Microplastics and nanoplastics are everywhere in our environment – including in our oceans and lakes, farmland, and even Arctic ice algae.

Microplastics have also been found inside of us – with studies detecting them in various tissues including in the lungs, blood, heart and placenta. Understandably, concern is rising about the potential risks of microplastics on our health.

However, while a growing body of research has focused on microplastics and nanoplastics, there’s still a lack of direct evidence that their presence in human tissues is harmful to our health – and it’s uncertain if they are related to particular diseases.

A new study has uncovered a correlation between microplastics and heart health, though. The researchers found that people who had detectable microplastics and nanoplastics in the plaque in their arteries had a higher risk of heart attack, stroke and death.

Heart health

The researchers looked at 257 people altogether. All of the patients were already undergoing preventative surgery to remove plaque from their carotid arteries (the main arteries that supply the brain with blood). This allowed the researchers to collect plaque samples and perform a chemical analysis. They then followed up with participants 34 months later.

Of the 257 participants, 150 were found to have the presence of microplastics and nanoplastics in their arterial plaque – mainly fragments of two of the most commonly used plastics in the world, polyethylene (used in grocery bags, bottles and food packaging) and polyvinyl chloride (used in flooring, cladding and pipes).

A statistical analysis of this data found that patients with microplastics and nanoplastics in their plaque had a higher risk of suffering a heart attack, stroke or death from any cause, compared with those who had no microplastics or nanoplastics in their plaque.

The researchers also analysed the macrophages (a type of immune cell that helps remove pathogens from the body) in the patients’ arteries. They found that participants who’d had microplastics and nanoplastics in their plaque also had evidence of plastic fragments in their macrophages.

They also looked at whether certain genes associated with inflammation (which can be a sign of disease) were switched on in the participants. They found that the participants who’d had microplastics and nanoplastics in their plaque also had signs of inflammation in their genes.

These results may suggest an accumulation of nanoplastics and microplastics in carotid plaque could partly trigger inflammation. This inflammation may subsequently change the way plaque behaves in the body, making it less stable and triggering it to form a blood clot – which can eventually block blood flow, leading to heart attacks and strokes.

Interestingly, the researchers also found the presence of nanoplastics and microplastics was more common in participants who had diabetes and cardiovascular disease. This raises a lot of questions which have yet to be answered – such as why microplastics were more common in these participants, and if there may be a correlation between other diseases and the presence of microplastics in the body.

Other health risks

This study only focused on patients who had carotid artery disease and were already having surgery to remove the build-up of plaque. As such, it’s unclear whether the findings of this study can be applied to a larger population of people.

However, it isn’t the first study to show a link between microplastics and nanoplastics with poor health. Research suggests some of this harm may be due to the way microplastics and nanoplastics interact with proteins in the body.

For example, some human proteins adhere to the surface of polystyrene nanoplastics, forming a layer surrounding the nanoparticle. The formation of this layer may influence the activity and transfer of nanoplastics in human organs.

Another study suggested that nanoplastics can interact with a protein called alpha-synuclein, which in mouse studies has been shown to play a crucial role in facilitating communication between nerve cells. These clumps of nanoplastics and protein may increase the risk of Parkinson’s disease.

My published PhD research in chicken embryos found that nanoplastics may cause congenital malformations due to the way they interact with a protein called cadherin6B. Based on the interactions myself and fellow researchers saw, these malformations may affect the embryo’s eyes and neural tube, as well as the heart’s development and function.

Given the fact that nanoplastics and microplastics are found in carotid plaque, we now need to investigate how these plastics got into such tissues.

In mice, it has been demonstrated that gut macrophages (a type of white blood cell) can absorb microplastics and nanoplastics into their cell membrane. Perhaps a similar mechanism is taking place in the arteries, since nanoplastics have been identified in samples of carotid plaque macrophages.

The findings from this latest study add to a growing body of evidence showing a link between plastic products and our health. It is important now for researchers to investigate the specific mechanisms by which microplastics and nanoplastics cause harm in the body.

Meiru Wang, Postdoctoral Researcher, Molecular Biology and Nanotoxicology, Leiden University

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

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.