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Research by Dr. Murray Ellis in Australia indicates NO antidepressant helps anxiety

serotonin

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#1 kurdishfella

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Posted 20 August 2017 - 05:15 PM


In 2000 or 2001 Dr. Murray Ellis published research indicating that those suffering from anxiety disorders have serotonin levels EIGHT TIMES HIGHER than normal. He went on to ask what I have been asking for 25 years now which is why are we giving drugs that increase serotonin (all antidepressants do this) when those suffering anxiety disorders already have elevated levels of serotonin. This is why the drugs make it worse.


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#2 Mind_Paralysis

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Posted 20 August 2017 - 09:23 PM

He's only one guy though, there are plenty of placebo-controlled trials which have shown that serotonergic antidepressants, multiple classes, do affect anxiety.

 

I've even used two myself, to great effect - Sertraline and Duloxetine worked like a charm, while I was on them.

 

 

More recent data have confirmed, that yes, there is at least a subset of anxious patients which have serotonergic hyperactivity as the main mechanism behind their anxiety - but that's NOT the only form of anxiety...! NMDA-antagonists shouldn't do SH*T if that was the case - but it works. SNRI's shouldn't be MORE effective than SSRI's if that was the case - but they work! So, obviously, norepinephrine must be involved as well.

(which is logical, NE is a stress-hormone - stress causes anxiety)

 

Reason I'm mentioning it, is because the more recent theory regarding how SSRI's treat anxiety is quite simple: homeostatic response.

Higher dosages of SSRI's are prescribed for anxiety than for depression, and when that is done, they actually work - by overloading the brain with serotonin, homeostatic response FINALLY kicks in, and the body realizes what's happening, and then summarily shuts down serotonin activity to a high degree - and VOILÀ! Anxiety starts going down.

 

Now then, there is a point though, that serotonergic antidepressants often do cause more anxiety at first, since it takes a while for serotonin to overload, so yeah, that can be a concern - but that's been a well-known fact for a long time, and is often why many Dr's plan for this event - by prescribing a benzodiazepine for the first week or so of treatment with the SSRI/SNRI. Some also use other agents.

There are other examples of how something which does the opposite can help - for instance, some kappa-agonistic medications should cause depression, yes? Because kappa-antagonists treats some forms of depression - well, not necessarily - there's evidence that slight agonisation of the Kappa-receptors does indeed, in the long run, cause the opposite to happen: the body responds with an overzealous form of homeostatic response, thereby downregulating kappa-receptors instead, leading to improved mood.

 

Point being - don't always focus on HOW a drug works - focus instead on whether it DOES work for the disease at hand.

 

 

Btw, have you checked out any of the alternative compounds and pathways towards treating anxiety, which I have mentioned, MULTIPLE times? I would have thought that HydroxyNorKetamine, Propanolol and Guanfacine would have been especially interesting to you, since they work by decreasing activity out of the amygdala...

 

Focus instead on obtaining these drugs, than warring against serotonergics (which I'm guessing didn't work for you?) which does help a lot of other people.


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#3 Finn

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Posted 21 August 2017 - 06:47 AM

He's only one guy though, there are plenty of placebo-controlled trials which have shown that serotonergic antidepressants, multiple classes, do affect anxiety.

 

 

 

I had hard time finding this "Murray Ellis" . It seems that Murray Esler has become victim of Ann Tracy Blake, who also falsely tried to represent her Ph.D status to gain more credibility, who also likes to "publish" poorly written anti-antidepressant rants full of typos.

 

http://www.gw.edu/_e...n_Ann_Tracy.pdf

 

https://famguardian....ort-DrTracy.pdf

 

http://www.drugaware...g/tag/insanity/

 

 

Esler certainly never  "went on to ask what I have been asking for 25 years now which is why are we giving drugs that increase serotonin (all antidepressants do this) when those suffering anxiety disorders already have elevated levels of serotonin." like she claimed

 

 

http://www.socialanx...7329-post6.html

 

 

Esler merely challenged theory of how SSRIs work, not if they work.

 

 

https://web.archive....-2000May13.html

 

The scientists tested the levels of the mood-regulating chemical serotonin in 20 patients who suffer panic attacks and found that, even on a good day, the average levels of the chemical in the brains of at least 15 of the patients were eight times higher than normal. ----- Professor Esler emphasised that the SSRIs were "great drugs" and should remain worldwide bestsellers. ---- First, the conventional view of how SSRIs operate has been challenged. It would appear that the drugs are effective because, over time, they somehow decrease, rather than increase, serotonin as originally thought.

 

 

Murray Esler's articles of  SSRIs helping with issues possibly related to increased serotonin turnover

https://www.research...e-inhibitor.pdf

 

 

 

 

Increased brain serotonin turnover in panic disorder patients in the absence of a panic attack: Reduction by a selective serotonin reuptake inhibitor

------

 

Support for this interpretation comes from the direct relationship which existed between serotonin turnover and illness severity, and the finding that SSRI administration reduced serotonin turnover. Serotonin transporter genotyping suggested that increased whole brain serotonin turnover most likely derived not from impaired serotonin reuptake, but from increased firing in serotonergic midbrain raphe neurons projecting to both subcortical brain regions and the cerebral cortex.

 

 

 

 

http://jamanetwork.c...larticle/482548

 

Elevated Brain Serotonin Turnover in Patients With Depression Effect of Genotype and Therapy

-----

 

Conclusions Brain serotonin turnover is elevated in unmedicated patients with MDD and is influenced by the 5-HTT genotype. The marked reduction in serotonin turnover following SSRI treatment and the accompanying improvement in symptoms suggest that high brain serotonin turnover may be a biological substrate of MDD.

 

 

 

 

Edited by Finn, 21 August 2017 - 07:08 AM.

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#4 Mind_Paralysis

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Posted 21 August 2017 - 09:54 AM

 

I had hard time finding this "Murray Ellis" . It seems that Murray Esler has become victim of Ann Tracy Blake, who also falsely tried to represent her Ph.D status to gain more credibility, who also likes to "publish" poorly written anti-antidepressant rants full of typos.

 

http://www.gw.edu/_e...n_Ann_Tracy.pdf

 

https://famguardian....ort-DrTracy.pdf

 

http://www.drugaware...g/tag/insanity/

 

 

Esler certainly never  "went on to ask what I have been asking for 25 years now which is why are we giving drugs that increase serotonin (all antidepressants do this) when those suffering anxiety disorders already have elevated levels of serotonin." like she claimed

 

 

http://www.socialanx...7329-post6.html

 

 

Esler merely challenged theory of how SSRIs work, not if they work.

 

 

https://web.archive....-2000May13.html

 

The scientists tested the levels of the mood-regulating chemical serotonin in 20 patients who suffer panic attacks and found that, even on a good day, the average levels of the chemical in the brains of at least 15 of the patients were eight times higher than normal. ----- Professor Esler emphasised that the SSRIs were "great drugs" and should remain worldwide bestsellers. ---- First, the conventional view of how SSRIs operate has been challenged. It would appear that the drugs are effective because, over time, they somehow decrease, rather than increase, serotonin as originally thought.

 

 

Murray Esler's articles of  SSRIs helping with issues possibly related to increased serotonin turnover

https://www.research...e-inhibitor.pdf

 

 

 

 

Increased brain serotonin turnover in panic disorder patients in the absence of a panic attack: Reduction by a selective serotonin reuptake inhibitor

------

 

Support for this interpretation comes from the direct relationship which existed between serotonin turnover and illness severity, and the finding that SSRI administration reduced serotonin turnover. Serotonin transporter genotyping suggested that increased whole brain serotonin turnover most likely derived not from impaired serotonin reuptake, but from increased firing in serotonergic midbrain raphe neurons projecting to both subcortical brain regions and the cerebral cortex.

 

 

 

 

http://jamanetwork.c...larticle/482548

 

Elevated Brain Serotonin Turnover in Patients With Depression Effect of Genotype and Therapy

-----

 

Conclusions Brain serotonin turnover is elevated in unmedicated patients with MDD and is influenced by the 5-HTT genotype. The marked reduction in serotonin turnover following SSRI treatment and the accompanying improvement in symptoms suggest that high brain serotonin turnover may be a biological substrate of MDD.

 

 

 

 

 

You are informative as always, Finn! = )

 

Thank you for bringing this to my attention - especially the info regarding Ann Tracy Blake... Pseudo-scientific people like this, which have a rather GROTESQUE* and irrational agenda, is a constant issue when discussing matters of science - everyone needs to know about such things, and how to filter out incorrect information.

 

I also hope that Farshad sees your post and accepts the facts in it, so that he can move on towards treating his issues in some way instead.

 

 

*Why grotesque, you ask? Because there is a HUGE contingent of the people against psychiatric medications, which are either SCIENTOLOGISTS themselves, or SHILLS for the Scientologists, which are actively trying to discredit science for their own ECONOMIC gains! You never know... she might be one of them.



#5 kurdishfella

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Posted 21 August 2017 - 10:45 AM

those are old studies not even gonna read them. you need to get on with the time and read the new ones. your souces from 20 years ago .......

 

 

'''''''''''"...New evidence puts into doubt the long-standing belief that a deficiency in serotonin - a chemical messenger in the brain - plays a central role in depression. In the journal ACS Chemical Neuroscience, scientists report that mice lacking the ability to make serotonin in their brains (and thus should have been "depressed" by conventional wisdom) did not show depression-like symptoms."

"...Interestingly, the mice were compulsive and extremely aggressive, but didn't show signs of depression-like symptoms. Another surprising finding is that when put under stress, the knockout mice behaved in the same way most of the normal mice did. Also, a subset of the knockout mice responded therapeutically to antidepressant medications in a similar manner to the normal mice. These findings further suggest that serotonin is not a major player in the condition, and different factors must be involved. These results could dramatically alter how the search for new antidepressants moves forward in the future, the researchers conclude."

http://www.medicalne...ases/281645.php

 

 

Benzodiazepines: anxiety-reducing activity by reduction of serotonin turnover in the brain.

https://www.ncbi.nlm.../pubmed/5064914

 

 

http://www.independe....-a7207421.html

serotonin Increases Anxiety And Suicide "...But, despite being prescribed as a treatment for anxiety, these ‘SSRI’ drugs designed to boost levels of serotonin in the brain had a strange and mysterious side-effect. In some cases, they initially made people feel more anxious or even suicidal. Now a new study, published in the journal Nature, has found that, contrary to the popular view serotonin only promotes goodfeelings, it also has a darker side."

"...Researchers in the US delivered a mild shock to the paws of mice and found this activated neurons that produce serotonin in an area of the brain known to be involved in mood and depression. Artificially increasing these neurons’ activity also appeared to make the mice anxious. Using sophisticate equipment to monitor the mice’s brains, the scientists, from North Carolina University’s medical school, then mapped what they described as an “essential” serotonin-driven circuit “governing fear and anxiety”.

 

 

Study confirms science behind serotonin and depression is backwards

"...The low-serotonin theory is the basis for commonly prescribed anti-depressant medications called selective serotonin re-uptake inhibitors, or SSRIs, which keep the neurotransmitter's levels high by blocking its re-absorption into the cells that release it. Those serotonin-boosting medications actually make it harder for patients to recover, especially in the short term, says lead author Paul Andrews, an assistant professor of Psychology, Neuroscience & Behaviour at McMaster...When depressed patients on SSRI medication do show improvement, it appears that their brains are actually overcoming the effects of anti-depressant medications, rather than being assisted directly by them. Instead of helping, the medications appear to be interfering with the brain's own mechanisms of recovery."

"...The best available evidence appears to show that there is more serotonin being released and used during depressive episodes, not less, the authors say. The paper suggests that serotonin helps the brain adapt to depression by re-allocating its resources, giving more to conscious thought and less to areas such as growth, development, reproduction, immune function, and the stress response."

http://www.sciencedi....49763415000287 https://www.scienced....0217114119.htm

 

 

Serotonin reverses dominant social status http://www.sciencedi....66432800003934

 

 

Children With Autism Have High Serotonin Levels

"...Another thing the study found out is the relationship of serotonin to ASD. The results show that about 30 percent of the total number of the correspondents, which are children having the disorder, have hyperserotonemia. When they have undergone tests, their blood exam showed they are positive to have an above normal level of serotonin. With the information gathered, Cascio and her group became certain of how hyperserotonemia affects people with ASD. And to know more about it, she said that the group is currently working to prove their hypothesis, which she believes will be a stable ground for future research."

http://www.parenther....m-disorder.htm

 

 

Serotonin antagonists (could) prevent / treat osteoporosis

"...Osteoporosis is a disease of low bone mass most often caused by an increase in bone resorption that is not sufficiently compensated for by a corresponding increase in bone formation. As gut-derived serotonin (GDS) inhibits bone formation, we asked whether hampering its biosynthesis could treat osteoporosis through an anabolic mechanism (that is, by increasing bone formation). We synthesized and used LP533401, a small molecule inhibitor of tryptophan hydroxylase-1 (Tph-1), the initial enzyme in GDS biosynthesis. Oral administration of this small molecule once daily for up to six weeks acts prophylactically or therapeutically, in a dose-dependent manner, to treat osteoporosis in ovariectomized rodents because of an isolated increase in bone formation. These results provide a proof of principle that inhibiting GDS biosynthesis could become a new anabolic treatment for osteoporosis."

https://www.ncbi.nlm...pubmed/20139991

 

 

Serotonin Antagonists Extend Lifespan, SSRI Dramatically Shorten It

"...Four compounds increased lifespan by 20%-30%: mianserin, mirtazapine, methioteptin and cyproheptadine (Fig. 1 and Supplementary Table 1). In humans, all four compounds are antagonists of serotonin 2 (5-HT2) receptor and, to a variable extent, of certain other biogenic amine receptors."

http://www.nature.co....ture05991.html

 

 

More On The Wrong Theory Of Depression And Serotonin

"... The corollary to the chemical imbalance theory, which implies that raising brain serotonin levels alleviates depression, has also been hard to prove. As mentioned previously, the serotonin-depleting drug reserpine was itself shown to be an effective anti-depressant in the 1950s, the same decade in which other studies claimed that reserpine caused depression-like symptoms. At the time, few psychiatrists acknowledged these conflicting reports, as the studies muddled a beautiful, though incorrect, theory. Tianeptine is another drug that decreases serotonin levels while also serving as a bona-fide anti-depressant. Tianeptine does just the opposite of SSRIs – it enhances serotonin reuptake. Wellbutrin is a third anti-depressant that doesn't increase serotonin levels. You get the picture. If you prefer your data to be derived more accurately, but less relevantly, from rodents, you might consider a recent meta-analysis carried out by researchers led by McMaster University psychologist Paul Andrews. Their investigation revealed that, in rodents, depression was usually associated with elevated serotonin levels. Andrews argues that depression is therefore a disorder of too much serotonin, but the ambiguous truth is that different experiments have shown "activation or blockage of certain serotonin receptors [to improve] or worsen depression symptoms in an unpredictable manner."

http://io9.gizmodo.c....ory-1686163236

 

Serotonin deficiency may not cause depression after all

http://www.salon.com....ssion_partner/

 

 

 

serotonin inhibits the senses

"...The inhibition of sensory responsivity is considered a core serotonin function, yet this hypothesis lacks direct support due to methodological obstacles. We adapted an optogenetic approach to induce acute, robust and specific firing of dorsal raphe serotonergic neurons. In vitro, the responsiveness of individual dorsal raphe serotonergic neurons to trains of light pulses varied with frequency and intensity as well as between cells, and the photostimulation protocol was therefore adjusted to maximize their overall output rate. In vivo, the photoactivation of dorsal raphe serotonergic neurons gave rise to a prominent light-evoked field response that displayed some sensitivity to a 5-HT1A agonist, consistent with autoreceptor inhibition of raphe neurons. In behaving mice, the photostimulation of dorsal raphe serotonergic neurons produced a rapid and reversible decrease in the animals' responses to plantar stimulation, providing a new level of evidence that serotonin gates sensory-driven responses."

http://journals.plos....l.pone.0105941

 

 

Individuals with social phobia have too much serotonin – not too little http://www.uu.se/en/...rticle/?id=4918

''''''''''''''''

 

(EDIT) just realised most of the links dont work but im sure you can find it if you just copy the text into google and you will find some sources.


Edited by farshad, 21 August 2017 - 10:50 AM.


#6 Finn

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Posted 21 August 2017 - 11:23 AM

those are old studies not even gonna read them. you need to get on with the time and read the new ones. your souces from 20 years ago .......

 

 

Uhmm, you cited 20 year old misinformation by Ann Tracy Blake in your original post, the only links in my post that were anywhere near that 20 years old, were the links to original article that Blake lied about, and to Blake's lies that you cited, and to Blake's history of lying about her degree. Esler's other articles were newer. 

 

Of those articles you posted, none of them shows that SSRIs don't help for those psychiatric conditions. They might only indicate that SSRIs help through different route that it was thought before, ie not by increasing serotonin but by decreasing serotonin turnover, like indicated in all those Esler's articles from 2007, 2008 and earlier.

 

Actually you even linked articles that supports SSRIs working for anxiety issues

 

Benzodiazepines: anxiety-reducing activity by reduction of serotonin turnover in the brain.

 

Like Esler and other have shown, in this aspect benzos and SSRIs are similar, SSRIs do the same thing, they reduce serotonin turnover , benzos also reduce serotonin turnover.


Edited by Finn, 21 August 2017 - 11:29 AM.

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#7 kurdishfella

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Posted 21 August 2017 - 11:32 AM

yes my point is  serotonin not all that good that everyone makes it out to be .







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