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Thread: Opioids for Depression: poppy tea, buprenorphine, methadone, and now trying tianeptine

  1. it's called a strawman when you misstate a person's views and then proceed to dispute the opinion you've just created. that's what you're doing, @jakemoe

    and then you recite a mantra from pharmaceutical company marketing material. my guess is you take those toxic drugs and it threatens your worldview to have it exposed here as a sham and a racket that makes people miserable. slaves can become very angry at being told they are slaves. they don't want to know.

    i didn't get my ideas from reading the books of Dr. Edward Shorter, but was very pleasantly surprised that he presented very strong evidence of the folly of so-called transmitter-deficiency theory of depression. read his books Before Prozac and Why Everyone Became Depressed.
    Last edited by Trampy; 3 Days Ago at 04:21 PM.
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  3. From the dustjacket of Before Prozac:

    An unsettling look at modern psychiatry, revealing how greed,lax regulation, and academic infighting have set the field back fifty years.

    Psychiatry today is a barren tundra, writes medical historian Edward Shorter, where drugs that don't work are used to treat diseases that don't exist. ... Shorter illuminated this dismal laandscape in a revealing and provocative account of why psychiatry is losing ground in the struggle to treat depression.

    Naturally, the book looks at such culprits as the pharmaceutical industry, which is not inclined to market drugs once the patent expires, leading to the introduction of new--but not necessarily better--drugs. But the heart of the book focuses on an unexpected villain: the FDA, the very agency charged with ensuring drug safety and effectiveness. Shorter describes how the FDA permits companies to test new products only against placebo. If you can beat sugar pills, you get your drug licensed, whether or not it is actually better than (or even as good as) current medications, thus sweeping from the shelves drugs that may be superior but have lost patent protection. ...
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  4. #23
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    You have a right to believe what you want @Trampy, I respect that from anyone. I know in some cases, chemicals are very beneficial to ones health.
    F**k the DEA

  5. Quote Originally Posted by jakemoe View Post
    You have a right to believe what you want @Trampy, I respect that from anyone. I know in some cases, chemicals are very beneficial to ones health.
    Oh I agree 100%. I'd rate opioids and endogenous opioids as the key to health and happiness. In Aldous Huxley's Brave New World the fictional drug named Soma had very strong mu- activity.

    From the old Jefferson Airplane song in the 60s: "One pill makes you larger, and one pill makes you small, but the one that mother gives you doesn't do anything at all."

    The old earth mother has been replaced by a partnership between government and big industry and they are the ones pushing the serotonin and norepinephrine drugs, which have no relation at all to Melancholia, Non-Melancholia, etc. a huge number of very diverse "depressions" all rolled into one these days as Major Depression.

    It's not politically correct to say that chronic unhappiness, low energy, low mood are often the result of an endogenous-opioid deficiency. Opiates are the Enemy, so they can't possibly be good for a patient.
    Last edited by Trampy; 3 Days Ago at 08:11 PM.
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  6. In a modern society of efficient worker slaves it's undesirable for them to have varying work hours depending on how they feel that day. Everyone is supposed to work the same schedule year round. But in nature everything follows cycles of growth and rest and then decay. Same for humans, We have period of high energy and these are naturally followed by a period of low energy.

    In the common hive mind, seasonal affective disorder is associated with a wintertime slump or cold-weather blues. Well, in my case it's not winter but high summer temperatures that make me feel sleepy and tired all day. Maybe it was just an unfortunate coincidence that my cat Romeo died after a week in the hospital when they tried to keep him alive after his bladder was punctured by an intoxicated veterinarian who performed a cystocentesis without my permission and without medical necessity. And he was so high it was obvious. And he gave me two paper scrips in a row with the drug name misspelled. I was so angry and then felt a big loss of companionship from his massive 19 pounds of soft cat who would circle around before coming to rest against my body touching me all along his spine if that was possible.

    So when it got hot here and the temp hit 99 F one day it was all I could do to feed my four remaining cats and keep their water bowls fresh and empty the catboxes for the 17-yr-old who does his business where he pleases while the others are put outside for looking at the catbox. There were days it was an effort to get off the couch and i'd fall asleep to take a surprise nap sometimes with a book in my hand, or even sitting in a armchair dozing off from fatigue and feeling tired all the time.

    That chronic fatigue is relieved by 10 mg of methadone.

    I believe that the serotonin drugs that began with Prozac will go down in history as one of the greatest and most profitable hoaxes in the history of medicine. Ever since Hippocrates the opium poppy plant has been the panacea for all those who are constitutionally sad. The Prohibition of alcohol from the Progressive Era--criticized so well by H.L. Mencken in his American Mercury--was rescinded but the war on drugs and drug users has only intensified.

    I'm sure there are many here who use opioids to self-medicate for low mood and chronic fatigue with them feeling energized by those drugs and medical science won't explore their use for those indications for political or religious reasons, but they don't realize it, because of the societal stigma against opiate users.

    Life is so precious. My cats brought home a small fledgling baby bird and it has two wounds on its back from being carried here and they played with it for an hour and then left it alone and so i'm holding it in my left hand and can feel its heartbeat and breathing where it's trying to live and it's probably made more comfortable from the warmth of my hand. It stopped chirping but it's staying alive. I never imagined that i'd live to the age i've achieved. It's a miracle.
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    Psychiatric Times
    Opioids to Treat Depression: The Jury Is Out
    Burns Woodward, MD
    December 1, 2016
    Volume: 33 Issue: 12
    Major Depressive Disorder, Addiction, Couch in Crisis, Depression, Opioid Related Disorders
    ©Lightspring/ Shutterstock


    Two recent clinical trials of opioid medication for depression and suicidality highlight the role of brain opioid systems in depression.1,2 Opioids treat pain, but depression and pain are often comorbid, and some antidepressants relieve neuropathic pain even in the absence of depression. Depression involves dysfunction in monoamine systems, the hypothalamus-pituitary-adrenal (HPA) axis, and hippocampal neurogenesis, but could it also be rooted in a deficit of endorphins, or even an endopharmacological withdrawal state?

    Before the modern antidepressant era, depression was often treated with opiates—with a sometimes heavy price of addiction. Would psychiatrists be contributing to the epidemic of opioid addiction if we started to treat depression with opioids?

    Brain opioid systems

    The best-understood endogenous opioids are the endorphins, which, like morphine, bind preferentially to mu-opioid receptors. Enkephalins bind to the delta-receptor, and dynorphins to the kappa-receptor. The less-studied endomorphins and nociceptin are structurally related to opioids; they also contribute to pain, anxiety, stress responses, and reward, and are targets for drug development.

    Human neuroimaging shows mu-receptor activity in brain areas involved in emotions, including the nucleus accumbens, ventral pallidum, amygdala, anterior cingulate, and posterior thalamus.2 More detailed information comes from animal research using mice genetically engineered with inactive opioid receptors; micro-infusion of drugs into key sites such as the nucleus accumbens; and models such as learned helplessness, forced swim, and tail suspension.3 Mu-, delta-, and kappa-opioid receptors have central roles in many mood-related functions, including the dopamine reward system, serotonin and noradrenergic pathways, and the HPA axis. Opioids also influence the survival and growth of neurons in the hippocampus.

    The Table summarizes some of the behavioral effects of opioids in animals. Mu-agonists relieve depression-like behavior acutely, but tolerance develops, and depression is worse on withdrawal from long-term administration. Delta-agonists appear to improve mood, while kappa-agonists worsen it.3-5 There is evidence that opioid dysfunction accounts for lack of pleasure in depression, while problems with dopamine impair motivation.6

    Opioid systems, then, participate in many mood-related functions. They are examples of evolutionary repurposing of neurotransmitters that originally evolved for one purpose to meet a variety of other needs.7,8 Like monoamines, opioids are neuromodulators; they affect excitability by slower second messenger effects.

    Recent research

    Yovell and colleagues1 report that ultra–low-dose buprenorphine markedly reduced suicidal ideation over 4 weeks in 62 patients with varying levels of depression; the majority also had borderline personality dis*order. The reduction in suicidality correlated only modestly with improvement in depressive symptoms. The investigators did not report any assessment of possible addictive responses to buprenorphine.

    The mean buprenorphine dosage in the study was only 0.44 mg daily, which is in the range used to treat pain. In mammals, such ultra-low dosages reduce separation distress. Below 2 mg, agonist effects predominate, and abuse can occur. At the much higher dosages of 8 mg to 24 mg daily used to treat addiction, buprenorphine is a mu-partial agonist, exerting mild mu-agonist effects while blocking other opioids from the receptor.

    This intriguing study originated in theoretical work by the neuroscientist Jaak Panksepp. Drawing on animal research, Panksepp8 has identified 7 basic emotional systems that underlie behavior, which he calls seeking, rage, fear, lust, care, panic/grief, and play. Each is associated with specific brain regions and neurotransmitters. Yovell, Panksepp, and colleagues1 hypothesized that patients’ depression, physical and mental pain, and suicidality were related to the panic/grief system and would be relieved by mu-opioid agonism.
    Helpful jaders Rated helpful
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    Safety, Tolerability, and Clinical Effect of Low-Dose Buprenorphine for Treatment-Resistant Depression in Midlife and Older Adults

    Jordan F. Karp, MD; Meryl A. Butters, PhD; Amy E. Begley, MA; Mark D. Miller, MD; Eric J. Lenze, MD; Daniel M. Blumberger, MD; Benoit H. Mulsant, MD; and Charles F. Reynolds III, MD

    J Clin Psychiatry 2014;75(8):e785–e793
    © Copyright 2014 Physicians Postgraduate Press, Inc.
    To view this item, select one of the options below.


    Objective: To describe the clinical effect and safety of low-dose buprenorphine, a ?-opioid receptor antagonist, for treatment-resistant depression (TRD) in midlife and older adults.

    Method: In an 8-week open-label study, buprenorphine was prescribed for 15 adults aged 50 years or older with TRD, diagnosed with the Structured Clinical Interview for DSM-IV, between June 2010 and June 2011. The titrated dose of buprenorphine ranged from 0.2–1.6 mg/d. We assessed clinical change in depression, anxiety, sleep, positive and negative affect, and quality of life. The Montgomery-Asberg Depression Rating scale (MADRS) served as the main outcome measure. Tolerability was assessed by documenting side effects and change in vital signs, weight, and cognitive function. Clinical response durability was assessed 8 weeks after discontinuation of buprenorphine.

    Results: The mean dose of buprenorphine was 0.4 mg/d (mean maximum dose = 0.7 mg/d). The mean depression score (MADRS) at baseline was 27.0 (SD = 7.3) and at week 8 was 9.5 (SD = 9.5). A sharp decline in depression severity occurred during the first 3 weeks of exposure (mean change = ?15.0 [SD = 7.9]). Depression-specific items measuring pessimism and sadness indicated improvement during exposure, supporting a true antidepressant effect. Treatment-emergent side effects (in particular, nausea and constipation) were not sustained, vital signs and weight remained stable, and executive function and learning improved from pretreatment to posttreatment.

    Conclusion: Low-dose buprenorphine may be a novel-mechanism medication that provides a rapid and sustained improvement for older adults with TRD. Placebo-controlled trials of longer duration are required to assess efficacy, safety, and physiologic and psychological effects of extended exposure to this medication.
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  9. Those two studies don't prove anything except that work is ongoing on using opioids for TRD. I met the criteria for TRD 20 years ago. It's not a disease; it's a personality type.
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  10. Bingo! D-methadone was fast-tracked for adjunctive use in refractory depression meaning it's not sposed to be used by itself by a prescriber (not meaning it has to be combo drug!). The methadone HCl used in medicine is racemic, ~50/50, varying somewhat by manufacturer just like with ketamine. That's the first article below, a company press release. The second, journal article is proposing the idea of using r-methadone (rather than 50/50 R-S or d-l) for pain and presumably MMT. So these two articles are about two new drugs based on the currently used racemic mixture. The methadone dispensed at clinics and made into tablets is racemic, half and half. There is interest in making patented drugs by essentially "separating" methadone HCl into its left and right enantiomers. Wow. I was on to this a long time ago and the science is catching up.

    Publish Date April 13, 2017

    REL-1017 exerts its action by inhibiting the activation of NMDA receptors while possessing no opioid activity

    The Food and Drug Administration (FDA) has granted Fast Track designation for d-Methadone (REL-1017 dextromethadone; Relmada) for the adjunctive treatment of major depressive disorder.

    REL-1017 is Relmada’s investigational, rapid-acting, oral N-methyl-D-aspartate (NMDA) receptor antagonist under development for the treatment of depression, neuropathic pain, and other potential CNS pathological conditions. The company has completed a Phase 1 study for REL-1017 and intends to initiate a randomized, double-blind, placebo-controlled Phase 2a trial in patients with major depressive disorder to assess its efficacy, safety, tolerability and pharmacokinetics.

    REL-1017, an enantiomer of racemic methadone, exerts its action by inhibiting the activation of NMDA receptors while possessing no opioid activity at therapeutic doses.

    For more information visit

    Addiction. Author manuscript; available in PMC 2013 Jul 25.
    Published in final edited form as:
    Addiction. 2011 Apr; 106(4): 687–688.
    doi: 10.1111/j.1360-0443.2011.03374.x

    R)-methadone versus racemic methadone: what is best for patient care?

    Methadone has been linked to cardiac arrhythmia. (R)-methadone appears to confer a lower risk of QT interval prolongation, resulting in debate over how best to treat patients needing this medication. A discussion of salient aspects of selecting therapy for opioid dependence and pain management and decision-making regarding methadone formulation follows.

    Since the groundbreaking work of Dole & Nyswander in the 1960s [1], methadone has been a life-saving treatment for heroin and, more recently, prescription opioid analgesic addiction. Methadone is used increasingly as a treatment for chronic pain, both malignant and non-malignant [2]. As methadone use has increased, associated toxicities and overdose deaths have risen. Methadone confers some risk for cardiac adverse events and sudden death. Its use has been associated with arrhythmias, particularly torsade de pointes [3]. This effect is mediated through the ability of methadone to bind to human Ether-à-go-go Related Gene (hERG) channels in cardiac myocytes [4], resulting in delayed repolarization. The risk is thought to result mainly from the use of a racemic methadone formulation that contains both (R)- and (S)-enantiomers. The (R)-enantiomer is a mu opioid agonist responsible for therapeutic effects. The (S)-enantiomer is a poor mu agonist and can block hERG channels to a greater degree than the (R)-enantiomer, which has been postulated to be responsible for cardiac adverse events in methadone use [5]. This information, in the context of recent studies showing a reduced effect of (R)- methadone on QTc interval [6] has generated discussion of the consideration of eliminating racemic methadone in favor of the exclusive use of (R)-methadone or buprenorphine as a means of resolving the cardiac safety issues related to current methadone treatment. However, this is a multi-faceted problem that deserves further consideration.
    Last edited by Trampy; 2 Days Ago at 04:27 PM.
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  11. #30
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    I would like to mention something I found which seems to help with depression. Its name is agmatine, its non habit forming, helps boost your mood and is good for you. They say it reduces your risk of cancer. Also its cheap and available otc.

    I use it now and then, if I feel cruddy in the morning I pop a 500 mg cap and an hour or so later feel more positive and energetic the rest of the day. Its not real strong, may not work for major depression but its worth a look. I also use st john's wort which also can help with mood
    Helpful jakemoe, jaders, trish5959 Rated helpful

  12. Thank You, @Gullible. I'll look into it. Sounds like it might be chemically similar to memantine or to the tianeptine that i'm still taking at 13 mg three or four times a day.

    This morning I waited as long as I could before taking some kratom, but it's immediately energizing. Medical science is slowly approaching the recognition that low levels of endogenous opioids can be the cause of so-called depression or a melancholic personality.
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  13. #32
    Ray Peat PhD has some interesting ideas on the whole "receptor" idea of communication. He seems to be more into the idea of thyroid deficiency and environment that has the greatest impact of well being. Lots of estrogen is being introduced into our systems by toxic oils like soybean, that in turn slow down thyroid and varnish cell wals to slow down cell to cell communication.
    Likes Stlgirl liked this post

  14. Thanks, @john66. Yeah, i've tried taking levothyroxine from India at lowest dose several times but all it ever did was cause anxiety. People have a natural tendency to tout whatever worked for them or someone close to them and so yeah, low thyroid can cause low energy. The way to test if that's your problem is a low-dose trial. Other things that can help are a sleeping pill because insomnia can cause daytime sleepiness and fatigue. Vitamin D I need to buy some ran out.

    Still feeling 1.5 grams of boosted kratom powder from 4 hours ago and yesterday took only 5 mg methadone, and no Suboxone and no tramadol. 50 grams remaining of boosted kratom powder and 10 methadone tablets remain. Looks like i'll need to buy some kratom because it really helps a lot.

    It's a terrible shame they follow the stigma and so many people rather be dead than be going to a methadone clinic. They really do die from their unhappiness, one way or another, suicide, overdose, or complications of opiate abuse. Or end up in prison for buying a medicine they need that doctors won't prescribe.
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  15. #34
    Quote Originally Posted by Trampy View Post
    Doctors work in the disease industry. They make money from people's poor health. If you feel lousy and are sleepy all the time do you think a doctor would ask you to describe your sleep? Heck no. They don't ask you don't ask you anything about your sleep or diet or digestion because that's considered blaming the victim. If you're tired all the time, first look at sleep, then diet, and for overall vitality you need to have a well-functioning digestive system to get the nutrition from your food and to avoid being full of crap. So that's number 1 priority if you're tired all the time. If you think a doctor can solve all your problems for you, go look for a shaman or witch doctor, not a licensed medical doctor.

    And if you're feeling miserable and think that this thread is a good justification for you to self-medicate with opiates, well good luck.
    Exactly. I went in last October for chronic fatigue that’d id been experiencing for a year. They said it’d take a month to have everything done. It’s now July ‘19 and I just did my “sleep test” in June. It’s been 4 weeks from that and the specialist Dr still hasn’t read my study results. I’ve been calling, as they told me I should if i hadn’t heard anything for 2 weeks. This entire time I’ve been tired and miserable. I know I don’t have sleep apnea, I don’t have any of the symptoms but they had to do the test because my Dr won’t do anything until the sleep study results are in. I’ve also been eating healthier and exercising more just as the Dr had suggested. Still no change.

    I feel like I’m going crazy because being “tired” is not something people take seriously. Neither my family or my doctors really seem to give a shit and they must think it’s all “in my head” or think I’m depressed. I wasn't depressed before, but I am NOW! After waiting 2 years for ANY kind of help and not receiving it can take its toll.

    I would LOVE to try the ketamine nasal spray. I have never reacted well to SSRIs or any anti depressants that basically change your brain composition, so it would be worth a shot for me. The best anti depressants I’ve ever used were Vicodin. They don’t make me tired but give me energy and motivation, which is what I need. Plus, I can control my use of them just to treat my symptoms.

    Sorry for the rant, I’m just so frustrated and alone. I would just love to try something that actually works, which I can’t get atm, because all of the drs are too scared to prescribe anything.
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  16. #35
    Quote Originally Posted by john66 View Post
    Ray Peat PhD has some interesting ideas on the whole "receptor" idea of communication. He seems to be more into the idea of thyroid deficiency and environment that has the greatest impact of well being. Lots of estrogen is being introduced into our systems by toxic oils like soybean, that in turn slow down thyroid and varnish cell wals to slow down cell to cell communication.
    Yeah, I have low T3 hormone and got an Rx for it but I’m still very fatigued. Thyroid issues are very common. It was one of my first tests when I complained of fatigue

  17. #36
    @Stlgirl, the sleep study seems like such a waste for everyone but the doctors who scam people into doing such a stupid procedure. If you spend the night in a strange place surrounded by machinery or if you wear some kind of devices at home, what could be learned conclusively? Nothing. It's just a silly scam to inflate doctors as gods and impose barriers to the prescribing of sleeping pills.

    Vicodin can be found. Ketamine in my opinion is just a fad that will blow over. It's an anesthetic so of course it will ease a person's pain but you can't be taking it every day because you go crazy as happened to John Lilly, in The Scientist, later editions of which were censored BTW, so get the 1st or 2nd edition.

    Today I was feeling a lot of sadness due to the aging of a person close to me. The heavy lethargy was not relieved by kratom today even after taking three doses of 1.5 grams, the amount taken yesterday that seemed beneficial immediately. I see my lethargic depression as sort of a chronic pain syndrome of the psyche. At 3:45 PM i took just 5 mg of methadone and took a nap and woke up feeling none of that psychic pain.

    Yes, I need to get hooked up with BTC in a wallet so I can buy from vendors that way. Opiates relieve my psychic pain, and when that suffering is allayed, I can function and be active and happy and healthy. Just 5 mg of methadone was tremendously beneficial to me this afternoon. So coinbase here I come.Lilly_TheScientist_1st_edition.jpg

    Sorry for the very large image of John Lilly dust jacket. But ketamine is something i've had around the house for decades now and even when my psychic pain is at its worst i don't use the ketamine. Once at the very beginning of this thread i took 20 or 25 mg by IM, whatever it was. But not again. Please forget about pipe dreams and fads like ketamine for depression. Unless you know that ketamine is good for you, stay away because if you have that nasal inhaler you'll be tempted to misuse it. And it's poison. No good. Crazy making. Vicodin or methadone or any other pure mu agonist is another story entirely.

    With Vicodin being 5/500, the maximum safe dose would be at most four a day if your liver is healthy, or 20 mg hydrocodone. I'm finding a strong response to just 5 mg of methadone. But oxycodone IR seems like there are way more sources and there's no APAP to worry about. Be safe and please forget about the ketamine because it's just a pipe dream pushed by snake oil salesmen. Pain killer opiate tablets are much safer and you know they work for you, because you said so yourself.
    Last edited by Trampy; 10 Hours Ago at 08:20 PM.
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  18. #37

    Default the war on opiates is pushing people to use ketamine instead of opiates for TRD

    The new s-ketamine nasal spray was approved by FDA for TRD in March 2019. It's named Spravato. Theoretically any doctor can prescribe it but plain old racemic ketamine might be more effective and cost pennies per dose if you get it by mail from Pakistan, or buy Spravato and pay big bucks out of pocket or from a Medical Savings Account pre-tax income.

    Esketamine's approval comes as more and more doctors have begun administering a generic version of ketamine for depression. Generic ketamine is approved as an anesthetic, not as an antidepressant. Even so, doctors can legally prescribe it for off-label medical uses.

    And as a growing number of studies have shown ketamine's effectiveness against depression, ketamine clinics have sprung up around the United States. These clinics often administer the drug in an intravenous infusion that can cost more than $500 per treatment.

    Many doctors who have become comfortable offering ketamine for depression probably won't switch to esketamine, said Dr. Demitri Papolos, director of research for the Juvenile Bipolar Research Foundation and a clinical associate professor at Albert Einstein College of Medicine.

    For the past 10 years, Papolos has been prescribing an intranasal form of ketamine for children and adolescents who have a disorder that includes symptoms of depression.

    "I'm very pleased that finally the FDA has approved a form of ketamine for treatment-resistant mood disorders," Papolos said. He said the approval legitimizes the approach he and other doctors have been taking.

    But he hopes that doctors who are currently using ketamine continue to do so. "It'll be a lot less expensive and a lot easier for their patients [than esketamine]," he said.

    And animal studies show it's possible that old-fashioned ketamine is a more potent antidepressant than esketamine, Papolos said.

    Esketamine "may not be as effective as a generic that any psychiatrist or physician can prescribe without restrictions," Papolos said.

    Johnson & Johnson said the wholesale cost of each treatment with esketamine will range from $590 to $885, depending on the dose. That means twice-weekly treatments during the first month will cost centers that offer the drug at least $4,720 to $6,785. Subsequent weekly treatments will cost about half as much.

    The drugmaker says those figures don't include administration and observation costs.

    Many psychiatrists and patients with depression are excited about the potential of esketamine nasal spray. But Alan Schatzberg, MD, warns that too little is known about ketamine for it to be used broadly. In this podcast, he talks about the dangers and unknowns of ketamine and the importance of additional studies before widespread adoption. Dr. Schatzberg is a professor of psychiatry and behavioral sciences and director of the Stanford Mood Disorders Center.
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