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  • Q&A with Australian Health Practitioners

    How do antidepressants work?

  • Find a professional to answer your question

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    beyondblue is a national, independent, not-for-profit organisation working to address issues associated with depression, anxiety and related disorders in Australia.beyondblue is a bipartisan initiative of ... View Profile

    Antidepressants are drugs that are used to treat depression and can be prescribed only by a doctor. Research shows that more severe forms of depression are associated with specific changes in the brain, including changes to some hormones and chemical message systems. In these forms of depression, there are alterations in the activity of the brain in areas under the influence of the brain chemicals serotonin and noradrenaline.

    There are different types of antidepressants which work in slightly different ways, but they all act on chemicals in the brain related to emotions and motivation.

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    My research interests include immunology and the mechanisms of amyloid formation. The latter has implications for people who are dealing with Alzheimer's Disease, Parkinson's Disease ... View Profile

    Typically antidepressants (ADs) work by increasing the levels of two neurotransmitters (serotonin and norepinephrine) in the brain.

    Neurotransmitters are chemicals which “send a message” across the gap (the “synapse”) between one neuron and another in the brain. Low levels of serotonin and norepinephrine are commonly associated with depression. Some classes of ADs are;

    (1) Selective serotonin reuptake inhibitors (SSRIs), eg Prozac. These block the removal of serotonin from the synapse.

    (2) Serotonin-norepinephrine reuptake inhibitors (SNRIs), eg Effexor). These block the removal of serotonin and norepinephrine from the synapse.

    (3) Noradrenergic and specific serotonergic antidepressants (NaSSAs), eg Remeron. These increase norepinephrine and serotonin neurotransmission.

    (4) Norepinephrine reuptake inhibitors (NRIs), eg Mazindol. These block the removal of norepinephrine from the synapse.

    For a technical explanation, more examples and references see http://en.wikipedia.org/wiki/Antidepressant .

    Typically it takes some time (weeks – months) for an AD to kick in fully.

    Also it can take some time for a health professional, working with his/her clients, to match the “right” AD to the “right” person. In the mental health community this is sometimes called “being on the medi-go-round”.

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    I am a Consultant Psychiatrist and Psychoanalytic Psychotherapist who specialises in Adult ADHD, Jungian Psychotherapy, and the Psychological Medicine aspects of Chronic Pain conditions. View Profile

    In the studies accrued over the decades, the evidence is that antidepressants do not work much better than placebo, and that placebo works quite well. The methodological problem has been that the pharmaceutical industry facilitates publication of positive studies but is under no obligation to publish negative studies. 

    It seems we sometimes can 'turn off' the software program for 'depression' in many cases through a meaningful relationship (placebo, psychotherapy), through ECT, through chemical means ('antidepressant medicines', ketamine), and through using a magnet treatment (TMS).

    My guess is that one day we will find the 'genes for depression', that code for the 'depression software program', and figure out what switches these genes, and these software programs, on or off.

  • Michael Beswick

    Healthshare Member

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    As a patient (and, at that, one who has been through many antidepressants that either did not work or made things profoundly worse), this is a simplistic view. The issue with antidepressants is that if they work, you can only expect them to make things more bearable. To allow you to do the hard psychological work on your own, now that you have the energy. Even if that energy comes with more anxiety and other strange effects on your psyche. But to say they are no more effective than placebo, based on a review of studies, is a typical professionals' response (no offense).

    They DO work. Just not very well. And you have to go through the merry-go-round to find one that makes the grade, but once you find it, you hold onto it like a drowning man holds on to a lifebuoy.

    I disagree with 'turning off' the mechanisms for depression but it's too complicated to discuss and I suppose you have a point. Thank you for mentioning ketamine and TMS, two treatments that need more research/sincere attention. (ECT.... not so much).

    Finding the genes for depression? Pot of gold at the end of a rainbow. You may find a few genes that produce more innervation/receptor density in certain parts of the brain, but even then, the interaction between that and the emotions, the life experiences, is too complicated to imagine. And switching those genes off will come with some unpredictable consequences.

    Actually (I'm almost done don't worry), that way of thinking frustrates me as a patient rather than a doctor. You always seem to be looking for the magic bullet. You will never find it. Alleviation - to a large degree, sure - is the best that can be hoped for. It is the search for the perfect way to fix X problem, especially mental illness, that leads to drugs created from incomplete information but based on a wonderful new idea, and therefore TD, anorgasmia and 'brain zaps', permanent sexual dysfunction from something like Propecia (and SSRIs but that's more controversial), etc. It is a trend amongst doctors and it has created a lot of problems and never a cure. Anyway.

    ~

    To the other two responses, I have some issues with the NA/SE proposition. Consider MAOIs, especially selegiline ('EMSAM' which unfortunately we do not have here in Aus); bupropion, and the recent interest in triple reuptake inhibitors. Dopamine is a large factor in depression and it has unfortunately been overlooked. It doesn't have the same broad effect of SE or NE but it is still an important neurotransmitter involved in the enjoyment of everyday life.

  • My research interests include immunology and the mechanisms of amyloid formation. The latter has implications for people who are dealing with Alzheimer's Disease, Parkinson's Disease ... View Profile

    Michael, quoting from you; "Finding the genes for depression?"

    People are trying to do this using what are called Genome-Wide Association Screens (GWAS). In a GWAS what is done is to recruit people (as many as possible) who have been diagnosed, in this context, with clinical depression and match them with other similar people who do not have that diagnosis.

    What is then done is to look for genetic differences between the two groups. In the context of clinical depression nothing particularly helpful has turned up yet, I suspect because clinical depression covers a multitude of conditions and different people with that blanket diagnosis may have, probably many, genetic differences compared to people who do not.

    This recent and very technical paper, which may be of interest to Dr Heffernan as well, raises some interesting ideas but whether they lead to improved therapeutic approaches remains to be seen.

    http://www.nature.com/articles/nature14659.epdf?referrer_access_token=kNCeZYK1mDAnId1MF_Q7RNRgN0jAjWel9jnR3ZoTv0O4ozQhgzDjVeO-iLPSTg4LfChQ1cQQi_Rh_bOejrCaUkinQWqKoI5VyZ9to2JC-wtF7jiXwpqNU93fTKW3hFSIc8Ttfb7ze5cLTNvJqb2EM3ENiOQCYrxsnPZdiio3bNe6b-CeF9nNpbTXDRBLTJ1tHOMoa-qe55hpXtw0SArLZ_tTuslCLC8og2BVjzNnsFY%3D&tracking_referrer=www.nature.com

     

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