This method is designed to pick up not only RAD but also the proposed new alternative categories of disorders of attachment. Causes
Although increasing numbers of childhood mental health problems are being attributed to genetic defects, reactive attachment disorder is by definition based on a problematic history of care and social relationships. Abuse can occur alongside the required factors, but on its own does not explain attachment disorder. It has been suggested that types of temperament, or constitutional response to the environment, may make some individuals susceptible to the stress of unpredictable or hostile relationships with caregivers in the early years. In the absence of available and responsive caregivers it appears that most children are particularly vulnerable to developing attachment disorders.While similar abnormal parenting may produce the two distinct forms of the disorder, inhibited and disinhibited, studies show that abuse and neglect were far more prominent and severe in the cases of RAD, disinhibited type. The issue of temperament and its influence on the development of attachment disorders has yet to be resolved. RAD has never been reported in the absence of serious environmental adversity yet outcomes for children raised in the same environment are the same.In discussing the neurobiological basis for attachment and trauma symptoms in a seven-year twin study, it has been suggested that the roots of various forms of psychopathology, including RAD, borderline personality disorder (BPD), and post-traumatic stress disorder (PTSD), can be found in disturbances in affect regulation.
Sphingolipidoses are a class of lipid storage disorders or degenerative storage disorders caused by deficiency of an enzyme that is required for the catabolism of lipids that contain ceramide, also relating to sphingolipid metabolism. The main members of this group are Niemann–Pick disease, Fabry disease, Krabbe disease, Gaucher disease, Tay–Sachs disease and metachromatic leukodystrophy. They are generally inherited in an autosomal recessive fashion, but notably Fabry disease is X-linked recessive. Taken together, sphingolipidoses have an incidence of approximately 1 in 10,000, but substantially more in certain populations such as Ashkenazi Jews. Enzyme replacement therapy is available to treat mainly Fabry disease and Gaucher disease, and people with these types of sphingolipidoses may live well into adulthood. The other types are generally fatal by age 1 to 5 years for infantile forms, but progression may be mild for juvenile- or adult-onset forms. Accumulated products
Gangliosides: Gangliosidosis
GM1 gangliosidoses
GM2 gangliosidoses
Tay–Sachs disease
Sandhoff disease
GM2-gangliosidosis, AB variant
Glycolipids
Fabrys disease
Krabbe disease
Metachromatic leukodystrophy
Glucocerebrosides
Gauchers disease

Comparison
Metabolic pathways
See also
Lipid storage disorder

References
External links

Sphingolipidoses at the US National Library of Medicine Medical Subject Headings (MeSH)