Q. My direct question follows *** below; this is lead-in information). I have a background in evolutionary neuroscience, and support the position that the adaptive neural/information-processing systems of the human neocortex are constructed during early childhood (but continue to be updated in an on-line fashion throughout the lifespan; see LaCerra and Bingham, Proc. Natl.Acad.Sci. USA, Vol 95, pp 11290-11294, September, 1998). As a consequence, while early social conditioning establishes patterns of behavior that are often recalcitrant to later interventions, I suspect that the problem is most probably due to 2 interrelated factors: 1) behavior emitted affects the way other people interact with an individual thereby predisposing him/her to similarly unsatisfactory behavior in the future; and 2) the individual continues to accrue an ever-growing database of experience that serves to generate future behavior; subsequent to intervention, behavioral generation is still arising most predominantly from the pre-intervention database. As such, I would expect that, owing to the positive effects on behavior subsequent to RET or other cognitive therapy, with time there should be improvement in BPD symptoms. 

From an information-processing perspective -- at least within the framework that I'm working with -- BPD symptoms appear to result from early self-other relational "neural representational networks" that give rise to predications that others cannot be counted on to provide for you or protect you (although the person might desperately wish someone would). In this light, one might say BPD is "biological problem", in the most pragmatic sense of the term, but it's hardly a disease state. The human behavioral intelligence system and the mind to which it gives rise are designed to estimate the outcome of behavior on the basis of past experience in the environment. Indeed, if your parent isn't trustworthy, why would you predict that strangers would be? 

My degrees are in biopsychology, and my training was in behavioral neuropsychopharmacology, with an emphasis on dopamine systems. While I can understand how anti-depressant therapy would ameliorate the problems associated with BPD, it seems to me that the primary therapeutic effect results from the anti-depressant alleviating depressive symptoms that are secondary to the effects of living with BPD; this would in turn, produce a direct effect by improving behavior and therefore improving the behavioral database. But, based on my understanding of monoaminergic control of the behavioral intelligence system, and rudimentary understanding of the behavioral symptomatology of BPD, I don't see any reason why one would think that increasing activity in dopaminergic, serotonergic or noradrenergic pathways would change the neural foundation of BPD symptoms.

***So here are my questions to you: 
1) Do you know of any research based on a neuropharmacological model of the normal/functional organization of the brain/mind that provides an explanation for BPD, and, consequently, the therapeutic mechanism of antidepressants?
2) What is your best guess as to the mechanism of BPD and the therapeutic effect of antidepressants?

I'm in the process of writing a book based on the model of the human neurocognitive architecture described in brief in the article I site above. At present, I've planned to discussed depression, mania, bipolar disorder, and MPD in light of the model, and would like to touch on BPD. Any insight you can provide would be appreciated. 

A. This is a very interesting question.  The truth is, no one knows what causes BPD. First, there is not one kind of BPD. There are parents who are salt of the earth, that adopt babies at the time of birth, raise them perfectly, and the babies become borderlines. There are many individuals--siblings of BPD patients-- that do not develop BPD. Your supposition that BPD is a learned phenomena may or may not be valid. I do not believe it is. It is also possible, that BPD is genetically preordained. A "hardwiring" with which one is born. It makes little sense to me that 
cognitively borderlines learn all kinds of other things logically--to wear cooler clothes in summer, warmer in winter, to toilet train, live in a nice home if possible, etc., yet do other things that are painful again and again. That is chemical. Seeing BPD behavior in these learning models in humans may be an epi-phenomena. The parents have the same disease which involves violence, sexually impulsive behavior, etc., and it is just passed on like eye color. You assume it is learned, when it is in fact already wired in as part of the genes.

Antidepressants do not change the hardwiring. They simply damp down the circuits to a point where many individuals can control their lives. Mood swings, somatic complaints, rage, irritability, binge eating, anxiety, and even black-white thinking are reduced significantly. The treatment now is crude compared to what we will do 10 to 15 years from now, but it works. I have seen virtually no data that therapy reverses the illness. While CBT helps a bit, it impacts on life is limited. I have seen no data that it reduces any of the things medications reduce. I think therapy is a good thing, but in all fields of medicine we use it after we fix what is broken, e.g., rehab (therapy) following heart surgery and weight training after ligaments in a knee have been repaired. Current forms of therapy need to be continually upgraded and reevaluated, just like I do with medications.

I am always galled by the concept of therapy prior to medications. It supposes if an individual really tried, they could be better. BPD is a debilitating biological illness. Talking to it is like talking to diabetes. First insulin, then therapy.