Nutritional status, body composition, and quality of life in community-dwelling sarcopenic and non-sarcopenic older adults: A case-control study

Verlaan, Sjors; Aspray, Terry; Bauer, Jüergen M.; Cederholm, Tommy; Hemsworth, Jaimie; Hill, Tom R.; McPhee, Jamie S.; Piasecki, Mathew; Seal, Chris; Sieber, Cornel; Borg, Sovianne ter; Wijers, S.; Brandt, Kirsten

doi:10.1016/j.clnu.2015.11.013

Cited by 212 publications

(241 citation statements)

References 31 publications

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“…We demonstrate that both aging and frailty associate with higher levels of MMA indicative of a higher prevalence of vitamin B12 deficiency in the Singapore Longitudinal Aging Study. A similar association was also recently demonstrated in a different human population with mobility deficits where sarcopenic patients had lower levels of circulating vitamin B12 compared with age‐matched elderly controls . Taken together, these observations strongly suggest that vitamin B12 deficiency could directly impact muscle performance and physical function in the elderly.…”

Section: Discussionsupporting

confidence: 83%

Vitamin B12 deficiency and impaired expression of amnionless during aging

Pannérec

Migliavacca

Castro

et al. 2017

J cachexia sarcopenia muscle

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BackgroundPhysical frailty and loss of mobility in elderly individuals lead to reduced independence, quality of life, and increased mortality. Vitamin B12 deficiency has been linked to several age‐related chronic diseases, including in the musculo‐skeletal system, where vitamin B12 deficiency is generally believed to be linked to poor nutritional intake. In the present study, we asked whether aging and frailty associate with altered vitamin B12 homeostasis in humans and investigated the underlying molecular mechanisms using preclinical models.MethodsWe analysed a subset of the Singapore Longitudinal Aging Study and stratified 238 participants based on age and Fried frailty criteria. Levels of methyl‐malonic acid (MMA), a marker for vitamin B12 deficiency, and amnionless, the vitamin B12 co‐receptor that anchors the vitamin B12 transport complex to the membrane of epithelial cells, were measured in plasma. In addition, vitamin B12 levels and the molecular mechanisms of vitamin B12 uptake and excretion were analysed in ileum, kidney, liver, and blood using a rat model of natural aging where nutritional intake is fully controlled.ResultsWe demonstrate that aging and frailty are associated with a higher prevalence of functional vitamin B12 deficiency that can be detected by increased levels of MMA in blood (ρ = 0.25; P = 0.00013). The decline in circulating vitamin B12 levels is recapitulated in a rat model of natural aging where food composition and intake are stable. At the molecular level, these perturbations involve altered expression of amnionless in the ileum and kidney. Interestingly, we demonstrate that amnionless can be detected in serum where its levels increase during aging in both rodents and human (P = 3.3e‐07 and 9.2e‐07, respectively). Blood amnionless levels negatively correlate with vitamin B12 in rats (r2 = 0.305; P = 0.0042) and positively correlate with the vitamin B12 deficiency marker MMA in humans (ρ = 0.22; P = 0.00068).ConclusionsOur results demonstrate that aging and frailty cause intrinsic vitamin B12 deficiencies, which can occur independently of nutritional intake. Mechanistically, vitamin B12 deficiency involves the physio‐pathological decline of both the intestinal uptake and the renal reabsorption system for vitamin B12. Finally, amnionless is a novel biomarker which can detect perturbed vitamin B12 bioavailability during aging and physical frailty.

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Section: Discussionsupporting

confidence: 83%

Vitamin B12 deficiency and impaired expression of amnionless during aging

Pannérec

Migliavacca

Castro

et al. 2017

J cachexia sarcopenia muscle

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“…Moreover, we observed no effect on plasma homocystein levels after reduced nutritional intake of vitamins B6/B12/folate, indicating that mice were not deficient. However, an age‐related increase in plasma homocystein was observed, which indicates that vitamin B metabolism is already affected by ageing per se . Similarly, GSH levels decreased with advanced age, indicative of increased systemic oxidative stress with ageing.…”

Section: Discussionmentioning

confidence: 97%

Reduced dietary intake of micronutrients with antioxidant properties negatively impacts muscle health in aged mice

Dijk

Hartog

et al. 2017

J cachexia sarcopenia muscle

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BackgroundInadequate intake of micronutrients with antioxidant properties is common among older adults and has been associated with higher risk of frailty, adverse functional outcome, and impaired muscle health. However, a causal relationship is less well known. The aim was to determine in old mice the impact of reduced dietary intake of vitamins A/E/B6/B12/folate, selenium, and zinc on muscle mass, oxidative capacity, strength, and physical activity (PA) over time.MethodsTwenty‐one‐month‐old male mice were fed either AIN‐93‐M (control) or a diet low in micronutrients with antioxidant properties (=LOWOX‐B: 50% of mouse recommended daily intake of vitamins A, E, B6, and B12, folate, selenium, and zinc) for 4 months. Muscle mass, grip strength, physical activity (PA), and general oxidative status were assessed. Moreover, muscle fatigue was measured of m. extensor digitorum longus (EDL) during an ex vivo moderate exercise protocol. Effects on oxidative capacity [succinate dehydrogenase (SDH) activity], muscle fibre type, number, and fibre cross‐sectional area (fCSA) were assessed on m. plantaris (PL) using histochemistry.ResultsAfter 2 months on the diet, bodyweight of LOWOX‐B mice was lower compared with control (P < 0.0001), mainly due to lower fat mass (P < 0.0001), without significant differences in food intake. After 4 months, oxidative status of LOWOX‐B mice was lower, demonstrated by decreased vitamin E plasma levels (P < 0.05) and increased liver malondialdehyde levels (P = 0.018). PA was lower in LOWOX‐B mice (P < 0.001 vs. control). Muscle mass was not affected, although PL‐fCSA was decreased (~16%; P = 0.028 vs. control). SDH activity and muscle fibre type distribution remained unaffected. In LOWOX‐B mice, EDL force production was decreased by 49.7% at lower stimulation frequencies (P = 0.038), and fatigue resistance was diminished (P = 0.023) compared with control.ConclusionsReduced dietary intake of vitamins A, E, B6, and B12, folate, selenium, and zinc resulted in a lower oxidative capacity and has major impact on muscle health as shown by decreased force production and PA, without effects on muscle mass. The reduced fCSA in combination with similar SDH activity per fibre might explain the reduced oxidative capacity resulting in the increased fatigue after exercise in LOWOX‐B mice.

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“…Huo et al reported that the number of selfreported falls was higher in sarcopenic obese older adults than either sarcopenic or obese alone groups. 34,35 Both ageing and obesity can result in disability by leading to decreased organ function, increased chronic diseases and inflammation. 32 The present study demonstrated that the mean scores for domains of the SF-36 questionnaire were lower in both obese and sarcopenic obese participants compared to the sarcopenic and non-sarcopenic non-obese participants.…”

Section: Discussionmentioning

confidence: 99%