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.

We’ve all wished we could forget, at one stage or another. We wish we could forget trivial embarrassments: the time we texted a booty call to our mum by mistake, or the time we vomited chunks of mushroom and merlot in the shadows of the nearest alleyway. We wish we could forget the heartbreaks, the failures, the things that make us cry.

For a long time, these wishes were purely that: a flight of fancy. So much so that Eternal Sunshine won the Saturn Award for Best Science Fiction Film the year it was released. Targeted memory erasure is, after all, a ludicrous concept, and one destined to exist only in fantasy and film—or so we thought.

The Human Memory System

The main reason targeted memory erasure seems so implausible is because our memories are incredibly complex. Rather than being located in one specific area of the brain, the human memory uses a number of different neural structures, reflecting the different types of memories we have.

First of all, we have our short-term memory. This refers to our ability to hold information in our mind over a short space of time, usually only a matter of seconds. Although individuals differ in their capacity, we can, generally speaking, hold 7± 2 chunks of information (partially why telephone numbers are seven digits long). Rehearsing information in our short-term memory results in it being consolidated into our long-term memory, where it can then later be retrieved.

Long-term memory can be categorised according to ‘declarative’ and ‘non-declarative’ systems. Declarative memories are those which we are explicitly aware of and are able to articulate, and can be either episodic or semantic. Episodic memories catalogue our past experiences, and are typically associated with a specific time and place. Semantic memories, on the other hand, refer to our knowledge for generic facts. These memories lack the temporal and contextual component that characterise episodic memories, so although we all know that a light year is exactly 9,460,730,472,580.8 kilometres, we are unlikely to remember the precise moment when we learnt this.

Non-declarative memories, on the other hand, are more implicit in nature. They include physical skills, like riding a bike or doing sweet karate moves; spatial knowledge, like how to find your way around your house in the dark; and emotional associations, like how the smell of matches reminds you of birthdays.

The difficulty in erasing a specific memory is twofold. Firstly, sensory information is stored accordingly throughout the brain. Visual details are stored in our visual cortex, auditory details in our auditory cortex, and emotional details in the areas associated with emotional processing.

Memory storage is further fragmented because different types of memories are stored in different parts of the brain, and any specific memory we have will typically involve these different types. Let’s take, for instance, our memory of the time our big brother handcuffed us to a shopping trolley and then ran away, leaving us there for two hours before our mother found us sobbing in the dog food aisle, our pants a sodden mess. This memory is likely to involve not only episodic information, but also semantic information like the name of the supermarket (New World); emotional associations, such as how the smell of dog food now makes you weep; and spatial information, like the layout of the different aisles and the convoluted path we took as we tearfully searched for help.

Every time we retrieve that sordid ordeal from the recesses of our brain, the neurons associated with this memory are simultaneously activated and, as a result, strengthened. This is best summarised by Hebb’s rule that ‘cells that fire together, wire together’. Every time a memory is activated, the relationships between the neurons associated with it grow stronger, making it easier to remember. This is why repetition works: the more practice those specific neurons have at communicating with each other, the more efficiently they can be retrieved. This process—by which the associations between neurons are strengthened—is called long-term potentiation, and is integral to remembering.

Every time we retrieve a memory, we reconsolidate (or re-save) it. The neural activity involved in this process mirrors that initial process of consolidating information: after all, we’re basically re-running that process of transferring information from our short-term to our long-term memory. During reconsolidation, however, the memory being retrieved is temporarily vulnerable to modification. We tend to give specific details greater emphasis, for example—we’re more likely to remember the ugly dress your boyfriend’s bitchy ex was wearing than her inane comment about the sociology paper she’s doing. Over time, our memories are slowly re-edited. Details are lost while others are retained.

This process of reconsolidation is key to targeted memory erasure. If disrupted, our memories might not get properly re-saved. In some cases, they might not get re-saved at all. Although a number of neurochemicals are involved in the processes of long-term potentiation and reconsolidation, the two enzymes PKMζ and αCaMKII play a particularly important role in the retention of our long term memories, and hence have been the focus of research thus far.

Bypassing Memory Lane

Despite the staggering complexity of our memory system, targeted memory erasure is well on its way to becoming a reality. Studies have found that blocking either PKMζ or αCaMKII result in specific memories being erased, presumably because it disturbs the reconsolidation process. Researchers have, for example, developed a drug called ZIP that blocks the activity of PKMζ in the brain. In one study, rats were trained to press a lever in order to get a treat of cheese. Typically, once rats learn this behaviour, they don’t forget it. When a single dose of ZIP was administered during the execution of a lever press (and hence the process of reconsolidation), however, the response stopped. The specific memory (knowing that pressing the lever resulted in food) ceased to exist.

It isn’t just classically conditioned behaviours either. Studies have also erased rats’ memories for spatial information, including their ability to navigate their way through a maze while avoiding areas resulting in mild electric shocks. Thus, when ZIP was administered, the rats forgot their previously learnt knowledge of the space, and paid the price for it.

Taste memory has also been manipulated in aversion studies, where rats were given sugar water that elicited the symptoms of food poisoning. As you’d expect, they quickly learnt to avoid drinking said water. One dose of ZIP later, though, and they were lapping it up again, oblivious to the negative consequences of doing so.

Although ZIP has only been used on rats so far, scientists speculate that it will operate in a similar fashion in the human brain. Theoretically, then, if you administered ZIP while retrieving a specific memory, that memory could be erased forever. All those painful memories—the unnecessary fight you had with your boyfriend last week or the time you (accidentally) called out Anne Tolley’s name in the throes of passion—wouldn’t just be a thing of the past, they’d be gone forever.

Hello oblivion, goodbye shame?

The implications of these findings are huge. Drugs like ZIP could potentially serve as a ‘cure’ for psychological disorders like post-traumatic stress disorder (PTSD) or drug addictions. But although their potential benefits are clear, whether such memories should be erased is another question altogether. We remember for a reason. We remember because it helps us learn, adapt, and ultimately, to survive.

Sure, we can forget that the homeless guy who sleeps in Central Park once cornered you and demanded that you hand over your wallet. And sure, maybe then we’ll stop shaking in fear every time that odious stench of bourbon, sweat and pee wafts past us. But if we forget, we fail to learn. If we forget, we live in a state of perpetual ignorance. Erasing traumatic memories means that we’ll continue to strut obscenely down that seedy stretch of road screaming “I’m rich, bitch!” and we won’t be a better person for it.

Erasing traumatic memories may offer an instant reprieve, but it will also hinder the natural process of recovery. If we erase these memories, we stunt our personal development, and our perception and understanding of the world becomes severely skewed: terrible things become less terrible, shameful acts seem less shameful, and we deny accountability for our actions.

Perhaps most importantly, erasing our memories means erasing a part of who we are, not just as individuals, but society as a whole. Our memories shape who we have become, without them we are vacuous vessels. Santayana’s observation that those who do not remember the past are doomed to repeat it springs to mind: what if, for instance, we erased everybody’s memories of the Holocaust?

Likewise, erasing the physical and psychological aspects of addiction sounds great—in theory. On the one hand, it has all the makings of an idyllic, addiction-free society. On the other hand, we become addicted for a reason. Providing the means through which addictions can be easily overcome may simply encourage greater experimentation, and an increased proclivity towards addictive behaviour.

Of course, many argue that the benefits of forgetting outweigh the costs. Walter Glannon at the University of Calgary maintains that “When a condition is intractable to other interventions, when it severely affects one’s quality of life, and when it poses a significant risk of harm to oneself and to others, considerations of immediate efficacy can override considerations of long-term safety.” The man has a point. PTSD can stem from horrific experiences like the time your dad made you bomb a small village in the South Island. The symptoms—which include flashbacks, nightmares, and depression—impact greatly on your ability to function in daily life. Nevertheless, rather than searching for a quick fix, emphasis should be placed more on addressing the actual experiences causing it. PTSD develops for a reason, and those reasons aren’t necessarily unavoidable.

Remembering the Past: Ro15-4513

The development of Ro15-4513 in 1984 raised similar ethical questions. Initially developed as an antidote to alcohol overdoses, commercialisation of Ro15-4513 was halted due to the legal issues surrounding its effects. Just as ZIP blocks the effect of PKMζ, Ro15-4513 was found to block the effect of ethanol without removing it from the bloodstream. In other words, you could knock back an entire bottle of whisky, do a little dance, realise you have a test in an hour, administer a dose of Ro15-4513 and sit your test sober (but fail because you didn’t actually study). The implications of this drug were concerning to say the least, largely due to its short half-life. Multiple doses were necessary for patients who were significantly intoxicated because the drug would wear off before the alcohol had metabolised in the body. There was, as a result, the possibility of a false sobriety. If alcohol was still being metabolised when the drug wore off, individuals would become incredibly drunk again, possibly resulting in serious accidents (like passing out on the motorway and plummeting to your death).

It’s not all bad though. One of the implications of ZIP is that it offers a starting point to develop a drug that enhances, rather than blocks, the activity of PKMζ or αCaMKII. If this is the case, the progression of neurodegenerative disorders that affect memory, like Alzheimer’s, could be slowed down. Of course, even the development of a drug like this poses a number of ethical issues: How much is too much?

A Possible Future Which Owes Naught to Memory

Picture this: The year is 2093. A new drug has been released into the market, aptly named ZIP. In townhouses all over the world, parents zealously crush up these pills on their Formica tabletops before sprinkling them carefully onto their kid’s cornflakes. They then wait impatiently, fervently hoping that their baby will become the next Stephen Hawking or Charles Xavier, minus the wheelchair.

Universities are swarming with lazy students who pop a couple ZIP at the beginning of their day. Cramming time is cut in half while drinking time triples. Weary lecturers keep jars of ZIP by their journals, their eyes darting suspiciously around as their shaky hands reach for yet another hit.

Meanwhile, in the back alleys of New York, a sweaty horse of a man clutches a handful of UnZIP as he waddles back to his loft. There, he greets his love. She stares back at him with muted eyes, her mumbling stifled behind the dirty rag tied roughly around her ashen cheeks. She squirms desperately in her chair as he descends upon her, but can do nothing as he crams the UnZIP down her throat. She whimpers as the memories of her captor melt away.

In a prison cell, a man grimly brings a bottle of UnZIP to his lips as he mentally relives the vicious stabbing of his son and his wife. Across the way, a rakish young lad shakes his head. “Has it come to this?” he asks.

The man gulps down a fistful of regret. “Yes.” He mutters hoarsely. “Yes, it has.”

Or not.

This is, of course, a future way beyond our grasp. Despite all the research, we still don’t know that much about the human brain, let alone our memory system. Although PKMζ and αCaMKII play a significant role in the retention of our memories, they’re not the only neurochemicals involved in this process, and the reality of targeted memory exposure is still a far way off. Indeed, Larry Squire, one of the leading researchers in the field of memory, warns that “It’s likely that any effects are reversible, temporary. You may be able to bring up a memory, weaken it, but eventually the memory comes back. The effect is more like interference than real change.”

The possibility of such a process is, however, there nonetheless, lurking in the shadows and sparkling in the sky. Be warned. Be prepared. And remember.

This article was first published in Craccum in 2009. Many, many thanks to Rosabel for her persmission to reprint this article. And thanks to Matt too. You guys rule.

The ASPAs are the biggest event on the student media calendar. Usual attire for student journalists include t-shirts boasting internet memes, jeans, hoodies, and generic sneakers. The ASPAs, however, call for something a little more formal.

“We made the dress standard this year ‘cocktail’, but I had a lot of people asking me what that meant,” said event organiser and fashion commentator Laura McQuillan. “I told them to wear what they’d wear to dinner with John Key.” Some took heed of Ms McQuillan’s advice. Others should never have dinner with John Key.

As the student media’s answer to the Oscars, the awards constitute only a small part of the evening. The Student Pants Association (SPA) were therefore out in full force, with two-time award-winning student journalist Sarah Robson and pancake enthusiast Rosabel Tan there to judge the fashion highs and lows.

In these recessionary times, looking like you got a lot of bling bling for not much ching ching is imperative. Several attendees sported dresses purchased from op-shops and vintage stores, but the Recessionista of the night was Salient arts editor Fiona McNamara. Robson commented that McNamara’s dress, which cost a minimal $6, “was beautifully offset by her spray-painted silver shoes.”

Also verring dangerously close to ‘frugal’ was the winner of the Best Accessory Award, Michael Oliver. Salient’s news editor sported a fluorescent green and orange plastic pipe which blew bubbles. “The pipe was a representation of my individuality and my love of personal freedom,” Oliver explained. Tan described his pipe—purchased from the $2 shop especially for the awards—as “setting off his otherwise stern outfit, hinting towards a playful lad under all that serious business.”

The highly sought-after Woody Allen Memorial Award went to Craccum’s Film Editor, Hugh Lilly. Lilly teamed skinny black jeans with a light blue t-shirt and a black pinstriped blazer, creating an understated, indie-cool vibe that complemented his thick-framed glasses and perfectly coiffed hair. Both Robson and Tan noted that he was the only attendee who was able to pull off the ‘t-shirt’ look at this high-class event.

The You-Could-Have-Done-Better-And-Had-The-Girls-Swooning Award went to Newsboy. After a good show at the ASPA Conference, expectations were high, but he failed to deliver on the fashion front. The judges reported feeling “quietly disappointed.”

Hairstyles are frequently overlooked when it comes to planning one’s outfit. However, the clear winner for The Most Super Sayian Use of Hair Product was Laura McQuillan. Her blonde locks defied gravity and provided attendees with a distraction from Barry Soper’s needless ranting. “I was hoping she would vanquish him with a ki blast,” Tan reported. “But then he might have fed her to the Rancor.”

For the most part, the judges were impressed with the editors’ fashion sense. Competition was immensely tough, and double first-equal placings were awarded. In the Best Dressed Editor (male) category, first equal was Jackson James Wood of Salient and Jon Andrew of Canta. An impressed Robson said of Wood,“He usually wears a hoodie and checkered vans.” He also sported a skinny black tie that his girlfirend had perfectly knotted. Both judges were impressed with Andrew’s neatly trimmed facial hair, a rarity in student media circles.

Best Dressed Editor (female) was awarded to Analiese Jackson of Satellite and Stacey Knott of InUnison. When questioned on the fact that they awarded the only two female editors first place, Robson and Tan declined to comment, muttering something about a booby prize.

Certain trends were also evident during the evening. For males, scruffiness seemed to be a recurring look, as was unkempt facial hair. Many also sported shoes from Number One Shoe Warehouse, which seems to be gaining momentum as more and more student journalists endorse their brand. Females seemed to enjoy looking pretty, and many wore strapless dresses, including Robson and Tan.

As modest beings, Robson and Tan thought it only fitting to award themselves a prize. The award for Retaining-the-ability-to-dress-well-despite-hanging-out-with-boys-who-taunt-and-mock-them-on-a-daily-basis was well-deserved by both, for their impeccable ability to coordinate outfits and simultaneously put up with inappropriate jokes.