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Does Testosterone Treatment Help Conserve Lean Body Mass in Dieting Men?

sharma-obesity-dexa-scan1Screen Shot 2016-05-29 at 9.03.11 PMLoss of muscle is an almost obligatory consequence of losing weight. This is particularly true during very restrictive diets resulting in rapid weight loss.

Now, a randomised controlled study by Mark Ng Tang Ful and colleagues, published in BMC Medicine, suggests that treatment with testosterone may help promote diet-induced loss of fat mass and limit loss of muscle mass.

The study included 100 middle-aged men with obesity, who had a total testosterone level of or below 12 nmol/L, the lower limit reported for healthy young men.

Subjects received 10 weeks of a very low energy diet (VLED) followed by 46 weeks of weight maintenance during which they were randomly assigned to 56 weeks of 10-weekly intramuscular testosterone undecanoate or placebo.

Of the 82 men, who completed the study, participants treated with testosterone had an about 3 Kg greater reduction in fat mass with a greater reduction in visceral fat.

While both groups lost the same amount of lean mass during the VLED, participants treated with testosterone, quickly regained the lean mass so that they had about 3.4 more lean mass than the controls at the end of the study, so that virtually all of the greater weigh loss by these participants over the course of the trial was attributable to fat loss.

These findings are consistent with what is known about testosterone function in men with obesity.

Thus, as the authors remind us,

“Experimental studies in humans suggest that fat-derived adipokines and pro-inflammatory mediators may play a role in central gonadal axis suppression. In addition, preclinical evidence has shown that testosterone deficiency promotes adipose tissue accumulation but reduces myogenesis via an androgen receptor mediated pathway.”

Thus, these findings suggest that dieting men may benefit from adjunct treatment with testosterone to promote fat loss and conserve muscle mass.

Edmonton, AB


5th Canadian Obesity Summit – Four More Days To Submit Your Abstracts!

banff-springs-hotelEvery two years the Canadian Obesity Network holds its National Obesity Summit – the only national obesity meeting in Canada covering all aspects of obesity – from basic and population science to prevention and health promotion to clinical management and health policy.

Anyone who has been to one of the past four Summits has experienced the cross-disciplinary networking and breaking down of silos (the Network takes networking very seriously).

Of all the scientific meetings I go to around the world, none has quite the informal and personal feel of the Canadian Obesity Summit – despite all differences in interests and backgrounds, everyone who attends is part of the same community – working on different pieces of the puzzle that only makes sense when it all fits together in the end.

The 5th Canadian Obesity Summit will be held at the Banff Springs Hotel in Banff National Park, a UNESCO World Heritage Site, located in the heart of the Canadian Rockies (which in itself should make it worth attending the summit), April 25-29, 2017.

Yesterday, the call went out for abstracts and workshops – the latter an opportunity for a wide range of special interest groups to meet and discuss their findings (the last Summit featured over 20 separate workshops – perhaps a tad too many, which is why the program committee will be far more selective this time around).

So here is what the program committee is looking for:

  • Basic science – cellular, molecular, physiological or neuronal related aspects of obesity
  • Epidemiology – epidemiological techniques/methods to address obesity related questions in populations studies
  • Prevention of obesity and health promotion interventions – research targeting different populations, settings, and intervention levels (e.g. community-based, school, workplace, health systems, and policy)
  • Weight bias and weight-based discrimination – including prevalence studies as well as interventions to reduce weight bias and weight-based discrimination; both qualitative and quantitative studies
  • Pregnancy and maternal health – studies across clinical, health services and population health themes
  • Childhood and adolescent obesity – research conducted with children and or adolescents and reports on the correlates, causes and consequences of pediatric obesity as well as interventions for treatment and prevention.
  • Obesity in adults and older adults – prevalence studies and interventions to address obesity in these populations
  • Health services and policy research – reaserch addressing issues related to obesity management services which idenitfy the most effective ways to organize, manage, finance, and deliver high quality are, reduce medical errors or improve patient safety
  • Bariatric surgery – issues that are relevant to metabolic or weight loss surgery
  • Clinical management – clinical management of overweight and obesity across the life span (infants through to older adults) including interventions for prevention and treatment of obesity and weight-related comorbidities
  • Rehabilitation –  investigations that explore opportunities for engagement in meaningful and health-building occupations for people with obesity
  • Diversity – studies that are relevant to diverse or underrepresented populations
  • eHealth/mHealth – research that incorporates social media, internet and/or mobile devices in prevention and treatment
  • Cancer – research relevant to obesity and cancer

…..and of course anything else related to obesity.

Deadline for submission is October 24, 2016

To submit an abstract or workshop – click here

For more information on the 5th Canadian Obesity Summit – click here

For sponsorship opportunities – click here

Looking forward to seeing you in Banff next year!

Edmonton, AB


How Strong Is The Physiological Drive To Regain Lost Weight?

Yo-Yo Rubber Band Feb 2014It is now well established that the almost non-existant rates of long-term weight loss are not because of lack of will power or lack of motivation. Rather, they are firmly embedded in human (and animal) physiology, that is designed to defend body weight at all costs through complex neuroendocrine homeostatic mechanisms that will eventually wear out even the staunchest dieter.

But just how strong is the physiological drive to defend and regain lost body weight? Or even more specifically, how much does an increase in appetite counteract weight loss?

This is the topic of a paper by David Polidori and colleagues, prepublished on bioRxiv*.

The researchers use data from a 52-week trial of canagliflozin, a sodium glucose co-transporter (SGLT2) inhibitor leads to a urinary glucose loss of approximately 90 g/day throughout the duration of treatment.

This amounts to a net daily energy loss of ~360 kcal/day that occurs without directly altering central pathways controlling energy intake and without the patients being directly aware of the energy deficit.

Based on the observed changes in body weight over time, the researchers used a validated mathematical method to calculate changes in daily energy intake using principles from engineering control theory.

The complex mathematical formula takes into account a wide range of parameters including changes in the energy expenditure rate and density of fat and fat-free mass, energy cost of fat and protein turnover, dietary and adaptive thermogenesis as well as changes in physical activity (no change in physical activity was assumed in this study).

Subjects in the treatment arm showed the typical initial weight loss (of about 5 Kg) followed by the maintenance of a weight-loss plateau throughout the remainder of the study, a pattern which, in light of a continuing daily energy loss of about 360 kcal is consistent with a proportional feedback control system that serves to limit the amount of weight loss and creates a drive towards weight regain (think of this as the tension that counteracts a steady pull  on a rubber band).

Based on their calculations, the amount of daily increase in caloric intake required to maintain the weight loss plateau (rather than continuing to lose weight), was in the order of about 100 Kg/day per Kg weight loss. This is substantially more than the reduction in metabolic rate generally seen with weight loss (of about 10-20% of body weight) is only about 30 kcal/day per Kg weight loss).

When applying these finding to the typical weight-loss curve seen in the usual commercial weight loss programs (an initial weight loss followed by gradual weight regain), the researchers show that the difference between the homeostatic drive to eat and the actual energy intake, a quantitative index of the ongoing effort to sustain the intervention in the face of the continuing biological signals to overeat, requires that subjects have to demonstrate a persistent effort to avoid overeating above baseline during the intervention even when the average energy intake returns to near baseline levels.

Despite the elegant use of real data, the authors caution about limitations of their study, which include the fact that all subjects had type 2 diabetes and the overall degree of weight loss was rather modest. Thus, the model may well look different in subjects without diabetes or more extreme weight loss.
Nevertheless, as the authors discuss,
“…homeostatic feedback control of energy intake is likely a primary reason why it is so difficult to achieve large sustained weight losses in patients with obesity. Rather, weight regain is typical in the absence of heroic and vigilant efforts to maintain behavior changes in the face of an omnipresent obesogenic environment. Unfortunately, there is no evidence that the energy intake feedback control system resets or relaxes with prolonged maintenance of lost weight – an effect similar to the long-term persistent suppression of energy expenditure in weight-reduced humans. Therefore, the effort associated with a weight loss intervention persists until either body weight is fully regained or energy intake increases above baseline to match the homeostatic drive to eat.”
Thus, the key to finding long-term obesity treatments that work, will be to find means of permanently subverting or countering this feedback control system (which is exactly how medications or surgery theoretically work).
No wonder, that will power alone will rarely result in sustainable weight loss and will always require on-going (heroic?) effort in the cases where it does.
Edmonton, AB
*Papers published on bioRxiv are “preprints” before peer review, thus allowing other scientists to see, discuss, and comment on the findings immediately. Readers should therefore be aware that articles on bioRxiv have not been finalized by authors, might contain errors, and report information that has not yet been accepted or endorsed in any way by the scientific or medical community.



My Critical Review Of Critical Fat Studies: Obesity In Canada

obesity-in-canada-coverA few weeks ago, I was invited by the Editor of The Lancet Diabetes & Endocrinology to review Obesity in Canada, a collection of articles by Canadian and Australian authors, who identify themselves as “fat scholars” engaging in “critical fat studies”. (Edited by Jenny Ellison, Deborah McPhail, and Wendy Mitchinson).

Obviously, I have had multiple interactions with “fat scholars” over the years and have certainly always learnt a lot.

Indeed, I would be the first to admit that many of my own ideas about obesity, including the issue of whether or not obesity is a disease and, if so, how to define the clinical problem of obesity in a manner that does not automatically label a quarter of the population as “diseased”, has been shaped by this discourse.

Similarly, my own notions about obesity management, with a primary goal to improve health and well-being rather than simply moving numbers on the scale, are clearly influenced by ideas that first emerged from the “fat acceptance camp” (not exactly the same, but close enough).

Thus, there was certainly much in this compendium that I was already quite familiar with – which certainly made the reading of this 500 page volume most enjoyable.

Nevertheless, it is important to realise that “fat scholars” do not just see themselves as “scientists” – rather, they see the practice of “fat studies” as a political work, tightly (some might say dogmatically) bound to a frame of reference that is reminiscent of political “activism” rather than “science”.

Fat scholars (at least the ones represented in this volume) are not just critical of, but also appear most happy to discard the entire biomedical and population health discourse around obesity, as nothing more than (I paraphrase), “a thinly-veiled conspiracy by the biomedical establishment to create a moral panic that justifies the reassertion of normative identities pertaining to gender, race, class, and sexuality.

Accordingly, some fat scholars appear to be of the rather strong opinion that there is in fact no “global obesity epidemic” and even if there are perhaps a few more fat people around today than ever before, the health consequences of obesity are vastly overblown, and any recommendations or attempts to lose weight are not only ineffective but actually harmful.

Now, before you simply roll your eyes and decide to file away the whole exercise in the drawer that you reserve for global-warming deniers and anti-vaxxers, let me assure you that there is indeed a lot to be learnt from the discourse (at least I did).

For one, there are absolutely fascinating chapters on the history of fat activism in Canada (which apparently dates back to the early 70s), enlightening perspectives on Indigenous People’s encounters with obesity, the issue of “mother blaming”, and even a chapter on fat authenticity and the pursuit of hetero-romantic love in Vancouver.

There are stories about how kids and families experience childhood obesity intervention programs and how primary school teachers themselves struggle with being thrust into a role of being role models while struggling with their own personal response to the pervasive obesity messages.

Obviously, there are some ideas that may be harder to swallow than others.

Take for e.g, the notion that the “root cause” of fat phobia (at least according to fat scholars who rely on postmodern feminism, psychoanalysis, and queer theories), is simply a reflection of the femininity ascribed to body fat: because women need fat to menstruate, body fat can be seen as female reproductive material that, in patriarchy, must be contained, restrained, and ultimately eliminated.

Personally, I can no doubt think of a wide range of other “root causes” that would result in “fat phobia” and “weight stigma” without having to quite delve into feminism or queer theories – but that’s another story.

Or the notion that there is in fact no link between body fat and diabetes – something that is easily refuted by a host of experimental animal studies and clinical observations  (which, in the world of “fat scholars” do not appear to exist or are for some opaque reason deemed entirely irrelevant for the discourse).

Nevertheless, these “peculiarities” aside, I do admit that I found the book a very timely, relevant and enlightening read for anyone who is seriously interested in the issue of obesity and bold enough to step out beyond the typical biomedical discourse.

I would most certainly recommend this volume to people working in health policy and public health but also to clinicians, who seek to better understand some of the social aspects of the obesity discourse as it relates to their patients.

There is much in the volume that I perhaps disagree with or rather, see from a different perspective (I am after all a clinician) – however, openness to entertaining alternative views and ideas, and willingness to shift your own opinion and beliefs when new evidence emerges, is the defining characteristic of good scholarship – and I certainly remain a lifelong student.

Edmonton, AB

Disclaimer: I was given a complimentary copy of Obesity in Canada to review by the Lancet Diabetes & Endocrinology


Higher BMI In Identical Twins Increases Risk of Diabetes But Not Heart Attacks?

sharma-obesity-blood-sugar-testing1Increased BMI is often touted as a major risk factor for cardiovascular disease. However, this relationship is not as straightforward as most of us believe.

Now a study by Peter Nordström and colleagues, published in JAMA Internal Medicine, reports that a higher BMI in identical twins is associated with a greater risk for type 2 diabetes but not myocardial infarction or death.

The researchers looked at data from 4,046 monzygous twin pairs with discordant BMIs (difference >0.01 units) from the nationwide Swedish twin registry.

During a mean follow-up of 12 years, the rate of myocardial infarcts and deaths were similar in the twins with lower BMI compared to their higher BMI co-twin (5.0% vs. 5.2% and 13.6% vs. 15.6%, respectively).

This lack of difference remained true even when the researchers compared the extremes of BMI discordance and only considered twins with BMI greater than 30.

In contrast, both higher BMI and greater increase in BMI since 30 years before baseline was associated with greater risk of incident diabetes.

Given that diabetes is such a powerful risk factor for cardiovascular disease, one can only wonder why this did not translate into a higher cardiovascular risk in the higher weight twins.

One possible explanation, offered by the authors is that cardiovascular risk may have been well managed in these individuals thus minimizing any increased risk due to diabetes (or other BMI associated risk factors such as dyslipidemia or hypertension).

Indeed, it would probably have required a far larger group of twins (or much longer follow-up) to fully rule out higher cardiovascular risk in these twins.

Let us also not forget that BMI is a rather lousy measure of overall cardiovascular risk.

Thus, which the study is certainly compatible with the (genetics-independant?) role of higher BMI in the risk for diabetes, it certainly should not be interpreted as demonstrating that this increased risk in benign in terms of cardiovascular disease.

Edmonton, AB