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Thread: SSRI'S vs. SNRI'S

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    Default SSRI'S vs. SNRI'S

    There's a great article I read recently (I deliberately left out the tables to reduce the length of the post) talking about SNRI's vs. SSRI's. I always thought they were different. Like, effexor was fundamentally different than prozac. It turns out, I was wrong. SNRI's are a lot like SSRI's and vice versa. It's the drug reps who want us to believe that effexor is "special".

    SSRI and SNRI: Are they misnomers? Common wisdom holds that SSRIs (selective serotonin reuptake inhibitors) and SNRIs (serotonin norepinephrine reuptake inhibitors) have different mechanisms of action. SSRIs act by blocking the serotonin reuptake pump (more technically referred to as the 5-HT transporter, or simply the 5-HTT), whereas SNRIs presumably block both 5-HTT and the norepinephrine transporter (NET). Blocking these transporters prevents the neuron from “vacuuming” up excess neurotransmitters, allowing more to remain in the synapse and stimulate postsynaptic receptors.

    According to standard dogma, SNRIs (Effexor and Cymbalta) increase concentrations of both 5-HT and NE, potentially leading to some clinical advantages, although the extent of these advantages is hotly debated.

    Unfortunately for this theory, it turns out that most “SSRIs” have a significant effect on NE as well, and the “SNRIs” behave much more like SSRIs than is appreciated.

    All the numbers are greater than one, showing that all these medications are much more selective for 5-HT than for NE. Even Cymbalta (duloxetine), proclaimed the most “balanced” of SNRIs, is twenty times more effective at blocking serotonin reuptake than norepinephrine reuptake. The other “SNRI,” venlafaxine, hardly deserves the name, since it is 120 times more effective at increasing 5-HT than NE. The only ADs that are meaningfully balanced in 5-HT and NE reuptake are the tricyclics, suggesting that they are the ones that should really be labeled “SNRIs” (J Clin Psychiatry 2003;64 (suppl 13):5-12). Given these reuptake profiles, it seems more logical to call all these medications “SRIs,” or serotonin reuptake inhibitors, reflecting their primary mode of action (acknowledgments to my colleague John J. Miller, M.D., Medical Director, Center for Health and Well-Being, Exeter, New Hampshire, for help in working out these concepts.)


    Of course, if your goal is to increase levels of all three monoamines (serotonin, norepinephrine, and dopamine), you should be prescribing MAOIs (monoamine oxidase inhibitors). MAOIs are not reuptake blockers at all; they increase neurotransmitter levels by inhibiting MAO, an enzyme that breaks down all three monoamines. Thus, MAOIs increase the levels of all three neurotransmitters thought crucial in depression, which may be why they are the only antidepressants generally agreed to have an efficacy advantage over others. (See APA’s latest practice guideline for major depression for references, available free at Page Not Found.)

    Serotonin receptors: What do we know? Regardless of how we choose to categorize them, antidepressants do a good job of increasing levels of monoamines in the synapses. This raises questions about what these much-vaunted chemicals do that helps our patients’ moods.

    The most exciting recent research has focused on 5-HT. There are currently about fifteen 5-HT receptors known. They are classified into seven main families (5-HT1 to 5-HT7) and broken down further into subtypes, each denoted by letters (5-HT2A, 5-HT2B, etc.)

    These 5-HT receptors are located in different parts of the body – some in the brain and the spinal cord, but many more in the gut. In fact, more than 90% of all 5-HT receptors are found in the GI tract. Serotonin stimulates gut motility (we all know that SRIs can cause diarrhea), and the latest medication approved for irritable bowel syndrome, Zelnorm (tegaserod), treats constipation by stimulating the 5-HT4 receptor. Researchers are great at discovering, naming, and locating 5-HT receptors (see a schematic of receptor locations at PubMed Central Homepage
    articlerender.fcgi?artid=1201318&rendertype=figure &id=f1). Unfortunately, they’ve been much less successful at figuring out how stimulating them might lead to an antidepressant response.

    We do know that most of them do whatever it is they do via G proteins, those monstrous molecules that coil seven times across neuron cell membranes and change in shape when 5-HT receptors are stimulated. This change in shape leads to downstream chemical events involving ATP and phosphorylation. These “second messengers” then lead to the activation of certain genes and the production of various proteins.

    One of the most intriguing findings of the STAR*D research helps us to understand the clinical relevance of one type of 5-HT receptor, 5-HT2A. Researchers sifted through the genes of about 2000 patients who had been given Celexa for depression, in an effort to see if there were any genetic markers predictive of antidepressant response. They found that patients who had a specific variant of the 5-HT2A receptor gene (the “AA” variant) were 16% more likely to respond to Celexa than patients with the “GG” variant. While this finding doesn’t tell us anything about how stimulating 5-HT2A relieves depression, it does suggest that this receptor subtype is involved in the antidepressant action of SSRIs.
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    Wow that's pretty interesting @QVC1212 I didn't know that all antidepressant drugs are almost the same!!!

    Well, that's not entirely true, since there are some subtle differences in efficacy across different 5HT receptor subtypes of which there are fifteen, but the knowledge of their similarity speaks to the power of marketing. Specifically, the power of the drug reps to market their drug as superior when, in truth, it's not much better than the old.

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    I've been involved in a situation where I had to dig through hundreds of thousands of pages of correspondence, emails, reports, etc., from a pharmaceutical company and I can unequivocally report that they haven't evolved very much from the old west snake oil peddlers. It's actually pretty scary how big pharma views us.
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    for some reason I can't take anti depressants they make me violent... I have tried at least seven or more different ones, and after about two to three months on them i get very violent to others and to myself... so don't take anything and hope for the best..

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    Cool article.

    Antidepressants are better than 'placebo' I can say that. However, they are so MISUNDERSTOOD, and further mystified by the marketing over 30+yrs that the prescribing and knowledge of them is dauntingly abysmal. Most people know what an AD is.. obviously.

    A large portion, by now, have heard of SSRI -- a smaller portion SNRI.. but the majority don't have a clue what they mean much less their action in the brain. Much less what a receptor even is.

    This isn't a greater is us..

    It just is how it is. The sad fact, is doctors don't know much more than these people. I have spoken to quite a few doctors whom knew less of AD's than I did. Which is fine, I have studied them for many years.. but they have the 'experience' of patients whom they prescribe and then the anecdotal reports to coincide... which leads them to their biases.

    Nonetheless.. point is with this type of blunt understanding of these receptor subtypes and calling out old vs new AD's for what they are -- (a little improvement sometimes.. but mostly a way to make money). --- Will lend better en mass knowledge,better general physician knowledge, and better treatment.

    Especially if we can ACCURATELY start using genetics to bypass the 'guessing game' which can be a little dangerous potentially , and often uncomfortable at least... of which AD will work?

    5-Hydroxytryptophan is everywhere.. and I liken it a bit similarly to Opiate receptors. They are both responsible for mood. They are both all over the body in great numbers. They both control muscle tone (and bowel motility). They both modulate pain. They both up and down regulate based on endogenous and exogenous intake, etc. Don't get me wrong they are night and day substances.. but I think this neurochemical being more 'complex' than just say (Dopamine, N-Epi, Serotonin, and GABA) AND it being more of a chemical in biology, found in high amounts in the brain. I believe that not too far down the road we will discover how much of this is across the body, and why.. and it may even link some of the symptoms of depression, anxiety, OCD, etc to a more physical foundation.

    The treatment of mental illness is arcane, abymsmal, and we haven't come very far since 1950. It is the biggest field of medicine that is 'lagging'. I know it isn't 'easy',.. but it is due for a breakthrough. Mental illness is a huge pandemic .
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