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.

A new brain scan shows what it looks like when a person runs out of patience or loses self-control.

It would explain why someone who works very hard not to take a second helping of lasagna at dinner winds up taking two pieces of cake at desert. The study could also modify previous thinking that considered self-control to be like a muscle.

University of Iowa neuroscientist William Hedgcock confirms previous studies that show self-control is a finite commodity that is depleted by use. Once the pool has dried up, we're less likely to keep our cool the next time we're faced with a situation that requires self-control.

But Hedgcock's study is the first to actually show it happening in the brain, using Functional Magnetic Resonance Imaging (FMRI) images that scan people as they perform self-control tasks, the Journal of Consumer Psychology reports.

The images show the anterior cingulate cortex (ACC) fires with equal intensity throughout the task. ACC is the part of the brain that recognises a situation in which self-control is needed and says: "Heads up, there are multiple responses to this situation and some might not be good."

However, the dorsolateral prefrontal cortex (DLPFC) fires with less intensity after prior exertion of self-control. DLPFC is the part of the brain that manages self-control and says: "I really want to do the dumb thing, but I should overcome that impulse and do the smart thing".

Hedgcock said that loss of activity in the DLPFC might be the person's self-control draining away. The stable activity in the ACC suggests people have no problem recognising a temptation. Although they keep fighting, they have a harder and harder time not giving in.

Researchers gathered their images by placing subjects in an MRI scanner and then had them perform two self-control tasks-the first involved ignoring words that flashed on a computer screen, while the second involved choosing preferred options.

Hedgcock says the study is an important step in trying to determine a clearer definition of self-control and to figure out why people do things they know aren't good for them.

One possible implication is crafting better programs to help people who are trying to break addictions to things like food, shopping, drugs, or alcohol.

A diet high in cholesterol may help people with a fatal genetic disease which damages the brain, according to early studies in mice.

Patients with Pelizaeus-Merzbacher disease struggle to produce a fatty sheath around their nerves, which is essential for function.

A study, published in Nature Medicine, showed that a high-cholesterol diet could increase production.

The authors said the mice "improved dramatically".

Pelizaeus-Merzbacher disease (PMD) is one of many leukodystrophies in which patients struggle to produce the myelin sheath. It protects nerve fibres and helps messages pass along the nerves.

Without the sheath, messages do not travel down the nerve - resulting in a range of problems including movement and cognition.

Researchers at the Max Planck Institute of Experimental Medicine, in Germany, performed a trial on mice with the disease and fed them a high cholesterol diet.
'Striking potential'

The first tests were on mice when they were six weeks old, after signs of PMD had already emerged. Those fed a normal diet continued to get worse, while those fed a cholesterol-enriched diet stabilised.

"This six-week-long cholesterol treatment delayed the decline in motor co-ordination," the scientists said.

Further tests showed that starting the diet early was more beneficial, leading the researchers to conclude that in mice "treatment should begin early in life and continue into adulthood".

This study was only in mice, meaning it is not known if there would be a similar effect in people - or if there would, how early treatment would have to start.

The authors of the report said: "Dietary cholesterol does not cure PMD, but has a striking potential to relieve defects."

It is thought the cholesterol frees up a "traffic jam" inside cells in the brain. The disease is caused by producing too much of a protein needed in myelin, which then becomes stuck inside the cells. It is thought the extra cholesterol helps to free up the protein.