miércoles, 15 de agosto de 2012

Obesity: Is Fast Food Responsible?

The reasons for obesity are multiple and complex.  Despite conventional wisdom, it is not simply a result of overeating.  Research has shown that in many cases, the significant underlying cause of morbid obesity is genetic. Studies have demonstrated that once the problem is established, efforts such as dieting and exercise programs have a limited ability to provide effective long-term relief. 

Science continues to search for answers but, until the disease is better understood, the control of excess weight is something patients must work at for their entire lives.  That is why it is very important to understand that all current medical interventions, including the Lap Band, Gastric Sleeve and Gastric Bypass procedures should not be considered medical cures. Rather, they are attempts to reduce the effects of excessive weight and alleviate the serious physical, emotional and social consequences of the disease. 
Contributing Factors 

The underlying causes of severe obesity are not known.  There are many factors that contribute to the development of obesity including genetic, hereditary, metabolic, environmental, and eating disorders.  There are also certain medical conditions that may result in some special type of obesity, such as the long term intake of steroids and some diseases such as hypothyroidism and hyper-adrenalism.
Genetic Factors 

Numerous scientific studies have established that your genes play an important role in your tendency towards excess weight gain.  The body weights of adopted children show no correlation with the body weights of their adoptive parents, who feed them and teach them how to eat.  However, their weight does have an 80 percent correlation with their genetic parents, whom they have never met.  As well, identical twins with identical genes, show a much higher similarity of body weights than do fraternal twins.

Certain groups of people, such as the Pima Indian tribe in Arizona and the growing Mexican-American population have shown a very high incidence of severe obesity. They also have significantly higher rates of diabetes and heart disease than other ethnic groups. 

We probably have a number of genes directly related to weight.  Just as some genes determine eye color or height, others can affect the appetite by increasing the amount of secretion of the Ghrelin Factor by the stomach, or the ability to feel full, satisfied, or have an early age-related change in metabolism. Our fat-storing ability, and our natural activity levels may even be affected by some predetermined gene.
Environmental Factors

Environmental and genetic factors are obviously closely intertwined.  If you have a genetic predisposition toward obesity, then the modern American lifestyle and environment may make controlling weight more difficult.  Fast food, long days sitting at a desk or in front of a TV screen or monitor, and suburban neighborhoods that require cars all magnify hereditary factors such as metabolism and efficient fat storage.   For those suffering from morbid obesity, anything less than a total change in environment usually results in failure to reach and maintain a healthy body weight. 
Metabolism

We used to think of weight gain or loss as only a function of calories ingested and then burned. Take in more calories than you burn, gain weight; burn more calories than you ingest, lose weight. But now we know the equation isn’t that simple.  Obesity researchers now talk about a theory called the “set point,” a sort of Thermostat in the brain that makes people resistant to either weight gain or loss. If you try to override the set point by drastically cutting your calorie intake, your brain responds by lowering metabolism and slowing activity. You then gain back any weight you’ve lost.
Eating Disorders & Medical Conditions

Weight loss surgery is not a cure for eating disorders. And there are medical conditions, such as hypothyroidism, that can also cause weight gain. That’s why it’s important that you work along with your doctor to find out whether you have any conditions that should be treated with medication and counseling.

ArturoRodriguez, MD
md@thebariatric.com
http://www.thebariatric.com
http://www.bandstersforum.com
Phone: 011-52-81-8378-3177
Twitter: @bandagastrica
Facebook: http://www.facebook.com/banda.gastrica

 

lunes, 13 de agosto de 2012

Strict laws on School Snacks

Adolescents in states with strict laws regulating the sale of snacks and sugary drinks in public schools gained less weight over a three-year period than those living in states with no such laws, a new study has found.

The study, published Monday in Pediatrics, found a strong association between healthier weight and tough state laws regulating food in vending machines, snack bars and other venues that were not part of the regular school meal programs. Such snacks and drinks are known as competitive foods, because they compete with school breakfasts and lunches.

The conclusions are likely to further stoke the debate over what will help reduce obesity rates, which have been rising drastically in the United States since the 1980s. So far, very little has proved effective and rates have remained stubbornly high. About a fifth of American children are obese, according to the Centers for Disease Control and Prevention.

Public health experts have urged local and state governments to remove competitive foods from schools, and in recent years states have started to pass laws that restrict their sale, either banning them outright or setting limits on the amount of sugar, fat or calories they contain.

The study tracked weight changes for 6,300 students in 40 states between 2004 and 2007, following them from fifth to eighth grade. They used the results to compare weight change over time in states with no laws regulating such food against those in states with strong laws and those with weak laws.

Researchers used a legal database to analyze state laws. Strong laws were defined as those that set out detailed nutrition standards. Laws were weak if they merely offered recommendations about foods for sale, for example, saying they should be healthy but not providing specific guidelines.

The study stopped short of saying the stronger laws were directly responsible for the better outcomes. It concluded only that such outcomes tended to happen in states with stronger laws, but that the outcomes were not necessarily the result of those laws. However, researchers added that they controlled for a number of factors that would have influenced outcomes.

Still, the correlation was substantial, researchers said, suggesting that the laws might be a factor. Students who lived in states with strong laws throughout the entire three-year period gained an average of 0.44 fewer body mass index units, or roughly 2.25 fewer pounds for a 5-foot-tall child, than adolescents in states with no policies.

The study also found that obese fifth graders who lived in states with stronger laws were more likely to reach a healthy weight by the eighth grade than those living in states with no laws. Students exposed to weaker laws, however, had weight gains that were not different from those of students in states with no laws at all.

The authors argued that the study offered evidence that local policies could be effective tools.

“Competitive-food laws can have an effect on obesity rates if the laws are specific, required and consistent,” said Daniel Taber, a fellow at the Institute for Health Research and Policy at the University of Illinois at Chicago, who was one of the authors of the study.

Still, many states have no laws at all regulating the sale of such foods, and the group that helped finance the study, the Robert Wood Johnson Foundation, argued that the results made the case for a strong national standard for snacks and beverages in schools. The United States Department of Agriculture has been developing new standards for some time, but they have yet to emerge.

Some experts argue that a real reduction in the obesity rate will come only when many more local governments adopt tough policies to change the food environment. Still others say that school is such a small part of a child’s day that healthier options will make little difference when coupled with a home environment with a lot of unhealthy choices.

nytimes.com

ArturoRodriguez, MD
md@thebariatric.com
http://www.thebariatric.com
http://www.bandstersforum.com
Phone: 011-52-81-8378-3177
Twitter: @bandagastrica
Facebook: http://www.facebook.com/banda.gastrica

jueves, 7 de junio de 2012

New brain target for appetite control identified

Researchers at Columbia University Medical Center (CUMC) have identified a brain receptor that appears to play a central role in regulating appetite. The findings, published today in the online edition of Cell, could lead to new drugs for preventing or treating obesity.

"We've identified a receptor that is intimately involved in regulating food intake," said study leader Domenico Accili, MD, professor of Medicine at CUMC. "What is especially encouraging is that this receptor is belongs to a class of receptors that turn out to be good targets for drug development, making it a highly 'druggable' target. In fact, several existing medications already seem to interact with this receptor. So, it's possible that we could have new drugs for obesity sooner rather than later."

In their search for new targets for obesity therapies, scientists have focused on the hypothalamus, a tiny brain structure that regulates appetite. Numerous studies suggest that the regulatory mechanism is concentrated in neurons that express a neuropeptide, or brain modulator, called AgRP. But the specific factors that influence AgRP expression are not known.

The CUMC researchers found new clues to appetite control by tracing the actions of insulin and leptin. Both hormones are involved in maintaining the body's energy balance, and both are known to inhibit AgRP. "Surprisingly, blocking either the insulin or leptin signaling pathway has little effect on appetite," says Dr. Accili. "We hypothesized that both pathways have to be blocked simultaneously in order to influence feeding behavior."

To test their hypothesis, the researchers created a strain of mice whose AgRP neurons lack a protein that is integral to both insulin and leptin signaling. As the researchers hypothesized, removing this protein — Fox01 — had a profound effect on the animals' appetite. "Mice that lack Fox01 ate less and were leaner than normal mice," said lead author Hongxia Ren, PhD, associate research scientist in Medicine. "In addition, the Fox01-deficient mice had better glucose balance and leptin and insulin sensitivity — all signs of a healthier metabolism."

Since Fox01 is a poor drug target, the researchers searched for other ways to inhibit the action of this protein. Using gene-expression profiling, they found a gene that is highly expressed in mice with normal AgRP neurons but is effectively silenced in mice with Fox01-deficient neurons. That gene is Gpr17 (for G-protein coupled receptor 17), which produces a cell-surface receptor called Gpr17.

To confirm that the receptor is involved in appetite control, the researchers injected a Gpr17 activator into normal mice, and their appetite increased. Conversely, when the mice were given a Gpr17 inhibitor, their appetite decreased. Similar injections had no effect on Fox01-deficient mice.

According to Dr. Accili, there are several reasons why Gpr17, which is also found in humans, would be a good target for anti-obesity medications. Since Grp17 is part of the so-called G-protein-coupled receptor family, it is highly druggable. About a third of all existing drugs work through G-protein-coupled receptors. In addition, the receptor is abundant in AgRP neurons but not in other neurons, which should limit unwanted drug side effects.

http://medicalxpress.com

ArturoRodriguez, MD
md@thebariatric.com
http://www.thebariatric.com
http://www.bandstersforum.com
Phone: 011-52-81-8378-3177
Twitter: @bandagastrica
Facebook: http://www.facebook.com/banda.gastrica