The paper: “Quantification of biological aging in young adults,” by Daniel Belsky, Avshalom Caspi, et al. was published in the Proceedings of the National Academy of Sciences. This paper served as a progress report on an aging study, the Dunedin Study, which is an ongoing longitudinal study funded by the New Zealand Health Research Council, U.S. National Institute on Aging, UK Medical Research Council, Jacobs Foundation and the Yad Hanadiv Rothschild Foundation. Much like the Framingham Heart Study that began in 1948 and has gone on to study subsequent generations’ cardiovascular health this study envisions studying the aging process over a lifetime.
The study covers the aging process in in a group of just over a thousand people born in 1972 or 1973 in Dunedin, New Zealand from age 26 to 38 years old and reports on 954 of the original 1,037 Dunedin study participants. Thirty of the subjects had died by age 38: 12 by illnesses, 10 by accidents and eight by suicide or drug overdose. Another 26 did not take part in the study at age 38 and twenty-seven participants had insufficient data to be included, but could be included in later years.
At age 38 in 2012 the study measured a panel of 18 biological measures that include such things as blood pressure, lung function, cholesterol, body mass index, inflammation and the integrity of their DNA (including the length of their telomeres) that were combined to determine whether people are aging faster or slower than their peers.
The aging process isn’t all genetic. Studies of twins have found that only about 20 % of aging can be attributed to genes. According to Dr. Belsky from the Center for the Study of Aging and Human Development at Duke University and the lead author of the paper, there’s a great deal of environmental influence in the aging process. It has long been known that socioeconomically disadvantaged populations suffer increased illness as they grow older and the poor die younger.
The study found that though most participants aged at a rate that was near to one biological year per calendar year, some participants were found to be aging as fast as three years per calendar year, and some were aging at zero years per year, in effect staying younger than their age. My apologies to those slow agers- you do exist.
Measuring aging is controversial. In the Dunedin Study they measured aging in two ways. First, they used a series of biomarkers that they calibrated on a large, mixed-age sample. Then they applied this algorithm to the biomarker data collected when the Dunedin Study participants were all chronologically 38 years old to calculate their “true” Biological Age. Second, the researchers performed a longitudinal analysis of 18 biomarkers in the participants when they were 26 years old, 32 years old and 38 years old. They used this longitudinal data to model how each individual changed over the 12-year study period to calculate their personal rate of aging.
Rate of aging and biological age are two different approaches to quantifying aging. The rate of aging captures real-time changes in human physiology across multiple body systems using all 18 biomarkers recorded in the Dunedin Study databank. The other approach, biological age, provides a point-in-time snapshot of physiological condition examined against the National Health and Nutrition Examination Survey (NHANES) cross-sectional data. NHANES is a program of CDC studies designed to assess the health and nutritional status of adults and children in the United States. Both approaches yielded consistent results.
The study participants with an older biological age also have shown a faster rate of aging over the preceding 12 years. The scientists estimate that about half of the difference between biological age and chronological age at 38 had accumulated over the past 12 years. Their analysis showed that biological age can provide a summary of accumulated aging at a single point in time.
Further, the biological measures of study participants’ aging were mirrored in their functional status, brain health, self-awareness of their own physical well-being, and their facial appearance. Study members who had an older biological age than their chronical age and who experienced a faster rate of aging scored lower on tests of balance, strength, and motor coordination, and reported more physical limitations. These biologically older participants also scored lower on IQ tests when they were aged 38 years, showed actual decline in full-scale IQ score from childhood to age-38 follow-up, and exhibited signs of elevated risk for stroke and for dementia measured from images of micro vessels in their eyes. Furthermore, those with an older biological age and who experienced a faster rate of aging reported feeling in worse health. People who did not know the study members beyond a facial photograph were able to see differences in the aging of their faces.
The Dunedin Study will continue to follow the study group. The next evaluation will be when they are 45. The researchers are charting the participants’ diet, exercise and other behaviors to try and evaluate which behaviors are working to slow down aging. The ultimate goal, of course, is to be able to intervene in the aging process itself, rather than addressing killers like heart disease or cancer in isolation, Dr. Belsky said; “As we get older, our risk grows for all kinds of different diseases. To prevent multiple diseases simultaneously, aging itself has to be the target. Otherwise, it’s a game of whack-a-mole.”
The greatest gift in life would be for my true love and I to grow old slowly together. I miss quote and take great liberties with Robert Browning’s poem “Rabbi Ben Ezra:”
Grow old along with me!
The best is yet to be,
The last of life, for which the first was made:
Our times are in His hand; trust God: be not afraid.
Henceforth I summon age,
Life’s journey having reached this stage
Once more upon our adventure fearless and unafraid.
Together: We shall face the last of life, for which the first was made.
CITATION: “Quantification of biological aging in young adults,” Daniel Belsky, Avshalom Caspi, et al. PNAS, July 7, 2015. DOI: 10.1073/pnas.1506264112