Dietary protein intake might be beneficial to physical function (PF) in the elderly. We examined the cross-sectional and prospective associations of protein intake of g/kg body weight (BW), fat mass (FM) and lean mass (LM) with PF in 554 women aged 65·3-71·6 years belonging to the Osteoporosis Risk Factor and Prevention Fracture Prevention Study. Participants filled a questionnaire on lifestyle factors and 3-d food record in 2002. Body composition was measured by dual-energy X-ray absorptiometry, and PF measures were performed at baseline and at 3-year follow-up. Sarcopaenia was defined using European Working Group on Sarcopenia in Older People criteria. At the baseline, women with higher protein intake (≥1·2 g/kg BW) had better performance in hand-grip strength/body mass (GS/BM) (P = 0·001), knee extension/BM (P = 0·003), one-leg stance (P = 0·047), chair rise (P = 0·043), squat (P = 0·019), squat to the ground (P = 0·001), faster walking speed for 10 m (P = 0·005) and higher short physical performance battery score (P = 0·004) compared with those with moderate and lower intakes (0·81-1·19 and ≤0·8 g/kg BW, respectively). In follow-up results, higher protein intake was associated with less decline in GS/BM, oneleg stance and tandem walk for 6 m over 3 years. Overall, results were no longer significant after controlling for FM. Associations were detected between protein intake and PF in non-sarcopaenic women but not in sarcopaenic women, except for change of GS (P = 0·037). Further, FM but not LM was negatively associated with PF measures (P < 0·050). This study suggests that higher protein intake and lower FM might be positively associated with PF in elderly women.
Better diet quality as measured by higher adherence to BSD and MED might reduce the risk of sarcopenia in elderly women.
Frailty is a syndrome of growing importance given the global ageing population. While frailty is a multifactorial process, poor nutritional status is considered a key contributor to its pathophysiology. As nutrition is a modifiable risk factor for frailty, strategies to prevent and treat frailty should consider dietary change. Observational evidence linking nutrition with frailty appears most robust for dietary quality: for example, dietary patterns such as the Mediterranean diet appear to be protective. In addition, research on specific foods, such as a higher consumption of fruit and vegetables and lower consumption of ultra-processed foods are consistent, with healthier profiles linked to lower frailty risk. Few dietary intervention studies have been conducted to date, although a growing number of trials that combine supplementation with exercise training suggest a multi-domain approach may be more effective. This review is based on an interdisciplinary workshop, held in November 2020, and synthesises current understanding of dietary influences on frailty, focusing on opportunities for prevention and treatment. Longer term prospective studies and well-designed trials are needed to determine the causal effects of nutrition on frailty risk and progression and how dietary change can be used to prevent and/or treat frailty in the future.
Low protein intake can lead to declined lean mass (LM) in elderly. We examined the associations of total protein (TP), animal protein (AP) and plant protein (PP) intakes with LM. The association of TP intake with LM change was further evaluated according to weight change status. This cross-sectional and prospective cohort study included 554 women aged 68 (sd 1·9) years from the Osteoporosis Risk Factor and Prevention – Fracture Prevention Study (OSTPRE-FPS). The intervention group (n 270) received daily cholecalciferol (800 IU; 20 μg) and Ca (1000 mg) for 3 years while the control group received neither supplementation nor placebo (n 282). Participants filled out a questionnaire on lifestyle factors and a 3-d food record in 2002 and underwent dual-energy X-ray absorptiometry for body composition measurements at baseline and 3 years. Multiple linear regressions evaluated the association between protein intake and LM, adjusting for relevant covariates. At the baseline TP and AP intakes were positively associated with LM and trunk LM, TP was associated also with appendicular LM (aLM). Follow-up results showed that in the total population and the intervention group, higher TP and AP were associated with increased LM and aLM (P ≤ 0·050). No such associations were observed in the control group. PP intake was also associated with aLM change in the total population. Overall, the associations were independent of fat mass. Further, among weight maintainers, TP intake was positively associated with LM, aLM and trunk LM changes (P ≤ 0·020). In conclusion, dietary TP, especially AP, intake may be a modifiable risk factor for sarcopenia by preserving LM in the elderly.
Knowledge regarding association of dietary branched-chain amino acid (BCAA) and type 2 diabetes (T2D), and the contribution of BCAA from meat to the risk of T2D are scarce. We evaluated associations between dietary BCAA intake, meat intake, interaction between BCAA and meat intake and risk of T2D. Data analyses were performed for 74 155 participants aged 50-79 years at baseline from the Women's Health Initiative for up to 15 years of follow-up. We excluded from analysis participants with treated T2D, and factors potentially associated with T2D or missing covariate data. The BCAA and total meat intake was estimated from FFQ. Using Cox proportional hazards models, we assessed the relationship between BCAA intake, meat intake, and T2D, adjusting for confounders. A 20 % increment in total BCAA intake (g/d and %energy) was associated with a 7 % higher risk for T2D (hazard ratio (HR) 1·07; 95 % CI 1·05, 1·09). For total meat intake, a 20 % increment was associated with a 4 % higher risk of T2D (HR 1·04; 95 % CI 1·03, 1·05). The associations between BCAA intake and T2D were attenuated but remained significant after adjustment for total meat intake. These relations did not materially differ with or without adjustment for BMI. Our results suggest that dietary BCAA and meat intake are positively associated with T2D among postmenopausal women. The association of BCAA and diabetes risk was attenuated but remained positive after adjustment for meat intake suggesting that BCAA intake in part but not in full is contributing to the association of meat with T2D risk.
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