Nov. 3 (Bloomberg) -- More American children are taking pills for diabetes, high blood pressure and cholesterol than ever before, reflecting a rise in chronic diseases related to obesity, a study found.

Use of drugs for type-2 diabetes, the form of the disease commonly seen in overweight adults, doubled in children ages 5 to 19 and cholesterol-lowering medications rose by 15 percent between 2002 and 2005, according to the report published today by the journal of the American Academy of Pediatrics.

A surge in obesity among children puts them at risk for diabetes, hypertension and other conditions, said researchers from Express Scripts Inc., the Pediatric Research Institute at St. Louis University and the Kansas Health Institute in Topeka who worked on the study. The report supports earlier data published in June by Harvard University researchers that found a fourfold increase in childhood obesity over three decades.

``Ten or 15 years ago we weren't even discussing these conditions, which were mainly in adults,'' said Emily Cox, a senior director of research at St. Louis-based Express Scripts, which provided data for the research. ``Now we are seeing a growing number of children being treated for chronic conditions that they are going to take into adulthood.''

The study tracked the prescription drug records collected by Express Scripts, which manages pharmacy benefits, for about 3 million children a year. Use of drugs for asthma, also linked to obesity, rose 47 percent and high blood pressure medicines rose 2 percent, the report said.

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Speed of eating 'key to obesity'

Wolfing down meals may be enough to nearly double a person's risk of being overweight, Japanese research suggests.

Osaka University scientists looked at the eating habits of 3,000 people and reported their findings in the British Medical Journal.

Problems in signalling systems which tell the body when to stop eating may be partly responsible, said a UK nutrition expert.

He said deliberately slowing down at mealtimes might impact on weight.

The latest study looked at the relationship between eating speed, feelings of "fullness" and being overweight.

Just under half of the 3,000 volunteers told researchers they tended to eat quickly.

Compared with those who did not eat quickly, fast-eating men were 84% more likely to be overweight, and women were just over twice as likely.

Those, who, in addition to wolfing down their meals, tended to eat until they felt full, were more than three times more likely to be overweight.

Stomach signals

Professor Ian McDonald, from the University of Nottingham, said that there were a number of reasons why eating fast could be bad for your weight.

He said it could interfere with a signalling system which tells your brain to stop eating because your stomach is swelling up.

He said: "If you eat quickly you basically fill your stomach before your gastric feedback has a chance to start developing - you can overfill the thing."

He said that rushing meals was a behaviour that might have been learned in infancy, and could be reversed, although this might not be easy.

"The old wives' tale about chewing everything 20 times might be true - if you did take a bit more time eating, it could have an impact."

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Waste From Gut Bacteria Helps Host Control Weight, Researchers Report

ScienceDaily (Oct. 19, 2008) — A single molecule in the intestinal wall, activated by the waste products from gut bacteria, plays a large role in controlling whether the host animals are lean or fatty, a research team, including scientists from UT Southwestern Medical Center, has found in a mouse study.

When activated, the molecule slows the movement of food through the intestine, allowing the animal to absorb more nutrients and thus gain weight. Without this signal, the animals weigh less.

The study shows that the host can use bacterial byproducts not only as a source of nutrients, but also as chemical signals to regulate body functions. It also points the way to a potential method of controlling weight, the researchers said.

"It's quite possible that blocking this receptor molecule in the intestine might fight a certain kind of obesity by blocking absorption of energy from the gut," said Dr. Masashi Yanagisawa, professor of molecular genetics at UT Southwestern and a senior co-author of the study, which appears online in Proceedings of the National Academy of Sciences.

Humans, like other animals, have a large and varied population of beneficial bacteria that live in the intestines. The bacteria break up large molecules that the host cannot digest. The host in turn absorbs many of the resulting small molecules for energy and nutrients.

"The number of bacteria in our gut far exceeds the total number of cells in our bodies," said Dr. Yanagisawa.

"It's truly a mutually beneficial relationship. We provide the bacteria with food, and in return they supply energy and nutrients," he explained.

Using mice, the researchers focused on two species of bacteria that break up dietary fibers from food into small molecules called short-chain fatty acids. Dr. Yanagisawa's team previously had found that short-chain fatty acids bind to and activate a receptor molecule in the gut wall called Gpr41, although little was known about the physiological outcome of Gpr41 activation.

The researchers disrupted communication between the bacteria and the hosts in two ways: raising normal mice under germ-free conditions so they lacked the bacteria, and genetically engineering other mice to lack Gpr41 so they were unable to respond to the bacteria.

In both cases, the mice weighed less and had a leaner build than their normal counterparts even though they all ate the same amount.

The researchers also found that in mice without Gpr41, the intestines passed food more quickly. They hypothesized that one action of Gpr41 is to slow down the motion that propels food forward, so that more nutrients can be absorbed. Thus, if the receptor cannot be activated, food is expelled more quickly, and the animal gets less energy from it.

Because mice totally lacking Gpr41 were still healthy and had intestinal function, the receptor may be a likely target for drugs that can slow, but not stop, energy intake, Dr. Yanagisawa said.

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http://www.sciencedaily.com/releases/2008/10/081018093223.htm