Butter unlikely to harm health, but margarine could be deadly

a block of butter 
Butter is not likely to kill you 

Saturated fat found in butter, meat or cream is unlikely to kill you, but margarine just might, new research suggests.

Although traditionally dieticians have advised people to cut down on animal fats, the biggest ever study has shown that it does not increase the risk of stroke, heart disease or diabetes.

However trans-fats, found in processed foods like margarine raises the risk of death by 34 per cent.

 “For years everyone has been advised to cut out fats,” said study lead author Doctor Russell de Souza, an assistant professor in the Department of Clinical Epidemiology and Biostatistics, at McMaster University in Canada.

“Trans fats have no health benefits and pose a significant risk for heart disease, but the case for saturated fat is less clear.

“That said, we aren’t advocating an increase of the allowance for saturated fats in dietary guidelines, as we don’t see evidence that higher limits would be specifically beneficial to health.”

Saturated fats come mainly from animal products, such as butter, cows’ milk, meat, salmon and egg yolks, and some plant products such as chocolate and palm oils.

In contrast Trans unsaturated fats or trans fats – are mainly produced industrially from plant oils for use in margarine, snack foods and packaged baked goods.

Guidelines currently recommend that saturated fats are limited to less than 10 per cent, and trans fats to less than one per cent of energy, to reduce risk of heart disease and stroke.

However the new research which looked at 50 studies involving more than one million people found there was no evidence that saturated fat was bad for health.

It backs up recent research from the University of Cambridge that found saturated fat in dairy foods might protect against diabetes.

Cheese counter at a shop
Cheese and other saturated fats are unlikely to be harmful to health   

Last year leading heart scientist Dr James DiNicolantonio of Ithica College, New York, called for health guidelines on saturated fats to be changed in an article in the British Medical Journal.

The “vilification” of saturated fats dates back to the 1950s when research suggested a link between high dietary saturated fat intake and deaths from heart disease.

But the study author drew his conclusions on data from six countries, choosing to ignore the data from a further 16, which did not fit with his hypothesis, and which subsequent analysis of all 22 countries’ data.

Nevertheless the research stuck and since the 1970s most public health organisations have advised people to cut down on fat.

However the new research found no clear association between higher intake of saturated fats and death for any reason, coronary heart disease, cardiovascular disease, ischemic stroke or type 2 diabetes.

In contrast, consumption of industrial trans fats was associated with a 34 per cent increase in death, a 28 per cent increased risk of death from coronary heart disease, and a 21 per cent increase in the risk of cardiovascular disease.

Despite the research British health experts cautioned against changing to a diet which was high in saturated fat.

Prof Tom Sanders, Emeritus Professor of Nutrition and Dietetics, King’s College London, said: “It would be foolish to interpret these findings to suggest that it is OK to eat lots of fatty meat, lashings of cream and oodles of butter.

“Death rates from CVD have fallen in the UK by about 55 per cent since 1997 despite the rise in obesity for reasons that remain uncertain but this may in part be due to changes in the food supply particularly fewer trans and more omega-3 fatty acids.”


Victoria Taylor, Senior Dietitian, British Heart Foundation, added: “While saturated fats were not robustly associated with total or deaths from CHD, this does not mean we should all go back to eating butter – the studies that this review is based on can’t show cause and effect.

“Rather, it highlights how difficult it is to understand the true relationship between diet and our health.

“Diets high in saturated fat are linked to raised cholesterol levels, a risk factor for CHD. But when one nutrient is reduced it will be replaced by another and, depending on what this is, it can have positive or negative health consequences.”

Source: British Medical Journal.

Here’s Proof That Facebook Knows You Better Than Your Friends

Your operating system knows you so well, says science

Facebook, for one. Researchers at the University of Cambridge and Stanford University studied how Facebook Likes matched up with people’s own answers on personality tests, as well as those of their close family and friends. With enough Likes of objects, brands, people, music or books, the computer was better at predicting a person’s personality than most of the people closest to them—with the exception of spouses. (They still know us best, it seems.)

Wu Youyou, a PhD student in the Psychometrics Center at the University of Cambridge, and her colleagues had previously investigated how computer models could predict demographic and psychological traits in people. But inspired by the movie Her, they were curious about how the models would do in evaluating personality traits. They asked 86,220 people on Facebook to complete a 100-question personality survey that determined where they stood on the so-called Big Five traits: openness, conscientiousness, extraversion, agreeableness and neuroticism. They then analyzed their Facebook Likes to generate a model in which Likes were linked to the traits. Likers of meditation, TED talks and Salvador Dali, for example, tended to score higher on openness, while those who liked reality star Snookie, dancing and partying were more extraverted.

On average, people on Facebook had 227 Likes, and this was enough information for the computer to be a better predictor of personality than an average human judge (in other words, a friend), and almost as good as a spouse. The more Likes, the better the computer got. It only took 10 Likes for the computer to outperform a work colleague, for instance, 70 to do better than a friend, and 150 to outscore a family member.


“We know people are pretty good at predicting people’s personality traits, because it’s such an important thing in all of our interactions,” says Youyou. “But we were surprised by how computers were able to do better than most friends by using just a single kind of digital data such as Facebook Likes.”

Computers are such good predictors because they can take all the Likes at face value and treat them equally, says Youyou’s co-author Michal Kosinski from Stanford’s department of computer science. People tend to forget information if it’s not top of mind and tend to give more weight to memorable or recent events, potentially biasing our evaluations. But computers can treat each piece of information objectively.


Still, the computer strategy isn’t always entirely accurate. It can’t account for changes in people’s moods and behaviors and outlooks, and given that people are notoriously dynamic, that could be a problem. (People who scored higher on the extraversion scale, for example, did like meeting new people but also inexplicably Liked Tiffany & Co., while those who were more conscientious expressed preferences for mountain biking and motorcycles.) But Kosinski thinks that this kind of computer modeling could help processes like career planning and job recruitment. People just entering the job market could benefit from such personality profiling, which could better link them to the right industries and jobs in those sectors. A free spirit who likes to travel, explore and take risks, for example, likely wouldn’t be happy as an accountant, while an introverted person wouldn’t be ideal for a marketing or public relations position.

Kosinski also speculates that computers could streamline job recruitment. Many companies use personality questionnaires, especially when seeking high-level executives, but such questionnaires can be inaccurate and unreliable, as candidates are incentivized to give the answers they think the company wants to see. Computers might be able to come up with a more accurate personality profile than these questionnaires, if the Facebook data are any indication.

Kosinski recognizes that applying such models is tricky. “We have to be really cautious and make sure we don’t upset people and don’t do anything that breaches the trust between the applicant and the employer, if the employer starts testing without explicit consent,” he says. “But we certainly hope that these technologies can be used to better human life.”


Hybrid-electric airplane, the first ever to be able to recharge its batteries in flight, has been successfully tested in the UK.

Scientists from the University of Cambridge, in association with Boeing, have successfully tested the first aircraft to be powered by a parallel hybrid-electric propulsion system.


In this hybrid aircraft an electric motor and petrol engine work together to drive the propeller. The demonstrator aircraft uses up to 30% less fuel than a comparable plane with a petrol-only engine. The aircraft is also able to recharge its batteries in flight, the first time this has been achieved.

Dr Paul Robertson of Cambridge’s Department of Engineering, who led the project, said:

“Although hybrid cars have been available for more than a decade, what’s been holding back the development of hybrid or fully-electric aircraft until now is battery technology.

Until recently, they have been too heavy and didn’t have enough energy capacity. But with the advent of improved lithium-polymer batteries, similar to what you’d find in a laptop computer, hybrid aircraft – albeit at a small scale – are now starting to become viable.”

Watch the video.URL: https://www.youtube.com/watch?v=VAjbfevv9D0


Prosthetic bladder ‘controls urine’

A device that could one day restore bladder function to patients with a severed spinal cord has been devised by UK researchers and tested in animals.

Nerve damage can leave no sense of when the bladder is full or control over when the contents are released.

A study, published in Science Translational Medicine, showed a device to read the remaining nerves’ signals could be used to control the organ.

The charity Spinal Research said this was “impressive and important” work.

The loss of bladder, bowel and sexual function after spinal cord injury is often rated by patients as having the biggest impact on quality of life.

Blocked signals

When the spinal cord is injured, signals passing up from the bladder cannot tell the brain when the bladder is full. Going the other way, signals from the brain cannot tell the bladder when it is time to go to the toilet.

Researchers at the University of Cambridge have devised a solution that uses the nerves still around the bladder.

Electrodes wrapped around bundles of nerves can interpret signals that say the bladder is full.

Continue reading the main story

“Start Quote

The ultimate aim is to regenerate the spinal cord, what we’re doing is restoring some function.”

Dr Daniel Chew Cambridge University

Stimulating other sets of nerves can get the bladder to contract on demand and prevent it emptying of its own volition.

One of the researchers, Dr Daniel Chew, told the BBC the device had worked on rats.

“It is very effective. The feasibility studies are done, we’re now limited by miniaturisation of the technology,” he said.

While the components that fit inside a rat could be converted for human use, the rest of the technology to process the information recorded currently needs a 6ft (2m) stack of equipment.

This needs to shrunk down to a handheld device that can inform a patient when the bladder is full and a trigger button to contract the bladder.

Bladder x-ray

Dr Chew added: “This device is not the ultimate goal, the ultimate aim is to regenerate the spinal cord. What we’re doing is restoring some function, not curing spinal cord injury.”

Dr Mark Bacon, the director of research at the charity Spinal Research, told the BBC: “Bladder dysfunction blights the life of many with spinal cord injuries and has a very major impact on their health and quality of life.

“This is impressive and important work addressing one of the major limitations found with existing options for electrical stimulation to control bladder emptying, namely the need to surgically destroy the sensory fibres coming from the bladder.

“Sparing and making use of sensory signals from a filling bladder adds a welcome degree of sophistication to elective voiding whilst retaining other functions normally lost such as erectile function – a distressing consequence of current methods.”

The skinny on cocaine. Insights into eating behavior and body weight in cocaine-dependent men.


There is a general assumption that weight loss associated with cocaine use reflects its appetite suppressing properties. We sought to determine whether this was justified by characterizing, in detail, alterations in dietary food intake and body composition in actively using cocaine-dependent individuals. We conducted a cross-sectional case-control comparison of 65 male volunteers from the local community, half of whom satisfied the DSM-IV-TR criteria for cocaine dependence (n = 35) while the other half had no personal or family history of a psychiatric disorder, including substance abuse (n = 30). Assessments were made of eating behavior and dietary food intake, estimation of body composition, and measurement of plasma leptin. Although cocaine users reported significantly higher levels of dietary fat and carbohydrates as well as patterns of uncontrolled eating, their fat mass was significantly reduced compared with their non-drug using peers. Levels of leptin were associated with fat mass, and with the duration of stimulant use. Tobacco smoking status or concomitant use of medication did not affect the significance of the results. Weight changes in cocaine users reflect fundamental perturbations in fat regulation. These are likely to be overlooked in clinical practice but may produce significant health problems when cocaine use is discontinued during recovery.



Children of obese mothers ‘have higher heart risk’.

Children born to obese and overweight mothers are more likely to die early of heart disease, a study has found.

Scottish research showed a 35% higher risk of dying before the age of 55 in adults whose mothers were obese in pregnancy.

It is not known how much of the link is down to genetics, influences in the womb or later lifestyle.

But the authors say their findings, in the British Medical Journal, are of “major public health concern”.

One woman in five in the UK is obese at their antenatal booking appointment.

Continue reading the main story

“Start Quote

This study emphasises the need for everyone, but in particular pregnant women, to try to eat healthily and be active”

Doireann MaddockBritish Heart Foundation

Premature deaths

The analysis included 28,540 women whose weight was recorded at their first antenatal check-up and their 37,709 children now aged between 34 and 61.

One in five mothers was classed as overweight with a body mass index (BMI) between 25 and 29.9 and 4% were obese with a BMI above 30.

There were 6,551 premature deaths from any cause and heart disease was the leading contributor.

The risk of premature death was 35% higher among people born to obese mothers compared with those whose mothers had had normal weight in pregnancy. This was after adjusting the results for factors such as the mother’s age at delivery, social class and infant birthweight.

The results also revealed that children born to obese mothers went on to be at 42% increased risk of being treated in hospital for a heart attack, stroke or angina.

Appetite control

Study leader Prof Rebecca Reynolds, of the University of Edinburgh, said the results highlighted the importance of current advice to maintain a healthy weight, eat sensibly and keep active during pregnancy.

She added that more work was needed to unpick the reasons for the increased risk and to look at the impact of weight gain over pregnancy.

“It would be nice to know how much of this risk is modifiable.”

Previous research has shown a link between obesity in pregnancy and changes in appetite control and metabolism in children.

Prof Sir Stephen O’Rahilly, of the University of Cambridge, warned that obesity runs in families.

“Obese people are at higher risk of heart disease, so it is very likely that the people in this study whose mothers were obese were fatter than those whose mothers were lean.”

‘Eat healthily’

The researchers did not measure or account for this.

The Royal College of Midwives said it was important for women to start their pregnancy at a normal weight.

But Louise Silverton, RCM director for midwifery, said not all pregnancies are planned and midwives work hard to support women avoid excess weight gain and lose weight sensibly after birth.

Drastic dieting is not recommended.

Doireann Maddock, senior cardiac nurse at the British Heart Foundation, which part-funded the study, said: “This study emphasises the need for everyone, but in particular pregnant women, to try to eat healthily and be active.”

Source: BBC


Genetic advance in Down’s syndrom.

US scientists say they have moved a step closer to being able to treat disorders caused by an extra chromosome.

They have “switched off” the chromosome that causes the symptoms of Down’s syndrome in human cells in the lab.

The research, published in Nature, could one day lead to new medical treatments for the condition.

Future work may be of real benefit to people with Down’s syndrome, said the UK Down’s Syndrome Association.

Humans are born with 23 pairs of chromosomes, including two sex chromosomes, making a total of 46 in each cell.

People with Down’s syndrome have three – rather than two – copies of chromosome 21.


 “Start Quote

This is an exciting breakthrough, but this process is still at a very early [cellular] stage and we are nowhere near seeing this procedure being used in the treatment of Down’s syndrome in people”

Dr Lucy RaymondUniversity of Cambridge

This causes symptoms such as learning disabilities and early-onset Alzheimer’s disease, as well as a greater risk of blood disorders and heart defects.

Gene therapy, which uses genes to treat illnesses, has been attempted for problems caused by a single defective gene. But until now, the idea of being able to silence the effects of a whole chromosome had appeared beyond the realms of possibility, even in the lab.

Now scientists at the University of Massachusetts Medical School have shown that, in theory, this might be possible but would take decades of research.

A team led by Dr Jeanne Lawrence inserted a gene called XIST into the stem cells of a person with Down’s syndrome grown in the lab.

‘Exciting research’

The gene plays a role in normal cell development by switching off one of the two X chromosomes present in female embryos, ensuring daughters avoid a double dose of X chromosome genes.

The experiments showed that the gene was able to silence the extra copy of chromosome 21, helping correct unusual patterns of growth in the cells.

Dr Lawrence told BBC News: “The research means that we have a new way – right away – to study the cellular basis for Down’s syndrome, that could help identify drugs for Down’s syndrome.

“At the same time we have made it conceivable – not necessarily possible or effective, that still needs to be proven – but conceivable that you could use just a single gene to correct the over-expression of the whole chromosome. So it makes genetic therapy for Down’s syndrome more conceivable where it really wasn’t before.”

Commenting on the study, Carol Boys, chief executive of the Down’s Syndrome Association, said it was exciting new research from a very well-respected team.

“The findings could have serious implications for future work that may be of real benefit to people with Down’s syndrome,” she said.

“We are a very long way from understanding how these findings might translate into clinical applications but it could be that they will be of great assistance in the search for conventional treatments for some of the health conditions that affect people with Down’s syndrome.”

Dr Lucy Raymond, from the department of medical genetics at the University of Cambridge, said the group had demonstrated an important proof of concept.

“This is an exciting breakthrough, but this process is still at a very early [cellular] stage and we are nowhere near seeing this procedure being used in the treatment of Down’s syndrome in people.”

Source: BBC

Turning Genes Up, Not On: A New View of the Myc Protein.

Acting as an amplifier, the Myc protein may increase the expression of all active genes in a cell.

One of the best studied proteins in cancer research is also one of the most mysterious.

Myc helps control genes involved in cell growth and is associated with many cancers. But, after thousands of studies, researchers still do not know important details about how Myc operates in normal cells and in cancer cells.

Two new studies, however, cast this large body of work in a new light, providing some answers and raising new questions. Myc, the studies found, apparently boosts the expression of nearly all active genes in a cell, rather than activating specific genes.

“Whatever a cell is doing, it will do that more intensely under the influence of Myc,” said Dr. David Levens of NCI‘s Center for Cancer Research, who co-led one study with Dr. Keji Zhao of the National Heart, Lung, and Blood Institute. Both studies appeared in Cell last week.

A New Perspective

Dr. Levens and his colleagues tracked the activity of Myc in white blood cells using molecular “tags.” This approach revealed that Myc does not preferentially interact with any specific gene; instead, the protein is present at nearly every gene that is already expressed.

Using different methods and types of cells, Dr. Richard Young of the Whitehead Institute for Biomedical Research and his colleagues reached a similar conclusion in a second study. “We came to realize that the primary role of Myc is to go to all the genes that are active in a cell and act like a rheostat, turning up their expression,” said Dr. Young.

These are very well done studies, noted Dr. Chi Van Dang, director of the Abramson Cancer Center at the University of Pennsylvania and a Myc researcher who was not involved in the work. “They provide an additional view of how a relatively powerful cancer gene works when it is deregulated.”

We came to realize that the primary role of Myc is to go to all the genes that are active in a cell and act like a rheostat, turning up their expression.

—Dr. Richard Young

But the model, he added, does not account for some well-documented observations about Myc.

“We know, for instance, that Myc inhibits the differentiation of cells,” Dr. Dang said. “So that means that instead of only amplifying the expression of active genes, the protein has to inhibit something in cells. These studies acknowledge that not all active genes are turned up; in fact, up to one-third are repressed.”

Another important question, Dr. Dang noted, is how high levels of Myc might contribute to cancer. “If you crank up Myc to very high levels and it still behaves as an amplifier, does that cause the expression of genes to occur in an imbalanced way and alter  [RNA in a way] that could lead to cancer?” he asked.

These and similar questions could keep researchers busy for a long time, noted the authors of an accompanying editorial. These “seminal” studies provide a first “glimpse of a coherent and holistic view of Myc,” wrote Dr. Gerard Evan and two colleagues at the University of Cambridge in the United Kingdom in the editorial.

This view of Myc suggests there will never be a single transcriptional signature—a set of genes consistently activated by the protein. This is because the activity of Myc depends entirely on the type of cell and which state the cell is in when Myc is activated, according to the new model.

Implications for the Future

If the new results are confirmed, they could have implications for cancer researchers. Drug developers might want to disrupt the cellular machinery involved in the amplification effect of Myc rather than focusing on specific genes, noted Dr. Young.

“If Myc is amplifying all of the active genes in a cell, the idea of targeting just some of those genes appears unlikely to succeed,” he said. “Going after Myc may be more fruitful.” He predicted that the new results could “reinvigorate efforts to drug Myc itself,” though Myc, like other transcription factors, has proven to be an elusive target.

Researchers have been looking for a pathway through which Myc operates for many years. “Our results suggest that Myc will cooperate with any oncogenic process,” said Dr. Levens.

Before launching this study, Dr. Levens wondered whether he could add anything new to the large scientific literature on Myc. He now sees the new model as bringing together and explaining many puzzling and often contradictory observations about the biology of Myc.

“Our study is more integrative than it is novel,” he said. “It’s hard to say something really new about this protein.”

Source: NCI