New aspirin risk to health say US researchers

About 1 in 4 adults may carry a gene, which when combined with taking aspirin may make them twice as likely to suffer a heart attack, according to US researchers.

Previous studies of aspirin, which is recommended to cut the risk of heart attack and stroke, have linked it to life-threatening internal bleeding. Others have cast doubt on whether healthy people should take aspirin as the risks could outweigh the benefits.

They have also found some do not appear to benefit from it, and while the risk of non-fatal heart attacks is reduced by 20 per cent, deaths from strokes and heart failure are not cut.

Dr Kathryn Hall, the report’s lead author, at Harvard Medical School said: ‘We need to look at ourselves as individuals, a certain constellation of genes, and to take that into consideration. If the research is validated in further study, it would be the logical next step to test everyone for these genes before giving them aspirin.’

In the UK last year30.9 million NHS prescriptions for aspirin were issued for those at risk of heart attacks and strokes.

The new US study involved examined 40,000 women over a ten-year period. Of those, 23 per cent carried a variation of the catechol-O-methyltransferase gene, which helps the body process stress hormones, linked to heart problems and stroke. And it was found that those who had the gene were naturally protected and were 34 per cent less likely to have heart attacks.

However, taking aspirin removed this protection and increased their risk of heart problems by 85 per cent – and, in some cases, by as much as three times.In contrast, another group who carried a different variation of the same gene were more likely to have a heart attack than those who did not carry the gene, but aspirin protected against this, cutting the number of heart attacks by 47 per cent.

The results raise the question whether aspirin should be given to all patients with risk factors for heart disease. And that doctors would be using modern genomics and genetics to identify those individuals for whom aspirin has the greatest benefit and the lowest risk of adverse effects. Tests for the genes are not currently available on the NHS.

Anyone with medical concerns should speak with their doctor rather than stopping to take their medication.

Gene cocktail creates beating heart cells

Los Angeles: A new technique, in which a gene cocktail, has been successfully to create beating heart cells, has been used on mice.

The new technique could also cut the need for transplants in people whose ailing hearts cannot mend themselves.

heart.bmpIf developed for use in human patients the new treatment could change the lives of many thousands of sick people.

The experiments, which were carried out on mice, are still in the early stages, but they offer fresh hope for the future.

They centre on the large muscular cells that allow the heart to beat and go about its vital work of pumping blood. Normally, the body has little or no way of replacing any that die or are damaged.

But researchers at the California’s Gladstone Institute of Cardiovascular Disease, have devised a cocktail of genes that trick other heart cells called fibroblasts into transforming into beating muscle cells called cardiomyocytes.

The journal Cell reports how fibroblasts treated with the cocktail in the lab turned into beating muscle cells after being transplanted into a mouse.

Masaki Ieda of the Gladstone Institute said: “Scientists have tried for 20 years to convert non-muscle cells into heart muscle. It turns out we just needed the right combination of genes in the right dose.”

Deepak Srivastava, senior study author from Gladstone, said: “The ability to re-programme fibroblasts into cardiomyocytes has many therapeutic implications.

“Half of the cells in the heart are fibroblasts, so the ability to call upon this reservoir of cells already in the organ to become beating heart cells has tremendous promise for cardiac regeneration.”

In time a drug that works in the same way as the cocktail of genes could be developed. Injected into damaged hearts, it would drive the growth of new muscle.

“That’s our long-term goal,” said Srivastava.

Every two minutes, someone, somewhere has a heart attack. Many go on to develop heart failure, in which the weakened heart gradually loses its ability to pump blood.

Up to 40 per cent of these die within a year of diagnosis – giving heart failure a worse survival rate than many cancers.

Other organs could be patched up in a similar way, the researchers believe.


Scientists identify “fat” gene

London: Scientists have identified an “obesity gene” which predisposes many people to desire fattening foods.

The obesity gene variant is present in 63% of the population, has been
shown to cause people to eat 100 extra calories, on average, at a single

A team at the University of Dundee conducted an eating test with 100
schoolchildren aged between 4 and 10 and found that the children with
the common variant on the `obesity gene’ FTO consumed the extra 100
calories. These children chose to eat food types that contained more
sugar and fats as opposed to more healthy options.

Results of the study are published in this week’s edition of the New England Journal of Medicine.

The research was led by Professor Colin Palmer at the University of Dundee, and included colleagues who are nowbased at the Universities of St Andrews, Brighton and Glasgow Caledonian.

The study measured the metabolism, adiposity (fat distribution),exercise and eating behaviours in the schoolchildren. They were given a test meal at school, which included a mix of options: ham, cheese, crackers, crisps, raisins, grapes, cucumber, carrot, chocolate buttons,water, orange juice and bread rolls. Investigators recorded the foodthat remained on each child’s tray. Importantly, each child wastested with this meal on three occasions to increase the reliability of the results.

Researchers found the gene had no impact on metabolic rates or measures
of physical activity. There was also no evidence that individuals carrying the obesity-related variant had any problem with satiety (knowing when to stop increased calorific intake from a greater consumption of the more fattening foods as opposed to the more healthy options.

“This work demonstrates that this gene does not lead to obesity without overeating and suggests that obesity linked to this gene could be modulated by careful dietary control,” said Professor Palmer, Chair of Pharmacogenomics in the Biomedical Research Institute at theUniversity of Dundee..

“What it effectively shows is that the people with the relevant variants on the gene have a trait which may lead them to eat more unhealthy, fattening foods. I would stress that this is a trait, and not an absolute occurrence.

“The findings do not change the dietary and lifestyle advice to people, which would be to eat relatively healthily and take regular exercise. Doing this will still have a positive effect whether you carry this gene variant or not.

“But these findings do also reinforce the hypothesis that the increase in obesity seen in children over recent years may be largely attributable to the widespread availability of inexpensive and highly energy dense foods, which may be more attractive to the large proportion of the population who carry this genetic variant,” said Professor Palmer.

The results in the newly-published study are also consistent with studies in animals that have shown that feeding or fasting turns the expression of this gene on and off in the regions of the brain that are known to control eating behaviours.

Professor Palmer was part of the large group of scientists from around the UK that discovered the obesity gene, FTO, in 2007. They found that individuals carrying one copy of the variant (49% of the population) have an approximately 30% increased risk of obesity and individuals carrying two copies of the variant (14% of the population) have almost 70% increased risk of obesity. This effect has since been confirmed in many populations around the world.

Work has been continuing to further explore how the gene works.

“What we are doing with this work is debunking the old myths which are still often repeated in relation to obesity: ‘I have big bones’,or ‘I have a slow metabolism’, or indeed ‘it is in my genes’.

While strong genetic effects have been found in extremely rare cases, most obesity is associated with rather weak genetic tendencies that are modifiable by diet and exercise,” said Professor Palmer.

“The genetics of obesity are complicated and it is likely that there are other genes which will have an effect. But we are now clearly seeing the effects of genetic variants like this one in FTO.”

Longevity genes hold key to ageing


Washington: A new discovery holds out the prospect of keeping old age at bay by targeting “longevity” genes.

Scientists have identified 25 genes that regulate lifespan in two organisms separated by 1.5 billion years of evolution.

They believe at least 15 are likely to have similar versions in humans. Affecting their activity could provide a way to slow down the ageing process and treat age-related conditions.

Dr Brian Kennedy, one of the researchers from the University of Washington in Seattle, US, said: “Now that we know what many of these genes actually are, we have potential targets to go after in humans.

“We hope that in the future we could affect those targets and improve not just lifespan, but also the ‘health span’ or the period of a person’s life when they can be healthy and not suffer from age-related illnesses.”

The two organisms studied by the scientists were yeast and the tiny roundworm Caenorhabditis elegans.

Both are commonly used laboratory tools. The researchers say finding genes that are conserved between them is important because they are so far apart on the evolutionary scale. Yeast and C. elegans are even more widely separated than C. elegans and humans.

Similar types of genes are known to exist in humans. Taken together, the evidence suggests that longevity genes are likely to influence human lifespan as well.

Several of the genes shown to be involved in ageing are also linked to a key nutrient pathway called the Target of Rapamycin, or TOR.

Calorie intake and nutrient response are believed to affect lifespan through TOR activity. Previous studies have shown that drastically restricting the diets of animals ranging from worms to monkeys can prolong lifespan and prevent age-related diseases.

Happiness – its mostly in your genes


Edinburgh: Happiness is in your genes, according to the latest research from the University of Edinburgh.

Fifty per cent of our disposition is genetic, with external factors such as money, career, health, relationships accounting for the rest, says the report in the journal Psychological Science.

Those who are lucky enough to inherit a happy disposition also have extra reserves for times of stress, the researchers who studied 900 sets of twins found.

Leader researcher Dr Alexander Weiss says: “Together with life and liberty, the pursuit of happiness is a core human desire. Although happiness is subject to a wide range of external influences we have found that there is a heritable component of happiness which can be entirely explained by genetic architecture of personality.”

Those who have inherited a poor set of genes have to work harder at being happy, they said.

Shorter women may live longer


Tel Aviv: A gene found in women of shorter stature is also linked to living a very long life — to 90 and beyond, according to researchers at the Albert Einstein College of Medicine of Yeshiva University.

Mutations in genes governing an important cell-signaling pathway influence human longevity. The findings are part of on-going research for genetic clues to longevity through a study of more than 450 Ashkenazi (Eastern European) Jews between the ages of 95 and 110.

Descended from a small founder group, Ashkenazi Jews are more genetically uniform than other groups, making it easier to spot gene differences that are present. In 2003, this study resulted in the first two “longevity genes” ever identified–findings that have since been validated by other research.

The present study focused on genes involved in the action of insulin-like growth factor (IGF-I), a hormone that in humans is regulated by human growth hormone. Affecting virtually every cell type in the body, IGF-I is crucially important for children’s growth and continues contributing to tissue synthesis into adulthood. The IGF-I cell-signaling pathway is triggered when IGF-I molecules circulating in blood plasma latch onto receptors on the surface of cells, causing a signal to be sent to the cell’s nucleus that may, for example, tell that cell to divide.

Animal research had shown that mutations to genes involved in the IGF-I signaling pathway cause two effects: Affected animals have impaired growth but also longer life spans. So the Einstein scientists reasoned that altered signaling in this pathway might also influence human longevity. To find out, they analyzed IGF-I-related genetic variations in 384 Ashkenazi Jewish centenarians.

And since plasma levels of IGF-I do not reflect their levels at a younger age, the researchers also looked at two other groups: the children of these centenarians, and a control group consisting of Ashkenazi Jews the same age as the centenarians’ children but with no family history of longevity.

Remarkably, the female children of the centenarians had IGF-I plasma levels that were 35 percent higher than female controls–perhaps a sign that the body was compensating for a glitch in IGF-I signaling by secreting increased amounts of the hormone. That suspicion was strengthened by two other findings: the daughters of centenarians were 2.5 cm shorter than female controls; and when the researchers analyzed the gene coding for the IGF-I cell-surface receptor molecule to which the IGF-I hormone binds, the receptor genes of centenarians and their daughters were much more likely to have a variety of mutations than were the receptor genes of the controls.

“Our findings suggest that, by interfering with IGF-I signaling, these gene mutations somehow play a role in extending the human life span, as they do in many other organisms,” says Dr. Nir Barzilai, senior author of the study and director of the Institute for Aging Research at Einstein.

Dr. Barzilai notes that a drug that decreases IGF-I action is currently being tested as a cancer treatment and could be useful in delaying aging. “Since the subjects in our study have been exposed to their mutations since conception, it is not clear whether people would need such a therapy throughout life or if it could help people who received it at a later time.”

This research is described in the March 4 issue of the Proceedings of the National Academy of Sciences.

Besides Dr. Barzilai, other Einstein scientists involved in the study were lead author Yousin Suh, Gil Atzmon and Mi-Ook Cho. Other researchers were David Hwang, Bingrong Liu and Pinchas Cohen of UCLA’s David Geffen School of Medicine and Daniel J. Leahy of the Johns Hopkins University School of Medicine.

UK’s first public debate on genetic screening to be held in London


London: Genetic screening for common diseases……..Fact or fiction?

The UK’s first public debate on genetic screening is being held at The Wellcome Institute, London, Thursday 8th November 6.30pm – 8.30pm. For more information go to

There has been so much in the press this year about the use of genetic screening as a powerful new diagnostic tool for predicting risk in areas such as:

Heart disease, thrombosis, hypertension, metabolism and obesity, osteoporosis, drug metabolism, and cancer predisposition, especially prostate, breast and ovarian cancers.

But is it really what it is cracked up to be? Is there a proven link between some gene polymorphisms and the onset of age related diseases.

Here for the first time an eminent group of doctors and scientists discuss the facts, the scientific evidence, and the potential application in the physician’s surgery.

For two hours on Thursday evening you can have a unique opportunity to hear, not only from leading researchers and clinicians, but also from doctors who have been using this exciting new tool for over two years in the UK.

The excellent speakers: Prof Stephen Bustin (Barts and The London), Prof Mark McCarthy (Oxford), Dr Paul Jenkins (Barts), Dr Lobo (Barts), Dr Brull (The Whittington).

This is the first event of its kind in the UK and a unique opportunity to learn about this powerful new diagnostic tool.

Places will be limited as the lecture hall only holds 150. So please book your place online as soon as you can, to be assured of your place. There will be a small exhibition alongside the meeting, a good opportunity to network and enjoy a glass of wine afterwards.

To register please call + 44 (0)20 8742 3789 so we can register you. For more information to or email

This event is sponored by the UK’s Genetic Health, Roche and the magazine Body Language.

Don’t let your past kill your future – get tested at Britain’s first private patient gene clinic


London: Genetic screening reveals a vital part of our life story: the part that was unknown until the discovery of the human genome – that is all the genes in each individual cell responsible for life. Now for the first time with genetic testing you can discover which genes you have been handed down – those responsible for protecting your body and which ones have the potential to harm you.

The aim of genetic testing is to foresee and with medical intervention prevent the “envelope of diseases” that may dispose certain individuals to debilitating and or life threatening illnesses such as heart disease, cancer, osteoporosis, diabetes and Alzheimer’s.

GeneticHealth is the first clinic in the UK – based in London’s Harley Street, to offer the latest scientific testing, analysis and medical intervention to prevent and protect individuals from the life-threatening diseases and illnesses they may have inherited.

The basis of GeneticHealth’s gene testing is a swab taken from the patient’s mouth which is used to analyse 45 genes that are clinically proven to have an effect on the way humans age and our resistance to age-related diseases. These are technically known as single nucleotide polymorphisms (SNPs) and, in particular, will tell you if you are prone to:

• Heart and cardiovascular disease
• Stroke
• Cancer
• Osteoporosis
• Obesity
• Diabetes
• Inflammation

Patients receive a 50-page report which examines in detail the state of their health, and includes a detailed results analysis and interpretation by our genetic doctors. Afterwards the client receives a medical consultation in which allows them to understand the implications of their individual genetic profile and what can be done to change their risk profile. GeneticHealth provides the opportunity for tailor made strategies to be developed to minimizing the risk of many of the diseases covered by the genetic analysis, especially cardiovascular disease. Your bespoke medical intervention programme is created with you by GeneticHealth’s medical experts.

The clinic’s Medical Director, Dr Paul Jenkins comments:

“I am convinced that the advent of effective genetic analysis will become increasingly relevant to individuals and clinicians seeking to minimise the burden of age-related diseases. For the first time, we are able to more accurately determine and individuals overall risk profile for many diseases by combining their genetic risk to that of lifestyle and environmental influences. Such an approach has enormous implications for healthcare and disease prevention in the 21st century.”

The results of the test are the basis for bespoke medical intervention including nutrition and other advice/therapies from the clinic’s experts. There are seven genetic tests to chose from and range in price from £180 to £825.

The clinic’s expert analytical team of medical experts and scientists in the field of genetics and healthy ageing includes:

• Dr Paul Jenkins MA, BChir, MD, FRCP – Reader in Endocrine Oncology, Honorary Consultant Physician, St Bartholomew’s Hospital, Queen Mary School of Medicine and Dentistry, University of London. He is Medical Advisor of the European Scanning Centre, which is one of only two centres in the UK to use an Electron Beam CT (EBCT) scanner. He leads an active research team and has published over 60 research papers in the field of hormones and genetic actions in the human body. He has a special interest in the role of genetics in disease prevention and ageing.

• Professor Stephen Bustin, BA,PhD – Professor of Molecular Medicine, Institute of Cell and Molecular Science, Queen Mary University of London. Stephen is a leading researcher in the genetic determinants of colonic cancer.

• Dr Lynette Yong, MAm MBBSm FRCSm LF Hom – Dr Yong studied medicine at Cambridge University and at St Mary’s Hospital, London. She completed her surgical fellowship in London with the Royal College of Surgeons of England. She has a special interest in the application of genetic analysis to the prescribing of hormones for men and women.

Patient information can be obtained by calling +44(0) 870 043 5551 email:

GeneticHealth is a clinically led company, based at 68 Harley Street, London W1, run by world-renowned doctors and genetic scientists.

Longevity – it’s all in the genes

LOS ANGELES – A World War 1 veteran has defied health experts by living until the age of 112, despite a diet of that included sausages and waffles.

George Johnson who lived in Richmond was considered California’s oldest living person at 112 until he died last Wednesday, as a result of pneumonia. Mr Johnson’s wife died in 1992 at the age of 92.

Dr L Stephen Coles, of the Gerontology Research Group at the University of California in Los Angeles said that Mr Johnson’s genes had contributed to his longevity.

Mr Coles commented: “A lot of people think or imagine that your good habits and bad habits contribute to your longevity. But we often find it is in the genes rather than lifestyle.”

Johnson, who was blind and living alone until his 110th birthday when a caregiver began helping him, built the Richmond house by hand in 1935 and got around using a walker in recent years.

Johnson was the only living Californian considered a “supercentenarian,” a designation for those ages 110 or older, Coles said. His group is now in the process of validating a Los Angeles candidate who claims to be 112 years old.

Coles participated in an autopsy Thursday that was designed to study Johnson’s health.

“All of his organs were extremely youthful. They could have been the organs of someone who was 50 or 60, not 112. Clearly his genes had some secrets,” Coles said.

“Everything in his body that we looked at was clean as a whistle, except for his lungs with the pneumonia,” Coles said. “He had no heart disease, he had no cancer, no diabetes and no Alzheimer’s.

“This is a mysterious case that someone could be so healthy from a pathology point of view and that there is no obvious cause of death.”

The family was in favor of an autopsy. Relatives said Johnson wanted them to allow it if it would help science.

Born May 1, 1894, Johnson’s father managed the Baltimore and Ohio Railway station in Philadelphia.

Johnson was working in 1917 as a mail sorter for the U.S. Post Office when he was drafted into the Army. The war ended a year later, and he never served in combat.

Two years later, he and his wife moved to Northern California.

“It was a great adventure in those days. We were young and wanted the experience,” Johnson said in a March interview with the Contra Costa Times.

The couple settled in Fresno and remained there until 1935, when they bought property in Richmond. They used lumber salvaged from dismantled buildings to build their house.

During World War II, Johnson worked at the Kaiser shipyard in Richmond and later managed the heating plant at Oak Knoll Naval Hospital in Oakland.

He remained in good health and continued driving until he was 102, when his vision began to fail.

Gerontology Research Group