ketamine & vitamine B12

Davinci schreef:Tussen vitamine B12 en ketamine zie ik echt geen verband...

Vinz schreef:iemand die bij de kruitvat werkt heb tog ook receptroen in zijn\haar hooft en als die jouw b12 verkoopt hebbn die dinge zeker met elkaar te make je moet probere buiten de doos te denke eistien

The Dude schreef:

Yeah, well, you know, that's just, like, your opinion, man.

An organic compound in which the hydrogen of the hydroxyl group of methyl alcohol is replaced by a metal.
tr.v. meth·yl·at·ed, meth·yl·at·ing, meth·yl·ates
1. To mix or combine with methyl alcohol.
2. To combine with the methyl radical.

Sometimes the provider might want to use ketamine. It is a dissociative anesthetic; in essence, a hallucinogenic. It is usually used for sedation, especially for short procedures like changing dressings on burns. In children – especially so-called difficult pediatric patients – it might be used to make starting an IV easier. Ketamine’s advantage is that it doesn’t depress respiration as other anesthetics might. It’s also easy to use; it can be given orally, intramuscularly, or intravenously. Typical side effects, however, include open eyes, nystagmus, increased salivation, and emergence delirium. Ketamine alters the patient’s sensory perception, which raises questions about its use for these children.

Special attention must be paid to the topic of nitrous oxide (“laughing gas”). It is one of the oldest anesthetics, and is still used for sedation in dental procedures. In addition, it is used on occasion as a carrier gas with sevoflurane in mask inductions. That is, nitrous oxide is utilized for a second-gas effect to increase the concentration of another inhaled anesthetic agent, thereby allowing the patient to get to sleep faster.

In the last decade, concerns have been raised about it: inactivation of methionine synthase, increase of post-operative nausea, relatively poor amnesic properties, and even as a contribution to greenhouse gases. Because of these concerns, nitrous oxide use in the operating room has dramatically declined in recent years.
Nitrous oxide might present specific problems for autistic children with common underlying conditions; it depletes the B12/folate system and deactivates methionine synthase, which is an enzyme that catalyzes the conversion of homocysteine and methyltetrahydrofolate to methionine and tetrahydrofolate. Such a deactivation in a patient with a defect in the MTHFR (methylenetetrahydrofolate reductase) gene, which is associated with diminished enzyme activity, could result in increased homocysteine levels, increased oxidative stress, and activated NMDA glutamate receptors. All of these could contribute to inflammation; additionally, nitrous oxide also might cause hematologic problems, neuropathy, and neurotoxic effects.5

For years, the anesthetic community was told that nitrous oxide was the perfect anesthetic. Now we know better. A study published in 2003 discussed the effects of two subsequent nitrous oxide exposures, MTHFR mutation, and the fatal neurological outcome due to a methionine deficiency.6 In 2007, Dr. Victor Baum presented a paper at a pediatric anesthesiology meeting that made us all rethink using nitrous oxide as an anesthetic.7
Methylation is important for detoxification, myelin (nerve sheath) formation, neurotransmitters and DNA synthesis. How can we help the anesthetic provider understand that compromised methylation is one of the underlying problems that we see in autism? That some of our children have genetic mutations such as CBS (cystathionine beta synthase) and MTHFR, which will affect how they detoxify drugs? That our children have increased oxidative stress as well as decreased methylation? That most of our children have gut problems that interfere with the absorption of many vitamin co-factors needed for methlylation and detoxification? That many developmentally delayed children have some type of mitochondrial dysfunction that might affect the provider’s choice of an anesthetic? That many anesthetic drugs affect autonomic nervous system function and can have untoward effects in the autistic population? How can we help them realize that their choices in the operating room might have detrimental effects on our child when they return home?

The best starting point is Dr. Martha Herbert’s well-reasoned 2005 article titled “Autism: A brain disorder or a disorder that affects the brain?”, which lays out the need to embrace a new paradigm in understanding autism.9

In addition, the 2004 article by Dr. S. Jill James and her colleagues, “Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism,” explains the methylation problems in autistic individuals which can lead to increased oxidative stress.10 These pathways were considered in other neurological diseases, but never linked to autism before Dr. James’ work. This article also discusses the use of B12, folinic acid, and betaine to increase methylation and reverse the effects of oxidative stress. This is critical information for anesthesia providers.

A recent article from 2008 by Dr. Richard Deth, et al. addresses the environmental and genetic factors that can lead to autism.11 The article describes a “redox/methylation hypothesis of autism,” in which oxidative stress, initiated by environmental factors in genetically vulnerable individuals, leads to impaired methylation and neurological deficits secondary to reductions in the capacity for synchronizing neural networks. The article underscores the need to minimize the oxidative stress that can result from anesthesia. Commonly used anesthetics might contribute to the toxic load, deplete B12, and affect methylation.

rI'm sticking this here so I can find it again later. I'm hoping for opinions about the benefits or dangers of stimulating glutamate in this way:

Ketamine: The best single agent for CFS/FMS and all other neurosomatic disorders. Known best as an NMDA receptor antagonist (the NMDA receptor is one of the several receptors for the excitatory amino acid glutamate), it increases dopamine in the limbic system, a very important objective in CFS. I

Dr. Jon Poling’s paper on developmental regression and mitochondrial dysfunction in autism (published in 2006) also helps to explain the overall impact anesthetic choice might have.12 The mitochondria provide energy to our cells, and are necessary for the Kreb’s cycle, fatty acid oxidation, metabolism of amino acids, and oxidative phosphorylation. The increased risk of certain anesthetics for patients with mitochondrial problems has been widely reported in anesthesia journals, and Dr. Poling’s conclusions are easily understood.

Claviceps schreef:

The Dude schreef:

Ik denk dat je deze quote zocht The Dude

Yeah, well, you know, that's just, like, your opinion, man.[
/quote]

Bunnie schreef:Dus als je meer VitaminaB12 heb heb je meer Methylation , heb je meer Melatonine dus dan heb je een betere Ketamine-trip.

Ketamine is metabolized by hepatic N-methylation to norketamine, which has approximately one third the activity of the parent compound.