Thursday, October 2, 2014

Shifting To Wellness

Practice Consultant at Association of New Brunswick Licensed Practical Nurses

Christie Ruff, Practice Consultant at Association of New Brunswick Licensed Practical Nurses

Yesterday, at the annual conference of the Canadian Occupational Health Nurses in Saint John, New Brunswick, I was delighted to hear a presentation by Christie Ruff, a nursing practice consultant for the Province of New Brunswick, who spoke on the impact of sleep and shift work on health and wellness.

As Ruff pointed out, shift work is “officially” defined as any work that happens on a regular basis outside of 8.00 am to 5.00 pm, Mondays to Fridays. Work includes any of the work you take home, any checking of work related e-mails or even carrying a pager so you can be reached.

Based on this definition, the vast majority of the working population is doing shift work. Yet, virtually none of us have any formal “education” on how best to deal with the many problems that regular shift work poses for our health and well-being.

One program that addresses this issue is a program called “Shifting to Wellness“, developed at Keyanu College in Fort MacMurray, Alberta, and provides a two-day workshop for employees, who work shifts. Ruff has been a Master Trainer for this program for over 10 years.

The program looks in detail at how better understanding natural circadian rhythms, can allow shift workers to better cope with burden of shift work – from catching up on sleep to healthy eating and physical activity patterns.

From an employer perspective, this is far from trivial. Shift workers are far more prone to making mistakes and having accidents (or simply clicking the “send” button a moment too soon). Many major workplace disasters were the direct result of workplace fatigue, inattention and errors made by shift workers often fatigued from lack of sleep.

Indeed, the presentation included a comprehensive review of the stages of sleep and how these are affected (and may be corrected) in shift workers.

The “crankiness” and “irritability” of shift workers is directly related to their lack of REM sleep, as is their higher rates of depression and decreased ability to deal with stressors.

These factors also affect other aspects including personal relationships and decisions.

As readers will be well aware, lack of sleep has also been linked to appetite and hunger as well as metabolic health.

No doubt, learning more about sleep, fatigue and how to address these issues is something that any health professional working in obesity prevention or management needs to pursue to better serve their clients (and themselves).

@DrSharma
Saint John

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Wednesday, October 1, 2014

How Does Stress Affect Eating Behaviour?

sharma-obesity-brainOne of the best recognized psychosocial factors tied to food intake is stress. However, this relationship is far from straightforward. While acute stress is often associated with loss of appetite, chronic stress is generally associated with an increase in appetite and weight gain.

Now, a series of articles assembled in Frontiers in Neuroendocrine Science by Alfonso Abizaid1 (Carlton University, Canada) and Zane Andrews (Monash University, Australia), describe in detail the rather complex neuroendocrine factors that link stress to changes in ingestive behaviour.

The series includes articles on the role of neuroendocrine factors like GLP-1, NPY, ghrelin, oxytocin, dopamin, and bombesin but also articles linking stress-related eating behaviours to adverse childhood experiences, perinatal influences, circadian rhythms and reward-seeking behaviours.

I look forward to some interesting reads over the next few days and hope to summarize some of these articles in subsequent posts.

@DrSharma
Saint John, NB

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Thursday, September 18, 2014

Efficacy of Vagal Blockade For Obesity Treatment Remains Vague

VBLOC

VBLOC

Regular readers may recall past posts on the use of intermittent electrical blockade of the vagus nerves (VBLOC) as a means of reducing food intake to promote weight loss.

Now a large randomised controlled study of vagal blocakade, published by Sayeed Ikramuddin and colleagues, published in JAMA, reports on rather disappointing outcomes with this treatment.

In this study (ReCharge), conducted  at one of 10 sites in the United States and Australia between May and December 2011, 239 participants with a BMI greater than 40 (or greater than 35 with at least one comorbidity), were randomised to receiving an active vagal nerve block device (EnteroMedics’ Maestro® Rechargeable (RC) System, n=162) or a sham device (n=77).

Over the 12-month blinded portion of the 5-year study (completed in January 2013), the vagal nerve block group lost about 9% or their initial body weight compared to only 6% in the sham group.

In addition to this rather modest difference in weight loss between the groups (about 3%), participants in the active treatment group also experienced a number of clinically relevant adverse effects (heartburn or dyspepsia and abdominal pain).

Thus, overall these rather disappointing results are in line with the previously disappointing observations in the smaller MAESTRO trial.

Based on these findings, it seems that intermittent electrical blockade of the vagal nerve may not hold its promise of a safe and effective long-term treatment for severe obesity after all.

@DrSharma
Edmonton, AB

ResearchBlogging.orgIkramuddin S, Blackstone RP, Brancatisano A, Toouli J, Shah SN, Wolfe BM, Fujioka K, Maher JW, Swain J, Que FG, Morton JM, Leslie DB, Brancatisano R, Kow L, O’Rourke RW, Deveney C, Takata M, Miller CJ, Knudson MB, Tweden KS, Shikora SA, Sarr MG, & Billington CJ (2014). Effect of reversible intermittent intra-abdominal vagal nerve blockade on morbid obesity: the ReCharge randomized clinical trial. JAMA, 312 (9), 915-22 PMID: 25182100

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Wednesday, September 3, 2014

Can Targeting Estrogen Receptors Alleviate Binge Eating Disorder?

sharma-obesity-mouse-eatingBinge eating disorder, a loss of control of food intake accompanied by dysphoric mood alterations, is more common in women than in men and may account for as much as 40% of severe obesity seen at bariatric centres.

Strangely enough, a new study by Xuehong Cao and colleagues from Baylor College of Medicine, Houston, Texas, published in the Journal of Clinical Investigation, shows that targeting estrogen receptors in the serotonergic neurons of brain centres involved in appetite regulation may alleviate this behaviour, at least in mice.

Previous observations in humans that women with binge eating often suffer from menstrual irregularity, presumably due to impaired functions of ovarian hormones (e.g. estrogens) and that circulating 17β-estradiol levels are inversely associated with binge eating, prompted these investigators to study the role of estrogen in binge eating behaviours in ovarectomised mice.

While estrogen administration resulted in markedly reduced binge eating behaviour in these mice, this effect was absent in genetically modified mice that lacked the estrogen receptor-α (ERα) in the dorsal raphe nuclei (DRN), an area particularly rich in serotonin (5-HT) neurons known to be important in appetite regulation (and sleep).

The researchers also showed that a conjugate that combines GLP-1 and estrogen into one molecule is far more effective in reducing binge eating behaviour than GLP-1 alone (again, this effect was much reduced in ERα KO mice) suggesting that such a conjugate may be used to specifically target GLP-1 receptor neurons, thereby perhaps avoiding any potential adverse effects of estrogen administration.

Obviously, there is a long way from such initial observations in mice to safe and effective treatments in humans.

Nevertheless, these observations should open a new field of interest in finding more effective pharmacological treatments for binge eating disorders or perhaps even more “common-garden-variety” obesity in humans.

@DrSharma
Gambach, Germany

ResearchBlogging.orgCao X, Xu P, Oyola MG, Xia Y, Yan X, Saito K, Zou F, Wang C, Yang Y, Hinton A Jr, Yan C, Ding H, Zhu L, Yu L, Yang B, Feng Y, Clegg DJ, Khan S, DiMarchi R, Mani SK, Tong Q, & Xu Y (2014). Estrogens stimulate serotonin neurons to inhibit binge-like eating in mice. The Journal of clinical investigation PMID: 25157819

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Monday, September 1, 2014

Guest Post: Emotional Distress And Weight Gain

Erik Hemmiingsson, PhD, Obesity Research Centre, Karolinska Institute, Stockholm, Sweden

Erik Hemmiingsson, PhD, Obesity Research Centre, Karolinska Institute, Stockholm, Sweden

Today’s guest post comes from Erik Hemmingsson, PhD,  a Group Leader at the Obesity Center, Department of Medicine, Karolinska Institute, Stockholm, Sweden. His group studies the role of psychological and emotional distress in weight gain and obesity by mapping life events that influence stress, metabolism and body weight. Erik has a PhD in Exercise and Health Sciences from the University of Bristol (2004) and a PhD in Medicine from Karolinska Institutet.

I work as a researcher in a specialized obesity treatment center at a university hospital in Sweden. My job is to develop new and more effective treatment and prevention methods so that we can hopefully confine obesity to the history books some day.

For many years I mostly did studies on behaviour therapy combined with low energy diets. Since this did not result in any major breakthroughs, I decided to try something a little different.

I had been aware of that many of our patients had experienced difficult childhoods. There were so many sad stories, but I didn’t fancy doing any research on the topic, it was too painful. But then my attitude gradually started to change about a year ago. It was clear that our current treatment methods were woefully ineffective, but I also became more receptive to all those troublesome stories from the patients. Enough was enough, it was time act. So, like Neo in the Matrix movies, I decided to take the red pill, and delve deeper into the very uncomfortable subject of childhood abuse and adult obesity.

I searched the literature and quickly saw that there were more than enough studies for a systematic review and meta-analysis. I enlisted the help of Dr Kari Johansson and Dr Signy Reynisdottir, and got to work.

What we found very much confirmed all those clinical observations, i.e. there was a very robust association between childhood abuse and adult obesity. The association was also very consistent across difference types of abuse, with an increased risk of about 30-40%. There was also a dose-response association, i.e. the more abuse, the greater the risk of obesity.

While this study confirmed something very important, it was also clear that not everyone who suffers childhood abuse develops obesity, or that all obese individuals have suffered childhood abuse, or the effects would have been even more pronounced. But for me, the study proved that stressful childhood experiences can easily manifest as obesity many years later. This led me even deeper down the rabbit hole. I wanted to know why.

I decided to try and piece together different ideas about how obesity develops in relation to stressful life events. This resulted in a new conceptual causal model consisting of six different developmental stages. Like many diseases, obesity development is more likely when there is socioeconomic disadvantage (applies mainly to Europe and North America). Socioeconomic disadvantage can very easily trigger a chain of events that include adult distress, a disharmonious family environment, offspring distress, psychological and emotional overload, and finally disruption of homeostasis through such mechanisms as maladaptive coping responses, stress, mental health problems, reduced metabolism, appetite up-regulation and inflammation.

Much more research is needed to validate the model, but if there is some truth to this theory, which the childhood abuse meta-analysis clearly suggests that there is, then my hope is that we can use this information to develop more effective treatment and prevention methods.

My other hope is that some of the truly horrendous stigma, shame and discrimination that the obese experience can gradually be alleviated, since there is clearly a lot more to obesity etiology than the commonly held preconception that obese individuals are merely lazy and overindulgent.

After having done all this work on obesity etiology, I would say that my top-3 reasons we have an obesity epidemic (in no particular order) are socioeconomic inequality, the junk food invasion, and psychological and emotional distress patterns (usually established at an early age). And when you combine all three you have the perfect storm for weight gain.

You can find more information at my blog at www.holisticobesity.com

Erik Hemmingsson,
Stockholm, Sweden

References:

Hemmingsson E, Johansson K, Reynisdottir S. Effects of childhood abuse on adult obesity: a systematic review and meta-analysis. Obesity Reviews (epub 15 August 2014).

Hemmingsson E. A new model of the role of psychological and emotional distress in promoting obesity: conceptual review with implications for treatment and prevention. Obesity Reviews 2014, 15:769-779.

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In The News

Diabetics in most need of bariatric surgery, university study finds

Oct. 18, 2013 – Ottawa Citizen: "Encouraging more men to consider bariatric surgery is also important, since it's the best treatment and can stop diabetic patients from needing insulin, said Dr. Arya Sharma, chair in obesity research and management at the University of Alberta." Read article

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