- RSS Channel Showcase 7674439
- RSS Channel Showcase 6029856
- RSS Channel Showcase 1921516
- RSS Channel Showcase 9076243
Articles on this Page
- 04/25/16--05:00: _Skinny Kids Eat Mor...
- 04/27/16--05:00: _Liraglutide Alters ...
- 04/28/16--05:00: _How To Interpret St...
- 05/25/16--05:00: _Stretching The Rubb...
- 06/23/16--05:00: _Arguments For Calli...
- 06/29/16--05:00: _Arguments For Calli...
- 09/08/16--05:00: _Can Planned Cheatin...
- 05/05/17--05:00: _Why Would Anyone Wa...
- 07/05/17--05:00: _Use of Low Calorie ...
- 07/11/17--05:00: _Alternate Day Fasti...
- 10/03/17--05:00: _Residential Schools...
- 12/07/17--05:00: _DIRECT Remission of...
- 01/22/18--05:00: _Taxing Sugar-Sweete...
- 01/23/18--05:00: _Counting Calories F...
- 04/25/16--05:00: Skinny Kids Eat More Candy
- 04/28/16--05:00: How To Interpret Studies On Screen Time And Eating Behaviour
- 05/25/16--05:00: Stretching The Rubber Band
- 06/29/16--05:00: Arguments For Calling Obesity A Disease #8: Can Reduce Stigma
- 09/08/16--05:00: Can Planned Cheating Help You Stick With Your Diet?
- 07/05/17--05:00: Use of Low Calorie Diets in Type 2 Diabetes
- 07/11/17--05:00: Alternate Day Fasting Is No Better Than Any Other Fad Diet
- 10/03/17--05:00: Residential Schools And Indigenous Obesity – More Than Just Hunger?
- 12/07/17--05:00: DIRECT Remission of Type 2 Diabetes in Primary Care?
- 01/22/18--05:00: Taxing Sugar-Sweetened Beverages To Prevent Obesity
- 01/23/18--05:00: Counting Calories For Weight Loss – More of The Same
A common assumption is that kids with obesity consume more high-caloric foods – which of course includes confectionary items like chocolate and non-chocolate sweets. Now, a study by Constantin Gasser and colleagues from Melbourne, Australia, in a paper published in the American Journal of Clinical Nutrition, present a systematic review and meta-analysis of confectionary consumption and overweight in kids. The researchers identified 19 studies fort their systematic review, 11 of which (∼177,260 participants) were included in the meta-analysis. Overall, odds of excess weight of kids in the highest category of sweets consumption was about 20% less than in the reference category. This inverse association was true for both chocolate and nonchocolate confectioneries. Furthermore, in the longitudinal studies and the randomised controlled trial included in the review, no associations were observed between confectionery consumption and overweight, obesity, or obesity-related outcomes. Thus, based on data from well over 175,000 kids, there appears to be no relationship between sweets consumption and excess weight – if anything, the relationship is the opposite of what one may expect. As so often, when data don’t fit the “accepted” hypothesis, the authors are also quick to point out that these findings could well be explained by reverse causality (overweight kids avoiding sweets) or underreporting by heavier kids (a polite way of saying that heavier kids may be less honest about their candy consumption). On the other hand, it may also well be that regular (non-restrictive) sweet consumption actually does in fact make kids less vulnerable to overeating, simply by ruining their appetite (just as grandma always warned you it would – as in, “No sweets before supper!”). Overall, the findings remind me of a previous study that failed to find any association between sugary pop consumption and body weight in Ontario and PEI kids (if anything skinny kids in PEI drank more pop than those with excess weight). Whatever the true answer may be, these findings certainly do not support the notion that sweet or chocolate consumption is a key factor in childhood obesity. @DrSharma Edmonton, AB
Liraglutide, a GLP-1 analogue now available for the treatment of obesity (as Saxenda) in North America, works by reducing appetite and increasing satiety, thus making it easier to lose weight and keep it off (with continuing treatment). Now, a study by Olivia Farr and colleagues, in a paper published in Diabetologia not only present data showing the presence of GLP-1 receptors in human cortex, hypothalamus and medulla, but also provide functional evidence for altered brain response to food cues. After documenting the presence of GLP-1 receptor in human brains using immunohistochemistry, the researchers conducted a randomised controlled placebo-controlled, double-blind, crossover trial in 18 individuals with type 2 diabetes who were treated with placebo and liraglutide for a total of 17 days each (0.6 mg for 7 days, 1.2 mg for 7 days, and 1.8 mg for 3 days). Using functional MRI neuroimaging studies, the researchers found that liraglutide remarkably decreased activation of the parietal cortex in response to highly desirable (vs less desirable) food images. They also observed decreased activation in the insula and putamen, areas involved in the reward system. Furthermore, using neurocognitive testing, the researchers showed that increased ratings of hunger and appetite correlated with increased brain activation in response to highly desirable food cues while on liraglutide. In contrast, ratings of nausea (a well-known side effect of liraglutide) correlated with decreased brain activation. As the authors note, “Our data point to a central mechanism contributing to, or underlying, the effects of liraglutide on metabolism and weight loss.” These findings no doubt match the reports from my own patients of experiencing less interest in highly palatable foods and finding it much easier to pass up on foods that they would have otherwise found hard to resist. Clearly, as we learn more about brain function in eating behaviour, we are thankfully moving towards treatments that are clearly proving to be far more effective than just telling patients to “simply eat less” (which I have often likened to telling people with depression to “simply cheer up”). @DrSharma Edmonton, Canada Disclaimer: I have received honoraria for speaking and consulting from Novo Nordisk, the maker of liraglutide
Much of the research on the contribution of screen time, sedentariness, food consumption and other factors comes from cross-sectional or longitudinal studies, where researchers essentially describe correlations and statistical “effect sizes”. To be at all meaningful, analyses in such studies need to be adjusted for known (or at least likely) confounders (or at least the confounders that happen to available). No matter how you turn and wind the data, such studies by definition cannot prove causality or (even less likely) predict the outcome of actual intervention studies. Nevertheless, such studies can be helpful in generating hypotheses. Thus, for example, I read with interest the recent paper by Lei Shang and colleagues from the University of Laval, Quebec, Canada, published in Preventive Medicine Reports. The researchers looked at cross-sectional data on 630 Canadian children aged 8-10 years with at least one obese biological parent. While the overall median daily screen time was about 2.2 hours, longer screen time was associated with higher intake of energy (74 kcal) and lower intake of vegetables & fruit (- 0.3 serving/1000 kcal). This unhealthy “effect” of screen time on diet appeared even stronger among children with overweight. Thus, there is no doubt that the study shows that, “Screen time is associated with less desirable food choices, particularly in overweight children.” The question of course remains whether or not this relationship is actual causal or in other words, does watching more television lead to an unhealthier diet (I am guessing no one assumes that eating an unhealthier diet leads to more TV watching). Unfortunately, this is not a question that can be answered by this type of research. Nor, is this type of research likely to predict whether or not reducing screen time will get the kids to eat better. Indeed, it doesn’t take a lot of imagination to come up with other explanations for these findings that would not require any assumption of a causal link between eating behaviours and television watching. For one, TV watching could simply be a surrogate measure for parenting style – perhaps parents that let their kids watch a lot of TV are also less concerned about the food they eat. And, for all we know, reducing TV time may (e.g. by cutting the kids off from TV – or cutting the parents off from a convenient babysitter) in the end make the kids eating behaviours even worse. Who knows – that’s… Read More »
I remember as a kid having a pair of pyjamas that were held up by an elastic rubber band. It must have been a pretty cheap rubber band, because every few months it would wear out and lose its stretch, so it had to be replaced it with a new band. Unfortunately, this is not what can be said about the rubber band that I used in my recent TEDx talk to demonstrate what happens when you try to lose weight. Unlike the cheap band in my pyjamas, the rubber band I used to represent our physiology trying to gain the weight back, never seems to lose its stretch. No matter how hard or how long we pull, the rubber band keeps wanting to bring our weight back to where we started. Yes, perhaps for some people, eventually the rubber band may relax (these would certainly be the exceptions) or may be the “muscles” that we use to pull on the band just grow stronger, which makes it seem easier to keep up the pull – but for all we know, in most people, this “rubber band” is of pretty good quality and seems to last forever. So, how do we take the tension out of the rubber band ? Well, we do know that people who have bariatric surgery have a much better chance of keeping the weight off in the long-term and we now understand that this has little to do with the “restriction” or the “malabsorbtion” resulting from these procedures but rather from the profound effect that this surgery has on the physiology of weight regain. Thus, we know that many of the hormonal and neurological changes that happen with bariatric surgery, seem to inhibit the body’s ability to defend its weight and perhaps even appears to trick the body into thinking that its weight is higher than it actually is. In other words, bariatric surgery helps maintain long-term weight loss by reducing the tension in the rubber band, thus making it far easier for patients to maintain the “pull”. And that is exactly how we think some of the anti-obesity medications may be working. For example, daily injections of liraglutide, a GLP-1 analogue approved for obesity treatment, appears to decrease the body’s ability to counteract weight loss by reducing hunger and increasing satiety, thus taking some of the tension out of that band. Think of it as sprinkling “magic dust” on that rubber band to reduce the… Read More »
Continuing in my miniseries on why obesity (defined here, as excess or abnormal body fat that affects your health) should be considered a disease, is the simple observation that obesity responds less to lifestyle treatments than most people think. Yes, the internet abounds with before and after pictures of people who have “conquered” obesity with diet, exercise, or both, but in reality, long-term success in “lifestyle” management of obesity is rare and far between. Indeed, if the findings from the National Weight Control Registry have taught us anything, it is just how difficult and how much work it takes to lose weight and keep it off. Even in the context of clinical trials conducted in highly motivated volunteers receiving more support than you would ever be able to reasonably provide in clinical practice, average weight loss at 12 – 24 months is often a modest 3-5%. Thus, for the vast majority of people living with obesity, “lifestyle” treatment is simply not effective enough – at least not as a sustainable long-term strategy in real life. While this may seem disappointing to many (especially, to those in the field, who have dedicated their lives to promoting “healthy” lifestyles as the solution to obesity), in reality, this is not very different from the real-life success of “lifestyle” interventions for other “lifestyle” diseases. Thus, while there is no doubt that diet and exercise are important cornerstones for the management of diabetes or hypertension, most practitioners (and patients) will agree, that very few people with these conditions can be managed by lifestyle interventions alone. Indeed, I would put to you that without medications, only a tiny proportion of people living with diabetes, hypertension, or dyslipidemia would be able to “control” these conditions simply by changing their lifestyles. Not because diet and exercise are not effective for these conditions, but because diet and exercise are simply not enough. The same is true for obesity. It is not that diet and exercise are useless – they absolutely remain a cornerstone of treatment. But, by themselves, they are simply not effective enough to control obesity in the vast majority of people who have it. This is because, diet and exercise do not alter the biology that drives and sustains obesity. If anything, diet and exercise work against the body’s biology, which is working hard to defend body weight at all costs. Thus, it is time we accept this reality and recognise… Read More »
Next, in this miniseries on arguments for and against calling obesity a disease, I turn to the issue of stigma. One of the biggest arguments against calling obesity, is the fear that doing so can increase stigma against people living with obesity. This is nonsense, because I do not think it is at all possible for anything to make stigma and the discrimination of people living with obesity worse than it already is. If anything, calling obesity a disease (defined as excess or abnormal body fat that impairs your health), could well serve to reduce that stigma by changing the narrative around obesity. The current narrative sees obesity largely as a matter of personal choice involving poor will power to control your diet and unwillingness to engage in even a modest amount of regular physical activity. In contrast, the term ‘disease’ conjures up the notion of complex biology including genetics, epigenetics, neurohormonal dysregulation, environmental toxins, mental health issues and other factors including social determinants of health, that many will accept are beyond the simple control of the individual. This is not to say that other diseases do not carry stigma. This has and remains the case for diseases ranging from HIV/AIDS to depression – but, the stigma surrounding these conditions has been vastly reduced by changing the narrative of these illnesses. Today, we are more likely to think of depression (and other mental illnesses) as a problem related to “chemicals in the brain”, than something that people can pull out of with sheer motivation and will power. Perhaps changing the public narrative around obesity, from simply a matter of motivation and will power, to one that invokes the complex sociopsychobiology that really underlies this disorder, will, over time, also help reduce the stigma of obesity. Once we see obesity as something that can affect anyone (it can), for which we have no easy solutions (we don’t), and which often requires medical or surgical treatment (it does) best administered by trained and regulated health professionals (like for other diseases), we can perhaps start destigmatizing this condition and change the climate of shame and blame that people with this disease face everyday. @DrSharma Edmonton, AB
Many diet plans praise the importance of strict adherence to whatever the storyline of the diet happens to be. This includes tips on what foods to avoid or to never eat. Indulging in these “forbidden” foods, is considered cheating and failure. Now, research by Rita Coelho do Vale and colleagues, published in the Journal of Consumer Psychology, explores the notion that planned “cheats” can substantially improve adherence with restrictive diets. Using a set of controlled dietary experiments (both simulated and real dieting), the researchers tested the notion that goal deviations (a more scientific term for “cheats”) in the plan helps consumers to regain or even improve self-regulatory resources along the goal-pursuit process and can thus enhance the likelihood that the final goal is attained. That, is exactly what they found: Compared to individuals who followed a straight and rigid goal, individuals with planned deviations helped subjects regain self-regulatory resources, helped maintain subjects’ motivation to pursue with regulatory tasks, and (3) has a positive impact on affect experienced, which are all likely to facilitate long-term goal-adherence. Thus, the authors conclude that, “…it may be beneficial for long-term goal-success to occasionally be bad, as long it is planned.” This is not really that new to those of us, who recommend or use planned “treats” as a way to make otherwise restrictive diets bearable. Good to see that there is now some research to support this notion. @DrSharma Edmonton, AB
Just imagine if the question in the title of this post was, “Why would anyone want access to prescription medications for diabetes?” (or heart disease? or lung disease? or arthritis? or, for that matter, cancer?) Why would anyone even ask that question? If there is one thing we know for sure about obesity, it is that it behaves just like every other chronic disease. Once you have it (no matter how or why you got it) – it pretty much becomes a life-long problem. Our bodies are so efficient in defending our body fat, that no matter what diet or exercise program you go on, ultimately, the body wins out and puts the weight back on. In those few instances where people claim to have “conquered” obesity, you can virtually bet on it, that they are still dealing with keeping the lost weight off every single day of their life – they are not cured, they are just treated! Their risk of putting the weight back on (recidivism) is virtually 100% – it’s usually just a matter of time. Funnily enough, this is no different from people trying to control any other chronic disease with diet and exercise alone. Take for e.g. diabetes. It is not that diet and exercise don’t work for diabetes, but the idea that most people can somehow control their diabetes with diet and exercise alone is simply not true. No matter what diet they go on or what exercise program they follow, sooner or later, their blood sugar levels go back up and the problems come back. You could pretty much say the same for high blood pressure or cholesterol, or pretty much any other chronic health problem (that, in fact, is the very definition of “chronic”). So why medications for obesity? Because, like every other chronic disease, medications can help patients achieve long-term treatment goals (of course only as long as they stay on treatment). Simply put, if the reason people virtually always regain their lost weight (no matter how hard they try to lose it) is simply because of their body’s ability to resist weight loss and promote weight regain, then medications that interfere with the body’s ability to resist weight loss and promote weight regain, will surely make it far more likely for them to not only lose the weight but also keep it off. Now that we increasingly understand many of the body’s mechanisms to defend… Read More »
Managing weight in patients with type 2 diabetes (most of who have significant overweight or obesity) is always challenging, not least because many medications used to treat diabetes can also promote weight gain. Now, a paper by Judy Shiau and colleagues from the University of Ottawa, in a paper published in the Canadian Journal of Diabetes, present the results of a retrospective cohort study (1992 to 2009) of weight, glycemic control and diabetes medications changes in 317 patients with obesity and type 2 diabetes at 6 months on a low-calorie diet program. The program (week 1 to week 26) included mandatory weekly group sessions led by a dietitian, behaviour therapist or exercise therapist. All patients received OPTIFAST ®900 as full meal replacements (MR) starting at week 2. Patients consume 4 MR shakes per day for a total of 900 kcal per day, a regimen that is high in proteins (90g/day) and moderate in carbohydrates (67 g/day). Patients with initial body mass indexes (BMIs) of 33 kg/m2 or higher commited to 12 weeks of full MRs, while patients with initial BMIs below 33 started with 6 weeks of full MRs and the option to increase to up to 12 weeks of full MRs. Once patients completed their full MR regimen, there was a 5-week transition period to regular food, typically followed by a maintenance diet, as determined in a one-on- one dietitian counselling session. As glycemic control improved with weight loss, anti-diabetes medications were adjusted or discontinued, thereby stopping any weight-gain-promoting medications first. As the authors note, “At 6 months, both groups had lost 16% of their weight, and the decreases or discontinuations of medications were 92% sulfonureas, 87% insulins, 79% thiazolidinediones, 78% alpha-glucosidase inhibitors, 50% meglitinides, 33% dipeptidyl peptidase-4 (DPP-4) inhibitors and 33% metformin. At 6 months, compared with baseline, A1C levels improved significantly and at 6 months, 30% of patients were no longer taking diabetes medications and had significantly better percentages of weight loss compared with those taking medications (18.6% vs. 16%; p=0.002).” Thus, this paper shows that, a low-calorie meal replacement program can substantially improve glycemic control and reduce the need for anti-diabetes medications. Unfortunately, as participants were transitioned to community care at 6 months, little is know about how long these effects last. Nevertheless, with the increasing availability and use of weight-neutral or even weight-reducing anti-diabetes medications, one may expect that some of these effects can be… Read More »
It seems that every year someone else comes up with a diet that can supposedly conquer obesity and all others health problems of civilization. In almost every case, the diet is based on some “new” insight into how our bodies function, or how our ancestors (read – hunters gatherers (never mind that they only lived to be 35) ate, or how modern foods are killing us (never mind that the average person has never lived longer than ever before), or how (insert remote population here) lives today with no chronic disease. Throw in some scientific terms like “ketogenic”, “guten”, “anti-oxidant”, “fructose”, or “insulin”, add some level of restriction and unusual foods, and (most importantly) get celebrity endorsement and “testemonials” and you have a best-seller (and a successful speaking career) ready to go. The problem is that, no matter what the “scientific” (sounding) theories suggest, there is little evidence that the enthusiastic promises of any of these hold up under the cold light of scientific study. Therefore, I am not the least surprised that the same holds true for the much hyped “alternative-day fasting diet”, which supposedly is best for us, because it mimics how our pre-historic ancestors apparently made it to the ripe age of 35 without obesity and heart attacks. Thus, a year-long randomised controlled study by John Trepanowski and colleagues, published in JAMA Internal Medicine, shows that alternate day fasting is evidently no better in producing superior adherence, weight loss, weight maintenance, or cardioprotection compared to good old daily calorie restriction (which also produces modest long-term results at best). In fact, the alternate day fasting group had significantly more dropouts than both the daily calorie restriction and control group (38% vs. 29% and 26% respectively). Mean weight loss was virtually identical between both intervention groups (~6 Kg). Purists of course will instantly critisize that the study did not actually test alternative-day fasting, as more people dropped out and most of the participants who stayed in that group actually ate more than prescribed on fast days, and less than prescribed on feast days – but that is exactly the point of this kind of study – to test whether the proposed diet works in “real life”, because no one in “real life” can ever be expected to be perfectly compliant with any diet. In fact, again, as this study shows, the more “restrictive” the diet (and, yes, starving yourself… Read More »
A recent CMAJ article, by Ian Mosby and Tracey Galloway from the University of Toronto argues that one of the key reasons why we see obesity and diabetes so rampant in Canada’s indigenous populations, is the fact that widespread and persistent exposure to hunger during the notorious residential school system may have metabolically “programmed” who generations toward a greater propensity for obesity and type 2 diabetes. There is indeed a very plausible biological hypothesis for this, “Hunger itself has profound consequences for childhood development. Children experiencing hunger have an activated hypothalamic–pituitary–adrenal stress response. This causes increased cortisol secretion which, over the long term, blunts insulin response, inhibits the function of insulin-like growth factor and produces long-term changes in lipid metabolism. Through this process, the child’s physiology is essentially “programmed” by hunger to continue the cycle of worsening effects, with their bodies displaying a rapid tendency for fat-mass accumulation when nutritional resources become available.” While the impact of hunger may well have been one of the key drivers or metabolic changes, the authors failed to acknowledge another (even more?) important consequence of residential schools – the impact on mental health. Oddly enough, in a blog post I wrote back in 2008, I discussed the notion that the significant (and widespread) physical, emotional, and sexual abuse experienced by the generations of indigenous kids exposed to the residential school system would readily explain much of the rampant psychological problems (addictions, depression, PTSD, etc.) present in the indigenous populations across Canada today. The following is an excerpt from this previous post: This disastrous and cruel [residential school] policy resulted in much pain and despair in the First Nations’, Inuit and Metis people that lasts to this day (known as the “generational effect”). Sexual, physical and mental abuse was widespread; students were broken in heart and spirit; culture and identities were destroyed. Much (if not all) of what ails the Aboriginal peoples of Canada can be traced back to this policy – including possibly issues that affect Aboriginal health to this day. It is no secret that obesity and its consequences (e.g. diabetes) are rampant amongst the Aboriginal peoples of Canada. While poverty, breakdown of traditional lifestyle and culture and even genetic factors (thrifty genotype) have all been implicated in this, I wonder how much the misery caused by the residential school program had to contribute. Early traumatic life experiences including sexual, mental and physical… Read More »
There is no reasonable argument against the fact that excess weight gain is one of the key drivers of diabetes risk, and it should come as no surprise to anyone, that losing weight (though bariatric surgery or otherwise) dramatically improves glycemic control in people living with type 2 diabetes. So what exactly can we learn from the DIRECT study published by Michael Lean and colleagues in The Lancet? For one, this is a large cluster-randomised trial of obesity intervention conducted entirely in a non-specialist primary care setting with significant weight loss (at least 15 Kg) and diabetes remission (defined as glycated haemoglobin (HbA1c) of less than 6·5% after at least 2 months off all antidiabetic medications) as the pre-defined primary outcome at 12 months. In the intervention centres, a nurse or dietitian (as available locally) was given a total of 8 h structured training by the study research dietitians experienced in the Counterweight-Plus program. Initial weight loss was induced with a total diet replacement phase using a low energy formula diet (825–853 kcal/day) for 3 months (extendable up to 5 months if wished by participant), followed by structured food reintroduction of 2–8 weeks (about 50% carbohydrate, 35% total fat, and 15% protein), and an ongoing structured programme with monthly visits for long-term weight loss maintenance. Given the primary care non-specialist setting of this trial, the key findings (as summarized by the authors), were perhaps surprising: “Just less than a quarter of participants in the intervention group achieved weight loss of 15 kg or more at 12 months, half maintained more than 10 kg loss, and almost half had remission of diabetes, off antidiabetic medication….Remission was closely related to the degree of weight loss maintained at 12 months, with achievement in 86% of participants with at least 15 kg weight loss, and 73% of those with weight loss of 10 kg or more. 28% of all eligible individuals volunteered to participate,17 and 79% completed the intensive total diet replacement phase…” In general, the intervention was well tolerated with 117 out of 150 participants (78%) in the intervention group completing the intervention. So here are the key learning from DIRECT: For one, there should no longer be any doubt that “remission” of Type 2 diabetes is possible in a substantial number of patients, if we can help them achieve and sustain significant weight loss – the odds of experiencing remission are directly proportional… Read More »
In addition to the series of article on long-term outcomes in bariatric surgery, the 2018 special issue of JAMA on obesity, also features several articles discussing the potential role of taxing or otherwise regulating the use of sugar-sweetened beverages (SSB) as a policy measure to address obesity. In a first article, Jennifer Pomeranz and colleagues discuss whether or not governments can in fact require health warnings on advertisements for sugar-sweetend beverages. The discussion focuses on an injunction issued by the Ninth Circuit Court on the enforcement of San Francisco’s requirement that sugar-sweetened beverage (SSB) advertisements display a health warning statement, finding that this law likely violated the First Amendment rights of advertisers of SSBs. The background for this court decision was the fact that San Francisco passed a law requiring SSB advertisers to display: “WARNING: Drinking beverages with added sugar(s) contributes to obesity, diabetes, and tooth decay. This is a message from the City and County of San Francisco.” In its decision, the court felt that the proposed warning label was not scientifically accurate, as it focussed exclusively on “added sugar(s)” rather than sugars overall. It appears that there is no scientific evidence suggesting that “added sugars” are any more (or less) harmful than the “natural” sugar occurring in any other foods or beverages). However, as the authors argue, warning on SSB may well be warranted as “In addition to being a major source of added sugar in the US diet, the liquid form of SSBs could enable rapid consumption and digestion without the same satiety cues as solid foods. SSBs also contain no relevant ingredients to provide offsetting health benefits, in comparison with sweetened whole grain cereals, nut bars, yogurt, or other foods with added sugars, which can have healthful components. Furthermore, the associations of SSBs with weight gain, obesity, type 2 diabetes, and heart disease are each stronger and more consistent than for added sugars in solid foods. In addition, compared with other foods containing added sugars, SSBs are the only source for which randomized controlled trials have confirmed the observational link to weight gain.” Another point of contention identified by the court was related to the fact that the warning stated harm irrespective of quantity and would have been more accurate had it included the term “overconsumption” or at leas the qualifier “may”. Here, the authors argue that, “health risks of SSBs increase monotonically. Thus, use of the word… Read More »
If there is one article in the 2018 special issue of JAMA on obesity that we could have well done without, it is surely the one by Eve Guth promoting the age-old notion that simply counting calories is a viable and effective means to manage body weight. As the author suggests: “It is better for physicians to advise patients to assess and then modify their current eating habits and then reduce their caloric ingestion by counting calories. Counseling patients to do this involves provision of simple handouts detailing the calorie content of common foods, suggested meal plan options, an explanation of a nutrition label, and a list of websites with more detailed information. Patients should be advised that eating about 3500 calories a week in excess of the amount of calories expended results in gaining 1 lb (0.45 kg) of body weight. If a patient reduces caloric ingestion by 500 calories per day for 7 days, she or he would lose about 1 lb of body weight per week, depending on a number of other factors. This is a reasonable and realistic place to start because this approach is easily understood and does not ask a patient to radically change behavior.” There is so much wrong with this approach, that it is hard to know exactly where to start. For one, this advise is based on the simplistic assumption that obesity is simply a matter of managing calories to achieve and sustain long-term weight loss. Not only, do we have ample evidence that these type of approaches rarely result in long-term sustained weight-loss but, more importantly this type of advice comfortably ignores the vast body of scientific literature that tells us that body weight is a tightly regulated physiological variable and that there are a host of complex neuroendocrine responses that will defend our bodies against long-term weight loss – mechanisms that most people (irrespective of whether they have obesity or not) will find it exceedingly hard to overcome with “will-power” alone. No doubt, caloric “awareness” can be an eye-opener for many patients and there is good evidence that keeping a food journal can positively influence dietary patterns and even reduce “emotional” eating. But the idea that cognitively harnessing “will-power” to count calories (a very “unnatural” behaviour indeed), thereby creating and sustaining a long-term state of caloric deficit is rather optimistic at best. In fact, legions of people who have been… Read More »