The core experiences of depression – changes in energy, activity, thinking and mood – have been described for more than 10,000 years. The word “depression” has been used for about 350 years.

Given this long history, it may surprise you that experts don’t agree about what depression is, how to define it or what causes it.

But many experts do agree that depression is not one thing. It’s a large family of illnesses with different causes and mechanisms. This makes choosing the best treatment for each person challenging.

Reactive vs endogenous depression

One strategy is to search for sub-types of depression and see whether they might do better with different kinds of treatments. One example is contrasting “reactive” depression with “endogenous” depression.

Reactive depression (also thought of as social or psychological depression) is presented as being triggered by exposure to stressful life events. These might be being assaulted or losing a loved one – an understandable reaction to an outside trigger.

Endogenous depression (also thought of as biological or genetic depression) is proposed to be caused by something inside, such as genes or brain chemistry.

Many people working clinically in mental health accept this sub-typing. You might have read about this online.

But we think this approach is way too simple.

While stressful life events and genes may, individually, contribute to causing depression, they also interact to increase the risk of someone developing depression. And evidence shows that there is a genetic component to being exposed to stressors. Some genes affect things such as personality. Some affect how we interact with our environments.

What we did and what we found

Our team set out to look at the role of genes and stressors to see if classifying depression as reactive or endogenous was valid.

In the Australian Genetics of Depression Study, people with depression answered surveys about exposure to stressful life events. We analysed DNA from their saliva samples to calculate their genetic risk for mental disorders.

Our question was simple. Does genetic risk for depression, bipolar disorder, schizophrenia, ADHD, anxiety and neuroticism (a personality trait) influence people’s reported exposure to stressful life events?

You may be wondering why we bothered calculating the genetic risk for mental disorders in people who already have depression. Every person has genetic variants linked to mental disorders. Some people have more, some less. Even people who already have depression might have a low genetic risk for it. These people may have developed their particular depression from some other constellation of causes.

We looked at the genetic risk of conditions other than depression for a couple of reasons. First, genetic variants linked to depression overlap with those linked to other mental disorders. Second, two people with depression may have completely different genetic variants. So we wanted to cast a wide net to look at a wider spectrum of genetic variants linked to mental disorders.

If reactive and endogenous depression sub-types are valid, we’d expect people with a lower genetic component to their depression (the reactive group) would report more stressful life events. And we’d expect those with a higher genetic component (the endogenous group) would report fewer stressful life events.

But after studying more than 14,000 people with depression we found the opposite.

We found people at higher genetic risk for depression, anxiety, ADHD or schizophrenia say they’ve been exposed to more stressors.

Assault with a weapon, sexual assault, accidents, legal and financial troubles, and childhood abuse and neglect, were all more common in people with a higher genetic risk of depression, anxiety, ADHD or schizophrenia.

These associations were not strongly influenced by people’s age, sex or relationships with family. We didn’t look at other factors that may influence these associations, such as socioeconomic status. We also relied on people’s memory of past events, which may not be accurate.

How do genes play a role?

Genetic risk for mental disorders changes people’s sensitivity to the environment.

Imagine two people, one with a high genetic risk for depression, one with a low risk. They both lose their jobs. The genetically vulnerable person experiences the job loss as a threat to their self-worth and social status. There is a sense of shame and despair. They can’t bring themselves to look for another job for fear of losing it too. For the other, the job loss feels less about them and more about the company. These two people internalise the event differently and remember it differently.

Genetic risk for mental disorders also might make it more likely people find themselves in environments where bad things happen. For example, a higher genetic risk for depression might affect self-worth, making people more likely to get into dysfunctional relationships which then go badly.

What does our study mean for depression?

First, it confirms genes and environments are not independent. Genes influence the environments we end up in, and what then happens. Genes also influence how we react to those events.

Second, our study doesn’t support a distinction between reactive and endogenous depression. Genes and environments have a complex interplay. Most cases of depression are a mix of genetics, biology and stressors.

Third, people with depression who appear to have a stronger genetic component to their depression report their lives are punctuated by more serious stressors.

So clinically, people with higher genetic vulnerability might benefit from learning specific techniques to manage their stress. This might help some people reduce their chance of developing depression in the first place. It might also help some people with depression reduce their ongoing exposure to stressors.

If this article has raised issues for you, or if you’re concerned about someone you know, call Lifeline on 13 11 14.

Jacob Crouse, Research Fellow in Youth Mental Health, Brain and Mind Centre, University of Sydney and Ian Hickie, Co-Director, Health and Policy, Brain and Mind Centre, University of Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.

It’s a Saturday afternoon at a kids’ birthday party. Hordes of children are swarming between the spread of birthday treats and party games. Half-eaten cupcakes, biscuits and lollies litter the floor, and the kids seem to have gained superhuman speed and bounce-off-the-wall energy. But is sugar to blame?

The belief that eating sugary foods and drinks leads to hyperactivity has steadfastly persisted for decades. And parents have curtailed their children’s intake accordingly.

Balanced nutrition is critical during childhood. As a neuroscientist who has studied the negative effects of high sugar “junk food” diets on brain function, I can confidently say excessive sugar consumption does not have benefits to the young mind. In fact, neuroimaging studies show the brains of children who eat more processed snack foods are smaller in volume, particularly in the frontal cortices, than those of children who eat a more healthful diet.

But today’s scientific evidence does not support the claim sugar makes kids hyperactive.

The hyperactivity myth

Sugar is a rapid source of fuel for the body. The myth of sugar-induced hyperactivity can be traced to a handful of studies conducted in the 1970s and early 1980s. These were focused on the Feingold Diet as a treatment for what we now call Attention Deficit Hyperactivity Disorder (ADHD), a neurodivergent profile where problems with inattention and/or hyperactivity and impulsivity can negatively affect school, work or relationships.

Devised by American paediatric allergist Benjamin Feingold, the diet is extremely restrictive. Artificial colours, sweeteners (including sugar) and flavourings, salicylates including aspirin, and three preservatives (butylated hydroxyanisole, butylated hydroxytoluene, and tert-Butrylhdryquinone) are eliminated.

Salicylates occur naturally in many healthy foods, including apples, berries, tomatoes, broccoli, cucumbers, capsicums, nuts, seeds, spices and some grains. So, as well as eliminating processed foods containing artificial colours, flavours, preservatives and sweeteners, the Feingold diet eliminates many nutritious foods helpful for healthy development.

However, Feingold believed avoiding these ingredients improved focus and behaviour. He conducted some small studies, which he claimed showed a large proportion of hyperactive children responded favourably to his diet.

Flawed by design

The methods used in the studies were flawed, particularly with respect to adequate control groups (who did not restrict foods) and failed to establish a causal link between sugar consumption and hyperactive behaviour.

Subsequent studies suggested less than 2% responded to restrictions rather than Feingold’s claimed 75%. But the idea still took hold in the public consciousness and was perpetuated by anecdotal experiences.

Fast forward to the present day. The scientific landscape looks vastly different. Rigorous research conducted by experts has consistently failed to find a connection between sugar and hyperactivity. Numerous placebo-controlled studies have demonstrated sugar does not significantly impact children’s behaviour or attention span.

One landmark meta-analysis study, published almost 20 years ago, compared the effects of sugar versus a placebo on children’s behaviour across multiple studies. The results were clear: in the vast majority of studies, sugar consumption did not lead to increased hyperactivity or disruptive behaviour.

Subsequent research has reinforced these findings, providing further evidence sugar does not cause hyperactivity in children, even in those diagnosed with ADHD.

While Feingold’s original claims were overstated, a small proportion of children do experience allergies to artificial food flavourings and dyes.

Pre-school aged children may be more sensitive to food additives than older children. This is potentially due to their smaller body size, or their still-developing brain and body.

Hooked on dopamine?

Although the link between sugar and hyperactivity is murky at best, there is a proven link between the neurotransmitter dopamine and increased activity.

The brain releases dopamine when a reward is encountered – such as an unexpected sweet treat. A surge of dopamine also invigorates movement – we see this increased activity after taking psychostimulant drugs like amphetamine. The excited behaviour of children towards sugary foods may be attributed to a burst of dopamine released in expectation of a reward, although the level of dopamine release is much less than that of a psychostimulant drug.

Dopamine function is also critically linked to ADHD, which is thought to be due to diminished dopamine receptor function in the brain. Some ADHD treatments such as methylphenidate (labelled Ritalin or Concerta) and lisdexamfetamine (sold as Vyvanse) are also psychostimulants. But in the ADHD brain the increased dopamine from these drugs recalibrates brain function to aid focus and behavioural control.

Why does the myth persist?

The complex interplay between diet, behaviour and societal beliefs endures. Expecting sugar to change your child’s behaviour can influence how you interpret what you see. In a study where parents were told their child had either received a sugary drink, or a placebo drink (with a non-sugar sweetener), those parents who expected their child to be hyperactive after having sugar perceived this effect, even when they’d only had the sugar-free placebo.

The allure of a simple explanation – blaming sugar for hyperactivity – can also be appealing in a world filled with many choices and conflicting voices.

Healthy foods, healthy brains

Sugar itself may not make your child hyperactive, but it can affect your child’s mental and physical health. Rather than demonising sugar, we should encourage moderation and balanced nutrition, teaching children healthy eating habits and fostering a positive relationship with food.

In both children and adults, the World Health Organization (WHO) recommends limiting free sugar consumption to less than 10% of energy intake, and a reduction to 5% for further health benefits. Free sugars include sugars added to foods during manufacturing, and naturally present sugars in honey, syrups, fruit juices and fruit juice concentrates.

Treating sugary foods as rewards can result in them becoming highly valued by children. Non-sugar rewards also have this effect, so it’s a good idea to use stickers, toys or a fun activity as incentives for positive behaviour instead.

While sugar may provide a temporary energy boost, it does not turn children into hyperactive whirlwinds.

Amy Reichelt, Senior Lecturer (Adjunct), Nutritional neuroscientist, University of Adelaide

This article is republished from The Conversation under a Creative Commons license. Read the original article.