Sure, I know exactly what you're referring to. In psychology that trance-like, complete engagement state of mind is just called <i>flow</i>. That's the main reason why I love certain video games. A great computer game (like Civilization 3) is like a surrogate for replicating the feeling of 'flow' that comes from successfully daytrading a volatile market. I can (sometimes) reach flow via trading or games, but don't enter anything resembling an altered state from therapeutic hypnosis. Anyways, I've done my part here in explaining the Endorphin-Depression-Opioid connection. I've already used it to save the life of one suicidal friend (no, I'm not talking about myself), am far more capable at properly treating depression than nearly all of the doctors*, and will have to continue helping others this way until the world catches up with me on this subject. *Actually, some psychiatrists <b>do</b> know that many 'incurable' depression patients can only find relief in opiates, but won't even let the patient know (let alone prescribe anything) due to fear of the uneducated DEA thugs who dictate to them exactly how they must practice medicine.
BTW, I shouldn't have used the word 'cure' at all in the title of this thread. 'Treatment option with high success rates' would be the correct wording. When doing research, and finally stumbling upon the fact that every single theory I've independently come up with about the Endorphin-Depression-Opioid connection <b>was not only true, but also proven via clinical trial</b>, I got pretty enthusiastic about the need to tell people about it, so they won't have to go through what I did.
I think its obvious that if you can achieve a certain state once, you can do it again. If you weren't able to in a therapeutic setting then it was probably an incompetent person sitting across from you and not a blow against your capacity or the validity of hypnotherapy. Dr. Milton Erickson was more than once confronted with patients who claimed they weren't able to be hypnotized or that they were 'immune' to his mind tricks. The results were quite funny (for students of his techniques) and healing (for the patient). Of course, the guy was a freakin' GOD when it came to hypnosis. And btw, Civ 4 is out. I've resisted buying it because I know I'll become more cloistered than a hermit for the next month if I do.
I've just discovered yet more scientific research to support my assertions: http://opioids.com/naloxone/depcrf.html The effect of naloxone on adrenocorticotropin and cortisol release: evidence for a reduced response in depression by Burnett FE, Scott LV, Weaver MG, Medbak SH, Dinan TG Department of Psychological Medicine, The Medical Colleges of St. Bartholomew's and the Royal London Hospitals, West Smithfield, UK. J Affect Disord 1999 Jun; 53(3):263-8 BACKGROUND: Endogenous opioid peptides inhibit the hypothalamic-pituitary-adrenal (HPA) axis by influencing the release of hypothalamic corticotropin releasing factors. This study examines whether increased activity of the HPA axis in major depression is associated with reduced opioid tone. METHODS: We measured the adrenocorticotropin (ACTH) and cortisol responses to an intravenous bolus of naloxone 0.125 microg/kg in 13 depressed outpatients and 13 healthy volunteers. RESULTS: The mean cortisol response was significantly reduced (P<0.05), and the ACTH response was also non-significantly reduced in the depressed subjects. CONCLUSIONS: These findings imply that the degree of inhibitory endogenous opioid tone is reduced in depression. Various mechanisms for the finding are discussed, including possible alteration in the function of alpha-adrenergic pathways. <b>CLINICAL IMPLICATIONS: Reduced endogenous opioid tone may explain why some depressed individuals self-medicate with opiates, and depression is associated with opiate withdrawal. Opioid pathways may have a role in the mechanism of action of antidepressant drugs, and may be of relevance in the development of novel antidepressants. </b>LIMITATIONS OF THE STUDY: The sample size was small, leading to a failure of the difference of the basal cortisol levels and also the delta ACTH between the groups to reach statistical significance.
http://opioids.com/antidepressant/history.html THE EFFECT OF MORPHINE ON SYMPTOMS OF ENDOGENOUS DEPRESSION Michael Feinberg, Jean-Paul Pegeron, and Meir Steiner NIDA Research Monograph Series 43, pp. 245-250, 1982. Resurgence of interest in the association between narcotics and mental illness suggests that a careful reading of the older clinical literature may point the way toward fruitful experiments which will shed light on the pathophysiology of some mental illnesses and may suggest radically new treatments. Comfort (1977) has briefly reviewed the literature written in English. We have reviewed the clinical literature on the treatment of melancholia with morphine or opium, covering the years from 1850 to 1960, to address several questions: Is morphine effective in relieving the symptoms of endogenous depression? If so, is this merely nonspecific sedation, or is there some more specific treatment of symptoms? Does the relief of symptoms persist after the administration of morphine is stopped? How do depressed patients respond to morphine? What dose is needed for relief of symptoms, or for sedation? What is the incidence of tolerance and dependence? <b>Nearly every author cited concluded that morphine provided symptomatic relief in melancholia, and some suggested that morphine cured the patient.</b> Kielholz (1959) compared opium with imipramine and concluded that opium produced symptomatic relief but that the symptoms might return if treatment were stopped. (It is interesting to note that this represents the current clinical wisdom about imipramine: the symptoms may return if administration of the drug is stopped too early.) Tigges (1864) was the only author who found opium useless in the treatment of melancholia. He described the treatment of 39 patients, and provided a good deal of information about each patient's history, symptoms, and treatment. He concluded that the poor response may have been caused by the patients' having chronic, rather than acute, melancholia. It is equally likely that the lack of response was due in part to the relatively low doses of opium used. Some older textbooks of psychiatry recommend opium as a sedative-hypnotic in endogenous depression (Bucknill & Tuke, 1858; Cramer et al., 1907, Maudsley, 1867), while others found it useless (Henderson and Gillespie, 1933). The latter did not comment on the doses used, and the former only occasionally provided guidelines for its use. Nearly all of the patients described were psychotic. Morphine had an antipsychotic effect out of proportion to its effect on other symptoms, such as depressed mood. Kielholz (1959), Mickle (1874), and Marce (1857) were quite specific about this, and Ziehen (1889) found that the presence of hallucinations predicted a good response to opium. These reports are even more interesting in light of the more recent finding that psychotically depressed patients may not respond to treatment with tricyclic antidepressants (Glassman et al., 1975). Some of the papers cited describe psychotic patients who probably did not have endogenous depression (Engelken, 1851; Knecht, 1872; Voisin, 1881; 1891); in these cases the antipsychotic effect was clearly separate from an antidepressant (or antimelancholic) effect. The antipsychotic effect of morphine, found in a wide variety of patients, is difficult to reconcile with the current theory that psychosis may be due to a functional excess of endorphins and be relieved by narcotic antagonists (Bloom et al., 1976; Berger et al., 1981). Gold et al. (1977) have suggested that morphine may have an antipsychotic effect, based on the morphine-induced increase in plasma prolactin. Voisin also described an increased sensitivity to morphine, which occurred suddenly when patients became well. He could find no reason for this, or for the wide range of sensitivity to morphine in his patients; he said that he'd asked Claude Bernard, who was similarly puzzled. CONCLUSIONS <b>The available evidence clearly suggests that morphine produces symptomatic relief in melancholic patients, </b>and that this relief is out of proportion to any sedative effects. These effects seen to be dose related, as authors using lower doses (<60 mg of morphine/day) reported fewer responses to treatment than did those using higher doses. It is likely that rather than being a cure, this is symptomatic relief similar to that provided by antidepressant drugs, although most of the authors do not give enough information to allow a clear decision.<b> This finding suggests that abnormal functioning of an endorphin "system" may be responsible for some of the symptom of melancholia. </b>It is tempting, and may be fruitful, to speculate that this abnormal functioning may underlie the illness itself. It is also possible that morphine, an artificial endorphin, acts to remedy symptoms caused by abnormal function elsewhere in the brain. The evidence suggests that we should mount a double-blind placebo-controlled study of morphine or other centrally acting endorphin agonist in patients with melancholia. Such a study should probably include a narcotic antagonist and one or more of the partial agonists. The drugs used should be selected for their differential effects on the several postulated endorphin receptors in the brain. AUTHORS Michael Feinberg, M.D., Ph.D.; Meir Steiner, M.D., Ph.D.; Jean-Paul Pegeron, M.D. Mental Health Research Institute and Adult Psychiatric Service, Dept. of Psychiatry, University of Michigan, Ann Arbor, Michigan 48109 _______________
Here's an anonymous writer, who came to the exact same conclusions as I did... about everything: http://opioids.com/index.html His write up is far better than anything I've done. "A significant minority of the population only feel truly well on opioids. In effect, they self-medicate, taking responsibility for their own mental health in defiance of medical orthodoxy.... Read the rest
Update: Buprenorphine doesn't just work on paper, <b>it works for me.</b> Today marks the seventh day I've been on Subutex, and therefore 100% oxy-free. (You can't physically use any other opiate in combination with buprenorphine, as it would be wasted. The bupe binds to the opioid receptors in one's brain, and doesn't allow other opiates to bind or have any effect at all.) Seven days means I'm now officially detoxed. Buprenorphine is <b>the holy grail of psychiatry</b>. Here's a medication which effectively treats even the most severe cases of refractory, suicidal depression. At this point, it's not even legal to prescribe bupe for this purpose, but once the truth is commonly known, the laws will be forced to change. You'll see... http://www.naabt.org/forum/topic.asp?TOPIC_ID=114
For the 13 people and one filthy troll who clicked the first poll option: Now that I'm fully detoxed off oxy, and my opinions haven't changed one iota, can I still be called "Another useles junkie trying to justify his habit"? ...or do you now understand that I was right all along?
Just found this thread. I hope people understand the most important point being made here; that you must take responsibility for your own health, because the special interest types have... no interest. Others have an interest but are too brainwashed to be able to do anything about it. Good luck - I hope this continues to work for you. I now have some insight into your comments on the drug trafficking thread.
Good luck with the bupe. Some see it as a "get-outta-jail-free" card. Some don't. (you know what I mean) If you want to no mutha fuxxing shit kick and leave it all behind then ....look into Ibogaine. If you don't want to kick then bupe is your answer. But it's almost like the 'done.....It'll keep ya on the hook but in a very quiet and insidious manner. Or so I'm told. Ask an anesthestiologist what they use bube for. http://www.ibogaine.org/