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5-HTP and SAMe
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Overview
Defining Complementary and Alternative Medicine (CAM)Complementary and Alternative Medicine PractitionersRising Popularity of Complementary and Alternative Medicine ApproachesThe Safety of Alternative Medicine
Anxiety
Anxiety IntroductionWell Supported Integrative Therapies for Anxiety - KavaIntegrative Therapies for Anxiety - Passion Flower (Passiflora incarnata)Integrative Therapies for Anxiety - Valerian (Valeriana officinalis)Integrative Therapies for Anxiety - Serotonin PrecursorsOther Therapies for Anxiety
Depression
Depression IntroductionWell Supported Natural Therapies for Depression - St. John's WortWell Supported Natural Therapies for Depression - ExerciseIntegrative Therapies for Depression - Omega-3 Fatty AcidsIntegrative Therapies for Depression - Serotonin Precursors - SAMeIntegrative Therapies for Depression - Serotonin Precursors - 5-hydorxytryptophan (5-HTP)Other Therapies for Depression
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Bipolar Disorder IntroductionIntegrative Therapies for Bipolar Disorder - Omega 3 Fatty Acids (Fish Oils)Other Therapies for Bipolar Disorder - Serotonin PrecursorsOther Therapies for Bipolar Disorder -B-Complex Vitamins
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Schizophrenia IntroductionIntegrative Therapies for Schizophrenia - Omega-3 fatty acids (Fish Oils) and GlycineIntegrative Therapies for Schizophrenia - Tryptophan and GinkgoOther Therapies for Schizophrenia
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Attention-deficit/hyperactivity disorder (ADHD) IntroductionIntegrative Therapies for ADHD - Omega-3 Fatty Acids (Fish Oils)Other Therapies for ADHDOther Therapies for ADHD Continued
Article References
Introduction and Anxiety ReferencesDepression ReferencesBipolar ReferencesSchizophrenia ReferencesADHD References
More Information
AcupressureAcupunctureAre You Considering Using Complementary and Alternative Medicine (CAM)?AromatherapyBiologically Based Practices: An OverviewChiropractic CareComplementary and Alternative MedicineConsumer Financial Issues in Complementary and Alternative MedicineDietary SupplementsEnergy Medicine: An OverviewGinkgo Biloba Fact SheetHerbalismManipulative and Body-Based Practices: An OverviewMeditationMind-Body Medicine: An OverviewWhat is Complementary and Alternative Medicine?Whole Medical Systems: An OverviewWise Counsel Interview Transcript: An Interview with James Gordon MD on Mind Body Medicine and His Book \'Unstuck\'
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U.S. Spending Millions to See if Herbs Truly WorkFDA Warns of Tainted Dietary Supplement ProductsMany With Brain Tumors Use Alternative TherapiesZen Meditation Can Help Bring Pain Under ControlCertain Formulations of Omega-3s Might Help With DepressionAcupuncture Really Does Help Relieve Pain: StudyTai Chi May Provide Arthritis ReliefAHA: Supplement Use High in Warfarin-Treated PatientsACR: Tai Chi Associated With Improvements in ArthritisFish Oil Supplements May Not Slow Alzheimer'sFish Oil Pills Don't Affect Postpartum Depression: StudyFibromyalgia Sufferers May Benefit From Yoga PracticeMouse Study Clarifies Fish Oil Anti-Inflammatory EffectTai Chi Shows Benefits in Treating FibromyalgiaPositive Brain Changes Seen After Body-Mind MeditationMeditation Appears to Boost Attention SpanHomeopathic Nasal Zinc Linked to Loss of SmellQigong and Tai Chi Have Multiple Health BenefitsFish Oil Usage Linked to Lower Risk of Certain Breast CancersNutraceutical Drug Use Often Ignored by CliniciansBrain Scans Show How Meditation Calms PainAcupuncture May Trigger Natural PainkillerMany Supplements Said to Contain Toxins, Make False Health ClaimsPregnant Women Using Herbals Despite Lack of Safety DataYoga's Benefits Outweigh Risks for Pregnant WomenYoga Eases Sleep Problems Among Cancer SurvivorsHerbal Supplements, Warfarin Can Be Hazardous MixParents of Autistic Children Turning to Alternative TreatmentsYoga Benefits African-American Heart Failure PatientsAcupuncture May Help Restore Lost Sense of SmellAcupuncture May Ease Anxiety Over Dental WorkMassage Fosters Healing in Bereaved RelativesComplementary Medicine Not Uncommon in Pediatric CancerMusic Soothes Anxiety as Well as Massage DoesAcupuncture May Ease Depression During PregnancyHerbals Not the Answer for Asthma, Study ShowsClinicians Need to Be Aware of Patient Use of Herbal ProductsOmega-3s May Reduce Risk of Developing Psychotic DisorderHerbal Remedies Can Cause Cardiac ProblemsOmega-3 Supplements Don't Reduce Risk of Preterm BirthKids' Use of Alternative Therapies Often Mimics Parents'Study Explores Alternative Medicine Use in ChildrenMedical Students Supportive of Alternative MedicineStudy May Explain Cardiac Benefit of Green TeaSt. John's Wort May Not Help Irritable Bowel SyndromeAcupuncture May Cut Hot Flashes, Boost Sex Drive in Breast Cancer Patients Ginkgo biloba May Not Reduce Cognitive Decline in Adults
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Yoga help Bipolar
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The Benefits of YogaComplementary and Alternative Medicine In The Treatment of Personality DisordersA Natural Approach to Treating Depression Web SeriesAn Interview with James Gordon, MD on Mind-Body Medicine and his book 'Unstuck'Should a Disabled Student Have the Right to a Service Dog in School?Mingo: Loss and Grief and Celebrating the Life and Work of a Service DogDangers of a Little Knowledge Revisited: Medications, Benefit or Just Money?Meditation: More BenefitsUpdated Alternative Medicine Topic Center
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Other Therapies for Bipolar Disorder - Serotonin Precursors
Scott Olson, ND Updated: Aug 7th 2009
Serotonin precursors are compounds used in the production of serotonin, dopamine, and norepinephrine, brain chemicals responsible for mood. A subset of people with bipolar disorder will respond to serotonin precursor treatment, but this intervention is still considered experimental. Both 5-hydorxytryptophan (5-HTP) and S-adenosyl-L-methionine (SAMe, pronounced "Sammy") are serotonin precursors that can be used in the treatment of bipolar disorder.
5-HTP is a compound made from the amino acid (protein) tryptophan and is primarily found in the brain. 5-HTP is one of the basic building blocks for serotonin, one of the neurotransmitters (brain chemical) responsible for mood regulation. Individuals who experience depression have reduced levels of serotonin in their brains.
Serotonin itself can be manufactured in the laboratory, but when taken as a supplement, it cannot reach the brain (it does not have the ability to cross from general blood circulation into brain circulation, because of a selective membrane that only allows certain chemicals into the brain). 5-HTP came into use in an effort to find a natural way to increase brain serotonin levels. Multiple research studies have demonstrated 5-HTP's ability to increase serotonin levels when taken as a supplement.
SAMe is a compound produced by the liver and used throughout the body in a chemical process called methylation. Methylation, essential to many chemical reactions in the body, is one of the last steps in the production of the brain chemicals serotonin, dopamine and norepinephrine (which regulate mood).
Because there are no foods that have high SAMe levels, our bodies must make this substance. Our liver usually creates SAMe from the amino acid (protein) methionine, which is found in many foods. Interestingly, supplementing with methionine does not work as well as supplementing with SAMe, because creating SAMe takes multiple steps and requires many co-factors (other nutrients, such as vitamin B12, folate and others) to ensure that the process is successful.
While the use of SAMe in your body is diverse (it participates in over 35 biochemical processes), the process of interest in bipolar disorder is the creation of the brain chemicals mentioned above (dopamine, serotonin and norepinephrine). SAMe slows the breakdown of these brain chemicals, allowing them to work longer. In addition, SAMe speeds production of the receptors which receive these neurotransmitters. The presence of additional receptors allows the neurotransmitters that are present to work more effectively. Some research suggests that SAMe may also make the existing receptors more responsive (better able to receive messages from neurotransmitters). All of these functions combine to create increased levels of neurotransmitters, which can decrease the symptoms of bipolar disorder.
http://www.mentalhelp.net/poc/view_doc.php?type=doc&id=11885&cn=15
Alternative Mental Health Medicine
Email a link to this page to:
Type the code into the box:
Resources
Basic Information
Overview
Defining Complementary and Alternative Medicine (CAM)Complementary and Alternative Medicine PractitionersRising Popularity of Complementary and Alternative Medicine ApproachesThe Safety of Alternative Medicine
Anxiety
Anxiety IntroductionWell Supported Integrative Therapies for Anxiety - KavaIntegrative Therapies for Anxiety - Passion Flower (Passiflora incarnata)Integrative Therapies for Anxiety - Valerian (Valeriana officinalis)Integrative Therapies for Anxiety - Serotonin PrecursorsOther Therapies for Anxiety
Depression
Depression IntroductionWell Supported Natural Therapies for Depression - St. John's WortWell Supported Natural Therapies for Depression - ExerciseIntegrative Therapies for Depression - Omega-3 Fatty AcidsIntegrative Therapies for Depression - Serotonin Precursors - SAMeIntegrative Therapies for Depression - Serotonin Precursors - 5-hydorxytryptophan (5-HTP)Other Therapies for Depression
Bipolar Disorder
Bipolar Disorder IntroductionIntegrative Therapies for Bipolar Disorder - Omega 3 Fatty Acids (Fish Oils)Other Therapies for Bipolar Disorder - Serotonin PrecursorsOther Therapies for Bipolar Disorder -B-Complex Vitamins
Schizophrenia
Schizophrenia IntroductionIntegrative Therapies for Schizophrenia - Omega-3 fatty acids (Fish Oils) and GlycineIntegrative Therapies for Schizophrenia - Tryptophan and GinkgoOther Therapies for Schizophrenia
ADHD
Attention-deficit/hyperactivity disorder (ADHD) IntroductionIntegrative Therapies for ADHD - Omega-3 Fatty Acids (Fish Oils)Other Therapies for ADHDOther Therapies for ADHD Continued
Article References
Introduction and Anxiety ReferencesDepression ReferencesBipolar ReferencesSchizophrenia ReferencesADHD References
More Information
AcupressureAcupunctureAre You Considering Using Complementary and Alternative Medicine (CAM)?AromatherapyBiologically Based Practices: An OverviewChiropractic CareComplementary and Alternative MedicineConsumer Financial Issues in Complementary and Alternative MedicineDietary SupplementsEnergy Medicine: An OverviewGinkgo Biloba Fact SheetHerbalismManipulative and Body-Based Practices: An OverviewMeditationMind-Body Medicine: An OverviewWhat is Complementary and Alternative Medicine?Whole Medical Systems: An OverviewWise Counsel Interview Transcript: An Interview with James Gordon MD on Mind Body Medicine and His Book \'Unstuck\'
Latest News
U.S. Spending Millions to See if Herbs Truly WorkFDA Warns of Tainted Dietary Supplement ProductsMany With Brain Tumors Use Alternative TherapiesZen Meditation Can Help Bring Pain Under ControlCertain Formulations of Omega-3s Might Help With DepressionAcupuncture Really Does Help Relieve Pain: StudyTai Chi May Provide Arthritis ReliefAHA: Supplement Use High in Warfarin-Treated PatientsACR: Tai Chi Associated With Improvements in ArthritisFish Oil Supplements May Not Slow Alzheimer'sFish Oil Pills Don't Affect Postpartum Depression: StudyFibromyalgia Sufferers May Benefit From Yoga PracticeMouse Study Clarifies Fish Oil Anti-Inflammatory EffectTai Chi Shows Benefits in Treating FibromyalgiaPositive Brain Changes Seen After Body-Mind MeditationMeditation Appears to Boost Attention SpanHomeopathic Nasal Zinc Linked to Loss of SmellQigong and Tai Chi Have Multiple Health BenefitsFish Oil Usage Linked to Lower Risk of Certain Breast CancersNutraceutical Drug Use Often Ignored by CliniciansBrain Scans Show How Meditation Calms PainAcupuncture May Trigger Natural PainkillerMany Supplements Said to Contain Toxins, Make False Health ClaimsPregnant Women Using Herbals Despite Lack of Safety DataYoga's Benefits Outweigh Risks for Pregnant WomenYoga Eases Sleep Problems Among Cancer SurvivorsHerbal Supplements, Warfarin Can Be Hazardous MixParents of Autistic Children Turning to Alternative TreatmentsYoga Benefits African-American Heart Failure PatientsAcupuncture May Help Restore Lost Sense of SmellAcupuncture May Ease Anxiety Over Dental WorkMassage Fosters Healing in Bereaved RelativesComplementary Medicine Not Uncommon in Pediatric CancerMusic Soothes Anxiety as Well as Massage DoesAcupuncture May Ease Depression During PregnancyHerbals Not the Answer for Asthma, Study ShowsClinicians Need to Be Aware of Patient Use of Herbal ProductsOmega-3s May Reduce Risk of Developing Psychotic DisorderHerbal Remedies Can Cause Cardiac ProblemsOmega-3 Supplements Don't Reduce Risk of Preterm BirthKids' Use of Alternative Therapies Often Mimics Parents'Study Explores Alternative Medicine Use in ChildrenMedical Students Supportive of Alternative MedicineStudy May Explain Cardiac Benefit of Green TeaSt. John's Wort May Not Help Irritable Bowel SyndromeAcupuncture May Cut Hot Flashes, Boost Sex Drive in Breast Cancer Patients Ginkgo biloba May Not Reduce Cognitive Decline in Adults
Questions and Answers
Yoga help Bipolar
Blog Entries
The Benefits of YogaComplementary and Alternative Medicine In The Treatment of Personality DisordersA Natural Approach to Treating Depression Web SeriesAn Interview with James Gordon, MD on Mind-Body Medicine and his book 'Unstuck'Should a Disabled Student Have the Right to a Service Dog in School?Mingo: Loss and Grief and Celebrating the Life and Work of a Service DogDangers of a Little Knowledge Revisited: Medications, Benefit or Just Money?Meditation: More BenefitsUpdated Alternative Medicine Topic Center
Videos
The Power of VisualizationTai Chi: The Dance of HealthAlternative Arthritis Therapies: Supplements
Links
[2] Associations[1] Government[6] Information[1] Other Sites[3] Videos
Book Reviews
BreathingBuddha's BrainComplementary and Alternative Therapies ResearchDepression-Free for LifeDr. Andrew Weil's Guide to Optimum HealthDr. Andrew Weil's Mindbody ToolkitEastern Body, Western MindEcological MedicineGood MedicineIntegrative MedicineMaui PilatesMeditation for Optimum HealthMindfulness for BeginnersNatural Healing for DepressionSnake Oil ScienceThe Jewel Tree of TibetThe Medical AdvisorThe Natural Pharmacist : Natural Health Bible from the Most Trusted Alternative Health Site in the World The PDR Family Guide to Natural Medicines & Healing TherapiesThe Pill Book Guide to Natural MedicinesThe Places That Scare YouTrick or Treatment
Community
Talk about this issue in our mental health support community
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Use our Advanced Search to locate a therapist outside of North America.
Related Topics
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Autism
o
ADHD
o
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o
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o
Bipolar Disorder
o
Conversion Disorders
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Depression (Unipolar)
o
Depression Primer
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Other Therapies for Bipolar Disorder - Serotonin Precursors
Scott Olson, ND Updated: Aug 7th 2009
Serotonin precursors are compounds used in the production of serotonin, dopamine, and norepinephrine, brain chemicals responsible for mood. A subset of people with bipolar disorder will respond to serotonin precursor treatment, but this intervention is still considered experimental. Both 5-hydorxytryptophan (5-HTP) and S-adenosyl-L-methionine (SAMe, pronounced "Sammy") are serotonin precursors that can be used in the treatment of bipolar disorder.
5-HTP is a compound made from the amino acid (protein) tryptophan and is primarily found in the brain. 5-HTP is one of the basic building blocks for serotonin, one of the neurotransmitters (brain chemical) responsible for mood regulation. Individuals who experience depression have reduced levels of serotonin in their brains.
Serotonin itself can be manufactured in the laboratory, but when taken as a supplement, it cannot reach the brain (it does not have the ability to cross from general blood circulation into brain circulation, because of a selective membrane that only allows certain chemicals into the brain). 5-HTP came into use in an effort to find a natural way to increase brain serotonin levels. Multiple research studies have demonstrated 5-HTP's ability to increase serotonin levels when taken as a supplement.
SAMe is a compound produced by the liver and used throughout the body in a chemical process called methylation. Methylation, essential to many chemical reactions in the body, is one of the last steps in the production of the brain chemicals serotonin, dopamine and norepinephrine (which regulate mood).
Because there are no foods that have high SAMe levels, our bodies must make this substance. Our liver usually creates SAMe from the amino acid (protein) methionine, which is found in many foods. Interestingly, supplementing with methionine does not work as well as supplementing with SAMe, because creating SAMe takes multiple steps and requires many co-factors (other nutrients, such as vitamin B12, folate and others) to ensure that the process is successful.
While the use of SAMe in your body is diverse (it participates in over 35 biochemical processes), the process of interest in bipolar disorder is the creation of the brain chemicals mentioned above (dopamine, serotonin and norepinephrine). SAMe slows the breakdown of these brain chemicals, allowing them to work longer. In addition, SAMe speeds production of the receptors which receive these neurotransmitters. The presence of additional receptors allows the neurotransmitters that are present to work more effectively. Some research suggests that SAMe may also make the existing receptors more responsive (better able to receive messages from neurotransmitters). All of these functions combine to create increased levels of neurotransmitters, which can decrease the symptoms of bipolar disorder.
Serotonin & the Pineal Gland
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http://www.antidepressantsfacts.com/pinealstory.htm
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SEROTONIN & THE PINEAL GLAND
Pineal Gland By Charly Groenendijk
The Netherlands
Oct 9, 2001 (updated March 11, 2003)
The Serotonergic System, the Pineal Gland & Side-Effects of Serotonin Acting Anti-Depressants -Part 1
Go to Serotonin & the Pineal Gland -Part 2
REFERENCE
The content of this article is based on and written in accordance with accepted theories in Bio-Psychiatry and should therefore be perceived as another theory.
Take notice that also non SSRI anti-depressants (such as SNRI's targeting the neurotransmitter nor-epinephrine (nor-adrenaline) and even Ritalin) may interact (primary or secondary) with the serotonergic system in the brain, causing serotonin deficiency symptoms.
1. Introduction: Neurons & Neurotransmitters
There are billions of working cells in our brain called Neurons and great variety in the kind of brain cells or neurons, with each group representing a specific cluster of functions. Neurons communicate with similar neurons by firing molecules from its nerve endings to the receiving nerve endings of the other neuron. The nerve endings of the firing part of the neuron are called axon terminals and the nerve endings of the receiving part of the neuron are called dendrites. The end of the axon terminals are called synapses. The synaptic cleft is the space where synapses and dendrites meet each other and where all the activity takes place. Each neuron is able to receive and fire molecules simultaneously. The molecules fired in the synaptic cleft are called neurotransmitters. Situated at the end of the axon terminals of the firing part of the neuron, the synapses work like "ball throwers." The dendrites of the receiving part of the other neuron, work like "catcher's mitts." They use receptor-molecules, or receptors, to capture the "thrown" neurotransmitters. (See Picture)
Re-Uptake
Once one neuron is firing neurotransmitters from it's synapse to the receiving dendrite of the other neuron, it is critically important that the "mis-fired" neurotransmitter left overs must be removed from the synaptic cleft. Any neurotransmitter which is not removed from the synaptic cleft, prevents further neurotransmitters from getting through. Re-uptake, the process of removing neurotransmitters after firing or release, allow these neurotransmitter left overs to be recycled for further use. Re-uptake is carried out by "transporter proteins" which bind to the mis-fired neurotransmitter and carry it across the plasma membrane back into the synapse of the firing neuron.
Medication classified "Re-Uptake Inhibitors" act on these transporter proteins and thereby inhibit the re-uptake of neurotransmitters back into the synapse of the firing neuron. SSRI-AntiDepressants or Selective Serotonin Re-uptake Inhibitors, belong to this class of medication. Each group of neurons fire specific neurotransmitter-molecules. The neurotransmitter Serotonin, also known as 5-Hydroxy-Tryptamine (5-HT) is such a molecule. SSRI-AntiDepressants inhibit the re-uptake of serotonin what means that more serotonin will be fired from synapse to dendrite in the synaptic cleft of every communicating serotonergic neuron in the brain.
2. The neurotransmitter "Serotonin"
In the brain, serotonin is synthesized from the amino acid precursor "Tryptophan". By enzymatic interaction, tryptophan converts into 5-HTP and eventually into serotonin. (see image) This neurotransmitter belongs to the group of serotonergic neurons which make the Serotonergic System in the brain. Levels of serotonin are highly concentrated in the Raphe Nuclei. Raphe Nuclei are present in the Medulla and Pons, 2 structures which are part of the Brainstem. From the Raphe Nuclei in the pons of the brainstem, also called "Rostral Raphe Nuclei", serotonin pathways project through parts of the Limbic System (like the Thalamus and Hypothalamus) into the Forebrain. (See Picture)
2.a. Serotonergic functioning
If you would believe the overwhelming advertisements of the pharmaceutical companies, you would think that serotonin primarily regulates mood. In fact, serotonin regulates a lot of other activities in the brain and body. In 1948, Maurice Rapport, a haematologist, found that serotonin tended to make blood form clots, and it tended to be a muscle- as well as a vasoconstrictor. Next to be a muscle- and vasoconstrictor, serotonin plays an important role in sleep, appetite, memory, aggression, sexual behaviour, cardiovascular activity, respiratory activity, motor output, sensory and neuroendocrine function, but most important, perception! Since 1988 the serotonin hype brought us several SSRI-AntiDepressants all stimulating this neurotransmitter. For about 11 years now, Dr. Ann Blake Tracy (Prozac: Panacea or Pandora?), persistently warns the public against raising serotonin levels. Doctor Tracy has taught us that an increase in serotonin produces rushes of insulin dropping sugar levels and chemically inducing hypoglycaemia (low blood sugar) in this way. Furthermore it has been established that too much serotonin damages blood vessels, particularly in the lungs, and may also harm heart valves. This would be due to the fact that serotonin is a powerful vasoconstrictor.
Affecting Mood or Mind?
But most alarming is the serotonin and perception connection. Doctor Tracy as well as other sources described how the hallucinogenic drug LSD strongly acts on this neurotransmitter serotonin. The numerous examples of human LSD experiences have learned us that serotonin plays a major part in perception, our sense of reality, how we experience our in- and outside world! Other examples of drugs acting on the serotonergic system are PCP and MDMA (Ecstasy). Most of the readers will recognize also these serotonergic drugs for their capability to produce "an altered state of consciousness" in human beings. In the way that the serotonergic system responds to serotonergic drugs, we may conclude that this system is heavily involved in the determination of ones perception and therefore ones thought processes and emotions. The advertisements from the pharmaceutical companies, promoting elevated serotonin levels as were they purely mood lifting, therefore seem to be rather misleading then informative. SSRI-AntiDepressants are to be considered mind-altering drugs and not primarily mood-altering.
In all these years since 1988, scientists are still not sure why serotonin boosters seem to "alleviate" depression. They assume that low serotonin levels could be a possible cause of endogenous depression, but it's still just a theory and not a proven fact! New research present us a different view on serotonin, which may not even have that connection with mood as previously thought. By experimental research, scientists discovered that a new drug, code-named MK-869, blocked a neuropeptide called " Substance P." By blocking this neuropeptide, people became less depressed. An interesting fact was, that blocking substance P did not affect the function of serotonin! This raises new concerns about the involvement of serotonin in mood and/or depression.
"But why do I hear people talking about benefits from these SSRI-AntiDepressants?", you might want to ask in this stage. "They surely must work somehow don't they?" The answer is yes, they "work" somehow, but not in a very proper way. The mechanism of action on serotonergic neurons implies a lot of other neuro- endocrine responses. What actually happens when you increase serotonergic neuronal activity or elevate your serotonin levels is this: the stress hormones "Cortisol" & "Adrenaline" (Epinephrine) in the brain and body are triggered by increased serotonergic activity or elevated serotonin levels. It is a natural reaction from the body to combat the excessive serotonin levels. These released hormones, cortisol and adrenaline, are secreted from the "Adrenal Glands." They give the human personality a boost, producing a euphoric state, which can last for a prolonged period of time. In this manner SSRI-AntiDepressants initially produce the deceptive results the doctor and "patient" are both expecting. *
If a patient continues to ingest a particular SSRI-antidepressant over a prolonged period of time, eventually the bodies Adrenal Glands may lose their efficiency and "Adrenal Exhaustion Syndrome" will be the end result. Adrenal Exhaustion causes levels of adrenaline initially to fall and levels of cortisol to rise. Ultimately, also cortisol levels fall. When untreated, Adrenal Exhaustion will lead to seriously declining physical health. Many (former) SSRI-AntiDepressant users reported fatigue as a long term side-effect or were diagnosed with "Chronigue Fatigue Syndrome." People suffering from stress are generally diagnosed with this disorder. Symptoms range from simple exhaustion to much more complex problems that are secondary to excessive output of adrenal hormones in the bloodstream, leading to Adrenal Exhaustion. Unlike the other hormones, it takes a long time before the Adrenal Glands have their adrenaline levels restored. Could we say that the SSRI-AntiDepressant "works" by slowly excavating the body's Adrenal Glands?
* [ Actually, when a family doctor (GP) or psychiatrist is observing a patient in a "euphoric" state of being, this should ring warning bells immediately! The drug induced (iatrogenic) conditions Akathisia & Mania are well documented in the medical litarature. Drug induced Mania, an abnormally elated mental state, typically characterized by feelings of euphoria, racing thoughts and talkativeness, is a "forerunner" of Akathisia, a neurologically driven agitation ranging from mild leg tapping, feeling "caffeinated" to severe panic, an extreme manic state and hyper-sensitivity of the nervous system. Akathisia can lead to suicidal, aggressive and/or homicidal thoughts and behaviours. When a doctor or psychiatrist is observing symptoms of mania and/or akathisia in a patient, SSRI-AntiDepressant use should be discontinued immediately! The pharmaceutical companies are well informed regarding above mentioned conditions and the capacity of their antidepressant inducing these symptoms. Therefore it is strongly advised to medical professionals, physicians, to monitor a patient very closely after prescription of (SSRI) anti-depressant treatment. In the field of Bio-Psychiatry it was a conventional common thought that hypothalamic-pituitary-adrenal (HPA) system dysregulation/hyperactivity (and thus excessive secretion of cortisol) played an important role in the pathophysiology of depression and that normalization of HPA axis hyperactivity could be achieved by (SSRI) anti-depressant treatment, and thus relief of depression. However, a study and a case report involving the non-SSRI antidepressant Remeron (mirtazapine) and a review show us that nor amelioration of HPA system dysregulation, nor reduction of cortisol secretion in depressed patients is correlated with relief of symptoms of depression. See: (1), (2), (3). Furthermore, a study developed by D. Jezova & R. Duncko, Laboratory of Pharmacological Neuroendocrinology, demonstrated that repeated SSRI-antidepressant treatment in healthy men does not inhibit, but enhances stress-induced pituitary hormone release (neuroendocrine activation). Cortisol levels failed to be modified by antidepressants. A simple search through available PubMed articles uncovers clearly that SSRI-antidepressants not only fail to modify cortisol, but actually stimulate/increase cortisol release. See: (1), (2), (3), (4), (5), (6). Initially the rise in cortisol & adrenaline (secreted from the Adrenal Glands) may create the illusion of a patient making progress in his/her situation, but a potential tragedy may be surfacing very soon. It is very well known that (SSRI-AntiDepressant induced) increased cortisol secretion can lead to violent suicidal behaviour.
(I would like to encourage you to use your discernment when viewing antidepressant involved suicide/homicide/violence cases represented by the media. In the section casualties of this website, these cases are carefully stored up to be a "silent" witness for the future, in order to testify regarding the devastating & powerful destructive effects these "legal drugs" exercised on children, adolescents and adults, not discriminating between men and women). ]
The Serotonin-Cycle: beaconing of conscious awareness and dream sleep?
One of the first significant discoveries about the serotonergic system in the brain was that it's activity was dramatically altered across the sleep-wake cycle. Serotonergic activity gradually decreases as one becomes drowsy and enter slow-wave sleep. An overall slowing of serotonergic activity is observed during slow-wave sleep known as non-REM sleep. During REM sleep (Rapid Eye Movement-the original dream sleep), serotonergic activity falls completely silent. Serotonergic activity returns to it's basic level several seconds prior to the end of REM sleep. REM sleep occurs in roughly 90-100 minute cycles, alternating with non-REM sleep (around 4 to 5 times during sleep). During non-REM sleep, there is lots of movement, but during REM sleep, only the eye muscles move. REM-dreaming turns on neurons in the medulla of the brainstem that inhibit all other motor activity. In this way it prevents the dreamer from sleepwalking and to act out his/her dreams in real time.
Another significant discovery was that, when during REM sleep the serotonergic neurons in the brainstem were "off" (silent), cholinergic neurons in the brainstem were "on" (firing)! Cholinergic neurons fire the neurotransmitter "Acetylcholine." Acetylcholine not only plays an important role in dreaming, but also in long-term memory processes. In the brainstem, the cholinergic "REM-on" neurons can only trigger REM sleep (and thus dreaming) when the serotonergic "REM-off" neurons are inactive. This happens because, in the brainstem, the serotonergic neurons inhibit the cholinergic neurons whilst we are awake. When, in the brainstem, the serotonergic neurons release their inhibitory constraint, only then, the cholinergic brainstem neurons will be able to get active, triggering the REM-dream sleep. Both the REM-on and the REM-off cells are localized in the brainstem. These brainstem mechanisms work as an "oscillator", which controls the transitions from waking to sleeping and further controls the REM/non-REM cycle, which occurs 4 to 5 times during sleep.
Now at this moment you might ask yourself, how it is possible that so many individuals report bizarre vivid lifelike dreams whilst on serotonin boosters, when an active serotonergic system suppresses REM sleep, and thereby dreaming? Serotonergic suppression of REM sleep in humans by acute dosage of SSRI-AntiDepressants was indeed confirmed. (see article) This is what Dr. Tracy is also been telling us for many years in her book. The PubMed article discusses rebound of REM sleep after abrupt withdrawal from an SSRI-AntiDepressant, but it still doesn't answer the question how it is possible that individuals are experiencing disturbing dreams and nightmares whilst they are taking an SSRI-AntiDepressant over a prolonged period of time. When I delved deeper into this matter I discovered some interesting facts. Although there is an important link between REM sleep and dreaming, they are in fact doubly dissociable states. That is, REM can occur without dreaming and dreaming can occur without REM. Although REM is triggered from the brainstem, it alone will not result in dream states. Dreams require input from the forebrain and structures in the limbic system. The forebrain mechanisms are the final common path to dreaming. The brainstem is just one of the many arousal triggers that can activate these forebrain mechanisms. Although REM sleep is controlled by the brainstem, dreaming seems to be controlled by these forebrain mechanisms. It is now acknowledged that REM sleep is not necessary for dreaming, that dreaming can also occur during non-REM sleep, and that dream-like experiences can even be elicited during quiet wakefulness! The controversial human reports of very vivid lifelike dreams whilst taking an SSRI-AntiDepressant could therefore be explained as existing outside and independent of the REM (dream) sleep! But, -now that we know that the forebrain is the final common path to dreaming, and SSRI-AntiDepressants suppress the brainstem's REM arousal system (which normally activates forebrain dreaming)- what kind of arousal triggers are then responsible for the activation of forebrain dreams during use of SSRI-AntiDepressants?
Forebrain Nightmares and Forebrain Seizures
An even more exciting discovery was that dreaming can also be induced by focal forebrain stimulation and by complex partial forebrain seizures during non-REM sleep, without the involvement of the brainstem's REM mechanism! There is a causal link between epileptic activity and recurring nightmares during non-REM sleep. This was demonstrated by neurosurgeon and researcher Wilder Penfield, who was able to reproduce these anxious experiences artificially in the form of waking "dreamy state" seizures. The causal link between forebrain seizures and recurring nightmares was confirmed by the fact that both the underlying seizure disorder and the nightmares responded to anticonvulsant therapy.
Here is an example of a recurring nightmare, caused by epileptic activity in the forebrain:
The patient [35 year old woman with idiopathic complex-partial seizures] reported a recurrent dream about her [dead] brother ... which has reappeared several times. The dream is as follows: "I am walking down the street. I meet him. He is with a group of people whom I know now. I feel that I will be so happy to see him. I say to him, `I'm glad you're alive,' but he'll deny that he is my brother and he'll say so, and I'll wake up crying and trying to convince him."' Electroencephalography revealed a poorly defined right anterior temporal / right temporal spike focus which appeared with the onset of drowsiness and light sleep (Epstein & Ervin 1957, p. 45).
Could it be that the bizarre vivid lifelike dreams, reported by SSRI-AntiDepressant users are epileptiform of nature? Notice the "poorly defined spike focus." Could it be that this is epileptic activity which remains undiscovered because it is barely detectable? Standard tests for epilepsy included?
3. The Pineal Gland
The Pineal Gland -also called the epiphysis- looks like a miniature pine cone and is situated in the middle of the brain beneath the two brain halves, surrounded by the ventricles, under the roof of the corpus callosum (cross-beam connecting the 2 brain halves). (see picture) This active organ has, together with the Pituitary Gland (see picture), the next highest blood circulation after the kidneys. It is not protected by the blood-brain barrier and therefore makes this gland fragile to any substance entering the bloodstream. It is, for instance, very sensitive to fluoride.
Another factor involved in affecting the Pineal Gland can be excessive high or even toxic levels of an SSRI-AntiDepressant in the bloodstream. Certain individuals have a metabolic deficiency in the metabolism of anti-depressant medication. In the liver, a group of enzymes named " cytochrome P-450" enzymes, particularly the "CYP2D6 enzymes" of this group of enzymes, metabolise SSRI-AntiDepressants. When not properly metabolised, because one has a metabolic deficiency, a daily therapeutic dose can build up to excessive high or even toxic levels in the bloodstream. Hence, the Pineal Gland would be an easy target, since it is not very well protected by the blood-brain barrier. It is it's connection to serotonin what makes this organ so very interesting.
3.a. The Pineal Gland-Serotonin connection
Nicholas Giarmin, a professor of pharmacology and Daniel Freedman, a professor of psychiatry, confirmed that the human brain manufactures serotonin at various sites in the brain. For example, in the Thalamus, they discovered 61 nanograms of serotonin per gram of tissue; in the Hippocampus, 56 ng.; in the Central Gray Section of the Midbrain, they found 482 ng. But in the Pineal Gland, they found 3140 ng. of serotonin per gram of tissue. The Pineal Gland was unmistakably the richest site of serotonin in the brain! This discovery implicates the Pineal Gland as an important site of serotonergic activity.
The neurohormone Melatonin & the Endocrine System
One of the neurotransmitters secreted by the Pineal Gland is Melatonin, also known as N-Acetyl-5-Methoxy-Tryptamine (NA-5-MT). In the Pineal Gland, serotonin converts into melatonin by enzymatic interaction. Melatonin is also an important hormone to the body, that's why it is called a neurohormone. It is necessary to regulate the function of all organs of the Endocrine System in the body. The organs or glands of the endocrine system are: the Pituitary Gland, situated in the brain; the Thyroid + Parathyroid Glands; the Thymus; the Pancreas; the Ovaries/Testes (see image). All of these endocrine organs/glands secrete their hormones to the blood. The Pituitary Gland stimulates the secretion of these hormones, while the Pineal Gland apply the brakes on them through it's neurohormone melatonin. If the endocrine organs/glands release too much of their hormones, for instance when we are stressed, then the Pineal Gland releases melatonin to counteract these hormones. Also serotonin gets released when stress is involved. The increased serotonin triggers the release of adrenaline, which allows the body to work through the stress.
The Pineal Gland is a magneto sensitive organ, what means that it is sensitive to electromagnetic fields (EMF). It is sensitive to electromagnetic waves from computer monitors, cellular phones, microwave ovens, high voltage lines, etc.. Electromagnetic fields suppress the activity of the Pineal Gland and reduce melatonin production. EMF also affect serotonin.
The neurohormone Melatonin & the Eye-SCN-Pineal Gland Axis
The Pineal Gland is also a photosensitive organ, what means that it is sensitive to light. It normally releases melatonin when it no longer receives light impulses. Just like serotonin, also melatonin has it's own day & night cycle (circadian rhythm) which begins where the cycle of serotonin normally ends. When serotonin reaches it's lowest level at night (in the dark) during slow wave sleep, the Pineal Gland starts to convert it's store of serotonin into melatonin to be released prior to REM sleep. Melatonin has it's peak around 02:00 AM. During daytime, the daylight inhibits the release of melatonin. This works as follows: when, during daytime, light reaches the eyes, then it's presence gets translated into nerve impulses, which travel through the optic nerve between the eyes and a region of the Hypothalamus called the "Suprachiasmatic Nucleus" (SCN). (see picture) The SCN in it's turn sends it's nerve impulses to the Pineal Gland. These impulses inhibit the Pineal Gland's production of melatonin until it gets dark, when it's to be released again.
Melatonin is not only present in the brain and body but also in the eye! One has speculated whether or not high melatonin levels in the eyes during daylight exposure, may bring damage to them over time. Visual/eye problems (light sensitivity, spots, blurred vision) are other symptoms, frequently reported by (former) SSRI-AntiDepressant users. I questioned myself if these problems could be related to elevated melatonin levels in the eye. When serotonin accumulates in the Pineal Gland, on account of an SSRI-AntiDepressant, then it would come under pressure to produce more melatonin out of the excessive amounts of serotonin. Hence, during daytime, melatonin levels in the eyes would be significantly higher then normally would occur... But, I had to revise this hypothesis. In a PubMed study, SSRI-AntiDepressants were found not to elevate melatonin levels in humans. Although "Luvox" and "Paxil" increases melatonin to a more or lesser amount, apparently this seemed not to be the case for the other SSRI-AntiDepressants. However, since the Pineal Gland does contain a complete map of the visual field of the eyes, could there be a correlation between visual/eye problems and a dysfunctional Pineal Gland?
A case, noted by Dr. Berman, could give us some more insight into this matter:
A child was brought to a German clinic suffering from eye trouble and headaches. He was five years old and very mature, and apparently had reached the age of adolescence. He was abnormally bright mentally, discussing metaphysical and spiritual subjects. He was strongly group-conscious and only happy when sharing what he had with others. After his arrival at the clinic, he rapidly grew worse and died in a month. An autopsy showed a tumour of the pineal gland. - Berman, Louis, M.D., The Glands Regulating Personality, p. 89.
Could it be that the visual/eye problems (light sensitivity, spots, blurred vision), frequently reported by (former) SSRI-AntiDepressant users, are caused by some element of Pineal Gland dysfunction?
Continue... Serotonin & the Pineal Gland -Part 2
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SEROTONIN & THE PINEAL GLAND
Pineal Gland By Charly Groenendijk
The Netherlands
Oct 9, 2001 (updated March 11, 2003)
The Serotonergic System, the Pineal Gland & Side-Effects of Serotonin Acting Anti-Depressants -Part 1
Go to Serotonin & the Pineal Gland -Part 2
REFERENCE
The content of this article is based on and written in accordance with accepted theories in Bio-Psychiatry and should therefore be perceived as another theory.
Take notice that also non SSRI anti-depressants (such as SNRI's targeting the neurotransmitter nor-epinephrine (nor-adrenaline) and even Ritalin) may interact (primary or secondary) with the serotonergic system in the brain, causing serotonin deficiency symptoms.
1. Introduction: Neurons & Neurotransmitters
There are billions of working cells in our brain called Neurons and great variety in the kind of brain cells or neurons, with each group representing a specific cluster of functions. Neurons communicate with similar neurons by firing molecules from its nerve endings to the receiving nerve endings of the other neuron. The nerve endings of the firing part of the neuron are called axon terminals and the nerve endings of the receiving part of the neuron are called dendrites. The end of the axon terminals are called synapses. The synaptic cleft is the space where synapses and dendrites meet each other and where all the activity takes place. Each neuron is able to receive and fire molecules simultaneously. The molecules fired in the synaptic cleft are called neurotransmitters. Situated at the end of the axon terminals of the firing part of the neuron, the synapses work like "ball throwers." The dendrites of the receiving part of the other neuron, work like "catcher's mitts." They use receptor-molecules, or receptors, to capture the "thrown" neurotransmitters. (See Picture)
Re-Uptake
Once one neuron is firing neurotransmitters from it's synapse to the receiving dendrite of the other neuron, it is critically important that the "mis-fired" neurotransmitter left overs must be removed from the synaptic cleft. Any neurotransmitter which is not removed from the synaptic cleft, prevents further neurotransmitters from getting through. Re-uptake, the process of removing neurotransmitters after firing or release, allow these neurotransmitter left overs to be recycled for further use. Re-uptake is carried out by "transporter proteins" which bind to the mis-fired neurotransmitter and carry it across the plasma membrane back into the synapse of the firing neuron.
Medication classified "Re-Uptake Inhibitors" act on these transporter proteins and thereby inhibit the re-uptake of neurotransmitters back into the synapse of the firing neuron. SSRI-AntiDepressants or Selective Serotonin Re-uptake Inhibitors, belong to this class of medication. Each group of neurons fire specific neurotransmitter-molecules. The neurotransmitter Serotonin, also known as 5-Hydroxy-Tryptamine (5-HT) is such a molecule. SSRI-AntiDepressants inhibit the re-uptake of serotonin what means that more serotonin will be fired from synapse to dendrite in the synaptic cleft of every communicating serotonergic neuron in the brain.
2. The neurotransmitter "Serotonin"
In the brain, serotonin is synthesized from the amino acid precursor "Tryptophan". By enzymatic interaction, tryptophan converts into 5-HTP and eventually into serotonin. (see image) This neurotransmitter belongs to the group of serotonergic neurons which make the Serotonergic System in the brain. Levels of serotonin are highly concentrated in the Raphe Nuclei. Raphe Nuclei are present in the Medulla and Pons, 2 structures which are part of the Brainstem. From the Raphe Nuclei in the pons of the brainstem, also called "Rostral Raphe Nuclei", serotonin pathways project through parts of the Limbic System (like the Thalamus and Hypothalamus) into the Forebrain. (See Picture)
2.a. Serotonergic functioning
If you would believe the overwhelming advertisements of the pharmaceutical companies, you would think that serotonin primarily regulates mood. In fact, serotonin regulates a lot of other activities in the brain and body. In 1948, Maurice Rapport, a haematologist, found that serotonin tended to make blood form clots, and it tended to be a muscle- as well as a vasoconstrictor. Next to be a muscle- and vasoconstrictor, serotonin plays an important role in sleep, appetite, memory, aggression, sexual behaviour, cardiovascular activity, respiratory activity, motor output, sensory and neuroendocrine function, but most important, perception! Since 1988 the serotonin hype brought us several SSRI-AntiDepressants all stimulating this neurotransmitter. For about 11 years now, Dr. Ann Blake Tracy (Prozac: Panacea or Pandora?), persistently warns the public against raising serotonin levels. Doctor Tracy has taught us that an increase in serotonin produces rushes of insulin dropping sugar levels and chemically inducing hypoglycaemia (low blood sugar) in this way. Furthermore it has been established that too much serotonin damages blood vessels, particularly in the lungs, and may also harm heart valves. This would be due to the fact that serotonin is a powerful vasoconstrictor.
Affecting Mood or Mind?
But most alarming is the serotonin and perception connection. Doctor Tracy as well as other sources described how the hallucinogenic drug LSD strongly acts on this neurotransmitter serotonin. The numerous examples of human LSD experiences have learned us that serotonin plays a major part in perception, our sense of reality, how we experience our in- and outside world! Other examples of drugs acting on the serotonergic system are PCP and MDMA (Ecstasy). Most of the readers will recognize also these serotonergic drugs for their capability to produce "an altered state of consciousness" in human beings. In the way that the serotonergic system responds to serotonergic drugs, we may conclude that this system is heavily involved in the determination of ones perception and therefore ones thought processes and emotions. The advertisements from the pharmaceutical companies, promoting elevated serotonin levels as were they purely mood lifting, therefore seem to be rather misleading then informative. SSRI-AntiDepressants are to be considered mind-altering drugs and not primarily mood-altering.
In all these years since 1988, scientists are still not sure why serotonin boosters seem to "alleviate" depression. They assume that low serotonin levels could be a possible cause of endogenous depression, but it's still just a theory and not a proven fact! New research present us a different view on serotonin, which may not even have that connection with mood as previously thought. By experimental research, scientists discovered that a new drug, code-named MK-869, blocked a neuropeptide called " Substance P." By blocking this neuropeptide, people became less depressed. An interesting fact was, that blocking substance P did not affect the function of serotonin! This raises new concerns about the involvement of serotonin in mood and/or depression.
"But why do I hear people talking about benefits from these SSRI-AntiDepressants?", you might want to ask in this stage. "They surely must work somehow don't they?" The answer is yes, they "work" somehow, but not in a very proper way. The mechanism of action on serotonergic neurons implies a lot of other neuro- endocrine responses. What actually happens when you increase serotonergic neuronal activity or elevate your serotonin levels is this: the stress hormones "Cortisol" & "Adrenaline" (Epinephrine) in the brain and body are triggered by increased serotonergic activity or elevated serotonin levels. It is a natural reaction from the body to combat the excessive serotonin levels. These released hormones, cortisol and adrenaline, are secreted from the "Adrenal Glands." They give the human personality a boost, producing a euphoric state, which can last for a prolonged period of time. In this manner SSRI-AntiDepressants initially produce the deceptive results the doctor and "patient" are both expecting. *
If a patient continues to ingest a particular SSRI-antidepressant over a prolonged period of time, eventually the bodies Adrenal Glands may lose their efficiency and "Adrenal Exhaustion Syndrome" will be the end result. Adrenal Exhaustion causes levels of adrenaline initially to fall and levels of cortisol to rise. Ultimately, also cortisol levels fall. When untreated, Adrenal Exhaustion will lead to seriously declining physical health. Many (former) SSRI-AntiDepressant users reported fatigue as a long term side-effect or were diagnosed with "Chronigue Fatigue Syndrome." People suffering from stress are generally diagnosed with this disorder. Symptoms range from simple exhaustion to much more complex problems that are secondary to excessive output of adrenal hormones in the bloodstream, leading to Adrenal Exhaustion. Unlike the other hormones, it takes a long time before the Adrenal Glands have their adrenaline levels restored. Could we say that the SSRI-AntiDepressant "works" by slowly excavating the body's Adrenal Glands?
* [ Actually, when a family doctor (GP) or psychiatrist is observing a patient in a "euphoric" state of being, this should ring warning bells immediately! The drug induced (iatrogenic) conditions Akathisia & Mania are well documented in the medical litarature. Drug induced Mania, an abnormally elated mental state, typically characterized by feelings of euphoria, racing thoughts and talkativeness, is a "forerunner" of Akathisia, a neurologically driven agitation ranging from mild leg tapping, feeling "caffeinated" to severe panic, an extreme manic state and hyper-sensitivity of the nervous system. Akathisia can lead to suicidal, aggressive and/or homicidal thoughts and behaviours. When a doctor or psychiatrist is observing symptoms of mania and/or akathisia in a patient, SSRI-AntiDepressant use should be discontinued immediately! The pharmaceutical companies are well informed regarding above mentioned conditions and the capacity of their antidepressant inducing these symptoms. Therefore it is strongly advised to medical professionals, physicians, to monitor a patient very closely after prescription of (SSRI) anti-depressant treatment. In the field of Bio-Psychiatry it was a conventional common thought that hypothalamic-pituitary-adrenal (HPA) system dysregulation/hyperactivity (and thus excessive secretion of cortisol) played an important role in the pathophysiology of depression and that normalization of HPA axis hyperactivity could be achieved by (SSRI) anti-depressant treatment, and thus relief of depression. However, a study and a case report involving the non-SSRI antidepressant Remeron (mirtazapine) and a review show us that nor amelioration of HPA system dysregulation, nor reduction of cortisol secretion in depressed patients is correlated with relief of symptoms of depression. See: (1), (2), (3). Furthermore, a study developed by D. Jezova & R. Duncko, Laboratory of Pharmacological Neuroendocrinology, demonstrated that repeated SSRI-antidepressant treatment in healthy men does not inhibit, but enhances stress-induced pituitary hormone release (neuroendocrine activation). Cortisol levels failed to be modified by antidepressants. A simple search through available PubMed articles uncovers clearly that SSRI-antidepressants not only fail to modify cortisol, but actually stimulate/increase cortisol release. See: (1), (2), (3), (4), (5), (6). Initially the rise in cortisol & adrenaline (secreted from the Adrenal Glands) may create the illusion of a patient making progress in his/her situation, but a potential tragedy may be surfacing very soon. It is very well known that (SSRI-AntiDepressant induced) increased cortisol secretion can lead to violent suicidal behaviour.
(I would like to encourage you to use your discernment when viewing antidepressant involved suicide/homicide/violence cases represented by the media. In the section casualties of this website, these cases are carefully stored up to be a "silent" witness for the future, in order to testify regarding the devastating & powerful destructive effects these "legal drugs" exercised on children, adolescents and adults, not discriminating between men and women). ]
The Serotonin-Cycle: beaconing of conscious awareness and dream sleep?
One of the first significant discoveries about the serotonergic system in the brain was that it's activity was dramatically altered across the sleep-wake cycle. Serotonergic activity gradually decreases as one becomes drowsy and enter slow-wave sleep. An overall slowing of serotonergic activity is observed during slow-wave sleep known as non-REM sleep. During REM sleep (Rapid Eye Movement-the original dream sleep), serotonergic activity falls completely silent. Serotonergic activity returns to it's basic level several seconds prior to the end of REM sleep. REM sleep occurs in roughly 90-100 minute cycles, alternating with non-REM sleep (around 4 to 5 times during sleep). During non-REM sleep, there is lots of movement, but during REM sleep, only the eye muscles move. REM-dreaming turns on neurons in the medulla of the brainstem that inhibit all other motor activity. In this way it prevents the dreamer from sleepwalking and to act out his/her dreams in real time.
Another significant discovery was that, when during REM sleep the serotonergic neurons in the brainstem were "off" (silent), cholinergic neurons in the brainstem were "on" (firing)! Cholinergic neurons fire the neurotransmitter "Acetylcholine." Acetylcholine not only plays an important role in dreaming, but also in long-term memory processes. In the brainstem, the cholinergic "REM-on" neurons can only trigger REM sleep (and thus dreaming) when the serotonergic "REM-off" neurons are inactive. This happens because, in the brainstem, the serotonergic neurons inhibit the cholinergic neurons whilst we are awake. When, in the brainstem, the serotonergic neurons release their inhibitory constraint, only then, the cholinergic brainstem neurons will be able to get active, triggering the REM-dream sleep. Both the REM-on and the REM-off cells are localized in the brainstem. These brainstem mechanisms work as an "oscillator", which controls the transitions from waking to sleeping and further controls the REM/non-REM cycle, which occurs 4 to 5 times during sleep.
Now at this moment you might ask yourself, how it is possible that so many individuals report bizarre vivid lifelike dreams whilst on serotonin boosters, when an active serotonergic system suppresses REM sleep, and thereby dreaming? Serotonergic suppression of REM sleep in humans by acute dosage of SSRI-AntiDepressants was indeed confirmed. (see article) This is what Dr. Tracy is also been telling us for many years in her book. The PubMed article discusses rebound of REM sleep after abrupt withdrawal from an SSRI-AntiDepressant, but it still doesn't answer the question how it is possible that individuals are experiencing disturbing dreams and nightmares whilst they are taking an SSRI-AntiDepressant over a prolonged period of time. When I delved deeper into this matter I discovered some interesting facts. Although there is an important link between REM sleep and dreaming, they are in fact doubly dissociable states. That is, REM can occur without dreaming and dreaming can occur without REM. Although REM is triggered from the brainstem, it alone will not result in dream states. Dreams require input from the forebrain and structures in the limbic system. The forebrain mechanisms are the final common path to dreaming. The brainstem is just one of the many arousal triggers that can activate these forebrain mechanisms. Although REM sleep is controlled by the brainstem, dreaming seems to be controlled by these forebrain mechanisms. It is now acknowledged that REM sleep is not necessary for dreaming, that dreaming can also occur during non-REM sleep, and that dream-like experiences can even be elicited during quiet wakefulness! The controversial human reports of very vivid lifelike dreams whilst taking an SSRI-AntiDepressant could therefore be explained as existing outside and independent of the REM (dream) sleep! But, -now that we know that the forebrain is the final common path to dreaming, and SSRI-AntiDepressants suppress the brainstem's REM arousal system (which normally activates forebrain dreaming)- what kind of arousal triggers are then responsible for the activation of forebrain dreams during use of SSRI-AntiDepressants?
Forebrain Nightmares and Forebrain Seizures
An even more exciting discovery was that dreaming can also be induced by focal forebrain stimulation and by complex partial forebrain seizures during non-REM sleep, without the involvement of the brainstem's REM mechanism! There is a causal link between epileptic activity and recurring nightmares during non-REM sleep. This was demonstrated by neurosurgeon and researcher Wilder Penfield, who was able to reproduce these anxious experiences artificially in the form of waking "dreamy state" seizures. The causal link between forebrain seizures and recurring nightmares was confirmed by the fact that both the underlying seizure disorder and the nightmares responded to anticonvulsant therapy.
Here is an example of a recurring nightmare, caused by epileptic activity in the forebrain:
The patient [35 year old woman with idiopathic complex-partial seizures] reported a recurrent dream about her [dead] brother ... which has reappeared several times. The dream is as follows: "I am walking down the street. I meet him. He is with a group of people whom I know now. I feel that I will be so happy to see him. I say to him, `I'm glad you're alive,' but he'll deny that he is my brother and he'll say so, and I'll wake up crying and trying to convince him."' Electroencephalography revealed a poorly defined right anterior temporal / right temporal spike focus which appeared with the onset of drowsiness and light sleep (Epstein & Ervin 1957, p. 45).
Could it be that the bizarre vivid lifelike dreams, reported by SSRI-AntiDepressant users are epileptiform of nature? Notice the "poorly defined spike focus." Could it be that this is epileptic activity which remains undiscovered because it is barely detectable? Standard tests for epilepsy included?
3. The Pineal Gland
The Pineal Gland -also called the epiphysis- looks like a miniature pine cone and is situated in the middle of the brain beneath the two brain halves, surrounded by the ventricles, under the roof of the corpus callosum (cross-beam connecting the 2 brain halves). (see picture) This active organ has, together with the Pituitary Gland (see picture), the next highest blood circulation after the kidneys. It is not protected by the blood-brain barrier and therefore makes this gland fragile to any substance entering the bloodstream. It is, for instance, very sensitive to fluoride.
Another factor involved in affecting the Pineal Gland can be excessive high or even toxic levels of an SSRI-AntiDepressant in the bloodstream. Certain individuals have a metabolic deficiency in the metabolism of anti-depressant medication. In the liver, a group of enzymes named " cytochrome P-450" enzymes, particularly the "CYP2D6 enzymes" of this group of enzymes, metabolise SSRI-AntiDepressants. When not properly metabolised, because one has a metabolic deficiency, a daily therapeutic dose can build up to excessive high or even toxic levels in the bloodstream. Hence, the Pineal Gland would be an easy target, since it is not very well protected by the blood-brain barrier. It is it's connection to serotonin what makes this organ so very interesting.
3.a. The Pineal Gland-Serotonin connection
Nicholas Giarmin, a professor of pharmacology and Daniel Freedman, a professor of psychiatry, confirmed that the human brain manufactures serotonin at various sites in the brain. For example, in the Thalamus, they discovered 61 nanograms of serotonin per gram of tissue; in the Hippocampus, 56 ng.; in the Central Gray Section of the Midbrain, they found 482 ng. But in the Pineal Gland, they found 3140 ng. of serotonin per gram of tissue. The Pineal Gland was unmistakably the richest site of serotonin in the brain! This discovery implicates the Pineal Gland as an important site of serotonergic activity.
The neurohormone Melatonin & the Endocrine System
One of the neurotransmitters secreted by the Pineal Gland is Melatonin, also known as N-Acetyl-5-Methoxy-Tryptamine (NA-5-MT). In the Pineal Gland, serotonin converts into melatonin by enzymatic interaction. Melatonin is also an important hormone to the body, that's why it is called a neurohormone. It is necessary to regulate the function of all organs of the Endocrine System in the body. The organs or glands of the endocrine system are: the Pituitary Gland, situated in the brain; the Thyroid + Parathyroid Glands; the Thymus; the Pancreas; the Ovaries/Testes (see image). All of these endocrine organs/glands secrete their hormones to the blood. The Pituitary Gland stimulates the secretion of these hormones, while the Pineal Gland apply the brakes on them through it's neurohormone melatonin. If the endocrine organs/glands release too much of their hormones, for instance when we are stressed, then the Pineal Gland releases melatonin to counteract these hormones. Also serotonin gets released when stress is involved. The increased serotonin triggers the release of adrenaline, which allows the body to work through the stress.
The Pineal Gland is a magneto sensitive organ, what means that it is sensitive to electromagnetic fields (EMF). It is sensitive to electromagnetic waves from computer monitors, cellular phones, microwave ovens, high voltage lines, etc.. Electromagnetic fields suppress the activity of the Pineal Gland and reduce melatonin production. EMF also affect serotonin.
The neurohormone Melatonin & the Eye-SCN-Pineal Gland Axis
The Pineal Gland is also a photosensitive organ, what means that it is sensitive to light. It normally releases melatonin when it no longer receives light impulses. Just like serotonin, also melatonin has it's own day & night cycle (circadian rhythm) which begins where the cycle of serotonin normally ends. When serotonin reaches it's lowest level at night (in the dark) during slow wave sleep, the Pineal Gland starts to convert it's store of serotonin into melatonin to be released prior to REM sleep. Melatonin has it's peak around 02:00 AM. During daytime, the daylight inhibits the release of melatonin. This works as follows: when, during daytime, light reaches the eyes, then it's presence gets translated into nerve impulses, which travel through the optic nerve between the eyes and a region of the Hypothalamus called the "Suprachiasmatic Nucleus" (SCN). (see picture) The SCN in it's turn sends it's nerve impulses to the Pineal Gland. These impulses inhibit the Pineal Gland's production of melatonin until it gets dark, when it's to be released again.
Melatonin is not only present in the brain and body but also in the eye! One has speculated whether or not high melatonin levels in the eyes during daylight exposure, may bring damage to them over time. Visual/eye problems (light sensitivity, spots, blurred vision) are other symptoms, frequently reported by (former) SSRI-AntiDepressant users. I questioned myself if these problems could be related to elevated melatonin levels in the eye. When serotonin accumulates in the Pineal Gland, on account of an SSRI-AntiDepressant, then it would come under pressure to produce more melatonin out of the excessive amounts of serotonin. Hence, during daytime, melatonin levels in the eyes would be significantly higher then normally would occur... But, I had to revise this hypothesis. In a PubMed study, SSRI-AntiDepressants were found not to elevate melatonin levels in humans. Although "Luvox" and "Paxil" increases melatonin to a more or lesser amount, apparently this seemed not to be the case for the other SSRI-AntiDepressants. However, since the Pineal Gland does contain a complete map of the visual field of the eyes, could there be a correlation between visual/eye problems and a dysfunctional Pineal Gland?
A case, noted by Dr. Berman, could give us some more insight into this matter:
A child was brought to a German clinic suffering from eye trouble and headaches. He was five years old and very mature, and apparently had reached the age of adolescence. He was abnormally bright mentally, discussing metaphysical and spiritual subjects. He was strongly group-conscious and only happy when sharing what he had with others. After his arrival at the clinic, he rapidly grew worse and died in a month. An autopsy showed a tumour of the pineal gland. - Berman, Louis, M.D., The Glands Regulating Personality, p. 89.
Could it be that the visual/eye problems (light sensitivity, spots, blurred vision), frequently reported by (former) SSRI-AntiDepressant users, are caused by some element of Pineal Gland dysfunction?
Continue... Serotonin & the Pineal Gland -Part 2
This website is designed for educational purposes only and does not intend to offer medical advice.
We are not affiliated with any organization or group. Also visit Dr Tracy's site DrugAwareness.org.
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All Truth passes through Three Stages: First, it is Ridiculed. Second, it is Violently Opposed... Third, it is Accepted as being Self-Evident. - Arthur Schopenhauer (1778-1860) By Charly Groenendijk Back to Side-Effects
The Netherlands
2000 - 2009
Toxicity and Brain Damage
"Who does Not Know the Truth, is simply a Fool...
Yet who Knows the Truth and Calls it a Lie, is a Criminal."
- In "Galileo Galilei" by Berthold Brecht (1898-1956)
Take notice that also non SSRI anti-depressants (and even Ritalin) may interact (primary or secondary) with the serotonergic (or serotoninergic) system in the brain.
PHYSICIANS REMEMBER... "FIRST DO NO HARM"...
SSRI/SSNRI-induced Toxicity & Brain Damage by disrupting the balance of Body & Brain Metabolism
SSRI's are "Selective Serotonin Re-Uptake Inhibitors." In contrast to the deceiving claim of the pharmaceutical companies that SSRI's or SSNRI's may correct some sort of "biochemical imbalance" of serotonin in the brain, all of these serotonergic agents actually cause major and dangerous imbalances in the brain and the body, evidenced by the many medical reports (below) of severe toxic neurological and physical side-effects. Neuronal re-uptake of neurotransmitters is metabolism. What serotonin re-uptake inhibitor actually means is that the SSRI-antidepressant interferes with ones ability to metabolise serotonin, so that can and will build up to toxic amounts after prolonged use. In other words, an SSRI-antidepressant impairs the ability of cells to metabolise serotonin, not only in the brain, but -since serotonin is widely distributed throughout the body- in the body as well! The greatest concentration of serotonin, around 90%, is not found in the brain, but is found in the gastrointestinal or digestive tract (human gut, intestines, bowels).
Originally, the neurotransmitter serotonin -thought to be secreted by the Pineal Gland- is called a neurohormone, because of it's specific regulatory effect on the activity of the Endocrine Glands in the human body. (1),(2) Affecting serotonin thus means also affecting the Glandular Endocrine System. Next to it, serotonin affects the Cardiovascular System and the Respiratory System, under which, the lungs. Serotonin is also found in blood platelets and stimulates platelet aggregation (blood clotting). Furthermore, serotonin is known to affect contraction of smooth muscles (such as those of the gut) and blood vessel elasticity (vasoconstriction and expansion). More information: Serotonin & the Pineal Gland
A recent study (25 sept, 2004) shows us clearly that serotonin toxicity can even appear rapidly in a few hours after taking a single therapeutic dose of SSRI medication. In Bio-Psychiatry it is a common thought that SSRI's are believed to have their effect by inhibiting the re-uptake of serotonin (downregulation of transporters) and thereby gradually increasing serotonin outside the tissue cell wall (extracellular) in the synaptic gap between brain cells (neurons) in the brain. In this important study, Zoloft (Lustral, sertraline) was given to monkeys for 4 weeks to establish how long it would take before Zoloft would have it's effect on serotonergic neurons and thus elevation of serotonin. In contrast with the commonly accepted SSRI theory, it was observed that serotonin levels raised NOT gradually, but rapidly and dramatically and kept on raising during these 4 weeks, an effect that can NOT be ascribed solely to a "re-uptake inhibition" of serotonin!
Antidepressant induced neurological and/or physical toxicity (body and/or brain damage) either as a result of prolonged inhibition of P450-2D6 liver-enzymes, or as a result of impairing serotonin metabolism, can take on many forms as described below. A few examples are: Hyperserotonemia, such as the lifethreatening condition the Serotonin Syndrome, Epileptiform Discharges, Epileptic Seizures and/or Epilepsy, Hypoglycaemia/Hyperglycemia (Low/Elevated Blood Sugar Imbalance), Stroke/Hemorrhagic Syndromes, Frontal Lobe Syndrome, Tardive Dyskinesia/Dystonia, Parkinsonism, Akathisia, Mania, etc...
Tardive Dyskinesia/Dystonia, Parkinsonism & Akathisia
SSRI & SSNRI antidepressants induced side-effects (Iatrogenic Extrapyramidal Symptoms) are
recognized to be similar to Neuroleptic (anti-psychotic) induced side-effects. These side-effects are known as Tardive Dyskinesia/Dystonia (severe body movement disorder, mostly permanent), Parkinsonism (a sign of future Parkinson's disease) and Akathisia (a Neurological driven severe mania/agitation that can lead to suicidality, suicide attempts, self-harm & suicide). It is well documented in the medical literature that these neuroleptic induced side-effects refer to damage at dopaminergic neurons in the "motor system" of the
"Basal Ganglia", a structure deep in the "Limbic System" of the brain. 1, 2, 3, 4, http://www.emedicine.com/EMERG/topic338.htm (scroll down)
Serotonin Syndrome
The Serotonin Syndrome is a potentially lethal condition caused by excessive serotonergic activity. It is a very dangerous and a potentially fatal side effect of the serotonergic enhancing drugs such as SSRI & SSNRI antidepressants and is diagnosed by the presence of at least 3 of 10 symptoms: mental status changes (confusion, hypomania), agitation, myoclonus, hyperreflexia, diaphoresis, shivering, tremor, diarrhea, incoordination, and fever. This "hyperserotonergic" toxic condition requires heightened clinical awareness in order to prevent, recognize, and treat the condition promptly. Promptness is vital because, as we just mentioned, the serotonin syndrome can be fatal and death from this side effect can come very rapidly. The Serotonin syndrome is brought on by excessive levels of serotonin and is difficult to distinguish from the "Neuroleptic Malignant Syndrome" because the symptoms are so similar. The "Neuroleptic Malignant Syndrome" is a serious condition brought on by the use of neuroleptic drugs (anti-psychotics).
Source: Prozac: Panacea or Pandora? by Dr Ann Blake Tracy http://members.aol.com/atracyphd/syndrome.htm
Source: Journal of Clinical Psychiatry
MEDICAL REPORTS OF SSRI/SSNRI ANTIDEPRESSANT INDUCED (IATROGENIC) SEVERE SYMPTOMS:
Go to: Newborn Baby (Neonatal) Neurological Damage & Withdrawal
Go to: General Physical & Mental Side-Effects
Go to: Body Movement Disorders (Dystonia) & Parkinsonism (future Parkinson's disease)
Go to: Akathisia, Mania, Restlessness & Restless Legs Syndrome
Go to: Serotonin Syndrome, Neuroleptic Malignant Syndrome
Go to: Blood/Organ Diseases, Stroke, Hemorrhage, TIA, Tumours & Bleedings
Go to: Hepato Toxicity (Liver Damage)
Go to: Cardiovascular Toxicity (Heart Damage) & Neurological Toxicity (Brain Damage)
Go to: Epileptiform Activity, Epilepsy, Seizures, REM Sleep/Memory/EEG Problems, Sleepwalking
Go to: Hypoglycemia (low blood sugar), Hyperglycemia (high blood sugar, Diabetes)
Go to: Urinary Incontinence, Dermatologic (Skin) Problems, Ocular (Eyes) Disturbances
Go to: Pain & Numbness, Swellings, Sexual (Organ) Problems, Hormonal Imbalances
Go to: Hyponatremia & Syndrome of Inappropriate Secretion of Antidiuretic Hormone (SIADH)
Go to: (Suicide Overdose)-Toxicity & Death
Go to: Suicide, Suicidality, Suicide Attempts & Self-Harm
Go to: Mental State, Perceptual, Emotional & Psychological Changes
Go to: Mental & Physical Side-Effects of Withdrawal/Discontinuation
Go to: Other Observations & Complications: Case Reports, Reviews & Studies
SSRI & SSNRI Antidepressants: NEWBORN BABY (NEONATAL) NEUROLOGICAL DAMAGE & WITHDRAWAL
2004
09/00
Case/Study Neonatal toxicity: Fluoxetine concentrations in cord & maternal serum
2004
08/09
WARNING Health Canada: Potential Neurological Adverse Effects of SSRI's on Newborns
2004
08/00
Case/Study Using an SSRI during pregnancy has Damaging Teratogenic Effects on the Fetus
2004
06/00
Case/Review Baby SSRI (withdrawal) side-effects: agitation, breathing & suction problems
2004
02/00
Case/Study SSRI's during pregnancy: Foetal Brain Damage (Neurobehavioral Disruptions)
2003
11/00
Case/Review Neonatal (baby) Large Intraventricular Haemorrhage with maternal use of Paxil
2003
08/00
Case/Review Baby SSRI (withdrawal) effects: hypoglycaemia, bradycardia, tachycardia, jaundice
2003
07/00
Case/Review Increased risk for neonatal problems after exposure to SSRI's in late pregnancy
2003
07/14
Case/Review SSRI's During Pregnancy May Cause Neurologic Symptoms in Newborns
2003
07/12
Case/Review Withdrawal symptoms in Baby after exposure to Effexor during pregnancy
2003
04/16
Case/Review Neonatal (baby) Convulsions & Subarachnoid Hemorrhage after exposure to Paxil
2001
09/00
Case/Review Neonatal Paxil withdrawal syndrome or actually serotonin syndrome?
2001
03/00
Case/Review Baby SSRI withdrawal syndrome lasting up to one month after birth
2001
03/00
Case/Review BABY Withdrawal Syndrome after exposure to SSRI's Celexa, Paxil & Prozac
2000
10/11
Case/Review Prozac Toxicity in preterm infant: marked motor automatism & skin manifestations
1999
11/00
Case/Study Breastfeeding while taking Prozac associated with reduced growth infants
1997
11/00
Case/Review SSRI's, Breast Milk and Baby Withdrawal Symptoms
Abnormalities in Brain Cells (Neurons)
2004
06/21
Animal Study SSRI disrupts development of neural circuitry during cortical synaptic formation
2002
04/15
Bio-Study Neuronal Cell Death induced by Fluoxetine (Prozac, Sarafem)
2000
02/29
Animal Study Prozac & other SSRI's cause Shriveled & Corkscrew Shaped Brain Cells
1999
09/25
Animal Study Prozac Induces Muscle Contractions and has other Molecular Targets Part2
1999
-1998
Dr Ann.B.Tracy SSRI induced hypoglycaemia & raised cortisol levels: Braincells Die 1, 2, 3, 4, 5
1998
09/01
Animal Study Brain cell (neuron) function in forebrain altered by prenatal exposure to Prozac
1998
08/00
Animal Study Reduced activity of rat dopaminergic neurons in the VTA may explain "Akathisia"
1997
00/00
Animal Study Prenatal exposure to Prozac produces changes in brain serotonin (5-HT) neurons
1992
10/00
Animal Study Site specific malformations in mouse embryos following exposure to SSRI's
Abnormalities in the "Motor System", deep in older part of the brain (basal ganglia of the limbic system).
2004
-2000
Antidepres.Facts SSRI induced Akathisia: a neurological state of restlessness and agitation
2004
01/16
The Hilltop Bruxism -Nocturnal TeethGrinding: Anti-depressants causing Damage to Teeth
2002
05/00
J.Clin.Psychiatry Case Report: Dystonia Induced by Mirtazapine (Remeron)
2001
07/00
J.Clin.Psychiatry Case Report: SSRI-Induced Akathisia & Nefazodone (Serzone)
2000
00/00
Dr Jos.Glenmullen SSRI induced "Parkinsonism", Muscle Spasms and "Tardive Dyskinesia"
1999
06/00
J.Clin.Psychiatry Case Report: SSRI-Induced Parkinsonism (future Parkinson's)
Neurological & Physical Side-Effects of dangerous condition "Hyperserotonemia"
2004
-2000
Antidepres.Facts The Serotonin Syndrome: a serious, dangerous & potentially fatal condition
2000
04/00
J.Ch.Adol.Psych. Child, 9; liver cytochrome P-450 2D6 deficiency; Prozac-related death
1999
-1998
Dr Ann.B. Tracy Increased Serotonin: psychosis, mania, aggression, autism, anorexia, abortions
1998
08/28
MIT News Too much Serotonin damages Blood Vessels, particularly in the Lungs
1994
00/00
Psychph.Bulletin SSRI Toxicity by inhibition of Cytochrome P450 Isoenzymes Related Link
(SSRI/SSNRI) Antidepressants
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Nefazodone: Serzone or Dutonin
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Trazodone: Trazodone or Desyrel
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All Truth passes through Three Stages: First, it is Ridiculed. Second, it is Violently Opposed... Third, it is Accepted as being Self-Evident. - Arthur Schopenhauer (1778-1860) By Charly Groenendijk Back to Side-Effects
The Netherlands
2000 - 2009
Toxicity and Brain Damage
"Who does Not Know the Truth, is simply a Fool...
Yet who Knows the Truth and Calls it a Lie, is a Criminal."
- In "Galileo Galilei" by Berthold Brecht (1898-1956)
Take notice that also non SSRI anti-depressants (and even Ritalin) may interact (primary or secondary) with the serotonergic (or serotoninergic) system in the brain.
PHYSICIANS REMEMBER... "FIRST DO NO HARM"...
SSRI/SSNRI-induced Toxicity & Brain Damage by disrupting the balance of Body & Brain Metabolism
SSRI's are "Selective Serotonin Re-Uptake Inhibitors." In contrast to the deceiving claim of the pharmaceutical companies that SSRI's or SSNRI's may correct some sort of "biochemical imbalance" of serotonin in the brain, all of these serotonergic agents actually cause major and dangerous imbalances in the brain and the body, evidenced by the many medical reports (below) of severe toxic neurological and physical side-effects. Neuronal re-uptake of neurotransmitters is metabolism. What serotonin re-uptake inhibitor actually means is that the SSRI-antidepressant interferes with ones ability to metabolise serotonin, so that can and will build up to toxic amounts after prolonged use. In other words, an SSRI-antidepressant impairs the ability of cells to metabolise serotonin, not only in the brain, but -since serotonin is widely distributed throughout the body- in the body as well! The greatest concentration of serotonin, around 90%, is not found in the brain, but is found in the gastrointestinal or digestive tract (human gut, intestines, bowels).
Originally, the neurotransmitter serotonin -thought to be secreted by the Pineal Gland- is called a neurohormone, because of it's specific regulatory effect on the activity of the Endocrine Glands in the human body. (1),(2) Affecting serotonin thus means also affecting the Glandular Endocrine System. Next to it, serotonin affects the Cardiovascular System and the Respiratory System, under which, the lungs. Serotonin is also found in blood platelets and stimulates platelet aggregation (blood clotting). Furthermore, serotonin is known to affect contraction of smooth muscles (such as those of the gut) and blood vessel elasticity (vasoconstriction and expansion). More information: Serotonin & the Pineal Gland
A recent study (25 sept, 2004) shows us clearly that serotonin toxicity can even appear rapidly in a few hours after taking a single therapeutic dose of SSRI medication. In Bio-Psychiatry it is a common thought that SSRI's are believed to have their effect by inhibiting the re-uptake of serotonin (downregulation of transporters) and thereby gradually increasing serotonin outside the tissue cell wall (extracellular) in the synaptic gap between brain cells (neurons) in the brain. In this important study, Zoloft (Lustral, sertraline) was given to monkeys for 4 weeks to establish how long it would take before Zoloft would have it's effect on serotonergic neurons and thus elevation of serotonin. In contrast with the commonly accepted SSRI theory, it was observed that serotonin levels raised NOT gradually, but rapidly and dramatically and kept on raising during these 4 weeks, an effect that can NOT be ascribed solely to a "re-uptake inhibition" of serotonin!
Antidepressant induced neurological and/or physical toxicity (body and/or brain damage) either as a result of prolonged inhibition of P450-2D6 liver-enzymes, or as a result of impairing serotonin metabolism, can take on many forms as described below. A few examples are: Hyperserotonemia, such as the lifethreatening condition the Serotonin Syndrome, Epileptiform Discharges, Epileptic Seizures and/or Epilepsy, Hypoglycaemia/Hyperglycemia (Low/Elevated Blood Sugar Imbalance), Stroke/Hemorrhagic Syndromes, Frontal Lobe Syndrome, Tardive Dyskinesia/Dystonia, Parkinsonism, Akathisia, Mania, etc...
Tardive Dyskinesia/Dystonia, Parkinsonism & Akathisia
SSRI & SSNRI antidepressants induced side-effects (Iatrogenic Extrapyramidal Symptoms) are
recognized to be similar to Neuroleptic (anti-psychotic) induced side-effects. These side-effects are known as Tardive Dyskinesia/Dystonia (severe body movement disorder, mostly permanent), Parkinsonism (a sign of future Parkinson's disease) and Akathisia (a Neurological driven severe mania/agitation that can lead to suicidality, suicide attempts, self-harm & suicide). It is well documented in the medical literature that these neuroleptic induced side-effects refer to damage at dopaminergic neurons in the "motor system" of the
"Basal Ganglia", a structure deep in the "Limbic System" of the brain. 1, 2, 3, 4, http://www.emedicine.com/EMERG/topic338.htm (scroll down)
Serotonin Syndrome
The Serotonin Syndrome is a potentially lethal condition caused by excessive serotonergic activity. It is a very dangerous and a potentially fatal side effect of the serotonergic enhancing drugs such as SSRI & SSNRI antidepressants and is diagnosed by the presence of at least 3 of 10 symptoms: mental status changes (confusion, hypomania), agitation, myoclonus, hyperreflexia, diaphoresis, shivering, tremor, diarrhea, incoordination, and fever. This "hyperserotonergic" toxic condition requires heightened clinical awareness in order to prevent, recognize, and treat the condition promptly. Promptness is vital because, as we just mentioned, the serotonin syndrome can be fatal and death from this side effect can come very rapidly. The Serotonin syndrome is brought on by excessive levels of serotonin and is difficult to distinguish from the "Neuroleptic Malignant Syndrome" because the symptoms are so similar. The "Neuroleptic Malignant Syndrome" is a serious condition brought on by the use of neuroleptic drugs (anti-psychotics).
Source: Prozac: Panacea or Pandora? by Dr Ann Blake Tracy http://members.aol.com/atracyphd/syndrome.htm
Source: Journal of Clinical Psychiatry
MEDICAL REPORTS OF SSRI/SSNRI ANTIDEPRESSANT INDUCED (IATROGENIC) SEVERE SYMPTOMS:
Go to: Newborn Baby (Neonatal) Neurological Damage & Withdrawal
Go to: General Physical & Mental Side-Effects
Go to: Body Movement Disorders (Dystonia) & Parkinsonism (future Parkinson's disease)
Go to: Akathisia, Mania, Restlessness & Restless Legs Syndrome
Go to: Serotonin Syndrome, Neuroleptic Malignant Syndrome
Go to: Blood/Organ Diseases, Stroke, Hemorrhage, TIA, Tumours & Bleedings
Go to: Hepato Toxicity (Liver Damage)
Go to: Cardiovascular Toxicity (Heart Damage) & Neurological Toxicity (Brain Damage)
Go to: Epileptiform Activity, Epilepsy, Seizures, REM Sleep/Memory/EEG Problems, Sleepwalking
Go to: Hypoglycemia (low blood sugar), Hyperglycemia (high blood sugar, Diabetes)
Go to: Urinary Incontinence, Dermatologic (Skin) Problems, Ocular (Eyes) Disturbances
Go to: Pain & Numbness, Swellings, Sexual (Organ) Problems, Hormonal Imbalances
Go to: Hyponatremia & Syndrome of Inappropriate Secretion of Antidiuretic Hormone (SIADH)
Go to: (Suicide Overdose)-Toxicity & Death
Go to: Suicide, Suicidality, Suicide Attempts & Self-Harm
Go to: Mental State, Perceptual, Emotional & Psychological Changes
Go to: Mental & Physical Side-Effects of Withdrawal/Discontinuation
Go to: Other Observations & Complications: Case Reports, Reviews & Studies
SSRI & SSNRI Antidepressants: NEWBORN BABY (NEONATAL) NEUROLOGICAL DAMAGE & WITHDRAWAL
2004
09/00
Case/Study Neonatal toxicity: Fluoxetine concentrations in cord & maternal serum
2004
08/09
WARNING Health Canada: Potential Neurological Adverse Effects of SSRI's on Newborns
2004
08/00
Case/Study Using an SSRI during pregnancy has Damaging Teratogenic Effects on the Fetus
2004
06/00
Case/Review Baby SSRI (withdrawal) side-effects: agitation, breathing & suction problems
2004
02/00
Case/Study SSRI's during pregnancy: Foetal Brain Damage (Neurobehavioral Disruptions)
2003
11/00
Case/Review Neonatal (baby) Large Intraventricular Haemorrhage with maternal use of Paxil
2003
08/00
Case/Review Baby SSRI (withdrawal) effects: hypoglycaemia, bradycardia, tachycardia, jaundice
2003
07/00
Case/Review Increased risk for neonatal problems after exposure to SSRI's in late pregnancy
2003
07/14
Case/Review SSRI's During Pregnancy May Cause Neurologic Symptoms in Newborns
2003
07/12
Case/Review Withdrawal symptoms in Baby after exposure to Effexor during pregnancy
2003
04/16
Case/Review Neonatal (baby) Convulsions & Subarachnoid Hemorrhage after exposure to Paxil
2001
09/00
Case/Review Neonatal Paxil withdrawal syndrome or actually serotonin syndrome?
2001
03/00
Case/Review Baby SSRI withdrawal syndrome lasting up to one month after birth
2001
03/00
Case/Review BABY Withdrawal Syndrome after exposure to SSRI's Celexa, Paxil & Prozac
2000
10/11
Case/Review Prozac Toxicity in preterm infant: marked motor automatism & skin manifestations
1999
11/00
Case/Study Breastfeeding while taking Prozac associated with reduced growth infants
1997
11/00
Case/Review SSRI's, Breast Milk and Baby Withdrawal Symptoms
Abnormalities in Brain Cells (Neurons)
2004
06/21
Animal Study SSRI disrupts development of neural circuitry during cortical synaptic formation
2002
04/15
Bio-Study Neuronal Cell Death induced by Fluoxetine (Prozac, Sarafem)
2000
02/29
Animal Study Prozac & other SSRI's cause Shriveled & Corkscrew Shaped Brain Cells
1999
09/25
Animal Study Prozac Induces Muscle Contractions and has other Molecular Targets Part2
1999
-1998
Dr Ann.B.Tracy SSRI induced hypoglycaemia & raised cortisol levels: Braincells Die 1, 2, 3, 4, 5
1998
09/01
Animal Study Brain cell (neuron) function in forebrain altered by prenatal exposure to Prozac
1998
08/00
Animal Study Reduced activity of rat dopaminergic neurons in the VTA may explain "Akathisia"
1997
00/00
Animal Study Prenatal exposure to Prozac produces changes in brain serotonin (5-HT) neurons
1992
10/00
Animal Study Site specific malformations in mouse embryos following exposure to SSRI's
Abnormalities in the "Motor System", deep in older part of the brain (basal ganglia of the limbic system).
2004
-2000
Antidepres.Facts SSRI induced Akathisia: a neurological state of restlessness and agitation
2004
01/16
The Hilltop Bruxism -Nocturnal TeethGrinding: Anti-depressants causing Damage to Teeth
2002
05/00
J.Clin.Psychiatry Case Report: Dystonia Induced by Mirtazapine (Remeron)
2001
07/00
J.Clin.Psychiatry Case Report: SSRI-Induced Akathisia & Nefazodone (Serzone)
2000
00/00
Dr Jos.Glenmullen SSRI induced "Parkinsonism", Muscle Spasms and "Tardive Dyskinesia"
1999
06/00
J.Clin.Psychiatry Case Report: SSRI-Induced Parkinsonism (future Parkinson's)
Neurological & Physical Side-Effects of dangerous condition "Hyperserotonemia"
2004
-2000
Antidepres.Facts The Serotonin Syndrome: a serious, dangerous & potentially fatal condition
2000
04/00
J.Ch.Adol.Psych. Child, 9; liver cytochrome P-450 2D6 deficiency; Prozac-related death
1999
-1998
Dr Ann.B. Tracy Increased Serotonin: psychosis, mania, aggression, autism, anorexia, abortions
1998
08/28
MIT News Too much Serotonin damages Blood Vessels, particularly in the Lungs
1994
00/00
Psychph.Bulletin SSRI Toxicity by inhibition of Cytochrome P450 Isoenzymes Related Link
(SSRI/SSNRI) Antidepressants
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Side-Effects
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Citalopram: Celexa or Cipramil
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Escitalopram: Cipralex or Lexapro
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Duloxetine: Cymbalta
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Venlafaxine: Effexor or Efexor
Antidepressant
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Paroxetine: Paxil, Seroxat, Aropax or Pexeva
Antidepressant
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Fluoxetine: Prozac or Sarafem
Antidepressant
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Mirtazapine: Remeron or Remergil
Antidepressant
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Nefazodone: Serzone or Dutonin
Antidepressant
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Trazodone: Trazodone or Desyrel
Antidepressant
Side-Effects
Bupropion: Wellbutrin or Zyban
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Wednesday, December 8, 2010
Erowid Methylphenidate (Ritalin)
http://www.erowid.org/pharms/methylphenidate/methylphenidate_info1.shtml
Summary of the Medical Uses of Methylphenidate
by Seth
Dec 2002
Methylphenidate is a prescription drug often used for attention deficit disorder (ADD), attention deficit hyperactivity disorder (ADHD), and narcolepsy. Although the FDA has not approved these uses, it is also used in mild to moderate depression, brain injury, HIV infection fatigue, post-stroke patients, and for anesthesia-related hiccups.
Prescription drugs that the are considered addictive or recreational are scheduled by how much control the government believes is necessary to reduce inappropriate uses pursuant to U.S. Code of Federal Regulations, Title 20 Part 1308.1 (1987). Methylphenidate has been put into Schedule II, the most restrictive medical category. Due to its schedule, prescriptions for methylphenidate may not be called in or faxed to a pharmacy except in an emergency situation.
Use of methylphenidate for ADD and ADHD is common but controversial. Many people feel that it is over prescribed. A new non-stimulant treatment for ADD and ADHD that will be named Straterra (a nor-epinephrine reuptake inhibitor) could dramatically decrease the use of stimulants. Dr. Mary Ann Block, author of "No More Ritalin: Treating ADHD Without Drugs" is one of the foremost critics of the use of Ritalin. She maintains that methylphenidate dose not correct the underlying causes of ADHD. These may include: hypoglycemia, allergies and sensitivities, environmental factors and hyperthyrodism. The Feingold Association of the United States (http://www.feingold.org) is an organization that works on drug-free approaches to ADD and ADHD.
Chemically, methylphenidate hydrochloride is methyl-alpha-phenyl-2-piperidineacetate hydrochloride. It is a white, odorless, fine crystalline powder with a chemical formula C14H20ClNO2. . It is slightly acidic. A 5% aqueous solution is neutral to litmus.. It is freely soluble in water and methanol, soluble in alcohol, and slightly soluble in chloroform and acetone. Its molecular weight is 269.77. pKa equals 8.9. LD50 in mice (the dose that is lethal to 50% of the mice studied) is 190mg/kg.
Methylphenidate is marketed under many names. Different companies have produced methylphenidate with a variety of delivery systems. These different systems are used to prevent children from having to take doses at school, to keep a steady level of the drug, or to cause the level to rise sharply at specific times. Novartis markets methylphenidate as Ritalin. Mallinckrodt markets it as Methylin, Alza calls it Concerta, and Medeva uses Metadate as their name.
The FDA has approved methylphenidate as part of a total treatment program in children with a behavioral syndrome characterized by moderate to severe distractibility, short attention span, hyperactivity, emotion lability, and impulsivity greater than that expected for a child that age. Stimulants are not for childen or adults who exhibit symptoms secondary to environmental factors or primary psyciatric disorders, including psychosis. When symptoms are associated with acute stress reactions, methylphenidate is usually not indicated.
The mode of action in people is not completely understood, but methylphenidate activates the brain stem arousal system and cortex to produce its stimulant effect. Mehtylphenidate is very similar to other amphetamines structurally. It appears to increase extracellular dopamine. This action is likely achieved through inhibition of dopamine transporter protein. Some research also shows that methylphendate inhibits serotonin transporter protein. This action may partially explain its antidepressant effects. Methylphenidate also increases norepinephrine (noradrenaline). Methylphenidate also affects regional cerebral blood flow in the cerebellar vermis.
Dosage should be individualized according to the needs of the patients.
Adult Dosages: #
Immediate release tablets should be given 2 or 3 times daily, preferabley 30-45 minutes before meals. Average dosage is 20 to 30mg daily. Some patients may require 40-60mg daily. In others 10 to 15mg will be adequate. Patients who are unable to sleep should take their last dose before 6 pm. Women appear to absorb methylphenidate better than men, and may need slightly lower dosages.
Time released preparations vary. Sustained-release tablets such as Ritalin SR have a duration of approximately 8 hours and may be used in place of regular tablets. These tablets must be swallowed whole, never crushed or chewed. Crushing or chewing causes the time release mechanism to fail, delivering all of the medication at once.
Concerta should be given once daily in the morning, without regard to meals. Doses start at 18mg in the morning and may range up to 54mg. Each tablet releases the drug over 12 hours.
Metadate CD is given once daily in the morning. Capsules should not be opened. 30% of the dose is immediate release with the remainder releasing slowly. Fatty foods may delay absorption.
Children's Dosages: #
(children over 6 years old)
A typical starting dose is 5mg twice daily (before breakfast and lunch) with gradual increase if necessary. The total dose should not exceed 60mg. If improvement is not observed after dosage adjustment over 1 month, discontinuation is recommended.
It is not uncommon for patients on methylphenidate to get worse. Remember, it is a stimulant.
It is recommended that methylphenidate should be discontinued periodically to assess the condition. Improvement may be sustained when the drug is either temporarily or permanently discontinued. Drug treatment should not be indefinite and usually may be discontinued after puberty.
Overdosage: #
Overdosage results primarily in overstimulation of the central nercous system and excessive sypathomimetic effects. Symptoms and signs of overdose may include: vomiting, agitation, tremors, hyperreflexia, muscle twitching, convulsion (may be followed by coma), euphoria, confusion, hallucinations, delirium, sweating, flushing, headache, hyperpyrexia (high fever), tachcardia, palpitations, cardiac arrhythmias, hypertension, mydriais, and dryness of mucous membranes.
Treatment of methylphenidate overdoses consists of supportive measures and symptomatic treatments. The patient should be protected against self-inury and against external stimuli that would aggravate overstimulation. Gastric contents may be evacuated by gastric lavage. In severe intoxication, use of a SHORT ACTING barbituate before lavage is indicated. Other measures to detoxify the gut include use of activated charcoal and cathartics. External cooling measures may be required. Peritoneal dialysis or extracorporeal hemodialysis has not had efficacy proven. Benzodiazepines are commonly used in emergency rooms to alleviate symptoms. In case of severe overdoses, standard measures to reduce hypertension and hypertensive crises are used.
Alternatives to using methylphenidate: #
There are a variety of amphetamines by prescription with similar side effects and uses. There has been some "off-label" use of modafinil (a novel stimulant) as a replacement for ritalin, but this use is not approved by the FDA and there is little anecdotal and no scientific evidence that it is effective as a replacement for methylphenidate for patients.
Straterra, a nor-epinephrine uptake inhibitor may also be used. It works similarly to Effexor.
DMAE (dimethylaminoethanol)--once available by prescription, this nutritional supplement is supportive for attention and concentration. It is a biological precursor to acetylcholine. As such, it is also useful for Alzheimer's disease. Most recently, topical DMAE has gained acceptance as a cosmetic ingredient to increase muscle tone in the face. DMAE is typically extracted from salmon. It is inexpensive. Twinlabs makes one that is $8.95 retail for 100. Blue Bonnet is $9.95 per 100 put typically offers a money back guarantee.
Essential Fatty Acids are perhaps the most important supplements for a person with concentration issues. One with a balance of omega 3, 6, and 9 fatty acids is ideal. Consider Total EFA by Health From the Sun (as they state on the label that theirs is cold pressed and hexane free) or Ultra 369 from KAL.
GABA Gamma-Aminobutyric Acid acts as an inhibiting amino acid. It may reduce anxiety, nervousness, etc… It is most ideal for those patients who have hyperactivity in addition to attention deficit.
Magnesium is supportive for concentration. It is essential for over 300 enzymatic reactions in people. If given in the evening, magnesium may also help with sleep.
Lifestyle Factors: #
Some alternative medicine experts believe the conditions treated with methylphendate can often be treated with less habituating, stimulating means. Avoidance of refined sugars, food additives and dyes may be helpful. For more info, see www.feingold.org . Food allergies may also be at play and patients considering methylphenidate might consider food allergy testing. Great Smokies Diagnostic Labs has my favorite test www.gsdl.com It tests for IgG and IgE antibodies.
Keeping on a schedule, getting regular sleep, consistently timed meals, and reducing chaotic stress can help reduce ADD/ADHD symptoms.
Biofeedback is helpful for many children and adults who would otherwise use methylphenidate. Some physicians recommend learning relaxation and meditation techniques.
Side Effects: #
The information in this document regarding side effects and warnings comes from Drugs.com and the Ritalin professional packet insert. The following side/adverse effects have been selected on the basis of their potential clinical significance (possible signs and symptoms in parentheses where appropriate)--not necessarily inclusive:
Symptoms requiring medical attention:
* More Common Symptoms
Hypertension (increased blood pressure), tachycardia (fast heartbeat)--especially with doses greater than 0.5 mg per kg of body weight (mg/kg)
* Less Common Symptoms
Angina (chest pain), arthralgia (joint pain), dyskinesia (uncontrolled movements of the body), fever, skin rash or hives, thrombocytopenia (rarely, unusual bleeding or bruising; black tarry stools; blood in urine or stools; pinpoint red spots on skin)--usually asymptomatic.
Note: Arthralgia, fever, skin rash or hives, and thrombocytopenia may be indicative of a hypersensitivity reaction to methylphenidate. Rarely, exfoliative dermatitis and erythema multiforme have occurred.
* Rare Symptoms
Blurred vision or other changes in vision, convulsions, muscle cramps, Tourette's syndrome (uncontrolled vocal outbursts and/or tics [uncontrolled repeated body movements]), With prolonged use or at high doses, Psychosis, toxic (changes in mood; confusion; delusions; depersonalization; hallucinations), weight loss --possibly more frequent in children.
Symptoms needing for medical attention only if they continue or are bothersome
# Common Symptoms
Anorexia (loss of appetite)--usually transient; possibly more frequent in children, CNS stimulation (nervousness; trouble in sleeping)--possibly more frequent in children
# Less Common Symptoms
Dizziness, drowsiness, headache, nausea, stomach pain --possibly more frequent in children
Symptoms indicating possible withdrawal and the need for medical attention if they occur after medication is discontinued:
Mental depression, severe, unusual behavior, unusual tiredness or weakness
Drug Interactions: #
The following drug interactions and/or related problems have been selected on the basis of their potential clinical significance (possible mechanism in parentheses where appropriate)--not necessarily inclusive (major clinical significance):
Combinations containing any of the following medications, depending on the amount present, may also interact with this medication.
Anticholinergics or other medications with anticholinergic activity (concurrent use may intensify anticholinergic effects because of secondary anticholinergic effects of methylphenidate).
arial'>Anticonvulsants, especially phenytoin, phenobarbital, and primidone or Anticoagulants, coumarin-or indanedione-derivative or Phenylbutazone (serum concentrations of these medications may be increased because of inhibition of metabolism by methylphenidate, possibly resulting in toxicity; dosage adjustments may be necessary)
Antidepressants, tricyclic, especially desipramine and imipramine (serum concentrations of these medications may be increased because of inhibition of metabolism by methylphenidate, possibly resulting in toxicity; also, concurrent use may antagonize the effects of methylphenidate)
Antihypertensives or Diuretics used as antihypertensives (hypotensive effects may be reduced when these medications are used concurrently with methylphenidate; the patient should be carefully monitored to confirm that the desired effect is being obtained)
CNS stimulation–producing medications, other (concurrent use with methylphenidate may result in additive CNS stimulation to excessive levels, causing nervousness, irritability, insomnia, or possibly seizures or cardiac arrhythmias; close observation is recommended)
Monoamine oxidase (MAO) inhibitors, including furazolidone, procarbazine, and selegiline (concurrent use may potentiate the effects of methylphenidate, possibly resulting in a hypertensive crisis; methylphenidate should not be administered during or within 14 days following the administration of MAO inhibitors)
Pimozide (methylphenidate may provoke tics; before therapy with pimozide is initiated, methylphenidate should be withdrawn to determine the cause of observed tics; pimozide is not indicated for the treatment of tics caused by other medications)
Vasopressors (pressor effects may be potentiated when vasopressors are used concurrently with methylphenidate)
Medical considerations/Contraindications The medical considerations/contraindications included have been selected on the basis of their potential clinical significance (reasons given in parentheses where appropriate)-- not necessarily inclusive (major clinical significance).
Except under special circumstances, this medication should not be used when the following medical problems exist: Anxiety, tension, or agitation, severe or Depressive disorder amenable to treatment with conventional antidepressants. Glaucoma or Motor tics other than Tourette's disorder (may be exacerbated).
Risk-benefit should be considered when the following medical problems exist.
Emotional instability, including history of drug dependence or alcoholism (increased potential for addiction or abuse).
Epilepsy or other seizure disorders (seizure threshold may be lowered)
Gastrointestinal Obstructions, pathologic or iatrogenic (increased chance of obstructions due to nondeformable controlled-release tablet design)
Gilles de la Tourette's syndrome, family history or diagnosis of (motor and vocal tics may be exacerbated; however, some patients, under close supervision, may benefit from cautious trials)
Hypertension (may be exacerbated)
Psychosis: (symptoms of behavior disturbance and thought disorder may be exacerbated in children with psychoses)
Sensitivity to methylphenidate
Patient monitoring
The following may be especially important in patient monitoring (other tests may be warranted in some patients, depending on condition; major clinical significance):
Assessment of amount and frequency of medication use (recommended at periodic intervals to detect signs of dependence or abuse during long-term therapy)
Blood pressure determinations (recommended at periodic intervals during therapy, especially for patients with hypertension)
Complete blood cell, differential, and platelet counts (recommended at periodic intervals for patients on prolonged therapy)
Monitoring of growth, both height and weight gain, in children (recommended during long-term therapy, since data are inadequate to determine whether chronic administration of methylphenidate may be associated with growth inhibition)
Reassessment of need for therapy for behavioral syndrome in children (interruption of therapy at periodic intervals is recommended to determine if a recurrence of behavioral symptoms is sufficient to continue therapy; tapering of dose may be necessary to prevent withdrawal symptoms)
References #
1. Prescribing Information, Ritalin hydrochloride. November 1999, Novartis Pharmaceuticals Corporation, East Hanover New Jersey
2. Greenblatt E.N., Osterberg A.C. J. Pharmacol. Exp. Ther. Toxicity Data 131, 115 (1961)
3. Merk Index, 11th Ed. Merck & Co., Rahway, NJ 1990
4. Drug Facts & Comparisons, Wolters Kluwer Company, St Louis, Missouri, 2002
5. http://www.acnp.org/sciweb/journal/Npp110602427/default.htm
6. http://www.drugs.com/xq/cfm/pageid_0/htm_001417/tgid_15/type_pros/bn_Ritalin/micrpro_medex/qx/index.htm
[ back to pharms ] [ back to methylphenidate ]
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Last Mod - Apr 21 2009
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Summary of the Medical Uses of Methylphenidate
by Seth
Dec 2002
Methylphenidate is a prescription drug often used for attention deficit disorder (ADD), attention deficit hyperactivity disorder (ADHD), and narcolepsy. Although the FDA has not approved these uses, it is also used in mild to moderate depression, brain injury, HIV infection fatigue, post-stroke patients, and for anesthesia-related hiccups.
Prescription drugs that the are considered addictive or recreational are scheduled by how much control the government believes is necessary to reduce inappropriate uses pursuant to U.S. Code of Federal Regulations, Title 20 Part 1308.1 (1987). Methylphenidate has been put into Schedule II, the most restrictive medical category. Due to its schedule, prescriptions for methylphenidate may not be called in or faxed to a pharmacy except in an emergency situation.
Use of methylphenidate for ADD and ADHD is common but controversial. Many people feel that it is over prescribed. A new non-stimulant treatment for ADD and ADHD that will be named Straterra (a nor-epinephrine reuptake inhibitor) could dramatically decrease the use of stimulants. Dr. Mary Ann Block, author of "No More Ritalin: Treating ADHD Without Drugs" is one of the foremost critics of the use of Ritalin. She maintains that methylphenidate dose not correct the underlying causes of ADHD. These may include: hypoglycemia, allergies and sensitivities, environmental factors and hyperthyrodism. The Feingold Association of the United States (http://www.feingold.org) is an organization that works on drug-free approaches to ADD and ADHD.
Chemically, methylphenidate hydrochloride is methyl-alpha-phenyl-2-piperidineacetate hydrochloride. It is a white, odorless, fine crystalline powder with a chemical formula C14H20ClNO2. . It is slightly acidic. A 5% aqueous solution is neutral to litmus.. It is freely soluble in water and methanol, soluble in alcohol, and slightly soluble in chloroform and acetone. Its molecular weight is 269.77. pKa equals 8.9. LD50 in mice (the dose that is lethal to 50% of the mice studied) is 190mg/kg.
Methylphenidate is marketed under many names. Different companies have produced methylphenidate with a variety of delivery systems. These different systems are used to prevent children from having to take doses at school, to keep a steady level of the drug, or to cause the level to rise sharply at specific times. Novartis markets methylphenidate as Ritalin. Mallinckrodt markets it as Methylin, Alza calls it Concerta, and Medeva uses Metadate as their name.
The FDA has approved methylphenidate as part of a total treatment program in children with a behavioral syndrome characterized by moderate to severe distractibility, short attention span, hyperactivity, emotion lability, and impulsivity greater than that expected for a child that age. Stimulants are not for childen or adults who exhibit symptoms secondary to environmental factors or primary psyciatric disorders, including psychosis. When symptoms are associated with acute stress reactions, methylphenidate is usually not indicated.
The mode of action in people is not completely understood, but methylphenidate activates the brain stem arousal system and cortex to produce its stimulant effect. Mehtylphenidate is very similar to other amphetamines structurally. It appears to increase extracellular dopamine. This action is likely achieved through inhibition of dopamine transporter protein. Some research also shows that methylphendate inhibits serotonin transporter protein. This action may partially explain its antidepressant effects. Methylphenidate also increases norepinephrine (noradrenaline). Methylphenidate also affects regional cerebral blood flow in the cerebellar vermis.
Dosage should be individualized according to the needs of the patients.
Adult Dosages: #
Immediate release tablets should be given 2 or 3 times daily, preferabley 30-45 minutes before meals. Average dosage is 20 to 30mg daily. Some patients may require 40-60mg daily. In others 10 to 15mg will be adequate. Patients who are unable to sleep should take their last dose before 6 pm. Women appear to absorb methylphenidate better than men, and may need slightly lower dosages.
Time released preparations vary. Sustained-release tablets such as Ritalin SR have a duration of approximately 8 hours and may be used in place of regular tablets. These tablets must be swallowed whole, never crushed or chewed. Crushing or chewing causes the time release mechanism to fail, delivering all of the medication at once.
Concerta should be given once daily in the morning, without regard to meals. Doses start at 18mg in the morning and may range up to 54mg. Each tablet releases the drug over 12 hours.
Metadate CD is given once daily in the morning. Capsules should not be opened. 30% of the dose is immediate release with the remainder releasing slowly. Fatty foods may delay absorption.
Children's Dosages: #
(children over 6 years old)
A typical starting dose is 5mg twice daily (before breakfast and lunch) with gradual increase if necessary. The total dose should not exceed 60mg. If improvement is not observed after dosage adjustment over 1 month, discontinuation is recommended.
It is not uncommon for patients on methylphenidate to get worse. Remember, it is a stimulant.
It is recommended that methylphenidate should be discontinued periodically to assess the condition. Improvement may be sustained when the drug is either temporarily or permanently discontinued. Drug treatment should not be indefinite and usually may be discontinued after puberty.
Overdosage: #
Overdosage results primarily in overstimulation of the central nercous system and excessive sypathomimetic effects. Symptoms and signs of overdose may include: vomiting, agitation, tremors, hyperreflexia, muscle twitching, convulsion (may be followed by coma), euphoria, confusion, hallucinations, delirium, sweating, flushing, headache, hyperpyrexia (high fever), tachcardia, palpitations, cardiac arrhythmias, hypertension, mydriais, and dryness of mucous membranes.
Treatment of methylphenidate overdoses consists of supportive measures and symptomatic treatments. The patient should be protected against self-inury and against external stimuli that would aggravate overstimulation. Gastric contents may be evacuated by gastric lavage. In severe intoxication, use of a SHORT ACTING barbituate before lavage is indicated. Other measures to detoxify the gut include use of activated charcoal and cathartics. External cooling measures may be required. Peritoneal dialysis or extracorporeal hemodialysis has not had efficacy proven. Benzodiazepines are commonly used in emergency rooms to alleviate symptoms. In case of severe overdoses, standard measures to reduce hypertension and hypertensive crises are used.
Alternatives to using methylphenidate: #
There are a variety of amphetamines by prescription with similar side effects and uses. There has been some "off-label" use of modafinil (a novel stimulant) as a replacement for ritalin, but this use is not approved by the FDA and there is little anecdotal and no scientific evidence that it is effective as a replacement for methylphenidate for patients.
Straterra, a nor-epinephrine uptake inhibitor may also be used. It works similarly to Effexor.
DMAE (dimethylaminoethanol)--once available by prescription, this nutritional supplement is supportive for attention and concentration. It is a biological precursor to acetylcholine. As such, it is also useful for Alzheimer's disease. Most recently, topical DMAE has gained acceptance as a cosmetic ingredient to increase muscle tone in the face. DMAE is typically extracted from salmon. It is inexpensive. Twinlabs makes one that is $8.95 retail for 100. Blue Bonnet is $9.95 per 100 put typically offers a money back guarantee.
Essential Fatty Acids are perhaps the most important supplements for a person with concentration issues. One with a balance of omega 3, 6, and 9 fatty acids is ideal. Consider Total EFA by Health From the Sun (as they state on the label that theirs is cold pressed and hexane free) or Ultra 369 from KAL.
GABA Gamma-Aminobutyric Acid acts as an inhibiting amino acid. It may reduce anxiety, nervousness, etc… It is most ideal for those patients who have hyperactivity in addition to attention deficit.
Magnesium is supportive for concentration. It is essential for over 300 enzymatic reactions in people. If given in the evening, magnesium may also help with sleep.
Lifestyle Factors: #
Some alternative medicine experts believe the conditions treated with methylphendate can often be treated with less habituating, stimulating means. Avoidance of refined sugars, food additives and dyes may be helpful. For more info, see www.feingold.org . Food allergies may also be at play and patients considering methylphenidate might consider food allergy testing. Great Smokies Diagnostic Labs has my favorite test www.gsdl.com It tests for IgG and IgE antibodies.
Keeping on a schedule, getting regular sleep, consistently timed meals, and reducing chaotic stress can help reduce ADD/ADHD symptoms.
Biofeedback is helpful for many children and adults who would otherwise use methylphenidate. Some physicians recommend learning relaxation and meditation techniques.
Side Effects: #
The information in this document regarding side effects and warnings comes from Drugs.com and the Ritalin professional packet insert. The following side/adverse effects have been selected on the basis of their potential clinical significance (possible signs and symptoms in parentheses where appropriate)--not necessarily inclusive:
Symptoms requiring medical attention:
* More Common Symptoms
Hypertension (increased blood pressure), tachycardia (fast heartbeat)--especially with doses greater than 0.5 mg per kg of body weight (mg/kg)
* Less Common Symptoms
Angina (chest pain), arthralgia (joint pain), dyskinesia (uncontrolled movements of the body), fever, skin rash or hives, thrombocytopenia (rarely, unusual bleeding or bruising; black tarry stools; blood in urine or stools; pinpoint red spots on skin)--usually asymptomatic.
Note: Arthralgia, fever, skin rash or hives, and thrombocytopenia may be indicative of a hypersensitivity reaction to methylphenidate. Rarely, exfoliative dermatitis and erythema multiforme have occurred.
* Rare Symptoms
Blurred vision or other changes in vision, convulsions, muscle cramps, Tourette's syndrome (uncontrolled vocal outbursts and/or tics [uncontrolled repeated body movements]), With prolonged use or at high doses, Psychosis, toxic (changes in mood; confusion; delusions; depersonalization; hallucinations), weight loss --possibly more frequent in children.
Symptoms needing for medical attention only if they continue or are bothersome
# Common Symptoms
Anorexia (loss of appetite)--usually transient; possibly more frequent in children, CNS stimulation (nervousness; trouble in sleeping)--possibly more frequent in children
# Less Common Symptoms
Dizziness, drowsiness, headache, nausea, stomach pain --possibly more frequent in children
Symptoms indicating possible withdrawal and the need for medical attention if they occur after medication is discontinued:
Mental depression, severe, unusual behavior, unusual tiredness or weakness
Drug Interactions: #
The following drug interactions and/or related problems have been selected on the basis of their potential clinical significance (possible mechanism in parentheses where appropriate)--not necessarily inclusive (major clinical significance):
Combinations containing any of the following medications, depending on the amount present, may also interact with this medication.
Anticholinergics or other medications with anticholinergic activity (concurrent use may intensify anticholinergic effects because of secondary anticholinergic effects of methylphenidate).
arial'>Anticonvulsants, especially phenytoin, phenobarbital, and primidone or Anticoagulants, coumarin-or indanedione-derivative or Phenylbutazone (serum concentrations of these medications may be increased because of inhibition of metabolism by methylphenidate, possibly resulting in toxicity; dosage adjustments may be necessary)
Antidepressants, tricyclic, especially desipramine and imipramine (serum concentrations of these medications may be increased because of inhibition of metabolism by methylphenidate, possibly resulting in toxicity; also, concurrent use may antagonize the effects of methylphenidate)
Antihypertensives or Diuretics used as antihypertensives (hypotensive effects may be reduced when these medications are used concurrently with methylphenidate; the patient should be carefully monitored to confirm that the desired effect is being obtained)
CNS stimulation–producing medications, other (concurrent use with methylphenidate may result in additive CNS stimulation to excessive levels, causing nervousness, irritability, insomnia, or possibly seizures or cardiac arrhythmias; close observation is recommended)
Monoamine oxidase (MAO) inhibitors, including furazolidone, procarbazine, and selegiline (concurrent use may potentiate the effects of methylphenidate, possibly resulting in a hypertensive crisis; methylphenidate should not be administered during or within 14 days following the administration of MAO inhibitors)
Pimozide (methylphenidate may provoke tics; before therapy with pimozide is initiated, methylphenidate should be withdrawn to determine the cause of observed tics; pimozide is not indicated for the treatment of tics caused by other medications)
Vasopressors (pressor effects may be potentiated when vasopressors are used concurrently with methylphenidate)
Medical considerations/Contraindications The medical considerations/contraindications included have been selected on the basis of their potential clinical significance (reasons given in parentheses where appropriate)-- not necessarily inclusive (major clinical significance).
Except under special circumstances, this medication should not be used when the following medical problems exist: Anxiety, tension, or agitation, severe or Depressive disorder amenable to treatment with conventional antidepressants. Glaucoma or Motor tics other than Tourette's disorder (may be exacerbated).
Risk-benefit should be considered when the following medical problems exist.
Emotional instability, including history of drug dependence or alcoholism (increased potential for addiction or abuse).
Epilepsy or other seizure disorders (seizure threshold may be lowered)
Gastrointestinal Obstructions, pathologic or iatrogenic (increased chance of obstructions due to nondeformable controlled-release tablet design)
Gilles de la Tourette's syndrome, family history or diagnosis of (motor and vocal tics may be exacerbated; however, some patients, under close supervision, may benefit from cautious trials)
Hypertension (may be exacerbated)
Psychosis: (symptoms of behavior disturbance and thought disorder may be exacerbated in children with psychoses)
Sensitivity to methylphenidate
Patient monitoring
The following may be especially important in patient monitoring (other tests may be warranted in some patients, depending on condition; major clinical significance):
Assessment of amount and frequency of medication use (recommended at periodic intervals to detect signs of dependence or abuse during long-term therapy)
Blood pressure determinations (recommended at periodic intervals during therapy, especially for patients with hypertension)
Complete blood cell, differential, and platelet counts (recommended at periodic intervals for patients on prolonged therapy)
Monitoring of growth, both height and weight gain, in children (recommended during long-term therapy, since data are inadequate to determine whether chronic administration of methylphenidate may be associated with growth inhibition)
Reassessment of need for therapy for behavioral syndrome in children (interruption of therapy at periodic intervals is recommended to determine if a recurrence of behavioral symptoms is sufficient to continue therapy; tapering of dose may be necessary to prevent withdrawal symptoms)
References #
1. Prescribing Information, Ritalin hydrochloride. November 1999, Novartis Pharmaceuticals Corporation, East Hanover New Jersey
2. Greenblatt E.N., Osterberg A.C. J. Pharmacol. Exp. Ther. Toxicity Data 131, 115 (1961)
3. Merk Index, 11th Ed. Merck & Co., Rahway, NJ 1990
4. Drug Facts & Comparisons, Wolters Kluwer Company, St Louis, Missouri, 2002
5. http://www.acnp.org/sciweb/journal/Npp110602427/default.htm
6. http://www.drugs.com/xq/cfm/pageid_0/htm_001417/tgid_15/type_pros/bn_Ritalin/micrpro_medex/qx/index.htm
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Vision problems and visualization
http://www.children-special-needs.org/vision_therapy/esophoria_reading_pf.html
Public Web Sites with Free Referrals - No Registration Required
www.optometrists.org - www.children-special-needs.org - www.visiontherapy.org
Vision & Reading
The following are excerpts from an article on Vision, Learning and Nutrition
by Donald J. Getz, OD, FCOVD, FAAO
This article by an eye doctor discusses children's problems with reading, learning, and behavior caused by convergence insufficiency, eye tracking problems, esophoria, exophoria, and other visual problems.
Vision and Eyesight
Eyesight is simply the ability to see something clearly, the so-called 20/20 eyesight (as measured in a standard eye examination with a Snellen chart). Vision goes beyond eyesight and can best be defined as the understanding of what is seen. Vision involves the ability to take incoming visual information, process that information and obtain meaning from it.
Two general statements can be made about vision. First, vision is learned. A child learns to see just like he learns to walk and talk. When learning to walk and talk, he has the added opportunity of imitating his parents and siblings. In addition, parents can observe their children to determine if walking and talking are developing properly. Vision development, however, generally proceeds without much concerned awareness on the part of parents. Because of these differences in development, no two people see exactly alike.
Vision Is Learned
Vision is learned; therefore vision is trainable. If a child does not possess the necessary visual skills, he can be taught to possess them through the proper Vision Therapy techniques.
Adequate Vision Is Critical to Learning
Since something like 75% to 90% of all a child learns comes to him via the visual pathways, it stands to reason that if there is any interference in those pathways, a child will not develop to his maximum potential.
Vision
The Visual Skills Needed for Academic Success
Visual Acuity: There are many visual skills which are important for academic success. One of the least important skills is termed visual acuity (clarity, sharpness). This is the so-called 20/20, 20/400, etc., eyesight. All that is meant by the notation 20/20 is that a person is capable of seeing clearly at a distance of twenty feet. Unfortunately, how well a child sees at twenty feet has little to do with how his vision functions at the reading and learning distance -- aproximately eleven to sixteen inches from the face. In fact, it is my opinion that the Snellen eye chart test which measures visual acuity actually does more harm than good. It gives both parents and teachers a false sense of security that vision is normal. There are many other important visual skills that might not be developed even though visual acuity at distance is normal.
Binocular Coordination: One of the more important visual skills is the ability to coordinate the two eyes together. A child is born with two eyes, but he must learn to team them together. Some children learn to do this properly while others do not. For example, some children develop a problem known as exophoria, which is a tendency for the eyes to deviate in an outward direction. This is not the same as a condition known as exotropia where the eye actually can be seen to be in an outward position.
Adequate Convergence: During the act of reading, the demand is for the two eyes to turn inward so that they are aimed at the reading task. If the eyes have a tendency to deviate outward, the child must use excess effort and energy to maintain fixation on the reading task. Most studies have shown that the greater the amount of effort involved in reading, the lower will be the comprehension and the lower will be the performance. When reading, the eyes do not move smoothly over a line of print. Rather, they make a series of fixations looking from word to word. When an exophoria exists, each time fixation is broken and moved to the next word, the eyes will tend to deviate outwards and they must be brought back in to regain fixation. Human nature being what it is, the child generally has an avoidance reaction to the reading task. This is compounded by the fact that anything the child doesn't do well, he would rather not do. This is the child who looks out the window rather than paying visual attention. He is commonly given labels. He is often accused of having a short attention span and not trying. He is told that he would do better if he tried harder, but he has tried harder to no avail. He is often labeled as having dyslexia, minimal brain dysfunction, learning disability, etc. Commonly, he loses his place while reading and/or uses his finger or a marker to maintain his place. While making the eye movements during the act of reading, he might not land on the next word, but rather land a few words further on. Consequently, he commonly omits small words or confuses small words. Often, he just adds a word or two to make the sentence make sense. If the two eyes are pointing at the same point in space, a person will see the fixated object as being single. Double vision or overlapping vision (Figure #3) results if the two eyes are not exactly pointing at the same point. Don't expect a child to tell you that his vision isn't clear. He has no yardstick of comparison to inform him that his vision differs from the vision of anyone else.
Figure 3
Astigmatism, Eye-Hand Coordination, Visual-Motor Problems and more: I have maintained for many years that I could walk into a classroom and pick out those children with coordination type visual problems. They get into distorted postures in an attempt to get one eye out of the act. They often put their head down on their arm, cover one eye with their palm or rotate their head so that the bridge of their nose interferes with the vision from one eye.
Esophoria: Another eye coordination problem is termed esophoria, which is a tendency for the eyes to turn inwards. The educational implication of this particular problem is that a child with esophoria sees things smaller than what they actually are. In order to see an object properly, it is necessary to make the object larger. The only means at the disposal of the child to make it larger is to bring it closer. Eventually, the child is observed with his head buried in a book and still not achieving.
Reading Skills and Binocular Visual Skills
One of the tests used in optometric offices is to have the child read words while looking into an instrument called a Telebinocular. The performance is compared between reading with either eye alone and with both eyes together. The difference in performance is often quite dramatic if there is an eye teaming problem. One eye performance might be quite satisfactory, but reading with both eyes together will be slower and many more errors will be made.
Other Visual Skills
Directionality: Directionality is another visual skill important for academic success. One test for this skill is illustrated in Figure #5. Look at Figure #5 and determine what you see. If the visual reflex is from left to right, a duck will be seen. However, if the visual reflex is from right to left, a rabbit will be seen. This is just one test out of a series to determine the directionality of the visual reflex.
Figure 5
It is just a convention of our culture that the English language proceeds in a left to right direction. Other languages proceed in a right to left direction and still others have a vertical orientation. Many people feel that it would make more sense if the language proceeded as illustrated in Figure #6. If a child does not visually proceed from left to right, through Vision Therapy he can be taught to develop this skill just like he can be taught to team his eyes together.
Figure 6
Form Perception: Form perception is another important visual skill for academic achievement. This can best be illustrated by referring to Figure #7. The child is shown these forms one at a time and he is simply asked to copy them. It is amazing to see some of the distortions that a child will make in attempting to copy these forms. If a child can't perceive and copy these simple geometric forms, it is unreasonable to assume that he will be able to perceive the wiggly lines which make up letters which in turn make up words, which in turn make up sentences which stand for abstract ideas. We see children often who can't tell the difference between a square and a rectangle or a circle and an oval. This is also a skill which can be improved through Vision Therapy.
Figure 7
Attention Span/Span of Perception: The Span of Perception is also related to success in school. Many children see just one word at a time with each eye fixation. Reading speed can be improved by learning to see two, three, or more words with each eye fixation. This could be compared to reading through a straw. This is illustrated in Figure #8. It is easy to see the difference in reading for meaning when the span of perception is wide.
Figure 8
Visualization: The ultimate visual skill is visualization. This is similar to being able to see things in the mind's eye. There are authorities that state that the ability to visualize is very closely allied to the ability to think. In other words, thinking is related to the ability to abstract from specifics and the ability to visualize is deeply involved in this process. Visualization is also a trainable skill.
There are many other visual skills that time and space do not permit me to mention. However, it is hoped that the reader will realize from the above discussion that there is a lot more to vision than just 20/20.
Nutrition and Vision
When I see a child with a learning problem, I feel very strongly that there usually is more than just a single cause. For example, when I find a visual problem, if I probe a bit further, a nutritional problem will be found as well. Children often walk into the office eating a candy bar or sipping on a cola or other soft drink. When they are asked what they had for breakfast, the response usually falls in the frosted, sugary flake category or the answer is that they had no breakfast at all.
When I am asked which nutrients are important for optimum visual functioning, I respond that the same nutrients essential for the rest of the body are the ones needed for vision. This is because vision does not operate independently of the rest of the body.
In all cases, a diet of high quality, nutrition-rich, unprocessed foods is important if we are going to be successful in Vision Therapy. Vision therapy involves a learning process and, as with any learning process, learning will be maximized if a healthy body and a healthy mind are brought to the learning task.
Reprinted with permission from The Journal of Applied Nutrition Volume 28, Winter, 1976
This complete article may be purchased by writing to College of Optometrists in Vision Development, 243 N. Lindbergh Blvd., Ste. 310, St. Louis, MO 63141-7851 and requesting the article: Getz, Donald J., O.D., "Vision and Perception Therapy," 1973.
Bibliography
Feingold, Ben F., M.D., Why Your Child Is Hyperactive, Random House, New York, 1975.
Lane, Benjamin. O.D., "Myopia," 1976. College of Optometrists in Vision Development
Ludlam, William, O.D., "Visual Evoked Response," 1974. College of Optometrists in Vision Development
McDonald, Lawrence W., O.D., "Visual Training," 1962-1963. Optometric Extension Program
Ott, John. Sc.D., Health and Light, The Effects of Natural and Artificial Light on Man and Other Living Things, Devin-Adair Co., 1973.
Skeffington, A.M., O.D., Continuous writings, Optometric Extension Program
________________________________________
To locate an eye doctor who provides comprehensive pediatric vision examinations and treatment, including Vision Therapy, request a referral through our Referral Directory: Find a Pediatric Eye Doctor.
All other images and text: copyright © 1996-2010 by Rachel Cooper. All rights reserved.
Public Web Sites with Free Referrals - No Registration Required
www.optometrists.org - www.children-special-needs.org - www.visiontherapy.org
Vision & Reading
The following are excerpts from an article on Vision, Learning and Nutrition
by Donald J. Getz, OD, FCOVD, FAAO
This article by an eye doctor discusses children's problems with reading, learning, and behavior caused by convergence insufficiency, eye tracking problems, esophoria, exophoria, and other visual problems.
Vision and Eyesight
Eyesight is simply the ability to see something clearly, the so-called 20/20 eyesight (as measured in a standard eye examination with a Snellen chart). Vision goes beyond eyesight and can best be defined as the understanding of what is seen. Vision involves the ability to take incoming visual information, process that information and obtain meaning from it.
Two general statements can be made about vision. First, vision is learned. A child learns to see just like he learns to walk and talk. When learning to walk and talk, he has the added opportunity of imitating his parents and siblings. In addition, parents can observe their children to determine if walking and talking are developing properly. Vision development, however, generally proceeds without much concerned awareness on the part of parents. Because of these differences in development, no two people see exactly alike.
Vision Is Learned
Vision is learned; therefore vision is trainable. If a child does not possess the necessary visual skills, he can be taught to possess them through the proper Vision Therapy techniques.
Adequate Vision Is Critical to Learning
Since something like 75% to 90% of all a child learns comes to him via the visual pathways, it stands to reason that if there is any interference in those pathways, a child will not develop to his maximum potential.
Vision
The Visual Skills Needed for Academic Success
Visual Acuity: There are many visual skills which are important for academic success. One of the least important skills is termed visual acuity (clarity, sharpness). This is the so-called 20/20, 20/400, etc., eyesight. All that is meant by the notation 20/20 is that a person is capable of seeing clearly at a distance of twenty feet. Unfortunately, how well a child sees at twenty feet has little to do with how his vision functions at the reading and learning distance -- aproximately eleven to sixteen inches from the face. In fact, it is my opinion that the Snellen eye chart test which measures visual acuity actually does more harm than good. It gives both parents and teachers a false sense of security that vision is normal. There are many other important visual skills that might not be developed even though visual acuity at distance is normal.
Binocular Coordination: One of the more important visual skills is the ability to coordinate the two eyes together. A child is born with two eyes, but he must learn to team them together. Some children learn to do this properly while others do not. For example, some children develop a problem known as exophoria, which is a tendency for the eyes to deviate in an outward direction. This is not the same as a condition known as exotropia where the eye actually can be seen to be in an outward position.
Adequate Convergence: During the act of reading, the demand is for the two eyes to turn inward so that they are aimed at the reading task. If the eyes have a tendency to deviate outward, the child must use excess effort and energy to maintain fixation on the reading task. Most studies have shown that the greater the amount of effort involved in reading, the lower will be the comprehension and the lower will be the performance. When reading, the eyes do not move smoothly over a line of print. Rather, they make a series of fixations looking from word to word. When an exophoria exists, each time fixation is broken and moved to the next word, the eyes will tend to deviate outwards and they must be brought back in to regain fixation. Human nature being what it is, the child generally has an avoidance reaction to the reading task. This is compounded by the fact that anything the child doesn't do well, he would rather not do. This is the child who looks out the window rather than paying visual attention. He is commonly given labels. He is often accused of having a short attention span and not trying. He is told that he would do better if he tried harder, but he has tried harder to no avail. He is often labeled as having dyslexia, minimal brain dysfunction, learning disability, etc. Commonly, he loses his place while reading and/or uses his finger or a marker to maintain his place. While making the eye movements during the act of reading, he might not land on the next word, but rather land a few words further on. Consequently, he commonly omits small words or confuses small words. Often, he just adds a word or two to make the sentence make sense. If the two eyes are pointing at the same point in space, a person will see the fixated object as being single. Double vision or overlapping vision (Figure #3) results if the two eyes are not exactly pointing at the same point. Don't expect a child to tell you that his vision isn't clear. He has no yardstick of comparison to inform him that his vision differs from the vision of anyone else.
Figure 3
Astigmatism, Eye-Hand Coordination, Visual-Motor Problems and more: I have maintained for many years that I could walk into a classroom and pick out those children with coordination type visual problems. They get into distorted postures in an attempt to get one eye out of the act. They often put their head down on their arm, cover one eye with their palm or rotate their head so that the bridge of their nose interferes with the vision from one eye.
Esophoria: Another eye coordination problem is termed esophoria, which is a tendency for the eyes to turn inwards. The educational implication of this particular problem is that a child with esophoria sees things smaller than what they actually are. In order to see an object properly, it is necessary to make the object larger. The only means at the disposal of the child to make it larger is to bring it closer. Eventually, the child is observed with his head buried in a book and still not achieving.
Reading Skills and Binocular Visual Skills
One of the tests used in optometric offices is to have the child read words while looking into an instrument called a Telebinocular. The performance is compared between reading with either eye alone and with both eyes together. The difference in performance is often quite dramatic if there is an eye teaming problem. One eye performance might be quite satisfactory, but reading with both eyes together will be slower and many more errors will be made.
Other Visual Skills
Directionality: Directionality is another visual skill important for academic success. One test for this skill is illustrated in Figure #5. Look at Figure #5 and determine what you see. If the visual reflex is from left to right, a duck will be seen. However, if the visual reflex is from right to left, a rabbit will be seen. This is just one test out of a series to determine the directionality of the visual reflex.
Figure 5
It is just a convention of our culture that the English language proceeds in a left to right direction. Other languages proceed in a right to left direction and still others have a vertical orientation. Many people feel that it would make more sense if the language proceeded as illustrated in Figure #6. If a child does not visually proceed from left to right, through Vision Therapy he can be taught to develop this skill just like he can be taught to team his eyes together.
Figure 6
Form Perception: Form perception is another important visual skill for academic achievement. This can best be illustrated by referring to Figure #7. The child is shown these forms one at a time and he is simply asked to copy them. It is amazing to see some of the distortions that a child will make in attempting to copy these forms. If a child can't perceive and copy these simple geometric forms, it is unreasonable to assume that he will be able to perceive the wiggly lines which make up letters which in turn make up words, which in turn make up sentences which stand for abstract ideas. We see children often who can't tell the difference between a square and a rectangle or a circle and an oval. This is also a skill which can be improved through Vision Therapy.
Figure 7
Attention Span/Span of Perception: The Span of Perception is also related to success in school. Many children see just one word at a time with each eye fixation. Reading speed can be improved by learning to see two, three, or more words with each eye fixation. This could be compared to reading through a straw. This is illustrated in Figure #8. It is easy to see the difference in reading for meaning when the span of perception is wide.
Figure 8
Visualization: The ultimate visual skill is visualization. This is similar to being able to see things in the mind's eye. There are authorities that state that the ability to visualize is very closely allied to the ability to think. In other words, thinking is related to the ability to abstract from specifics and the ability to visualize is deeply involved in this process. Visualization is also a trainable skill.
There are many other visual skills that time and space do not permit me to mention. However, it is hoped that the reader will realize from the above discussion that there is a lot more to vision than just 20/20.
Nutrition and Vision
When I see a child with a learning problem, I feel very strongly that there usually is more than just a single cause. For example, when I find a visual problem, if I probe a bit further, a nutritional problem will be found as well. Children often walk into the office eating a candy bar or sipping on a cola or other soft drink. When they are asked what they had for breakfast, the response usually falls in the frosted, sugary flake category or the answer is that they had no breakfast at all.
When I am asked which nutrients are important for optimum visual functioning, I respond that the same nutrients essential for the rest of the body are the ones needed for vision. This is because vision does not operate independently of the rest of the body.
In all cases, a diet of high quality, nutrition-rich, unprocessed foods is important if we are going to be successful in Vision Therapy. Vision therapy involves a learning process and, as with any learning process, learning will be maximized if a healthy body and a healthy mind are brought to the learning task.
Reprinted with permission from The Journal of Applied Nutrition Volume 28, Winter, 1976
This complete article may be purchased by writing to College of Optometrists in Vision Development, 243 N. Lindbergh Blvd., Ste. 310, St. Louis, MO 63141-7851 and requesting the article: Getz, Donald J., O.D., "Vision and Perception Therapy," 1973.
Bibliography
Feingold, Ben F., M.D., Why Your Child Is Hyperactive, Random House, New York, 1975.
Lane, Benjamin. O.D., "Myopia," 1976. College of Optometrists in Vision Development
Ludlam, William, O.D., "Visual Evoked Response," 1974. College of Optometrists in Vision Development
McDonald, Lawrence W., O.D., "Visual Training," 1962-1963. Optometric Extension Program
Ott, John. Sc.D., Health and Light, The Effects of Natural and Artificial Light on Man and Other Living Things, Devin-Adair Co., 1973.
Skeffington, A.M., O.D., Continuous writings, Optometric Extension Program
________________________________________
To locate an eye doctor who provides comprehensive pediatric vision examinations and treatment, including Vision Therapy, request a referral through our Referral Directory: Find a Pediatric Eye Doctor.
All other images and text: copyright © 1996-2010 by Rachel Cooper. All rights reserved.
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