▣ 2.5 Comorbidities of IBM.

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 First it is important to understand what comorbidity is; it is where a patient has two or more distinct diseases at the same time. Usually it is assumed that the diseases are independent of each other. For example, the patient may have two diseases by chance alone. There are also other situations, for example, disease one may directly cause disease two. Another situation is by associated risk; we'll use the example of smoking. Many smokers also drink, therefore smoking and drinking are correlated risk factors. You may get COPD from smoking and have a higher risk for liver disease from alcohol consumption, thus, smoking and drinking make it a higher risk that these associated diseases will occur together. In another example, the symptoms of disease one and disease two may be each due to a third distinct disease (see Valderas, Starfi, & Sibbald, 2009). Comorbidities are associated with aging; more than 50 percent of older adults show occurrences of three or more chronic conditions (American Geriatrics Society, 2012).

 Comorbidity is complicated by the lifestyle of IBM patient. For example, due to their disability, many IBM patients are sedentary — not moving around very much, thus muscle disuse becomes a factor. Most people gain weight in this situation. People often consume a high-fat, high sodium, low-protein diet and eat too much. Thus they gain weight and often have high blood fat levels. These lifestyle factors put IBM patients at risk for diseases like type II diabetes. If you have IBM and develop type II diabetes, you now have the burden of both illnesses. In this situation it may be difficult to sort out what symptoms are from which disease, because both IBM and type II diabetes are associated with muscle issues.

 A study done by Keshishiana, Greenberg and others in 2018 showed that several diseases are comorbid with IBM. Patients with IBM are at an increased risk of cardiovascular disease compared to matched non-IBM patients, as indicated by associations with hypertension, diabetes, dyslipidemia, myocardial infarction and congestive heart failure. Prevalences of hypertension (65.9 percent) and diabetes (25.2 percent) were found. Other IBM comorbidities may include muscle and joint pain, and pulmonary complications.

 It appears that IBM and type II diabetes mellitus both have impacts on muscle. For example, diabetes affects the muscles’ ability to contract under performance. It is thought that this may be related to problems with microcirculation of blood through the skeletal muscle fibre. (Frisbee, Lewis, & Wiseman, 2019).

 Chronic diseases such as type II diabetes reduce the oxidative capacity as skeletal muscles. The increased death of mitochondria (mitophagy) is also related to symptoms often seen in common diseases. For example, factors such as hypoxia, inflammation, the disuse of muscles, and iron deficiencies all contribute to increasing mitophagy. There is a tight balance between mitochondria dying off and mitochondria being produced. It is likely that muscle disuse is an important early trigger of mitophagy, probably as part of a normal physiological adaptation to adjust mitochondrial content to the reduced energy demand associated with lower physical activity levels. Interventions to combat the loss of muscle oxidative capacity targeted directly at mitophagy signaling should be approached with the highest caution. A reduction in mitophagy will not only rescue healthy mitochondria but result in an increased number of dysfunctional mitochondria as well, which could aggravate the decrease in muscular health even more (Leermakers & Gosker, 2016).

 Type II diabetes is also associated with muscle wasting. Despite differences in pathogenesis and disease-related complications, there are reasons to believe that some fundamental underlying mechanisms are inherent to the muscle wasting process, irrespective of the pathology. Recent evidence shows that inflammation, either local or systemic, contributes to the modulation of muscle mass and/or muscle strength, via an altered molecular profile in muscle tissue. However, it remains ambiguous to which extent and via which mechanisms inflammatory signaling affects muscle mass in disease (Dalle & Koppo, 2020).


 American Geriatrics Society Expert Panel on the Care of Older Adults with Multimorbidity. Guiding principles for the care of older adults with multimorbidity: an approach for clinicians. J Am Geriatr Soc. 2012; 60:E1–E25. https://doi.org/10.1111/j.1532-5415.2012.04188.x

 Dalle, S., & Koppo, K. (2020). Is inflammatory signaling involved in disease-related muscle wasting? Evidence from osteoarthritis, chronic obstructive pulmonary disease and type II diabetes. Experimental Gerontology, 137(April), 110964. https://doi.org/10.1016/j.exger.2020.110964

 Frisbee, J. C., Lewis, M. T., & Wiseman, R. W. (2019). Skeletal muscle performance in metabolic disease: Microvascular or mitochondrial limitation or both? Microcirculation, 26(5), e12517. https://doi.org/10.1111/micc.12517

 Keshishian, A., Greenberg, S. A., Agashivala, N., Baser, O., & Johnson, K. (2018). Health care costs and comorbidities for patients with inclusion body myositis. Current Medical Research and Opinion, 34(9), 1679–1685. https://doi.org/10.1080/03007995.2018.1486294

 Leermakers, P. A., & Gosker, H. R. (2016). Skeletal muscle mitophagy in chronic disease. Current Opinion in Clinical Nutrition & Metabolic Care, 19(6), 427–433. https://doi.org/10.1097/MCO.0000000000000319

 Valderas, J. M., Starfi, B., & Sibbald, B. (2009). Defining Comorbidity: Implications for Understanding Health and Health Services. Annals Of Family Medicine, 357–363. https://doi.org/10.1370/afm.983


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