Does Ralph Lauren Care About Anorexia?
I am fully aware that this blog is generally dedicated to discussing topics relevant to obesity prevention and management. Readers may therefore be surprised to see that today’s post deals with anorexia. However, regular readers will probably recall previous posts on this topic and on how the problem of eating disorders in general can be promoted by ridiculous beauty ideals promoted by the media and the fashion and beauty industry in particular (see Dr Eyecandy for more on this topic). Recently, one fashion designer has been caught promoting particularly ridiculously photoshopped advertisements to promote his ware. A widespread outcry resulted in retraction and apologies, but several other photoshopped images from the same designer remain in use. As a result, Darryl Roberts, the producer and director of America the Beautiful, an award-winning documentary on fashion-dictated beauty ideals, has called for a boycott on Ralph Lauren that is receiving worldwide attention. The declared goal is to have at least 10,000 registered fans on a facebook group specifically started to demonstrate the massive support for this call by the end of this week! I encourage all readers to visit the facebook site and join the call by clicking here: ATB Action Network Boycott of Ralph Lauren Please make sure you invite your friends to do the same! AMS Edmonton, Alberta
Genetic Obesity Clears Parents of Blame?
As obesity is widely believed to be a condition resulting from people’s poor lifestyle choices, it is only normal to also believe that childhood obesity is simply the result of poor parenting skills. Thus, in severe cases, childhood obesity has been likened to childhood abuse and there are cases where obese children have been brought to the attention of social services and child protection agencies. As now reported by the BBC, at least a few such parents have recently been exonerated after the discovery that the severe obesity that resulted in their children being formally placed on the social services ‘at risk’ register on the assumption that the parents were deliberately overfeeding the kids, were removed from the register after the discovery of a new genetic defect that largely explained the kids’ excess weight. This new genetic defect, consisting of large chromosomal deletions associated with severe early-onset obesity, was reported by Elena Bochukova and colleagues from the University of Cambridge, UK, in an early online publication in NATURE. In their study of 300 Caucasian patients with severe early-onset obesity, 143 of whom also had developmental delay, the researchers identified several rare copy number variants that were recurrent in patients but absent or at much lower prevalence in controls. Five patients had overlapping deletions on chromosome 16. Two patients harboured a larger de novo chromosome 16 deletion, extending through a 593-kilobase region previously associated with autism and mental retardation. In an independent sample of 1,062 patients with severe obesity, the smaller chromosome 16 deletion was found in an additional two patients. All deletions include SH2B1, which is involved in leptin and insulin signaling. All deletion carriers exhibited hyperphagia and severe insulin resistance disproportionate for the degree of obesity. Not only does this study point to an important role of this region of chromosome 16 (and possibly SH2B1) for rare cases of early-onset hyperphagic obesity, but it also shows that even genetic obesity is a remarkably heterogeneous disorder. This study certainly serves as a reminder that jumping to conclusions about peoples lifestyle “choices” based simply on their appearance is never a good idea. AMS Edmonton, Alberta
Outfoxing the Fasting Response
One of the best ways to increase your hunger, slow down metabolism and increases spontaneous physical search activity is to simply stop eating or to even just reduce caloric intake. This is called the adaptive response to fasting and it is of course this hyopthalamic response that limits the long-term effectiveness of weight loss strategies. A new study by Jose Silva and colleagues from New York’s Rockefeller University, published this week in NATURE identifies forkhead box transcription factor (Fox-a2) as a key molecule in the regulation of this response. Using mice models, the researchers now showed that the stimulation of the lateral hypothalamic area (the main ‘feeding centre’ that regulates food intake, arousal and motivated behaviour) through the actions of orexin and melanin-concentrating hormone (MCH), neuropeptides that are released during fasting, are regulated by Fox-a2. This transcription factor incidentally is also a target of insulin signaling. During fasting, Fox-a2 binds to MCH and orexin promoters and stimulates their expression thereby increasing hunger and increasing spontaneous activity. In fed and in hyperinsulinemic obese mice, insulin signalling leads to nuclear exclusion of Foxa2 and reduced expression of MCH and orexin, thereby decreasing hunger and increasing activity. Activation of Fox-a2 increases orexin and MCH production leading to mice that eat more, are more physically active and have improved insulin sensitivity. Turning on Foxa2 in obese mice also increases lean body mass and reduces their fat content. Thus, the researchers appear to have identified a key molecule that may prove to be a useful pharmacological target for medications that can help increase spontaneous physical activity and improve health. AMS Edmonton, Alberta
Are Healthy Obese People Healthy?
In clinical practice, it is not uncommon to meet individuals who, despite meeting the BMI criteria for obesity, appear metabolically healthy: their glucose, lipid and blood pressure levels are well within the normal range. According to the Edmonton Obesity Staging System (EOSS), we would refer to these individuals as having “Stage O” obesity. But are these apparently metabolically healthy obese individuals really healthy in that they have a lower mortality risk than obese individuals with metabolic abnormalities? This question was addressed by Jennifer Kuk and colleagues from York University, Toronto, Canada, in a paper just published in Diabetes Care. Kuk and colleagues examined data from 6,011 men and women from the Third National Health and Nutrition Examination Survey (NHANES III) where metabolically abnormal was defined as having insulin resistance (IR) or two or more metabolic syndrome (MetS) criteria. A total of 30% of obese subjects had IR, and 38.4% had two or more MetS factors, whereas only 6.0% (or 1.6% of the whole population) were free from both IR and all MetSyn factors. Based on the mortality data over 8 years, both the metabolically healthy and metabolically abnormal obese individuals had around the same roughly 2.5 to 3-fold elevation in mortality risk compared to the metabolically normal normal-weight individuals. The authors conclude that even in the absence of overt metabolic aberrations, excess weight is associated with increased all-cause mortality risk. Thus, as I’ve said before, it appears that there is no such thing as “benign” obesity. Eventually excess weight will increase the risk for a wide range of health problems including cancers, osteoarthritis and obstructive sleep apnea. This is why it is critical to include the assessment of all four Ms in patients presenting with excess weight. So how do these findings impact on weight loss recommendations in obese individuals who appear metabolically normal (EOSS 0)? As blogged before, the first step in weight management is prevention of weight gain. As a rule, this will require substantial changes in diet and activity levels as well as mitigation of any underlying root causes of positive energy balance – this alone can be difficult enough to achieve. With current conservative obesity treatments only a small minority of patients will achieve and maintain clinically relevant weight loss – the vast majority of weight-losers will simply yo-yo back to their excess weight. I therefore maintain that for most obese individuals weight stabilization may be… Read More »
Does White Hat Bias Confound Obesity Research?
Readers of these pages may be following the current “Climategate” uproar about the leaked (or rather hacked) correspondence between leading climate researchers, who it now appears were quite actively bending the truth to ensure that evidence in support of global warming was overblown, while publication of data that failed to support this idea was actively suppressed. No doubt, the researchers working at the Climatic Research Unit at the University of East Anglia (from where the e-mails were leaked), may well have believed that their deeds were justified as a means given their own (ideological?) convictions regarding the potentially catastrophic effects of man-made climate change. It now turns out that climate research may not be the only area of research where some scientists appear to happily misrepresent scientific evidence (by overblowing data that support their ideas while underplaying or ignoring contradictory data) for what they may well perceive to be righteous ends. Thus, in a paper just published by Mark Cope and David Allison from the University of Birmingham, Alabama, USA, in the International Journal of Obesity, it appears that this ‘white hat bias’ (WHB) may also play a role in the community of obesity researchers. To assess the role of WHB, Cope and Allison examined how findings on the potential relationship between obesity and sugary beverages (as a risk factor) or breast feeding (as a protective factor) were reported and discussed in the obesity literature. Their analyses illustrates convincingly how citation bias (citing positive articles while ignoring or misrepresenting negative articles), publication bias (increased likelihood of publishing positive findings) and miscommunication in press releases (where inconclusive data are presented as conclusive, while contradictory or non-supportive data is ignored or under played) suggests that some obesity researchers may well be driven more by their feelings of righteous zeal or indignation toward certain aspects of industry, than by what the data actually shows. Thus, the papers analysed by Cole and Allison provide many examples where the putative relationship between the obesity promoting effects of sugary drinks and the obesity preventing effects of breast feeding are presented as far more robust than the actual data would suggest. Paradoxically, while much concern has been raised about the potential bias resulting from industry sponsored trials, according to Cope and Allison, publication bias and misrepresentation of data appears to be particularly rampant in non-industry sponsored studies (perhaps reflecting the anti-industry bias of non-industry funded researchers?). Clearly it… Read More »
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