Obesity as injurious to health as smoking/New discovery may help reduce obesity complications

06/01/2010
Obesity as injurious to health as smoking
Obesity is no less injurious to health than smoking, says a recent study. Researchers from Columbia University and The City College of New York calculate that the Quality-Adjusted Life Years (QALYs) lost due to obesity is now equal to, if not greater than, those lost due to smoking, both modifiable risk factors.



QALYs use preference-based measurements of Health-Related Quality of Life (HRQOL), which allow a person to state a relative preference for a given health outcome.

Since one person may value a particular outcome differently than another, these measures capture how each respondent views his or her own quality of life.

The 1993-2008 Behavioural Risk Factor Surveillance System (BRFSS), the largest ongoing state-based health survey of US adults, has conducted interviews of more than 3.5 million individuals.



This survey, conducted by Haomiao Jia and Erica I. Lubetkin, includes a set of questions that measures HRQOL, asking about recent poor health days and tracking overall physical and mental health of the population.

The authors analysed these data and converted the measures to QALYs lost due to smoking and obesity, said a Columbia release. From 1993 to 2008, when the proportion of smokers among US adults declined 18.5 percent, the proportion of obese people increased 85 percent. Smoking had a bigger impact on deaths while obesity had a bigger impact on illness. These findings are slated for publication in the February issue of the American Journal of Preventive Medicine.

Source: IANS

05/02/2010
New discovery may help reduce obesity complications
A research team led by an Indian-origin scientist has identified a potential target that may reduce complications of obesity.


According to Dr Suneil Koliwad, Gladstone Institute of Cardiovascular Disease, when individuals become obese from overeating, cells called adipocytes located in the fat tissue fill up with dietary fats and begin to die. Immune cells called macrophages move out of the blood stream and into this tissue, where they accumulate around dying adipocytes.

As the macrophages work to clear away the dead cells, they are exposed to large amounts of dietary fat that can result in unwanted consequences.

Exposure to saturated fats, in particular, causes the macrophages to enter an inflammatory state. In this state, the macrophages secrete cytokines, such as tumour necrosis factor (TNF) alpha, that encourage the development of insulin resistance, diabetes, and heart disease.

They hope that enhancing the capacity of macrophages to store dietary fats might alter this process.


The researchers focused their study on an enzyme called DGAT1, which makes triglycerides from dietary fats for storage as cellular energy reserves.

They examined a transgenic strain of mice (aP2-Dgat1) that make large amounts of DGAT1 in both adipocytes and macrophages.

On a high-fat diet, these mice became obese, but the macrophages in their fat tissue did not undergo inflammatory activation, and the mice were protected from developing systemic inflammation, insulin resistance, and fatty livers, all problems that were profound in the control mice.

"We found in experimental mice that a single enzyme, DGAT1, in macrophages is involved in many of the problems associated with obesity," said Koliwad.

"This is exciting because humans have this enzyme as well, providing the potential for a therapeutic target to examine," he added.

Source: Indian Express