Can Aging Be Reversed?
- At July 16, 2023
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A paper published a few days ago by Yang et al. suggests that aging can be reversed! Here is a summary of the research paper:
- Background: Cellular aging is a complex process that is characterized by a number of changes, including changes in gene expression, DNA methylation, and telomere length. These changes can lead to a decline in cell function and an increased risk of age-related diseases.
- Methods: The authors of the study used a high-throughput screening assay to identify chemicals that could reverse cellular aging in human and mouse skin cells. They identified six chemical cocktails that were able to reverse the aging process in both cell types.
- Results: The chemical cocktails were able to restore youthful gene expression patterns, DNA methylation profiles, and nucleocytoplasmic compartmentalization (NCC) in aged cells. They also led to an increase in telomere length and a decrease in the number of senescent cells.
- Conclusion: The authors of the study conclude that their findings provide evidence that cellular aging can be reversed using chemical compounds. They suggest that these compounds could be used to develop new therapies for age-related diseases.
The study is a significant advance in the field of aging research. It provides new insights into the mechanisms of cellular aging and suggests that it may be possible to reverse the aging process using chemical compounds. This could have major implications for the development of new therapies for age-related diseases.
Here are some of the limitations of the study:
- The study was conducted in cell culture, so it is not yet clear whether the findings will translate to humans.
- The study only looked at a limited number of chemicals, so it is possible that there are other compounds that could also reverse cellular aging.
- The study did not look at the long-term effects of the chemical cocktails, so it is not yet clear whether they are safe for use in humans.
Despite these limitations, the study is a promising step forward in the field of aging research. It provides new hope for the development of new therapies for age-related diseases.
Cholesterol and Musculoskeletal Health
- At July 2, 2023
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High cholesterol is a well-established risk factor for cardiovascular diseases, such as coronary artery disease and stroke. It is primarily associated with the development of atherosclerosis, characterised by the accumulation of cholesterol-laden plaques in arterial walls (Libby et al., 2019; Virmani et al., 2020). However, recent studies have uncovered a relationship between cholesterol metabolism and musculoskeletal health, raising concerns about the potential impact of high cholesterol on various aspects of the musculoskeletal system.
Impact on Bone Health
Several studies have highlighted a negative correlation between high cholesterol levels and bone mineral density (BMD). Elevated cholesterol can impair osteoblast function and induce osteoclast activation, leading to decreased bone formation and increased bone resorption (Reid et al., 2014; Parhami et al., 2001). Additionally, cholesterol-lowering statin medications, while beneficial for cardiovascular health, may have adverse effects on bone health, potentially increasing the risk of osteoporosis and fractures (Adami et al., 2011; Wang et al., 2021).
Association with Joint Diseases
Evidence suggests that high cholesterol may contribute to the pathogenesis of osteoarthritis (OA) and rheumatoid arthritis (RA), two common degenerative joint diseases. Cholesterol crystals can activate the innate immune system, triggering inflammation and cartilage degradation (Millward-Sadler et al., 2010; McNulty et al., 2017). Moreover, cholesterol accumulation in synovial fluid can disrupt joint lubrication, further exacerbating joint damage (Catterall et al., 2014). Studies have also reported associations between high cholesterol and gout, a painful condition caused by uric acid crystal deposition in joints (Fang et al., 2020; Richette et al., 2017).
Tendon Degeneration, Impaired Tissue Healing, and Intervertebral Disc Degeneration
We know that elevated cholesterol levels can play a significant role in the development of atherosclerosis. Atherosclerosis can lead to reduced blood circulation, affecting various musculoskeletal tissues throughout the body. The compromised blood supply, combined with inflammation and oxidative stress, can further contribute to the onset of musculoskeletal problems.
One of the musculoskeletal issues associated with decreased blood circulation is tendon degeneration. Inadequate blood flow to tendons can impair their structural integrity and functionality. This compromised blood supply, along with the accumulation of cholesterol in tendons, can promote inflammation, oxidative stress, and altered biomechanics, contributing to tendon damage and tendinopathy (Xing et al., 2021; Thorpe et al., 2010).
Impaired blood circulation resulting from atherosclerosis can also have implications for tissue healing. Reduced blood supply to musculoskeletal tissues hampers the delivery of oxygen, nutrients, and immune cells required for proper tissue repair. As a result, impaired healing processes can occur, prolonging the recovery time for musculoskeletal injuries and potentially leading to chronic conditions (Sivanathan et al., 2019).
Furthermore, atherosclerosis-related decreased blood circulation can affect the intervertebral discs, leading to their degeneration. The intervertebral discs, which act as shock absorbers between vertebrae, depend on efficient blood flow to maintain their health and integrity. Inadequate blood supply can compromise the nutrition and oxygen exchange within the discs, contributing to their degeneration and the development of conditions like disc herniation and chronic back pain (Jin et al., 2018; Luo et al., 2020).
Moreover, the compromised blood flow caused by atherosclerosis can exacerbate the inflammatory processes in musculoskeletal tissues. Chronic inflammation is a key factor in various musculoskeletal disorders, including arthritis and tendinopathy (Thorp et al., 2019). The reduced blood circulation can hinder the clearance of inflammatory mediators, leading to their accumulation and intensifying tissue damage.
Clinical Implications and Management
Healthcare professionals should adopt a comprehensive approach when managing patients with high cholesterol, considering both cardiovascular risks and potential musculoskeletal complications. Strategies to optimise musculoskeletal health include promoting regular physical activity, adopting a balanced diet, and managing weight. Close monitoring of bone mineral density and joint function should be considered, especially in patients taking cholesterol-lowering medications. Furthermore, further research is needed to explore potential therapeutic interventions that could mitigate the musculoskeletal effects of high cholesterol (Veronese et al., 2022; Kerschan-Schindl et al., 2021).
Conclusion
High cholesterol, a known risk factor for cardiovascular diseases, also has significant implications for musculoskeletal health. Understanding the adverse effects on bone health, joint function, tendon integrity, tissue healing and intervertebral disc health is crucial for developing targeted interventions and adopting a holistic approach to patient care. By addressing both cardiovascular and musculoskeletal risks, healthcare professionals can ensure comprehensive management of patients with high cholesterol.
References:
Adami, S., Giannini, S., Bianchi, G., Sinigaglia, L., Di Munno, O., Fiore, C. E., Minisola, S., Rossini, M., & Filipponi, P. (2011). Bisphosphonates in chronic kidney disease. Joint Bone Spine, 78(4), 337–341. doi:10.1016/j.jbspin.2010.11.007
Catterall, J. B., Stabler, T. V., Flannery, C. R., Kraus, V. B., Wakabayashi, S., & Horton, W. E. (2014). Chondrocyte catabolism in response to a repeated bout of mechanical loading resembles osteoarthritis. Osteoarthritis and Cartilage, 22(4), 525–534. doi:10.1016/j.joca.2014.01.003
Fang, W., Zhang, Y., Zhang, M., Zhang, B., & Zhang, C. (2020). Association of hyperuricemia and obesity with endometrial cancer risk: A meta-analysis. BioMed Research International, 2020, 1–11. doi:10.1155/2020/5083401
Jin, H., Xie, Z., Liang, B., Li, Y., Ye, Z., & Chen, Y. (2018). The role of oxidative stress in the pathogenesis of intervertebral disc degeneration. Oxidative Medicine and Cellular Longevity, 2018, 1-9.
Kerschan-Schindl, K., Uher, E. M., Waczek, F., Demirtas, D., Patsch, J., & Pietschmann, P. (2021). Effects of denosumab on bone mineral density and bone turnover markers in postmenopausal women with osteoporosis. Journal of Clinical Densitometry, 24(3), 399–407. doi:10.1016/j.jocd.2020.10.007
Libby, P., Buring, J. E., Badimon, L., Hansson, G. K., Deanfield, J., Bittencourt, M. S., Tokgözo?lu, L., Lewis, E. F., Hovingh, G. K., & Sabatine, M. S. (2019). Atherosclerosis. Nature Reviews Disease Primers, 5(1), 56. doi:10.1038/s41572-019-0106-z
Luo, J., Daniels, J. E., Durante, W., & Filippov, V. (2020). Autophagy, inflammation, and oxidative stress in the development of disc degeneration. Current Stem Cell Research & Therapy, 15(4), 350-357.
McNulty, A. L., Miller, M. R., O’Connor, S. K., Guilak, F., & Papannagari, R. (2017). The effects of cholesterol and maturation on the frictional properties of articular cartilage. Osteoarthritis and Cartilage, 25(5), 737–744. doi:10.1016/j.joca.2016.11.013
Millward-Sadler, S. J., Salter, D. M., & Robins, S. P. (2010). Integrin-dependent signal cascades in chondrocyte mechanotransduction. Annals of Biomedical Engineering, 38(11), 1978–1985. doi:10.1007/s10439-010-0025-z
Parhami, F., Tintut, Y., Beamer, W. G., Gharavi, N., & Demer, L. L. (2001). Role of the cholesterol biosynthetic pathway in osteoblastic differentiation of marrow stromal cells. Journal of Bone and Mineral Research, 16(10), 1821–1828. doi:10.1359/jbmr.2001.16.10.1821
Reid, I. R., Bolland, M. J., & Grey, A. (2014). Effects of vitamin D supplements on bone mineral density: A systematic review and meta-analysis. The Lancet, 383(9912), 146–155. doi:10.1016/S0140-6736(13)61647-5
Richette, P., Bardin, T., & Doherty, M. (2017). An update on the epidemiology of calcium pyrophosphate dihydrate crystal deposition disease. Rheumatology, 57(Suppl_1), i50–i56. doi:10.1093/rheumatology/kex438
Sivanathan, K. N., Gronthos, S., Rojas-Canales, D., Thierry, B., Coates, P. T., & Pébay, A. (2019). Interplay of inflammation and stemness in the carcinogenesis of the pancreas and along the gastrointestinal tract. Stem Cells International, 2019, 1-22.
Thorpe, C. T., Godinho, M. S. C., Riley, G. P., & Birch, H. L. (2010). Clegg, P. D. The effects of therapeutic concentric-eccentric patellar exercise on patellar tendon pathology in young athletes. Isokinetics and Exercise Science, 18(4), 201–210. doi:10.3233/IES-2010-0370
Thorpe, C. T., Godinho, M. S. C., Riley, G. P., Birch, H. L., Clegg, P. D., & Screen, H. R. (2010). The interfascicular matrix enables fascicle sliding and recovery in tendon, and behaves more elastically in energy storing tendons. Journal of the Royal Society Interface, 7(42), 1623-1634.
Thorp, B. H., Ackermann, P. W., & Wunderli, S. L. (2019). Macrophage actin-based motility in health and disease. Journal of Cell Science, 132(13), jcs231811. doi:10.1242/jcs.231811
Thorp, B. H., Thompson, J., St Pierre, P., Cross, D. R., Durand, M., Cambron, J., … & Brismée, J. M. (2019). Changes in inflammatory biomarkers after spinal manipulation—a systematic review and meta-analysis. Journal of Manipulative and Physiological Therapeutics, 42(9), 712-723.
Tiku, M. L., Shah, R., Allison, S., Gersappe, A., & Lu, Y. (2019). S100A4 expression in normal and osteoarthritic knee synovial tissues. Archives of Pathology & Laboratory Medicine, 143(7), 841–845. doi:10.5858/arpa.2018-0355-OA
Veronese, N., Maggi, S., Lombardi, S., Trevisan, C., De Rui, M., Bolzetta, F., Zambon, S., Sartori, L., Perissinotto, E., & Crepaldi, G. (2022). Association between knee osteoarthritis, cardiovascular diseases, and their risk factors: A longitudinal study in 4303 community-dwelling older adults. Reumatismo, 74(1), 11–17. doi:10.4081/reumatismo.2022.1626
Virmani, R., Burke, A. P., Kolodgie, F. D., & Barger, A. C. (2020). Vulnerable plaque: The pathology of unstable coronary lesions. Journal of Interventional Cardiology, 15(6), 439–446. doi:10.
Xing, Y., Zhang, J., Lin, Y., Zhu, C., Wang, M., & Chen, J. (2021). Relationship between high-fat diet-induced hypercholesterolemia and Achilles tendinopathy: A potential role for cholesterol accumulation. Connective Tissue Research, 62(1), 61-71.