraced by the already fit, ignored by the people who need them most?

Will it increase weight-based discrimination at the workplace - the thin people are walking, the overweight are not - no one stops to ask why - back pain? osteoarthritis? depression? plantar fasciitis? - excuses, excuses! Who cares!

Although is seems like a good way to reintroduce activity into the workplace, it is still "useless" activity, i.e. you are not actually paid to walk - or in other words, you don't really have to walk to get your job done.

While I personally would probably not mind having this device, I can see all sorts of problems - anyone out there who's experienced this or a similar device - I'd love to hear how this has influenced intra-office dynamics.

I will maintain my scepticism on this being the answer till I see some actual data.

AMS
Edmonton, Alberta

Mitochondria and Obesity Revisited

Several months ago I blogged about the results from a Finnish twin study that found lower mitochondria numbers and disturbed mitochondrial energy metabolism activity in fat cells from identical twins who were leaner than their genetically identical co-twins. These impairments correlated with critical clinical measures of obesity including liver fat accumulation, reduced whole-body insulin sensitivity, hyperinsulinemia, hypoadiponectinemia and adipocyte hypertrophy.

In this month's issue of OBESITY, Tomas Gianotti and colleagues from the University of Buenos Aires, Argentina, report a significantly lower mitochondrial-to-nuclear DNA ratio (mtDNA/nDNA) in insulin resistant (IR) adolescents recruited out of a subset (n=175) of a cross-sectional, population-based study of 934 high school students. In this study, the mtDNA/nDNA ratio was also inversely correlated with HOMA index, a crude but simple measure of insulin resistance.

This study is very much in line with the notion that obesity-prone individuals may have impaired mitochondrial number and/or function resulting in increased risk for obesity.

From the aforementioned twin study, we know that the decreased number and function is not corrected by weight loss.

Indeed the question is whether or not mitochondrial number and function can be increased by prescribing higher activity levels? If yes, how much activity will be needed to reverse these changes? And most importantly, will people with impaired mitochondrial function actually be able to enjoy exercise enough to actually stick with this prescription?

Perhaps it is not obesity that causes impaired mitochondrial function but rather impaired mitochondrial number and/or function that predisposes to obesity. This impairment could be genetic but also due to intrauterine programing or perhaps simply luck of the draw (remember - all mtDNA comes from your mom).

Of course this is not an "excuse" for obesity as is often misinterpreted when data on the genetics and biology are presented. However, it is clear that if you have impaired mitochondrial number and/or function you are much more likely to become obese in an environment that promotes sedentariness than if you were dependent on physical activity to meet your basic needs for survival.

Remember, there were times, not too long ago, when people were actually paid to be physically active. Today, choosing to be physically active actually costs money (not to mention time).

AMS
Edmonton, Alberta

Obesity: It's Not TV - It's TV Dinners

People who watch more TV tend to be heavier that people who don't. The question, however, is whether it is the lack of physical activity associated with TV watching or the snacking that often goes with it that accounts for the weight gain.

This question was recently addressed by Verity Cleland and colleagues from the Menzies Research Institute, Hobart, Tasmania, Australia, in a paper just out in the American Journal of Clinical Nutrition.

This study involved a cross-sectional analysis of data from 2001 Australian adults aged 26-36 y. Waist circumference (WC) was measured at study clinics, and TV viewing time, frequency of food and beverage consumption during TV viewing, leisure time physical activity, and demographic characteristics were self-reported.

In both men and women, watching more than 3 hrs of TV per day was associated with a roughly two-fold higher risk of abdominal obesity compared to men or women watching an hour or less per day.

Interestingly, adjusting for leisure time physical activity did not change this relationship, whereas adjusting for food and beverage consumption during TV viewing did.

The authors conclude that the impact of TV viewing on weight is more likely due to the associated snacking than due to the sedentariness of sitting in front of the TV.

So if you do watch a lot of TV, watch out for those snacks and drinks.

Remember, one of the best weight management tips has always been: do not eat in front of the TV!

AMS
Edmonton, Alberta

Lifestyle not a Determinant of Obesity in Teens?

Now here is a counter intuitive finding from Catherine Sabiston, of McGill University, and P.R.E. Crocker, of the University of British Columbia (UBC) published in the Journal of Adolescent Health earlier this year.

In their study of 900 Vancouver-area 16-18 year-old teenagers in Grades 10 through 12, neither was there a link between body mass index (BMI) values and levels of physical activity nor did the physically active teens eat a markedly healthier diet than their less-active counterparts.

If anything, the heavier teens were actually the ones making healthier food choices while the teens with “healthier” BMI values were no more likely to be physically active than those with higher, “unhealthier” values.

According to Dr. Sabiston (quoted in a press release from McGill University)

“A lot of people are surprised, but when you think about it, BMI doesn’t have a huge impact on physical activity. And in terms of diet, it actually makes sense that someone who is not happy with their body might try to eat more healthily. What this study really says, is that one cannot assume that someone who is physically active necessarily eats a healthy diet – or the reverse, that someone who is more sedentary or has a high BMI by definition eats a diet of junk food."

To me the findings aren't all that surprising. I have always maintained that health cannot be simply deducted from the number on your scale and that for every overweight kid who eats mostly junk food and spends every spare minute on his Xbox, there's a skinny kid out there who's no better.

The simple truth is that eating healthy and exercising is important at any weight!

On the other hand, just as simply eating poorly and not exercising by no means guarantees weight gain - simply eating healthy and exercising does not guarantee a so-called "healthy" weight.

When everyone eats too much and no one moves, it's likely the poor kids with the "wrong" genes that pack on the pounds - the kids with the "right" genes are simply lucky and can apparently get away with their lousy lifestyles - who says life has to be fair!

Of course, the words "wrong" and "right" in the previous sentence refer to these genes in today's world. Until not all too long ago in the history of mankind, the "wrong" genes would have been just "right" and vice versa (talking of thinking in circles).

AMS
Edmonton, Alberta

[Hat tip to Michael Dwyer of CIHR for sending me the McGill press release]

Back Surgery Does Not Cure Obesity

Immobility, due to pain or otherwise, is certainly a major contributor to weight gain. Pain is indeed often presented by overweight and obese patients as a factor limiting their ability to lose weight.

Given the widely-held (but false!) belief that exercise is the most effective way to lose weight, the general expectation of both patients and health professionals is probably that restoring mobility by relieving pain will enable patients to be more physically active and thereby lose weight.

But is this actually the case?

This issue was recently addressed by Ryan Garcia and colleagues from the Department of Orthopaedic Surgery, Case Western Reserve University, Cleveland, OH in a study just out in the Journal of Bone and Joint Surgery.

Garcia and colleagues examined weight changes in 63 overweight and obese patients with neurogenic claudication who experienced substantial pain relief after lumbar decompression surgery for spinal stenosis. Although Zurich Claudication Questionnaire (ZCQ) Symptom Severity and Physical Function scores significantly improved by a mean of 56.4% and 53.0%, respectively, body weight and BMI significantly increased by 2.48 kg and 0.83 kg/m(2), respectively.

Overall, an average 34 months after surgery, 35% of the patients had actually gained at least 5% of their preoperative body weight while only 6% of the patients weighed at least 5% less than before their operation. The vast majority (59%) remained within 5% of their preoperative body weight.

This study, consistent with several previous studies on joint surgery, nicely documents that increased mobility after pain-alleviating surgery does not necessarily translate into weight loss - in fact, most people will either continue to gain weight or simply stay the same.

Obviously, this should not be an argument against alleviating pain in obese patients - no one deserves to live with pain. It just goes to show that increased mobility alone is not likely to substantially lower body weight - at best, it may prevent further weight gain (difficult enough even at the best of times).

This is probably something patients should be counseled about to not raise any false expectations.

On the other hand, it is important to note that this was not a weight-loss study. This means, that patients were not expressly counseled for weight loss or offered obesity treatments.

The question therefore remains whether or not improving mobility in patients by alleviating pain would improve efficacy of obesity management strategies (which I believe it would).

That is obviously a study that remains to be done.

AMS
Edmonton, Alberta

Stop Walking to Gain Belly Fat

As regular readers of my blog know, I love walking (at least when I have to!).

To find out how important walking actually is to help control your weight, apparently all you need to do is stop.

This was exactly what Rasmus Olsen and colleagues from the University of Copenhagen convinced 18 healthy male subjects to do. Participants were instructed to reduce daily steps by using elevators instead of stairs and riding in cars instead of walking or bicycling while maintaining their habitual food intake (JAMA, March 19).

The first set of eight men decreased their pedometer recorded daily steps from a mean value of 6,203 to 1,394 over 22 days. The second set of ten men decreased their mean daily steps from 10,501 to 1,344 over 2 weeks.

While body weight was not reported for the first eight men, they had a marked rise in insulin area-under-the-curve (AUC) following the glucose tolerance test (interpreted as reduced insulin sensitivity).

But even more interestingly, in the second group, although BMI DECREASED(!) from 22.1 to 21.8, intra-abdominal (visceral) fat INCREASED by 7% (as measured by MRI). Lean body mass (as measured by DEXA) decreased by 1.2 Kg while both the insulin and triglyceride response to the tolerance tests were adversely affected.

Not bad for just two weeks of not walking! And these were healthy lean young men to start with - my guess is that the effects in older overweight folks would be even more dramatic.

So why spend money at McDonalds? Just walking less will "supersize" your abdomen as nicely.

AMS
Edmonton, Alberta

Obesity: It's all in Your Cells?

Yesterday I blogged about a remarkable Finnish twin study, in which the investigators went to the considerable trouble of finding monozygotic twin pairs who showed marked differences in body weight. The biggest predictor of weight gain in these genetically identical but weight-discordant co-twins was a markedly lower physical activity level, which in turn, declined even further as the obese co-twins packed on the pounds.

Assuming that this was not just a bunch of "lazy" co-twins, I wondered about what biological factors could possibly be causing these co-twins to be less physically activity. The answer to this question may lie in the results of another study by the same investigators in the same set of twins published in the open access journal PLoS Medicine.

In this study, Kirsi Pietiläinen and colleagues compared the genetic expression profiles in fat cells and macrophages between the obese and non-obese co-twins. Because, by design, the twins were genetically identical, they were able to normalise expression patterns for differences in genetic background, gender and age - thereby cutting through the considerable noise generally associated with expression studies.

In short, the authors found that the fat tissue from the obese co-twins showed a significant up-regulation of inflammatory pathways, significantly reduced mitochondrial DNA copy number, and disturbed mitochondrial energy metabolism—statistically most significantly, the decreased catabolism of branched-chain amino acids (BCAA). These impairments correlated with critical clinical measures of obesity including liver fat accumulation, reduced whole-body insulin sensitivity, hyperinsulinemia, hypoadiponectinemia and adipocyte hypertrophy.

In one individual, who the investigators were able to study before and after an additional weight gain of around 11 Kg over 3 years, mtDNA copy number was further reduced while serum BCAA concentrations and inflammatory activity increased even further.

Although the authors acknowledge that correlations do not prove causality, it is clear from the tone of their discussion that they believe that the metabolic derangements and low mtDNA copy count are a consequence of the obesity and are thus amenable to treatment by diet and exercise (the "politically correct" conclusion).

This is where I wonder if not the reverse may be true. I am no expert on mitochondrial biology, but I would assume that a key consequences of a reduction in mtDNA copy number is a decreased maximal capacity for oxidative phosphorylation, i.e., utilization of fat for energy production.

Assuming for a moment that these findings are also present in skeletal muscle, it would not be hard to imagine that these individuals are likely to find exercise more difficult and tiring than their co-twins with a normal mitochondrial population - less exercise means further weight gain and further decline in mitochondrial function - a nice little vicious cycle, if I ever saw one.

It is hard for me to image that in all 14 obese co-twins lack of physical activity alone was able to bring about the reduced mtDNA copy number, increased inflammation and reduced BCAA metabolism - somehow I find it easier to imagine that it was rather a malfunction in their mitochondria which significantly affected their ability to be (and enjoy being) physically active in the first place.

But of course, this is a chicken-or-egg question that cannot be resolved by the present study.

So the obvious questions now are: Can these co-twins be "rescued" by prescribing higher activity levels? How much activity will be needed to reverse these changes? And most importantly, will these co-twins stick with this prescription?

It's probably hard to enjoy exercise when there's a problem with your fuel cell.

AMS

Activity Determines Discordant Obesity in One-Egg Twins

So for Easter I wanted a posting with "Egg" in the title. What better paper to choose than the recent publication by Kirsi Pietiläinen and colleagues from Helsinki University published in last month's OBESITY?

In this remarkable study, Pietiläinen and colleagues went to the considerable effort of screening 1,870 young adult twin pairs to find 658 monozygotic (MZ) pairs, of whom only 14 (!) pairs reported a BMI difference of at least 4 kg/m2, with one twin being non-obese (BMI approximately 25 kg/m2) and the other obese (BMI approximately 30 kg/m2).

This effort alone shows how rare it is to find MZ twins that are discordant for weight, clear evidence for the well-known fact that body weight is one of the most heritable complex traits found in man, in fact, only marginally less heritable than height.

Nevertheless, the investigators were able to further characterize at least 10 of the 14 BMI-discordant twin pairs and readily identified the difference in physical activity as the key determinant of the discordance. Virtually all of the co-twins who ultimately became obese reported having been less physically active in adolescence than their non-obese co-twins. Furthermore, as they grew heavier, the obese co-twins' physical activity levels declined even further as did their self-perceived physical fitness. Based on accelerometer recordings, the obese co-twins had less than half the daily activity of their non-obese co-twins

In contrast, in the weight-concordant reference MZ twin pairs, physical activity patterns and fitness changed little during adolescence and were similar in the co-twins.

Thus, this paper appears to suggest that even in genetically identical individuals, large amounts of physical activity (or lack thereof) can "override" the genetic determinants of BMI.

What the paper, however, fails to tell us is why in these rare instances (only 14 out of 658 or 2% of MZ pairs) the obese co-twins were less active than their non-obese counterparts.

Why, as discussed in a previous posting on this blog, if the disposition to be physically active is such an 'innate" trait, did these 14 co-twins behave so differently from their siblings? Was it lack of interest, competing hobbies, sibling rivalry, injury?

Or was it epigenetics - i.e. post-conceptional modification of DNA that may involve paramutations, bookmarking, imprinting, gene silencing, X chromosome inactivation, position effects, reprogramming, transvection or maternal (intrauterine) effects - all of which could impact character traits or behaviour in later life?

So, while the paper shows that even in genetically identical individuals the heritability of BMI can be overridden by marked differences in physical activity, it does not provide the answer to whether or not this level of activity can be cognitively induced or, rather, happens as a result of rare quirks of nature.

Clearly, there are a few more eggs to crack before we fully understand why some people "chose" to be physically active and others don't.

Happy Easter!

AMS

Obese Folks: on Your Feet!

One of the most common accusations faced by people with weight problems is that they are simply lazy and just lack the motivation to be active (the other one is that they simply eat too much!).

It turns out that some obese people may in fact be less active than lean individuals. For e.g., a recent study by Darcy Johannsen and colleagues from Iowa State University published in OBESITY, used state-of-the-art activity monitoring technology (IDEAA) to examine in detail the activity patterns of 20 free-living lean and obese women over 14 days. Total energy expenditure was measured using doubly labeled water, body composition was measured using dual energy X-ray absorptiometry.

The main finding was that even after correction for increased body mass, obese women on average expended around 300 KCal less in physical activity per day than their lean counterparts. Overall, obese women sat 2.5 hrs more each day and stood 2 hrs less than the lean women. They also spent only half the time being physically active compared to lean women.

This finding is not new. Previous studies have noted that obese individuals spend less time on their feet and expend less energy through non-exercise thermogenesis (fidgeting). Importantly, intervention studies have shown that this is not corrected by weight loss - rather, the tendency to be less active appears to be innate, i.e. not due to the excess weight.

Well, as usual, Johannson and colleagues conclude their paper with the profound insight that if only obese women adopted the activity pattern of lean women, they wouldn't be obese - and that is where the logic breaks down.

In fact, this is very much like saying that, "if only depressed people could be less sad and, like "normal" people, show more interest in things, they'd be so less depressed".

The issue is not whether or not obese people move less - the question is why they do so. If the tendency to be less physically active and spend less time on their feet is innate - i.e. a character trait that is determined largely by genetics, then trying to get someone with this trait to be more physically active is likely to be difficult.

Perhaps one way of thinking about this is to reverse the argument. If, for a moment, we assumed that being lean was really the problem, then we'd have to teach lean people to really try to sit down more and to focus on being less active, so that they could gain weight. Anyone who believes that it would probably be difficult to teach lean people to sit still, to stop fidgeting and to simply be less active, should realise that for exactly the same reasons it may be unreasonable to expect the opposite of people with excess weight.

Not to say it is impossible - but in both cases it would take a special focus, a lot of resolve and perhaps constant reminding as it goes against their "natural" disposition.

While in today's obesogenic environment the natural disposition to fidget and rush around works to the advantage of lean people, the natural disposition to sit down and not rush around (indeed a "sensible" behaviour in a calorically frugal environment) is a handicap.

Again, the results of such studies should not be interpreted in the sense of: "Aha, so now we know what is "wrong" with people who have obesity - they are indeed lazy!". Rather they should be interpreted in the sense of: "Aha, so that is why people with obesity have such a hard time keeping their weight off - they are simply "programmed" against a senseless waste of energy".

This of course is not an excuse to do nothing - it just means that we must appreciate the extra effort that is required.

In other words, when lean people run around - that's just their nature, they can't help it - it's not because they are extra smart or better people. In fact, now that we have seen this research we should realise that when people who have obesity run around (even a little) this is certainly highly commendable, as we now know that they have to consciously make this extra effort despite their innate tendency to preserve energy.

Creating an environment that fosters time on your feet will serve everyone - the lean people will love it (or not care), those with weight problems will benefit without having to make a conscious effort. Time for more stand-up meetings?

AMS

Exercise Resistance

Recently I blogged about how few people actually take up the advise to be physically active, even when delivered by a health professional (e.g. click here).

A new study in the Lancet now shows how difficult it is, even with the greatest effort, to get a substantial proportion of people moving.

In this study by Kinmonth and colleagues from the General Practice and Primary Care Research Unit, University of Cambridge, 365 sedentary adults with a parental history of type 2 diabetes were randomly assigned to either receiving just a brief advise leaflet in the mail or a 1-year behaviour-change program, delivered either by trained facilitators in participants' homes or to the same program delivered by telephone. The program was designed to alter behavioural determinants, as defined by the theory of planned behaviour, and to teach behaviour-change strategies.

Surprisingly, at 1 year, the physical-activity ratio of participants who received the intervention, by either delivery route, did not differ from the ratio in those who were simply given the brief advice leaflet.

The bottom line of this relatively large randomised trial is clear: A facilitated theory-based behavioural intervention, even when delivered with professional home trainers and individual counseling is no more effective than simply providing an advice leaflet for promotion of physical activity in an at-risk group.

I can only imagine how disappointed the investigators must have been having to conclude that health-care providers should remain cautious about commissioning behavioural programmes into individual preventive health-care services.

This seems very much in line with the large body of evidence that states that people will either exercise or they will not - those who like activity and have done it before will do it again - those who don't - will refuse to do it (in the long term), no matter what.

Of course there will always be some exceptions, but these are likely to be few and far between - the majority is simply resistant to change.

Having predictors of who is likely to adopt exercise and who is not may be important in order to target advise (and resources) to those most likely to actually do it (and persist).

Once again - one-size is unlikely to fit all.

AMS