Obesity Promotes Musculoskeletal Problems in Kids
Not that this study should come as a surprise – indeed, regular readers of this blog will be well aware of the link between excess weight and bone and joint problems. Perhaps, what is surprising about this study is that it comes from The Netherlands, one of the leanest countries in Europe, which is a obviously also starting to have obesity problems of its own. In this study, just published in the Annals of Family Medicine, Marjolein Krul and colleagues from the University of Rotterdam, compared the frequency of musculoskeletal problems in overweight and obese children with that in normal-weight children in a cross-sectional database and face-to-face interview study that included 2,459 children aged 2 to 17 years from Dutch family practices. Overweight and obese children in both age-groups (2 to 11 years and 12 to 17 years) reported significantly more musculoskeletal problems (OR = 1.86 and OR = 1.69, respectively) than normal-weight children. In general children who were overweight or obese were almost twice as likely to report ankle and foot problems than children who were of normal weight. Overweight and obese children aged 12 to 17 years were also twice as likely to consult their family physicians with lower extremity problems than normal-weight children. So much for the notion that “chubbiness” in childhood is something that is cute and just a sign of a “healthy” appetite. What can the poor kids do? More often than not, excess weight is a problem that affects more than one member in the family and may well require family-based interventions. Simply telling the overweight kid to exercise more (especially with already existing musculoskeletal problems) is probably not the solution. AMS Edmonton, Alberta
Is Obesity a Risk Factor for Tendinopathy?
Without question, people carrying extra weight are at high risk for mechanical injury to their musculoskeletal system and need to be careful when attempting any form of physical activity to not inadvertently promote injury and subsequent immobility with all its detrimental consequences for further weight gain and loss of fitness. Apart from the excess mechanical pressures on the joints and ligaments, new research suggests that obesity may also play an important, hitherto largely unrecognized role, in tendinopathies, a common painful condition that affects the tendons rather than the joints. (Tedons are the ligament-like structures that attach muscles to bone and are thus the key tissues responsible for transferring muscle strength to the skeletal system.) In a systematic review published in this month’s issue of Arthritis and Rheumatism, James Gaida and colleagues from Deakin University, Melbourne, Australia, examined studies that compared adiposity between subjects with and without tendon injury or examined adiposity as a predictor of conservative treatment success. They identified 4 longitudinal cohorts, 14 cross-sectional studies, 8 case-control studies, and 2 interventional studies (28 in total), providing a total of 19,949 individuals. Overall, the studies suggest a substantially increased risk for tendon injury associated with obesity, although there was some heterogeneity in study findings depending on study populations and mode of assessment. This finding has some important implications: 1) it would be interesting to see if obesity treatment can indeed reduce the risk of tendon injury; 2) clinicians making exercise recommendations to individuals with excess weight must be fully aware of the increased potential for tendon injury and design exercise routines with this in mind. Anyone, who has experienced tendon injury is well aware that once established, this condition is notoriously hard to treat and often results in chronic pain ultimately reducing mobility and thus further increasing the potential for weight gain. Another good reason, why exercise professionals working with obese clients (as blogged before) need a sound understanding not just of exercise physiology but also of musculoskeletal pathology. AMS Edmonton, Alberta
Poor Muscle Strength Predicts Immobility in Obese Elderly
Students and residents in my clinic are often surprised when I refer to my severely obese patients as olympian athletes – most people I know, who consider themselves fairly athletic, would be unable to even stand up out of their chairs let alone walk 10 steps were they to suddenly weigh 400 lbs or more. For the same reason I consider Jillian and Bob the biggest losers on the Biggest Loser show, as neither of them would last even 5 minutes doing any of their exercises and drills wearing a 200 lb fat suit (something they regularly expect of their poor contestants). That said, losing some of that incredible muscle (or lean body mass) in an obese individual is always a reason for grave concern – I have previously referred to it as a medical emergency. We routinely see severely obese patients, who were fully mobile on their own prior to admission, unable to even stand on their own after a few days in a hospital bed. This offloading-atrophy is a major complication and frequent cause of extended immobility in severely obese patients. That losing lean body mass (for whatever reasons) is never a good sign, not even for obese individuals, who generally have plenty of muscle to go around, is shown in a new study by Sari Stenholm and colleagues from the National Institute on Aging, Baltimore, MD, published in this month’s issue of the International Journal of Obesity. This study examined whether older obese persons with low muscle strength experience significantly greater declines in walking speed and mobility than comparable persons with only obesity or low muscle strength. The study population consisted of 930 community-dwelling adults aged 65 years or older living in the Chianti geographic area (Tuscany, Italy) and were followed for 6 years (inChianti study). Obesity was defined as BMI equal or greater than 30 and low muscle strength as lowest sex-specific tertile of knee extensor strength. Walking speed and self-reported mobility disability (ability to walk 400 m or climb one flight of stairs) were assessed at baseline and at 3- and 6-year follow-up. As expected, at baseline, obese persons with low muscle strength had lower walking speed compared with all other groups. More importantly, in the longitudinal analyses, obese participants with low muscle strength at baseline had a much steeper decline in walking speed and substantially higher risk of developing new mobility disability over the… Read More »
Don’t Spare the Protein
To anyone trying to lose weight, avoiding the virtually obligatory reduction in lean body mass is always a challenge. Not only does “offloading” as the body gets lighter reduce the actual “weight-bearing” work resulting in loss of muscle mass, but also the fact that most dietary recommendations tend to also reduce protein intake to maintain a “balanced” diet can promote a protein catabolic state. As skeletal muscle is a major determinant of energy expenditure, losing muscle mass eventually limits the amount of weight that can be lost at any given caloric deficit, resulting in an early plateau. Furthermore, as lost lean body mass tends to be replaced with fat during weight regain (catch-up fat), you end up with a greater fat mass than before your diet. The importance of maintaining protein intake during diet-induced weight loss was again illustrated in a recent study by Melanie Bopp and colleagues from Wake Forest University School of Medicine, Winston-Salem, NC, published in the Journal of the American Dietetic Association. The authors investigated the association between dietary protein intake and loss of lean mass during weight loss in postmenopausal women through a retrospective analysis of a 20-week randomized, controlled diet and exercise intervention in women aged 50 to 70 years. Weight loss was achieved by differing levels of caloric restriction and exercise. The diet-only group reduced caloric intake by 2,800 kcal/week, and the exercise groups reduced caloric intake by 2,400 kcal/week and expended approximately 400 kcal/week through aerobic exercise. Lean mass was measured using DEXA. Average weight loss was 10.8+/-4.0 kg, with an average of 32% of total weight lost as lean mass. While protein intake averaged 0.62 g/kg body weight/day (range=0.47 to 0.8 g/kg body weight/day), participants who consumed higher amounts of dietary protein lost less lean mass. These associations remained significant after adjusting for intervention group and body size. The authors conclude that inadequate protein intake during caloric restriction may be associated with adverse body-composition changes in postmenopausal women. I would dare to add that the same is probably true for anyone undergoing a dietary weight loss intervention that does not maintain adequate protein intake. AMSEdmonton, Alberta
I’ll Take Catch-Up With Those Fries
Yesterday, I attended the “Crosstalk” symposium at ECO 2008 here in Geneva. Once again, I was fascinated by Abdul Dulloo’s (Co-Chair of the Symposium) talk on the phenomenon of “catch-up” fat. Simply stated, this phenomenon describes the preferential accumulation of fat tissue as part of any weight-gain process that follows an energy deprived state (See Dulloo’s excellent 2008 review for more on this topic). Interestingly, this phenomenon occurs irrespective of whether the energy-deprived state is caused by voluntary or enforced starvation, dieting, anorexia or severe illness including sepsis or cancer. In fact, it even occurs in small-for-gestational-age babies, who manage to rapidly make up for their low birth weight by rapidly tucking away those calories in those chubby fat depots. Even more interestingly, data suggest that the excess calories that are tucked away are only partly derived from increased caloric intake. Most of them come from preferential partitioning of energy to the fat stores, largely by dramatically turning down skeletal muscle thermogenesis. This means than even if you are careful not to “overfeed”, your lean tissue will happily deprive itself for the benefit of those fat depots. In animal experiments, high-fat refeeding appears to make this phenomenon even more pronounced. All of this appears to be related to substantial insulin resistance that occurs during this “regain” phase and researchers are still trying to figure out what exactly makes the muscle “slow down” in order for the fat to accumulate. Teleologically all of this makes sense. The idea perhaps is to rapidly take up those calories (following the famine or illness) and store them away – let’s worry about rebuilding the lean mass later. Unfortunately, at least in animals, this process may be detrimental in the long term. There is now a fairly consistent body of evidence that shows “catch-up” growth to be a risk factor for the development of cardiometabolic risk factors including abdominal obesity, type 2 diabetes, and dyslipidemia – all eventually leading to heart disease. As regular readers may recall, I recently blogged about the apparent increased risk for the metabolic syndrome with weight cycling – perhaps a reflection of this phenomenon. Whatever the causes and consequences of catch-up weight, the phenomenon is very real – people tend to get fatter with every diet; patients recovering from cancer tend to put on massive amounts of fat when they recover – most interesting indeed. What if abdominal obesity is… Read More »
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