Showing posts with label The Lancet. Show all posts
Showing posts with label The Lancet. Show all posts

Wednesday, July 31, 2013

Childhood Obesity: How many extra calories does it take?

Overweight kids may be consuming far more calories than their doctors or parents realize, a new study suggests.

The study, which is published in the July 30 online issue of The Lancet Diabetes & Endocrinology, updates the mathematical model doctors use to calculate the daily calorie needs of children and adolescents.

The new model tries to more accurately estimate the energy requirements for growing girls and boys.

It also accounts for kids' higher metabolisms, relative to adults, and takes into account the drop in physical activity that happens with age as frenetic toddlers turn into sluggish teens.

Lastly, study authors factor in the increased energy required to maintain a bigger body size with age.

In sum, the model predicts that it takes far more calories for children to gain weight than experts had realized.

For example, the old model estimates that for a girl who's a normal weight at age 5 to become 22 pounds overweight by the time she's 10, she'd need to eat around 40 extra calories a day—the equivalent of the calories in a small apple.

The new model predicts that she'd actually need to eat far more than that—about 400 extra calories a day, or the calories in a medium serving of fast-food french fries—to get the same result.

That's one case, but the number of calories it takes to gain weight is slightly different for boys and girls at every age.

"It's a bit of a moving target," admitted study author Kevin Hall, a senior investigator at the U.S. National Institute of Diabetes and Digestive and Kidney Diseases.

"The point of these examples is that the excess calorie consumption is much larger than most folks would have suggested in the past."

Using historical data collected by the U.S. Centers for Disease Control and Prevention, Hall and his co-authors calculated that children today are an average of 13 pounds heavier than kids were in the late 1970s, before the start of the obesity epidemic.

To gain those extra pounds, kids have consumed about 200 more calories a day. At different ages, and depending on the amount of weight a child has gained, the differences can be even more stark.

For example, the model estimates than an 11-year-old boy who is about 18 pounds overweight has eaten roughly 320 more calories a day than his healthy-weight peers.

Meanwhile, a girl who is the same age and also 18 pounds overweight has taken in an extra 301 daily calories.

Hall said the new numbers give parents and doctors a road map for "how we got here" with overweight and obese kids, but they aren't exactly the way back to a normal weight.

Kids who cut calories by the amount their currently overeating may stop gaining, for example, but they'd likely need to cut even more to shed their extra pounds.

Dr. David Katz, director of the Yale Prevention Research Center, praised the new model, and said it clarifies energy intake levels needed to achieve public health goals.

"Importantly, given the rather large calorie excesses fueling childhood obesity, this model is a rebuttal to the food industry arguments that exercise alone can be the answer," said Katz, who is also editor of the journal Childhood Obesity.

"For our kids to achieve healthy weight, control of calories in, not just calories out, will have to be part of the formula," said Katz, who was not involved in the research. But there's some good news in the new numbers, too.

As doctors and parents have long suspected, some kids appear to be able to outgrow their extra pounds when they shoot up in height during puberty, though that feat may be easier for boys than girls, because boys gain more calorie-burning muscle during puberty than girls.

"If you haven't reached puberty and haven't yet reached that growth spurt, that might be the ideal time to institute a weight management intervention to harness the power of the growth to decrease fat mass and increase fat-free mass," said study author Hall.

Sunday, March 31, 2013

Cystic fibrosis bug 'can spread between patients'

A dangerous infection which is becoming more common in people with cystic fibrosis can spread between patients, UK researchers say in The Lancet.

Doctors previously thought the Mycobacterium abscessus bacteria could only be caught from water and soil.

But hospitals around the world may now have to change the way patients are treated, the study says.

Around 3-10% of cystic fibrosis patients in Europe and the US are infected with the hard-to-treat bug.

There are around 9,000 people with cystic fibrosis in the UK although around one-in-25 people carries the faulty gene which causes the condition.

It affects the internal organs, especially the lungs and digestive system, by clogging them with thick sticky mucus which makes it hard to breathe and digest food.

Researchers writing in The Lancet do not know exactly why Mycobacterium abscessus - which is distantly related to the bacteria that causes tuberculosis - is more likely to infect people with cystic fibrosis but it could be related to problems with the immune system.

It causes lung damage, and can be incredibly hard to treat with infected patients needing months of treatment with toxic drugs.

Mycobacterium abscessus bacteria
Although the infection has been on the rise over the past decade, doctors always believed it could not spread between humans.

But by looking at DNA from almost 170 samples of the bacterium, and using that to create a family tree, researchers found that it can indeed spread from person to person.

Infection control
Study leader Dr Andres Floto, research director of the Cystic Fibrosis Unit at Papworth Hospital in Cambridge, UK and principal investigator at the Cambridge Institute for Medical Research, said the results had prompted them to completely rethink their infection control, despite already having strict policies in place.
He explained they already treated all in-patients in individual rooms without exposing them to other patients and out-patient clinics were set up so individuals did not have direct contact with each other.

"But despite that we were seeing transmission events in hospital which tells us that transmission is likely to be indirect," Dr Floto said.

Dr Andres Floto
"We are doing more research into that but we believe it gets aerosolised, for example, when people cough and because this bacteria is tough it hangs around in the air."

All inpatients at Papworth are now treated in negative pressure rooms to prevent the spread of airborne bugs and those with the infection are cared for away from the cystic fibrosis unit.

"And in outpatients for people with this bug, we use clinic rooms only once and then not for other patients until the next day when it has been deep cleaned."

Dr Floto said his team had already been in touch with hospitals in the UK and abroad to inform them of their findings and encourage them to change their practices and prevent the infection spreading as much as possible.

"Our results will help to protect patients from this serious infection."

Co-author Professor Julian Parkhill, head of pathogen genomics at the Wellcome Trust Sanger Institute, said: "By sequencing the complete genomes of bacteria we can accurately describe where they have emerged from and how they pass from person to person.

"This new information has led to rapid changes in how people with cystic fibrosis are cared for in hospital to protect them from this emerging threat."

Jo Osmond, director of Clinical Care and Commissioning at the Cystic Fibrosis Trust (UK), said: "We will work closely with clinicians and the NHS to ensure appropriate measures are in place to deal with this issue.

"It is reassuring that this issue has been picked up early and that we are working positively to put in place measures to ensure cross-infection risks are reduced to a minimum.

"People with cystic fibrosis who have concerns about this issue should speak to their clinician."

Sunday, July 15, 2012

Developmental Dyslexia - The Lancet

Dyslexia is a neuro-developmental disorder that is characterised by slow and inaccurate word recognition.

Dyslexia has been reported in every culture studied, and mounting evidence draws attention to cross-linguistic similarity in its neurobiological and neurocognitive bases.

Much progress has been made across research specialties spanning the behavioural, neuropsychological, neurobiological, and causal levels of analysis in the past 5 years.

From a neuropsychological perspective, the phonological theory remains the most compelling, although phonological problems also interact with other cognitive risk factors.

Work confirms that, neurobiologically, dyslexia is characterised by dysfunction of the normal left hemisphere language network and also implicates abnormal white matter development.

Studies accounting for reading experience demonstrate that many recorded neural differences show causes rather than effects of dyslexia. Six predisposing candidate genes have been identified, and evidence shows gene by environment interaction.