– relatively

Back up, back up.

Even my own glasses can be rose tinted, at times. Human nature, self-preservation, mental masochism – whatever the reason, I’m just as prone as anyone else to imagining a past more perfect than the present. It probably does me no good.

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Prologue II

I knew it was the paroxetine; I knew, but I didn’t want to admit that, because then the bliss could leave at any moment, the childlike and childish joy in my heart would be contingent on this daily capsule. I knew it was the paroxetine, but secretly hoped that I’d got plugged directly into the heart of God. That it would be as I felt; eternal, oceanic, forever and ever.

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Under all this sound and fury

Sharing the stuff I wrote in my early 20s is probably a terribly embarrassing idea, but it does give some kind of insight into my mental health across time. And at least I’ve not shared all the stuff I wrote when I thought I was Jesus.

I’m moving out of London soon – this city might not send me crazy, but leaving it sure will help keep me sane. At least for a little while. Now seems an opportune time – I’ve no job holding me here, my studies will either finish soon or be postponed for a year. I’ve family in Sheffield. Family is good for me, as are the Pennines, as is home.

I’m being unusually pro-active about it – usually when moving I leave everything to the last minute, but I’m seeing this as a chance to declutter. You go through life, you pick up so much crap, so much stuff. I moved down here with a rucksack… now I’m going to need a car for my return.

Still. May as well get of as much as I can stand to. Almost all my books are going, and I suspect a fair few clothes will end up with charity shops. But of course in clearing out you find forgotten bits of life. And if you have a habit of writing – sometimes in fits and starts, sometimes consistently for years – you find a lot of forgotten bits of life. All dusty and discoloured. And with hindsight you can return to all those years ago, with new eyes, and wonder how some things managed to escape your attention for so damn long.

What follows are a few brief extracts – with the exception of the first one, which I’ve reproduced pretty much in its entirety since it does such a good job of evoking my frustration, confusion, and despair at the time – and how much the city (Leeds) was getting to me.

Jan 2002

(Age 20)

Clever dykes and clever dicks, how to get ahead in relationships. How to not care what women want. How to worry over what men want; how to walk past beggars and only feel a twinge of guilt, how to ignore Big Issue vendors.

How to dance and hardly care who’s watching.

“You know about helping yourself?” the woman in the cafe asks.



The exams are coming and I’m too busy smashing crockery and whimpering on the kitchen floor to do anything about it.

And outside the rain’s still pouring and the poor bastards with no homes to go to are crouching by the light, wrapped in sodden blankets with nothing but a handful of coppers in their McDonald’s cups.

And I walk by thinking poor bastard.

And I walk by thinking I want to run away.

And I walk by thinking maybe this next car.

And I walk by.

I’m plummeting. I can feel the world slip by and I slip down.

No, really. I can.

Nausea and vertigo. I wish I could throw up.

I don’t feel too good.

I’m breaking up. I no longer relate to myself. This time it’s serious, I don’t think we’re getting back together, but I don’t care. Who needs him anyway?

“Do you know about helping yourself?”

 In Border’s the coffee tastes of vanilla, and the lights are bright and anonymous.

Anonymous is a word for limericks. A nonny mouse.

My head still hurts with awesome pressure and my legs are still weary tho I don’t know why, The world is still swirling in my head.

It’s only 7:30. I’ve no desire to go home. I’ve no desire to communicate in anything other than wails and tears and screams.

Whale ant ears and cream.

Let me out.

Laugh and the world laughs with you;

Cry and you cry alone.

For this sad old earth sees little of mirth

And has troubles enough of its own


Summer 2002

(Age 21)

For the first time I can remember, I look into my future and every part of me, every fibre of my body and soul is saying yes.

Some of it is in baritone, so deep it’s a feeling more than a sound. Some so excited the sound is a babysqueal of joy. Some are so simple it’s as if the answer is so obvious it’s a non-question.  Now it all looks so simple. All the fear has left me now.

November 2007

(Age 26)

I’m flirting with depression again. Flirting, because it comes and goes, and I’m still functioning OK, for the main part.

Before, I’ve just got wound iup and more depressed about it. That’s a bad strategy. Before I get too bad and wound up, I need to deconstruct this and take some pro-active action.

  1. What do I think has triggered this?
  2. What maintains it?
  3. What makes it worse?
  4. What can I do?
  5. What can I think?

February 2008

(Age 27)

I’m sorry

I’m sorry

I’m sorry

I’m sorry

I’m so sorry

March 2009

(Age 28)

I’m sat on my bed, in my tidied-last-week (becoming messy) room, listening to Gaydar Radio.

I’m feeling OK.

Or, something’s making me feel OK. 40mg of citalopram might be involved. The exercise I did yesterday might be involved. And the alcohol I drank last night and the poor sleep I’ve had and coffee might be involved. Brains are complicated like that.

The music on the radio is sending ripples of hypomania through me. Am I bipolar or is it the drugs? That strange, pressured joy and expansive bliss.

Expansive bliss is something I’ve had for years, now and then. The first time, in mum and dad’s garden, on a summer evening, with the dark sky and violet flowers and sweet air.

E x p a n s i v e  B l i s s

March 2009

(Age 28)

I miss my past. Because in my past I only look at the good bits. In my memory everything was perfect.

Who are you, Phil? Under all this sound and fury, who are you? Can you stand still?

June 2009

(Age 28)

Sat upstairs in the Wellington, drink by my side and pen in my had, trying to write poetry and only finding commentary.

Memories insistent as rain, I shudder sometimes from little earthquakes. You don’t know where you end and the drugs begin. All those ticktock phrases gone, evaporated in the sun; all those loops, looping loops lost. Left with memories, soft and insistent as raindrops on skin.

I’m feeling good, ultimately. Sanity is underrated.


In June 2012 I visited a friend in Cardiff. He was worried about my mental health and invited me up for a break.

Leaving, we hugged, and I pulled him close, tight, kneading his flesh. Began to sob, hysterical.

I’m going to do itI’m so scared, I think I’m going to do it.

The next day I was picked up by the police and taken to hospital.

Life is full of ups and downs, as they say.


‘Ticktock phrases’ and ‘looping loops’ refers to the persistent, insistent thoughts and phrases of violence, suicide and grief which beat obsessively in my mind when I’m depressed. ‘Memories soft as rain’ refers to the side effect I get, occasionally, with antidepressants – their strange habit of bringing up old memories, neutral, long forgotten memories, often of childhood.

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.


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.

Always be beautiful

I feel…

I feel. You don’t know, you can’t know. How this feels. I feel.


Like the world…


Like my heartbeat… Like my soul…

I feel the world, my heartbeat, my soul. I see this majesty, this glorious, wild, passionate world. I want to grab, to pull, to claw the world. To kiss. Deep. To leave my marks, red and raw and burning. Bloody, primal, rare.

To devour. This world dripping with promise and passion and fury and chaos and love, and love, and love, and lust.

I step from the pharmacy, holding a blister pack of lamotrigine in my hand, and look to the sky; a sunset glorious and impossible and free. A breeze teasing and sensual, and playful, and exultant. Clouds, golden, blazing.

I step from the pharmacy and look at the blister pack in my hand. Do you know how it feels? You can’t know. To feel so miserable, to feel to wretched and useless and bleak and ruined, to then see the world blossom out in breathless beauty; to move so swiftly from putrid misery to… to…

To this.

To glory.

And to be told this glory is folly, to be told to swallow these pills to take the fierce, untamed beauty from the world. To be told you must turn down Nirvana. Attenuate Heaven. You can’t know.

I walk, I smoke a cigarette. Catch the tube.

You can only hide so long. I suspected, ever since 2008, that the reason SSRI medication worked ‘so well’ for me was that they pushed me into a kind of hypomania. Paroxetine threw me into wild abandon – true mania, light speed and ecstatic and frightening and free; Sertraline, giddy and loose, the time I decided I needed to start dealing shares and learn Latin. Citalopram… Citalopram, like the bed of baby bear, just right. Citalopram, not too wild, just wild enough.

And yeah, sometimes I felt so free I could fly. Sometimes, even without the drugs, I could embark on wonderful new ideas and projects and schemes and it would always, always be beautiful. And I could dance in the street and dance in the gym because honestly, honestly, sometimes I can hear the music and feel the music, feel the music like a kiss. Not the gentle kiss of romance but music lustful, electric, abandoned; which grabs your neck and your body and pulls you in, devouring, devouring, hard and dangerous and fierce.

You give too much away, eventually. The records they keep are surprisingly detailed. “Would you be open to a mood stabiliser?” the psychiatrist asks. I say yes, eventually, for my own nefarious reasons.

Hypomanic episodes have less than ideal long term effects. Cognitive decline, possible neurological disruption. Still.


You can’t know how it feels. To be told this has to be taken from you, for your own good. The blinding brilliance of hypomania, when the world makes sense and you make sense and everything, oh everything is glorious, to be told everything that is glorious is a lie, the real world is a watery reflection, the real world a muted song. Take this pill. Save yourself. Turn down the world.

Would you take the pill?

I get off at Waterloo.

I take the pill.


I turned up to the GP, the other week. New GP, same old spiel; history of depression, not feeling great, suicidal ideation. Yes, there’s something of a family history. Tend to respond well to citalopram. Can I have some?

Of course, the GP says, and has me fill in a PHQ-9 while he taps a prescription out.

(The ‘Patient Health Questionnaire – Section 9’ is the standard test they give to – I think – anyone turning up to a GP’s office with suspected depression. It’s somewhat similar to something called the Beck Depression Inventory, which is used in research. It’s ten questions about your mood and thoughts over the past week, each scored 1 – 5, which map roughly onto the DSM-IV and ICD-10 definitions of major depressive disorder. I’ve filled in more PHQ-9s than I’ve had hot dinners)

Problematically, I don’t look depressed.

I know, I know – those twee fucking jpegs that do the Facebook and Twitter rounds, ‘Spot the depressed person OMG THEY LOOK JUST LIKE NORMAL PEOPLE’, as if those experiencing depression are some kind of alien stealth attack force. But by the time I make it to a doctor’s office, I am usually in a bad way. For weeks I will have been failing to claw my way out of this hole even as the ground crumbles beneath my feet; I’ll have gone from unremarkable, to tired-looking, to vacant and miserable; unshaven, matted hair, somehow smaller. I finally get into the doctor’s office, away from the eyes of the world, and I sink into whispering, eyes bobbing like dead fish in water. Mouth closed, open. Closed. In those moments I do not look just like anyone else. I look like one profoundly depressed bastard.

When you turn up looking like that, sounding as I do when I’m bad – slow, quiet, halting – then GPs are happy to fire anything at you. When you turn up obviously, profoundly depressed, and say you’ve been here before and say you’ve been helped by drugs before, doctors have no problem in handing you a script and also – in my experience – will ask what dose you’ve previously been on.

So, I don’t look depressed; I’m sat straight, speaking and gesticulating easy, eye’s maintaining contact; bright. Because I’ve been sensible, and this time I’ve gone to get drugs before I get really, really, really bad.

And this is problematic, because I get to the pharmacy and see I’ve been prescribed half my effective dose. This isn’t a huge issue in the moment, since I can simply double dose. This becomes an issue later on, when I finish the script early and have not arranged a further appointment to sort it out because – hey, depression, mind scramble, strobe light impulsivity.

It becomes an issue now, when I’ve run out.


So, just over a week into citalopram; the nausea has subsided, the strange yawning-stretching-crawling pulses are becoming more infrequent. My teeth still chatter, slightly. The turbulence of takeoff.

Sleep. Sleep is one of my two big sticking points with SSRI medications. I’m naturally a lark, one of those insufferable early-to-bed, early-to-rise people, up by 8am at the latest on weekends, unable to lie in. Except while on meds.

Antidepressants increase bed gravity like you wouldn’t believe. And this is the first time I’ve taken them when I’ve not had to get up first thing (to get into work), which has allowed me, for the past few days, to lie, just lie, and bob on drifts of sleep. Which means this is the first time I’ve realised – this is a terrible thing for me to do!

If I can’t get started first thing, turns out I can barely get started at all. I climb out of sleep and bed hazy and befuddled, clunk aimlessly downstairs and muddle about for a few hours, until I can no longer put off going into the lab and into the gym; shove myself, sulking, out the house. Wonder what the point of it all is.

This morning I forced myself up; I need to get to Dean Street for a checkup anyway, I’ve got shopping to do and then (obviously) lab and gym on top of that. And it’s not as if I’ve nothing to do – a mountain of study which I’ve been ignoring, my room is a tip (a few weeks worth of depression will do that). And Jesus, I feel better for getting up. Must remember this. Must try harder. It’d be absurd if a side effect of the antidepressants I’m taking made me more depressed…

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.