Oxytocin

Post Reply New Topic

It is characterized by a distinctive, "elvish" facial appearance, along with a low nasal bridge; an unusually cheerful demeanor and ease with strangers, coupled with unpredictably occurring negative outbursts; mental retardation coupled with unusual (for persons who are diagnosed as mentally ret*d) language skills; a love for music; and cardiovascular problems, such as supravalvular aortic stenosis and transient hypercalcaemia. Williams syndrome shares some features with autism (such as difficulty understanding the state of mind of conversational partners[1]) and Fetal alcohol syndrome (e.g., certain facial features, possible mental retardation, and negative potential outbursts),[2] although persons with Williams generally possess very good social skills, such that this condition is sometimes called "cocktail-party syndrome". Temple Grandin, author of Thinking in Pictures, has claimed that the brain abnormalities of Williams syndrome are the opposite of those of autism.[3] There also appears to be a higher prevalence of left-handedness and left-eye dominance in those with Williams,[4] and cases of absolute pitch appear to be significantly higher amongst those with the condition.[5]

Another symptom of Williams syndrome is lack of depth perception and an inability to visualize how different parts assemble into larger objects (in assembling jigsaw puzzles, for example). This problem is caused by a defect in the brain that creates a sparsity of tissue in the visual systems of the brain. A team of researchers at the National Institute of Mental Health used functional magnetic-resonance imaging (fMRI) to watch the blood flow of the brains of test subjects while they were performing two tasks involving spatial relations. People with Williams Syndrome showed weaker activity in the section of the brain associated with spatial relations. Scans of brain anatomy of test subjects with Williams indicated a deficit of brain tissue in an area of the same section of the brain mentioned above. This deficit partly blocks transmission of visual information to the spatial-relations region of the brain. In the test, all participants of the study measured in the average intelligence range, to remove the possibility that the retardation aspect of Williams syndrome would have an effect on the visual systems of the tested individuals.

Damasio also points to some pretty interesting hypotheses about well-known pathologies, including autism and William's syndrome. The first is characterized by a relative lack of social bonding and trust; William's syndrome patients "approach strangers fearlessly and indiscriminately." He raises the question of whether this level of trust may come from excessive oxytocin release. One may alternatively ask whether it comes from an alteration in the underlying neural structures affected by oxytocin, but whether it is the first of the second, it seems likely that the trust-related mechanisms of the brain require both a structural and neurochemical input

1: J Control Release. 2007 Apr 2;118(2):185-8. Epub 2006 Dec 9.
Links
Topical iodine facilitates transdermal delivery of insulin.
Sintov AC, Wormser U.

Department of Clinical Pharmacology and School of Pharmacy, Ben-Gurion University of the Negev, Beer Sheva 84105, Israel.

Transdermal delivery of insulin is a non-invasive alternative to the subcutaneous injection of insulin in diabetic patients. It has been found that skin pretreatment with iodine followed by a dermal application of insulin results in reduced glucose and elevated hormone levels in the plasma. Topical iodine protects the dermally applied insulin presumably by inactivation of endogenous sulfhydryls such as glutathione and gamma glutamylcysteine which can reduce the disulfide bonds of the hormone. Thus, the effect of iodine is mediated by retaining the potency of the hormone during its penetration via the skin into the circulation. The proposed procedure might be applicable for additional disulfide-containing peptides such as calcitonine, somatostatin, oxytocin/vasopressin and their analogs.

PMID: 17270303 [PubMed - in process]

SIDE EFFECTS: May cause some nasal irritation, runny nose, or tearing of the eyes.

Where can u get this stuff? And could u possibly get prescribed this as a medication for being an aspie??

i thought oxycontins were used to treat cancer and aids

6-01-07 12:22
Taking dose 13 & 14

Day 2
6-02-07 00:06
Taking dose 1 & 2

6-02-07 01:42
Taking dose 3 & 4

6-02-07 05:18
I napped from 2am-5am and did not walk my dogs. This maybe a result of
for geting my prozac dose. Anyway taking dose 5 & 6.

6-02-07 06:35
Maybe unrelated but I have been eating lots of high fat/protein food

the last 2
days.

6-02-07 07:35
Taking dose 7 & 8.

6-02-07 10:05
Taking dose 9 & 10.

6-02-07 12:45
Taking dose 11 & 12

6-02-07 14:10
Taking dose 13 & 14

6-03-07 3:03
Taking dose 1 & 2 woke up about 2 AM about to walk dogs.

6-03-07 5:17
Taking dose 3 & 4 Back from walk.

6-03-07 5:59
Taking dose 5& 6 might try larer amounts now till negative effects are

noted.

6-03-07 6:36
Taking dose 7 & 8.

6-03-07 7:16
Taking dose 9 & 10.

6-03-07 12:28
Napped many hours Taking dose 11 & 12

6-03-07 14:19
Taking dose 13,14,15,16

Trust-Building Hormone Short-Circuits Fear In Humans

A brain chemical recently found to boost trust appears to work by reducing activity and weakening connections in fear-processing circuitry, a brain imaging study at the National Institutes of Health's (NIH) National Institute of Mental Health (NIMH) has discovered. Scans of the hormone oxytocin's effect on human brain function reveal that it quells the brain's fear hub, the amygdala, and its brainstem relay stations in response to fearful stimuli. The work at NIMH and a collaborating site in Germany suggests new approaches to treating diseases thought to involve amygdala dysfunction and social fear, such as social phobia, autism, and possibly schizophrenia, report Andreas Meyer-Lindenberg, M.D., Ph.D., NIMH Genes Cognition and Psychosis Program, and colleagues, in the December 7, 2005 issue of the Journal of Neuroscience.

"Studies in animals, pioneered by now NIMH director Dr. Thomas Insel, have shown that oxytocin plays a key role in complex emotional and social behaviors, such as attachment, social recognition and aggression," noted NIH Director Elias Zerhouni, M.D. "Now, for the first time, we can literally see these same mechanisms at work in the human brain."

"The observed changes in the amygdala are exciting as they suggest that a long-acting analogue of oxytocin could have therapeutic value in disorders characterized by social avoidance," added Insel.

Inspired by Swiss scientists who last summer reported1 that oxytocin increased trust in humans, Meyer-Lindenberg and colleagues quickly mounted a brain imaging study that would explore how this works at the level of brain circuitry. British researchers had earlier linked increased amygdala activity to decreased trustworthiness2. Having just discovered decreased amygdala activity in response to social stimuli in people with a rare genetic brain disorder that rendered them overly trusting of others, Meyer-Lindenberg hypothesized that oxytocin boosts trust by suppressing the amygdala and its fear-processing networks.

To test this idea, he asked 15 healthy men to sniff oxytocin or a placebo prior to undergoing a functional magnetic resonance imaging (fMRI) scan, which reveals what parts of the brain that are activated by particular activities. While in the scanner, the men performed tasks known to activate the amygdala — matching angry or fearful faces and threatening scenes.

As expected, the threatening pictures triggered strong activation of the amygdala during the placebo scan, but markedly less activity following oxytocin. The difference was especially pronounced in response to threatening faces, suggesting a pivotal role for oxytocin in regulating social fear. In addition, oxytocin dampened the amygdala's communication with sites in the upper brainstem that telegraph the fear response. The results mirrored findings in rats 3, reported earlier this year by European scientists.

"Because increased amygdala activation has been associated with social fear in social phobia, genetic risk for anxiety and depression, and possibly with social fear in autism assessed during faces processing, this dual mode of action of oxytocin in humans suggests a potentially powerful treatment approach toward socially relevant fear," suggest the researchers.

People with autism characteristically avert their gaze from faces. A fMRI study4 reported earlier this year by NIMH grantee Richard Davidson, Ph.D., University of Wisconsin, and colleagues, found over-activation of the amygdala in people with autism when they were looking at faces. Meyer-Lindenberg said future studies may test oxytocin as a treatment for such social anxiety symptoms in children with autism.

"Future research may also examine how oxytocin affects the amygdala in women, the mode of action of related hormones such as vasopressin, and how genetic variants in these hormones and their receptors affect brain function," he added.

Also participating in the research were: Peter Kirsch, Christin Esslinger, Daniela Mier, Stefanie Lis, Harald Gruppe, Bernd Gallhofer, Justus-Liebig University, Giessen, Germany; Qiang Chen, Sarina Siddhanti, Venkata Mattay, NIMH Genes Cognition and Psychosis Program.

Functional magnetic resonance imaging data (red) superimposed on structural MRI scans. Frightful faces triggered a dramatic reduction in amygdala activity in subjects who had sniffed oxytocin, suggesting that oxytocin mediates social fear and trust via the amygdala and related circuitry.

Source: NIMH Genes, Cognition and Psychosis Program
Kosfeld M, Heinrichs M, Zak PJ, Fischbacher U, Fehr E. Oxytocin increases trust in humans. Nature. 2005 Jun 2;435(7042):673-6.
Winston JS, Strange BA, O'Doherty J, Dolan RJ. Automatic and intentional brain responses during evaluation of trustworthiness of faces. Nat Neurosci. 2002 Mar;5(3):277-83.
Huber D, Veinante P, Stoop R. Vasopressin and oxytocin excite distinct neuronal populations in the central amygdala. Science. 2005 Apr 8;308(5719):245-8.
Dalton KM, Nacewicz BM, Johnstone T, Schaefer HS, Gernsbacher MA, Goldsmith HH, Alexander AL, Davidson RJ. Gaze fixation and the neural circuitry of face processing in autism. Nat Neurosci. 2005 Apr;8(4):519-26. Epub 2005 Mar 6.

Intranasal Oxytocin in the Treatment of Autism

This study is currently recruiting patients.
Verified by Mount Sinai School of Medicine June 2007Sponsored by: Mount Sinai School of Medicine
Information provided by: Mount Sinai School of Medicine
ClinicalTrials.gov Identifier: NCT00490802



Purpose
The purpose of this study is to learn whether or not the drug called Oxytocin is helpful in improving mood and social functioning in adults with autism. Condition Intervention Phase
Autism Drug: Oxytocin Phase II


MedlinePlus related topics: Autism

Study Type: Interventional
Study Design: Treatment, Randomized, Double-Blind, Placebo Control, Parallel Assignment, Safety/Efficacy Study
Number of arms in study: 2

Official Title: Intranasal Oxytocin in the Treatment of Autism
Further study details as provided by Mount Sinai School of Medicine:
Primary Outcome Measures:
Clinical Global Impressions Scale (CGI) [Time Frame: Baseline visit, week 2, 4, and 6 visits]
Diagnostic Analysis of Nonverbal Accuracy, Adult Paralanguage Test (DANVA2-AP) [Time Frame: Baseline and week 6 visits]
Repetitive Behavior Scale (RBS) [Time Frame: Baseline visit, week 2, 4, and 6 visits]
Event Contingent Reporting [Time Frame: Baseline, week 2 and 6 visits]

Secondary Outcome Measures:
Yale-Brown Obsessive-Compulsive Scale (YBOCS) [Time Frame: Baseline visit, week 2, 4, and 6 visits]
Social Responsivity Scale (SRS) [Time Frame: Baseline visit, week 2, 4, and 6 visits]

Study start: June 2006

Definition: Extended description of the protocol, including information not already contained in other fields, such as comparison(s) studied.

Autism is a developmental disorder characterized by abnormalities in speech and communication, impaired social functioning, and repetitive behaviors and restricted interests (American Psychiatric Association, 2000). A number of researchers have suggested that the neuropeptide oxytocin may be implicated in the etiology of autism (Hollander et al., 2003; Insel et al., 1999; Lim et al., 2005; McCarthy & Altemus, 1997; Modahl et al., 1992; Waterhouse et al., 1996).

Given the likely possibility of dysregulated oxytocin in autism, the goal of this pilot study is to investigate the long-term therapeutic effects of oxytocin in the treatment of autism. One practical issue with oxytocin is that it does not exist in a pill form. Only the intravenous form is available in the US and this form may or may not pass the blood-brain barrier. In addition, IV oxytocin is not practical for treatment studies. One alternative is intranasal oxytocin; this form of administration is known to pass the blood-brain barrier, and it is easy for participants to self-administer. Although not available in the US, we are in the process of receiving an IND exemption for its use and can import it from Europe.

Thus, this pilot investigation will explore daily intranasal oxytocin in the treatment of autism. Also, there are very few, if any, outcome measures to assess social functioning in the “real world” in the context of clinical trials; yet, this is a major target for intervention, especially in autism. Thus, a final goal of this study will be to explore the use of Event Contingent Recording (ECR) to index changes in social functioning and affect. ECR is a methodology developed by personality/social psychologists, which allows participants to report on symptoms, affect, and behavior close in time to experience. In addition, to enabling more sensitive assessments, this methodology allows for the assessment of more diverse (e.g., at home versus work) and more detailed measurements of mood and behavior.

Finally, a portion of this study aims to perform gene expression profiling using fresh whole blood to explore the molecular mechanisms underlying oxytocin therapy and oxytocin efficacy in adults with high functioning autism or Asperger’s syndrome. The systemic effects of oxytocin therapy and the molecular basis for a positive treatment response to oxytocin are not well understood. An understanding of the former may help predict those persons who may suffer side-effects from treatment and the latter may help provide easily accessible peripheral biomarkers that could predict treatment response.

Eligibility
Ages Eligible for Study: 18 Years - 60 Years, Genders Eligible for Study: Both
Criteria

Inclusion Criteria:
Male or female outpatients 18 to 60 years of age.
Meet DSM-IV-TR (Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision). The diagnosis will be confirmed with Autism Diagnostic Interview–Revised (ADI-R) and ADOS .
Have a Clinician’s Global Impression–Severity (CGI-S) score ≥ 4 (moderately ill) at Screening and Baseline.
If already receiving stable nonpharmacologic educational, behavioral, and/or dietary interventions, have continuous participation during the preceding 3 months prior to Screening and will not electively initiate new or modify ongoing interventions for the duration of the study.
Have normal physical examination and laboratory test results at Screening. If abnormal, the finding(s) must be deemed clinically insignificant by the Investigators.
The patient must be able to speak and understand English sufficiently to understand the nature of the study and to allow for the completion of all study assessments.
Have a normal IQ (>70) supported by the Wechsler Abbreviated Scales of Intelligence (WASI).

Exclusion Criteria:
Patients born prior to 35 weeks gestational age.
Patients with any primary psychiatric diagnosis other than autism at Screening: a history of ADHD, bipolar disorder, psychosis, posttraumatic stress disorder, schizophrenia, or major depressive disorder.
Patients with a medical history of neurological disease, including, but not limited to, epilepsy/seizure disorder (except simple febrile seizures), movement disorder, tuberous sclerosis, fragile X, and any other known genetic syndromes, or known abnormal MRI/structural lesion of the brain.
Pregnant female patients.
Patients with a medical condition that might interfere with the conduct of the study, confound interpretation of the study results, or endanger their own well-being. Patients with evidence or history of malignancy or any significant hematological, endocrine, cardiovascular (including any rhythm disorder), respiratory, renal, hepatic, or gastrointestinal disease.
Patients taking psychoactive medication(s) (e.g., stimulants, antidepressants, antipsychotics, antiepileptics, anxiolytics, clonidine).
Patients who plan to initiate or change nonpharmacologic interventions during the course of the study.
Patients unable to tolerate venipuncture procedures for blood sampling.
Patients who, in the Investigator’s opinion, might not be suitable for the study.

Location and Contact Information
Please refer to this study by ClinicalTrials.gov identifier NCT00490802

Jessica Cuellar, BA 212-241-2993 [email protected]

United States, New York
Mount Sinai School of Medicine, New York, New York, 10029-6574, United States; Recruiting
Evdokia Anagnostou, MD, Principal Investigator
Jennifer Bartz, PhD, Sub-Investigator

Study chairs or principal investigators

Evdokia Anagnostou, MD, Principal Investigator, Mount Sinai School of Medicine

More Information

http://www.mssm.edu/psychiatry/autism/r ... rams.shtml
Study ID Numbers: GCO#: 06-0230 0001 02 PS*
Last Updated: June 22, 2007
Record first received: June 22, 2007
ClinicalTrials.gov Identifier: NCT00490802
Health Authority: United States: Food and Drug Administration
ClinicalTrials.gov processed this record on July 25, 2007

An fMRI Study of the Effect of Intravenous Oxytocin vs. Placebo on Response Inhibition and Face Processing in Autism

This study is currently recruiting patients.
Verified by Mount Sinai School of Medicine April 2007Sponsored by: Mount Sinai School of Medicine
Information provided by: Mount Sinai School of Medicine
ClinicalTrials.gov Identifier: NCT00263796



Purpose
To study the effect of oxytocin on face processing and response inhibition in autistic adults by fMRI.Condition Intervention Phase
Autism Drug: Oxytocin Phase I


MedlinePlus related topics: Autism

Study Type: Interventional
Study Design: Treatment, Randomized, Double-Blind, Placebo Control, Parallel Assignment, Safety/Efficacy Study

Official Title: An fMRI Study of the Effect of Intravenous Oxytocin vs. Placebo on Response Inhibition and Face Processing in Autism
Further study details as provided by Mount Sinai School of Medicine:

Total Enrollment: 30

Study start: March 2006
Autism is a developmental disorder affecting approximately 60/10,000 individuals. It is characterized by social and language deficits and repetitive behaviors/restricted interests. Functional imaging is becoming a very useful tool in trying to understand the neurobiology of autism. Oxytocin is a hormone produced by the brain to assist with labor and lactation. Recent evidence suggests that it may be involved in social attachment and in repetitive behaviors. In this project, we will study how oxytocin changes the way the brain of autistic adults processes faces, and deals with response inhibition (the ability to interrupt ongoing responses should they prove ineffective or interfering with attaining a goal). There is currently no functional imaging data assessing the effect of oxytocin on the brain. We will explore the activation patterns in response to oxytocin across circuits involved in social cognition (face fusiform area) and response inhibition (caudate, orbitofrontal and dorsolateral cortex) by administering a specific fMRI task activating those circuits before and during an oxytocin infusion. We will also explore the effect of oxytocin in these areas by administering specific cognitive testing not associated with fMRI before and during oxytocin infusion.

Eligibility
Ages Eligible for Study: 18 Years - 50 Years, Genders Eligible for Study: Both
Criteria

Inclusion Criteria:
Meet DSM-IV, ADI, or ADOS criteria for autism spectrum disorder.
Age 18-50.
Be seen as outpatients
IQ>80
5. Demonstrate capacity to provide authorized informed consent or provide consent for participation by an approved surrogate on the autistic individual’s behalf

Exclusion Criteria:
Subjects who are pregnant or nursing mothers. Sexually active women of childbearing potential who are not using adequate birth control measures.
Subjects with epilepsy.
Subjects with a history of schizophrenia, schizoaffective disorder or other Axis 1 mental disorders, such as bipolar disorder.
Subjects reporting history of encephalitis, phenylketonuria, tuberous sclerosis, fragile X syndrome, anoxia during birth, neurofibromatosis, hypomelanosis, hypothyroidism, Duchenne muscular dystrophy, and maternal rubella
Subjects who have received depot neuroleptic medication, or other psychoactive drugs within the past 5 weeks.
Subjects with renal or liver disease or abnormalities in blood chemistry.
Any metallic prosthesis such as plates, pins and screws, shrapnel, metallic foreign body, vascular or neurosurgical clips that may be incompatible with the MRI and any electrical devices such as a pacemaker or a defibrillator
Claustrophobia

Location and Contact Information
Please refer to this study by ClinicalTrials.gov identifier NCT00263796

Kate Stamper, BA 212-241-7098 [email protected]
Evdokia Anagnostou, MD 212-241-4229 [email protected]

United States, New York
Mount Sinai School of Medicine, New York, New York, 10029-6574, United States; Recruiting
Evdokia Anagnostou, MD, Principal Investigator

Study chairs or principal investigators

Evdokia Anagnostou, MD, Principal Investigator, Mount Sinai School of Medicine

More Information
Study ID Numbers: GCO # 04-0749 (2)
Last Updated: April 18, 2007
Record first received: December 7, 2005
ClinicalTrials.gov Identifier: NCT00263796
Health Authority: United States: Institutional Review Board
ClinicalTrials.gov processed this record on July 25, 2007

Please be aware that street drugs supress oxytocin production, which is why (ab)users(especially marijuana and cocaine (ab)users) become paranoid.