In the average charismatic church, from the time you park your car in the parking lot, to the time the music starts at the beginning of the service, the smiles of at least a hundred people beam at you, and at least one third of those smiles are also attached to enthusiastic handshakes and exhortations like, “Isn’t it great to be in church this morning!”
When you’re a Christian, especially at the happy-clappy end of the church spectrum, you’re supposed to be constantly full of the Holy Spirit and experiencing the joy of the Lord.
Which is why for most church-goers, putting the terms “Christian” and “depression” in the same sentence just doesn’t seem natural, even though depression affects a lot more of the church than the church is aware of.
So, how much of the church is affected by depression? The lifetime prevalence (how likely you are to suffer from depression at one stage through your life) is about twenty-five percent, or about one in four people. The point prevalence (those who are suffering from clinical depression at any particular time) is about six percent.
I used to attend a church which had a regular congregation of about 2500 people. So statistically, one hundred and fifty people in that congregation are suffering from depression every Sunday, and more than 600 will experience depression in their lifetime.
And by ‘depression’, we’re not talking about feeling a little sad … that Bill Shorten might become Prime Minister one day, or Ben Hunt can’t catch, or that One Direction isn’t the same without Zayn. Sadness for genuine reasons … you broke up with a long term partner, someone stole your purse out of your bag, or there’s the threat of redundancies at your office … also doesn’t mean you’re depressed.
The DSM5 is the current standard for psychiatric diagnoses around the world. I’ve included the full definition of depression at the end of this blog, but suffice to say, depression is more than just unhappiness. Proper depression symptoms “cause clinically significant distress or impairment in social, occupational or other important areas of functioning.” In other words, you’re so low that your social life or work is affected, and for more than two whole weeks. It’s also important to know that depression isn’t just low mood but can also be experienced as “Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day”.
Depression has a number of causes and correlations. People who are chronically unwell, be that from chronic pain, long term illness such as cancer or autoimmune disease, or life threatening illnesses such as those who’ve suffered from heart attacks or meningitis, have a higher rate of depression. People who have experienced significant physical or psychological trauma also have a higher rate of depression. In fact, stress of any form is highly correlated with depression (that is, people who suffer from any severe stress are more likely to develop depression).
This observation led to a theory about the development of depression, called the Stress Exposure Model of depression  – You develop depression because you’ve suffered from stress. This is one of the most common assumptions about depression in our society, and there are some important consequences from this line of thinking. Like, if being stressed is the cause of depression then the cure for depression is simply reducing stress. This is probably why most people assume that depression is a choice, or a simple weakness, and why depressed people are often told just to snap out of it.
But there’s more to depression than just better dealing with stress. Fundamentally, I understand depression as the end result of the brains capacity to deal with the demands of life. Too many demands or not enough resources overwhelms the brain and low mood is the end result.
Some depression is predominantly biological. People with biological depression can’t effectively deal with even a normal amount of demand on their system, because their brain doesn’t have the resources to process the incoming signals correctly or efficiently. The main biological cause is a deficiency of a growth factor called BDNF, which is needed for the nerve cells to grow new branches, which enable the brain to process new information. This theory is called the Neurotrophic Hypothesis of Depression  (‘neuro’ = nerve and ‘trophic’ = growth). BDNF isn’t the only critical factor in the biological story of depression. There are many others, including the stress hormone system , the serotonin system  and the dopamine/rewards system .
Some depression is predominantly psychological. There are certain situations in which there’s so much going on and so much change and adaptation is required, and the brains coping systems simply can’t cope. So, severe and sudden stressors would fit into this category. For example, people trying to cope with natural disasters, or a tragedy like a massive house fire.
Most of the time, depression is a combination of both biological and psychological. Genetic factors change our capacity to handle the incoming. The nerve cells don’t have enough BDNF and are slow to grow new branches. Genetics are also important in determining other mechanisms of resilience, and people with poor resilience are also more prone to depression [6-8]. Genetic factors also determine other factors involved in the way we process the incoming stream of sensory input – our personality. People with the neurotic personality type, the classical introverts/pessimists, are more prone to depression, because of the way their brain naturally biases the flavour of the incoming information . What’s also very interesting is that these tendencies to depression also tend to create more stress [1, 10]. So stress is important to the risk of depression, but ironically, it is the risk of depression which influences the risk of stress.
The risk of depression is related to an increased tendency towards stress, and poor processing of that stress because of personality factors and a reduced capacity to cope. All three of these factors are influenced by a broad array of genetic factors.
What’s also important to see here is that being depressed isn’t because of “toxic thinking” or because of “negative confessions”. What we say and what we think are signs of what is going on underneath, not the cause of it. And more importantly, you can make as many faith-filled confessions as you like, but if they don’t help you to change your capacity to cope, then they’re just hot air.
In the next instalment, we’ll look at ways to handle depression, and what the Bible says about being depressed.
 Liu RT, Alloy LB. Stress generation in depression: A systematic review of the empirical literature and recommendations for future study. Clinical psychology review 2010 Jul;30(5):582-93.
 Duman RS, Li N. A neurotrophic hypothesis of depression: role of synaptogenesis in the actions of NMDA receptor antagonists. Philosophical transactions of the Royal Society of London Series B, Biological sciences 2012 Sep 5;367(1601):2475-84.
 Hauger RL, Risbrough V, Oakley RH, Olivares-Reyes JA, Dautzenberg FM. Role of CRF receptor signaling in stress vulnerability, anxiety, and depression. Annals of the New York Academy of Sciences 2009 Oct;1179:120-43.
 Caspi A, Hariri AR, Holmes A, Uher R, Moffitt TE. Genetic sensitivity to the environment: the case of the serotonin transporter gene and its implications for studying complex diseases and traits. The American journal of psychiatry 2010 May;167(5):509-27.
 Felten A, Montag C, Markett S, Walter NT, Reuter M. Genetically determined dopamine availability predicts disposition for depression. Brain and behavior 2011 Nov;1(2):109-18.
 Karatsoreos IN, McEwen BS. Resilience and vulnerability: a neurobiological perspective. F1000prime reports 2013;5:13.
 Wu G, Feder A, Cohen H, et al. Understanding resilience. Frontiers in behavioral neuroscience 2013;7:10.
 Russo SJ, Murrough JW, Han M-H, Charney DS, Nestler EJ. Neurobiology of resilience. Nature neuroscience 2012 November;15(11):1475-84.
 Hansell NK, Wright MJ, Medland SE, et al. Genetic co-morbidity between neuroticism, anxiety/depression and somatic distress in a population sample of adolescent and young adult twins. Psychological medicine 2012 Jun;42(6):1249-60.
 Boardman JD, Alexander KB, Stallings MC. Stressful life events and depression among adolescent twin pairs. Biodemography and social biology 2011;57(1):53-66.
The DSM5 Formal Diagnostic Criteria for Depression
A. Five (or more) of the following symptoms have been present during the same 2- week period and represent a change from previous functioning; at least one of the symptoms is either (1) depressed mood or (2) loss of interest or pleasure.
(Note: Do not include symptoms that are clearly due to a general medical condition, or mood-incongruent delusions or hallucinations.)
- Depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad or empty) or observation made by others (e.g., appears tearful). Note: In children and adolescents, can be irritable mood.
- Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as indicated by either subjective account or observation made by others).
- Significant weight loss when not dieting or weight gain (e.g., a change of more than 5 percent of body weight in a month), or decrease or increase in appetite nearly every day. Note: In children, consider failure to make expected weight gains.
- Insomnia or hypersomnia nearly every day.
- Psychomotor agitation or retardation nearly every day (observable by others, not merely subjective feelings of restlessness or being slowed down).
- Fatigue or loss of energy nearly every day.
- Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not merely self-reproach or guilt about being sick).
- Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or as observed by others).
- Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide.
B. The symptoms cause clinically significant distress or impairment in social, occupational or other important areas of functioning.
C. The symptoms are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g., hypothyroidism).
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