Red Lion Group

DNA pioneer says red tape hinders drug trials and a cure could be found within five or ten years if more risks were taken

At 82, you might imagine James Watson would be taking life easy. After a spectacular scientific career, during which he was part of a duo which made, as his fellow Nobel Laureate Sir Peter Medawar described it, "the greatest achievement of science in the 20th century," a relaxing retirement might be in order. Not so for Watson, it seems.

Speaking at University College Cork this week, while presenting the inaugural cancer lecture of the Cork cancer research centre (CCRC), Watson told a packed audience about his ongoing research into finding a cure for cancer at the Cold Spring Harbor laboratory in New York where he is now Chancellor Emeritus.

Striking a highly optimistic note, the Nobel Laureate bemoaned some pessimistic cancer researchers who he said were more interested in merely researching cancer and didn't realise that they had an obligation to cure people and save lives.

"I got real annoyed with someone … at the end of his talk he said, 'we're going to get somewhere over the next ten to twenty years'. He could have said twenty to forty or why didn't he say five to ten?"

"We should try and cure cancer now, not ten to twenty years from now," Watson warned. "It would be sort of irresponsible to all those people who would die of cancer if we don't try and do it now."

"We are nearly there", was his message for the evening, having suggested that the medicines to do the job might already be in use for other ailments, but that doctors and scientists may not have recognised their anti-cancer properties yet.

"People are so frightened by being wrong," he continued, "I figure that it doesn't matter if you're wrong, if you're sometimes right. The main thing is to try."

Watson explained how he initially became interested in cancer research early on in his career. So much so, that he included a whole chapter on cancer in the first edition of his seminal textbook Molecular Biology of the Gene, which was originally published in 1965.

Prior to receiving an Honorary Doctorate from University College Cork, Watson told journalists that he was in favour of less regulation for clinical trials as this could speed up the process of finding a cure for cancer: "We're terribly held back on clinical tests by regulations which say that no one should die unnecessarily during trials; but they are going to die anyway unless we do something radical. I think the ethics committees are out of control and that it should be put back in the hands of the doctors. There is an extraordinary amount of red tape which is slowing us down. We could go five times faster without these committees."

In his introductory address, Professor Gerald O'Sullivan of CCRC praised Watson saying, "his accomplishments and contributions transcend boundaries, disciplines, and generations. One of the greatest scientists ever, he is also a respected leader, a gifted administrator, a brilliant author and a beacon in the Gaelic diaspora."

O'Sullivan continued, "hopefully mankind will also constructively use its increasing technical capability to live peacefully. If so, the humans in future millennia may not know of many from our time but they will know of the structure of DNA and of Watson and Crick as by then the ramifications of its discovery will have impinged on life in ways that we cannot yet imagine".

• Eoin Lettice is a lecturer in the School of Biological, Earth & Environmental Sciences at University College Cork, Ireland.

He blogs on the Communicate Science blog

Studies shows that test subjects with good strength, speed and balance are likely to outlive their weaker peers

If you have a firm grip and can stand on one leg, it may indicate that you are heading for a long life, according to a new study.

Grip strength and single leg balance are two of four markers for physical ability examined by researchers from the Medical Research Council's unit for lifelong health and ageing. The other factors were speed of rising from a chair and walking pace.

People who were faster, stronger or better balanced in these tests, say the researchers today in a paper published online by the British Medical Journal, were likely to outlive their slower and weaker peers.

The object of the research was to work out whether these simple physical measures could be used to identify older people living in their own homes who might need more help.

The MRC team reviewed 57 studies that had measured people's abilities in one of these four tests and had gone on to record their subsequent death. The team excluded any studies of people who were suffering from specific diseases.

In one of the tests – grip strength, which is measured by squeezing a handle as hard as possible – studies in people aged under 60 had been carried out.

The team found there was a link between weaker performance in the tests and earlier death. "We have found evidence of associations between all four measures of physical capability investigated (grip strength, walking speed, chair rises and standing balance) and all cause mortality," they write. "People in community dwelling populations who perform less well in these tests were consistently found to be at higher risk for death."

They found that the stronger the performance in the tests, the more likely the participant was to live longer.

In 14 studies (involving 53,500 people) that dealt with grip strength, the death rate among the weakest was 1.67 times greater than among the strongest, after taking age, sex and body size into account.

In five studies (involving 14,700 people) that dealt with walking speed, the death rate among those who were slowest was 2.87 times greater than among the people who were fastest, after similar adjustments. In five studies (involving 28,000 people) that dealt with the speed at which seated volunteers stood up and sat down again), the death rate of those who were slowest was almost twice the rate of the fastest.

The researchers say there are several possible explanations for the findings – one of which is possible skewing of the results because, for instance, the studies did not record and adjust for the socioeconomic circumstances and physical activity levels of the participants.

Secondly, it is possible that the results simply reflected the general health status and underlying disease of the volunteers.

But, they point out, the same association between performance and mortality risk was seen in the grip strength studies, which included a younger and presumably healthier population.

The MRC team would like to see further trials done in younger people, to find out whether it is possible to spot those who may be at risk of an earlier death.

But ultimately, they would like to know whether physical interventions – such as exercise programmes to improve people's fitness, grip strength, walking speed and so on – would result in longer lives.

Dr Rachel Cooper of the ageing unit said: "Simple noninvasive assessment measures like these, that are linked to current and future health, could help doctors identify those most vulnerable to poor health in later life and who may benefit from early intervention to keep them active for longer."

Some participants in Oxford University trial see their neurological decline reduce by as much as 50% after using vitamin B tablets

Taking daily supplements of B vitamins may delay the onset of Alzheimer's disease, scientists have claimed.

The discovery that people in the early stages of failing memory can retain more of their mental faculties for longer if they take the tablets regularly could lead to treatments for the condition. Some participants in the Oxford University trial saw their neurological decline reduced by as much as half after using B vitamins.

That breakthrough has raised hopes that the vitamins, which are sold in chemists and health food stores, could at least slow down, if not prevent, the shrinkage that affects many older people's brains.

Vitamin B tablets are popular among vegans, because they shun some of the foods in which vitamin B is found – fish, meat and milk – and among sufferers of pernicious anaemia.

"It is our hope that this simple and safe treatment will delay the development of Alzheimer's in many people who suffer from mild memory problems," said David Smith, a professor emeritus in Oxford University's pharmacology department and co-leader of the study. About 1.5m people over 70 in the UK who suffer from mild cognitive impairment (MCI) – who have a 50/50 chance of going on to develop full-blown dementia within five years – could benefit from the discovery, Smith added. But while the results were "immensely promising", it was not yet certain, he stressed, if B vitamins could slow or prevent the development of Alzheimer's. [See footnote]

Healthy middle-aged people hoping to avoid dementia and older people exhibiting early signs of memory loss might now be tempted to start routinely taking the vitamins, he said. But they should not do without first talking to their doctor, as the tablets could help stimulate the growth of early-stage cancer, he warned.

Chris Kennard, chair of the neurosciences and mental health board at the Medical Research Council, said the findings "bring us a step closer to unravelling the complex neurobiology of ageing and cognitive decline and hold the key to the development of future treatments for conditions like Alzheimer's disease."

Rebecca Wood, chief executive of the Alzheimer's Research Trust, said: "These are very important results, with B vitamins now showing a prospect of protecting some people from Alzheimer's in old age. The strong findings must inspire an expanded trial to follow people expected to develop Alzheimer's, and we must hope for further success."

Some 820,000 people in the UK have dementia, predominantly Alzheimer's, and their numbers are expected to soar as the population ages.

Smith and his colleagues at the Oxford Project to Investigate Memory and Ageing gave one group of people with MCI daily tablets comprising folic acid, vitamin B6 and vitamin B12, and another group a placebo. The vitamins were chosen because they control the amounts of an amino acid called homocysteine in the blood. High levels of homocysteine have been linked to a greater risk of Alzheimer's.

After two years participants' brains were examined using MRI scanners and their mental faculties assessed using tests of cognition. They found that those who had been receiving the supplements had experienced on average 30% less brain atrophy than those receiving the dummy pills. The former saw their brains shrink by 0.76% a year, while the placebo group saw theirs reduce by 1.08%. Those who started the trial with the highest levels of homocysteine experienced the greatest benefit – 50% less brain shrinkage.

• This footnote was added on 9 September 2010. The study findings were published in an open-access journal, Public Library of Science ONE. A reference in the story text to vegans has been amended to make clear that fish, meat and milk are not the only foods containing significant amounts of vitamin B.

Poor physical fitness and working more than 45 hours a week is potentially lethal combination for men aged 40-59

Unfit, middle-aged men who work more than 45 hours a week are more than twice as likely to die of heart disease as those who devote less time to their jobs, new research medical research warns today.

It identifies the combination of poor physical fitness and working for unusually long hours as a potentially lethal combination for men aged between 40 and 59. However, men who manage to remain physically active into middle age are not at risk, emphasising the health benefits of regular exercise.

The findings in the study, in the medical journal Heart, reinforce the health risks being run by men in that age group who are part of Britain's long hours culture. Working excessive hours is thought to damage cardiovascular health by causing someone's heart rate and blood pressure to go up and stay raised for long periods. This happens whether the work itself is physically demanding or not.

The heart health and physical fitness levels of some 5,000 Danish men aged 40-59 working for 14 companies was examined for 30 years by a team from the National Research Centre for Denmark's Working Environment.

Participants did cycling tests to indicate how fit they are and disclosed how many hours they worked a week. More than two-thirds worked between 41 and 45 hours, but almost one in five clocked up more than 45 hours.

Among unfit men, those who were in the latter category were more than twice as likely to die of heart trouble than those who worked for less than 40 hours.

Heart health campaigners said that the study underlined the need for middle-aged men to maintain a good level of fitness by taking part in regular physical exercise, despite the pressures on their time.

Dr Jane Landon, deputy director of the National Heart Forum, a coalition of 65 health organisations which aims to reduce the damage done by poor heart health, said: "Men in this age group don't need to be doing extreme sports but they do need to be keeping physically fit by, for example, walking or cycling or even doing gardening or DIY, which all contribute to a good level of fitness."

Men's risk of developing heart trouble increases as they head into middle age, and is heightened if they put on weight, or have a poor diet or are unfit. The research's conclusion that fit men of the same age and working patterns as those who are unfit proved the protective effects of regular exercise, she said.

Cathy Ross, senior cardiac nurse at the British Heart Foundation, said that men should try to be physically active for at least 30 minutes at a time five times a week. "We already know that working long hours can increase blood pressure, a known risk factor for cardiovascular disease."Being physically active helps to control your blood pressure and previous studies have shown that being physically fit can help you cope with the demands of long hours, physically demanding jobs and shift work," she said.

"This study adds to these findings by demonstrating that men who are physically active as part of their everyday life do not increase their risk of coronary heart disease, irrespective of the number of hours they work."

Rare childhood cancers are the subject of an award-winning essay by Nicola Harris in this year's Max Perutz prize

My palms are sweaty and my mouth is dry, but it's more excitement than nerves, though of course the nerves are there, too. I've got my cells out of the incubator and now I just can't resist having a quick glance at them down the microscope – will I see more dead cells floating in one set than the other? I know I can't tell properly till I add some staining solution and analyse them accurately, but that will take hours and I just can't wait that long to find out: has it worked or not?

If you've ever held that envelope of exam results and been desperate to tear them open and find out how you did, but also terrified to look in case you didn't get what you were hoping for, then you'll know exactly the sort of feelings I'm talking about.

I'm working on tumour cells from two childhood cancers, called neuroblastoma and Ewing's sarcoma. These are both very hard to treat, with less than half the children surviving for five years after their diagnosis. That's the problem with treating cancer: some patients do brilliantly on a particular drug, but for others it'll have little effect. At the moment, it's often a case of trial and error working out which drug is going work – and some people simply run out of time before we can find the right one. So what I'm trying to find out is what causes the differences in responses and how can we use that to our advantage.

The drug I'm using is called fenretinide, and it's similar to vitamin A (the vitamin found in carrots). It's able to kill cancer cells, while normal cells remain healthy. It works by causing a build-up of oxidants in the cells (you'll all probably have seen the adverts for beauty creams offering anti-oxidant properties to get glowing skin – that's because oxidants are bad news for cells!). Normal, healthy cells should be able to cope with the presence of a few oxidants, but cancer cells will already be exposed to high levels as they're produced when cells divide, and so they can't cope with the extra oxidants produced from fenretinide treatment.

Due to its similarity to vitamin A, fenretinide can get into receptors meant for that vitamin and so the main side effect with fenretinide treatment is that the patients get what's called night-blindness; basically, you can't see very well in the dark. This makes it particularly suitable for treating childhood cancers as it's a much easier side effect to deal with than many other treatments – it's easier to give a five-year-old a night light than to comfort them as they're losing their hair. The problem is that fenretinide seems to work really well for some neuroblastoma and Ewing's sarcoma tumours, but not others. And I want to know why!

I've found that some of the tumours have more of an enzyme called CYP26 than others, and this enzyme helps to metabolise fenretinide in the body. Usually, you'd expect the patients to do worse if their body is breaking down the drug, but fenretinide is a little different. As well as the drug itself being able to kill cancer cells (what we call an "active" compound), one of the metabolites of fenretinide is also active. This means there could be an extra hit from this second compound to those cancer cells where there is metabolism occurring. This is the reason I'm desperately hoping to see more dead cells in some of my flasks than others – these should hopefully be the cells with more CYP26.

So what would it mean if I'm right about the link between CYP26 and how many cancer cells die? There are a few options, actually – we could be selective and only give the drug to those whose cancer has been tested and shown to have CYP26, or there are other drugs that have been shown to increase concentrations of CYP26 in the body, so alternatively these could be used in combination with fenretinide. The important point is that we could decide on which drug or combination of drugs to use based on what should work for each particular patient, and that's what this is all about – taking the guesswork out of cancer treatment.

I've already analysed these cells to see how much CYP26 they have, and then I've added the drug and left them to grow for a few days (having a quick peek every day to see how they're getting on). Now it's the moment of truth, as I look down the microscope and bring the cells into focus...

The prize

The Max Perutz Science Writing Award, now in its 13th year, encourages young Medical Research Council scientists to communicate their research to a wider audience. The competition is open to all MRC-funded PhD students and asks them to describe the importance and excitement of their research.

The 2010 award received a record number of submissions, with 114 entries. Twelve essays were shortlisted and judged by the MRC's outgoing chief executive, Sir Leszek Borysiewicz, the Guardian's science and environment correspondent Alok Jha; the head of the MRC Centre, Cambridge, Dr Megan Davies; the former winner Dr Jacqueline Maybin; and the author and broadcaster Dr Alice Roberts.

• Nicola Harris is at the Northern Institute of Cancer Research, Newcastle University