What's the appropriate use for antidepressants?

False.

Which is the point of a therapy.

Sorry, but that’s nonsense. It would not deal with the underlying problem at all. If you have a philadelphia chromosome, you have a philadelphia chromosome. The therapy doesn’t change that at all. It merely makes sure that cells with such a genetic aberration don’t kill you, and hopefully die out. Not the least, progress is being made on addressing issues of synaptic plasticity that are thought to be involved in the more permanent forms of mood disorders.

False in the first part and irrelevant in the second. The testing isn’t done inside pharmaceutical companies, but in hospitals, ALL ACROSS THE WORLD. The results are published and reviewed. Saying that they ‘choose what results to report’ is hogwash. The fact what huge ruckus was created by a single case of death in a trial for genetic therapy and cases of leukemia in others shows quite well that problems get out, quite simply because the doctors who conduct the trial do not defer to the company first and foremost, but to the public, and because people start to ask serious questions when seriously weird things happen.

Thanks for demonstrating you had no idea what I was talking about. Your insinuations and putting things into my posts that aren’t there merely show you have no factual arguments whatsoever. I suggest reading a bit about genomics and proteomics.

I would suggest you stop making claims and simply dancing around ‘You’re wrong’ and ‘You’re oversimplifying’ when all you do is just that. You hardly show that I am wrong by simply claiming so. Neither do you show that I am wrong, nor do you make suggestions what, in fact, is the case. I would suggest reading some medical literature, rather than just making feel-good statements. I already provided several quotes from peer-reviewed literature. I can provide more once you’re through reading them. For that matter, I’ll give you some more rightaway:

Neurochem Res 2003 Jun;28(6):965-76 ‘Central GABAergic systems and depressive illness.’

Brain Res Mol Brain Res 2003 Apr 10;112(1-2):82-9 ‘Effect of chronic estradiol, tamoxifen or raloxifene treatment on serotonin 5-HT(1A) receptor.’

Eur J Neurosci 2003 Mar;17(5):917-28 ‘Alpha2A and alpha2C-adrenoceptor regulation in the brain: alpha2A changes persist after chronic stress.’

Cogn Affect Behav Neurosci 2001 Mar;1(1):96-104 ‘Enhancement of serotonin uptake by cortisol: a possible link between stress and depression.’

Curr Opin Pharmacol 2003 Feb;3(1):33-40 ‘Brain plasticity and pathology in psychiatric disease: sites of action for potential therapy.’

Biol Psychiatry. 2003 Apr 15;53(8):707-42 ‘Enhancing neuronal plasticity and cellular resilience to develop novel, improved therapeutics for difficult-to-treat depression.’

No, I am generating this statement from the lecture of scientific publications in the field.

It is funny that you accuse me not to know anything about an issue and claim once more that I am incorrect without even once suggesting what is, in fact, the case. As long as you don’t do so, it is YOU who demonstrably doesn’t know anything about the issue you are talking about. Because otherwise, you could say more than just ‘You’re wrong, you’re wrong, you’re wrong’

I didn’t say that therapy with drugs is always successful, I said addressing the chemical imbalance will help in all cases described. That means addressing the specific balance given in each case.

Says who? You?

One that the body is capable of regulating in either direction itself. You see, that’s what balance means: equilibrium between several states, or as merriam webster puts it 'equipoise between contrasting, opposing, or interacting elements '.

But I take it that you consider a scale balanced when you dump a sack of rice on one side, and nothing on the other?

Seriously, I would suggest that when you are given cites, you actually read them rather than simply claiming someone has no idea what he is talking about despite the fact he references his opinion to scientific literature. You’re not doing yourself a favor just denying that the world is round and circling round the sun.

They do, but a noted phenomenon is that many go into psychiatry and psychology because they, themselves, have suffered or are suffering through psych disorders. By learning about the mind, they often are better able to help themselves work through their own problems.

Nah, SSRIs don’t produce euphoria. In large doses, they’re more likely to produce apathy and a sense of flatness, rather than an increase in emotion that would be analagous to a euphoric high. Prescription doses vary; for example, those with OCD tend to take fairly high doses of SSRIs, compared to much lower doses for those suffering minor depression.

**

Cocaine is a dopamine reuptake inhibitor; its major effect is not based on serotonin, as with Prozac. In general (though this is far too simplified), dopamine tends to “excite”, where serotonin tends to “calm”. The feelings by Prozac are nothing like those produced by cocaine. Further, the reason that cocaine is not legal is that it has a high potential for abuse. Cocaine lasts less than half an hour, typically; as it wears off, a crash is experienced. This crash often leads the user to take more cocaine. As this cycle continues, the crashes become worse, and when the coke is gone, the user feels like crap. Basically, its unsustainable and short-acting; as well, it tends to provoke undesired behavior (compulsions, aggression, etc.) – things you wouldn’t want to have somebody who’s already depressed have to deal with. Prozac and company are long-acting, without this cycle of nasty ups and downs. They tend to make the user more “normal”, cliched as this may sound.

The other drugs you mentioned all have problems that make them unsuited for treatment of depression. With most recreational drugs, the issue is that they make it difficult for the user to function in everyday society; yeah, being drunk or stoned can alleviate depression, but you’re going to have trouble functioning while in this state. Hence, not too useful.

Wow, great explanation, occ. The SSRI detractors in this thread seem to think that’s all lies, but they remain suspiciously silent on the exact details of this supposedly hidden “truth”. I’m still waiting to hear about all these horrible “dangers” that folks keep alluding to.

I agree with TVAA on his point that we don’t know what are the underlying causes of mood disorders, and, OliverH your posts actually support TVAA.

Your statement, which I quoted above, is compromised with fudge phrases: “progress is being made”, “[issues] that are thought to be involved”. In other words, synaptic plasticity is speculated by some researchers to be “involved” in mood disorders. That’s pretty much the same as saying we don’t know what the cause is.

This year the hot research topic might be synaptic plasticity. So what? Some people think cortisol and the hypothalamic-pituitary-adrenal axis are implicated. Others are convinced that a combination of sertonin/noradrenaline receptors were involved (hence the drugs venlafaxine, reboxetine, and buspirone), and still others point to dopamine (hence the drug amineptine).

Just a few years ago the ideal was the selective serotonin reuptake inhibitors – in other words, they thought that only one neurotransmitter needed to be affected. The monoamine hypothesis for depression is over 30 years old and it, like all current ideas, is only a hypothesis.

All of the theories are failing to account for one or another important aspect of depression. For example, we can raise your serotonin levels in one hour with an SSRI, but it takes weeks for the clinical effect to manifest. Another example: significant percentages of people do not respond to the monoamine chemicals. If depression were one entity, they would all respond. Another example: many people show paradoxical reactions to current drugs. I think the most amazing thing about modern drugs is how widely people vary in their reactions to them. Zoloft stimulates one person, and calms down another.

There are other theories about depression. What about calcium channels? What about the fact that depression often results from left frontal lobe damage, which argues for a more global level of organization than neurotransmitters?

All of your statements are only hypotheses no matter how much you, personally, believe in them. TVAA is right.

It is defined in the DSM. For some reason people like to pick on social anxiety as somehow being false, or unworthy of attention. Your arguments about it are completely misinformed. If someone is happy being alone, then they will not seek medical attention. If someone is very unhappy with their anxiety in social situations, and has few relationships and job prospects as a result, then what’s wrong with getting treatment for it?

Only where it’s the serotonin levels that are a problem. An SSRI does not help with bipolar disorders, although there is some overlap in symptoms between that and depression in the depressive part of the bipolar cycle.

How about another comparison? Parkinson’s disease is caused by a depletion of dopamine generating cells in a particular region of the brain. You would think that L-Dopa, which keeps dopamine in circulation longer (much as SSRI’s do for serotonin) would provide perfect symptom management - but it doesn’t. Simply pouring more dopamine into the brain has strange effects, produces definite unwanted side effects, and in general is not a satisfactory solution.

Likewise, simply dumping more serotonin into a brain is unlikely to restore a perfectly natural balance. What about all the other neuro-transmitters? Don’t all these chemical affect each other? Is the patient deficient or over-supplied with others? These question are not answered.

Who determines what is “proper” signalling? What is a “normal” level, or range of levels? Do we even know what normal is?

Something that either kills ALL the cancer cells and leaves ALL the healthy cells intact, or a treatment that repairs the damage to cancer cells and converts them back to normal.

And the inconvenient detail that it doesn’t alway work - there are some patients who just don’t get better and no one knows why.

In what sense are you using “effects on the brain”? An addict knows that if he takes a particular substance it will tend to have a particular effect, and he/she just doesn’t care what the specific chemical reactions are - the addict is looking for a feeling, not a particular “chemical balance”. Are they kidding themselves? Sometimes. Sometimes they are surprisingly knowledgable about what they are doing.

Nonsense. My father worked for several major drug companies, mostly in quality control, and he often expressed frustration about his work.

Right now, I’m working with a medical research institution. Yes, I have a better than average view of how much work it takes to bring a drug to market.

Yes, there is an enormous difference from the manufacturer’s or the researcher’s viewpoint - but not from the end user’s. You know, the lay public.

Maybe that’s why I don’t read the stuff on the web and stick to peer-reviewed journals.

Actually, I was talking about the American medical insurance industry, which will pay for a lifetime of Prozac but won’t pay for six months of psychotherapy or inpatient therapy, even where a medical professional recommends it.

That’s like saying the bubonic plague and the flu are the same thing because they both cause a fever.

Sure, there may be subtle chemical differences between various mental disorders, but at least in this country diagnosis is based on symptoms, by behaviors manifested in patients, not by sampling cerebral-spinal fluid or performing brain biopsies.

If it’s measured in “hours or days” it’s NOT clinical depression, it’s ordinary grief, sadness, or similar emotion. After the death of a loved one normal grief does last weeks, even a year. Other criteria are needed, like is a person functional? Are they manifesting a depressed mood after a tragedy but still maintaining personal hygiene, job performance, etc? Or do they lie in bed all day, unwashed, hair uncombed, the shades drawn, etc? Those are two different circumstances. One requires treatment, the other typically does not.

Except the American medical insurance industry is increasingly unwilling to pay for anything but drugs. Policies are written with lifetime caps as low as $20,000 for mental illness. An SSRI can be administered indefinately by an MD with no protest, but for psychotherapy treatment may be authorized for only 90 days, and subject to adminsitrative review by the insurance company to be paid beyond that. Inpatient treatment may not even be covered, even for those actively suicidal, or restricted in time (such as 72 hours). That’s not a push towards drugs over other therapies?

I am famillar with clinical trials. I am also famillar with the fact that results can be inconclusive, trials poorly designed, researchers biased, and so on. Not to mention legitimate differences of opinion when observing the same person. Is a given patient rude - or open and honest? Is the patient meticulous and careful - or obessive and compulsive? Where is the line drawn?

In the 19th Century women who enjoyed sex “too much” had their clitorises removed, or were committed. Now - we worry abut women who don’t enjoy sex enough and administer drugs. Who is/was right?

But it does happen.

I’m talking about ads on TV discussing a new use for a drug such as Zoloft or other SSRI urging people to “talk to your doctor” if “you ever feel uncomfortable in social situations”. I’m talking about full-page ads in the mainstream press trumpeting the wonders of a prescription drug to get you through the normal stresses of life.

Perhaps if you do not live in the United States you do not see these things… in which case, of course you have no idea what I’m talking about.

Let’s review what I actually wrote, hmm?

I was not talking about the truly non-functional socially avoiding personality - the people who lock themselves in their room, become hermits even though they would like to be more social, and otherwise meet the DSM criteria. I was talking about people who, although not as social as the norm, are nonetheless content with their lives but, with the wording of various ads now blitzing the media, such people are pushed into the realm of pathological. They aren’t - they’re just on one end of the normal spectrum.

It’s also undeniable that some people’s social problems come from their own problems that have more to do with conduct than some innate chemical imbalance. They require better manners rather than a drug.

And then there are people who are disfigured or handicapped and unfairly shunned by many in society. No drug for them is going to improve their social lives. The brutal fact is, right or wrong, if a person is facially disfigured, or both blind and deaf, they may wind up almost completely isolated no matter how wonderful their personality. In which case, a link to the internet and a selection of message boards may have to do for their social life.

And certainly there are people manifesting a mental illness in this regard.

Again, the symptom of social isolation is a symptom - one that may have more than one root cause. And may require more than one solution. Or combination of solutions.

A few decades ago, psychopharmacologists would brag about how many neurotransmitter systems their drugs would affect. The more, the better, right?

Now drugs are marketed based on their selectivity. After all, we only want to target the specific neurotransmitter system responsible for the condition. Of course, there’s a drug that targets practically every neurotransmitter system we know about – we can’t be too careful, after all.

And there’s no way to determine which will be helpful in any particular case except to try them. If one doesn’t work, we have to keep trying with a higher dose in case that works. We have to find the right drugs by trial-and-error because our understanding of mental illness and neurochemistry is so profound. Our knowledge of psychiatry has expanded so much that we have dozens of new drugs to try.

(I’ve really got to stop posting to this thread before my head explodes… channeling all this sarcasm can’t be good for me.)

As a therapist, I can say this:

For some people prozac alone IS what’s needed, they take it, they’re fine, don’t need to revisit their daddy issues.

For others, the prozac (or whatever) will give them a fair shot at dealing with whatever patterns get and keep them depressed.

For others, medication isn’t going to help anything, and really need to work out issues, change patterns of behavior, have a catharsis, etc.

It’s a spectrum thing.

For all of these arguments against drug therapy for depression, you could substitute “allergies” for “depression” and have the same conversations.

Allergy drugs only treat the symptoms!

Some doctors prescribe allergy drugs without clinical tests to determine if there really is an allergy involved!

Some doctors believe that if the symptoms respond to the drug, you’ve identified it as an allergy!

Not all allergies respond to the same drugs!

How do you know the person really has an allergy and doesn’t just have a cold?

It seems that people are eager to attack drug treatment for certain symptoms, but have little to say when the symptoms are a runny nose or itchy eyes.

Why? As has already been said in this thread, I think it’s to do with so many people’s perception of mental illness.

Many insurance companies won’t pay for a lifetime of Prozac. They’ll pay for half a lifetime. The deductibles and copayments are often twice what they are for other drugs–even allergy drugs. :smiley:

Julie

No, it isn’t.

But thanks for showing that posting references here is a waste of time.

Question: Do you actually know what synaptic plasticity is?

Sorry, but I think you are grossly confused about the ‘depression as one entity’ thing. I never claimed the effect to be monocausal, but being based on specific principles. That cancer is an aberration of cell growth and death doesn’t make it a ‘single entity’ in terms of what drugs work, or what specific processes are going haywire. I think you seriously underestimate the multitude of approaches a given signal can be modulated.

Except, of course, that nothing you said supports TVAA in any way, or contradicts me in any way. It merely suggests a serious lack of understanding of the underlying science.

Excellent post, JS.

I know of someone for whom the doctor had determined that the best drug to treat her anxiety was one that also happened to be useful as an aid to stop smoking, although smoking was not an issue in her treatment. The insurance wouldn’t cover it since they did not cover anti-smoking aids, and they covered a reduced amount for therapy also.

Dumb on 2 counts. Even if she DID need it as an anti-smoking treatment, it was apparently more cost-effective in the long run to risk having to pay for a few years of lung cancer treatment than to pay for the possible prevention.

Personally, I think that if the people making insurance decisions were not isolated from the people they are denying, they might make different decisions, if not from an empathetic point of view, then from a personal safety point of view <insert grin here>. “I’m out of <estrogen, Prozac, Paxil, Wellbutrin>, dammit, and I’ve got a gun!”

I am a published author in neuroscience. Your posts are simple minded and do not address the issues raised by others. If you do not understand how my post supports TVAA, then it merely suggests a serious lack of intelligence.

Yes. I know what synaptic plasticity is – the concept has been around for at least 30 years. I’m guessing that you’re still a student.

I am guessing that you are simply bragging. After all, aside from insults, such as suggesting a lack of intelligence on my part, you have nothing to offer. Not one citation, not one piece of evidence, just claims. You claim to be a published author in neuroscience, but completely ignore the references I posted. That raises serious doubts as to the accuracy of your claims. As does the fact that you consider careful phrasing as ‘compromising’. The attitude you display here is thoroughly unacademic.

You claim you know what synaptic plasticity is, but at the same time try to display receptor response as something fundamentally distinct from synaptic plasticity. Never mind the numerous publications on synaptic plasticity in the dopamine system. Nevermind the effects of long-term serotonin depletion on glutamate receptor subunits. Nevermind that norepinephrine, the role of which you specifically contrast with synaptic plasticity, has been cited precisely in the context of plasticity e.g. in J Neurochem 2002 Dec;83(5):1054-64.

It seems your arguments don’t quite hold up to the state of knowledge in the community. The fact that we have drugs to address specific receptors is totally uncontradictory to addressing synaptic plasticity.

I would suggest you swallow your insults and finally come up with some solid arguments -and most importantly, read the references you were given. Because until then, your claim of being a published author has little credibility. Not the least, I would suggest you actually read what I say, instead of just making arguments you claim refute me and then throwing insults when I say they don’t.

By the way: No, I am not ‘still a student’.

Of course the situation will only get better if serotonin levels are a problem. I was referring to addressing the specific problem in a given case.

Well, temporary and spatial gradients matter a lot in cellular signaling. Just ‘keeping it in circulation longer’ is worth a try, but is not a catch-all.

No, but they can be. And even if it alone doesn’t solve all the problems, it might enable our physiological system to solve the rest of the problems by itself, or with a little bit of further aid. Someone who fixes a broken leg for you doesn’t solve all the problems. But he sure as heck helps you, and enables you to lumber to the doctor on a crutch.

Sure. There are levels our body can handle, and there are levels it can’t handle. An overload of a specific signal can lead to the shutting down of a given signal pathway, as can deprivation of signals. That can be temporary or permanent, and it can be useful or harmful, depending on the circumstances.

And that’s precisely why I said such a treatment will never exist. You’d have to define what a cancer cell is vs. a healthy cell. By the time you’re 65, plenty of cells in your body will have some kind of genomic damage. That doesn’t necessarily mean they are cancerous, but that they can easily become cancerous, depending on where that damage is. As such, what is a healthy cell? One that has no damage whatsoever? One that only has slight damage? One that has no damage in checkpoint-relevant genes?

As for repairing the damage, while there are key genes frequently damaged in cancer, even a given tumor is frequently not a single entity. Repairing specific damage will only help with those cells that actually have it, not those having a different type.

Um, I just described one reason why it doesn’t work with some people. Cf. eg http://irweb.swmed.edu/newspub/newsdetl.asp?story_id=568

How many people who take ecstasy know they are seriously damaging their brain in a permanent fashion?

No, it isn’t. Not in any meaningful fashion. We’re not talking infecteous diseases.

That is precisely what I referred to when talking about yesterday’s medicine being practiced today. A while ago, we were at the same stage with cancer diagnosis. Yet today, we have molecular assays for numerous types of cancer, and more are constantly being developed.

Never said anything to the contrary.

Single patient results are hardly relevant on the global scale, as are biased researchers. And your arguments can easily be generalized for any and all clinical trials, not just in the mental field.

Question: How many women who don’t enjoy sex ‘enough’ were drugged against their explicit will?

Yes, it does happen. It also happens that people take out the wrong kidney. It also happens that people amputate the wrong leg. Sht happens, even when it should not. People get fired. Happens all the time. But even doing nothing would not prevent sht from happening. As such, I hardly see a sense in not helping those who can be helped just because sh*t occasionally happens.

The Zoloft website suggests Zoloft for depression, OCD, panic disorders and PTSD. I have seen numerous spots for Zoloft, and all I did was shrug. That despite the fact that there are numerous types of social situations I feel uncomfortable in. If your problem is that the public jumps at every advertisement and ‘needs to have it’, I think your beef is with the wrong people, and I think you would do better in curbing fundamentalism and conformism.

I have just returned from a stint in the US that took several years, at a major medical research institution. Yes, I have seen those spots over there, and no, I don’t see them over here, because advertisement for prescription drugs is (as of yet, with heavy lobbying going on) only allowed in medical journals. But while I consider that a good thing, seriously, I think your beef is with the wrong people. You’d probably do society a bigger favor by trying to combat gullibility, since the effect would reach far wider than mental health treatments.

I made no such claim, but rather I pointed out that there have been a variety of hypotheses over the years by others. I was discussing the history of confident pronouncements about the cause of depression. At the time that each hypothesis was new, i.e. the hot topic, researchers who were involved in the work truly felt that they were beginning to understand depression (and I prefer to stick to depression as an example), but the clinical results have been mixed – and sometimes very disappointing.

Hence, your enthusiasm for a few papers published within the last two years has nothing to do with the OP. There is a gap in the level of analysis of the problem; this year’s research papers rarely translate to effective clinical results and policies in the same year. Most doctors are not researchers, and wait for a long time before they adjust their practices.

Invariably, historically, the precious hypotheses have had many flaws when applied in individual clinical situations. They have to work in individual clinical situations or the work is of purely academic interest. My perspective is that hypotheses come and go out of fashion. If your point is that mood is related to chemistry, no one is arguing against that. If you are arguing that synapses change, no one is arguing against that.

Here’s what you did say:

That, sir, is the monoamine hypothesis, or some variant of it. You didn’t mention anything about the complexities of synaptic plasticity there did you? No, you stated that the simple “level of neurotransmitters” is what’s important. Your statement implies that you know which neurotransmitter levels make us feel certain emotions. Can you list the neurotransmitter levels that make us feel: anxious, afraid, friendly? Your statement was simplistic especially considering the research articles you yourself posted.

By the way, I used an insulting tone in my last post in order to mirror your own insulting and arrogant manner, and to provoke a response from you about it. But look at your previous posts and you will see that you began the ad hominems where you called AHunter3 a moron, and you continued in other subtle forms. If you don’t like insults, and I certainly don’t, then examine your own behavior and clean up your act.

You all might enjoy taking a look at Blaming the Brain by Elliot Valenstein. It’s a pretty balanced examination of the history of biological psychiatry.

Couldn’t get your link to work.

I think the bottom line of these debates lies in answering the question of: Where and What is Consciousness?

If an individual is considered mentally ill and out of control, medications seem to help. But don’t really, because when they are stopped the illness returns. All medication does is prevent the body from operating normally and at full capacity.

If consciousness is not a product of the brain, medication will never effect any cures. Although it may be helpful until a cure is found.

I believe that depression is easily cured when the cause is understood. We will have to look into the spiritual nature of man for our cures.

http://ndeweb.com/info01.htm

Too bad there’s no cure for being full of shit.:rolleyes:

I think psychotropic drugs in many situations are like a wheelchair. Most people would see a requirement to use as wheelchair as “confinement” as “confined to a wheelchair” and a terrible thing. On the other hand, a parapelegic might see a wheelchair as liberating since it enables the person to move about the world. Still, folks would consider it wrong to force a person to use a wheelchair when it’s not necessary, and if a person can be rehabilitated enough to not need a wheelchair that’s a good thing.

However, at this point in time, there is a contingent that is doing the equivalent of insisting on wheelchairs for people with broken legs when crutches would do, and making no effort to get folks out of the wheelchairs. Yes, the SSRI’s and others (including even such things as Thorazine for extreme cases of psychosis) are wonderful tools. But, on general principals, I think it is best if multiple approaches are considered, even tried, and that the best course is to use the lowest level of pharmaceuticals required to produce the desired benefit. If behavioral modification, “talking cures”, and other approaches reduce maladaptive patterns in a person, resulting in a lower dose of drug, that’s all to the good. But the people footing the bill find it ever so much easier to just hand out pills, and the pharceutical companies love it, and to heck with the ultimate good of the patient.

Very few - unfortunately. But even if they did, I’m not sure it would change the behavior. They are not, of course, looking for brain damage - they’re looking for the feeling they get from ecstasy, the emotional high. Many of the users are young, still in the stage where they feel immortal. By the time they learn otherwise the damage will already be done.

(It’s rather like some individuals I know who, when young, thought very little of falling off a motorcycle at high speed and breaking bones, but are now, in their 70’s, haunted by the long-term effects on bones and joints.)

This is one of the major differences between street drugs and licensed pharmaceuticals. Not only are street drugs of questionable purity and quality, but major side effects and damage are tolerated by dealer and user that would never be permitted in a therapeutic drug. And that’s assuming all parties are even aware of these problems, which often they are not.

Single patient results are not relevant in research but when you move to treating the general population the doctor deals with nothing BUT individuals.

Yes, my statement applies to ALL clinical trials. That does not make it irrelevant to the discussion here.

We’re getting off-track here, but —

I know from personal experience that doctors can have a very ridgid notion of what consitutues “normal” in the female reproductive system and can be quite agressive at medicating women to achieve that standard. (Possibly TMI: my cycle runs several days longer than “normal” and I’ve had at least a half dozen doctors in my life pressure me quite strongly to go on the Pill to “correct” this “problem” - it’s nothing pathological (in fact, a common trait in my family) and why the heck would I want to bleed every four weeks instead of every five? To be “normal”? Normality, at least in that sense, is highly overrated)

How many post-menopausal women were put on hormones for extended periods? One of the justifications used (in addition to supposedly stronger bones and protection against heart disease) was that it would keep a woman interested in sex and her vagina lubricating better – in other words, better able to serve a man’s desires. Nevermind that treating a woman with respect and love, and a tube of lubricant, will achieve the same effect with less potential for side effects. And cheaper, too. Just one more example of how our society would rather medicate the symptoms (lack of interest, vaginal dryness) with a pharmaceutical that has effects on the entire body rather than direct the solutions to the primary causes alone.

I do my part… but as the Straight Dope banner says about fighting ignornace, it’s taking longer than we thought.

I wish we could go back to that… I absolutely hate the direct-to-consumer advertising.

Well, I’m not quite sure how I got appointed to the position of “saving society” here, but in fact my company does try to educate people. It’s an uphill battle, though, because we just do not have the dollars of the big pharmaceutical companies and, of course, like everyone else, we are perceived to be biased. And when it comes to medicine you are often dealing with frightened, desparate people who are functioning more with emotions than intellect.