Article

Dietary protein intake is associated with lean mass change in older, community-dwelling adults: the Health, Aging, and Body Composition (Health ABC) Study.

Sticht Center on Aging, Wake Forest University School of Medicine, Winston-Salem, NC 27157-1207, USA.
American Journal of Clinical Nutrition (Impact Factor: 6.92). 01/2008; 87(1):150-5.
Source: PubMed

ABSTRACT Dietary surveys suggest that many older, community-dwelling adults consume insufficient dietary protein, which may contribute to the age-related loss of lean mass (LM).
The objective of the study was to determine the association between dietary protein and changes in total LM and nonbone appendicular LM (aLM) in older, community-dwelling men and women.
Dietary protein intake was assessed by using an interviewer-administered 108-item food-frequency questionnaire in men and women aged 70-79 y who were participating in the Health, Aging, and Body Composition study (n=2066). Changes in LM and aLM over 3 y were measured by using dual-energy X-ray absorptiometry. The association between protein intake and 3-y changes in LM and aLM was examined by using multiple linear regression analysis adjusted for potential confounders.
After adjustment for potential confounders, energy-adjusted protein intake was associated with 3-y changes in LM [beta (SE): 8.76 (3.00), P=0.004] and aLM [beta (SE): 5.31 (1.64), P=0.001]. Participants in the highest quintile of protein intake lost approximately 40% less LM and aLM than did those in the lowest quintile of protein intake (x+/-SE: -0.501+/-0.106 kg compared with -0.883+/-0.104 kg for LM; -0.400+/-0.058 kg compared with -0.661+/-0.057 kg for aLM; P for trend<0.01). The associations were attenuated slightly after adjustment for change in fat mass, but the results remained significant.
Dietary protein may be a modifiable risk factor for sarcopenia in older adults and should be studied further to determine its effects on preserving LM in this population.

0 Bookmarks
 · 
97 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Many diets and nutritional advice are circulating, often based on short- or medium-term clinical trials and primary outcomes, like changes in LDL cholesterol or weight. It remains difficult to assess which dietary interventions can be effective in the long term to reduce the risk of aging-related disease and increase the (healthy) lifespan. At the same time, the scientific discipline that studies the aging process has identified some important nutrient-sensing pathways that modulate the aging process, such as the mTOR and the insulin/insulin-like growth factor signaling pathway. A thorough understanding of the aging process can help assessing the efficacy of dietary interventions aimed at reducing the risk of aging-related diseases. To come to these insights, a synthesis of biogerontological, nutritional, and medical knowledge is needed, which can be framed in a new discipline called 'nutrigerontology'. © 2014 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.
    Aging cell 12/2014; · 7.55 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Poor vitamin K status is linked to greater risk of several chronic diseases. Age, sex, and diet are determinants of circulating vitamin K; however, there is still large unexplained interindividual variability in vitamin K status. Although a strong genetic component has been hypothesized, this has yet to be examined by a genome-wide association (GWA) study. The objective was to identify common genetic variants associated with concentrations of circulating phylloquinone, the primary circulating form of vitamin K. We conducted a 2-stage GWA meta-analysis of circulating phylloquinone in 2 populations of European descent from the Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium Nutrition Working Group. Circulating phylloquinone was measured by using reversed-phase high-performance liquid chromatography. Results from adjusted cohort-specific discovery GWA analyses were meta-analyzed with inverse variance weights (n = 2138). Associations with circulating phylloquinone at P < 1 × 10(-6) were then evaluated in a second-stage analysis consisting of one independent cohort (n = 265). No significant association was observed for circulating phylloquinone at the genome-wide significance level of 5 × 10(-8). However, from the discovery GWA, there were 11 single-nucleotide polymorphism (SNP) associations with circulating phylloquinone at P < 1 × 10(-6), including a functional variant previously associated with warfarin dose and altered phylloquinone metabolism. These SNPs are on 5 independent loci on 11q23.3, 8q24.3, 5q22.3, 2p12, and 19p13.12, and they fall within or near the candidate genes APOA1/C3/A4/A5 cluster (involved in lipoprotein metabolism), COL22A1, CDO1, CTNAA2, and CYP4F2 (a phylloquinone oxidase), respectively. Second-stage analysis in an independent cohort further suggests the association of the 5q22.3 locus with circulating phylloquinone (P < 0.05). Multiple candidate genes related to lipoprotein and vitamin K metabolism were identified as potential determinants of circulating phylloquinone. Further investigation with a larger sample is warranted to verify our initial findings and identify other loci contributing to circulating phylloquinone. Trials related to this study were registered at clinicaltrials.gov as NCT00005121 (Framingham Offspring Study) and NCT00005487 (Multi-Ethnic Study of Atherosclerosis). © 2014 American Society for Nutrition.
    American Journal of Clinical Nutrition 12/2014; 100(6):1462-9. · 6.50 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Sarcopenia is characterized by decreases in both muscle mass and muscle function. The loss of muscle mass, which can precede decrements in muscle function, is ultimately rooted in an imbalance between the rates of muscle protein synthesis and breakdown that favors a net negative balance (i.e., synthesis < breakdown). A preponderance of evidence highlights a blunted muscle protein synthetic response to dietary protein, commonly referred to as “anabolic resistance,” as a major underlying cause of the insipid loss of muscle with age. Dietary strategies to overcome this decreased dietary amino acid sensitivity include the ingestion of leucine-enriched, rapidly digested proteins and/or greater protein ingestion in each main meal to maximally stimulate muscle anabolism. Anabolic resistance is also a hallmark of a sedentary lifestyle at any age. Given that older adults may be more likely to experience periods of reduced activity (either voluntarily or through acute illness), it is proposed that inactivity is the precipitating factor in the development of anabolic resistance and the subsequent progression from healthy aging to frailty. However, even acute bouts of activity can restore the sensitivity of older muscle to dietary protein. Provided physical activity is incorporated into the daily routine, muscle in older adults should retain its capacity for a robust anabolic response to dietary protein comparable to that in their younger peers. Therefore, through its ability to “make nutrition better,” physical activity should be viewed as a vital component to maintaining muscle mass and function with age.
    Advances in Nutrition 09/2014; 5(5):599S-607S. · 3.20 Impact Factor