These studies were apparently conducted to support extensive clinical experience, with the hope of scientifically validating a seemingly efficacious treatment method for an increasingly prevalent and costly illness. The purpose of the studies was to investigate the possibility that some cases of pediatric asthma are the result of a greater than normal number of bonding disruptions “near or at the time of birth”, and that such disturbances and the resulting asthma can be successfully treated using a targeted therapeutic approach. The studies further attempted to show that a considerable measure of success in alleviating asthma symptoms in the children can be obtained by treating only the mother, with additional improvements with treatment of children past the preverbal stage.

The first article of the three (Madrid & Schwartz, 1991) describes the second study in the series, in which 30 mothers of asthmatic children and 30 mothers of well children were interviewed using the Maternal Infant Bonding Survey (M.I.B.S.) in order to discover whether bonding disruptions were more prevalent in the histories of asthmatic children than those of well children. The researchers’ premise was that bonding disruptions such as the physical or emotional separation of mother and infant soon after birth affect the emotional attachment between mother and child and that the absence of this attachment, or “non-bonding”, rather than maternal rejection and/or over-protection, as postulated by previous researchers, is what underlies some cases of pediatric asthma.
The authors claim that they derived the definition of the term “non-bonding” from Klaus and Kennell’s research, referenced in their book Maternal-Infant Bonding (1976). While Klaus, Kennell and Klaus are well-known authorities and advocates of optimal birth in the facilitation of better mother-infant bonding, Madrid and Schwartz appear to have relied for their definitions solely on this book, while apparently disregarding seminal work on attachment by researchers such as Bowlby (1969, 1973, 1988), (Ainsworth (Ainsworth, Blehar, Waters, & Wall, 1978), and Stroufe (Stroufe, Fox, & Pancake, 1983). Such writers distinguish between “bonding”, as a descriptor of mothering behaviors towards the infant, and “attachment”, describing the biologically-driven process by which the infant forms a relationship with its mother, and further distinguish between different styles of attachment: Secure, Avoidant, Resistant/ambivalent (Ainsworth, Blehar, Waters, & Wall, 1978) and Disorganized/disoriented (Main and Solomon, 1990). Unfortunately, Klaus and Kennell did not, themselves, define their terms too clearly: despite the title of their book, they use the words “attachment” and “bonding” interchangeably throughout the book, without discriminating between their application to mother or child.

Madrid and Schwartz (1991) further make the assumption that “non-bonding” exists and, indeed, is commonplace in mother-child pairs in which the child has asthma (86% in this study!). Other writers in the field of attachment research, including Main (Main & Solomon, 1990) believe that it is rare for infants not to attach at all (children in certain orphanages might exemplify those who may not have the opportunity to form an attachment): it is certainly more likely that a mother may have difficulty bonding with her infant. While Madrid and Schwartz state clearly that their study “did not attempt to provide a comprehensive, operational definition of bonding” (p. 354) they write “Mothers who do not bond with their children . . “ in one paragraph, and three paragraphs later report that they used raters “to categorize the children as bonded or non-bonded . . .” (p. 54). Thus they state in the same article, indeed, on the same page, that bonding is something the mother does, something the child does, and something that takes place “between mother and child”! They do not clarify whether it is, in fact, probable that a child could be “non-bonded” as opposed to having a dysfunctional attachment to their mother. Since there has apparently been no study demonstrating that “non-bonding” exists in children predominantly raised by their mothers or another significant caregiver, the study stands on shaky ground in using the term as it does. Credibility would have been enhanced by using terms such as “disrupted bonding” or “dysfunctional attachment” to describe either the experience of mother or child, respectively, or the effects of certain events on the interpersonal process between mother and child. In addition to the above, the article uses additional terms that are not clearly defined (e.g. “soon after birth”).

A second problem with this study is that no explanation is given for the lack of citations later than the 70s and 80s: all but one of the later ones being those of colleagues from the same facility. In fact, there was apparently little or no relevant research regarding the etiology of pediatric asthma during the 80s and 90s. A recent study (Celano, 2001) stated:

The salience of psychogenic and family factors in asthma faded in the 1980s and 1990s as asthma was redefined as a medical (not a psychosomatic) problem (Mrazek & Klinnert, 1988). Although a small but consistent scientific literature continued to explore the role of psychological or family interaction influences in asthmatic episodes or disease course, the prevailing perspective was that family processes affect morbidity only via asthma management behaviors.

A similar sentence included in the article would have gone far to justify the lack of more recent citations in support of Madrid’s hypothesis.

The selection of subjects for the study is inadequately described so the reader is left unclear as to the recruitment method, selection procedures, or whether the mothers and children in the experimental and control groups were matched for age, race, severity of illness, socioeconomic status, etc. There is also no indication of how children were diagnosed and whether a physician’s letter or report was utilized in this regard. Since one-third of the experimental group were already clients of the Erickson Institute and others were referred by study participants, while control group participants were also referred through personal contacts, there is no pretense that the subjects are unbiased, and this bias is s a major weakness of the study. A study in which recruitment of new subjects was framed around a request that permitted participants to be unbiased as to the study’s hypothesis would have produced far more credible results.

A fourth problem with this study lies in the use of an unvalidated instrument, the M.I.B.S. This was apparently developed and administered by staff of the Erickson Institute, which includes the authors of this study, and thereby reflects their bias. A 19-item checklist, it seems to be neither comprehensive nor objective enough to be administered and scored by untrained personnel, introducing considerable researcher bias into the interview process and the rating of the results, despite the additional use of quantitative analysis. In fact, it is stated that the two raters for the study disagreed on a significant number of cases (12 out of 30) and discussions towards an agreed-upon rating did not involve an unbiased third party, casting further doubt on the accuracy and validity of the findings.
The questions on the M.I.B.S., themselves, while apparently intended to identify factors that might disrupt bonding or attachment, exclude a number of possible events that might contribute to this, or be in themselves causes of pediatric asthma. For example, there are no questions concerning whether the mother or anyone in the household smoked while she was pregnant, there is no question regarding whether the infant was resuscitated, suctioned or intubated at birth, or what the Apgar scores were (a subjective, but universally used measure of a newborn’s condition at one and five minutes after birth, based on five observable factors). There is no question regarding other birth interventions (chemical induction/augmentation, forceps or vacuum extraction, hypoxia, narcotic use, diagnosis at birth of respiratory distress, etc.) that would be traumatic for the infant and therefore could affect the early ability to attach, or whether there were any significant heart-rate decelerations during the delivery. There is no question regarding whether a cesarean section was scheduled or emergent, or whether the child’s umbilical cord was clamped before he/she had taken the first breath. Remarkably, there is also no question about whether or when the mother first breastfed her child, although breastfeeding success is correlated throughout the literature with enhanced bonding. In addition, since childbirth is such an intense and in some cases overwhelming experience, many women might be unable to identify certain complications which affected their baby and could influence its subsequent attachment. There are also only two questions concerning events in the prenatal period: inadequate to identify some competing emotional factors on the part of the mother or infant: for example, there is no question regarding whether the child was planned or wanted or how supported the mother was during the pregnancy. While some women will be very forthcoming in response to a request such as “Please describe any conditions you experienced”, others might require more specific prompting before they are able to identify relevant factors. A more comprehensive form of the survey would undoubtedly reveal other factors that may contribute to or cause pediatric asthma, therefore their omission, and the use of biased interviewers and raters, cast serious doubt on the veracity of the postulated causes of the illness. Thus the study described in this article contains some serious methodological flaws, while offering a tantalizing glimpse of a plausible explanation and a potentially valuable treatment for the problem of pediatric asthma.

The second article (Madrid & Pennington, 2000) appears from its structure and headings to be more a brief review of the literature than the description of a research study. Its purpose seems to be to repair the deficit in the previous article of failing to build an adequate case from the literature for its hypothesis before describing the research conducted by its authors to support the introduction of the treatment protocol developed in conjunction with their studies. A single case example from the Erickson Institute’s clinical experience is described, which apparently gave rise to the notion that treating the mother for bonding disruptions resulted in reduction or cessation of symptoms in the child. Pennington’s own dissertation study is awarded a mere paragraph, while the article’s purpose seems to be to provide support for the hypothesis of a relationship between disruptions or failures in bonding and pediatric asthma, and to call for the examination of a targeted treatment protocol to repair disrupted bonding. The article continues to rely on Klaus and his associates to define bonding—this time as a “biological, psychological, and emotional . . . intricate dance” (p. 280) between mother and child during a period of impressionability shortly after birth. However, since Klaus and associates are explicitly describing the mother’s experience of the events and the relationship with her infant, little attention is paid to the infant’s part in this dance either in their writing, or in this article and the associated research. Such a focus would justify the bias towards the use of the term “bonding” rather than “attachment”, however this article continues the mistake of the previous one in continuing to allude to “non-bonded babies” (p. 284). In this case, they are described as “often colicky and may dislike being cuddled” as well as “difficult to please,” “fidgety,” and “not really comfortable with people” (pp. 284-285) when older. No criteria are described for identifying these behaviors, nor are other causes of such behaviors ruled out. While these behaviors may be associated with non-bonding, there are many perinatal factors other than bonding disruptions that can contribute to their formation.

In describing previous research the authors state that “it has become widely accepted that separation of mother and child is good for neither” but cite no studies as examples. This optimistic perspective is far from today’s reality and some degree of mother-infant separation is still routine practice in many hospitals throughout the country. It would take very little effort, unfortunately, to find hospitals at which studies similar to those they describe as having been conducted 20 years ago could still be done. Like the previous article, this one does not address whether adequate bonding can take place later.

This article also represents a missed opportunity to provide a more thorough description of Feinberg’s research, for which neither the number of participants in the study nor the degree of significance of the results was provided. It might also have offered the details of Pennington’s study, which, though apparently interesting in its findings of four specific “non-bonding” events found to occur significantly more often in the histories of asthmatic children, and correlating with Klaus and Kennell’s findings, is given short shrift.

What is surprising is that, with their reliance upon Klaus and Kennell’s work for their fundamental premise and the basic elements of their survey, Madrid and Pennington did not appear to have reviewed the updated version of their book (Klaus, Kennell & Klaus, 1995), in which the information provided on bonding is much expanded as a result of, the authors say, 13 years of NICDH grant funding.

This article does assist the reader in understanding the findings of the M.I.B.S. by reporting that in Schwartz’s study (1988) “twenty percent of well children had two or more non-bonding events in their mother’s histories. For asthmatic children, the corresponding figure was 70%.” (p. 287). Unfortunately, since the raters were biased, the identification of these non-bonding events appears to be purely subjective.

In this article, two new terms are introduced: “intrinsic asthma” and “responding asthma”, in conjunction with the summary of Schwartz’s results. Unfortunately, neither term is defined, nor sources cited, leaving the reader wondering, since there was found to be no difference in incidence of non-bonding events between the two, why the terms were introduced in this brief summary in the first place!

It was valuable to find here (p. 287) a sentence stating clearly that “all non-bonded children do not have asthma and that all asthmatic children are not non-bonded.” Belatedly, this sets a context for the body of work by these authors. However, in the conclusion of the article, an additional study (Mrazek, Klinnert, Mrazek & Macey, 1991) is cited (pp. 287-288), apparently to support the argument for the relationship between “failures in bonding” and pediatric asthma, which introduces the term “genetically predisposed asthmatic children” as those studied with their mothers by these researchers. However, whether or not asthma can be transmitted genetically is never addressed here or elsewhere in the article, leaving an additional unanswered question on the table, and detracting from the case the authors attempt to build for further study of the phenomenon of interest.

It is stated at the beginning of the third article (Madrid, Ames, Skolek & Brown, 2000), that its purpose is to formalize the examination of the research hypothesis and the presentation of findings, thus attempting to remedy the shortcomings of the previous two articles and the studies described therein. It follows the standard format for journal publication of the findings of research in which the authors conducted a small pilot study to test the effectiveness of a treatment approach in repairing bonding disruptions between mothers and their asthmatic children. Since many of the citations in this article are of the authors’ colleagues, and these colleagues’ citations are not explicitly referenced, it is still unclear how many non-related writers have addressed the issue of strained mother-child relationships. There is also still no explanation provided for the lack of citations (other than those of colleagues) from the 80s and 90s.

The six subjects for the study were those who completed the study from an initial pool of 19 who volunteered to participate in response to announcements in schools and health centers in a named specific geographical area. Mothers who volunteered were sent a research package that included the M.I.B.S., a Mother’s Report: a nine-item questionnaire adapted from a similar document already in use and requesting objective data on the child’s asthmatic condition, and a Child’s Report, another nine-item questionnaire designed to permit the child to evaluate his or her own breathing under specific conditions. Mother’s report and Child’s report were both administered three times: before the study began, two weeks after completion of the mother’s treatment, and one month after the child’s treatment was completed. In two cases the children in question were too young to respond to this questionnaire. A Clinical Scoring Check List, developed by the researchers who provided the original of the Mother’s Report, was used with the Mother’s Report “for some presentations of the data in order to determine the changes in the severity of asthma.” (p. 95) Treatment was conducted first on the mother, and then on the child if he/she was old enough to participate. It would appear that the methodology for this study was designed to provide somewhat more objective measures that could also be cross-checked by comparing mother and child’s reports.

Subject selection still appeared problematic, in that “two mothers did not wish to participate because they did not think the hypothesis for this study was valid,” while a third “was not comfortable with the theoretical assumptions.” (p. 93). Properly framed, the invitation to participate should ideally have attracted participants regardless of whether they agreed with the hypothesis or not, although issues concerning birth, bonding, and parenting can be extremely sensitive for some parents, who might have resistance to certain concepts no matter how neutral their presentation. A larger number of subjects would have made for a study with greater reliability, but possibly would also have exceeded the allotted research budget.

Despite the addition of some more objective measures, the continued use of the M.I.B.S., an unvalidated and rudimentary instrument, requiring the expertise of the Senior Investigator, Madrid, to rate participants bonded or non-bonded, renders the substance of the study highly subjective due to overwhelming investigator bias, while permitting no adequate way of ruling out other possible causes of pediatric asthma in the child subjects.

The study is handicapped by the absence of a control group. In this case, such a group should have responded to the questionnaires but received some form of education session(s), rather than the full treatment process, to rule out any improvements as a result of simply receiving researcher attention. On the other hand, the detailed description of the treatment process, clearly calling for considerable expertise in the techniques used, and clearly tailored to the history of each individual mother-child dyad, conveys the potential potency of the procedure employed, while highlighting the fact that therapy itself is not something easily standardized or quantified and may therefore be more amenable to qualitative, rather than quantitative, research. A purely quantitative approach might have called for a standardized protocol, or script, for the treatment itself, and while this method might have accomplished some of the treatment goals, it is likely that results would be less convincing with the absence of the art of therapy itself, and the experience and convictions of the therapist conducting the sessions.

While the greater improvement was shown consistently following treatment of the mother, further improvement was shown in several cases after treating the child. It is possible that the child may make some significant contribution to the bonding disruption, in concert with the development of the asthma, yet virtually no attention is given to this possibility, just as the study makes no attempt to relate its terminology to that of the body of research concerning disordered infant attachment. The authors quote the statements of mothers who feel unbonded to their infants, yet repeatedly ascribe “bonded” or “nonbonded” to the infants themselves. In addition, the study does not explicitly address the distinction and relationship between maternal bonding and infant attachment, nor define the limitations of the study to the mother’s part in bonding disruptions.

While mention is made of a delayed improvement in one child, there was apparently no specific longer-term follow-up incorporated into the study, which might have had considerable value in indicating whether the effects of treatment in alleviating asthma symptoms were enduring, while being reasonable simple to implement using the same measures as were used during the study.

Statistically, the number of subjects in this study is too small for the results to have great significance, although the use of the Chi-square analysis helps to indicate whether the study’s findings have statistical validity and it is therefore worth replicating. The article’s concluding discussion asserts, justifiably, that the study indicated that the researchers’ Maternal-Infant Bonding therapy alleviates children’s asthma symptoms by improving mother-child bonding. An additional hypothesis emerged from the study: that “impaired bonding may be easier to remedy at a younger age” (p. 110), particularly with regard to the developmental tasks of adolescence, which would be in direct conflict with efforts to strengthen the mother’s connection to her child. The limitations of the study are addressed explicitly here, and a larger study, with “stronger objective measures” is called for (p. 111). The authors also emphasize the importance, however, of the subjective experiences of the participants, stressing the value of a quick and effective solution to the suffering pediatric asthma imposes on the families who experience it.

While there were major deficiencies in the three articles’ reviews of the literature, some serious methodological flaws in the earlier studies and significant limitations in the later one, and poorly defined and inaccurate terms on which the studies’ hypotheses were founded, the cumulative outcomes of these researchers’ attempts nevertheless present an intriguing approach to the resolution of some cases of pediatric asthma, and represent the  all too rare efforts of clinicians to document the potentially valuable outcomes of their clinical explorations and experience.

References

Ainsworth, M. D. S., Blehar, M. C., Waters, E., & Wall, S. (1978). Patterns of attachment: A psychological study of the Strange Situation. Hillsdale, N.J.: Erlbaum.
Bowlby, J. (1969). Attachment and loss: Vol. 1. Attachment. New York: Basic Books.
Bowlby, J. (1973). Attachment and loss: Vol. 2. Separation and anger. New York: Basic Books.
Bowlby, J. (1988). A secure base: Clinical applications of attachment theory. London: Routledge.
Celano, M. P. (2001). Family systems treatment for pediatric asthma: Back to the future. Families, Systems & Health: The Journal of Collaborative Family HealthCare, l (19) (Issue 3), 285-290.
Klaus, M., & Kennell, J. (1976). Maternal-infant bonding. St. Louis: Mosby.
Klaus, M., Kennell, J., & Klaus, P. (1995). Bonding: Building the foundations of secure attachment and independence. Reading, MS: Addison-Wesley.
Madrid, A. & Schwartz, M. (1991). Maternal-infant bonding and pediatric asthma: An initial investigation. Pre- and Perinatal Psychology, 5 (4), 347-358.
Madrid, A. & Pennington, D. (2000). Maternal-infant bonding and asthma. Journal of Prenatal and Perinatal Psychology and Health, 14 (3-4), 279-289.
Madrid, A., Ames, R., Skolek, S. & Brown, G. (2000). Does Maternal-infant bonding therapy improve breathing in asthmatic children? Journal of Prenatal and Perinatal Psychology and Health, 15(2), 90-117.
Main, M., & Solomon, J. (1990). Procedures for identifying infants as disorganized/disoriented during the Ainsworth Strange Situation. In M. T. Greenberg, D, Cicchetti, & E. M. Cummings (Eds.), Attachment in the preschool years: Theory, research, and intervention, 121-160. Chicago: University of Chicago Press.
Mrazek, D., Klinnert, M., Mrazek, P., & Macey, T. (1991). Early asthma onset: Consideration of parenting issues. Journal of the American Academy of Child and Adolescent Psychiatry, 30, 2.
Stroufe, L. A., Fox, N. E., & Pancake, V. R. (1983). Attachment and dependency in the developmental perspective. Child Development 54, 1615-1627.

Photo: NASA/GSFC, MODIS Rapid Response

Just wow!

The caption on the BBC News website states: “This striking image taken by Nasa’s Terra satellite on 7 January shows the UK deep in the clutches of the current cold snap.”

This photograph is of something I do not ever remember happening in the twenty-plus years I lived in the UK growing up. I don’t know if this is symptomatic of global warming, global cooling or what, but it’s definitely something!

The UK maybe small compared to the US or Canada, but isn’t it unusual for the entire country to experience exactly the same weather like this? I hope my family and friends back in Britain are keeping toasty warm (or at least having fun in the snow!!) Weather like this is a great excuse for hot chocolate, hot buttered rum and a few other cold weather treats!

The focus of my dissertation research study was, as you can see by the above title, an exploration of whether there is any relationship between the use of Pitocin (artificial oxytocin) to start or speed up labor, and the way children born with its use function individually and in their relationships when they are three years old. I was interested in Pitocin use because what I read suggested that around two-thirds of inductions are now for non-medical reasons, but there wasn’t a lot of research to tell us whether there were any specific consequences to the child of this use.

Before starting this research I first interviewed six therapists who work with babies, children, and adults to resolve issues arising fromchallenging prenatal or birth experiences. All the therapists had worked with clients who had been born with the use of Pitocin. The therapists told me what they had observed and learned about their clients and the role they thought Pitocin played in their functioning. I performed a content analysis on the interview transcripts, and about two years later, had a long list of “items” that eventually became the raw material for a survey to be conducted with mothers of three-year-old children. I sent this list to the six therapists with a voting form, and they helped me select which items best represented the various areas of functioning about which I planned to ask the mothers.

Eventually, this list became the survey that participants were invited to complete. Ultimately, I had 498 completed surveys that could be analyzed to see if Pitocin use appeared to be related to a difference in how three-year-olds functioned.  The following is a summary of the findings that were statistically significant.

1.      Receiving Pitocin resulted in more negative recollections of labor and delivery, suggesting that mothers who received it had a more challenging experience than those who didn’t. However, there was a similar finding for the use of epidural anesthesia and for pain medication, both of which tend either to precede or follow the use of Pitocin.

2.      Mothers who received Pitocin spent less time with their babies in the first hour after delivery, and were less likely to feed their babies exclusively at the breast in the first six months. In other words, babies who were born without Pitocin were more likely to be fed exclusively at the breast in the first six months than those born with Pitocin

3.      Two factors distinguished children born with Pitocin from those born without Pitocin.

The first was called “Assertiveness”, which describes a socially appropriate way that babies and children communicate their need for help and comfort when they are feeling uncomfortable or unsafe. Typically, crying, using facial expressions and physical gestures, and later, verbalizing their thoughts and feelings, elicits helpful responses from parents, who try to identify and meet the need the baby or child is expressing. However, babies born with Pitocin, whose mothers reported having had a more challenging time during labor and delivery, appear to have a higher need to be assertive because they seem to experience more discomfort, but are apparently less effective in asserting their needs and getting them met when they feel unsafe or uncomfortable.

The second factor was called “Need to Control Environment” and this summarizes what seems to be a higher level of discomfort or insecurity, particularly in response to “outside-in” influences (e.g., reacting to food with digestive problems or being picky eaters; problems coping with other people’s timing and structure, refusing help from others) and increased or exaggerated efforts to control their environment, resulting in behaviors that may be more challenging to their mothers/family. There appears to be some continuity of effects between infancy and age three: for example, children who were described as picky eaters, or as having digestive problems at three, were likely to have been colicky, fussy babies. Interestingly, the hormone oxytocin is very involved in the digestive process: it plays a role in the production of digestive enzymes and as we enjoy our meal, in a positive feedback loop, we produce more oxytocin.

It may be that a process described as “hormonal imprinting”, identified in a considerable number of animal studies since the 1970s, is the mechanism that accounts for these differences between children exposed to Pitocin and those who were not. Using Pitocin to initiate labor may “flood” the available oxytocin receptors in mother and baby, apparently affecting children’s internal comfort levels and how they interact with others, although how this takes place in the babies has not yet been studied. Since both mother and baby receive Pitocin during labor and delivery, it is as yet unclear to what degree each contributes to challenges in their mutual relationship.  

Santa Barbara Graduate Institute

July 2008 

 Use these links to download a .pdf of the Powerpoint presentation of this material:

 Microsoft PowerPoint – 6 slides per page

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I am posting this link because the story has beautiful elements that clearly pertain to prenatal and perinatal psychology and illustrates eloquently how children remember and communicate their early memories.

I wondered if I had an overly morbid fascination with fires. I keep the television on, listen to the radio in my car, check the web for updates, and search for interactive maps that show the movement of flames and the growth of the area involved. Then I realized that, really, it’s my weak attempt to control the uncontrollable—defaulting to my left brain as I usually do when overwhelmed, I feel less helpless, less awed by the terrible power of wildfires, when I have facts and figures: the location of the fire’s edges, the percentage of containment— 154,000 acres burned, 78 structures lost, 2 firefighters killed, 3 injured—natural causes or arson? (apparently, 90% are the latter—although Buckweed was started accidentally by a child playing with matches while the Santa Anas were blowing).

Ironic that, when talking and writing about birth, I am all for allowing Mother Nature to prevail, to trust that, when protected and undisturbed, mothers and babies know how to do this thing called birth with very few problematic outcomes. In birth, “civilization” has taken too much control and outcomes have worsened proportionately. Yet with these terrifying wildfires I want more control. I want Mother Nature tamed and safe. And even then, perhaps fewer homes would be endangered by fire if we paid more attention in selecting where to build: they are tucked into steep, wooded canyons, clustered in the foothills of forested mountains—places that are rich in fuel in this hot, dry climate—beautiful, but potentially deadly. I’m grateful that there has been no significant wind during this fire—it would have spread so much faster and done so much more damage, but the lack of wind also kept the haze from dispersing. *Click*–another shot of pink sun seen through brown smoke.

Physically safe though I may be, the fire preoccupies me every day. Periodically, I try to plan what to pack if I had to evacuate and feel rising panic as I realize what might be considered non-essentials in a hurried departure: my books—a sizeable collection since I completed my Ph.D. and continue to collect publications whose contents fascinate me and/or whose information I hope to use in future scholarly articles or a book, computer, jewelry, boxes of photographs, as well as more accepted essentials: personal documents (insurance policies, passports, birth certificate, etc.), clothes, shoes, medications . . . how would I ever find and pack everything in the urgency of an immediate evacuation?!

I notice ashes on my car in the morning. A colleague posts on Facebook “I’m scared! May have to evacuate!” I stop outside my hairdresser’s to photograph helicopters flying above flames. I drive to work watching for the columns of smoke noting the direction of movement of the fire.

*Click*–a shot of the haze over the desert. *Click*–a photograph of the amazingly white cumulonimbus clouds formed by the heat of the smoke and flames.

I breathe smoke going from car to buildings, I watch and take more pictures of the colors of the sky: pink, brown, grey, orange—anything but the usual intense Southern California blue.

I wonder if I will ever again relax by a fireplace and truly enjoy the crackle and smell of burning wood. I complain with my colleagues about the bad air and the triple-digit temperatures. I cough and rub my stinging eyes, and fall asleep to dream of green places: tall trees in forests, rivers and lakes, the fragrance of pine and juniper, wild ocean waves, rain . . .

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Postscript: We have learned that this fire was the result of arson.

Bumpers!

Yes, those invisibly color-coordinated bits of cars back and front that are expected to protect passengers (and cars) in rear- and front-end crashes.

What the hell happened?!!!

When I learned to drive, umpteen decades ago, bumpers were big, black, rubbery-looking things that could withstand a fair amount of impact without damage to the car. On a visit back home to England I remember my cousin and her daughter laughing as they squeezed the car into a tight spot, tapping the bumper behind them in the act. Immediately, cousin and daughter laughed and announced in unison “Bumpers are for bumping!”

Today, lightly tapping the part of a car laughably called a bumper will cost you at the very least a couple of hundred to fix the paint, likely points on your record, and possibly, if the tap was less than light, a couple thou to fix the dent. Dent? What happened to “bumper”?!!! Oh, and not to mention the possibility of an additional claim for whiplash! So much for protecting car and passengers!

My previous car, the Mazda 323 I owned for 15 of its 16 years, had solid-looking black bumpers. They had survived one being knocked off kilter by a car skidding across black ice on a Vancouver corner (just had to pop it back on to its mounts—no harm done), countless minor bumps and scrapes over years of driving and parking–mine and others, protected me from possible whiplash injuries in a couple of fender-benders—and never once required dent removal or painting. Actually, I thought they made my little car look sturdy, a little more macho, and trustworthy, living up to the AAA inspector’s description of the car as “bullet-proof”—figuratively speaking, of course.

So what happened to bumpers that work—that do the job they were originally designed to do? Was it just valuing cosmetic appeal over safety that made them disappear? Another way to make money off the hapless consumer? Despite the matching paint, do they do as good a job of protecting car and passengers? Did they make the rules more lax and begin to rely instead on airbags?

I simply don’t understand. All the slick, uniformly painted cars on the road today (mine included) just don’t compare to a car with great, chunky, reassuringly black bumpers. Who do I have to talk to to bring them back?

www.reducinginfantmortality.com

For a country that spends so much money on pregnancy and childbirth, our infant mortality rates are appalling. Listen to obstetricians, doulas, neonatologists, midwives, psychologists, pediatricians, and other physicians explain how our health care system is failing babies and mothers and what we can do about it.

Please view the film, then share it with your colleagues and friends, show it in your community, and send it to your legislators. Our babies (and their parents) will thank you!

Here is a link to President Obama’s committee on health care reform. You can send the link to the video directly to the committee–the more of us sending the link, the better chance it will be recognized as an important issue for consideration in the re-visioning of our health care system.

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There is currently a lively discussion going on about the order given to nurses to “Pit to distress”, apparently with the intention of causing fetal distress that can then result in an emergency cesarean.  Two days following the original post it went viral with well over 11,000 hits.  I do encourage you to read this discussion, since the trend is alarming and another very clear example of a health care system in crisis putting the safety and needs of mothers and babies last.  I feel no need to add to what has already been said by The Unnecesarean, Keyboard Revolutionary , and others, so I will only make a brief comment here about the perinatal psychological implications of this:

What astonishes me over and over again is that no-one ever, ever seems to consider (well, actually Sarah Buckley does) what it may mean to motherbaby to have a massive overdose of Pitocin binding with oxytocin receptors at a time when oxytocin is supposed to be surging ready for post-birth bonding, not to mention all the consequences of distressed babies, crash sections and traumatized mothers and babies. Michel Odent said somewhere: “When human beings release adrenaline, they cannot release oxytocin.” Why do we settle for so little? The “at least you have a healthy baby” offered as the consolation following a cesarean is questionable itself, unless “is breathing and has a pulse” is all you need to meet the criteria for “healthy”.

What does it mean to begin life with life-threatening trauma entirely as a result of someone who is too impatient to allow nature to take its course? Assuming that the cesarean ensuing from “Pit to Distress” is successful and there are no lasting physical problems for mother or baby (which, of course, we can’t assume in all cases!), what is it like to have adrenaline and cortisol flooding your system, likely an overnight stay in the nursery, a mother in recovery from major surgery, and delayed or failed breastfeeding, instead of basking in abundant endorphins and oxytocin, nursing and falling in love?

Animal studies have suggested that interfering with the oxytocin system at birth may have enduring consequences: for digestion (in which oxytocin is involved) and social functioning.  We also know that the oxytocin system is implicated in autism spectrum disorders and schizophrenia.  Now that is not to imply a causal relationship between the two–I’d be the last to suggest this, but I do wonder about social functioning when birth becomes disruptive to the hormones involved in the primary attachment relationship.  Rixa Freeze, in her own discussion of this issue, Pitocin Protocol and emergency cesareans, cited a recent study, Hospital’s Oxytocin Protocol Change Sharply Reduces Emergency C-Section Deliveries which noted that “As oxytocin utilization declined from 93.3% to 78.9%, emergency cesarean deliveries decreased from 10.9% to 5.7%”. I know I’m not the only person shocked that a hospital would consider 78.9% oxytocin use a good percentage!!  That means more than 3/4 of women birthing at that hospital are being given Pitocin! Does this mean that 3/4 of American women are incapable of giving birth without chemical help? Are their bodies “broken”?  Or is it the health care system?

What will it mean for all these babies/children/people to have started life rushed into the world with the wrong chemicals flooding their newborn bodies? What will it mean for their mothers: oxytocin receptors flooded with a synthetic  that, while a perfect chemical copy of oxytocin, cannot replicate its multiple functions at birth, in our bodies, and in our daily relationships.  And what will it mean for society?

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Here is a link to flow-chart of typical consequences of Pitocin use:

http://www.birthinternational.com/parents/obstetric/diagram.html

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 Imagine then that this same experience happens unpredictably for a number of months: perhaps only occasionally, perhaps daily or even more often. This may be what it is like to be a fetus exposed to maternal substance abuse: particularly a substance like methamphetamine. The fetus is also exposed to its mother’s stress hormones–adrenaline, cortisol, norepinephrine—depending on her circumstances: there may be domestic violence, she may be homeless, prostituting, and not eating well. She is unlikely to get regular prenatal care and her baby may come early, and spend time in the N.I.C.U., where its already hypersensitized nervous system is further assaulted by the standard care that infants receive in most neonatal intensive care units: no warnings before a diaper change, a bath, or a needle being poked into a vein: if they are lucky, a nurse will speak softly to them, if not, sounds, lights, sensations and medical procedures can be exhausting and overwhelming. In addition, many of these children are detained from their mothers at birth and find themselves in the care of others: perhaps family members, or strangers. Some of the babies not detained at birth show up in the child welfare system months or years later: victims of neglect and possibly abuse.  

 By age three many of these children are being “suspended” or “expelled” from their preschool or day care for their aggressive behaviors, their resistance to following directions, their disruptiveness and their inability to relax and sit quietly through an activity or story. Many also have problems with falling or staying asleep, which may add to their irritability. By five, many of them will have been diagnosed with Disruptive Behavior Disorder, AD/HD, Oppositional Defiant Disorder and other similar childhood diagnoses. Some will begin on medication early, sometimes for a lack of alternative treatments (such as occupational therapy for sensory processing and/or regulatory disorders that often co-occur with AD/HD), or to keep their teachers happy and keep them in school, perhaps making it possible for them to avoid being placed in Special Education classes or classes for “emotionally disturbed children.”

 I have a theory. I wonder if the sensations of angry feelings inside a preschooler are experienced as similar to the sensation of drugs in their bloodstream prenatally. I wonder if these children therefore believe that they cannot control angry feelings (the very big angry feelings common in 3-5-year-olds) because they couldn’t control the sensations of the drugs entering their fetal bodies carried by blood from their mother through the umbilical cord (although apparently many try—they instinctively contract the muscles around the umbilicus in a vain attempt to squeeze off the offending substance, but of course, can’t do this with complete effectiveness because they’d also be reducing their oxygen levels. These children tend to have constipation as infants and gait problems when they begin to walk from this chronic pattern of muscle contraction.  I wonder if each time they experience feeling angry and frustrated they also feel the terror of possibly being annihilated by those sensations, just as they formerly feared the very real possibility of dying as a result of a huge overdose of a drug for the size of the fetal body. I wonder if their hyperactivity and inability to settle and focus results from the hardwired need to be hypervigilant, to watch out at all times for the next possible threat to their survival. I wonder if their aggressive behaviors are the result of the fight/flight system having become the dominant operating system at such a young age. Not necessarily that they are just plain aggressive, but that they perceive every stick to be a snake, every movement around them to be a potential source of danger.

 I wonder what these souls seek in such a life experience. What makes them survive circumstances that might result in miscarriage for another fetus in a similar situation? They used to say that our fears for “crack babies” were overstated and that many turned out just fine. A psychiatrist I know said that prenatal drug exposure is such a random process it affects the brain like scattershot, so the damage is like Swiss cheese: little pockets of damage concealed among normal brain tissue.  You may see the effects right away or not until later on. And no two children so affected are affected in quite the same way, though there are commonalities in many (see above).  Is it treatable?  Yes, I think so, in most cases. But whether the appropriate treatments are available and affordable varies by location and family circumstances. And then there are the families. Some are in denial that there is any problem. Others simply don’t notice anything out of the ordinary until later on. Some have limited resources. Some are misled by practitioners who are unaware of the possibilities for helping such children into thinking there is little or nothing they can do. Many children ultimately get medication, which treats symptoms, but not the source.

 I would so love to find out what’s being done for these little ones around the country, and around the world. I’ll bet there are pioneers all over the place, some of whom are doing marvelous, brilliant things. I only wish they were right here where I live and work!

Here is a link to a report of a recent study on prenatal methamphetamine exposure: http://tinyurl.com/lgf5do

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At the end of his life, looking less than robust and possibly continuing a long-standing addiction to narcotics, once again he was under tremendous pressure to perform—in 50 concerts, for heaven’s sake! And again, by powerful, intimidating father figures in the form of his financial backers who expected him to sing and dance his way out of monstrous debt while making them a handsome profit. Whether these individuals were truly intimidating or not doesn’t matter: Michael would have experienced them that way—that’s part of the recapitulation. Terror induces trauma and similar situations may trigger trauma memories on a physiological level. The expectation was essentially to equal or surpass his performances at his prime—and make no mistake, Michael Jackson at 50 was no Mick Jagger at 64—the robust Jagger’s life story is a very different one. While he clearly longed to be back on stage and adored, and was working hard to prepare for it, perhaps Michael knew there was no way he could meet those expectations and struggled with the anxiety of attempting to do so, or perhaps he just “lost heart” for such a crazy endeavor and felt as trapped and helpless as the little boy he was when all this began. What fascinates me is how he managed to manifest such a sadly similar experience at the end of his life as he had experienced as a child. What a brilliant, shining star he was, and what a truly tragic life he lived! I really hope he is at peace now.

Here is a link to a related article describing Jackson’s life: http://www.cnn.com/2009/SHOWBIZ/06/26/michael.jackson.spotlight/index.html