Written by Dr. Gabriel Fries
The concept of “accelerated aging” was first introduced after researchers started studying biological markers of aging and realized that sometimes the age that is detected in the laboratory does not concur with the actual age of a person. In this sense, it’s important that we define two different but important concepts: ‘chronological age’ and ‘biological age’. By definition, a chronological age measures the time elapsed since birth. Accordingly, individuals born on the same day will share the same chronological age throughout life, regardless of lifestyle, disease, or health. In contrast, individuals of identical chronological age may have different biological ages. Biological age is intended to measure the decline in the function of tissues and organism, and more often than not, both of these ages do not line up.
Of note, the problem is not to have your chronological and biological ages out of sync; the problem is when you have a biological age that’s actually older than your chronological age (“premature aging”). The ultimate goal of our research is to find ways to prevent premature aging, since it may increase the risk for aging-related diseases (cardiovascular disease, hypertension, cancer, osteoarthritis, diabetes, osteoporosis, dementia, among others) and contribute to an early decline in physical function.
There are no statistics on the prevalence of premature aging in the American population or in any other population. We do know from studies that by 2050 the American 85 years old and over population will triple, and so will the burden of the public health community to attend to this growing population. The possibility of younger people having an older biological age may indicate that these estimations are actually not completely accurate; in fact, we might be underestimating the burden that the premature aging of society as a whole may have in the future.
Thankfully, there are several strategies that have been scientifically suggested to prevent accelerated aging to some extent. One of the strongest evidence is on the effects of caloric restriction on lifespan, i.e., eating less can actually help us live longer1. Other studies also suggest the beneficial effects of an overall healthier eating habit, exercising, having a good night’s sleep, avoiding drugs, tobacco, and alcohol, among others. All of these have been proven to prevent accelerated aging to some extent.
The fact that some medical conditions can contribute to accelerated aging is not really new to Medicine. Doctors have been aware of rare genetic disorders known to cause premature aging and shorten life expectancy for years, such as the progeroid syndromes. What is fairly novel is the fact that common chronic diseases can also contribute to accelerated aging mechanisms. For instance, there is evidence to suggest that this is the case for some types of cancer, cardiovascular disease, heart failure, diabetes, liver cirrhosis, chronic obstructive pulmonary disease, systemic lupus, among others. With the support from the UTHealth Consortium on Aging and of The University of Texas Houston Retiree Organization (UTHRO), the Translational Psychiatry Program in the Department of Psychiatry and Behavioral Sciences at UTHealth has been studying how psychiatric disorders, specifically bipolar disorder, can also contribute to accelerated aging. We have evidence that some patients with bipolar disorder show features of accelerated biological aging compared to healthy people2. While this is something that’s not carved in stone, still needs to be replicated by other research groups, and may not be true for all patients, it emphasizes the importance of carefully thinking of anti-aging strategies for these patients.
As discussed before, we could all be taking the effort to maintain healthy eating habits, exercise, prevent smoking habits, etc, and according to what we are finding in our studies this may be particularly important for patients with chronic conditions, such as bipolar disorder. Overall, we should be mindful that our lifestyle choices may be contributing to our biological age, especially if we already have a pre-existing condition that may make us more vulnerable to accelerated aging mechanisms.
1Balasubramanian P, Howell PR, Anderson RM. Aging and Caloric Restriction Research: A Biological Perspective With Translational Potential. EBioMedicine. 2017;21:37-44.
2Fries GR, Bauer IE, Scaini G, Wu MJ, Kazimi IF, Valvassori SS, Zunta-Soares G, Walss-Bass C, Soares JC, Quevedo J. Accelerated epigenetic aging and mitochondrial DNA copy number in bipolar disorder. Transl Psychiatry. 2017;7(12):1283.
Gabriel R. Fries, PhD, is a translational researcher in the field of biological psychiatry. His research focuses on the epigenetic basis of mood disorders, with a particular interest in bipolar disorder and molecular mechanisms of stress. Dr. Fries’ studies use basic science and investigation of cells, (epi)genomes and clinical datasets to better understand disease mechanisms and transmission, with the ultimate goal of designing novel medications and improving the lives of patients.