{"id":33252,"date":"2013-02-11T20:58:34","date_gmt":"2013-02-12T01:58:34","guid":{"rendered":"http:\/\/1boringoldman.com\/?p=33252"},"modified":"2013-02-11T20:58:34","modified_gmt":"2013-02-12T01:58:34","slug":"too-big-a-hurry","status":"publish","type":"post","link":"https:\/\/1boringoldman.com\/index.php\/2013\/02\/11\/too-big-a-hurry\/","title":{"rendered":"too big a hurry…"},"content":{"rendered":"\n
The Human Genome Project was declared complete in April 2003. An initial rough draft of the human genome was available in June 2000 and by February 2001 a working draft had been completed and published followed by the final sequencing mapping of the human genome on April 14, 2003…<\/strong><\/sup><\/em><\/div>\n
The Human Genome Project, Wikipedia<\/a><\/strong><\/sup><\/em><\/div>\n

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Abbot Gregor Mendel’s genetic studies on the inheritance of traits in the pea plant at the time of our Civil War and my own Zoology 101 eye color experiment crossbreeding fruit flies as a college freshman came out just right. I expect those Tennessee fruit flies’ descendents are still amazing students at my alma mater even today. Later, at the Sickle Cell Center in Memphis, I’d wager those endless genograms we drew for Sickle Cell Anemia and Thalassemia continue to confirm Mendel’s Laws of Inheritance, just like they did 50 years ago during my tenure. But later, when I got to psychiatry, I read about diseases that ran in families<\/em> like Manic Depressive Insanity and Schizophrenia – but those genograms looked a lot different. Inheritance required statistics on large populations and twin studies to show evidence of the genetic component, but paid little attention to Mendel’s Laws. Here are a couple of summary slides showing the familial associations in Schizophrenia [left] and Manic-Depressive Illness [right]:<\/div>\n
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The diagnosis of Major Depressive Disorder is less precise to my mind so I haven’t posted some summary slide. But notice that in the graph on the right, black is for the Bipolar Phenotype and the open bar is using the standard of [Bipolar + Recurrent Unipolar Depression + Suicide] and it approaches 100% in monozygotic [identical] twins. The study below is a meta-analysis of the studies in Major Depressive Disorder [as of 2010] looking at the attempts to translate the runs in family<\/em> information into studies that look at the actual genetic data available in the post-Human-Genome era: <\/div>\n
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Overview of the Genetics of Major Depressive Disorder<\/a>
Falk W. Lohoff<\/sup>
Current Psychiatry Reports<\/font><\/strong>. 2010 12[6]: 539–546.
[full text on-line<\/a>]<\/div>\n

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Abstract: Major depressive disorder [MDD] is a common psychiatric illness with high levels of morbidity and mortality. Despite intensive research during the past several decades, the neurobiological basis and pathophysiology of depressive disorders remain unknown. Genetic factors play important roles in the development of MDD, as indicated by family, twin, and adoption studies, and may reveal important information about disease mechanisms. This article describes recent developments in the field of psychiatric genetics, with a focus on MDD. Early twin studies, linkage studies, and association studies are discussed. Recent findings from genome-wide association studies are reviewed and future directions discussed. Despite all efforts, thus far, no single genetic variation has been identified to increase the risk of depression substantially. Genetic variants are expected to have only small effects on overall disease risk, and multiple genetic factors in conjunction with environmental factors are likely necessary for the development of MDD. Future large-scale studies are needed to dissect this complex phenotype and to identify pathways involved in the etiology of MDD.<\/strong><\/sup><\/div>\n