buffb2
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Can Dopamine Make Your Future Look Brighter? - TIME
just thought it was interesting.
Wanted to share with friends on AM
just thought it was interesting.
Wanted to share with friends on AM
Is there any application for low dose naltrexone to improve the side effect of decreased libido from antidepressant treatment?The real problem is that affecting dopamine centers leads to addiction and other issues. It isn't a good idea to modify dopamine centers unless you have an underlying issue such as schizophrenia, Parkinson's or some other psychotic disorder. It is unfortunate that we don't understand more of these areas but basically what happens is the VTA extends dopamine neurons through the mesolimbic and mesocortical centers. Overactivity of one causes dependence and underactivity of the other causes dependence. You also have seratonin, dopamine, GABA, and nicotinic receptors attached to these neurons which have various positive/negative effects, it is very complex.
Anti-Dopaminergic side effects are also very nasty. When using an agonist you can definitely downregulate receptors so that when you can come off it is similar to antagonism. The sides are called EPS (extra pyramidal side effects) and the worst of which is something called tardive dyskinesia and is very sad to see when patients start to exhibit it. The other problem with taking L-dopa is that most of it is metabolized in the periphery so you aren't really getting the effects you are looking for unless you combine it with a D-decarboxylase inhibitor like carbidopa.
Bottom line, I wouldn't mess with anything that alters dopamine transition unless you truly do have an underlying issue such as schisophrenia and some aspects of bipolar disorder.
Psychoneuroendocrinology. 1989;14(1-2):103-11.
Endorphins in male impotence: evidence for naltrexone stimulation of erectile activity in patient therapy.
Fabbri A, Jannini EA, Gnessi L, Moretti C, Ulisse S, Franzese A, Lazzari R, Fraioli F, Frajese G, Isidori A.
Institute of V Clinica Medica, University of Rome La Sapienza, Italy.
In the present study we evaluated whether naltrexone administration could stimulate sexual function in 30 male patients, ages 25 to 50 years, with idiopathic impotence of at least one year's duration and not of organic etiology. The patients received naltrexone (50 mg/day) or placebo, on a random basis for two weeks. Sexual performance, expressed as the number of full coitus/week, was assessed before (time 0) and during (on days 7 and 15) each treatment. The naltrexone therapy significantly increased the number of successful coitus compared to placebo after 7 and 15 days of treatment: improvement of sexual performance was evident in 11 out of the 15 treated patients. All the patients experienced a significant increase in morning and spontaneous full penile erections/week. No significant side effects were reported. Endocrine studies revealed no significant modification of plasma LH, FSH or testosterone by naltrexone, suggesting that the positive effect of the drug on sexual behavior was exerted at a central level. A two-month follow-up, at which time patients were off treatment, erectile capacity had returned to baseline in 10 patients, while five reported complete recovery of their sexual ability. We hypothesize that an alteration in central opioid tone is present in idiopathic impotence and is involved in the impairment of sexual behavior.
PMID: 2543996 [PubMed - indexed for MEDLINE]
J Androl. 1993 Nov-Dec;14(6):407-10.
Treatment of idiopathic erectile dysfunction in men with the opiate antagonist naltrexone--a double-blind study.
Brennemann W, Stitz B, Van Ahlen H, Brensing KA, Klingmüller D.
Department of Clinical Biochemistry, University of Bonn, Germany.
Opiate antagonists can indirectly stimulate the secretion of luteinizing hormone (LH) and testosterone, as well as sexual functions in animals and humans. We therefore treated 20 otherwise healthy men with idiopathic erectile dysfunction aged 46.3 +/- 2.7 years (mean +/- SE, range 23.9-63.3) in a double-blind study with an opiate antagonist, naltrexone, or placebo. The erectile dysfunction of these men had persisted for 3.6 +/- 0.5 years despite libido maintenance; standard procedures had excluded any organic causes. Trial duration was 12 weeks overall. After a 4-week forerun, the patients received at first 25 mg naltrexone/day orally or placebo for 4 weeks followed by 4 weeks of a 50-mg dose of naltrexone/day or placebo. Each day the patients filled out a questionnaire detailing libido, degree of erection, frequency of sexual intercourse, and spontaneous morning erections. Serum concentrations of gonadotropins and testosterone were determined radioimmunologically in the initial stage and at the end of each phase. Both patient collectives had similar initial factors. The group treated with naltrexone showed a significant rise in spontaneous early morning erections during the treatment: from 2.8 +/- 0.3 to 4.2 +/- 0.3 a week (P < 0.001). The placebo group showed no significant change in spontaneous erections (2.4 +/- 0.3 and 2.6 +/- 0.3, respectively). The subjective parameters, however, such as libido, degree of erection, and frequency of sexual intercourse showed no significant difference within each group. There was no difference in LH, follicle-stimulating hormone, or testosterone concentrations in both groups. Thus, treatment with naltrexone significantly raises the rate of spontaneous early morning erections when compared to controls.(ABSTRACT TRUNCATED AT 250 WORDS)
Hope this helps. Gotta run.Eur Urol. 1995;28(3):246-50.
Opiate antagonists in erectile dysfunction: a possible new treatment option? Results of a pilot study with naltrexone.
van Ahlen H, Piechota HJ, Kias HJ, Brennemann W, Klingmüller D.
Department of Urology, University of Münster, Germany.
Opioids have an inhibitory effect on sexual functions in both animals and humans. Twenty patients with idiopathic, nonvascular, nonneurogenic erectile dysfunction were treated with the opiate receptor antagonist naltrexone in a randomized, placebo-controlled, double-blind study for 8 weeks. Libido and frequency of sexual intercourse were not significantly altered, but early-morning erections increased significantly under naltrexone therapy. This response was not related to levels of androgens or gonadotropins, neither was it dose dependent. There was no change in any of the measured parameters under placebo. Further clinical studies with the substance should be conducted to evaluate its possible role in the oral treatment of male impotence.
PMID: 8536780 [PubMed - indexed for MEDLINE]
Repeated amphetamine (AMPH) exposure in nonhuman primates produces a chronic state of monoamine dysregulation and long-lasting changes in behaviors elicited by acute AMPH (including tracking, grasping "at thin air," manipulating nonapparent stimuli, and hypervigilance) in a manner that bears a marked resemblance to symptoms of both amphetamine psychosis and paranoid schizophrenia. These abnormal responses have historically been referred to as psychotomimetic or hallucinatory-like. In contrast to negative symptoms and cognitive deficits, the positive symptoms of schizophrenia including hallucinations have not traditionally been linked to prefrontal dysfunction.The dorsomedial (9/8B), dorsolateral (46/8A), and inferior (45/12) sectors of prefrontal cortex were lesioned, singly or in combination. Lesioned and nonlesioned control monkeys were sensitized over a 6-week period using an intermittent schedule of escalating low doses of AMPH. Behavioral responses to acute AMPH after chronic exposure were compared with preexposure responses.Bilateral lesions of prefrontal cortex performed before subchronic AMPH suppressed the sensitization of hallucinatory-like behaviors but markedly enhanced locomotor sensitization compared with control animals.These findings indicate that the primate prefrontal cortex may be a substrate for the development of the full complement of behaviors elicited by AMPH sensitization, including hallucinatory-like behaviors.
I think you guys are getting a bit confused about the schizophrenic brain. Obviously there is A LOT we don't know about psychosis based disorders, however, here is what we currently know. There is a mesolimbic area that goes from the VTA (ventral tegmental area) to the NAc (nucleus accumbens) and a mesocortical area that protrudes from the VTA to the cerebral cortex. There is too much dopamine release in the mesolimbic area that controls impulse and addictive cravings and the mesocortical region seems to be deficient in dopamine. The mesolimbic area is what is typically causes the positive symptoms such as hallucinations and the mesocortical controls more of the negative symptoms such as anhedonia. It may seem confusing at first as to why there can be increases in one area and deficiencies in others but the reason is because these two dopamine neurons split off from the VTA and go opposite directions, but there is actually another interneuron that connects from the cortex to the NAc that that inhibits the mesolimbic area. This means that there is less inhibition on the mesolimbic area allowing it to become interactive.To Dumbhick3, who said "Schizophrenics have brains that are practically bathing in dopamine and not in the "pleasure" areas alone; their prefrontal cortex is flooded with it which is where most thought-perception occurs (I think)."
It has been hypothesized that those with schizophrenia actually have much less dopamine in the prefrontal cortex (hypofrontality theory of schizophrenia). Many functionial magentic resonance imaging studies have supported this hypothesis, showing decreased activity in the region. This leads to many of the negative symptoms of the disorder. It is likely responsible for the distorted ability to plan ahead and for some loss of executive functioning. It also causes the brain to send signals to other parts of the brain to produce more dopamine to compensate. This overcompensation leads to excess dopamine in the mesolimbic system leading to positive symptoms, such as hallucinations and delusions, and to negative ones such as inappropriate response to emotion.
I do agree with you that it is not impossible for those prescribed stimulants and other amphetamines to become addicted. The theory behind this is that they will not become as easily addicted if they are not altering the dose and they will not be satisfying the craving to get high. A key feature of addiction is the need to get even higher the next time. If this is not present, then some will argue that it is not an addiction.
What about selegiline "slo-gel" (transdermal L-Dopa) that my TRT / anti-aging doc prescribed 2 years ago? I take 3mg a day via gel on forearms and it seems to have brightened my step somewhat.The real problem is that affecting dopamine centers leads to addiction and other issues. It isn't a good idea to modify dopamine centers unless you have an underlying issue such as schizophrenia, Parkinson's or some other psychotic disorder. It is unfortunate that we don't understand more of these areas but basically what happens is the VTA extends dopamine neurons through the mesolimbic and mesocortical centers. Overactivity of one causes dependence and underactivity of the other causes dependence. You also have seratonin, dopamine, GABA, and nicotinic receptors attached to these neurons which have various positive/negative effects, it is very complex.
Anti-Dopaminergic side effects are also very nasty. When using an agonist you can definitely downregulate receptors so that when you can come off it is similar to antagonism. The sides are called EPS (extra pyramidal side effects) and the worst of which is something called tardive dyskinesia and is very sad to see when patients start to exhibit it. The other problem with taking L-dopa is that most of it is metabolized in the periphery so you aren't really getting the effects you are looking for unless you combine it with a D-decarboxylase inhibitor like carbidopa.
Bottom line, I wouldn't mess with anything that alters dopamine transition unless you truly do have an underlying issue such as schisophrenia and some aspects of bipolar disorder.
Too lateDon't let life give you anhedonia.
Well first off selegiline is not l-dopa it is actually an MAOI. I have no idea why a doctor would prescribe you this for anti-aging though. There has been research recently that show it "possibly" helps with Parkinsons and that it may be anti-apoptotic or anti-oxidant but that would definitely not warrant the use of an MAOI.What about selegiline "slo-gel" (transdermal L-Dopa) that my TRT / anti-aging doc prescribed 2 years ago? I take 3mg a day via gel on forearms and it seems to have brightened my step somewhat.
I was able to wean off Zoloft (old doc had me on 100mg/day for 5 years) and didn't miss a beat.
BTW, I'm 53 yo and my daughter has been diagnosed with bipolar though I don't think I exhibit such symptoms.
Yes, you are right on Athletix. lithium has worked wonders for my daughter (unfortunately after dealing with many docs who only wanted to prescribed depakote, ablifiy, zoloft, etc.) Turns out the "cheap drug" did all the heavy lifting.Well first off selegiline is not l-dopa it is actually an MAOI. I have no idea why a doctor would prescribe you this for anti-aging though. There has been research recently that show it "possibly" helps with Parkinsons and that it may be anti-apoptotic or anti-oxidant but that would definitely not warrant the use of an MAOI.
Was the sertraline (Zoloft) not working for you? AD's are completely hit or miss and if one doesn't work you should try another as it may help. If your daughter has bipolar disorder I sure hope she is on lithium for the mania, it is very important to keep the mania from showing its ugly face.
You can't really diagnose yourself with bipolar disorder but mania is obviously what sets it apart from depression. The high euphoria you get intermittently.
If you were hypomanic (BP), you would probably have trouble noticing the symptoms in yourself, depending on subjectivity and level of insight. If you are in full blown mania, you would possibly lack any insight (at the time anyway), but it would be apparent to anyone who knows you I would think.You can't really diagnose yourself with bipolar disorder but mania is obviously what sets it apart from depression. The high euphoria you get intermittently.
Wow, surprised she used aripiprazole for you. I am sort of opposed to the use of anti-psychotics unless you are schizophrenic or other anti-depressents are not working but typically there is a trial of at least three drugs before they would even think about going that route. If you have ADHD then the aripiprazole could make it worse as it will decrease dopamine as opposed to increase it. Methylphenidate (ritalin) and amphetamine both increase seratonin and dopamine.Yes, you are right on Athletix. lithium has worked wonders for my daughter (unfortunately after dealing with many docs who only wanted to prescribed depakote, ablifiy, zoloft, etc.) Turns out the "cheap drug" did all the heavy lifting.
Had another daughter who recently died of CF. I had been taking Zoloft for years (over 10) to help with gnawing depression as she fought the fatal disease. It helped at first, then I thoought it was diminishing. Went to a hormone doc who prescribed testosterone (which helped) and selegiline (not sure - feel kind of "active" when first applied). He thought selegiline would help on dopamine side of depressions - apparently there are some studies. But things I have read - just like what you posted, have made he put it on the shelf.
I've just started with a great pyschiatrist. She thinks I may also have ADHD - took many tests, can't concentrate, walk away in the middle of conversations, etc. She said Zoloft probably isn't the right drug for me as it effects only serotonin, me problem may be more on dopamine side. So she just started weaning me off Zoloft and added 5mg Abilify. If that doesn't do it she may add vyvanse into the picture next week (yes, I know all about vyvanse, even tried it once, was a miracle drug for me I thought).
It can be hard to be 100% honest (you suceeded!) with your psychiatrist and expect monthly amphetamine scripts (Vyvanse is a CII amphetamine), especially when you haven't already been legitimately taking an amphetamine (no "legitimate drug history" rapport in a sense). People with ADHD are more inclined to try illegal drugs prior to being treated for ADHD (e.g. undiagnosed/untreated adults), and I am not a fan of prescibed stimulants for 3 year olds (5 or 6 years maybe if it is severe; otherwise, when it becomes significantly hindering to your life), so it is a tad hypocritical. They do have a high potential for abuse, but if you haven't abused any drugs in years, and have even had the opportunity too but declined, then you have little to worry about.I'm glad I came across this thread because you guys obviously know what you are talking about. I need help...
So now this pyschiatrist has added Strattera to my mix. Right now I'm taking Zoloft 100mg, Abilify 10mg, and now Strattera 40mg (up to 80). She didn't put me on Zoloft - I was already on that, but she said maybe we could wean that off once the Strattera kicks in. I am legit Adult ADHD - took all the tests. This pysch said she would never prescribe me an amphetamine because I admitted to trying cocaine 25 years ago! My oldest daughter is ADHD and switched from Adderall to Vyvanse a while ago which helps her a lot. I admitted to the pysch that I tried the Vyvanse (30mg) a month ago for 3 days with my daughter's permission and that it worked wonders for my concentration. I know that was stupid but I was just trying to be honest. She let me have it and said because I did that it just reinforced her decision never to put my on an amphetamine.
So what do you think of this mix? Strattera? Her decision never to let me try Vyvanse even though it worked?
My libido is non-existent but she said the Strattera may help. I was hornier than a dog on Vyvanse. What do you guys think??
I really like what I read about Wellbutrin. In my case it seems it would do better things for my symptoms (depression, ADHD, lack of energy and libido) than Zoloft without the Zoloft sides (or maybe even maintain a smalle Zoloft dose say, 50mg, from 100mg). I think this is one anti-stim that I will bring up to (new) doc. Thanks. Thoughts?Have you tried Wellbutrin? It's an atypical antidepressant and may or may not help you ADHD and isn't a controlled substance.
I already saw a new doctor today!!! - he had a cancellation. He told me to chuck the Strattera script (I never had it filled) and also come off the the Abilify (just started last week). He is starting Wellbutrin 150mg for a week and 300mg thereafter. Told me to stay on Zoloft for the time being (I have been on it for years) and wants to titrate that down to 50mg over a few months (from 100mg) but then stay on that 50mg dose w/ the Wellbutrin.It has a chance of helping your ADHD whereas I doubt any SSRI like Zoloft is going to be of much use. Wellbutrin does lower the seizure threshold, so you may have to come off of strattera and/or zoloft, but it's possible that it could help with depression, lack of energy, libido, and ADHD. I don't want to get your hopes up on the one hand, but it definitely doesn't have any significant negative effects on libido and energy like those 2 drugs. It is sometimes called a "stimulating antidepressant" b/c it does in fact have some dopaminergic effects along with serotonergic effects. Strattera and zoloft do nothing significant in the land of dopamine.
I took Wellbutrin at the same time that I was taking methylphenidate/ritalin (before going back to amphetamine) in order to quit smoking (same ingredient as Zyban but insurance companies won't pay for "Zyban"). I tolerated it well even alongside the stimulant. I don't recommend drinking on it as alcohol also increases the chance of seizures and I noticed that I had worse hangovers in college while taking it (don't drink anymore so its not an issue).
I think it is definitely worth a shot and has a better side effect profile than the 2 drugs mentioned above.
Thanks for all your help dumbhick, and your informative PM. I appreciate it.You found a good psych. Stick with him; if the wellbutrin doesn't work out, then you can always try the stims later on.
Your last psych is stuck in the middle ages or dark ages (a shame, really, but that's her problem now, not yours).
Your comment about not giving up hits close to home with me. I'll spare you the details, but it took 6 months of agonizing pain, numerous doctors and visits, etc, before I found a doctor who (A) gave a d@mn about my pain, AND (B) was willing to do something about it. Though I no longer need pain medicine or take it, that doctor is definitely a keeper and knows what appropriate medical care constitutes (and isn't a "feel good" doctor-very judicious actually).
Wow, this thread is old.so i could say then that dopamine is the pleasure neurotransmitter?
old?Wow, this thread is old.
What you say is a vast oversimplification, but you can say whatever you like.