Weight Loss - Obesity

[Michael Scally MD]

Re: Weight-Loss

The prevalence of obesity (body mass index [BMI {calculated as weight in kilograms divided by height in meters squared}]) has risen markedly since 1976, now exceeding 30% among US adults. Obesity has well-known associations with morbidity and disability, resulting in unhealthy life-years and increased health care costs. Although many studies have examined obesity treatment (weight loss through lifestyle intervention, pharmacotherapy, or surgery), research on obesity prevention (preventing or decreasing the amount of weight gain) is less abundant.

Public health guidelines recommend regular physical activity to minimize age-related weight gain, implying that weight gain may be prevented by maintaining high activity levels over time. However, these recommendations are largely based on cross-sectional observational and short-term clinical evidence that cannot account for the changing risk of weight gain with increasing age. Data on the amount of activity necessary for prevention of weight gain are also sparse. Although a 2008 report from the US Department of Health and Human Services (HHS) advocates at least 30 minutes of moderate-intensity activity 5 days per week, a recent study observed that HHS-recommended activity levels were insufficient for weight gain prevention in middle-aged women (mean, 54.2 years at baseline). It is unclear if federal activity guidelines are sufficient to prevent weight gain, particularly in the transition from young adulthood to middle age, when the highest risk of weight gain occurs.

This study evaluates the relationship between maintaining higher activity levels, including HHS-recommended levels, and changes in BMI and waist circumference over 20 years in young adults. Because participation in activity varies by race, sex, and weight status, this study also examines if these factors modify the relationship between activity and weight gain. Maintaining high activity levels through young adulthood may lessen weight gain as young adults transition to middle age, particularly in women.


Hankinson AL, Daviglus ML, Bouchard C, et al. Maintaining a High Physical Activity Level Over 20 Years and Weight Gain. JAMA. 2010;304(23):2603-10. Maintaining a High Physical Activity Level Over 20 Years and Weight Gain, December 15, 2010, Hankinson et al. 304 (23): 2603 — JAMA

Context Data supporting physical activity guidelines to prevent long-term weight gain are sparse, particularly during the period when the highest risk of weight gain occurs.

Objective To evaluate the relationship between habitual activity levels and changes in body mass index (BMI) and waist circumference over 20 years.

Design, Setting, and Participants The Coronary Artery Risk Development in Young Adults (CARDIA) study is a prospective longitudinal study with 20 years of follow-up, 1985-1986 to 2005-2006. Habitual activity was defined as maintaining high, moderate, and low activity levels based on sex-specific tertiles of activity scores at baseline. Participants comprised a population-based multicenter cohort (Chicago, Illinois; Birmingham, Alabama; Minneapolis, Minnesota; and Oakland, California) of 3554 men and women aged 18 to 30 years at baseline.

Main Outcome Measures Average annual changes in BMI and waist circumference.

Results Over 20 years, maintaining high levels of activity was associated with smaller gains in BMI and waist circumference compared with low activity levels after adjustment for race, baseline BMI, age, education, cigarette smoking status, alcohol use, and energy intake. Men maintaining high activity gained 2.6 fewer kilograms per year (+0.15 BMI units; 95% confidence interval [CI], 0.11-0.18 vs +0.20 in the lower activity group; 95% CI, 0.17-0.23), and women maintaining higher activity gained 6.1 fewer kilograms per year (+0.17 BMI units; 95% CI, 0.12-0.21 vs +0.30 in the lower activity group; 95% CI, 0.25-0.34). Men maintaining high activity gained 3.1 fewer centimeters in waist circumference per year (+0.52 cm; 95% CI, 0.43-0.61 cm vs 0.67 cm in the lower activity group; 95% CI, 0.60-0.75 cm) and women maintaining higher activity gained 3.8 fewer centimeters per year (+0.49 cm; 95% CI, 0.39-0.58 cm vs 0.67 cm in the lower activity group; 95% CI, 0.60-0.75 cm).

Conclusion Maintaining high activity levels through young adulthood may lessen weight gain as young adults transition to middle age, particularly in women.

 

[Michael Scally MD]

Re: Weight-Loss

Ioannides-Demos LL, Piccenna L, McNeil JJ. Pharmacotherapies for obesity: past, current, and future therapies. J Obes;2011:179674. Pharmacotherapies for Obesity: Past, Current, and Future Therapies

Past therapies for the treatment of obesity have typically involved pharmacological agents usually in combination with a calorie-controlled diet. This paper reviews the efficacy and safety of pharmacotherapies for obesity focusing on drugs approved for long-term therapy (orlistat), drugs approved for short-term use (amfepramone [diethylpropion], phentermine), recently withdrawn therapies (rimonabant, sibutamine) and drugs evaluated in Phase III studies (taranabant, pramlintide, lorcaserin and tesofensine and combination therapies of topiramate plus phentermine, bupropion plus naltrexone, and bupropion plus zonisamide). No current pharmacotherapy possesses the efficacy needed to produce substantial weight loss in morbidly obese patients. Meta-analyses support a significant though modest loss in bodyweight with a mean weight difference of 4.7 kg (95% CI 4.1 to 5.3 kg) for rimonabant, 4.2 kg (95% CI 3.6 to 4.8 kg) for sibutramine and 2.9 kg (95% CI 2.5 to 3.2 kg) for orlistat compared to placebo at >/=12 months. Of the Phase III pharmacotherapies, lorcaserin, taranabant, topiramate and bupropion with naltrexone have demonstrated significant weight loss compared to placebo at >/=12 months. Some pharmacotherapies have also demonstrated clinical benefits. Further studies are required in some populations such as younger and older people whilst the long term safety continues to be a major consideration and has led to the withdrawal of several drugs.

 

[Michael Scally MD]

Re: Weight-Loss

The following are recent summaries for current obesity management. The FDA, IMO, will be pushed to approve some form of treatment besides medical devices.


Yao F, MacKenzie RG. Obesity Drug Update: The Lost Decade? Pharmaceuticals 2010;3(12):3494-521. http://www.mdpi.com/1424-8247/3/12/3494/pdf

The growing worldwide obesity epidemic and obesity-related disorders present a huge unmet medical need for safe and effective anti-obesity medications. The discovery of leptin in 1994 was rapidly succeeded by a wave of related discoveries leading to the elaboration of a hypothalamic melanocortinergic neuronal circuit regulated by leptin and other central and peripheral signaling molecules to control energy homeostasis. The identification of specific neuronal subtypes along with their unique connections and expression products generated a rich target menu for anti-obesity drug discovery programs. Over the course of the last decade, several new chemical entities aimed at these targets have reached various stages or successfully completed the drug discovery/regulatory process only to be dropped or taken off the market. There are now in fact fewer options for anti-obesity drug therapies in late 2010 than were available in 2000. The challenge to discover safe and effective anti-obesity drugs is alive and well.


Halpern B, Oliveira ESL, Faria AM, et al. Combinations of drugs in the Treatment of Obesity. Pharmaceuticals 2010;3(8):2398-415. http://www.mdpi.com/1424-8247/3/8/2398/pdf

Obesity is a chronic disease associated with excess morbidity and mortality. Clinical treatment, however, currently offers disappointing results, with very high rates of weight loss failure or weight regain cycles, and only two drugs (orlistat and sibutramine) approved for long-term use. Drugs combinations can be an option for its treatment but, although widely used in clinical practice, very few data are available in literature for its validation. Our review focuses on the rationale for their use, with advantages and disadvantages; on combinations often used, with or without studies; and on new perspectives of combinations being studied mainly by the pharmaceutical industry.


Isidro ML, Cordido F. Approved and Off-Label Uses of Obesity Medications, and Potential New Pharmacologic Treatment Options. Pharmaceuticals 2010;3(1):125-45. http://www.mdpi.com/1424-8247/3/1/125/pdf

Available anti-obesity pharmacotherapy options remain very limited and development of more effective drugs has become a priority. The potential strategies to achieve weight loss are to reduce energy intake by stimulating anorexigenic signals or by blocking orexigenic signals, and to increase energy expenditure. This review will focus on approved obesity medications, as well as potential new pharmacologic treatment options.

 

[Michael Scally MD]

Re: Weight-Loss

Obesity and overweight have reached epidemic proportions in the U.S. and increasingly around the world. A number of studies have suggested that protein is the most satiating macronutrient and promotes the retention of lean body mass. Meals with increased protein to carbohydrate ratios have been demonstrated to increase satiety and decrease food intake by comparison to standard protein intake. Increased protein intake results in both improved weight loss and improved maintenance of weight loss. Therefore, protein enriched or supplemented meal replacements have found their way into weight management practice.

There has been some concern that the long-term use of high protein diets may damage liver function, renal function, or reduce bone density. While there are studies of the effects of increased intake of animal protein in the diet, protein-enriched meal replacements have not been evaluated in comparison to standard meal replacements in terms of effects on liver function, renal function, and bone mineral density in free-living populations.

Meal replacement (MR) is an important strategy in designing structured diets for weight management due to their simplicity, low cost, and convenience of protein-enriched meal replacement shakes by comparison to fast food meals. Meal replacements are as effective as structured weight-loss diets. MR simplifies the weight loss plan by replacing one or two meals a day with a product of defined nutrient and calorie content. MR leads to increased weight losses over twelve weeks compared to simply restricting the intake of favorite food, and weight losses have been shown to be maintain for up to 4 years with the inclusion of one MR per day. The present study was designed to recommend isocaloric weight management programs through the inclusion of either a protein or a carbohydrate supplement to a standard meal replacement powder to make either a standard or protein-enriched meal replacement.

These studies demonstrate that protein-enriched meals replacements as compared to standard meal replacements recommended for weight management do not have adverse effects on routine measures of liver function, renal function or bone density at one year.

Li Z, Treyzon L, Chen S, Yan E, Thames G, Carpenter CL. Protein-enriched meal replacements do not adversely affect liver, kidney or bone density: an outpatient randomized controlled trial. Nutr J 2011;9(1):72. http://www.nutritionj.com/content/pdf/1475-2891-9-72.pdf

BACKGROUND: There is concern that recommending protein-enriched meal replacements as part of a weight management program could lead to changes in biomarkers of liver or renal function and reductions in bone density. This study was designed as a placebo-controlled clinical trial utilizing two isocaloric meal plans utilizing either a high protein-enriched (HP) or a standard protein (SP) meal replacement in an outpatient weight loss program. Subjects/methods: 100 obese men and women over 30 years of age with a body mass index (BMI) between 27 to 40 kg/m2 were randomized to one of two isocaloric weight loss meal plans 1). HP group: providing 2.2 g protein/kg of lean body mass (LBM)/day or 2). SP group: providing 1.1 g protein/kg LBM/day. Meal replacement (MR) was used twice daily (one meal, one snack) for 3 months and then once a day for 9 months. Body weight, lipid profiles, liver function, renal function and bone density were measured at baseline and 12 months.

RESULTS: Seventy subjects completed the study. Both groups lost weight (HP -4.29 +/- 5.90 kg vs. SP -4.66 +/- 6.91 kg, p<0.01) and there was no difference in weight loss observed between the groups at one year. There was no significant change noted in liver function [AST (HP -2.07 +/- 10.32 U/L, p=0.28; SP 0.27+/- 6.67 U/L, p=0.820), ALT (HP -1.03 +/- 10.08 U/L, p=0.34; SP -2.6 +/- 12.51 U/L, p=0.24), bilirubin (HP 0.007+/-0.33, U/L, p=0.91; SP 0.07+/-0.24 U/L, p=0.120), alkaline phosphatase (HP 2.00+/- 9.07 U/L, p=0.240; SP -2.12+/- 11.01 U/L, p=0.280)], renal function [serum creatinine (HP 0.31 +/- 1.89 mg/dL, p=0.380; SP -0.05+/- 0.15 mg/dL, p=0.060), urea nitrogen (HP 1.33 +/- 4.68 mg/dL, p=0.130; SP -0.24+/- 3.03 mg/dL, p=0.650), 24 hour urine creatinine clearance (HP -0.02 +/- 0.16 mL/min, p=0.480; SP 1.18+/- 7.53 mL/min, p=0.400), and calcium excretion (HP -0.41 +/- 9.48 mg/24 hours, p=0.830; SP -0.007+/- 6.76 mg/24 hours, p=0.990)] or in bone mineral density by DEXA (HP 0.04 +/- 0.19 g/cm2, p=0.210; SP -0.03+/- 0.17 g/cm2, p=0.320) in either group over one year.

CONCLUSIONS: These studies demonstrate that protein-enriched meals replacements as compared to standard meal replacements recommended for weight management do not have adverse effects on routine measures of liver function, renal function or bone density at one year.

 

[Michael Scally MD]

Re: New Weight Loss Drugs

VIVUS Provides Regulatory Update on QNEXA NDA
http://ir.vivus.com/releasedetail.cfm?ReleaseID=544917

MOUNTAIN VIEW, Calif., Jan. 21, 2011 /PRNewswire/ -- VIVUS, Inc. (Nasdaq: VVUS) today announced that it held an End-of-Review meeting with the Food and Drug Administration (FDA) for the New Drug Application (NDA) for QNEXA®, an investigational drug for the treatment of obesity. The meeting occurred on January 19th at the FDA's offices in Maryland and was attended by senior members of the FDA and VIVUS' management and consultants. At this meeting the FDA requested that VIVUS assess the feasibility of analyzing existing healthcare databases to determine the historical incidence of oral cleft in offspring of women treated with topiramate for migraine prophylaxis (100 mg).

Based on discussions at the meeting, VIVUS believes the FDA's additional request stems from two published reports which cited two oral clefts in the UK Epilepsy and Pregnancy Register (Hunt et al., July 2008) and four, including two isolated cleft lips, from the North American AED Pregnancy Registry (Hernandez-Diaz et al., June 2010). In the QNEXA® studies, which included 15 births from women exposed to QNEXA® or topiramate, there were no reports of any fetal malformations. The timing of the planned resubmission of the QNEXA® NDA will be determined after agreement with the FDA is reached on the feasibility assessment. VIVUS anticipates continued dialog with the FDA on the planned resubmission of the QNEXA® NDA.

 

[Maxximal]

Re: New Weight Loss Drugs

The Obesity is a epidemic all over the world the people loves eat junk food all day

 

[Michael Scally MD]

Re: Weight-Loss

The Claim: Chia Seeds Can Help You Lose Weight [But it does make you grow crazy little hairs from all of your body pores!!!]
http://www.nytimes.com/2011/01/25/health/25really.html

By ANAHAD O’CONNOR
Published: January 24, 2011

THE FACTS

Chia Pets — those terra-cotta figurines that sprout fuzzy green hair — made the chia plant a household name. But chia has gained an entirely new reputation as a diet supplement.

Diet books and fitness gurus promote the plant’s seeds as an appetite suppressant, and health food stores and Web sites sell them by the pound. Chia seeds, which are native to Mexico and Guatemala and were cultivated by the Aztecs, are certainly chock-full of nutrition: a single serving, about an ounce (28 grams), delivers 4 grams of protein and 11 grams of fiber, which is supposedly the key to its weight-loss magic.

But there is little evidence that it lives up to that claim. In one study in 2009, a team of researchers randomly split 76 overweight and obese men and women into two groups. One group was given 25 grams of chia seeds twice a day, and the other was given a placebo. After 12 weeks, the scientists found no significant difference between the groups in appetite or weight loss.

Another team that reviewed the scientific evidence on chia came to a similar conclusion: There was no indication of “any effects” on weight loss. Nor did the researchers find much evidence supporting other health claims linked to the plant, like cardiovascular benefits. They noted that while chia is generally safe for consumption and a healthy addition to most diets, “further rigorous examination” of its effects as a supplement is needed.

THE BOTTOM LINE

There is little evidence that chia seeds or supplements promote weight loss.


Nieman DC, Cayea EJ, Austin MD, Henson DA, McAnulty SR, Jin F. Chia seed does not promote weight loss or alter disease risk factors in overweight adults. Nutr Res 2009;29(6):414-8. Chia seed does not promote weight loss or alter di... [Nutr Res. 2009] - PubMed result

The objective of this study was to assess the effectiveness of chia seed (Salvia hispanica L) in promoting weight loss and altering disease risk factors in overweight adults. The hypothesis was that the high dietary fiber and alpha-linolenic (ALA) contents of chia seed would induce a small but significant decrease in body weight and fat and improve disease risk factors. Subjects were randomized to chia seed (CS) and placebo (P) groups, and under single-blinded procedures, ingested 25 g CS or P supplements mixed in 0.25 L water twice daily before the first and last meal for 12 weeks. Ninety nondiseased, overweight/obese men and women between the ages of 20 and 70 years were recruited into the study, with 76 subjects (n = 39 CS, n = 37 P) completing all phases of the study. Pre- and poststudy measures included body mass and composition (dual energy x-ray absorptiometry), inflammation markers from fasting blood samples (C-reactive protein, interleukin 6, monocyte chemoattractant protein 1, and tumor necrosis factor alpha), oxidative stress markers (trolox equivalent antioxidant capacity and plasma nitrite), blood pressure, and a serum lipid profile. Plasma ALA increased 24.4% compared to a 2.8% decrease in CS and P, respectively (interaction effect, P = .012). No group differences were measured for changes in plasma eicosapentaenoic acid and docosahexaenoic acid (interaction effects, P = .420 and .980, respectively). Pre-to-post measures of body composition, inflammation, oxidative stress, blood pressure, and lipoproteins did not differ between CS and P for both sexes. In conclusion, ingestion of 50 g/d CS vs P for 12 weeks by overweight/obese men and women had no influence on body mass or composition, or various disease risk factor measures.

 

[Michael Scally MD]

Re: OnLine First

This drug has had some serious setbacks for FDA approval. Many of these are found at the company website, Arena Pharmaceuticals - Arena Pharmaceuticals . I do NOT see approval. [Email me for the full-text article.]


Martin CK, Redman LM, Zhang J, et al. Lorcaserin, A 5-HT2C Receptor Agonist, Reduces Body Weight by Decreasing Energy Intake without Influencing Energy Expenditure. J Clin Endocrinol Metab. http://jcem.endojournals.org/cgi/content/abstract/jc.2010-1848v1

Context: Lorcaserin, a selective 5-hydroxytryptamine (5-HT)2C receptor agonist, reduces body weight. It is unclear whether weight loss is due to reduced energy intake (EI) or also to enhanced energy expenditure (EE).

Objective: This study tested the effect of lorcaserin on EI and EE.

Design, Participants, and Intervention: In a double-blind, randomized, placebo-controlled trial, 57 (39 women) overweight and obese (body mass index, 27-45 kg/m(2)) adults were randomized to placebo (n = 28) or 10 mg twice daily lorcaserin (n = 29) for 56 d. Weight maintenance was imposed during d 1-7. Beginning on d 8, participants followed a diet and exercise plan targeting a 600 kcal/d deficit.

Outcomes: At baseline and after 7 and 56 d of treatment, we measured body weight, body composition (dual x-ray absorptiometry), blood pressure, heart rate, EI at lunch and dinner, subjective appetite ratings, and 24-h EE and 24-h-respiratory quotient (RQ), measured by indirect calorimetry in a respiratory chamber.

Results: After 7 d of weight maintenance, EI was significantly (P < 0.01) reduced with lorcaserin but not placebo (mean +/- SEM for lorcaserin, -286 +/- 86 kcal; placebo, -147 +/- 89 kcal). After 56 d, lorcaserin resulted in significantly larger reductions in body weight (lorcaserin, -3.8 +/- 0.4 kg; placebo, -2.2 +/- 0.5 kg; P < 0.01), EI (lorcaserin, -470 +/- 87 kcal; placebo, -205 +/- 91 kcal; P < .05), and appetite ratings than in placebo. Changes in 24-h EE and 24-h RQ did not differ between groups, even after 24-h EE was adjusted for body weight and composition. Compared with placebo, lorcaserin had no effect on systolic or diastolic blood pressure or heart rate after 56 d.

Conclusions: Lorcaserin reduces body weight through reduced EI, not altered EE or RQ.

 

[Michael Scally MD]

Re: New Weight Loss Drugs

FDA Issues Complete Response to New Drug Application for Contrave® for the Management of Obesity
http://finance.yahoo.com/news/FDA-Issues-Complete-Response-prnews-3262225145.html

SAN DIEGO and OSAKA, Japan, Feb. 1, 2011 /PRNewswire/ -- Orexigen® Therapeutics, Inc. (Nasdaq:OREX - News) and Takeda Pharmaceutical Company Limited (Takeda) (TSE:4502.to - News) announced today that the United States Food and Drug Administration (FDA) has issued a complete response letter dated January 31, 2011 regarding the New Drug Application for Contrave® (naltrexone HCl/bupropion HCl) extended-release tablets for the treatment of obesity, including weight loss and maintenance of weight loss.

The FDA noted concern about the cardiovascular safety profile of naltrexone/bupropion when used long-term in a population of overweight and obese subjects. Specifically, the letter stated that "before your application can be approved, you must conduct a randomized, double-blind, placebo-controlled trial of sufficient size and duration to demonstrate that the risk of major adverse cardiovascular events in overweight and obese subjects treated with naltrexone/bupropion does not adversely affect the drug's benefit-risk profile."

"We are surprised and extremely disappointed with the Agency's request in light of the extensive discussion and resulting vote on this topic at the December 7 Advisory Committee meeting," said Michael Narachi, President and CEO of Orexigen. "We plan to work closely with the Agency to gain more information to determine the appropriate next steps regarding the Contrave application."

Contrave, an investigational combination therapy of naltrexone HCl and bupropion HCl, was studied for its ability to help people with obesity initiate and sustain weight loss of at least 5 percent of their starting body weight in one year. Contrave was submitted for U.S. regulatory approval in March 2010. The original submission was based on multiple clinical trials that evaluated Contrave in more than 4500 patients.

 

[Michael Scally MD]

Re: Weight-Loss

Today’s Lab Rats of Obesity: Furry Couch Potatoes
http://www.nytimes.com/2011/02/20/health/20monkey.html?hp

February 19, 2011
By ANDREW POLLACK

HILLSBORO, Ore. — Like many these days, Shiva sits around too much, eating rich, fatty foods and sipping sugary drinks. He has the pot belly to prove it, one that nearly touches the floor — when he’s on all fours, that is.

Shiva belongs to a colony of monkeys who have been fattened up to help scientists study the twin human epidemics of obesity and diabetes. The overweight monkeys also test new drugs aimed at treating those conditions.

“We are trying to induce the couch-potato style,” said Kevin L. Grove, who directs the “obese resource” at the Oregon National Primate Research Center here. “We believe that mimics the health issues we face in the United States today.”

The corpulent primates serve as useful models, experts say, because they resemble humans much more than laboratory rats do, not only physiologically but in some of their feeding habits. They tend to eat when bored, even when they are not really hungry. And unlike human subjects who are notorious for fudging their daily calorie or carbohydrate counts, a caged monkey’s food intake is much easier for researchers to count and control.

“Nonhuman primates don’t lie to you,” said Dr. Grove, who is a neuroscientist. “We know exactly how much they are eating.”

To allow monitoring of their food intake, some of the obese monkeys are kept in individual cages for months or years, which also limits their exercise. That is in contrast to most of the monkeys here who live in group indoor/outdoor cages with swings and things to climb on.

While this research is not entirely new and has been the target of some animal rights’ group complaints, demand for the overweight primates is growing as part of the battle against the nation’s obesity epidemic, according to Dr. Grove and other researchers working with such monkeys in Florida, Texas and North Carolina, and also overseas.

Some tests have already produced tangible results. Rhythm Pharmaceuticals, a start-up company in Boston, tested its experimental diet drug on some of the Oregon monkeys. After eight weeks, the animals reduced their food intake 40 percent and lost 13 percent of their weight, without apparent heart problems.

“We could get a much better readout on chronic safety and efficacy early,” said Bart Henderson, the president of Rhythm, which now plans to move into human testing.

In another study, a group of academic researchers is using the monkeys to compare gastric bypass surgery with weight loss from forced dieting. One goal is to try to figure out the hormonal mechanisms by which the surgery can quickly resolve diabetes, so that drugs might one day be developed to have the same effect. To that end, the study will do what cannot be done with people — kill some of the monkeys to examine their brains and pancreases.

The primate center here, which is part of Oregon Health and Science University, has more than 4,000 monkeys, mostly rhesus macaques. About 150 of them are the rotund rhesuses. Some receive daily insulin shots to treat diabetes, and some have clogged arteries. One monkey died of a heart attack a few years ago at a fairly young age.

Shiva, a young adult, gained about 15 pounds in six months and weighs about 45 pounds, twice the normal weight for his age. Like other monkeys with a weight problem, he carries much of the excess in his belly, not his arms and legs.

The monkey’s daily diet consists of dried chow pellets, with about one-third of the calories coming from fat, similar to a typical American diet, Dr. Grove said, though the diet also contains adequate protein and nutrients.

They can eat as many pellets as they want. They also snack daily on a 300-calorie chunk of peanut butter, and are sometimes treated to popcorn or peanuts. Gummy bears were abandoned because they stuck to the monkeys’ teeth.

They also drink a fruit-flavored punch with the fructose equivalent of about a can of soda a day. In all, they might consume about twice as many calories as a normal-weight monkey.

Dr. Grove and researchers at some other centers say the high-fructose corn syrup appears to accelerate the development of obesity and diabetes.

“It wasn’t until we added those carbs that we got all those other changes, including those changes in body fat,” said Anthony G. Comuzzie, who helped create an obese baboon colony at the Southwest National Primate Research Center in San Antonio.

Still, about 40 percent do not put on a lot of weight.

Barbara C. Hansen of the University of South Florida said calories, but not high fat, were important. “To suggest that humans and monkeys get fat because of a high-fat diet is not a good suggestion,” she said.

Dr. Hansen, who has been doing research on obese monkeys for four decades, prefers animals that become naturally obese with age, just as many humans do. Fat Albert, one of her monkeys who she said was at one time the world’s heaviest rhesus, at 70 pounds, ate “nothing but an American Heart Association-recommended diet,” she said.

Mice and rats remain the main animals for medical research, but the effects on rodents often do not mirror those in people.

Rinat Neuroscience had an experimental drug that sharply reduced appetite in rodents. But obese baboons in San Antonio doubled or tripled their food intake when they got the drug.

The surprising result prompted Pfizer, which acquired Rinat, to explore whether the drug instead could promote weight gain, perhaps for cancer patients or others suffering from wasting.

Some companies see no need to use primates to study obesity and diabetes, saying it is almost as easy to do human studies.

Monkey studies can cost up to several million dollars. The animals are so precious that only a small number can be used. And there are ethical reviews before a study can begin.

“Doing primate studies is about as difficult as doing human studies from an ethical standpoint,” said Dr. Lee M. Kaplan, director of the weight center at Massachusetts General Hospital, who is one of the researchers in the bariatric surgery study here.

Animal rights activists say primate studies subject animals to needless suffering, like the stress of being caged. Two activists got jobs here in the last decade and presented evidence of what they said were mistreated and unhealthy monkeys.

Jim Newman, a spokesman for the primate center, said the accusations were unfounded and that after both instances, inspectors from the Department of Agriculture found no violations of rules.

Activists also question whether the studies are needed.

For example, they point to studies in the last two years by Dr. Grove and colleagues showing that when pregnant monkeys ate the high-fat diet, their offspring had metabolic problems. The babies were also more prone to anxiety when confronted with threatening objects, like a Mr. Potato Head with huge eyes.

“Terrorizing Monkeys with Mr. Potato Head is Research?” Alisa Mullins of People for the Ethical Treatment of Animals wrote in November. She noted that in the study, fetuses were taken from wombs and killed so their brains could be dissected. She also questioned the need to study fat monkeys: “Gee, couldn’t he have hung out at the local McDonald’s and learned the same thing?”

Dr. Grove said he understood the protesters’ view: “I applaud them for that pressure because it makes us do our job better.”

But he said the study found the diet induced chemical changes in the brains of fetuses that might be responsible for the problems in the offspring. The findings might also apply to humans but could not be studied in people.

The studies also found something else that could be important for people — that eating a healthy diet during pregnancy reduced troubles in the offspring. That suggests, he said, that the diet of a pregnant woman matters more than whether she is obese.

He also defended keeping the animals in some studies in individual cages. Not all labs do. At Wake Forest University, the monkeys are housed in pairs and separated only at meal times so that researchers can monitor what each monkey eats.

“These are social animals,” said Janice D. Wagner, a professor of pathology there. “We think they are happier that way.”

But Dr. Grove said he needed the animals separated at all times so they could snack between meals, since that is an important reason people gain weight. And allowing them outside, even one at a time, would mean they would exercise more.

“Our research model is a sedentary lifestyle with calorically dense diets,” he said.

As pharmaceutical companies move some research to less expensive countries, the obese monkeys are following. “This is a booming industry in China,” said Dr. Grove. “They have colonies of thousands of them.”

 

[Michael Scally MD]

Re: Weight-Loss

When Man's Best Friend Is Obese
Pets Are Getting Fatter; Owners Find It Tricky to Count Kitty Calories, Cut Kibble
When Man's Best Friend Is Obese - WSJ.com

As more Americans confront their own weight issues, furry housemates increasingly struggle alongside them. New data due out this week indicate the problem is reaching epidemic proportions, with more than half of U.S. dogs and cats now overweight or obese. Of pets considered to be "obese"—defined as 30% above normal weight—one-fifth of dogs and cats fit the bill, according to the Association for Pet Obesity Prevention, which conducted the survey with Mars Inc.'s Banfield Pet Hospital, the nation's largest general veterinary practice.

[ame=http://online.wsj.com/video/news-hub-why-fat-cats-or-dogs-are-no-joke/0769DA28-25A4-4852-87F1-C25483CDF2C6.html]Video - News Hub: Why Fat Cats or Dogs Are No Joke - WSJ.com[/ame]

 

[Michael Scally MD]

Re: Weight-Loss

The Jury Is Still Out on Impact of Menu Labeling
FDA Law Blog: The Jury Is Still Out on Impact of Menu Labeling

March 09, 2011
By Susan J. Matthees –

The USDA’s Economic Research Service (“ERS”) recently published an article titled “Will Calorie Labeling in Restaurants Make a Difference?” that considers the potential impact of the new menu labeling requirements for chain restaurants. As we previously reported (here and here), § 4205 of the Patient Protection and Affordable Care Act requires chain restaurants and retail food establishments to include calorie information on their menus. In an effort to determine the potential impact of the law, ERS reviewed studies of consumer food choices conducted in geographical areas with menu labeling requirements already in place as well as studies on consumer eating behavior. The studies had conflicting results, and ERS was inconclusive as to whether the menu labeling requirements will have any impact on consumer food choices.

According to the article, studies suggest that Americans generally underestimate the calorie and fat content in restaurant menu items. It would seem to follow that disclosing nutrition information on menus would lead Americans to choose lower calorie and lower fat foods, but ERS researchers found that this is not necessarily the case. The article cites studies showing that people’s knowledge about health and nutrition has less impact on what they choose to eat when they are away from home than when they eat at home, and people dieting tend to choose less healthy options when eating out. Also, the article points to two experiments that suggest that consumers may be primed to believe that foods that are identified as low in fat are not as satisfying as non-low fat foods.

The article also points to conflicting results of studies of New York City’s calorie labeling law as an indication that it may be too soon to tell how federal law will change consumers’ habits. New York City began requiring chain restaurants to disclose calorie information on their menus in 2008, and studies on the impact of the law have found conflicting results. One study conducted in low-income, minority neighborhoods in New York City and similar neighborhoods in Newark, NJ, before and after the law went into effect, showed that although 88% of consumers in New York City said they were purchasing fewer calories, receipts from their purchases showed that people in New York City purchased about the same number of calories before and after the law took effect and about the same amount as people in Newark. Research by Stanford University, however, showed that mandatory calorie posting lead to a 6% decrease in calories per transaction for food purchases at Starbucks in New York City.

FDA intends to publish regulations implementing the menu labeling requirements by March 23. Some in industry believe the regulations could cost in the hundreds of millions of dollars to implement, and for now, it seems it will be wait and see as to whether the regulation will have any impact on consumer’s food choices.

 

[Michael Scally MD]

Re: Weight-Loss

Hoping to Avoid the Knife
http://www.nytimes.com/2011/03/17/health/research/17devices.html

By ANDREW POLLACK
Published: March 16, 2011

In November, the prestigious Cleveland Clinic hailed a “scar-less” weight-loss surgery as one of the top 10 medical innovations expected this year.

Developed by a company aptly called Satiety Inc., the procedure shrinks the stomach by using a stapler inserted through the mouth, rather than by cutting open a person’s belly.

But when the results of a clinical trial came in, the procedure resulted in the shedding of far fewer pounds for patients than the company had hoped. Venture capitalists who had invested $86 million in Satiety over a decade shut the company down.

The failure of the procedure, called transoral gastroplasty, pushes back the availability of any incision-less procedure to millions of obese Americans for several years, a disappointment to companies trying to find the next best thing to major surgery. The setback also further restricts options for those who are overweight, because it is occurring on top of federal rejections of a new generation of diet pills.

These defeats are not for lack of effort. Entrepreneurs are developing all manner of odd and ingenious ideas aimed at replacing bariatric surgery. These include a pill taken before meals that would swell up in the stomach, pacemakers that deliver jolts of electricity to the stomach wall, and tubes that line the inside of the small intestine, letting food slide through without being absorbed.

Device makers hope that by going in through the mouth using an endoscope, they can eliminate the infection risk from incisions, and possibly the need for general anesthesia, thereby lowering the current $12,000 to $30,000 cost for bariatric surgery. If weight loss could be made less forbidding and less expensive, many more people might undergo such procedures, including people who are less than severely obese. Even though more than 20 million Americans are heavy enough to qualify for bariatric surgery, only about 200,000 have the operation each year.

“There’s definitely a need for something for the other 99 percent,” said Hugh Narciso, chief executive of Baronova, whose experimental device slows the movement of food out of the stomach.

But bringing a device to market can be difficult. The digestive tract, with all its acids and movements, is an inhospitable place for a medical device. Bariatric surgery, meanwhile, has become safer because it is now done through tiny incisions. Just recently, the Food and Drug Administration lowered the weight requirement for Allergan’s Lap-Band, making more than 26 million additional people eligible to have it implanted.

Other companies besides Satiety have had problems. Leptos Biomedical went out of business last year. Industry executives say that ReShape Medical has cut many workers; company executives and directors did not return calls. Gastric pacemakers from EnteroMedics and Transneuronix failed in clinical trials. The Transneuronix failure occurred only months after the company was acquired by the device giant Medtronic for $269 million.

“Right now, it doesn’t look like anything is on the horizon that will replace surgery,” said Dr. Ninh Nguyen, chief of gastrointestinal surgery at the University of California, Irvine.

There are two main types of surgery. The gastric bypass, which restricts the stomach and bypasses part of the small intestine, can cause people to lose as much as 80 percent of their excess weight. In many cases it can also quickly resolve diabetes, a frequent companion disease to obesity.

Gastric banding, like the Lap-Band, involves putting an inflatable ring around the stomach to restrict food intake. It is less complicated than bypass, with a fatality rate during surgery of about one in 1,000, or about one-third that of bypass. But banding does not result in weight loss as significant as that of bypass, and carries potential complications after surgery.

A third approach, sleeve gastrectomy, is starting to gain popularity. The procedure involves stapling the stomach into a narrow tube so that less food can be ingested. The excess part of the stomach is then cut out.

A potential improvement on sleeve gastrectomy is gastric imbrication or plication. The stomach is narrowed by folding and sewing it in place, much like the pleating used to narrow a pair of pants. Those tucks eliminate the need to remove the excess stomach.

Still, entrepreneurs hope that devices through the mouth will be safer and cheaper.

Perhaps the simplest idea is a balloon inserted through the mouth and inflated in the stomach, creating a sense of fullness. Allergan and some other companies sell balloons in Europe, where rules for device approval are easier.

But balloons lose their effectiveness over time, because the stomach expands to accommodate them. And there are risks. A balloon used in the 1980s in the United States caused complications, including potentially fatal blockages, when it accidentally deflated and traveled into the small intestine.

Spatz FGIA of Jericho, N.Y., is developing an adjustable balloon that can be inflated further after the stomach has expanded, providing another jolt of weight loss. It also has an anchor to keep the balloon in the stomach should it deflate.

Gelesis, a start-up in Boston, is testing a capsule that would be swallowed before meals. The capsule contains particles that swell to hundreds of times their size in the stomach by absorbing water, then eventually shrink and are excreted.

In a demonstration, a spoonful of the particles was put into a glass of water. A few minutes later, the glass was filled with a heavy slush.

One big challenge for this idea is that someone anticipating a delicious feast might simply skip the pill.

HourGlass Technologies of Redwood City, Calif. is trying to mimic banding from within. Instead of clamping a ring around the outside of the stomach, it inserts a device through the mouth that sucks in the stomach and clamps it in place.

GI Dynamics of Lexington, Mass., has approval in Europe for the EndoBarrier, which mimics part of bypass surgery. It is a tube, inserted through the mouth, that lines the inside of the small intestine. Food going through the intestine cannot pass through the intestinal wall.

One drawback for devices embedded in the digestive tract is that they should be removed after six months or a year to prevent health problems from developing. Some surgeons question the value of these devices compared with permanent surgery.

“You remove it and there’s nothing to prevent the person from going back to the way they were,” said Dr. Gregg Kai Nishi, a weight loss surgeon in Beverly Hills, Calif.

Some manufacturers, however, argue that the devices can spur people to change their lifestyles. “It’s like nicotine patches,” said James McKinley, chief executive of Endosphere, an obesity device developer.

Not all the new devices circumvent incisions. Vibrynt, of Redwood City, Calif., is developing a device shaped like the stomach that is implanted next to the real stomach and compresses it.

Gastric pacemakers are implanted under the skin in the abdomen, with wires leading to the stomach wall. The electric pulses are believed to somehow dampen appetite. IntraPace, of Mountain View, Calif., recently won approval of its pacemaker in Europe.

Even the devices approved in Europe are several years from the market in the United States. Many of the companies have not yet reached agreement with the F.D.A. on the clinical trials needed to win approval.

“There is no clear path to an approval in the U.S.,” said Mr. Narciso of Baronova. “The investment community is getting very nervous about obesity right now.”

A spokeswoman for the F.D.A. said the agency wanted devices to result in weight loss that was 15 to 25 percentage points greater than a control group’s weight loss. In addition, the F.D.A. wants to measure this weight loss six months after the device is taken out, because of the potential for regaining weight.

Some executives say they have been told they need a difference of 25 percentage points, which could be tough. If the control group loses 15 percent of its excess weight, the treated group would need to lose 40 percent. That is more than the median weight loss of 32 percent median achieved by the Lap-Band when it was approved, in a trial without a control group.

Some device makers say they should not be held to the same standards as procedures that involve incisions. “Because this is a less invasive and less risky approach, something with a lower weight loss may be very helpful and accepted by patients,” said Darin Buxbaum, chief executive of HourGlass.

Satiety’s procedure resulted in nearly 40 percent loss of excess weight in an early trial without a control group. But in the main trial, it was compared with the results from patients who underwent a simulated procedure, in which a device was briefly inserted down the throat but no stapling was done.

Executives would not provide specific results but the weight loss was far less than in the earlier studies. Satiety executives speculated that patients, not knowing if they had really had the procedure, did not change their diets accordingly.

The failure has “thrown some cold water on the field,” said Dr. Richard Rothstein, chief of gastroenterology at Dartmouth Medical School. He is helping to organize a meeting later this year in which industry executives, doctors and the F.D.A. will discuss standards for trial design and approval of obesity devices.

 

[HeadDoc]

Re: Weight-Loss

Well - Tara Parker-Pope on Health
March 14, 2011, 5:34 pm
Forget the Treadmill. Get a Dog.
By TARA PARKER-POPE
Kevin Moloney for The New York Times UNLEASHED Among dog owners who went for regular walks, 60 percent met federal criteria for regular moderate or vigorous exercise, a new study says.

If you’re looking for the latest in home exercise equipment, you may want to consider something with four legs and a wagging tail.

Several studies now show that dogs can be powerful motivators to get people moving. Not only are dog owners more likely to take regular walks, but new research shows that dog walkers are more active over all than people who don’t have dogs.

One study even found that older people are more likely to take regular walks if the walking companion is canine rather than human.

“You need to walk, and so does your dog,” said Rebecca A. Johnson, director of the human-animal interaction research center at the University of Missouri College of Veterinary Medicine. “It’s good for both ends of the leash.”

Just last week, researchers from Michigan State University reported that among dog owners who took their pets for regular walks, 60 percent met federal criteria for regular moderate or vigorous exercise. Nearly half of dog walkers exercised an average of 30 minutes a day at least five days a week. By comparison, only about a third of those without dogs got that much regular exercise.

The researchers tracked the exercise habits of 5,900 people in Michigan, including 2,170 who owned dogs. They found that about two-thirds of dog owners took their pets for regular walks, defined as lasting at least 10 minutes.

Unlike other studies of dog ownership and walking, this one also tracked other forms of exercise, seeking to answer what the lead author, Mathew Reeves, called an obvious question: whether dog walking “adds significantly to the amount of exercise you do, or is it simply that it replaces exercise you would have done otherwise?”

The answers were encouraging, said Dr. Reeves, an associate professor of epidemiology at Michigan State. The dog walkers had higher overall levels of both moderate and vigorous physical activity than the other subjects, and they were more likely to take part in other leisure-time physical activities like sports and gardening. On average, they exercised about 30 minutes a week more than people who didn’t have dogs.
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Dr. Reeves, who owns two Labrador mixes named Cadbury and Bella, said he was not surprised.

“There is exercise that gets done in this household that wouldn’t get done otherwise,” he said. “Our dogs demand that you take them out at 10 o’clock at night, when it’s the last thing you feel like doing. They’re not going to leave you alone until they get their walk in.”

But owning a dog didn’t guarantee physical activity. Some owners in the study did not walk their dogs, and they posted far less overall exercise than dog walkers or people who didn’t have a dog.

Dog walking was highest among the young and educated, with 18-to-24-year-old owners twice as likely to walk the dog as those over 65, and college graduates more than twice as likely as those with less education. Younger dogs were more likely to be walked than older dogs; and larger dogs (45 pounds or more) were taken for longer walks than smaller dogs.

The researchers asked owners who didn’t walk their pets to explain why. About 40 percent said their dogs ran free in a yard, so they didn’t need walks; 11 percent hired dog walkers.

Nine percent said they didn’t have time to walk their dogs, while another 9 percent said their dogs were too ill behaved to take on a walk. Age of the dog or dog owner also had an effect: 9 percent said the dog was too old to go for walks, while 8 percent said the owner was too old.

“There is still a lot more dog walking that could be done among dog owners,” Dr. Reeves said.

And the question remains whether owning a dog encourages regular activity or whether active, healthy people are simply more likely to acquire dogs as walking companions.

A 2008 study in Western Australia addressed the question when it followed 773 adults who didn’t have dogs. After a year, 92 people, or 12 percent of the group, had acquired a dog. Getting a dog increased average walking by about 30 minutes a week, compared with those who didn’t own dogs.

But on closer analysis, the new dog owners had been laggards before getting a dog, walking about 24 percent less than other people without dogs.

The researchers found that one of the motivations for getting a dog was a desire to get more exercise. Before getting a dog, the new dog owners had clocked about 89 minutes of weekly walking, but dog ownership boosted that number to 130 minutes a week.

A study of 41,500 California residents also looked at walking among dog and cat owners as well as those who didn’t have pets. Dog owners were about 60 percent more likely to walk for leisure than people who owned a cat or no pet at all. That translated to an extra 19 minutes a week of walking compared with people without dogs.

A study last year from the University of Missouri showed that for getting exercise, dogs are better walking companions than humans. In a 12-week study of 54 older adults at an assisted-living home, some people selected a friend or spouse as a walking companion, while others took a bus daily to a local animal shelter, where they were assigned a dog to walk.

To the surprise of the researchers, the dog walkers showed a much greater improvement in fitness. Walking speed among the dog walkers increased by 28 percent, compared with just 4 percent among the human walkers.

Dr. Johnson, the study’s lead author, said that human walkers often complained about the heat and talked each other out of exercise, but that people who were paired with dogs didn’t make those excuses.

“They help themselves by helping the dog,” said Dr. Johnson, co-author of the new book “Walk a Hound, Lose a Pound,” to be published in May by Purdue University Press. “If we’re committed to a dog, it enables us to commit to physical activity ourselves.”
A version of this article appeared in print on March 15, 2011 on page D6.

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[HeadDoc]

Re: Weight-Loss

The Dose of Intervention and the Land of Dr. Oz
Written on March 7, 2011 by GT in diets, Dr. Oz, glycemic index, News, Obesity and weight regulation, weightloss diets

Today marks my appearance on the Dr. Oz Show, which was, let’s just say, an interesting experience and leave it at that. It was the show, though, that (finally) prompted me to address an issue I’ve wanted to address for quite some time.

The Dr. Oz Show is one part health advice and discussion and quite a few parts entertainment, as Oz’s producers kept telling me in the days before we taped the episode. To make for what they consider good television they played me up as the second coming of Atkins – a persona that my wife likes to refer to as “meat boy” — while Oz got to play the role of the harvest king, extolling the healing virtues of fruits, vegetables and whole grains. This made it more difficult than I would have liked to get across the important messages from my books, but television is television and I certainly knew what they had in store for me.

My message and the message of Why We Get Fat was not that we should all be eating nothing but animal products – and certainly not the unappetizing meat and eggs that Oz’s crew prepared as props — but that carbohydrate-rich foods are inherently fattening, some more so than others, and that those of us predisposed to put on fat do so because of the carbs in the diet. That’s why I called the book Why We Get Fat rather than some variation on The Miracle 24-Hour (or 14-Day or Three Week or Three month) Diet Cure, which is more the norm for lay books in the nutrition genre.

The idea despite all the controversy is pretty simple. I’m arguing, as others have before me, that the same thing that makes our fat cells fat is what makes us fat — a fat person, after all, is a person with a lot of overstuffed fat cells — and what makes our fat cells fat is fundamentally the hormone insulin. Raise insulin levels and we accumulate more fat in our fat cells. Lower insulin and fat is released from the fat cells and the cells of our lean tissue can burn it for fuel.

There’s nothing particularly controversial about the science involved. If you doubt insulin regulates fat accumulation in fat cells, you can literally look it up in any good biochemistry or endocrinology (the study of hormones and related disorders) textbook – the latest editions, say, of Lehningers Principles of Biochemistry or Williams Textbook of Endocrinology, which are the authoritative texts in their respective fields. Look up the word adipocyte (the technical term for fat cell) and this is what you’ll find:

First Williams (and I’ll translate the technical terminology immediately after):

The activity of LPL within individual tissues is a key factor in partitioning triglycerides among different body tissues. Insulin influences this partitioning through its stimulation of LPL activity in adipose tissue. Insulin also promotes triglyceride storage in adipocytes through other mechanisms, including inhibition of lipolysis, stimulation of adipocyte differentiation and escalation of glucose uptake.

To understand what this means you have to know that LPL is the enzyme (in less technical language, the thing) that works to pull fat from the circulation into whatever cell it happens to be sitting on. If that cell is a muscle cell, the fat is used for fuel. If it’s a fat cell, the fat is stored. Triglycerides are the form that fat is stored in fat cells and transported through the blood stream in lipoproteins. Adipose tissue is fat tissue and adipocyte is the fat cell.

So what Williams says is that fat is stored in different tissues (partitioned) depending on how this enzyme LPL is distributed on the cells of those tissues, and its insulin that to a large extent determines this. Then it adds that insulin promotes fat storage through other mechanisms as well — it creates new fat cells (stimulation of adipocyte differentiation), and it inhibits the escape of fat from the fat cell and its use for fuel (lipolysis), and it also increases the uptake of blood sugar (glucose) into the fat cell, which might not be relevant but the authors of the textbook don’t apparently know this, and neither did I when I wrote Good Calories, Bad Calories.

Now here’s Lehningers Principles of Biochemistry:

High blood glucose elicits the release of insulin, which speeds the uptake of glucose by tissues and favors the storage of fuels as glycogen and triaglycerols, while inhibiting fatty acid mobilization in adipose tissue.

Lehningers uses the other spelling of triglyceride – triaglycerol – to denote the fat in the blood and in our fat cells, and we get high blood glucose by consuming carbohydrate rich foods, which end up as glucose (a carbohydrate) in our blood stream. We also tend to have high blood glucose when we have a condition called insulin resistance, which is the underlying defect in obesity, diabetes and heart disease. When Lehningers says insulin inhibits fatty acid mobilization that’s pretty much the equivalent of what Williams is saying about insulin inhibiting lipolysis.

The point of both is simple. Insulin puts fat in fat cells. That’s what it does. And our insulin levels, for the most part, are determined by the carb-content of our diet — the quantity and quality of the carbohydrates consumed. (Or if Jenny Brand Miller and her colleagues are right, also by our fat content — the lower the fat in the diet, the higher the insulin and vice verse.) The way to get fat out of fat cells and burn it, which is what we want to do with it, is to lower insulin. This has been known since the early 1960s.

One point I make in Why We Get Fat is that we all respond to this carbohydrate/insulin effect differently. Some of us can eat carbohydrate-rich meals and burn them off effortlessly. We’re the ones (like Oz) who partition the carbs we consume into energy. (This is the fuel gauge metaphor that I use in WWGF and that Oz’s producers reproduced wonderfully on the show.) And some of us partition the carbs we consume into fat for storage, and that partitioning depends on a lot of different enzymatic and hormonal factors — mostly relating to insulin and LPL as Williams Textbook of Endocrinology said).

There are a few obvious dietary means to reduce the amount of insulin we secrete and ultimately the level of insulin in our circulation day in and day out. One is to eat fewer carbohydrates; one is to improve the quality of the carbs we do eat, which means eating carbs that are less refined (their glycemic index is low or at least lower) and carbs that come with a lot of fiber attached (green leafy vegetables), and then eating less sugars, by which I mean both sucrose and high fructose corn syrup.

And this brings us to the point of controversy on the show – where Oz and I disagree. (Okay, one of the many points on which we disagree, but the one that needs clarification sooner rather than later). This is also the point that public health authorities, physicians and nutritionists almost religiously refuse to accept or even understand, because one implication of what I’m saying is that the good Dr. Atkins was right all along, and they just can’t get it through their head, as Oz can’t, that a diet of the kind Atkins recommended might be not only healthy but the medically appropriate treatment for the condition – in this case, obesity.

There are a couple of helpful ways to think about the role of carbohydrates in obesity and chronic disease, and one of them (the other I’ll discuss at the end of this post) is that some of us are more tolerant to the refined and easily digestible carbs and sugars in our diet than others. The more we can tolerate them the less we have to avoid them. Hence, the dose of carb-restriction that’s necessary to be lean and (probably) healthy is a small one. Again here’s how I put this issue of individual variation in WWGF:

…Multiple hormones and enzymes affect our fat accumulation, and insulin happens to be the one hormone that we can consciously control through our dietary choices. Minimizing the carbohydrates we consume and eliminating the sugars will lower our insulin levels as low as is safe, but it won’t necessarily undo the effects of other hormones—the restraining effect of estrogen that’s lost as women pass through menopause, for instance, or of testosterone as men age—and it might not ultimately reverse all the damage done by a lifetime of eating carbohydrate- and sugar-rich foods.

This means that there’s no one-size-fits-all prescription for the quantity of carbohydrates we can eat and still lose fat or remain lean. For some, staying lean or getting back to being lean might be a matter of merely avoiding sugars and eating the other carbohydrates in the diet, even the fattening ones, in moderation: pasta dinners once a week, say, instead of every other day. For others, moderation in carbohydrate consumption might not be sufficient, and far stricter adherence is necessary. And for some, weight will be lost only on a diet of virtually zero carbohydrates, and even this may not be sufficient to eliminate all our accumulated fat, or even most of it.

Oz and physicians like him think that there’s so much to be gained by eating whole grains and fruits (we agree on the green vegetables, although I do so less because of any compelling scientific evidence than because my mother insisted they were good for me) that they think this should be recommended to anyone and everyone and a diet that restricts them can’t possibly be healthful.

Oz implies on the show that everyone can benefit sufficiently by improving the quality of the carbs they eat and getting rid of the sugars, that any more significant restriction isn’t necessary. And he thinks any significant amount of carb restriction will cause problems because a) people won’t stay on such a restricted diet; b) they’ll replace these foods in their diet with high fat, high saturated fat meats and eggs and so increase their risk of heart disease (a point I discuss at length in both my books and is obviously critical), and c) they’ll develop diseases like cancer that Oz believes can be prevented by eating fruits and vegetables and maybe even whole grains.

As I point out on the show (or at least I did when the segment was taped, but it may or may not make it to the air as our taping session ran long), there’s precious little clinical trial evidence to support this last contention, but Oz and authorities like him believe in the healing power of fruits and vegetables, and they’re not all that bothered by the lack of clinical trials to support it.

This is the same take on the problem used by physicians and nutritionists who recommend low glycemic index diets instead of carbohydrate-restricted diets. They think this is enough to improve the quality of the carbs we consume, and the implicit assumption is that if we cut back on the quantity of carbs to any great extent we’ll either eat too much fat (or too much meat, period) or we won’t stick to the diet and any benefits will be lost.

What I’m arguing is that for many of us who run to fat, cutting down on the refined carbs and starchy carbs (potatoes, for instance) and on the added sugars will help, but it probably won’t help enough. The dose of carb-restriction won’t be sufficient to deal with the problem. We may stay fat. We may even get fatter. A blanket recommendation to eat fruits and vegetables and whole grains, as Oz prescribes and now Weight Watchers and the U.S. Dietary Guidelines, ignores this aspect of human variability completely. It assumes that people who are predisposed to fatten can tolerate the same foods and benefit from the same very mild dose of carb-restriction that the naturally lean can.

I don’t think that’s true. It’s that simple. I think that if we’re so predisposed to fatten that we’re already obese, we’re probably among those who have to restrict carbs far more severely – have a much greater dose of the intervention – to get even relatively lean, which means relatively healthy. So for some of us and maybe most of us, even fruit, the nutritionist’s darling of the early 21st century, can be fattening , and if it’s fattening, it means it’s probably causing far more problems than whatever antioxidants or phtyochemicals it contains may be preventing. (As even Wikipedia says, as of March 6th 2011 anyway, “While there is abundant scientific and government support for recommending diets rich in fruits and vegetables, there is only limited evidence that health benefits are due to specific phytochemicals.”)

The way I see it, Oz, who’s naturally skinny, can eat fruits and vegetables and whole grains to his hearts content and remain lean. For him, they can be the bulk of his diet and he can tolerate them and burn them off. They give him energy. They don’t make him fat. But most of his audience is not naturally lean, and they probably can’t. I’d argue that many of them have probably been living on diets very similar to the diet Oz is prescribing and it hasn’t helped them or certainly not to any significant degree. I get e-mails all the time now from people who tell me they were getting fatter and fatter on just those “heart healthy” diets.

Assuredly some proportion of the population and so Oz’s audience will lose a little weight eating as Oz recommends and getting rid of the refined grains and sugars in their diet, and they’ll be a little healthier for the effort. Getting rid of the sugars alone might make a significant difference on both counts. But it’s an insufficient dose of the intervention for a serious medical issue that typically requires far more. For those who are obese and want to be anything close to lean and stay that way, they’re likely to be better off getting rid of all the grains and much or most of the fruit, and then eating more of whatever foods they happen to eat or like that provide protein and fat – pulses, for instance, and tofu (a more complicated issue than I have time for here) for the vegetarians and vegans and animal products (meat, fish, fowl and eggs) for the rest.

This also speaks to a question I’ve been asked numerous times in e-mails from readers. Simply put, what about nuts and what about fruit? And here’s my answer: Nuts are not only Oz’s snack of choice, but the snack of choice of many low-carbers. And nuts and fruit are fine if your body can tolerate them. If you’re still heavier than you’d like, maybe it can’t. It’s a trade-off. If I eat fruit, other than maybe a handful of blueberries a day, I start to gain weight, so I don’t eat it. If I was fatter than I wanted to be — which I’m not — I’d consider giving up both the blueberries and the almonds I eat and see what happens. If it didn’t make any difference, I’d go back to them. If it did, I could decide how much I missed them and whether the trade-off of weight vs. fruits and nuts was worth it. You can look at any number of the nutrition websites to see which nuts have the lowest carb content and which fruits have the lowest sugar content and glycemic index and use that as a guide. But there’s no website or diet book that will tell you what your body can tolerate.

Finally, here’s the other way to look at carbohydrate-restricted diets, and it speaks to Oz’s belief that saturated fats are the cause of heart disease. As I explain in WWGF and did so on the Oz show, it’s almost assuredly the case that the same foods that make us fat are the same foods that cause heart disease and diabetes and cancer, etc. — the diseases that associate with obesity. These are the foods that were absent from human diets during the 2.5 million years of evolution leading up to the agricultural era, and so we’re still poorly adapted to dealing with these foods — easily digestible starches, refined carbs and sugars. When we remove these foods from our diets, we get healthier. Insulin levels come down and with them a host of metabolic disturbances normalize.

It was an email from my friend Bob Kaplan a few days before I taped the Oz show that reminded me of how best to phrase this argument. So I’m going to end with Bob’s e-mail because he said it as well or better than I ever could.

I was just thinking about the “beneficial effects” of a low-carb diet and how it’s essentially a misnomer.

When we eat low-carbohydrate diets, our “good” HDL tends to go up, our LDL becomes larger and fluffier (less atherogenic), our blood pressure goes down, and our triglycerides plummet. Does this mean a low-carbohydrate diet is beneficial to health?

Yes and no. While it appears “beneficial,” for me, it’s more of an indicator of our serum lipids “correcting” to levels that we are supposed to find in a healthy individual. In other words, if we look at a population of people who are chronically over-consuming sugar and refined carbohydrates, their serum lipids are going to be abnormal. When they go on a low-carbohydrate diet, they’re correcting the abnormality and the associated lipids will become more “favorable” (while I would argue that they’re just trending toward a normal, healthy human being) depending on which MD or researcher you ask.

So it is with weight “loss,” water “loss,” lipid and metabolic “benefits” of a low-carbohydrate diet. There is nothing magical about restricting carbohydrates, rather it’s closer to the kind of diet that we’ve been eating and are presumably genetically adapted to eat, and any loss of weight and water, any beneficial effects on serum lipids are just a correction rather than an improvement in health.

Benefits v. Correction:

A restricted-carbohydrate diet doesn’t make you lose weight; it corrects your weight.

A restricted-carbohydrate diet doesn’t make you lose water weight; it corrects your water weight.

A restricted-carbohydrate diet doesn’t improve serum lipids; it corrects serum lipids.

A restricted-carbohydrate diet doesn’t improve health; it corrects unhealthiness.

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Calories, fat or carbohydrates? Why diets work (when they do).
Written on December 13, 2010 by GT in bad science, diets, Obesity and weight regulation, weightloss diets

Last September, the Williams College psychologist Susan Engel had an opinion piece in the New York Times on the value of standardized testing as a means of assessing the quality of a child’s education. Engel argued that there was scant evidence that these tests were of any value at all, and that they should be…

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The Inanity of Overeating
Written on December 4, 2010 by GT in bad science, calories-in-calories-out, Obesity and weight regulation

My new book is coming out at the end of the month. It’s called Why We Get Fat and the subtitle is What To Do About it. The book concentrates more on the first because once you understand why we get fat, the what to do about it part is pretty obvious. And the problem…

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[Michael Scally MD]

Re: Weight-Loss

OUTLINE

REALITIES IN TREATING AN OBESE PATIENT
MODEL FOR ADDRESSING THE PROBLEM
DIET AND THE TREATMENT OF OBESITY
Very-Low-Calorie Diets
Balanced-Deficit Diets
Low-Fat Diets
Low-Carbohydrate Diets
High-Protein Diets
Comparison of Diets with Different Macronutrient Composition

MEDICATIONS AND THE TREATMENT OF OBESITY
Mechanisms Underlying Drug Therapy of Obesity
Drugs Approved in the United States for the Treatment of Obesity
Drugs Used to Treat Obesity but Not Approved for This Purpose
Drugs in Clinical Trials

CONCLUSION


Bray GA. Medical therapy for obesity. Mt Sinai J Med 2010;77(5):407-17. Medical Therapy for Obesity - Bray - 2010 - Mount Sinai Journal of Medicine: A Journal of Translational and Personalized Medicine - Wiley Online Library

Obesity results from a prolonged small positive energy imbalance, and treatment needs to reverse this imbalance. Many different diets have been tried to treat obesity, and weight loss occurs with all of them. There is currently no evidence that supports the superiority of one macronutrient composition for diets over any other. The principal effect seems to be the degree of adherence to the prescribed calorie reduction. Obesity drugs have been developed that tap brain mechanisms for controlling feeding and the gastrointestinal tract and its peptides. Orlistat blocks intestinal lipase and produces modest weight loss. Sibutramine is a serotonin-norepinephrine reuptake inhibitor that has a warning on its label from the US Food and Drug Administration because of cardiovascular risk. Its marketing has been suspended in Europe. Several drug combinations are on the horizon for treatment of obesity.

 

[Michael Scally MD]

Re: Weight-Loss

Although obesity in adulthood is a well-documented risk factor for both type 2 diabetes and coronary heart disease, it remains unclear whether a longer history of relative overweight, starting earlier in life, poses an additional risk. Furthermore, whereas the trajectory of weight and height from birth to adolescence is well documented, the progression of body-mass index (BMI) from adolescence into adulthood is less well described. Obese children probably have higher odds of becoming obese adults. Moreover, although an elevated BMI in childhood or adolescence may not necessarily represent adiposity, childhood obesity is associated with classic cardiometabolic risk factors, as is the case in adults. Some studies — though not all — have shown that elevated BMI in childhood or adolescence is associated with an increased risk of disease or death later in life. What is lacking is knowledge of how childhood BMI interacts with the particular pathologic mechanisms of obesity-related diseases and whether it does so even within the BMI range that is now considered normal.

Given the current obesity pandemic, it is important to determine whether elevated BMI in childhood, adolescence, or adulthood, or an increase in BMI during the transition from adolescence to adulthood, contributes independently to the risk of disease. Increases in BMI in childhood and adolescence may be closely associated with a higher incidence of coronary heart disease and type 2 diabetes mellitus in young adults. In fact, the occurrence of these diseases in the third to fifth decades of life may be the result of distinct associations with risk factors that are overlooked when the diseases are studied later in life.

To address these points, researchers used data from the Metabolic, Lifestyle, and Nutrition Assessment in Young Adults (MELANY) study of the Israel Defense Forces (IDF) Medical Corps and followed more than 37,000 apparently healthy young men whose BMI was measured at adolescence and into early adulthood, in order to identify incident cases of type 2 diabetes and angiography-proven coronary heart disease.


Tirosh A, Shai I, Afek A, et al. Adolescent BMI Trajectory and Risk of Diabetes versus Coronary Disease. New England Journal of Medicine 2011;364(14):1315-25. MMS: Error

BACKGROUND - The association of body-mass index (BMI) from adolescence to adulthood with obesity-related diseases in young adults has not been completely delineated.

METHODS - We conducted a prospective study in which we followed 37,674 apparently healthy young men for incident angiography-proven coronary heart disease and diabetes through the Staff Periodic Examination Center of the Israeli Army Medical Corps. The height and weight of participants were measured at regular intervals, with the first measurements taken when they were 17 years of age.

RESULTS - During approximately 650,000 person-years of follow-up (mean follow-up, 17.4 years), we documented 1173 incident cases of type 2 diabetes and 327 of coronary heart disease. In multivariate models adjusted for age, family history, blood pressure, lifestyle factors, and biomarkers in blood, elevated adolescent BMI (the weight in kilograms divided by the square of the height in meters; mean range for the first through last deciles, 17.3 to 27.6) was a significant predictor of both diabetes (hazard ratio for the highest vs. the lowest decile, 2.76; 95% confidence interval [CI], 2.11 to 3.58) and angiography-proven coronary heart disease (hazard ratio, 5.43; 95% CI, 2.77 to 10.62). Further adjustment for BMI at adulthood completely ablated the association of adolescent BMI with diabetes (hazard ratio, 1.01; 95% CI, 0.75 to 1.37) but not the association with coronary heart disease (hazard ratio, 6.85; 95% CI, 3.30 to 14.21). After adjustment of the BMI values as continuous variables in multivariate models, only elevated BMI in adulthood was significantly associated with diabetes (?=1.115, P=0.003; P=0.89 for interaction). In contrast, elevated BMI in both adolescence (?=1.355, P=0.004) and adulthood (?=1.207, P=0.03) were independently associated with angiography-proven coronary heart disease (P=0.048 for interaction).

CONCLUSIONS - An elevated BMI in adolescence — one that is well within the range currently considered to be normal — constitutes a substantial risk factor for obesity-related disorders in midlife. Although the risk of diabetes is mainly associated with increased BMI close to the time of diagnosis, the risk of coronary heart disease is associated with an elevated BMI both in adolescence and in adulthood, supporting the hypothesis that the processes causing incident coronary heart disease, particularly atherosclerosis, are more gradual than those resulting in incident diabetes.

 

[Michael Scally MD]

Re: Weight-Loss

[It is VERY important to note that the authors of the study are beneficiaries of VVUS largess!]

Patients Lose Weight With Rejected Combo Pill
Medical News: Patients Lose Weight With Rejected Combo Pill - in Primary Care, Obesity from MedPage Today

A combination drug denied FDA approval for treating obesity led to significantly better weight loss compared with placebo, according to a large phase III clinical trial.

In the 52-week randomized trial of more than 2,400 patients, significantly more participants lost at least 5% of their body weight on the combo pill of phentermine and topiramate (Qnexa) than they did on a placebo pill, Kishore Gadde, MD, of Duke University, and colleagues reported in The Lancet.

The paper marks the formal publication of data that the FDA used in its review and rejection of the agent last year, along with two other anti-obesity drugs: lorcaserin (Lorqess) and a combination of bupropion and naltrexone (Contrave).

The current data come from the phase III CONQUER trial, conducted between November 2007 and June 2009.

The trial was encompassed 2,487 patients who were overweight or obese (body mass index [BMI] 27 kg/m2 to 45 kg/m2) and who had at least two comorbidities: hypertension, dyslipidemia, diabetes, or prediabetes.

Patients were randomized to either placebo or to one of two doses of the drug -- 7.5 mg phentermine plus 46 mg topiramate, or 15 mg phentermine plus 92 mg topiramate.

The primary endpoint was change in body weight and the proportion of patients achieving at least 5% weight loss.

The researchers found patients lost significantly more weight on either dose of the drug than on placebo -- losing 1.4 kg (or 3.08 lb) for placebo, versus 8.1 kg (almost 18 lb) for the lower dose, and 10.2 kg (or 22.48 lb) for the higher dose, P<0.0001, Gadde and colleagues reported.

As well, significantly more patients achieved the marker of at least 5% weight loss (21% of those on placebo versus 62% on the lower dose, and 70% on the higher dose, P<0.0001).

And more patients on the drug achieved greater than 10% weight loss (7% versus 37% and 48%, respectively, P<0.0001).

The researchers added that improvements in risk factors were most pronounced among patients with pre-existing comorbidities.

For instance, hypertensive patients had greater reductions in systolic blood pressure when taking the drug compared with placebo. They were also more likely to come off antihypertensives with the drug.

Patients with hypertriglyceridemia had greater improvements in concentrations of triglycerides and HDL cholesterol on drug than on placebo, Gadde's team wrote.

Diabetic patients had greater reductions in glycated hemoglobin levels, and those with prediabetes had greater reductions in fasting plasma glucose and insulin.

Fewer patients progressed to full-blown diabetes if they were on the drug, the researchers added.

The most common adverse events were dry mouth (2% in the placebo group vs 13% in the low-dose and 21% in the higher dose group), paraesthesia (2% vs 14% and 21%), constipation (6% versus 15% and 17%), insomnia (5% versus 6% and 10%), dizziness (3% versus 7% and 10%), and dysgeusia (1% versus 7% and 10%).

Depression-related events occurred in 4% of those on placebo, in 4% of those on the low dose, and in 7% of those on the higher dose, and anxiety-related events occurred in 3%, 5%, and 8%, respectively.

There was a small increase in mean heart rate with both doses of the drug, and a greater proportion of patients these patients had increases of more than 10 bpm at two consecutive visits, the researchers said.

One of the main concerns with the next-generation anti-obesity drugs is cardiovascular problems, given that many of the once-available pharmacologic treatments (including Fen-Phen and sibutramine [Meridia] were pulled from the market because of suspected adverse cardiovascular effects.

Another concern has been psychiatric issues.

Gadde and colleagues wrote that psychiatric adverse events "occurred mainly during the early phase of treatment, generally resolved on drug discontinuation, and occurred at a higher frequency with the drug in a dose-dependent manner."

They cautioned that patients with significant depression were excluded from the study, "and a cautious approach is warranted when considering administration of this treatment to patients with mood disorders."

Overall, however, the researchers said the side effect profile of the combo pill is similar to that of other diet drugs.

Peter Tam, president of Vivus, the drug's manufacturer, told MedPage Today and ABC News that the company is working to re-submit the drug application.

"We have an upcoming meeting to discuss the specific information they need for that resubmission and I'm confident based on our ongoing communications that we will be able to resubmit in the second half of this year," Tam said.

He noted that since sibutramine was removed from the market, only one drug -- orlistat (Alli, Xenical) -- remains approved for the treatment of obesity.


Gadde KM, Allison DB, Ryan DH, et al. Effects of low-dose, controlled-release, phentermine plus topiramate combination on weight and associated comorbidities in overweight and obese adults (CONQUER): a randomised, placebo-controlled, phase 3 trial. The Lancet. Effects of low-dose, controlled-release, phentermine plus topiramate combination on weight and associated comorbidities in overweight and obese adults (CONQUER): a randomised, placebo-controlled, phase 3 trial : The Lancet

Background - Obesity is associated with a reduction in life expectancy and an increase in mortality from cardiovascular diseases, cancer, and other causes. We therefore assessed the efficacy and safety of two doses of phentermine plus topiramate controlled-release combination as an adjunct to diet and lifestyle modification for weight loss and metabolic risk reduction in individuals who were overweight and obese, with two or more risk factors.

Methods - In this 56-week phase 3 trial, we randomly assigned overweight or obese adults (aged 18—70 years), with a body-mass index of 27—45 kg/m2 and two or more comorbidities (hypertension, dyslipidaemia, diabetes or prediabetes, or abdominal obesity) to placebo, once-daily phentermine 7•5 mg plus topiramate 46•0 mg, or once-daily phentermine 15•0 mg plus topiramate 92•0 mg in a 2:1:2 ratio in 93 centres in the USA. Drugs were administered orally. Patients were randomly assigned by use of a computer-generated algorithm that was implemented through an interactive voice response system, and were stratified by sex and diabetic status. Investigators, patients, and study sponsors were masked to treatment. Primary endpoints were the percentage change in bodyweight and the proportion of patients achieving at least 5% weight loss. Analysis was by intention to treat. This study is registered with Clinical Trials.gov, number NCT00553787.

Findings - Of 2487 patients, 994 were assigned to placebo, 498 to phentermine 7•5 mg plus topiramate 46•0 mg, and 995 to phentermine 15•0 mg plus topiramate 92•0 mg; 979, 488, and 981 patients, respectively, were analysed. At 56 weeks, change in bodyweight was ?1•4 kg (least-squares mean ?1•2%, 95% CI ?1•8 to ?0•7), ?8•1 kg (?7•8%, ?8•5 to ?7•1; p<0•0001), and ?10•2 kg (?9•8%, ?10•4 to ?9•3; p<0•0001) in the patients assigned to placebo, phentermine 7•5 mg plus topiramate 46•0 mg, and phentermine 15•0 mg plus topiramate 92•0 mg, respectively. 204 (21%) patients achieved at least 5% weight loss with placebo, 303 (62%; odds ratio 6•3, 95% CI 4•9 to 8•0; p<0•0001) with phentermine 7•5 mg plus topiramate 46•0 mg, and 687 (70%; 9•0, 7•3 to 11•1; p<0•0001) with phentermine 15•0 mg plus topiramate 92•0 mg; for ?10% weight loss, the corresponding numbers were 72 (7%), 182 (37%; 7•6, 5•6 to 10•2; p<0•0001), and 467 (48%; 11•7, 8•9 to 15•4; p<0•0001). The most common adverse events were dry mouth (24 [2%], 67 [13%], and 207 [21%] in the groups assigned to placebo, phentermine 7•5 mg plus topiramate 46•0 mg, and phentermine 15•0 mg plus topiramate 92•0 mg, respectively), paraesthesia (20 [2%], 68 [14%], and 204 [21%], respectively), constipation (59 [6%], 75 [15%], and 173 [17%], respectively), insomnia (47 [5%], 29 [6%], and 102 [10%], respectively), dizziness (31 [3%], 36 [7%], 99 [10%], respectively), and dysgeusia (11 [1%], 37 [7%], and 103 [10%], respectively). 38 (4%) patients assigned to placebo, 19 (4%) to phentermine 7•5 mg plus topiramate 46•0 mg, and 73 (7%) to phentermine 15•0 mg plus topiramate 92•0 mg had depression-related adverse events; and 28 (3%), 24 (5%), and 77 (8%), respectively, had anxiety-related adverse events.

Interpretation - The combination of phentermine and topiramate, with office-based lifestyle interventions, might be a valuable treatment for obesity that can be provided by family doctors.

 

[Michael Scally MD]

Re: Weight-Loss

Weight-Loss Drugs Alli and Xenical Should Be Removed From the Market, Public Citizen Tells FDA
Xenical and Alli Can Cause Severe Injury to Liver, Pancreas, Kidneys
Public Citizen Press Room

WASHINGTON, D.C. – The over-the-counter weight-loss drug Alli and its prescription form Xenical should be removed from the market immediately because they not only can damage the liver, but also, based on new information obtained from FDA adverse reaction files, have been associated with 47 cases of acute pancreatitis and 73 cases of kidney stones, Public Citizen said today in a petition to the Food and Drug Administration (FDA).

http://www.citizen.org/documents/1942.pdf

 

[Michael Scally MD]

Re: Weight-Loss/Obesity

Stigma Weighs Heavily on Obese People, Contributing to Greater Health Problems
Stigma weighs heavily on obese people, contributing to greater health problems

ScienceDaily (Apr. 16, 2011) — The discrimination that obese people feel, whether it is poor service at a restaurant or being treated differently in the workplace, may have a direct impact on their physical health, according to new research from Purdue University.

"Obesity is a physiological issue, but when people have negative interactions in their social world -- including a sense of being discriminated against -- it can make matters worse and contribute to a person's declining physical health," said Markus H. Schafer, the doctoral student in sociology and gerontology who led the study. "We found that around a third of the severely obese people in the United States report facing some form of discriminatory experience, and the experience of weight discrimination plays into people's own perspective about their weight. It seems that many people are internalizing the prejudice and stigma they feel, and it contributes to stress, which ultimately affects their health."

Whether someone is overweight or obese is determined by the body mass index scale, which accounts for height, weight, and gender. The Centers for Disease Control and Prevention report that 34% of U.S. adults are overweight and another 34% are obese. Being overweight is a predisposition for obesity, which puts people at risk for cancers, heart disease, diabetes, and other complications and quality of life issues.

The Purdue team's findings are published in the March issue of Social Psychology Quarterly. Schafer, along with Kenneth F. Ferraro, a distinguished professor of sociology, compared body mass indexes to people's health and perceptions of weight discrimination. More than 1,500 people, ages 25-74, were surveyed in 1995 and 2005 about issues related to aging and health equality as part of the National Survey of Midlife Development in the United States.

"As expected, those who were obese fared worse in overall health when they were followed up with 10 years later," Schafer said. "But we found there was a difference among those who felt they were discriminated against and those who didn't."

About 11% of those who were moderately obese and 33% of those who were severely obese reported weight discrimination, and these were the individuals who had the sharpest decline over time in their functional abilities, such as the capacity to climb stairs or carry everyday items. Functional ability is a key measure for health status, Schafer said.

"We've seen considerable progress to address racial and gender discrimination in the United States, but the iceberg of weight discrimination still receives relatively little attention," said Ferraro, who studies obesity and aging. "This is an interesting paradox because as the rates of obesity rise in this country, one might expect that anti-fat prejudice would decline. Public health campaigns for weight control are needed, but the stigma that many obese persons experience also exacts a toll on health."

Schafer and Ferraro are affiliated with the Department of Sociology and the Center on Aging and the Life Course. Schafer, who will be an assistant professor of sociology at the University of Toronto this fall, is currently studying social relationships and health among retirement community residents. Ferraro, who is director of the Center on Aging and the Life Course, is continuing to work on obesity issues related to aging.


Schafer MH, Ferraro KF. The Stigma of Obesity. Social Psychology Quarterly 2011;74(1):76-97. The Stigma of Obesity

Obesity is widely recognized as a health risk, but it also represents a disadvantaged social position. Viewing body weight within the framework of stigma and its effects on life chances, we examine how perceived weight-based discrimination influences identity and physical health. Using national survey data with a 10-year longitudinal follow-up, we consider whether perceptions of weight discrimination shape weight perceptions, whether perceived weight discrimination exacerbates the health risks of obesity, and whether weight perceptions are the mechanism explaining why perceived weight discrimination is damaging to health. Perceived weight discrimination is found to be harmful, increasing the health risks of obesity associated with functional disability and, to a lesser degree, self-rated health. Findings also reveal that weight-based stigma shapes weight perceptions, which mediate the relationship between perceived discrimination and health.