Typically, patients with minor depression were treated by watchful waiting, prescribed antidepressants, and given brief supportive counseling, but Problem-Solving Treatment for Primary Care (PST-PC) is a Cognitive-Behavioral Therapy that has gained popularity. In one study, PST-PC and Paroxetine, an antidepressant, were shown to be equally effective in significantly reducing symptoms. In another study, PST-PC was compared with the more typical care of the time and shown to reduce symptoms more quickly. Although the use of antidepressants has been widely used, not all agree that it is an appropriate treatment for some minor depression disorder settings.Another alternative that has been researched is the use of St. Johns wort (Hypericum perforatum). This herbal treatment has been studied by various groups with various results. Some studies show evidence of the treatment being helpful to treat minor depression, but others show that it does no better than the placebo. History
At its core, minor depressive disorder is the same illness as major depressive disorder with its symptoms being less pronounced. This ties its history closely to that of major depressive disorder. Depression in the past has largely been shrouded in mystery, as its causes and appropriate treatment were largely unknown. By the 1950s, it was clear that depression could be both a mental and largely physical disease, thus being able to be treated through both psychotherapy and medication. When the DSM-IV-TR was created and major depressive disorder was spelled out more clearly, there still seemed to be an uncategorized range of depression.
Mental retardation, short stature, headaches, unsteady gait, and collapsing or fainting are common. Psychiatric problems (such as anxiety, rapid mood changes, delusions, and hallucinations) may also result. Causes
Hartnup disease is inherited as an autosomal recessive trait. Heterozygotes are normal. Consanguinity is common. The failure of amino-acid transport was reported in 1960 from the increased presence of indoles (bacterial metabolites of tryptophan) and tryptophan in the urine of patients as part of a generalized aminoaciduria of the disease. The excessive loss of tryptophan from malabsorption was the cause of the pellagra like symptoms. From studies on ingestion of tryptophan it seemed that there was a generalized problem with amino-acid transport. In 2004, a causative gene, SLC6A19, was located on band 5p15.33. SLC6A19 is a sodium-dependent and chloride-independent neutral amino acid transporter, expressed predominantly in the kidneys and intestine. Diagnosis
The defective gene controls the absorption of certain amino acids from the intestine and the reabsorption of those amino acids in the kidneys. Consequently, a person with Hartnup disease cannot absorb amino acids properly from the intestine and cannot reabsorb them properly from tubules in the kidneys. Excessive amounts of amino acids, such as tryptophan, are excreted in the urine. The  body is thus left with inadequate amounts of amino acids, which are the building blocks of proteins.