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Five Sobering Facts About Ghrelin And Emotional Eating

Have you ever wondered about why some people turn to food when stressed while others don’t? Now, a study by Kate Raspopow and colleagues from Carlton University, Ottawa, published in Appetite provides some important new insights. The study was conducted in 103 undergraduate women who completed measures of emotional eating, were assigned to anticipate either a stressful (public speaking) or non-stressful event. Here are the main findings: 1. Anticipation of the stressor increased cortisol and ghrelin secretion in all participants. 2. Emotional eaters displayed lower basal ghrelin levels compared to non-emotional eaters. 3. Emotional eaters did not display a postprandial decrease of ghrelin levels. 4. Emotional eaters ate more than non-emotional eaters irrespective of stressor condition. 5. Percent body fat mediated the relationship between emotional eating and basal ghrelin. As the authors note, “The similarity of the ghrelin profile of emotional eaters to that of binge eaters and obese individuals, raises the possibility that disturbed ghrelin response might be a risk factor for such conditions.” As the best way to suppress ghrelin is by not letting yourself go hungry (weight loss regularly increases ghrelin levels), regular eating to avoid hunger may be a particularly important weight management strategy in emotional eaters. Clinically, I can certainly attest to the impression that emotional eaters appear far more prone to loss-of-control when restricting their food intake than non-emotional eaters. On the other hand this study also shows the importance of stress in this response. Clearly, better stress-coping skills may well lead to less emotional eating. I wonder if a “relax and eat more” strategy may ultimately help emotional eaters eat less? @DrSharma Edmonton, AB Kate Raspopow is a CON Obesity Research Bootcamp Graduate – for more on the Bootcamp – click here. Raspopow K, Abizaid A, Matheson K, & Anisman H (2014). Anticipation of a psychosocial stressor differentially influences ghrelin, cortisol and food intake among emotional and non-emotional eaters. Appetite, 74, 35-43 PMID: 24295926   .


Do Ghrelin-Stabilizing Antibodies Contribute to Obesity?

Readers are probably well aware of ghrelin, the primary hunger hormone released from the gut (largely stomach). Now, Tagaki and colleagues from Rouen University, France, in a paper published in Nature Communications, suggests that some people may have more pronounced and extended hunger due to to ghrelin-stabilizing immunoglobulins (IgG). In their experiments in mice showed that ghrelin degradation is inhibited by certain anti-ghrelin IgG with increased binding affinity foundnin the plasma of obese but not of anorectic or non-obese individuals. They also showed that repeated injections of ghrelin together with IgG from ob/ob mice resulted in increase food intake, meal frequency and total lean body mass of normal mice. These findings suggest that ghrelin-specific IgG may play a role in modulating hunger and food intake in obese humans and animals. This would not be the first example of such interactions between auto-antibodies and hormones, but does point to a new passible pathway to explain why some people, despite having “normal” ghrelin levels may experience more hunger than others. While these findings may not lead directly to a better treatment for obesity, they do remind us of the complexity of hunger and the physiology of ingestive behaviour. I guess, when you are hungry, pushing away from the table is simply not an option. @DrSharma Edmonton, AB Takagi K, Legrand R, Asakawa A, Amitani H, François M, Tennoune N, Coëffier M, Claeyssens S, do Rego JC, Déchelotte P, Inui A, & Fetissov SO (2013). Anti-ghrelin immunoglobulins modulate ghrelin stability and its orexigenic effect in obese mice and humans. Nature communications, 4 PMID: 24158035   .


Do Changes in Leptin, Ghrelin or Insulin Predict Weight Regain?

One of the main reasons why keeping weight off, is because of the complex neuroendocrine response to weight loss, which serve to promote weight regain. While some of the players involved in these responses are known, whether or not measuring them would help predict who may have a harder time losing weight or who is more likely to regain weight is not. As paper by Stohacker and colleagues from Brown University, Rhode Island, USA, published in the International Journal of Obesity suggests that this may be more complicated than some may think. In their review of 12 studies reporting changes in leptin, ghrelin or insulin during intentional weight loss with a follow-up period to assess regain, no consistent relationship was found between any of these factors and weight regain. Indeed, if anything, the data on this issue is more than confusing. For e.g. as the authors note, “…two of the nine studies examining leptin suggested that larger decreases were associated with great regain, three studies found the opposite (smaller decreases were associated with regain) while four studies found no significant relationship”. Similarly, “One study suggested that improvements in insulin resistance were associated with weight gain, but five subsequent studies reported no association.” Thus, the notion that simply measuring some of the hormones associated with weight loss is unlikely to predict weight regain in a given individual. This should come as no surprise. Not only, are these only three of a whole array of possible biological mediators of weight regain but, as the authors point out, there may also be important behavioural and environmental (and I would add psychological and medical) reasons why some people may find it easier to sustain weight loss than others. And of course, genetic factors as well as past weight-loss history may also play a role in this. Overall, there does not appear to be any simple test that clinicians can use to predict who is likely to regain weight and who is not. On the other hand, given that the vast majority of people who lose weight ultimately put it back on (perhaps with the exception of those undergoing bariatric surgery – but even there regain may happen), this question may not be the most pressing – after all, spotting weight regain when it happens is not rocket science. @DrSharma Edmonton, AB Strohacker K, McCaffery JM, Maclean PS, & Wing RR (2013). Adaptations of leptin,… Read More »


Ghrelin Growls at Glucose Tolerance

Regular readers of these pages probably recall that the hormone ghrelin, released largely from the stomach, is a key regulator of hunger and energy metabolism. A recent study by Jenny Tong and colleagues from the University of Cincinnati, published in DIABETES, now shows that ghrelin also plays an important role in suppressing the insulin response to a glucose load. In order to examine the effect of ghrelin on glucose metabolism, the researchers infused ghrelin at different doses (0.3, 0.9 and 1.5 nmol/kg/h) in 12 healthy participants (8 male/4 female). In addition, they performed an intravenous glucose tolerance test and measured insulin response. Although ghrelin infusion did not alter fasting plasma insulin or glucose, it did result in a dose-dependent suppression in the insulin release to the acute glucose load. As the authors point out: “This is a robust proof-of-concept study showing that exogenous ghrelin reduces glucose-stimulated insulin secretion and glucose disappearance in healthy humans.” Interestingly, ghrelin levels are markedly reduced in patients who undergo sleeve gastrectomies or gastric bypass surgery, and this finding may explain why, in many cases, these operations so dramatically improve diabetes. As I have said before, bariatric surgery is really endocrine surgery – and we have yet to fully understand exactly how it works. As readers will also readily appreciate, perhaps finding a drug that blocks ghrelin may provide a new treatment not just for obesity but also for diabetes. AMS Edmonton, Alberta Hat tip to Andrey for bringing this paper to my attention. Tong J, Prigeon RL, Davis HW, Bidlingmaier M, Kahn SE, Cummings DE, Tschöp MH, & D’Alessio D (2010). Ghrelin suppresses glucose-stimulated insulin secretion and deteriorates glucose tolerance in healthy humans. Diabetes, 59 (9), 2145-51 PMID: 20584998


The Power of Placebo In Weight-Loss Trials

Placebos are powerful – even when people know they’re on placebo! This scientific fact has been long established and probably accounts for much of the hype and “success stories” around dietary supplements and a host of “alternative” medicines, which often lack any demonstrable “biological” effect (other than placebo). Although placebo-controlled trials are generally considered the highest-quality evidence, it is often wrongly assumed that the placebo group is not receiving treatment, when it actually is. Thus, contrary to a common belief, taking a placebo is a form of “active” treatment, and cannot be equated to “doing nothing” (which is perhaps why even study participants randomised to a “placebo” or “control” group in clinical trials  often do so much better than individuals who are not in a trial). Now a paper by Kevin Fontaine and colleagues, in a paper published in OBESITY,  look at the problems around the use of “placebos” in weight-loss trials. As the authors note, “It is becoming increasingly clear that placebo responses operate not merely from believing one is ingesting a bioactive compound or undergoing a legitimate medical procedure but also from environmental and psychosocial factors embedded within clinical and research encounters. These encounters may engage several potential conscious and non-conscious mechanisms, including expectations, conditioning, anxiety reduction, interactions with practitioners/research staff (e.g., emotional support, empathy), and so on. Collectively, placebo-related factors may promote improved outcomes even when participants do not receive a bioactive treatment and regardless of whether they are aware of this.” The authors cite a number of studies that have specifically looked at the power of “placebo” in weight loss trials. In one study, …participants consumed identical 380-calorie milk shakes. On one occasion, the label said it contained 140 calories (“sensible shake”), and on another, the label said it contained 620 calories (“indulgent shake”). The “indulgent” condition produced a steeper decline in ghrelin (a satiety hormone) and greater self-reported satiety compared to the “sensible” condition.” In another, “…all participants [received] a placebo pill and [were] then randomized to conditions in which they were told that they had taken either a placebo or weight loss pill. Those who were told that they had taken a weight loss pill ate more during a taste test and preferred larger quantities of sugary drinks compared to those who were told that they had taken a placebo. The findings suggest that those who believed that they took the weight loss pill may have perceived… Read More »