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Recent research published in the medical journal Laryngoscope lends further credence to the belief that supplemental antioxidants may protect the inner ear from traumatic and age-related hearing loss.1

In a study conducted at Southern Illinois University, scientists studied the effects of supplemental vitamin E on hearing loss induced by a potent anticancer drug, cisplatin. Rats receiving vitamin E before an injection of cisplatin sustained far less damage to the sensory hairs of the inner ear than rats that did not receive vitamin E. Scientists believe that cisplatin damages hearing in much the same way that normal aging erodes hearing; both conditions are believed to be the result of free-radical damage.2,3 Scientists hypothesize that vitamin E and other antioxidants are able to neutralize damaging free radicals before they affect sensitive sensory hairs in the inner ear.

The study’s findings echo similar research published in recent years. In 2002, Yale University researchers determined that hearing loss correlates with both age and noise exposure. They found that subjects with higher vitamin E levels tend to suffer less loss of hearing than patients with low vitamin E levels.4 Likewise, in a study conducted in Israel in 2003, human subjects with sudden hearing loss of unknown origin were more likely to recover their hearing after treatment with supplemental vitamin E than patients who did not receive the antioxidant.5

Other recent studies have noted a hearing-protective effect for other supplemental antioxidants, including resveratrol,6 vitamin C, melatonin,2 and acetyl-l-carnitine and alpha-lipoic acid.3

—Dale Kiefer

A considerable increase in early human life span may have been a key factor in shaping modern civilization, according to a new fossil study published July 5, 2004, in the Proceedings of the National Academy of Sciences.

Scientists at the University of Michigan and University of California, Riverside, analyzed the ratio of older to younger adults in 750 hominid tooth samples from successive time periods, assessing the significance of differences in rates of molar wear. Their findings showed that the number of people surviving to an older age more than quadrupled during the early Upper Paleolithic Period around 30,000 BC, when Homo sapiens was becoming established in Europe.

In the study, the researchers defined “old” to be at least double the age of reproductive maturation. “While the age of reproductive maturation may have varied in early human groups, if it were 15, then age 30 would be the age at which one could theoretically first become a grandmother,” Caspari noted.

The jump in longevity may have been a key factor in the shaping of modern civilization. Larger numbers of older people provided distinct evolutionary advantages such as tighter social relationships and kinship bonds, as well as allowing greater efficiency in the accumulation and transmission of more specialized knowledge from older, experienced individuals to younger generations. This so-called “grandmother hypothesis” posits that grandmothers are useful because of the knowledge they pass on to reproductive-age daughters and their daughters’ offspring.

Longer life span would also have increased the number of years available for reproduction, working to promote population expansion, and creating social pressures that led to the growth of trade networks, increased mobility, and more complex systems of cooperation and competition.

“There has been a lot of speculation about what gave modern humans their evolutionary advantage. This research provides a simple explanation for which there is now concrete evidence: Modern humans were older and wiser,” the study’s co-authors wrote.

—Dean S. Cunningham, MD, PhD

Researchers at the Mayo Clinic in Rochester, MN, were searching for genetic causes of cancer when they stumbled on something unexpected—a gene that controls important aspects of aging.*

According to findings published in the journal Nature Genetics, the scientists discovered that mutant mice lacking a certain gene, dubbed BubR1, die of old age five times faster than normal mice. This glaring discrepancy in life span suggests that the protein coded by BubR1 is involved in maintaining normal life span. Mice without this protein show numerous early signs of accelerated aging, including thinning skin, a weakening immune system, infertility, cataracts, and spinal abnormalities.

Turning their attention to normal mice—which have the gene and thus the BubR1 protein—researchers discovered that BubR1 protein levels normally decrease with age. This prompted speculation that a decline in BubR1 protein may be responsible for at least some of the physiological decline associated with aging.

Because BubR1 protein levels dwindle in the testis and ovaries of normal mice with advancing age, scientists hypothesize that the protein decrease may be responsible for infertility and certain age-associated birth defects, such as Down’s syndrome, in humans. BubR1-lacking mutant mice are infertile due to an inability to pass the correct number of chromosomes to reproductive germ cells. Down’s syndrome and other common birth defects associated with advanced age in humans result when a fertilized egg contains an incorrect number of chromosomes.

This intriguing discovery provides new insight into the complexities of aging and may help scientists to better understand and eventually treat some of the disorders associated with human aging.

—Dale Kiefer