Thursday, September 16, 2010

UNASKED QUESTIONS ABOUT SYNTHETIC OXYTOCIN

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PRIMAL HEALTH RESEARCH
A NEW ERA IN HEALTH RESEARCH
Published quarterly by Primal Health Research Centre
Charity No.328090
72, Savernake Road, London NW3 2JR
michelodent@googlemail.com
Summer 2010 Vol 18. No1
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www.primalhealthresearch.com
(Free access to the Primal Health Research Data Bank)
www.wombecology.com
(The importance of pre- and perinatal ecology)
BETWEEN THE MIDATLANTIC AND THE MIDPACIFIC CONFERENCES
(Topics for the future: see below)


UNASKED QUESTIONS ABOUT SYNTHETIC OXYTOCIN
A labouring woman was puzzled and even anxious when she received a drip of synthetic oxytocin, The midwife immediately reassured her that oxytocin is not like a drug: it is “natural”. Perhaps this is why we ignore many questions regarding what is undoubtedly the most common medical intervention in childbirth on all five continents. Today, all over the world, most women giving birth vaginally get such a drip (called Syntocinon or Pitocin) including those with an eventual operative delivery by forceps or ventouse. Most women who undergo a caesarean section during labour have had such a drip before the decision to operate, and this drip is usually continued for some hours after the surgery. Even during and after a pre-labour c-section, synthetic oxytocin is included in many hospital protocols to facilitate uterine retraction. Furthermore, the rates of labour inductions are currently high, and induction almost always involves the use of synthetic oxytocin.

Preliminary questions
This new situation raises important questions. We must first wonder why modern women need substitutes for the hormone that is naturally released by the posterior pituitary gland. Is it because their oxytocin system is disturbed? Is the capacity to effectively release oxytocin depleted from generation to generation, as a result of several aspects of modern life, particularly medicalised birth? This is a vital question for the future of civilisation, since the oxytocin system is involved in sociability, capacity to love, and potential for aggression. Is it mostly cultural conditioning in a context of industrialised childbirth? In this latter case the current situation might be reversible. If it is simply a matter of environment at birth, we need to improve our understanding of the birth process. In fact, we must explore the possible contribution of multiple factors.

Other questions address the substances that might cross the placenta and reach the unborn baby. For example, the kind of fluid used to transport synthetic oxytocin. In earlier times, glucose drips were routine during labour. These infusions were not benign because simple sugar molecules rapidly cross the placenta while the mother’s insulin—released in response—fails to reach the fetal bloodstream. There is thus a risk of excessive insulin production generated by the baby's pancreas in response to these circulating high blood sugar levels. Extensive research has confirmed the risks of neonatal hypoglycemia.(1 to 7) These studies led to the replacement of glucose drips during labour by other liquids, such as Ringer’s solution. The results of such studies also apply to labouring women without a drip of synthetic oxytocin if they are encouraged to consume sugar or soft drinks. This is not always understood by the natural childbirth groups. Furthermore, if labour progresses spontaneously, adrenaline type hormone levels are low, voluntary muscles are at rest, and these women don’t need added energy.8

Can synthetic oxytocin cross the placenta?

When we finally acknowledge that all over the world most women receive synthetic oxytocin while giving birth, we can no longer deny problems arising from the possible transfer of oxytocin via the placenta. One can wonder why it remains an unexplored issue. The main reason, as we have suggested, might be that oxytocin is not considered a “real” medication because chemically the synthetic form is no different from the natural hormone: it is a simple molecule (a nonapeptide). However, the problem is not simple because the amount of oxytocin reaching the maternal blood stream via an intravenous drip is enormous compared with the amount of natural oxytocin the posterior pituitary gland can release. Furthermore, natural oxytocin is released through pulsations, while synthetic oxytocin is delivered continuously. Another reason for ignoring this issue might be the discovery of enzymes that metabolize oxytocin (oxytocinases) in the placenta. This finding might have led to a hasty, tacit conclusion that synthetic oxytocin does not reach the baby.

Until now, there has been only one serious article published on this subject.9 A team from Arkansas concluded that oxytocin crosses the placenta in both directions—after measuring concentrations of oxytocin in maternal blood, in the blood of the umbilical vein and umbilical arteries, and also after perfusions of placental cotyledons. More precisely, the permeability is higher in the maternal-to-fetal direction than in the reverse. Eighty percent of the blood reaching the fetus via the umbilical vein goes directly to the inferior vena cava via the ductus venosus, bypassing the liver, and therefore reaching the fetal brain immediately: it is all the more direct since the shunts (foramen ovale and ductus arteriosus) are not yet closed.

Since there is a high probability that a significant amount of synthetic oxytocin can reach the fetal brain, we must investigate the permeability of the so-called blood brain barrier at this phase of human development. This “barrier” implies a separation of circulating blood from cerebrospinal fluid in the central nervous system. It restricts the diffusion of microscopic particles, including bacteria, and molecules such as oxytocin. However, Australian researchers presented evidence that the developing brain is more permeable to small lipid-insoluble molecules and that specific mechanisms, such as those involved in transfer of amino acids, develop gradually as the brain grows.10 Furthermore, it appears that the permeability of the blood-brain barrier can increase under the influence of oxidative stress11,12,13, that commonly results when a synthetic oxytocin drip is administered during labor.14 Therefore, we have serious reasons to be concerned if we consider the widely-documented concept of “oxytocin-induced desensitization of oxytocin receptors”.15,16,17,18 It is probable that, at a quasi-global level, we routinely interfere with the development of the oxytocin system of human beings at a critical phase for gene-environment interaction. Within the framework of accepted scientific knowledge, we must acknowledge the important role of oxytocin, particularly in sociability, the capacity to love (of others and love of oneself) as well as the potential for aggression (aggression towards oneself and towards others).19 Interfering in normal reproductive physiology raises critical issues. For example: “Is there a link between the increased incidence of disorders associated with documented alterations of the oxytocin system (such as autism20,21 and anorexia nervosa22,23) and the widespread use of intravenous drips during labour?” “What will be the impact on the evolution of our civilizations?” We may even wonder if the widespread use of synthetic oxytocin can induce an unprecedented cultural revolution.

Such questions should inspire a new generation of research.

Plastic related substances

Of course, one cannot ignore the toxic effects of phtalates, which are added to plastics such as polyvinyl chloride (PVC) to increase their flexibility, transparency, and longevity. The National Institute of Environmental Health Sciences and the National Toxicology Program began studying phthalates following a discovery that blood stored in PVC plastic bags for transfusions contained significant concentrations of phthalates.24 The most common phthalate is di-ethylhexyl phthalate, or DEHP. In bags for intravenous drips and tubing, additives like DEHP can make up 40 or 50 percent of the product.

There are several reasons why this issue is critical. The first is that the effects of phtalates on intellectual development have already been demonstrated, in particular by an authoritative South Korean study.25 The authors found that high urinary concentrations of phthalate metabolites were associated with lower intellectual quotients (IQ) among 667 children at nine elementary schools. Another reason for serious concern is that today most women spend hours with an intravenous drip while giving birth. There is an accumulation of data confirming the transplacental transfer of phtalates among mammals in general26,27 and humans in particular.28 Most babies probably receive some amount of phtalates during the critical period surrounding birth. Is this amount negligible or dangerous? What are the possible long-term consequences? It is essential to emphasize that these phtalates pass directly into the fetal bloodstream, with no possibility of degradation in the digestive tract. Very sensitive tests today can find a millionth of a gram, or even less, of certain substances in blood or urine. This measurement process is called biomonitoring. In July 2006, an expert committee of the National Academy of Sciences (NAS) published the results of a comprehensive study of biomonitoring. The committee stated that, “In spite of its potential, tremendous challenges surround the use of biomonitoring, and our ability to generate biomonitoring data has exceeded our ability to interpret what the data mean to public health.”

Today, even the experts confess that they are in the dark.

References
1 - Mendiola J, Grylack LJ, Scanlon JW. Effects of intrapartum maternal glucose infusion on the normal fetus and newborn. Anesth Analg. 1982 Jan;61(1):32-5
2 - Lucas A, Adrian TE, Aynsley-Green A, Bloom SR. Iatrogenic hyperinsulinism at birth. Lancet. 1980 Jan 19;1(8160):144-5.
3 - Kenepp NB, Kumar S, Shelley WC, Stanley CA, Gabbe SG, Gutsche BB. Fetal and neonatal hazards of maternal hydration with 5% dextrose before caesarean section. 1982 May 22;1(8282):1150-2.
4 - Carmen S. Neonatal hypoglycemia in response to maternal glucose infusion before delivery. J Obstet Gynecol Neonatal Nurs. 1986 Jul-Aug;15(4):319-23
5 - Grylack LJ, Chu SS, Scanlon JW. Use of intravenous fluids before cesarean section: effects on perinatal glucose, insulin, and sodium homeostasis. Obstet Gynecol. 1984 May;63(5):654-8.
6 - Kenepp NB, Shelley WC, Kumar S, Gutsche BB, Gabbe S, Delivoria-Papadopoulos M. Effects of newborn of hydration with glucose in patients undergoing caesarean section with regional anaesthesia. Lancet. 1980 Mar 22;1(8169):645.
7 - Singhi S, Sharma S. Neonatal hypoglycemia following maternal glucose infusion prior to delivery. Indian J Pediatr. 1991 Jan-Feb;58(1):43-9.
8 - Odent M. Laboring women are not marathon runners. Midwiferytoday
9 - Malek A, Blann E, Mattison DR. Human placental transport of oxytocin. J Matern Fetal Med. 1996 Sep-Oct;5(5):245-55.
10 - Saunders NR, Habgood MD, Dziegielewska KM. Barrier mechanisms in the brain, II. immature brain. Clin. Exp. Pharmacol. Physiol. 1999;26(2):85–91
11 - Noseworthy M, Bray T. Effect of oxidative stress on brain damage detected by MRI and in vivo 31P-NMR. Free Rad. Biol. Med. 1998;24:942–951
12 - Agnagnostakis D, Messaritakis J, Damianos D, Mandyla H. Blood-brain barrier permeability in healthy infected and stressed neonates. J. Pediatr. 1992;121:291–294.
13 - Noseworthy M, Bray T. Zinc deficiency execerbates loss in blood–brain barrier integrity induced by hyperoxia measured by dynamic MRI. PSEBM. 2000;231:175–182.
14 - Schneid-Kofman N, Silberstein T, Saphier O, Shai I, Tavor D, Burg A. Labor augmentation with oxytocin decreases glutathione level. Obstet Gynecol Int. 2009;2009:807659. Epub 2009 Apr 16.
15 - Robinson C, Schumann R, Zhang P, Young R. Oxytocin-induced desensitization of the oxytocin receptor. Am. J. Obstet. Gynaecol. 2003;188:497–502.
16- Gimpl G, Fahrenholz F. The oxytocin receptor system: structure, function and regulation. Physiol. Rev. 2001;81:642–643.
17 - Phaneuf S, Rodríguez Liñares B, TambyRaja RL, MacKenzie IZ, López Bernal A. Loss of myometrial oxytocin receptors during oxytocin-induced and oxytocin-augmented labour. J Reprod Fertil. 2000 Sep;120(1):91-7.
18 - Phaneuf S, Asboth G, Carrasco M, Lineares B, Kimura T, Harris A, et al. Desensitization of oxytocin receptors in human myometrium. Hum. Reprod. Update. 1998;4:625–633.
19 - Odent M. The Scientification of Love. Free Association Books. London 1999.
20 - Modahl C, Green L, et al. Plasma oxytocin levels in autistic children. Biol Psychiatry 1998; 43 (4): 270-7.
21- Green L, Fein D, et al. Oxytocin and autistic disorder: alterations in peptides forms. Biol Psychiatry 2001; 50 (8): 609-13.
22 - Demitrack MA, Lesem MD, Listwak SJ, et al. CSF oxytocin in anorexia.nervosa and bulimia nervosa: clinical and pathophysiologic considerations. Am J Psychiatry 1990 Jul;147(7):882-86
23 – Odent. Autism and anorexia nervosa: two facets of the same disease? Med Hypotheses 2010. doi:10.1016/j.mehy.2010.01.039
24 - Baker RW. Diethylhexyl phthalate as a factor in blood transfusion and haemodialysis. Toxicology.1978 Apr;9(4):319-29.
25 - Cho SC, Bhang SY, Hong YC, et al.. Relationship Between Environmental Phthalate Exposure and the Intelligence of School-Aged Children. Environ Health Perspect. 2010 Mar 1. [Epub ahead of print]
26 - Saillenfait AM, Payan JP, Fabry JP, et al. Assessment of the developmental toxicity, metabolism, and placental transfer of Di-n-butyl phthalate administered to pregnant rats. Toxicol Sci. 1998 Oct;45(2):212-24.
27- Kihlström I, Placental transfer of diethylhexyl phthalate in the guinea-pig placenta perfused in situ. Acta Pharmacol Toxicol (Copenh) 1983 Jul;53(1):23-7.
28 - Mose T, Knudsen LE, Hedegaard M, et al. Transplacental Transfer of Monomethyl Phthalate and Mono(2-ethylhexyl) Phthalate in a Human Placenta Perfusion System.0. International Journal of Toxicology 2007; 26(3): 221-229.

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BETWEEN THE MID-ATLANTIC AND THE MID-PACIFIC CONFERENCES
The Mid-Atlantic Conference on Birth and Primal Health Research – which attracted 1250 participants from 39 countries – has been a successful rehearsal before the Mid-Pacific Conference.
The Mid-Pacific Conference will occur on October 26-28, 2012, in Honolulu. The venue will be the prestigious Hawaii Convention Center, as the meeting point between Western and Eastern cultures.
Once more, the main objective of the conference will be to phrase new questions after presenting an overview of technical and scientific advances that will influence the history of childbirth. As in Las Palmas, the participation of Pr. Michael Stark, the “father” of the new simplified technique of cesarean, will symbolize technical advances, while the participation of Pr Kerstin Uvnas-Moberg, as an expert in behavioural effects of oxytocin, will symbolize scientific advances. The need to think globally will be emphasized by the participation of Dr Mario Merialdi, coordinator for maternal and perinatal health at WHO.
The Mid-Pacific conference will be characterized by the emergence of new important themes, such as the transgenerational effects of early experiences (during the “primal period”), the expected importance of economical factors in the evolution of medicine in general and obstetrics in particular, and also by the great diversity of renewed practical topics presented during the thirty concurrent sessions and through posters.
During these three days, inspired by our logo and surrounded by the foams of the oceanic waves, we’ll be in an ideal place to dream of and to work for the Rebirth of the Goddess of Love.
Aloha means Love!
Michel Odent and Heloisa Lessa

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