Vallium and zen

zenI’ve started meditating. I spend approximately 1/5th of my adult life starting meditating. Hopefully one of these days it’ll stick.

I first started when I was a teenager, mum had a ‘teach yourself yoga’ book which lay about the house. I picked it up, started doing the occasional asana on the days I was off school / the days I couldn’t be bothered to go into school (by my mid teens these were many). On the occasions I bother to look, I’ve got fond memories of dipping into that tatty book, hidden inside in the autumn and winter sun, hiding from school.

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I was born in 1981.
I’m now 33.
A lot has changed in those 33 years.

So I’m taking these at the moment.
PEP medication
For all the Matrix like excitement of taking a red pill and a blue pill, they’re actually fairly boring. Tales abound about how you’ll be laid out for weeks with symptoms akin to a persistent norovirus, or flu, or foul food poisoning. Alas, for me at least, they’re not even that exciting.

I get a bit nauseous the first few days. Then again, they give you anti-nausea pills, too. So I’m sorted.

I’m told they’re very powerful drugs but then, they tell me the mood stabilisers and antidepressants are also very powerful drugs. Frankly, unless I’m tripping balls within half an hour of swallowing them I have difficulty believing that claim.

They do clever and intricate things to do with DNA replication and integration. For all their apparent innocence, they are both absolute, undisputed marvels of 20th and 21st century biology, biotechnology, pharmacology and medical research.

They’re anti HIV pills.

I don’t even think I have HIV.


PEP, for those of you who don’t know, stands for Post Exposure Prophylaxis. They’re handed out after suspected HIV exposure and consist of standard anti HIV medication – the exact drugs vary depending on what other medication you’re taking and any pre-existing conditions. The idea is to slam the virus down before it takes hold, before it inserts itself into your own DNA and becomes a permanent resident within your immune system.

Treatments for HIV these days are, like I say, a marvel of modern medical research. HIV first came to attention around the time I was born; now, in my thirties, an individual living with HIV can generally expect a normal lifespan. There are exceptions, and there is variability in response; but from talking to most (heterosexual) people, the impression I get is that their perception of HIV is over fifteen years out of date. For many in the UK the tombstone adverts of the ’80s still loom large in their minds. Most, let’s be fair, never think of it at all.

HIV never went away. It just became old news, and old news is no news. But in the gay community, such as it is, it remains; a permanent resident. For gay men in London, if you’ve had unprotected sex with anyone at all whose status you’re unaware of, then you’re usually offered PEP. You’re presumed to have been exposed.


Sexual health counsellors are amazing.

OK, I only saw one, the one time, but she was amazing. Half her hair cropped tight, the other half waved wild, streaked green; torn jeans and flannel shirt and big, big boots.

She laughed lots.

“It’s your choice. You’re a smart guy; you know exactly the risks you’re taking. Even when you go out, get pissed, get high, you know the risks you will take. You keep on like this, you probably will get HIV.

“Your call”

Ever since 2008, my libido’s been fucked. And really, honestly, I don’t know why any more. Maybe the psychiatric meds. Maybe the depression. Maybe my own neurosis about sex, built up during the episode and now difficult to tear down again; am I any good, will they be disappointed, will they think I’m too fat, too thin, too boring, too kinky? Rejection hurts, it’s easier to say no. Or ensure no one ever even asks.

Unless I’m wasted.

When you’re wasted, everything’s easy, except thinking and talking and life. But pleasure, but desire, but lust… these things are easy. And when you’re wasted, who cares about the rest?

Fucking is easy when you’re wasted.

Lust is fierce when you’re wasted.

Who wants to use condoms, when you’re wasted?

I only have sex when I’m wasted.


Amongst gay men, there’s a degree of prejudice around barebacking (sex without a condom). To a degree, this is understandable; the safer sex message was naturally targeted intensely at our community, and of course there are those who remember the decimation of the ’80s. For a long while, the message was condoms or not at all. This prejudice is unfortunate, because gay guys – an increasing number of gay guys – bareback. We do it for many, often complex reasons. Often it’s just the one time; we’re drunk, we’re high. We always use condoms but we might slip up. Or maybe we’re with a partner and we both last tested negative. Or maybe we only fuck when high or otherwise disinhibited, meaning we never, or rarely, use protection. Or maybe, maybe just fuck it, because sex without condoms just feels better, and we’re fucking horny, and it’s fucking horny, fucking like that, cumming like that.

Turning around to that vast, varied swathe and saying, “what’s wrong with condoms” – well we’ve been doing that for decades, and still we have HIV, inserted into our lives. It’s as absurd as telling people to ‘just say no’ to drugs. It’s tone deaf, idealistic to the point of idiocy, and presumes a perfect, predictable world. Sorry sugar – the world isn’t like that. People aren’t like that.

The messages of moral superiority, ‘just say no’, that barebacking is stupid, hurts. It hurts the individuals who do it, and it hurts the community it’s supposedly aimed at protecting. It results in the people who bareback  – for whatever reason – not talking about it, not understanding the options now available, picking up hearsay and horror stories about the medications available. It plays a part in fuelling anti HIV prejudice, which is still all to prevalent not only in the wider world but in our community. You’d think that we of all people would understand that this never solves anything; that communication is better than silence, understanding better than judgement.

Your call.

The promise of lust

Partial list of side effects from citalopram information sheet I don’t know exactly when it shifted, and I definitely don’t know why. I tend to put a definite cut off around 2008, since the 2008-09 episode was so profound, lasted so long, and smothered me; like sleep, under morphine.

At first I blamed the drugs. That was comforting and easy, because after all a side effect of SSRIs is loss of libido. It also held out the promise that once I was off the drugs, I’d be up and running again. I was willing to put up with a flatlining sex drive for a while, for the relief the antidepressants gave me. They were only temporary, after all.

And then I came off the drugs, and I looked forward to the promise of torrential lust. Being young and gay in London with no strong desire for sex is… frustrating. I wanted that part of my life back. So I waited, and I waited, and it never came.

Oh sure, I could get drunk and horny. But that’s missing the point, isn’t it? Drunken lust is clumsy, grasping and loose. Temporary, and soon forgotten. Being young and gay in London with no strong desire for sex is more than a little alienating.

I still blamed the drugs, or maybe I blamed the depression, or both. Blamed some kind of permanent rewiring of the circuits of sexual desire. Maybe they’d burned out? Maybe they’d atrophied? We live in a culture saturated by sex – gay subcultures especially are sodden with it. But for all that, we seem to have little real regard for it. For most of us, sex is important, beyond hedonism and lust and beyond even passion. It’s important for contact, for happiness. For relationships and belonging and feeling a broad and deep range of emotion, sensation.

And I wasn’t getting any.


“Loss of libido” is thrown away in the patient information sheet which details side effects of SSRIs, alongside “failure to reach / maintain an erection (in men)”* and “Anorgasmia (failure to reach orgasm)”. I guess in the grand scheme of things, these aren’t profoundly worrying side effects – the other drug I’m on, lamotrigine, lists Stevens-Johnson syndrome (a potentially fatal loss of skin) and disseminated intravascular coagulation (DIC, AKA Death Is Coming) as it’s potential side effects. Yes, I’d rather have no sex drive and shit orgasms than die horribly from my skin sloughing from my body. Still. Hardly a fair comparison.

Sex is important. And when you’re prone to depression, not having a full – or any – sex life, and thus no romantic life, is dangerous. It denies you a source of pleasure, emotional soil in which to grip your roots to the world. “Protective factors”, in the dry but honest language of a psychiatric consultation. The fewer roots you have the more likely you are to wither. The easier it becomes to simply take the hand you’ve been dealt, and fold.

Sex is important. I really, really don’t think the wider psychiatric community appreciate just how important it is, largely oblivious to how antidepressants can deeply wound a life.


Of course, I’m human, and humans excel at making simple things complicated. Maybe the depression led to a plummeting libido. Maybe SSRIs turned down too many switches inside my head. But people are more complicated than just brains. After so long without a shag, the whole issue takes a life of it’s own, entwining with sexual confidence and body confidence, until it becomes impossible to know if you’re not having sex because you don’t want to, or because you’re afraid to.

I hope this problem is nice and simple and neurological. I hope my bottomed out libido can be blamed on a zapped out reward pathway, or a scrambled endocrine system, or anything other than high level psychology. Because if it’s up to psychology, I really can’t see it being resolved any time soon. Sex is important. Without it I don’t meet guys, I don’t date. I must be the only gay man in London who has never met anyone off Grindr. Seriously. My last online hookup was in 2008. This. Is getting. Tiring.


“Would you be open to a mood stabiliser?” The psychiatrist asks.

I’ve been rumbled. They want to take the hypomania from me.

“Which one?” I ask. They know I study neuroscience. It’s in the file. An awful lot is in the file.

“Lamotrigine”

I’ve heard of it, but beyond it being a mood stabiliser I know nothing. I don’t want the sluggishness that can come with some psychiatric meds (paroxetine destroyed me with sleep; and I’ve seen the effects of olanzapine – an antipsychotic – second hand). Will it place a final nail in the coffin of my libido? I’m wary. I want to know it’s mode of action, I want to know if…

“Like I say; I think the SSRIs work because they make me slightly hypomanic. If you take that away… What’s left?”

He reassures me; “just a trial”

It’s ultimately up to me. Naturally I go online and look up the mode of action (voltage gated sodium channel blocker, calcium channel blocker, glutamate modulator). I look up personal experiences.

Rise in libido.

Not everyone, not all the time. And sometimes the reverse – maybe it could be the final nail in the coffin. And sometimes the rise is due to activation of mania, sometimes fades after a few weeks. Still. It hangs there, glowing on my iPad screen. The promise of lust. Rise in libido.

I say yes.

I take the pill.


*Seriously, this is how it’s phrased. I love the fact they felt the need to specify.

Ring the alarm!

My twitter feed has been somewhat abuzz today with this story about the ‘discovery’ of the chemical responsible for depression and anxiety, dubbed the ‘misery molecule’ by various sections of the press and reported on in a confused and hard-to-follow manner, with the main take home message being ‘more drugs (maybe)’.

First things first – I know this may come as a shock to many of you, but the reporting of this in the media is overblown and misguided. The headline from the Independent serves as a good guide to the misunderstandings present in the reporting of this story:

Scientists discover the molecule responsible for causing feelings of depression 

From this you might surmise that a new molecule has been discovered, and that it is responsible for causing feelings of depression; the implication of the rest of the article is that this molecule has a role to play in pathological depression. Lest you think I’m being too harsh (journalists aren’t responsible for headlines, after all), the body of the article contains the sentence

…scientists have now discovered that the protein receptor CRF1 is responsible for releasing hormones which can cause anxiety and depression over extended periods of time

Similar stories have cropped up in the Times, the Daily Mail, and various other news sources (notably, the reporting in the Financial Times was much better).

Unfortunately for these stories, this is not a previously unknown molecule, and it’s role in either feelings of depression or depressive disorder is  complicated and uncertain.

Human experience, complex emotions and mental health not reducible to a single molecule – surprise!

What has been discovered is the structure of the molecule – this gives us a better chance at figuring out how it works and makes designing drugs which work on it easier. The molecule in question is called CRF1, and it’s a receptor – it sits on the surface of cells and transmits information from outside the cell to inside it. Even on a very reductionist understanding, it is not responsible for feelings of depression, any more than your tongue is responsible for the taste of sugar.

CRF1 is part of a pathway called the Hypothalamic Pituitary Adrenal (HPA) axis. The interaction of all the bits and pieces of this pathway are involved in the ‘stress’ response; it’s a good example of how the brain and rest of the body work together, and it’s a pathway which is often found to be disrupted not only in people with depression, but also in those with psychosis. It involves – as you might expect – the hypothalamus, the pituitary, and the adrenal glands.

The hypothalamus is a small structure which sits deep in your brain and is a kind of ‘master switch’ for all the body’s hormones – long-distance messengers which diffuse signals throughout the body. One of the hormones controlled by the hypothalamus is cortisol, although this being biology nothing is simple; cortisol is not released by the hypothalamus, or even by the brain, but by the adrenal glands which sit atop the kidneys. The hypothalamus itself, while it acts as a master switch, gets it’s neighbour – the pituitary – to do most of the heavy lifting.

Various other parts of the brain, notably the amygdala and the hippocampus, send signals to the hypothalamus which provide information about any potential threats. If it gets such a signal, the hypothalamus releases a chemical messenger known as Corticotrophin Releasing Factor (CRF), which tells the pituitary to release a further messenger, Adrenocorticotropin Releasing Hormone (ACTH), into the bloodstream. ACTH acts on receptors on the adrenal cortices – remember these are the glands which sit on top of the kidneys, and which release cortisol in response to ACTH. Cortisol goes on to have many, many effects on various tissues throughout the body, effects which are mediated through a couple of receptors called the Glucocorticoid Receptor (GR) and the Mineraloreceptor (MR).

You might think this is a roundabout way of doing things (and you’d be right), but each additional step allows for modulation and modification of the signal – in biology, more steps make for a better dance.

So – what’s this all got to do with depression? Well, being constantly stressed all the time isn’t nice, and nor is it good for the brain – cortisol is great for adding a boost to the engine, but you’d soon wear the machine out if the boost was constantly applied. To prevent this from happening, neurons in both the hypothalamus and the pituitary express glucocorticoid receptors; when cortisol acts on these receptors, the activity of the HPA axis is inhibited. This ensures the cortisol alarm is short lived – so long as the receptors on the hypothalamus and pituitary are doing their job.

As you might have guessed, in at least some types of depression this feedback loop fails. There are good reasons for thinking that when this system malfunctions, it’s the glucocorticoid receptors which are the weak link in the chain, and this leads to abnormally long ‘recovery times’ after stress exposure. It’s as if, when it comes to the racket made by the cortisol alarm, your brain is a little bit deaf. The alarm keeps on going on, and on, and on.

Worse, the cortisol alarm actually seems to damage cells in the hippocampus, leading to lower hippocampal volume in some depressed patients. The hippocampus is best known for its role in memory formation but, as I say, it also sends input to the hypothalamus. The nature of this input is inhibitory – that is, it helps turn down the alarm (the amygdala, meanwhile, helps turn it up – which makes sense when you think about the amygdala’s role in fear and anxiety). Of course, if pathologically raised levels of cortisol are damaging the hippocampus, that could well damage its ability to turn down the alarm. As the amygdala doesn’t appear to experience any such damage, you end up with a circuit which is easy to turn on and easily turned up, but resists being turned down or off. Can you imagine a car alarm like that?!

(As an aside, memory problems are a known symptom of major depressive disorder, and it’s extraordinarily tempting to link the lower hippocampal volume seen in depressed individuals with these memory problems; it’s certainly not going to help, but just as there’s more to mood than molecules, there’s more to memory than the hippocampus; depressed individuals also have problems with attention and concentration, both of which could conceivably lead to problems with memory via a different route).

What are the wider effects of this raised alarm? That is a trickier question to answer; the safest response is that there is an association between disrupted cortisol regulation and some (but not all) forms of depression. Current antidepressants do not act directly on the HPA axis, although successful treatment with them seems to have beneficial effects on both the cortisol response and hippocampal volume (we really don’t know much about their mechanisms of action at all, either on the HPA axis or on the brain more generally – a post for another time, perhaps).  Wouldn’t it be great if we could design some drugs which could turn off this runaway alarm directly, and so maybe resolve depression?

And here, at last, we get to the point of this paper. The receptor CRF1 is found on cells of the pituitary gland; they respond to the first ‘go’ signal from the hypothalamus, the chemical messenger CRF (CRF binds to CRF1, see?). Knowing the structure of this receptor makes it a lot easier to design drugs that can inhibit it’s function, working to turn down the alarm. The reasoning goes lower HPA axis activity, a miracle happens, then no depression.

As you can see, it’s a theory that needs a bit of work. But hey – you never know until you try.

Mirtazapine, intense as in

Peaches! It's a visual metaphor, maybe.So last week I asked for my prescription to be changed.

I’ve been on citalopram for about a year now – it’s is a common-or-garden antidepressant which has a very similar cellular action to Prozac – they’re both what you may or may not know as ‘selective serotonin reuptake inhibitors’ (SSRIs). I won’t go into the nuances of SSRI treatment here, save to say they work to an extent, and for some people more than others. I’m fortunate – citalopram seems to work very, very well with me. So why change?

Side effects.

The side effects of SSRIs are usually not too bad – the worst I’ve ever had, or seen anyone have, is an immense tiredness, which can be enough to lead people to quit. But the tiredness I experience on citalopram isn’t anything troubling to me; I need an afternoon nap and that’s pretty much it. Given how profound and dangerous the depths of my depression can be, a few piddling side effects really aren’t worth worrying over, not in the heat of the moment (or, rather, the depths of the dark).

After a while tho, when all is sunny and well, what had been niggling side effects take on a change in character; specifically, the rock-bottom libido I’ve lived with for a few years now, notwithstanding alcohol inebriation. SSRIs are known to sometimes muck about with sex drive, and after mirtazapine was brought to my attention I thought it worth a punt.

Even so, I don’t have great hopes for this ‘working’; that is, delivering some miraculous return of my sex drive. Libido is complicated and impacted by a whole range of factors, from depression itself to past sexual and romantic history, confidence, self-perception, all the way up to culture and subculture, and perception of one’s own role within that wider context. Even if my predicament was initially brought on by a simple chemically-induced neurobiological change, it will be far from simple now. Brains are complex, and people even more so. Still, this is low hanging fruit (fnar), and you have to make a start somewhere – this is a start, of a kind.

And what a kind! My GP looked surprised at my request, pointing out that mirtazapine is usually prescribed for more anxious-depressive types, those filled with a worrying energy. The drug, he explained, can have quite profound sedative effects. Take at night. You might have difficulty waking. Dreams may come.

Dreams did come, and they’re still coming, though I’m told they’ll eventually, probably, fade. Some claustrophobic, some vertiginous, some icy and frightening, all suffocating, intense. Intense as in seeming profound, only to tatter away with a moments thought. Intense as in teenage crush, primal and primary, confusing. Intense as in shrooms, hilarious because, hilarious because hilarious, because. Haunting, and like ocean waves dragging you down as you wake, as you surface, only thrashing and gasping and drowning again into dreaming, and again, and again into dreaming.

The first day, my eyes opened and I got up, I drank strong coffee and more strong coffee but never really awoke, napped for hours before exhausted went to bed, another twelve hours, awoke to dreaming, awoke to dreaming, awoke.

The second day – strange and a world full of echoes and space, but more awake. I think I’m lucky – the tiredness fading fast and swift now, even if the dreams still boil away at night; while waking is still a confused surfacing it’s getting easier. During the day I can write, read, I can even talk and think, and it’s been less than a week. That’s some quick neuroadaptation!

Maybe I’ll even get my libido back.testosterone