The past decade witnessed major strides in our understanding and treatment of affective disorders in adults, children and adolescents. One of the baffling problems in child and adolescent psychiatry was the question of psychiatric illness spanning a lifetime. The existence of depressive disorders in prepubertal children has been generally recognized and acknowledged since the 1960s; however, only in the last decade did evidence become available that supports the notion that depression in different ages represents the same entity, albeit manifesting different clinical symptoms in each developmental period (Cytryn and others 1986).
A clinical similarity is already evident in 5- to 6-year-old children, which permits to diagnosing mood disorders at this age using modified adult rating scales and unmodified adult diagnostic criteria. A developmental continuity is also suggested by the fact that many biological markers found in major depressive disorders approximate adult values with advancing age. These include: EEG sleep patterns, hypersecretion of cortisol, diminished growth hormone to an insulin tolerance test and diminished 24-hour 3-methoxy-4-hydroxy phenylglycol (MHPG) excretion in the urine (Cytryn, McKnew 1980).
In addition, several follow-up studies indicate that (1) prepubertal mood disorders often continue into adolescence and adulthood (Asarnow and colleagues; Kovacs and others); (2) many children who develop depressive disorders in childhood will have at least one relapse before the age of 15 (Weissman and others); (3) dysthymic disorder, the most common form of mood disorder in prepubertal children, frequently converts to major depressive disorder in adolescence and usually has a protracted, chronic course (Kovacs and coworkers). In fact, it has been suggested that early onset of a depressive disorder may foretell a more severe course of the illness, similar to that found in juvenile forms of rheumatoid arthritis and diabetes; and (4) bipolar disorder is being diagnosed in children with increasing frequency, and of those with a severe unipolar disorder before puberty, at least 20% become bipolar during late adolescence.
The modern understanding of genetic factors started with the discovery of the deceptive simplicity of our genetic code, based on a variable arrangement of only four organic bases-adenine, guanine, thymine and cytosine. This discovery opened the way for the remarkably rapid progress in genetic research, aided by impressive advances in molecular genetics in the last two decades. In rapid succession, the discovery of restriction enzymes, followed by such ingenious breakthroughs as the polymerase chain reaction and genetic sequencing, generated a dizzying speed in the process of gene mapping, i.e., identification and correct localization of up to 100,000 human genes.
This gigantic effort has been appropriately recognized and nurtured by the Human Genome Project, started in the 1980s by the National Institute of Health. It was originally estimated that the process of mapping the entire human genome may not be completed until several decades into the 21st century. However, as the rapid pace of genetic discoveries continues, abetted by the involvement of the private sector, the completion of the task looms much closer on the horizon. Some estimates are a mere several years after the turn of the century, providing a fitting entry into the third millennium.
1. Asarnow JR, Carlson GA, Perdue S, et al. Childhood-onset of depressive disorders: A follow-up study of rates of rehospitalization and out-of-home placement among child psychiatric inpatients. J Affect Disord. 1988;15:245-253.
2. Cytryn L, McKnew DH. Affective disorders in childhood. In: Kaplan HI, Friedman AM, Sadock BH, eds. Comprehensive Textbook of Psychiatry II, Vol. III. Baltimore: Williams & Wilkins; 1980.
3. Cytryn L, McKnew DH, Zahn-Waxler C, et al. Developmental issues in risk research: The offspring of affectively ill parents. In: Rutter M, Izard CE, Read PB, eds. Depression in Young People: Clinical and Developmental Perspectives. New York: Guilford Press; 1986.
4. Kendler KS, Kessler RC, Neale MC, et al. The prediction of major depression in women: Toward an integrated etiologic model. Am J Psychiatry. 1993;150:1139-1148.
5. Kovacs M, Feinberg TL, Crouse-Novak MS, et al. Depressive disorders in childhood, II. A longitudinal study of the risk for a subsequent major depression. Arch Gen Psychiatry. 1984;41:643-649.
6. Plomin R, Owen MJ, McGuiffin P. The genetic basis of complex behavior. Science. 1994;264:1733-1739.
7. Reiss D, Plomin R, Hetherington EM. Genetics and psychiatry: An unheralded window on the environment. Am J Psychiatry. 1991;48:283-291.
8. Rieder R, Gershon ES. Genetic strategies in biological psychiatry. Arch Gen Psychiatry. 1978;35:866-873.
9. Weissman MM, Gammon GD, John K, et al. Children of depressed parents: Increased psychopathology and early onset of major depression. Arch Gen Psychiatry. 1987;44:847-853.