Men With A Peer Support System Live Longer, Study Shows

Hebrew U scientists learn why DNA breaks down in cancer cells; American Cacner Society invites Israeli site to global fellowship.

Having a good peer support system at work may help you live longer than those who lack such backing, according to a new study by Tel Aviv University researchers who published recently in the American Psychological Association’s journal Health Psychology.

This effect of peer support on the risk of mortality was most pronounced among those between 38 and 43. But similar support from workers’ supervisors had no effect on mortality, the researchers found. In addition, men who felt they had control and the authority to make decisions at work also experienced this “protective effect,” according to the study. Surprisingly, such authority increased the risk of mortality among women in the sample.

“Peer social support, which could represent how well a participant is socially integrated into his or her employment context, is a potent predictor of the risk of all causes of mortality,” the researchers wrote. The researchers rated peer social support as high if participants reported that their co-workers were helpful in solving problems and were friendly. Control and decision-making authority were rated high if participants said they were able to use their initiative, had opportunities to decide how best to use their skills, and were free to make decisions on how to accomplish the tasks assigned.

Dr. Arie Shiron, the lead researcher, and TAU colleagues looked at the medical records of 820 adults who were followed from 1988 to 2008. The workers were drawn from people who had been referred to a health fund for routine health screening. The employees, who came from some of Israel’s largest firms in finance, insurance, public utilities, healthcare and manufacturing, reported working on average 8.8 hours a day. One-third of them were women; 80 percent were married with children; and 45% had at least 12 years of formal education.

The researchers controlled for the physiological, behavioral and psychological risk factors of total cholesterol, triglycerides, glucose levels, blood pressure, body mass index, alcohol consumption, smoking, depressive symptoms, anxiety and past hospitalizations. Participants were also given another questionnaire that measured job demands, control at work and peer and supervisor support. Over the 20-year period, 53 participants died.

Asked why workplace control was positive for men but not women, Shirom said that for employees in blue-collar jobs (and most respondents belonged to this category), high levels of control were found in jobs typically held by men, rather than by women. “Providing partial support to our finding, a past study found that for women in blue-collar jobs, having low levels of control does not increase their risk of becoming ill with stress-related disorders,” he added.

One limitation of the study was that the researchers did not have data on changes in workload, control or support during the 20-year period. “Still, we argue that other researchers have consistently found that workload, control and support tend to be stable across time,” Shirom said.

Why DNA breaks down in cancer cells

The common denominator of all kinds of cancer cells is damage to the genes’ normal DNA. Although it is already known that cell damage is caused by stress to their DNA replication when cancerous cells invade, the molecular basis remained unclear.

But now, reportedly for the first time, Hebrew University scientists have shown that in early cancer development, cells suffer from insufficient building blocks to support normal DNA replication. It is possible to halt this by externally supplying the “building blocks,” resulting in reduced DNA damage and the cells’ significantly lower liklihood of developing cancerous features. Thus, it is hoped that eventually this will provide protection against cancer development.

Prof. Batsheva Kerem of the Alexander Silberman Institute of Life Sciences and her Ph.D. student Assaf Bester showed that abnormal activation of cellular proliferation that drives many different cancer types leads to insufficient levels of the DNA building blocks (nucleotides) needed to support normal DNA replication.

Then, using lab cultures to which cancerous cells were introduced, the researchers were able to show that through external supply of those DNA building blocks it is possible to reactivate normal DNA synthesis, thus negating the damage caused by the cancerous cells. This work, documented in the journal Cell, raises the possibility of new approaches for protection against precancerous development, even possibly creating a kind of treatment to decrease DNA breakage.
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