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July 12, 2010 | by  | in Features |
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She’s Got the No Pussy Blues

When Viagra was introduced to the mass market in 1998, it changed the way people thought about sex. Flagging male libido no longer posed a barrier to gettin’ down and dirty—all it took was one little blue pill and hello sailor, no more cold lonely nights half-heartedly watching Sky One porn. Twelve years on, and German drug company Boehringer-Ingelheim claim to have developed its female equivalent: flibanserin, the first drug to specifically target low sex drive in females, or what is clinically referred to as hypoactive sexual desire disorder.

So, what, it’s a pill to treat frigidity?

Not quite. To be diagnosed with hypoactive sexual desire disorder, an individual must satisfy the following criteria as outlined in the Diagnostic and Statistical Manual of Mental Disorders IV:
1. Persistently or recurrently deficient (or absent) sexual fantasies and desire for sexual activity. The judgement of deficiency or absence is made by the clinician, taking into account factors that affect sexual functioning, such as age and the context of the person’s life.
2. The disturbance causes marked distress or interpersonal difficulty.
3. The sexual dysfunction is not better accounted for by another Axis 1 disorder (except another sexual dysfunction) and is not due exclusively to the direct physiological effects of a substance (e.g. a drug of abuse, a medication) or a general medical condition.
The emphasis here is that a lack of sexual desire in itself doesn’t warrant a diagnosis; the individual has to be significantly distressed by their low libido as well.

Maybe She’s Just Not That Into You

The etiology of hypoactive sexual desire disorder varies depending on whether it’s life-long or acquired, as well as whether it’s situational or generalised. Broadly speaking, however, sexual response (and thus dysfunction) involves an interaction between biological factors, the physiological mechanisms involved in sexual response; psychological factors, the affective and cognitive processes that sustain that response; and relational factors, interactions promoting intimacy and mutually satisfying experiences.

Drugs for sexual dysfunction address the biological processes involved in sexual arousal, but sex differences make it harder to target females. For males, the physiological basis of arousal is an erection: the arteries of the penis open, causing pressurised blood to rush into the corpus cavernosa, a spongy tissue running the length of the organ. At the same time, the veins leading out of the penis constrict, trapping the pressurised blood and thus elongating and stiffening the penis. Drugs like Viagra simply facilitate this process by increasing blood flow.

For females, sexual dysfunction is more difficult to diagnose. Physiological indicators of sexual arousal for females are diverse, and include vaginal lubrication, increased blood flow to the vulva, and the enlargement and erection of the clitoris. However, whereas men typically experience sexual desire in association with an erection, there is little evidence for a correlation between genital response and women’s subjective experience of arousal. Because of this, flibanserin doesn’t target any of these specific physical processes. Instead, it takes two steps back and targets the neurochemical processes involved in sexual arousal.

The Sexual Chemistry of the Brain

The classic linear model of sexual response involves four phases: desire, arousal, orgasm and resolution. At each stage, interactions between certain neurotransmitters and hormones play an integral and complex role, primarily in the hypothalamic and limbic systems of the brain. Sexual arousal results from an interaction between the excitatory and inhibitory sexual neural systems. Both systems are evolutionary and fundamentally adaptive: the former, allowing individuals to seek out sexual partners and reproduce; the latter, allowing individuals to minimise engagement in sexual behaviours that could potentially result in negative outcomes (having sex with the wart-ridden homeless man who lives outside Pak’n’Save), or to allow for a post-ejaculatory refractory period during which sperm can be generated for subsequent ejaculations (for better baby-making results). Arousal results from either direct activation of the excitatory system, or through suppression of the inhibitory system, or a combination of both.

The Excitatory System

The excitatory system is integral to the first three phases of sexual response, and the neurotransmitter dopamine plays the most significant role in modulating sexual desire. Studies have found that increased dopamine levels enhance the subjective sense of excitement associated with, and the motivation to engage in, activity geared towards attaining sexual rewards. Other key neurochemicals involved in the sexual excitatory system are norepinephrine, which plays a vital role in general arousal, and the sex hormones testosterone, estrogen, and progesterone.

The Inhibitory System

The mechanisms of sexual inhibition are typically exhibited post-orgasm, but can also be activated by situational variables such as stress, psychological processes such as specific thought processes, or through drugs operating on relevant neurochemicals. Activation of this system is characterised by shifting or minimising attention away from sexual incentives as well as inhibiting sexual responses where these incentives are attended to. So, for example, your 3am drunk self may feel that sleeping with your ex-boyfriend is a great idea, but thankfully the memories of him cheating on you come flooding back as you’re unbuttoning his shirt, and before he can prematurely ejaculate as per usual, you’re tripping over yourself to get the fuck out of there.

Opioids play a key role in this system by mediating sexual reward states. To take (not literally) a synthetic example, opiates like heroin produce a huge rush of euphoria, followed by a prolonged period of relaxation. Induction of this state is associated with a dramatic decline in sexual arousal and an inability to orgasm (if you get that far into the piece). So, you know, if you ever wanted to know what heroin feels like, it feels like a three-hour orgasm. Or something. High levels of opioids in the brain therefore reduce your motivation to seek out further sexual rewards, since you already feel awesome.

Endicannabinoids also play a role, inducing sedation. You become less responsive to stress-provoking stimuli, and experience a general sense of sleepiness. Yes, as if you just smoked a fat joint or, you know, violently came. Finally, serotonin promotes feelings of satiation, muscular relaxation, and a general sense of well-being. In other words, when the inhibitory system is activated, you feel pretty good and have no reason to seek further pleasure.

WANT TO WANT? TRY FLIBANSERIN OR YOUR MONEY BACK GUARANTEED!*

Flibanserin enhances sexual desire by increasing dopamine and norepinephrine levels (activating the excitatory system) and reducing serotonin levels (suppressing the inhibitory system). In support of its efficacy, a 24-week long clinical trial of the drug last year reported an increase in sexual desire, as well as what they termed “sexually satisfying events” from 2.8 to 4.5 per month, compared to 2.7 to 3.7 per month for those given a placebo.

*Money back not guaranteed

Despite these results, the Food and Drug Administration voted ten to one late last month against the approval of the drug, based on conclusions that it wasn’t significantly better than a placebo, and that the benefits of the drug failed to outweigh its side effects. These include dizziness, nausea, fatigue and insomnia. The panel did, however, acknowledge its potential benefits and encouraged the company to continue researching and developing the drug.

Sex sells sex sells sex sells sex

The drug in itself has a lot of potential, sure, but as with any company, Boeringer-Ingelheim’s ultimate aim is to turn a profit, and this involves pushing their product into as many eager mouths as possible. David Fitzhenry and Leslie Sandberg, in their overview of female sexual dysfunction in Nature in 2005, predicted that the market value of a successful drug treating female sexual dysfunction “could exceed US$4 billion in the US alone, with only 15 per cent of patients captured on therapy”. That’s a lot of super yachts. Or 114 trips to the moon if you book through Space Adventures (www.spaceadventures.com).

The attempted introduction of the drug into the market has raised eyebrows and sparked widespread debate, largely due to the company’s pre-emptive marketing campaign: this included a Discovery Channel documentary educating the public about hypoactive sexual desire disorder (though critics argue that reported prevalence rates—estimated to be around 1 in 10 for females—are exaggerated, and many prevalence studies have been funded by none other than Boehringer-Ingelheim), which in itself could create or enhance insecurities among women about their libido, inducing distress, the second diagnostic criteria of the disorder. A publicity tour was also launched starring the one and only Lisa Rinner, former Playboy model and actress on Days of Our Lives and Melrose Place (though embarrassingly, I recognise her only as ‘Logan’s mum on Veronica Mars’).

Classes for practising clinicians were also implemented: in one session, clinicians were given a case study describing a 42-year-old working mother who has to take care of her three children as well as her sick mother, and who no longer has any desire for sex. The diagnosis? Potential hypoactive sexual desire disorder. Obviously.

Leonore Tiefer, associate professor of psychiatry at New York University, expresses her concerns about the implications of introducing and marketing a drug like Flibanserin: “The much larger group of women without any medical reason for their sexual distress will inevitably be misinformed and misled into thinking that there is a pill that can get them the sex life they read about, the one they think everyone else is having.” Annemarie Jutel, associate professor of medical sociology at Otago Polytechnic, agrees: “On the one hand consumer culture is based on perpetuating feelings of sexual inadequacy; on the other, the industry has recognised an opportunity for exploitation, and has designed and presented a remedy: also for sale.”

Finger-Pointing Part Deux

Ultimately, you have to look beyond Boehringer-Ingelheim: they’ve invested into the development of this drug because there’s a genuine market for it. Societal attitudes now dictate that hypersexuality is the norm. Not wanting sex is not normal, and the medicalisation of low libido, Jutel comments, “reinforces an inadequately challenged combination of assumptions and observations about sexual function which consequently serve as a basis for commercial exploitation”.

Pathologisation of female sexuality—in what is arguably an attempt to control and moderate it—is in no way new; the direction has simply changed. In 1873, Edward Clarke, Professor of Psychiatry at Harvard, declared that women should not be able to pursue an academic life beyond secondary education, because it would shunt blood from their uterus to their brain, making them depressed, infertile and irritable. During this same period, French neurologist Jean-Martin Charcot concluded that most mental disease in females resulted from abnormalities or over-excitation of their genitalia. Masturbation was believed to be the cause of a whole host of psychological disorders, ranging from insomnia and exhaustion to epilepsy, depression, paralysis and insanity. Cliterodetomies were introduced as a cure for these ailments, and the acclaimed surgeon Isaac Baker Brown, whose practices led to the death of his career—although alarmingly not due to disapproval of his practice but reportedly jealousy over his commercial success—wrote about a series of clitoridectomies he had conducted, which successfully “cured” everything from one woman’s desire to divorce her husband, to treating a 20-year-old woman’s proclivity for sending visiting cards to men she liked and spending too much time in serious reading.

We’ve come a long way, true, but have we gone too far?

Societal attitudes towards female sexuality have since flung itself squarely into liberation, or so we like to think. But beneath the medicalisation of sexual desire lurk more sinister undertones. The diagnostic criteria for hypoactive sexual desire disorder is in itself problematic, since the necessary experience of distress is ultimately dependent on societal constructions of normative sexual behaviour. While laden with good intentions, pathologising low sex drive as a psychological disorder inadvertently perpetuates a norm of hypersexuality: You gotta want to fuck, now and always, else you’ve got a problem.

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