A recent open access paper describing efforts to measure degenerative aging in people in their twenties and thirties age bracket has been doing the rounds in the media. It is interesting to see people making an effort to create definitive measurements of aging in earlier age groups. The signs should certainly be there to see, given discriminating enough biotechnologies: the underlying damage that causes aging occurs at all ages. I'm also very much in favor of anything that might make the younger people in the audience feel more like they have skin in the game. In my experience one of the great ironies in persuading people to care about aging, to speak out for the cause and help fund research, is that the young think it isn't their problem, and the old think that there is no point in helping given that meaningful results will only arrive in the decades ahead. Everyone looks to their own lawn and little beyond.
Nonetheless, the young age too. Aging is a process of damage accumulation, accelerating to greater obvious results in later life due to interactions between damage that cause problems greater than the sum of the parts, and also due to declining repair and maintenance mechanisms. Damage feeds on damage in any machine: the more of it there is, the faster it arrives, and old, damaged machines see a rapid decline in mean time to failure. There are numerous types of cellular and molecular damage at the roots of aging, some of which can be repaired by our cells, were they operating at best capacity, and others that cannot. Aging is thus caused by a mix of two types of harm. On the one hand there is a slow and relentless accumulation of some types of defect: consider cross-links in the extracellular matrix that cannot be broken down by any of the enzymes we produce, generated as comparatively rare byproducts of metabolic operation, or mitochondrial mutations that can evade cellular quality control mechanisms and result in a growing population of dysfunctional cells packed with dysfunctional mitochondria. On the other hand there is a constant, ongoing, rapid creation of other types of defect that is matched by an equally rapid and capable set of repair processes. Unfortunately that repair effort itself winds down over time, allowing damage to get ever further ahead. Here you might think of plain old tissue maintenance by stem cell populations, as the decline of stem cell activity in aging is an important concern in medical research these days.
I think that much further work would need to be done in order to validate that the methods of measuring aging used by these researchers hold up well enough, and in fact correlate usefully with outcomes. Telomere length in particular is very flaky as usually measured in white blood cells, prone to all sorts of interesting and apparently contradictory outcomes in various different studies.
Researchers introduced a panel of 18 biological measures that may be combined to determine whether people are aging faster or slower than their peers. The data comes from the Dunedin Study, a landmark longitudinal study that has tracked more than a thousand people born in 1972-73 in the same town from birth to the present. Health measures like blood pressure and liver function have been taken regularly, along with interviews and other assessments. "We set out to measure aging in these relatively young people. Most studies of aging look at seniors, but if we want to be able to prevent age-related disease, we're going to have to start studying aging in young people."
The progress of aging shows in human organs just as it does in eyes, joints and hair, but sooner. So as part of their regular reassessment of the study population at age 38 in 2011, the team measured the functions of kidneys, liver, lungs, metabolic and immune systems. They also measured HDL cholesterol, cardiorespiratory fitness, lung function and the length of the telomeres -- protective caps at the end of chromosomes that have been found to shorten with age. The study also measures dental health and the condition of the tiny blood vessels at the back of the eyes, which are a proxy for the brain's blood vessels.
Based on a subset of these biomarkers, the research team set a "biological age" for each participant, which ranged from under 30 to nearly 60 in the 38-year-olds. The researchers then went back into the archival data for each subject and looked at 18 biomarkers that were measured when the participants were age 26, and again when they were 32 and 38. From this, they drew a slope for each variable, and then the 18 slopes were added for each study subject to determine that individual's pace of aging.
Most participants clustered around an aging rate of one year per year, but others were found to be aging as fast as three years per chronological year. Many were aging at zero years per year, in effect staying younger than their age. As the team expected, those who were biologically older at age 38 also appeared to have been aging at a faster pace. A biological age of 40, for example, meant that person was aging at a rate of 1.2 years per year over the 12 years the study examined.
At present, much research on aging is being carried out with animals and older humans. Paradoxically, these seemingly sensible strategies pose translational difficulties. The difficulty with studying aging in old humans is that many of them already have age-related diseases. Age-related changes to physiology accumulate from early life, affecting organ systems years before disease diagnosis. Thus, intervention to reverse or delay the march toward age-related diseases must be scheduled while people are still young. Early interventions to slow aging can be tested in model organisms. The difficulty with these nonhuman models is that they do not typically capture the complex multifactorial risks and exposures that shape human aging. Moreover, whereas animals' brief lives make it feasible to study animal aging in the laboratory, humans' lives span many years. A solution is to study human aging in the first half of the life course, when individuals are starting to diverge in their aging trajectories, before most diseases (and regimens to manage them) become established. The main obstacle to studying aging before old age - and before the onset of age-related diseases - is the absence of methods to quantify the Pace of Aging in young humans.
We studied aging in a population-representative 1972-1973 birth cohort of 1,037 young adults followed from birth to age 38 y with 95% retention: the Dunedin Study. When they were 38 y old, we examined their physiologies to test whether this young population would show evidence of individual variation in aging despite remaining free of age-related disease. We next tested the hypothesis that cohort members with "older" physiologies at age 38 had actually been aging faster than their same chronologically aged peers who retained "younger" physiologies; specifically, we tested whether indicators of the integrity of their cardiovascular, metabolic, and immune systems, their kidneys, livers, gums, and lungs, and their DNA had deteriorated more rapidly according to measurements taken repeatedly since a baseline 12 y earlier at age 26. We further tested whether, by midlife, young adults who were aging more rapidly already exhibited deficits in their physical functioning, showed signs of early cognitive decline, and looked older to independent observers.
We developed and validated two methods by which aging can be measured in young adults, one cross-sectional and one longitudinal. Our longitudinal measure allows quantification of the pace of coordinated physiological deterioration across multiple organ systems (e.g., pulmonary, periodontal, cardiovascular, renal, hepatic, and immune function). We applied these methods to assess biological aging in young humans who had not yet developed age-related diseases. Young individuals of the same chronological age varied in their "biological aging" (declining integrity of multiple organ systems). Already, before midlife, individuals who were aging more rapidly were less physically able, showed cognitive decline and brain aging, self-reported worse health, and looked older. Measured biological aging in young adults can be used to identify causes of aging and evaluate rejuvenation therapies.
I absolutely disagree with the author's position that intervention to reverse aging and age-related disease must happen while people are young. It will be certainly be much easier to achieve medical control of aging when people are young, as therapies will then have to successfully repair far less damage and a much smaller variety of damage. But, and this is crucial, the whole point of developing methods of repair for the causes of aging rather than methods of merely slowing it down is so that the old can be rescued - so that we create rejuvenation. This is no small point: it is a core part of the plan for SENS and other repair-based rejuvenation strategies.