As a society, we aren’t getting as much exercise as we should. In fact, current activity guidelines state that adults should get at least 150 minutes of moderately intense activity – or 75 minutes of vigorous activity – every week. But research has found that one in four adults aren’t active enough.
It’s easy to see why. Many of us drive to work instead of walking – and for those of us who work desk jobs, many are often so focused on what we’re doing we rarely get up from our desks except to visit the bathroom or get a drink. In short, though we might be busy, we aren’t moving very much. But after dealing with the stress of work week after week, it’s easy to daydream about unwinding on a warm beach, doing nothing but lounge around for a fortnight. But this might not be what our bodies need. In fact, it might actually be more harmful than we realise.
Our research looked at what effect even short periods of physical inactivity had on our bodies. We found that even just two weeks of low activity actually increased participants’ risk of later developing serious health conditions such as cardiovascular disease.
We know that physical activity is good for us. This is irrefutable, and we’ve known this for a long time. As far back as the 1950s, the link between day-to-day physical activity and health was first identified in the London transport workers study.
The study found that bus drivers were more likely to experience a heart attack compared to their bus conductor counterparts. The main difference between these two groups was that conductors spent their working day on their feet collecting fares from commuters, while bus drivers spent their days sitting down.
Since then, some have branded physical activity a “miracle cure” for cardiovascular risk. Yet, as a society, we are more sedentary than ever, and cardiovascular-related deaths remain the leading cause of death worldwide.
While we know that having a physically active lifestyle will improve our health, surely we aren’t doing any additional harm, even if we choose not to be physically active? We decided to examine exactly what the harmful effects of being physically inactive are.
For our study, we recruited young (aged 18-50 years), healthy weight (BMI less than 30), physically active individuals (meaning that they take more than 10,000 steps per day on average). After carrying out assessments to measure blood vessel health, body composition and blood sugar control, we asked them to become inactive for two weeks.
To achieve this, participants were provided with a step counter and asked not to exceed 1,500 steps per day, which equates to approximately two laps of a full sized football pitch. After two weeks, we reassessed their blood vessel health, body composition and blood sugar control to examine what effects two weeks of inactivity had on them. We then asked them to resume their usual routine and behaviours. Two weeks after resuming their normal daily lifestyles, we checked participants’ health markers to see if they’d returned to where they were when they’d started the trial.
Our group of participants successfully reduced their step count by an average of around 10,000 steps per day and, in doing so, increased their waking sedentary time by an average of 103 minutes per day. Artery function decreased following this two-week period of relative inactivity, but returned to their normal levels after two weeks following their usual lifestyles.
We were interested in seeing how activity levels influenced blood vessel health, since this is where most cardiovascular disease starts. Most of us don’t realise that our blood vessels are a complex system. They’re lined with muscle and constantly adapt to our needs by dilating (opening) and constricting (closing) to distribute blood where it’s most needed. For example, during exercise vessels feeding organs such as the stomach will constrict, as it is inactive at this time, and so blood is redistributed to our working muscles to fuel movement. One of the earliest detectable signs of cardiovascular risk is a reduced function of this dilatory capacity.
To measure this, we used an imaging technique called flow-mediated dilation or FMD. FMD measures how well the arteries dilate and constrict, and it has been found to predict our future cardiovascular risk.
We found that after as little as two weeks of inactivity there was a reduction in artery function. This indicates the start of cardiovascular disease development as a result of being inactive. We also observed an increase in traditional risk factors, such as body fat, waist circumference, fitness and diabetes markers, including liver fat, and insulin sensitivity.
Something we also observed – which we initially weren’t researching – was that resuming normal activity levels following two weeks of being physically inactive was below baseline. That is to say, our participants did not return back to normal within two weeks of completing the intervention.
This is interesting to consider, especially regarding the potential longer-term effects of acute physical inactivity. In real-world terms, acute physical inactivity could mean a bout of flu or a two-week beach holiday – anything that can have a potential longer-term effect on our usual habits and behaviour.
These results show us that we need to make changes to public health messages and emphasise the harmful effect of even short-term physical inactivity. Small alterations to daily living can have a significant impact on health – positively, or negatively. People should be encouraged to increase their physical activity levels, in any way possible. Simply increasing daily physical activity can have measurable benefits. This could include having a ten-minute walk during your lunch hour, standing from your desk on an hourly basis to break up sitting time or parking your car at the back of the supermarket car park to get more steps in.
The impact of spending a large proportion of the day being inactive has received a lot of research in recent years. In fact, it has become a hot point of discussion among exercise scientists. As technology advances and our lives become increasingly geared towards convenience, it’s important this kind of research continues.
The health consequences of sedentary behaviour are severe and numerous. Moving more in everyday life could be key in improving your overall health.
As we age, our bodies inevitably deteriorate. Some changes, like grey hair and wrinkles, are easily visible. Others, like high blood pressure, often go unnoticed, but can be deadly.
Just as our body shows signs of ageing, so does our genome. Damage comes from chemical reactions that alter our DNA, and from errors introduced when it is copied. Our cells protect against these ravages, but these mechanisms are not foolproof and cells gradually accumulate DNA damage over a lifetime.
As a consequence of this damage, your genome is not the same in every cell; you are a patchwork of cells with subtle differences in their DNA. When a cell divides it will pass on these changes, and as they accumulate there is more and more likelihood that there will be consequences.
If these changes – we call them mutations – chip away at the systems that govern cell proliferation and survival, this can lead to cancer.
Our latest research, published today in the journal Blood, provides new clues about how our cells protect their genome and guard against cancer.
Nearly 10% of cancers have a familial component. Genes like BRCA1 and TP53 are among the best known cancer susceptibility genes, and both are involved in coordinating the cell’s response to DNA damage.
BRCA1 helps to repair a specific type of DNA damage, in which both strands of DNA are broken. Inheriting a defective BRCA1 gene elevates the lifetime risk of both breast and ovarian cancer.
When DNA repair mechanisms break down, cells can accumulate staggering numbers of mutations, and cancer becomes almost inevitable.
Beyond genetics, a complex mix of environmental and lifestyle factors modify cancer risk.
When we read the genome of a cancer it is possible to attribute mutations to certain types of stress. UV radiation, for example, will fuse certain DNA bases. The UV damage signature is writ large in melanoma, a cancer linked to sun exposure.
Lung cancers from smokers and non-smokers have different mutation patterns because of the action of chemicals in cigarette smoke that attack the DNA.
We can also use this approach to diagnose defective DNA repair, as each defect triggers a characteristic pattern of mutations. In this way, mutation signatures can help us understand why a cancer has developed.
Smoking, UV radiation and X-rays all damage your DNA, but damage also comes from reactive molecules present within the cell. These molecules are fundamental to the chemistry of life – take water, for example.
Water is a very reactive molecule and can do damage to our DNA. One of the most common mutations, either in cancer or in normal cells, results from water molecules reacting with methylated DNA.
DNA methylation is a small chemical modification that acts as a signpost on top of our genetic code. It helps to control which genes are switched on or off. This fine-tuning is essential for normal development, but methylation also makes DNA more susceptible to damage. Most of these events are quickly repaired, but the damage is unrelenting and some sneak through.
Methylation damage is the most prominent feature of an ageing genome. It’s so pervasive and reliable it has been proposed as a molecular clock that marks ageing. But our new research shows this process occurs more rapidly in some people.
We found and studied three people whose pathways to repair methylation damage had broken down. They all lacked a DNA repair protein called MBD4, which led to a marked accumulation of methylation damage – as though their cells were ageing prematurely.
All three developed an aggressive form of leukaemia in their early 30s, a cancer which usually wouldn’t be seen until the person is in their 60s or 70s.
Methylation damage plays a role in most cancers, but in these cases it was the primary driver of the disease.
While complete inactivation of MDB4 – as occurred in the three participants – is extremely rare, our findings raise the question of how more subtle differences in DNA repair shape cancer risk, particularly in the context of ageing.
Ageing contributes to cancer risk in myriad ways. While we’ve focused here on the buildup of DNA damage, our immune system also plays an important role and tends to fade as we get older.
Lifestyle factors – such as obesity, stress and diet – also provide a cumulative risk that builds over a lifetime.
Understanding the interplay between these factors is key to finding strategies that will effectively diffuse the health consequences associated with ageing.
Our research is helping to tease apart the contribution of DNA damage in different disease processes. Our findings suggest that some people accumulate more DNA damage than others – their clocks are ticking a little faster – and measuring these differences may help to spot people at risk of developing cancer, or help match them with more effective treatments.
Ian Majewski, Laboratory Head & Victorian Cancer Agency Fellow, Cancer & Haematology Division, Walter and Eliza Hall Institute and Edward Chew, PhD candidate, Cancer and Haematology Division, Walter and Eliza Hall Institute
The series of earthquakes in North Lombok and others further east goes on. But hopefully the worst is over and the intensity will recede from now.
Hundreds of people have been killed and a lot more injured, many of them seriously. Nearly all this human suffering was caused by collapsing buildings. The subsequent homelessness will go on for many months for hundreds of thousands of people.
But a lot of this suffering need not have happened.
The strongest quake on August 5, 6.9 in magnitude and at a relatively shallow depth, is large by any standard. But, as photos and video footage show, not all buildings collapsed. Among the landscape of devastation are many buildings that appear to have suffered little if any damage.
According to one estimate, 70% of buildings suffered serious damage, which means 30% did not. In many parts of the world, such as Japan, New Zealand and Chile, buildings are designed to withstand earthquakes of this scale and many of them do, repeatedly.
Traditional buildings in most of Indonesia, including northern Lombok, were built of timber framing with thatched roofs. In an earthquake they flex and sway but rarely collapse. If they do, it is likely to happen slowly and incompletely and any falling roofing is relatively light and soft.
But over recent decades, building materials and methods have changed. Timber and thatch have become scarce and expensive and popular tastes have shifted towards houses that look, at least superficially, like those of the global modern middle class – little villas with plastered walls, glass windows and tiled roofs.
But underneath the (often picturesque) facades, the construction is of brick or concrete blocks, held together only with weak mortar and supported by little or no framing. The better ones may have some concrete framing, but the quality of the concrete is usually poor and the steel reinforcing, especially at joints, is minimal. These facades do not reliably support infill materials and they are heavy when they fall.
Roof tiles are only loosely secured and ceilings below them are too light to catch them. If one had to design a system of construction for easy collapse and maximum injuries, this would be the perfect model.
In Yogyakarta, in central Java, in May 2006, at least 150,000 houses of exactly this kind collapsed in less than a minute of shaking caused by a lesser earthquake than the largest in Lombok. Nearly 6,000 people were killed and thousands more injured. Farm animals housed in traditional buildings mostly survived.
A massive international humanitarian aid response and significant government programmes followed and within a year Yogyakarta was largely rebuilt – an astonishing result in the circumstances. Both government and international agencies went to considerable lengths to design safer methods, educate people about them and offer support, materials and incentives to “build back better”.
An expert report ten years later (unfortunately not yet published) concluded that:
The overall poor quality of construction however has almost certainly placed more people at increased risk of larger, heavier building elements collapsing upon them.
Northern Lombok has not had this kind of experience in recent decades and, because it is a relatively poor part of Indonesia, until 20 years ago, many people outside the urban areas lived in traditional houses. However, over recent years, partly as a result of tourism revenues, many houses have been built or extended in the new style and construction.
Here too, construction standards tend to be low, and even lower for poorer households. The video evidence shows exactly the kind of failures as in Yogyakarta 12 years ago, because of exactly the same basic weaknesses of design. The next earthquake, wherever it may be in Indonesia, will almost certainly have the same effects.
A recent article makes similar points and blames inadequate enforcement of building codes and lack of government commitment. Unfortunately the reality is not so simple.
The Yogyakarta experience shows that even with a massive campaign by government and international agencies, and with the fear of earthquakes still fresh in people’s minds, the rebuilding was little better than what it replaced. Building codes do exist in Indonesia, but they are rarely followed, easily evaded, and rarely enforced, least of all at the level of owner-built local housing.
Even if there were a serious effort to implement codes, it would be undermined by well-known levels of bureaucratic inefficiency and corruption, as well as public resistance and evasion. It would also have unintended consequences, including making decent housing even less affordable, especially for poorer people.
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There will be no easy solutions, but national education in basic structural design principles, subsidised design, production and distribution of cheap and simple hardware for mitigating the most common failures of design and financial incentives for appropriate construction might be worthwhile places to start.
The links below are to articles reporting on a major earthquake that hit New Zealand today, measuring 6.9 and located between the two islands in Cook Strait.
For more visit:
– New Zealand hit by quake of magnitude 6.9, minor damage | Reuters
A large number of earthquakes have hit the New Zealand area in recent days.
A reasonably strong earthquake (5.6) has just struck South Australia’s outback – basically in the desert. From what I understand there is a small town located 10 minutes from the suspected epicentre of the earthquake. There is potential for significant damage within that sort of radius of the earthquake, but thankfully it has struck a fairly remote region. It is of a similar magnitude to the earthquake that struck Newcastle in 1989.
The following article includes a number of ‘very good’ photos of damage caused by the tornadoes in the USA. These photos show very graphically the amount of damage and heartache caused by these destructive storms.
A major aftershock/earthquake has struck Christchurch, causing more damage to the devastated city.
The following are articles from Compass Direct News from the period I was on my break: