As in 2018, 1 in 4 in Scotland and 1 in 8 in England are now prescribed antidepressant here is their effect and read research at 2019
The medication of depression, is justified by the belief, in an unproven theory, that depression, is caused by seronergic neurons, releasing too little serotonin into the synaptic gap, making the serotonegic pathways underactive.
Antidepressants, purport to bring serotonin levels up to ‘normal’
But, a normal level of serotonin is unknown, and, there is no scientific evidence that depression, is in fact caused by a serotonin imbalance.
And Germany will not licence Prozac as the trial data is insufficient above the placebo
And the latest 2017 data shows here it has no effect over placebo takers.
Despite this over 57 million antidepressant prescriptions were issued in England in 2013- a rise of over 500% since 1992.
11% of all women and 6% of men in England take them.
Yet trials show little effect over a placebo.
So what will increasing serotonin via antidepressants, do to their brains ?
And, as serotonin acts, in, as yet unknown ways, on different parts of our infinitely complex brain, on a person’s bodily functions ?
In the same way, as anti psychotics, change the pathology of the brain, and make it super sensitive to dompamine, causing psychosis, anti depressants increase serotonin, triggering pathological changes to the serotonergic system, which actually causes and/or worsens depression.
Prior to being medicated, a ‘depressed’ person, has no known chemical imbalance, anti depressants, then increase the level of serotonin in the brain, by stopping its normal removal from the synapses.
This triggers a cascade of changes, and several weeks later, which is why, it take weeks, for the medication to kick in, the serotonergic pathway is operating in a very abnormal way.
To compensate for the fact, the serotonin reuptake channels are blocked ,the presynaptic neuron produces more serotonin
After a few weeks, the saturation of increased serotonin exacerbated by blocked removal from the synapses, causes the postsynaptic neurons to become desensitised to serotonin.
And, then this drug induced neuropathology, appears to cause depression, as clinical trials have shown antidepressants, worsen, depressive epitodes
And this is also borne out, by the depression epidemic in the USA, the escalation of which, co insides with the increased use of antidepressants. .
In 1955, 38,200 were in mental hospitals due to depression, today, a major depressive disorder, is the leading cause of disability in the USA , affecting 15 million adults, and in 2008, the John Hopkins School of Public Health reported, that 58% of this group were ‘severely impaired’.
Global depression is up 18% since 2005.
In addition to causing depression, anti depressants cause a multitude of side effects, including aggression, agitation, suicidal thoughts, sexual dysfunction, suppression of REM sleep, muscle tics, fatigue, emotional blunting- no highs or lows- apathy, memory impairment, problem solving difficulties, loss of creativity, and learning difficulties.
So all this physical and mental damage is caused for what benefit ?
None, that by NICE standards is ‘clinically significant’.
Pre Prozac, the NIMH reviewed the old antidepressants- monamine oxidase inhibitors MAOIs and tricyclics, and found, the ‘more stringently controlled the study, the lower the improvement rate reported for a drug’.
In well controlled studies, 61% of drug related patients improved versus 46% of placebo patients.
This minimal efficacy, led researchers to wonder, if the placebo response, rather than the drug, accounted for small improvement.
They conducted seven studies comparing a tricyclic, to an ‘active’ placebo, ie one with a side effect, and in six out of the seven there was no difference in outcomes.
But Prozac PR had been building up big time, read how Eli Lilly,’s Dr John Virapen, secured this blockbuster drug, and then turned whistle blower, and wrote the best seller ‘Side effect death: corruption in the pharmaceutical industry”.
But Eli Lilly’s sales hype and marketing, did not bear up to independent scrutiny.
Arif Khan reviewed the data submitted to the Federal Drug Agency for 7 SSRIs, and concluded symptoms were reduced by 42% by tricycles, 41% by SSRIs, and 31% in the placebo group.
As with second generation atypical antipsychotics, the new ‘wonder drugs’ were no more efficient than the old ones.
A review of Erick Turner from Oregon Health and Science University, of FDA data for 12 anti depressants approved between 1987 and 2004
showed 36 of the 74 trials, had failed to show any statistical benefit, and there were as many trials that had produced negative, or questionable results, as positive ones.
In 2008 Irving Kirsch at University of Hull, found that in trials of Prozac, Effexor, Serzone, and Paxil, symptoms in those medicated, dropped 9.6 points on the Hamilton Rating Scale of Depression, versus 7.8 points for the placebo group.
NICE states a 3 point difference, is needed to demonstrate, a ‘clinically significant benefit’, this was 1.8.
In 2009 The British Journal of Psychiatry stated there was ‘limited valid evidence’ for the use of the drugs.
A group of European psychiatrists affiliated with the World Health Organisation conducted a review of Paxil’s clinical data, and concluded that ‘among adults with moderate to severe major depression’, this popular SSRI, was not superior to placebo in terms of overall treatment effectiveness and acceptability.
Yet our political cross party consensus, this year recommends, that even more of our NHS budget be spent on medicating us with these ‘mood enhancers’.