SUGARED SODA CONSUMPTION CELL AGING ASSOCIATED

Sugar-sweetened soda consumption might promote disease independently from its role in obesity, according to UC San Francisco researchers who found in a new study that drinking sugary drinks was associated with cell aging.

The study revealed that telomeres -- the protective units of DNA that cap the ends of chromosomes in cells -- were shorter in the white blood cells of survey participants who reported drinking more soda. The findings were reported online October 16, 2014 in the American Journal of Public Health.

The length of telomeres within white blood cells -- where it can most easily be measured -- has previously been associated with human lifespan. Short telomeres also have been associated with the development of chronic diseases of aging, including heart disease, diabetes, and some types of cancer.

"Regular consumption of sugar-sweetened sodas might influence disease development, not only by straining the body's metabolic control of sugars, but also through accelerated cellular aging of tissues," said Elissa Epel, PhD, professor of psychiatry at UCSF and senior author of the study.

"This is the first demonstration that soda is associated with telomere shortness," Epel said. "This finding held regardless of age, race, income and education level. Telomere shortening starts long before disease onset. Further, although we only studied adults here, it is possible that soda consumption is associated with telomere shortening in children, as well."

The authors cautioned that they only compared telomere length and sugar-sweetened soda consumption for each participant at a single time point, and that an association does not demonstrate causation. Epel is co-leading a new study in which participants will be tracked for weeks in real time to look for effects of sugar-sweetened soda consumption on aspects of cellular aging. Telomere shortening has previously been associated with oxidative damage to tissue, to inflammation, and to insulin resistance.

Based on the way telomere length shortens on average with chronological age, the UCSF researchers calculated that daily consumption of a 20-ounce soda was associated with 4.6 years of additional biological aging. This effect on telomere length is comparable to the effect of smoking, or to the effect of regular exercise in the opposite, anti-aging direction, according to UCSF postdoctoral fellow Cindy Leung, ScD, from the UCSF Center for Health and Community and the lead author of the newly published study.

The average sugar-sweetened soda consumption for all survey participants was 12 ounces. About 21 percent in this nationally representative sample reported drinking at least 20 ounces of sugar-sweetened soda a day.

"It is critical to understand both dietary factors that may shorten telomeres, as well as dietary factors that may lengthen telomeres," Leung said. "Here it appeared that the only beverage consumption that had a measurable negative association with telomere length was consumption of sugared soda."

The finding adds a new consideration to the list of links that has tied sugary beverages to obesity, metabolic syndrome, type 2 diabetes, and cardiovascular disease, and that has driven legislators and activists in several U.S. jurisdictions to champion ballet initiatives that would tax sugar-sweetened beverage purchases with the goal of discouraging consumption and improving public health.

The UCSF researchers measured telomeres after obtaining stored DNA from 5,309 participants, ages 20 to 65, with no history of diabetes or cardiovascular disease, who had participated in the nation's largest ongoing health survey, called the National Health and Nutrition Examination Survey, during the years 1999 through 2002. They found that the amount of sugar-sweetened soda a person consumed was associated with telomere length, as measured in the laboratory of Elizabeth Blackburn, PhD, professor of biochemistry at UCSF and a winner of the 2009 Nobel Prize in Physiology or Medicine for her telomere-related discoveries.

Additional study authors include, from UCSF, Nancy E. Adler, PhD, professor of psychiatry and director of the Center for Health and Community, and Jue Lin, PhD, an associate researcher with Blackburn's lab; from UC Berkeley, Barbara A. Laraia, PhD, director of public health nutrition; from the University of Michigan, Belinda Needham, PhD, assistant professor of epidemiology; and from Stanford University, David H. Rehkopf, ScD, assistant professor of medicine.

Major funding for the study was provided by the National Institutes of Health. Lin is a shareholder of Telomere Diagnostics, Inc.

HIGH FAT DIET POSTPONES BRAIN AGING IN MICE

New Danish-led research suggests that signs of brain aging can be postponed in mice if placed on a high-fat diet. In the long term, this opens the possibility of treatment of children suffering from premature aging and patients with Alzheimer's and Parkinson's disease. The research project is headed by the Center for Healthy Aging, University of Copenhagen and the National Institute of Health.

When we get older, defects begin to develop in our nervous system, our brain loses some of its intellectual capacity, and the risk of developing diseases such as Parkinson's and Alzheimer's increases. Alzheimer's disease is currently the fastest-growing age-related disease.

Throughout our lives, it is important that our cells -- to the extent possible -- keep our DNA undamaged, and, therefore, the cells have a system that repairs the damage that occurs all the time. Humans age when the repair system ceases to function. In diseases such as Alzheimer's, the researchers also see damage to the DNA

A new research project headed by the Center for Healthy Aging, University of Copenhagen and the National Institute of Health has studied mice having a defect in their DNA repair system. In humans, this defect causes the disorder Cockayne syndrome, where patients prematurely age as children and die at an age of 10-12 years. The study shows that placing a mouse model of Cockayne syndrome on a high-fat diet will postpone aging processes such as impaired hearing and weight loss.

Fat putting a stop to premature aging

"The study is good news for children with Cockayne syndrome, because we do not currently have an effective treatment. Our study suggests that a high-fat diet can postpone aging processes. A diet high in fat also seems to postpone the aging of the brain. The findings therefore potentially imply that patients with Alzheimer's and Parkinson's disease in the long term may benefit from the new knowledge," says Professor Vilhelm Bohr from the Center for Healthy Aging, University of Copenhagen and the National Institute of Health, who has headed the study.

Our brain has a constant need for fuel in the form of either sugar or so-called ketones. Ketones are the brain's fuel reserve, and, in particular, play an important role in periods of low blood sugar levels, e.g. if you are fasting. This is because the body breaks down fat if it needs sugar, and during this process it produces ketones. The researchers see a particular positive effect when the mice are given the so-called medium chain fatty acids -- e.g. from coconut oil.

Brain cells need extra fuel

"In cells from children with Cockayne syndrome, we have previously demonstrated that aging is a result of the cell repair mechanism being constantly active. It eats into the resources and causes the cell to age very quickly. We therefore hope that a diet with a high content of coconut oil or similar fats will have a beneficial effect, because the brain cells are given extra fuel and thus the strength to repair the damage," says postdoc Morten Scheibye-Knudsen from the National Institute of Health.

The study has just been published in the scientific journal Cell Metabolism.

ON OFF SWITCH FOR AGING CELLS DISCOVERED BY SCIENTISTS

Scientists at the Salk Institute have discovered an on-and-off “switch” in cells that may hold the key to healthy aging. This switch points to a way to encourage healthy cells to keep dividing and generating, for example, new lung or liver tissue, even in old age.

In our bodies, newly divided cells constantly replenish lungs, skin, liver and other organs. However, most human cells cannot divide indefinitely–with each division, a cellular timekeeper at the ends of chromosomes shortens. When this timekeeper, called a telomere, becomes too short, cells can no longer divide, causing organs and tissues to degenerate, as often happens in old age. But there is a way around this countdown: some cells produce an enzyme called telomerase, which rebuilds telomeres and allows cells to divide indefinitely.

In a new study published September 19 in the journalGenes and Development, scientists at the Salk Institute have discovered that telomerase, even when present, can be turned off.

“Previous studies had suggested that once assembled, telomerase is available whenever it is needed,” says senior author Vicki Lundblad, professor and holder of Salk’s Ralph S. and Becky O'Connor Chair. “We were surprised to discover instead that telomerase has what is in essence an ‘off’ switch, whereby it disassembles.”

Understanding how this “off” switch can be manipulated–thereby slowing down the telomere shortening process–could lead to treatments for diseases of aging (for example, regenerating vital organs later in life).

Lundblad and first author and graduate student Timothy Tucey conducted their studies in the yeast Saccharomyces cerevisiae, the same yeast used to make wine and bread. Previously, Lundblad’s group used this simple single-celled organism to reveal numerous insights about telomerase and lay the groundwork for guiding similar findings in human cells.

“We wanted to be able to study each component of the telomerase complex but that turned out to not be a simple task,” Tucey said. Tucey developed a strategy that allowed him to observe each component during cell growth and division at very high resolution, leading to an unanticipated set of discoveries into how–and when–this telomere-dedicated machine puts itself together.

Every time a cell divides, its entire genome must be duplicated. While this duplication is going on, Tucey discovered that telomerase sits poised as a “preassembly” complex, missing a critical molecular subunit. But when the genome has been fully duplicated, the missing subunit joins its companions to form a complete, fully active telomerase complex, at which point telomerase can replenish the ends of eroding chromosomes and ensure robust cell division.

Surprisingly, however, Tucey and Lundblad showed that immediately after the full telomerase complex has been assembled, it rapidly disassembles to form an inactive “disassembly” complex — essentially flipping the switch into the “off” position. They speculate that this disassembly pathway may provide a means of keeping telomerase at exceptionally low levels inside the cell. Although eroding telomeres in normal cells can contribute to the aging process, cancer cells, in contrast, rely on elevated telomerase levels to ensure unregulated cell growth. The “off” switch discovered by Tucey and Lundblad may help keep telomerase activity below this threshold.