Guest guest Posted August 9, 2011 Report Share Posted August 9, 2011 From: Owens <lwo@...> Sultana, I studied this area quite a few years ago, but I think the two posts I wrote back then might answer your question. >Date: Wed, 21 May 1997 11:36:03 +0000 >SJU Autism and Developmental Disablities >List <AUTISM@...> >From: Walter & Owens <lwo@...> >Subject: Re: Pitocin causing autism? > >Listmates, > >I had a few thoughts on the pitocin issue related to my recent studies of >CCK. Thanks Kay, for posting the article you saw. I feel that the fact >that pitocin was needed to complete these pregnancies may speak of some >issues of biochemistry going on in mom that made her natural oxytocin >ineffective (pitocin is a manufactured oxytocin), and that those same >issues of biochemistry could have been an influence on development in >utero that may have nothing to do with direct effects of pitocin use. > >I mentioned in an earlier post that it is possible that opiate excess and >sulfation problems could alter the body's use or manufacture of CCK. CCK >administered outside the brain can produce both the stimulation of >corticotrophin releasing hormone and oxytocin secretion from both the >pituitary and the hypothalamus. This is believed to happen through the >activation of the vagal nerve which has two brands of CCK receptors, the >type typically found in the brain, and the type typically found in the >gut, but the ones involved in oxytocin seem to be the type receptors more >common to the gut. They know that sulfated CCK8 will give rise to >increases in Fos protein in both the brain stem and in nerves known to >encourage oxytocin production in the hypothalamus. Involved in this >process is the appearance of a chemical called C-fos which is what they >call an immediate early gene. Interestingly, unsulfated CCK8 will engage >the right CCK receptors, but is incapable of stimulating this early gene >expression that is necessary to produce oxytocin. It might just get in >the way and I suppose could make pitocin less effective. > >So, what does it mean? I think it may mean that if mother has poor >sulfation, she may have trouble in labor, because her body may be >producing adequate CCK to encourage the production of oxytocin, but it >might not work well if unsulfated CCK ends up engaging and blocking the >receptors needed to encourage the production of oxytocin. It just might >be very inefficient and might perhaps lead to stalled or slow labors. > >Since CCK has some poorly understood functions in the brain that happen >primarily after the brain has already produced most of its neurons towards >the end of the second trimester, when the brain becomes more active in >making connections, then it may be that if mom has opiate excess problems >and sulfation problems, it may have some influence on how the brain >develops. Two events that are not directly related could occur together >because they have a common factor causing each event. The areas that show >the most response to peripheral CCK are the hypothalamus, the amygdala, >and the brainstem. We've heard of them before. > >Now, just for comparison, here is a snapshot of my experience with >pitocin, and I DEFINITELY have had opiate excess problems, and have been >happily off wheat and milk for over twenty months. My second daughter is >not autistic, but did have developmental delays which have resolved since >she quit eating wheat and milk. > >Both of my girls were delivered with pitocin. My first daughter had >already died in utero of unknown cause, but she was just at that magic age >when things in the brain's development switch over to new >priorities. After my cervix had ripened somewhat my doctor gave me a >prostaglandin cream that didn't work, and then he used pitocin. My blood >pressure dropped suddenly, but quickly recovered, and the rest of the >delivery was very straightforward. > >When Grace was born, I had lots of slow or pre-labor all day, but I was >scheduled for induction the next morning, so at 2:00 a.m. we got to the >hospital. Sometime that morning when labor was quite active, the nurse >turned me on my side causing great pain, and my labor stopped cold. That >is when they used pitocin, and Grace came I'd guess six or seven hours >later (sorry, don't remember exactly the timing--I was too busy being >angry with that nurse!) > >Another interesting angle is that I had great trouble getting my milk to >come in and required the help of a lactation consultant. Another function >of oxytocin is acting on the mammary glands to stimulate the production of >milk. > >Hope this helps! > > > >PS. , are you listening? This article had the following >interesting quote: > >It is relevant that CCKA receptors have been located in the area postrema >(Hill et al.m, 1987) an area devoid of the blood brain barrier, and it is >likely that CCK-8S is acting primarily on receptors in this area to >stimulate IEG expression in the CNS. > >I haven't studied neurobiology yet, but I have a textbook lying around, >and this postrema looks like it might be located at the back where the >head meets the neck. My migraines form a lump right there. Do you think >that could be related, or do I have my geography right? > >PPS. Does anyone know if pitocin is already sulfated which is used for >labor or for the social phobia business mentioned in the Newsweek article? > > >Reference: Day HEW; McKnight AT; Poat JA; J. (1994) Evidence >that Cholecystokinin Induces Immediate Early Gene Expression in the >Brainstem, Hypothalamus and Amygdala of the Rat by a CCKA Receptor >mechanism. Neuropharmacology, 33:6, pp. 719-727. ========================= Dana, I heard some research at the NIH's special meeting this fall on the role of cell signalling in autism that confirms what you are saying. They said that those with autism do tend to focus in on the mouth instead of the eyes. I think those of us who have a hard time relating to that difference could spend some useful time trying hard to look at mouths instead of eyes, and see how uncomfortable we become! At this meeting, some studies were presented where they talked about the way that the hormone oxytocin (low in autism) changes the parts of the brain that are used to understand and analyze a sensory signal that usually gives social information. A different group explored this by creating an animal missing the oxytocin gene, and watched the animal's response to various social situations. They did the same trial after giving the animal oxytocin,. The oxytocin normalized the way the animal used his brain to process social signals and normalized his behavior. Oxytocin, which is the hormone of labor (pitocin) and milk production, is also called " the social hormone " , when you describe its more everyday job. The last article below suggests even another " talent " of this hormone. Oxytocin is a neuropeptide that is made by a certain type of neuron after it has been signalled by sulfated cholecystokinin, another neuropeptide. The sulfation problems common to autism may weaken that signal from cholecystokinin considerably, which may explain the decreased levels of oxytocin that have been found in autism. Of course, a rat, when he is considering social information, gets most of his input from smell, so those are the regions of his brain that " light up " . The areas of the brain in humans sensitive to this hormone are very different from the rat, but quite relevant. The abstracts from these talks are at my office, so I can't get more specific than that tonight, but I thought it might be interesting to know that there may be a biochemical explanation for why you prefer to look at the mouth and are uncomfortable looking at the eyes. I've put some older studies below that talk about this issue in one way or another. I think the important message is this: the knockout studies showed that the difference in this social information processing did not come from abnormal connections, or abnormal brain structure, or abnormal experience, but instead came from abnormal biochemistry. That conclusion was drawn since the differences in brain processing went away completely when the hormonal deficit was corrected artificially. Again, this was research presented which is in progress, and not yet published. By the way, an appetite for salt can also be caused by oxytocin deficiency. PS. Both my daughter with SI and I have sulfation problems. My labor for her wimped out and I needed pitocin(oxytocin), but after that my milk had a very difficult time coming in, but eventually, in a couple of weeks, I caught up, and my milk was fine. The difficult time at first probably happened because I was having a hard time making oxytocin since labor probably exhausted my sulfate chemistry. A history of needing pitocin for labor has been noticed so much in women whose children end up developing autism that it has been suggested that pitocin might CAUSE autism. I think that is VERY unlikely, but sulfation problems in mom may lead to sulfate deficits in her newborn child. Couple that with infant vaccination, and a series of ear infections or whatever, and it becomes very hard for the sulfate chemistry to " catch up " . 1: J Neurosci 2001 Oct 15;21(20):8278-85 Oxytocin in the medial amygdala is essential for social recognition in the mouse. Ferguson JN, Aldag JM, Insel TR, Young LJ. Center for Behavioral Neuroscience and the Department of Psychiatry and Behavioral Sciences, Emory University, Atlanta, Georgia 30322, USA. Oxytocin (OT) knock-out mice fail to recognize familiar conspecifics after repeated social exposures, despite normal olfactory and spatial learning abilities. OT treatment fully restores social recognition. Here we demonstrate that OT acts in the medial amygdala during the initial exposure to facilitate social recognition. OT given before, but not after, the initial encounter restores social recognition in OT knock-out mice. Using c-Fos immunoreactivity (Fos-IR) as a marker of neuronal activation in this initial encounter, we found similar neuronal activation in the wild-type (WT) and OT knock-out mouse in olfactory bulbs, piriform cortex, cortical amygdala, and the lateral septum. Wild-type, but not OT knock-out mice exhibited an induction of Fos-IR in the medial amygdala. Projections sites of the medial amygdala also failed to show a Fos-IR induction in the OT knock-out mice. OT knock-out, but not WT, mice showed dramatic increases in Fos-IR in the somatosensory cortex and the hippocampus, suggesting alternative processing of social cues in these animals. With site-specific injections of OT and an OT antagonist, we demonstrate that OT receptor activation in the medial amygdala is both necessary and sufficient for social recognition in the mouse. PMID: 11588199 [PubMed - indexed for MEDLINE] 1: Brain 2001 Oct;124(Pt 10):2059-73 Face processing occurs outside the fusiform 'face area' in autism: evidence from functional MRI. Pierce K, Muller RA, Ambrose J, G, Courchesne E. Department of Neurosciences, University of California, San Diego, USA. Processing the human face is at the focal point of most social interactions, yet this simple perceptual task is difficult for individuals with autism, a population that spends limited amounts of time engaged in face-to-face eye contact or social interactions in general. Thus, the study of face processing in autism is not only important because it may be integral to understanding the social deficits of this disorder, but also, because it provides a unique opportunity to study experiential factors related to the functional specialization of normal face processing. In short, autism may be one of the only disorders where affected individuals spend reduced amounts of time engaged in face processing from birth. Using functional MRI, haemodynamic responses during a face perception task were compared between adults with autism and normal control subjects. Four regions of interest (ROIs), the fusiform gyrus (FG), inferior temporal gyrus, middle temporal gyrus and amygdala were manually traced on non-spatially normalized images and the percentage ROI active was calculated for each subject. Analyses in Talairach space were also performed. Overall results revealed either abnormally weak or no activation in FG in autistic patients, as well as significantly reduced activation in the inferior occipital gyrus, superior temporal sulcus and amygdala. Anatomical abnormalities, in contrast, were present only in the amygdala in autistic patients, whose mean volume was significantly reduced as compared with normals. Reaction time and accuracy measures were not different between groups. Thus, while autistic subjects could perform the face perception task, none of the regions supporting face processing in normals were found to be significantly active in the autistic subjects. Instead, in every autistic patient, faces maximally activated aberrant and individual-specific neural sites (e.g. frontal cortex, primary visual cortex, etc.), which was in contrast to the 100% consistency of maximal activation within the traditional fusiform face area (FFA) for every normal subject. It appears that, as compared with normal individuals, autistic individuals 'see' faces utilizing different neural systems, with each patient doing so via a unique neural circuitry. Such a pattern of individual-specific, scattered activation seen in autistic patients in contrast to the highly consistent FG activation seen in normals, suggests that experiential factors do indeed play a role in the normal development of the FFA. [warning: the " interpretation " of the data might not be right!] PMID: 11571222 [PubMed - indexed for MEDLINE] 2: J Cogn Neurosci 2001 Feb 15;13(2):232-40 Abnormal processing of social information from faces in autism. Adolphs R, Sears L, Piven J. Department of Neurology, University of Iowa Hospitals and Clinics, University of Iowa, Iowa City, 52242, USA. ralph-adolphs@... Autism has been thought to be characterized, in part, by dysfunction in emotional and social cognition, but the pathology of the underlying processes and their neural substrates remain poorly understood. Several studies have hypothesized that abnormal amygdala function may account for some of the impairments seen in autism, specifically, impaired recognition of socially relevant information from faces. We explored this issue in eight high-functioning subjects with autism in four experiments that assessed recognition of emotional and social information, primarily from faces. All tasks used were identical to those previously used in studies of subjects with bilateral amygdala damage, permitting direct comparisons. All subjects with autism made abnormal social judgments regarding the trustworthiness of faces; however, all were able to make normal social judgments from lexical stimuli, and all had a normal ability to perceptually discriminate the stimuli. Overall, these data from subjects with autism show some parallels to those from neurological subjects with focal amygdala damage. We suggest that amygdala dysfunction in autism might contribute to an impaired ability to link visual perception of socially relevant stimuli with retrieval of social knowledge and with elicitation of social behavior. PMID: 11244548 [PubMed - indexed for MEDLINE] 2: Exp Neurol 2001 Oct;171(2):323-8 Enhanced salt intake in oxytocin deficient mice. Puryear R, Rigatto KV, Amico JA, M. Department of Pharmacology and Toxicology, State University School of Medicine, Dayton, Ohio, 45401 The maternal roles of oxytocin (OT) are well known, but recent work suggests that OT is also a vital component in fluid balance regulation. To explore the role of OT in salt/volume regulation, we studied NaCl intake in a genetically modified mouse strain lacking OT. Using male control and OT knockout mice (OTKO), we determined the circadian pattern of salt and water intake under need-free conditions. For the study of intake, a two-bottle choice system was used to provide access to water and 2% NaCl with computerized monitoring of licking activity. Salt licking activity (licks/24 h) for controls was 59 +/- 22 vs 380 +/- 105 in OTKO (P < 0.05). The volume of salt consumed (ml/24 h) was 0.4 +/- 0.1 in controls vs 1.8 +/- 0.4 in OTKO (P < 0.01). There was no statistical difference in the consumption of water between the groups. However, the initiation of water intake was shifted, with an advancement of almost 3 h in OTKO (P < 0.01). Differences in the timing of salt intake could not be determined due to the low volume of salt consumed by controls. Taken together, these data show that removal of OT amplifies the salt-seeking behavior associated with normal daily fluid fluctuations. The fact that OTKO voluntarily consume a normally aversive salt solution further implies that OT is a powerful regulator of circadian salt appetite. Copyright 2001 Academic Press. PMID: 11573985 [PubMed - in process] 4: Nat Genet 2000 Jul;25(3):284-8 Social amnesia in mice lacking the oxytocin gene. Ferguson JN, Young LJ, Hearn EF, Matzuk MM, Insel TR, Winslow JT. The Center for Behavioural Neuroscience, Department of Psychiatry and Behavioural Sciences and Yerkes Regional Primate Research Center, Emory University School of Medicine, Atlanta, Georgia, USA. The development of social familiarity in rodents depends predominantly on olfactory cues and can critically influence reproductive success. Researchers have operationally defined this memory by a reliable decrease in olfactory investigation in repeated or prolonged encounters with a conspecific. Brain oxytocin (OT) and vasopressin (AVP) seem to modulate a range of social behaviour from parental care to mate guarding. Pharmacological studies indicate that AVP administration may enhance social memory, whereas OT administration may either inhibit or facilitate social memory depending on dose, route or paradigm. We found that male mice mutant for the oxytocin gene (Oxt-/-) failed to develop social memory, whereas wild-type (Oxt+/+) mice showed intact social memory. Measurement of both olfactory foraging and olfactory habituation tasks indicated that olfactory detection of non-social stimuli is intact in Oxt-/- mice. Spatial memory and behavioural inhibition measured in a water-maze, Y-maze, or habituation of an acoustic startle also seemed intact. Treatment with OT but not AVP rescued social memory in Oxt-/- mice, and treatment with an OT antagonist produced a social amnesia-like effect in Oxt+/+ mice. Our data indicate that OT is necessary for the normal development of social memory in mice and support the hypothesis that social memory has a neural basis distinct from other forms of memory. PMID: 10888874 [PubMed - indexed for MEDLINE] 5: Adv Exp Med Biol 1998;449:231-40 Targeted reduction of oxytocin expression provides insights into its physiological roles. Young WS 3rd, Shepard E, DeVries AC, Zimmer A, LaMarca ME, Ginns EI, Amico J, RJ, Hennighausen L, Wagner KU. Laboratory of Cellular and Molecular Regulation, National Institute of Mental Health, Bethesda, land, USA. scott@... Oxytocin is a nonapeptide hormone that participates in the regulation of parturition and lactation. It has also been implicated in various behaviors, such as mating and maternal, and memory. To investigate whether or not oxytocin (OT) is essential for any of these functions, we eliminated, by homologous recombination, most of the first intron and the last two exons of the OT gene in mice. Those exons encode the neurophysin portion of the oxytocin preprohormone which is hypothesized to help in the packaging and transport of OT. The homozygous mutant mice have no detectable neurophysin or processed oxytocin in the paraventricular nucleus, supraoptic nucleus or posterior pituitary. Interestingly, homozygous mutant males and females are fertile and the homozygous mutant females are able to deliver their litters. However, the pups do not successfully suckle and die within 24 hours without milk in their stomachs. OT injection into the dams or rescue with the rat OT gene restores the milk ejection in response to suckling. OT is also needed for post-partum alveolar proliferation. These results indicate an absolute requirement for oxytocin for successful milk ejection, but not for mating, parturition and milk production, in mice. Furthermore, homozygous mutant mice show reduced aggression in some tests. PMID: 10026810 [PubMed - indexed for MEDLINE] 6: Horm Behav 1997 Jun;31(3):221-31 Gene targeting approaches to neuroendocrinology: oxytocin, maternal behavior, and affiliation. Young LJ, Winslow JT, Wang Z, Gingrich B, Guo Q, Matzuk MM, Insel TR. Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia 30322, USA. lyoun03@... Transgenic technology affords exciting new opportunities in the field of behavioral neuroendocrinology. We have extended our research into the behavioral function of oxytocin in maternal and social behavior using two transgenic approaches: (i) targeted deletion of the oxytocin gene in mice and (ii) augmented oxytocin receptor expression in the brain. Mice genetically deficient in oxytocin can mate, give birth, and display normal maternal behavior; however, milk ejection and certain aspects of social behavior are affected. Comparative studies of oxytocin receptors have led to the observation that species differences in social organization are associated with differences in receptor distribution. Specifically, monogamous prairie voles and nonmonogamous, asocial montane voles exhibit different patterns of OT receptor expression in the brain. Transgenic mice have been created with a reporter gene driven by the prairie vole oxytocin receptor gene promoter. Analysis of the expression pattern suggests that it should be possible to manipulate receptor expression in the vole brain in order to examine the effects of receptor distribution on behavior. Publication Types: Review Review, Tutorial PMID: 9213136 [PubMed - indexed for MEDLINE] 1: Biol Psychiatry 1998 Feb 15;43(4):270-7 Plasma oxytocin levels in autistic children. Modahl C, Green L, Fein D, M, Waterhouse L, Feinstein C, Levin H. Boston University School of Medicine, Massachusetts, USA. BACKGROUND: Social impairments are central to the syndrome of autism. The neuropeptide oxytocin (OT) has been implicated in the regulation of social behavior in animals but has not yet been examined in autistic subjects. METHODS: To determine whether autistic children have abnormalities in OT, midday plasma samples from 29 autistic and 30 age-matched normal children, all prepubertal, were analyzed by radioimmunoassay for levels of OT. RESULTS: Despite individual variability and overlapping group distributions, the autistic group had significantly lower plasma OT levels than the normal group. OT increased with age in the normal but not the autistic children. Elevated OT was associated with higher scores on social and developmental measures for the normal children, but was associated with lower scores for the autistic children. These relationships were strongest in a subset of autistic children identified as aloof. CONCLUSIONS: Although making inferences to central OT functioning from peripheral measurement is difficult, the data suggest that OT abnormalities may exist in autism, and that more direct investigation of central nervous system OT function is warranted. Publication Types: Clinical Trial PMID: 9513736 [PubMed - indexed for MEDLINE] 3: Ann N Y Acad Sci 1997 Jan 15;807:501-3 Neurohumoral brain dynamics of social group formation. Implications for autism. Freeman WJ. Department of Molecular & Cell Biology, University of California at Berkeley 94720, USA. Brains are dynamic systems in which learning tends towards isolation by increasing specialization of cognitive skills. Induction of social skills for cooperative behavior requires " unlearning " in social contexts. A hypothesis is proposed by which oxytocin and related neuropeptides play a key role in meltdown of prior learning in preparation for new learning. This has implications for clinical management of disorders of the socialization processes in children. PMID: 9071382 [PubMed - indexed for MEDLINE] At 01:51 AM 11/30/2001 +0000, you wrote: > > > Do any of your kids have problems looking at people > > in the eye? .... >I am AS...Eye contact - when a person is speaking, I look at that person's >mouth. Now I have learned about eye contact, so most times I >compromise and try to look at the nose. Looking directly into the eyes >is very uncomfortable for me, sometimes even makes my skin crawl. Can someone help me understand the relationship between pitocin and oxytocin? I have been reading, and have heard at A1, that nasal oxytocin is beginning to show positive results in autistic kids by alleviating social impairments. Yet, I have also read that pitocin should be avoided during induction/delivery as there are so many induced/pitocin births that resulted in children affected by autism. ????? Also, if anyone has had experience with oxytocin, could you share? I am wondering if the " increased trust " the treatment brings out, while allowing kids to be more socially comfortable, might also make them frighteningly vulnerable. Thanks. Sheri Nakken, R.N., MA, Hahnemannian Homeopath Vaccination Information & Choice Network, Washington State, USA Vaccines - http://www.nccn.net/~wwithin/vaccine.htm or http://www.wellwithin1.com/vaccine.htm Vaccine Dangers, Childhood Disease Classes & Homeopathy Online/email courses - next classes start October 28 & 29 http://www.wellwithin1.com/vaccineclass.htm or http://www.wellwithin1.com/homeo.htm Quote Link to comment Share on other sites More sharing options...
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