Tag Archives: prozac

Prozac : 50% Placebo Effect?


It goes by names – Fluoxetine, Rapiflux, Sarafem, Selfemra, Oxactin, Ranflutin – but it is best known as Prozac.  Prozac is a Selective Serotonin Reuptake Inhibitor (SSRI).  SSRI’s are a class of drugs intended to block reuptake of serotonin, a mood regulating neurotransmitter, at the synapse.  The inhibition of the reuptake process is believed to cause an increase in the concentration of the neurotransmitter, in this case Serotonin, at the synapse.  (Kelsey, Newport, & Nemeroff, 2006, p. 28)  Other examples of this class of drugs include Citalopram (Celexa), Escitalopram (Lexapro), Fluvoxamine (Luvox), Paroxamine (Paxil), and Sertaline (Zoloft). (Kelsey et al., 2006, p. 47)

The history of SSRIs is one laden with concerns about side effects of their antidepressant predecessor,  Tricyclic Antidepressants (TCAs), and before them, Monoamine Oxidase Inhibitors (MAOIs).  Both classes of drugs are laden with side effects because they possess “rich pharmacology” as compared to the more targeted and selective SSRIs.  “In 1983, the first SSRI, fluvoxamine (Luvox), debuted in Switzerland.  Five years later, Fluoxetine (Prozac) was introduced in the United States.  The SSRIs revolutionized the treatment of depression.”  (Kelsey et al., 2006, p. 54)  SSRIs improved safety and tolerability – removing much of the stigma of taking an antidepressant.

SSRI’s are not without side effects, particularly because serotonin is so widely distributed in the brain.  Despite the fact that SSRIs have an overall effect of increasing and stabilizing mood for most people, they may also produce abdominal discomfort, sexual dysfunction, and anxiety.  (Kelsey et al., 2006, p. 54)  The response one can expect from an SSRI is highly individualized – every patient or client responds differently.  When starting an SSRI it is important to titrate (or gradually increase) dosages to avoid abrupt increases in serotonin.  Abrupt increases have led to headache, sleep issues, anxiety, and a host of other (mostly tolerable and short-term, comparatively speaking) side effects.  Longer term side effects include delayed orgasm, impotence, and decreased desire to have sexual relations.  It bears mentioning this can be a nice perk for men who are prone to premature ejaculation.  Abruptly stopping SSRIs can produce a constellation of symptoms affectionately called “serotonin discontinuation syndrome.”  (SDS) (Kelsey et al., 2006, p. 55)  Nausea, abdominal pain, irratibility, anxiety, and “shock-like sensations are among the most common signs and symptoms of SDS.  Aside from depression, the disorder for which SSRIs are primary intended, some SSRIs have proven to be effective in the treatment of Dysthymic Disorder, the depressive phase of Bipolar Disorder, Premenstrual Dysphoric Disorder, Panic Disorder, Social Phobia, OCD, Bulimia Nervosa, and Binge-Eating Disorder.  (Kelsey et al., 2006, p. 55)

Prozac holds a number of unique qualities within the more general category of SSRIs.  Aside from being the most prescribed antidepressant in the world for many years, it is notable for its long half life.  This longer action causes the “washout time” to take longer, but is undoubtedly a positive for clients who periodically miss a dose due to poor compliance.  There is also a once-a-week depot type dose for those individuals that do not wish to take pills daily.  Dosages range from 20mg-80mg once daily, usually in the morning.  (Kelsey et al., 2006, p. 55)

The prognosis or expected outcome from this drug is hard to predict because every individual patient responds differently to it.  Common side effects are addressed above, but if side effects are intolerable, or the positive effects are not clinically significant – the most likely scenario is “try a different one.”  Long story short – antidepressants are a crap shoot.  The patient should expect to get a markedly uptake in mood after taking Prozac for 4 weeks.  Discontinuation symptoms are rare when compared with other SSRIs.  Half of people who take Prozac may be just as well off with a sugar pill due to the placebo effect, with as little as 25% of Prozac users actually responding to the drug itself.  (Kirsch & Sapirstein, 1998)  Some believe that the field has inappropriately ignored the overshadowing role of the placebo effect and have rushed to declare victory for SSRIs, but not everyone is so hip on that hypothesis.  (Beutler, 1998)  There is no shortage of controversy around this particular article, however, including concerns about the absence of no-treatment effect sizes and other questionable statistical methodology.  (Dawes, 1998)  It should also be noted that the data is almost 15 years old.  More recent research failed to support the hypothesis that avoidance enhancement would be enhanced by Prozac (in goldfish).  The implications on the treatment of other vertebrates remains to be seen since it is hypothesized that serotonin mechanism may be higher conserved in vertebrate evolution.  (Beulig & Fowler, 2008)  The bottom line – your mileage may vary – consult with a psychiatrist.

 

References

Beulig, A., & Fowler, J. (2008). Fish on prozac: Effect of serotonin reuptake inhibitors on cognition in goldfish. Behavioral Neuroscience, 122(2), 426-432. doi: 10.1037/0735-7044.122.2.426

Beutler, L. E. (1998). Prozac and placebo: There’s a pony in there somewhere. Prevention & Treatment, 1(2). doi: 10.1037/1522-3736.1.2.13c

Dawes, R. M. (1998). Listening to prozac but hearing placebo: Commentary on kirsch and saperstein. Prevention & Treatment, 1(2). doi: 10.1037/1522-3736.1.1.15c

Kelsey, J. E., Newport, D. J., & Nemeroff, C. B. (2006). Principles of psychopharmacology for mental health professionals. Hoboken, NJ: John Wiley & Sons.

Kirsch, I., & Sapirstein, G. (1998, Jun). Listening to Prozac but hearing placebo: A meta-analysis of antidepressant medication. Prevention & Treatment, 1(2). doi: 10.1037/1522-3736.1.1.12a

Eating Disorders = BIG BUSINESS


“Weight discrimination and the resulting obsession with thinness are rampant and recalcitrant.  I believe that, in order to make any kind of a dent in this field, we all need to combat these pernicious influences.”  (Netherton, Holmes, & Walker, 1999, p. 412)  Amen.  The weight of the media, the “diet food industry,” and the purveyors of a “healthy lifestyle” propagate this issue… without a doubt.  Losing weight is BIG BUISINESS, and there are huge profits to be made for those that offer obese people the glimmer of a stereotypically thin body.

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I also appreciated the acknowledgement on the pressure exerted by managed care.  Eating disorders appear to be particularly “deep seated” and ill suited for half a dozen one hour sessions.  Correcting inaccurate perceptions, relabeling cognitions of visceral and affective states, and redrawing boundaries… this kind of work takes time… more time than managed care often provides.  This is yet another example of the effect managed care will continue to have for as long as it is the primary method of seeking out psychological assistance.

I was suitably surprised at the long-term mortality rate… suggested to be over 10%.  (Netherton et al., 1999, p. 399)  With a roughly 1 in 10 shot of succumbing to starvation, suicide, or electrolyte imbalance; you would think this particular set of disorders would get more research attention.  The fact that there is still limited epidemiological data is frustrating… perhaps the difficulty obtaining the data is related to the relative secrecy and shame associated with the disorders themselves?

Like the BM text, NHW jumps on the multi-determined etiology bandwagon.  It’s hard to disagree with since biological, familial, sociocultural, and personality factors all seem to be plausible.  The differences in family characteristics were particularly interesting.  “Bulimic families tend to be characterized as disengaged, chaotic, and highly conflictual and as having a high degree of life stress.”  Conversely, “anorexic families tend to be characterized as enmeshed, overprotective, and conflict avoidant.”  (Netherton et al., 1999, p. 400)  That’s a strange clinical picture that seems to suggest that there might be a single underlying biological cause for EDs in general, but that familial and personality factors may play a role in its manifestation.

The list of comorbid disorders we need to consider during the assessment process is long and fairly inclusive.  “Depression, anxiety disorders, dissociative disorders, substance abuse, and personality disorders” are on the forefront of the disorders we should be checking for.  (Netherton et al., 1999, p. 401)  Furthermore, NHW suggest we assess treatment history, as well as suicide attempts and self mutilative behaviors (cutters).

Pharmacological interventions employing antidepressants have been particularly successful.  This text only cites 3 studies that have employed SSRI class antidepressants, but they report “significant improvement with 60-80 mg dosages (of Prozac) compared to placebo.”  (Netherton et al., 1999, p. 407)  I think I am going to dig deep into some more recent research to see of this trend holds up, there has to be more than three studies on it by now.

I like the idea of a behavioral contract… not just for eating disorders, but for any disorders which involve “behavior.”  I am inclined to agree with the statement “the contract provides structure and predictability.  Expectations, rewards, and consequences are delineated so that all people involved (patient, treaters, families) know what is expected at all stages of treatment.”  (Netherton et al., 1999, p. 407)  My question is this… realistically, what “consequences” are there if we are dealing with outpatient treatment?

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Reference

Netherton, S. D., Holmes, D., & Walker, C. E. (1999). Child and adolescent psychological disorders: A comprehensive textbook. Oxford, NY: Oxford University Press.