The concept of aging is one that we are all too familiar with. Aging is something that, no matter how hard they try, nobody can avoid. As we age, it is not uncommon to hear something along the lines of “You’re only as old as you feel.” And while your number of laps around the sun may not show it, this saying is rooted in truth. In this article, we will introduce the topic of biological aging in comparison to the traditional and better-known concept of chronological aging. It’s a classic game of how you feel on the inside versus how many years you’ve been alive. Let’s get into it.
Biological Age vs Chronological Age
We all age, but at different rates. The amount of time passed does not manifest in everyone the same way. You may feel and seem younger or older than how long you’ve been alive would predict.
By early adulthood, human physiological development is complete. From then onwards, the aging process starts and physiological functions begin to slowly decay. Aging can be defined as the time-related decline of the physiological functions necessary for survival. But this decline is not linearly caused by the time that has passed since you were born, but rather by the cellular damage that has accumulated throughout your life [1].
Aging is not linearly caused by the time that has passed since you were born, but rather by the cellular damage that has accumulated throughout your life.
The number of years you’ve been alive is your chronological age—it’s a measure of time passed. But that’s not an accurate measure of how old your cells and tissues are—that’s your biological age. In general, chronological and biological aging are correlated, but biological aging can be accelerated or decelerated by individual physiological and lifestyle factors [2,3]. Biological age is an indication of the functional health of your body and its susceptibility to age-related disorders. Therefore, it’s a more accurate indication of healthspan and of how long you may remain healthy [4].
Biological age is an indication of the functional health of your body and its susceptibility to age-related disorders.
If you lead a healthy lifestyle and are notably fit for your age, your biological age may be lower than your chronological age. On the other hand, if you're unhealthy and in poor physical condition, your biological age may be higher.
Biological Aging Starts at The Cellular Level
Biological aging happens at the cellular level. The signs of age you see on the outside — wrinkles, gray hair, physical decline — are all consequences of what happens in cells and how it affects the function, integrity, and health of tissues and organs.
Cellular aging refers to a gradual decline in cell function and an increase in the probability of cell death [5]. It underlies the decline in tissue and organ function that defines biological aging. If cells are aging at a higher rate, so are you, and the more likely it becomes to develop age-related dysfunctions. Biological aging is the main risk factor for such conditions.
Biological aging is characterized by a number of cellular and molecular changes known as the twelve hallmarks of aging [6]:
- Genomic instability
- Telomere attrition
- Epigenetic alterations
- Loss of proteostasis
- Deregulated nutrient-sensing
- Mitochondrial dysfunction
- Cellular senescence
- Stem cell exhaustion
- Altered intercellular communication
- Disabled macroautophagy
- Chronic inflammation
- Dysbiosis
All twelve hallmarks of aging are strongly related to each other. Some of them are regarded as initiating triggers whose damaging consequences progressively accumulate with time (e.g., genomic instability, telomere attrition, epigenetic alterations), whereas others may have beneficial functions in some conditions, but become progressively negative with age, in part due to other hallmarks (e.g., cellular senescence, mitochondrial dysfunction/mitohormesis). Other hallmarks arise when the accumulated damage cannot be compensated by tissue homeostatic mechanisms (e.g., stem cell exhaustion, dysbiosis) [6,7].
Together, these age-related changes can hinder the body’s capacity to adequately respond to stress, repair and regenerate tissues, and maintain long-term homeostasis, thereby driving the progressive deterioration of health that is linked to the aging process [6,8].
How to Measure Your Biological Age
To measure biological aging, it is necessary to have methods to objectively quantify cellular and functional decline. These are known as predictors of biological age or biomarkers of aging.They predict the rate of aging, healthspan, and lifespan by monitoring changes in molecules, processes, or physical functions associated with or affected by the aging process. They are usually assessed by a simple, harmless test, such as a blood test, an imaging technique, or physical assessment [9,10]. Currently, there is no single test that accurately determines biological age, but there are several markers that can be used to estimate it [11].
There are several clinical measurements that are often used as indicators of biological age, such as maximal oxygen consumption during physical exertion, grip strength, systolic blood pressure, waist circumference, body composition, microbiome analysis, immune signaling mediators, lipid profile, glucose metabolism profile, kidney function markers, and other blood biomarkers [11,12]. Functional age estimators can also be used as indices of biological aging. These are not based on blood biomarkers, but rather on the measurement and scoring of frailty and functional capacity, such as the Frailty Index [10].
There are also molecular measurements that assess genetic changes associated with aging, such as telomere length. Telomeres are DNA sequences at the ends of chromosomes that shorten slightly each time a cell divides, meaning they get shorter as we age [13]. Telomere length is usually assessed in white blood cells. Telomere length has been recognized as one of the best biomarkers of aging. However, recent research indicates that telomere length per se only allows for a rough estimate of biological age. Nevertheless, it is a valuable marker for determining biological age when used in combination with other markers [14].
Another genetic marker of biological age is DNA methylation [11]. At any given time, you have genes that are turned on, meaning they’re being expressed and used to produce proteins, and others that are turned off, meaning they’re silenced. The process that turns genes on or off is called DNA methylation. It doesn't change or mutate genes, it just modifies their expression. DNA methylation is part of a set of mechanisms that regulate gene expression based on lifestyle and environment called epigenetic modifications [15]. Several studies have identified specific age-related patterns in DNA methylation that can be measured in the blood and used as markers of biological age [16–18]. These are known as epigenetic clocks and they are regarded as one of the most accurate and promising estimates of biological age [19–21]. Companies that offer these types of biological age tests include TruDiagnostic and Clock Foundation.
Given the complexity of the aging process, biological age estimation based on only one biomarker is often insufficient. Better biological age estimates can be obtained from combinations of a few biomarkers [4].
Nature vs Nurture
Genes certainly play a part in how fast we age, and those are beyond our control, but our environment and lifestyle choices are also key determinants of biological aging. As an example, in a first-of-its-kind study, an eight-week comprehensive diet and lifestyle program was able to decrease biological age—assessed using an epigenetic clock—by almost 2 years [22]. Some of the main lifestyle factors that influence cellular and biological aging include:
Diet
Unhealthy diets high in processed foods, trans fats, added sugar, and salt can accelerate biological aging by promoting oxidative stress, unhealthy immune signaling, and metabolic deregulation. Adopting healthy dietary patterns, rich in fruits, vegetables, nuts, seeds, seafood, and healthy fats such as olive oil can help to slow the progression of biological aging [23,24].
Exercise
A sedentary lifestyle can accelerate the physical decline that comes with age, such as losses in metabolic function, muscle function, and cardiovascular and respiratory fitness, resulting in a premature deterioration of health. Maintaining physical activity and exercising regularly can help to mitigate the impact of several promoters of aging, including mitochondrial dysfunction, abnormal immune signaling, and oxidative stress, and thereby help to prevent or delay age-related health decline [25,26].
Stress
Prolonged psychological stress leads to an excessive production of stress hormones that can influence cell and tissue function and dysregulate physiological responses in the body and brain. These changes have physical and molecular consequences that influence the immune, endocrine, and central nervous systems in ways that can accelerate aging and compromise healthy aging [27,28].
Sleep
Sleep quality tends to worsen with aging [29]. Poor sleep can accelerate biological aging and age-associated health decline by promoting persistent changes in systemic signaling that can affect every major physiological system within the body, including immune, metabolic, thermoregulatory, endocrine, and cardiovascular functions [30–32].
How to Slow Your Biological Clock
You have no control over your chronological age, but you can have some control over biological aging by making positive changes. Our environment and lifestyle choices are key determinants of biological aging and how healthy you stay into old age.
Here are a few simple lifestyle changes that may help to slow biological aging:
- Adjusting your diet by adding more fruits, vegetables, lean meats, and water is a simple intervention to support healthy aging and extend healthspan [7].
- Maintaining physical activity and exercising regularly—even just by walking more—can help to prevent or delay physical and cognitive manifestations of age-related health decline [33–35].
- Adopting interventions for stress reduction and management such as yoga, slow paced breathing, meditation, or any other calming and relaxing activity may help you cope with stress and counteract its pro-aging effects [36–38].
- Improving your sleep hygiene by setting a sleep schedule, turning off electronic devices one hour before bedtime, and creating a sleep-promoting environment—dark, silent, relaxing, and at a cool but comfortable temperature [39,40].
- And, of course, if you smoke, quit smoking [41].
Dietary Supplements for Healthy Aging
Qualia’s healthy aging line offers three products that help to support healthy cell and tissue function and whole-body health as we age.
Qualia Life is designed to comprehensively support the molecules, processes, and pathways involved in health at the cellular level. A central goal was foundational support for cellular energy generation so that individual cells can better do all the things they need to do to support better aging.* Learn more about it in Qualia Life: Putting the Healthy Aging Puzzle Together.
NAD+ is a central molecule of energy production and signaling pathways critical for cellular health. NAD+ levels decrease as we get older and this decline contributes to poorer health [42]. Qualia NAD+ supports NAD+ maintenance by providing several substrates for NAD+ biosynthesis, as well as supporting rate-limiting steps in the different pathways of NAD+ production.* You can learn more about it in The Formulator's View of the Qualia NAD+ Ingredients.
Biological aging can be accelerated by the existence of persistent age-related conditions driven by cellular senescence, but alleviating cellular senescence may help mitigate functional decline as we age.* Qualia Senolytic was developed to support healthy aging by helping to bring the creation and clearance of senescent cells back into a healthy balance.* Learn more about Qualia Senolytic in The Formulator's View of the Qualia Senolytic Ingredients.
*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.
References
[1]V.N. Gladyshev, S.B. Kritchevsky, S.G. Clarke, A.M. Cuervo, O. Fiehn, J.P. de Magalhães, T. Mau, M. Maes, R. Moritz, L.J. Niedernhofer, E. Van Schaftingen, G.J. Tranah, K. Walsh, Y. Yura, B. Zhang, S.R. Cummings, Nat Aging 1 (2021) 1096–1106.
[2]X. Li, A. Ploner, Y. Wang, P.K. Magnusson, C. Reynolds, D. Finkel, N.L. Pedersen, J. Jylhävä, S. Hägg, Elife 9 (2020).
[3]L. Ferrucci, G.A. Kuchel, J. Am. Geriatr. Soc. 69 (2021) 610–612.
[4]M.R. Hamczyk, R.M. Nevado, A. Barettino, V. Fuster, V. Andrés, J. Am. Coll. Cardiol. 75 (2020) 919–930.
[5]M. Ogrodnik, Aging Cell 20 (2021) e13338.
[6]C. López-Otín, M.A. Blasco, L. Partridge, M. Serrano, G. Kroemer, Cell 186 (2023) 243–278.
[7]C. López-Otín, M.A. Blasco, L. Partridge, M. Serrano, G. Kroemer, Cell 153 (2013) 1194–1217.
[8]C. López-Otín, G. Kroemer, Cell 184 (2021) 1929–1939.
[9]J. Jylhävä, N.L. Pedersen, S. Hägg, EBioMedicine 21 (2017) 29–36.
[10]T. Lohman, G. Bains, L. Berk, E. Lohman, Gerontol Geriatr Med 7 (2021) 23337214211046419.
[11]V.V. Erema, A.Y. Yakovchik, D.A. Kashtanova, Z.V. Bochkaeva, M.V. Ivanov, D.V. Sosin, L.R. Matkava, V.S. Yudin, V.V. Makarov, A.A. Keskinov, S.A. Kraevoy, S.M. Yudin, Int. J. Mol. Sci. 23 (2022).
[12]J. Bortz, A. Guariglia, L. Klaric, D. Tang, P. Ward, M. Geer, M. Chadeau-Hyam, D. Vuckovic, P.K. Joshi, Commun Biol 6 (2023) 1089.
[13]J.W. Shay, Curr. Opin. Cell Biol. 52 (2018) 1–7.
[14]A. Vaiserman, D. Krasnienkov, Front. Genet. 11 (2020) 630186.
[15]L.D. Moore, T. Le, G. Fan, Neuropsychopharmacology 38 (2013) 23–38.
[16]J.T. Bell, P.-C. Tsai, T.-P. Yang, R. Pidsley, J. Nisbet, D. Glass, M. Mangino, G. Zhai, F. Zhang, A. Valdes, S.-Y. Shin, E.L. Dempster, R.M. Murray, E. Grundberg, A.K. Hedman, A. Nica, K.S. Small, MuTHER Consortium, E.T. Dermitzakis, M.I. McCarthy, J. Mill, T.D. Spector, P. Deloukas, PLoS Genet. 8 (2012) e1002629.
[17]H. Heyn, N. Li, H.J. Ferreira, S. Moran, D.G. Pisano, A. Gomez, J. Diez, J.V. Sanchez-Mut, F. Setien, F.J. Carmona, A.A. Puca, S. Sayols, M.A. Pujana, J. Serra-Musach, I. Iglesias-Platas, F. Formiga, A.F. Fernandez, M.F. Fraga, S.C. Heath, A. Valencia, I.G. Gut, J. Wang, M. Esteller, Proc. Natl. Acad. Sci. U. S. A. 109 (2012) 10522–10527.
[18]G. Hannum, J. Guinney, L. Zhao, L. Zhang, G. Hughes, S. Sadda, B. Klotzle, M. Bibikova, J.-B. Fan, Y. Gao, R. Deconde, M. Chen, I. Rajapakse, S. Friend, T. Ideker, K. Zhang, Mol. Cell 49 (2013) 359–367.
[19]P.D. Fransquet, J. Wrigglesworth, R.L. Woods, M.E. Ernst, J. Ryan, Clin. Epigenetics 11 (2019) 62.
[20]R. Duan, Q. Fu, Y. Sun, Q. Li, Ageing Res. Rev. 81 (2022) 101743.
[21]S. Horvath, K. Raj, Nat. Rev. Genet. 19 (2018) 371–384.
[22]K.N. Fitzgerald, R. Hodges, D. Hanes, E. Stack, D. Cheishvili, M. Szyf, J. Henkel, M.W. Twedt, D. Giannopoulou, J. Herdell, S. Logan, R. Bradley, Aging 13 (2021) 9419–9432.
[23]L.J. Dominguez, N. Veronese, E. Baiamonte, M. Guarrera, A. Parisi, C. Ruffolo, F. Tagliaferri, M. Barbagallo, Nutrients 14 (2022).
[24]C. Capurso, F. Bellanti, A. Lo Buglio, G. Vendemiale, Nutrients 12 (2019).
[25]M. Izquierdo, J.E. Morley, A. Lucia, BMJ 368 (2020) m402.
[26]P.L. Valenzuela, A. Castillo-García, J.S. Morales, M. Izquierdo, J.A. Serra-Rexach, A. Santos-Lozano, A. Lucia, Compr. Physiol. 9 (2019) 1281–1304.
[27]M. Moreno-Villanueva, A. Bürkle, Exp. Gerontol. 68 (2015) 39–42.
[28]K.M.M. Hasan, M.S. Rahman, K.M.T. Arif, M.E. Sobhani, Age 34 (2012) 1421–1433.
[29]B.A. Mander, J.R. Winer, M.P. Walker, Neuron 94 (2017) 19–36.
[30]K.K. Petrov, A. Hayley, S. Catchlove, K. Savage, C. Stough, Mech. Ageing Dev. 192 (2020) 111388.
[31]M.R. Irwin, M.R. Opp, Neuropsychopharmacology 42 (2017) 129–155.
[32]M.R. Irwin, Annu. Rev. Psychol. 66 (2015) 143–172.
[33]M. Izquierdo, R.A. Merchant, J.E. Morley, S.D. Anker, I. Aprahamian, H. Arai, M. Aubertin-Leheudre, R. Bernabei, E.L. Cadore, M. Cesari, L.-K. Chen, P. de Souto Barreto, G. Duque, L. Ferrucci, R.A. Fielding, A. García-Hermoso, L.M. Gutiérrez-Robledo, S.D.R. Harridge, B. Kirk, S. Kritchevsky, F. Landi, N. Lazarus, F.C. Martin, E. Marzetti, M. Pahor, R. Ramírez-Vélez, L. Rodriguez-Mañas, Y. Rolland, J.G. Ruiz, O. Theou, D.T. Villareal, D.L. Waters, C. Won Won, J. Woo, B. Vellas, M. Fiatarone Singh, J. Nutr. Health Aging 25 (2021) 824–853.
[34]B.K. Pedersen, B. Saltin, Scand. J. Med. Sci. Sports 25 Suppl 3 (2015) 1–72.
[35]P.G. Rossi, B.F. Carnavale, A.C.S. Farche, J.H. Ansai, L.P. de Andrade, A.C. de M. Takahashi, Arch. Gerontol. Geriatr. 93 (2021) 104322.
[36]A.L. Francis, R.C. Beemer, Complement. Ther. Med. 43 (2019) 170–175.
[37]Y.-Y. Tang, B.K. Hölzel, M.I. Posner, Nat. Rev. Neurosci. 16 (2015) 213–225.
[38]B. Stubbs, D. Vancampfort, S. Rosenbaum, J. Firth, T. Cosco, N. Veronese, G.A. Salum, F.B. Schuch, Psychiatry Res. 249 (2017) 102–108.
[39]M. Sejbuk, I. Mirończuk-Chodakowska, A.M. Witkowska, Nutrients 14 (2022).
[40]O. Troynikov, C.G. Watson, N. Nawaz, J. Therm. Biol. 78 (2018) 192–203.
[41]G. Radmilović, V. Matijević, D. Mikulić, D. Rašić Markota, A.R. Čeprnja, Tob. Induc. Dis. 21 (2023) 161.
[42]A.J. Covarrubias, R. Perrone, A. Grozio, E. Verdin, Nat. Rev. Mol. Cell Biol. 22 (2021) 119–141.
No Comments Yet
Sign in or Register to Comment