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WHAT IS IT? Legitimate use How is it used? What else is it called? What does it look like? What can it be cut with? WHAT DOES IT DO?
When ketamine blocks the NMDA neuroreceptor, the cell is unable to absorb glutamate; without glutamate the cell will not permit the passage of calcium or sodium ions through its membrane. As a consequence, this cell does not pass information to any neighbouring cells. The effect of this lack of communication is anaesthetization-or the high you experience after inhaling ketamine. Other effects of this lack of communication are changes in the normal production of other neurotransmitters--a decrease in production of gamma-aminobutyric acid (GABA) and an increase in the transmission of dopamine. How does it make you feel physically? How does it affect you after you use it? How long will the effects last? WHAT ARE THE RISKS? Short-term Risks?
You need about 2.2 mg of ketamine per 1 kg of body weight to put you into a K-hole-give or take, depending on who you are and the conditions under which you take your drugs. A bump of ketamine from a bullet is anywhere from 30 to 50 mg-although this can vary greatly from bullet to bullet (read more at erowid). If you are going to use ketamine, it's a good idea to figure out the math, so that you have an idea of where your lines are. For example, if a 77 kg person is using a bullet to inhale a bump of ketamine he or she would be consuming anywhere from about .38mg/kg to about .65mg/kg. A single bump is liable to give this 77kg person a buzz of some kind-the intensity will depend on a host of factors-the size of the bullet, the temperature, the person's tolerance. A second or third bump would bring the dosage close to what is required for a K-hole-particularly close if you've been dancing for a while, are dehydrated, overheated, or have taken other drugs. Under these conditions, the threshold for a K-hole could be much lower. In practical terms, this means that doing multiple bumps for most of us is probably not a good idea. Unless you're into passing out. For those who don't do metric: a K-hole is about 1mg of ketamine per pound of body weight. Seizures Seizures are the result of the way ketamine inhibits the production of the GABA neurotransmitter. GABA is an inhibitory neurotransmitter-it keeps brain cells quiet and operating within their normal limits of activity. With no GABA around to protect it, cells are easily activated by any stimulus (in this case, the presence of other neurotransmitters). In short, the cell gets all fired up and doesn't have a chance to relax or recoup. When this occurs, the cell ends up using all its recourses and eventually dies. We experience the death of brain cells as seizures. Other significant short-term risks (which may or may not be part of a k-hole) include hallucinations, vivid dreams, rapid heart rate and high blood pressure. Also be ware that a severe overdose would result in coma with respiratory depression (decreased breathing) and possibly apnea (no breathing) - not simply a "k-hole". Medium-term Risks Long-term Risks
Brain damage associated with ketamine is in the form of what are called Olney's lesions (also called NMDA antagonist neurotoxicity or NAN). These lesions occur in particular areas of the brain (posterior cingulate cortex and retrosplenial cortex) that are associated with multi-sensory thinking, new learning, visual perception, and possibly sense of smell. Differently, these parts of the brain support higher functioning and thinking-the ability to process complex information and what is called long term potentiation (i.e., the ability to learn new ideas). In animal studies, the dose at which irreversible brain damage occurs is around 40 milligrams of ketamine per 1 kilogram of body weight (Olney et al. 1989; Allen et al. 1990, Jensen 2000). Jensen (2000) summarizes research on ketamine and brain cell death in relation to primates, noting that there is no evidence that ketamine causes brain damage at the cellular level in primates. He cites research, which found no permanent effects on cell structure were found at doses of 10mg/kg of body weight.
Read more about ketamine here.
So while there is no evidence that ketamine causes cell death in primates, bear in mind that this research is based on anesthetic doses, not recreational doses. Recreational doses lead to over-active neurological processes-and it is this overactivity that causes cell death. Second, while there is not much clear evidence of cellular change in primate brains, there is evidence of persistent changes on primate brain functioning. Ketamine leads to changes in the regulation of the neurotransmitters dopamine and glutamate, which help in the production of memory systems. "Repeated chronic doses of ketamine result in persistent alterations .that might result in a loss of efficiency in memory systems that is not apparent as a change in cell structure"(Jensen 2000: 427). The effects of ketamine appear to be worse for women and gets worse as you get older (Jevtovic-Todorovic et al. 2000). WHAT ARE THE HARM REDUCTION TECHNIQUES FOR THIS DRUG?
Think about frequency, duration, and dose and your body weight. Be conscious about what is acceptable to you given the dose guidelines we've suggested. This can take any number of forms: taking only so much K with you, taking smaller bumps, or limiting yourself to a pre-determined number of bumps. Limit you dose to once every two days (yes, every two days-this is the length of time it took lab animals to return to "normal"). Taking minor sedatives might help in reducing the risk of brain damage-although
we don't recommend you take drugs to reduce the dangers associated with
other drugs. A healthy diet and nutrition might be useful. As a rule,
don't bother megadosing on vitamins or herbals-what your body doesn't
use goes to waste. And when it comes to herbals, there is simply no
research or evidence indicating how Special K interacts with herbals. Snorting your drugs has risk too. How will I feel at first if I'm starting to get into trouble? What are the contraindications? What drugs shouldn't I mix
with this drug? Anti-depressants of any kind are not a good idea when it comes to ketamine. Anti-depressants work either by limiting a brain cell's absorption of some neurotransmitters or by reducing the rate at which neurotransmitters are broken down. In the end, what this means is that while using anti-depressants, your brain is floating in a lot of neurotransmitters already - taking ketamine will only complicate or exacerbate the effects of these neurotransmitters on your brain cells. For example, some anti-depressants lead to an increase in the amount of dopamine your brain cells are exposed to - with this increased dopamine level and the decreased GABA production associated with ketamine, you are more prone to experience brain damage. Taking ketamine with large amounts of sugars may increase free radical damage - bear this in mind as you're drinking cranberry juice. If you are at all susceptible to seizures for any reason, put the K away and think about something else.
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Buzzcode provides meaningful harm reduction strategies for gay men who use party drugs. THERE IS NO SAFE WAY TO USE DRUGS. Our aim is to help you reduce the risks inherent in taking drugs. Please read our policies and terms of use before proceeding. All works featured on this sight are copyrighted © 2003 by VGMHRI. You may not use this material without express written authorization. |