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Getting A Grip On Mortality

jamar dynamometerThere are many clinical measures that predict increased risk of cardiovascular and all-cause mortality (e.g. having a high blood pressure).

However, it turns out that perhaps one of the most powerful predictors of mortality is a simple and inexpensive assessment of grip strength – something rarely assessed in clinical practice.

Now, a study by Darryl Leung and colleagues, in a paper published in The Lancet, reports that grip strength does just that.

The paper presents data from the Prospective Urban-Rural Epidemiology (PURE) study, a large, longitudinal population study done in 17 countries of varying incomes and sociocultural settings involving nearly 150,000 individuals.

During a median follow-up of 4·0 years, grip strength (as a simple measure of muscular strength) was found to be inversely associated with all-cause mortality (hazard ratio per 5 kg reduction in grip strength 1·16), cardiovascular mortality (1·17), non-cardiovascular mortality (1·17), myocardial infarction (1·07), and stroke (1·09).

In fact, grip strength was a stronger predictor of all-cause and cardiovascular mortality than systolic blood pressure.

In contrast, grip strength was not associated with diabetes, hospital admission for pneumonia or COPD, injury from fall, or fracture.

Interestingly, the association between grip strength and cardiovascular mortality is not new – however, the association with all-cause mortality and the consistency of this findings across populations and economic strata is remarkable.

Obviously, these findings beg the question whether increasing grip strength (or rather muscular strength in general) through resistance training and adequate protein intake will lower mortality – a question that would take a rather large randomised controlled study to answer.

Till then, it is prudent to remember that association does not prove causation – it would thus be premature to conclude that your weak handshake is killing you.

@DrSharma
Edmonton, AB

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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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Are Weight-Cycling Elite Athletes Predisposed To Weight Gain?

powerliftingMy recent reading of the paper by Dulloo and colleagues on post-dieting weight gain in non-obese individuals, reminded me of my clinical observation that a surprisingly large proportion of patients I see in our bariatric clinic report a history of competitive sports.

When I have previously discussed this observation with colleagues, the answer I often get is that this weight gain is simply due to the fact that active athletes are used to eating a lot, which they continue to do after their activity levels decline, thus resulting in weight gain – a theory, I don’t quite buy largely because it appears far too simplistic (and I have yet to see any evidence to support it).

Rather, if the phenomenon of weight-cycling induced weight gain is real, one would assume that not all athletes are at risk, but rather that this phenomenon would be limited to athletes in disciplines where weight cycling (e.g. to meet certain weight criteria), often referred to as “weight cutting”, is part of the culture of that sport. Examples of such sports include wrestling, boxing, and weight lifting.

It turns out that this very issue has been studied by Saarni and colleagues, who, in a paper published in the International Journal of Obesity, report their findings on a large national cohort of 1838 male elite athletes who had represented Finland in major international sport competitions in 1920-1965.

This cohort included 370 men engaged in sports in which weight-related performance classes are associated with weight cycling (boxers, weight lifters and wrestlers) and 834 matched control men with no background in athletics.

Over the 20+ years of follow-up, the weight-cycling gained a whooping 5.2 BMI units from age 20 years to their maximum mean weight (at around age 60) conpared to only 3.3 BMI units in non-weight-cycling athletes or just 4.4. BMI units in the non-athletic controls.

Indeed, weight-cycling athletes were about three times as likely to develop obesity (defined as a BMI > 30), than their non-weight cycling colleagues or controls.

This enhanced risk of developing obesity in weight-cycling athletes remained significant even after correction for a number of potential confounders including health habits (smoking, alcohol use, use of high-fat milk or physical activity) or weight at age 20 years.

While this paper does not prove causality, or for that matter, provide any insights into possible biological mechanisms that would promote weight gain, it is certainly consistent with the hypothesis that repeated cycles of weight loss and regain in people who start out with a normal weight (in this case elite athletes) strongly predicts subsequent weight gain and the development of obesity.

Or, as the authors put it,

“The weight cycling behavior of the former athletes engaged in power sports at a young age resembles that of young dieters who lose weight temporarily and soon regain it. The present observations concerning the enhanced weight gain of these athletes raise the concern that the repeated cycles of weight loss and regain caused by dieting at a young age could similarly affect weight in the long term.”

@DrSharma
Edmonton, AB

ResearchBlogging.orgSaarni SE, Rissanen A, Sarna S, Koskenvuo M, & Kaprio J (2006). Weight cycling of athletes and subsequent weight gain in middleage. International journal of obesity (2005), 30 (11), 1639-44 PMID: 16568134

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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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Epode’s Canada Obesity Forum

Epode canadaAs part of the 4th Canadian Obesity SummitEPODE Canada presents its first Canadian Regional Forum. This one-day workshop is designed for program managers, local community coordinators or program advisors of childhood obesity prevention programs, and to share knowledge and practical advice between EPODE and Canadian programs.

Senior members of the EPODE global team including program managers from programs in Belgium and the Netherlands will share their practical experience on program design, social marketing actions, private public partnerships and program evaluation. Canadian program managers will report on their experience and learnings and discuss barriers and levers to working in the Canadian context. A special workshop on program evaluation, chaired by Dr. Emile Levy of Hospital St. Justine in Montreal will discuss practical approaches to evaluating process and outcomes. A special luncheon presentation on kids and nutrition will be given by the founders of Real Foods for Real Kids. A networking event will be held afterwards for more informal discussion or questions. By attending this landmark event you will find ideas that can help you improve the efficiency and effectiveness of your childhood obesity prevention program.

The cost of the full day workshop includes lunch and the networking event. Attendees can choose to attend only the EPODE Canada workshop or to continue on with the full Summit program and presentations. Program members of the EPODE International Network may attend at a significantly reduced rate.

Learning objectives:

Through these presentations and workshops, participants will learn to improve the efficiency and effectiveness of a community-based childhood obesity prevention program by learning:

  1. The 23 year evolution of the EPODE methodology and its critical success factors. e.g. the four pillars.
  2. Best practices from community-based programs around the world in program design, social marketing actions, private public partnershipsand program evaluation methodologies.
  3. Valuable insights into barriers and opportunities in the Canadian context via experts in the field presenting their findings and experience.
  4. Participants will share knowledge with other similar programs, and become part of a Canada-wide network of childhood obesity prevention programs.

Who should attend:

Anyone interested in improving the efficiency and effectiveness of implementing a childhood obesity prevention programs. This includes:

    • program managers
    • local community coordinators
    • program advisors (academics, health care professionals) of childhood obesity prevention programs

Topics include:

See a full list of topics in our schedule (as of January 19th 2015).

Registration (ends April 28, 2015)

Members of EPODE Canada and the Canadian Obesity Summit receive discounts on registration! Become a member of the EPODE International Network today!

General – $350

EPODE Network members- $225

Registration is now open!  

@DrSharma
Edmonton, AB

 

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