MinireviewCarotenoids as protection against sarcopenia in older adults
Section snippets
Oxidative stress and sarcopenia
Oxidative stress has been implicated as a central mechanism in the pathogenesis of sarcopenia [30]. Oxidative damage to DNA, proteins, and lipids increases in human skeletal muscle with age. Biopsy studies demonstrate that 8-hydroxy-2-deoxyguanosine, protein carbonyls, and malondialdehyde (markers of oxidative damage to DNA, protein, and lipids, respectively) are elevated in human skeletal muscle in older adults [31], [32], [33], [34]. Animal models also show that increased oxidative damage to
Inflammatory cytokines and sarcopenia
Reactive oxygen species can damage muscle tissue directly, but they also provide a trigger for the expression of inflammatory cytokines such as interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and IL-6. In sepsis, cachexia, and chronic inflammatory conditions, inflammatory cytokines are associated with loss of muscle mass and strength, but whether long-term, low level elevations in proinflammatory cytokines in aging adults cause sarcopenia requires further investigation [1]. Redox-sensitive
Dietary carotenoids in older adults
Given the importance of ROS and redox-sensitive signaling in the upregulation of inflammatory cytokines, what is the relative role of antioxidant nutrients in oxidative stress and inflammation? The six major dietary carotenoids (α-carotene, β-carotene, β-cryptoxanthin, lutein, zeaxanthin, and lycopene) comprise an important component of the antioxidant defense system in humans, and the major dietary sources of carotenoids are fruits and vegetables. Carotenoids are hydrophobic molecules, and
Evidence for role of carotenoids in sarcopenia
New investigations are emerging that show that low serum/plasma carotenoids are independently associated with poor skeletal muscle strength and impaired physical performance. Among 669 women aged 70–79 years in the Women’s Health and Aging Studies (WHAS) I and II, low serum carotenoid levels were associated with poor muscle strength [62]. In multivariate models adjusting for age, race, smoking, cardiovascular disease, arthritis, and serum IL-6, low total carotenoids were associated with low
Carotenoids and other related outcomes in adults
The relationships that have been observed between serum/plasma carotenoids and sarcopenia in epidemiological studies should be seen in the broader context of other outcomes such as inflammation and cardiovascular disease. Carotenoids are considered the best biological marker for fruit and vegetable intake [66], and recent large epidemiological studies show that a higher intake of fruits and vegetables is associated with a lower risk of cardiovascular disease [67], [68], [69], disability [70],
Conclusions
Recent epidemiological studies suggest that carotenoids or carotenoid-rich foods are protective against a decline in muscle strength and walking disability among older community-dwelling adults. This line of investigation also suggests that the possible health benefits of carotenoids or carotenoid-rich foods extend beyond hypertension, atherosclerosis, and cardiovascular disease, the clinical outcomes that are conventionally examined in relationship to dietary factors. Further work is needed to
Acknowledgments
This work was supported by National Institute on Aging Contracts N01-AG-916413, N01-AG-821336, N01-AG-5-0002, and NIA Grant R01 AG027012. This research was supported in part by the Intramural Research Program, National Institute on Aging, NIH.
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2023, Experimental GerontologyPlasma lutein and zeaxanthin concentrations associated with musculoskeletal health and incident frailty in The Irish Longitudinal Study on Ageing (TILDA)
2023, Experimental GerontologyCitation Excerpt :As such, it will be interesting to explore these relationships further in future Waves of TILDA. The mechanisms by which carotenoids may affect muscle function are unclear, but are mainly hypothesised to relate to attenuated age-related skeletal muscle mitochondrial DNA damage resulting from oxidative stress, leading to the atrophy, loss and impaired function of muscle fibres (McKenzie et al., 2002; Semba et al., 2007). There is also some recent evidence that lutein may influence synaptic function independent of its antioxidant activity, in conditions of mitochondrial dysfunction (Maglioni et al., 2022).
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