Women are more likely to suffer from anxiety than men

Tuesday June 7 2016

Everyone gets anxious, but persistent anxiety can affect daily life

"Women twice as likely as men to experience anxiety, research finds," The Guardian reports. A new review that attempts to get a global snapshot of the prevalence of anxiety disorders identifies a number of vulnerable groups.

There are various types of anxiety disorder, but generally they involve feelings of unease, such as worry or fear, that can be mild or severe and affect daily life. Having an overwhelming sense of anxiety that "takes over your life" is described as having a generalised anxiety disorder.

There are many factors that can trigger an anxiety disorder, such as stress, physical conditions, genetic background and hormonal imbalances.

The researchers found that women, young people and those with other chronic diseases were disproportionally affected. Across countries, women were found to be twice as likely to be affected as men.
 
The researchers call for further research to be carried out on the illness, as well as investigating which type of interventions have the greatest benefit. There is also a need for further study of anxiety prevalence in developing and under-developed parts of the world, as there was a lack of representation.

Although feelings of anxiety at certain times are completely normal, you should see your GP if anxiety is affecting your daily life or causing you distress.

Where did the story come from?

The study was carried out by researchers from the University of Cambridge and Westminster City Council. It was funded by the UK National Institute for Health Research. The study was published in the peer-reviewed clinical journal Brain and Behavior. It is available on an open-access basis and is free to read online.

While the media coverage was generally accurate, both the Mail Online and The Times claimed that the reasons why younger women had higher levels of anxiety were down to many of them being working mothers. This claim seems to be based on opinions, rather than any hard evidence presented in the study.

What kind of research was this?

This was a systematic review that aimed to collate evidence from other systematic reviews which had explored the prevalence of anxiety, to describe the burden of disease across population subgroups.

As the researchers mention, anxiety disorders contribute to significant disability and impairment to quality of life, and are the most prevalent mental health conditions in Europe. They place increasing demand upon health services across the globe, and are recognised as important determinants of poor health. This is the first reported study to attempt to provide a comprehensive synthesis of the findings from reviews undertaken on the global burden of anxiety.

Systematic reviews are one of the highest levels of evidence, but they are only as good as the studies they contain. The included reviews varied widely in their methods, the studies they had included and populations examined. Due to this variation, the researchers did not attempt to carry out a meta-analysis of their findings. Instead, they report the findings across the individual reviews.

What did the research involve?

The researchers searched three literature databases up to May 2015 to identify systematic reviews and meta-analyses that had reported the burden of anxiety across the globe.

Reviews could have looked at any anxiety disorder, including generalised, social anxiety or obsessive compulsive disorder, and use any method to assess anxiety. The researchers specifically searched for reviews including individuals suffering from other medical or mental health conditions (chronic or infectious disease, psychiatric conditions, and addiction) as well as those from vulnerable populations. Reviews on the treatment of anxiety were excluded.

Two researchers assessed the quality of the reviews and eligibility for inclusion, and extracted data.

The reviews included studies of people of all ages, from young children to people of old age, with the overall number of studies and individual study sample sizes varying. The method of anxiety assessment also varied between studies, from structured and unstructured interviews to self-reported questionnaires.

What were the basic results?

Results from the 48 studies were gathered to describe the global distribution of anxiety disorders. The main results were as follows:

• The general prevalence of anxiety disorders in healthy populations ranged from 3% to 25%.
• Women were found to be twice as likely to be affected as men (female: male ratio of 1.9:1). This was consistently the case across different countries and co-existing health conditions.
• Young adults under the age of 35 were also more often affected (2.5% to 9.1%).
• Prevalence was found to be highest in North America (7.7%, 95% confidence interval [CI] 6.8 to 8.8) and in North Africa/Middle East (7.7%, 95% CI 6.0 to 10.0).
• The lowest prevalence was found in East Asia (2.8%, 95% CI 2.2 to 3.4).

The prevalence was then described according to five common themes:

• addiction
• other mental and neurological disorders
• chronic physical diseases
• trauma
• vulnerable population subgroups

They found that, compared to healthy populations, the prevalence was higher in individuals with chronic conditions, who had a prevalence ranging from 1.4% to 70%.

How did the researchers interpret the results?

The researchers concluded: "Despite epidemiologic advances in this field, important areas of research remain under- or unexplored. There is a need for further studies on the prevalence of anxiety disorders. These recommendations can serve to guide the research agenda, and most importantly, help develop tailored and timely interventions."

Conclusion

This systematic review of previously gathered data compiled evidence from 48 studies to describe the global prevalence of anxiety disorders, which are placing increasingly high demand upon health services across the globe. The review gives us a general picture of the prevalence of these conditions worldwide and notes several themes.

It found that anxiety disorders are common across all population groups, but women and young people seem to be disproportionally affected. Anxiety prevalence was also higher in individuals with chronic conditions, though it is not possible to say whether mental health problems could be a contributing factor or a consequence.

Reviews were assessed for eligibility against a validated quality assessment tool. However, the researchers highlight the large variability in the methods of the reviews and the studies they included, which makes comparison of prevalence figures between the studies difficult.

For example, there was wide variation between reviews in:

• the overall number of studies they included and their sample sizes
• the ages of participants, with some reviews looking at older individuals and some looking at children (aged 6+)
• whether they were general population samples or those with specific physical or mental health conditions
• the tools used to assess anxiety
• whether they took account of other health, environmental or lifestyle factors

While this review is a useful indicator of the prevalence of anxiety disorders, it is unable to suggest causation – for example, why prevalence may be higher in women or younger adults. It is possible that this could be down to a complex interaction of biological and lifestyle factors. However, the direction of effect or the extent of influence of different factors remains unknown.

The researchers call for further research to be carried out on the course of the illness, as well as anxiety levels pre- and post-treatment. They also note the need for further study into developing and under-developed parts of the world, as there was a lack of representation of those areas, and for specific study into vulnerable subgroups of society.

Visit the NHS Choices Moodzone for more information about stress, anxiety and depression, and methods you can try to cope with and combat these feelings.  

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'Friendly' virus repairs damaged liver cells (but only in mice)

Friday June 3 2016

There are more than 100 different types of liver disease

"Have scientists found a cure for alcoholism?," the Mail Online asks, missing the point of the research entirely.

Researchers were able to improve liver damage in mice, but this does not amount to curing an addiction to alcohol.

The study showed it was possible to create "bespoke friendly" viruses to infect cells known as myofibroblasts, which are cells associated with tissue repair. The virus passed on instructions that transformed the myofibroblasts into healthy liver cells in mice who had fibrosis (scarring) of the liver, known as cirrhosis.

Not all the experiments in the mice worked, but in those that did, the transformed liver cells looked and behaved normally, replaced some of the diseased liver cells, and led to less liver scarring.

Researchers will now attempt to refine this technique before seeing if it works in humans.  

Right now, this technique is not available as a new treatment. It represents one of the earliest stages of treatment discovery and development, which can take decades from start to finish.

If you do have a lifestyle that increases your risk of liver disease, such as heavy alcohol consumption, being obese, or injecting drugs, you should ask your GP for a liver function test. The symptoms of liver disease often only occur once it is too late to undo the damage.

Taking action to reduce your risk before this happens could restore your liver back to good health.

Where did the story come from?

The study was carried out by researchers from The University of California and funded by grants from the US National Institutes of Health.

The study was published in the peer-reviewed science journal Cell – Stem Cell.

The Mail Online's reporting was poor, failing on three main points.

Firstly, it asked an inappropriate question in its headline – "Have scientists found a cure for alcoholism?". A cure, or at least a partial repair, of liver damage would not amount to a cure for alcohol addiction. The headline confused alcohol with its main health consequence – alcoholic liver disease. There are many other consequences of chronic alcohol misuse – be it social, financial or mental health-related.

Secondly, nowhere in the article (let alone in the headline) did it mention that the study was on mice, so readers might naturally assume it involved people.

Thirdly, there are other causes of liver disease aside from alcohol, such as obesity (non-alcoholic fatty liver disease) or infection with the hepatitis C virus. The mice studied didn't have alcohol-induced liver disease.

What kind of research was this?

This was a laboratory study investigating a potential new treatment approach for liver fibrosis.

Liver fibrosis is the scarring and demise of your liver, following repeated cell damage and inflammation. Fibrosis can have many causes, including viruses (like hepatitis B and C), alcohol misuse, and fatty liver disease.

Despite the liver's somewhat unique ability to recover and regenerate, when liver cells are repeatedly damaged, such as through sustained heavy alcohol use, they gradually die and the organ stops working. Part of the damage is the build-up of collagen, which causes scarring and restricts blood flow.

The poorly functioning liver and restricted blood flow causes symptoms including jaundice, weight loss, swelling of the abdomen, vomiting blood and, ultimately, death.

The only cure for severe liver scarring, where the liver loses most of its functioning ability (liver failure), is a liver transplant. But there are not enough organs to meet demand, so medical researchers are always looking for alternatives.

What did the research involve?

The researchers reprogrammed types of cells called myofibroblasts into liver cells by injecting reprogramming instructions, via a "designer virus", into mice with liver disease.

Myofibroblasts were chosen as the target, as they produce the excess collagen which causes scarring.

The researchers carefully analysed whether the reprogrammed cells behaved like normal liver cells in the lab and had similar DNA and protein profiles. They also tested whether once injected they were able to grow, repair and replace some or all of the liver damage.

Part of the challenge was devising a safe and effective way to deliver the reprogramming instructions to the mice myofibroblast cells. They used adeno-associated virus 6 (AAV6) vectors to act as delivery vehicles.

This involved taking the packaging of a virus and modifying it, so instead of infecting a mouse and causing disease, it infects the mouse and makes the modifications they wanted – in this case, turning myofibroblasts into liver cells. This involves replacing and modifying the virus DNA – that instructs the virus cell – with DNA encoding instructions you want.

What were the basic results?

The researchers overcame the delivery and reprogramming challenges to influence some cells to change from myofibroblasts into liver cells by injecting the reprogramming instructions into the bloodstreams of the mice using different AAV vectors.

Not all of the vectors worked. But in those that did, not only did some cells change, they appeared to function like normal liver cells, were able to grow and multiply, and reduced the amount of problematic collagen.

This partially alleviated two of the main causes of liver fibrosis – liver cell death and collagen build up – in mice with liver disease.

How did the researchers interpret the results?

The researchers concluded: "Our study establishes the feasibility of in vivo reprogramming of myofibroblasts into fully functional hepatocytes [liver cells] using AAV vectors, a gene delivery tool that proved to be safe and effective in clinical trials of liver-directed gene therapy".

Conclusion

This study showed it was possible to engineer and inject instructions that transform myofibroblasts into liver cells in mice with liver disease, which is quite a feat. Not all delivery mechanisms, called vectors, worked, but in those that did, the new liver cells looked normal, replaced some of the dying cells, and led to less damage due to collagen build up.

Despite the alcoholism-related headline, the mice did not have alcohol-induced liver damage – although this is a major cause of liver damage in people.

This study serves to prove this approach is feasible, and was successful in doing this. Researchers will now need to refine the technique before testing to see if it works in human trials.  

The good news is the vector delivery system has been used in human trials before – although not containing the same liver cell transformation message – so has a better chance than normal of working in people.

Right now this technique is not available as a new treatment. It represents one of the earliest types of treatment development, which can take decades from start to finish.

Currently the only cure for severe liver scarring is an organ transplant, but many die while waiting for a transplant as need far outstrips supply. If you are not on the register, you could save lives by joining the NHS Organ Donor Register today.

The liver is tough and can regenerate itself, but it can only take so much damage. Moderating your alcohol consumption, maintaining a healthy weight, and reducing your risk of contracting hepatitis C (mainly spread by injecting drugs), will do much to keep your liver healthy. 

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Could cannabis damage DNA that is then passed down generations?

Thursday May 26 2016

One of the active ingredients in cannabis may damage DNA

"Smoking cannabis can alter a person's DNA, causing mutations that expose a user to serious illnesses," the Mail Online reports.

A new review has looked at the role cannabis may play in what is known as chromothripsis.

A relatively recent discovery, chromothripsis is when the DNA of a cell suffers large-scale damage, but not enough to kill the cell. It has been linked to some types of cancer and birth defects.

In this review, researchers considered the evidence about whether one of the active ingredients in cannabis – tetrahydrocannabinol (THC) – could trigger chromothripsis, which could potentially cause cancer and other illnesses.

The researchers also raised the possibility that the DNA damage could be passed down to later generations.

There is a great deal of uncertainty about how the included studies were chosen, so there is a possibility not all relevant research was considered.

This type of study serves to stimulate debate and further research. It is not reliable enough to form the foundation of policy change on its own.

Arguably, a longer-term study would be needed to see if cannabis use could have an intergenerational effect.

We do know that cannabis, a class B illegal drug, is known to contain cancer-causing chemicals (carcinogens) and has previously been linked with lung cancer, psychosis, schizophrenia and fertility problems.

Find out more facts about cannabis.

Where did the story come from?

The review was carried out by two researchers from the University of Western Australia. There was no external source of funding.

It was published in the peer reviewed journal, Mutation Research: Fundamental and Molecular Mechanisms of Mutagenesis.

The Mail Online's headline, "Smoking cannabis can alter a person's DNA, causing mutations that expose a user to serious illnesses", made it sound like the researchers' hypothesis was proven by newly uncovered evidence, which is not the case.

The headline and article did largely reflect the researchers' findings, but failed to add any notes of caution, balance or discussion about the limitations of the research, instead taking it at face value.

What kind of research was this?

This was an evidence-informed narrative review of research exploring the hypothesis that cannabis use causes errors in human DNA, potentially leading to cancer and affecting brain development in unborn babies.

Non-systematic reviews like this are useful for summarising scientific research in a particular area, but can miss relevant research and counter-arguments.

Without a clear and systematic review of the published and unpublished science, there is a risk the authors cherry-picked the evidence, consciously or unconsciously, to fit their views. 

Such a one sided-argument has its place in stimulating debate, but should not be viewed on a par with a systematic review, one of the highest levels of evidence.

A systematic review of well-designed long-term cohort studies would be one of the best ways to assess the causal links between cannabis and DNA damage and disease.

What did the research involve?

The research is a narrative review of evidence that presents the idea that cannabis can disrupt a person's DNA, potentially raising their risk of cancer and causing genetic toxicity that could be passed from one generation to the next.

The review assembled data from 189 research articles. However, it had no reported methods. As such, we cannot assume the researchers employed systematic review methodology.

As the authors didn't mention how they found the articles, the study risks being biased to fit a coherent story, or may have missed other relevant research.

Some limitations in the evidence were presented, although quite briefly. The relative strength and balance of evidence for and against their hypothesis is not clear.

What were the basic results?

The review starts by providing scientific background on key moments in cell division – a complex and crucial process of normal cell growth and tissue maintenance.

It then outlines evidence that cannabis disrupts this process at specific points, leading to potentially cancer-causing DNA mutations.

This is a relatively recent discovery known as chromothripsis, which in a literal Greek translation means "chromosomes shattering into pieces".

Some of the main points revolve around the effects of cannabis on cancer and foetal abnormalities.

It also touches on the possibility that genetic mutations may be passed down through generations – meaning a child who has never touched cannabis could be negatively affected because of their parents' past use.

Cannabis and cancer

The review describes several observational studies linking cannabis to cancer, including brain, prostate and lung. Many also showed the higher the cannabis use the higher the cancer risk, a tentative sign of causation.

The authors acknowledge that other studies showed no link, but suggest this might be because the participants were quite low cannabis users, making a link easier to detect, or that the link only exists after a certain threshold is passed.

For example, one study reported "heavy cannabis use" as more than 0.89 joints in one day, which may not have been enough to cause DNA damage.

Cannabis and foetal abnormalities

The review discusses several studies showing a positive link between cannabis use and foetal abnormalities such as spina bifida or low birth weight as a result of disruptions in cell growth.

As before, the authors pointed out that harms were generally found when cannabis use was high (around 50-300mg/kg) – although the definition of this was variable. 

Other addictive substances

The review says that the effects of other addictive substances – alcohol, opioids, tobacco and benzodiazepines – on the development of tumours and foetal abnormalities are similar to cannabis. In other words, they all disrupt the cell cycle in a similar way.

The harmful link between alcohol consumption and tobacco use during pregnancy has long been known.

Cannabis use and future generations

Transmission of cannabis-related genetic damage from parent to child has been shown in rat and human studies, as well as for damage caused by alcohol, cocaine and opioids.

As this type of research has only just scratched the surface, the review authors said it was "an exciting time" for continuing research in this area.

How did the researchers interpret the results?

The researchers concluded that cannabis use was likely associated with cancers and other serious illnesses because it causes DNA damage in a person's cell during and around cell division.

The authors highlighted that this was an important finding as the use of cannabis is increasing globally, as is the strength of cannabis, while many countries are starting to legalise its use.

Conclusion

This review presents a useful summary of evidence backing the idea that cannabis can disrupt cell division, causing genetic damage, potentially leading to the development of cancer and foetal abnormalities.

The review was transparent in exploring the evidence behind one theory. And while this is a valuable body of research, a systematic review would have been more reliable, providing a more balanced view of the evidence.

Because of the uncertainty about how the included studies were chosen, there is a possibility that not all the relevant research was considered.

The strength of the included evidence was also not discussed. So we don't know whether it was generally strong or weak, or how it stacks up against counter-evidence. Results are only as good as the studies included, and this can vary depending on study design and assessment.

This type of study serves to stimulate debate and further research. It is not systematic or reliable enough to form the foundation of policy change on its own.

Read more about the potential harms of cannabis use.

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Healthier lifestyles 'could cut cancer death rates'

Friday May 20 2016

A few hours exercise a week can cut cancer risks

"Half of all cancer deaths could be avoided if people simply adopted a healthier lifestyle," the Daily Mail reports.

A new study adds to the weight of evidence that says combining simple lifestyle changes can dramatically cut cancer death rates.

More than 100,000 health professionals from the US were asked to complete questionnaires about their lifestyle and cancer status every two years, and diet every four years.

The researchers compared cancer rates between people with low- and high-risk lifestyle factors, and also compared rates in the low-risk group with the general white population in the US.

They found a large number of cancer cases and deaths could be attributed to a high-risk lifestyle, such as an individual being overweight, smoking, drinking heavily, or being physically inactive.

The researchers estimated between a quarter and a third of all cancer cases in this population group could be attributed to poor lifestyle factors.

These findings are in agreement with past research and the understanding that a healthier lifestyle may reduce the risk of various types of cancer.

But this study has limitations, including the population group, which only involved white American health professionals, and the possibility that the estimates are inaccurate. 

The study would appear to confirm that any small lifestyle changes you can make, such as quitting smoking, could considerably reduce your risk of developing cancer. And the more of these small changes you can combine, the greater the effect.

Read more about how lifestyle changes can help prevent cancer.

Where did the story come from?

The study was carried out by researchers from Harvard Medical School and was funded by the US National Institutes of Health.

It was published in the peer-reviewed journal, JAMA Oncology.

The Daily Mail reported on the study fairly accurately, but did not present any of its limitations.

It's nice to see that the article included clear recommendations from the research team about how a person can reduce their risk of cancer.

However, the headline figure of "half of all cancer deaths" seems a bit of a fudge, as the study presented a range of different results for specific cancer types.

What kind of research was this?

This prospective cohort study followed a large population group over time, and assessed the incidence of cancer and related deaths.

The researchers looked at how these cancer outcomes were related to various lifestyle factors, and then estimated the proportion of cancers that could be attributed to these factors.

The observational nature of this type of study means it is not able to prove causation, but it can find links and potential risk factors.

This type of study has strengths in terms of being able to follow a large number of participants over a long period of time, but the number of people who become non-responsive to follow-up assessments may increase over the years.

What did the research involve?

The researchers recruited participants from two cohort studies:

• The Nurses' Health Study – which started in 1976 and enrolled female nurses aged 30 to 55
• The Health Professionals Follow-up Study – which started in 1986 and enrolled male health professionals aged 40 to 75

Participants completed questionnaires about their medical history and lifestyle at the beginning of the study and every two years thereafter. Dietary information was collected every four years using a validated food frequency questionnaire.

The researchers split the participants into two groups according to the level of health risk associated with their lifestyle.

To be considered low risk, a participant had to meet the following requirements:

• have never smoked or be a past smoker more than five years ago
• drink no or a moderate amount of alcohol – no more than one drink a day for women and two for men
• have a body mass index (BMI) of at least 18.5 and lower than 27.5
• do at least 75 minutes of vigorous-intensity or 150 minutes of moderate-intensity aerobic physical activity a week

If all of these requirements were not met, the participant would be considered high risk.

The outcomes of interest were the incidence of total and major individual cancers and associated deaths. Cancer was self-reported in the questionnaires. Where a participant failed to respond, the National Death Index was used to identify deaths.

The researchers compared the cancer rates between the low- and high-risk groups. They then compared cancer rates in the low-risk group with cancer rates in the general population using national surveillance data.

They used this information to help them calculate population-attributable risk (PAR).

This is an estimate of the proportion of all cancer cases that can be attributed to poor lifestyle factors, or the number of cancers that would not occur in a population if the risk factor – in this case, a high-risk lifestyle – was eliminated.

For example, a PAR could be used to estimate how many people in a given population would not die of lung cancer if nobody in that population smoked.

What were the basic results?

A total of 135,910 people were included in the study (89,571 women and 46,339 men). The low-risk group contained 21% of all participants (12% women and 9% men) with the remaining 79% classed as high risk (54% women and 25% men).

The incidence of cancer per 100,000 people was 463 for women and 283 for men in the low-risk groups, compared with 618 for women and 425 for men in the high-risk groups.

From this, the researchers estimated that 25% of cancers in women and 33% of cancers in men could be attributed to high-risk lifestyle factors. For cancer-related deaths, 48% of cancer deaths in women and 44% of cancer deaths in men could be attributed to a high-risk lifestyle.

For individual cancers, the proportion of cancers estimated to be caused by high-risk lifestyle factors were:

• lung – 82% for women, 78% for men
• bowel – 29% for women, 20% for men
• pancreas – 30% for women, 29% for men
• bladder – 36% for women, 44% for men

Estimates were similar for cancer death, though there were additional associations for some other sites, including breast (12%), womb (49%), kidney (48% in men), and oral and throat (75% in women and 57% in men) cancers.

The general US populations were at higher risk than the whole study population, meaning that the PARs for these cancers resulting from a poor lifestyle were even higher than the researchers' estimates – for example, the PAR for bowel cancer jumped to 50%. 

How did the researchers interpret the results?

The researchers concluded that, "In this cohort study of a portion of the US white population, about 20-40% of cancer cases and about half of cancer deaths can be potentially prevented through lifestyle modification.

"These figures increased to 40-70% when assessed with regard to the population of US whites, and the observations are potentially applicable to broader segments of the US population." 

Conclusion

This prospective cohort study assessed the number of cancer cases and related deaths associated with poor lifestyle factors in a sample of US health professionals.

As the findings demonstrate, a large number of cancer cases and deaths in both men and women can be attributed to a high-risk lifestyle, such as being overweight, smoking, drinking heavily, or being physically inactive.

Worryingly, a poor lifestyle was estimated to account for an even greater number of cancers in the general population.

These findings are in agreement with much research, which has found that a healthier lifestyle may reduce the risk of various cancers.

The study has both strengths and limitations to consider. It contained a large number of participants and excluded types of cancer where incidence may be related to environmental factors rather than lifestyle, both adding strength to the findings.

It did have limitations, however:

• The use of questionnaires for collecting information is prone to bias, either by people reporting what they think they should be doing rather than what they are doing, or because of difficulty recalling information over a period of time.
• Only medical professionals were included in the study. This group are potentially more health conscious, so may not be a good reflection of the whole population. This is supported by the fact that even the high-risk study group were healthier than the US population overall, and PAR estimates for cancer from poor lifestyle factors were higher in the general population.
• Only including a white population means these findings may not necessarily apply to other ethnicities.
• These results are only estimates: though informed by careful analysis of this population and their lifestyle factors and cancer rates, it's possible that the proportion of cancers attributed to poor lifestyle factors is inaccurate, particularly for wider populations.

Despite these limitations, it is well known that unhealthy lifestyle factors could increase your risk of developing cancer, as well as various other health problems. Any small changes you can make to your lifestyle could considerably reduce your risk.

Read more about how to prevent cancer.

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Are broken bones, loneliness and poor sleep really hidden killers?

Wednesday May 18 2016

A broken bone can affect other areas of wellbeing

"Revealed, the five hidden killers that could send you to an early grave," the Daily Mail reports. These "hidden killers" include loneliness and poor sleep. But this is a simplistic take on complex research aiming to identify new ways of classifying health and wellbeing.

The research assessed the health and lifestyle of 3,000 US adults aged 57 to 85 years, then reassessed how many were incapacitated or had died five years later.

The researchers then compared two models to see which better categorised the participants' health status and risk.

The first mainly looked at the presence of diseases. The second model was more comprehensive, and included wider measures such as psychological wellbeing, mobility and health behaviours.

Overall, two-thirds of the sample was classed as being in "robust" good health when using the medical disease model, but many of these fell into more vulnerable risk groups when using a more comprehensive risk model.

The comprehensive model identified poor mental health, including depression, isolation and memory problems, and frailty and mobility problems as being predictive of mortality – "hidden killers" in newspaper speak – factors that would be largely overlooked if you only focused on physical diseases.

The findings suggest a comprehensive view of a person's health and wellbeing is needed when looking at their risk status and trying to target appropriate medical care and support.

Wellbeing and quality of life is not simply a case of whether or not someone has a physical illness. 

Where did the story come from?

The study was carried out by researchers from the University of Chicago, and was funded by the same institution and the US National Institute of Aging.

It was published in the peer-reviewed journal, PNAS, and the article is openly available for access.

The Daily Mail, The Sun and Metro articles are generally representative of the study's findings on loneliness, fractures and mobility problems.

But none of the papers grasped the point of the study – an attempt to create more complex and subtle models of wellbeing.

What kind of research was this?

This cohort study aimed to look at the best way of defining population health.

The researchers explained how the World Health Organization (WHO) defines health as a "state of complete physical, mental and social wellbeing and not merely the absence of disease or infirmity".

However, despite this there has been little rigorous attempt to use this definition to measure and assess population health. More often, what is described as the "medical model" is used to measure health, which focuses solely on disease diagnoses.

The researchers propose a "comprehensive model" that also considers psychological wellbeing and function as being a better fit to the WHO classification.

The researchers applied both of these models to US survey data to see how population health was defined by the different methods.   

What did the research involve?

The research involved a large, nationally representative sample of 3,005 older US adults aged 57 to 85 years who lived in the community and were taking part in the National Social Life, Health and Aging Project (NSHAP).

The participants were interviewed and completed a questionnaire about their health and lifestyle, as well as having body measures taken.

The researchers then used two different models to categorise the state of a person's health.

The medical model looked at specific diseases:

• heart disease
• cancer
• lung disease
• stroke
• diabetes
• kidney disease
• liver disease
• arthritis
• high blood pressure
• asthma
• thyroid disease

The comprehensive model also included 35 additional measures that encompassed five broad dimensions of health and wellbeing:

• health behaviour – smoking, exercise, sleep
• psychological health – depression, memory
• sensory abilities – vision, hearing
• neuroimmunity – chronic inflammation
• mobility or frailty – including fractures

The researchers followed these people up five years later. They then identified a few distinct health classes or categories within these models that encompassed several of the disease and wellbeing features, and most reliably indicated a person's health and mortality risk.  

What were the basic results?

The researchers identified five distinct health classes within the medical model that had significant and independent effects on mortality.

The first two classes were people who had undiagnosed high blood pressure (hypertension) and a single non-cardiovascular disease. These were the least vulnerable, or most "robust", health groups.

The intermediate (third) risk group were those with poorly controlled diabetes. The two most vulnerable groups (four and five) were those who had both cardiovascular disease and diabetes, or who had extensive medical illnesses.

People in the first two robust classes had around a 15% risk of being physically incapacitated or dead after five years, compared with 35% in the top extensive illness group.   

In the comprehensive model, six distinct classes arose – again, the first two classes were the least vulnerable, or most robust; classes three and four had an intermediate risk; and five and six were the most vulnerable.

The six classes were:

1. robust obese – obese but generally in good health
2. one minor condition – stomach ulcer, thyroid problems, bladder problems
3. broken bones – people with osteoporosis
4. poor mental health – depression, poor memory and loneliness
5. diabetes, hypertension and immobility
6. extensive medical illnesses and frailty

Almost a quarter of this older US population (22%) were in the first robust obese group. These people often had undiagnosed hypertension as measured by a home device, but, other than this, few other diseases and only a 6% risk of dying after five years.

The second group were not obese and had a minor condition – one not considered to have high mortality risk – and a 16% risk of death.

The two middle classes of the comprehensive model – those with fractures or osteoporosis and poor mental health – included 28% of this US population, despite being, as the researchers say, "largely ignored" by the medical model.   

The last two, most vulnerable, classes had the most compatibility with the vulnerable classes of the medical model, but still more people were reclassified as vulnerable when using the comprehensive model.

People in the most vulnerable sixth group had a 44% risk of dying within five years.

Overall, the medical model classified two-thirds of the older US population as being in robust health. Only half of these people went into the robust classes of the comprehensive model.

These findings suggest that factors such as poor mental health, bone fractures, and sensory and mobility problems are very important to consider when categorising vulnerability and mortality risk.

How did the researchers interpret the results?

The researchers concluded that the comprehensive model identifies new classes of people with mortality risk, such as those with broken bones or poor mental health, who are largely overlooked by medical models that only focus on disease.

They said that: "This approach provides a method for broadly reconceptualising health, which may inform health policy", with implications for medical care, prevention and resource allocation.   

Conclusion

As the researchers say, the WHO definition of health encompasses physical, mental and social wellbeing – not just the presence or absence of disease.

But how often are these extra dimensions taken into account when assessing a person's health status?

In this sample of older adults, just looking at their disease status puts the majority of them into an apparently "robust" health group.

Yet when you consider the additional dimensions of psychological health and wellbeing, you seem to get a much better indication of those who were at higher or lower risk of dying or being incapacitated in the coming five years.

The "hidden killers" the media refer to are factors such as frailty and fractures, and depression and loneliness, which would be overlooked if you looked at disease diagnoses alone.  

This suggests that a comprehensive view of a person's health and wellbeing is needed if you are looking at their risk status, and trying to target appropriate medical care and support.

But you can't say from the results of a study like this that these factors are being overlooked within healthcare.

For example, just because a medical risk model looking at physical diseases alone hasn't looked at these factors as a risk indicator doesn't necessarily mean that the people with these conditions have not been diagnosed in medical practice and are not receiving appropriate care and treatment.

The media term "hidden" in this context is therefore a bit misleading – as is the term "killer".

Of course, factors like loneliness and depression aren't necessarily going to lead to death directly, but could be associated with other poor health factors that together contribute to mortality risk.

Although this is a large, nationally representative sample, these are all older US adults. The six predictive classes the researchers identified to indicate robust, intermediate or vulnerable risk status may not be the same if people from another country were examined, or a population of middle-aged or younger adults.

It would be interesting and useful if researchers carried out a similar analysis on various groups within the UK population.

The study is a valuable contribution to how we define health and wellbeing. However, whether it has any direct implications in terms of health assessment, screening and diagnosis is unknown at this stage.  

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from NHS Choices: Behind the headlines http://ift.tt/1OzQefd

Women who regularly attend religious services 'live longer'

Tuesday May 17 2016

Churchgoing women were more likely to be non-smokers

"Going to church could save your life," reports the Daily Mail, adding that, "Women who worship once a week are '25 per cent less likely to die early'."

Perhaps surprisingly, while the first part of the headline is overly simplistic, it may not technically be wrong – according to new research from the US, anyway. Whether or not divine providence is responsible for the increase in lifespan is still up for debate.

A large Harvard study showed that predominantly white Christian nurses who attended religious services more than once a week had a 33% lower relative risk of dying over a 16-year period compared with similar women who did not attend religious services.

A sizeable chunk of the link was explained by social support (23%), smoking rates (23%) and, to a lesser extent, optimism differences (9%) between attenders and non-attenders.

The study was very large, precise, and as robust to bias and confounding as you could reasonably expect, so it can be considered reliable. But the lifestyle and social differences between the groups can't go unnoticed.

It's therefore possible that the regular pattern of social interaction associated with being part of a religious community, and the benefits this brings, is mainly responsible for the outcome seen in this research, rather than any specific religious or spiritual aspects.

Atheists who regularly attend humanist gatherings, or just those who go to weekly bingo sessions, may also experience similar benefits.

Read more about the benefits of connecting with others.

Where did the story come from?

The study was carried out by researchers from the Harvard T. H. Chan School of Public Health in the US.

It was funded by the John Templeton Foundation, which, according to its website, funds research on the "big questions of human purpose and ultimate reality". The foundation has a stated aim of using scientific methods to explore the alleged spiritual aspects of reality.

The study was published in the peer-reviewed Journal of the American Medical Association: Internal Medicine.

Generally, the media covered the story accurately, citing the possible reasons why attending religious services might be good for you in terms of boosting social support, happiness and optimism.

For example, The Independent reported advice from the researchers, who said: "Our results do not imply that healthcare professionals should prescribe attendance at religious services, but for those who already hold religious beliefs, attendance at services could be encouraged as a form of meaningful social participation." 

What kind of research was this?

This cohort study looked at the links between religious service attendance and subsequent death in female nurses.

This type of study is appropriate to investigate this link.

But many factors can influence death rates, and potentially also be linked to church attendance – for example, more resilient social networks can help people cope in times of hardship.

Teasing out any clear causal links from the vast mix of influencing factors is tricky.

What did the research involve?

This study analysed self-reported religious service attendance information from 1996 to 2012 and linked death records from the same time period.

The researchers analysed information from 74,534 female US nurses who had been answering health and lifestyle questionnaires every two years from 1992 to 2012 as part of the Nurses' Health Study, a rich ongoing source of epidemiological research.

From 1992 and every four years thereafter, women were asked how often they go to religious meetings or services. Responses included more than once a week, once a week, one to three times a month, less than once a month, and never (or almost never).

The researchers' main analysis looked at the death rates of women with different frequency of religious attendance, comparing them with those who did not attend.

They adjusted for a lot of confounders to try to isolate the single effect of religious attendance, including:

• age
• alcohol consumption
• physical exercise
• multivitamin use
• high blood pressure
• high cholesterol
• use of hormonal replacement therapy
• healthy eating scores
• smoking status
• body mass index
• husband's education level
• physical impairment
• social integration score – composite of marriage status, group participation, number of close friends or relatives
• living alone
• family income
• geographic region in the US
• depression in 1992
• religious attendance in 1992

The researchers also performed a "mediator" analysis, which helps understand how much each of the confounders is contributing to the main link of interest – in this case, religious service attendance and death.

What were the basic results?

Most women were either Roman Catholic or belonged to other Christian denominations, and 97% or more were white. There was a small minority of Jewish women and no Hindu or Muslim women.

There was a consistent pattern between religious service attendance and lower rates of death from any cause, cardiovascular disease and cancer.

There were 13,537 deaths over the study period, giving a base rate of death of 18.1 %. Compared with women not attending religious services, women who attended a service more than once a week had 33% less risk of dying from any cause during the 16-year study (hazard ratio 0.67, 95% confidence interval [CI] 0.62 to 0.71).

Those attending regularly in both 1996 and 2000 – a sign of long-term, regular attendance – had an even lower relative risk at 45% (95% CI 0.52 to 0.59) less than non-attenders.

Looking at potential mediators, the researchers picked out depressive symptoms, smoking, less social support and optimism as the most important.

Social support explained the highest proportion of the link (23%), with smoking a close second (22%). Optimism accounted for around 9%.

The link appeared consistent over time, as well as for religion (although there wasn't much variety), geography and other potentially influential factors.

How did the researchers interpret the results?

The researchers said that: "Frequent attendance at religious services was associated with significantly lower risk of all-cause, cardiovascular, and cancer mortality among women.

"Religion and spirituality may be an underappreciated resource that physicians could explore with their patients, as appropriate." 

Conclusion

This study showed that white Christian women who attended religious services more than once a week had a lower risk of dying from any cause, cancer, and cardiovascular disease specifically compared with similar women who did not attend religious services.

This link was at least partially explained by social support, smoking rates, and optimism differences between attenders and non-attenders.

As the study was very large, it gives precise estimates of relative risks. The researchers pointed out there are other factors that could potentially mediate the link that they couldn't measure in their study, like psychosocial resilience, religious coping mechanisms, a sense of a purpose in life, and self-discipline.

But their interesting stats also showed that biases from these or other sources would have to be very large to affect the result in a meaningful way, suggesting the study's conclusions are quite solid.

The study mainly involved white women who mostly identified as Christian, so we don't know if the same effects would be seen for men of a similar faith, or adults or children from other religions or with no religion.

Non-religious groups could argue having a purpose in life, self-discipline and many other aspects that potentially mediate the link are not the sole preserve of the religious, but there is no doubt that for many people this comes from practising a faith.

But it's possible the same effect could be achieved in other ways, too. While the researchers tried to account for social factors associated with religious attendance, there could well be other unmeasured, or possibly unconsidered, effects associated with regular social group interaction.

A similar study could have noted reduced mortality among people attending any community activity groups or societies, both for people of all faiths as well as people with none.

As we discussed last month, people with a history of cancer who regularly attended a choir session showed evidence of improved immune function.

Human beings are social animals, so enjoying regular social activities with others is probably a good way, among others, to improve both your physical and mental wellbeing.

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from NHS Choices: Behind the headlines http://ift.tt/1TGfYYG

Dad's age, diet and drinking habits may impact on birth defect risks

Monday May 16 2016

Age, diet and drinking can damage sperm quality

"Men are being warned to become fathers by 40 or face a greater risk of having children with serious illnesses," the Daily Mail reports after a new review looked at some of the evidence about paternal influences on the risk of childhood diseases.

The review discusses several research findings found previously, including some reports that children born to fathers over the age of 40 have higher rates of conditions like autism spectrum disorder – and that stress, smoking and alcohol may also cause heritable changes.  

But this is an opinion piece. We don't know how the researchers selected the evidence they reviewed, and it is possible that not all relevant research was considered.

The review should not be taken as firm evidence that there is such a thing as a "male biological clock" and fathers are putting their children at risk by delaying fatherhood until middle age.

Still, men trying for a baby should avoid smoking, excessive alcohol consumption and eating a poor diet. It may not boost your sperm's health, but it will definitely improve your health.  

Where did the story come from?

The study was carried out by researchers from Georgetown University Medical Centre in the US, and was funded by the US National Institutes of Health.

It was published in the peer-reviewed American Journal of Stem Cells. This is an open-access journal, so the study can be downloaded for free as a PDF.

Neither the Daily Mail nor The Times recognise the important limitations of this review: namely, that is it is not a systematic review, so it carries far less weight in terms of evidence.

Also, the Mail talks about men being "warned" about delaying fatherhood – but, as far as we can tell, the only people actually issuing any warning based on this review is the Mail itself.

What kind of research was this?

This appears to be a narrative review discussing whether how a man's age and environmental exposures may alter his genes and so be passed on to his offspring.

The article centred on epigenetics, the idea that, though a person's DNA sequence may not change, their exposures over the course of a lifetime may lead to changes in their gene activity and expression that can be passed on to their children.

This happens through mechanisms such as DNA methylation, where methyl groups (types of molecules) are added to the building blocks of the DNA, or where small RNA molecules (miRNA) are added to the DNA – both of which alter gene activity.

This review discusses how epigenetics in the father have an effect on the offspring, focusing on age and environmental exposures. The researchers discuss these theories, referencing various publications, but this does not appear to be a systematic review. 

The research team did not provide any information about how they identified and selected the evidence they reviewed. As such, it is possible that not all relevant research has been examined and so this must largely be considered to be an opinion piece.      

What does the research say about a father's age?

The researchers say that past research has shown that a father's age has a significant effect on a child's characteristics and the likelihood of them having congenital abnormalities.

Some studies have linked increasing paternal age (over 40 or so years) with higher rates of conditions like autism and schizophrenia. Others have observed increased rates of birth abnormalities, such as heart defects, musculoskeletal abnormalities, and Down's syndrome.

Mouse studies also support this. Studies have shown that mice born to "old" fathers (over two years old) performed poorly on tests of learning and memory, and also had a reduced lifespan and less reproductive success themselves. Mice with slightly younger fathers (10 months old) were less social.

The researchers say that although the mechanism behind this is not established, most evidence points in the direction of DNA methylation. Animal studies have shown higher rates of DNA methylation in the sperm cells of older rats compared with younger rats.

What does the research say about environmental exposure?

The effect of environmental exposures on offspring is less clear, although there is some evidence of this. Some studies have shown that people with little available food have demonstrated some changes that can be passed on to their children, though not necessarily bad ones.

It's reported that children born to fathers who had low food availability during pre-adolescence were less likely to die from cardiovascular disease. And those whose grandparents had little food were less likely to have diabetes.

Other studies have suggested stress induces DNA changes that could be passed on. Mouse fathers who were subject to the stress of food deprivation before mating had offspring with lower blood glucose levels.

Mice exposed to other psychological stressors – such as cage changes and fox smell – had offspring that displayed blunted stress responses, indicating some form of behavioural defect.

Smoking and alcohol may also have effects. Smoking has been shown to alter the DNA in sperm.

And three-quarters of babies with foetal alcohol syndrome – birth defects normally associated with maternal consumption of alcohol during pregnancy – are reported to have fathers with alcohol use problems.

Chronic alcohol use in the father is said to again affect DNA methylation. In rats, offspring from fathers given alcohol were more likely to have a low birthweight or spatial learning problems when put in a maze test.

Studies in mice also found those whose fathers were given alcohol were more likely to have cognitive and mobility problems. 

How did the researchers interpret the results?

The researchers say their review findings support the concept of the epigenetic inheritance of paternal experiences across generations.

They say their review highlights "the possible links between birth defects and paternal age, environmental factors, and alcohol consumption" and the need for future research in this area.

Conclusion

This narrative review summarises past research on DNA changes that may occur as a result of a father's age and exposures that could be passed on to his children.

In particular, the review discusses animal and human studies that have linked changes in offspring with increasing paternal age, stress and substance use.  

But this review must largely be considered to only be an opinion piece. We don't know how the researchers identified, appraised and selected the studies they discussed.

As such, there is a strong possibility that not all animal and human research relevant to the issue of paternal epigenetic inheritance will have been reviewed and discussed here.  

There are also no clear methods or results provided for the studies that are discussed, with only a few brief sentences given for each study. We are not able to critique the quality and strength of evidence linking a father's age or any other exposure with the outcome reported. 

For example, people would likely be concerned by reports that increased rates of autism or congenital defects have been observed in children born to fathers over the age of 40. But we have nothing more to go on than this – no firm risk figures are given.

And the observational studies themselves are likely to have been influenced by various unknown sources of bias and confounding, like the report that three-quarters of babies with foetal alcohol syndrome have a father with alcohol use problems.

This doesn't tell us anything about what the mother is doing. It could be that many of these babies had a mother who also had alcohol use problems – alongside her partner – and used alcohol during pregnancy, and has directly exposed the developing baby.

This study will add to the research on how parental exposures may be passed on to a child through epigenetics.

However, given the limitations of this review and the lack of methods given, this opinion piece should not be taken as firm evidence that fathers are putting their children at risk by delaying fatherhood.

These limitations aside, advice that men hoping to become fathers should avoid known bad lifestyle behaviours, such as smoking, drinking too much, not exercising and eating a poor diet seems sensible.

Read more about what both men and women can do to protect their fertility.

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from NHS Choices: Behind the headlines http://ift.tt/1siAFUc