Friday, June 20, 2014

Your Body Thinks Obesity Is A Disease

sharma-obesity-adipose-tissue-macrophageYesterday, the 4th National Obesity Student Summit (#COSM2014) featured a debate on the issue of whether or not obesity should be considered a disease.

Personally, I am not a friend of such “debates”, as the proponents are forced to take rather one-sided positions that may not reflect their own more balanced and nuanced opinions.

Nevertheless, the four participants in this “structured” debate, Drs. Sharon Kirkpatrick and Samantha Meyer on the “con” team and Drs. John Mielke and Russell Tupling on the “pro” team (all from the University of Waterloo) valiantly defended their assigned positions.

While the arguments on the “con” side suggested that “medicalising” obesity would detract attention from a greater focus prevention while cementing the status quo and feeding into the arms of the medical-industrial complex, the “pro” side argued for better access to treatments (which should not hinder efforts at prevention).

But a most interesting view on this was presented by Tupling, who suggested that we only have to look as far as the body’s own response to excess body fat (specifically visceral fat) to determine whether or not obesity is a disease.

As he pointed out, the body’s own immunological pro-inflammatory response to excess body fat, a generic biological response that the body uses to deal with other “diseases” (whether acute or chronic) should establish that the body clearly views this condition as a disease.

Of course, as readers are well aware, this may not always be the case – in fact, the state of “healthy obesity” is characterized by this lack of immunological response both locally within the fat tissue as well as systemically.

Obviously, it will be of interest to figure out why some bodies respond to obesity as a disease and others don’t – but from this perspective, the vast majority of people with excess weight are in a “diseased” state – at least if you asked their bodies.

While this is a very biological argument for the case – it is indeed a very insightful one: it is not the existence of excess body fat that defines the “disease” rather, how the body responds to this “excess” is what makes you sick.

As readers, are well aware, there are several other arguments (including ethical and utilitarian considerations) that favour the growing consensus on viewing obesity as a disease.

Of course,  calling obesity a disease should not detract us from prevention efforts, but, as I often point out, just because be treat diabetes or cancer as diseases, does not mean that we do not make efforts to prevent them.

If calling obesity a disease increases resources towards better dealing with this problem and helps take away some of the shame and blame – so be it.

@DrSharma
Waterloo, Ontario

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Wednesday, June 18, 2014

4th Canadian Obesity student Meeting (COSM 2014)

Uwaterloo_sealOver the next three days, I will be in Waterloo, Ontario, attending the 4th biennial Canadian Obesity Student Meeting (COSM 2014), a rather unique capacity building event organised by the Canadian Obesity Network’s Students and New Professionals (CON-SNP).

CON-SNP consist of an extensive network within CON, comprising of over 1000 trainees organised in about 30 chapters at universities and colleges across Canada.

Students and trainees in this network come from a wide range of backgrounds and span faculties and research interests as diverse as molecular genetics and public health, kinesiology and bariatric surgery, education and marketing, or energy metabolism and ingestive behaviour.

Over the past eight years, since the 1st COSM was hosted by laval university in Quebec, these meetings have been attended by over 600 students, most presenting their original research work, often for the first time to an audience of peers.

Indeed, it is the peer-led nature of this meeting that makes it so unique. COSM is entirely organised by CON-SNP – the students select the site, book the venues, review the abstracts, design the program, chair the sessions, and lead the discussions.

Although a few senior faculty are invited, they are largely observers, at best participating in discussions and giving the odd plenary lecture. But 85% of the program is delivered by the trainees themselves.

Apart from the sheer pleasure of sharing in the excitement of the participants, it has been particularly rewarding to follow the careers of many of the trainees who attended the first COSMs – many now themselves hold faculty positions and have trainees of their own.

As my readers are well aware, I regularly attend professional meetings around the world – none match the excitement and intensity of COSM.

I look forward to another succesful meeting as we continue to build the next generation of Canadian obesity researchers, health professionals and policy makers.

You can follow live tweets from this meeting at #COSM2014

@DrSharma
Waterloo, Ontario

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Tuesday, June 10, 2014

Surgical Weight Loss Reduces Sympathetic Nerve Activity

sharma-obesity-verticalsleevegastrectomyOK, to some folks this may not be all that new a finding – after all the drop in sympathetic nerve activity with weight loss is one of the main reasons that weight loss reduces blood pressure. Unfortunately, it is also one of the main reasons that metabolic rate is reduces with weight loss.

For anyone, who wonders what happens to sympathetic activity following surgical weight loss, a study by Gino Seravalle and colleagues from the University of Milan, Italy, published in HYPERTENSION has some answers.

Their study in patients undergoing sleeve gastrectomy, studied before as well as six and twelve months post surgery not only shows a respectable drop in blood pressure and heart rate but also a marked and persistent decrease in leptin levels and in muscle sympathetic activity as measured by microneurography. They also showed a significant improvement in baroreceptor sensitivity.

Together these data certainly provide strong evidence that massive weight loss (in this case 9 BMI units) induced by sleeve gastrectomy, triggers profound sympathoinhibitory effects, associated with a stable and significant reduction in plasma leptin levels.

Obviously, much of this can be achieved with non-surgical weight loss, except that finding subjects who lose that amount of weight and keep it off for 12 months without surgery is far more difficult (but not impossible) and therefore much harder to study.

@DrSharma
Edmonton, AB

Hat tip to Bill Colmers for pointing me to this study.

ResearchBlogging.orgSeravalle G, Colombo M, Perego P, Giardini V, Volpe M, Dell’Oro R, Mancia G, & Grassi G (2014). Long-Term Sympathoinhibitory Effects of Surgically Induced Weight Loss in Severe Obese Patients. Hypertension PMID: 24866140

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Wednesday, May 28, 2014

Hypertension: Cut The Sugar?

sugarAnyone interested in blood pressure will have gotten the message that cutting salt may well be beneficial, especially in someone who has high blood pressure.

Indeed, there is little doubt that a substantial proportion of the population (although not everyone), may be “salt-sensitive” (this used to be my area of research before I switched to obesity).

Now, a paper by Lisa Te Morenga and colleagues, in a paper published in the American Journal of Nutrition, suggests that sugar may be as (if not more) potent than salt in increasing blood pressure levels.

The researchers conducted a systematic review and meta-analysis of 12 randomized controlled trials that examined effects of the modifying dietary free sugar on blood pressure and found that increased sugar intake could increase systolic and diastolic blood pressure by  almost 7 and 6 mmHg, respectively – this effect was greatest in trials ≥8 wk in duration and was not explained by a change in body weight.

This is certainly impressive, as these numbers even exceed what is generally quoted for blood pressure effects of sodium.

While no convincing explanation for the biological basis for these findings are given, they are indeed intriguing as these are findings from randomised intervention trials in human volunteers. No doubt, these findings are certainly far more convincing than the usual “‘X’ causes ‘Y’” nonsense, that we so often see derived from epidemiological studies.

Given the current “moral panic” about sugar (which has pretty much replaced the previous “moral panic” about fat), it should not be hard to get funding to figure out how this actually works.

@DrSharma
Sofia, Bulgaria

ResearchBlogging.orgTe Morenga LA, Howatson AJ, Jones RM, & Mann J (2014). Dietary sugars and cardiometabolic risk: systematic review and meta-analyses of randomized controlled trials of the effects on blood pressure and lipids. The American journal of clinical nutrition PMID: 24808490

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Monday, May 26, 2014

Does Short-Term Weight Loss Reduce Cardiovascular Risk?

sharma-obesity-weight-gainIf you believe recent media headlines describing the findings of a paper published in The Lancet last week, you may be convinced that any weight loss – even if you don’t keep the weight off – reduces your risk for cardiovascular disease.

The study, reports on the relationship between lifelong patterns of BMI and cardiovascular risk a 60-64 year-old British  birth cohort born in 1946.

Participants were classified as normal weight or overweight or obese based on heights and weights measured during childhood (at ages 2, 4, 6, 7, and 11 years) and adulthood (at ages 36, 43, 53 and 60–64 years).

As may be expected, various measures of cardiovascular and metabolic risk factors were positively related to extent and duration of adiposity.

There were, however, two findings that may seem rather unexpected:

Firstly, adiposity in childhood did not seem to matter as a predictor of CV risk in adulthood.

Secondly, it appeared that individuals who dropped at least one BMI category at any time during adulthood, irrespective of whether or not this weight loss was maintained, had lower cardiovascular (but not diabetes) risk than did those who never lost weight.

From these findings the authors conclude that,

…cardiovascular benefit might arise from weight loss in adulthood, irrespective of when this weight loss is achieved, and support public health policies for lifestyle modifications for prevention and management of overweight and obese individuals at all ages.

While it is easy to see why sustaining weight-loss as an adult (particularly if you have risk factors for cardiovascular disease) may well be beneficial, it is hard to imagine a plausible biological pathway that would link a “short-term” weight loss to long-term improvements in cardiovascular risk.

Indeed, the authors provide no explanation for their findings. They also provide no further information on the people who lost weight compared to the people who did not.

My first response would be to look for biological plausible confounders – were people who lost weight at anytime as adults perhaps more conscious or concerned about their health than those who did not? Or, were they more metabolically healthy to start with?

Let us also not forget that this was merely an observational study – association does not prove causality.

This is not to say that the findings are entirely implausible. There is some literature on the long-term “legacy effect” of lifestyle interventions on metabolic risk factors – but the biological basis for this is unknown and some colleagues doubt wether this effect really exists.

Given that weight regain is rather common after weight loss, it will be interesting to see if other studies can demonstrate lasting benefits of short-term weight loss.

At this time some scepticism may well be warranted.

@DrSharma
Edmonton, AB

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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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