Snoring heavily almost doubles the risk of developing rheumatoid arthritis, a new study shows.

Researchers found patients diagnosed with the snoring-related condition sleep apnoea were nearly twice as likely to suffer the joint-damaging disease.

The discovery, which comes from research carried out in Taiwan, is something of a surprise as rheumatoid arthritis - which affects around 350,000 people in the UK - is thought to be triggered when something goes wrong with the immune system.

The same study found a similar increase in the risk of other so-called autoimmune disorders, where the body's defences start to attack healthy tissues.

Scientists said they believe the explanation lies in the fact that chronic sleep apnoea can lead to inflammation in blood vessels throughout the body, which may act as a catalyst for arthritis.

Although previous studies have suggested sleep apnoea may raise the risk of heart attacks, the latest investigation is the first to show a link with arthritis.

An estimated three million people in Britain suffer with sleep apnoea, though many more may remain undiagnosed.

As sleep begins, the muscles in the airway relax. For most people this does not pose a problem but in sleep apnoea, it leads to a complete collapse which shuts off breathing for at least ten seconds.

It also disrupts breathing and triggers the sound of snoring as air vibrates against the soft tissue that stands in its way.

Once the brain realises breathing has stopped it sends out a signal for the airway muscles to contract again.

This opens the airway and the sufferer normally wakes with a jolt. In mild sleep apnoea, this can happen about once every ten minutes. If it's severe, it means sleep can be disturbed every couple of minutes.

Very few people remember waking up at all because they fall asleep again within seconds.

Yet the cumulative effect is that they feel exhausted during the day, putting them at increased risk of accidents. Being overweight is one of the major risk factors.

In the latest study, by experts at the Taipei Medical University, 1,411 sleep apnoea patients were compared to a 7,000-strong group of healthy adults.

Over a five-year period, researchers monitored how many in each group went on to develop rheumatoid arthritis, ankylosing spondylitis and systemic lupus erythematous - all conditions where the immune system goes haywire and causes swollen, painful joints and flu-like symptoms.

The results, published in the journal Sleep Medicine, showed the snoring-affected group were 91 per cent more likely to develop one of the three conditions.

However, the researchers stressed that the absolute risk of falling ill was still small. Out of the snoring patients, only 2.91 percent experienced arthritis-related problems.

In a report on their findings the researchers said: 'Our study is the first to investigate the association between sleep apnoea and the development of autoimmune diseases.

'We think this may have gone unnoticed in clinical settings because these cases are relatively rare and may not be reported.

'But the potential link between these two conditions should not be overlooked. Among the diseases we studied, rheumatoid arthritis had the highest risk of developing in sleep apnoea patients.'

As well as inflamed and swollen joints, arthritis sufferers also experience flu-like symptoms. In very severe cases, they can end up crippled and unable to live a full life.

But diagnosing the condition can be difficult as the early signs can be as innocuous as a slight stiffness in hand joints, often early in the morning.

Staying highly active may protect against breast cancer whether it's walking, running, or anything in between, researchers found.

Women who got around 2 hours of exercise a day most days of the week were about 30% less likely to develop breast cancer whether pre- or post-menopausal in a population-based study by Lauren E. McCullough, MSPH, of the University of North Carolina in Chapel Hill, and colleagues.

High-intensity exercise didn't appear any better than low-intensity activity, the group reported online in Cancer.

"Given that three-quarters of the U.S. population participates in some physical activity, it is conceivably one of the most important lifestyle risk factors associated with the incidence of breast cancer," they wrote.

The study included 1,504 women with cancer and 1,555 without it in the population-based Long Island Breast Cancer Study Project.

Simply getting some physical activity outside of work didn't appear to have much impact on breast cancer risk, with an odds ratio of 0.94 (95% CI 0.79 to 1.12).

Reproductive status did seem to matter. Exercise during the reproductive years -- between the birth of a first child until menopause -- or after menopause had the biggest influence.

Even then, less than average activity levels (9 or 10 hours) were not significantly protective in either group.

Only the third quartile in both showed statistically significant benefits in terms of reduced breast cancer risk.

Women who got 10 to 19 hours of exercise a week during their reproductive years showed an odds ratio of 0.67 for breast cancer compared with inactive women (95% CI 0.48 to 0.94).

Women in their childbearing years who got more than 19 hours of activity a week showed a reduced odds ratio of 0.86 as well but with a wide, nonsignificant CI.

With regard to activity levels after menopause, women in the quartile that got 9 to 17 hours a week of physical activity had an odds ratio of 0.70 for breast cancer (95% CI 0.52 to 0.95). Those who got more than 17 hours again tended to have reduced risk but not significantly so (OR 0.84, 95% CI 0.63 to 1.13).

The lack of a linear dose-response "could be interpreted as weak evidence of an association" but a J- or U-shaped curve is also possible, McCullough's group noted.

Sustained activity can generate cellular and DNA damage and depress immune function, they pointed out.

Results were similar for in situ and invasive cancer and across hormone receptor status.

Every weight category showed lower breast cancer risk with more activity versus none.

Substantial weight gain after menopause appeared to eliminate the benefits of exercise for breast cancer risk, though still apparently better than a big gain without staying active (OR 1.02 versus 1.28).

"Collectively, these results suggest that women can still reduce their breast cancer risk later in life by maintaining their weight and engaging in moderate amounts of activity," the researchers wrote.

The group noted that exercise's benefits likely come from cutting down on insulin resistance and inflammation by keeping energy balance and obesity under control.

They cautioned that the study cohort was richer and better educated than typical in the U.S. and included few women who didn't have children, which may have an impact on generalizability.

Fathers who smoke pass on damaged DNA to their children raising the risk of cancer, research shows.

A study found that smoking harms the father's DNA, and these damaged genes can be inherited by his children.

This raises the risk of youngsters developing childhood cancers, particularly leukaemia, warn researchers at the University of Bradford.
Because a fertile sperm cell takes three months to fully develop, fathers should kick the habit 12 weeks before conceiving to avoid the risk, Dr Diana Anderson said.
She added: 'Smoking by fathers at the time around conception can lead to genetic changes in their children. These changes may raise the risk of developing cancer.'
Meanwhile scientists at the University of Glasgow have also found that men who drink lots of tea are far more likely to develop prostate cancer.

They found that those who drank seven or more cups a day had a 50 per cent higher risk of contracting the disease than men who had three or fewer.

The warning comes after researchers tracked the health of more than 6,000 men for four decades.

Their findings run counter to previous research, which had suggested that tea-drinking lowers the risk of cancer, as well as heart disease, diabetes and Parkinson's disease.

It is estimated that one in seven American adults live alone. An international study of stable outpatients who were either at risk of or suffered from arterial vascular disease, such as coronary disease or peripheral vascular disease has now discovered that individuals who live alone have a higher risk of mortality and cardiovascular mortality. The study, published Online First in JAMA's Archives of Internal Medicine reveals that social isolation may be linked to poor health outcomes.

According to the study's background information, epidemiological evidence indicates that social isolation could have various implications, such as influencing health behavior and effecting access to health care. It can also potentially change neurohormonal-mediated emotional stress, which can either be linked to or lead to the development of cardiovascular risk.

Jacob A. Udell, M.D., M.P.H., from Brigham and Women's Hospital at the Harvard Medical School in Boston and his team decided to assess whether living alone was linked to a higher risk of mortality and cardiovascular (CV) disease. They evaluated data obtained from the global REduction of Atherothrombosis for Continued Health (REACH) Registry and found that 8,594 people or 19% lived alone from a total of 44,573 REACH participants.

Their results revealed a four-year mortality rate of 14.1% in those living alone, compared with 11.1% in those who lived with others. The risk of cardiovascular disease was 8.6% for those living alone, compared to 6.8% for those who did not.

In terms of age, people between the ages from 45 to 65 years who lived alone were linked to a higher death risk (7.7%) than those who lived with others (5.7%), whilst participants between the ages of 66 to 80 years had a 13.2% higher risk, compared to a 12.3% risk respectively. The results also demonstrate that those above the age of 80 who lived alone had a lower increased risk of mortality, i.e. 24.6%, compared with those who lived with someone else (28.4%).

The researchers state:

"In conclusion, living alone was independently associated with an increased risk of mortality and CV death in an international cohort of stable middle-aged outpatients with or at risk of atherothrombosis. Younger individuals who live alone may have a less favorable course than all but the most elderly individuals following development of CV disease, and this observation warrants confirmation in further studies."

Scientists including one of an Indian origin have found new clues to why some urinary tract infections recur persistently after multiple rounds of treatment.

Their research, conducted in mice, suggested that the bacteria that cause urinary tract infections take advantage of a cellular waste disposal system that normally helps fight invaders.



In a counterintuitive finding, the researchers at Washington University School of Medicine in St. Louis learned that when the disposal system was disabled, the mice cleared urinary tract infections much more quickly and thoroughly.

"This could be the beginning of a paradigm shift in how we think about the relationship between this waste disposal system, known as autophagy, and disease-causing organisms," said senior author Indira Mysorekar, PhD, assistant professor of obstetrics and gynaecology and of pathology and immunology.

"There may be other persistent pathogens that have found ways to exploit autophagy, and that information will be very useful for identifying new treatments," she explained.

Urinary tract infections are very common, particularly in women.. Scientists believe 80 percent to 90 percent of these infections are caused by the bacterium Escherichia coli (E. coli).

Data from the new study and earlier results have led Mysorekar and her colleagues to speculate that E. coli that cause recurrent urinary tract infections may hide in garbage-bin-like compartments within the cells that line the urinary tract.

These compartments, found in nearly all cells, are called autophagosomes. They sweep up debris within the cell, including harmful bacteria and worn-out cell parts. Then, they merge with other compartments in the cell that are filled with enzymes that break down the contents of autophagosomes.

"We think, but can't yet prove, that the bacteria have found a way to block this final step. This would transform the autophagosome from a death trap into a safe haven where the bacteria can wait, hidden from the immune system, for their next chance to start an infection," Myosrekar said.

In the new research, Mysorekar teamed with colleagues at the School of Medicine who had developed mice in which both copies of an important autophagy gene, Atg16L1, were impaired. Co-author Herbert W. Virgin, MD, PhD, Edward Mallinckrodt Professor and head of the Department of Pathology and Immunology, and others created the mice to study Crohn's disease, a chronic bowel inflammation associated with mutations in Atg16L1.

Co-lead authors Caihong Wang, DVM, PhD, a staff scientist, and Jane Symington, an MD/PhD student in the Mysorekar group, infected the mice with E. coli. The researchers found that bacteria levels in the urinary tracts of the modified mice decreased much more rapidly after infection than they did in normal mice. Cells lining the urinary tract in mice with the mutated gene also had significantly fewer dormant reservoirs of E. coli than in normal mice.

The scientists identified structural changes in urinary tract cells of the mice with Atg16L1 mutations that may help explain their unexpected results. These changes may have made it much more difficult for the bacteria to find and break into autophagosomes, Mysorekar says.

The altered gene also was associated with changes in the immune system. In the modified mice, E. coli infections in the urinary tract led cells to produce more inflammatory immune factors and prompted additional bacteria-fighting immune cells to come to the site of the infection.

"The immune system appears to be primed to attack at the slightest provocation in the mice with mutations. This may be why mutations in Atg16L1 are also connected with Crohn's disease, which involves immune cells erroneously attacking beneficial microorganisms in the gut," Mysorekar stated.

Mutations in Atg16L1 are quite common, according to Virgin, although not everyone who has a mutated form of the gene will get Crohn's disease.

"These new results may help explain why the mutations have persisted for so long in the general population. They don't just put the carrier at risk of Crohn's disease, they also may have a protective effect that helps fight infections," he said.

Mysorekar plans to investigate how E. coli takes advantage of a fully functioning autophagy system in mice with urinary tract infections.

The results will be published in the early online edition of The Proceedings of the National Academy of the Sciences.