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Depression: Dopamine vs. Serotonin: Which Is More Important?

Based on the symptoms experienced as a result of lower levels of dopamine, it is thought that dopamine plays just as big of a role as serotonin in treating depression. Why then are medications used to treat depression primarily dealing with targeting serotonin only? Because people have been brainwashed by pharmaceutical companies? Maybe. It could be though that many people simply have not tried increasing their dopamine to determine whether they notice an antidepressant effect.

Depression itself is pretty subjective and can have a number of causes. It could be caused by trauma, a difficult childhood, abuse, drug usage, and other external events. It can also be caused by genetics and biological factors. Someone may have experienced developmental problems in the womb or have been exposed to certain toxins. This may lead to the development of depression. There is absolutely no clear cut evidence that low neurotransmitter levels even cause depression.

However, many people believe that “serotonin” may have something to do with depression because SSRI’s are the primary class of drugs used to treat it. Although serotonin may be the neurotransmitter most talked about when it comes to depression, my guess is that dopamine plays just as big of a role – if not a bigger role in depression.

Low dopamine vs. low serotonin… Which causes depression?

The reason I tend to think dopamine plays a huge role in treating depression is because if you look at individuals with low dopamine, they have difficulties with memory, thinking, organization, and experience an inability to feel pleasure. Many people with schizophrenia have abnormally low dopamine and as a result aren’t able to get motivated or stay productive.

Low dopamine: Tends to result in symptoms similar to Parkinson’s disease. People with abnormally low levels of dopamine may have difficulties with thinking, memory, and have slow reaction times. They may also experience anhedonia or lack of ability to feel pleasure. They may also feel similar to individuals with negative symptoms of schizophrenia in regards to having no motivation (avolition).

  • Source: http://europepmc.org/abstract/MED/6324981

Low serotonin: Results in OCD-like symptoms including obsessive thoughts and compulsive behaviors. It also may result in impulsivity, feeling suicidal, aggressive behavior, etc. Lower levels of serotonin are linked to mood swings, sugar cravings, worrying, insomnia, and sadness.

There is some overlap between serotonin and dopamine that cannot be ignored. Some people do respond very well to SSRI’s and the increase in serotonin may be helping. With that said, many drugs like Paxil may indirectly affect dopamine receptors in the brain and actually improve them. So there can be certain links between SSRI’s and dopamine.

Dopamine vs. Serotonin for Depression Treatment

I tend to think that in most cases, people who respond well to SSRI antidepressants should just stay on them – they have been proven to work. With that said, there are many people for whom these drugs do not work very well. They also come with unwanted side effects and many people have gone through the entire wringer of medications only to find no relief. What ends up happening is that people end up staying on these medications and come off them with abnormally low levels of serotonin.

So the withdrawal is overwhelmingly difficult and the people have a difficult time coping with low serotonin. In many cases, the original problem wasn’t necessarily low serotonin, it may have been abnormally low dopamine. In this case, now the individual has abnormally low serotonin as well as low dopamine. If the individual would have targeted their dopamine first, they may have had success than experimenting with drugs that primarily affect serotonin.

I have had success in using Adderall for depression as well as anxiety. My personal experience is that some individuals with depression and/or anxiety may respond very well to medications that deal with dopamine more than they do serotonin.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/17187269
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/8099801

Triple Reuptake Inhibitors: New Antidepressants

It seems as though researchers are catching on though and are trying to develop medications that target serotonin, norepinephrine, as well as dopamine. I tend to think that although this development could be useful, it sounds a bit overcomplicated. Many people do not need to tinker with all three neurotransmitters at the same time.

It would be much more favorable to simply target either dopamine or serotonin in my opinion and determine which class of drugs works better. The triple reuptake of neurotransmitters serotonin, norepinephrine, and dopamine sounds more and more like taking an illicit drug. I can only imagine how horrendous the withdrawal would be from something that tinkers with that many neurotransmitters.

The major difference between these medications and older ones is that they include the reuptake inhibition of dopamine. Although Wellbutrin can inhibit reuptake dopamine, it does it to a very little degree. Most dopamine reuptake inhibitors are weak in their reuptake of actual dopamine. With that said, this could be a reason why using Wellbutrin for ADHD works in some cases.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/19702555
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/19702555

Medications that may work for depression

  • SSRI’s (Serotonin): These are considered the first line of treatment for depression among psychiatrists. Various popular medications include: Prozac, Paxil, and Zoloft. They work by preventing the reuptake of serotonin in the brain. The thought is that by increasing serotonin, an antidepressant effect will be produced in the brain.
  • SNRI’s (Serotonin + Norepinephrine): A few examples of this medication class would be Effexor, Pristiq or Cymbalta. All three medications work by inhibiting the reuptake of serotonin and norepinephrine at the same time. However, these do not directly have an impact upon dopamine.
  • NDRI’s (Norepinephrine + Dopamine): This is a medication class like Wellbutrin (Bupropion) which is widely regarded as one of the best antidepressants. A medication like Wellbutrin that works on both norepinephrine and dopamine can have a profound effect on improving depressive symptoms.  Source: http://www.ncbi.nlm.nih.gov/pubmed/19272288
  • NRI (Norepinephrine): This is a class of medications that focus strictly on inhibiting the reuptake of norepinephrine. A common example would be the ADHD medication Strattera. Many argue that this medication works exceptional for treating depression. This primarily works on inhibiting the reuptake of norepinephrine (neither serotonin nor dopamine).
  • Psychostimulants (Dopamine): Various stimulants like Adderall may work awesome for depression if it is caused by primarily low dopamine levels. Psychostimulants may also be an effective class of medication for someone trying to cope with treatment-resistant depression. In either case, these drugs can help increase dopamine levels and thus take away depression.  They also can have an effect on the reuptake of serotonin as well as that of norepinephrine. Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3005101/

Conclusion: Dopamine needs more credit in regards to depression

I think many people simply are not aware of the fact that abnormally low levels of dopamine could be the culprit for their depression and possibly their anxiety. Unfortunately the only time this neurotransmitter is going to get a bunch of hype is when the newer class of “triple reuptake inhibitor” medications hits the pharmacies.

Then we are going to have a bunch of scientific information and testimonials about the importance of dopamine in treating depression. Most people that think outside the box know that dopamine plays a role in depression. Serotonin-based medications work well in some cases to treat symptoms, but do not work for everyone. The reason that most psychostimulant medications aren’t used to treat depression is because they have a high addiction potential.

Giving someone with severe depression a psychostimulant medication tends to work pretty well (and quickly) at alleviating symptoms. Obviously there are psychiatrists that have become more liberal in what they prescribe, which is why some will prescribe a SSRI with a stimulant as an antidepressant augmentation strategy. Many people find that the antidepressant effect of Adderall wears off and the person builds up a tolerance to the drug.

With that said, most people notice that it works quite well for the first few weeks of taking it. When these stimulants end up in the wrong hands, the individual may build a tolerance, develop an addiction, and use it to get a “high.” The abuse potential is very high if it ends up in the wrong hands. Additionally, many people may not be able to handle the stimulant crashes (e.g. Adderall crash).

The goal of this article was not to say that dopamine is the magic cure for depression and serotonin levels don’t play a role. It simply was written to address the fact that dopamine hasn’t been discussed as much as serotonin in regards to depression.

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34 thoughts on “Depression: Dopamine vs. Serotonin: Which Is More Important?”

  1. Thank you for the blog entry. I tend to agree that, objectively, dopamine is more of a determinant than serotonin for depression. I suspect that the discovery of dopamine’s role in addiction has been one factor for researchers avoiding it. I recently compiled numerous clinical studies (to share with my doctor) and noted that the pharma industry in the 60s and 70s DID directly target dopamine for depression.

    The ultimate results of many of the drugs were bizarre, completely unexpected (e.g. critical blood cell crises, etc). Most of them were taken off the market. If you look at what happens when you tamper with the body’s dopamine production systems, the sequence is HIGHLY complex and difficult to influence. Serotonin’s production, on the other hand, is easier to understand and manipulate.

    Since serotonin is easier–and some people benefit from altering it – the pharma industry has really sold this as the thing to hit for depression. Even some health professionals reflexively aim for serotonin instead of understanding their patient’s actual clinical needs. -Je

    Reply
  2. Thank you for a very informative article, I’d like to share this with my students, as part of my class on antidepressants for Pharmacology in Nursing. As someone who has experienced depression, this article really was relatable. I’ve had a history of depression, going way, way back to the old days of Imipramine (Tofranil) for my one time major depressive disorder, to, 10 years later, Paroxetine (Paxil) for a shorter-term PPD, and finally another 10 years later, I am now on Bupropion (Wellbutrin) for my third round of (mild to moderate) depression. Wellbutrin is working very well, with none of the SSRI side effects that I had on the SSRI Paxil. I hope it is Ok with you to use your article in my class.

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  3. I really appreciate this blog. I myself have struggled with ADHD/depression and now RLS as well as elevated prolactin levels. I unfortunately feel as if I just get pushed from psychologist to endocrinology to primary. When after my own research has brought me to dopamine issues with all of the things. I look forward to meeting with my primary care physician tomorrow to see what she says.

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  4. Interesting article. You and I both know that the real issue in treating depression arises from lack of sufficient effort towards determining the underlying cause. Although this can be difficult to do, available resources are not being utilized. When one walks into the psychiatrists office, many times, are placed on antidepressants without even taking a depression inventory test. SSRI’s are utilized first line due to safety. Adderall is not only frowned upon due to addiction potential, it can raise BP and pulse also.

    It can heighten anxiety (dose dependent) also, at higher percentages relative to anti-depressants. In your article you write wellbutrin as one of the best anti-depressants. There is no such thing as a best anti-depressant. They all tend to drop HAM-D scores by around 50% or > in about 45-60% of patients. Some work better on different people for various reasons. Dopamine is a tricky compound to play with and used often in neuroleptics. If it was so successful in augmenting MDD, I would think there would be more SDRI’s on the market in comparison to SNRI’s.

    What’s interesting is Stimulants like adderall should not really be used in schizophrenia, however DRI’s are used to treat schizophrenia. I believe adderall causes more release of dopamine rather than being a reuptake inhibitor, such as Provigil or Wellbutrin. I think the neuroleptics also perform more as a DRI. This might mean it is safer to utilize DRI’s in depression rather than stimulants like adderall or ritalin.

    I think when a patient walks into the psych’s office he or she sould take inventory tests for ADD, Bipolar, Depression, Anxiety, Schizo, & Eating disorders. If depression inventory sticks out, they should get lab work done prior to med treatment. TSH, with T4 reflex, Vitamin D, B12, and Folate, and CBC for anemia. If those are normal, you still might have a folate/b12 methylation issue.

    You would check for a MTHFR mutation. If those are normal then think about medication. Does the patient have cardiovascular disease, diabetes, or any metabolic conditions. DNRI, SNRI’s, Stimulants, and neuroleptics can effect BP, Pulse, or triglycerides, Cholesterol. Thus making SSRI’s a very popular first line agent.

    The benefit of a stimulant is immediate effect. However, remember it is meth, missing a few methyl groups. It actually depletes dopamine fast. If your underlying issue is low dopamine, meaning your body does not make much of it, then why would you want to use up your stores so quickly? A re-uptake inhibitor, or augmenting the dopamine pump with some SAM-E or Methylated Folate might be a better route.

    Reply
    • Hi Tim, Great comment you wrote. I recently went on Wellbutrin and I was afraid that it might deplete my dopamine stores so I am glad that this is not so. I have a COMT mutation are you aware of it’s effects and what it means when I take Wellbutrin? In the long term I’d like to be on supplements potentially but on the other hand the results with meds are more predictable.

      I appreciate you posting the other tests that a useful to do with a doc before going on psych meds. Could you elaborate on the difference between Provigil and Wellbutrin? Are there any long-term negatives on staying on a DNRI like wellbutrin? Thank you very much for your thoughts.

      Reply
    • This comment made sense to me as an outside observer in my son’s journey w/depression & ADHD. He did not respond well to the typical stimulants used to treat ADHD and actually developed depression after the Vyvanse (tried concerta, adderall, and several others with bad side effects). Looks like stimulants actually quickly deplete his already low dopamine stores leading to depression on top of ADHD.

      He currently takes Prozac 60 mg paired w/guanfacine ER 4mg. He is okay with them as far as behavior reg and depression but they don’t help w/the ADHD side. His dad thinks they negatively impact his sports performance and wants to try Wellbutrin instead. Having been the main person dealing with this for 3 years, I am reluctant to try something new when this is working for most of the problems.

      Your post about Wellbutrin being a reuptake inhibitor rather than a depletor like the stimulants has made me more open to the idea of trying Wellbutrin.

      Reply
  5. I have depression and don’t take an SSRI as I find they don’t help, as my issue is with motivation and drive. I have (luckily) also gotten the diagnosis of of ADHD and take vyvanse (another DRI like adderall just longer half life, smoother onset edge). I mainly take it for depression. (Sometimes I smoke doobage as it yields a shorter attention span and as a byproduct creativity… it has its time and place sometimes even outside recreation).

    To those whom it may concerned. I am extremely honest with my psychiatrist and I leave nothing relevant out. I’m writing an undergraduate research paper on depression, finding a good source for this topic has been difficult, and I’m very thankful to be able to site your first hand experience. Many thanks, good luck and days, Brinks

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  6. They’re out there. Agomelatine (Valdoxan) is a norepinephrine–dopamine disinhibitor (NDDI) and is used at least in Europe and Australia to treat depression. I have heard that it is very effective. Also Selegiline at low doses is a good way to increase dopamine (as in Parkinson’s treatment), though sleep can be an issue since it has a ~40 day duration of action.

    Reply
    • Re: Aglomelatine in Australia – is this something that’s been made available relatively recently? When living overseas my best insurance for high functioning with OCD, Depression and Anxiety was a combo of Wellbutrin, Sodium Valproate and Clonazepam for at night, ad hoc. When I moved back to Australia discovered I couldn’t get the Wellbutrin (Zyban) except as a smoking cessation aid and thus my treatment was turned onto its head.

      The only dopamine-related option my doctor could come up with that wouldn’t cost as much as the Wellbutrin off script (which was $139 for 45 days!) was Repreve (ropinerole) plus Pristiq, creating a triple reuptake effect as described in the article. I definitely respond better to dopamine options than SSRIs so am unsure why this one you mention was never proposed. Will have to look into it!

      Reply
  7. The hallmark of schizophrenia is a High Level of dopamine in the brain, not low levels. Also, re-uptake inhibitors do nothing to increase systemic levels of neurotransmitters, but only hold a particular neurotransmitter in the neuronal cleft through out the effective period of the medication.

    Have you noticed that no one is talking about the CAUSE of low or high neurotransmitter levels in the first place. They only talk about a temporary chemical fix to alleviate the problem. Triple the re-uptakes and you will triple the misunderstanding of how neurotransmitters are suppose to work naturally (IMHO).

    Reply
    • We know how neurotransmitters work naturally. If we didn’t we wouldn’t make medications that increase or decrease their activity resulting in the desired effects. Also the reason that people aren’t talking about the cause of low or high neurotransmitters is that there can be so many factors contributing to it. It can take years and thousands of dollars to find the root cause and even then the treatment would be the same.

      Reply
  8. Hello. “Many people with schizophrenia have abnormally low dopamine and as a result aren’t able to get motivated or stay productive.” Could you please reference where you got this information, it is my understanding that schizophrenia results from high levels of dopamine, low levels are associated with ADHD and like you say and I believe, depression.

    Reply
    • Dopaminergic transmission in cases of schizophrenia may be subject to interindividual variation… That said, the dopamine hypothesis of schizophrenia suggests abnormally low dopaminergic transmission in mesocortical pathways, and hyperactive dopaminergic transmission in mesolimbic pathways. The former may be responsible for avolition / blunted affect, while the latter may yield hallucinations / delusions.

      Reply
  9. Thank you. I also appreciate the scientific research provided here to back up my experience throughout my 20+ year ‘journey’ & struggles with depression and especially avolition (which I hadn’t realized was a proper term for how I felt prior to reading this). I’ve been diagnosed with everything from bipolar (despite never having a manic episode) to depression with anxiety and ADD which runs in my family and have struggled with intermittent stimulant abuse and addiction over these 20+ years.

    I have recently been researching the effects of depleted dopamine and have been shocked to learn the symptoms mirror almost everything I’ve struggled with, including distractibility, restless leg syndrome, apathy, lessened eye contact (which I never had known why I had this problem). To here you mention the industry of pharmaceuticals and their role in the over medicating those like me who have had minimal relief from these symptoms after taking an array of SRI and/or SNRI’S etc., is both difficult to swallow and a relief to understand the madness behind it.

    I often vehemently argued with practitioners my relief from my symptoms while taking Adderall, only to be informed it’s not a medication that treats depression and having to explain my understanding (having been an R.N.), that, that may not be it’s labeled use but that it has been one of the only medications that have made me feel ‘normal’. That being said, I am glad to see the information regarding the downsides of stimulant medications and their high addictive potential. I have experienced all these things with stimulant medications, including the Adderall Crash which is truly awful.

    I am now at a point I hope to change my brain chemistry through healthier choices and scientific research. Exercise is one of the other most significant effects on my mood improvement second to stimulants that I have experienced and hope to force myself to do all the while fighting my brain that gives my body the message I don’t want to do anything…but along with hopeful research and articles such as yours I hope at the age of 42 I might finally be on the path to improve and relieve my suffering. Thank you.

    Reply
  10. I really think you should research my chemical imbalance. I produce triple the amount of dopamine of an average person and almost no serotonin.

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  11. I want to thank you for this report. I have been suffering from OCD my whole life and had my first really bad depression when I was 11. I was out of school for 3 quarters of a year and I don’t remember much of the worst times I had because I was so distant from everything. My teenage years became a roller-coaster like no other. I suffered from “on and off” depression and my OCD came to visit me several times each year.

    I was first diagnosed after I had my son in 2013 – when I was 20 years old. They told me I had OCD, GAD and a case of depression. I had no idea about the GAD but knew about the other two. After I was diagnosed I was given Zoloft. I took it for a year. My highest dose was 150mg, but that made me incapacitated so I ended up at about 125 and then gradually weaned off it and quit in april this year. Although Zoloft did help me cope a bit with my OCD I had absolutely no energy at all. In fact, my energy levels were even lower than before (which I didn’t think was even possible as I was struggling with low energy already).

    I was given Lexapro a couple of months ago, but as expected that just caused me to be more tired than usual so I quit that one too. Now I’m on Wellbutrin (150mgs for two days now). I’m hoping this one will help since it covers dopamine instead of serotonin, but I’m afraid it might not be enough. Unfortunately I live in a country (Sweden) which does not prescribe medications meant for other illnesses as antidepressants. I doubt that I could be given Adderall or Concerta for my issues here.

    Reply
  12. I take Effexor XR (Venlafaxine / SNRI) 75 mg and Metadate ER (Methylphenidate / DNRI) 20 mg daily upon waking. The combination works like a triple reuptake inhibitor. I had previously tried Prozac and Wellbutrin together but they did not work as well for me.

    Reply
  13. I’m very glad to see an article shedding some light on this situation. For about 5 years now I’ve had treatment-resistant depression and have tried almost every antidepressant (Celexa, Effexor, Cymbalta, Wellbutrin, and Parnate.) The only 2 that helped were Wellbutrin and Parnate which both increase dopamine but I couldn’t tolerate the side-effects.

    Wellbutrin destroyed my memory (the nicotinic receptor it blocks which aids in smoking cessation is also necessary for learning and brain plasticity.) Parnate helped with depression but I started getting leg swelling and always had a headache & nausea. The best combination I’ve found, which I’m on now, is Adderall and Mirapex (a dopamine agonist usually used for Parkinson’s Disease). The Adderall has helped a lot with motivation, better decision making, and an interest in achieving long term goals again.

    The Mirapex seems to be keeping me from developing too much of a tolerance to Adderall and has a somewhat calming effect and makes me not have a “crash” between Adderall doses. Also, while most literature advices against prescribing stimulants to persons with a history of substance abuse, I was drinking heavily to alleviate anxiety prior to this combination and now have been sober for over two years. I was lucky enough to find a psychiatrist who trusted my insight enough to let me try this.

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  14. It’s a disgusting shame that content like this is only being heavily talked about by the few. Some countries and their therapists may very well be more ‘liberal’ but many countries and their therapists are not. What needs to also be looked at, is that there are a large number of people with depression who do “get high” because it makes them feel more normal. “Symptoms” such as being more talkative and having motivation shouldn’t be illegal – if the alternative is so much worse. I am one of those people who has been ‘put through the ringer’ by SSRI medication – and can happily say I accidentally found relief with Tramadol (an SNRI that also releases Dopamine).

    I am now thankfully SSRI free and am so glad to be free of their side-effects, such as premature-ejaculation which took years to pass – and a ‘numbness’ towards life which also took a long time to pass. I felt like an utter guinea-pig and when mentioning these side-effects to my doctor, which also included waking every night covered in sweat and a large rash around my groin and arm-pits I was told “well maybe you should ask yourself what’s worse, the side-effects or the depression. The mental alterations that ‘legal’ drugs can do is more criminal than those out there who know how to properly self-medicate.

    Reply
    • I got a little off topic in part of that post – but to summarise, I completely agree with the author here and many of the people commenting. I didn’t mean to advocate the use of illegal substances – but was instead complaining about countries and physicians who are not willing to look into dopaminergics – for example the only use of Wellbutrin in my country is for a short term course for those people giving up cigarette smoking. When people try the dopamine angle for themselves they are very often breaking the law. In the past I found very small micro doses throughout the day of Tramadol would keep my depression at bay, however I did not have a prescription for it.

      Reply
      • I also find that a very small amount of Tramadol helps greatly with my depression. When prescribed Celexa, Zoloft etc. I have found my depression much worse.

        Reply
  15. I really appreciate this blog. I have been struggling with a diagnosis of Schizo-Affect Bipolar type for years. I’m afraid to reveal my method for staying healthy, I have an idea the majority would like to squash dopamine treatment for judicial purposes. Dopamine chemicals are highly sought after by the law because everybody seems to be using some form of them to get high. I don’t get high but I do realize there possible benefits.

    Tyro-sine 500 mg in the morning, 40mg of Strattera at noon and 1.5mg of olanzapine at night for sleep. An assortment of vitamin also, inositol, b-12, acidophilous probiotic. I can seem to narrow my symptoms down to anxiety, then simply pop a fish oil gel capsule. What a pain in the ass though. Straight stimulant drugs work the best. Keep working on this idea dopamine is a better solution for depression, you get my vote. Thanks for the blog.

    Reply
    • I agree. I didn’t know about the dopamine, serotonin and norepinephrine details. I’m still going to research the norepinephrine. I’ve been on every anti depressant since 2002. I hated Effexor, made me numb. I lived on Lexapro for years! Until it stopped working and went to Celexa (citalaprolam). After my 2nd kid, it was as effective so the Dr put me on Wellbutrin.

      I hated taking 2 meds, but they worked. Recently, he asked if I’d like to “come off” the Celexa. Having tried this multiple times and feeling like I could not, I always started my dosage again. This time, my husband is very supportive in the process and has been an exceptional pillar. I am still taking the 150mg of Wellbutrin but thought I should research vitamin supplements to help me along this process.

      There are different ones to take whether you want to increase serotonin or dopamine. So, I went out and purchased them. I am hopeful that there is another way out instead of being dependent on Rx medication. I am grateful for the stability these drugs have given me over the past 13 years. Keep doing your research and keep informing people.

      It drives me crazy that Dr’s write Rx so easily. They are allowed to come up with all these “cocktails” making you so loopy and dependent. God forbid you don’t take them all as required, you wind up becoming worse, being labeled something else with yet another new Rx.

      Reply
  16. I’m confused by all of this. I have been on a daily dosage of Buproprion HCI 150mg and Sertraline 100mg for several years now. They don’t seem to be getting me to where I want to be as far as motivation goes, though. Any advice as to what I should say to my doctor to point him in a better direction for my case?

    Reply
    • Try supplementing with fairly high doses of tyrosine. I’ve been on an SSRI for years and just added tyrosine a couple weeks ago. It increases dopamine production. It’s completely changed me. The SSRI helped, but I still had several hours a day where I’d be depressed. And I had much lower energy. Tyrosine has greatly helped with both of those.

      Reply
  17. Amen! SSRIs might work for some cases of depression only because the drugs treat anxiety. Anxiety seems to have a greater link to low serotonin levels than depression.

    Additionally, a high serotonin state is not “good”. It leads to sluggishness, drowsiness, apathy and (when REALLY high, such as in early pregnancy or cancer patients getting chemotherapy) nausea, vomiting and diarrhea. I’m not endorsing high dopamine states however, as it can cause mania, compulsive behavior, etc. But the serotonin theory of depression is indeed outdated and not supported by good science.

    Reply
    • Hold up there a second, the article states how serotonin does affect aggression and sadness (the latter a well known part of depression) and this neurotransmitter is involved with mood (and feeds into the hippocampus, which is the store for memory and feeling). Dopamine runs mainly ito the frontal cortex and affects your state of reward, as well as things like euphoria.

      Low serotonin = aggro, sadness etc. Low dopmanine = no reward, “what’s the point?” and reduced cheer. Of course dopamine might work in some people’s depression, serotonin in others, norepinephrine in others again, and SNRI’s in others, and psychiatry isn’t just “lets treat the depression” but also “what leads to your depression.” Short story, my history includes parental neglect, sexual assault (resultant PTSD) and psychotic episode, and depression not diagnosed until after starting on antipsychotics.

      At a stretch, I could be considered ADHD but I have no classic childhood history. As psychosis seems to be due to over elevated dopamine, the psych I just started seeing has put me on SNRI’s, as a dopamine reuptake inhibitor or an amphetamine might trigger a second psychotic episode. I’ve believed I was under surveillance and could decode number plates once, and that was enough.

      Just because drug companies want yo make a buck does not mean it’s a conspiracy to boost everybody’s serotonin levels.

      Reply
  18. If antidepressants are supposed to make you feel better, how do SSRIs cause sexual dysfunction unlike dopamine drugs such as wellbutrin, it’s not so simple because they are different dopamine receptors.

    In Parkinson’s dopamine agonists are used because of defective receptors, dopamine antagonist’s are used for mental illness also which is odd, however agonist’s can make the brain less sensitive to dopamine and antagonist’s more sensitive, reuptake inhibitors keep it in place, and they have releasing agents.

    In addition atypical anti psychotics also block histamine and serotonin receptors, so some arguments in favor are puzzling. Cocaine does stimulate all three I believe but is more like a rep-uptake inhibitor.

    Reply
    • It’s a result of serotonin reuptake inhibition… that’s really all we know. SSRI’s cause sexual dysfunction and other classes that act more on dopamine or norepinephrine do not.

      Reply
      • Its because serotonin helps regulate sexual function at a particular level, or inhibit it. From what I’ve looked at via google searches from increased aggression, low serotonin also seems to lead to an increased sex drive. So, conversely, upping serotonin or lengthening the time serotonin remains active in the brain seems to lead to heightened inhibition, end result, reduced sex drive.

        On the side, the reason an SSRI/SNRI’s might make you nauseous or give you diarrhea because serotonin is also in your gut, and when you get an irritant (bad food etc), its the hormone that speeds up digestion to get the irritant out the back (diarrhea) or purge it frontwards (nausea and ultimately vomit).

        Reply

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