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Source for ADs as anti-histamines


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Hi all, long history w psych med drugging and Lyme disease that I will update soon.


i have a fundamental question though.  Can someone provide me with a good baseline source that states that Antidepressants have anti-histamine properties?  I can find pub med articles about TCAs being anti- Histamine, but not other ADs like Effexor, Paxil, Prozac etc.


i have a couple of docs involved in my care and they are unfamiliar with ADs being antihistamines.  I want to provide them with so e sources that they can rely on.  Everything I am finding is just folks statements that “ADs have antihistamine properties.”





Update 2018 (been away awhile!)

Early 2014: Diagnosed with Lyme disease, confections Bartonella, Babesia so spent 2014 treating w/ local LLMD with antibiotics, antiparasitics and supplements.  Symptoms just worsened.  Also consulted with autonomic neurologist and underwent vestibular therapy.

2015 - 2016: Switched to “big gun” LLMD in Washington D.C. who treated with further ABX, antiparasitics, supplements, antifungals, T3 treatment.  No improvement, but worsening over 2 years

2017: Switched to local LLMD and functional medicine doc who diagnosed sub clinical mast cell activation disorder (9 month trial of cromalyn did not help); allergies to serotonin, norepinephrine, epinephrine, estrogen, progesterone and leutenizing hormone

2018: Continue to work with local LLMD, but do not think Lyme is the issue.  Believe that long term use of fludrocortisone, Effexor, and then gut ruining ABX for years for Lyme is cause of symptoms rendering me bedridden.  In February, underwent autologous stem cell therapy at Infusio Beverly HIlls to heal nervous system, strengthen immune system, strengthen vascular system so that over the next year I can taper off Effexor and Fludorcortisone.


Current Dx: POTS, chronic dizziness / vestibular migraine, hypotension, Lyme, Bartonella / babesia, SSRI withdrawal syndrome, hormone allergies, neurotransmitter allergies, iron deficiency anemia, Vit D deficiency, cognitive dysfunction


Treatment:  mostly vegan diet, daily meditation, SVF stem cell therapy (2/18).  Supplements: Histamine Scavenger, DAO, zeolite clay, psyllium seed, CBS / BHMT Assist, castor oil packs, epsom salt baths.


2011 - 2013:  Bad reaction to Effexor generic in Jan. 2011 resulted in multiple med changes 2011 - 2012 including prozac, klonopin (10/11 - 4/12 @ .125; jumped 4/12), Pdoc increased my Effexor to 112.5 b/c of K withdrawal, then put on 1.5 mg Ativan 4/24/12 (.05 3 x day) for anxiety caused by Effexor updose. Ativan put me in bed for two months, so I tapered 15% per week, jumped 7/23/12 (way too fast)

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  • 2 weeks later...
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Newer-generation antidepressants are not anti-cholinergic, as the tricyclics were, except for paroxetine.

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

"It has become appallingly obvious that our technology has surpassed our humanity." -- Albert Einstein

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a few examples in my binding profile document include these i excerpted and linked below.  track down their references to get to the bottom of what they are meaning.  better or more appropriate sources may exist, but these are things i had on hand:


"All SSRIs have a great affinity for the 5-HT reuptake carrier in the synaptic cleft in the central nervous system, with much less affinity for the noradrenaline (norepinephrine) reuptake carrier, and for alpha- and beta-adrenergic, dopamine, histamine, 5-HT and muscarine receptors." Found at: http://www.ncbi.nlm.nih.gov/pubmed/8384945


"Secondary properties within the class of SSRIs include some combination of actions at noradrenergic, dopaminergic, muscarinic cholinergic, histaminergic and sigma receptors." Found at: https://www.ncbi.nlm.nih.gov/pubmed/24930682 -- the most interesting of the three


"Duloxetine is a potent and selective inhibitor of serotonin and noradrenaline transporters, and a weak inhibitor of dopamine transporters. It has a low affinity for neuronal receptors, such as alpha(1)- and alpha(2)-adrenergic, dopamine D(2), histamine H(1), muscarinic, opioid and serotonin receptors, as well as ion channel binding sites and other neurotransmitter transporters, such as choline and GABA transporters. It does not inhibit monoamine oxidase types A or B." Found at: https://www.ncbi.nlm.nih.gov/pubmed/19480470


while a lot of these newer antidepressants have markedly less affinity for histamine (relative to their other targets and to many other drugs), they still do act on it.  using multiple drugs, having a history of drug use, and other factors can impact how histaminergically relevant drugs like SSRIs and SNRIs can be for someone.  even drugs that are not TCAs or paroxetine can entail histaminergic effects during use and also as withdrawal or rebound symptoms.  they tend to be less prominent than effects caused through a focus on certain other binding targets, but it is also important to keep in mind that the central nervous system is interregulatory, meaning that impacting one neurotransmitter system can have implications regarding the functioning of others.


it is further relevant to mention that sustained use can entail different results than single-time use or short-term use, and that the active metabolites of an antidepressant may feature a different binding profile and also the potential to synergize with the parent molecule.  tests run to discern the particular effects of these drugs rarely research all of these angles, and ones researching at least a few tend to measure affinities and impacts in ways which do not translate directly into actual patient experiences.  while not generally marked in the immediate sense, the histaminergic influences of drugs like SSRIs are not outright irrelevant.


SSRIs and SNRIs essentially have a shared history with drugs considered 'antihistamines' rather than 'antidepressants', and some drugs could be easily seen as one or the other.  the distinction is commonly one of marketing rather than one of binding affinities, just as the category "antidepressant" is in general.  TCAs and antipsychotics both stemmed from experimentation with antihistamines as well.  while particularities of individual drug binding profiles can make a drug more tenable as one 'class' of drug rather than another, the basic thing to mind here is that these kinds of drugs tend to act pretty widely.


as for hardcore research, look on pubmed to find the studies where cell cultures, rat brains, human brains, and other things are studied.  there are a variety of different ways that binding affinities are approximated, and it is worth synthesizing the varied data rather than looking only to one source or another.  one should remember how these methods are not a true and full representation of what goes on and why, and also that the implications of binding are not explained just by talking about affinity.  having a high or low affinity does not tell us what the outcome is of that level of binding, particularly when different areas of the CNS utilize neuron subtypes differently.


so, it is absolutely established that SSRIs and the like can have a histaminergic influence...but the exact nature of that influence is not entirely clear.  neuroscience is a pretty nascent field, even though it is a popular and popularly storied one.  you may want to track down references indirectly.  for instance, check out table 3 from this article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4047306/  it lists some sources which are commonly cited for these kinds of claims.  sometimes academics just cite sources within easy reach or considered canon even if they arent the most accurate or most up to date, so dont settle for what comes up most easily.  dig around a bit if you want to present something solid and multidimensional to your professional team.


and if you were asking about the history of SSRIs and such, dig into well-referenced articles or plain ol books that document the development of TCAs, TeCAs, SSRIs, SNRIs, and so forth.  even well-liked figures such as david healy have some good writings on these topics.

from 2005-2012, i spent 7 years taking 17 different psychotropic medications covering several classes.  i would be taking 3-7 medications at a time, and 6 out of the 17 medications listed below were maxed or overmaxed in clinical dosage before i moved on to trying the next unhelpful cocktail.
antidepressants (SSRIs, SNRIs, NDRIs, tetracyclics): zoloft, wellbutrin, effexor, lexapro, prozac, cymbalta, remeron
antipsychotics (atypical): abilify, zyprexa, risperdal, geodon
sleep aids (benzos, off-label antidepressants & antipsychotics, hypnotics): seroquel, temazepam, trazodone, ambien
anxiolytics: buspar
anticonvulsants: topamax
i tapered off all psychotropics from late 2011 through early 2013, one by one.  since quitting, ive been cycling through severe, disabling withdrawal symptoms spanning the gamut of the serious, less serious, and rather worrisome side effects of these assorted medications.  previous cross-tapering and medication or dosage changes had also caused undiagnosed withdrawal symptoms.
brainpan addlepation

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  • 3 weeks later...
Do you still have symptoms? How about Lyme disease treatment?

2012 March- low anxiety, I started sertraline and I got adverse reaction. -.I got depression, ss thoughts and other bad symptoms 2012 May I was put on Clonozepam & paroxetine- it helped. I stopped clonozepam after 4 months with no issue. 2012- 2016 paroxetine 20 mg/ 30 mg

10/2016-02/2017 I tappered paroxetine and during this I was feeling wonderfull. 3 months without paroxetine and withdrawal syndrome appeared. I went back to paroxetine but I couldn't stabilise. CRASH
01/08/2016--Bridge to fluoxetine. fluoxetine 20 mg , triticco / trazadone 75 mg , clonozepam 0,5mg
September 2016 I was diagnosed with Lyme disease. I did test in two different laboratories- both positive 04.03.2017. from 20.11.2017 I started tapper from 0.5 to 0.125 mg- when I got some relief from Lyme treatment. I crashed on 01.02.2018, I slowed down tappering.
20/03/2019-  clonozepam 0,0062 mg,  fluoxetine 20 mg, trazadone 75 mg
28/06/2019- clonozepam 0,0023 mg, trazadone 75 mg, fluoxetine 20 mg
29/07/2019- clonozepam 0,0012 mg trazadone 75 mg, fluo-20 mg
13/08/2019 clonozepam 0,0006 mg I cut trazadone to 50 mg bcs of terrible fatique- big MISTAKE- 21.08.2019 updosed trazadone to 62 mg-still WD- 28.08.2019 oryginal dosage 75 mg
26/09/2019 OFF clonozepam, fluoxetine 20 mg, trazadone 75 mg
06/05/2023 OFF clonozepam, fluoxetine 17 mg, trazadone 25 mg HOLD from 20.11.2021
FROM WD of paroxetine 2017 I have not recovered. I was diagnosed with Lyme, Bartonella , mold, I have low dao (Diamine oxidase). I don't know why but I have some relief from resweratrol, ginger, famotidine (Pepcid)
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