Antidepressants Can Cause Long-Term Depression

[Guest guest]

This may be old news but a patient brought this in and I thought it was worth

sharing - Bill Harney

http://www.huffingtonpost.com/dr-peter-breggin/antidepressants-long-term-depress\

ion_b_1077185.html

New Research: Antidepressants Can Cause Long-Term Depression

Shortly after Prozac became the best-selling drug in the world in the early

1990s, I proposed that there was little or no evidence for efficacy, but

considerable evidence that the drug would worsen depression and cause severe

behavioral abnormalities. I attributed much of the problem to " compensatory

changes " in neurotransmitters as the brain resists the drug effect. Since then,

in a series of books and articles, I've documented antidepressant-induced

clinical worsening and some of its underlying physical causes. Now the idea has

gained ground in the broader research community and has recently been named

" tardive dysphoria. "

It has been apparent for many years that chronic exposure to SSRI

antidepressants frequently makes people feel apathetic or less engaged in their

lives, and ultimately more depressed. In my clinical experience, this is a

frequent reason that family members encourage patients to seek help in reducing

or stopping their medication. SSRI-induced apathy occurs in adults and includes

cognitive and frontal lobe function losses. (See Barnhart et al., 2004; Deakin

et al., 2004; Hoehn-Saric et al., 1990). It has also been identified in

children. Adults with dementia are particularly susceptible to

antidepressant-induced apathy.

A recent scientific study by El-Mallakh and his colleagues reviewed the

antidepressant literature and concluded that any initial improvements are often

followed by treatment resistance and worsening depression. They compare this

problem to tardive dyskinesia, caused by antipsychotic drugs, and call it

tardive dysphoria, " an active process in which a depressive picture is caused by

continued administration of the antidepressant. " Based on rat studies, they

hypothesize that " dendrite arborization " -- an increased branching growth of

nerve cells -- caused by chronic antidepressant exposure, may be the cause.

In a meta-analysis of 46 studies, s et al. (2011) found the relapse rate

for antidepressant-treated patients (44.6 percent) was much higher than for

placebo-treated patients (24.7 percent). s also found that the more potent

antidepressants caused an increased risk of relapse on drug discontinuation. A

2010 Minnesota evaluation of patient care in the state found that only 4.5

percent of more than 20,000 patients were in remission at 12 months, indicating

that they had become chronically afflicted with depression during and probably

as a result of their treatment.

s et al. (2011), like El-Mallakh et al. (2011), stress what I had first

described as compensatory mechanisms. SSRI antidepressants block the removal of

serotonin from the synapses between neurons, in effect trying to flood these

synapses with serotonin. Many studies confirm that the brain attempts to

compensate for the impact of the SSRIs by reducing the brain's capacity to

respond to serotonin. This leads to a loss of serotonin receptors that can reach

60 percent. Blockade of serotonin reuptake causes a potentially harmful adaptive

response in the form of a persistent hypertrophy of the reuptake mechanism.

Additional studies show persistent biochemical changes in the brain following

exposure to SSRI antidepressants.

In addition, I have been describing direct toxic effects on the brain that can

account for the emotional deterioration of these patients. Prolonged SSRI

antidepressant use can produce abnormal cell growth in the rat brain

(neurogenesis) and decreased thalamic volumes in children (tissue shrinkage from

cell death). Thus far, most researchers have not yet begun to take into account

or to face these more gross threats to the integrity of the patient's brain

after prolonged exposure to antidepressants. Meanwhile, drug-induced changes in

brain cell structure and number, when found as a result of taking illegal drugs,

are always touted as a reason not to take these drugs.

Antidepressants are the second most prescribed group of drugs in America. Yet

evidence continues to converge on the dangerousness of antidepressant drugs.

Given the difficulty showing any effectiveness even in the short-term, the use

of these drugs becomes more and more problematic. On top of that, the

antidepressants produce serious withdrawal reactions, making it difficult and at

times life-threatening to withdraw from them, even with the recommended clinical

supervision and slow taper. Psychiatry has always been slow to respond to

scientific evidence that its treatments are harmful. Often, as in this case,

psychiatry flouts science. The public will have to develop its own resistance to

taking antidepressant drugs.

R. Breggin, M.D. is a Harvard-trained psychiatrist and former full-time

consultant with NIMH who is in private practice in Ithaca, New York. Dr. Breggin

is the author of more than twenty books including the bestseller Talking Back to

Prozac and the medical book Brain-Disabling Treatments in Psychiatry, Second

Edition. His most recent book is Medication Madness, the Role of Psychiatric

Drugs in Cases of Violence, Suicide and Crime. He is also the author of dozens

of peer-reviewed scientific articles, many in the field of psychopharmacology.

On April 13-15, 2012 in Syracuse, New York, the annual conference of Dr.

Breggin's 501c3 nonprofit international organization, The Center for the Study

of Empathic Therapy, will present a panel of lawyers, experts, survivors and

families concerning antidepressant-induced violence and crime. Conference

information is available on www.EmpathicTherapy.org.