Why aging is one of the biggest public health problems of our time
Preventing aging may be one of the most strategic ways to combat major chronic diseases globally. Here’s why.
Aging is a hot topic right now. We’ve all heard of anti-aging skin creams and special longevity diets. But is the goal of preventing aging just to keep ourselves looking beautiful as we grow older? Here I’m going to explain why preventing aging may be one of the most strategic and important preventative public health measures we can take as a society.
The world is growing older
Human life expectancy has increased dramatically in the past two centuries. In the United Kingdom (UK), life expectancy has nearly doubled. While those born in the UK in 1841 on average lived until around 40 years old, people born in the UK can now on average expect to live until roughly 80 years old. And these numbers are projected to continue growing. Worldwide, the number of people that live to 80 or older is expected to triple between 2020 and 2050 (1). So as a global society, humans are living longer than ever before, and this increase in life expectancy has been happening quickly. But does that necessarily mean that we are becoming healthier as a society?
Aging fast and aging slow
While living longer sounds great, these increases in lifespan over the past 200 years have not necessarily lead to us enjoying longer disease-free lives (healthspan) (2). Aging involves a progressive loss of bodily function and integrity over time, such as a weakened immune system or physical frailty. This makes us increasingly vulnerable to disease and, ultimately, death. From mid-life onwards, physiological aging includes loss of bone and muscles mass, as well the accumulation of abdominal fat (3). This in turn leads to increases in blood pressure, inflammation, changes in hormone levels, and a decrease in sensitivity to hormones such as insulin (4). All of these changes directly impact our health and our ability to lead healthy lifestyles.
On the biological level, researchers have identified twelve hallmarks of aging that seem to be shared across many animal species, including humans (5). These include:
- A reduced ability of our cells to communicate with each other
- Chronic inflammation
- Gut health imbalance (dysbiosis)
- Genomic instability
- Shortening of telomeres (protective caps on ends of DNA)
- Epigenetic changes (e.g., altered DNA methylation)
- Loss of protein stability (proteostasis)
- Disabled ability to eradicate damaged cells and proteins (macroautophagy)
- Changes to metabolism and nutrient sensing
- Dysfunction of our mitochondria (energy powerhouses in our cells)
- Loss of cells’ ability to multiply (senescence)
- Stem cell damage and regeneration
Over time, aging entails degradation to all twelve of these biological systems and mechanisms. Many of these cellular hallmarks of aging have been shown to lead to chronic activation of our inflammation systems (which some call “inflammaging”) (6).
While we all grow older every year, we vary in how quickly and extensively we experience the kinds of biological and physiological decline described above. This can be described as variation in rates of aging. Or to put it in other terms, some people age “faster” than others. How “fast” we age ultimately shapes the extent of middle and late life disease and disability, and determines whether we die earlier than the average life expectancy where we live (premature mortality) or whether we live extremely long lives (longevity).
How “fast” we age can result in major differences between calendar age and so-called biological age. Two persons born on the same day may differ substantially in biological age. One could be relatively healthy, whereas the other could already be far down a path of age-related physiological, cognitive, and biological decline. When your biological age is older than your chronological age, this is what we call biological age acceleration. Even within the same individual, different tissues (e.g., heart, brain) can age at different rates and through different mechanisms (7). One really cool area of research right now is in creating biological “clocks” using biological data like DNA methylation, blood proteins, or blood biochemistry data. There are a few good recent review papers out there on the technology and methods used to build biological clocks (7,8) and a few direct-to-consumer commercial products already exist that will measure your biological age using a blood sample.
Aging is the biggest contributor to most common chronic diseases
Now let’s get to the real point of all of this. Put simply, aging is the single most important risk factor for nearly all common chronic diseases (9). Major chronic diseases such as cardiovascular disease, diabetes, cancer, and neurodegenerative disease all show increasing rates with age (10). And each of these major chronic diseases has been linked to the aging-related physiological changes described above and the twelve hallmarks of biological aging (5,9–11). This means that aging, as a set of biological and physiological mechanisms, is at the root of most of the major chronic diseases worldwide.
This also helps us to identify why the number of people who have two or more diseases simultaneously (multimorbidity) is rising globally (12). As global populations are growing older, the aging-related causes of one chronic disease are the same ones that will likely cause another chronic disease. As people continue to get older and older, the same underlying problems associated with aging continue to lead to the development of disease after disease. For a great comprehensive review on multimorbidity and the challenges and solutions that lie ahead, I recommend a recent article published in Nature Medicine.
Why are chronic diseases such a large public health concern, and why should we care about preventing them? Because the development of chronic diseases and multimorbidity are the major causes of death worldwide. In fact, all of the top 10 causes of death in the global population over 70 years are chronic diseases (13). And those with multimorbidity or blood markers of chronic disease die up to 20 years younger than those without multimorbidity and/or low levels of disease markers (14,15).
Opportunities
Unfortunately, historical evidence from the past several decades in the UK and the Netherlands indicates that as populations are starting to live longer, they are spending more time in poor health (16). Our aim as a society should be moving towards promoting healthy aging. This would mean an extension of healthy, disease-free life (healthspan) and longevity. For example, those who survive to over 100 or even 110 years show progressively later onset of major disease and shorter duration of disease late in life (17,18).
Now think for a moment about the opportunity that addressing aging presents. If most chronic diseases share in common the same underlying aging mechanisms and patterns, then if we focus our preventative efforts on aging itself this would result in prevention of most chronic diseases simultaneously. With one fell swoop, preventative efforts would touch cardiovascular diseases, diabetes, dementias, chronic liver and kidney diseases, cancer, and many others.
By addressing aging, we also address the burden that prolonged periods of chronic disease and disability creates on our health infrastructures and economies. Reducing the length and severity of late-life morbidity will have a major impact on the economic burden of age-related diseases on society. In the United States alone, the value of slowing aging and increasing life expectancy by 1 year has been estimated to be US$ 38 trillion, whereas the value of slowing aging by 10 years would be US$ 367 trillion (19).
In a world as complex and interconnected as ours, we need a strategic plan to move forward and make the world better. In terms of improving global health, curtailing rising rates of multimorbidity, and avoiding premature deaths worldwide, I can think of few more strategic and widely beneficial approaches as targeting aging itself.
Austin Argentieri is researcher at Harvard and the Broad Institute. His work is focused on using big data, machine learning, and biological data to better understand human aging and predict age-related diseases. Austin can be found online at austinargentieri.com, as well as on Twitter and LinkedIn.
References
1. United Nations, Department of Economic and Social Affairs, Population Division. World Population Ageing 2019: Highlights. (2019).
2. Crimmins, E. M. Lifespan and Healthspan: Past, Present, and Promise. Gerontologist 55, 901–911 (2015). https://doi.org/10.1093/geront/gnv130
3. Belsky, D. W. et al. Quantification of biological aging in young adults. Proc Natl Acad Sci U S A 112, E4104–4110 (2015). https://doi.org/10.1073/pnas.1506264112
4. Chahal, H. S. & Drake, W. M. The endocrine system and ageing. J Pathol 211, 173–180 (2007). https://doi.org/10.1002/path.2110
5. López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M. & Kroemer, G. Hallmarks of aging: An expanding universe. Cell 186, 243–278 (2023). https://doi.org/10.1016/j.cell.2022.11.001
6. Franceschi, C., Garagnani, P., Parini, P., Giuliani, C. & Santoro, A. Inflammaging: a new immune-metabolic viewpoint for age-related diseases. Nat Rev Endocrinol 14, 576–590 (2018). https://doi.org/10.1038/s41574-018-0059-4
7. Rutledge, J., Oh, H. & Wyss-Coray, T. Measuring biological age using omics data. Nat Rev Genet (2022). https://doi.org/10.1038/s41576-022-00511-7
8. Horvath, S. & Raj, K. DNA methylation-based biomarkers and the epigenetic clock theory of ageing. Nat Rev Genet 19, 371–384 (2018). https://doi.org/10.1038/s41576-018-0004-3
9. Niccoli, T. & Partridge, L. Ageing as a risk factor for disease. Curr Biol 22, R741–752 (2012). https://doi.org/10.1016/j.cub.2012.07.024
10. Partridge, L., Deelen, J. & Slagboom, P. E. Facing up to the global challenges of ageing. Nature 561, 45–56 (2018). https://doi.org/10.1038/s41586-018-0457-8
11. Kennedy, B. K. et al. Geroscience: linking aging to chronic disease. Cell 159, 709–713 (2014). https://doi.org/10.1016/j.cell.2014.10.039
12. Langenberg, C., Hingorani, A. D. & Whitty, C. J. M. Biological and functional multimorbidity-from mechanisms to management. Nat Med 29, 1649–1657 (2023). https://doi.org/10.1038/s41591-023-02420-6
13. Collaborators, G. A. Global, regional, and national burden of diseases and injuries for adults 70 years and older: systematic analysis for the Global Burden of Disease 2019 Study. BMJ 376, e068208 (2022). https://doi.org/10.1136/bmj-2021-068208
14. Crimmins, E. M., Kim, J. K. & Seeman, T. E. Poverty and biological risk: the earlier “aging” of the poor. J Gerontol A Biol Sci Med Sci 64, 286–292 (2009). https://doi.org/10.1093/gerona/gln010
15. Barnett, K. et al. Epidemiology of multimorbidity and implications for health care, research, and medical education: a cross-sectional study. Lancet 380, 37–43 (2012). https://doi.org/10.1016/S0140-6736(12)60240-2
16. Westendorp, R. G. What is healthy aging in the 21st century? Am J Clin Nutr 83, 404S-409S (2006). https://doi.org/10.1093/ajcn/83.2.404S
17. Andersen, S. L., Sebastiani, P., Dworkis, D. A., Feldman, L. & Perls, T. T. Health span approximates life span among many supercentenarians: compression of morbidity at the approximate limit of life span. J Gerontol A Biol Sci Med Sci 67, 395–405 (2012). https://doi.org/10.1093/gerona/glr223
18. Christensen, K., McGue, M., Petersen, I., Jeune, B. & Vaupel, J. W. Exceptional longevity does not result in excessive levels of disability. Proc Natl Acad Sci U S A 105, 13274–13279 (2008). https://doi.org/10.1073/pnas.0804931105
19. Scott, A. J., Ellison, M. & Sinclair, D. A. The economic value of targeting aging. Nature Aging 1, 616–623 (2021). https://doi.org/doi:10.1038/s43587-021-00080-0
