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Can exercise offset some of the harms of regular drinking?

NHS Choices - Behind the Headlines -

"Adults who booze regularly but exercise for five hours a week are no more likely to die than teetotallers," the Mail Online reports.

A study suggests exercise may compensate for some, but certainly not all, of the harms associated with excessive alcohol consumption. This latest study looked at deaths from cancer and cardiovascular disease, as well as premature death in general (usually judged to be dying before the age of 75).

Researchers looked at around 10 years' worth of national survey data from UK adults aged over 40. Unsurprisingly, they found links between all-cause and cancer mortality in inactive people. But they also found increasing levels of physical activity generally removed the association with drinking habits. In fact, occasional drinking was associated with a significant reduction in all-cause mortality for the most active of people.

Although the study had strengths in its large sample size and regular follow-up, we can't be sure that any links observed were solely down to the interaction between alcohol and exercise. For example, people who are physically active may also avoid smoking and consume healthy diets. It is difficult to completely control for such influences when analysing data like this.

While regular exercise may mitigate against some of the harms associated with excessive alcohol consumption it certainly won't make you immune. Many world-class sportspeople, such as George Best and Paul Gascoigne, have had both their careers and lives blighted by drinking.

 

Where did the story come from?

The UK-based study was carried out by an international collaboration of researchers from Canada, Australia, Norway and the UK. The health surveys on which the study was based were commissioned by the Department of Health, UK. Individual study authors also reported receiving funding from the National Health and Medical Research Council and University of Sydney. 

The study was published in the peer-reviewed British Journal of Sports Medicine. 

The media coverage around this topic was generally overly optimistic, highlighting that by exercising, individuals can completely undo the harm caused by excessive alcohol consumption, which is untrue.

In particular, the Mail Online claimed "Adults who booze regularly but exercise for five hours a week are no more likely to die than teetotallers" which could send out the wrong message to the public.

 

What kind of research was this?

This cohort study analysed data from British population-based surveys: Health Survey for England (HSE) and the Scottish Health Survey (SHS) to investigate whether physical activity is able to moderate the risk between alcohol consumption and mortality from cancer and cardiovascular diseases.

Cohort studies like this are useful for assessing suspected links between an exposure and outcome. However, there are potentially other factors that have a role to play in such associations and therefore the study design doesn't allow for confirmation of cause and effect.

 

What did the research involve?

The researchers collected data on 36,370 men and women aged 40 or above from Health Survey for England (1994; 1998; 1999; 2003; 2004; and 2006) and the Scottish Health Survey (1998 and 2003). Among other things, the participants were asked about their current alcohol consumption and physical activity.

Alcohol intake was defined by six categories (UK units/week):

  • never drink (lifetime abstainers)
  • ex-drinkers
  • occasional drinkers (haven't drank anything in past seven days)
  • within (previous) guidelines: <14 units (women) and <21 units (men)
  • hazardous: 14-15 units (women) and 21-19 units (men)
  • harmful: >35 (women) and >49 (men)

Frequency and type of physical activity in the past four weeks was questioned and converted into metabolic equivalent task-hour (MET-hours, which are an estimate of metabolic activity) per week according to national recommendations:

  • inactive (≤7 MET-hours)
  • lower level of active (>7.5 MET-hours)
  • higher level of active (>15 MET-hours)

The surveys were linked to the NHS Central Register for mortality data and the participants were followed up until 2009 (HSE) and 2011 (SHS). There were 5,735 recorded deaths; deaths from cancer and cardiovascular disease were of most interest for this study.

The data was analysed for associations between alcohol consumption and the risk of death from all-causes, cancer and cardiovascular disease. The results were then analysed according to levels of physical activity.

Potential confounders (such as sex, body mass index and smoking status) were controlled for.

 

What were the basic results?

Overall, the study found a direct link between all levels of alcohol consumption and risk of cancer mortality. It also found that increasing levels of physical activity reduced this association with cancer mortality, and also reduced the link with death from any cause.

  • In individuals who reported inactive levels of physical activity (≤7 MET-hours), there was a direct association between alcohol consumption and all-cause mortality.
  • However, in individuals who met the highest level of physical activity recommendations a protective effect of occasional drinking on all-cause mortality was observed (hazard ratio: 0.68; 95% confidence interval (CI): 0.46 to 0.99). It should be noted that this result just skimmed the cut-off point for statistical significance.
  • In this high activity group, there was no link between all-cause mortality and alcohol consumption within guidelines, or even hazardous amounts, but the risk was still increased for those drinking harmful amounts.
  • The risk of death from cancer increased with the amount of alcohol consumed in inactive participants, ranging from a 47% increased risk for those drinking within guidelines to 87% increased risk for those with harmful drinking.
  • In people with higher activity levels (above 7.5 MET hours) there was no significant link between any amount of alcohol consumption and cancer mortality.
  • No association was found between alcohol consumption and mortality from cardiovascular disease, although a protective effect was observed in individuals who reported the lower and higher levels of physical activity (>7.5 MET-hours) and (>15 MET-hours) respectively.

 

How did the researchers interpret the results?

The researchers concluded "we found evidence of a dose–response association between alcohol intake and cancer mortality in inactive participants but not in physically active participants. [Physical activity] slightly attenuates the risk of all-cause mortality up to a hazardous level of drinking."

 

Conclusion

This study aimed to explore whether physical activity is able to moderate the risk between alcohol consumption and mortality from cancer and cardiovascular diseases. It found that increasing levels of physical activity reduced the association for death from both all-causes and cancer.

This study has strengths in its large sample size, comprehensive assessments and long duration of follow-up. The findings are interesting, but there a few points to bear in mind:

  • As the authors mention, cohort studies such as this are unable to confirm cause and effect. Though the researchers have tried to account for various potential health and lifestyle confounding variables, there is the possibility that others are still influencing the results. A notable one is dietary habits which weren't assessed. Also, for example, the former drinkers may have quit due to other health issues which may have introduced bias.
  • The study was unable to look at binge drinking levels of alcohol consumption which would have likely had important health implications.
  • Additionally, there is always the possibility with self-reported surveys that the participants either under or over-reported their drinking habits which can increase the chance of misclassification bias.
  • Though having a large sample size, fewer people reported harmful drinking levels, so links within this category may be less reliable.
  • The study has only looked at the link between alcohol and actually dying from cancer or cardiovascular disease. Links may be different if they looked at associations between alcohol and just being diagnosed with cancer or heart disease, for example.
  • The study is also only representative of adults over the age of 40.

Overall, maintaining a healthy lifestyle seems to be the best bet for reducing the risk of any chronic disease, be it through physical activity, balanced diet or reasonable alcohol consumption.

Current alcohol recommendations for both men and women are to drink no more than 14 units per week.  

Links To The Headlines

How exercise undoes the harm from drinking: Adults who booze regularly but exercise for five hours a week are no more likely to die than teetotallers. Mail Online, September 8 2016

Two hours a week of exercise could offset the dangers of alcohol. The Daily Telegraph, September 8 2016

Exercise can cut risk from alcohol-related diseases, study suggests. The Guardian, September 8 2016

Links To Science

Perreault K, Bauman A, Johnson N, et al. Does physical activity moderate the association between alcohol drinking and all-cause, cancer and cardiovascular diseases mortality? A pooled analysis of eight British population cohorts. British Journal of Sports Medicine. Published online August 31 2016

Could Parkinson's disease start in the gut?

NHS Choices - Behind the Headlines -

"Parkinson's disease 'may start in gut'," BBC News reports. New research involving mice suggests that bacteria in the gut may lead to a greater decline in motor function in patients with Parkinson's disease.

The study involved a mouse model of Parkinson's disease. The researchers gave some of the mice gut bacteria from people with Parkinson's disease, some were given gut bacteria from healthy individuals, and some mice were not given any bacteria.

They found that gut bacteria seemed necessary to trigger Parkinson's-like symptoms. There was greater decrease in motor function in mice infected with gut bacteria compared with those who remained germ-free, with the greatest decline seen in mice given bacteria from people with Parkinson's.

The researchers suggest that the presence of gut bacteria may cause the build-up of proteins called alpha-synuclein, which is found in patients with Parkinson's disease.

The study does not prove that Parkinson's is essentially a gut disorder and could potentially be treated or prevented with antibiotics or probiotics. And, humans aren't identical to mice, so the study findings may not apply to people.

The study arguably raises more questions than answers. But it could pave the way for further studies in people, with the hope of finding potential new treatments for Parkinson's.

 

Where did the story come from?

The study was carried out by researchers from a variety of institutions, mainly from the US and Sweden, including the California Institute of Technology, Rush University Medical Center in Chicago and Chalmers University of Technology in Sweden.

It was funded by the Knut and Alice Wallenberg Foundation and the Swedish Research Council.

The study was published in the peer-reviewed scientific journal Cell. It's available on an open-access basis and is free to read online.

Generally the UK media coverage on this topic was balanced, although the Mail Online did say this study "could overhaul medical research and treatment of Parkinson's" which is possibly over optimistic. 

 

What kind of research was this?

This was an animal study which aimed to investigate a possible link between gut bacteria and brain diseases such as Parkinson's disease.

Parkinson's is a disease of unknown cause where there is a loss of dopamine-producing cells in the brain. This leads to progressive decline in brain and motor function. Typical symptoms include slow movements, stiff muscles and involuntary shaking. There are also often mental health effects such as depression and dementia.

Past evidence has suggested that gut bacteria could influence the development of brain diseases such as Parkinson's by causing build-up of the protein alpha-synuclein (α-synuclein).

However, there was a lack of studies investigating the link through cellular research, an issue the researchers wanted to address.

Animal studies are useful early stage research which can indicate how processes in the body may work. On the other hand, mice and humans are quite different in biology so what works in mice may not necessarily be the same in humans. And even if the findings do apply, they may not provide the whole answer to the causes of diseases such as Parkinson's.

 

What did the research involve?

The research involved two groups of mice aged 12-13 weeks. One group of mice was genetically programmed to produce the protein alpha-synuclein (α-synuclein), which is thought to build up in people with degenerative brain conditions like Parkinson's. Another group of "normal" mice acted as controls.

Within these two groups, the gut composition of the mice was changed. Some mice remained germ-free, some were given gut bacteria from "healthy" donors, and others were given gut bacteria from people with Parkinson's.

The brain and motor function was tested over time in all groups of mice, along with gastrointestinal tests, up to the age of 24-25 weeks. Standardised testing, used for mice, was used to assess motor function.

The test results were compared between the different groups of mice to see whether gut bacteria composition, in combination with the protein, had any effect on the onset of Parkinson-like symptoms.

 

What were the basic results?

Overall, they found that a decrease in motor function for mice with gut microbes compared with those who remained germ-free.

  • The presence of gut bacteria promoted the decline in motor function caused by α-synuclein. Mice genetically modified to produce this protein and then given gut bacteria generally performed the worst in the motor function tests. Gut bacteria from people with Parkinson's caused the greatest decline in motor dysfunction.
  • Mice producing α-synuclein who remained germ-free still showed a decline in motor function by 24-25 weeks old, but the onset was significantly slower compared to the mice with gut bacteria. 
  • The researchers found that gut microbes seemed to be affecting brain function via the action of short-chain fatty acids. The microbes produce short-chain fatty acids. The acids then cause an inflammatory response in the brain's immune cells (microglia) which leads to the dysfunction. 
  • In the germ-free mice there was no fatty acid signalling, limited inflammatory effect and limited motor dysfunction.

 

How did the researchers interpret the results?

The researchers concluded: "remarkably, colonization of aSyn-overexpressing mice with microbiota from [people with Parkinson's] enhances physical impairments compared to microbiota transplants from healthy human donors.

"These findings reveal that gut bacteria regulate movement disorders in mice and suggest that alterations in the human microbiome represent a risk factor for Parkinson's disease."

 

Conclusion

This study aimed to investigate a possible link between gut bacteria and degenerative brain diseases such as Parkinson's.

In the animal model of Parkinson's, researchers found that the presence of gut bacteria seems to enhance the brain's inflammatory response and lead to greater decrease in motor function.

And gut bacteria from people with Parkinson's seemed to have the greatest effect.

But does this mean that Parkinson's is essentially a gut disorder and could potentially be treated or prevented with antibiotics? Unfortunately the answer isn't so simple.

Although these are interesting findings, biological function in mice isn't exactly the same as in humans, so you can't necessarily apply these findings to the human population.

Even if they are applicable in part, this still may not provide the whole answer as to how the disease process of Parkinson's starts. However, it does act as useful early stage research which could pave the way for further studies in humans.

Dr. Arthur Roach, Director of Research and Development at Parkinson's UK commented on this study: "This paper shows for the first time a way in which one of the key players in Parkinson's, the protein alpha-synuclein, may have its actions in the brain modified by gut bacteria. It is important to note however that this study has been done in mice and we would need further studies in other model systems and in humans to confirm that this connection is real … There are still many questions to answer but we hope this will trigger more research that will ultimately revolutionise treatment options for Parkinson's."

Find support in your area for people affected by Parkinson's.

Links To The Headlines

Parkinson's disease 'may start in gut'. BBC News, December 2 2016

Parkinson's could start in the GUT not the brain: Study finds first ever link between the disease and gut microbes. Mail Online, December 1 2016

Links To Science

Sampson TR, Debelius JW, Thorn T, et al. Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson’s Disease. Cell. Published online December 1 2016

'Not enough over-50s' taking aspirin to prevent heart disease

NHS Choices - Behind the Headlines -

"Aspirin a day could dramatically cut cancer and heart disease risk … study claims," the Mail Online reports.

U.S. researchers ran a simulation of what might happen if all Americans over 50 years old took aspirin on a daily basis. Their results found that people would live about four months longer on average, adding 900,000 people to the US population by 2036.

The study was designed to demonstrate the possible long-term effects of more people taking aspirin to prevent cardiovascular disease.

It should be pointed out that there is an important difference between UK and US guidelines. In the UK low-dose aspirin is usually recommended for people with a history of heart disease or stroke. In the US this advice is extended to people who are at risk of cardiovascular disease but don't have it yet.

We already know that aspirin reduces the risk of heart disease and strokes caused by blood clots (ischaemic stroke). There's some evidence it may reduce some types of cancer. However, aspirin also increases the risk of stroke caused by bleeding (haemorrhagic stroke) and increases the chances of bleeding in the stomach or gut.

So should you be taking low-dose aspirin? Without knowing your individual circumstances it is impossible to provide an accurate response. You need to ask your GP.

 

Where did the story come from?

The study was carried out by researchers from the University of Southern California and a company called Analysis Group. The authors received no funding for the study.

The study was published in the peer-reviewed journal PLOS One, on an open-access basis so it's free to read online.

The Mail Online reports the study as if the findings about aspirin reducing cardiovascular disease and potentially extending lifespan were new, while they have actually been known for some time.

The report says taking aspirin "would save the US $692 billion in health costs," which seems to be a misunderstanding. Health costs would actually increase, because of people living longer.

However, the researchers assigned a value of $150,000 to each additional year of life lived, which is how they arrived at the $692 billion figure.

 

What kind of research was this?

This was a "microsimulation" study, which used a modelling system to project possible outcomes under different scenarios, using information from health surveys. This type of modelling can throw up some interesting possibilities, but because it relies on so many assumptions, we have to be cautious about taking the results too literally.

 

What did the research involve?

Researchers used data from cohort studies to predict average life expectancy, cardiovascular events, cancers, disabilities and healthcare costs for people in the US aged 50 and over. They predicted what would happen with the current numbers of people taking aspirin, then with everyone currently recommended to take aspirin doing so, then with everyone over 50 taking aspirin.

They compared the results of their modelling, to see what effect it would have on average lifespan, the US population, costs and benefits.

Cohort studies providing data included the National Health and Nutrition Examination Survey (NHANES), Health and Retirement Study of Americans, Medical Expenditure Panel Survey and Medicare Current Beneficiary Survey.

The model included an assumption that more people would have gastrointestinal bleeding as a result of taking aspirin. It also modified the results using quality of life measures, so that additional life years were adjusted for quality of life.

 

What were the basic results?

The researchers found that, if everyone advised by US guidelines to take aspirin did so, the:

  • numbers of people with cardiovascular disease would fall from 487 per 1,000 to 476 per 1,000 (11 fewer cases, 95% confidence interval (CI) -23.2 to -2)
  • numbers with gastrointestinal bleeding would rise from 67 per 1,000 to 83 per 1,000 (16 more cases, 95% CI 3.6 to 30)
  • years of life expectancy at age 51 would rise from 30.2 years to 30.5 years, an additional four months of life (0.28 year, 95% CI 0.08 to 0.5)
  • life expectancy without disability would rise from 22.8 years to 22.9 years, an additional one month of life (0.12 year, 0.03 to 0.23)

The model found no reduction in the numbers of strokes or cancers.

The model shows there could be an additional 900,000 people (CI 300,000 to 1,400,000) alive in the US in 2036, who would otherwise have died.

Using the figure of $150,000 per quality-adjusted life year to represent benefits, the researchers say the value of extra life gained by 2036 would be $692 billion.

 

How did the researchers interpret the results?

The researchers said: "Expanded use of aspirin by older Americans with elevated risk of cardiovascular disease could generate substantial population health benefits over the next twenty years, and do so very cost-effectively."

 

Conclusion

This study doesn't really tell us anything we didn't already know. Aspirin has been used for many years to prevent heart attacks and strokes in people with cardiovascular disease. Aspirin's wider use is controversial, because of the potential side effects.

What this study does add is an estimate of what might happen if all people in the US who were advised to take aspirin under US guidelines, actually did so. (The researchers say that 40% of men and 10% of women advised to take aspirin don't take it).

The study assumes that people would get the same benefits as those seen in clinical trials of aspirin. This is unrealistic, because most studies find that people tend to do better in clinical trials than when being treated in the real world.

The average results – showing an additional one month of disability-free life for every 1,000 people – may sound trivial. However, it's important to remember that averages don't work like that in real life. Many people will get no benefit from aspirin, while a smaller group will avoid a heart attack or stroke, and so live many more months or possibly years, as a result of taking aspirin.

If you've already had a heart attack or stroke, or if you have angina or another heart or circulation problem, your doctor has probably prescribed low dose aspirin. There's good evidence that aspirin (or similar drugs, for those who can't take aspirin) can help prevent a second heart attack or stroke.

Find out more information about aspirin.

Links To The Headlines

Aspirin a day could dramatically cut cancer and heart disease risk - and even extend lifespan, study claims. Mail Online, November 30 2016

Links To Science

Agus DB, Gaudette E, Goldman DP, Messali A. The Long-Term Benefits of Increased Aspirin Use by At-Risk Americans Aged 50 and Older. PLOS One. Published online November 30 2016

'No need to wait to try again after miscarriage' advice

NHS Choices - Behind the Headlines -

"Women who suffer a miscarriage should try for a baby again within six months, a major study has found," the Daily Mail reports.

Current guidance from the World Health Organization recommends couples wait at least six months before trying to conceive again after a miscarriage. But the researchers decided to investigate the validity of this recommendation as it was based on a single study from women in the developing world.

The researchers looked at information taken from around 1 million women from 11 different countries around the world. It found no more adverse outcomes for women who get pregnant less than six months after a miscarriage compared to those who wait. Moreover, a reduced risk of miscarriage and preterm birth was found for these women.

So this study suggests these guidelines should be reviewed and that couples be advised that delaying pregnancy doesn't necessarily improve outcomes.

If you have had a miscarriage, you should avoid having sex until all of your miscarriage symptoms have gone. Your periods should return within four to six weeks of your miscarriage, although it may take several months to settle into a regular cycle.

Not every woman will feel physically and/or emotionally ready to try for another pregnancy. Charities such as the Miscarriage Association can provide advice and support about trying for another pregnancy.

Where did the story come from?

The study was carried out by researchers from the University of Malta and the University of Aberdeen and did not receive any funding.

The study was published in the peer-reviewed medical journal Human Reproduction Update and the authors declare no conflict of interest.

The media generally reported the story accurately, acknowledging that women are more likely to have a successful pregnancy if they conceive sooner after a miscarriage, rather than waiting.

The Daily Mail suggests that women who have a miscarriage "should try for a baby again within six months". However not all women will feel emotionally ready to try again for a baby so soon.

 

What kind of research was this?

This was a systematic review and meta-analysis aiming to see if becoming pregnant less than six months after miscarriage is associated with adverse outcomes in the next pregnancy, compared with getting pregnant more than six months later.

Meta-analyses are a useful way of summarising many studies looking at the same outcomes, in this case adverse pregnancy outcomes.

However, this type of study will only ever be as good as the individual studies included, and weaknesses from these studies will be brought into the analyses.

The studies included were 13 cohort studies and three randomised controlled trials, from 11 different countries.

Cohort studies are a good way of looking at a link between two factors, but cannot prove that one – falling pregnant before six months – causes another – future pregnancy outcomes.

 

What did the research involve?

Researchers compared the results of 1,043,840 women from 16 trials. They then pooled the results of 10 similar trials, involving 977,972 women. They compared the difference in pregnancy-related outcomes between women who fell pregnant less than six months after having a miscarriage, and those who fell pregnant more than six months after miscarriage.

They looked at outcomes, including:

The results were analysed and the risk of each outcome for the two groups of women (less than six months to pregnancy or more than six months to pregnancy) was calculated.

 

What were the basic results?

Results showed that in women with less than six months between miscarriage and pregnancy compared to those with a six months or more interval, there was a:

  • decreased risk of further miscarriage of 18% (risk ratio (RR) 0.82, confidence interval (CI) 0.78 to 0.86)
  • decreased risk of preterm delivery of 21% (RR 0.79, 95% CI 0.75 to 0.83)

There was no significant difference between women with less than six months or more than six months between miscarriage and pregnancy for still birth, low birthweight or pre-eclampsia.

 

How did the researchers interpret the results?

The researchers concluded: "The results of this systematic review and meta-analyses show that an IPI [inter-pregnancy interval] of less than six months is associated with no increase in the risks of adverse outcomes in the pregnancy following miscarriage compared to delaying pregnancy for at least six months."

In fact, there is some evidence to suggest that chances of having a live birth in the subsequent pregnancy are increased with an IPI of less than six months.

They go on to add: "there is now ample evidence to suggest that delaying a pregnancy following a miscarriage is not beneficial and unless there are specific reasons for delay couples should be advised to try for another pregnancy as soon as they feel ready."

 

Conclusion

This study shows that getting pregnant sooner after a miscarriage results in no more adverse outcomes compared to waiting for more than six months.

In addition, there appear to be better outcomes in terms of a lower risk of further miscarriage and possibly preterm birth. It should be pointed out that for preterm birth the result only reached statistical significance when one of the relevant studies was excluded, which limits our confidence in this result.

This study has strengths as it included a large number of women from many different countries. However, it also has limitations:

  • The way data was collected from the original studies varied. Some used mother's recall while others gained information from databases – therefore the quality of data varied.
  • Studies had different definitions of miscarriage. While some included only spontaneous abortion (miscarriage), others did not distinguish between spontaneous and induced abortion.

However, there are a number of confounding factors that influence pregnancy outcomes, including:

  • maternal age
  • ethnicity
  • social class
  • smoking
  • alcohol
  • BMI
  • previous obstetric history

Other than maternal age, the included studies varied in addressing these potential confounding variables, which could have led to an over- or under-estimation of results.

Miscarriages are fairly common. Among women who know they're pregnant, it's estimated one in six of these pregnancies will end in miscarriage.

Recurrent miscarriages (losing three or more pregnancies in a row) are far less common, affecting only around 1 in a 100 women.

If you do want to get pregnant again, you may want to discuss it with your GP or hospital care team. Make sure you are feeling physically and emotionally well before trying for another pregnancy.

The Miscarriage Association provides more advice about trying for another pregnancy.

Links To The Headlines

Women who lose their baby to miscarriage told to try again within six months because it can reduce the risk by a fifth. Daily Mail, November 30 2016

Successful pregnancy more likely sooner after miscarriage, say researchers. BBC News, November 30 2016

Try again for a baby within six months of miscarriage for best chance of success – new research. The Daily Telegraph, November 30 2016

Women who conceive within six months of miscarriage are 'more likely to get pregnant', study finds. The Independent, November 30 2016

Links To Science

Kangatharan C, Labram S, Bhattacharya S. Interpregnancy interval following miscarriage and adverse pregnancy outcomes: systematic review and meta-analysis. Human Reproduction Update. Published online November 17 2016

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