Congenital myopathies include, but are not limited to:
(G71.2) nemaline myopathy (characterized by presence of "nemaline rods" in the muscle),
(G71.2) multi/minicore myopathy (characterized by multiple small "cores" or areas of disruption in the muscle fibers),
(G71.2) centronuclear myopathy (or myotubular myopathy) (in which the nuclei are abnormally found in the center of the muscle fibers), a rare muscle wasting disorder
(G71.3) Mitochondrial myopathies, which are due to defects in mitochondria, which provide a critical source of energy for muscle
(G72.3) Familial periodic paralysis
(G72.4) Inflammatory myopathies, which are caused by problems with the immune system attacking components of the muscle, leading to signs of inflammation in the muscle
(G73.6) Metabolic myopathies, which result from defects in biochemical metabolism that primarily affect muscle
(G73.6/E74.0) Glycogen storage diseases, which may affect muscle
(G73.6/E75) Lipid storage disorder
(G72.89) Other myopathies
Brody myopathy
Congenital myopathy with abnormal subcellular organelles
Fingerprint body myopathy
Inclusion body myopathy 2
Megaconial myopathy
Myofibrillar myopathy
Rimmed vacuolar myopathy

Acquired
(G72.0 - G72.2) External substance induced myopathy
(G72.0) Drug-induced myopathy
Glucocorticoid myopathy is caused by this class of steroids increasing the breakdown of the muscle proteins leading to muscle atrophy. (G72.1) Alcoholic myopathy
(G72.2) Myopathy due to other toxic agents - including atypical myopathy in horses caused by toxins in sycamore seeds and seedlings. (M33.0-M33.1)
Dermatomyositis produces muscle weakness and skin changes. The skin rash is reddish and most commonly occurs on the face, especially around the eyes, and over the knuckles and elbows. Ragged nail folds with visible capillaries can be present. It can often be treated by drugs like corticosteroids or immunosuppressants. (M33.2)
Polymyositis produces muscle weakness.
Epidemiology
The estimated percentage of the population with a vitamin D deficiency varies based on the threshold used to define a deficiency. Recommendations for 25(OH)D serum levels vary across authorities, and probably vary based on factors like age; calculations for the epidemiology of vitamin D deficiency depend on the recommended level used.A 2011 Institute of Medicine (IOM) report set the sufficiency level at 20 ng/mL (50 nmol/L), while in the same year The Endocrine Society defined sufficient serum levels at 30 ng/mL and others have set the level as high as 60 ng/mL. As of 2011 most reference labs used the 30 ng/mL standard. : 435 Applying the IOM standard to NHANES data on serum levels, for the period from 1988 to 1994 22% of the US population was deficient, and 36% were deficient for the period  between 2001 and 2004; applying the Endocrine Society standard,  55% of the US population was deficient between 1988 and 1994, and 77% were deficient for the period between 2001 and 2004.In 2011 the Centers for Disease Control and Prevention applied the IOM standard to NHANES data on serum levels collected between 2001 and 2006, and determined that 32% of Americans were deficient during that period (8% at risk of deficiency, and 24% at risk of inadequacy). History
The role of diet in the development of rickets was determined by Edward Mellanby between 1918 and 1920. In 1921, Elmer McCollum identified an antirachitic substance found in certain fats that could prevent rickets.