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Toxins in environment might make you older than your years

May 28, 2014
Courtesy of Cell Press
and World Science staff

Why are some 75-year-olds down­right spry while oth­ers can barely get around? Part of the ex­plana­t­ion, say re­search­ers in a new stu­dy, is dif­fer­ences in ex­po­sure to harm­ful sub­stances in the en­vi­ron­ment, chem­i­cals such as ben­zene, cig­a­rette smoke, and even stress.

While the birth date on your driver’s li­cense can tell you your chron­o­log­i­cal age, that might mean lit­tle in terms of your body’s bi­o­log­i­cal age. The re­search­ers say that what we need now is a bet­ter un­der­stand­ing of the chem­i­cals in­volved in ag­ing and “biomark­ers” to meas­ure their ef­fects.

“The rate of phys­i­o­logical, or mo­lec­u­lar, ag­ing dif­fers be­tween in­di­vid­u­als in part be­cause of ex­po­sure to ‘geron­to­gens’, i.e., en­vi­ron­men­tal fac­tors that af­fect ag­ing,” said Nor­man Sharp­less from the Uni­vers­ity of North Car­o­li­na, Chap­el Hill. “We be­lieve just as an un­der­stand­ing of car­cino­gens has in­formed can­cer bi­ol­o­gy, so will an un­der­stand­ing of geron­to­gens ben­e­fit the study of ag­ing. By iden­ti­fy­ing and avoid­ing geron­to­gens, we will be able to in­flu­ence ag­ing and life ex­pect­an­cy.”

The study is pub­lished May 28 in the jour­nal Trends in Mo­lec­u­lar Med­i­cine.

In the fu­ture, blood tests eval­u­at­ing biomark­ers of mo­lec­u­lar age might be used to un­der­stand dif­fer­ences amongst in­di­vid­u­als in ag­ing rates. Those tests might meas­ure key path­ways in­volved in the pro­cess of cel­lu­lar se­nes­cence or chem­i­cal modifica­t­ions to DNA. In fact, Sharp­less said in the in­ter­est of full dis­clo­sure that he has founded a com­pa­ny to com­mer­cial­ize mo­lec­u­lar tests of ag­ing.

From a pub­lic health per­spec­tive, cig­a­rette smoke is likely the most im­por­tant geron­to­gen, Sharp­less said. Cigarettes are linked with can­cers but al­so with ath­er­o­scle­rosis, pul­mo­nary fi­bro­sis, and oth­er age-associated dis­eases. UV radia­t­ion from the sun makes us old­er too, and Sharp­less and his col­leagues re­cently showed that chemoth­erapy treat­ment is al­so a strong geron­to­gen. With the aid of a mouse mod­el that they de­vel­oped, his team is pre­pared to study these geron­to­gens and oth­ers in much great­er de­tail.

The re­search­ers call for a con­cert­ed re­search ef­fort to un­der­stand the clin­i­cal uses for mo­lec­u­lar tests of ag­ing. “We be­lieve the com­par­i­son of mo­lec­u­lar mark­ers of ag­ing to clin­i­cal out­comes should beg­in in earnest,” Sharp­less said. For ex­am­ple, he asked, can biomark­ers to ag­ing pre­dict tox­i­city from sur­gery or chemoth­erapy in pa­tients in whom chron­o­log­i­cal age is al­ready a known risk fac­tor?

Sharp­less does cau­tion against mak­ing tests of mo­lec­u­lar age availa­ble to con­sumers and pa­tients di­rect­ly. “The po­ten­tial for mis­com­mu­nica­t­ion and oth­er harm seems real,” he said.


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Why are some 75-year-olds downright spry while others can barely get around? Part of the explanation, say researchers in a new study, is differences in exposure to harmful substances in the environment, chemicals such as benzene, cigarette smoke, and even stress. While the birth date on your driver’s license can tell you your chronological age, that might mean little in terms of the biological age of your body. The researchers say that what we need now is a better understanding of the chemicals involved in aging and “biomarkers” to measure their effects. “The rate of physiologic, or molecular, aging differs between individuals in part because of exposure to ‘gerontogens’, i.e., environmental factors that affect aging,” said Norman Sharpless from the University of North Carolina, Chapel Hill. “We believe just as an understanding of carcinogens has informed cancer biology, so will an understanding of gerontogens benefit the study of aging. By identifying and avoiding gerontogens, we will be able to influence aging and life expectancy at a public health level.” The study is published May 28 in the journal Trends in Molecular Medicine. In the future, blood tests evaluating biomarkers of molecular age might be used to understand differences amongst individuals in aging rates. Those tests might measure key pathways involved in the process of cellular senescence or chemical modifications to DNA. In fact, Sharpless said in the interest of full disclosure that he has founded a company to commercialize molecular tests of aging. From a public health perspective, cigarette smoke is likely the most important gerontogen, Sharpless said. Cigarettes are linked with cancers but also with atherosclerosis, pulmonary fibrosis, and other age-associated diseases. UV radiation from the sun makes us older too, and Sharpless and his colleagues recently showed that chemotherapy treatment is also a strong gerontogen. With the aid of a mouse model that they developed, his team is prepared to study these gerontogens and others in much greater detail. The researchers call for a concerted research effort to understand the clinical uses for molecular tests of aging as well as the epidemiology of accelerated aging. “We believe the comparison of molecular markers of aging to clinical outcomes should begin in earnest,” Sharpless said. For example, he asked, can biomarkers to aging predict toxicity from surgery or chemotherapy in patients in whom chronological age is already a known risk factor? Sharpless does caution against making tests of molecular age available to consumers and patients directly. “The potential for miscommunication and other harm seems real,” he said.