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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… Read More »

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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). ┬áI 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┬áabundantly 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┬áage. They then extensively characterized a subset of 97 children┬áwith 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… Read More »

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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… Read More »

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Vitamin D Substitution after Roux-en-Y Gastric Bypass

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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Lorcaserin for Obesity

Serotonin plays an important role in the regulation of ingestive behaviour. Lorcaserin (APD356), a potent, selective 5-HT(2C) agonist is currently under development by ARENA pharmaceuticals for the treatment of obesity. In this month’s issue of OBESITY, Steven Smith and colleagues from the Pennington Biomedical Research Centre, Baton Rouge, LA (where I happen to be visiting today), report on the safety and efficacy of lorcaserin for weight reduction in obese patients. The randomized, double-blind, placebo-controlled, parallel-arm study enrolled 469 men and women between ages 18 and 65 and with BMI 30-45 . Patients received placebo, lorcaserin 10 mg q.d., lorcaserin 15 mg q.d., or lorcaserin 10 mg b.i.d. for 12 weeks, and were counseled to maintain their usual diet and activity. Safety analyses included echocardiograms at Screening and day 85/study exit. Lorcaserin was associated with progressive weight loss of 1.8 kg, 2.6 kg, and 3.6 kg at 10 mg q.d., 15 mg q.d., and 10 mg b.i.d., respectively, compared to placebo weight loss of 0.3 kg (P < 0.001 for each group). The proportions of completers achieving >5% of initial body weight were 12.8, 19.5, 31.2, and 2.3% in the 10 mg q.d., 15 mg q.d., 10 mg b.i.d., and placebo groups, respectively. The most frequent adverse events were transient headache, nausea, and dizziness. Echocardiograms showed no apparent drug-related effects on heart valves or pulmonary artery pressure. This short-term study shows that lorcaserin was well tolerated and efficacious for weight reduction. Obviously, 12 weeks is too short to determine the full efficacy or safety of this compound. Nevertheless, the results appear promising and it will be interesting to see how longer-term studies that combine locaserin with behaviour modification turn out. AMS Baton Rouge, LA Disclaimer: I have served on the locaserin echocardiography data safety monitoring board for ARENA and have received honoraria in this capacity.

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Bypassing Breast Cancer?

The strong link between obesity and many forms of cancer is well documented. Not surprisingly, previous studies on obesity surgery have shown dramatic reductions (up to 60%) in overall cancer mortality. These data are supported by yet another study, this time from Nicolas Christou and colleagues from McGill University in Montreal. Apart from being a renowned Canadian bariatric surgeon, Christou is also the Past-President of the Canadian Association of Bariatric Physicians and Surgeons. In this study, published in in the latest issue of Surgery for Obesity and Related Diseases, Christou and colleagues conducted an observational 2-cohort study consisting of a treatment cohort of 1035 patients who had undergone bariatric surgery from 1986 to 2002 and a control group consisting of 5746 age- and gender-matched morbidly obese patients identified from an administrative database. The cohorts were followed up for a maximum of 5 years. While the patients who underwent bariatric surgery (mostly gastric bypass) experienced a weight loss of around 31%, their rate of any cancer diagnosis was only 23% of that in the control group (77% risk reduction!). The biggest risk reductions were seen for breast (83%) and colorectal (68%) cancers. Thus, while bariatric surgery has long been documented to remarkably improve a host of obesity-related disorders including type 2 diabetes, dyslipidemia, heart disease, sleep apnea, osteoarthritis and pain, the reduction in cancer morbidity and mortality has perhaps been less well recognized. I wonder just how much the ÔÇ£Run for the CureÔÇØ has contributed to research on obesity and bariatric surgery to date? AMS Edmonton, Alberta

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