Sarcopenia may also cause reduced strength, functional decline and increased risk of falling. Sarcopenia may also have no symptoms until it is severe and is often unrecognized. Research has shown, however, that hypertrophy may occur in the upper parts of the body to compensate for this loss of lean muscle mass Therefore, one early indicator of the onset of sarcopenia can be significant loss of muscle mass in the anterior thigh and abdominal muscles. Causes
There are many proposed causes of sarcopenia and it is likely the result of multiple interacting factors. Understanding of the causes of sarcopenia is incomplete, however changes in hormones, immobility, age-related muscle changes, nutrition and neurodegenerative changes have all been recognized as potential causative factors.The degree of sarcopenia is determined by two factors: initial amount of muscle mass and rate at which muscle mass declines. Due to variations in these factors across the population, the rate of progression and the threshold at which muscle loss becomes apparent is variable. Immobility dramatically increases the rate of muscle loss, even in younger people. Other factors that can increase rate of progression of sarcopenia include decreased nutrient intake, low physical activity, or chronic disease. Additionally, epidemiological research has indicated that early environmental influences may have long-term effects on muscle health. For example, low birth weight, a marker of a poor early environment, is associated with reduced muscle mass and strength in adult life.
Causes
The genetic cause of ULD is known, but research has led to new areas of study that may lead to an increase in knowledge of what causes ULD. Genetic factors
The cause of ULD is known to be a mutation of the gene that produces cystatin B. The disease is autosomal recessive, so both parents of an individual must be carriers of the recessive CSTB gene for the individual to inherit it, and for an individual to show symptoms of ULD, they must have both recessive CSTB genes. Siblings of affected individuals who only have one recessive gene have been monitored and generally do not show the signs of ULD, though in some cases mild symptoms may be present. New developments
New research shows that cystatin B may not be the only factor involved in Unverricht–Lundborg disease. In a study, it was determined that patients with ULD had more dopamine receptors in certain areas of their brain than unaffected individuals. The researchers chose to investigate dopamine receptors because they are known to be a factor in myoclonus, which are a significant part of the symptoms of ULD. The results of this study indicate that the cause of ULD may be more complex than currently thought. Mechanism
While the genetic cause of Unverricht–Lundborg disease is known, the mechanism by which it works is not fully known. Current research has provided promising results that may lead to a confirmation of the mechanism.