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Measures of body mass such as weight and body mass index (BMI) have long been practically used as a measure for the prediction of health risks and outcomes. Although of some value, these measurements do not address an individual’ s variability in body composition (i.e. lean versus adipose tissue). Abnormalities in body composition such as low muscle mass are powerful predictors of morbidity and mortality. The term “ sarcopenia”  has often been used to describe low muscle mass in clinical settings, but now widely accepted to also include measures of strength, muscular performance, or physical performance in context of ageing.

The concurrent appearance of low muscle mass with high adiposity (also termed sarcopenic obesity) is the new face of an old problem, common in people who face chronic diseases. This condition has a compounding impact on health and outcomes. To date, medical practice relies on measures of body size such as BMI; however, BMI does not necessarily relate to muscle mass, making the measure problematic

Low muscle mass in hospitalized patients is a prevalent phenomenon that worsens with increased time spent admitted to a hospital. This is led by a variety of reasons ranging from hyper-catabolism, inadequate food intake and/or immobility Low muscle mass is an economic burden to the health care system, as this condition is associated with an average increase of over $14,000 in total hospital costs per patient undergoing major abdominal surgery compared to patients with normal muscle amounts. Post-surgical complications such as sepsis, infection, prolonged ventilation and pneumonia are reported to occur at a higher rate and survival is shorter in individuals with low muscle mass undergoing different types of surgery.

Obesity is a risk factor for heart disease, and many patients, therefore, have obesity at disease presentation. However, body weight may be artificially elevated due to oedema and can conceal underlying low muscle mass. This influences body composition measurement since hydration may affect some measures of muscle mass. Nevertheless, the presence of low muscle mass is estimated to occur in almost 20% of patients with stable heart failure. It is associated with a decline in several functional parameters such as strength (handgrip and quadriceps), total peak VO2 , walking distance (6-meter walk tests), abnormal cardiac parameters and cardiac perfusion.

In individuals with chronic kidney disease (CKD), systemic inflammation, transient catabolic comorbidities, nutrient losses during dialysis, endocrine abnormalities (such as resistance to insulin, growth hormone and insulin-like growth factor), hyperglycemia, hyperparathyroidism and loss of blood during hemodialysis are prevalent. Additionally, reduced protein diets of 0.6– 0.8 g/kg/day may be recommended to patients, not on dialysis. These factors contribute to muscle wasting, which is usually reported under the auspices of protein-energy wasting.

Recent clinical evidence demonstrates that individuals with COPD with higher muscle mass (measured by DXA) experienced better outcomes (e.g. improved forced expiratory volume and COPD assessment test score and reduced dyspnea) and lower occurrence of osteopenia/osteoporosis than COPD patients with low muscle mass. Importantly, the prevalence of low muscle mass was higher in men with COPD compared to matched males with normal lung function. There was a relationship between muscle mass and airflow limitation, which suggests that disease severity may induce or exacerbate muscle loss in individuals with COPD.

Therefore, the potential clinical benefits of preventing and reversing low muscle mass in patients are likely to impact not only patient outcomes but also resource utilization/health care costs. Currently, body composition measurement tools (e.g. DXA, CT) although available to specific clinical settings are not widely available to the general population highlighting why BMI is a poor tool and alternative measures should be explored.

 

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