The diathesis–stress model specifies that depression results when a preexisting vulnerability, or diathesis, is activated by stressful life events. The preexisting vulnerability can be either genetic, implying an interaction between nature and nurture, or schematic, resulting from views of the world learned in childhood. American psychiatrist Aaron Beck suggested that a triad of automatic and spontaneous negative thoughts about the self, the world or environment, and the future may lead to other depressive signs and symptoms.Adverse childhood experiences (incorporating childhood abuse, neglect and family dysfunction) markedly increase the risk of major depression, especially if more than one type. Childhood trauma also correlates with severity of depression, poor responsiveness to treatment and length of illness. Some are more susceptible than others to developing mental illness such as depression after trauma, and various genes have been suggested to control susceptibility. Genetics
Family and twin studies find that nearly 40% of individual differences in risk for major depressive disorder can be explained by genetic factors. Like most psychiatric disorders, major depressive disorder is likely influenced by many individual genetic changes. In 2018, a genome-wide association study discovered 44 genetic variants linked to risk for major depression; a 2019 study found 102 variants in the genome linked to depression. Research focusing on specific candidate genes has been criticized for its tendency to generate false positive findings. There are also other efforts to examine interactions between life stress and polygenic risk for depression.
Retroperitoneal fibrosis or Ormonds disease is a disease featuring the proliferation of fibrous tissue in the retroperitoneum, the compartment of the body containing the kidneys, aorta, renal tract, and various other structures. It may present with lower back pain, kidney failure, hypertension, deep vein thrombosis, and other obstructive symptoms. It is named after John Kelso Ormond, who rediscovered the condition in 1948. Causes
The association of idiopathic retroperitoneal fibrosis with various immune-related conditions and response to immunosuppression led to a search for an autoimmune cause of idiopathic RPF. Many of these previously idiopathic cases can now be attributed to IgG4-related disease, an autoimmune disorder proposed in 2003. Otherwise, one-third of cases are secondary to malignancy, medication (methysergide, hydralazine, beta blockers), prior radiotherapy, or certain infections.Other associations include:

connective tissue disease
Riedels thyroiditis
sclerosing cholangitis
membranous nephropathy
ankylosing spondylitis
inflammatory bowel disease
ANCA-associated vasculitis
autoimmune pancreatitis
sarcoidosis
primary biliary cirrhosis
inflammatory abdominal aortic aneurysm

Diagnosis
The diagnosis of retroperitoneal fibrosis cannot be made on the basis of the results of laboratory studies. CT is the best diagnostic modality: a confluent mass surrounding the aorta and common iliac arteries can be seen. On MRI, it has low T1 signal intensity and variable T2 signal. Malignant retroperitoneal fibrosis usually gives uneven MRI signals, is bulky, extends above the origins of renal arteries, or displaces the aorta anteriorly.