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Two health physiology researchers discuss the latest obesity news, research, and weight loss products.
Travis Saunders, MSc
106 posts
Peter Janiszewski, PhD
3 posts
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by Travis Saunders, MSc in Obesity Panacea
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 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.... Read more »
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
by Travis Saunders, MSc in Obesity Panacea
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).... Read more »
Saunders, T. (2011) Potential Contributors to the Canadian Pediatric Obesity Epidemic. ISRN Pediatrics, 1-10. DOI: 10.5402/2011/917684
by Travis Saunders, MSc in Obesity Panacea
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.... Read more »
Saunders, T. (2011) Potential Contributors to the Canadian Pediatric Obesity Epidemic. ISRN Pediatrics, 1-10. DOI: 10.5402/2011/917684
by Travis Saunders, MSc in Obesity Panacea
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.... Read more »
Saunders, T. (2011) Potential Contributors to the Canadian Pediatric Obesity Epidemic. ISRN Pediatrics, 1-10. DOI: 10.5402/2011/917684
by Travis Saunders, MSc in Obesity Panacea
Just because one study finds a relationship between A and B, does not mean that other studies will be able to replicate that finding, or that it will extend to other situations. On the face of it, this seems like an incredibly obvious statement. And yet it’s something that newspapers often forget, and which I think could have some very negative consequences.... Read more »
Goldfield, G., Kenny, G., Hadjiyannakis, S., Phillips, P., Alberga, A., Saunders, T., Tremblay, M., Malcolm, J., Prud'homme, D., Gougeon, R.... (2011) Video Game Playing Is Independently Associated with Blood Pressure and Lipids in Overweight and Obese Adolescents. PLoS ONE, 6(11). DOI: 10.1371/journal.pone.0026643
Carson, V., & Janssen, I. (2011) Volume, patterns, and types of sedentary behavior and cardio-metabolic health in children and adolescents: a cross-sectional study. BMC Public Health, 11(1), 274. DOI: 10.1186/1471-2458-11-274
by Travis Saunders, MSc in Obesity Panacea
Some exciting news this week - the world’s first systematic review on the relationship between sedentary behaviour and health in school-aged children has just been published online in the International Journal of Behavioural Nutrition and Physical Activity. I am one of 8 authors on the review (nestled nicely in the middle), which was created to inform the Canadian Sedentary Behaviour Guidelines, released earlier this year.... Read more »
Tremblay, M., LeBlanc, A., Kho, M., Saunders, T., Larouche, R., Colley, R., Goldfield, G., & Connor Gorber, S. (2011) Systematic review of sedentary behaviour and health indicators in school-aged children and youth. International Journal of Behavioral Nutrition and Physical Activity, 8(1), 98. DOI: 10.1186/1479-5868-8-98
by Travis Saunders, MSc, CEP in Obesity Panacea
Image by mhowry
Travis’ Note: Today’s post comes from PhD Student Ash Routen. You can find out more about Ash and his work at the bottom of this post.
Consistent with the majority of developed countries, a significant proportion of children here in the UK are overweight or obese (around 30% of 10-11 year olds as of 2010). How do we know this? Well, since 2005 the UK Department of Health have been operating the ‘National Child Measurement Programme’ (NCMP) a nationwide public health surveillance initiative, which to the best of my knowledge is the biggest in Europe. Annually over one million children (aged 4-5 and 10-11 years) have their height and weight measured by teams of school nurses, these measures are then used to calculate body mass index (BMI), and then BMI determined weight status. This data is used to inform local planning and delivery of weight intervention/healthy lifestyle services, and to produce national overweight and obesity prevalence figures.
As BMI differs between genders and increases with age during childhood, the NCMP categorise the children’s weight status as underweight, healthyweight, overweight or obese, by comparing their BMI to children the same age and gender using a BMI growth reference chart. So, children above the 91st percentile (91% of all children used in the reference sample) are defined as overweight, and above the 98th as obese. In most regions, the child’s weight status is fed back to the parent’s and children by letter, with information on local weight management initiatives if they are categorised as underweight, overweight, or obese. Of course you can imagine the furore of some parent’s and thus the NCMP has attracted quite a lot of negative media attention (e.g.http://www.telegraph.co.uk/health/children_shealth/7514267/Letter-to-fat-four-year-old-prompts-complaint-from-obesity-group.html) as a result. As such there is great onus on ensuring the quality of data and identifying any sources of potential ‘error’, which include human (i.e. reliability of the nurses measurements), technical (i.e. reliability of the scales/height measuring device) and biological ‘error’(i.e. both daily and monthly variation in BMI).
I was interested in the impact of the time of day when the measurements are conducted. The nurses follow a standardised protocol, but can take the measurements at any time of day (and indeed the month of measurement may also vary). We know that our weight fluctuates throughout the day, and that we shrink a little after rising due to gravity pushing us back down! What we didn’t know was if combined variation in these measures would result in a change in BMI. Who cares right? they would be at no more or less risk of adverse health if their BMI shifts a little…but could it be enough for those whom are on the cusp of a BMI weight category (e.g. 90.5 percentile) to be differently classified due to the time of day they are measured?
What did we do?
To investigate this issue we took a sample of 74 children (aged 10-11 years) and measured their height and weight in the morning (0900-1045 hr) and again in the afternoon (1300-1500). From this we calculated their BMI, BMI percentile and weight status category using two set’s of BMI percentile cut-off’s, namely clinical cut-off’s (overweight: 91st and obese: 98th) as used by the NCMP and clinicians, and population monitoring cut-off’s as used mainly by researchers (85th and 95th centiles).
What did we find?
Not surprisingly in the afternoon all the children were shorter (-0.5 cm), however only girls were heavier (+0.1 kg), and BMI (+0.12 kg.m2), and BMI percentile was greater (+2.5 centiles) in all children. In relation to weight status categories there were no shifts in the number of people in each category from morning to afternoon, but on an individual level there were some interesting findings. When applying the clinical BMI cut-off’s we saw that one girl moved from healthyweight to overweight, and using the population monitoring cut-off’s , two girls moved from the healthyweight to overweight category, and one moved from the overweight to obese category with BMI increases of only 0.30, 0.55 and 0.26 kg/m2, respectively.
What are the implications?
We saw that it only takes a height loss of about 1 cm and an increase in weight of about 150g to shift a girls BMI category if they are near to the cut-off threshold. As only a few individuals changed (and this was a small sample) the results may seem inconsequential. However both on an individual and national level there may be some impact. Nationally, comparison of prevalence data (and thus future direction of resources) between schools and regions (and this is where I speculate) may be may be clouded if they measure a greater proportion of their children either in the morning or the afternoon. Whilst the extrapolation of the present observations using the clinical BMI cut-off’s (which the NCMP use in parental feedback) to the potential impact on the national NCMP data is tenuous, it is worthy of consideration. As the time of day when measurements are taken is not standardised, or recorded by the NCMP it could be supposed that 50% of the measurements taken are performed in the morning and 50% in the afternoon. If one in every 27 (3.7%) healthy weight girls (as we found in our sample) were on the cusp of overweight in samples measured in the morning they could well have been categorised as overweight had they been measured in the afternoon. Out of the 162,640 healthyweight girls measured by the NCMP in 2009/10 this would represent 6017 girls being classified as overweight instead of healthyweight, which hinders a ‘true’ assessment of prevalence data.
Arguably of more importance is that potentially 6017 parents and children would be informed that their child is overweight, due to their misfortune of being measured in the afternoon as opposed to the morning. We know that children labelled as overweight may be at greater risk of stigmatisation, teasing and anxiety; it is not unimaginable therefore that such a letter could trigger unhealthy activity and dietary habits and unnecessary parental intervention. For all the useful information such screening programmes provide us researchers, we must be cognisant of the discourse surrounding the issue of childhood obesityand consider the impact of such surveillance programmes on individual children and families (see Michael Gard’s work for a thought provoking viewpoint: http://bod.sagepub.com/content/13/4/118.extract).
What can we do?
In our paper we conclude that arguably, to increase data reliability the time of day in which the measurements are performed should be standardized (to either morning or afternoon) by the NCMP and indeed any public health surveillance programme that does not standardise measurement – this would at least ensure that all children are treated equitably. We do not have one ‘true BMI’, but fluctuate about a mean value on a daily and weekly basis. Therefore for the purposes of comparison, and analysis of trends year-on year, we should choose either to measure in the morning or afternoon. However, on the individual level it appears wise to ensure that children are measured in the morning to avoid unfavourable shifts in weight category and associated psychosocial implications of labelling. Standardisation of the timing of taking the measurements is one simple revision to the procedures of such surveillance programmes that could help to limit the impact of at least one potential ‘error’ variable.
Ash Routen
About the author: Ash Routen is in the final months of his doctoral studies at the University of Worcester, UK examining the impact of pedometer interventions on habitual PA in kids, with an interest in the assessment of body composition and objective physical activity measurement in kids. He can be found on Twitter @AshRouten.
... Read more »
Routen, A., Edwards, M., Upton, D., & Peters, D. (2011) The impact of school-day variation in weight and height on National Child Measurement Programme body mass index-determined weight category in Year 6 children. Child: Care, Health and Development, 37(3), 360-367. DOI: 10.1111/j.1365-2214.2010.01204.x
by Travis Saunders, MSc, CEP in Obesity Panacea
Earlier this year I posted an infographic on the health impact of sedentary behaviour which has generated plenty of discussion both here and elsewhere. Many people are understandably skeptical about the relationship between sedentary behaviour and mortality, so I was excited about the recent publication of two recent systematic reviews focusing on just this issue.
The first, published in the American Journal of Preventive Medicine by Karin Proper and colleagues, focused on the prospective association between sedentary behaviour and obesity, CVD and diabetes risk, as well as mortality. Somewhat surprisingly, they found little evidence that sedentary behaviour was associated with increased body weight or other health risk factors, despite consistent associations between sedentary behaviour and risk of death. From the paper:
Weight Gain:
Based on the inconsistent findings among the [3] prospective studies identified, there is insufficient evidence for a longitudinal relationship between sedentary behavior and body weight/BMI gain.
Risk of Being Overweight or Obese:
Based on the inconsistent findings among the [4] studies, there is insufficient evidence for the relationship between sedentary behavior and the risk for overweight or obesity.
Increased Waist Girth:
Based on this single study, there is insufficient evidence for the relationship between sedentary behavior and waist gain.
Risk of Developing Diabetes:
Based on the consistent findings of… two low-quality studies, there is moderate evidence for a significant positive relationship between the time spent sitting and the risk for type 2 diabetes.
Risk of Cardiovascular Disease:
Based on the findings of the 4 studies identified, there is insufficient evidence for a significant relationship between sedentary behavior and various CVD risk factors.
Endometrial Cancer:
Based on the inconsistencies found between and within the two studies identified, there is insufficient evidence for the relationship between sedentary behavior andendometrial cancer.
As I said, there’s really not much evidence so far that sedentary behaviour is prospectively linked with these various markers of health. However, it does seem to be associated with increased risk of death from various causes:
Based on the findings of the two high-quality studies, there is strong evidence for a relationship between sedentary behavior and mortality from all causes and from CVD, but no evidence for the relationship between sedentary behavior and mortality from cancer.
Another review published late last year focused specifically on sedentary behaviour and cancer outcomes. It’s conclusions were a bit stronger than the review above, but the evidence for a relationship between sedentary behaviour and cancer still seems pretty weak. From the review:
The literature review identified 18 articles pertaining to sedentary behavior and cancer risk, or to sedentary behavior and health outcomes in cancer survivors. Ten of these studies found statistically significant, positive associations between sedentary behavior and cancer outcomes. Sedentary behavior was associated with increased colorectal, endometrial, ovarian, and prostate cancer risk; cancer mortality in women; and weight gain in colorectal cancer survivors. The review of the literature on sedentary behavior and biological pathways supported the hypothesized role of adiposity and metabolic dysfunction as mechanisms operant in the association between sedentary behavior and cancer.
What’s the take-home message?
Sedentary behaviour seems very likely to be associated with increased risk of all-cause and cardiovascular disease mortality, while the relationship between sedentary behaviour and cancer mortality remain quite speculative. Interestingly, prospective studies have yet to find much strong evidence linking sedentary behaviour with prospective risk of cardiovascular disease, despite being associated with increased risk of cardiovascular disease mortality. Clearly there’s still a lot to be worked out here, especially given that so few prospective studies have been performed to date. Further, 17 of 19 studies in the Proper review used self-report measures of sedentary behaviour, which can be dramatically different from directly measured sedentary behaviour.
The prospective relationships between sedentary behaviour and risk markers is likely to become more clear with time. In the meantime, it seems reasonably clear that the more you sit, the greater your risk of mortality.
Standing workstation, anyone?
Travis
Proper, K., Singh, A., van Mechelen, W., & Chinapaw, M. (2011). Sedentary Behaviors and Health Outcomes Among Adults American Journal of Preventive Medicine, 40 (2), 174-182 DOI: 10.1016/j.amepre.2010.10.015
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... Read more »
Proper, K., Singh, A., van Mechelen, W., & Chinapaw, M. (2011) Sedentary Behaviors and Health Outcomes Among Adults. American Journal of Preventive Medicine, 40(2), 174-182. DOI: 10.1016/j.amepre.2010.10.015
by Travis Saunders, MSc, CEP in Obesity Panacea
Image by Editor B
A few weeks ago our friend Colby Vorland of Nutritional Blogma emailed me an article titled “The Chocolate Milk Diet“, which he had come across via Twitter. The article (which was written and published last year by the editor-in-chief of Men’s Health and Women’s Health David Zinczenko) got both of our BS detectors going, and we thought it would be a good idea to tag-team a post deconstructing the arguments in the original article (Given that Colby is far more knowledgeable about nutrition than I am, the lion’s share of this post – and all of the good parts - is his). You can also read the post on his blog, which is definitely worth checking out if you’re not already. Enjoy!
Usually I (Colby) ignore these kind of things, but the article was so nonsensical that I felt it needed to be critiqued, especially considering the huge audience it probably reached and influenced (it received over 2,000 Facebook likes on Yahoo alone! And think of the reach of the Men’s Health magazine). Articles like this really do health professionals a disservice, as they spread bad nutrition information around like wildfire; it is no wonder people don’t know what advice to follow. And of course many other health and fitness organizations including Goodlife, Running Room, and Livestrong.com are also on the chocolate milk bandwagon (the latter two are proudly mentioned in this press release from the Dairy Farmer’s of Canada), such that it is almost impossible to avoid the the chocolate milk media machine. In the face of a barrage of such one-sided information, we can sometimes benefit from a reminder that, as Yoni Freedhoff puts it, “milk is not a magic fairy food that confers the health of immortal unicorns”. So here is our passage-by-passage rebuttal to The Chocolate Milk Diet (emphasis ours).
“Imagine if everything you needed to know about weight loss, you learned in kindergarten.”
Most of us continued learning after kindergarden, Mr. Zinczenko. (OK, no more zingers, only science)
“Well, if your teacher gave you chocolate milk as a lunchtime treat, she was (unknowingly) giving you one of the most powerful weight-loss tools in the nutritional universe. Turns out this childhood staple may be the ideal vehicle for your body’s most neglected nutritional needs. Each bottle delivers a package of micro- and macronutrients that can help you shake off body flab and replace it with firm muscle. And when you served it ice-cold, the creamy sweetness flows across your tongue with all the pleasure of a milk shake. Yum.”
Sure, chocolate milk tastes good- the lowfat (that Zinczenko recommends) version has about 25 grams of sugar per 8 oz. serving (1) (Zinczenko recommends 3 servings per day), twice as much as 1% white. Per glass, the Calorie content is about 158, giving you about 474 Calories per day, just from chocolate milk (1). Let’s see how he thinks adding chocolate milk will help you lose weight:
“That’s the crux of what I’m calling “The Chocolate Milk Diet,” which isn’t a diet at all. It’s essentially three eight-ounce servings of chocolate milk consumed at key points throughout your day: one when you wake up, a second before you exercise, and a third directly after your workout. Or, if it’s your day off, just pattern them for morning, afternoon, and night. Sounds good, right? It is, and that’s why it’s so easy. But is this a free ticket to eat as much fried chicken as you want throughout the rest of the day? Unfortunately not, but alongside a healthy diet, it can help you drop lots of belly fat fast. Here are the four reasons why:
Secret #1: The Calcium Effect
Researchers have known for years about the role that calcium plays in building strong bones, but a more recent development deals with they way it affects your belly. A series of studies have shown that calcium can actually impede your body’s ability to absorb fat, and when researchers in Nebraska analyzed five of these studies, they were able to estimate that consuming 1,000 mg more calcium can translate to losing nearly 18 pounds of flab. What’s more, other studies have shown that dairy foods offer the most readily absorbable calcium you can find. Knock back three servings of brown cow and you’ll reach that crucial 1,000 mg threshold. At that point, any other calcium that you eat or drink is a bonus.”
Zinczenko refers (vaguely of course, who is going to take the time to look any of these up, right?) to 1 review paper from 2000 (2). His claim, however, that you can lose nearly 18 pounds of fat with 1,000 mg of calcium is not supported by this paper. Even in the abstract it states that: “Estimates of the relationship indicate that a 1000-mg calcium intake difference is associated with an 8-kg difference in mean body weight and that calcium intake explains 3% of the variance in body weight.” This result is estimated from statistical analysis of 4 observational studies in the review.
Since this was published, more research has been done in this area. Luckily, a new meta-analysis on randomized controlled trials with calcium and weight was just published by Onakpoya and colleagues (18). Of 24 trials, they included 7 in one analysis (all of which were on overweight or obese subject- important to keep in mind), and concluded that calcium supplementation for at least 6 months reduced body weight by only 0.74 kg, with no relationship between dose and weight loss. The authors note that “the clinical relevance [...] is debatable.” Most trials are small thus it will be important for larger studies to see if this effect is an artifact or not. Note that this is calcium per se, independent of the calories in milk. Also note that they needed to exclude studies from their analysis because of poor design and/or result reporting. It is necessary to survey all research in an area to get a more accurate picture instead of cherry picking results like Zinczenko tries to do to support his ideas. Notably, this meta-analysis was supported by Heaney in an editorial, who has done a lot of the research in this area (and was involved in the 2000 review that Zinczenko cited).
Another recent meta analysis (19) published in in 2009 supports the idea that dairy calcium may prevent fat absorption (e.g. you poop out more fat; this is one mechanism in which calcium may exert a small effect on weight loss), although the magnitude of this effect is pretty tiny. From the review paper:
We estimated that increasing the dairy calcium intake by 1241 mg day-1 resulted in an increase in faecal fat of 5.2 (1.6–8.8) g day-1.
So how much milk would you need to drink in order to get that much calcium? 1 cup of 1% white milk has 290 mg of calcium, which means that you would need to drink roughly 1 L (4.4 cups) in order to get 1290 mg. It should be pointed out that this will mean ingesting more than 400 calories, all so that you can hopefully poop out an extra 81 calories of fat (there are 9 calories per gram of fat). Now if you were to drink chocolate milk as the Men’s Health article suggests, you would need to drink nearly 700 liquid calories in order to excrete 81 calories! Clearly, the math doesn’t quite add up.
While there is biological plausibility that calcium may have a small effect on weight (other potential mechanisms have been identified as well), Zinczenko’s logic does not agree with research and common sense.
“Secret #2: The Vitamin D Factor
All the calcium in the world isn’t going to help you if you don’t get a good dose of vitamin D to go with it. That’s because vitamin D is responsible for moving calcium from your food to your body, which means if you’re running low on D, you’re probably also missing the calcium you need to stay slim.”
Yes, vitamin D promotes calcium absorption, but you need a lot more than what you can get from milk- see below.
“Other symptoms of the D deficiency are weak muscles, easily breakable bones, and depression—not a great combo for success... Read more »
Onakpoya, I., Perry, R., Zhang, J., & Ernst, E. (2011) Efficacy of calcium supplementation for management of overweight and obesity: systematic review of randomized clinical trials. Nutrition Reviews, 69(6), 335-343. DOI: 10.1111/j.1753-4887.2011.00397.x
by Travis Saunders, MSc, CEP in Obesity Panacea
Image by cloudchaser32000
Travis’ Note: Today’s guest post comes from our friend and colleague Dr Ashlee McGuire. The study that Ashlee discusses in this post can be found here. More details on Ashlee and her work can be found at the bottom of this post.
I am sure that most people have heard that some physical activity is better than none and that any increase in physical activity is associated with health benefits. However, when considering a change in physical activity habits to improve health, many people still think that longer bouts of structured exercise (i.e., 30 minutes of moderate to vigorous physical activity on a treadmill) are the only way to gain meaningful improvements.
Unfortunately, this is an overwhelming amount of daily physical activity for someone who typically accumulates none outside of their activities of daily living and as a consequence, this person either a) attempts to engage in a structured physical activity program 5 days per week for a short period before giving up because it is too difficult or b) decides to continue living an inactive lifestyle without attempting to change.
This is a very disheartening and unfortunately common situation.
Thus, I was interested in exploring the association of cardiorespiratory fitness (CRF) with incidental physical activity – non-purposeful physical activity that is accumulated through activities of daily living and is generally low intensity (it is easy) and/or sporadic (it lasts less than 10 minutes in duration). CRF was chosen as the health outcome of choice for 2 main reasons: 1) moderate to high levels of CRF are associated with a significant reduction in morbidity and mortality, and 2) current recommendations suggest that to improve CRF physical activity must be at least moderate intensity and must be accumulated in sustained bouts of at least 10 consecutive minutes.
To examine this issue we investigated a sample of 135 abdominally obese, inactive men and women who had completed a maximal treadmill test to exhaustion to determine CRF and had worn an accelerometer (which objectively measures physical activity) for one week. First, incidental physical activity was quantified in average minutes per day using the accelerometer data. Then, to determine whether the intensity of incidental physical activity was important, it was further broken down into average minutes of light physical activity (e.g., preparing food, strolling through a park) and sporadic moderate physical activity (e.g., higher intensity activities that last less than 10 minutes in duration such as a quick sprint to stop your baby from ingesting a non-edible item or running a block to catch the bus).
What did we find?
Incidental physical activity was a significant predictor of CRF however it only explained a very small amount of variance in the regression model. This suggested that the total volume of incidental physical activity doesn’t have a huge role in determining CRF. However, when incidental physical activity was broken down into light and sporadic moderate physical activity, we found that light physical activity was not associated with CRF, whereas sporadic moderate physical activity was a significant predictor (explaining 20% of the variance in the regression model) and remained so after consideration for gender and body mass index. This suggests that, contrary to current recommendations, physical activity does not need to be accrued in sustained bouts to improve CRF.
What does this mean in terms of risk reduction? To determine this, we split participants into tertiles based on amount of sporadic moderate physical activity and compared CRF values. Between tertiles 1 (average accumulation of 6 minutes of moderate physical activity per day) and 3 (average accumulation of 34 minutes of moderate physical activity per day) there was a 1 MET (3.5 ml/kg/min) difference in CRF. While this number sounds small and insignificant, it was recently demonstrated (Kodama, 2009) that every 1 MET increase in CRF was associated with a 13% and 15% reduction in risk for all-cause mortality and cardiovascular disease, respectively. Thus, in our sample, a difference of approximately 30 minutes of sporadically obtained moderate physical activity may be associated with a significant reduction in morbidity and mortality.
What’s the take-home message?
These results are encouraging and suggest that random, short duration physical activity, which may be more feasible and enjoyable for inactive individuals attempting to engage in physical activity for health benefit, is indeed beneficial.
This study was cross-sectional therefore we unfortunately cannot state that the physical activity caused the improvement in CRF. Also, our study sample was homogenous with respect to phenotype and physical activity levels. Thus, further studies (preferably prospective) are required in a more heterogeneous population.
Nonetheless, I encourage everyone to attempt to increase both the duration and intensity of their incidental physical activity (as Travis and Peter have previously) throughout the day by taking more frequent trips to the water fountain and washroom, paying colleagues personal visits instead of sending emails, and parking further from the building entrance. Every little bit does indeed count!
About the author: Ashlee McGuire recently completed her doctoral studies at Queen’s University (Congrats Ashlee!), where she examined the association of incidental physical activity, sedentary behaviour, and sleep with cardiometabolic risk factors in men and women. Ashlee is also involved in projects aimed at improving access to healthy lifestyle choices within the community and is an avid long distance runner.
McGuire, K., & Ross, R. (2011). Incidental Physical Activity Is Positively Associated With Cardiorespiratory Fitness Medicine & Science in Sports & Exercise DOI: 10.1249/MSS.0b013e31821e4ff2
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McGuire, K., & Ross, R. (2011) Incidental Physical Activity Is Positively Associated With Cardiorespiratory Fitness. Medicine , 1. DOI: 10.1249/MSS.0b013e31821e4ff2
by Peter Janiszewski, Ph.D. in Obesity Panacea
A commonly held belief among many athletes and coaches (particularly male ones) is that sexual intercourse the evening before a competition spells disaster on the big day. Thus, many high-level athletes practice abstinence prior to competition. Muhammad Ali was an outspoken proponent of this rule, as was Marv Levy, head coach of the Buffalo Bills, who separated his athletes from their partners leading up to the SuperBowl.
My fiancée, Marina, and I are running 10k and 5k races this weekend in Ottawa, respectively. During our jog today we were discussing what we should do to maximize our efforts during the run, and in jest, I suggested that we sleep in separate beds leading up to the event. After we came home, I decided to look into this issue more seriously and see if there is any scientific evidence to back up the idea that knockin’ boots pre-competition might negatively influence performance.
Despite what I consider to be a very interesting and valid scientific query, PubMed and Google Scholar revealed little research on the matter (hint: if you are a graduate student in health science or kinesiology and you’re looking for a neat thesis topic – you’re welcome!).
A decent editorial by McGlone and Schrier published in 2000 discussed the evidence available at that time and came up with 3 studies.
According to these authors,
“All of these studies suggested that sex the night before competition does not alter physiological testing results.”
For example, in one study, 14 married males performed a maximum grip strength test the morning after an evening of horizontal mambo with their wives, and the same test after at least 6 days of abstinence. No differences were found between the 2 conditions. Other studies have similarly suggested no effect of bumpin’ uglies on outcomes such as balance, reaction time, aerobic power (stair-climbing exercise), and VO2max.
The two commonly suggested reasons why intercourse may reduce subsequent performance are physical exertion and a decreased testosterone level among men. First, despite the extravagant stories exchanged between males in locker rooms, a normal session of business time between married partners results in the expenditure of only 25-50 calories, and it’s thus unlikely to influence next day energy stores. Keep in mind, however, that the physiological response to sex with a new partner is markedly different and may results in a few extra calories being consumed. In terms of testosterone level, the evidence I could find suggested no influence of intercourse.
While the above studies certainly suggest no physiological change in response to recent coitus, athletic performance also depends on psychological status. It has been suggested that levels of aggression might be reduced after intercourse, and aggression is thought to influence athletic performance. Unfortunately, I am unaware of research either supporting or debunking this hypothesis.
Thus, until evidence to the contrary becomes available, a good wrestle in the sheets with your loved one is unlikely to affect your athletic performance the following day.
Peter
McGlone, S., & Shrier, I. (2000). Does Sex the Night Before Competition Decrease Performance? Clinical Journal of Sport Medicine, 10 (4), 233-234 DOI: 10.1097/00042752-200010000-00001
... Read more »
McGlone, S., & Shrier, I. (2000) Does Sex the Night Before Competition Decrease Performance?. Clinical Journal of Sport Medicine, 10(4), 233-234. DOI: 10.1097/00042752-200010000-00001
by Peter Janiszewski, Ph.D. in Obesity Panacea
Rita Chretien, a Canadian woman survived being stranded inside a vehicle in Nevada for 48 days, by eating only some trail mix and candy, and drinking water from a stream. Apparently, she and her husband were following their GPS instructions on their way to Las Vegas from British Columbia when they took a rural road that essentially turns to a bog in the winter months. Their van eventually got stuck in the mud in the middle of nowhere, and they both waited for help for 3 days without sighting anyone. At this point, Albert Chretien, the husband, left to seek out help, while Rita remained inside the van. When she was found by a group of hunters just last week, she was nearly dead and had lost some 30lbs. Her husband remains to be found.
This recent story of near complete starvation highlights the human ability to survive for long periods of time without sustenance.
Due to obvious ethical concerns, there is not a whole lot of credible scientific data on the topic of starvation and survival. Instead, there are many accounts of either voluntary or involuntary cases of complete or near-complete starvation that allow us to make some very general conclusions.
One of the most well known cases of voluntary starvation, is the hunger strike of Mahatma Ganhdi. During his protest, Gandhi ate absolutely no food and only took sips of water for 21 days, and survived. What extraordinary about this case is the fact that Gandhi was very lean when he started his hunger-strike, thus not having much energy reserve from the outset. Also, it must be noted that during his life, Gandhi is reported to have performed a total of 14 hunger strikes.
In a 1997 editorial in the British Medical Journal, Peel briefly reviewed the available literature regarding human starvation. Generally, it appears as though humans can survive without any food for 30-40 days, as long as they are properly hydrated. Severe symptoms of starvation begin around 35-40 days, and as highlighted by the hunger strikers of the Maze Prison in Belfast in the 1980s, death can occur at around 45 to 61 days.
The most common cause of death in these extreme cases of starvation is myocardial infarction or organ failure, and is suggested to occur most often when a person’s body mass index (BMI) reaches approximately 12.5 kg/m2.
Of course, one would expect marked variability between 2 individuals in their ability to endure starvation. As suggested in a Scientific American article by Alan Lieberson,
The duration of survival without food is greatly influenced by factors such as body weight, genetic variation, other health considerations and, most importantly, the presence or absence of dehydration.
I would add that body composition would also likely play a key role; for the same body weight, the individual with a greater percentage of body fat has a greater on-board storage of calories. Also, a lower muscle mass would generally be associated with reduced caloric consumption. This by extension would suggest that females may have a survival advantage over males due to their greater relative fat stores.
Most important factor of all, however, appears to be hydration.
In the example that started this post, Rita Chretien survived her 48 day ordeal in large part due to the availability to some melted snow for drinking. Indeed, had no water been available, Rita may not have fared as well. In examples of hospitalized individuals who are in a persistent vegetative state, who become cut off from artificial sustenance, death ensues within 10-14 days. Keep in mind that these individuals are in a coma and completely immobile, thereby consuming the lowest amount of energy possible. It can thus be surmised that the same conditions (no food or water) in a person who is at least somewhat active, and who may perspire, would only lead to a much swifter end.
For individuals who like to get out into the wilderness, and who upon reading accounts of other’s misadventures (Into the Wild, 127 Hours, etc.) are not in the least discouraged from following suit (present company included), ensuring to always have a reasonable supply of water should be priority number one. Additionally, as is well documented in the eventual demise of Christopher McCandless (Into the Wild) the avoidance of eating unknown plants and shrubs can also be a key survival strategy.
Peter
Peel M (1997). Hunger strikes. BMJ (Clinical research ed.), 315 (7112), 829-30 PMID: 9353494
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Peel M. (1997) Hunger strikes. BMJ (Clinical research ed.), 315(7112), 829-30. PMID: 9353494
by Peter Janiszewski, Ph.D. in Obesity Panacea
Due to the increasing obsession with quick solutions to excess fat mass, liposuction has become one of the most popular cosmetic procedures.
And as far as simply removing large volumes of subcutaneous fat from one’s body, it just may be the most effective method – certainly, far superior to diet/exercise or bariatric surgery.
But there are a few catches.
As I have previously discussed, in contrast to losing weight via lifestyle modification or bariatric surgery, liposuction does not make an obese person healthier. In fact, the removal of benign subcutaneous fat stores may actually make you worse off in terms of metabolic health.
Also, as I suggested in an earlier post, there was some very preliminary evidence suggesting that after the removal of fat from the buttocks, thighs, and abdomen, women see a compensatory increase in the fat deposition in other places – namely, their breasts. A 2-for-1 deal, if you will.
However, a hot-off-the-press study by Hernandez and colleagues suggests something less ideal than this scenario. Indeed, the authors found that a year after liposuction was performed the fat initially removed is basically all replaced, but not necessarily where you’d want it to go.
Specifically, while fat removed from the thighs and buttocks tended to stay ‘off’, abdominal fat increased to essentially compensate for any initial fat reduction (regardless of whether or not abdominal fat was removed during the procedure). There was a particularly significant growth of fat in the visceral depot.
So, essentially liposuction can permanently reduce fat stores in areas that may be beneficial to metabolic health (butt, hips and thighs) but increase fat stores in areas known to lead to metabolic problems (abdominal, specifically visceral fat).
Not good.
Finally, as was suggested by other studies, the women who underwent liposuction in the current study did not experience any metabolic benefits from the procedure.
To sum up, liposuction will:
1) not improve your health
2) not permanently reduce fat mass
3) redistribute body fat from good to bad areas of your body
Peter
Hernandez, T., Kittelson, J., Law, C., Ketch, L., Stob, N., Lindstrom, R., Scherzinger, A., Stamm, E., & Eckel, R. (2011). Fat Redistribution Following Suction Lipectomy: Defense of Body Fat and Patterns of Restoration Obesity DOI: 10.1038/oby.2011.64
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Hernandez, T., Kittelson, J., Law, C., Ketch, L., Stob, N., Lindstrom, R., Scherzinger, A., Stamm, E., & Eckel, R. (2011) Fat Redistribution Following Suction Lipectomy: Defense of Body Fat and Patterns of Restoration. Obesity. DOI: 10.1038/oby.2011.64
by Travis Saunders, MSc, CEP in Obesity Panacea
Image from Gamebike.com
Active gaming (aka exer-gaming) is the term used for video games that involve some level of physical activity. I’ve discussed active gaming on Obesity Panacea in the past, and while I don’t doubt that it can be an effective tool for promoting physical activity in certain specific situations (eg as a form of physiotherapy), I remain skeptical about it’s ability to increase physical activity levels for the vast majority of children.
Unfortunately for active gaming enthusiasts, a study recently published in Applied Physiology, Nutrition and Metabolism suggests that my skepticism may have been well-founded. In this new study (available free to Canadians here) researchers at the Children’s Hospital of Eastern Ontario examined the impact of the GameBike on exercise adherence, energy expenditure, aerobic fitness, and metabolic health in overweight and obese adolescents with at least one metabolic complication.
Briefly, the GameBike is an exercise bike that attaches to any video-game console and allows people to compete in racing games by pedaling the bike. The faster you pedal, the better your score. I haven’t played it myself, but I will admit that it does sound more fun that simply riding an exercise bike.
In this study, the authors compared the impact of the GameBike with the impact of simply listening to music (on the radio, a CD, or personal music player). In both conditions, participants were asked to attend the lab twice a week for 10 weeks. Each session lasted for 60 minutes, and while the participants had to remain in the lab for that time, the amount of time spent cycling was completely up to them.
What happened?
Somewhat surprisingly, listening to music was actually more effective than the GameBike in a number of important categories. Participants in the music group missed fewer sessions (8% vs 14%), spent nearly twice as much time exercising at a vigorous intensity in each session (25 min vs 14 min), and cycled 2.3 kilometers (~1.5 miles) farther every session. Both groups saw significant increases in fitness over the course of the intervention, while neither group saw changes in metabolic profile (although there was a reduction in total cholesterol when the groups were collapsed).
I will readily admit that this study doesn’t suggest that the GameBike is completely ineffective – but it does appear to be substantially less effective than simply listening to music. This is somewhat surprising given that the GameBike website claims immodestly that the GameBike:
…has changed the world as we know it.
And let’s not forget that listening to music is incredibly cheap, while the Game Bike costs $1500-2000. Certainly not the most cost-effective strategy for promoting physical activity, and one more reason to think that active gaming may not be the panacea for the childhood inactivity crisis.
Travis
Adamo KB, Rutherford JA, & Goldfield GS (2010). Effects of interactive video game cycling on overweight and obese adolescent health. Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme, 35 (6), 805-15 PMID: 21164552
... Read more »
Adamo KB, Rutherford JA, & Goldfield GS. (2010) Effects of interactive video game cycling on overweight and obese adolescent health. Applied physiology, nutrition, and metabolism , 35(6), 805-15. PMID: 21164552
by Travis Saunders, MSc, CEP in Obesity Panacea
Regular readers of Obesity Panacea will know that one of my favourite topics (and the focus of my PhD) is the health impact of sedentary behaviour. Last fall computational biologist Larry Parnell left a comment linking to a recent paper of his exploring how genes modify the health impact of sedentary behaviour. The paper was fascinating, but since genes aren’t my area of expertise I wasn’t sure that I could do it justice on my own. Luckily, Larry put me in touch with the study’s lead author Caren Smith, who did a fantastic job of explaining the study in terms that non-geneticists like me can understand! Below are my questions and Caren’s answers.
1. Could you briefly summarize the findings of your study in lay-terms?
This study, and other “gene-environment interaction” studies are based on growing awareness that our health status is based not only on our genes or only on our environment (diet, activity level, smoking, alcohol), but on the ways in which these two components “interact” with each other. For example, depending on genetic makeup, some people may be more sensitive than others to the effects of physical inactivity. The current study examines the effects of physical inactivity (quantified as computer time and television time or ‘screen time’) on HDL (the ‘good cholesterol’). Depending on the version of a particular gene that a person carries, inactivity may be more or less likely to adversely affect (eg, lower) the individual’s HDL.
2. What is a genetic polymorphism?
A genetic polymorphism is a variation of a specific gene at a specific location in the DNA. The word polymorphism means ‘many shapes’, reflecting that at a given position, there are different varieties of a particular segment of DNA . Although overall we (as humans, and even as higher primates) are much more genetically similar than we are different, at least xxxx polymorphisms have been identified in people. Some of these are associated with health-related traits such as diabetes, heart disease or lipid levels, although our understanding of the consequences of polymorphisms or even how many exist across all of the world’s people is still quite limited.
3. Your results showed a significant interaction between screen time, genotype and HDL-cholesterol levels in women, but not men. Why do you think the interaction was only seen in women? Does this mean that men don’t need to worry about screen time, at least when it comes to HDL?
The reasons for our detection of the interaction only in women are unclear. We know that HDL differs, overall between men and women, with women having higher HDL on average. Several earlier (non-genetic) studies reported similar relationships between television viewing and risk of disease which were limited to women. These differences could be related to gender-specific biology, but could also be related to broader issues, such as differences in the ways men and women spend their leisure time, or what kind of work they perform inside or outside the home.
With respect to the issue of exempting men from any concern about screen time and HDL, we need to emphasize that we examined a single polymorphism in a single (relatively small) group of white individuals living in the US Midwest. Our observations are therefore incomplete, and may not be generalizable to all individuals. Further, HDL is a ‘complex trait’ which is determined not only by a single gene and a single exposure (eg, physical activity) but in fact by many genes and many other exposures including smoking, drinking alcohol and body weight. Other genes (we only studied one) may be more important in men.
4. What is the clinical significance of the relationship between screen time, genotype, and HDL cholesterol that you observe in your findings? Should people be worried about their genotype in addition to the amount of time that they spend being sedentary?
When we think about clinical significance of a genetic finding, we often look at the amount of difference between the two genotype groups, and/or between the two environment groups (low and high inactivity, in this case). In the current study, women with high screen time and the ‘higher risk’ genotype had an average HDL of 48 whereas women with the same genotype but low screen time had an average HDL of 57. A difference of 9 units for HDL would be considered clinically relevant, since even an increase of 1 unit will substantially reduce risk of cardiovascular disease. With respect to worrying about genotype vs. worrying about sedentary behavior, at the moment we know more about the overwhelmingly beneficial effects of physical activity than we do about the effects of interactions with certain genotype. While it is likely that some people derive greater benefits than others from exercise (or conversely, at put at higher risk through inactivity), the vast majority of people would benefit from increasing their overall physical activity.
5. This paper examined endothelial lipase, but other work in animals suggests that sedentary behaviour also has a dramatic influence on lipoprotein lipase activity. For example, this study suggests that 6 hours of muscle inactivity reduces LPL activity by roughly 50% in animal models. Could the polymorphisms examined in this study be related to LPL activity as well as endothelial lipase?
The specific polymorphism that we examined was in the gene that ‘codes’ for the enzyme called ‘endothelial lipase’. That is: this gene contains instructions which are used to construct this enzyme, specifically, and not other enzymes. However, you bring up an important point which is that many other enzymes (such as LPL ( lipoprotein lipase)), or proteins within metabolic pathways are affecting HDL level. It is also possible that an individual with the endothelial polymorphism might also have polymorphisms in the genes encoding any of these other components, and that these polymorphisms could affect HDL or any other health-related trait, either directly or through interaction with an environmental exposure. The full range of polymorphisms which affect even the single trait of HDL is unknown.
6. What is the next step as far as research is concerned?
The best way to continue research in this area would be to carry out an ‘intervention trial’. In this kind of study, people volunteer to enroll in a controlled study for a specified period of time and to agree to the terms of the study. For example, the design of the study might specify periods of activity and periods of inactivity (or record these very precisely using a device that quantifies movement), and also control for other factors which influence HDL (see the next answer below). Before enrolling in the study, people would be tested (genotyped) to see whether they have the polymorphism that we studied, to make sure that there are similar numbers of people with and without the polymorphism to compare. The intervention trial is a more reliable design for establishing ‘causality’ – that is, for being more certain that the effects we see are due to gene-screen time interactions, and not to some other (unknown) factor.
7. What is the take-home message for people who want to improve their HDL cholesterol levels? [feel free to speculate wildly here ]
For most people reading this interview, the single most important factor affecting HDL is body weight or waist size. The majority of people in the US are overweight or obese. HDL levels are very sensitive to extra weight which tends to decrease HDL levels, especially if the weight is concentrated in the abdomen. The same is true for another lipid in the blood called triglyceride, which increases in response to extra weight. The combination of high triglycerides and low HDL is associated with a pre-diabetes condition called ‘metabolic syndrome’ which affects more and more people in the US. Physical activity helps in the maintenance of a healthy body weight, leading not only to healthier HDL but also to an overall prevention of metabolic and other diseases.
Other lifestyle factors which affect HDL are smoking and drinking alcohol. Smoking decreases HDL (perhaps for some people more than others, which may depend on their genes). Cigarette smoking also increases triglycerides, so that improving blood lipids represents yet one more reason to stop smoking. Moderate use of alcohol can i... Read more »
Smith, C., Arnett, D., Tsai, M., Lai, C., Parnell, L., Shen, J., Laclaustra, M., Junyent, M., & Ordovás, J. (2009) Physical inactivity interacts with an endothelial lipase polymorphism to modulate high density lipoprotein cholesterol in the GOLDN study. Atherosclerosis, 206(2), 500-504. DOI: 10.1016/j.atherosclerosis.2009.03.012
by Travis Saunders, MSc, CEP in Obesity Panacea
As many of our readers will know Canada is in the midst of an election campaign and the major parties are putting out a number of policy ideas on a daily basis. One idea proposed by Conservative leader Stephen Harper was to expand the Canadian Children’s Fitness Tax Credit (CFTC). As it currently stands, the CFTC offers a $500 non-refundable tax credit that parents can receive by enrolling their child in an approved physical activity program. If I understand it correctly, this means that if your income is $50,000, claiming this credit would effectively reduce your taxable income to $49,500.
While a $500 tax credit may sound pretty large, at the end of the day parents only save a maximum of $75 per child (this saving can be increased by another $75 if the child has a disability). And keep in mind that parents still need to be able to afford the full $500 fee up front – they don’t get the $75 saving until tax season. So if Junior’s soccer fees come to $500 and you only have $425 dollars, you’re out of luck. You need to be able to pay that full $500 fee and then wait until the following spring to have your tax-bill reduced by $75.
Mr Harper is proposing that the current CFTC be expanded to offer a $1,000 tax-credit per child, as well as offering a similar $500 tax-credit for adults (an important detail being that these credits won’t be until the budget is balanced… which is projected to be 2015 at the earliest). This would mean that parents could now save up to $150 per child, and an additional $75 for themselves…. once the budget is balanced.
These types of tax-credits seem to be catching on with politicians on both sides of the political spectrum as similar credits have been enacted or expanded by the Liberal government here in Ontario, the New Democratic Party in Manitoba, the Progressive Conservative Party in Nova Scotia, the Yukon Party in the Yukon and the Saskatchewan Party in (you guessed it) Saskatchewan (one key difference for the Saskatchewan program being that it is fully refundable). Similar credits are rumored to be in the works in both Australia and the USA as well.
So, since are these types of tax-credits seem to be increasing in popularity among politicians, and given the limitations described above, is there any evidence that they actually increase physical activity levels? Luckily, a recent paper by John Spence and colleagues at the University of Alberta looked at this exact question.
In this new paper, Dr Spence et al. surveyed a representative sample of 2,135 Canadian adults to ask them if they were aware of the CFTC, if they had claimed it/planned to claim it, and whether they believed that the CFTC led to their child being more involved in physical activity programs.
I have inserted 2 figures of their most telling results below. I graphed it twice and wasn’t sure which way did a better job of breaking it down, so I have included both.
Figure 1. Result by Income Quartile (Q1 = lowest income, Q4 = highest income).
Data from Spence et al., 2010
Figure 2. Results by question.
Data from Spence et al. 2010
Not surprisingly, both graphs suggest that the individuals with a higher income were much more likely to report having a child involved with organized physical activity (68% in Q4 vs 40% in Q1). Similarly, these high income individuals were much more likely to have knowledge of the CFTC, and have claimed it in 2007 or plan to claim it in 2008. The proportion of individuals in Q3 and Q4 who claimed the CFTC in 2007 was double the proportion of individuals in Q1. The authors also note that among those who claimed the CFTC in the past only 15% said that it led to their children being more involved in organized physical activity.
Given these findings Dr Spence and colleagues conclude that:
More than half of Canadian parents with children have claimed the CFTC. However, the tax credit appears to benefit the wealthier families in Canada.
Clearly, if increasing enrollment in organized physical activity is the goal, this type of tax-credit seems unlikely to make much of a difference. Based on the results of this paper, it seems that the current CFTC is of benefit to people who can already afford to put their kids in organized sport, but is of little use to the children who need it the most.
I would argue that for the same amount of money, we could get far more children involved in sport by funding programs directly, or by working out a system whereby children from low-income families simply have to pay lower registration fees compared to those from high-income families. I know that many sports programs, such as the Fredericton Youth Hockey Association, already have systems like this in place by reducing registration fees and/or providing free equipment to children in financial need. If getting kids involved in organized activities is the goal then I would argue that this type of program is much more likely to make an actual difference than the fitness tax credits that are popping up around the country (Full disclosure – my dad is heavily involved with the FYHA and its program for kids with financial need, although I’d be a fan of the program even if he wasn’t).
All that to say that while expanding the CFTC isn’t necessarily a bad thing, it’s probably not going to do much to increase enrollment in organized physical activity among those who need it most.
For an excellent explanation of why the CFTC isn’t terribly effective from an economic perspective, I suggest this Globe and Mail article by Kevin Milligan.
Hat tip to Meghann Lloyd for letting me know about the plans to expand the CFTC (if/when the budget is balanced).
Travis
Spence, J., Holt, N., Dutove, J., & Carson, V. (2010). Uptake and effectiveness of the Children’s Fitness Tax Credit in Canada: the rich get richer BMC Public Health, 10 (1) DOI: 10.1186/1471-2458-10-356
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Spence, J., Holt, N., Dutove, J., & Carson, V. (2010) Uptake and effectiveness of the Children's Fitness Tax Credit in Canada: the rich get richer. BMC Public Health, 10(1), 356. DOI: 10.1186/1471-2458-10-356
by Peter Janiszewski, Ph.D. in Obesity Panacea
Breakfast is the most important meal of the day, or so goes the old adage. However, in today’s fast-paced society, people are cutting corners at every turn to save some time. One of these oft-cut corners during the morning rush is breakfast.
While some individuals skip breakfast in an effort to curb their daily calorie intake and thus lose weight, others simply don’t give themselves enough time in the morning before they’re off for the day. Whatever the case, research suggests breakfast skippers are doing more damage than good.
For example, many cross-sectional findings have suggested that breakfast skipping is associated with a higher body weight. However, due to the nature of the analysis it is difficult to ascertain what preceded what: the excess weight or the skipping breakfast.
A new study in the International Journal of Obesity evaluated the prospective relationship between skipping breakfast and change in weight over a 2 year period among 68,606 Chinese grade school children.
Of all the kids assessed, approximately 5% of both the boys and girls were skipping breakfast. As suggested by prior studies, when assessed at one time-point those who were skipping breakfast also tended to be heavier.
In the prospective analises, the authors found that those kids who were skipping breakfast in grade 4 tended to gain significantly more weight by grade 6 than those who ate breakfast. This observation was particularly strong among kids who also skipped lunch.
That is, kids who skipped breakfast and also lunch had the highest risk of gaining weight over the 2 year follow-up period.
I realize it is a bit counter-intuitive that skipping meals, therefore cutting calorie intake would result in weight gain rather than loss, but there are a few plausible reasons for such an observation.
For example, it has been suggested that breakfast-skippers are more likely to eat between meals and also that these in-between-meals tend to be of high fat/sugar/calorie composition. I know from personal experience that when on occasion I would miss breakfast, by the time 10:30am came around I was ravenous with particular craving for specific foods, namely of the greasy, high-calorie variety.
Alternatively, kids and adults who skip breakfast may be less likely to be physically active throughout the day, thereby reducing caloric expenditure.
Whatever the mechanism, one thing is certain: skipping breakfast is not likely to have the intended result of reduced body weight.
Peter
Tin, S., Ho, S., Mak, K., Wan, K., & Lam, T. (2011). Breakfast skipping and change in body mass index in young children International Journal of Obesity DOI: 10.1038/ijo.2011.58
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Tin, S., Ho, S., Mak, K., Wan, K., & Lam, T. (2011) Breakfast skipping and change in body mass index in young children. International Journal of Obesity. DOI: 10.1038/ijo.2011.58
by Travis Saunders, MSc, CEP in Obesity Panacea
Photo by cupcakes2
Human Chorionic Gonadotropin (hCG) is the most thoroughly debunked weight loss gimmick in medical history. We have known since the mid-1970′s that hCG has no impact on body weight whatsoever. I’ve discussed it a number of times, and it always amazes me just how much evidence there is that hCG is no better than a placebo. My favourite hCG-related quote comes from this systematic review, which sums things up pretty nicely:
“there is no scientific evidence that hCG is effective in the treatment of obesity; it does not bring about weight loss or fat redistribution, nor does it reduce hunger or induce a feeling of well-being”.
And don’t forget that it comes from the urine of pregnant women who are often misled into thinking that it is going to be used for fertility treatments (a legitimate use of hCG). Seriously. From the same review as above:
“hCG is obtained from the urine of pregnant women who donate their urine idealistically in the belief that it will be used to treat an entirely different condition, namely infertility”
So when it comes to body weight, it seems pretty clear that hCG is nothing but a placebo. An expensive placebo that is obtained by misleading pregnant women into donating their urine, but a placebo nonetheless. It couldn’t get any worse for proponents of hCG for weight loss, right?
Actually, it could.
It turns out that urine-derived fertility treatments like hCG could transmit prions, the misfolded proteins responsible for brain-wasting diseases like mad cow disease, and it’s human equivalent, Creutzfeldt-Jakob disease.
These findings come from a paper published in PLoS One earlier this week. As I mentioned in passing up above, hCG and other gonadotropin hormones are derived from the urine of pregnant women to be used as a legitimate fertility treatment. In this new paper Alain Van Dorsselaer and colleagues examined hCG and these other urine-derived treatments for the presence of non-gonadotropin protein. They found that prion protein was a major source of non-gonadotropin protein in urine-derived hCG. In other words, prions have made their way from the donors into the hCG.
So there are prions in the urine-derived hCG – should we be concerned? From the paper (emphasis mine):
Current urine collection systems pool the urine of thousands of donors and, unlike the blood collection system, do not allow for donor tracing. There is also no mechanism of ensuring that the designated donor is actually the one who provides the urine, as donation is normally done at home. However, even if donor management and tracing were flawless, the fact that prionuria may exist well before the onset of clinically overt prion disease, without being detectable by current methods, remains a cause for concern. Furthermore, the now indisputable detection of prions in urine of experimental animals, the lack of a species barrier for human-to-human transmission, the relative efficiency of the intramuscular injection route for prion transmission, and the young age of fertility drug recipients all support application of the ‘precautionary principle’ for urinary derived pharmaceuticals. As risk management paradigms shift towards more proactive approaches intended to ‘anticipate and prevent’ emerging risks [23]–[26], a careful examination of the risk of transmission of human prion disease through the use of urine-derived hormones and peptides would appear to be warranted.
Now I personally don’t know much about prions, but I’m taking this to mean that we should probably investigate this more closely if we’re going to continue giving people urine-derived hCG for any reason. Also, we should stop giving hCG to people who don’t need it! Interestingly, this exact issue was discussed in the February issue of the West Virginia Medical Journal (what, you don’t read WVMJ?). Although his editorial was published before the new paper in PLoS ONE, Dr Roger Toffle argues that prions could theoretically be passed from donor to recipient resulting in Creutzfeld-Jakob disease, and cites the initial discontinuation of human-derived gonadotropins as being due to concerns over this very issue (Dr Toffle also explains that increased demand for hCG among people trying to lose weight has resulted in shortages and increased costs for those attempting to procure it for legitimate fertility-related purposes – yet another downside to the promotion of hCG for weight loss).
In their new PLoS ONE paper, Dr Van Dorsselaer and colleagues are quick to point out that while these new results suggest that it is theoretically plausible that prions could be transmitted through urine, there have not been any documented cases of it actually happening. Still, we have now arrived at an odd situation where a common weight loss gimmick may have a better chance of giving you mad cow disease than helping you lose weight.
Let’s just briefly recap:
hCG is obtained by misleading pregnant women who think they are donating their urine to help people get pregnant,
hCG is no better than a placebo in promoting weight loss,
The (nonsensical) demand for hCG in the treatment of obesity has resulted in increased costs for people who need hCG for legitimate uses, and finally
hCG may give you mad cow disease
The cost-benefit ratio clearly doesn’t make sense when it comes to hCG for weight loss.
Travis
Van Dorsselaer, A., Carapito, C., Delalande, F., Schaeffer-Reiss, C., Thierse, D., Diemer, H., McNair, D., Krewski, D., & Cashman, N. (2011). Detection of Prion Protein in Urine-Derived Injectable Fertility Products by a Targeted Proteomic Approach PLoS ONE, 6 (3) DOI: 10.1371/journal.pone.0017815
... Read more »
Van Dorsselaer, A., Carapito, C., Delalande, F., Schaeffer-Reiss, C., Thierse, D., Diemer, H., McNair, D., Krewski, D., & Cashman, N. (2011) Detection of Prion Protein in Urine-Derived Injectable Fertility Products by a Targeted Proteomic Approach. PLoS ONE, 6(3). DOI: 10.1371/journal.pone.0017815
by Travis Saunders, MSc, CEP in Obesity Panacea
Dr Angelo Tremblay
It’s time for part 2 in our series on obesity prevention with Universite Laval obesity researcher Angelo Tremblay (Part 1, which focused on the relationship between sleep and obesity, can be found here).
In today’s episode he discusses the important role that mental work and stress have on appetite, and therefore energy balance. He also explains ways that we can reduce the impact of mental work on energy balance, either by reducing the amount of mental work that children must deal with on a daily basis (e.g. less class time) or increasing the amount of physical activity in our daily lives. He also explains his strategy of “running meetings”, which got his lab featured in Runner’s World magazine.
As with last week, the presentation can be listened to as a typical audio-only podcast, or it can be viewed as a webinar with powerpoint slides. This week’s presentation is just over 15 minutes.
View more webinars from TravisSaunders
A reminder that email subscribers can listen to the podcast here on the blog, and can also download it directly by clicking here (it’s released with a creative commons license, so feel free to embed or sample it on other sites however you please). And to have all of our podcasts delivered directly to your ipod, you can also subscribe via itunes. To view all of our former podcasts, click here.
As always, we’d love to hear your thoughts and comments. Enjoy the podcast, and don’t forget to check-in for next week’s podcast on the impact of mental work on appetite and food intake!
Travis
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CHAPUT, J., & TREMBLAY, A. (2007). Acute effects of knowledge-based work on feeding behavior and energy intake Physiology & Behavior, 90 (1), 66-72 DOI: 10.1016/j.physbeh.2006.08.030
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CHAPUT, J., & TREMBLAY, A. (2007) Acute effects of knowledge-based work on feeding behavior and energy intake. Physiology , 90(1), 66-72. DOI: 10.1016/j.physbeh.2006.08.030
by Peter Janiszewski, Ph.D. in Obesity Panacea
There are few of us who can honestly say they are not stressed out at least some of the time. Too much to do, not enough time, looming deadlines, financial concerns, health problems, etc. can all cause us to feel on edge.
Your heart rate and blood pressure soar, you start perspiring, sleeping becomes a challenge, you’re irritable, and so on.
As you might have imagined, chronic psychological stress negatively impacts on your physical health, increasing the chances of countless chronic diseases. Additionally, stress can also reduce your lifespan.
Findings on a more cellular level suggest that psychological stress expedites the aging process of your body’s cells. Specifically, stress has been correlated with telomere shortening of a cell’s chromosomes. Every time a cell divides, and it replicates and shares the genetic information wound up in its chromosomes with its new copy, the new cell retains a slightly smaller end section of the chromosome, termed the telomere. When the telomere gets to a critical length, the cell reaches a point it can no longer divide properly.
When this begins to occur on a systemic level, you are in trouble.
And this is essentially what happens with aging, leading to cellular senescence.
So what effect, if any, does exercise have on this negative impact of psychological stress on cellular aging?
A recent study investigated this very question in a sample of 63 healthy post-menopausal women who were assessed for stress via questionnaire, physical activity levels over a 3 day period, and telomere length via a process I barely understand, so I won’t try to explain (it is Friday, after all).
For purposes of comparison, the women were divided into sedentary (< 33 minutes during the 3 days) or active (>33 minutes during the 3 days) – not a very high bar for activity.
Not surprisingly, participants with higher levels of stress were less likely to exercise, have higher BMI, less years of education, and shorter telomere length.
In terms of exercise protecting you from the negative cellular effects of stress, the authors found the following:
Among sedentary individuals, a 1 unit increase in perceived stress was associated with a 15-fold increased risk of having short telomeres (in the lower tertile of telomere length in the entire sample).
Among active individuals, a 1 unit increase in perceived stress had NO RELATIONSHIP with telomere length.
In other words, those who are active (and just barely so, based on the categorization in this study: 11 mins per day) seem to be protected against the cellular damage caused by cognitive stress
Keep in mind these analyses accounted for differences in BMI, education, age, and anti-oxidant use.
Bottom line:
Just in case you needed another reason to be physically active, regular activity may protect your cells from the damage caused by daily stresses of modern life. Unfortunately, those people who could benefit the most from physical activity – stressed individuals – are least likely to be active.
Peter
Puterman, E., Lin, J., Blackburn, E., O’Donovan, A., Adler, N., & Epel, E. (2010). The Power of Exercise: Buffering the Effect of Chronic Stress on Telomere Length PLoS ONE, 5 (5) DOI: 10.1371/journal.pone.0010837
... Read more »
Puterman, E., Lin, J., Blackburn, E., O'Donovan, A., Adler, N., & Epel, E. (2010) The Power of Exercise: Buffering the Effect of Chronic Stress on Telomere Length. PLoS ONE, 5(5). DOI: 10.1371/journal.pone.0010837
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