February 2nd, 2012
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Most US middle and high schools sell soft drinks, candy and chips to their students. These practices have been widely criticized as contributing to childhood and adolescent obesity. However, a new study followed approximately 19,450 children from fifth to eight grade. Researchers found the children’s weight gain was not associated with the introduction or the duration of exposure to competitive foods. This did not vary by gender, race/ethnicity or family socioeconomic status. Possible explanations are that children’s food preferences and dietary patterns are firmly established before adolescence. Also, schools are highly structured whereas home life may have more opportunities for snacking. http://www.asanet.org/images/journals/docs/pdf/soe/Jan12SOEFeature.pdf.
November 23rd, 2011
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The National Heart, Lung and Blood Institute has issued guidelines endorsed by the American Academy of Pediatrics. They are directed to all primary pediatric care providers to address the known risk factors of cardiovascular disease, including obesity, blood pressure, cholesterol, tobacco and lipids.
The report notes that longitudinal data on non-white populations are lacking and that “Clinically important differences in prevalence of risk factors exist according to race and gender, particularly with regard to tobacco-use rates, obesity prevalence, hypertension, and dyslipidemia.”
The report notes, “Obesity tracks more strongly than any other risk factor, among many reports from studies that have demonstrated this fact…Tracking data on physical data is more limited.”
Regarding overweight and obesity, the report states,
“The dramatic increases in childhood overweight and obesity in the United States since 1980 are an important public health focus. Despite efforts over the last decade to prevent and control obesity, recent reports from the National Health and Nutrition Examination Survey show sustained high prevalence: 17% of children and adolescents have a BMI at the >95th percentile for age and gender. The presence of obesity in childhood in childhood and adolescence is associated with increased evidence of atherosclerosis at autopsy and of subclinical measures of atherosclerosis on vascular imaging. Because of its strong association with many of the other established risk factors for cardiovascular disease, obesity is even more powerfully correlated with atherosclerosis; this association has been shown for BP, dyslipidemia, and insulin resistance in each of the major pediatric epidemiologic studies. Of all of the risk factors, obesity tracks most strongly from childhood into adult life.”
Given that physical activity is a primary prescription for preventing childhood and adolescent obesity, it is interesting to read what the expert panel has to say about its utility:
“A moderate number of RCTs (randomized controlled clinical trials) have evaluated the effect of interventions that addressed only physical activity and/or sedentary behavior on prevention of overweight and obesity. In a small number of these studies, the intervention was effective. It should be noted that these successful interventions often addressed reduction in sedentary behavior rather than attempts to increase physical activity. In a majority of these studies there was no significant difference in body-size measures. Sample sizes were often small and follow-up was often short (frequently < 6 months). ..Overall, the expert panel concluded that on the basis of the evidence review, increasing activity in isolation is of little benefit in preventing obesity. By contrast, the review suggests that reducing sedentary behavior might be beneficial in preventing the development of obesity.”
The report identifies populations at special risk for obesity: children with a BMI between the 85 and 95th percentiles;children in whom there is a positive family history of obesity in 1 or both parents; early onset of increasing weight; excessive weight gain during adolescence; children who have been very active and become inactive. See Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents- NHLBI, NIH
November 4th, 2011
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Every now and then a study appears and you realize no one has ever done this before. Here’s one which may have profound impact. A group from Kings College London looked at 1,000 women aged 45-68 years who were annually checked for BMI. Now, at this point, most studies would report the mean or average BMI. But they went further. They looked at each individual’s weight trajectory, i.e. did their weight change or stay the same. What they found was a great stability in individual BMI during the years of follow-up. 30% had no change in their weight. Nonetheless, weight increased in 58%, decreased in 11.4%. The authors note that simply combining all individuals into groups and overlooking the distinctive patterns of BMI change may lead to biased inferences in epidemiologic and etiologic research in the future. Longitudinal study of variation in body mass ind… [Age (Dordr). 2011] – PubMed – NCBI
I have been sending this paper to a number of researchers, suggesting they look at databases available to them, such as the placebo arms of intervention studies, to replicate this study. If it is replicated, it may have a great effect on future clinical trials. The authors of the paper call for an examination of genetic polymorphisms according to this weight paradigm. This might mean that future clinical trials might be able to exclude those expected to naturally lose weight and concentrate on those likely to gain weight. This may be doubly important if the FDA requires more studies of cardiovascular endpoints. Such studies, like the SCOUT trial, necessitate an older population, some of whom, it appears, are losing weight naturally.
October 28th, 2011
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Antidepressant usage is the topic of a recent data brief from the Centers for Disease Control and Prevention. The paper shows that 11% of Americans over 12 years of age take antidepressants. More than 60% taking antidepressants do so for 2 years or longer with 14% taking the medication for 10 years or more. Less than 1/3 taking one antidepressant has been seen by a mental health professional in the past year. Usage is heaviest among white women. Products – Data Briefs – Number 76 – October 2011
Why is this important for obesity? Because most antidepressants cause weight gain. According to a recent meta-analysis, amitriptyline, mirtazapine and paroxetine were associated with weight gain. Weight loss was associated with fluoxetine and bupropion. Antidepressants and body weight: a compreh… [J Clin Psychiatry. 2010] – PubMed – NCBI
On average, there is a 1-3kg average weight gain on antidepressants. Weight gain, obesity, and psychotropic prescribing. [J Obes. 2011] – PubMed – NCBI. Thus, the continuing high usage of the antidepressants which cause weight gain and the long duration of weight with low medical oversight indicates a point of intervention to prevent further health problems in the population taking these drugs. Click here for information on other FDA approved drugs which cause weight gain.
October 7th, 2011
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The “obesity paradox” refers to a phenomenon in which overweight and obese patients with established cardiovascular disease have a better prognosis than normal weight patients. This has been a controversial finding in several studies, indicating to some that weight loss is worse than weight gain. Now, researchers from the Veterans Affairs Palo Alto Health Care System, examined 3,834 male vets. They did find that weight loss was related to higher mortality and weight gain was related to lower mortality, compared to stable weight over 7 years.
However, 60% of the deaths in the weight loss group were attributable to conditions associated with muscle wasting, including cancer and heart disease. These conditions arose during the seven year period. This study underscores that the obesity paradox may be explained by the distinction between intentional v. unintentional weight loss. As the authors note, clinically supervised intentional weight loss has shown extensive benefits including lowers incidence of cardiovascular events, better overall survival, marked reduction in the metabolic syndrome, inflammatory markers, lipids, prevalence of hypertension and better glucose tolerance. The obesity paradox and weight loss. [Am J Med. 2011] – PubMed – NCBI
Even very obese adults can improve their cardiometabolic risk factors. Researchers of the Louisiana Obese Subjects Study (LOSS) found most parameters improved with 5% weight loss or more among 390 extremely obese men and women, followed for one year. The intervention group was under primary medical care, using meal replacements, weight loss medications, especially sibutramine and behavioral counseling. Those in the intervention group lost an average of 13% of their weight while the ususal care group lost an average of 0.9%. 20.7% of participants had substantial weight loss (10%-19.9%) and 15.4% lost over 20%. There was a “precipitous” decrease in fasting plasma glucose among patients with type 2 diabetes who achieved at least modest weight loss. Systolic and diastolic blood pressure decreased inconsistently. With modest weight loss, patients achieved 22% improvement in triglyceride levels. Only 53% of subjects stayed in the program for evaluation at one year. Incremental weight loss improves cardiometabolic ri… [Am J Med. 2011] – PubMed – NCBI
October 3rd, 2011
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So what actually is wrong with fat-bashing? Everyone does it. Isn’t it a good thing to embarrass and ridicule people into healthy behavior? Well, yes. I guess. If it worked. The round of vitriol directed at Chris Christie for his weight is nothing which millions of persons with obesity haven’t experienced in their own families or workplaces or just walking down the street. The problem with telling a person with obesity to eat a salad and take a walk ,like the Washington Post’s Eugene Robinson did, is like telling a person with Parkinson’s disease to just stop shaking or a drug addict to just say no. It ignores the complexity of disease focusing only on the visible end point of a long and complex biological and social process.
Given the context of the fat-bashing regarding New Jersey Governor Chris Christie, it is useful to revisit Dr. Jeffrey Friedman’s 2003 commentary, “Make War on Obesity, not the Obese.”
Jeffrey Friedman and Douglas Coleman’s names came up this weekend as possible contenders for the Nobel Prize in Medicine. (They would have my vote if I had a vote) for their work in the discovery of leptin in 1994. Their work revolutionized obesity research, showing how a hormone produced by fat tissue plays a key role in body weight regulation.
Friedman’s commentary is still timely and deserves revisiting while obesity, especially extreme or severe obesity, is in the news. I think it remains one of the best scientific explanations of obesity and should give pause to anyone who wants to throw a stone or two.
His major points are:
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“There can be no meaningful discussion of obesity until we resist the impulse to assign blame. Nor can we hold to the simple belief that with willpower alone, one can consciously resist the allure of food and precisely control one’s weight.“
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The facts are these “(i) the increasing incidence of obesity in the population is not reflected by a proportionate increase in weight; (ii) the drive to eat is to a large extent hardwired, and differences in weight are genetically determined; and (iii) obesity can be a good thing depending on the environment in which one (or one’s ancestors) finds oneself.”
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The change in weight attributable to any recent changes in diet or a more sedentary life-style is much smaller than the enormous differences in weight, often numbering in the hundreds of pounds, that can be observed among individuals living in today’s world.”
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“Twin studies, adoption studies, and studies of familial aggregation confirm a major contribution of genes to the development of obesity. Indeed, the heritability of obesity is equivalent to that of height and exceeds that of many disorders for which a genetic basis is generally accepted. It is worth noting that height has also increased significantly in Western countries in the 20th Century.”
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“In general, obesity genes encode the molecular components of the physiologic system that regulates energy balance. This system precisely matches energy intake (food) to energy expenditure to maintain constant energy stores, principally fat. That there must be a system balancing food intake and energy expenditure is suggested by the following analysis. Over the course of a decade, a typical persons consumes approximately 10 million calories, generally with only a modest change in weight. To accomplish this, food intake must precisely match energy output within 0.17% over that decade. This extraordinary level of precision exceeds by several orders of magnitude the ability of nutritionists to count calories and suggests that conscious factors alone are incapable of precisely regulating caloric intake.”
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“Feeding is a complex motivational behavior, meaning that many factors influence the likelihood that the behavior will be initiated. These factors include the unconscious urge to eat that is regulated by leptin and other hormones, the conscious desire to eat less (or more), sensory factors such as smell or taste, emotional state, and others. The greater the weight loss, the greater the hunger and, sooner or later for most dieters, a primal hunger trumps the conscious desire to be thin.”
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The increase in weight is not evenly distributed in the population. “In modern times, some individuals have manifested a much greater increase of BMI than others, strongly suggesting the possibility that in our population (species) there is a subgroup that is genetically susceptible to obesity and a different subgroup that is relatively resistant.”
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“Obesity is not a personal failing. In trying to lose weight, the obese are fighting a difficult battle. It is a battle against biology, a battle that only the intrepid take on and one in which only a few prevail.” A war on obesity, not the obese. [Science. 2003] – PubMed – NCBI.
September 27th, 2011
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Are persons with obesity different? The question is fraught with implications.
Much of obesity policy is premised on the assumption that persons with obesity are just like normal weight persons but with less self-control. The assumption is that education and awareness will overcome their lack of awareness and result in more self-control, just like normal weight persons. Of course, a genetic basis for obesity is counter to this assumption. How does this genetic pre-disposition express itself? Two recent studies may provide insights. In one, overweight persons show a higher capacity for storing fats but a lower capacity for ridding themselves of them, using the radioactive isotope carbon-14. Cell dysfunction linked to obesity and metabolic disorders | ScienceBlog.com
In another study, the brains of persons with obesity were found to create a greater desire for high-calorie foods than normal-weight subjects which would explain why people who become overweight tend to remain overweight. Study: Obese people’s brains may crave high-calorie foods – USATODAY.com
September 5th, 2011
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The Agency for Healthcare Research and Quality is undertaking a comparative effectiveness review of approaches to weight maintenance in adults. Information is available at Approaches to Weight Maintenance in Adults: A Comparative Effectiveness Review | AHRQ Effective Health Care Program The paper cites a recent Cochrane review of workplace diet and physical activity which found a rather minimal decrease in weight of 2.8 pounds or .5 BMI unit at 6-12 months.
