Stress can raise your risk of cancer, other diseases

Tel Aviv University scientist honored at research conference in Florida; until now there wasn't direct evidence of stress' effect on telomere length.

By JUDY SIEGEL-ITZKOVICH
Stress worried smoking cigarette 311 (R) (photo credit: TIM WIMBORNE / Reuters)
Stress worried smoking cigarette 311 (R)
(photo credit: TIM WIMBORNE / Reuters)
Although Israeli researchers were not involved in groundbreaking research presented over the weekend by the American Association for Cancer Research, the population here – exposed on a daily basis to the stress of security dangers, economic and family pressures and tension at the workplace – would be well advised to take note.
For the first time, a direct link between stress and damage to the chromosomes in every cell has been shown, with the ends – called telomeres – shortening as people are more exposed to chronic emotional stress.
Although telomere length generally shortens as one ages, lifestyle and not only genetic differences can make these structures longer or shorter and thus affect one’s risk and timing of diseases from cancer to cardiovascular disease and stroke to diabetes.
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Two pieces of research related to telomeres were unveiled at a Saturday press conference at the AACR’s 102nd annual meeting, in Florida, that aroused much interest around the world.
The studies were simultaneously published in Cancer Prevention Research.
In the first, a study led by Prof. Edward Nelson, division chief of the department of hematology/oncology at the University of California, Irvine, lent credence to the idea that improving quality of life affects stress-related biological markers and possibly the health of cancer patients.
Until now, there was only epidemiological but not direct evidence that stress and not only aging can affect telomere length.
“We are trying to understand the interconnections between the mind and the body; that is, how does the diagnosis and treatment of cancer impact patients not only psychologically, but also physiologically and how can we improve their outcome.
Cancer drives a chronic stress response in some patients,” said Nelson.

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Telomeres have been described like the plastic or metal ends of shoelaces that prevent them from unraveling or fraying. They protect the chromosome from deteriorating, breaking apart or joining with other chromosomes, which can lead to mutations.
Chromosomal rearrangements are seen in cancers and provided a biological reason to investigate this link, said Nelson.
“For this study, we wanted to know if chronic stress was associated with accelerated telomere shortening in cancer patients, and if a psychosocial intervention that modulates the stress response could also modulate telomere length,” he said.
In this retrospective study, the researchers took biological samples from 31 women with cervical cancer who had been randomized to one of two groups – those who received six counseling sessions by telephone and those who received usual care without counseling.
The six sessions consisted of a quality of life and psychosocial profile, managing stress and emotions, enhancing health and wellness, addressing relational and sexual concerns, and integrating and summarizing the information.
At enrollment and after four months, the researchers obtained biological samples from both groups and investigated changes over time to see if psychological counseling had any physical effects.
“Improved quality of life and reduced stress response was associated with changes in telomere length,” Nelson said.
Nelson’s study was the first study of telomere length and chronic stress in a cancer population, and the first longitudinal analysis of whether changes in quality of life and changes in the stress response would be associated with modulating the telomere length, he said. Giving backing to the mind/body approach in cancer treatment, he said there is “no doubt that offering psychological services has the potential to improve quality of life and outcomes of patients, but “whether we can draw conclusions or make recommendations about the capacity of a behavioral intervention to modulate telomere length remains an open question.”
AACR president and 2009 Nobel Prize laureate biologist and physiologist Elizabeth Blackburn of the University of California, San Francisco, wrote an editorial in the AACR journal.
“[The study] has shed light on the biology of early cancers and their initiating events.
These advances now create unprecedented opportunities for novel approaches directed at prevention and early interception of cancer’s deadly trajectory,” Blackburn wrote.
Although she stressed that the effect of interventions to lengthen telomeres would need to be tested in prospective studies, she said the finding was a major research advancement.
The other published study was written by University of Texas epidemiologist Prof. Jian Gu, who with his team linked both longer telomeres on the chromosome and a 19-percent reduction in the risk of bladder cancer.
Of some 300,000 SNPs – DNA sequence variations – in 459 healthy participants, it was found that 15,120 of them were associated with telomere length. The team also found that smoking especially augmented the risk of bladder cancer in those people having the other genetic variant, which was associated with shorter telomeres. Gu said that a common genetic variation links to both bladder cancer risk and to the length of protective caps found on the ends of chromosomes.
Although not part of the studies, Tel Aviv University Sackler School of Medicine cancer researcher Prof. Yosef Shiloh was highly honored by receiving the G.H.A.
Clowes Memorial Award at the Florida conference for his work on damage response and the rare genomic instability syndrome ataxiatelangiectasia (A-T).
AACR chief executive Dr.
Margaret Foti said that the Israeli’s discovery, “along with his subsequent work, has played a critical role in increasing our understanding of DNA damage response and repair, which has important implications for cancer and other diseases.
Dr. Shiloh is a truly exceptional scientist, and we congratulate him on receiving the G.H.A. Clowes Memorial Award.”
Patients with A-T exhibit progressive neurodegeneration, immunodeficiency, striking cancer predisposition and chromosomal fragility.
The disease is caused by a profound defect in a major mechanism that maintains genomic stability – the cellular response to DNA double strand breaks.
Shiloh, who spoke to The Jerusalem Post before leaving for Orlando, has for three decades been investigating AT and the defect in the DNA damage response that leads to this disease. He changed the field when his lab identified the A-T gene in 1995 and successfully cloned it.