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Updated: 18 hours 6 min ago

Menopause 'may mix up exercise reward pathways in the brain'

Fri, 2016-07-29 07:30

"Menopause 'crushes your motivation to exercise'," the Mail Online reports. But before you bin your gym card, the study it reports on involved rats, not women.

The female rats were genetically engineered to have either a high or low exercise capacity.

Those who had their ovaries removed to model human menopause showed lower activity on a running wheel over the following 11 weeks compared with those who hadn't.

And surprisingly the rats that had prior high exercise capacity had no protection – in fact, their activity levels declined more than the rats who'd been less active to start with.

The reason seemed to be because lack of oestrogen alters dopamine activity in the brain's motivation and reward centre.

In simplistic terms, dopamine is often described as a "feel-good" chemical and has been linked to many addictive activities, such as gambling.

The findings may give a possible explanation for why some women going through the menopause may feel less motivated to exercise.

But humans aren't genetically engineered rats, and we don't know that our biological mechanisms work in exactly the same way.  

Also, the rats were not given any type of hormone replacement therapy (HRT) to boost oestrogen levels, so these finding may not be applicable for women who choose to have HRT.

Physical activity is recommended at all stages of life, and many postmenopausal women enjoy very active lifestyles.

The best thing for people to do is to follow physical activity recommendations where possible, doing what feels comfortable for them.

Where did the story come from?

The study was carried out by researchers from the University of Missouri and the University of Kansas Medical Center, and received funding from the US National Institutes of Health.

It was published in the peer-reviewed journal, Physiology and Behavior.

The Mail's headline boldly states that the findings directly relate to menopausal women – only hidden well down in the article does it say that it involved rats.

What kind of research was this?

This animal research in genetically engineered rats aimed to see whether those bred to have high exercise capacity are better protected from losing interest in physical activity after they have their ovaries removed, compared with rats bred to have low exercise capacity.

As the researchers say, most people fail to meet physical activity recommendations. Rats bred to have high or low running capacity have also been shown to have different behaviour on a voluntary running wheel.

The researchers think this may be because of differences in dopamine pathways in a brain region called the nucleus accumbens, which control self-motivated activity and reward.  

Oestrogen has been shown to stimulate dopamine receptors and maintain activity in rats.

A loss of oestrogen from the rat's ovaries being removed – modelling human menopause – may be expected to reduce activity. This is what the researchers aimed to examine.

Animal studies can give a good insight into biological mechanisms that may be similar in humans, but we are not genetically engineered rats.

What did the research involve?

The research involved two types of rats – those bred to have either a high or low exercise capacity.

There were 40 female rats in each group, who were then randomised to either have their ovaries removed or a sham operation. 

After one week of recovery they were given access to a voluntary running wheel. Their wheel running was monitored weekly for 11 weeks.

The rats also had other assessments of body composition and blood glucose control. Their brain tissue was examined after death, paying close attention to dopamine activity in the nucleus accumbens.

What were the basic results?

The high exercise capacity rats ran more on the wheel compared with the low capacity rats.

Ovary removal significantly reduced activity in both groups compared with rats who received the sham procedure.

Strangely, while the high capacity rats who had their ovaries removed demonstrated a weekly reduction in the distance they ran on the wheel over the 11 weeks, the low capacity rats with their ovaries removed actually increased the amount they ran each week.

This meant that by the end of the 11 weeks there was no difference in running between the high and low capacity rats who had their ovaries removed. 

Brain examination showed that high capacity rats had greater dopamine activity than the low capacity rats.

Removing the ovaries was associated with increased dopamine blocking in the high capacity rats, but was linked to reduced dopamine blocking in the low capacity rats.

How did the researchers interpret the results?

The researchers concluded that the dopamine system in the brain's nucleus accumbens plays an important role in motivation to run in female rats.

High capacity rats run significantly more than low capacity rats, which is the result of a higher ratio of excitatory to inhibitory dopamine receptors.

The researchers say that despite greater inherent motivation to run, high capacity rats are not protected against the effect that ovary removal has upon dopamine activity.

It reduces the ratio of excitatory to inhibitory dopamine activity, "for which intrinsic fitness does not confer protection".


This research uses an animal model of human menopause – surgically removing the ovaries – to see what effect this would have on rats bred to have either high or low exercise capacity.  

As oestrogen has been shown to have an effect on dopamine activity in the brain's motivation centre, the researchers expected that ovary removal would have an effect on the rats' activity.

However, what was unexpected was that having prior high exercise capacity seemed to give no protection – these rats seemed to decrease their activity much more than rats that had low activity to start with.

These findings could be stretched to explain a possible reason why women who've been through natural or induced menopause (such as having their ovaries removed) may feel less motivated to exercise, particularly if they were very active previously – because of changes in dopamine activity in the brain.

However, humans are obviously not genetically engineered rats running on a wheel. Animal studies can give a good insight into biological mechanisms that may be similar in humans, but we don't know that things work exactly the same.

We also don't know whether these are permanent changes that would persist in the long term, or whether they're only short-term changes around the time of menopause. 

Overall, the findings are of interest, but they do not have any preventative or therapeutic implications.

Physical activity is recommended at all stages of life, and many postmenopausal women enjoy very active lifestyles.

Exercise can be especially important at this time, as it can help boost bone strength, which can weaken during the menopause.

The best thing for people to do is follow physical activity recommendations where possible, doing what feels comfortable for them.

For all adults, including people over 65 who are generally fit and healthy, this is at least 150 minutes of moderate aerobic activity every week (such as cycling or walking) combined with strength exercises that work all muscle groups on two or more days a week. 

Links To The Headlines

How menopause 'crushes your motivation to exercise': Brain changes mean 'many women feel less pleasure and reward from their workout in later life'. Mail Online, July 29 2016

Links To Science

Park YM, Kanaley JA, Padilla J, et al. Effects of intrinsic aerobic capacity and ovariectomy on voluntary wheel running and nucleus accumbens dopamine receptor gene expression. Physiology & Behavior. Published online June 11 2016

Categories: News

New weapon in superbug war may be right under our noses

Thu, 2016-07-28 09:40

"Antibiotic resistance: 'snot wars' study yields new class of drugs," BBC News reports.

Researchers studying a type of bacteria found in many people's nostrils have used this knowledge to develop a possible new antibiotic called lugdunin.

While it has not yet been tested in humans, this is a development not to be sniffed at.

Lugdunin was found to eradicate Staphylococcal aureus bacteria, which is carried naturally on the human body, including inside the nostrils.

Staph. aureus wasn't always a concern in most cases, as it usually only caused mild skin infections such as boils. But in recent decades some strains of the bacteria have developed resistance to commonly used antibiotics.

These types of strains are known as methicillin-resistant Staphylococcus aureus (MRSA) and can be challenging to treat. They can also pose a significant threat to people with weakened immune systems.

Researchers found another bacterial strain called Staph. lugdunensis, which lives alongside Staph. aureus and so competes for resources, produces antibacterial enzymes to kill off its competitor – the so-called "snot wars" described by the BBC.

They identified the genetic mechanisms behind this, and from there developed a purified compound called lugdunin that had the same antibacterial activity.

First in human blood samples, and then in rodents and human nasal swabs, they demonstrated that lugdunin can reduce Staph. aureus colonisation.

These are undoubtedly promising findings, but this is early-stage research. There are many testing stages to go.

And Staph. aureus isn't the only resistant microbe out there, so it wouldn't provide the whole answer to antimicrobial resistance – but this research does provide a new avenue for exploration.

Where did the story come from?

The study was carried out by researchers from the University of Tübingen in Germany, and was funded by the German Research Council and the German Center for Infection Research.

It was published in the peer-reviewed journal, Nature.

The UK media's reporting is generally accurate, though headlines talking about a "new class of drugs" may suggest these drugs are already available when they're actually still in the very early stages of development and have not yet been tested in humans.

What kind of research was this?

This laboratory study aimed to develop a new type of antibiotic that prevents Staph. aureus bacterial colonisation.

Antibiotic resistance is a global health problem. A well-known example is methicillin-resistant Staph. aureus (MRSA) – so called because it doesn't respond to methicillin, an old type of penicillin antibiotic.

As the number of infections that do not respond to antibiotics continues to rise, increasingly stronger antibiotics have to be used to treat them.

But this puts us at risk of coming to a point where infections can't be treated, as our strongest antibiotics no longer work.

This means there is an urgent need to develop new antibiotics that can tackle resistant infections – but there is a limit on how quickly they can be developed.

The vast majority of severe infections in people who have weak immune systems or have had major surgery or trauma, for example, are caused by bacteria that are normally carried on the body by healthy people.

Staph. aureus is present in the nose of around a third of the population. 

Bacteria that are naturally present in the body are in constant competition with other types of bacteria.

It has been found some actually produce antibacterial-type substances to kill off the competing bacteria. This is what this research aimed to build on.   

What did the research involve?

The researchers first screened multiple types of Staphylococcal bacteria to see which had antibacterial activity against Staph. aureus.

They found one particular bacterial strain, Staph lugdunensis, was able to prevent growth of Staph aureus.

They investigated the way it did this and identified a cluster of genes called lug, which were responsible for producing a group of antibacterial enzymes.

They then used genetic engineering techniques to amplify the activity of these antibacterial genes to produce a purified compound, which they called lugdunin.

This compound was analysed in the laboratory to confirm its chemical structure and that it had the same antibacterial activity as the original bacteria.

The researchers then moved on to laboratory, animal and human experiments to test how effective it actually was.   

What were the basic results?

When tested in human blood samples in the lab, the researchers found lugdunin had strong antibacterial activity against several resistant bacteria, including MRSA – and this was without causing damage to the human blood cells.

Further analysis showed it seemed to be breaking down the bacteria's energy resources.

Staph. aureus didn't develop resistance to lugdunin, even when repeatedly exposed to low levels of the compound (not enough to kill the bacteria) over the course of 30 days.

They then tested mouse skin infected with Staph. aureus. Mice were treated with lugdunin one to two days after infection. This showed that lugdunin was able to reduce or completely eradicate the bacteria.

They then moved into tests in cotton rats, which are said to be an established animal model for investigating Staph. aureus nasal colonisation.

These animals were infected with both Staph. aureus and the original bacteria, Staph. lugdunensis. This confirmed that production of the antibiotic compound can reduce Staph. aureus colonisation.

This was repeated by testing nasal swabs from 187 hospitalised patients. The researchers found about a third of samples carried Staph. aureus, while 10% carried its opponent, Staph. lugdunensis.

The number of Staph. aureus bacteria present was about six times lower in the swabs also carrying Staph. lugdunensis.

Further tests showed all Staph. aureus were also susceptible to the new compound lugdunin.

How did the researchers interpret the results?

The researchers concluded that, "Lugdunin or lugdunin-producing commensal bacteria could be valuable for preventing staphylococcal infections."

They further say the bacteria naturally carried by humans "should be considered as a source for new antibiotics".


This valuable research has found a possible new avenue in the battle against antibiotic resistance – by harnessing the mechanisms that our own natural bacteria use to compete against other bacteria.

Multi-resistant Staph. aureus bacteria are responsible for many severe infections in hospitalised and immunosuppressed people.

This research found Staph. lugdunensis bacteria produce antibacterial substances, and from this researchers managed to develop a new purified compound that carries these antibacterial properties: lugdunin.

These are undoubtedly promising findings, but it's important not to jump too far ahead. This is currently only an experimental compound in the early stages of development.

Many more stages of testing would be needed before it is better known whether this antibiotic could be effective in humans and how it could be used.

For example, we need to find out whether the antibiotic would be used for just reducing Staph. aureus colonisation on the skin or in the nose, or whether it could actually be given to treat severe infections that have infected the body.

We would also need to know it is safe.

The study has only demonstrated the effects of this compound against Staph. Aureus, not against confirmed MRSA strains, so we don't know if it would definitely combat the well-known superbug.

Staph. aureus aren't the only resistant microbes out there, nor are they responsible for all infections.

This means this single discovery doesn't provide the whole answer to antimicrobial resistance. What it does provide is a new avenue for exploration.

While the possible developments from this research are as yet unknown, there are things you can do to fight antibacterial resistance.

This includes recognising that many simple coughs, colds and tummy upsets are viral and self-limiting. They will likely get better on their own and neither need, nor respond to, antibiotics.

If you are prescribed antibiotics – or any other antimicrobial, for any reason – it is important that you take the full course, even when you start to feel better.

Not taking the full course will expose bacteria to the antibiotic but not kill them off, allowing them to build resistance to it.

Read more about how you can help combat the threat of antibiotic resistance.

Links To The Headlines

Antibiotic resistance: 'Snot wars' study yields new class of drugs. BBC News, July 28 2016

Scientists sniff out new antibiotic – inside the human nose. The Guardian, July 27 2016

Antibiotics that could fight superbugs produced from bacteria in human nose. The Daily Telegraph, July 27 2016

Links To Science

Zipperer A, Konnerth MC, Laux C, et al. Human commensals producing a novel antibiotic impair pathogen colonization. Nature. Published online July 27 2016

Categories: News

An hour of exercise a day may compensate for an 'office lifestyle'

Thu, 2016-07-28 08:30

"Office workers must exercise for an hour a day to counter death risk," The Daily Telegraph reports.

A major new study suggests that at least an hour's exercise a day may compensate for the risks of a sedentary lifestyle.

The study, which looked at previous research involving more than a million people, delivered a "bad news, good news" analysis. The bad news is that sitting for long periods may increase the chance of dying earlier. The good news is that doing at least an hour of moderately intense activity (such as cycling or brisk walking) each day may eliminate that risk.

The people in the study who were least active and sat for more than eight hours a day were 59% more likely to have died during the study follow-up than people who exercised most and sat for less than four hours a day. Sitting for longer than four hours a day increased the chance of death for everyone not in the highest activity category. However, people who did the most physical activity did not have an increased risk of death, regardless of how many hours a day they spent sitting.

This type of research cannot prove cause and effect but it certainly seems that daily physical activity brings long-term benefits.

The current activity advice for adults is to do at least 30 minutes of physical activity a day. Increasing that to 60 minutes may be a good idea if you do have a "9-5 office lifestyle".


Where did the story come from?

The study was carried out by researchers from institutions in many different countries, including the Norwegian School of Sports Sciences, University of Cambridge, University of Queensland, Oslo University Hospital, Swinburne University of Technology in Melbourne, Sydney University and Harvard Medical School. It received no direct funding.

The study was published in the peer-reviewed journal The Lancet on an open-access basis so it is free to read online (although you need to register).

Some UK media outlets took the study very literally. The Daily Mail tells readers "adults who sit down for at least eight hours every day must do at least an hour's daily exercise to undo all the harm." The study does not prove that exercise will "undo the harm" of sedentary behaviour.

It also ignores the study findings that people who were moderately active for about half an hour to an hour had only a slightly raised risk of death associated with sitting for longer periods. While the advice to exercise more is sound, people might think there's no point in exercising for less than an hour a day, and so give up altogether. It is very much the case that "every little helps" when it comes to exercise.

Experts in sports and exercise medicine were mostly welcoming of the study, describing it as "excellent quality" and "very interesting". However, one expert in evidence based medicine warned of the study's limitations and that it had not sufficiently controlled for factors such as socioeconomic status. 


What kind of research was this?

This study was a systematic review and meta-analysis of prospective cohort studies. The researchers went back to the authors of the studies and asked them to re-analyse their data according to a standardised protocol, which allowed them to make direct comparisons between groups.

This is a good way to get a better idea of the relative importance of sitting and physical activity in terms of length of life. However, observational studies cannot tell us whether certain factors (sitting time or physical activity) directly cause another (chances of death). They can only tell us that the factors may be linked. 


What did the research involve?

Researchers searched the literature for studies that included information on sitting time, exercise and mortality. They added two studies that had not been published but which had relevant data.

They asked the original study authors to rework their data according to a standardised protocol which divided people into categories of physical activity and sitting time. They then pooled the data to look at how the two factors were linked to length of life. They also looked separately at time spent watching television, and at deaths from cardiovascular disease and cancer.

By applying a standardised protocol, the researchers were able to make direct comparisons across groups according to specific categories of sitting time (less than four hours a day, four to six hours, six to eight hours, and more than eight) and of physical activity. Physical activity was measured by metabolic equivalent of task (MET) hours a week. MET is a measurement of how much energy the body is likely to consume during specific physical activities.

MET levels were divided in four groups:

  • less than 2.5 (equivalent to five minutes a day of moderate intensity physical activity)
  • 16 (25 to 35 minutes a day, as recommended by many guidelines)
  • 30 (50 to 65 minutes a day)
  • more than 35.5 (60 to 75 minutes a day)

Researchers took the people who did the most physical activity and had the least sitting time as the baseline, and looked to see how more sitting time affected that, for people in the different categories of physical activity.

The same calculations were repeated using daily hours of TV viewing time, from less than one to five or more.


What were the basic results?

For people who did the least physical activity, sitting for more than four hours a day was linked to an increased chance of dying during the study. For these people, sitting for eight hours a day or more increased the chances of death by 27% (hazard ratio (HR) 1.27, 95% confidence interval (CI) 1.22 to 1.32), compared to if they'd been sitting four hours a day or less. Compared to people who did the most exercise and sat for less than four hours a day, they had a 59% increased risk of death (HR 1.59, 95% CI 1.52 to 1.66).

People who were physically active for between half an hour and an hour also had a raised chance of death linked to sitting for eight hours a day compared to four hours a day, of 10% to 12%. But for people who exercised the most, time spent sitting did not increase the risk of death.

High levels of physical activity were clearly linked to lower chance of death. People who did the most activity but sat for eight hours or more were less likely to die than those who did the least activity but sat for four hours or less.

Television viewing time showed similar results, but in this case even the highest amount of physical activity did not cancel the raised risk of watching five hours or more of television. The least active people had a 44% higher risk of death if they watched five or more hours of television, compared to less than one hour (HR 1.44, 95% CI 1.34 to 1.56).

Results were similar when the researchers looked at the chances of dying from cardiovascular disease or cancer.


How did the researchers interpret the results?

The researchers concluded: "These results provide further evidence on the benefits of physical activity, particularly in societies where increasing numbers of people have to sit for long hours for work" and suggest the study should be taken into account when public health recommendations are made.



This study helps to disentangle the effects of having a sedentary lifestyle and being physically active. Previous studies have had conflicting results, with some saying that sitting for long periods can be counteracted by taking exercise, while others disagreed.

The advantage of this study is that it looks at time spent sitting as well as time spent being physically active, and calculates how both are linked to mortality and to each other.

The study has many strengths, not least its size. It includes data from 1,005,791 people from 16 studies. The researchers applied a standardised protocol and asked study authors to provide re-analysed data. This meant they could pool information and make direct comparisons between groups sub-divided by sitting time and activity levels, to a higher degree of accuracy than would otherwise have been possible.

However, there are limitations. The authors only included English-language papers, so other relevant studies may have been excluded.

The authors tried to account for what is called reverse causation – in this case that illness may have prevented people from being physically active – by including studies of apparently healthy adults. However they admit that this factor was not completely ruled out.

In addition, the data came from participants' own estimates of time spent sitting, watching TV and being physically active. Not only is this reliant on accurate (and honest) self-assessment, it was only measured at one time point, so may not be representative over time.

Although the original studies included controls for most other confounding factors, such as smoking, most did not include socio-economic data, which could have a big impact on the results. For example, watching a lot of television could be linked to being on a low income, or unemployed, which are themselves linked to poor health.

Conversely, going to the gym is expensive, so this type of physical activity may be more common among people who are better-off. That makes it hard to know whether TV watching or exercise are the factor causing the difference in death rates, rather than being a marker for something else.

We know that sedentary lifestyles are linked to poorer health. For many people, work (or travelling to work) involves sitting down for long periods. While some people may be able to change this, for example by using a standing desk or cycling to work, for others it's not so easy. So it's heartening to know that taking exercise and being physically active in your free time may help.

However, it's interesting to note that the levels of activity linked to eliminating the risk of a sedentary lifestyle are higher than those usually recommended. The most active people spent the equivalent of 60 to 75 minutes doing moderately intense physical activity – higher than the usually recommended 30 minutes a day.

It may be that compensating for a desk job requires us to be more physically active than most of us currently manage.

You don't need to join a gym to increase your activity levels. Read more about how you can get fitter for free.

Links To The Headlines

Office workers must exercise for an hour a day to counter death risk. The Daily Telegraph. July 28 2016

Hour's activity 'offsets sedentary day'. BBC News, July 27 2016

One hour of activity needed to offset harmful effects of sitting at a desk. The Guardian, July 27 2016

A desk job could make you 60% more likely to die earlier: Hour's exercise every day is needed to help beat deadly effects of working 9 to 5. Daily Mail, July 28 2016

Links To Science

Ekelund U, Steene-Johannessen J, Brown WJ, et al. Does physical activity attenuate, or even eliminate, the detrimental association of sitting time with mortality? A harmonised meta-analysis of data from more than 1 million men and women. The Lancet. Published online July 27 2016

Categories: News