Why our brain needs sleep, and what happens if we don’t get enough of it

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Sleep is the time for our brain to reboot.
Hernan Sanchez/Unsplash, CC BY-SA

Leonie Kirszenblat, The University of Queensland

Many of us have experienced the effects of sleep deprivation: feeling tired and cranky, or finding it hard to concentrate. Sleep is more important for our brains than you may realise.

Although it may appear you’re “switching off” when you fall asleep, the brain is far from inactive. What we know from studying patterns of brain electrical activity is that while you sleep, your brain cycles through two main types of patterns: rapid eye movement (REM) sleep and slow-wave sleep.

Slow-wave sleep, which occurs more at the beginning of the night, is characterised by slow rhythms of electrical activity across large numbers of brain cells (occurring one to four times per second). As the night progresses, we have more and more REM sleep. During REM sleep we often have vivid dreams, and our brains show similar patterns of activity to when we are awake.

Read more – Health Check: three reasons why sleep is important for your health

What are our brains doing while we sleep?

Sleep serves many different functions. One of these is to help us remember experiences we had during the day. REM sleep is thought to be important for emotional memories (for example, memories involving fear) or procedural memory (such as how to ride a bike). On the other hand, slow-wave sleep is thought to reflect the storing of so-called “declarative” memories that are the conscious record of your experiences and what you know (for example, what you had for breakfast).

We also know experiences are “replayed” in the brain during sleep – the memories of these experiences are like segments from a movie that can be rewound and played forward again. Replay occurs in neurons in the hippocampus – a brain region important for memory – and has been best studied in rats learning to navigate a maze. After a navigation exercise, when the rat is resting, its brain replays the path it took through the maze. Replay helps to strengthen the connections between brain cells, and is therefore thought to be important for consolidating memories.

While we’re asleep our brain does a tidy-up, only keeping what it needs.
Sashank Saye/Unsplash

But is it that important for you to remember what you had for breakfast? Probably not – that’s why the brain needs to be selective about what it remembers. Sleep allows the brain to sift through memories, forgetting certain things so as to remember what’s important. One way it may do this is by “pruning away” or “scaling down” unwanted connections in the brain.

A leading theory of sleep function – the “synaptic homeostasis hypothesis” – suggests that during sleep there is a widespread weakening of connections (known as “synapses”) throughout the brain.

This is thought to counterbalance the overall strengthening of connections that occurs during learning when we are awake. By pruning away excess connections, sleep effectively “cleans the slate” so we can learn again the next day. Interfering with this scaling down process can, in some cases, lead to more intense (and perhaps unwanted) memories.

The importance of sleep for keeping our brains optimally active may be reflected in our changing sleep patterns as we age. Babies and children sleep much more than adults, probably because their developing brains are learning much more, and being exposed to new situations.

Later in life, sleep declines and becomes more fragmented. This may reflect either a reduced need for sleep (as we are learning less) or a breakdown in sleep processes as we age.

Read more – Children and sleep: How much do they really need?

Sleep is also needed to do a bit of brain “housekeeping”. A recent study in mice found sleep cleanses the brain of toxins that accumulate during waking hours, some of which are linked to neurodegenerative diseases. During sleep, the space between brain cells increases, allowing toxic proteins to be flushed out. It’s possible that by removing these toxins from the brain, sleep may stave off neurodegenerative diseases like Alzheimer’s.

What happens if we have a bad night’s sleep?

Getting enough sleep is important for attention and learning during our waking hours. When we are sleep deprived, we can’t focus on large amounts of information or sustain our attention for long periods. Our reaction times are slowed. We are also less likely to be creative or discover hidden rules when trying to solve a problem.

When you haven’t had enough sleep, your brain may force itself to shut down for a few seconds when you’re awake. During this “micro-sleep” you may become unconscious for a few seconds without knowing it. Drowsiness while driving is a leading cause of motor vehicle accidents, with sleep deprivation affecting the brain just as much as alcohol. Sleep deprivation can also lead to fatal accidents in the workplace – a major issue in shift workers.

Read more – Explainer: how much sleep do we need?

The beneficial effects of sleep on attention and concentration are particularly important for children, who often become hyperactive and disruptive in class when they don’t have enough sleep. One study found getting just one hour less sleep per night over several nights can adversely affect a child’s behaviour in class.

What are the long-term effects?

The longer-term effects of sleep deprivation are more difficult to study in humans for ethical reasons, but chronic sleep disturbances have been linked to brain disorders such as schizophrenia, autism and Alzheimer’s. We don’t know if sleep disturbances are a cause or symptom of these disorders.

The ConversationOverall, the evidence suggests having healthy sleep patterns is key to having a healthy and well-functioning brain.

Leonie Kirszenblat, Postdoctoral research fellow, The University of Queensland

This article was originally published on The Conversation. Read the original article.


Research Check: can ‘Lightning Process’ coaching program help youths with chronic fatigue?

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About 1% of youths will suffer from chronic fatigue.
from http://www.shutterstock.com

John Malouff, University of New England

Chronic fatigue syndrome involves experiencing a disabling level of fatigue for at least three months, where medical tests fail to show a biological cause. Adults, adolescents, and children can experience chronic fatigue syndrome. About 1% of youths develop the syndrome, which greatly affects their mood and decreases school attendance.

A research article published recently in the journal Archives of Disease in Childhood reported the effects of an intervention called the “Lightning Process”. The study found the Lightning Process added significantly to the effects of the usual treatment in the UK for chronic fatigue syndrome in youths.

The results immediately attracted media attention. But while the study did show a positive outcome, there are a few limitations that may have affected these results and should be mentioned.

Read more – Explainer: what is chronic fatigue syndrome?

The Conversation, CC BY-ND

What is the Lightning Process?

The Lightning Process is a psychological intervention developed by British osteopath Phil Parker. The 12-hour intervention, provided over three days, was developed for chronic fatigue syndrome, as well as other disorders.

The intervention, which can cost up to a few thousand dollars, involves three components that were outlined in the study:

  1. Instruction on the stress response, on how the mind and body interact, and on how thoughts can have positive or negative effects;

  2. Group discussion about these topics and about what trainees can change;

  3. Individual identification of a relevant goal each participant wants to achieve, and the thinking that might help the person achieve the goal, such as walking more.

The Lightning Process has generated controversy because of claims of its effectiveness in the absence of solid evidence. It has also attracted criticism because it is a psychological intervention for a medical problem, which some sufferers perceive as undermining the severity of their symptoms.

What exactly did the study find?

The study was the first randomised controlled trial (meaning half the people in the study were allocated to receive the intervention, and half were not) of Lightning Process for chronic fatigue syndrome in youths aged 12 to 18. It compared the usual treatment in the UK, which involves gradually increasing activity level, to the usual treatment plus 12 hours of Lightning Process.

The results showed better outcomes for the group receiving Lightning Process. These better outcomes involved fatigue, physical functioning, anxiety, and school attendance over periods of six to 12 months. Participants in the usual treatment group also improved significantly over time, but not as much as those who received the Lightning Process.

Half of the youths in the trial received usual treatment, half had the usual treatment plus the Lightning Process.
from http://www.shutterstock.com

How well done was the study?

The study procedures were published prior to the start of the study, making it hard to change methods to produce a desired finding. Participants were assessed using mostly well-validated measures before the intervention and for many months after.

The study had three notable weaknesses in its methods. These weaknesses limit how much can be made of the findings.

First, both the therapists and the clients knew which treatment they received. Hence, the zeal of the therapists or the desire of participants to please the researchers could have helped produce results in favour of the Process. Placebo effects may also have occurred: when participants think they’re getting a new, experimental treatment, placebo effects can lead to real or imagined improvements.

Second, the school attendance reports came from the young people themselves. It would have been more valuable to gather this information from official records.

Third, the Process participants received 12 extra hours of treatment. Hence, it’s not clear whether they improved more due to the content of that extra treatment or due to receiving more treatment.

What questions might be answered in the future?

The study showed a general problem in treating chronic fatigue: most of the potential participants with chronic fatigue syndrome who were contacted about entering the study chose not to enter. Also, some who entered the study failed to complete the intervention. No treatment works for someone who does not receive it. Attracting more young people with chronic fatigue to treatment remains a challenge.

The study did not compare Lightning Process with cognitive behavioural therapy (CBT) for chronic fatigue. Of all treatments for chronic fatigue syndrome, CBT has the most evidence of producing positive effects. A meta-analysis of many studies showed that CBT tends to lead to moderate benefits. The Process intervention has instructional, cognitive, and behavioural components that are commonly included in CBT. So the Lightning Process could produce similar outcomes, given that many of these components overlap.

What comes next?

The study findings are important enough to suggest that more research on the Lightning Process is warranted. But the findings are from a single study, with a single set of researchers. As such, they do not justify a conclusion that someone with the disorder ought to seek this specific treatment.

We shouldn’t change treatment off the back of one study. Especially one with limitations.
from http://www.shutterstock.com

If other studies with different researchers find something similar, then we might consider the intervention empirically supported for use in paediatric chronic fatigue syndrome.

A trial comparing Lightning Process to CBT would be valuable. Parents of young people suffering from chronic fatigue would like solid evidence about which treatment is most likely to help. – John Malouff

Peer review

I agree with the Research Check that this study has limitations, but I would perhaps be stronger in my criticisms of the study, as I think there are a few that haven’t been mentioned.

The treatment options the participants received were not standardised, and so because of the variety of treatment options available it’s difficult to evaluate what treatment worked best. All individuals also received a different number of sessions, which would have also impacted on the results from the study.

One point I would also raise is that the criteria used for diagnosing those in the study with chronic fatigue were very broad and did not take into account other criteria that are recognised in diagnosing chronic fatigue.

For these reasons, I think more research is needed before we can say this treatment has a benefit. Participants in the study should follow a standardised treatment and should not know which group they belong to in order to avoid a placebo effect. I would also make the suggestion researchers consider using a better method for establishing these individuals do suffer with chronic fatigue. – Lynette Hodges

Statement from the study author, Esther Crawley

The ConversationI did a press briefing because it was important to me that the limitations and implications of this study were clear. For example, it was important to me that children with CFS/ME [chronic fatigue syndrome/myalgic encephalomyelitis] and their parents understood that we have only tested LP [Lightning Process] in addition to specialist medical care. And that we could not say anything about adults with CFS/ME. I wanted it to be clear that many eligible children did not take part and some said this was because they didn’t want LP. I think most of these points were picked up by the press and on the whole, I was pleased with the reporting.

John Malouff, Associate Professor, School of Behavioural, Cognitive and Social Sciences, University of New England

This article was originally published on The Conversation. Read the original article.

No, depression won’t literally break your heart (but have a heart check anyway)

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Depression doesn’t lead to heart disease, as some people suggest, but it’s a sign that you might be at risk of it.
Paola Chaaya/Unsplash, CC BY-SA

Jennifer Welsh, Australian National University and Ellie Paige, Australian National University

Some people say depression leads to a broken heart. It’s a catchy expression, but is it really true?

There is certainly a link between depression and heart disease, the most common cause of a heart attack. People with depression are 30% more likely to develop heart disease than those without it.

It seems logical then that depression could, quite literally, break your heart.

Read more: Depression can break your heart, literally

However, our new research suggests rather than cause heart disease, depression in people aged 45 or older can signal the early signs of the disease and the need for a heart check.

How are depression and heart disease linked?

To say one thing causes another, we first need to understand how the two things are linked, including which comes first.

Does depression lead to an event like a heart attack? Or are there early signs of heart disease – which make people much more likely to have a heart event – that lead to depression?

We know depression has physical effects on the body, some of which may harm the heart. Depression can increase inflammation, heart rate and blood pressure, all of which are involved in developing heart disease.

However, it’s also true people with early heart disease can feel physically lousy long before a life threatening heart event.

Read more: Women have heart attacks too, but their symptoms are often dismissed as something else

Half of people who survive a heart attack say they had heart disease symptoms leading up to it. The most common early signs were fatigue, shortness of breath and pains in the chest, arm, neck or back. If experienced for long periods of time these symptoms can leave a person feeling depressed.

Depression can also be linked to heart disease through behaviours and other chronic diseases. Smoking, not exercising enough, heavy drinking and poor diet, and chronic conditions like diabetes, are all more common in people with depression. These are all also factors involved in developing heart disease.

So before we can claim depression breaks your heart, we must account for the fact some behaviours and chronic diseases are more common in this group, and some people may have depression because of the early signs of heart disease.

This is exactly what our study did.

What our study found

We used data from more than 150,000 people 45 years or older who had not already had a heart attack or stroke.

At the start of the study people reported their level of psychological distress, a commonly used measure of symptoms of depression and anxiety. We then followed them over five years to see how many developed heart disease.

Read more: What causes depression? What we know, don’t know and suspect

People with the highest levels of psychological distress were 70% more likely to go on to have a heart event (like a heart attack) within the next few years than people with the lowest levels of psychological distress.

After taking smoking, exercise, alcohol, weight and diabetes into account, this dropped to just 40%.

When we excluded people with early signs of heart disease, there was little evidence psychological distress increased the risk of developing heart disease at all.

This suggests it’s more helpful to view depression as something that signals a higher risk of heart disease, rather than as a direct cause of the disease.

This is in line with findings from other large-scale studies and robust trials. These have found treating depression does not reduce the risk of developing heart disease. If depression caused heart disease, we would have expected treating depression to have reduced the chance of developing heart disease.

If you have depression, get a heart check

The finding that depression is unlikely to cause heart disease suggests depression in people aged 45 or older might be an important sign of other things going on.

If you experience depression, talk to your doctor about it and how treatments can help.

If you’re 45 or older, while you’re with your doctor, ask for a heart check. This is the first step to assessing your future risk of heart disease. It also helps your doctor find the best way to lower your risk.

The ConversationIf you think you may be experiencing depression or another mental health problem, contact your general practitioner or in Australia, contact Lifeline 13 11 14, beyondblue 1300 22 4636 or SANE Australia 1800 18 7263.

Jennifer Welsh, PhD Candidate, Australian National University and Ellie Paige, Research Fellow, Australian National University

This article was originally published on The Conversation. Read the original article.

What causes depression? What we know, don’t know and suspect

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When thinking about what causes depression it’s important to remember some depression is a normal mood state.
Benjamin Combs/Unsplash, CC BY-SA

Gordon Parker, UNSW

The term and even diagnosis of “depression” can have different meanings and consequences. Depression can be a normal mood state, a clinical disorder, and even a disease.

If your favourite soccer team loses, you might feel emotionally depressed for a few minutes. If you were a player on the team and you brought about the loss, your state of depression and self-criticism might last much longer. Both can be viewed as normal “depressed mood” states.

Such states are common, with a study of university students finding that 95% of individuals had periods of feeling depressed, being self-critical and feeling hopeless every 6-8 weeks. So we should accept that a “depressed mood” is a universal and common experience. For most, the depressed mood is transient because the person will come to terms with the cause, or its cause will cease to exist over time, or be neutralised in some way.

Read more: Explainer: what is depression?

There’s no precise boundary between “depressed mood” states and “clinical depression”, but differences lie in impairment, symptoms and duration. Clinical depression is associated with distinct impairment (such as “absenteeism” with the individual unable to get to work, or “presenteeism” where the individual gets to work but the depression compromises their performance). Symptoms common in clinical depression include loss of appetite, sleep and libido changes, an inability to be cheered up, an inability to experience pleasure in life and a lack of energy. Clinical depression generally lasts months or years if untreated.

Current formal classification manuals tend to view clinical depression as a single condition simply varying by severity (major depression versus a set of minor depressions, regrettably including normal depressive moods). For the sake of discussing the causes of depression, I’ll look at two distinct types of depression: melancholia and the situational depressions.

Biological and disease-like depression

The key “biological” depressive disorder is melancholia. For some 2000 years, this was more viewed as a movement disorder rather than a mood disorder due to it showing “psychomotor disturbance”. This means the individual is slow to move or speak, lacking energy and unable to be cheered up, or agitated – wringing their hands, pacing up and down and repetitively uttering phrases. In addition, those with melancholia lose the capacity to find pleasure in life or be cheered up. They also lack energy and experience appetite and sleep changes.

Read more – Back to black: why melancholia must be understood as distinct from depression

A small percentage of those with melancholic depression develop “psychotic depression”. This is where an individual experiences delusions or hallucinations, often of derogatory voices telling them they’re worthless and better off dead, or of pathological guilt. For those with a bipolar disorder, most depressed episodes are melancholic or psychotic depression in type.

Melancholia has a strong genetic contribution, with a study quantifying a three times greater history of depression in family members of those with melancholia. If one parent has melancholia, their child has a 10% chance of developing the same; if both parents have melancholia, the chance is approximately 40%.

Once termed “endogenous depression” as it seemed to come from “within” rather than being caused by external stressors, episodes are generally more severe and persistent than would be expected from depression caused by environmental stressors. It doesn’t respond to counselling or psychotherapy and requires medication (most commonly an antidepressant drug but also perhaps other drug types). The psychotic form requires an antipsychotic drug in addition to an antidepressant.

There are a number of differing classes of antidepressants. The SSRIs (selective serotonin reuptake inhibitors) are viewed as increasing levels of the neurotransmitter serotonin in the brain and so correct the “chemical” disturbance underlying many depressive conditions. However, in melancholia it’s thought that there are also disturbances in other neurotransmitters such as noradrenaline and dopamine. Melancholia is therefore more likely to respond to the broader action antidepressant drugs such as the serotonergic and noradrenergic reuptake inhibitors (SNRIs) and tricyclics (TCAs), with the latter targeting all three implicated neurotransmitters.

In recent years, studies have not only implicated dysregulation in brain chemicals (“neurotransmitters”), but also in brain network circuits in those with melancholia. Disruptions in the circuits linking the basal ganglia (situated at the base of the forebrain and associated with emotion) and the pre-frontal cortex (the brain region implicated in personality expression and social behaviour) result in depressed mood, impaired cognition and psychomotor disturbance. These are, in essence, the key features of melancholia.

Brain imaging studies have also identified disrupted function in circuits and networks linking the insula (a brain region associated with awareness of our emotions) to other regions in the frontal cortex. These indicative findings are being progressively advanced by highly technical brain imaging strategies, and so in future years should clarify the multiple functional and structural changes that occur in the brain for those with melancholia.

There’s no “test” to diagnose biological depression, with former methods falling out of fashion due to inaccuracy, so diagnosis relies on the doctor identifying its characteristic features, excluding environmental factors and weighting a family history of depression.

Psychological and social depression

Non-melancholic depression is generally induced by a social stressor. A diagnosis of “reactive depression” captures a clinical, non-melancholic disorder caused by the individual experiencing a social stressor that impacts and compromises self-esteem. This could be a boyfriend or employer berating a young woman to the point where she feels worthless.

Read more: Biology is partly to blame for high rates of mental illness in women – the rest is social

In many ways, such scenarios are similar to a “normal” depressed mood state, but more severe. Here we would expect the individual to come to terms with or neutralise the stressor, or even spontaneously improve across all clinical parameters after weeks. A chronic environmentally or socially driven non-melancholic depression generally reflects an ongoing stressor that the individual cannot escape. An example would be a wife who lives with a constantly abusive husband, but is unable to leave him due to having a number of young children and no money of her own.

Other non-melancholic disorders are principally driven by psychological or personality-based factors – with actual episodes generally triggered by social stressors. Research has identified a number of personality styles that put people at risk:

  1. those with high levels of general anxiety who are at risk of depression because of their worrying, catastrophising propensities, and their tendency to take things too personally

  2. “shy” people who are often this way due to having been bullied or humiliated in their early years. They often view social interactions with others as threatening in comparison to the safety of their own company

  3. those who are “hypersensitive” to judgement by others. This could be praise or
    feeling (perhaps inappropriately) they are being rejected or abandoned. These people often respond by sleeping more and craving certain foods that may settle their emotional dysfunction

  4. “self-focused” individuals who are hostile and volatile with others, blame others when things go wrong and prioritise their own needs. When depressed, they tend to show a “short fuse” and create collateral damage for those around them

  5. those who were neglected or abused in their early years and who therefore have low basic self-worth. They often repeat such cycles of deprivation and abuse in their adult relationships, and so readily become depressed

  6. perfectionists who are prone to self-criticism and a loss of pride. They may also have a limited range of adaptive strategies to stress.

There are several brain regions implicated in these non-melancholic mood states and disorders. A key site is the amygdala (an almond-shaped region in the brain that processes emotional reactions) which shows a heightened response when an individual is depressed.

If there is “chemical” dysfunction in the non-melancholic disorders, serotonin is the most likely neurotransmitter implicated. We suspect serotonin has a role to play but we can’t be sure yet and further studies are needed.

The ConversationSo, we should reject a “one size fits all” model for considering “depression” and instead favour a “horses for courses” model. There are multiple types of depression (normal and clinical), with the latter reflecting differing biological, psychological and social causes and therefore requiring treatments that address the primary causal factor.

Gordon Parker, Scientia Professor, UNSW

This article was originally published on The Conversation. Read the original article.

Smartphone apps can be memory aids for people with brain injuries, and everyone else

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Calendar apps can be useful to people with and without memory problems.
Darren Grove/Shutterstock

Dana Wong, Monash University

Smartphone apps allow us to outsource remembering appointments or upcoming tasks. It’s a common worry that using technology in this way makes our brain’s memory capacity worse, but the reality is not that simple.

In fact, these platforms can be useful, not only for people with memory impairments, but also the general population.

Over two studies, we set out to explore the potential of smartphones as memory aids by investigating how people with traumatic brain injuries (TBI) or with stroke use them.

We surveyed 29 people with TBI and 33 non-injured people for our TBI study. For the stroke study, we surveyed 29 participants with stroke and 29 with no history of neurological conditions.

We found that memory apps like calendars can be helpful for people with brain injuries. And while it was a small sample, we also found that for participants without brain injury, there was no relationship between memory app use and memory ability.

This finding requires further analysis, but it is not consistent with the idea that memory aids make our brains lazy. Rather, such apps can free our minds to focus on other things, without using up mental resources worrying about what needs to be remembered.

How does brain injury affect memory?

Memory difficulties are common after acquired brain injuries such as a stroke. Everyday problems include forgetting appointments, names and details, losing track of conversations and misplacing personal items.

Research on rehabilitation of memory after brain injury supports the use of compensatory strategies. These include internal or mental strategies such as mentally rehearsing a speech and external strategies, such as calendars, lists, notes, alarms and photos.

Traditionally, external memory aids have been in paper-based formats such as diaries and notes, which are bulky and easily lost. Research shows early technological aids such as pagers and Personal Digital Assistants were helpful in approving improving memory function, but unfamiliar and difficult to learn to use for many people with brain injury.

Smartphones have the potential to address the limitations of earlier devices. They are familiar to most people, at least in the developed world, and are highly portable.

Are smartphones useful memory aids?

In both studies, we found that the majority of people both with and without brain injury used smartphones for three main reasons: for communication, as a memory aid and for internet access.

When asked about the biggest benefit of using a smartphone, users with TBI and stroke most often cited its helpfulness as a memory aid. This contrasted with those with no history of brain injury, who instead listed portability, convenience and access to the internet as the main benefits.

The memory apps used most often by participants with TBI and stroke were calendars, alarms, contacts lists, reminder text messages, notes, cameras, and to-do lists. These apps help the user remember appointments, tasks, details and locations without relying on their internal memory capacity.

A cerebral infarction (ischemic stroke) at the brain’s left hemisphere .
Puwadol Jaturawutthichai/Shutterstock

For people with TBI and those without any neurological conditions, there was no relationship between use of memory apps and performance on objective memory tests requiring recall of a list of words. This suggests that relying on memory aids did not influence intrinsic memory ability.

This result was important in counteracting the fear expressed by some TBI and stroke survivors that using a memory aid may make their memory abilities worse, just like using a wheelchair may make leg muscles weaker.

Our results indicate that this idea does not apply to memory among our sample group – rather, using memory aids is helpful for people who struggle to remember things by supporting their injured brains without causing any further damage.

For stroke survivors, more frequent use of memory apps also seems to be associated with higher productivity, as measured by their engagement in work, study and volunteer activities. This may mean that using smartphone memory apps enabled them to be more productive by supporting them to remember and organise tasks.

What are the barriers to using memory apps?

In both studies, we found that younger participants were more likely to use smartphones, suggesting that older adults may require more support in using them.

TBI and stroke survivors were also more likely to have difficulty learning to use their smartphone, and preferred being directly shown how to use it rather than learning by trial and error. Stroke survivors with motor (physical) symptoms used memory apps less frequently.

To further increase access to the benefits of smartphone memory apps, we now need to work out how to help users with brain injuries who may find them difficult to learn.

The ConversationOur future research will aim to work out the most effective methods for teaching smartphone memory apps to people with memory impairment.

Dana Wong, Senior Lecturer in Clinical Neuropsychology, Monash University

This article was originally published on The Conversation. Read the original article.

We know too much sugar is bad for us, but do different sugars have different health effects?

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The type of sugar in popular soft drinks varies from country to country even if the brand name is the same.
from shutterstock.com

Bronwyn Kingwell, Baker Heart and Diabetes Institute; Pia Varsamis, Baker Heart and Diabetes Institute, and Robyn Larsen, Baker Heart and Diabetes Institute

Our recent article published in the Medical Journal of Australia found that Australian and European soft drinks contained higher concentrations of glucose, and less fructose, than soft drinks in the United States. The total glucose concentration of Australian soft drinks was on average 22% higher than in US formulations.

We compared the composition of sugars in four popular, globally marketed brands – Coca-Cola, Fanta, Sprite and Pepsi – using samples from Australia, Europe and the US. While the total sugar concentration did not differ significantly between brands or geographical location, there were differences between countries in the concentrations of particular sugars, even when drinks were marketed under the same trade name.

Sucrose is made up of one glucose molecule and one fructose molecule.
from shutterstock.com

Whether these differences have distinct effects on long-term health is currently unclear. Certainly, over-consumption of either glucose or fructose will contribute to weight gain, which is associated with a host of health conditions such as type 2 diabetes and heart disease. And because the body metabolises glucose and fructose in different ways, their effects may differ.

Sucrose, glucose and fructose

Soft drinks, as they are referred to in Australia, or “sodas” in the US and “fizzy drinks” in the UK, are non-alcoholic, carbonated, sugar-sweetened beverages. Australia ranks seventh out of the top ten countries for soft drink sales per capita.

Sugars are the chief ingredient in soft drinks and include glucose, fructose and sucrose. The source of sugars in popular soft drinks varies between global regions. This is because sugars are sourced from different crops in different areas of the world.

Soft drinks in Australia are primarily sweetened with sucrose from sugar cane. Sucrose, often referred to as “table sugar”, is composed of one glucose molecule and one fructose molecule joined by chemical bonds. This means equal amounts of glucose and fructose are released into the bloodstream when sucrose is digested.

Overseas, soft drinks are sweetened with sucrose-rich sugar beet (Europe) or high-fructose corn syrup (US). High-fructose corn syrup is also made up of glucose and fructose, but contains a higher fructose-to-glucose ratio than sucrose.

Do they have different health impacts?

Fructose over-consumption is known to contribute to fatty liver disease. Fatty liver disease affects about one in ten people in the West. Non-alcoholic fatty liver disease is the leading cause of liver disease.

Some researchers have suggested too much fructose in the diet can harm the liver in a similar fashion to alcohol. However, this concern is related to added fructose in the diet, not natural sources. Natural sources of fructose, such as fruit, honey and some vegetables, are not generally over-consumed and provide other important nutrients, such as dietary fibre and vitamins. So, fruit does not generally pose a risk for fatty liver disease.

Natural sources of fructose, such as fruit, are generally not over-consumed.
from shutterstock.com

High glucose consumption rapidly elevates blood glucose and insulin. This may affect brain function, including mood and fatigue. Because high blood glucose is linked to diabetes, consumption of high-glucose drinks may also raise the risk of diabetes and cardiovascular (heart) disease.

All soft drinks are considered energy-dense, nutrient-poor and bad for health. However, one of the inherent challenges in the field has been an inability to determine the actual dose of glucose or fructose in these drinks.

Studies that follow people over time, and link soft drink consumption to adverse health effects, are complicated by not knowing whether individuals in these studies are simply eating too many energy-rich foods, and whether soft drink consumption coincides with other poor health behaviours. So, further research is required to determine whether soft drinks containing different concentrations of fructose and glucose are associated with differing health risks.

Soft drink policies

There is still much to learn about the differences in composition of sugars and patterns of soft drink intake between countries. A small number of countries, including Mexico and France, have already implemented taxation on soft drinks. It remains to be determined whether these actions reduce the incidence of obesity, diabetes and heart diseases.

Over-consumption of any kind of sugar leads to weight gain.
from shutterstock.com

Australian policymakers are yet to take action to reduce soft drink consumption. A range of intervention strategies have been considered, including banning sugary soft drinks in schools and hospitals, taxation, and regulating beverage marketing.

The ConversationThe New South Wales Health Department has just announced sugary drinks will be phased out of vending machines, cafes and catering services in the state’s health facilities by December. This is a great move. Importantly, we must continue to increase public awareness of the adverse health effects of sugary soft drinks.

Bronwyn Kingwell, Head, Metabolic and Vascular Physiology NHMRC, Senior Principal Research Fellow, Baker Heart and Diabetes Institute; Pia Varsamis, PhD Student, Metabolic and Vascular Physiology, Baker Heart and Diabetes Institute, and Robyn Larsen, Postdoctural Research Fellow in Nutritional Biochemistry, Baker Heart and Diabetes Institute

This article was originally published on The Conversation. Read the original article.

Explainer: what causes alopecia areata and can you treat this type of hair loss?

Rodney Sinclair, University of Melbourne

Alopecia is the medical term for hair loss and comes from the Greek word alōpekía referring to the skin condition, mange, in foxes. Alopecia areata causes a unique form of hair loss different to the more common age-related male and female pattern hair loss.

It’s also the most common autoimmune disease (when the body’s immune system attacks its own tissues), more common than insulin-dependent diabetes, rheumatoid arthritis or thyroiditis (inflammation of the thyroid).


Alopecia areata affects people of all ages including young children. It produces circular patches of hair loss that appear overnight. More patches appear over time and eventually about 5% of people affected lose every hair on their body. This includes eyebrows, eyelashes and even nose hairs. In some people, hair grows back, either in the same place or on a previously unaffected part of the scalp or body.

If alopecia areata is the most common autoimmune disease, why have most people never heard about it?

There are two likely reasons. One is that it’s embarrassing and distressing. Wherever possible, people try to hide it with clever hairstyles and cosmetic camouflage. The other reason is it often comes and goes, and once gone people would rather forget they had it.

So people only tend to see severe cases where people have lost all their hair. Even then people can mistake the condition for the hair loss seen after chemotherapy.

Bouts of alopecia areata generally come and go.
Duncan Creamer/Flickr, CC BY

The distress can be severe, especially in boys whose short hair makes it more difficult to conceal the patches of hair loss. Suicide among young boys affected by alopecia areata is more common than we would expect for a condition that essentially affects appearance, rather than people’s physical health.


Alopecia areata occurs when the body’s immune system mistakes hair follicles as foreign and attacks them. This causes the hairs to fall out. This specific form of autoimmunity is a lifelong tendency that can be inherited from either parent.

It’s what geneticists call a “complex polygenic disease” meaning it arises due to an interaction between multiple genes as opposed to a mutation in a single gene. More than 17 genes have been associated with alopecia areata and scientists expect there are still more genes to be discovered.

While your genes are pretty much fixed from birth, alopecia areata tends to come and go, especially in the early stages. This suggests something in our environment triggers individual episodes.

Doctors, patients and their families have hunted for this elusive trigger hoping its discovery would allow people to avoid relapses. However, no convincing dietary or lifestyle modification has emerged that changes the risk of relapse.

While people regularly blame stress as a trigger, in my experience of treating patients, the condition causes the stress.

Current treatment

For 40 years, there has been little progress in its treatment. Mild cases usually respond to cortisone injections into the bald scalp. Cortisone suppresses inflammation and stops white blood cells from attacking the hair follicles and promotes hair regrowth.

Some patients respond to cortisone tablets or other anti-inflammatory tablets but the results are by no means guaranteed. Some doctors are reluctant to prescribe these medications for fear of side-effects such as weight gain, mood disturbance, diabetes, hypertension and increased risk of infection.

Severe cases, where the scalp is completely bald (called alopecia areata totalis) or where every hair on the body vanishes (called alopeica areata universalis) rarely recover without treatment. These types of hair loss tend to be long lasting or even permanent.

For millions of people worldwide affected by alopecia areata, nothing has helped and for many a wig is the only option.

For many people a wig is the only option.
Lwp Kommunikáció/Flickr, CC BY

Future treatments

Many of the 17 genes associated with alopecia areata are involved in a particular inflammatory pathway called the JAK/STAT pathway. Drugs targeting this pathway, known as JAK inhibitors or JAKs, are already in development or are available, but for other conditions.

Some JAK inhibitors are already available on prescription in Australia, Europe and the USA to treat other diseases such as rheumatoid arthritis and myelofibrosis (a blood disorder). But in Australia and elsewhere they are not yet approved for use to treat alopecia areata.

Clinical trials are taking place to see whether the drugs work in alopecia areata patients, who in particular will benefit the most and to see whether the benefits of treatment outweigh the risks.

The ConversationSide effects of JAK inhibitors identified so far include stomach upset, an increase in chest and skin infections and transaminaitis (an alteration in liver function identified by blood testing). Mild skin and upper respiratory tract infections have been reported in 25% of patients. Very few patients with alopecia areata elect to stop the medication as a result of side effects. Nevertheless patients receiving these medications require close medical supervision.

Rodney Sinclair, Professor of Dermatology, University of Melbourne

This article was originally published on The Conversation. Read the original article.

Explainer: what is traumatic brain injury?

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People with traumatic brain injuries, say after a car accident or an assault, can have behavioural problems long after their physical injuries have healed.
from www.shutterstock.com

Travis Wearne, UNSW and Emily Trimmer, UNSW

Adam was fortunate to survive a major car accident three years ago. He was in hospital for several months but had no ongoing physical injuries. He looked like he made a full recovery. But he was argumentative, childish, vulgar and his family said he “was not the same person”. Adam had a severe traumatic brain injury.

What is traumatic brain injury?

A traumatic brain injury is when the brain is damaged by an external mechanical force, like the type you may have in a car accident, if you fall, play sport or if you are assaulted.

These injuries are usually in the news when sports players have a concussion; or in relation to drug and alcohol fuelled assaults where a blow to the head results in a damaging, sometimes fatal, fall to the ground (the coward’s punch or king hit).

Mostly, it’s young adults, particularly men, who are affected. But many elderly people may get a traumatic brain injury when they fall.

Australia has a growing population of survivors of traumatic brain injury. This is due to the young age of most victims and decreased death rates due to better treatment. Traumatic brain injury is expected to be a major cause of disability by 2020.

How does it affect people?

Few traumatic brain injuries are the same and the outcomes of two similar injuries can be different in different people. Injuries can affect the way people think, feel, behave and relate to everyday situations.

People with moderate to severe injuries can have problems communicating, paying attention, processing thoughts quickly, learning, remembering, planning, problem-solving, meeting goals, and thinking abstractly or flexibly.

Damage to the part of the brain called the frontal lobes affects people’s ability to regulate their thoughts, emotions and behaviour. It can cause people to be impulsive, irritable, aggressive, have reduced drive, be apathetic, to have excessive emotions or a flattened mood.

Difficulties understanding the emotions and intentions of others (known as social cognition) may cause reduced empathy and socially inappropriate behaviour. Reduced self-awareness can also result in lack of insight into their abilities and the changes others perceive.

Traumatic brain injury can change an individual’s personality to the point where they “may no longer be the same person” that they were before. Given that many of these difficulties can occur without physical problems, they fall under the umbrella of an “invisible disability”.

How does traumatic brain injury affect the brain?

Injuries can be due to the immediate effect of the impact (known as primary injuries) or ones that follow these (secondary complications).

Primary injuries include: lacerations, when the brain tissue is cut or torn; contusions, when the brain is bruised; rupturing of blood vessels; and axonal injury, where neurons are stretched and torn.

These can occur where the object hits the head (a focal injury) or throughout the brain (diffuse injury). Parts of the brain known as the frontal and temporal lobes are most susceptible to both of these types of injuries. This is because of their large size and as they are close to the hard and uneven surfaces of the skull that can cause damage.

The frontal and temporal lobes of the brain, shown here, are particularly susceptible to injury.
from www.shutterstock.com

Secondary complications include brain lesions (damaged brain tissue); brain swelling, increased intracranial pressure (pressure inside the skull), herniation (movement of brain tissue), tissue death, hypoxia (oxygen deprivation) and infection.

How long someone loses consciousness initially and how long they’re confused for (known as post-traumatic amnesia) are used to classify traumatic brain injury as mild, moderate or severe. Most (about 80%) hospitalisations are for mild injuries.

How is it managed?

People with a traumatic brain injury can be treated while staying in hospital (as an in-patient) or after they’re discharged into the community (as an out-patient).

In-patient rehabilitation focuses on immediate medical and functional issues, with a range of health professionals involved, like physiotherapists, speech pathologists, neuropsychologists (psychologists who specialise in assessing, diagnosing and treating disorders of the brain) and occupational therapists. Typically, a personalised rehabilitation plan is drawn up to help the patient to move back into the community.

Out-patient rehabilitation focuses more on the context of daily living. Here, there is a shift to helping patients establish life roles and successfully complete everyday tasks, like making meals, showering and travelling.

What are the challenges ahead?

Recovery from a traumatic brain injury varies from person to person. Some people can easily resume their lives while others can struggle adjusting to their limitations, new lifestyle and new self. Some can have trouble living independently, fulfilling life goals and finding a meaningful place in society.

Behavioural and emotional difficulties are significant barriers to long-term recovery. These challenges may not become obvious until the person is in the community, discharged from rehabilitation services and completely dependent on their carers and/or families.

Behavioural and personality issues also make traumatic brain injury difficult to manage, placing burden on carers and result in difficulties finding and keeping a job.

Family members and friends can pull away, leading to further social isolation and loneliness, making survivors more susceptible to mental health problems and institutionalisation. Sadly, these problems worsen as years pass, despite improvements made during early recovery.

The ConversationIf you or someone you know is a survivor of traumatic brain injury, contact Brain Injury Australia, Synapse or the Centre for Research Excellence in Brain Recovery for more information and support.

Travis Wearne, Postdoctoral Research Fellow, UNSW and Emily Trimmer, Postdoctoral Research Fellow, UNSW

This article was originally published on The Conversation. Read the original article.

Melanoma: Taming a migratory menace

Richard Neubig, Michigan State University

The deadliest cancer of the skin is cutaneous melanoma. In 2017 over 160,000 Americans are expected to be diagnosed with melanoma, and over half will have invasive disease, or one that has gone beyond the skin and which carries greater risk of recurrence. About 9,700 people are expected to die from melanoma this year.

Unlike most common cancers, such as breast and lung cancer, the incidence of melanoma continues to increase, mainly in young people below the age of 30. There has been a more than 50 percent increase in melanoma in young women since 1980.

The vast majority of melanomas are caused by exposure to UV light from sun or indoor tanning. Reducing these exposures by changing habits or using sun protection – sun screens and clothing coverage – is the best way to avoid melanoma and other skin cancers.

As a researcher who studies what makes melanoma spread, or metastasize, I’m acutely aware of how hard this deadly cancer is to tame. To be sure, advances have been made. Former President Jimmy Carter – probably the most high-profile melanoma survivor in history – benefited from new treatments resulting from immunotherapy, a technique my lab and many others are using to combat cancer.

A challenging cancer

For reasons that aren’t fully understood, even quite small melanomas can spread in the body, or metastasize. Detection very early, when the tumor is less than 1 millimeter thick, allows surgery that provides a near cure.

Survival with the earliest Stage 0 or 1A melanomas, or local disease, is greater than 95 percent at ten years after diagnosis. This fact has prompted the Melanoma Research Foundation to promote its #GETNAKED campaign for monthly skin checks to identify new moles or skin changes that might be an early indication of melanoma. Catching it early is critical because once it spreads, melanoma can become a monster.

Let’s consider the process of cancer metastasis, which involves at least four distinct steps.

First the cancer cells have to leave the vicinity of the primary tumor. They do this by invading through tissue barriers that sustain the normal tissue architecture.

Second, they need to invade through the blood vessel wall to get into the bloodstream.

These two steps are called intravasation, which means “into the blood stream.” Once there, the cancer cells need to survive.

Most cells in normal tissues require cell attachment, or contact with surfaces or other cells, to survive. When normal cells are detached from those contacts, they usually undergo a type of cell suicide called anoikis. This process of cell suicide is lost in many cancers.

The cancer cells then need to leave the bloodstream by invading through the wall of the blood vessel in a process called extravasation. This third step allows the cancer cells to spread to other parts of the body.

Finally, the cancer cells need to adapt and grow in the new environment, such as in the lung or brain.

One unique characteristic of melanoma is that it is not uncommon to have melanoma metastases show up after 10 or more years with no evidence of disease.

These late recurrences may be due to several underlying mechanisms, but one explanation is a process called cellular dormancy. While in this dormant state, cells can not be detected, and it is thought that the patient may have been cured.

Finding a way to prevent dormancy could reduce the chances of a late recurrence of metastatic disease.

Recent advances bring hope

Beyond prevention of the cancer in the first place, which is the best approach, there have been tremendous advances in the treatment of cutaneous melanoma. A critical development was the discovery in 2002 that over half of cutaneous melanomas have a mutation in the BRAF gene.

The mutation of this gene plays a key role in melanoma cell growth and proliferation. The BRAF protein is a member of the protein kinase family which has become a major target class for drug development in the pharmaceutical sector.

In 2010, remarkable results were presented on clinical benefits of a BRAF inhibitor, vemurafenib.

In the same year, a major advance in immune therapy for melanoma was reported where ipilimumab, an antibody that enhances the body’s immune responses, showed a significant survival benefit in patients with diffuse metastatic melanoma. These were the first breakthroughs in melanoma treatment in more than a decade.

In addition to these two early developments, other drugs acting like vemurafenib as well as improved immunotherapies have been developed. These have further improved therapy of cutaneous melanoma. Immune modulation has even resulted in long-term survival in a fraction (10-20 percent) of patients.

Limits to new treatments

Despite these advances, however, there are still key problems with current therapies. Many rapidly lose effectiveness; drugs like vemurafenib that were controlling the tumor stop working through the development of resistant cancer cells, often within less than one year.

Also, the immune therapies only benefit a fraction of patients. When combinations of two immune therapy drugs are used to give a better effect on the cancer, the patients’ immune systems begin attacking normal tissues, which leads to autoimmune side effects.

Consequently, we need new approaches to prevent or treat the progression of melanoma and especially the development of metastases.

Work in our lab and that of others has identified a cellular mechanism similar to the BRAF pathway that appears to play a role in the migration and metastasis of melanoma. A pathway is a series of biological steps that lead to changes in cell function, such as growth or migration.

If we could confirm this new pathway as a possible drug target, we may be able to develop a therapy to prevent metastasis.

A protein to examine

In the BRAF pathway, a small protein called Ras works upstream of BRAF to activate it. Ras is one of the most commonly mutated genes in all of cancer biology. The particular version in melanoma is called NRAS. It is mutated and activated in about 20 percent of melanomas. Combined, mutations in BRAF and NRAS are found in 80-90 percent of melanomas. This is why the BRAF pathway is a prime target for therapy.

The new pathway we have identified starts with something called the Rho protein, which is very closely related to Ras.

When this Rho mechanism is activated, cancer cells move more actively and will invade the tissue that surrounds a tumor.

Along with Rho, a second critical player is a protein called MRTF that turns on gene expression (i.e. the production of RNA and proteins) when it is activated. Rho activates MRTF by driving it into the nucleus of the cell, where it can turn on gene expression.

We found that this Rho/MRTF pathway is activated in some melanoma tumors but not others. When it is turned on, the MRTF protein is in the nucleus and the cells migrate very quickly and form large lung metastases when injected into mice.

Our lab, in collaboration with Dr. Scott Larsen at the University of Michigan, has developed some chemical inhibitors of the Rho/MRTF pathway. In our recent publication, we showed that one of these compounds was able to reduce melanoma cell migration and invasion in lab studies and to reduce metastasis of a human melanoma to the lung in a mouse model. We observed a remarkable decrease in the number and size of lung metastases in this study.

Our current studies are trying to determine whether measurements of Rho/MRTF pathway activity can be used to predict which melanoma tumors will metastasize and which early-stage melanomas are more likely to recur. If so, identification of high activity would trigger the need for very close clinical monitoring after surgery or possible drug treatment with existing drugs, or our compounds if they become available for clinical use.

We are also trying to determine whether we can prevent metastases only before the cancer cells have arrived in the lung, for example. Alternatively, if we prevent dormancy so that the cells die before setting up shop in the distant tissue or prevent the reactivation of the dormant cells in their new environment, the compounds might work even after the earliest stage of tumor spread.

The road from studies in mice to the clinic is long and full of pitfalls. We are continuing efforts to demonstrate that these compounds are safe enough for human studies in a few years. There are still many questions, but this approach could add a new arrow in the quiver of cancer treatment specialists.

The Conversation

Richard Neubig, Professor of Pharmacology and Toxicology, Michigan State University

This article was originally published on The Conversation. Read the original article.

The science is in: gardening is good for you

Chris Williams, University of Melbourne

As the weather warms and days lengthen, your attention may be turning to that forgotten patch of your backyard. This week we’ve asked our experts to share the science behind gardening. So grab a trowel and your green thumbs, and dig in.

“That’s all very well put,” says Candide, in the final line of Voltaire’s novel of the same name, “but we must go and work our garden.”

I studied this text at high school before I became a gardener and professional horticulturist. We were taught that Candide’s gardening imperative was metaphorical not literal; a command for finding an authentic vocation, not a call to take up trowels and secateurs.

In fact, Voltaire himself really believed that active gardening was a great way to stay sane, healthy and free from stress. That was 300 years ago.

As it turns out, the science suggests he was right.

The science of therapeutic horticulture

Gardens and landscapes have long been designed as sanctuaries and retreats from the stresses of life – from great urban green spaces such as Central Park in New York to the humblest suburban backyard. But beyond the passive enjoyment of a garden or of being in nature more generally, researchers have also studied the role of actively caring for plants as a therapeutic and educational tool.

“Therapeutic horticulture” and “horticultural therapy” have become recognised treatments for stress and depression, which have served as a healing aid in settings ranging from prisons and mental health treatment facilities to schools and hospitals.

Gardening and school

Studies of school gardening programs – which usually centre on growing food – show that students who have worked on designing, creating and maintaining gardens develop more positive attitudes about health, nutrition and the consumption of vegetables.

They also score better on science achievement, have better attitudes about school, and improve their interpersonal skills and classroom behaviour.

Research on students confirms that gardening leads to higher levels of self-esteem and responsibility. Research suggests that incorporating gardening into a school setting can boost group cohesiveness.

Gardening and mental health

Tailored gardening programs have been shown to increase quality of life for people with chronic mental illnesses, including anxiety and depression.

Another study on the use of therapeutic horticulture for patients with clinical depression sought to understand why gardening programs were effective in lessening patient experience of depression. They found that structured gardening activities gave patients existential purpose. Put simply, it gave their lives meaning.

In jails and corrective programs, horticultural therapy programs have been used to give inmates positive, purposeful activities that lessen aggression and hostility during and after incarceration.

In one detailed study from a San Francisco program, involvement in therapeutic horticulture was particularly effective in improving psychosocial functioning across prison populations (although the benefits were not necessarily sustained after release.)

Gardening has been shown to help improve the lives of military veterans and homeless people. Various therapeutic horticulture programs have been used to help people with learning difficulties, asylum seekers, refugees and victims of torture.

Gardening and older people

As populations in the West age, hands-on gardening programs have been used for older people in nursing homes and related facilities.

A systematic review of 22 studies of gardening programs for older adults found that gardening was a powerful health-promoting activity across diverse populations.

One study sought to understand if patients recovering from heart attack might benefit from a horticultural therapy program. It concluded:

[Our] findings indicate that horticultural therapy improves mood state, suggesting that it may be a useful tool in reducing stress. Therefore, to the extent that stress contributes to coronary heart disease, these findings support the role of horticultural therapy as an effective component of cardiac rehabilitation.

Horticulturist and nurse Steven Wells talks about his work at Austin Health.

While the literature on the positive effects of gardening, reflecting both qualitative and quantitative studies, is large, most of these studies are from overseas.

Investment in horticultural therapy programs in Australia is piecemeal. That said, there are some standout success stories such as the Stephanie Alexander Kitchen Garden Foundation and the work of nurse Steven Wells at the Royal Talbot Rehabilitation Centre and beyond.

Finally, without professionally trained horticulturists none of these programs – in Australia or internationally – can take place.

The Conversation

Chris Williams, Lecturer in urban horticulture, University of Melbourne

This article was originally published on The Conversation. Read the original article.