Originally Posted by Soph
---- No, I didn't say it was just you and now you're stating its 50% . I said you 'stated that because you have a side effect everyone else will' then you bring up a citation for 50 %.
---- Also you are making a common error of quoting 1999 data as a representation for the entire class. Using your 'Celexa' which is much more refined than say the original prozac, the incidence of impotence was 2.8% versus a placebo of < 1%. Placebo controlled directly from the PI.
Sexual dysfunction encompasses a lot more ground than just impotence. You talk about me using poor logic but you're being VERY selective in the data you present and yet you choose to lecture me about the very same thing. Where's your data and multiple studies at multiple dosages (to use your words)?
My initial post included both my personal experience with the drugs and a statement of what I knew to be fact and is widely accepted among doctors, despite what the PI says. Every single independant study conducted on SSRIs for people with no history of sexual dysfunction shows results in the 30-50% range. I had no intentions of getting in to big thing and didn't know at the time of my original post that I was required to supply multiple sources. I also didn't think that the rest of the forum would be particularly interested in reading a bunch of abstracts from journal articles.
You clearly know less about the subject than you pretend to otherwise there's no way you would have posted information from the PI as "proof". I can't imagine any reason why a pharmaceutical company would structure questions in such a way as to minimize the negative impact of their drug on sexual activity
Here's the full excerpt from the PI. It even says that the data likely represent an underestimate of the actual incidence rate, which you chose to leave out in an attempt to prove yourself right:"Although changes in sexual desire, sexual performance, and sexual
satisfaction often occur as manifestations of a psychiatric disorder,
they may also be a consequence of pharmacologic treatment.
In particular, some evidence suggests that SSRIs can
cause such untoward sexual experiences.
Reliable estimates of the incidence and severity of untoward
experiences involving sexual desire, performance, and satisfaction
are difficult to obtain, however, in part because patients and
physicians may be reluctant to discuss them. Accordingly, estimates
of the incidence of untoward sexual experience and performance
cited in product labeling, are likely to underestimate their
The table below displays the incidence of sexual side effects
reported by at least 2% of patients taking Celexa in a pool of
placebo-controlled clinical trials in patients with depression.
Treatment Celexa Placebo
(425 males) (194 males)
Abnormal Ejaculation 6.1% 1%
(mostly ejaculatory delay) (males only) (males only)
Libido Decreased 3.8% <1%
(males only) (males only)
Impotence 2.8% <1%
(males only) (males only)
In female depressed patients receiving Celexa, the reported incidence
of decreased libido and anorgasmia was 1.3% (n=638
females) and 1.1% (n=252 females), respectively.
There are no adequately designed studies examining sexual dysfunction
with citalopram treatment.
Priapism has been reported with all SSRIs.
While it is difficult to know the precise risk of sexual dysfunction
associated with the use of SSRIs, physicians should routinely
inquire about such possible side effects."
You do understand that within FDA guidelines (which aren't perfect), a pharmaceutical company will do what it can to maximize the perceived benefits and minimize the negative effects. They don't operate in a void and they want their drug to be prescribed by doctors instead of their competitors. If you don't believe this happens then I don't know what to say...
Here's an abstract from a journal article that addresses the issue of testing in pre-marketing clinical trials. It supports my earlier reference and to make you happy it's from 2006. I can only give abstracts since I'm not at my university and don't have access to the full-text."OBJECTIVE: The incidence of sexual dysfunction due to antidepressant drugs reported in pre-marketing clinical efficacy trials is often several times lower than in subsequent clinical experiences and independent reports. Although it is commonly believed that the reason for this discrepancy is that the nonleading questions employed in conventional clinical trials underestimate sexual dysfunction while the direct questioning used in independent trials provides more accurate data, few studies have actually compared these 2 methods. METHOD: In this study, 119 patients with a DSM-IV-defined major depressive episode (82 women and 37 men) who had been treated with but not responded to a selective serotonin reuptake inhibitor (SSRI; either citalopram or paroxetine) were assessed regarding sexual functioning by means of open-ended questions and direct questioning at baseline (after SSRI treatment only) and after 4 weeks of SSRI treatment plus buspirone or placebo. RESULTS: More patients reported sexual dysfunction in response to direct questioning (41%) as compared with spontaneous report (6%) (p < .001). Sexual dysfunction correlated with the duration of the depressive episode, but not with age, dose of SSRI, plasma level of SSRI, duration of SSRI treatment, or any measurement of depression. No statistically significant differences regarding the incidence of sexual dysfunction were found between the citalopram and the paroxetine groups. CONCLUSION: Open-ended questions are an insufficient tool to estimate sexual dysfunction, and premarketing clinical trials should therefore include basic explicit assessments. The failure to find a correlation between treatment duration and sexual dysfunction adds to the notion that sexual side effects due to SSRIs do not abate over time."
Incidence of sexual side effects in refractory depression during treatment with citalopram or paroxetine., J Clin Psychiatry. 2005 Jan;66(1):100-6
And another which again shows that the reality is vastly different from the PI."OBJECTIVE: Sexual dysfunction is a common side effect of antidepressant treatment, but recognition of the problem is variable. The aim of this study was to estimate the prevalence and impact of sexual dysfunction during antidepressant treatment in 2 European countries. METHOD: A cross-sectional survey of 502 adults in France and the United Kingdom. All participants were diagnosed with depression and taking a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI), starting within the previous 3 months. Information was gathered about other medications and conditions known to impair sexual functioning, recent changes in sexual functioning, and the impact of any changes. The Medical Outcomes Study 12-Item Short-Form Health Survey and the Arizona Sexual Experience Scale were administered to measure health status and sexual functioning. Data were collected from June to July of 2002. RESULTS: Applying a prevalence estimate algorithm, 26.6% of the French sample and 39.2% of the U.K. sample were classified as having antidepressant-induced sexual dysfunction; 34.2% of men and 32.5% of women were classified with antidepressant-induced sexual dysfunction. There was no clear pattern of antidepressant-induced sexual dysfunction related to specific antidepressants. Patients with antidepressant-induced sexual dysfunction reported that changes in sexual functioning negatively affected their self-esteem, mood, and relationships with sexual partners. 23.8% of the French sample and 25.2% of the U.K. sample reported that they perceived that their partner was dissatisfied with their sex life. CONCLUSION: The prevalence of antidepressant-induced sexual dysfunction in this study is similar to previous estimates reported in the literature. The impact of antidepressant-induced sexual dysfunction is substantial and negatively affects quality of life, self-esteem, mood, and relationships with sexual partners."
Estimating the prevalence and impact of antidepressant-induced sexual dysfunction in 2 European countries: a cross-sectional patient survey.,J Clin Psychiatry. 2006 Feb;67(2):204-10.
And lastly one that compares citalopram to an snri, since you claim the side-effects are so minimal..."The objective of this study was to compare efficacy and tolerability of the selective noradrenaline reuptake inhibitor reboxetine with the selective serotonin reuptake inhibitor citalopram, in the treatment of major depressive disorder (MDD). In total, 357 outpatients with MDD were randomized to treatment with reboxetine 8-10 mg or citalopram 20-40 mg per day during 24 weeks. Primary end-point was change from baseline in the Hamilton Depression Rating Scale (HAM-D, 21 items). Sexual function/dysfunction was measured by the Sexual Function scale (SF). Observed case analysis showed that both treatments yielded a gradual reduction of HAM-D scores: reboxetine with -21.4 and citalopram with -22.1 points (NS). LOCF analysis showed a greater reduction of the HAM-D scores with citalopram compared with reboxetine (-19.6 vs. -17.8; P = 0.034). The response rate was 90.3% for reboxetine and 92.7% for citalopram (NS). The most common side effect in the reboxetine group was dry mouth, and in the citalopram group sexual dysfunction. At week 24, anorgasmia was reported by 5.9% of the sexually active women in the reboxetine group vs 39% in the citalopram group. The dropout number was 91 in the reboxetine group, and 54 in the citalopram group. To summarize, both treatments gave a satisfactory antidepressant effect. The side effect profile differed between the groups, with a notably high prevalence of sexual dysfunctions in the citalopram group. The high number of dropouts in the reboxetine group, is considered as a result of the non-titration starting dose of 8 mg reboxetine per day, which gave a high incidence of early side-effects."
Efficacy and tolerability of reboxetine compared with citalopram: a double-blind study in patients with major depressive disorder.,J Clin Psychopharmacol. 2006 Apr;26(2):121-7.
--- My why not try it obviously for those who are appropriate for it.
I am quoted twice as saying in this particular kid's issue:
You FAILED again to copy what I wrote right after 'Why not try it?
My quote, ***"So why not try it. But in this case he should have a sex cons."***
My bad, I glossed over the sex cons part. Unlike you, I can admit when I'm in error. I still don't think he needs to see anyone. And no, I'm not intentionally deleting anything.
4. Pharmaceutical companies suggest a dosage which will be effective for the highest percentage of patients with an acceptable side effect profile. Yes, it's obviously approved by the FDA, but a good doctor should tailor the dosage to the individual. Often times the recommended starting dosage is too high for an individual and they get more side effects than are necessary. I'm not saying it's too high in that it's dangerous, just that it's higher than it needs to be for certain individuals and can cause unnecessary side-effects. This is particularly true for SSRIs because some people are super sensitive to them and can see improvements with very small doses. If you can't wrap your mind around that then I don't know what to say...
--- Please. You stated, "pharmaceutical companies habit of suggesting starting doses which are too high"?"
---This is simply not an accurate statement you have made.
Now you are altering your over the top comments to at least some form of sanity. You should grasp not me. I don't make inaccurate, over the top claims and I don't misquote people.
Maybe my original wording was poor but you're now preaching to me about my original intent. I once read an article about a doctor that had prescribed antidepresants to herself and started experiencing really bad side-effects. She couldn't understand because she was taking the minimum dose recommended by the drug manufacturer. She spoke to some of her colleagues and they were equally perplexed. Eventually someone figured out to lower the dosage below the minimum suggested dose and she began to respond to treatment without all the nasty side-effects. Specialists generally know better, but a lot of ADs are prescribed initially by a GP that unfortunately doesn't keep-up with the literature, even though it's widely available. I'm not trying to fault anyone because there are good reasons for a higher starting dose, BUT it is influenced by marketing and sales. Drug companies are profit driven. I read another article which showed that some patients responded to as little as 2.5mg or 5mg (i forget for which drugs, both were SSRIs) a day when the the starting dosage is typically 4-10 times that.
The main thing is your heart is in the right place
Likewise, but there is obviously a very large disconnect between when you and I think that therapy and/or drugs should be employed. Someone that finished in 10 minutes is in need of neither. That's really all i wanted to say in this thread.