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.
The biguanide metformin is widely used for the treatment of type 2 diabetes. Metformin has also been shown to slow the progression from pre to full-blown type 2 diabetes. Moreover, metformin can reduce weight gain associated with psychotropic medications and polycystic ovary syndrome.
Now, a randomised controlled trial by M P van der Aa and colleagues from the Netherlands, published in Nutrition & Diabetes suggests that long-term treatment with metformin may stabilize body weight and improve body composition in adolescents with obesity and insulin resistance.
The randomised placebo-controlled double-blinded trial included 62 adolescents with obesity aged 10–16 years old with insulin resistance, who received 2000 mg of metformin or placebo daily and physical training twice weekly over 18 months.
Of the 42 participants (mean age 13, mean BMI 30), BMI was stabilised in the metformin group (+0.2 BMI unit), whereas the control group continued to gain weight (+1.2 BMI units).
While there was no significant difference in HOMA-IR, mean fat percentage reduced by 3% compared to no change in the control group.
Thus, the researcher conclude that long-term treatment with metformin in adolescents with obesity and insulin resistance can result in stabilization of BMI and improved body composition compared with placebo.
Given the rather limited effective options for addressing childhood obesity, this rather safe, simple, and inexpensive treatment may at least provide some relief for adolescents struggling with excess weight gain.
Continuing in my miniseries on arguments that support calling obesity a disease, is the simple fact that, once established, it behaves like a chronic disease.
Thus, once people have accumulated excess or abnormal adipose tissue that affects their health, there is no known way of reversing the process to the point that this condition would be considered “cured”.
By “cured”, I mean that there is a treatment for obesity, which can be stopped without the problem reappearing. For e.g. we can cure an ear infection – a short course of antibiotics and the infection will resolve to perhaps never reappear. We can also cure many forms of cancer, where surgery or a bout of chemotherapy removes the tumour forever. Those conditions we can “cure” – obesity we cannot!
For all practical purposes, obesity behaves exactly like every other chronic disease – yes, we can modify the course or even ameliorate the condition with the help of behavioural, medical or surgical treatments to the point that it may no longer pose a health threat, but it is at best in “remission” – when the treatment stops, the weight comes back – sometimes with a vengeance.
And yes, behavioural treatments are treatments, because the behaviours we are talking about that lead to ‘remission’ are far more intense than the behaviours that non-obese people have to adopt to not gain weight in the first place.
This is how I explained this to someone, who recently told me that about five years ago he had lost a substantial amount of weight (over 50 pounds) simply by watching what he eats and maintaining a regular exercise program. He argued that he had “conquered” his obesity and would now consider himself “cured”.
I explained to him, that I would at best consider him in “remission”, because his biology is still that of someone living with obesity.
And this is how I would prove my point.
Imagine he and I tried to put on 50 pounds in the next 6 weeks – I would face a real upward battle and may not be able to put on that weight at all – he, in contrast, would have absolutely no problem putting the weight back on.
In fact, if he were to simply live the way I do, eating the amount of food I do, those 50 lbs would be back before he knows it.
His body is just waiting to put the weight back on whereas my biology will actually make it difficult for me simply put that weight on.
This is because his “set-point”, even 5 years after losing the weight, is still 50 lbs higher than my “set-point”, which is around my current weight (the heaviest I have ever been).
Whereas, he is currently working hard against his set-point, by doing what he is doing (watching what he eats, following a strict exercise routine), I would be working against my set-point by having to force myself to eat substantially more than my body needs or wants.
That is the difference! By virtue of having had 50 lb heavier, his biology has been permanently altered in that it now defends a weight that is substantially higher than mine.
His post-weight loss biology is very different from mine, although we are currently at about the same weight.
This is what I mean by saying he is in “remission”, thanks to his ongoing behavioural therapy.
Today, we understand much of this biology. We understand what happens when people try to lose weight and how hard the body fights to resist weight loss and to put the weight back on.
This is why, for all practical purposes, obesity behaves just like every other chronic disease and requires ongoing treatment to control – no one is ever “cured” of their obesity.
Not even people who have bariatric surgery – reverse the surgery and before you know it, the weight is back.
So, if for all practical purposes, obesity behaves like a chronic disease, why not just call a spade a spade?
For an illustration on why obesity acts like a chronic disease watch this short TEDx talk
Are you an impulsive eater? Do you have a hard time meal planning or keeping a food journal? Do you find it hard to remember if you had breakfast or not (never mind what you actually ate)? Do you start every new diet or exercise program with super enthusiasm, only to lose interest a few days later? Does your day lack a routine (for no good reason)?
These are just some of the ways in which Attention Deficit Hypertactivity or just Attention Deficit Disorder (ADHD/ADD) can sabotage your efforts to control your weight.
Now, an article by Philip Asherson and colleagues from Kings College London, UK, published in The Lancet Psychiatry discuss important conceptual issues regarding the diagnosis and management of ADHD/ADD in adults.
Although ADHD/ADD is largely thought to be a problem in kids and youth, it remains a considerable and often undiagnosed issue in adults.
Thus, as the authors point out,
“…treatment of adult ADHD in Europe and many other regions of the world is not yet common practice, and diagnostic services are often unavailable or restricted to a few specialist centres.”
This is all the more surprising (and disappointing) given that adult patients respond similarly to current drug and psychosocial interventions, with the same benefits seen in children and adolescents.
With regard to diagnosis it is important to note that,
“Symptoms of ADHD cluster together into two key dimensions of inattention and hyperactivity-impulsivity, are reliably measured, and are strong predictors of functional impairments, but they reflect continuous traits rather than a categorical disorder.”
“Of particular relevance to adult ADHD is the relative persistence of inattention and improvements in hyperactive-impulsive symptoms during development, so that many patients who had the combined type presentation of ADHD as children present with predominantly inattentive symptoms as adults.”
“In clinical practice, the continuous nature of ADHD should not present diagnostic difficulties in moderate-to-severe cases, but might cause difficulties in mild cases with more subtle forms of impairment. Careful attention is needed to assess the effect of ADHD symptoms on impairment and quality of life, including an understanding of the broader range of problems linked to ADHD (eg, executive function [self-regulation] impairments, sleep problems, irritability, and internal restlessness), in addition to functional impairments such as traffic accidents and occupational underachievement. Therefore, some individuals, who seem to function well, might nevertheless suffer from a substantial mental health problem related to ADHD.”
Key criteria according to DSM-5 include:
- Mind seems elsewhere, even in the absence of any obvious distraction
- Starts tasks, but quickly loses focus and is easily side-tracked
- Fails to finish tasks in the workplace
- Reporting unrelated thoughts
- Problems returning calls, paying bills, keeping appointments
- Difficulty in managing sequential tasks; difficulty in keeping materials and belongings in order; messy, disorganised work
- Poor time management
- Tends to fail to meet deadlines
- Feeling restless
- Unable or uncomfortable being still for an extended time, such as in restaurants or meetings
- Might be perceived by others as being restless and difficult to keep up with
- Butts into conversations or activities, might start using other people’s belongings without permission, might intrude into or take over what others are doing
Other common features, that do not quite rise to level of diagnostic criteria include include poor concentration, distractibility, restlessness, over-talkativeness, sleep problems, irritability, impulsiveness, and low self-esteem.
It is important to note that other mental or physical disorders can mimic some of the symptoms of ADHD. These include anxiety, depression, bipolar disorder, hyperthyroidism and sleep apnea.
While the paper does not mention obesity or difficulties managing weight as a possible “complication” of ADHD, in my experience, identifying and treating ADHD in bariatric patients can often make all the difference.
Thus, I concur with the authors’ conclusions that,
“…ADHD should be recognised in the same way as other common adult mental health disorders, and that failure to recognise and treat ADHD is detrimental to the wellbeing of many patients seeking help for common mental health problems.”
The nature of chronic diseases is that they are (by definition) rarely (if ever) “cured”, meaning that the best you can generally hope for is “control”, which in some cases may only amount to “stabilisation” or “slowing of progression”.
In the context of obesity, one could perhaps define “control” as achievement AND maintenance of your “best weight”; “stabilisation” could be defined as prevention of further weight gain; “slowing of progression” would be defined as continuing to gain weight but at a slower rate than before.
Now, a paper by Janelle Coughlin and colleagues published in OBESITY, shows (surprise, surprise!) that continued intervention involving personal contact leads to better weight-loss maintenance (at five years) than time-limited self-directed management.
The paper describes the results of the the Weight Loss Maintenance (WLM) Trial, in which participants were essentially randomised to either a personal contact (PC) intervention or a self-directed (SD) group over 30 months with continued follow-up for another 30 months (for a total of 5 years).
Overall, the WLM had 3 phases. Phase 1 was a 6-month weight loss program. In Phase 2, those who lost ≥4 kg were randomized to a 30-month maintenance trial. In Phase 3, PC participants (n = 196, three sites) were re-randomized to no further intervention (PC-Control) or continued intervention (PC-Active) for 30 more months; 218 SD participants were also followed.
In the study overall at 5 years, mean weight change was −3.2 kg in those originally assigned to PC (PC-Combined) and −1.6 kg in SD (this rather modest amount of weight loss maintenance is unfortunately typical for all behavioural weight-management interventions, highlighting the ongoing need for better treatments!).
None of this is surprising.
As with any chronic disease, personal contact interventions by a trained health professional are likely to be superior to patients trying to manage on their own (self-directed).
At some point (the time may well be 30 months), continued regular intervention for everyone will likely provide diminishing returns.
This is evident from the finding in this study that in the PC group, continued intervention after 30 months did not appear to provide a significant additional benefit in terms of weight-loss maintenance.
In fact, one would probably want to vary frequency and intensity of any further intervention for patients who are relapsing (i.e. regaining their weight faster than expected).
This is not unlike patients in a diabetes or hypertension clinic. After an initial phase of a more intense intervention during which patients are titrated to a target blood pressure or HbA1c level, frequency of on-going follow-up should naturally be tailored to how well the patient in managing.
Some individuals will need more attention more often than others – this need will also be expected to vary over time for individual patients.
For many patients with chronic diseases, proper education and development of self-management skills (such as regular self-monitoring of blood pressure or blood sugar levels), may often allow on-going support to be limited to brief encounters largely involving brief assessments and prescription renewals.
As I have said before, long-term management of obesity is no different than managing any other chronic disease.
Tailoring the intensity and rate of follow-up to each patient’s specific needs should be no different in obesity management than in managing someone’s hypertension or diabetes.