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A science writer probes the one risk factor shared by a bevy of devastating diseases

Borrowed Time: The Science of How and Why We Age

Sue Armstrong
Bloomsbury
2019
272 pp.
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Chronic disease states—including diabetes, most cancers, and cardiovascular and neurodegenerative syndromes—have become the leading drivers of morbidity and mortality. Medicine has set out to develop therapies for each condition separately, and yet they share a common denominator: aging. This has led to the revolutionary idea that interventions that slow aging will have the biggest impact on our collective health: not just extending life span but also delaying or preventing the onset of many diseases and improving functional parameters later in life.

But what causes aging, and how do we intervene? In Borrowed Time, Sue Armstrong describes proposed hallmarks of aging—which include accumulation of cellular damage, loss of stem cell function, cellular senescence, and others—and makes a cogent case for the role of each in driving age-associated dysfunction. Along the way, she describes the origins and development of the aging research field.

Many early scientists, we learn, came to the discipline via unusual routes. Armstrong recounts these individuals’ stints in lion taming and grave digging, with a nearly naked trek across India thrown in for good measure. Rather than a motley crew, one senses a common element: a fascination with biology and knowledge for its own sake. This is refreshing in an increasingly translation-centric world.

Alzheimer’s hijacks the latter half of the book. While it is probably the disease we fear most as we age, it is not likely more related to aging than are a myriad of diseases, making its emphasis a bit at odds with the book’s objective.

Nonetheless, Armstrong admirably takes a holistic approach to Alzheimer’s, comparing mainstream interventions that largely involve therapies designed to remove plaques and tangles with more controversial strategies that involve multimodal alleviation of risk factors—including abnormal metabolism, altered levels of micronutrients, enhanced inflammatory factors, and unhealthy behaviors—to prevent disease progression. Although the Alzheimer’s story is informative, one cannot help but see this in part as a missed opportunity to better define aging, which is not a set of diseases but rather a set of intrinsic biological processes that together confer systemic changes with age, making us susceptible to disease.

As part of her research for this book, Armstrong interviewed futurists who strive for dramatic increases in life span or even immortality, but she dismisses them as “exasperatingly narcissistic.” She draws a distinction between this group and scientists who aim for more modest benefits to human longevity. Indeed, the concept of modified aging is being thought of and pursued in myriad ways; however, the differences in viewpoints are narrowing between futurists and more mainstream scientists, and both likely provide valuable insights into the future of human aging. Borrowed Time would have benefited from efforts to seek common ground among the two groups.

Interventions to extend human health and life span are now being tested in a variety of shapes and forms, and although no one knows which ones will be the most successful or how best to validate them in humans, an influx of public- and private-sector resources has resulted in an armada of possible approaches. These include everything from drugs and supplements to longevity-based diets and lifestyle management schemes.

Equally interesting is the recent explosion of molecular biomarkers, which have emerged largely from artificial intelligence–based analysis of deep datasets. Armstrong describes perhaps the most well-known of these biomarkers: the epigenetic clock, which uses DNA methylation levels detected in cells from saliva or blood as aging predictors.

One path forward in human studies of aging will be to test whether interventions delay the onset of multiple chronic diseases simultaneously, as was the goal of the well-publicized “TAME” trial (Targeting Aging with Metformin) (1). Others are seeking to determine whether interventions delay or reverse the progression of aging biomarkers.

In Borrowed Time, Armstrong lays open the pathways that govern aging and describes some of the approaches to test aging interventions in humans. However, as interest and investments in this field grow, progress in the latter area may move faster than she (or many others) expect.

ACKNOWLEDGMENTS
B.K. is board chair of Mt. Tam Pharmaceuticals, a board member and scientific adviser for PDL Pharma, a scientific adviser for Affirmativ Health, and a board member of L-Nutra. B.K. is named on patents held by PDL Pharma related to aging interventions.

References

  1. N. Barzilai et al., Cell Metab. 23, 6 (2016).

About the author

The reviewer is at the Departments of Biochemistry and Physiology, National University of Singapore; Centre for Healthy Ageing, National University Health System, Singapore; Singapore Institute for Clinical Sciences, A*STAR, Singapore; and Buck Institute for Research on Aging, Novato, California, USA.