Friday, August 8, 2014

Healthy Obesity: More Questions Than Answers?

sharma-obesity-visceral-fat-mriRegular readers will be well aware of the evidence that a subset of people living with obesity can be remarkably healthy despite carrying a rather large amount of body fat.

This issue of “healthy obesity” was the topic of the 13th Stock Conference of the International Association of the Study of Obesity, the proceeding of which are now published in Obesity Reviews.

As the authors note,

“The ‘healthy obese’ phenotype was described in the 1980s, but major advancements in its characterization were only made in the past five years. During this time, several new mechanisms that may be involved in health preservation in obesity were proposed through the use of transgenic animal models, use of sophisticated imaging techniques and in vivo measurements of insulin sensitivity. However, the main obstacle in advancing our understanding of the metabolically healthy obese phenotype and its related long-term health risks is the lack of a standardized definition.”

The latter is a real problem because finding people with obesity, who are truly metabolically and otherwise healthy becomes harder the higher the BMI gets – this makes the study of this phenomenon rather challenging.

Nevertheless,

“One of the most consistent characteristics of metabolic health in obesity across studies in humans is reduced liver lipid. This is likely the consequence of increased capacity for storing fat coupled with improved mitochondrial function in adipose tissue and decreased de novo lipogenesis in liver. This can also result in decreased deposition of lipids, including bioactive species, in skeletal muscle. Decreased adipose tissue inflammation with decreased macrophages and a unique T-cell signature with an anti-inflammatory circulating milieu were also suggested to characterize metabolic health in obesity. Anecdotal data support a possible role for healthier lifestyle, including increased level of physical activity and healthier diet. It remains to be established whether a favourable metagenomic signature is a characteristic of metabolic health in obesity.”

Finland’s, Dr Kirsi Pietiläinen explained that,

“..three energy dissipation pathways, oxidative phosphorylation, fat oxidation and amino acid catabolism showed preserved pathway activities in subjects who are MHO at a level similar to their lean counterparts. In contrast, these pathways were significantly down-regulated in adipose samples from obese twins with metabolic disturbances. Another potential hallmark of metabolic health, a favourable inflammatory profile of the adipose tissue was also observed in the MHO twins. Also, the fat cells of the MHO twins were smaller with evidence of more active differentiation processes within the fat tissue. As multiple mitochondrial pathways are vital in adipocyte differentiation [29], it is possible that mitochondrial malfunction impairs the development of new fat cells, which in turn results in an inability of the adipose tissue to expand under conditions of energy excess. This failure of fat cell proliferation has long been suspected to constitute the framework for ectopic fat storage, insulin resistance and type 2 diabetes.”

Other speakers discussed other aspects including immune function and microbiata in this phenomenon.

Finally, the authors concluded that,

“identifying underlying factors and mechanisms associated with this phenotype will eventually be invaluable in helping the scientific and medical community understand factors that predispose, delay or protect obese individuals from metabolic disturbances. It is essential to underscore that the MHO concept presently only address the cardio-metabolic risks associated with obesity; it is therefore important that patients who are MHO are still very likely to present many other obesity-related complications such as altered physical and/or physiological functional status, sleep problems, articulation and postural problems, stigma, etc. Importantly, the MHO concept supports the fact that classification based on excess adiposity per se (e.g. BMI or body composition if available) should be supplemented with obesity-related comorbidities, e.g. with fasting insulin as proposed by the Edmonton obesity classification system.”

Certainly a space to watch as we learn more and more about the “healthy obesity” phenotype.

@DrSharma
Edmonton, AB

ResearchBlogging.orgSamocha-Bonet D, Dixit VD, Kahn CR, Leibel RL, Lin X, Nieuwdorp M, Pietiläinen KH, Rabasa-Lhoret R, Roden M, Scherer PE, Klein S, & Ravussin E (2014). Metabolically healthy and unhealthy obese – the 2013 Stock Conference report. Obesity reviews : an official journal of the International Association for the Study of Obesity PMID: 25059108

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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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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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