Diet, exercise alone not sufficient obesity treatment for most

Researchers suggest that obesity is a chronic disease with a number of biological causes that make it impossible to be cured with diet and exercise alone in a recently published comment in The Lancet Diabetes & Endocrinology.

Eighty percent to 95% of people with obesity who lose weight eventually regain it. Several biological systems are triggered when caloric intake is reduced, which drives people to eat more high-calorie foods and, in turn, gain or regain weight. According to the researchers lifestyle changes are not enough to override the fat-loss defense for most individuals with sustained obesity.

“Although lifestyle modifications may result in lasing weight loss in individuals who are overweight, in those with sustained obesity, bodyweight seems to become biologically ‘stamped in’ and defended,” Christopher N. Ochner, PhD, assistant professor of pediatrics and psychiatry at Icahn School of Medicine at Mount Sinai and a research associate at the New York Obesity Nutrition Research Center at Columbia University Medical Center, said in a press release. “Therefore, the current advice to eat less and exercise more may be no more effective for most individuals with obesity than a recommendation to avoid sharp objects for someone bleeding profusely.”

Biological adaptations that occur with the development of obesity and undermine health weight loss effors can persist even in people who were are formerly obese and achieve a healthy bodyweight through dieting.

“Few individuals ever truly recover from obesity; rather they suffer from ‘obesity in remission,’” Ochner said in the press release. “They are biologically very different from individuals of the same age, sex and bodyweight who never had obesity.”

The researchers suggest that biological factors should be addressed to help sustain long-term weight loss, but current biologically-based interventions are limited to antiobesity drugs, weight loss surgery and intra-abdominal vagal nerve block. According to the researchers these interventions do not permanently correct the biological factors adaptations undermine healthy weight loss efforts. However, during use, the interventions alter neural or hormonal signaling associated with appetite, which can yield a 4% to 10% reduction in weight.

“Many clinicians are not aware of the reasons individuals with obesity struggle to achieve and maintain weight loss,” Ochner said. “Obesity should be recognized as a chronic and often treatment-resistant disease with both biological and behavioral causes that may require biologically-based interventions, such as pharmacotherapy or surgery, in addition to lifestyle modification. Ignoring the biological adaptations that undermine healthy weight loss efforts and continuing to rely solely on behavioral modification will surely result in the continued inability to treat obesity effectively and the premature deaths of millions of individuals each year.” 

Tomado de:Halo.org

Ochner CN, et al. Lancet Diabetes Endocrinol. 2015;doi:10.1016/S2213-8587(15)70010.

Obesity experts recommend weight loss drugs, surgery as supplement to lifestyle interventions

The  Endocrine Society today issued a Clinical Practice Guideline (CPG) on strategies for prescribing drugs to manage obesity and promote weight loss

The CPG, entitled "Pharmacological Management of Obesity: An Endocrine Society Clinical Practice Guideline," was published online and will appear in the February 2015 print issue of the Journal of Clinical Endocrinology and Metabolism (JCEM), a publication of the Endocrine Society.

Obesity is a worsening public health problem. According to the 2012 National Health and Nutrition Examination Survey, about 33.9 percent of adults ages 19-79 were overweight, 13.4 percent were obese and 6.4 were extremely obese.

The Food and Drug Administration has approved four new anti-obesity drugs -- lorcaserin, phentermine/topiramate, naltrexone/bupropion and liraglutide -- in the past two years. Medications like these can be used in combination with diet and exercise to help people lose weight.

"Lifestyle changes should always be a central part of any weight loss strategy," said Caroline M. Apovian, MD, of Boston University School of Medicine and Boston Medical Center, and chair of the task force that authored the guideline. "Medications do not work by themselves, but they can help people maintain a healthy diet by reducing the appetite. Adding a medication to a lifestyle modification program is likely to result in greater weight loss."

In the CPG, the Endocrine Society recommends that diet, exercise and behavioral modifications be part of all obesity management approaches. Other tools such as weight loss medications and bariatric surgery can be combined with behavioral changes to reduce food intake and increase physical activity. Patients who have been unable to successfully lose weight and maintain a goal weight may be candidates for prescription medication if they meet the criteria on the drug's label.

Other recommendations from the CPG include:

• If a patient responds well to a weight loss medication and loses 5 percent or more of their body weight after three months, the medication should be continued. If the medication is ineffective or the patient experiences side effects, the prescription should be stopped and an alternative medication or approach considered.

• Since some diabetes medications are associated with weight gain, people with diabetes who are obese or overweight should be given medications that promote weight loss or have no effect on weight as first- and second-line treatments. Doctors should discuss medications' potential effects on weight with patients.

• Certain types of medication -- angiotensin converting enzyme inhibitors, angiotensin receptor blockers and calcium channel blockers -- should be used as a first-line treatment for high blood pressure in obese people with Type 2 diabetes. These are effective blood pressure treatments that are less likely to contribute to weight gain than the alternative medication, beta-adrenergic blockers.

• When patients need medications that can have an impact on weight such as antidepressants, antipsychotic drugs and medications for treating epilepsy, they should be fully informed and provided with estimates of each option's anticipated effect on weight. Doctors and patients should engage in a shared-decision making process to evaluate the options.

• In patients with uncontrolled high blood pressure or a history of heart disease, the medications phentermine and diethylpropion should not be used.

The Hormone Health Network offers resources on weight and health at

http://www.hormone.org/diseases-and-conditions/weight-and-health.

Tomado de: sciencedaily.com

Journal Reference: Caroline M. Apovian, Louis J. Aronne, Daniel H. Bessesen, Marie E. McDonnell, M. Hassan Murad, Uberto Pagotto, Donna H. Ryan, Christopher D. Still.Pharmacological Management of Obesity: An Endocrine Society Clinical Practice Guideline. The Journal of Clinical Endocrinology & Metabolism, 2015; jc.2014-3415 DOI: 10.1210/jc.2014-3415

Obesity: exploring the causes, consequences and solutions

The World Health Organization estimates that global levels of obesity have doubled since 1980. In 2012, more than 40 million children under the age of 5 were estimated to be overweight or obese, which is an issue of serious concern as excess body weight is believed to be the driver of many non-communicable diseases, namely type 2 diabetes, cardiovascular disease and some types of cancer.

To tackle what is, in most cases, a preventable condition, there is increasing focus on research into understanding the mechanisms behind obesity, including our genetics and the influence of lifestyle and the environment. There is also now increased focus on introducing public health initiatives to aid long-term weight loss, which range from improving public, patient and healthcare provider education to policy reform regarding the sale of pre-packaged and processed foods.

To focus on these issues, BMC Medicine has launched an article collection that aims to explore the main contributing factors and possible solutions to tackle the worldwide impact of obesity.

Which are the culprits – sugars, starches or fats?

How much of what we eat makes us fat? This is an ongoing debate, fuelled most recently byRobert Lustig and his focus on sugar. On the question of sugar, a further debate arises – is itsucrose or fructose that has the most impact on obesity?

In an editorial to introduce the article collection in BMC Medicine, Jack Winkler, former Professor of Nutrition Policy at London Metropolitan University, and currently Director of Food & Health Research, discusses why it is so hard to measure which food components are associated with obesity.

Prof Winkler explains one of the many problems with this field is that data derived from large-scale studies depends on reliable and consistent reporting. However, this is a limiting factor simply because these studies rely on self-reported energy intake surveys, and as Prof Winkler reminds us, people are good at lying about how much they are actually eating.

“The lies people tell about their food may be white lies, but they are large lies….. In one study of soft drinks, subjects in the National Diet and Nutrition Survey claimed to be drinking barely a quarter of the products that manufacturers reported they were selling”

The consequences of obesity

There is no question that obesity places a burden on healthcare services. Earlier this year,Gillian Reeves and colleagues showed that elevated body mass index (BMI) in UK women is associated with increased hospital admissions equating to around 420,000 extra admissions annually, indicating that current obesity levels are directly impacting UK healthcare services.

Primary care physicians are usually the first in line to treat patients with obesity related diseases, although patients may not be visiting their GP to directly ‘treat’ their obesity. As David Haslam, a GP and physician specializing in obesity at the Centre for Obesity research explains, the role of primary care in managing obesity is complicated in the UK by ineffective or contradictory policies. In his commentary published as part of this article collection, Prof Haslam starkly points out:

“Obesity prevention has failed. If nobody in the UK gains another single ounce, there are enough already obese people to make epidemics of diabetes, then heart disease then premature death inevitable.”

Prof Haslam, who also serves as Chair of the National Obesity Forum, highlights that obesity can be most effectively managed by individualization of care, which should be implemented through effective screening and risk management. After all, not all patients will benefit from weight loss. Prof Haslam discusses the obesity paradox in his commentary, and recent evidence on this includes a meta-analysis we published this year by Wie Nie and colleagues, showing that an obesity paradox exists for pneumonia – i.e. obese individuals have an increased risk of pneumonia but a decreased risk of pneumonia mortality, indicating a survival advantage for obese individuals.

However, in most cases, obesity and diet are considered as a causal risk factor for chronic diseases such as type 2 diabetes. Recently, Elin Hall and colleagues showed that exposing pancreatic islet cells to the free fatty acid palmitate results in differential gene expression and epigenetic modifications, which may influence type 2 diabetes risk through impaired insulin secretion in these treated cells.

In an Opinion article, Naveed Sattar and Jason Gill discuss the plausible link between type 2 diabetes and ectopic fat around organs such as the liver and pancreas. In their article, they explain that studies have shown accumulation of ectopic fat around the liver leads to insulin resistance, and they also hypothesize that fat around the pancreas could lead to β-cell dysfunction. Prof Sattar and Dr Gill ask a very provocative question: can type 2 diabetes be reversed by loss of ectopic fat around key organs?

Taking action on obesity

So, what should be done about the rising levels of obesity? One of the physicians leading the issue is John Wass, a consultant physician and endocrinologist, and also Chair of the Working Party for Action on Obesity.

I interviewed Prof Wass about the goals of the working party, which aims to tackle the rise of obesity in the UK  by filling current gaps in knowledge and support within the healthcare and medical education systems. Prof Wass highlights that educating the public about healthy eating, and collaborations with the food industry on how to responsibly sell and label foods, is key to improving public health.

There is also ongoing debate about whether or not obesity should be considered as a disease. On this, Prof Wass explains that as obesity is a condition that needs to be actively managed it can be labelled as a disease, and unless it is recognized as such, prevention and management strategies will not be taken seriously.

Tomado de: 

http://blogs.biomedcentral.com/

Sabina Alam on August 26

PODCAST

http://media.biomedcentral.com/content/movies/supplementary/johnwass-audio-v1.mp3

High dependency predicts BMI increase during smoking cessation

Smokers who are heavily addicted to nicotine are significantly more likely to gain weight when they try to quit, researchers report.

Investigators studying 186 patients who successfully quit smoking after receiving nicotine replacement therapy at an outpatient clinic found that mean body mass index increased significantly from 23.5 kg/m² at an initial consultation to 23.9 kg/m² at 3 months after the start of therapy. A high Fagerstrom Test for Nicotine Dependence (FTND) score, indicating severe dependency, was found on multivariate analysis to be the strongest predictor of increase (using a gender-adjusted standardized coefficient).

Dr. Maki Komiyama of Kyoto (Japan) Medical Center and colleagues reported their findings online Aug. 21 in the open access journal PLoS One (PLoS One 2013 Aug. 21[doi:10.1371/journal.pone.0072010]).

The findings are important because, while smoking cessation is known to reduce cardiovascular and cancer risk and to reduce all-cause mortality, associated weight gain is linked with greater risk of glucose intolerance and a reduction in the beneficial effects that quitting has on pulmonary function. Concerns about weight gain also can lead to a failure to quit smoking, they said.

"Even if one is expected to experience post-cessation weight gain, quitting smoking still leads to a reduced cardiovascular risk. However, there is also a possibility that if one can prevent post-cessation weight gain, then this will further reduce the cardiovascular risk due to having ceased smoking," they wrote

Thus, they continued, the ability to predict which patients are likely to gain weight during smoking cessation therapy – and performing weight control accordingly at the outset – could lead to improved outcomes, and the findings of this study may be useful for discriminating such patient groups.

Study participants were 132 men and 54 women with a mean age of 59.6 years who visited the smoking cessation clinic at the National Hospital Organization Kyoto Medical Center between July 2007 and November 2011 and successfully quit smoking.

Other factors found on univariate analysis to be significantly associated with BMI increase included triglyceride level, high-density lipoprotein cholesterol, and daily cigarette consumption. "To further investigate ... we performed multivariate analysis. The results demonstrated that the triglyceride level and FTND score were factors determining the post-cessation BMI increase, and that the FTND score was the strongest one," the investigators wrote.

An FTND score of 8 or more (on a scale of 1-10) was associated with larger postcessation BMI increase, and the increase was statistically significant when compared with the level of BMI increase in those with a score of 7 or less, they noted.

"The result that a high FTND score was the most important determinant of a BMI increase supports the hypothesis that post-cessation weight gain is one of the nicotine withdrawal symptoms," they said.

As for the association between triglyceride elevation and weight gain, the mechanism is not clearly understood and requires further study, they noted.

With the exception of two patients who did not receive medical treatment, study participants were treated with either oral varenicline (95 patients) or nicotine patch (89 patients). No difference was seen between the varenicline and nicotine patch groups with respect to BMI increase, but the varenicline group had higher nicotine dependency.

They also noted that, in their study, "although a significant increase in BMI was confirmed after smoking-cessation therapy, the BMI increase was only 0.4 kg/m² (1.1 kg), which is much smaller than reported in previous studies for people who quit smoking on their own initiative (2.8-3.8 kg)."

Additional study is needed to determine the appropriate timing for initiating interventions against post–smoking cessation weight gain, they noted.

This study was supported by a grant-in-aid for clinical research from the National Hospital Organization and the Pfizer Health Research Foundation. The authors reported that one study drug (varenicline) is manufactured by Pfizer but confirmed "that this does not alter their adherence to all the PLoS One policies on sharing data and materials."

Tomado de:familypracticenews.com

La inflamación del tejido adiposo multiplica el riesgo de patologías asociadas a la obesidad

Un estudio del CIBERobn revela que el aumento de la muerte celular por apoptosis favorece el desarrollo de enfermedades metabólicas.

Un estudio llevado a cabo por especialistas del Centro de Investigación Biomédica en Red-Fisiopatología de la Obesidad y la Nutrición (CIBERobn), dirigidos por el investigador del Hospital Virgen de la Victoria de Málaga Francisco Tinahones, ha revelado que la inflamación es una de las principales causas de la muerte celular por apoptosis en el tejido adiposo. Con ello, se abre una nueva vía de actuación en la lucha contra la obesidad. El estudio ha sido publicado en la revista Diabetes Care.
     Según ha informado este martes el propio CIBERobn, junto a la constatación de que la inflamación es la responsable de que las células del tejido adiposo sean más propensas a la muerte, el hallazgo revela también que un incremento en el peso conlleva un aumento de apoptosis en el tejido adiposo. Esto, a su vez, "provoca un efecto adverso, pues si se produce un mayor aporte de energía se requieren más adipocitos para almacenarla; y una disminución de células adiposas en esas circunstancias eleva el riesgo de enfermedades metabólicas", sostiene Tinahones.
     La apoptosis, una forma de muerte celular programada que se desencadena a partir de señales celulares controladas genéticamente, es fundamental en el desarrollo de órganos y sistemas. Su función más importante es la destrucción de las células dañadas genéticamente, evitando que su reproducción provoque el desarrollo de enfermedades. Así, se produce apoptosis cuando una célula está deteriorada y no puede ser reparada o cuando sufre una infección vírica. Si una célula dañada no se 'apoptosiza', se continúa dividiéndo sin restricción alguna, lo que puede derivar en cáncer.
     Este tipo de muerte celular sigue un proceso regular y muy riguroso, por lo que el exceso o defecto de apoptosis puede desencadenar múltiples patologías con diferentes niveles de gravedad. "En los sujetos obesos hacen falta más células adiposas para almacenar una mayor cantidad de grasa, y en la mayoría de ellos se produce inflamación en el tejido adiposo que genera un exceso de muerte por apoptosis".
     "Por tanto", prosigue, "el tejido adiposo se vuelve insuficiente para almacenar grasa y debe almacenarla en otros tejidos, como el hígado, músculo, etcétera, lo que da lugar a las enfermedades metabólicas asociadas a la obesidad".
     El tejido adiposo es el tejido con más capacidad para aumentar su tamaño, además de constituir la principal reserva energética del organismo, pues las células que lo conforman (adipocitos) son responsables del almacenamiento de grasas. Asimismo, este tejido cumple una doble función: por un lado, sirve como amortiguador, ya que protege a los órganos internos, y por otro desempeña una función metabólica, de regulación de la ingesta y el gasto energético.
Hiperplasia e hipertrofia
     Se trata, en suma, del encargado de mantener el equilibrio entre la energía consumida y la utilizada. "Se cree que este tejido responde al exceso de energía a través de la hiperplasia, esto es, aumenta el tamaño del tejido como consecuencia del incremento del número de adipocitos; este aumento es un balance entre los que se forman nuevos y de los que mueren por apoptosis".
     "Cuando se altera ese balance no puede producirse hiperplasia del tejido y se produce hipertrofia, crece el volumen del tejido porque aumenta el tamaño de las células adiposas, pero no la cantidad. Por lo tanto el tejido pasa a tener células más grandes pero no nuevas y esta situación favorece el desarrollo de enfermedades metabólicas", concluye el especialista.
     En la mayoría de los obesos se genera una inflamación que causa un aumento de muerte celular por apoptosis y se reduce de forma considerable el número de células de ese tejido. Este decrecimiento de la celularidad disminuye la capacidad de almacenamiento del tejido adiposo y, por lo tanto, impide que éste realice correctamente sus funciones, dando lugar al desarrollo de patologías metabólicas asociadas a la obesidad, como la diabetes o el hígado graso.
Diabetes Care (2012); doi: 10.2337/dc12-0194

Tomado de jano.es

Target for Obesity Drugs Comes Into Focus

      Researchers at the University of Michigan have determined how the hormone leptin, an important regulator of metabolism and body weight, interacts with a key receptor in the brain.

Leptin is a hormone secreted by fat tissue that has been of interest for researchers in obesity and Type 2 diabetes since it was discovered in 1995. Like insulin, leptin is part of a regulatory network that controls intake and expenditure of energy in the body, and a lack of leptin or resistance to it has been linked to obesity in people.

Although there can be several complex reasons behind leptin resistance, in some cases the underlying cause is malfunction of the leptin receptor in the brain. An understanding of how leptin and its receptor interact could lead to new treatments for obesity and metabolic disorders, but the structure of this signaling complex has evaded researchers for years.

Georgios Skiniotis, a faculty member at the Life Sciences Institute and assistant professor in biological chemistry at the U-M Medical School, employed electron microscopy to obtain the first picture of the interaction between leptin and its receptor.

Skiniotis also traced similarities between the leptin receptor and other receptors of the same family, which may provide insight into new targets for treatment of other hormone-related diseases.

"It is exciting not only because it might help with developing new drugs," Skiniotis said. "We now better understand the design and mechanisms of signaling through this class of receptors, which brings us to a whole new set of intriguing questions."

In the paper "Ligand-Induced Architecture of the Leptin Receptor Signaling Complex," published electronically ahead of print on Oct. 11 in Molecular Cell, Skiniotis and his co-authors explain how the receptor is formed by two hinged legs that can swivel until they encounter leptin, which binds to the legs and makes them rigid.

Once the two legs of a receptor become rigid by binding to leptin, they signal to an enzyme called the Janus kinase. A number of drugs have been studied for treatments related to the Janus kinases; inhibiting it may lead to improvement of conditions like rheumatoid arthritis, psoriasis and metabolic disorders that are linked to inflammation.

Alan Saltiel, director of the Life Sciences Institute and a widely cited researcher who works on diabetes, obesity and metabolic disorders, sees a range of possibilities in the work of Skiniotis.

"This study may help solve an important issue we've been struggling with for some time," he said. "Since leptin is a master regulator of appetite, understanding why resistance to its effects develops in obesity has been a major obstacle to discovering new drugs for obesity and diabetes. Developing a clear picture of how leptin can bind to its receptor may be the first step in overcoming leptin resistance."

Tomado de: University of Michigan. "Target for obesity drugs comes into focus." ScienceDaily, 11 Oct. 2012. Web. 28 Nov. 2012.

Visceral fat, not adiposity, marker of prediabetes, type 2 diabetes in obese adults

     Among obese adults, excess visceral fat and insulin resistance — not necessarily adiposity — are independently associated with incident prediabetes and type 2 disease.

     Ian J. Neeland, MD, of the University of Texas Southwestern Medical Center, and colleagues conducted a study involving 732 obese adults (BMI ≥30) aged 30 to 65 years without diabetes or cardiovascular disease. Patients were enrolled in the Dallas Heart Study between 2000 and 2002.

     The following measurements were obtained: BMI (using DXA and MRI); circulating adipokines and biomarkers of insulin resistance; dyslipidemia and inflammation; and subclinical atherosclerosis and cardiac structure and function (using CT and MRI), according to the study.

     The primary outcome was diabetes incidence during a median 7 years of follow-up. Researchers also determined the incidence of composite prediabetes or diabetes in a subgroup of 512 patients with normal fasting glucose at baseline.

     More than 10% of patients developed diabetes (11.5%) during the study. Results of a multivariable analysis revealed that several factors were independently associated with diabetes, including: higher baseline visceral fat mass (OR=2.4; 95% CI, 1.6-3.7); fructosamine level (OR=2.0; 95% CI, 1.4-2.7); fasting glucose level (OR=1.9; 95% CI, 1.4-2.6); family history of diabetes (OR=2.3; 95% CI, 1.3-4.3); systolic BP (OR=1.3; 95% CI, 1.1-1.5); and weight gain during follow-up (OR=1.06; 95% CI, 1.02-1.10).

     However, BMI, total body fat and abdominal subcutaneous fat were not associated with diabetes. Results from the subgroup analysis demonstrated that the composite of prediabetes or type 2 diabetes occurred among 39.1% of patients and was independently associated with baseline levels of: visceral fat mass, fasting glucose, insulin and fructosamine; older age; non-white race; family history of disease; and weight gain during follow-up (P<.05 for each).

     Similarly, however, there was no association with general adiposity measurements, they wrote.“These findings suggest that clinically measurable markers of adipose tissue distribution and insulin resistance may be useful in prediabetes and diabetes risk discrimination among obese individuals and support the notion of obesity as a heterogeneous disorder with distinct adiposity subphenotypes.”

Neeland IJ. JAMA. 2012;308:1150-1159.

Tomado de  Healio.com

Obesity linked to coronary artery calcification in patients without diabetes

     Coronary artery calcification was linked to obesity, but not impaired fasting glucose, according to results from a community-based study of the offspring and third-generation cohorts of the initial Framingham Heart Study.

     “In the US population, approximately one in three nondiabetic adults has impaired fasting glucose (IFG) and one in three has obesity. IFG is known to be related to all components of the metabolic syndrome, including strong associations with obesity,” researchers wrote.

     Using multidetector computed tomography in 3,054 patients (mean age of 50 years; 49% women; 29% impaired fasting glucose [IFG] and 25% obese), researchers compared the coronary artery calcification (CAC) of patients with normal fasting glucose and IFG. Comparisons were also completed on the CAC of patients with and without obesity. Researchers aimed to determine if CAC differences were independent of important confounders.

Martin K. Rutter, MD, from the cardiovascular research group within the School of Biomedicine at the University of Manchester in the United Kingdom, and colleagues said the relationships of IFG and obesity to CAC in the general population has been ambiguous until now.

“Although this is cross-sectional observational data, our work may have public health implications because it has suggested the possible importance of targeting obesity over IFG for preventing subclinical atherosclerosis in the general population,” the researchers wrote.

Data confirmed that high CAC was significantly related to IFG in an age- and sex-adjusted model (OR=1.4; 95% CI, 1.1–1.7), and after additional adjustments for obesity, high CAC still showed a relation to IFG (OR=1.3; 95% CI, 1–1.6).

However, IFG was not associated with high CAC in multivariable-adjusted models before (OR=1.2; 95% CI, 0.9–1.4) or after adjustment for obesity, they wrote.

Moreover, obesity was linked to higher CAC in age- and sex-adjusted models (OR=1.6; 95% CI, 1.3–2.0) and in multivariable models, including IFG (OR=1.4; 95% CI, 1.1–1.7), according to data.

Finally, researchers used a spline regression model to explore the nonlinear relationships linking CAC with BMI, fasting glucose and waist circumference.

“This suggested that there is a J-shaped multivariable-adjusted relationship between BMI and CAC with significant nonlinearity in the nonobese BMI range.”

Despite consistent evidence for improved risk prediction by CAC, Rutter and colleagues said that CHD screening using CAC currently is not recommended to improve clinical outcomes.

Rutter M. Diabetes Care. 2012; doi: 10.2337/dc11-1950.

Tomado de: healio.com

Big Girls Don’t Cry: Overweight Teens Who Are Satisfied With Their Bodies Are Less Depressed, Less Prone to Unhealthy Behaviors

A study to be published in the June 2012 issue of Journal of Adolescent Health looking at the relationships between body satisfaction and healthy psychological functioning in overweight adolescents has found that young women who are happy with the size and shape of their bodies report higher levels of self-esteem. They may also be protected against the negative behavioral and psychological factors sometimes associated with being overweight.

A group of 103 overweight adolescents were surveyed between 2004 and 2006, assessing body satisfaction, weight-control behavior, importance placed on thinness, self-esteem and symptoms of anxiety and depression, among other factors.

"We found that girls with high body satisfaction had a lower likelihood of unhealthy weight-control behaviors like fasting, skipping meals or vomiting," said Kerri Boutelle, PhD, associate professor of psychiatry and pediatrics at the University of California, San Diego School of Medicine. Boutelle added that the positive relationship shown in this study between body a girl's happiness with her body and her behavioral and psychological well-being suggests that improving body satisfaction could be a key component of interventions for overweight youth.

"A focus on enhancing self-image while providing motivation and skills to engage in effect weight-control behaviors may help protect young girls from feelings of depression, anxiety or anger sometimes association with being overweight," said Boutelle.

Additional contributors included first author Taya R. Cromley, PhD, of UCLA; Stephanie Knatz and Roxanne Rockwell, UC San Diego; and Dianne Neumark-Sztainer, PhD, MPH, RD and Mary Story, PhD, RD, University of Minnesota, Minneapolis.

This study was supported by a University of Minnesota Children's Vikings Grant.

University of California, San Diego Health Sciences. "Big girls don’t cry: Overweight teens who are satisfied with their bodies are less depressed, less prone to unhealthy behaviors."ScienceDaily, 28 Apr. 2012. Web. 8 May 2012.

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