Nutrition as the foundation for successful aging: a focus on dietary protein and omega-3 polyunsaturated fatty acids

Abstract Skeletal muscle plays a critical role throughout the aging process. People living with sarcopenia, a progressive and generalized loss of skeletal muscle mass and function, often experience diminished quality of life, which can be attributed to a long period of decline and disability. Therefore, it is important to identify modifiable factors that preserve skeletal muscle and promote successful aging (SA). In this review, SA was defined as (1) low cardiometabolic risk, (2) preservation of physical function, and (3) positive state of wellbeing, with nutrition as an integral component. Several studies identify nutrition, specifically high-quality protein (eg, containing all essential amino acids), and long-chain omega-3 polyunsaturated fatty acids (n-3 PUFAs), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA), as positive regulators of SA. Recently, an additive anabolic effect of protein and n-3 PUFAs has been identified in skeletal muscle of older adults. Evidence further suggests that the additive effect of protein and n-3 PUFAs may project beyond skeletal muscle anabolism and promote SA. The key mechanism(s) behind the enhanced effects of intake of protein and n-3 PUFAs needs to be defined. The first objective of this review is to evaluate skeletal muscle as a driver of cardiometabolic health, physical function, and wellbeing to promote SA. The second objective is to examine observational and interventional evidence of protein and n-3 PUFAs on skeletal muscle to promote SA. The final objective is to propose mechanisms by which combined optimal intake of high-quality protein and n-3 PUFAs likely play a key role in SA. Current evidence suggests that increased intake of protein above the Recommended Dietary Allowance and n-3 PUFAs above the Dietary Guidelines for Americans recommendations for late middle-aged and older adults is required to maintain skeletal muscle mass and to promote SA, potentially through the mechanistical target of rapamycin complex 1 (mTORC1).