As humans age, the ability of their organs to function well becomes limited [1]. This deterioration manifests in several conditions, including sarcopenia, osteoporosis, and hypertension. A greater understanding of the biological mechanisms of aging will help the medical and scientific communities better address these conditions. 

One of the most common aging-related conditions is sarcopenia [1]. Sarcopenia is defined as “the severe loss of muscle mass and function” related to aging [1]. Many biological mechanisms influence the progression of sarcopenia [1]. Older bodies exhibit increased rates of mitochondrial mutation, which may affect the body’s ability to clear out dying tissue [2, 3]. Decreased sex hormone levels and malfunctioning satellite cells can also inhibit muscle protein synthesis and reduce the body’s ability to destroy muscle tissue [4, 5]. As a result, older bodies tend to have more ineffectual muscle and a diminished ability to replenish healthy muscle tissue [1]. 

Another contributor to aging is osteoporosis. While sarcopenia describes diminished, malfunctioning muscle mass, a weakening of bones and a general reduction in bone mass are the biological mechanisms underlying the aging-related phenomenon of osteoporosis [6]. The two conditions’ tendency to occur simultaneously leads to them being considered components of the same hybrid disease [1]. Indeed, they are informed by many of the same biological mechanisms, but their ability to occur separately suggests that it may be valuable to consider them as such [1].  

The body continually remodels the bones throughout life to maintain strength, sustain homeostasis, and renew weakened bones [7]. Osteoporosis limits the body’s ability to remodel existing bone, create new bone, and remove worn bone [7]. Indeed, researchers have noted that older people exhibit an imbalance between resorbed bone and newly formed bone [7]. Periosteal bones exist in excess, while endosteal and trabecular bone supply decreases [7]. The cause of these changes is related to osteoclast and osteoblast function [7]. Osteoclasts are the only cells known to be capable of resorbing used bone, while osteoblasts are key to forming new bone matrix [7]. People with osteoporosis contain more ineffectual versions of these cells, resulting in weakness and easier bone breakage, both of which are prominent characteristics of aging [7].  

One other condition that is related to aging is hypertension, which also is associated with various biological mechanisms. Beyond its association with myocardial infarction and strokes, hypertension is also dangerous because of its collateral effects [8]. These include falls, fractures, physical disability, and dementia [8]. As a result, it is essential to understand the physiology of hypertension. Diastolic blood pressure (DHP) tends to increase as people age [9]. Many biological phenomena are involved in this increase, two of which are large artery stiffness (LAS) and peripheral vascular resistance (PVR) [9]. LAS occurs when smooth vascular muscle cells change in composition such that collagen accumulates in the arteries [9]. Alternatively, when PVR occurs in small vessels, blood flow slows, and pressure rises [9]. Researchers note how these structural changes to the cardiovascular system parallel those found elsewhere in the body as aging progresses, suggesting the possible existence of a positive feedback loop between aging and hypertension [9]. 

Many other biologically significant diseases associated with aging are worth considering as well. These include dementia, osteoarthritis, diabetes, cancer, cardiovascular disease, and several chronic diseases [10]. As their unique biological influences continue to be studied, the prospect of curing them becomes more feasible. 

References 

[1] M. E. Csete, “Basic Science of Frailty—Biological Mechanisms of Age-Related Sarcopenia,” Anesthesia & Analgesia, vol. 132, no. 2, p. 293-304, February 2021. [Online]. Available: https://doi.org/10.1213/ANE.0000000000005096. 

[4] M. Maggio, F. Lauretani, and G. P. Ceda, “Sex hormones and sarcopenia in older persons,” Current Opinion in Clinical Nutrition and Metabolic Care, vol. 16, no. 1, p. 3-13, January 2013. [Online]. Available: https://doi.org/10.1097/MCO.0b013e32835b6044.  

[5] S. E. Alway, M. J. Myers, and J. S. Mohamed, “Regulation of Satellite Cell Function in Sarcopenia,” Frontiers in Aging Neuroscience, vol. 6, no. 246, p. 1-15, September 2014. [Online]. Available: https://doi.org/10.3389/fnagi.2014.00246. 

[3] L. Guarente, “Mitochondria–A Nexus for Aging, Calorie Restriction, and Sirtuins?,” Cell, vol. 132, no. 2, p. 171-176, January 2008. [Online]. Available: https://doi.org/10.1016/j.cell.2008.01.007. 

[2] N. Sun, R. J. Youle, and T. Finkel, “The Mitochondrial Basis of Aging,” Molecular Cell, vol. 61, no. 5, p. 654-666, March 2016. [Online]. Available: https://doi.org/10.1016/j.molcel.2016.01.028. 

[6] J. Paintin, C. Cooper, and E. Dennison, “Osteosarcopenia,” British Journal of Hospital Medicine, vol. 79, no. 5, p. 253-258, May 2018. [Online]. Available: https://doi.org/10.12968/hmed.2018.79.5.253. 

[7] N. M. Iñiguez-Ariza and B. L. Clarke, “Bone biology, signaling pathways, and therapeutic targets for osteoporosis,” Maturitas, vol. 82, no. 2, p. 245-255, October 2015. [Online]. Available: https://doi.org/10.1016/j.maturitas.2015.07.003. 

[9] E. Pinto, “Blood pressure and aging,” Postgraduate Medical Journal, vol. 83, no. 976, p. 109-114, February 2007. [Online]. Available: https://doi.org/10.1136/pgmj.2006.048371. 

[8] T. W. Buford, “Hypertension and Aging,” Aging Research Reviews, vol. 26, p. 96-111, March 2016. [Online]. Available: https://doi.org/10.1016/j.arr.2016.01.007. 

[10] E. Jaul and J. Barron, “Age-Related Diseases and Clinical and Public Health Implications for the 85 Years Old and Over Population,” Frontiers in Public Health, vol. 5, no. 335, p. 1-7, December 2017. [Online]. Available: https://doi.org/10.3389/fpubh.2017.00335.