Senescent cells, also known as "zombie cells" once vibrant and active components of our body, undergo a unique transformation as they cease to multiply but persist, releasing a cascade of chemicals called cytokines that produce inflammation. This phenomenon, often overlooked, plays a pivotal role in the aging process. In this blog, we delve into the intriguing world of senescent cells, unraveling the mysteries behind their persistence and the repercussions they bring.
The Paradox of Senescence: Stagnation without Demise
Senescent cells defy the typical life cycle, halting their replication while eluding the natural process of cell death. This paradoxical state raises questions about the underlying mechanisms that govern this phenomenon-the mitochondria.
Mitochondria are living organisms that respire (breath), requiring oxygen to produce energy called ATP. Mitochondria repair oxidative DNA damage and clean up zombie cells and making way for new healthy cells. Damage and subsequent dysfunction in mitochondria is an important factor in a range of human diseases causing metabolic dysfunction. Mitochondrial disorders often present as neurological disorders, including autism. They can also manifest as muscle degenerative disease, cancer, endocrine disorders like hypothyroidism and diabetes and a variety of other systemic disorders (Palmer et al., 2019; Pradeepkiran & Reddy, 2020).
Chemical Dispatch: Inflammation as a Consequence
Zombie cells, rather than gracefully exiting the cellular stage opt for a different role – that of chemical messengers. Similar to renewable energy like solar versus toxic energy from fossil fuels, zombie cells don’t die off and renew but rather hang around producing a concoction of molecules which are inflammatory in nature. This continuous release can trigger a chronic inflammatory environment often referred to a "cytokine storm" contributing to various age-related conditions.
Senescence and Aging: A Symbiotic Relationship
Aging happens as we increase mitochondrial death and accumulate zombie cells. As these cells accumulate over time, their impact becomes more pronounced, potentially accelerating the overall aging trajectory of the organism. Eventually, when our mitochondria die out so does the energy necessary for cellular function killing its host.
The Culprits Within: Identifying Senescence Triggers
Factors that induce cellular senescence, include DNA damage from free radicals in our internal and external environment. Telomere shortening is directly related to processed foods and excess of starchy carbohydrates and sugars, emotional trauma and stressors that trigger an imbalance in hormones. Understanding these triggers is crucial for developing strategies to mitigate the formation of senescent cells called hormesis.
Hormesis is the body's balanced state in which it perfectly promotes death of zombie cells and new cell growth. Promoting hormesis comes down to lifestyle.
Senolytics: Breaking the Chain
Enter the realm of senolytics, a burgeoning field of research focused on eliminating or rejuvenating senescent cells. Below are some potential interventions and therapies that aim to disrupt the persistence of these cells and alleviate the associated inflammatory burden:
1. Eating a diet rich in phytochemicals that come from the rainbow of vegetables and fruits lengthen telomeres through epigenetics.
2. Disallowing processed foods and sugars promote a cleaner burn encouraging your mitochondria to draw from essential fatty acids and amino acids rather than unessential starchy carbohydrates.
3. Practicing tricks that create a therapeutic window of oxidative stressors such as HIT exercise or fasting or time restricted eating allows your body to clean up its zombie cells and promotes decreased inflammation and insulin levels.
4. Getting the right amount of uninterrupted sleep encourages your body’s natural circadian rhythm to take over multiple processes in the body necessary for cellular turn over.
5. Meditation is more powerful than you know. Simply put energy crates mass. If you are having trouble mediating try listen to soothing music in theta (4-7Hz) while encouraging positive thinking and restfulness.
6. Finally, there are a few supplements worth mentioning with strong evidence that support mitochondrial function such as Ubiquinol COQ10, Resveratrol, Quercetin and Urolithin A (UA). UA is produced by gut microflora from foods rich in ellagitannins. UA has been shown to improve mitochondrial health in humans but not everyone has a microbiome capable of producing UA, making supplementation with UA an appealing strategy.
Conclusion:
Senescent cells, with their peculiar nature of ceasing multiplication but persisting in the body, emerge as silent contributors to the inflammaging process. By comprehending the intricacies of senescence, we open avenues for innovative therapies and interventions that may redefine the way we age. In this journey into the world of senescent cells, we discover not only the challenges they pose but also the promise they hold for a healthier and more resilient aging process.
References
Palmer, A. K., Xu, M., Zhu, Y., Pirtskhalava, T., Weivoda, M. M., Hachfeld, C. M., Prata, L. G., Dijk, T. H., Verkade, E., Casaclang‐Verzosa, G., Johnson, K. O., Cubro, H., Doornebal, E. J., Ogrodnik, M., Jurk, D., Jensen, M. D., Chini, E. N., Miller, J. D., Matveyenko, A., . . . Kirkland, J. L. (2019). Targeting senescent cells alleviates obesity‐induced metabolic dysfunction. Aging Cell, 18(3), e12950-n/a. https://10.1111/acel.12950
Pradeepkiran, J. A., & Reddy, P. H. (2020). Defective mitophagy in Alzheimer’s disease. Ageing Research Reviews, 64, 101191. https://10.1016/j.arr.2020.101191
Excellent article-sooo juicy. Much to jump in to and explore. Exciting stuff-thank you Dr. Davina!!