Abstract
This narrative review provides mechanistic insight into the biological link between smoking and/or chronic excess alcohol consumption, and increased risk of developing sarcopenia. Although the combination of excessive alcohol consumption and smoking is often associated with ectopic adipose deposition, this review is focused on the context of a reduced caloric intake (leading to energy deficit) that also may ensue due to either lifestyle habit. Smoking is a primary cause of periodontitis and chronic obstructive pulmonary disease that both induce swallowing difficulties, inhibit taste and mastication, and are associated with increased risk of muscle atrophy and mitochondrial dysfunction. Smoking may contribute to physical inactivity, energy deficit via reduced caloric intake, and increased systemic inflammation, all of which are factors known to suppress muscle protein synthesis rates. Moreover, chronic excess alcohol consumption may result in gut microbiota dysbiosis and autophagy-induced hyperammonemia, initiating the up-regulation of muscle protein breakdown and down-regulation of muscle protein synthesis via activation of myostatin, AMPK and REDD1, and deactivation of IGF-1. Future research is warranted to explore the link between oral healthcare management and personalised nutrition counselling in light of potential detrimental consequences of chronic smoking on musculoskeletal health outcomes in older adults. Experimental studies should investigate the impact of smoking and chronic excess alcohol consumption on the gut-brain axis, and explore biomarkers of smoking-induced oral disease progression. The implementation of behavioural change interventions and health policies regarding smoking and alcohol intake habits may mitigate the clinical and financial burden of sarcopenia on the healthcare system.
Highlights
Smoking and chronic excessive alcohol consumption are lifestyle choices that represent major risk factors for comorbidities in older adults, including heart disease, cirrhosis, alcoholic hepatitis, chronic obstructive pulmonary disease (COPD), and various forms of cancer[1]
Accumulating evidence suggests that health implications of smoking and chronic excessive alcohol consumption extend to the musculoskeletal system, as mediated by the down-regulation of metabolic pathways that regulate muscle protein metabolism and subsequent increased risk of sarcopenia
Chronic use of tobacco products may contribute to undernutrition through oral health and dopamine receptor dysfunction and, combined with systemic inflammation, may impair basal rates of muscle protein synthesis (MPS)
Summary
Smoking and chronic excessive alcohol consumption are lifestyle choices that represent major risk factors for comorbidities in older adults, including heart (fatty liver) disease, cirrhosis, alcoholic hepatitis, chronic obstructive pulmonary disease (COPD), and various forms of cancer[1]. It has been proposed that increased oxidative stress from aldehydes, carbon monoxide, ROS and reactive nitrogen species circulate to the skeletal muscle and activate the p38 and ERK mitogen-activated protein kinase (MAPK), and the nuclear factor κB (NF-κB) signalling pathway[123,124,125] This overexpression of MAPK may up-regulate the muscle-specific E3 ubiquitin ligases and lead to a greater inflammatory response and up-regulation of MPB in smokers, accelerating risk of sarcopenia[126,127,128]
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