Tuesday, December 16, 2008

Thanks for Voting!

Today’s post is just to thank all my avid readers for voting Dr. Sharma’s Obesity Notes the 2nd Best Canadian Health Blog.

The competition was stiff. The well-deserved winner was Yoni Freedhoff’s Weighty Matters - truly my favorite nutrition blog of all time. The competition was extremely close with Marijke: Nurse turned writer, who received only 6  votes less than I did. Kudos also to runners up Salted Lithium and Ottawa Street Dental, who came in #4 and #5, respectively.

Thanks to all who voted (no matter for whom) – simply knowing my readers care (enough to bother to vote) is all I need to keep me going.

AMS
Edmonton, Alberta

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Monday, December 15, 2008

Paying for Weight Loss?

This post is not about the incredible sums of money you can pay for the often incredulous weight-loss products or services offered by the weight-loss industry.

No, this post is literally about someone paying YOU for losing weight (and keeping it off).

Incentive-based weight-loss programs have been around for a while (see my previous post on Lifescales, a Toronto-based company that helps employers provide weight-loss incentives). But how effective are these kind of programs in practice?

This question was now examined in a randomized controlled trial by Kevin Volpp and colleagues from the Veterans Affairs Medical Center, Philadelphia, PA, just published in JAMA.

In this study, 57 healthy participants aged 30-70 years with a body mass index of 30-40 were randomized to 3 weight loss plans: monthly weigh-ins, a lottery incentive program, or a deposit contract that allowed for participant matching, with a weight loss goal of 1 lb (0.45 kg) a week for 16 weeks. No formal behavioural interventions or treatments for weight loss were provided.

After 16 weeks, the incentive groups lost significantly more weight than the control group (albeit only around 4 lbs more). The lottery group lost a mean of 13.1 lbs and the deposit contract group lost a mean of 14.0 lbs. About half of those in both incentive groups met the 16-lb target weight loss, while this was achieved by only 10% of participants in the control group.

Although the net weight loss between enrollment in the study and at the end of 7 months was larger in the incentive groups than in the control group (4.4 lb), these differences were not statistically significant. However, incentive participants weighed significantly less at 7 months than at the study start whereas controls did not.

The authors conclude that the of economic incentives produced significant weight loss during the 16 weeks of intervention that, however, was not fully sustained.

To me, this study raises several important issues:

1) I am not comfortable with the ethics of sending otherwise healthy (albeit overweight/obese) people off to try and lose weight on their own – given the recidivism of this condition, my advise to the participants would have been to first and foremost STOP GAINING WEIGHT and to focus on being as active and eating as healthy as they possibly can. Remember, we currently have no evidence to support the notion that otherwise healthy overweight or moderately obese individuals will indeed experience any health benefits from simply losing weight.

2) The idea of providing a financial incentive for weight loss reeks of weight bias and discrimination – Are we paying smokers to quite smoking and to never touch a cigarette again? Are we paying patients with diabetes to religiously measure their blood sugars and inject their insulins? Are we paying heart attack victims to exercise regularly and take their medications? Why single out patients with obesity for this kind of program?

3) The whole concept that obesity is something that can be “conquered” if only people were motivated enough (in this case by providing a financial incentive) further reinforces the prevailing notion that people are generally obese due to “choice” (read: their own idiocy, lack of motivation, indulgence, sloth). I have previously blogged on how the promotion of “healthy lifestyles” only serves to reinforce weight bias and discrimination.

Not lost on me is the fact, that even after only 16 weeks, all groups regained a significant amount of the weight lost (anyone can lose weight – see my post on weight-loss challenges).

When will folks recognize that obesity truly is a chronic condition that requires long-term treatment? Any strategy based on a short-term intervention (such as this incentive program), is senseless and doomed to failure.

AMS
Edmonton, Alberta

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Friday, December 12, 2008

Is FTO the Junk-Food Gene?

Regular readers of my blog will by now be familiar with my “Six Natural Laws of Weight Gain” (the title of the best seller that I will hopefully one day write).  I have argued that these laws are nothing less than a finely tuned genetic program for survival – in today’s obesogenic environment – a perfect prescription for weight gain.

Now, while I fully recognize that such a complex genetic program is not determined by any single gene, but rather, is the result of 100s if not 1000s of genes working in concert while interacting with the environment – I am also confident that occasionally we will find a gene that plays an important role in these processes.

According to a paper by Joanne Cecil and colleagues from the University of Dundee, Scotland, published in this week’s New England Journal of Medicine, the FTO gene may just be such a candidate.

As some readers may know, the FTO gene has so far shown the most robust associations with common obesity. This well-conserved gene, whose ancestors are over 450 million years old (found in fish and chicken), is abundantly present in feeding-related nuclei of the mammalian brainstem and hypothalamus, where it is significantly up-regulated after 48-h of food deprivation. It is therefore fair to assume that the FTO plays a role in the central control of energy homeostasis (see Fredriksson et al. for details).

In the present study, Cecil and colleagues first confirmed the relationship between the FTO gene (the “A” allele of variant rs9939609 to be precise) and increased weight in 2726 Scottish children, 4 to 10 years of age.

They then extensively characterized a subset of 97 children with and without the relevant genetic FTO variant for body composition, energy expenditure and food intake. To make a long story short, while the A allele was associated with increased body fat, this increase was not accounted for by decreased energy expenditure. Kids with the A allele also did not eat more food, however, by making the “wrong” choices, they ended up eating significantly more calories.

Thus, this gene appears to affect body weight by promoting “poor” food choices or in other words, a preference for energy-dense foods.

Reader of my blog will immediately recognize this as a candidate gene for Natural Law #2: “Always go for the gravy”.

So now what?

While many (including Columbia University’s Rudolph Leibel in an accompanying editorial) will suggest that all that carriers of this gene will need to do is make healthier lifestyle “choices”, the real point here is that we are obviously not all made equal in terms of our “resistance” to energy-dense foods.

Thus, while some of us obviously have no problem “passing the gravy” others may have a much harder time resisting and may in fact be unconsciously draw to exactly the high-energy-density junk foods that allow them to pack on the pounds.

Remember, just a few weeks ago, I blogged about the brain imaging studies that suggested that some people may simply need more chocolate to get the same level of stimulation of their “reward centres” than others.

Based on these recent studies, anyone who still believes that simply saying “no” to crappy foods is as easy for one person as it is for the next, simply does not understand the complexity of how our genetics interact with our environment.

It seems that perhaps people who couldn’t care less for junk food are not really “smarter” than those who love it – I guess they simply don’t have the “junk-food” gene.

AMS
Edmonton, Alberta

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Thursday, December 11, 2008

When will Health Professionals Understand Obesity?

With all the talk about obesity and its increasing role as the root cause of many chronic diseases (type 2 diabetes, osteoarthritis, and sleep apnea to name a few), you would think that health professionals are now regularly counseling their patients to manage their weight.

Well, this clearly does not seem to be the case, at least according to a new study by Jean Ko and colleagues from Johns Hopkins, Baltimore, MD, just published in Preventive Medicine.

Not only does this national (US) cross-sectional survey in over 1800 obese adults show that only around 40% of individuals reported being advised by their physicians to lose weight (this advise was more likely to occur in women and in people who also had chronic diseases), but that the advice given clearly did not reflect much understanding of obesity management.

Thus, although ample data show that exercise is NOT the most effective way to lose weight, this was exactly the advise given to 86% of the subjects. In contrast, changing diet, the best way to lose weight, was only recommended in 64%. Overall only 60% received the recommendation to both change their diet and to increase physical activity.

But the really scary finding of this study was the amount of weight loss recommended: 21%!

To put this into perspective – the average long-term result of the best behavioral intervention studies is 3-5% weight-loss, while adding pharmacotherapy to lifestyle results in long-term weight loss (while treatment continues) of only 10-15%. Sustained weight loss of 21% is in fact at the lower end of the average weight loss achieved by bariatric surgery (long-term weight loss in the SOS study was only 16%), which is generally in the 20-30% range.

I can well understand, when patients have ridiculous ideas about sustainable weight loss, but for health professionals to be advising unrealistic weight loss targets that are inconsistent with the ample evidence to the contrary is simply embarrassing!

I am convinced that few health professionals actually appreciate that for a 200 lb individual to lose 20% (=40 lbs), they are talking about a SUSTAINED energy deficit of 140,000 KCal. For a daily energy deficit of 500 KCal – difficult enough to achieve, let alone sustain – this would require at least 280 days (~ 9 months) of “dieting”.

In reality, because of the obligatory homeostatic counter-regulation that occurs with weight loss, to sustain this degree of weight loss, patients would need to maintain a diet that is generally well over 500 KCal less than they started out with. Always remember, that many of the successful weight-loss maintainers of the National Weight Control Registry are surviving on 1200-1400 KCal per day! (not very different from the effective caloric intake of a post-bariatric surgery patient).

As I have blogged before, managing your patients’ weight-loss expectations is sometimes more difficult than managing their weight.

For those who are not familiar with my recommendations:

1. The first step in weight management is STOP THE GAIN!

2. 5-10% sustained weight loss has clear health benefits.

3. The challenge in weight management is not losing the weight – it is keeping it off!

AMS
Edmonton, Alberta

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Wednesday, December 10, 2008

Vitamin D Substitution after Roux-en-Y Gastric Bypass

Vitamin D 

Vitamin D

Earlier this week, I visited Drs. Jeffery Genaw and Arthur Carlin, bariatric surgeons, at the Henry Ford Hospital in Detroit, MI. I would not only like to thank them for their great hospitality and allowing us to see their new bariatric surgical unit but would also like to take the time to highlight a piece of recent research done by Carlin and colleagues, just published in SOARD.

As some readers of this blog may be aware, vitamin D (VidtD) depletion is a common finding (up to 60%) in patients with morbid obesity presenting for surgery. Currently, despite recommended daily supplementation with 800 IU VitD and 1500 mg calcium after Roux-en-Y gastric bypass (RYGB), VitD depletion persists in almost one half (44%) of patients.

Carlin and colleagues now performed a randomized controlled study in 60 VitD-depleted morbidly obese women who were given conventional supplementation or an additional 50,000 IU of VitD weekly after RYGB.

At 1 year after RYGB, only 14% in the high-dose VitD group showed VitD depletion compared to 85% in the regular dose group. The high-dose group also showed a significant 33% retardation in hip bone mineral density decline and a significantly greater resolution of hypertension (75% versus 32%).

No significant adverse effects were encountered from pharmacologic VitD therapy.

The authors conclude that 50,000 IU of VitD weekly after RYGB safely corrects VitD depletion in most women, attenuates cortical bone loss, and improves resolution of hypertension.

I am particularly intrigued by the observation that high-dose VitD improved hypertension, as failure of hypertension resolution after bypass surgery has been a puzzling finding of the SOS trial. Perhaps VitD status is the answer? Certainly an observation that warrants further study.

AMS
Baton Rouge, LA

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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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