Congratulations to Miami Dolphins wide receiver Brandon Marshall for publicly discussing his treatment for borderline personality disorder. He joins the ranks of brave individuals in public eye who have talked about their struggles with mental illness in order to fight the stigma that still attaches to problems like Bipolar I disorder (Patty Duke) and Bipolar II disorder (Catherine Zeta-Jones), postpartum depression (Brooke Shields, Gwyneth Paltrow), and obsessive-compulsive disorder (Howie Mandel, David Beckham.

“My purpose moving forward is to raise awareness of this disorder — how it not only affects the patient but the families and the people in the community,” he has said.

My colleague and friend, Dr. Virginia Willour has just published a paper in the research journal Molecular Psychiatry announcing the discovery of an association between suicidal behavior in patients with bipolar disorder and a gene called ACP1.  The scientific approach is called a Genome-wide Association Study (GWAS.) In a GWAS, many thousands of genetics markers are tested in persons with the characteristic being investigated (in this case, suicidal behavior in volunteers with bipolar disorder) and compared to the markers in volunteers with that characteristic. Dr. Willour compared the marker pattern in 1201 bipolar (BP) subjects with a history of suicide attempts to the the pattern in 1497 BP subjects without a history of suicide attempts and used those findings to ask the same question in another sample of volunteers. The combined analysis of the two sample sets produced a significant “association signal” in an area on chromosome 2 containing the ACP1 (acid phosphatase 1) gene. There have been a number of other findings of genetic “signals” in bipolar disorder that no other research teams have been able to repeat (replicate.) However, other studies have show that the ACP1 gene is more activated in BP subjects who have completed suicide. Furthermore, the ACP1 protein influences a pathway in neurons called “Wnt signaling,” a pathway that is known to be regulated by lithium. Add this to the fact that lithium is known to have a specific protective effect against suicide, and you have the ingredients for a lot of excitement about this finding, which has been announced in many different media outlets. Congratulations, Ginny!!

If you are planning to attend this years symposium, I and my colleagues, Ray DePaulo, Kay Jamison and Dean MacKinnon will be available to sign copies of our books. The authors’ table will open at 3:30. Please stop by and say hello!

Borderline Personality Disorder: New Reasons for Hope is, like my other books, a comprehensive, compassionate  guide to a potentially devastating psychiatric disorder. More details will follow as the publication date nears.

I’m proud to announce that the Johns Hopkins University Press has accepted a book proposal that I submitted with my colleague Patrick Kelly, M.D., also of Johns Hopkins. It is tentatively titled “Borderline Personality Disorder: A Guide for Patients, Families and Practitioners.” Details will follow. Pat and I are VERY excited!

I will be talking to the Depression and Bipolar Support Alliance-National Capital Area Chapter on March 26. The talk is titled “Manic-depression to Bipolar NOS: 100 Years of Mood Disorders,” and I will be reviewing the history of the diagnosis and treatment of mood disorder over the centuries. I will also review promising future treatment developments. The talk will be in the George Washington University Hospital Auditorium, 900 23rd Street, Washington DC. Hope to see you there!

A current controversy in the treatment of bipolar disorder is how antidepressant medication(s) should be used to treat symptoms. A recent research article in the New England Journal of Medicine stated that “The use of adjunctive, standard antidepressant medication, as compared with the use of mood stabilizers, was not associated with increased efficacy.” In other words, antidepressant medication did not help these patients over the longer term. This study also reported that taking antidepressants was not associated with “increased risk of treatment-emergent affective switch,” that is, they did not trigger the development of manic or mixed symptoms, either. However, the patients in this study were only followed for about 6 months. In another study, which followed patients for one year, antidepressants were found to raise the risk of a switch to mania or hypomania. This is more in line with my clinical experience, which is that antidepressants often cause more cycling in patients with bipolar disorder and can induce mild mixed states where people have bouts of “rage” and irritability. Some patients describe these symptoms as “anxiety,” but close questioning often reveals the tense, “wired,” pressured feelings of a mixed state.

In a research article in the British Journal of Psychiatry, researchers from Germany reported that they measured the size of a particular brain area in patients with major depression and found that this area was significantly smaller in men who later had a relapse than in those who stayed well. The brain area they measured was, as you might have guessed, the hippocampus. It’s been know for several years that depressed persons tend to have shrinkage of this brain area compared to persons without depression. This study is the first one to show that in men who get well and stay well from depression, the hippocampus is larger and more like that seen in persons without depression problems. You can read about the study here. It’s interesting to note that this was not true of the women in the study. The researchers concluded that “Hippocampal reduction is a gender-specific factor” in the cause of depression.

…of the third edition of my book Depression, the Mood Disease. Read it here. Among other nice things, the reviewer (Kevin M. Purday, Principal of the Shanghai Rego International School) writes “Comprehensiveness is allied to readability to make this both a useful and a reader-friendly guide,” and “This is a highly comprehensive account and is to be recommended to sufferers and professionals in the mental health field.”

Thank you, Professor Purday!

In a recent article in the journal Science, researchers working in Italy announced that giving laboratory rats fluoxetine (AKA: Prozac)had the effect of turning on the development of brain cells in the visual area of the animals’ brains. You may be asking yourself “What does that have to do with making depression better!?” If so, you are probably still thinking about mood disorders as “chemical imbalances.” Well, that idea is so-o-o 20th Century! There is now a lot of evidence that new brain cells (neurons) are constantly being born in certain areas of the the brain (the most important is the hippocampus) and that the growth and development of these new cells is needed for normal mood control. One way to think about this process is that this area of the brain must constantly reprogram itself by bringing new neurons on line and making and re-making the connections between these new and the older neurons. The ability to do this remodeling is called neuroplasticity (remember that the original definition of “plastic” is “capable of being molded, or of receiving form.”

These researchers took advantage of a well-known fact regarding the development of the brain’s visual system, namely that this brain area needs visual stimulation just after birth to develop properly. If the visual cortex does not receive this stimulation, this area of the brain doesn’t organize its connections properly and individuals cannot see properly. You may have heard of “lazy eye” (amblyopia) being treated in children by covering their “good” eye with a patch, essentially over-stimulating the “lazy” eye so it can catch up. It’s important to know that the “catching up” happens in the brain, not the eyeball. Also, as individuals mature, this ability to catch up is lost. This brain area loses its plasticity. It used to be thought that the ability of the visual area of the brain to organize in response to this stimulation (its plasticity) completely and irretrievably disappeared in adulthood.

These researchers artificially created a “lazy eye” problem (really, for the reasons stated above, it should be called “lazy brain” or better yet: “lazy visual cortex”) in young rats by covering one of their eyes. As the rats approached adulthood, they gave some of them fluoxetine for several weeks, and they switched the eye patch to the other eye in all the rats. In the rats that did not receive the antidepressant, the artificially created “lazy visual cortex” never recovered when the eye was uncovered. The brain had lost its plasticity, and could no longer respond to the signals from the now opened eye. The rats that had received the antidepressant for two weeks, on the other hand, recovered their vision completely! The fluoxetine had turned on the brain’s ability to adapt. Brain plasticity was restored.

It’s been hypothesized for some years that antidepressants increased plasticity in the hippocampus, but it’s been hard to measure this increase. This study is different, because the researchers looked at an area of the brain (the visual cortex) that completely loses its plasticity in adulthood. Proving that antidepressant treatment restored plasticity to this brain area in adult brains is further evidence that this process is crucial to how antidepressants work.