Thanks to my friend Yoni, I found out that I have been nominated for the Best Health Blog Category in the Canadian Blog Awards!
There are two rounds to voting: the first round began a couple of days ago and ends Nov. 30th.
The other health blogs nominated include:
Dear Readers,
As of Aug 11, my blog has moved to my home page - you can read today's post here.
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Looking forward to your continuing interest, comments and support,
AMS
Edmonton, Alberta
Dear Readers,
As of Aug 11, my blog has moved to my home page - you can read today's post here.
- If you subscribe by email, you will need to update your email subscribtion here!
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Should you experience any problem cancelling your subscription to the old site, please do not hesitate to contact me at amsharm@ualberta.ca
Looking forward to your continuing interest, comments and support,
AMS
Edmonton, Alberta
Dear Readers,
As of Aug 11, my blog has moved to my home page - you can read today's post here.
- If you subscribe by email, you will need to update your email subscribtion here!
- If you subscribe by RSS, your feed should redirect automatically.
- Please change your bookmarks (and any web links) to point to drsharma.ca!
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Should you experience any problem cancelling your subscription to the old site, please do not hesitate to contact me at amsharm@ualberta.ca
Looking forward to your continuing interest, comments and support,
AMS
Edmonton, Alberta
Dear Readers,
As of Aug 11, my blog has moved to my home page - you can read today's post here.
- If you subscribe by email, you will need to update your email subscribtion here!
- If you subscribe by RSS, your feed should redirect automatically.
- Please change your bookmarks (and any web links) to point to drsharma.ca!
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Should you experience any problem cancelling your subscription to the old site, please do not hesitate to contact me at amsharm@ualberta.ca
Looking forward to your continuing interest, comments and support,
AMS
Edmonton, Ablerta
Dear Readers,
As of Aug 11, my blog has moved to my home page - you can read today's post here.
- If you subscribe by email, you will need to update your email subscribtion here!
- If you subscribe by RSS, your feed should redirect automatically.
- Please change your bookmarks (and any web links) to point to drsharma.ca!
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Should you experience any problem cancelling your subscription to the old site, please do not hesitate to contact me at amsharm@ualberta.ca
Looking forward to your continuing interest, comments and support,
AMS
Edmonton, Ablerta
Dear Readers,
As of Aug 11, my blog has moved to my home page - you can read today's post here.
- If you subscribe by email, you will need to update your email subscribtion here!
- If you subscribe by RSS, your feed should redirect automatically.
- Please change your bookmarks (and any web links) to point to drsharma.ca!
- Old posts have already been transfered to the new location and soon the content at this location will no longer be updated.
Should you experience any problem cancelling your subscription to the old site, please do not hesitate to contact me at amsharm@ualberta.ca
Looking forward to your continuing interest, comments and support,
AMS
Edmonton, Ablerta
Dear Readers,
As of Aug 11, my blog has moved to my home page - you can read today's post here.
- If you subscribe by email, you will need to update your email subscribtion here!
- If you subscribe by RSS, your feed should redirect automatically.
- Please change your bookmarks (and any web links) to point to drsharma.ca!
- Old posts have already been transfered to the new location and soon the content at this location will no longer be updated.
Should you experience any problem cancelling your subscription to the old site, please do not hesitate to contact me at amsharm@ualberta.ca
Looking forward to your continuing interest, comments and support,
AMS
Edmonton, Ablerta
Dear Readers,
As of Aug 11, my blog has moved to my home page - you can read today's post here.
- If you subscribe by email, you will need to update your email subscribtion here!
- If you subscribe by RSS, your feed should redirect automatically.
- Please change your bookmarks (and any web links) to point to drsharma.ca!
- Old posts have already been transfered to the new location and soon the content at this location will no longer be updated.
Should you experience any problem cancelling your subscription to the old site, please do not hesitate to contact me at amsharm@ualberta.ca
Looking forward to your continuing interest, comments and support,
AMS
Edmonton, Ablerta
Dear Readers,
As of Aug 11, my blog has moved to my home page - you can read today's post here.
- If you subscribe by email, you will need to update your email subscribtion here!
- If you subscribe by RSS, your feed should redirect automatically.
- Please change your bookmarks (and any web links) to point to drsharma.ca!
- Old posts have already been transfered to the new location and soon the content at this location will no longer be updated.
Should you experience any problem cancelling your subscription to the old site, please do not hesitate to contact me at amsharm@ualberta.ca
Looking forward to your continuing interest, comments and support,
AMS
Edmonton, Ablerta
Dear Readers,
As of Aug 11, my blog has moved to my home page - you can read today's post here.
- If you subscribe by email, you will need to update your email subscribtion here!
- If you subscribe by RSS, your feed should redirect automatically.
- Please change your bookmarks (and any web links) to point to drsharma.ca!
- Old posts have already been transfered to the new location and soon the content at this location will no longer be updated.
Looking forward to your continuing interest, comments and support,
AMS
Edmonton, Ablerta
Dear Readers,
As of Aug 11, my blog has moved to my home page - you can read today's post here.
- If you subscribe by email, you will need to update your email subscribtion here!
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- Please change your bookmarks (and any web links) to point to drsharma.ca!
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Looking forward to your continuing interest, comments and support,
AMS
Edmonton, Ablerta
p.s. if you have already subscribed to the "new blog" and are still receiving this message - please remember to unsubscribe to this message. If you experience any difficulty (or are confused), simply e-mail me at amsharm@ualberta.ca
Dear Readers,
As of today, my blog has moved to my home page - you can read today's post here.
- If you subscribe by email, you will need to update your email subscribtion here!
- If you subscribe by RSS, your feed should redirect automatically.
- Please change your bookmarks (and any web links) to point to drsharma.ca!
- Old posts have already been transfered to the new location and soon the content at this location will no longer be updated.
Looking forward to your continuing interest, comments and support,
AMS
Edmonton, Ablerta
Kidneys are exquisitely sensitive to many risk factors that can also accelerate atherosclerosis and heart disease. Thus, high blood pressure and diabetes are well-established risk factors for chronic kidney disease (CKD).
Because both hypertension and diabetes are in turn linked to obesity, the question is: does obesity increase the risk for CKD?
This questions was now addressed by Meredith Foster and colleagues from the National Heart, Lung, and Blood Institute, Framingham, MA, USA, who studied the relationship between Stage 3 CKD (= moderately reduced kidney function) and BMI in the Framingham Offspring participants (n = 2,676; 52% women; mean age, 43 years) free of stage 3 CKD at baseline who participated in examination cycles 2 (1978-1981) and 7 (1998-2001). (Am J Kidney Dis)
While there was no increased risk of kindey disease in overweight participants, obese individuals had a 68% increased odds of developing Stage 3 CKD (estimated glomerular filtration rate < 59 mL/min/1.73 m(2) for women and < 64 mL/min/1.73 m(2) for men).
However, this relationship became non-significant when data was adjusted for diabetes, systolic blood pressure, hypertension treatment, current smoking status, and high-density lipoprotein cholesterol level.
The authors rightly conclude that the link between obesity and CKD is largely explained by the effect of obesity on other cardiovascular risk factors like hypertension or diabetes.
Clearly, if your excess weight is raising your blood pressure and/or making you diabetic, you may need to start worrying about your kidneys.
AMS
Edmonton, Alberta
Yes, there's a childhood and adolescent obesity epidemic out there. The word on the street now is that "this is the first generation of kids, who will not outlive their parents".
But is this really true? Where is the data showing that childhood obesity is really a risk factor for early death?
This question is now answered by perhaps the largest study on this issue to date published by Tone Bjørge and colleagues from the University of Bergen, Norway, in the American Journal of Epidemiology.
Bjørge and colleagues studied the relationship between BMI (measured height and weight) and mortality in 227,000 adolescents (aged 14-19 years) recruited in Norwegian health surveys in 1963-1975. During follow-up (8 million person-years), 9,650 deaths were observed. Cause-specific mortality was compared among individuals whose baseline BMI was below the 25th percentile, between the 75th and 84th percentiles, and above the 85th percentile in a US reference population with that of individuals whose BMI was between the 25th and 75th percentiles.
Risk of death from endocrine, nutritional, and metabolic diseases and from circulatory system diseases was increased in the two highest BMI categories for both sexes. Relative risks of ischemic heart disease death were 2.9 for males and 3.7 for females in the highest BMI category compared with the reference. There was also increased risk of death from colon cancer (males: 2.1; females: 2.0), respiratory system diseases (males: 2.7; females: 2.5), and sudden death (males: 2.2; females: 2.7).
The authors conclude that adolescent obesity is related to increased mortality in middle age from several important causes.
Clearly not a good sign for what awaits our sons and daughters unless we get a hold on the obesity crisis.
AMS
Edmonton, Alberta
Sibutramine (Meridia) is a serotonin and norepinephrine reuptake inhibitor (SNRI) licensed as a prescription drug for obesity treatment.
Although sibutramine has been available for around a decade in over 70 countries and has been shown to reduce weight and improve comorbidities and risk factors in patients with obesity, its potential to increase blood pressure in some patients has remained an important barrier to its widespread use.
In the most recent issue of Diabetes Obesity and Metabolism, together with other colleagues from the Executive Steering Committee, we now publish an analysis of blood pressure changes associated with sibutramine during the 6-week lead-in period of the sibutramine cardiovascular outcomes trial (SCOUT), an ongoing, double-blind, randomized, placebo-controlled trial in over 10,000 overweight/obese patients at high risk of a cardiovascular event.
During the 6-week lead-in period, 10,742 patients received sibutramine and weight management. At entry, approximately 50% of patients were hypertensive and 26% were high-normal.
In hypertensive patients, blood pressure decreased by median of -6.5 mmHg systolic and -2.0 mmHg diastolic (p < 0.001). Even hypertensive patients with no weight loss or with weight gain had median decreases of -3.5 mmHg systolic and -1.5 mmHg diastolic (p < 0.001). Approximately 43% of patients initially categorized as hypertensive had a lower blood pressure category at end-point.
On the other hand, normotensive patients had median increases of 1.5 mmHg systolic and 1.0 mmHg diastolic (p < 0.001) which was attenuated with increasing weight loss.
As expected, pulse rates were uniformly elevated (median 1-4 bpm, p < 0.001) across blood pressure and weight change categories.
Although it must be remembered, that all patients received sibutramine during the lead-in period and therefore some decrease in blood pressure may be due to regression to the mean, the data confirm that even in patients at high risk for cardiovascular events, the vast majority of patients (especially if hypertensive) will experience a reduction in blood pressure.
Whether or not treatment with sibutramine will also reduce cardiovascular mortality of course remains to be seen when the study finishes sometime next year.
In the meantime, these data reinforce the notion that sibutramine can indeed be used in the vast majority of patients with controlled hypertension without having to fear an increase in blood pressure.
Obviously, in the few patients who do happen to experience an increase in blood pressure, adjustments in antihypertensive medications or discontinuation of sibutramine should be considered.
AMS
Edmonton, Alberta
Conflict of Interest: I am on the Executive Steering Committee of the SCOUT trial and am reimbursed for my time and effort by Abbott Laboratories, the maker of sibutramine
In the August 4 issue of the Globe and Mail, the science journalist Andre Picard puts forth the argument (as discussed at the International AIDS conference) that AIDS treatment is prevention because treated patients are less likely to transmit the disease.
The same, if not more, could be said about treating obesity. Not only is obesity a major driver of a laundry list of mental and physical health issues, including type 2 diabetes, osteoarthritis, and cancer – its treatment has been well documented to help prevent, and in some instances, even cure these conditions. Thus, for example, obesity treatment not only prevents type 2 diabetes, but can often reverse it to the point of cure. Obesity surgery also reduces cancer deaths by 60%.
But obesity treatment is perhaps also the most effective prevention for obesity itself. There is now accumulating evidence that genetic modifications that occur in the womb and during the first months of life in the offspring of overweight and obese mothers, essentially programs their kids for obesity later in life. Perhaps the best example of how aggressive obesity treatment in women can prevent obesity in their kids comes from a Laval University study where the children of obese women, who had undergone obesity surgery, were far less likely to become obese than expected.
Many experts now believe that perhaps our best handle on the childhood obesity epidemic is to also aggressively target the parents for obesity treatments – indeed, there is little evidence that treating the kids without doing the same for the parents is likely to be successful in the long term.
Furthermore, the recent observation that obesity may be “contagious” amongst peers, has also prompted serious discussions about whether targeting obese individuals would prevent the spread of this disorder to friends and family.
Thus, while we wait for policy makers and individuals to make important inroads into obesity prevention by changing our obesogenic environment and lifestyles, we need to also seriously step up our investments in obesity treatments – not only for the sake of the individuals who struggle with this condition – but also for the sake of their families and friends.
AMS
Edmonton, Alberta
I spent all of last week at the 2008 Obesity Boot Camp co-organized by the Canadian Obesity Network (CON) and the Merck-Frosst/CIHR Obesity Chair at the University of Laval, QC.
As in the two previous camps, this year's camp once again brought together some of the best and brightest students and new professionals from across Canada for over 100 hours of education and social activities (including the Tree Top Adventure, Kayaking, tour of Quebec City and the obligatory late night excursions to DD).
Overall I have no doubts that, as in previous camps, some friendships have been forged for life - both personal and professional.
For my part, I again learnt a lot from listening and interacting with the students and faculty. While there continue to be no easy solutions to obesity in sight, there certainly are reasons for optimism, seeing the enthusiasm with which the students are preparing to face the challenge of solving one of the greatest global health problem of our times.
The Canadian Obesity Network is grateful to all of the faculty and supporters who made this camp possible.
Personally, I look forward to continuing interactions with the Boot Camp Alumni over the coming months and years.
AMS
Edmonton, Alberta
Physical activity has numerous beneficial effects on mental and physical health. With the reduced need for physical activity to ensure our basic needs (utilitarian activity), it is increasingly up to the individual to compensate by consciously engaging in recreational (non-utilitarian) activity, generally referred to as exercise.
Numerous barriers exist to engaging in exercise, including time limitations, lack of motivation, and pain or injury. Researchers have therefore pursued the idea of being able to mimic the beneficial effects of exercise with the help of drugs that induce the same gene-expression patterns and metabolic changes seen with exercise.
In yesterday's issue of CELL, Vihang Narkar and colleagues from the Salk Institute, La Jolla, CA report on their findings that the combination of an orally active AMPK agonist with a PPARβ/δ agonist can induce metabolic genes and dramatically enhance running endurance in sedentary mice. Furthermore, the PPARβ/δ agonist in combination with exercise synergistically induced fatigue-resistant type I fibers and mitochondrial biogenesis, ultimately enhancing physical performance
These results demonstrate that AMPK-PPARδ pathway can be targeted by orally active drugs to enhance training adaptation or even to increase endurance without exercise.
Obviously, treatments that work in mice may not be as effective or safe in humans. Furthermore, the researchers did not actually demonstrate that the induction of metabolic genes and increased endurance actually improves the health of the mice.
But the results are promising and certainly a major step towards developing a pharmacological alternative to exercise.
In the meantime, however, there is no alternative to being as physically as you can. As Angelo Tremblay, presenting today to the students at the CON Obesity Boot Camp emphasized, increased participation in physical activity is a key characteristic of individuals who lose weight and manage to keep it off.
AMS
Duschesnay, Quebec
Clip art licensed from the Clip Art Gallery on DiscoverySchool.com
The following quote is taken from a recent article in the ECONOMIST on the discontent of Americans with the economic state of their country:
Petrol prices, despite their recent retreat, hurt nearly everyone. Adam Julch, an enormous former college football star who is now a manager at a trucking firm in Omaha, Nebraska, complains that he had to trade in his pickup truck for a little Honda Civic. “I’m 350 pounds,” he says, “I feel like I’m in a clown car.”Two aspects of this quote deserve comment:
Body mass index (BMI) is currently widely recommended and used as the best measure of obesity both in population and clinical studies. It dates back to the Belgian statistician Adolphe Quételet, who between 1830 and 1850 described this index as a way to characterize the level of adiposity in sedentary adults.
But how accurate is this index really to identify individuals with excess body fat?
This question was recently addressed by Abel Romero-Corral and colleagues from the Mayo Clinic, MN, USA, who analysed the relationship between BMI and body fat percent (BF%) as measured by bioelectrical impedence in 13,601 subjects (age 20-79.9 years; 49% men) from the Third National Health and Nutrition Examination Survey (Int J Obesity).
In this study, the authors defined obesity based on the World Health Organization (WHO) reference standard for obesity of BF%>25% in men and >35% in women.
BMI-defined obesity (>=30) was present in 19% of men and 25% of women, while BF%-defined obesity was present in 44% of men and 52% of women.
A BMI>=30 had a high specificity (men=95%, women=99%), but a poor sensitivity (men=36%, women=49%) to detect BF%-defined obesity. This means that while the BMI definition does identify the vast majority of men and women who have increased body fat, it also misses a significant number of individuals who have high percent body fat and would be considered obese by the BF% definition.
The diagnostic performance of BMI diminished as age increased and in the intermediate range of BMI (25-29.9), BMI failed to discriminate between BF% and lean mass in both sexes.
The authors conclude that accuracy of BMI in diagnosing obesity is limited, particularly for individuals in the intermediate BMI ranges, in men and in the elderly. Thus, the currently recommended BMI cutoff of >=30 kg for obesity has good specificity but misses more than half the people with excess fat.
The scary part of these results of course is in the fact that based on actual BF% the prevalence of obesity in this population doubled! On the other hand, we know that %body fat or body composition alone is not a particularly reliable measure of health.
I prefer to continue using my operational clinical definition of obesity: the presence of excess body fat that threatens or affects your health.
Given the wide variation in the inter-individual susceptibility to develop adiposity-related health problems, the diagnosis of obesity and the question of whether or not reducing the proportion of body fat will indeed benefit your health will always remain a matter of clinical judgement.
AMS
Duschesnay, Quebec
Yesterday was the beginning of the 3rd Annual Obesity Boot Camp co-hosted by the Canadian Obesity Network (CON) and the Merck-Frosst/CIHR Obesity Chair at the University of Laval, QC. The annual Boot Camp is one of CON’s most successful capacity-building initiatives as evidenced by the continuing enthusiastic feedback from the over 50 students and new professionals who have so far attended the camp.
Contrary to what the name suggests, this is not a weight-loss camp for students challenged by excess weight (in fact given the quality of the food at the camp – keeping weight off is a challenge). Rather, the 9-day camp is a teaching and networking exercise, offered to 24 of the top young obesity researchers in the country (this year’s attendees come from 19 different universities across Canada).
This year’s Boot Camp was again kicked off by Ian Janssen from Queen’s University (Kingston, ON), who talked about the definition and epidemiology of obesity. Apart from presenting a succinct overview of the topic, he also presented some of his original research on the health costs related to obesity.
New to the camp this year was Diane Finegood, Director of the CIHR Institute of Nutrition, Metabolism and Diabetes and Professor at Simon Fraser University (Vancouver, BC), who spoke on complex adaptive. Some key properties of complex systems include heterogeneity, nonlinearity, feedback, learning, evolution, stochastics, relevance of tails, interdependence and emergence.
According to Finegood, the obesity pandemic needs to be viewed as an emergent property of people living in our current obesogenic environment. Because emergent properties, by definition, emerge when parts of a system do together what they would not do by themselves, they are generally not best understood or tackled using a reductionistic approach. Thus, it would be quite difficult to reliably predict the obesity epidemic or find solutions simply by studying individual components of our environment (e.g. urban sprawl) or any single component of human biology (e.g. genetics) in isolation.
Given the complexity of the issues, her take home messages were: all individuals matter; we need to match complexity to capacity; manage expectations; establish networks and teams; create competition and feedback loops; build intersectoral trust; monitor behaviours; measure effectiveness; adopt a whole-of-government approach (no single ministry can solve the problem).
Definitely a great kick-off to the 2008 Obesity Boot Camp.
AMS
Duchesnay, Quebec
Don't worry - I am not going to take off on a discussion about whether obesity is a disease or "simply" a risk factor. I am also not going to discuss again obesity definitions - anthropometric or otherwise.
Today's post is simply about an analogy that may help sharpen our clinical thinking around excess weight.
Think of someone who has an elevated plasma creatinine level (a marker of kidney failure) - the elevated creatine definitely tells us that there is something "wrong" with the kidneys, but that's about it. From the creatine level alone we can certainly tell that the kidneys are failing in their excretory function, but we cannot tell what is causing the kidneys to fail - is it a pre-renal, intra-renal or post-renal problem? We can probably list a 100 reasons why kidneys could fail and obviously the treatment (apart from some very general principles) will very much depend on the cause, i.e. the actual diagnosis.
In many ways, one can look at excess body fat simply as a sign or symptom of the fact that there is a something "wrong" with energy homeostasis. The excess body fat tells us nothing about what the problem is - sure, it's either excessive food intake or reduced energy expenditure - but that is like saying that the creatinine levels are elevated because the kidney is not excreting properly. I can think of a long list of reasons or factors that would contribute to excessive caloric intake or reduced energy expenditure: sociocultural factors, psychological factors, biomedical factors - figuring out what exactly is causing the energy imbalance is the real problem.
Only when we find what is causing the excessive intake will we have made a diagnosis of what is causing the problem - a few specific examples could include: poor meal planning, peer pressure, hedonic overeating, depression, obesogenic medications, binge eating disorder, defective satiety signaling, etc. The point is that till we know what is causing the overeating, we can't fix it, which means we will have little success in treating the weight problem and will be limited to a "symptomatic" approach - just eat less!
Similarly, when the problem appears to be lack of activity, again the question is what exactly is causing the problem. Obviously if the problem is lack of time our approach will hopefully be very different than if the problem is back pain or lack of motivation (a possible symptom of sleep apnea, exhaustion or depression). A "symptomatic" but useless approach would be to simply recommend 10,000 steps. No better than offering an ice-pack to someone with a fever.
Just as the term "kidney failure" only tells us that there is something "wrong" with the kidneys the term "obesity" only tells us that there is something "wrong" with energy homeostasis.
In itself, neither the term "kidney failure" nor "obesity" is a real diagnosis - they are only helpful if they prompt further investigation into what might have or is still causing the problem. Only when we find the cause will we be on our way to solving the problem.
AMS
Edmonton, Alberta
Nonalcoholic fatty liver disease (NAFLD), is now the most common cause of liver disease in children.
Although this condition is associated with insulin resistance its impact on other features of the "metabolic syndrome" is less clear.
In the July 15 issue of Circulation, Jeffrey Schwimmer and colleagues from the University of California, San Diego report on their findings from a case-control study of 150 overweight children with biopsy-proven NAFLD and 150 overweight children without NAFLD.
Children with NAFLD had significantly higher fasting glucose, insulin, total cholesterol, low-density lipoprotein (LDL) cholesterol, triglycerides, systolic blood pressure, and diastolic blood pressure than overweight and obese children without NAFLD.
Not only do these findings support the notion that, as in adults, NAFLD in overweight and obese children is strongly associated with multiple cardiovascular risk factors, they also show that as in adults, weight alone is not a reliable measure of cardiovascular or metabolic risk factors in kids.
Identification of NAFLD in a child should prompt global counseling to address nutrition, physical activity, and avoidance of smoking to prevent the development of cardiovascular disease and type 2 diabetes.
AMS
Edmonton, Alberta
Feet are remarkably complex structures exquisitely designed to buffer and carry the weight of our bodies. Whether standing, running, jumping, hopping, skipping - the feet do it all. Not surprisingly, painful feet affect the whole organism.
Interestingly, not much is known about the impact of increased body weight on foot architecture in kids. This knowledge is of course of great importance for orthopaedic and paediatric physicians with regard to prevention, clinical treatment and management of foot problems but also of obesity.
Now, Marlene Mauch and colleagues from the University of Tuebingen, Germany, studied the foot morphology of normal, underweight and overweight children in 1450 boys and 1437 girls aged 2-14 years (Int J Obesity). Foot morphology was measured using a three-dimensional (3D) foot scanner (Pedus, Human Solutions Inc., Germany) in a bipedal upright position. Twelve relevant 3D foot measures were recorded, as well as the children's age, gender, height and mass.
Five foot types were identified: flat, robust, slender, short and long feet. While normal weight children displayed an almost equal distribution of all foot types throughout childhood, overweight and obese children were more likely to have flat and robust feet, whereas underweight children tended to have slender and long feet.
The authors not only conclude that excess weight may have a significant effect on foot morphology but may also increase the risk for foot discomfort as a result of various musculoskeletal disorders. This in turn may keep the overweight children from being active thereby further promoting weight gain.
Clearly, the role of foot morphology and the maintenance of foot health in overweight and obese kids deserves more attention and further study.
I would add that careful analysis of foot morphology and recommendation of proper footwear, orthotics and exercises should be part of every assessment of an overweight kid - damage to feet resulting from well-meant but ill-advised physical activity at an early age could precipitate lifelong foot problems and prove a major obstacle to long-term weight management.
AMS
Edmonton, Alberta
Big news for patients with severe obesity in Ontario. As part of a $741 Million announcement for a provincial diabetes strategy, the Ontario Health Minister yesterday announced $75 Million in funding for Bariatric Centres of Excellence.
As outlined in the press release:"Obesity is one of the main risk factors associated with diabetes. More than 50 per cent of type 2 diabetes cases in Ontario are associated with obesity. The government is improving access to bariatric surgery - a procedure that modifies the gastrointestinal tract to reduce food intake. This $75 million initiative will increase Ontario's capacity for bariatric surgery several-fold within two years and it will continue to increase thereafter. In 2006/07 169 procedures were performed in Ontario and 485 patients were funded for surgery out of country.
Clearly, a first sign of relief for Ontarians who have thus far had to travel South of the border or scrape together the money for private bariatric surgery.
Ontario will enhance capacity for bariatric surgery in the province by:
- Providing bariatric education and training to health care providers
- Expanding bariatric surgical capacity
- Establishing pre and post bariatric surgery programs that will be linked to surgical programs"
What I particularly like about the announcement is the emphasis on training health care providers and making sure both pre- and post-surgical care is in place. As I have blogged before, obesity surgery is not just about surgery. The actual operation is only a small technical piece in a complex life-long management plan.
I am particularly pleased by the announcement, because I believe that my past efforts in Ontario, including lobbying of the Government to provide better bariatric care, may in part have led to this announcement. As some readers may know, not only have I been quite vocal about this, but I was also the Clinical Co-Chair of the Health Technology Utilization Guidelines group that was contracted by the Ontario Health Ministry to prepare recommendations for Bariatric Surgery in Ontario.
We made it clear in this guideline document that bariatric care requires an interdisciplinary team and needs to take a chronic disease management rather than an acute-care approach to dealing with this issue.
Given that there is nothing different in the magnitude of the problem or the desperate need for bariatric care between Ontario and other regions of Canada, I can only hope that this announcement will be rapidly followed by similar announcements from other provinces.
Here in Alberta, we certainly have many of the components already in place (at least in the Edmonton Region) - and of course we'd be more than happy to share our experience with our colleagues in Ontario - the sooner we can get the services in place across all of Canada, the better for everyone.
AMS
Edmonton, Alberta
Regular readers of my blog know about my issues with a weight-based definition of obesity. As I have repeatedly pointed out, good health is possible over a wide range of body weights and weight alone is a rather poor measure of overall health.
Not surprisingly the same appears true for the Japanese. At least according to a paper just out in OBESITY, in which Atsushi Hozawa and colleagues from the Shiga University of Medical Science, Otsu, Japan, examined the relationship between BMI and all-cause mortality in 8,924 Japanese men and women without stroke or heart disease.
During 19 years of follow-up, 1,718 deaths were observed. As in other populations, the relationship between BMI and fatal events was U-shaped. Risk of total mortality was highest in participants with BMI <18.5 and lowest in participants with BMI 23.0-24.9. These findings persisted even after excluding the first 5 years of follow-up with a focus on healthy participants. For both the full sample and healthy participants, all-cause mortality risk did not differ between BMI ranges 21.0-22.9 and 23.0-24.9.
These data are particularly of interest because recent recommendation from the WHO and others suggest that a BMI > 23.0 should be considered overweight in Asian populations.
This would obviously make little sense if mortality is in fact lowest in individuals with BMI between 23.0-24.9.
Once again, this study illustrates the problem with BMI-based definitions of obesity which fail to take into account the huge inter-individual variability in the impact that excess body fat can have on health.
While there is no doubt that some Japanese with a BMI as low as 23 may have a full blown "metabolic syndrome", others (perhaps the majority) at the same BMI may be perfectly healthy.
Clearly it is time for a health-based rather than a solely anthropometric classification of obesity.
AMS
Edmonton, Alberta
The obesity epidemic is costing employers. Earlier this year, The Conference Board estimated that obesity-related health problems cost US companies an estimated $45 Billion each year in medical coverage and absenteeism - more than smoking or problem drinking.
Not surprisingly, employers and health care plans have long recognized the importance of promoting and perhaps even coddling employees into participating in "wellness" efforts. The idea is a no-brainer: healthier employees are more productive - a great investment for any company.
But with any good idea, the devil is in the details. The legal limits and potential for well-meant wellness programs (especially when promoted by health-care plans and payers) for promoting discrimination are discussed in a recent article by Michelle Mello and Meredith Rosenthal from the Harvard School of Public Health published in the July 10 issue of the New England Journal of Medicine.
In their analysis, Mello and Rosenthal focus on the impact of the nondiscriminatory provisions of the US Health Insurance Portability and Accountability Act (HIPPA) of 1996, which bars health plans and issuers of group health insurance from discriminating on the basis of a health factor.
The general rule is that no person can be denied or charged more for coverage than other "similarly situated" persons because of health status, genetic history, evidence of insurability, disability, or claims experience. In this context "similarly situated" refers only to an employment-based classification, such as full-time or part-time, not on health factors.
As a result of this, health plans can only opt not to provide coverage for particular health conditions, if this applies to all "similarly situated" individuals and is not based on whether or not people actually have that health condition.
While HIPAA is designed to prevent health discrimination, it does allow insurers and health plans to reward members for participating in health-promotion programs (e.g. reduced premiums, payouts, etc.) as long as the reward is open to all members (irrespective of whether or not they actually have a health problem). HIPAA, however, makes it particularly difficult for plans to tie these rewards to actually achieving an individual health target - i.e. it allow rewards for participation but not success.
In the rare cases that insurers do tie rewards to achieving health targets, there are important restrictions in place. In this regard, the provision that in cases where it is "unreasonably difficult" or "medically inadvisable" for a person to satisfy the health standard owing to a "medical condition" must be offered a reasonable alternative standard.
As pointed out by Mello and Rosenthal, the problem with this restriction is that no definition of "medical condition" is provided. So whether or not someone with overweight or obesity can be expected to achieve a target weight ultimately depends on whether or not the prior presence of excess weight is defined as being a "medical condition" or not - obviously, this leaves the room wide open for weight-based discrimination. It is certainly easier for someone with little excess weight to achieve an arbitrary "ideal weight" than for someone with a lot to lose - no matter that actually keeping the weight off becomes an exponentially bigger challenge the more you lose.
It is clear that whether or not excess weight in a given individual is caused by genetic predisposition, psychosocial factors, comorbidities or obesogenic medications, or, is simply a matter of poor "choices" and "sloth" will in most cases remain a matter of debate.
To me, the overall problem remains in the focus of employers, insurers and policy makers in general on the promotion of individual changes rather on than shifting society as a whole to a healthier lifestyle for everyone.
Given the multidimensional sociocultural, psychological and biomedical nature of obesity, answering "chicken and egg" questions or trying to pinpoint the primary causal factor is nigh impossible.
Perhaps one solution is to take "weight" out as a measure of health - either as a promoting factor or as a target.
As I have pointed out repeatedly, good health is possible over a surprisingly wide range of body weights and there is a wide variation in individual susceptibility to "weight-related" health problems. No one weight cuttoff will work for everyone - clearly, we have no idea what a good weight target should be, as our definitions of healthy weight are entirely defined on the presence or absence of comorbidites and/or functional limitations in a given individual or on actuarial morbidity and mortality statistics that, in turn, are simply not helpful when dealing with individuals.
I certainly do not envy the lawyers and policy makers who have to address this complex issue with "legalese". I am glad I am just a simple clinician helping patients conquer their obesity one step at a time.
Look forward to any comments on workplace wellness and its legal framework in Canada (or in Germany from my German readers).
AMS
Edmonton, Alberta
Last week, I blogged about the results of a study showing an association between vital exhaustion and weight gain.
This blog posting prompted Sharon Kirkey (award-winning health journalist and diligent reader of my blog) to explore this issue further by actually talking to the researchers themselves. Her article appeared yesterday via the Canwest News Service and contains far more details than I bothered to report in my blog.
For e.g. Sharon lists the actual questions Bryant and colleagues used to explore the presence of vital exhaustion. I found them most interesting so I list them below:
- Do you often feel tired?
- Do you wake up repeatedly during the night?
- Do you have the feeling that you have not been accomplishing much lately?
- Do you believe that you have come to a 'dead end'?
- Do you lately feel more listless than before?
- Do little things irritate you more than they used to?
- Does it take more time to grasp a difficult problem than it did a year ago?
- Do you have increasing difficulty in concentrating on a single subject for long?
While to me none of these questions seem particularly specific and are likely to get a "yes" response from a lot of people (hey, even I have to say "yes" to some), I guess when you have to say "yes" to most or all of them, you are probably not hopping around like the Energizer Bunny or scrambling to follow diet plans.
Sharon quotes me as saying: "Nobody is claiming all of obesity is exhaustion, but if people are clearly eating more than they need the question is not (just) how to get them to stop, but why, exactly, are they doing that. Maybe you're losing your job. Or you're overworked. Or it's some private issue that needs to be addressed. You don't fix obesity by giving people a copy of Canada's food guide. You have to try to understand what it is that's contributing to the weight gain."
Exactly! Obesity is a symptom of overeating, which in turn is a symptom of something else that's going on: it can be that you simply lack the knowledge about healthy nutrition or caloric content of foods, but it can also be a symptom of emotional (e.g. depression, vital exhaustion) or biological (e.g. MC-4 receptor defect) issue, medications (e.g. clozapine) or any number of other reasons I can think of.
Always remember: overeating (and/or sedentariness) is not a diagnosis - overeating (and/or sedentariness) is a symptom!
AMS
Edmonton, Alberta
Two days ago I reminded readers that not too long ago, people were actually paid to be physically active. Today, choosing to be physically active actually costs money (not to mention time).
So the big challenge is, how do we reintroduce activity into the work place so that people can actually be physically active at work again (allowing them to lounge around the couch in front of the TV when they get home).
Well, one obvious solution is to create a workspace where someone can get a workout in while on the computer. That is exactly the idea behind the "Walk Station" a desk that comes matched with a treadmill instead of a chair.
The device, the science (and the hype) behind it are described in an article from the Edmonton Journal from which I quote:The device allows people to work on their computers while walking on a treadmill at a slow speed of up to three kilometres per hour, enabling small amounts of movement that supporters say have the potential to reap big health benefits.
So here are my questions:
The product, made by Details, a unit of Michigan-based office furniture maker Steelcase, is selling 30 to 40 units per week, according to company president Bud Klipa.
The Walkstation was unveiled last year based on research from James Levine, a researcher at the Mayo Clinic, who contends that fitness can be improved through small, modest movements for people who are otherwise sedentary.
Levine's research indicates that people who use the Walkstation can increase energy expenditure by 100 calories per hour when walking at a 1.6 kilometres (one mile) per hour, helping weight loss.
The treadmill, which costs around $4,500 for a base model, never exceeds a speed of three kilometres per hour, which, according to the manufacturer, allows most people to use it for a few hours each day.
Where is the evidence that this device will actually promote weight loss?
What will prevent this device from going down the same path as previous workplace health initiatives - embraced by the already fit, ignored by the people who need them most?
Will it increase weight-based discrimination at the workplace - the thin people are walking, the overweight are not - no one stops to ask why - back pain? osteoarthritis? depression? plantar fasciitis? - excuses, excuses! Who cares!
Although is seems like a good way to reintroduce activity into the workplace, it is still "useless" activity, i.e. you are not actually paid to walk - or in other words, you don't really have to walk to get your job done.
While I personally would probably not mind having this device, I can see all sorts of problems - anyone out there who's experienced this or a similar device - I'd love to hear how this has influenced intra-office dynamics.
I will maintain my scepticism on this being the answer till I see some actual data.
AMS
Edmonton, Alberta
Increased visceral fat or "ectopic" fat deposition is associated with insulin resistance and increased cardiovascular risk.
Traditionally, the term visceral fat has been used to describe the omental and mesenteric fat located inside the abdomen. Over the last several years, this concept has been expanded to include other "ectopic" fat depots including the liver and the heart.
Recognition that the fat located around the heart can be a marker of visceral fat was pioneered by Gianluca Iacobellis, who joined me as a clinical research fellow a few years ago at McMaster University and has since been recruited to their faculty.
In this month's issue of OBESITY, Iacobellis reports on work we collaborated on just before I left McMaster to relocate to the University of Alberta demonstrating that epicardial fat is a sensitive marker of changes in visceral fat associated with weight loss.
In this study in 20 severely obese subjects who underwent a 6-month very low calorie diet weight loss program resulting in a 20% loss of original body weight, waist circumference decreased by 23% whereas epicardial fat thickness decreased by 32% of baseline.
Based on this finding, we suggest that measurement of echocardiographic epicardial fat thickness may provide an additional tool in understanding the metabolic risk associated with variation in fat distribution. Perhaps, more importantly, echocardiographic measurement of epicardial fat can serve as a simple and relatively inexpensive tool to assess changes in visceral fat with weight loss (or gain) in clinical practice.
Certainly beats simply measuring waist circumference (a rather crude surrogate measure of intra-abdominal fat) or the rather more expensive CAT or MRI study.
AMS
Edmonton, Alberta
p.s Thanks to Navneet Singh and Sean Wharton for their great help with this study and to all the patients who volunteered their time for these measurements
Several months ago I blogged about the results from a Finnish twin study that found lower mitochondria numbers and disturbed mitochondrial energy metabolism activity in fat cells from identical twins who were leaner than their genetically identical co-twins. These impairments correlated with critical clinical measures of obesity including liver fat accumulation, reduced whole-body insulin sensitivity, hyperinsulinemia, hypoadiponectinemia and adipocyte hypertrophy.
In this month's issue of OBESITY, Tomas Gianotti and colleagues from the University of Buenos Aires, Argentina, report a significantly lower mitochondrial-to-nuclear DNA ratio (mtDNA/nDNA) in insulin resistant (IR) adolescents recruited out of a subset (n=175) of a cross-sectional, population-based study of 934 high school students. In this study, the mtDNA/nDNA ratio was also inversely correlated with HOMA index, a crude but simple measure of insulin resistance.
This study is very much in line with the notion that obesity-prone individuals may have impaired mitochondrial number and/or function resulting in increased risk for obesity.
From the aforementioned twin study, we know that the decreased number and function is not corrected by weight loss.
Indeed the question is whether or not mitochondrial number and function can be increased by prescribing higher activity levels? If yes, how much activity will be needed to reverse these changes? And most importantly, will people with impaired mitochondrial function actually be able to enjoy exercise enough to actually stick with this prescription?
Perhaps it is not obesity that causes impaired mitochondrial function but rather impaired mitochondrial number and/or function that predisposes to obesity. This impairment could be genetic but also due to intrauterine programing or perhaps simply luck of the draw (remember - all mtDNA comes from your mom).
Of course this is not an "excuse" for obesity as is often misinterpreted when data on the genetics and biology are presented. However, it is clear that if you have impaired mitochondrial number and/or function you are much more likely to become obese in an environment that promotes sedentariness than if you were dependent on physical activity to meet your basic needs for survival.
Remember, there were times, not too long ago, when people were actually paid to be physically active. Today, choosing to be physically active actually costs money (not to mention time).
AMS
Edmonton, Alberta
Orlistat is a gastrointestinal lipase inhibitor sold as a prescription drug under the brand name Xenical and is also available in some countries (including the US) as an over-the-counter (OTC) weight-loss aid under the brand name Alli.
Orlistat has been around for almost a decade and has been extensively studied. No question, when used appropriately with recommeded dietary and lifestyle changes it aids in achieving about 5% weight loss and clinically relevant improvements in cardiometabolic risk factors (high blood pressure, low HDL, high blood sugars, etc.). As with all obesity drugs, weight is generally regained when the medication is discontinued - nothing new here!
Because the action of orlistat is limited to the gut (it is not absorbed in relevant amounts), it is promoted as not having any "systemic" side effects. The main side effects are fully explained by its impact on fat digestion and are generally limited to diarrhea, oily discharge and abdominal discomfort - unpleasant for sure, but certainly not a major health concern.
There is also some interference with the absorption of fat-soluble vitamins (ADEK) but this should not be a problem with a healthy balanced diet or proper intake of vitamin supplements. There is however, also a significant impact on lipid-soluble medications (e.g. ciclosporine A) and patients on these medication may need some readjustment of the dose.
All of the above is well known, extensively studied and not really of great concern for most patients.
But here is one side effect I'd be worrying about if I belonged to the people who tend to get kidney stones - there is a distinct chance that orlistat can increase urinary oxalate excretion thereby potentially promote formation of oxalate stones - anyone who's ever experienced a kidney colic knows exactly why this is something you want to avoid.
The cause of this potential side effect is related to the simple fact that the unabsorbed fat and bile acids resulting from the use of orlistat may react with calcium in the intestinal lumen, limiting the amount of free calcium binding with oxalate and thereby raising intestinal oxalate absorption leading to hyperoxaluria, which in turn can promote formation of oxalate stones.
This rather complex-sounding but rather straightforward state of affairs was first proposed based on a marked increase in urinary oxalate excretion observed in rats given orlistat together with a high-fat diet in a study by Renato Ribeiro Ferraz and colleagues from the Universidade Federal de São Paulo published in KIDNEY INTERNATIONAL in 2004.
In 2007, Ashutosh Singh and colleagues from the University of Tennessee described the case of a female patient with chronic kidney disease, who developed acute oxalate nephropathy with the use of orlistat (Am J Kidney Dis). Urine sediment showed abundant calcium oxalate crystals and 24-hour urine oxalate concentration was significantly elevated. Kidney biopsy showed deposition of calcium oxalate crystals within the tubular lumens. A repeat biopsy one month after discontinuing orlistat no longer showed signs of oxalate and renal function slowly recovered to baseline.
Now, in this month's issue of OBESITY, Kemal Sarica and colleagues from the Memorial Hospital in Istanbul, Turkey, report the data from a study in 95 obese patients (57 men, 38 women) randomly assigned to treatment with orlistat for 6 months vs. no specific medication. In the treatment group, two-thirds of patients showed a marked increase in urinary oxalate excretion at 3 months, which largely persisted at 6 months. Although no kidney stones were noted, the authors commented that the increase in oxalate excretion would have been enough to promote oxalate stone formation in susceptible individuals.
Nothing dramatic here - unless of course you are someone who happens to be at risk for oxalosis and oxalate kidney stones.
If you are, perhaps best to avoid orlistat or at least cut down on the concomitant use of high oxalate foods like rhubarb, spinach, strawberries, chocolate, wheat bran, nuts, beets, and tea and drink plenty of water.
AMS
Edmonton, Alberta
OK, we know stress, lack of time, low socioeconomic status, poor locus of control and poor sleep promote obesity - but here is a new one (at least for me): Vital Exhaustion.
The term Vital Exhaustion (VE) has three defining characteristics: (1) feelings of excessive fatigue and lack of energy, (2) increasing irritability, and (3) feelings of demoralization.
People often attribute these feelings to overwork, or to problems at work or in other important life areas that the person has not been able to solve, or to a real or symbolic loss. Therefore, it has been suggested that VE is a mental state at which people arrive when their resources for adapting to stress are broken down.
Now Maria Bryant and colleagues from the University of Leeds, UK in a paper just out in OBESITY, examined the relationship between VE and BMI cross-sectionally and after 3 and 6 years of follow-up among the 13,727 participants in the Atherosclerosis Risk in Communities (ARIC) study.
BMI was significantly higher among both white and African-American men and women in the highest VE quartile compared to those with no VE. Similarly, high VE at baseline was associated with higher BMI 3 and 6 years later. Baseline VE predicted future excess weight gain in white men and women, but not in African Americans.
Clearly, if this relationship is causal, identifying the factors contributing to VE and addressing them may help prevent and reduce the burden of obesity - certainly easier said than done.
Anyone who thinks we will solve the obesity crisis by handing out diet plans and chasing people around the block are kidding themselves.
AMS
Edmonton, Alberta
The recommended dietary allowance (RDA) is an estimate of the minimum average dietary intake level that meets the nutrient requirements of nearly all (~97%) healthy individuals.
According to this recommendation, the RDA for protein is 0.8 g/kg/d
Interestingly, as pointed out in a recent commentary by Robert Wolfe and Sharon Miller from the University of Arkansas published in the June 25 issue off JAMA, the term “recommended dietary allowance” is misleading as it is often misinterpreted as being the “optimal” rather than the “minimal” dietary requirement.
In fact, as illustrated in the commentary, if protein requirements are calculated based on a recommended proportion of energy intake [i.e. 10 to 35%], for a 70 Kg man requiring 3067 kg calories per day, 10% of energy as protein would translate into a protein intake of 0.95 g/kg/d whereas 35% of energy intake would translate to 3.3 g/kg per day. These values are obviously substantially higher than the RDA.
As blogged before, given the importance of maintaining appropriate protein intake to maintain muscle mass, strength and function, the issue of ensuring adequate protein intake during a caloric restricted diet becomes even more challenging. This means that caloric restricted diets need to at least provide a protein intake at the higher end of the Dietary Reference Intakes [DRI] or around 35% of total caloric intake and should perhaps err on the side of too high rather than too low.
The issue of maintaining appropriate protein intake is particularly important as close monitoring of body composition to detect disproportionate loss of lean body mass during weight loss is not routine part of patient monitoring during obesity treatment.
Perhaps, as recommended by Wolfe and Miller, the term “recommended dietary allowance” should be replaced by the term “minimal dietary requirement” to more accurately reflect the functional definition of RDA and avoid confusion regarding what is considered adequate protein intake.
AMS
Edmonton, Alberta
Yesterday, newspapers reported widely about the UK conservative leader David Cameron calling on the obese, the idle, and even the poor to accept some responsibility for their plight.
According to Cameron, society has become "far too sensitive" to people's feelings, with no one prepared to say "what needs to be said." "We talk about people being 'at risk of obesity' instead of people who eat too much and take too little exercise".
Great stuff! So all fat people eat too much and are lazy - they deserve their plight! In other words, let's stop coddling them and let's certainly not bother providing them with any health services for their plight.
Perfect. Let's next stop providing services for all smokers who get heart attacks or cancer, no more trauma surgery for anyone who gets injured driving above the speed limit or, God forbid, gets run over jay walking. No more health services for anyone coming down with influenza who did not get his flu shot, no more medical freebies for people spraining their ankles at sports, and obviously definitely no more medical help with "lifestyle diseases" like diabetes, high cholesterol, hypertension, osteoporosis, osteoarthritis and back pain.
Everyone is the master of their own destiny.
Thank you Mr. Cameron for saying what needed to be said.
Anyone feeling depressed? Suck it up!
AMS
Edmonton, Alberta
As unequivocally documented by twin studies, obesity is one of the most heritable complex traits. However, so far only a handful of genes that may play a role in the common "garden variety" of obesity (i.e. not just the rare monogenic forms) have been identified .
This week, a large research team led by Philippe Froguel (Picture) that included scientists from France, Denmark, Sweden, Germany and the UK report in Nature Genetics that relatively common variants of the PCSK1 gene, which codes for the proconvertase enzyme are associated with higher BMI. This enzyme is responsible for producing fully functioning versions of hormones such as insulin and glugagon that play important roles in carbohydrate metabolism but also for melanocortin, a key regulator of satiety.
Although the identified variants of the PCSK1 gene cause only relative minor functional changes in this enzyme, the effect on the relevant hormones is quite significant.
Obviously, no single gene or variant thereof can account for all of obesity and there is no reason to believe that all obesity is the same. Rather, it is clear that the heritability of obesity must be due to the distribution of a large number of variants of numerous genes in the population.
So when do we begin using genetic testing in our obesity clinics - not for a while I am guessing, i.e. till we can actually show that specific genes also predict better (or worse) outcomes with specific treatments.
In the dark, all cats are grey.
AMS
Edmonton, Alberta
As elsewhere in Europe, obesity is on the rise in Germany. According to government statistics, two-thirds of all German men between the ages of 18 and 80 are overweight and almost half of all women have a weight problem. These numbers add up to about 37 million adults and 2 million children and teenagers suffering from some kind of weight related disorders.
In response, the German government has now embarked on a new obesity initiative prepared by Health Minister Ulla Schmidt in cooperation with Food, Agriculture and Consumer Protection Minister Horst Seehofer. The program's initiative is to cut diseases related to obesity drastically by the year 2020, and foresees spending 30 million euros ($46.7 million) over the next two years.
As everywhere else, in Germany too, the government recognizes that the epidemic is not only a result of poor nutritional habits and lack of exercise but also wide-ranging societal and infrastructural factors. It therefore calls on politicians, scientists, health-care providers, unions and the food industry to help educate and promote healthier lifestyle approaches. As one may guess the ideas include: education on healthy eating and physical activity, tougher standards on school food programs, better product labeling by the food industry, reduced advertising by the makers of sweets and junk food that target children, i.e. essentially the usual list of initiatives.
As everywhere else, in Germany too, the government largely ignores one major consequences of the fact that 37 Million Germans are already living with this chronic disease, namely that this also calls for an immediate need to provide improved access to evidence-based obesity treatments with expansion of the resources to do so.
As in most other countries (the UK being a remarkable exception), access to professional obesity treatment that includes behavioural therapy, anti-obesity medications and surgery remains limited to a ridiculously small number of individuals, mostly those who can afford "private" payments for these services.
As I have blogged before - promoting obesity prevention (and hoping for these to kick in) should not be an excuse to deny obesity treatments to those already affected by this condition.
AMS
Edmonton, Alberta
p.s. incidentally, my blog is now also available in German
Image Rainer Zenz
Metabolic syndrome or syndrom X (recently refered to as Xyndrome) is the combination of abdominal obesity, high trigylcerides, low HDL cholesterol, high blood pressure and elevated levels of fasting blood glucose. This concept has been widely promoted as helping to clinically identify individuals at increased risk for heart disease.
While the concept appears intuitively sound (as all five components of this syndrome have been individually associated with increased cardiovascular risk), there is a continuing debate on whether the concept of this "syndrome" is any better in identifying individuals at risk for heart disease than looking at each individual risk factor on its own.
To address the issue of whether or not the "metabolic syndrome" is indeed a risk factor for heart disease, Naveed Sattar and colleagues from University of Glasgow examined the relationship between the metabolic syndrome and incident cardiovascular disease and type 2 diabetes in in 4812 non-diabetic individuals aged 70-82 years from the Prospective Study of Pravastatin in the Elderly at Risk (PROSPER). They corroborated these data in a second prospective study (the British Regional Heart Study [BRHS]) of 2737 non-diabetic men aged 60-79 years. (The Lancet)
In PROSPER, metabolic syndrome was not associated with increased risk of cardiovascular disease over 3.2 years but was associated with a 4-fold increased risk of diabetes. In contrast elevated fasting glucose alone was associated with an 18-fold increased risk for diabetes.
Likewise, in BRHS, metabolic syndrome was only modestly associated with incident cardiovascular disease despite a strong association with diabetes.
Importantly, in both studies, body-mass index or waist circumference, triglyceride, and glucose cutoff points were also not associated with risk of cardiovascular disease, but all five components were associated with risk of new-onset diabetes.
The authors conclude that while metabolic syndrome and its components are associated with type 2 diabetes, they only have a weak to no association with vascular risk in elderly individuals. Their recommendation is that the clinical focus should remain on establishing optimum risk algorithms for each individual risk factor rather than lumping them together as a putative "syndrome".
Obviously, one could argue that there may still be some use for the concept of the metabolic syndrome in younger individuals, but, as discussed in this paper, the same group (and others) have also not found the metabolic syndrome to be a strong predictor of heart disease in younger individuals.
Irrespective of whether or not the concept of the metabolic syndrome is helpful, it should be remembered that obesity treatment is the only intervention that can simultaneously have beneficial effects on all five components of this syndrome. Thus, while conventional care continues to aggressively target the individual risk factors, only aggressive obesity treatment will indeed improve all features of this putative syndrome.
Unfortunately, with the exception of obesity surgery, we still lack outcome studies confirming that obesity treatment will indeed decrease cardiovascular mortality.
Remember, the assumption that losing weight (without surgery) will save lives is not based on hard evidence from randomised controlled trials. My guess is that till we have better data on this issue, physicians, payers and policy makers will continue to question the benefits of tackling obesity with the same resources and enthusiasm as for other chronic diseases.
AMS
Edmonton, Alberta
