Can Dopamine Make Your Future Look Brighter? - TIME
just thought it was interesting.
Wanted to share with friends on AM
Can Dopamine Make Your Future Look Brighter? - TIME
just thought it was interesting.
Wanted to share with friends on AM
The study results are somewhat interesting. Dopamine is arguably one of the most complicated to understand neurotransmitters in the brain.
L-dopa increases dopamine in general in the various dopaminergic areas of the brain. This is good for Parkinson's patients because they suffer from both mental and physical problems from their low dopamine levels in particular areas of the brain. 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). In fact, one of the symptoms of L-dopa toxicity in Parkinson's patients is hallucinations and psychotic type phenomena-it happens over time as the doses get into the grams/day level. Then they have to switch to carbidopa, etc.
As the article points out, l-dopa isn't really associated with being "happier", which the study probably defined as a euphoria-type happiness since it is easiest to measure on an established scale (I dunno-but that's not really "happiness" anyway).
On the other hand, administration of amphetamines and cocaine cause a bit more of a targeted effect and typically cause an almost giddy euphoria in the majority of study patients given one or the other. They don't do too many of those studies anymore! However, I remember one study from the 70's (academic database) that would be unethical per the APA today. A person was administered IV (!) 10mg of dextroamphetamine (they don't even make IV amphetamines anymore) every hour on the hour and reactions noted. Initially, euphoria, etc. But within 24 hours and 240mg of IV amphetamine given (a freakin ton), he was in pretty much full blown toxic psychosis. It went away after a day or three as the drug left his system and he went to sleep, etc.
The same is true for the opioids and other abuseable drugs, including steroids. Pretty much anything that is rewarding and/or causes that momentary euphoria is associated with the release of dopamine in very specific parts of the brain only. These parts are mainly in the hindbrain (nucleus accumbens, ventral tegmental something-or-other, etc) which is the most primative part of the human brain and which is why rats/cats/dogs/etc respond to amphetamine/cocaine/opioids/etc as well and are often studied. It is also why junkies act like animals; they function on a very primative level in that, as the article alludes to, dopamine is associated with learned behaviors. "Roll over, sit up, etc" = "Get more smack, inject more smack, get more cash, repeat". That try a drug once and you are hooked stuff is generally non-sense; it is a learned behavior. People who are "hooked" from the first use of anything generally have very weak will power or other psychological issues such as depression.
Some drugs like crack (no, I've never used crack before) only give you a few get-out-of-jail-free cards in this respect before you inadvertently acquire a new learned behavior that intensifies with each additional use of the drug so the hole you dig gets deeper and deeper. To pick on crack heads some more, they will often choose crack over food b/c it is much more mentally rewarding and though that next rock only gets them high for 5 minutes, they are immediately looking forward to that next crack rock and how to get it, even after they really can't even get a buzz anymore-the mental drive is just that strong.
The learned behaviors can be a good or a bad thing depending on what you are learning and whether you are using drugs as well. Heroin addicts often inject saline solution when they are out of the drug because the brain is used to an injection followed by a profound euphoria. Dopamine levels actually rise briefly to euphoric levels in anticipation of that euphoria though no post-injection euphoria is experienced. Again, a learned behavior. The ritual of smoking cigarettes (packing them, lighting them, drawing on them, inhale, exhale, etc) is another example.
And for the bodybuilders of course. Steroids have definitely been shown to be associated with psychological cravings and sometimes physical dependence phenomena due to the myriad hormonal changes in the body and the Post cycle depression if present (don't get me wrong; I use them too). This is why some people literally never stop using steroids-30 week cycles and then you are so effed up that you need some test just to function since you have zilch. This applies to oral and injectable steroids, but I think that injectable steroids, relative potencies not being a factor, would be even more associated with psychological dependence than orals for this reason. Some steroids are inherently somewhat euphoric as well (some are dysphoric like good ole M1T).
The learned behavior of the ritual of steroid injections. Wipe the top of the vial with an alcohol wipe before inserting drawing needle, draw 3 cc's of oil with vial upside down (or right side up), remove needle from vial, flick syringe needle up, squeeze out air bubbles, aspirate slightly, take off dull needle, replace with new needle, wipe injection site with a new wipe, don't unsterilize the syringe and needle to be injected (unless you recapped it and put it on a sterile surface), squeeze skin taut if applicable, inject needle somewhat forcefully deep into the muscle, steady pressure on the plunger, remove needle with a pretty fast, smooth, motion, put a sesame street band-aid on if actually needed, repeat daily or weekly. That is a hell of a lot of learned behavior and ritual (necessary), and add to that the expectation of great gains in the gym and you have quite a mentally reinforcing package (esp. when the gains do come rapidly in the gym). Thankfully, steroids aren't exactly as addictive as crack, but it is little wonder that users are often looking forward to that next injection or that next cycle or whatever. Or people who never quit either one long cycle (wrestlers) or cycle after cycle their whole life.
The real question is at what point does it become deleterious to your life and do you stop using them at that point or do you continue on in spite of the effects they might be having on your life or health?
But it isn't all bad. Bodybuilding itself is very rewarding and in a healthy way. You work hard in the gym and you are rewarded for your hard efforts and you don't necessarily have unrealistic expectations as far as gains go (though you probably do if you have dabbled in steroids and seen the results) and you are pleased with the results. And you have less mental stress and are in better physical condition, etc. So this can be quite a healthy, learned behavior. I am not saying don't use steroids (or use them); it is just easier to look at one variable at a time.
I always felt like that when I left the gym anyways, even if I came in with a crappy mood. Probably the endogenous opioid release from the pain of working out ("runner's high"); of course endogenous opioids have a direct affect on the mood but also have a dopaminergic effect as described above.
But the body is good at regulating itself in healthy manner if you aren't taking drugs that try to circumvent your body's built-in protection system. The dopamine rush associated with sex or a good workout or both (LOL) is quick and fleeting because the dopamine transporter quickly mops up the free dopamine molecules which are reabsorbed into the neurons of the brain (ready for round number 2?-LOL!). Cocaine blocks the dopamine transporter from doing its job so the elation is unnaturally prolonged; amphetamine just floods the synapses (spaces between neurons) with dopamine, but the end result is similar. Both drugs exert most of their effects in the dopamine neuron heavy areas of the brain. Think of it as free testosterone versus total testosterone if you want.
It kind of ties in to the whole argument for taking low dose naltrexone. Basically the naltrexone helps with sensitizing the dopamine receptors. Which in turn will help with happiness, memory, etc. i just read about it on a blog. can't find it right now tho'.
There is a naltrexone/steroid enhancement article on Primordial Performance's website.
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.
The only other psychiatric disorder that warrants toying with dopamine is ADHD. I've had it all my life, but was only diagnosed as an adult when I started to flop in electrical engineering despite my best efforts.
ADHD is one of those contentious disorders b/c it is both underdiagnosed and overdiagnosed (and some people think it doesn't exist, etc), leading to undertreatment of the population that actually has the disorder, kind of similar to opioids and chronic pain (an even more heated issue, of which I have also had the displeasure), but stimulants are easier to get a "script" for. Lots of scripts are written for stimulants. But many of those people don't have ADHD (some doctors just want the money and have you fill out a 1 page/10 question sheet and then give you your adderall-I saw it frequently in college-a terrible thing-I saw a lot of addicts too).
However, the above post still holds true in many ways. It is a MYTH that people with ADHD cannot get high or become psychologically dependent/addicted to stimulants like Ritalin and Adderall-even some "medical" sites still perpetuate this BS. If you abuse them for any amount of time, you can pretty much count on becoming addicted for some period of time, ADHD or not. In ADHD and in all people, stimulants lose their euphoric effect at the same dose level within a few weeks of starting them.
With ADHD patients, beneficial effects are still derived and even over the long-term in my experience (though I had to try 5-6 different stimulants to find one that I could tolerate for more than 1 month to a year without unbearable side effects).
It is possible that a non-ADHD person could use the same dose over a long period of time and derive some cognitive enhancement beyond their baseline as well (never really been studied), but in either case, abuse will lead to dependence (been there, done that more than once). Escalate the dose, you will get high again for a brief period of days, and off you go into the bowels of addiction.
Some people are able to use them very intermittently for cram sessions in college and have no cravings, but I have seen people turn into addicts of varying degrees as well. Maybe because you can be a little lazier depending on your major in college, go drink more, and then catch up for 2 days before the exam, etc. I know it wasn't peculiar to my university, but stimulant use/abuse like this is rampant in almost every school. I guess it's that competitive edge or sheer laziness, and there are some parallels to the increase in young person steroid use too (and at the pro level if it hasn't already reached a critical mass, LOL).
That is exactly right it is overtreated when in regards to parents who think their three year old is hyperactive blind to the fact that all three year olds are hyperactive, yet statistically it is severely undertreated and if I remember the statistic correctly only around 2-3% of those with ADHD are actually treated for it.
Stimulants are still the mainstay therapy for ADHD but you can use atypical or typical antipsychotics and some antidepressents as well. It is actually MUCH rarer these days to see anyone on AP's if they have ADHD due to the side effects of blocking dopamine. However, stimulants such as amphetamine and methylphendiate effect both NE and DA. Doses are kept rather low though for ADHD with stimulants because there is a hairline threshold plasma concentration that starts showing the euphoric side effects.
There is a reason dopaminergic drugs feel good too, DA runs the pleasure centers of the brain so again the bottom line is you really don't want to mess with regulation of dopamine. If you want a quick release of dopamine just have sex .
Despite their woes, stimulants are much safer than antipsychotics-unless you are psychotic, unless the psychosis is secondary to acute amphetamine intoxication in which case it should pass.
I think plasma concentrations are irrelevant in terms of euphoria for amphetamines. I've taken massive amounts of prescribed Concerta before and nothing but severe side effects (say 60mg of it a day). A 10mg Ritalin would produce a tinge of euphoria in contrast. And I took both of them separately, and together at different times, all prescribed and at the scripted dose. Dose matters, but how quickly dopamine is released in the pleasure centers matters much more in terms of producing euphoria.
Have you ever taken an amphetamine or methylphenidate family compound before? The euphoric effects start at very low doses (5mg Adderall or 5mg Dex in an amphetamine naive person who isn't on SSRIs or other mood modulators; I have seen someone go hypomanic or manic off of 2.5mg and be fine 6 hrs later), and increase as the dose is titrated up to the terminal efficacious/target dose. Higher, single doses intensify the euphoria, to a point. Regardless of the dose though, whether 5mg/day or 60mg a day (I used to take that much Adderall) or 300mg in 3 days (don't ask-but again, why plasma levels are irrelevant for the most part), tolerance develops to the euphoric effects within a few days to a few weeks and the only way to sustain it is to increase the dose. Otherwise, no more euphoria. If you take it abusively every day (say 60-90mg single dose), you will hit a wall where you cannot get high anymore (even sleeping every day or every other day) due to the side effects limiting the dose (chest pains, arrythmias, etc).
And BTW, I stopped taking Adderall 30mg bid once for a week and when I started back I took a whole 30mg pill (my normal dose which didn't cause euphoria) and I was so high for about 20 hours that it was absurd. I had pre-cum in my pants, saucer pupils, couldn't sit still for long, was gregarious, and basically drowning in euphoria. And then at 4AM the next day trying to go to bed I had the worst stomach cramps I've ever had. I guess a week is plenty of time for your receptors to downregulate and for your dopamine pools to be replenished.
I would say that the doses are kept low for other reasons. Like most people don't need more than 40-60mg of amphetamine per day to control ADHD. Amphetamines are also neurotoxic in high doses. High doses also tend to deplete the large dopamine vesicles/neurons/whatever and cause the release of dopamine from the smaller vesicles/neurons/whatever as well as the release of serotonin which starts to all add up to a nasty psychotic state and a temporary but profound neurotransmitter depletion (DA and NE mainly).
And plain amphetamine has more cardiovascular effects than methamphetamine which is much more CNS active due to its increased lipid solubility and brain penetration and so the body can only tolerate so much plain amphetamine before your heart starts trying to escape from your chest. It takes longer for these effects to accrue with methamphetamine, so you have free reign to dig yourself a deeper hole, stay higher for longer with less sides (initially), and a 2-3 day "grace period" before you realize how big of an idiot you are (if you do) and pay the consequences or stay up for the next week or month or whatever your masochistic threshold happens to be.
Desoxyn/d-methamphetamine has some heavy binders in it to keep it from absorbing too rapidly and giving legit users too much euphoria. Everyone that has taken both the prescription and the relatively pure street version (that I know of) agrees that Desoxyn isn't even close to just ingesting crystal methamphetamine directly. Just like routes of administration intensify the euphoria of many drugs (PO, parental, etc), likewise for amphetamine, and I guess the ~100% version dissolves in the stomach much quicker than the hard 5mg pill version. Of course, this drug is just rarely prescribed period due to the stigma associated with methamphetamine (much of it deserved) and its even higher abuse potential than plain d-amp. But people can use either responsibly or irresponsibly for ADHD. It mind over matter or vice versa.
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]
I guess that you have tried yohimbe, viagra, cialis, levitra, etc? Apomorphine is another experimental treatment that seems to work for some, albeit with side effects (just like every other medication). Athletix probably can give you a more educated response than me.
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.
Truthfully, I know very little about schizophrenia relative to ADHD and amphetamines. Except that giving amphetamines to schizophrenics is a bad idea, and that heavy amphet abuse produces a temporary toxic psychosis that is essentially indistinguishable from schizophrenia. I had an acquaintance in college who abused Adderall like nobody's business (took an entire bottle, 480mg, in 24 hours once...)-he got misdiagnosed as schizophrenic somewhere along his amphetamine career and then they realized it was the massive doses of Adderall he was taking. He'd devour his bottle and buy somebody else's!
If you don't increase your prescribed dose of amphetamine ever, then there is a low to zilch chance of becoming addicted. However, if you cross the line and abuse it just once or twice, you have a high potential for liking the euphoria enough to do it a bit more, and pretty soon, you are on your way to full-blown amphetamine addiction. Especially when you end up staying up all night, and taking more to delay crashing because you have to go to class or something (or just want to stay high for as long as possible. The majority of people that I knew in college who had ADHD and were taking amphetamines had abused them and become addicted at one point or another and when/if they recovered, they would often stay on the drug and effectively treat their ADHD (nobody tells their psych that they are addicted to and abusing their monthly script if they are). Some would relapse into old habits; others would learn their lesson. And that is, don't ever abuse these drugs if unless you want to face a real risk of addiction that is extremely difficult to break out of and of course very deleterious to one's mental and physical health.
BTW, I know it's not impossible for someone prescribed stimulants to become addicted to them.
I can't say that I agree with your definition of addiction (sounds very subjective too). I have read a lot about addiction over the years and been through it over the years quite a few times as well; addiction is a much more complex phenomena than what you describe.
When I was addicted to cigarettes, I wasn't trying to get higher and higher, so by your logic, I probably wasn't addicted in the first place. A pack a day for 2 years and 5 months of withdrawal and cravings says otherwise.
Also, amphetamines are both simple and VERY complicated in terms of effects, good and bad, short term and long term, abusing and non-abusing populations, etc. Here is a grab bag study abstract that relates to amphetamines, the PFC, and schizophrenia-type symptoms (see below). I can't post links quite yet, but go to wwwamphetaminescom, click on the image, and you will find a plethora of interesting dopamine / stimulant / adhd / schizophrenia / you name it abstracts. The parent site is wwwbiopsychiatrycom which espouses some chemical based hedonistic philosophical approach to obtaining happiness, but the index and refs cover all drugs (even non-abusable (typically) drugs like anti-psychotics) and psychiatric disorders (such as addiction) and more. I have frequented that site over the course of many years for all the research abstracts. It is very technical and pretty addictive if you are a knowledge fiend like me. Anyway, you will find useful info galore there if you are interested.
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.
Now if it were only that easy lol. The problem comes in that there are a myriad of other receptors that seem to be present on these neurons and we don't yet know what the interneurons actually are, what kind they are. There is 5HT2A/C that seems to be inhibitory at the end of the dopamine neurons in the mesocortical neurons and there seems to be some GABA/enkephalin/opioid receptors and neurons that have effects in the VTA.
Typical psychotics seem to work best on the positive symptoms due to D2 blockade but of course cause some pretty nasty extra pyramidal effects while the newer atypical antipsychotics seem to help more with negative symptoms but cause sides such as severe weight gain, it is a lose/lose.
Doctor of Pharmacy
www.athetixsports.com - What you want, no bull
L-dopa treatment for Parkinson is not all that great as it increases dopamine everywhere and not just in the basal ganglia. but it is a step in the right direction. They need a selective dopamine drug that crosses the blood brain barrier
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.
Too lateDon't let life give you anhedonia.
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.
Doctor of Pharmacy
www.athetixsports.com - What you want, no bull
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).
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.
I read in a book once upon a time that for children with ADHD, if they had comorbid depression/MDD and were taking an SSRI, and then a stimulant was added, symptoms of hypomania could emerge in some cases (it suggested to watch for signs of hypomania and adjust/terminate the stimulant if needed). Would anyone care to explain if (A) this makes sense as put forth and (B) would a hypomania from SSRI+stimulant imply an underlying BP disorder (as opposed to stopping one or both drugs and the problem goes away completely)? I am stretching it here, but I am thinking of how it has been suggested (and I have seen one instance of this in college) that someone who is prodromal schizophrenic can be launched right into fullblow schizophrenia after taking acutely or chronically hallucinogens like LSD and shrooms. But the premise is that it would have happened anyway; the chemical just sped up the process. Amphetamines are slightly manic/hypomanic in their initial mood effects and if esp. if abused (very manic), so their contribution isn't too much of a strech.
I would definitely get rid of the doctor who prescribed you the MAOI (selegiline) that is just crazy. It cannot be used if you have suicidal thoughts or any sort of eating disorder. I don't want you to post any of your history here on the forum but just putting that out there.
Doctor of Pharmacy
www.athetixsports.com - What you want, no bull