~ 091608 Lifestyle Improvements Enhance Telomerase Activity

An article appearing online on September 16, 2008 in The Lancet Oncology reports a pilot study conducted by Dean Ornish, MD and colleagues which found that adopting positive lifestyle changes increases the activity of telomerase, the enzyme responsible for maintaining telomeres. Telomeres are DNA-protein complexes that cap the ends of chromosomes, aiding in their stabilization. Telomere length is associated with cellular age, and adequate telomere length is vital to maintaining cells, including immune system cells which protect the body against a number of diseases, such as cancer. Longer telomere length has been associated with increased resistance to disease and premature death in prostate, breast, lung and colorectal cancers.

The current study involved 24 patients with low-risk prostate cancer. Dr Ornish, of the Preventive Medicine Research Institute in Sausalito, and his associates at the University of California, San Francisco, conducted a three day intensive residential retreat followed by a three month comprehensive lifestyle modification program. Participants were asked to adopt diets that limited fat to 10 percent of their calorie intake, and which contained a low amount of refined carbohydrates, abundant amounts of whole grains, fruit and vegetables, and supplemental soy protein powder, fish oil, vitamin E, selenium, and vitamin C. The subjects were also asked to engage in moderate aerobic exercise for one half hour per day and one hour stress management periods for six days per week, in addition to a one hour weekly group support session. Blood samples were analyzed for telomerase activity and other factors, and psychological distress was evaluated at the beginning of the study and at the end of the three month treatment period.

Participants reported close adherence to the lifestyle recommendations. By the end of the study, telomerase levels in peripheral blood mononuclear cells had increased by 29 percent, and low-density lipoprotein (LDL) cholesterol levels declined from an average of 3.2 to 2.3 micromoles per liter. Additionally, psychological distress, body mass index, waist circumference, and systolic blood pressure were reduced.

Scientists are investigating the role of the telomerase in combating aging-related diseases, yet the enzyme may sometimes have an opposing role in the quest for a longer life because it helps maintain immortalized cancer cells. However, in the current study, prostate specific antigen (PSA), which is a marker of prostate cancer progression, slightly improved, as did free PSA. Additionally, there was no clinical evidence in disease progression in the study's subjects.

The authors remark that oxidative stress and inflammation are the most common causes of accelerated telomere shortening, and that both processes stem from poor nutrition, insufficient exercise, obesity, metabolic syndrome, and stress: conditions that the current study's program was designed to combat. The program could have positive effects on many chronic diseases and conditions associated with aging, including certain cancers, cardiovascular disease, diabetes and dementia.

"To our knowledge, we have reported here the first longitudinal study showing that comprehensive lifestyle changes--or any intervention--are significantly associated with increases in cellular telomerase activity levels and telomere maintenance capacity in immune system cells," the authors conclude. "The implications of this study are not limited to men with prostate cancer. Comprehensive lifestyle changes may cause improvements in telomerase and telomeres that may be beneficial to the general population as well."

Related Health Concern: Prostate Cancer Overview

Malignant tumors develop multiple genetic abnormalities that accumulate progressively in individual cells during the course of tumor evolution. For example, abnormalities involving p53 generally occur early in the development of invasive breast cancers.220 What biological situation(s) or conditions allow p53 or other DNA repair proteins, the guardians at the gate, to become mutated enough to allow such expressions? If we know what steps are involved in this process(es), we can avoid or reduce them and prevent initiation or promotional events.

The conditions favoring the above appear to include inflammatory situations that are associated with metabolic products that favor the development of dysplasia and neoplasia. These biologically inflamed situations are characterized by the production of reactive oxygen species (ROS) that damage cell membranes, that is, free radicals. For example, we know that ROS, or free radicals, cause oxidative damage to LDL cholesterol to eventuate in atheromatous plaques that are major factors in coronary artery disease. ROS damage the lipid membranes of the cell by means of an oxidative reaction called lipid peroxidation. The cell membrane is critical to the cell's integrity; it is involved in the selective entry and exit of substances (ligands) that interact at the membrane border by means of a chemical reaction with docking sites called receptors.

Damage to structures like the cell membrane allows the tumor cell access to vital cell functions. Tumor cells, or what causes them, along with viruses, inactivate other parts of the surveillance mechanisms of the healthy organism. The interferon-signaling pathway (ISP) is often knocked out by tumor cells because interferons are molecules that actively patrol against viruses and cancer cells. In situations where cancer has developed, the ISP is often damaged or inactivated. Therefore, tumor-promoting situations are ones in which there is vulnerability of the organism due to inflammatory conditions incited by events that lead to damage of the surveillance mechanisms and result in access to vital cell functions.

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