Airline Seats Revisited
BEST HEALTH BLOG FINALIST: The second round of voting is on – please vote AGAIN for your favourite health blog by clicking here Last week I blogged about the recent Supreme Court ruling mandating that airlines accommodate oversized passengers. This ruling was picked up by international media, especially in the US, where in light of their own obesity epidemic, this ruling attracted substantial attention. In fact, I was interviewed by MSNBC for my take on this, especially with regard to the question how airlines should determine who would qualify for an extra seat and who would not. My simple solution, as reported by MSNBC was as follows: “You can’t bring it down to a BMI. People’s body shapes are different.” Instead, the chair of obesity research at the University of Alberta suggests a solution inspired by the baggage sizers already in place at many airports. Instead, Sharma would like airlines to place an airplane seat in the terminal — “somewhere that offers travelers a bit of privacy.” Then, if it’s not obvious that a traveler won’t fit in one seat, they can sit in the sample seat. “If they don’t fit in the seat, then they’re too big and they’ll need to have that extra seat. At no cost. It’s not rocket science.” Obviously, other “experts” had other suggestions including bringing in doctors’ notes or simply increasing the seat sizes for everybody. For a full report on this story click here. If readers of this blog have any other suggestions – I’d love to hear them. AMS Edmonton, Alberta
A-Drop-In the Obesity Ocean?
BEST HEALTH BLOG FINALIST: The second round of voting is on – please vote AGAIN for your favourite health blog by clicking here Yesterday, I blogged about NAPEs, which are molecules secreted by the gut that affect food intake. Today, I draw attention to another newly discovered molecule called adropin (encoded by a gene called Enho), which is secreted by the liver in response to a high fat meal (adropin is also expressed in parts of the brain that regulate energy metabolism). In this study, just out in CELL METABOLISM, Ganesh Kumar and colleagues from the Pennington Biomedical Research Centre (PBRC), Baton Rouge, LA, fed mice with a high-fat diet, resulting in increased secretion of adropin. However, as animals gained weight on the high-fat diet and developed insulin resistance and fatty livers, adropin levels dropped. Interestingly, in genetically altered mice that expressed high levels of adropin or with administration of exogenous adropin, animals were less likely to develop insulin resistance and fatty livers. Together, the findings from this study suggest that adropin generation in the liver may play a role in the metabolic adaptation to high dietary fat intake. Previous studies have shown that obese individuals show impaired metabolic flexibility and do not efficiently match fat oxidation with consumption. If adropin is indeed a metabolic signal to adapt substrate metabolism with fat intake, then the decline in adropin synthesis with obesity may be a factor in the impaired ability to match lipid metabolism with dietary fat intake, leading to the development of fatty livers, dyslipidemia, and glucose intolerance. Given their findings, the authors conclude that adropin (or its target) may lead to new treatments for obesity-related metabolic disorders. Obviously, it is still a long way from these findings in mice to treatments that are safe and effective in humans. Nevertheless, this study could be another stepping stone towards better understanding obesity and finding treatments that work. AMS Edmonton, Alberta Hat Tip to Dennis Vance for bringing this study to my attention.
Another Gut Hormone Reduces Food Intake
BEST HEALTH BLOG FINALIST: The second round of voting is on – please vote AGAIN for your favourite health blog by clicking here Anyone, who is even vaguely familiar with gut physiology, by now knows that besides being an exocrine organ (=secreting digestive fluids into the gut lumen), the gut also secretes a vast array of molecules into the blood stream that act at remote areas – simply said, the gut is also an endocrine organ and the term “incretins” is often used to describe the various hormones secreted by the gut. In this week’s issue of CELL, Matthew Gillum and colleagues from Yale University School of Medicine, New Haven, CT, report that a relatively abundant group of plasma lipids molecules with the unpronounceable name N-acylphosphatidylethanolamines (or better called “NAPEs”) are secreted into the circulation from the small intestine in response to ingested fat and that systemic administration of the most abundant circulating NAPE, at physiologic doses, decreases food intake in rats. They also showed that NAPE enters the brain and is particularly concentrated in the hypothalamus (a key area in the regulation of hunger and satiety) and that intracerebroventricular infusions of nanomolar amounts of NAPE reduce food intake. Not surprisingly, chronic NAPE infusion in rats results in a reduction of both food intake and body weight, suggesting that NAPE and long-acting NAPE analogues may be novel therapeutic targets for the treatment of obesity. Thus, we can now add another molecule to the long list of gut-derived hormones that have been shown to affect food intake. While this discovery emphasizes the importance of better understanding gut physiology and how it interacts with the regulation of food intake, we must be cautious of jumping to conclusion that this is the new “magic bullet” for obesity. The history of obesity pharmacology is littered with promising lead compounds and targets that failed to deliver safe drugs that work – however, every new avenue that holds promise is welcome – if NAPE analogues can be developed and prove to be safe and effective even in a subset of obese individuals, it would represent a major leap forward in our ability to treat this chronic and debilitating condition. AMS Edmonton, Alberta
Pain in Older Obese Adults
BEST HEALTH BLOG FINALIST: The second round of voting is on – please vote AGAIN for your favourite health blog by clicking here Last night I gave a talk to General Practitioners at the Medical School in Victoria, BC (hosted by Dr. Brad Amson, General/Bariatric Surgeon). I spoke about the importance of carefully assessing patients for contributors and barriers to weight management. As blogged yesterday, pain is one of the most common issues in patients with excess weight and can be both a contributor and barrier to weight gain and severely obese patients appear at particular risk for pain catastrophizing. But how common is pain and how great is the incident risk in overweight and obese patients? This issue was addressed in a recent study by Noor Heim and colleagues from the VU University, Amsterdam, The Netherlands, published in OBESITY. This prospective study investigated the relationship between measured BMI and waist circumference with prevalent and incident pain in 2000 participants of the Longitudinal Aging Study Amsterdam, aged 55-85 years at baseline (1992-1993) and after after 3 years (N = 1,478) and 6 years (N = 1,271) of follow-up. The overall prevalence of pain was 33% at baseline and increased significantly with higher quartiles of BM. After adjustment for age, education, depression, smoking, physical activity, and chronic diseases, both men and women in the highest quartile of BMI were around twice as likely to present with pain than individuals in the lowest BMI quartile. Of the participants without pain at baseline, those in the highest quartile of BMI had a 2-fold increased odds for incident pain after 3 years of follow-up and around 2.5-fold after 6 years. The association with BMI was independent of waist circumference, suggesting that absolute weight rather than weight distribution was important for pain. This longitudinal study also answers the question whether or not pain in obesity is the chicken or the egg – it appears that obesity increases the risk for incident pain, rather than vice-versa. But what about weight loss and its effect on pain? This issue, interestingly, has not been widely studied and results have been inconsistent. Apart from the rather dramatic improvement in pain and mobility reported in surgical obesity treatment, the effect of non-pharmacological or pharmacological weight loss on pain incidence or progression is not clear (though my guess is that weight loss can’t hurt – no pun intended). Given the tendency… Read More »
Pain Catastrophizing in Severe Obesity
BEST HEALTH BLOG FINALIST: The second round of voting is on – please vote AGAIN for your favourite health blog by clicking here Pain is one of the most common and debilitating problems in patients challenged by severe obesity. Not just a consequence of mechanical complications of obesity (osteoarthritis, back pain, plantar fasciitis, fibromyalgia, etc.), pain is often a key barrier to physical activity and thus weight management. In fact, excess pain can promote psychological (e.g. depression, anxiety) and behavioural (e.g. binge eating) factors that may further promote weight gain. This issue is of even more importance in patients who display the now well-described phenomenon of pain catastrophizing, or the maladaptive responses to pain (tendency to focus on and magnify pain sensations with an intense sense of unbearable suffering and helplessness) that plays an extremely important role in how pain is perceived and processed. Pain catastrophizing now accounts for a substantial proportion of pain-related disability. Studies in patients with fibromyalgia show that pain catastrophizing is associated with increased activity in brain areas related to anticipation of pain (medial frontal cortex, cerebellum), attention to pain (dorsal ACC, dorsolateral prefrontal cortex), emotional aspects of pain (claustrum, closely connected to amygdala) and motor control. Thus, catastrophizing influences pain perception through altering attention and anticipation, and heightening emotional responses to pain. In another recent study by Tamara Somers and colleagues from Duke University, morbidly obese patients with osteoarthritis (OA) reported higher levels of pain catastrophizing than OA patients in the overweight and obese category. The severely obese patients who engaged in a high level of pain catastrophizing reported having much more intense and unpleasant pain, higher levels of binge eating, lower self-efficacy for controlling their eating and lower weight-related quality of life. The relationship between pain catastrophizing and eating behaviour is of particular interest, as high-fat and high-sucrose foods have been shown to increase pain tolerance. Thus, binging on highly-palatable foods may be a compensatory response to emotional distress and pain. It is not difficult to see how patients can enter into a vicious cycle of pain, increased eating, weight gain, more pain, more eating, and so on. In routine practice, pain catastrophizing can be easily and reliably assessed with questionnaires like this one, which can be scored like this. Fortunately, pain catastrophizing is responsive to cognitive behavioural therapy, with clinically relevant improvements in upto 50% of individuals. I would have little doubt that failure to recognize and… Read More »
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