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Post-Weight Loss Fat Gain in US Rangers

army-rangersAnd finally, to conclude this week’s discussion of evidence to support the notion that weight cycling predicts weight (fat) gain especially in normal weight individuals, I turn back to the paper by Dulloo and colleagues published in Obesity Reviews, which quotes these interesting findings in US Rangers:

“…U.S. Army Ranger School where about 12% of weight loss was observed following 8–9 weeks of training in a multi-stressor environment that includes energy deficit. Nindl et al. reported that at week 5 in the post-training recovery phase, body weight had overshot by 5 kg, reflected primarily in large gains in fat mass, and that all the 10 subjects in that study had higher fat mass than before weight lost. Similarly, in another 8 weeks of U.S. Army Ranger training course that consisted of four repeated cycles of restricted energy intake and refeeding, Friedl et al. showed that more weight was regained than was lost after 5 weeks of recovery following training cessation, with substantial fat overshooting (∼4 kg on average) representing an absolute increase of 40% in body fat compared with pre-training levels. From the data obtained in a parallel group of subjects, they showed that hyperphagia peaked at ∼4 weeks post-training, thereby suggesting that hyperphagia was likely persisting over the last week of refeeding, during which body fat had already exceeded baseline levels.”

Obviously, association (even in a prospective cohort) does not prove causality or, for that matter, provide insights into the physiological mechanisms underlying this observation.

All we can conclude, is that these observations in US Rangers (and the other studies cited in Dulloo’s article) are consistent with the notion that weight loss in normal weight individuals can be followed by significant weight gain, often overshooting initial weight.

Incidentally, these findings are also consistent with observational studies in women recovering from anorexia nervosa, famine, cancer survivors and other situations resulting in significant weight loss in normal weight individuals.

Certainly enough evidence to consider a work of caution against “recreational” weight loss, especially in individuals of normal weight.

@DrSharma
Edmonton, AB

ResearchBlogging.orgDulloo AG, Jacquet J, Montani JP, & Schutz Y (2015). How dieting makes the lean fatter: from a perspective of body composition autoregulation through adipostats and proteinstats awaiting discovery. Obesity reviews : an official journal of the International Association for the Study of Obesity, 16 Suppl 1, 25-35 PMID: 25614201

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Did Dieting Make You Fat? Blame Your ‘Proteinstat’

Skeletal muscle

Skeletal muscle

Yesterday, I posted on the intriguing finding (now documented in 15 prospective studies) that dieting can make you fat – especially if you start out with a normal weight.

In the paper by Dulloo and colleagues published in Obesity Reviews, the authors attribute part of this effect to the so far elusive “proteinstat” – a system, similar but different from the “adipostat” – that is designed to protect your lean body mass.

As the paper nicely delineates, the problem with post-dieting weight regain is that the fat comes back first but that the drive to eat does not cease till you have also regained the lost lean body mass (muscle).

It appears as though there are two complimentary biological systems that regulate weight regain.

The better known system is the “adipostat” that worries about protecting and restoring fat mass – the neuroendocrine players include leptin and perhaps other signals derived from fat tissue that signal fat stores to the brain. This system works (primarily through dropping metabolic rate but also through effects on appetite) to very quickly and effectively restore the depleted fat mass after dieting.

The less known system is the “proteinstat”, that apparenty worries about restoring lean body mass. The system works slower than the “adipostat” but continues its activity (often reaching its peak) even after all the lost fat has been regained and you are back to your original weight. In fact, it continuous working (primarily through appetite and cravings) till lean body mass is restored, even if this means gaining even more fat in the process.

In their careful reanalysis of starvation studies, Dulloo and colleagues also come up with an explanation why this process of “weight overshoot” results in more gain the skinnier the individual is to begin with.

“…the lower the initial adiposity, the greater the proportion of energy mobilized as body protein (referred to as P-ratio) during weight loss. The steep part of the negative exponential curve lies between 8–20% body fat, and a shift from the upper to the lower values in this range, generally considered to reflect a ‘normal’range of adiposity for men living in affluent societies, results in 2.5- to 3-fold increase in the P-ratio; the latter constitutes a proxy of the fraction of weight that is lost as FFM since protein belongs to the FFM compartment. This extremely high sensitivity of the P-ratio with regard to the initial body composition emphasizes the critical importance of even small differences in the initial percentage body fat in dictating the individual’s energy-partitioning characteristic and, hence, the pattern of lean and fat tissue deposition during weight loss and subsequent
weight regain, in turn, determining the extent of fat overshooting.”

In other words, lean dieters are far more susceptible to mobilising energy (and thus losing mass) from their muscle than from their fat stores, resulting in a much greater likelihood of overshooting their original weight.

Eventually, as these dieters get fatter with every diet cycle, they get less and less susceptible to this effect, which matches well with the finding that dieting is a far better predictor of long-term weight gain in people with lower fat percentages than in those who already have overweight or obesity).

As for exactly how the “proteinstat” works, much remains unclear. Early work focussed on the notion that certain amino acids may serve as signals of protein stores, however, now work is focussing on the far more plausible theory that some of the over 100 molecules now known to be secreted by skeletal muscle (myokines) may play a role in this system.

Certainly a topic that will be interesting to watch develop over the coming years.

@DrSharma
Calgary, AB

ResearchBlogging.orgDulloo AG, Jacquet J, Montani JP, & Schutz Y (2015). How dieting makes the lean fatter: from a perspective of body composition autoregulation through adipostats and proteinstats awaiting discovery. Obesity reviews : an official journal of the International Association for the Study of Obesity, 16 Suppl 1, 25-35 PMID: 25614201

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Plan Your Personalized Program For The Canadian Obesity Summit Now

Summit15appIf you are planning to attend the 4th Canadian Obesity Summit in Toronto next week (and anyone else, who is interested), you can now download the program app on your mobile, tablet, laptop, desktop, eReader, or anywhere else – the app works on all major platforms and operating systems, even works offline.

You can access and download the app here.

(To watch a brief video on how to install this app on your device click here)

You can then create an individual profile (including photo) and a personalised day-by-day schedule.

Obviously, you can also search by speakers, topics, categories, and other criteria.

Hoping to see you at the Summit next week – have a great weekend!

@DrSharma
Gurgaon, Haryana

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All Behavioural Interventions Carry Risks

sharma-obesity-kids-scale1Following the recent release of the Canadian Task Force on Preventive Health Care guidelines for prevention and management of adult obesity in primary care, the Task Force yesterday issued guidelines on the prevention and management of childhood obesity in the Canadian Medical Association Journal (CMAJ).

Key recommendations include:

  • For children and youth of all ages the Task Force recommends growth monitoring at appropriate primary care visits using the World Health Organization Growth Charts for Canada.
  • For children and youth who are overweight or obese, the Task Force recommends that primary health care practitioners offer or refer to formal, structured behavioural interventions aimed at weight loss.
  • For children who are overweight or obese, the Task Force recommends that primary health care practitioners not routinely offer Orlistat or refer to surgical interventions aimed at weight loss.

The lack of enthusiasm for the prevention of childhood obesity is perhaps understandable as the authors note that,

“The quality of evidence for obesity prevention in primary care settings is weak, with interventions showing only modest benefits to BMI in studies of mixed-weight populations, with no evidence of long-term effectiveness.”

leading the Task Force to the following statement,

“We recommend that primary care practitioners not routinely offer structured interventions aimed at preventing overweight and obesity in healthy-weight children and youth aged 17 years and younger. (Weak recommendation; very low-quality evidence)”

Be that as it may, the Task Force does recommend structured behavioural interventions for kids who already carry excess weight based on the finding that,

“Behavioural interventions have shown short-term effectiveness in reducing BMI in overweight or obese children and youth, and are the preferred option, because the benefit-to-harm ratio appears more favourable than for pharmacologic interventions.”

What caught my eye however, was the statement in the accompanying press release which says that,

“Unlike pharmacological treatments that can have adverse effects, such as gastrointestinal problems, behavioural interventions carry no identifiable risks.” (emphasis mine) 

While I would certainly not argue for the routine use of orlistat (the only currently available prescription drug for obesity in Canada) in children (or anyone else), I do take exception to the notion that behavioural interventions carry no identifiable risks – they very much do.

As readers may be well aware, a large proportion of the adverse effects of medications is attributable to the wrong use of these medications – problems often occur when they are taken for the wrong indication, at the wrong dose (too high or too low), the wrong frequency (too often or too seldom), and/or when patients are not regularly monitored. In a perfect world,  many medications that often lead to problems would be far less problematic than they are in the real world.

Interestingly, the same applies to behavioural interventions.

Take for example diets – simply asking a patient to “eat less” can potentially lead to all kinds of health problems from patients drastically reducing protein, vitamin and mineral intake as a result of going on the next “fad” or “do-it-yourself” diet. Without ensuring that the patient actually follows a prudent diet and does not “overdo” it, which may well require ongoing monitoring, there is very real potential of patients harming themselves. There is also the real danger of promoting an eating disorder or having patients face the negative psychological consequences of yet another “failed” weight-loss diet. Exactly how many patients are harmed by well-meant dietary recommendations is unknown, as I am not aware of any studies that have actually looked at this.

The same can be said for exercise – simply asking a patient to “move more” can result in injury (both short and long-term) and coronary events (in high-risk patients).  Again, ongoing guidance and monitoring can do much to reduce this potential harm.

In short when patient apply behavioural recommendations at the wrong dose (too much or too less), wrong frequency (too often or too seldom), and/or are not regularly monitored, there is indeed potential for harm – I would imagine that this potential for harm is of particular concern in kids.

This is not to say that we should not use behavioural interventions – we should – but we must always consider the potential for harm, which is never zero.

I’d certainly be interested in hearing from anyone who has seen harm resulting from a behavioural intervention.

@DrSharma
Edmonton, AB

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Exercise Reduces Cravings For Sugar?

sharma-obesity-exercise2I have long postulated that the benefits of exercise in weight management have little to do with burning calories. Rather, I am pretty sure that when people lose weight with exercise, they do so because of the impact that exercise may have on their food intake (I call it exercising to ruin your appetite!).

Thus, I am happy to acknowledge my affirmation bias in paosting about the recent study by Larissa Ledochowski and colleagues from the University of Innsbruck, Austria, published in PLOS One on the outcome of a randomised controlled trial of brisk walking on cravings for sugary snacks.

The study was conducted in 47 overweight volunteers who reported habitually consuming a fair share of sugary snacks. Following 3 days of “chocolate abstinence” subjects were randomised (using a within-subject design) to a 15-min brisk walk or passive control.

On each occasion, subjects were then stressed using the Stroop color–word interference task after which they reported their urges for sugary snacks using the State Food Craving Questionnaire [FCQ-S] adapted for sugary snacks.

Compared to the control situation, brisk walking resulted in a significant and relevant reduction in the urge for sugary snacks and attenuated the increase in sugar-cravings under trigger conditions (stress).

Although the authors are careful about not over-interpreting their findings from this acute study (that did not actually measure sugary-snack intake), they do make the following speculation regarding clinical relevance,

“This study adds to the increasing evidence that physical activity can somehow help to regulate the urge to consume snack food. It may be easy for overweight people to fit in short bouts of low-moderate intensity physical activity, instead of being sedentary, to elevate affective activation and valence and reduce high energy food cravings which may be triggered by stress and the presence of snack foods.”

While I am certain that more intense exercise may well trigger a hunger response, it appears that even a short bout of brisk walking may help dispel those cravings for sugary snacks (let me know if you have experienced this).

@DrSharma
Edmonton, AB

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