5 chapter 5 Attachment Mother
ONCE A CHILD, ALWAYS A CHILD
ATTACHMENT AND MY MAD MEAN MOTHER
Gunderson & Lyons-Ruth 2008
Abstract & article called in – McLean Hospital, Harvard Medical School, Belmont, MA 02478, USA.
BPD’s interpersonal hypersensitivity phenotype: a gene-environment-developmental model.
Abstract: This paper explores the development of BPD as it might emerge in the child’s early interpersonal reactions and how such reactions might evolve into the interpersonal pattern that typifies BPD.
t begins to bridge the relevant bodies of clinical literature on the borderline’s prototypic interpersonal problems with the concurrently expanding relevant literature on early child development.
We will start by considering how a psychobiological disposition to BPD is likely to include a constitutional diathesis for relational reactivity, that is, for hypersensitivity to interpersonal stressors.
Data relevant to this disposition’s manifestations in adult clinical samples and to its heritability and neurobiology will be reviewed. We then consider how such a psychobiological disposition for interpersonal reactivity might contribute to the development of a disorganized-ambivalent form of attachment, noting especially the likely contributions of both the predisposed child and of parents who are themselves predisposed to maladaptive responses, leading to an escalation of problematic transactions.
Evidence concerning both the genetics and the developmental pathways associated with disorganized attachments will be considered. Emerging links between such developmental pathways and adult BPD will be described, in particular the potential appearance by early- to middle-childhood of controlling-caregiving or controlling-punitive interpersonal strategies. Some implications from this gene-environment interactional theory for a better developmental understanding of BPD’s etiology are discussed.
I want to start this chapter on attachment by looking at my mother’s attachment to her mother, and my attachment “breakdowns” in relation to my mother. Studying this information, however, leaves me feeling contaminated and damaged – tapping into some level of perversion as if I am responsible, somehow! It leaves me feeling damaged, as if the trajectory established at my birth, or before, leaves me today so far off course from “good and normal” as to make my being almost desolate and hopeless, damaged, broken. Especially when considering genetics – if our very DNA is WRONG, how can we be right?
I know throughout the whole process of researching for this book I have tried to go against the mainstream and find the positive in what is labeled “dysfunctional” and “mentally ill.” I have tried to find the adaptational advantages and tie them into the bigger picture of what our species needs to retain within its widest format in order to ensure longevity and continuance of the species against all odds.
When I leave that bigger picture and take my observations down to home, within my own life, my own body – and into what happened in my childhood and in my mother’s, it is hard to maintain that positive and hopeful perspective – and it seems easy to slip into the ooze of what went wrong, what is wrong.
A “morphology of damage” just doesn’t seem remotely helpful! I want to celebrate my mother’s survival and endurance, somehow because by doing that I can allow myself to celebrate my own. Condemn her, I condemn myself? I want no part of either.
I cannot write this book from any point of view other than my own. I can describe where many, many branches on the topic take off in their own direction. Yet in the end I can only follow the one that seems to closest to best describing my own experience growing up with my mad mean mother.
This is not unlike following the road back to our homestead in the early days. We passed everybody else’s home on our way until we passed the last one and there were no more driveways until we reached our own. Well, actually there was an unused road that continued up the mountain after our own turn, but nobody actually ever lived there, so we were the last homesteaders on the road.
As attachment experts describe all the variations of both infant and resulting attachment patterns, the do so looking objectively at what they can see from the outside. I am writing of what I know about attachment from the inside of me and with what personal information I know and strongly suspect about my mother. Experts write about generalities. I am writing about my own specifics. It does me no good to dilute my story or to take a turn off before I get to the end of the road where the description of the particulars about our family deviate from any generalization the experts might try to apply to our story.
If I am good enough at writing this, I can take you down the road with me, stop the jeep and let you off at your own driveway so that you will at least know where to start looking for the information that best applies to you. But I know in the end that my story takes place in a place so private and distinct that there’s nobody else in that story but myself and my mother. My own story is that different even from the one my siblings would be able to tell you, though we grew up under the same roof. My mother had, as it were, a very special room in her life reserved just for me.
This will be equally true for any of you readers who happened to be the Chosen One in your family, the child singled out for the most horrendous abuse. Ours is a particular story, and so far through all my research it is not a story that anyone talks about. That’s why we need to do it ourselves. Ours are the most terrible and terrifying stories. The only ones worse are the ones that cannot possibly be told because the teller is either dead, or so far gone from the basics of being human that they have no words left to match up with the details of their tale.
Our stories are so awful that most people will have a hard time even believing that they are real. Ours are beyond reasoning, reason or reasonableness. But I am driven to find the reason, the sense of the madness because I believe it is there. It’s just that the others are so far removed from the reality of our childhoods that they can’t see the proverbial forest for the trees. They lose their footing and their bearings when they try to peer into that inky blackness. They are met with their own disbelief, their own denial, their own magical thinking that tells them nothing could ever possibly be that bad, certainly not for a newborn infant, not for a tiny young child.
We need to find our voice and speak clearly back to them with a loud steady voice, “Yes, it can be that bad. We are the living survivors, and this is what we have to say.” And with our words comes a terrible sadness, nearly more than a human being is meant to bear. It fills the air that carries the sound of our voices envelopes our words, weighs them down so they are threatened with sinking into the dark moistness of the forest floor before they can escape into the clearing where most other people stand, the ones we need to hear us.
And what of the words themselves? What vocabulary exists that can allow us to speak the unspeakable? Words are merely invisible containers with meaning inside them. Our species evolved for millions of years before we even had them. We take them so fore granted now, but they really are new to us, at most 140,000 years old. There was much we had to learn and do before we became ready in our brains and in our bodies to let them be born.
We then spent 70,000 years in Africa learning to use them, and another 70,000 years once our species left Africa making them our allies. Yet for some of us where things matter the most, we have no words to speak our own reality. Until now as the words and the vocabulary that we can use to talk about the truth of our own early lives can finally be found as they are being used in science.
For a word to have meaning it has to make sense to both our most ancient right limbic emotional brain and our later developing sequential left brain. Our species did not invent a new brain for language. We first developed all the infrastructure through millions of years of evolution, doing things in the world as it did things to us. Once all the necessary structures were built and as the operated language could use those structures and brain systems to include language with all the abilities we already had.
Far under and far older than what we like to call our left brain logical abilities and our left brain language abilities lies an entire structure of mirror neurons. Within the mirror neuron system we first began to read motion and gesture, built entire systems of understanding movement by watching that led to the beginning understandings about tools and their uses. As we watch another performing an action with an object the same mirror neurons are firing in our brain that are firing in theirs though we are not performing any physical action that we can see. Useful actions are not random. They follow sequence and pattern.
It was our ability to use the special form of empathy our mirror neuron system allows that built our brain’s underlying abilities to eventually make use of the FOXP2 gene mutation that gave us the ability to form and use words. While we very early evolved the ability to read one another’s facial expressions and to use emotional information to better our chances of survival, as we began to use worlds not only our brains but also our throat structure had to change in the process.
Our social interactions also began to change. Experts know that our species used gesture, music and dance, all deeply tied to our mirror neuron systems, to communicate with one another long before we had the ability to speak words. There are language experts who believe that language evolved directly from our mutual grooming behaviors so that more people in larger groups could be included in these meaningful social interactions. That means even our human “chit chat” has meaning as a way to involve ourselves in larger group cohesiveness.
Two crucial neuropeptides, oxytocin and vasopressin, are involved in human bonding on all levels, including bonding between mothers and infants. I therefore suspect that researchers will find that these two neuropeptides must have been involved in human language abilities from the beginning. I also believe that it was the safety and security that our species must have experienced that allowed mothers to have time with their infants safe and secure enough to have allowed them to foster language related development in their infants. We know that women have evolved a specific “baby talk” voice, unique in pitch, which attracts the attention and engages infants in language learning processes far more than does a man’s deeper voice and pattern of speech interaction with infants. Language, then, evolved and is fostered in a safe and secure world of mother infant interactions that has at its bedrock hormonal and neuropeptide underpinnings of social bonding.
Once our species had the ability to use words our brain and our species moved to a whole new level. It didn’t happen over night. Even in that 70,000 years we developed and used language before we migrated out of Africa, we only gradually moved from “show me” interactions that required involvement of the mirror neuron system to “tell me” so that our hands were free and our minds were freer to move, hunt, gather, protect ourselves, and raise our offspring in ever more adaptive, creative, inventive and expanding ways.
Yet we never lost the abilities we had to communicate long before we had spoken word “vessels” to convey meaning. Emotional expression, gesture, dance, music – which carried over to the pitch, rhythm, prosody of speech — are also tied into our human intelligence system and together reflect what I will describe to you later as reproductive fitness indicators. We have always been able to read the whole and bigger picture about one another. Fitness indicators tell us not ONLY about a single person, but tell us about the condition of the world that person developed in from before conception. As a species we have always been able to read the bigger picture and to understand what it meant. We understood about the condition of the world by being able to read the condition of one another. Words came to us so much later as to become simply the icing on the cake.
There have always been times and conditions where words were inadequate to convey the full extent of what an individual might need to or want to communicate. I have a hard time imagining a group of twenty hunters succeeding at a mammoth kill while losing half their numbers trying to calmly express the fullness of that entire experience calmly within the limitations of spoken words. There are times when communication requires expression that cannot be confined to an invisible vessel full of words.
The capacity of the human brain to feel, imagine and convey information is far, far more ancient than words, and they will always fail us on occasion. We are capable of experiencing and understanding, even within our imaginations, far more than what the limitation of words will allow us to express. So I imagine a word threshold, a point where experience crosses over into a place that words cannot follow. The realities of severe infant and child abuse exist in that place, the place without words. Yet we continue to grow and evolve as a species and our vocabulary and understanding is growing along with us. One of the most important cutting-edge places where our vocabulary is expanding along with our knowledge and understanding is in the area of science.
I see the evolution of language in the field as science as being no different than any other invention. The invention of the wheel, of the plow, of the printing press, of the cotton gin, changed the face of civilization. But always there are the gray shades as the inventions are gradually moved into greater and greater areas of human experience, with wider and wider effects not unlike ripples from a stone thrown into a pond full of water.
The discoverers, inventors and scientists always know first not only about the new “tools” but also are the first to know the language that goes along with them. One of the current new “tools” that will change the way humans live on this planet lies within the field of genetics, which of course was dependent upon the technology of computers before we could access this hidden information.
Paralleling the molecular discoveries on the level of our genetics are the advancements being made in imaging technologies that allow us ever more detailed visual scans of the world inside our bodies including our brains.
It is because of these new advances, along with the new facts and the new vocabulary that they bring to us, that we can begin to finally actually think about and talk about the realities of how harmful experiences during crucial developmental stages affects us as people.
I could describe to you in detail the actual specific events that I remember from my childhood. I could follow along in the footsteps of all the people before me and around me now in the world that might want to talk about what kind of “mental illness” my mother had, or what was wrong with her “psychologically” that meant she could do to me the things that she did. I could talk until I ran out of words about my “inner child,” my “adult child,” about being a victim or a survivor. I could talk in terms of “dysfunctional” and “recovery,” about addictions, about defense mechanisms like projection and splitting. I could talk about inheritance and “bad genes” and bad luck and “getting better.” I could use the words of guilt and shame and blame and forgiveness.
But I won’t. These are all self help words based on psychological concepts that come up only to the threshold of what I need to tell you and you need to know. They do not cross over. Given the reality of the 18 years I spent growing up under my mother’s constant violence and abuse of me from birth, these words don’t even begin to come close to telling you what happened to me. They don’t scratch the surface. And they sure don’t come close to telling you about what happened to my mother to make her that way. We would be better off relying solely on my mother’s own ten year old words she wrote in her stories as she tried to make sense of her world.
What we need to know is very real, and it happens in the body. What happened to me happened to my body, within my body, and in the 57 years of my life the experiences of my childhood have never left me. Nor will they as long as I am alive in this body. The same is true for you. All of the experiences of our lifetime are recorded in our bodies, in interaction with the genetic material given to us at our conception that contains our portion of the memories of our species, which is itself being continually told how to manifest within our bodies. And this means NOW.
It is with this information and understanding that we are now ready to cross over that threshold where words from the past have limited our abilities to talk about the traumas of infant and child abuse. If we hold only to the old words, the old vocabulary, we will make no progress. If you are anything like me, you have waited your whole life up until this moment to understand what really happened to you if you were traumatized from birth (or before) and in childhood.
We have not stood idly at the gate with patience. We have done our best to come to terms with the horror of our experiences and what those have done to us. But for all of the words, the advice, the theories, we have remained confused and empty knowing there is more that we haven’t been told, no matter how hard we have “worked” to get “better,” to “be better.” Many of us have thought that gate had opened as we followed the shining star above the horizon that gave us hope and help in the form of pharmaceuticals. We rely on them, but the unanswered questions still hound us at our heels. “Who am I and what went so terribly wrong?”
Using the new vocabulary we can begin to understand that absolutely nothing “went wrong.” Everything that we are is biological — with the exception of our soul if you believe in one – and even that is dependent on the body in this physical world of the here and now — and biology always makes perfect sense. The world of nature operates according to – Surprise! Surprise! – natural laws, and nothing about us as a species is an exception. We are confined in our lifetime to all the laws that operate in governing our bodies as part of the biological world. Our freedom comes from learning as much as possible about these laws and how they operate, so that we can consciously use our minds, working within the parameters, limitations and potentials of these laws, to affect positive changes for ourselves.
How is this new thinking different from the old thinking? First of all, let me say that we have to understand that we can never return to a state or recover something we never had in the first place. This is where we must draw the line between the “haves” and the “have nots,” or more accurately between the “hads” and the “had nots” while at the same time realizing that we can be both at the same time.
If you were fortunate enough to receive the most wonderful combination of genetic factors that were able to manifest themselves in a safe, secure and benevolent world, then you are a “have.” But in the new vocabulary we also now know that if you are conceived with those exact same genes but they have to manifest themselves in a far less safe, in fact toxic and dangerous malevolent world, you will end up being a different person from the basement on up.
Take this same parallel for those born with some risky genes that get to manifest in a benevolent world versus that same genetic combination manifesting in a malevolent world. Some Oops! Is bound to happen with the latter.
Now take someone conceived with a down right hazardous genetic combination. The environmental interactions those genes are required to manifest within are still going to alter how those genes manifest.
The fact also is that gene combinations that have some incredibly marvelous goodness potential in a benevolent world can be risk factors themselves in toxic conditions. Genes that might be less advantageous in a benevolent world, can in fact allow survival to occur in terrible circumstances when other supposed good genes would have been of no assistance whatsoever.
So the new thinking is that nothing is as simple, clear cut or straight forward as we might be used to thinking they are. The wizardry of genetics is that the potential for adaptation in an ever changing environment is extremely complex. Very few genes act in isolation but are, so to speak, members of teams. Which genes are part of which team can change according to circumstances. What they do and how they operate also changes according to conditions. We are not simply handed a package of chromosomes from our father and one from our mother at conception and then carry them with us to the grave.
Mechanisms tell our genes what to do according to signals from the environment in a continual ongoing process of interactive communication every nanosecond we are alive. In fact chemical signals within the mother are already giving the egg and the sperm information and directions even before we are formally conceived. Interactive signals between the environment both within and without our bodies tell every cell what to do from conception onward, and this process is still in high gear when we are born. It remains in high gear during the crucial developmental stages of our early infancy and early childhood.
If things go well from the beginning, then around age one we have all that we need to move our physical body out into the world away from our early primary caregivers. By age two our body is ready for the operation of a young but fundamentally intact individual self to take effect. Our ongoing development continues through a series of critical stages on through adolescence and into early adulthood where by around age 25-30 our highest functioning cortical brain regions finally complete their growth cycle. From then on out the only new brain cells we will get are in the hippocampus related to forming new memories, and in the neurons responsible for our sense of smell.
What we have to understand is that not only do all the regions of our brain grow in interaction with signals from the environment from birth, but how the brain regions communicate with one another is also established during the time frames that critical growth windows are open. During these early months and years we grow the brain regions and establish the networks, pathways and circuits that we will use to think with for the rest of our lives.
During this time our bodies are also growing the rest of the nervous system that the brain is a part of, the stress response systems, the hormonal systems, and the immune system at the same time. All these interactive systems, while receiving constant information from the environment, are in constant communication with each other and are in the continual process of making the best adaptations to the environment possible. Because of this, given the exact same genetic material in the beginning, a body that is evolving, growing and developing in a safe, secure and benevolent world will NOT be the same as it would if it went through those processes in a toxic, traumatic, threatening malevolent world. That is the law of nature.
Even the simplest single cell organism has a way to protect itself, its boundaries, from attack. No organism could survive without an ability to protect itself from threats in its environment. I believe that it is fundamentally our immune system response that allows our bodies to grow and develop in relationship to its environment, especially making changes that allow us to survive in the harshest circumstances. For this reason I believe that toxic environments, with corresponding requirements of our bodies to adapt within that environment, result in changes to what is called our phenotype. A phenotype is the visible (even if only on a molecular level) manifestation of what the genetic code allows.
Many genotypes appear in straightforward fashion. I have genes for blue eyes so I my genotype directly manifested as a blue eyed phenotype (remember genotype as genes, and phenotype as “finished” or the final form that shows). Many important phenotypes, however, are anything but cut and dried. They are outward manifestations rooted in complicated genetic complexes that are themselves told what to do and how to appear based on information that the environmentally interactive instruction mechanisms tells them. Did you get that? Reread that last sentence, it’s important. These interactive, informational, signaling communication processes and the mechanisms that then tell the genes what to do, make us far more specifically suited for our environments than our “simple” inherited genetic code could ever provide for us.
Think of it this way. You walk into a kitchen #1 hungry and there’s three food items there (the genotype): milk, eggs and bread. The resulting phenotype you could come up with would resemble some version of an American breakfast. Any other person in the same situation (with those genes to work with) would come up with pretty much the same thing. In fact, we could predict the outcome with good accuracy.
Now imagine you walked into kitchen #2 and there are forty different types of food items to work with. You could come up with a creative phenotype of any number of different meals. Any other person could work with those food items and come up with an entirely combination resulting in a different phenotype. Given the increased complexity of the situation, we would have a hard time predicting what meal would come out of kitchen #2.
Now imagine that each different person going into kitchen #2 was given a specific set of cooking instructions to use and with equal skill everyone followed them. We could again predict the phenotype to come out of kitchen #2 fairly accurately. But here’s where things get even more complicated and interesting. Same food items in the kitchen (same genes) but different instructions tailored for every single person. OK, so if they all followed their instructions and we knew what those instructions were we could again predict the outcome.
Enter into our thinking the idea of the process of epigenetics. We could stock the kitchen the same, send different people in there with the same or different instructions – but wait! What if the kitchen’s on fire? What if there’s no electricity or no appliances or the kitchen is flooded? What if the food is all spoiled? What if the kitchen is filled with poisonous gases? How do we include and account for the possible range of environmental factors that can and will influence the cooking process in that kitchen, and therefore the outcome, or phenotype? Where now are our powers of prediction? This is my point exactly.
The instructional mechanisms that tell our genes what to do as they determine the phenotype, are themselves able to adapt and adjust themselves so what they tell the genes to do varies in accordance with environmental factors. If everything is just fine in an optimal benevolent world, the best case conditions will allow for the best case outcome. But if the environment is just plain nasty, something less than best will come out of the kitchen. Unless…….
OK, now let’s think about how we appear to one another in the world, not knowing what went on behind the scenes. Let’s pretend the test is about life or death and not about how good things might look from the outside to somebody else. Let’s imagine we never know before hand the condition of the kitchen but you better come out with something good to eat or you are going to die. One person might rush into that kitchen and come stumbling out empty handed, starving to death but nearly overcome by noxious fumes.
Another person might rush into that same condition kitchen and walk calmly out again with a bag of fresh carrots from the refridgerator, first having to stop and take off their gas mask before they can eat them. Who could have told beforehand that they had a gene in the mix for a gas mask? If they’d never walked into that kitchen in the first place maybe they never would have known they had it.
And then there are all the “ignorant” people outside the scenario. They could say, “Well, how stupid! Why is that person wearing a gas mask? There’s no gas out here and absolutely no need for them to be so prepared for a threat that doesn’t exist.” But what if that person can never remove the gas mask once faced with the threat that required them to use it in the first place? Are they going to die of starvation anyway? How fair is that?
That’s the problem with epigenetics. The flexible possibilities of adaptation only go so far. Maybe it wasn’t just a single gas mask gene that was triggered by the environmental threat. Maybe it was some combination of a number of unrelated genes that, once combined in a certain adaptive way based on adaptive demand from the environment told that group of genes to produce a gas mask. The awesome fact about epigenetics is that memory of the situation that required a gas mask phenotype to be created can itself be remembered so that the pattern can be passed down the generations not as an actual change in DNA code, but as a change in the instructional mechanisms that tell the DNA what to do.
I don’t think scientists have much of a clue yet about exactly how these adaptive changes happen in the first place, and less information about how they are passed down through the offspring. They just know that it happens. Researchers have found that rats exposed to certain fungicides used in vineyards pass on adaptive changes through epigenetics over 4 or 5 generations through the males, resulting in serious adult onset diseases. Many adaptations to toxic environments have a cost attached and a price to be paid, sometimes for generations into the future. That, my friends, takes genetic memory to a whole new level. Considering the recent massive changes we have made in our environment on every level, we had better figure all of this out and quickly. The lives of our children and their children may depend on it.
But let’s get back to our kitchen for a moment. Let’s say once someone walked in there they were faced not only with poisonous gases but also with a floor covered with water and charged with hot electrical current. Their genes might provide them not only with a gas mask but also with an insulated rubber body suit. Out they come safely with their bad of carrots, exposed to an unknowing crowd of fellow humans this time absolutely dumb founded at the sight of them. What a phenotype would that make?
And on and on we could go, limited only by the possibilities of environmental conditions of threat and human genetic potential to adapt and survive in these contexts. If genes that get triggered in the hostile childhood conditions of growing up in a toxic kitchen do not match the benevolent conditions everyone else lives when we escape outside, we are going to have big troubles fitting in to their world. Sure, the genes allowed us to survive, but to what end? Once we grow up and those changes become a part of who be became, the process does not go backwards. Nature has its limits. In a way, we get what we wish for assuming that our goal was to survive through those horrible times.
This is a most important point. Our bodies adjust as they grow and develop from conception, through signals received from the environment — which include the condition our mother’s body is in based on her interactions with the world, signaled to us through her hormones and nutrients (and possible toxins) she passes to us. Our body prepares itself for the conditions of the future world based on information it receives from the present world as it is developing. It cannot operate any other way. If the world is bad enough as you develop, you are enabled to prepare for a bad world in the future to that you can survive it. If the world is good enough as you develop, you are allowed to prepare for a good world in the future so that you can thrive in it.
Humans are born well before they have reached maturity. Their early infant and childhood developmental experiences are merely a continuation of the same environmental interactive preparation processes they have been experiencing since conception. If an infant is born into a hostile world full of terrible interactions with caregivers, their developing body will on all levels continue to make whatever adjustments possible and necessary in order to continue to endure.
We can think about all the environmental impacts on an infant’s and child’s development in terms of the good, the bad and the ugly. There has to be a whole lot of good resources available to an infant to outweigh the bad, and a whole lot more resources for the good to balance against the ugly. We all know and can imagine what the needs of a tiny infant are. They have to come from somewhere and that means to an infant, from someone. We are born with an innate attachment system that operates through our opioid receptors. A safe and secure needs-being-met infant will have its opioid receptors full and it will feel good. When it needs something its opioid receptors are empty. Proper and adequate caregiver responds, opioid receptors fill up again. That’s the root level, the bedrock of where being a human member of a social species starts. It’s that simple, unless….
We can all imagine what the “unless” means. We no longer live in a naïve world; we know the worst that can happen to the helpless and the innocent and taboos against thinking and talking about it have to dissolve. We know the worst continues to happen. Not only does it happen to infants, it happens to very young toddlers, to children, to preteens on up.
In 2003 there were over a million confirmed cases of child maltreatment in the United States. It’s not going to get better until we make it, and that won’t happen until we understand the roots of what is going on. I believe that the more we legislate against physical abuse of children, the more we are pushing the problem under ground. Researchers are finding that verbal and emotional abuse of children is more harmful in its longterm consequences than is any other single form of abuse. We need the new vocabulary that science is giving us so that we can talk about the devastation of lives that is happening from infant and child abuse and neglect on the level that matters most — firstly and most fundamentally on the level of molecules and genes. I kid you not.
On the level of molecules and genes we must understand that harm against offspring was never normal except under the most severe environmental conditions. We have to stretch our thinking so that we can obtain the same kind of past-present-future thinking that our genes know all about if we are going to understand what the roots of severe child abuse are about. Information from the past, contained in our genetic memory codes, is always being transformed in the present in preparation for the future.
We never passed some magical line in the timeline of development (evolution) of our species where we decided as a group to leave behind some collection of archaic genetic material that we now no longer needed. We didn’t clean house one day, clean our genetic garage and decide to throw away what was useful then and stupid now. I think we remember almost all of it going back millennium upon millennium. Our computer chip technology cannot begin to equal the capacity that exists within our species to remember information that we knew in the past and might need again in the future.
I also believe that access to this information is on a need to know basis. If you are not going to get electrocuted in your kitchen without an insulated rubber suit, then you won’t need to remember that you have one. If there are no noxious fumes, forget you have access to a gas mask. But if your experiences in the world during your early developmental stages both required of you to make drastic adjustments for immediate survival and told you that the world to come was not going to get any better, then I suspect that you have access to a wealth of primitive and very ancient survival information that few of your neighbors can even imagine. You survived because you remembered how to. In the process your body prepared you for more of the same.
Maybe what makes developmental trauma the hardest is that we don’t stay in that kind of a world that developed us in the first place. The biggest problems arise when the world that we developed to live in doesn’t match the one we find ourselves living in once the future actually arrives. Now that we are still alive because of what we remembered and the adaptations our bodies made, we cannot forget. We can never return to who we would have become if we had been able to develop in a much nicer wholesome world. It’s not that we developed to know the battle plan. We developed to BE the battle plan.
Bodies talk back to infants and young children as they develop through deprivation, trauma and abuse, saying, “If it’s survival in the toughest world you want, then it’s survival you will get.” That’s how our species took over the planet in the first place. It didn’t happen because we were soft, cushy and nice. It happened because we are a species of fierce predatory warriors determined to stay alive no matter what. Eventually when we encountered soft, cushy and nice along our evolutionary pathway, we were flexible enough to adapt to those conditions as well, and we expanded our genetic horizons to include those potentials. But those times did not happen first and we never forgot the hard times. Never.
In our modern world we might want to believe that we can consciously select those aspects of being human that we want to live with and show to the world as if we are at some grand buffet of pickiness. We would probably like to be able to do the picking and choosing for our loved ones and neighbors as well. But when dealing with the longterm adaptive changes that early and chronic severe infant and child abuse create, we have to be more practical and realistic.
Everyone’s phenotype is established through forces beyond our control. What we can eventually choose to do within the parameters of our phenotype is a challenge all of us share in common, abused or not. What we need to understand, however, is that early abuse and neglect can create a different phenotype, a trauma survivor phenotype, which in its adjustment for endurance in a malevolent world has corresponding alterations regarding abilities to access conscious awareness, self reflection, “free will” and choice. Scientific advances in brain imaging now allow us to see how these changes physiologically operate.
There isn’t a single level of being a self in a body that wasn’t impacted by our abusive experiences during our early developmental stages, especially those that happened to us before the age of seven. We paid a price for our survival equal to the extent that the body we developed in adaptation to our traumas deviates from the more ideal blue print body we would have developed in a more ideal world. Developing a different kind of body, both in its design to deal with the immediate trauma of our childhood and in its preparation for a hostile world in the future, means that we ended up with a different kind of nervous system including our brains, different stress response systems and a different immune system.
On the extreme end of the trauma adaptation phenotype spectrum, we end up with people like my mother. Given the combination of her particular genetic makeup and the adaptations her body had to make to allow her to endure, her altered trauma adaptation phenotype ate up and swallowed whole who she would have become had she been raised in a benevolent environment that would have been able to meet her needs. It did so as effectively as you or I could swallow a small paper spit ball. I know this as surely as I know my own name.
My whole, healthy, potentially resplendent mother died nearly as soon as she was born, as I did. The environments we were both born into had no tolerance for who we could have become. Instead our environments were toxic to us, nourishing only enough and in ways that allowed our bodies to survive, but not without us having to pay a heavy price for that right. We did not have early caregivers who cared about who we were or who we could become as our own unique and beautiful selves.
I know I survived with more of my own potential intact than she did, though I also know the conditions she created for me were to outward appearances far harsher than the ones she endured in her own childhood. Our traumas and their contexts were very different. Somehow I was able to access more good resources, both internally and externally, to balance out the ugliness during my childhood than she could. As a result, her survivor phenotype became much more dangerous, destructive and toxic than mine did.
My mother’s survivor phenotype lacked the ability to empathize or to self reflect and therefore lacked the ability to learn, grow, and change or to celebrate herself as a person. There was not enough goodness in her childhood to balance out the bad and the ugly. Once I was born and her psychosis took to full bloom, she could no longer feed herself enough on goodness to keep any inner balance. Her alternative was to try to lighten things up on the side of badness, so she took it out of herself and dumped it on me instead. Well, hey! How well did that plan work out? Not good for me, I’ll tell you. Not good at all.
From a psychological point of view I could say that she projected onto me her own unacceptable and intolerable pain of badness within her psyche that told her she was unlovable and unacceptable. It was a doomed and never ending procedure that meant I was absolutely invisible to her as a person. I could not become a separate individual, unique self. That would have destroyed her chances of redemption and salvation.
For some reason her cross was not too much for me to bear, but the adjustments my developing brain and body had to make in order to survive the ordeal of being her child changed me permanently and created for me my own survivor phenotype that is quite different from hers. For all the walking I was made to do in her footsteps of badness, she never could never actually swallow me whole. But neither did I come out of that horrible childhood being whole myself. It was not humanly possible. I ended up with a changed brain just as she had, but mine changed differently.
I know that if my mother was alive today, and researchers scanned her brain and mine as they operated on different tasks, they would be able to see how differently our actual brains operate. The other part of this is that if they compared either her brain or mine to a brain that developed in an optimal benevolent environment my brain would be far less normal than normal. Believe me, that’s a sobering realization.
So in talking about our species’ abilities to adapt to horrifyingly difficult situations from birth (or before), I want to share with you the bigger picture of what I suspect is truly happening on the extreme ends of the human potential continuum. Remember I talked about how our species still carries our ancient evolutionary adaptive information in our genes along with their instructional mechanisms? The information in these genetic memories is not something that we will necessarily consciously know that we have remembered.
The information is contained in our bodies and can operate on the behavioral level without us having either any direct clue about or control over what either we or our bodies do with it. It would be like the reverse of mind control – call it body control directives. The body has the memories and acts them out. In the “olden times” when conditions in the environment were at their harshest, it was not a good time to give birth to offspring, no matter how much our species needed them. The genetic memory actions given to men and women during such times would be different based on the differences in our physiological makeup.
These ancient memories can be so alive in a survivor phenotype that very little of a conscious free will self is left to change how the memories operate in the body. In extremely harsh times when survival was threatened and death was closer than tomorrow, a female would not breed. If she accidentally bore young during a time when the environment was inadequate to support both her and her young, she would either kill or abandon all her offspring or all but the strongest and most fit to survive. Women’s major sphere of influence evolved close to the hearth where the babies were and not so far a field where the men hunted and fought. A woman’s ancient survival memory is therefore most likely to manifest itself close to home in the domestic arena.
A male’s drastic ancient survival memory concerns actions taken further out into the environment. These memories, which can even now be activated through early experiences of deprivation and maltreatment during crucial developmental stages just as a woman’s can be, trigger entirely different hormonal and brain changes that gear him to take different severe threat to survival actions. In ancient times of severe environmental crisis, a male would find food, fight the enemy, gain more territory and impregnate as many females as possible. In today’s world if these actions occur outside the law we call them crimes.
The conditions of the environment are clearly reflected in the operation of a woman’s body and not as visibly in the body of a man. A woman’s hormones provide important reproductive communication signals about her condition in the environment which we ignore today. Yet I don’t believe that we could find an instance of a mother’s severe abuse of her offspring, even to the point of killing them, without also finding severe fetal and/or early child deprivation and maltreatment in that mother’s developmental history. Given severe enough trauma and deprivation during her early developmental years, that mother will have evolved into a survivor phenotype that can be far more rooted in close connections to our ancient ancestral survival information than it is to the more newly evolved mental abilities of conscience and reason.
In fact, in most survivor phenotypes the brain regions in control of our higher executive functions do not develop the same way as they do in benevolent phenotypes. Remember when I said we get a changed brain? I meant it. When a mother, even mine, severely harms her offspring isn’t it time we start asking the right questions about a mother’s past that really enlighten us about the facts of an action rather than waste our time blaming her, hating her, or wringing our hands? Whether we want to acknowledge the fact or not, higher (or would you call them lower?) laws are in action when severe threat to life has stolen the show and now directs the action. The scene is set for competition for resources needed for immediate survival and the mother’s survival becomes most important because she is ready to reproduce immediately as soon as environmental conditions improve.
We might not like it, but we are mammals and our genetic memory knows how to act on the facts. Passing time and changing circumstances may have distanced us from our ancient genetic past, but we have not forgotten how to survive. Those genes have not abandoned us nor have we abandoned them. That they, along with their corresponding actions should surface occasionally among members of our modern civilization should not surprise us. These actions are a form of extreme immune system defensive reactions hell bent on survival, designed for and developed in and by the worst case scenarios. We would know that if we opened our minds and took a good long cold look at the same facts our bodies already know and some remember.
If we want to erase the possibility that violent crimes are committed by people whose phenotypes have been altered through early developmental deprivations and trauma, so that we can then clearly blame the individual with absolute assurance that their crimes were committed only through conscious acts of free will and choice, then we better eliminate the toxic circumstances of fetal and infant maltreatment at least until age two that can lead to these altered developmental outcomes. I will go toe to toe, eye to eye, nose to nose with anyone about this.
Having been raised by a mother that hated me from birth and abused me in some way nearly every day for 18 years gives me all the credentials I need to stand up in my own abusive mother’s defense and say, “There but for the grace of God go I.” Every human being has a breaking point even if that point be death, especially if the goodness of one’s early life was not enough to balance out the bad and the ugly. The required goodness necessary to provide protection and build resiliency is becoming less of a mystery as researchers are identifying those crucial factors. If they don’t have them the wounded become broken. If they do have them the wounded become damaged but they do not break. I am damaged but I am not broken. My mother was broken. God bless her soul.
In my mother’s case, when I say “Once a child, always a child” I am speaking a fact. I know now absolutely because I have the proof of her stories. This little yellowed fragile paper school composition book has traveled thousands of miles, through hundreds of moves over more than 70 years to end up in my hands intact except for its cover just as I was researching this book. The words are written in her child’s hand, sometimes pressed hard with dark lead lines across the pages, sometimes written with pencil lines so light and faint it takes effort to read them. But her words are here.
Her child’s voice, her child’s mind, her imagination and gift for writing lie intact in my hands after all of these years. I have to make the choice to either let the words come to you exactly the way she wrote them, most often without punctuation or capitalization, or to alter her stream of thought by adding these proper aspects myself. I choose to leave her writing alone if for no other reason than to honor the child she was.
I believe these stories are a gift to all of us by offering us the chance to glimpse the inner mind of a child who was to develop at best a severely violent borderline personality disorder. I know that I will have to give you some specific details about her life to provide context for her stories. But before I do that I want to tell you about the most freeing moment of my life.
It happened about six months ago as I was writing. Suddenly a thought came to me that felt like the light of a new dawn. I realized that at a minimum if I added up the number of severe beatings that I received by my mother’s hand, which would be considered assault should she step out the door of my house and into my neighborhood and raise such a hand to any single adult or child she might encounter there, the lightest combined sentence that a court of law would levy against her would be no less than 14,200 years.
At the moment of my realization I knew that this would not account for all of the beatings. It would not take into account the verbal or emotional abuse, would not include the thousands of face slappings, mouth washings, hair pullings, finger nails dug into my arms until they bled. It would not take into account the thousands of hours she stood me in corners or banished me to lie in bed like I was in a coffin for days on end, or the days she locked me in the shed or….. the list of her specific harms done to me would fill volumes. My point is that as soon as the 14,200 years made itself completely clear in my mind as a justified minimum sentence I was able to let go in a way I had never done before. I realized that there is no human way possible to hold parents who commit such crimes of abuse against their children accountable.
At that instant I was able to know fully and consciously in the bright light of day what I have always known in the hidden corners of my mind – that there was something so terribly wrong with my mother than it is humanly impossible to blame her for what she did to me. It is equally as impossible for me to describe or explain to you the reality of my childhood with her. It all happened to me in a different world, long ago and far away.
But the damage that she did to me lies in every cell of my body. It changed the development of my nervous system, my brain, what I perceive about the world and how. It changed how my senses operate in relation to my body and how I relate to other people. It changed the way my brain formed and how it operates. It changed my immune system. It changed the processes that lead to my feelings; it changed how I feel my feelings. Her abuse of me changed how I developed and it changed who I have become. Worst of all it changed how I remember myself in my own life and hence changed my relationship with my self.
But it did not break me. I have never crossed that line. If you pay attention you will see in my mother’s last story when it happened to her, when she crossed that line and became broken herself. It could have happened at any other moment of her life other than the one that found her with a pencil in her hand writing that story. Everything that had happened to her leading up to that moment prepared her for this break.
I see the image of a loved one crashing through the ice on a river and being swept away in the current, unreachable and unable to be saved. I see a flash of someone standing whole and in the next split second disappearing in an explosion or hit by a speeding car or falling to the ground with a parachute unwilling to open.
Yet the way her break happens in this story is as silent now as it was when it happened. Her body lived for another 65 years, but the person who could have lived in it vanished as the story’s words appeared across the lines of her paper. I am filled with sorrow for that little girl who lost what she had of herself that day. In reading her story we are witnesses to the moment her child’s mind broke. This is a moment as sacred as the moment of birth and the moment of death, this awesome moment that was paired with the dissolution of a human’s potential for growth and self realization.
My mother wrote all the first stories the fall before her 11th birthday and the last one just after. In the final story it’s as if she portrays the stopping of her personal clock. The hands of the clock remain frozen there in time, as if the child who picked up the pencil and began to write that day was not the same child who put the pencil down and went on with her life after the words were written. But nobody noticed. Nobody paid any attention. I don’t think anyone else ever read that story until I did after my mother died 65 years later. As soon as I read her words I knew that I had found my real mother. I knew when and where I had lost her. I just didn’t know how or why. I have a pretty good idea now. Her life had become more than a conscious self could handle. Her self was overwhelmed and it gave up trying to find a place in her own life. Her body took over with its ancient genetic memory of how to survive what a self cannot endure.
I believe that day my mother fully became a survival phenotype, whatever we choose to call it. Her final story conveys to us that transformational process. It has no ending and leaves us without resolution. That child, always a child, was left wandering the labyrinth searching for her Minotaur while her body went right on living without her. There was no other option.
I would say of her parents the same thing I say of my own: “Forgive them, Father, for they know not what they do.” But we are running out of excuses. That’s why I wrote this book, and that’s why you are reading it. “Times, they are a’changin.” I know it and so do you.
I am describing three main divisions of phenotypes. The first division includes people who were able to develop without major interferences caused by having to adapt to toxic environments.
The second type, what I call endurance phenotypes had to make these adjustments, but the connection between the body and the self is still available.
The third type, what I call the survival phenotype, includes people whose adjustments to hostile environments created a fundamental breech or break between the body and an operational self.
Abstract – Department of Psychiatry, The University of British Columbia, Vancouver, Canada. firstname.lastname@example.org
Toward a genetically-informed model of borderline personality disorder.
This article describes a conceptual framework for describing borderline personality disorder (BPD) based on empirical studies of the phenotypic structure and genetic architecture of personality.
The proposed phenotype has 2 components:
(1) a description of core self and interpersonal pathology-the defining features of personality disorder-as these features are expressed in the disorder; and
(2) a set of traits based on the anxious-dependent or emotional dysregulation factor of the four-factor model of PD.
Four kinds of traits are described:
emotional (anxiousness, emotional reactivity, emotional intensity, and pessimistic-anhedonia),
interpersonal (submissiveness, insecure attachment, social apprehensiveness, and need for approval),
cognitive (cognitive dysregulation), and
self-harm (behaviors and ideas).
Formulation of the phenotype was guided by the conceptualization of personality as a system of interrelated sub-systems. The psychopathology associated with BPD involves most components of the system.
The trait structure of the disorder is assumed to reflect the genetic architecture of personality and individual traits are assumed to be based on adaptive mechanisms.
It is suggested that borderline traits
are organized around the trait of anxiousness and that an important feature of BPD is
dysregulation of the threat management system
leading to pervasive fearfulness and unstable emotions.
The interpersonal traits
are assumed to be heritable characteristics
that evolved to deal with interpersonal threats
that arose as a result of social living.
The potential for unstable and conflicted interpersonal relationships that is inherent to the disorder is assumed to result from the interplay between the adaptive structure of personality and psychosocial adversity.
The etiology of the disorder is discussed in terms of biological and environmental factors associated with each component of the phenotype.
Ni et al 2006
Abstract – Neurogenetics Section, Centre for Addiction and Mental Health, 250 College Street, Toronto, Ont., Canada M5T 1R8. email@example.com
Association between serotonin transporter gene and borderline personality disorder.
Borderline personality disorder (BPD)
is characterized by a pervasive pattern of instability in regulation of emotion, interpersonal relationships, self-image, and impulse control beginning in early adulthood.
BPD affects about 1-2% of the general population
and has a high mortality rate as a result of suicide and impulsive behavior. And avoidance of care for medical conditions.
And wow to be raised by a mother with such a rare condition?
The serotonin transporter gene (5-HTT)
is considered as a candidate gene for BPD as multiple lines of evidence have suggested that it plays an important role in suicide, impulsive behavior, and emotional liability.
To test for an association between 5-HTT and BPD, we genotyped three common polymorphisms: the serotonin transporter linked promoter region (5-HTTLPR); a variable number of tandem repeat (VNTR) in intron 2, and a single nucleotide variant (A/G) within the LPR region. Eighty-nine Caucasian patients with BPD and 269 Caucasian healthy controls were analyzed. The program UNPHASED was used to compare allele and haplotype frequencies between cases and controls.
Significant differences in allele frequencies of the VNTR marker (p=0.012) and haplotype frequencies (p=0.002)
between patients and controls were found.
Compared with healthy controls, patients with BPD showed higher frequencies of the 10 repeat of the VNTR marker and the S-10 haplotype, and lower 12 repeat and L(A)-12 haplotype.
Our results suggest that the serotonin transporter gene may play a role in the aetiology of borderline personality disorder.
New et al 2008
Abstract – The Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1217, New York, NY 10029, USA. firstname.lastname@example.org
Recent advances in the biological study of personality disorders.
While it is premature to provide a simple model for the vulnerability to the development of either borderline (BPD) or schizotypal (SPD) personality disorder, it is clear that these heritable disorders lend themselves to fruitful neurobiological exploration.
The most promising findings in BPD suggest that a diminished top-down control of affective responses, which is likely to relate to deceased responsiveness of specific midline regions of prefrontal cortex, may underlie the affective hyperresponsiveness in this disorder.
In addition, genetic and neuroendocrine and molecular neuroimaging findings point to a role for
in this affective disinhibition.
Pascual et al 2007
Abstract – Psychiatry Department, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona , Barcelona, Spain.
Association between the serotonin transporter gene and personality traits in borderline personality disorder patients evaluated with Zuckerman-Zuhlman Personality Questionnaire (ZKPQ).
The serotoninergic system seems to be implicated in characteristic symptoms of borderline personality disorder (BPD) such as affective instability, impulsivity or suicide. Some studies suggest an association between serotonin transporter gene (5-HTT) polymorphisms and some BPD symptoms. Short allele (S) of the 5-HTTLPR polymorphism in the promoter region has been shown to be associated with impulsivity, aggressive behavior, anxiety and neuroticism. Of the variable number of tandem repeat (VNTR) polymorphism in intron 2, BPD patients showed higher frequencies of the allele with the 10 repeats.
The aim of this study was to determine the association between 5- HTTLPR and VNTR polymorphism of 5-HTT and personality traits in borderline personality disorder. METHOD: A total of 65 BPD patients diagnosed by means of semi-structured interviews SCID-II and DIB-R were included. Two common polymorphisms of 5-HTT were genotyped: the 5-HTTLPR in the promoter region and VNTR in intron 2. Personality traits were assessed by the Zuckerman-Kuhlman Personality Questionnaire (ZKPQ).
RESULTS: Patients with L allele (L/S or L/L) in the 5-HTTLPR polymorphism showed lower scores on the subscale of liking parties and friends.
Patients with the allele with 10 repeat of the VNTR polymorphism,
showed lower scores in impulsivity, sensation seeking
and in the subscale liking of parties and friends.
CONCLUSIONS: The results suggest a significant association between the 5-HTT gene and some personality traits in BPD. This gene may play a role in the etiology of borderline personality disorder.
Kazantseva et al 2008
Abstract – Institute of Biochemistry and Genetics, Ufa Scientific Center, Russian Academy of Sciences, Prospekt Oktyabrya, Ufa, Russia. Kazantsa@mail.ru
Polymorphisms of the serotonin transporter gene (5-HTTLPR, A/G SNP in 5-HTTLPR, and STin2 VNTR) and their relation to personality traits in healthy individuals from Russia.
OBJECTIVE: Numerous studies have reported association of the serotonin transporter gene (5-HTT) polymorphisms
and traits characterizing sociability and activity.
This study aimed to define a single genotype effect of
three polymorphic markers in the 5-HTT gene
A/G SNP in 5-HTTLPR and
and to check possible association of the 5-HTT haplotypes and personality traits
[assessed with Eysenck Personality Inventory (EPI) and Temperament and Character Inventory (TCI) questionnaires] in 301 healthy young individuals. METHODS: To investigate single genotype and haplotype effects of all polymorphic markers, multivariate analysis of variance and haplotype trend regression analyses were conducted correspondingly.
RESULTS: Individuals with STin2.10 allele scored significantly lower on Neuroticism (EPI) (P=0.007) and Harm Avoidance (P=0.005) in the overall sample.
The same pattern of association was reported in women: carriers of STin2.10 allele scored lower on Harm Avoidance (TCI) (P=0.008).
Haplotype trend regression analyses revealed that carriers of S12 haplotype had lower sociability-related traits such as Extraversion (EPI) and Novelty Seeking (TCI), whereas Harm Avoidance (TCI) (anxiety-related trait) was higher.
Opposite association was observed for S10 haplotype: Extraversion (EPI) score was higher, whereas Harm Avoidance (TCI) score was lower in carriers of this haplotype.
CONCLUSION: As single polymorphism effect of STin2 was observed in relation to anxiety-related traits, opposite S10 and S12 haplotype effects on Neuroticism and Harm Avoidance could be explained by the larger impact of STin2 polymorphism. Controversially, we consider that the
variance in sociability-related traits is related to specific haplotypes of 5-HTT gene.
Hard to understand all of this!
Sen, Burmeister & Ghosh 2004
Abstract – Neuroscience Program, University of Michigan, Ann Arbor, Michigan 48109, USA. email@example.com
Meta-analysis of the association between a serotonin transporter promoter polymorphism (5-HTTLPR) and anxiety-related personality traits.
Anxiety-related personality traits,
such as NEO neuroticism and TCI/TPQ harm avoidance, have been shown to have significant genetic components.
To date, however, no specific genetic variants that contribute to these traits have been conclusively identified. At least 26 studies have investigated a putative association between a functional serotonin transporter promoter polymorphism (5-HTTLPR) and anxiety-related personality traits. The results of these studies have been inconsistent with some studies finding evidence for an association, and others not. We performed a meta-analysis of all applicable studies investigating this association. In the overall analysis (N = 5,629 subjects), we found suggestive evidence for an
association between the 5-HTTLPR short allele (s) and increased anxiety-related personality trait scores (P = 0.087). However, we also found strong evidence for heterogeneity. This heterogeneity is largely explained by substantial variation between the studies in the inventory used. When the analysis was stratified by inventory type, there was a
significant association between 5-HTTLPR and NEO neuroticism (P = 0.000016),
a non-significant association between 5-HTTLPR and TCI/TPQ harm avoidance (P = 0.166),
and no association between 5-HTTLPR and other anxiety-related personality traits (P = 0.944).
There was no evidence that these results were either due to publication bias or accounted for by any one single study. We conclude that there is a strong association between the serotonin transporter promoter variant and neuroticism as measured in the NEO personality inventory and that non-replications are largely due to small sample size and the use of different inventories.
Abstract – Department of Psychology and Scheinfeld Center for Genetic Studies in the Social Sciences, Mount Scopus, Hebrew University, Jerusalem, Israel. firstname.lastname@example.org
The molecular genetic architecture of human personality: beyond self-report questionnaires.
Molecular genetic studies of personality began with two high impact papers in 1996 that showed provisional associations between the dopamine DRD4 exon III repeat region and Novelty Seeking/Extraversion. These first two reports were shortly followed by an investigation linking Neuroticism/Harm Avoidance with the serotonin transporter (SLC6A4) promoter region polymorphism (5-HTTLPR).
In the ensuing decade, thousands of subjects have been studied for association between these genes and personality, assessed by using self-report questionnaires, with erratic success in replication of the first findings for Novelty Seeking (DRD4) and Harm Avoidance (5-HTTLPR). Small effect sizes characteristic of non-Mendelian traits, polygenic patterns of inheritance and true heterogeneity between studies confound attempts to reach a consensus regarding the role of common polymorphisms in contributing to personality domains.
Nevertheless, the current state of personality genetics is far from being bleak. Several new paradigms especially functional neuroimaging or ‘imaging genomics’ have strengthened the connection between
5-HTTLPR and anxiety-related personality traits.
The demonstrations that early environmental information can considerably strengthen and even uncover associations between genes and behavior (Caspi’s seminal studies and more recently the demonstration that early environment impacts on
DRD4 and Novelty Seeking)
are notable and herald a new era of personality genetics. Finally, consideration of the broader phenotypic expression of common polymorphisms (e.g. the ‘social brain’, altruism, etc.) and the use of new experimental paradigms including neurophysiological, neuropsychological and computer games that go beyond the narrow self-report questionnaire design will enable a deeper understanding of
how common genetic polymorphisms modulate human behavior.
Human personality, defined by Webster as the quality or state of being a person or the complex of characteristics that distinguishes an individual, surely requires a more encompassing view towards understanding its complex molecular genetic architecture.
5-HTTLPR and anxiety-related personality traits.
DRD4 and Novelty Seeking
Are these 2 genetic influences and their common genetic polymorphisms at the root of the hawk and dove phenotypes?
Prunetti et al 2008
Abstract – Casa di Cura Villa Margherita, Vicenza, Italy. email@example.com
Attachment disorganization and borderline patients’ metacognitive responses to therapists’ expressed understanding of their states of mind: A pilot study.
This study explores the relationship between psychotherapists’ validation interventions and patients’ metacognitive responses at the beginning of treatment of borderline personality disorder (BPD).
A model of BPD based on disorganized attachment provides the hypothesis that, before patients’ internal working model of attachment has been corrected within the therapeutic relationship, therapist interventions that are likely to activate patients’ attachment system are also likely to induce temporary disorganization of patients’ metacognitive functions.
Any validation intervention implies that therapists openly display an understanding and accepting attitude when they comment on patients’ reported experiences and is, therefore, likely to activate the patients’ attachment system.
I believe a disorganized attachment system is ALWAYS activated – that is part of its disorganization – it is impossible to regulate it normally, and hence it is activated all of the time – or so nearly constantly that it would be nearly impossible to determine when it is NOT activated.
Linehan’s (1993) manual of dialectic-behavioral therapy (DBT) was used as a guideline to assess validation interventions adopted by therapists. The transcripts of the second individual session in the psychotherapy of 19 consecutive patients were analyzed. Checklists based on the DBT manual were used to identify therapists’ validating, supportive, and neutral interventions. The Metacognitive Assessment Scale was used to assess changes in specific aspects of patients’ metacognitive processes during therapeutic dialogues.
Following validation interventions,
patients’ responses revealed significantly higher rates
of temporary metacognitive failure
in comparison to the responses solicited by neutral intervention.
How are they translating this “temporary metacognitive failure” as a sign that the attachment system has been activated? I don’t have the article to find out – I guess I better get it.
Abstract – University of Sydney, Westmead, NSW, Australia. firstname.lastname@example.org
The extended mind and borderline personality disorder.
I have thought about my work on the computer as a mind extension – along the lines of meta cognition. This was an interesting abstract to come across.
It also makes me think of the discovery of mother’s childhood stories, and of the content of her homesteading journals. And, of my writing a book that I would hope would become an extension of somebody else’s mind – in a helpful way.
Extended mind theory, a recent development in the field of cognitive philosophy, suggests that the information and processes contained in external objects such as notebooks and computers can be considered as much a part of a person’s mind as the processes contained within the brain itself.
This paper aims to outline extended mind theory, and to explore how it might be applied to an understanding of psychiatric conditions such as borderline personality disorder (BPD).
CONCLUSION: Those with BPD have a deficit in their ability to perform certain high-level cognitive tasks, such as regulation of affect and impulse control. They incorporate the brains of people close to them, to supplement their own brains when performing these tasks. I have referred to this, especially while undergoing chemotherapy – that my “attachment figure’s” brains were like my external hard drives.
Using an external object or person as part of one’s own cognitive apparatus demands nearly constant proximity and an exceptionally intimate informational bond.
This would account for the BPD sufferer’s panic and despair in the face of abandonment—
when abandonment means literally losing one’s mind,
it could seem worth any effort or risk to avoid such a loss. Further application of extended mind theory to other psychiatric phenomena is also considered.
Abstract – Devon Partnership Trust and Peninsula Medical School, North Devon District Hospital, UK. email@example.com
Borderline personality disorder and the search for meaning: an attachment perspective.
OBJECTIVE: To explore the links between the attachment theory-derived concept of disorganized attachment, and the psychiatric diagnosis of borderline personality disorder (BPD).
METHOD: Literature search for characteristics of disorganized attachment. Clinical case material from psychotherapeutic work with patients suffering from BPD. RESULTS:
can be understood in terms of an approach-avoidance dilemma for infants for whom stressed or traumatized/traumatizing caregivers are simultaneously a source of threat and a secure base.
Interpersonal relationships in BPD including those with caregivers is similarly seen in terms of an approach-avoidance dilemma, which manifests itself in disturbed transference/countertransference interactions between therapists and BPD sufferers.
Borderline personality disorder sufferers
lack meaning in their lives
because [strange logic here] they are unable to
play ‘language games’
with their potential intimates,
resorting to actions rather than
words to express feelings.
Mother could write. She had a command as a child of words and images – but perhaps she had no real person to talk to. It is likely that she did not, and lived entirely in her own imagination, having no real alternative available to her.
I think the stories show that she tried to make sense of the world the best that she could. But she did not have anything from “outside” to work with. There was no “meta,” nothing bigger, nothing outside of her own child’s mind.
CONCLUSIONS: Possible ways of handling these phenomena are suggested, based on Main’s (1995) notion of ‘meta-cognitive monitoring’, in the hope of re-instating meaning and more stable self-structures, in these patients’ lives.
You can’t re-install something that was NEVER THERE in the first place! How stupid is that idea? I know that I have a disorganized attachment, but I never until now thought about mother as having one – though it makes perfect sense to me now. I always thought she had a preoccupied insecure attachment – but now I wonder if going down the ladder each more damaging insecure attachment pattern includes all the parameters of the one “above it” until at the very bottom where disorganized lives, there is nothing left of normal organization at all. There are just disorganized fragments of what was supposed to be an ability to participate equally as a member of a social species.
Buchheim et al 2008
Abstract – Department of Psychosomatic Medicine and Psychotherapy, University Ulm, Am Hochstraess 8, 89081 Ulm, Germany. firstname.lastname@example.org
Neural correlates of attachment trauma in borderline personality disorder: a functional magnetic resonance imaging study.
Functional imaging studies have shown that individuals with borderline personality disorder (BPD) display prefrontal and amygdala dysfunction while viewing or listening to emotional or traumatic stimuli.
The study examined for the first time the functional neuroanatomy of attachment trauma in BPD patients using functional magnetic resonance imaging (fMRI) during the telling of individual stories. A group of 11 female BPD patients and 17 healthy female controls, matched for age and education, told stories in response to a validated set of seven attachment pictures while being scanned.
Group differences in narrative and neural responses to “monadic” pictures (characters facing attachment threats alone) and “dyadic” pictures (interaction between characters in an attachment context) were analyzed.
Behavioral narrative data showed that monadic pictures were significantly more traumatic for BPD patients than for controls.
As hypothesized BPD patients showed significantly more anterior midcingulate cortex activation in response to monadic pictures than controls.
In response to dyadic pictures patients showed more activation of the right superior temporal sulcus and less activation of the right parahippocampal gyrus compared to controls.
Our results suggest evidence for potential neural mechanisms
of attachment trauma underlying interpersonal symptoms
of BPD, i.e.
fearful and painful intolerance of aloneness,
hypersensitivity to social environment, and
reduced positive memories of dyadic interactions.