Heavy drinking 'can double the risk of cancer' (?)

More epidemiological speculation. Suspicious that wine drinkers were not affected. Social class is the probable cause of the differences observed. Lower class people probably drink more irresponsibly and indulge in other risky behaviours, such as drug abuse. And Canada is very multi-ethnic. Were differences due to that ruled out? Blacks tend to have poorer health and may drink more so was it all just a racial effect?

Heavy drinkers have another reason to drown their sorrows. They face almost double the usual risk of developing certain cancers, according to research. The bad news is for those who frequently down large amounts of spirits or beer. Drinkers who prefer wine do not appear to face the same risk.

Heavy beer and spirits drinkers increase their risk of developing cancer of the oesophagus, liver and lung, the research claims. Doctors found 'statistically significant' links between heavy consumption of alcohol and seven different cancers in all. However moderate drinking - less than daily - and wine consumption did not show the same effects.

'We compared people who drank heavily to our reference group, who abstained or drank only very occasionally,' said Dr Andrea Benedetti from the department of medicine at McGill University in Montreal. 'We also looked for trends across our categories: non-drinkers, weekly drinkers and daily drinkers. The results were astounding. 'We saw increased risk for oesophageal cancer, stomach cancer, colon cancer, liver cancer, pancreatic cancer, lung cancer and prostate cancer. 'The strongest risk was for oesophageal and liver cancer.'

The research, published in the medical journal Cancer Detection and Prevention, used data originally collected for a massive occupational cancer study in Montreal in the 1980s. The information was a treasure-trove, said Dr Benedetti.

She continued: 'Lifetime interviews were conducted with people about their job histories and detailed information about all the things they could have been exposed to was collected. 'As it turns out, the data also included information about non-occupational factors such as drinking alcohol, smoking cigarettes, diet and socio-economic status. 'For the most part we showed that light drinkers were less affected or not affected at all. It is people who drink every day or multiple times a day who are at risk. 'This adds to the growing body of evidence that heavy drinking is extremely unhealthy in so many ways.'

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Discovery of epilepsy gene paves way for more effective treatments

A genetic defect that could be responsible for up to half of all cases of epilepsy has been identified by scientists. In about 50 per cent of cases, the onset of epilepsy is linked with an obvious cause, such as a head injury, brain tumour or another neurological disease. In most other cases the condition is believed to have a genetic basis — but so far little progress has been made in identifying the genes responsible. The latest study, which is published today in the journal PNAS (Proceedings of the National Academy of Sciences), shows that a mutation in a gene called ATP1A3 can lead to a severe form of epilepsy in mice. If the findings translate to human beings, they could pave the way for more effective treatments.

The team behind the study has already begun screening a large archive of DNA samples from epileptic patients to ascertain whether the same genetic flaw predisposes people to the disease. They say that the 99 per cent match between the mouse and human versions of the gene means there is a good chance that it also plays a role in human epilepsy.

In both species the gene is involved in regulating levels of sodium and potassium in the brain. Imbalances in these chemicals have already been linked with epilepsy in humans.

In epilepsy sufferers, the brain is hyperexcitable, meaning that when stimulated there is a much bigger increase in neuronal firing than in a normal brain. Sodium and potassium affect how easily neurons fire.

“It’s equivalent to salty water conducting electricity better than tap water. When there’s more sodium present in the brain, the conductivity of neurons increases and they fire more often,” said Steve Clapcote, a neuroscientist from the University of Leeds, who led the study.

The ATP1A3 gene regulates the levels of sodium and potassium in the brain by producing an enzyme that works as a sodium-potassium pump. In a strain of mouse called Myshkin, which has been bred to have epilepsy, a defect in the ATP1A3 gene means that an inactive version of the enzyme is produced, leading to sodium and potassium imbalances. As a consequence the mice have regular seizures.

The study went a step farther in isolating the cause of the epilepsy by cross-breeding the epileptic mice with normal mice that had been genetically engineered to have an extra copy of the ATP1A3 gene. The extra copy compensated for the faulty version, resulting in offspring that were free of epilepsy and had normal levels of the sodium-potassium pump enzyme.

“An imbalance of sodium and potassium levels has long been suspected to lead to epileptic seizures, but our study is the first to show beyond any doubt that a defect in this gene is responsible,” Dr Clapcote said.

Epilepsy affects about 1 in 200 people in Britain. But despite being a relatively common condition, anticonvulsive medication — the most common treatment — is ineffective in more than 30 per cent of cases. Its side-effects can also have a big impact on quality of life.

If the study’s findings translate to humans, it could open up new avenues for treatment. One possibility would be to give patients a synthetic version of the sodium-potassium pump enzyme to help to regulate levels of these chemicals in their brain. Alternatively, drugs could be designed to stimulate the inactive enzyme.

Designing specifically tailored drugs will be a long-range project, says Professor Mark Rees, a specialist at the University of Swansea, who is also involved in the DNA screening project. “But any piece of the jigsaw that takes us a step towards designing the drugs is to be welcomed,” he said.

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