Addict goes doctor shopping

Just a little rant against Doctors
« on: September 25, 2017, 07:50:51 pm »

[Buddie]

So I wasn’t sure where else to put this, but just wanted to get it off my chest. I went to see my 2nd p-doc within the last month in order to attempt to obtain a legitimate prescription to valium for the purposes of tapering. Also was looking for a script to remeron, since my sleep is still pretty bad even after reinstating. I made the mistake of mentioning tapering down, and switching over from the klonopin that I had previously been on. Big mistake. In the US, doctors just don’t get it. He actually said “well if there’s an addiction, we need to stop the benzos. You’ll feel a little anxiety for a few days, but then you’ll be ok” Lol. He then said but if you have GAD, and valium or klonopin seem to work for you, then we can go that route. I immediately said yes, I think I’ve have GAD. You see, docs just don’t want to get involved in the whole tapering business. It’s messy. I’m not sure if they’re completely ignorant to protracted WD, or if they just don’t want to get involved in a tapering schedule. With them, everything HAS to have a diagnosis. And if it’s benzo dependancy (addiction or not), than they are apparently almost never willing to write a script to taper. Because if it’s dependance, the solution is to get off the drug right NOW, find some other diagnosis, and put you on some other med that probably won’t help, and will likely make things worse. Long story short.. I get ONE WEEKS supply of valium and remeron, and have to go back in a week (another $150) to re-evaluate. I’m just going to stick to my GAD diagnosis and taper on my own. Hopefully he will trust me enough to change the visits to once a month.

Here is the real kicker: In the whole visit, he offered me gabapentin, paxil, effexor, anafranil (which I’d be willing to retry at some point b/c it of positive past with it). And the most outrageous of all.. He actually offered me buprenorphine (Suboxone) to help treat DEPRESSION!! Are you kidding me?? I was trying to be as personable and friendly as I could, so I just said “hmmm.. I haven’t been on opiates in about 8 months. That might have made a little more sense if I made the transition back then, but at this point, I’m not sure what the benefit would be?”. Come to find out, their have actually been clinical trials using buprenophine for depression, and it’s soon going to be a new depression treatment! What’s next? Oxycodone for depresssion? It makes you feel good, right? Anyway, he just refused to believe or accept that I’m trying to allow my brain to slowly recover from years of addictive psychotropic drugs. And that it takes time. But that’s just not how they think. It can’t last that long, they say. There must be some underlying condition that needs to be treated with a new drug. That’ll fix it. Sigh. Western medicine.. I guess that’s how they stay in business.

First question: “How do I find a doctor (who will give me benzos)? I fucking love them!”

My first question to everyone...
« on: February 26, 2017, 08:24:34 pm »

[Buddie]

How do I find a doctor that will taper me over a long period of time. All three tapers I have tried were between 1 and 3 months. And they all resulted badly, severe depression and anxiety along with cognitive effects and pain.
It seems like every doctor knows how to prescribe Benzos and I can’t find one to taper me off them without crashing me.
3mg clonazapam for 17 years. Was great for the first year and the years after just got worse and worse. It has changed me for the worse in so many ways.

Kooks push intravenous ketamine

Recreational use of ketamine

Ketamine is a prescription anesthetic that is federally regulated (e.g., U.S. Schedule III, U.K. Class B) that functions as a dissociative anesthetic, and so has seen use as a recreational drug. Originating in the United States in the 1970s, the recreational use of ketamine has since spread to Europe, Canada, Asia, and Australia. Attempts are made to use the drug at sub-anesthetic doses; contexts for use include both private settings and at club venues (raves and parties), where it initially gained popularity. Despite its emergence as a club drug, users may eventually relegate their use to more private settings

Ketamine interacts with a variety of other drugs, most pronounced with alcohol, opioids (potentiation), and barbiturates, and with drugs that increase blood pressure (e.g., stimulants, SNRI antidepressants, and especially MAOIs). The latter may have an additive effect on the user’s blood pressure, causing tachycardia, palpitations and potentially serious arrhythmias.[not verified in body] Ketamine use as a recreational drug has been implicated in a small but greatly exaggerated number of annual deaths, the majority of which are youth or young adults, which have, taken together, led to increasing stringency of its regulation worldwide.

As a consequence of its drug interactions and adverse effects, including the ability to cause confusion and amnesia, and adverse reactions that occur during emergence from anaesthesia, some cases are known from the media that involved irresponsibly high dosages and accidents in people who were not prepared for the experience and/or took other drugs at the same time, despite ketamine being a physically very safe substance in comparison to other psychoactives like opioids or even alcohol. But ketamine can leave users vulnerable to date rape (i.e., because of the associated confusion and amnesia).

Due to the complexity of its chemical synthesis, ketamine supplies for recreation use must be diverted from licit medical sources, though there have been reports of industrial-scale illicit ketamine manufacture in China and India.

Effects

Mortality
Ketamine’s use as a recreational drug has contributed to more than 90 fatalities—the majority among young adults—in England and Wales in the years of 2005-2013, including accidental poisonings, drownings, and traffic accidents. This has led to its increasingly stringent regulation (e.g., upgrading ketamine from a Class C to a Class B banned substance in the U.K.).

Drug interactions
Ketamine may increase the effects of other sedatives, including, but not limited to: alcohols, benzodiazepines, opioids, and barbiturates. Other drugs which increase blood pressure may interact with ketamine, having an additive effect on blood pressure; such agents include stimulants, SNRI antidepressants, and MAOIs.[citation needed] Increase blood pressure and heart rate, palpitations, and arrhythmias may be potential effects.[citation needed]

Adverse reactions
Ketamine is generally safe even for those critically ill, when administered by trained medical professionals. The dosages used recreationally are somewhat lower than a fully anaesthetic dosage, making the substance physically relatively safe in comparison to other psychoactive drugs.[44] Still, even in these cases, there are known side effects that include one or more of the following:

  • Cardiovascular: abnormal heart rhythms, slow heart rate or fast heart rate, high blood pressure or low blood pressure; and
  • Central nervous system: increased intracranial pressure (ICP), leading to intracranial hypertension.

In addition there are dermatologic adverse reactions (ARs; transient erythema, transient morbilliform rash), gastrointestinal ARs (anorexia, nausea, increased salivation, vomiting), neuromuscular and skeletal ARs (Increased skeletal muscle tone, i.e., tonic-clonic movements), ocular ARs (double vision, increased intraocular pressure, nystagmus), respiratory ARs (airway obstruction, apnea, increased bronchial secretions, respiratory depression, laryngospasm), as well as local pain or exanthema (e.g., at injection sites) and possible anaphylaxis and dependence.

In 10-20% of patients at anesthetic doses, adverse reactions are experienced that occur during emergence from anesthesia, reactions that can manifest as seriously as hallucinations and delirium. These reactions may be less common in some patients subpopulations, and when administered intramuscularly, and can occur up to 24 hours postoperatively; the chance of this occurring can be reduced by minimizing stimulation to the patient during recovery and pretreating with a benzodiazepine, alongside a lower dose of ketamine. Patients who experience severe reactions may require treatment with a small dose of a short- or ultrashort-acting barbiturate.

Non-lethal manifestations

Ketamine produces effects similar to phencyclidine (PCP) and dextromethorphan (DXM). Unlike these other well-known dissociatives, ketamine is very short-acting, its hallucinatory effects lasting tens of minutes when inhaled (insufflated) or injected, and hours when ingested. With ketamine, intensities of hallucinations are dose-dependent. Like other dissociative anaesthetics, hallucinations caused by ketamine are fundamentally different from those caused by serotonergic psychedelic (classic) hallucinogens.

The specific dissociative state produced by ketamine is characterised by a sense of detachment from one’s physical body and the external world that is known as depersonalization and derealization. At sufficiently high doses, users may experience what is called the “K-hole”, a state of extreme dissociation with phenomenology of schizophrenia (e.g., visual and auditory hallucinations).

John C. Lilly, Marcia Moore and D. M. Turner (amongst others) have written extensively about their own entheogenic use of and psychonautic experiences with ketamine. Both Moore and Turner died prematurely (due to hypothermia and drowning respectively) during presumed unsupervised ketamine use.

Overdose management

As the recreational dosages used are always below the fully anaesthetic threshold and thus lower than those medically administered, the term ‘overdose’ needs to be seen a bit differentiated from other drugs. While with continued use, people may build up some degree of tolerance, leading to the use of higher dosages than medically advised, it is technically somewhat difficult to overdose on ketamine. An even higher dosage will just lead to full anaesthesia, amnesia, but no physical danger from the drug itself as long as the environment isn’t dangerous. The user will become catatonic when fully dissociated, not experiencing any pain but also unable to move his/her body.

There is no known effective antidote used to treat ketamine overdose, and treatment generally focuses on the maintenance of respiratory and circulatory function until the patient is capable of breathing under their own power and all cardiac abnormalities have subsided. Unlike many other anaesthetics, ketamine has a minimal effect on respiratory drive and tidal volume; while pulse oximetry is always essential it rarely drops enough to require mechanical ventilation or supplemental oxygen, except in the most massive of overdoses and in cases of mixed-drug-overdose.

Verbal reassurance and a calming environment (i.e. dim lights, calming music, and the presence of supportive individuals in the room) should be provided when possible to calm the patient and/or prophylacticly to prevent agitation. Occasionally it may become necessary to restrain highly agitated patients during recovery should they become violent, experience panic attacks, or otherwise present a threat to themselves or others.

Even after all vital signs have normalized and the patient appears functional it is advised to require the patient to be driven home as residual impairment of motor skills may persist for up to a day after apparent resolution.

Dependence

Ketamine’s potential for dependence has been established in various operant conditioning paradigms, including conditioned place preference and self-administration; further, rats demonstrate locomotor sensitization following repeated exposure to ketamine. Increased subjective feelings of ‘high’ have been observed in healthy human volunteers exposed to ketamine.[63] Additionally, the rapid onset of effects following smoking, insufflation, and/or intramuscular injection is thought to increase the drug’s recreational use potential. The short duration of effects promotes bingeing, tolerance can develop, and withdrawal symptoms, including anxiety, shaking, and palpitations, may be present in some daily users following cessation of use.

Due to its primary NMDA-antagonist effect, sudden withdrawal in severely addicted users will result in overexcitability, manifesting as increased sensitivity to stress, anxiety and pain. There are speculations about possible excitotoxicity resulting from the rebound surge in glutamate, but this has not yet been proven or disproven in humans and it doesn’t seem to be a huge concern in healthy adults. Unlike GABAergic sedatives however, overexcitation secondary to ketamine withdrawal is not life-threatening as long as no underlying seizure disorders are present and even very tolerant users will likely suffer, at worst, only minor neurological sequela following the abrupt discontinuation of the drug. Some titration or the administration of anti-excitatory agents like memantine could be of benefit.

Ketamine can cause a variety of urinary tract problems that are more likely to occur with heavier and/or higher dosed use, especially in those not watching for a healthy lifestyle, according to a UK study.

See also: K-Hole (“K-hole” is a slang term for the subjective state of dissociation from the body commonly experienced after sufficiently high doses of the dissociative anesthetic ketamine. This state may mimic the experiences such as catatonic schizophrenia, out-of-body experiences (OBEs) or near-death experiences (NDEs), and is often accompanied by feelings of extreme derealization, depersonalization and disorientation, as well as temporary memory loss and vivid hallucinations.)

https://en.wikipedia.org/wiki/Recreational_use_of_ketamine

https://en.wikipedia.org/wiki/Ketamine

Benzo Buddies addict goes from binging on pills to binging on donuts

You mean chocolate donuts are not good for you?
« on: November 13, 2016, 02:11:42 am »

[Buddie]

I’m writing as kind of a confessional and I wasn’t sure where to even post this. Maybe a blog is in order but I am not good at tending to a blog, I think. And I don’t have a therapist at the moment. There is someone I spoke with on the phone but I owe her money and, well, I think I have to use BB forum as my therapist. It sure has been more helpful than anything or anyone else. Except for chocolate donuts.

So less than 2 months off, I’m beginning to see where my habits as a person are now not serving the person that needs help. I won’t get too into this too much – but I come from a family that left me emotionally scarred and very insecure. I have run the gamut of ADs and Ativan. Lunesta was the last. So now, as a woman in her 50s in the midst of w/d, I have to take care of myself.

I was rather undisciplined before all this with a lot of self-doubt and self-sabotage. I practice alot of fear-based emotional responses to the brain fogged/sleep deprived state that I know I must survive in spite of the fear I have that it may never end. I know I am not alone in this.

Of course I am depressed and tired. “Of course you deserve 6 of these chocolate donuts” I think. You can’t drink, smoke, drug. You feel like s**t. More donuts. I write because I want to begin taking care of myself. I mean really want to. I want to do my little p.t. excercises tired without complaint and quit chasing my beautiful organic veggies with sabotaging chocolate donuts (or other). They are a kind of metaphor. I practice self care and dash it with something or some behavior not good for me. I rebel at self-discipline. Why must I hate myself? It’s time. Thanks WBB
« Last Edit: November 14, 2016, 03:15:06 am by [Buddie] »