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 every other day is “restrictive”), the greater the dropout rate.
Unfortunately, what counts in real life is not what people should be doing, but what people actually do. The question really is not whether or not alternate-day fasting is better for someone trying to lose weight but rather, whether or not “recommending” someone follows an alternate-day fasting plan (and them trying to follow it the best they can) is better for them. The clear answer from this study is “no”.
So why are all diets the same (in that virtually all of them provide a rather modest degree of long-term weight loss)?
My guess is that no diet (or behaviour for that matter) has the capability of fundamentally changing the body’s biology that acts to protect and restore body fat in the long-term. Irrespective of whether a diet leads to weight loss in the short term and irrespective of how it does so (or how slow or fast), ultimately no diet manages to “reset” the body-weight set point to a lower level, that would biologically “stabilize” weight loss in the long-term.
Thus, the amount of long-term weight loss that can be achieved by dieting is always in the same (rather modest) ballpark and it is often only a matter of time before the biology wins out and put all the weight back on.
Clearly, I am not holding my breath for the next diet that comes along that promises to be better than everything we’ve had before.
My advice to patients is, do what works for you, but do not expect miracles – just find the diet you can happily live on and stick to it.
Readers may by now be familiar with the GLP-1 analogue liraglutide, which has now been approved at the 3 mg dose (Saxenda(R)) for long-term obesity treatment in a growing number of countries.
Now, Novo Nordisk, the maker of liraglutide, announced preliminary results from their long-acting GLP-1 analogue semaglutide, suggesting a rather remarkable ~14% weight loss in a one-year double-blind placebo controlled dose-finding study.
According to the company’s press release,
In the trial, 957 people with obesity were randomised to treatment with doses of semaglutide between 0.05 to 0.4 mg/day or placebo. Liraglutide 3.0 mg/day was included for comparison. Approximately 100 people were included in each active treatment arm in combination with diet and exercise. All people in the trial were treated for 52 weeks followed by a 7-week follow-up period.
From a mean baseline weight of around 111 kg and a body mass index of approximately 39 kg/m2, a weight loss up to 17.8 kg was observed after 52 weeks of treatment with semaglutide. This corresponded to an estimated 13.8% weight loss compared to the weight loss of 2.3% achieved by diet, exercise and placebo alone, with all treatment arms adjusted for people discontinuing treatment in the study. The results from the liraglutide 3.0 mg treatment arm were broadly in line with previously reported data.
Side effects were mainly reported as gastro-intestinal, as expected from this class of hormone analogues.
Clearly, if borne out by the final publication and confirmed in larger and longer studies, semaglutide may well prove to be even more effective than liraglutide.
It may be worth noting, that the ~14% weight loss reported in this trial comes very close to the mean ~15% weight loss seen with adjustable gastric banding, a bariatric surgical technique that is now increasingly seen as obsolete due to long-term complications and loss of effectiveness.
I’m guessing it’s now on to Phase 3 for this promising anti-obesity drug.
Disclaimer: I have received speaking and consulting honoraria from Novo Nordisk, the maker of liraglutide and semaglutide
Last week I was an invited plenary speaker at the 1st International Diabetes Expert Conclave (IDEC2017) held in Pune, India.
This 3-day event, organised by Drs. Neeta Deshpande (Belgaum), Sanjay Agrawal (Pune) and colleagues, brought together well over 900 physicians from across India for a jam-packed program that covered everything from diabetic food disease and neuropathy to the latest in insulin pumps and devices – all in a uniquely Indian context.
I, of course, was there to speak on obesity, which featured prominently in the program. Topics on obesity ranged from the potential role of gut bugs to bariatric surgery. While Dr. Allison Goldfine, former Director of Clinical Research at the Joslin Diabetes Center in Boston spoke on the latest developments in anti-obesity pharmacotherapy (delivering her talk via Skype), I spoke about obesity as a chronic disease and the need to redefine obesity based on actual indicators of health rather than BMI.
During my visit in Pune, I also had the opportunity to visit with my friend and colleague Dr. Shashank Shah, whose bariatric surgical center in Pune alone performs about 75 to 100 bariatric operations per month – a remarkable number by any standards.
Of course, the overwhelming number of talks were given by Indian faculty (there being only a handful of select invited international faculty at the meeting), and I did come away most impressed by the breadth and depth of knowledge presented by the local speakers.
Diabetes care certainly appears to be in good hands although the sheer number of patients with diabetes (estimated at about 70 million, which I assume to be a rather conservative assessment), would provide a challenge to any health care system.
On the obesity front, things are a lot less rosy, given that (as everywhere else) obesity has yet to receive the same level of professional attention and expertise afforded to diabetes or other chronic diseases.
Thanks again to the organisers for inviting me to this exciting meeting and congratulations on an excellent event that bodes well for the 2nd Conclave planned for 2018.
The third item on the disease definition modification checklist developed by the Guidelines International Network (G-I-N) Preventing Overdiagnosis Working Group published in JAMA Internal Medicine, pertains to the issue of why modify the disease definition at all?
With obesity being increasingly recognize as a chronic disease, it should be evident to anyone, that the current BMI-based definition of obesity, although simple (or rather simplistic), would label a substantial number of individuals as “diseased”, who may be in rather good health and, therefore, very unlikely to benefit from any obesity treatments (overdiagnosis).
On the other hand, the current BMI-based definition excludes a vast number of people, who may very well have health impairments attributable to abnormal or excess body fat, and may thus benefit from obesity treatments (underdiagnosis).
Although there have been many suggestions for replacing BMI with other anthropometric measures (e.g. waist-to-hip ratio, ponderal index, abdominal sagittal diameter, etc.), none of these measures would guarantee that the individuals identified by such measures, would indeed have health impairments attributable to abnormal or excess weight – their sensitivity and specificity, although perhaps marginally better than BMI in identifying individuals with excess body fat, would still not pass the sniff-test for a reliable diagnostic test of an actual disease.
In fact, given the diversity and heterogeneous nature of adipose tissue, even more precise measures of actual body composition (including sophisticated imaging techniques) would still not be enough to determine whether or not body fat in a given is in fact impairing health and warrants obesity treatment.
In contrast, a definition of obesity that requires the actual demonstration of health impairments (likely) attributable to abnormal or excess body fat, via a clinical assessment, would ensure that obesity is only diagnosed in individuals, who actually have a health problem and would therefore likely benefit from obesity treatments. This may well include individuals below the current BMI cut-off.
Thus, continuing to use BMI (or any other anthropometric measure or more sophisticated estimate of body fat) is simply not an option if we are serious about calling obesity a disease.
Following in the footsteps of other organisations like the American and Canadian Medical Associations, the Obesity Society, the Obesity Medical Association, and the Canadian Obesity Network, this month, the World Obesity Federation put out an official position statement on recognising obesity as a chronic relapsing progressive disease.
The position statement, published in Obesity Reviews, outlines the rationale for recognising obesity as a chronic disease and is very much in line with the thinking of the other organisations that have long supported this notion.
In an accompanying commentary, Tim Lobstein, the Director of Policy at the World Obesity Federation notes, that recognising obesity as a disease can have the following important benefits for people living with this disease:
1) A medical diagnosis can act to help people to cope with their weight concerns by reducing their internalized stigma or the belief that their problems are self-inflicted and shameful.
2) A classification of obesity as a disease, or disease process, may help to change both the public and professional discourse about blame for the condition, the latter hopefully encouraging greater empathy with patients and raising the patient’s expectations of unbiased care.
3) Recognition of obesity as a disease may have benefits in countries where health service costs are funded from insurance schemes that limit payments for non-disease conditions or risk factors.
While all of this is great, and I am truly delighted to see the World Obesity Federation come around to this statement, I do feel that the policy statement seems rather tightly locked into the notion that obesity (or at least most of it) is a disease “caused” primarily by eating too much, with the blame placed squarely on the “toxic obesogenic environment”.
Personally, I would rather see obesity as a far more etiologically heterogenous condition, where a wide range of mental, biological and societal factors (e.g. genetics, epigenetics, stress, trauma, lack of sleep, chronic pain, medications, to name a few) can promote weight gain in a given individual.
Although these factors may well operate through an overall increase in caloric consumption (or rather, a net increase in energy balance), they, and not the act of overeating per se must be seen as the underlying “root causes” of obesity.
Thus, I tend to see “overeating” (even if promoted by an obesogenic food environment) as a symptom of the underlying drivers rather than the “root cause”.
Thus, saying that obesity is primarily caused by “overeating” is perhaps similar to saying that depression is primarily caused by “unhappiness”. Readers would probably agree that such a statement regarding the etiology of depression would make little sense, as “unhappiness” is perhaps a symptom but hardly the “cause” of depression, which can be promoted by a wide range of biological, environmental and societal factors, all resulting in the underlying biology that results in the mood disorder.
Similarly, I would say that there are indeed a number of complex socio-psycho-biological factors that underly the biology that ultimately results in overeating and excess weight gain (the food environment clearly being one of these factors).
While this may seem like semantics, I do think that a more differentiated look at the underlying etiology of obesity at the individual level (rather than simply blaming it all on “overeating”), is essential for promoting a more sophisticated view of this complex chronic disease both at the level of the individual and the population.