Manuella Kaster and colleagues begin their fascinating paper with the sentence: “Repeated stress elicits neurochemical and morphological changes that negatively affect brain functioning. “ They go on to demonstrate that caffeine acts to prevent some of the negative effects of stress on the brain, and to detail the neurochemical pathways that are involved. Although their experiments were conducted on mice, this is important research with interesting implications for human mental health and wellbeing – as well as being good news for people who love coffee.
We do indeed know that chronic stress affects people very badly. In mice, the (rather unpleasant) stressful situations in this experiment included such things as damp bedding, sharing living space with others, food and water deprivation, cold baths and cages tilted at 45°. And these poor mice unsurprisingly showed the behavioural and neurological consequences of this stress. In humans, stress can also have disastrous consequences. In my department at the University of Liverpool, my colleagues have demonstrated that the economic crisis in the years between 2008 and 2010 can be blamed for as many as 1000 people in the UK taking their own lives. We do, absolutely, need to understand how stress affects us. And we definitely need to find ways to help people (and mice) affected by stress.
But, while research like this is both fascinating and positive (except, perhaps, for the mice), I do have a scintilla of worry. And that worry is brought into focus in Kaster and colleagues’ final sentence; “Thus we prompt the suggestion that the up-regulated A2AR might be an effective target to correct brain disorders that involve a synaptic dysfunction, as now observed for the maladaptive responses to chronic stress.” I’m not completely sure about this. While I don't doubt (within the parameters of peer-reviewed science) that Kaster and colleagues have revealed something fascinating about how the brain responds to chronic stress, it’s a little less certain that this reflects either “synaptic dysfunction” or “maladaptive responses”, much less a “brain disorder”. As I understand Kaster and colleagues’ paper, the mice (and their brains) were responding normally to an abnormal – stressful – situation. It’s good to know how the brain works. It would be unfortunate to extrapolate that understanding to infer that such a response is a sign of abnormality, especially in humans.
Stressful events make us stressed, emotionally and physically; they have negative cognitive, emotional, physical and behavioural consequences. Given that we process information in the brain, using neurotransmitters, it's obvious that there will be a neurological route or pathway. It's great to know more about that pathway, and maybe that will even help us become more resilient or recover faster from stressful life events.
The neurological pathway itself isn't (or at least isn't necessarily) the ‘cause’ of our response to stress. It's a pathway, not a cause.
An analogy might help. If a driver swerves and crashes a car, we don't usually regard the steering wheel as the 'cause' of the crash. The steering wheel was absolutely necessary (almost certainly the steering wheel was a necessary part of the causal chain), but it didn't "cause" the crash. OK, we can imagine a weird scenario where a fault in the steering wheel (grease on the grip, perhaps) might be to blame. But such scenarios are vanishingly rare. Essentially, the wheel is a part of a mechanism whereby the cause (the driver's swerve) translates into the crash.
For both the mice, and for us humans for whom the findings may be extended, the neurological mechanism isn't the cause. People are stressed by events. We - because we're biological beings - use our biological brains to respond to stressful events. But the biology enables our human response it doesn't entail it or determine it. Here, the mice were stressed by events (rather nasty events) - damp bedding, shared living spaces, food and water deprivation, cold baths, cages tilted at 45°, inescapable shock and light/dark cycle inversion (a mouse equivalent of jet lag). These are the causes of stress. The mechanisms are, I would argue, something else.
So it's fantastic that this research has been conducted. It's genuinely important and potentially useful. But it doesn't necessarily mean that these molecular pathways are the "cause" of psychological distress. It's probably better to think of them as enabling our normal human responses, not causing them. This is important. The unfortunate tendency to label undesirable emotions as ‘symptoms’ of ‘illness’ may well cause us to treat people with less empathy than we should, to ignore the root causes of distress, and to turn to inappropriate medical treatments. I’m all in favour of understanding how our brains work. I’m slightly less keen on mistaking mechanisms for causes.