People concerned about heart disease and diabetes should simply take their height and waist measurements to figure out their risk, say British researchers.
Ideally, all should aim to keep their waist measurement less than half that of their height, found the scientists.

That means a 6ft (72 inch) tall man should aim to keep his waist less than 36 inches, while a 5ft 4in (64 inch) woman should keep hers under 32 inches.

They have found that the easy-to-calculate ratio between the two is a better predictor of risk than the most widely measure of obesity, called body mass index (BMI).

The team, who analysed the health of some 300,000 people, found this ratio was a better predictor of high blood pressure, diabetes and cardiovascular events like heart attacks and strokes than body mass index.

While BMI is used almost universally in the medical profession, most people are unfamiliar with it, partially because it is not a straightforward calculation.
BMI is calculated by taking one's mass in kilograms and dividing it by the square of one's height in metres.

Dr Margaret Ashwell, former science director of the British Nutrition Foundation, and now an independent consultant, spearheaded the study. She is presenting the research at the European Congress on Obesity in Lyon, France, on Saturday.

"Keeping your waist circumference to less than half your height can help increase life expectancy for every person in the world," she said.

The ratio was also better than just taking a waist measurement, she added, as it took into account differing height between individuals and ethnic groups.

While BMI was a useful indicator, it failed to take into account the distribution of fat throughout the body.

Abdominal fat, around the heart, liver and kidneys, has been found to be worse than that on the bottom and hips, in terms of heart disease and diabetes.

Dr Ashwell suggested the waist-to-height ratio should be considered as a screening tool.

Children who get up at night and sneak into bed with their parents may be healthier as they are less likely to become overweight, a new study has revealed.

Disturbed sleep is associated with obesity because it interferes with hunger hormones but research conducted in Denmark suggested the opposite may be true for children.

A study of 497 children between the ages of two and six found children who always stayed in their own beds were three times more likely to be overweight than children who got into bed with their parents every night, the Telegraph reported.

Dr Nanna Olsen, at the Research Unit for Dietary Studies, Institute of Preventive Medicine, at Copenhagen University Hospitals said it might be because these children have a greater sense of security by cuddling up to their parents.

The findings were presented at the European Congress on Obesity in Lyon, France.

"The results may suggest that elements of parental social support or other types of positive psychosocial responses if being allowed to enter parents' bed during night may protect against overweight, whereas types of negative psychosocial responses such as feelings of rejection when not being allowed to enter parents' bed may lead to overweight," Dr Olsen said.

Lupus patients may develop more severe symptoms if their vitamin D levels are low, says an Australian study.
Known as systemic lupus erythematosus (SLE), lupus is an autoimmune disease, which prompts an attack on tissues of the body by its own immune system, affecting more than five million people worldwide. It can also lead to kidney disease.
Although its cause is unknown, the results can be disastrous as the body stops producing normal antibodies, which becomes instrumental in an attack on healthy tissues.
Eric Morand, professor and head of the Monash lupus clinic, who led the study, said although avoiding the sun is important for lupus patients, as sunlight can aggravate the condition, but this can also lead to vitamin D deficiency and contribute to its severity, according to a Monash statement.
"Instances of vitamin D deficiency can be seen in cultural groups where clothing covers the body, in people with dark skin tone who have lower absorption, and those who practice sun avoidance" Morand said.
"Although it's too soon to draw conclusions about the long-term safety and effectiveness of vitamin D supplements in lupus, a clinical trial is the next step proving that supplementing vitamin D makes lupus better," added Morand.

The tantalising prospect of treating a range of brain diseases, such as Alzheimer's and Parkinson's, all with the same drug, has been raised by UK researchers.

In a study, published in Nature, they prevented brain cells dying in mice with prion disease.

It is hoped the same method for preventing brain cell death could apply in other diseases.

The findings are at an early stage, but have been heralded as "fascinating".

Many neuro-degenerative diseases result in the build-up of proteins which are not put together correctly - known as misfolded proteins. This happens in Alzheimer's, Parkinson's and Huntington's as well as in prion diseases, such as the human form of mad cow disease.
Turn off

Researchers at the University of Leicester uncovered how the build-up of proteins in mice with prion disease resulted in brain cells dying.

They showed that as misfolded protein levels rise in the brain, cells respond by trying to shut down the production of all new proteins.

It is the same trick cells use when infected with a virus. Stopping production of proteins stops the virus spreading. However, shutting down the factory for a long period of time ends up killing the brain cells as they do not produce the proteins they actually need to function.

The team at the Medical Research Council laboratory in Leicester then tried to manipulate the switch which turned the protein factory off. When they prevented cells from shutting down, they prevented the brain dying. The mice then lived significantly longer.

Each neuro-degenerative disease results in a unique set of misfolded proteins being produced, which are then thought to lead to brain cells dying.

Prof Giovanna Mallucci told the BBC: "The novelty here is we're just targeting the protein shut-down, we're ignoring the prion protein and that's what makes it potentially relevant across the board."

The idea, which has not yet been tested, is that if preventing the shut down protects the brain in prion disease - it might work in all diseases that have misfolded proteins.

Prof Mallucci added: "What it gives you is an appealing concept that one pathway and therefore one treatment could have benefits across a range of disorders.

"But the idea is in its early stages. We would really need to confirm this concept in other diseases."
'Fascinating'

The study has been broadly welcomed by other scientists although many point out that the research is in its infancy.

Professor of Molecular Neurobiology at King's College London, Roger Morris, said it was a "breakthrough in understanding what kills neurons".

He added: "There are good reasons for believing this response, identified with prion disease, applies also to Alzheimer's and other neuro-degenerative diseases.

"And because it is such a general response, we already have some drugs that inhibit this response."

Prof Andy Randall, from the University of Bristol, said: "This is a fascinating piece of work.

"It will be interesting to see if similar processes occur in some of the common diseases with such deposits, for example Alzheimer's and Parkinson's disease.

"Furthermore, if this is the case, can modulating this same pathway be a route to new therapeutic approaches in these more prevalent conditions that afflict many millions of sufferers around the world? Ultimately only more research will tell us this."

Dr Eric Karran, the director of research at Alzheimer's Research UK, said: "The findings present the appealing concept that one treatment could have benefits for a range of different diseases; however the idea is in its early stages.

"The research focuses on the effects of the prion protein and we would need to see the same results confirmed in Alzheimer's and Parkinson's to really strengthen the evidence."

British scientists claim to be for the first time growing human body parts at a laboratory at the University College London, which they say could soon make organ donation a thing of the past.

A team, led by Prof Alexander Seifalian of the varsity's Department of Nanotechnology and Regenerative Medicine, claims it's actually focussing on growing replacement organs and body parts to order, using a patient's own cells.

"This is a nose we're growing for a patient next month. It's a world first. Nobody has ever grown a nose before," Prof Seifalian was quoted by the 'Daily Mail' as saying.

In fact, the scientists say that when the the nose is transferred to the patient, it doesn't go directly onto the face but will be placed inside a balloon inserted beneath the skin on their arm.

After four weeks, during which time skin and blood vessels can grow, the nose can be monitored, then it can be transplanted to the face, they say.

Added Adelola Oseni, a team member: "Other groups have tried to tackle nose replacement with implants but we've found they don't last. They migrate, the shape of the nose changes. But our one will hold itself completely, as it's an entire nose shape made out of polymer."

Looking like very thin Latex rubber, the polymer is made up of billions of molecules, each measuring just over one nanometre (a billionth of a metre), or 40,000 times smaller than the width of a human hair. Working at molecular level allows the material itself to be intricately detailed.

"Inside this nanomaterial are thousands of small holes. Tissue grows into these and becomes part of it. It becomes the same as a nose and will even feel like one," Seifalian said.

Other parts in the making include the trachea -- windpipe -- to be used in the world's first synthetic organ transplant, and an artery, say the scientists.

"We are the first in the world working on this. We can make a metre every 20 seconds if we need to. However, the full success of these implants needs to be tested with a larger number of patients in clinical trials," said Seifalian.