Henriksson et al. (2005) states statistically that the stressors are of one-half related to parental issues and one-third in peer issues.One hypothesis about Adjustment disorder is that it may represent a sub-threshold clinical syndrome. Subtypes and Their Symptoms
Adjustment disorder has six different subtypes, and they are all based on what the main symptoms are.Those subtypes are as follows:
With depressed mood: depression, hopelessness, lack of interest or joy from previously enjoyed hobbies, tearfulness
With anxiety: anxiousness, being overwhelmed, trouble concentrating, worry, separation anxiety (common in children)
With anxiety and depressed mood: combination of symptoms from both subtypes above
With disturbance of conduct: acting destructive, reckless behavior, rebellious
With mixed disturbance of emotions and conduct: combination of symptoms from both subtypes above
Unspecified: symptoms that do not fall into above subtypes; often include physical symptoms and withdrawal from everyday activities

Risk factors
Those exposed to repeated trauma are at greater risk, even if that trauma is in the past. Age can be a factor due to young children having fewer coping resources and because they are less likely to realize the consequences of a potential stressor.A stressor is generally an event of a serious, unusual nature that an individual or group of individuals experience. Adjustment disorders can come from a wide range of stressors that can be traumatic or relatively minor, like the loss of a girlfriend/boyfriend, a poor report card, or moving to a new neighborhood. It is thought that the more often the stressor occurs, the more likely it is to produce Adjustment disorder.
Deletion of the entire D4Z4 repeat array does not result in FSHD because then there are no complete copies of DUX4 to be expressed, although other birth defects result. One contracted D4Z4 repeat array with an adjoining 4qA allele is sufficient to cause disease, so inheritance is autosomal dominant. De novo (new) mutations are implicated in 10 - 30% of cases, 50% of which exhibit somatic mosaicism.It has been proposed that FSHD1 undergoes anticipation, a trend primarily associated with trinucleotide repeat disorders in which disease manifestation worsens with each subsequent generation. As of 2019, more detailed studies are needed to definitively show whether or not anticipation plays a role. If anticipation does occur in FSHD, the mechanism is different than that of trinucleotide repeat disorders, since D4Z4 repeats are much larger than trinucleotide repeats, an underabundance of repeats (rather than overabundance) causes disease, and the repeat array size in FSHD is stable across generations. FSHD2
FSHD without D4Z4 contraction is classified as FSHD2, which constitutes 5% of FSHD cases. Various mutations cause FSHD2, all resulting in D4Z4 hypomethylation, at which the genetic mechanism converges with FSHD1. Approximately 80% of FSHD2 cases are due to deactivating mutations in the gene SMCHD1 (structural maintenance of chromosomes flexible hinge domain containing 1) on chromosome 18. SMCHD1 is responsible for DNA methylation, and its deactivation results in hypomethylation of the D4Z4 repeat array. Another cause of FSHD2 is mutation in DNMT3B (DNA methyltransferase 3B), which also plays a role in DNA methylation.