spring can really hang you up the most

spring-bluebell_3213910bIt looks like the warm summer weather is finally here in the UK, and certainly everything is blossoming like mad. This is a good time for sufferers of Seasonal Affective Disorder (SAD) – the hours of daylight are long, and the sun shines brightly.

But if you feel particularly low at this time, or like me experience fleeting stabs of absolute desperation even when all seems well, you are not alone.  It seems counter-intuitive but spring is the peak period for suicide. The reasons are not well understood.

Get help

I will write more about suicide at a later point, but for now, if you are feeling suicidal, talk to somebody and get help. In the UK email or call the Samaritans on 0845 790 9090 (24 hours a day), or go to A&E if you need to be in a safe place.


Whatever you do, don’t listen to sad songs like this!


Further reading

Jong-Min Woo, Olaoluwa Okusaga and Teodor Postolache Seasonality of Suicidal Behavior 2012

David Dobbs Clues in the Cycle of Suicide 2014





A seasonal suicide peak in spring is highly replicated, but its specific cause is unknown. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3315262/


other reading http://well.blogs.nytimes.com/2013/06/24/clues-in-the-cycle-of-suicide/?_r=0

‘depression is a chemical imbalance’ a myth: so what?

The Daily Mail published an article last month with the headline

Depression is NOT caused by low serotonin levels and most drugs used to treat it are based on a myth, psychiatrist claims

DavidHealysmall1The story was based on an editorial in the British Medical Journal (BMJ) by psychiatrist David Healy (pictured), who argued that the popularity of SSRI antidepressants such as Prozac is based on a myth, grown from the notion that ‘SSRIs restored serotonin levels to normal, a notion that later transmuted into the idea that they remedied a chemical imbalance’.

In fact, whilst levels of serotonin may be linked to depression, it is not known exactly how, and nor is it understood how SSRI antidepressants really work.

According to Healy, the strength of the chemical imbalance myth means that SSRIs are often prescribed at the expense of more effective treatment, and with no regard to individual characteristics of a patient’s depression. But he says:

Serotonin is not irrelevant. Just as with noradrenaline, dopamine, and other neurotransmitters, we can expect it to vary among individuals and expect some correlation with temperament and personality.


Is the ‘depression is a chemical imbalance’ idea really incorrect?

prozacThe academics and medics who commented on the BMJ piece seem to be clear that the science has moved on a long way since SSRIs were introduced, and that the causation of depression is much more complicated than too much or too little of one neurotransmitter in the brain. So it is way too simplistic to say that SSRIs correct a chemical imbalance.

An article on the website io9 gives some background into how the chemical imbalance ‘myth’ took root and grew. It also summarises where the scientific thinking on depression is now:

Depression’s wide range of symptoms can be linked to myriad overlapping factors, from genetic vulnerability, to deficiency of certain neurotransmitters, to disruptions in circadian rhythms, to factors that can alter the survival and growth of neurons.

The birth of new neurons, for example, is a hallmark of a healthy brain; a prominent new theory about how SSRIs work has connected elevated serotonin levels to the elevated birth of neurons.

But the science still has a ways to go.  It is also obvious that psychological stress and so-called early lifetime stress can cause depression.

Poul Videbach, professor of psychiatry at Aarhus University Hospital in Denmark (Levi Gayde, io9)


So it’s a myth, so what?

The many comments on the Daily Mail and io9 articles illustrate the two main issues arising from all this: 1. SSRIs are overprescribed because patients and doctors have bought into the myth; 2. SSRIs really do help a lot of depressed people

If Prozac, or any of the SSRIs (Cipramil, Cipralex, Faverin, Seroxat, Lustral are the others used in the UK) improve your symptoms and side effects aren’t a problem, does it matter if we don’t really know how they work? No. Keep taking the tablets.

But if sorting out serotonin levels isn’t the answer, or not the whole answer anyway, to managing depression, it makes sense to keep doing the other things that help: healthy sleep, good diet, social contact, exercise, mindfulness, anti-ruminatory activity, exposure to sunshine.


References and further reading

Daily Mail 22.4.15  Depression is NOT caused by low serotonin levels and most drugs used to treat it are based on a myth, psychiatrist claims

David Healy Serotonin and depression: The marketing of a myth British Medical Journal, April 2015 (comments via BMJ 2015;350:h1771)

Levi Gayde The Most Popular Antidepressants Are Based On An Outdated Theory [UPDATED] io9 website

Jonathan Leo and Jeffrey Lacasse  A Reply to Peter Kramer: Do Serotonin Imbalances Cause Depression? April 2015

NHS Choices Selective serotonin reuptake inhibitors (SSRIs) 

exercise for depression: how to get the benefits without the pain

There is plenty of evidence that suggests regular exercise is good for our mental (and physical) health. It makes sense for most people with depression to include exercise as one of the strategies they use for getting and staying well.

Physical exercise, particularly aerobic exercise, has pronounced long-term antidepressant effects and can produce euphoria in the short-term. Numerous systematic reviews suggest that regular aerobic exercise (at sufficient intensity and duration) has comparable antidepressant efficacy to standard pharmaceutical antidepressants in treating depression. Consequently, current medical evidence supports the use of aerobic exercise as a treatment for depression. [Source: wikipedia]

pizzarunBut what if you hate exercising, or really can’t do it, for whatever reason? Is it possible to get the mental benefits of exercise through a different route?


Effect of exercise on the brain

Short-term euphoria aside, the main antidepressant effects of consistent aerobic exercise (30 minutes a day) seem to relate to neuroplasticity as well as healthy alterations in gene expression in the brain.  Some of these long-term effects include increased neuron growth, increased neurological activity, improved stress coping, enhanced cognitive control over behaviour, improved memory, and structural and functional improvements in brain structures and pathways associated with cognitive control and memory.  [Source: wikipedia]


Exercise the mind

Sound familiar? This post discusses mindfulness and how it promotes new neural activity and neuroplasticity. Mindfulness also improves cognitive performance (even after just 20 minute daily sessions for four days) and mood (Zeidan et al, 2010).  So if running or other physical exercise is not an option for you, try mindfulness. Or better still, do both.


But don’t give up on physical exercise unless you have to…

I wouldn’t want to talk anyone out of physical exercise, since the overall health benefits are so rewarding as this animated video 23 and 1/2 hours: What is the single best thing we can do for our health? shows so well.

Like anything we find difficult, it takes skill and and self-awareness to start and maintain an exercise habit. Dick Talens, co-founder of fitness website Fitocracy, says the only way to succeed is to create positive feedback loop – ie make sure you can feel or believe in the benefits of what you are doing in the short-term, so you feel encouraged to keep going.

NHS Choices has some 10 minute workouts that don’t involve running or leaving the house, and there are plenty of online resources for people with limited mobility who need low impact workouts (eg Launchpad)


References and further reading

S Rosenbaum et al Physical Activity Interventions for People With Mental Illness: A Systematic Review and Meta-Analysis 2014

F Zeidan et al Mindfulness meditation improves cognition: Evidence of brief
mental training 2010

K Erickson The Aging Hippocampus: Interactions between Exercise, Depression, and BDNF 2011

Dick Talens The Myth of Willpower and “Eat Less, Move More”

mindfulness-based cognitive therapy for recurrent depression – new research

The Guardian and others reported on a study published this week which compared relapse rates between two groups of patients who had experienced three or more previous major depressive episodes and were on a therapeutic dose of maintenance antidepressants. One group continued with their medication as before whilst the other received mindfulness-based cognitive therapy (MBCT) plus support to taper or discontinue antidepressant treatment (MBCT-TS).

The researchers had done a pilot study and were anticipating the results of this larger trial would show that MBCT-TS was more effective than anti-depressants, but this was not the case:

We found no evidence that MBCT-TS is superior to maintenance antidepressant treatment for the prevention of depressive relapse in individuals at risk for depressive relapse or recurrence. Both treatments were associated with enduring positive outcomes in terms of relapse or recurrence, residual depressive symptoms, and quality of life. (Kuyken et al, 2015)

NHS Choices has a very readable analysis of the study here.

The researchers, and especially the burgeoning mindfulness industry, are doubtless disappointed that the findings don’t establish mindfulness as a cast-iron cure for depression.  However, for those of us who suffer from major recurrent depression, the research does at least provide evidence that antidepressants are not the only way to stay well.


References and further reading

W. Kuyken et al Effectiveness and cost-effectiveness of mindfulness-based cognitive therapy compared with maintenance antidepressant treatment in the prevention of depressive relapse or recurrence (PREVENT): a randomised controlled trial 2015

DM Davis and JA Hayes What Are the Benefits of Mindfulness? A Practice Review of Psychotherapy-Related Research 2011

D Derbyshire Should we be mindful of mindfulness? 2014

fighting depression: a Sisyphean task

Why is it so easy to be knocked off course? Any distraction, or dip in confidence, or minor upset seems to mess up my routine and my resolve to do the Things That Help me stay well. This past week I have been completely absorbed by an argument about a duck on a statue, so that my healthy habits and depression experiments have fallen by the wayside; the week before it was hormones disturbing me.

escalatorAnd sure enough,  my early-warning system is picking up little signs of an impending depressive spell: listlessness, poor concentration, house extra untidy, inbox unmanageable, starting to avoid seeing friends, waking up at 4 in the morning.

Time to re-group, urgently and energetically. Get up early, record dreams, 5 minutes of mindfulness, record mood scores, go for a run, healthy breakfast, work on Depression Lab research/experiments, trombone practice, housework habit, walk with a friend, proper meals, bat work, more mindfulness, early night. And repeat.

This depression thing is like being stuck on a moving walkway taking you slowly but surely in the wrong direction. Got to keep going just to stand still. Think I know how Sisyphus must have felt.


depression and dreaming: when mental digestion leaves a bad taste in the mood

Sleep and depression

raisin asleepSleep disturbance is a key symptom of depression – difficulty in falling asleep at night and/or waking up too early in the morning is very common. The importance of sleep was discussed in a previous post; this one looks at the role of dreaming. But first, some background. Studies show that the sleep architecture – patterns of sleep throughout the night (see below) – in depressed people is different:

Compared with normal controls, sleep continuity of depressed subjects is often impaired, with increased wakefulness (more frequent, and longer periods of wakefulness), and reduced sleep efficiency. Sleep onset latency is significantly increased and total sleep time reduced. Rapid eye movement (REM) latency is often shortened, and the duration of the first REM period is increased. The number of eye movements in REM is also increased.

The total amount of slow wave sleep is often decreased in depression, compared with normal controls…   Also the normal pattern of slow wave activity in the brain decreasing from the first to the last NREM episode is disrupted. (Nutt, 2008)


Sleep ‘architecture’ (source: wikipedia)

  • non REM (NREM) stage 1: This is a stage of sleep that usually occurs between sleep and wakefulness, and sometimes occurs between periods of deeper sleep and periods of REM. The muscles are active, and the eyes roll slowly, opening and closing moderately.
  • NREM stage 2: In this stage, sleepers become gradually harder to awaken.
  • NREM stage 3: Formerly divided into stages 3 and 4, this stage is called slow-wave sleep. The sleeper is less responsive to the environment; many environmental stimuli no longer produce any reactions.
  • REM: The sleeper now enters rapid eye movement (REM) where most muscles are paralysed. REM sleep is turned on by acetylcholine secretion and is inhibited by neurons that secrete serotonin.

605px-Sleep_Hypnogram.svgAn adult [normally] reaches REM approximately every 90 minutes, with the latter half of sleep being more dominated by this stage. REM sleep occurs as a person returns to stage 1 from a deep sleep. The function of REM sleep is uncertain but a lack of it impairs the ability to learn complex tasks.

Sleep proceeds in cycles of REM and NREM, usually four or five of them per night, the order normally being N1 → N2 → N3 → N2 → REM. There is a greater amount of deep sleep (stage N3) earlier in the night, while the proportion of REM sleep increases in the two cycles just before natural awakening.


The role of dreaming

Dreaming probably occurs throughout the sleep cycle but is mostly associated with REM sleep. There isn’t scientific consensus on the role of dreams but one plausible proposal with relevance to depression is that dreams help regulate mood.  Emotionally charged events that happen during the day are woven into dreams at night that incorporate memories of similar events and emotions, allowing the brain to compare past events and their impact with the new one, and to file the memory.  Sort of mental digestion, processing emotions while we sleep.

When some disturbing waking experience is reactivated in sleep and carried forward into REM, where it is matched by similarity in feeling to earlier memories, a network of older associations is stimulated and is displayed as a sequence of compound images that we experience as dreams.

This melding of new and old memory fragments modifies the network of emotional self-defining memories, and thus updates the organisational picture we hold of “who I am and what is good for me and what is not.”

In this way, dreaming diffuses the emotional charge of the event and so prepares the sleeper to wake ready to see things in a more positive light, to make a fresh start. This does not always happen over a single night…..[it] may take many nights. (Cartwright, 2010)


Dreaming and depression

Cartwright’s research with depressed people going through divorce found that those who dreamt about their ex-spouse – angry, emotional dreams – generally recovered from their depression. Those who were passive and unemotional in their dreams did not fare so well, leading her to suggest that ‘dream collection might become a screening tool useful in determining a patient’s psychological resiliency’.

Dreams also show a progression through the night: whilst negative dreams occurring early in the night may reflect a within-sleep mood regulation process taking place, those that occur later may indicate a failure in the completion of this process (Cartwright, 1998)

The University of Hertfordshire has taken this mood-regulation idea a step further by exploring whether the emotional nature of dreams can be influenced, and whether this in turn affects waking mood. The Dream:On smartphone app has been developed so you can try it for yourself (not available on android, sadly).

The final dream of the night influences people’s morning mood, and so making that dream more positive may well help thousands face the day with a smile on their face.

In addition, sleep scientists have long known that the dreams of those diagnosed with depression are especially long, frequent, and negative. It’s possible that dream influence will become a radically new therapeutic tool in the fight against depression. It’s early days, but we’re very excited about the potential power of dream control.  (Wiseman, Dream:On)


So what?

There is a lot to think about here. I will reflect on these in particular:

  • does more sleep mean more dreaming, and therefore more emotional processing?
  • might be worth doing a dream diary for a while, noting any association between dreams and mood
  • might be worth trying to replicate the Dream:On idea of influencing the pre-wake dream
  • how much I love this song…


References/further reading

Rosalind Cartwright (2010) The Twenty-four Hour Mind Oxford University Press

Rosalind Cartwright (1998) Role of REM sleep and dream variables in the prediction of remission from depression

David Nutt (2008) Sleep disorders as core symptoms of depression



genetic vulnerability to depression a blessing in disguise: the orchid and dandelion hypothesis

The serotonin transporter gene has been fingered in a previous post as linked to depression, with two variations of the gene apparently conferring increased vulnerability to it. The optimum conditions for depression to thrive seem to be a combination of the dodgey gene plus a difficult, stressful environment.

A theory currently gaining ground suggests that natural selection would have wiped out the ‘depression’ gene if it was all bad, and that in a good, supportive environment, people with the gene can live happy, productive lives. So, it is argued, there must be some evolutionary advantage in keeping the gene.

LARGE-WHITE-ORCHID-H99-848x1000_905In this theory – the Orchid and Dandelion Hypothesis – people without the genetic sensitivity to their environment (the dandelions), will thrive anywhere whereas those with it (the Orchids) can, in optimal conditions, bloom spectacularly.  And, of course, wilt dismally in poor conditions.

Winston Churchill and Abraham Lincoln – two great leaders who suffered from depression – perhaps illustrate that, whilst they may not have been very happy, they were important for the survival of the species.

So my depressed friends: sort out your environment, and be brilliant. No excuses, your species needs you 🙂


Further reading

David Dobbs (2009) The Science of Success

See also Dobbs’ blog on genetics Smooth Pebbles

Nassir Ghaemi (2009) A First Rate Madness: Why mental illness enhances crisis leadership

Glenn Wilson (2013) The Black Dog: Causes and Cures for Depression




mindfulness for depression: pay attention, this is important

What mindfulness is

A ‘working definition’ of mindfulness is awareness that arises from:

  • paying attention, on purpose
  • in the present moment
  • non-judgmentally

(says Jon Kabat-Zinn in the video below)

It is difficult to pay attention like this without a great deal of practice.

pushupsOne way of practising is to decide to give all your attention to your breath for x minutes, and really be aware of the air coming in and going out for this amount of time. Whenever the mind wanders, as it will, bring attention gently back to the breath. Sort of mental press ups – the more you do it, the easier it gets.

But mindfulness is not about the breath per se; it’s about the paying attention to what is happening right now.

The non-judgment element of mindfulness is suspending judgement (of whether it’s good or bad for your mind to keep wandering, for example) – just experiencing things without assigning a label and an opinion.

How mindfulness alleviates depression

In other words, mindfulness is about developing the ability to become detached controllers and observers of our own minds (this is sometimes called ‘meta-awareness).  This enables us to:

  • focus our minds on, say, helpful rather than unhelpful things if we so choose
  • be aware of what our minds are doing and understand that the thoughts that pop into our heads are just thoughts: they are not us, and they are not necessarily true
  • control the meaning we give to thoughts, feelings and experiences

After repeated mindfulness practice – ie this deliberate paying attention – changes start to occur in the structure of the brain, through a process called neuroplasticity. The neural pathways that have developed in our brains over the years to govern thoughts, feelings and behaviours can be rewired when we forge new pathways through mindfulness.

This video explains neuroplasticity:

Here’s Ruby Wax on neuroplasticity (she starts talking about it at 4:51 after a preamble about what lead her to neuroplasticity, which you may have heard before):


Further reading

Peter Malinowski Meditation and Neuroplasticity: Five key articles 2014

my childlessness: a promise kept

Of all the things depression has prevented me from doing over the years, having children is perhaps the most poignant. But since you can’t really miss something you never had, it’s no biggy.

16201305-silhouette-of-pregnant-womanI mention it now because these last few months of getting my depression more or less under control has made me wonder what my life could have been if I’d got my act together sooner. And of course it’s Mother’s Day tomorrow, which, for all us childless women, rubs it in every year.

The decision not to have children happened when I was a schoolgirl, 14 or 15 years old, and desperate at feeling so miserable all the time. I could not risk passing this anguish on to my own children, as I perceived my mother had to me (since nothing other than genetics could have caused it, I reasoned). I made my future self promise not to have children, by writing a little song that I reckoned would stick with me through any changes of heart later.

Was it the right decision? Risk-wise, yes.  My children would have been 4 or 5 times more likely than the average person to suffer from depression. Terrible odds. If I had packed up drinking and tackled my depression 20 years ago, would I have broken the promise to my 14 year old self? Probably. But as they say a lot in AA: woulda, coulda, shoulda. Best not to dwell on it.

The lack of public discourse about this surprises me, although it probably shouldn’t, given the stigma still attached to mental illness.   Having just seen Still Alice, a film about a linguistics professor (played by Julianne Moore, below) who is diagnosed with early onset Alzheimer’s aged 50, the choices people make concerning their genetic inheritance seem familiar.  (Take a bow, Angelina Jolie.)

Julianne Moore in Still Alice: a great central performance in a 'televisual' film.

The following is taken from Stanford University School of Medicine’s Major Depression and Genetics page:

How do we know that genes play a role in causing depression? Scientists look at patterns of illness in families to estimate their “heritability,” or roughly what percentage of their cause is due to genes. To do this we find people with the disease who have a twin, and then find out whether the twin is also ill. Identical (monozygotic) twins share 100% of their genes, while non-identical (“fraternal” or dizygotic) twins share 50% of their genes. If genes are part of the cause, we expect a patient’s identical twin to have a much higher risk of disease than a patient’s non-identical twin. That is the case for major depression. Heritability is probably 40-50%, and might be higher for severe depression.

This could mean that in most cases of depression, around 50% of the cause is genetic, and around 50% is unrelated to genes (psychological or physical factors). Or it could mean that in some cases, the tendency to become depressed is almost completely genetic, and in other cases it is not really genetic at all. We don’t know the answer yet.

We can also look at adoption studies, to see whether an adopted person’s risk of depression is greater if a biological parent had depression. This also seems to be the case.

What about non-genetic factors? There are probably many non-genetic factors that increase risk of depression, many of which are probably not yet known. Severe childhood physical or sexual abuse, childhood emotional and physical neglect, and severe life stress are probably all risk factors. Losing a parent early in life probably also increases risk to some extent.

If someone has a family history of depression, are they at very high risk? If someone has a parent or sibling with major depression, that person probably has a 2 or 3 times greater risk of developing depression compared with the average person (or around 20-30% instead of 10%).

The situation is a little different if the parent or sibling has had depression more than once (“recurrent depression”), and if the depression started relatively early in life (childhood, teens or twenties). This form of depression is less common – the exact percentage of the population is not known, but is probably around 3-5%. But the siblings and children of people with this form of depression probably develop it at a rate that is 4 or 5 times greater than the average person.


cogitus interuptus: break the thought-mood-behaviour cycle

It’s odd but i feel like I’m under a spell, like in the song That Old Black Magic 

When that elevator starts its ride
Down and down I go,
Round and round I go
Like a leaf that’s caught in the tide

Unlike in the song, in my case it’s not love doing this. It’s terrible listlessness, lack of focus, inability to concentrate (hence the lack of posts here recently). Although this listlessness is a symptom of depression, I don’t feel particularly low. Frustrated with myself maybe, but not low.

So, how to snap out of it? My routine has gone to pot. Raisin has developed a (sporadic) hopping limp that makes me nervous for her recovery, so no early morning runs. No cleaning small areas of the bathroom after each trip to the loo. Very little trombone practice. Minimal mindfulness practice.


Cogitus interuptus

CBTblue-newLast week’s mindfulness class was all about disrupting old patterns of thought and behaviour using the CBT theory that thoughts can make you feel bad, which makes you behave in ways that aren’t helpful, which makes the thoughts worse and so it goes, in a spin.

The week before we looked at how thoughts are just random neurons firing in your head (my words, not official mindfulness-speak), with no inherent power to do anything. They can’t hurt you if you don’t let them. So one technique in this disruption strategy is to see thoughts for what they are – miniscule arrangements of dancing chemicals or whatever. Not big, and not scarey.

Another technique is to change your behaviour when you feel bad:

  • don’t withdraw socially: interact with other people
  • don’t mope around: do something that gives a sense of achievement
  • don’t just feel miserable: do something you usually enjoy

I baulked at this advice in the class because it’s really difficult to do this stuff when you are depressed. During my recent low patch these things – usually part of my routine – became impossible, even though I believed they would help. The answer is simple, I was told: lower your expectations. Don’t expect to be able to get out for a run – think of a short walk (or whatever) as an achievement when you are not well.

So there we are.

My snap out of it plan for today is to listen to Ella Fitzgerald doing That Old Black Magic, really loudly, every time I start to spin.

Take it away Ella