Close Concerns: Bariatric Care
Earlier this week, the influential healthcare information firm Close Concerns published a rather lengthy interview regarding my take on a wide range of issues related to the future of obesity management. The interviews were conducted by Joseph Shivers, Vincent Wu, Lisa Vance, and Kelly Close, who certainly challenged and stimulated my thinking with their well-informed questions. The following is another excerpt from this interview published in their newsletter Closer Look: JOSEPH: That certainly isn’t something that we hear talked about very much. It seems like stopping weight gain is much easier. How would you ballpark your own clinic’s success rate in that regard? DR. SHARMA: We would be hitting 80%, if not more, on stopping the weight gain. In every single case where a patient continues to gain weight, we know there’s a problem that we’ve not yet identified and have not yet addressed. JOSEPH: Like one of the underlying psychological or metabolic disorders that you talked about? DR. SHARMA: Yes, there’s something going on; something happening with this patient such that they are trying things and coming to the clinic but not able to do what it takes to stop gaining weight. For these patients, there’s no way that you’re going to get sustainable weight loss. On the other hand, stopping the gain is actually quite easy, because when you stop gaining weight, your body doesn’t go into starvation mode, so you don’t have to deal with any of those counter-regulatory mechanisms that make it challenging to keep weight off. The minute I start losing weight, all those systems will kick in and try to get my weight back to where it was. Hence, it is much, much easier and takes very little effort actually to stabilize people’s weight. If you look at any of the drug studies or even surgical studies over very long periods of time, you’ll see people’s weight stabilizing. For example, if you take SCOUT and forget about the sibutramine arm, and just look at the placebo arm, you’ve got people who’ve lost roughly 2 kg (4.4 pounds), and they’re keeping these 2 kg off for almost five years with virtually no intervention. The lifestyle intervention for both arms consisted essentially of seeing these patients, you’d give them a pedometer or a healthy eating brochure, but the key thing was that you were just seeing people. So you get some advice typically from the doctor… Read More »
ISORAM Day 1: FTO, Micro RNA, KO-Mice, and Big Fat Cells
Yesterday, the 2nd International School on Obesity Research And Management (ISORAM), kicked off with a series of brief overviews of the basic sciences in obesity. Yvonne Böttcher (Leipzig) provided an update of obesity genetics. Although there are now 33 common genetic risk variants for BMI, even when combined, these markers explain only a small proportion (<10%) of the total heritability of obesity. Perhaps, there is a bigger than expected role for rare and low frequency genetic variants with highly penetrant effects (albeit in a smaller number of obese people). In addition, there may also be an important role for deletions and copy number variability that may contribute to the obesity phenotype. Nora Klöting (Leipzig) explained how animal models are essential to better understanding of the pathogenesis, genetics and mechanisms of human obesity as the basic physiology of molecules associated with obesity and obesity related diseases can frequently only be investigated in such models. In fact, it was the study of animal models of obesity that led to the discovery of leptin and a host of other important molecules that regulate energy homeostasis and metabolism. There is no doubt that generation and characterization of transgenic animal models will continue adding pieces to the puzzle, allowing us to better understand the pathophysiology of adipose tissue, obesity, lipodystrophy, and insulin resistance. Maria Keller (Leipzig) next spoke about the importance of epigenetics, which may explain many of the gene x environment interactions. Thus, while these interactions do not change the genetic code, they very can very much influence tissue specific gene expression patterns that significantly alter metabolism and other function. Mechanisms that can lead to epigenetic modification of genes include DNA methylation, micro RNAs, or modifications of histonses. These mechanisms may not only play a role in fetal programming but may also be influenced by factors such as diet, physical activity, or environmental toxins. Isabel Wagner (Leipzig) rounded off this first session by discussing the many roles of adipose tissue, particularly in the development of childhood obesity. She pointed out that fat mass can increase both by hyperplasia (increase in cell number) and hypertrophy (increase in cell size), the latter being most often associated with insulin resistance, adipose tissue inflammation, and other alterations that may contribute to obesity related health problems. The many bioactive adipokines, secreted by fat cells can act locally and systemically through autocrine, paracrine and endocrine effects that can modulate a… Read More »
Simulating Bariatric Care
Readers may recall a previous post on the new University of Alberta’s Health Sciences Education and Research Commons, which will include a state-of-the-art bariatric simulation suite, designed to teach health professionals in the care of patients with severe obesity. In the following short videos, I discuss some of the thoughts that went into creating this rather unique training facility. Appreciate all comments. AMS Las Vegas, NV p.s. Congratulations to the University of Alberta for maintaining its position on the Times Top 50 Medical School list
Should Causality Matter In The Edmonton Obesity Staging System?
One of the questions many readers and colleagues have asked, is whether or not the issue of ‘causality’ should matter in the the context of the Edmonton Obesity Staging System (EOSS). In other words, should only conditions be counted that are ‘causally’ linked to obesity or is it enough that these conditional are merely more common in people with excess weight. There are essentially two important but distinct aspects to this question that ultimately relate to how EOSS is to be used in clinical practice. If the primary purpose of EOSS is to identify patients who would benefit from weight loss, then, yes, it matters whether or not the co-morbidities considered, are ‘causally’ related to obesity and can be reversed or ameliorated by reducing and sustaining a lower body weight. However, if the primary purpose of EOSS is merely to identify obese patients, who are at high risk and need to be prioritized within the health care system in order to receive the appropriate care for their conditions (irrespective of whether or not this ‘care’ involves weight loss or just better management of their comorbidities), then the question of causality is really irrelevant. Thus, in the first case, one would only count ‘comorbidities’ that are actually ‘causally’ related to excess weight – an example being sleep apnea. There is ample evidence that weight loss reduces symptoms of sleep apnea (while weight gain makes it worse) and so sleep apnea would count as an important comorbidity that can be addressed by obesity treatment. In the second case, it does not actually matter if the comorbidity is in any way related to excess weight. All that really matters, is whether this comorbidity is present or not. An e.g. would be depression, which, while not caused by obesity and not likely to improve with weight loss (it may sometimes even get worse), may, when present, help identify obese patients, who do have a higher risk of premature death. So while in the first example, EOSS would be used to decide who needs to lose weight, in the second example, EOSS simple serves to identify obese people, who are at highest risk of complications and death. Apart from the second scenario being the real reason that EOSS was developed, it is also a far more practical approach to using EOSS, because for many comorbidities it may be impossible to answer the ‘chicken or egg’… Read More »
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