NHS Choices

Does moderate drinking reduce heart failure risk?

NHS Choices - Behind the Headlines - Tue, 20/10/2015 - 12:10

"Seven alcoholic drinks a week can help to prevent heart disease," the Daily Mirror reports. A US study suggests alcohol consumption up to this level may have a protective effect against heart failure.

This large US study followed more than 14,000 adults aged 45 and older for 24 years. It found those who drank up to 12 UK units (7 standard US "drinks") per week at the start of the study had a lower risk of developing heart failure than those who never drank alcohol.

The average alcohol consumption in this lower risk group was about 5 UK units a week (around 2.5 low-strength ABV 3.6% pints of lager a week).

At this level of consumption, men were 20% less likely to develop heart failure compared with people who never drank, while for women it was 16%.

The study benefits from its large size and the fact data was collected over a long period of time.

But studying the impact of alcohol on outcomes is fraught with difficulty. These difficulties include people not all having the same idea of what a "drink" or "unit" is.

People may also intentionally misreport their alcohol intake. We also cannot be certain alcohol intake alone is giving rise to the reduction in risk seen.

Steps you can take to help reduce your risk of heart failure – and other types of heart disease – include eating a healthy diet, achieving and maintaining a healthy weight, and quitting smoking (if you smoke).

 

Where did the story come from?

The study was carried out by researchers from Brigham and Women's Hospital in Boston, and other research centres in the US, the UK and Portugal.

It was published in the peer-reviewed European Heart Journal.

The UK media generally did not translate the measure of "drinks" used in this study into UK units, which people might have found easier to understand.

The standard US "drink" in this study contained 14g of alcohol, and a UK unit is 8g of alcohol. So the group with the reduced risk actually drank up to 12 units a week.

The reporting also makes it seem as though 12 units – what is referred to in the papers as "a glass a day" – is the optimal level, but the study cannot not tell us this.

While consumption in this lower risk group was "up to" 12 units per week, the average consumption was about 5 units per week. This is about 3.5 small glasses (125ml of 12% alcohol by volume) of wine a week, not a "glass a day".

And the poor old Daily Express got itself into a right muddle. At the time of writing, its website is actually running two versions of the story. 

One story claims moderate alcohol consumption was linked to reduced heart failure risk, which is accurate. 

The other story claims moderate alcohol consumption protects against heart attacks, which is not accurate, as a heart attack is an entirely different condition to heart failure.

 

What kind of research was this?

This was a large prospective cohort study looking at the relationship between alcohol consumption and the risk of heart failure.

Heavy alcohol consumption is known to increase the risk of heart failure, but the researchers say the effects of moderate alcohol consumption are not clear.

This type of study is the best way to look at the link between alcohol consumption and health outcomes, as it would not be feasible (or arguably ethical) to randomise people to consume different amounts of alcohol over a long period of time.

As with all observational studies, other factors (confounders) may be having an effect on the outcome, and it is difficult to be certain their impact has been entirely removed.

Studying the effects of alcohol intake is notoriously difficult for a range of reasons. Not least is what can be termed the "Del Boy effect": in one episode of the comedy Only Fools and Horses, the lead character tells his GP he is a teetotal fitness fanatic when in fact the opposite is true – people often misrepresent how healthy they are when talking to their doctor.

 

What did the research involve?

The researchers recruited adults (average age 54 years) who did not have heart failure in 1987 to 1989, and followed them up over about 24 years.

Researchers assessed the participants' alcohol consumption at the start of and during the study, and identified any participants who developed heart failure.

They then compared the likelihood of developing heart failure among people with different levels of alcohol intake.

Participants came from four communities in the US, and were aged 45 to 64 years old at the start of the study. The current analyses only included black or white participants. People with evidence of heart failure at the start of the study were excluded.

The participants had annual telephone calls with researchers, and in-person visits every three years.

At each interview, participants were asked if they currently drank alcohol and, if not, whether they had done so in the past. Those who drank were asked how often they usually drank wine, beer, or spirits (hard liquor).

It was not clear exactly how participants were asked to quantify their drinking, but the researchers used the information collected to determine how many standard drinks each person consumed a week.

A drink in this study was considered to be 14g of alcohol. In the UK, 1 unit is 8g of pure alcohol, so this drink would be 1.75 units in UK terms.

People developing heart failure were identified by looking at hospital records and national death records. This identified those recorded as being hospitalised for, or dying from, heart failure.

For their analyses, the researchers grouped people according to their alcohol consumption at the start of the study, and looked at whether their risk of heart failure differed across the groups.

They repeated their analyses using people's average alcohol consumption over the first nine years of the study.

The researchers took into account potential confounders at the start of the study, including:

  • age
  • health conditions, including high blood pressure, diabetes, coronary artery disease, stroke and heart attack
  • cholesterol levels
  • body mass index (BMI)
  • smoking
  • physical activity level
  • educational level (as an indication of socioeconomic status)

 

What were the basic results?

Among the participants:

  • 42% never drank alcohol
  • 19% were former alcohol drinkers who had stopped
  • 25% reported drinking up to 7 drinks (up to 12.25 UK units) per week (average consumption in this group was about 3 drinks per week, or 5.25 UK units)
  • 8% reported drinking 7 to 14 drinks (12.25 to 24.5 UK units) per week
  • 3% reported drinking 14 to 21 drinks (24.5 to 36.75 UK units) per week
  • 3% reported drinking 21 drinks or more (36.75 UK units or more) per week

People in the various alcohol consumption categories differed from each other in a variety of ways. For example, heavier drinkers tended to be younger and have lower BMIs, but be more likely to smoke.

Overall, about 17% of participants were hospitalised for, or died from, heart failure during the 24 years of the study.

Men who drank up to 7 drinks per week at the start of the study were 20% less likely to develop heart failure than those who never drank alcohol (hazard ratio [HR] 0.80, 95% confidence interval [CI] 0.68 to 0.94).

Women who drank up to 7 drinks per week at the start of the study were 16% less likely to develop heart failure than those who never drank alcohol (HR 0.84, 95% CI 0.71 to 1.00).

But at the upper level of the confidence interval (1.00), there would be no actual difference in risk reduction.

People who drank 7 drinks a week or more did not differ significantly in their risk of heart failure compared with those who never drank alcohol.

Those who drank the most (21 drinks per week or more for men, and those drinking 14 drinks per week or more for women) were more likely to die from any cause during the study.

 

How did the researchers interpret the results?

The researchers concluded that, "Alcohol consumption of up to 7 drinks [about 12 UK units] per week at early middle age is associated with lower risk for future HF [heart failure], with a similar but less definite association in women than in men."

 

Conclusion

This study suggests drinking up to about 12 UK units a week is associated with a lower risk of heart failure in men compared with never drinking alcohol.

There was a similar result for women, but the results were not as robust and did not rule out the possibility of there being no difference.

The study benefits from its large size (more than 14,000 people) and the fact it collected its data prospectively over a long period of time.

However, studying the impact of alcohol on outcomes is fraught with difficulty. These difficulties include people not being entirely sure what a "drink" or a "unit" is, and reporting their intakes incorrectly as a result.

In addition, people may intentionally misreport their alcohol intake – for example, if they are concerned about what the researchers will think about their intake.

Also, people who do not drink may do so for reasons linked to their health, so may have a greater risk of being unhealthy.

Other limitations are that while the researchers did try to take a number of confounders into account, unmeasured factors could still be having an effect, such as diet.

For example, these confounders were only assessed at the start of the study, and people may have changed over the study period (such as taking up smoking). 

The study only identified people who were hospitalised for, or died from, heart failure. This misses people who had not yet been hospitalised or died from the condition.

The results also may not apply to younger people, and the researchers could not look at specific patterns of drinking, such as binge drinking.

Although no level of alcohol intake was associated with an increased risk of heart failure in this study, the authors note few people drank very heavily in their sample. Excessive alcohol consumption is known to lead to heart damage.

The study also did not look at the incidence of other alcohol-related illnesses, such as liver disease. Deaths from liver disease in the UK have increased 400% since 1970, due in part to increased alcohol consumption, as we discussed in November 2014.

The NHS recommends that:

  • men should not regularly drink more than 3-4 units of alcohol a day
  • women should not regularly drink more than 2-3 units a day
  • if you've had a heavy drinking session, avoid alcohol for 48 hours

Here, "regularly" means drinking this amount every day or most days of the week.

The amount of alcohol consumed in the study group with the reduced risk was within the UK's recommended maximum consumption limits.

But it is generally not recommended that people take up drinking alcohol just for any potential heart benefits. If you do drink alcohol, you should stick within the recommended limits.

Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.

Links To The Headlines

Seven alcoholic drinks a week can help to prevent heart disease, new research reveals. Daily Mirror, January 20 2015

A drink a day 'cuts heart disease risk by a fifth' researchers claim...so don't worry about having a dry January. Mail Online, January 19 2015

A drink a night 'is better for your heart than none at all'. The Independent, January 19 2015

Glass of wine a day could protect the heart. The Daily Telegraph, January 20 2015

Daily drink 'cuts risk' of middle-age heart failure. The Times, January 20 2015

Drinking half a pint of beer a day could fight heart failure. Daily Express, January 20 2015

Links To Science

Gonçalves A, Claggett B, Jhund PS, et al. Alcohol consumption and risk of heart failure: the Atherosclerosis Risk in Communities Study. European Heart Journal. Published online January 20 2015

Categories: NHS Choices

Antidepressant use in menopause linked to broken bones

NHS Choices - Behind the Headlines - Fri, 26/06/2015 - 14:30

"Taking antidepressants like Prozac to counter mood changes in menopause 'raises risk of broken bones'," the Daily Mail reports. A new study suggests that using selective serotonin reuptake inhibitors (SSRIs) during the menopause may increase the risk of bone fracture by around 76%.

While this may sound alarming, the baseline risk of bone fracture is relatively small so the 76% figure represents a small, if statistically significant, increase in risk.

The study in the spotlight looked at the risk of bone fractures in women taking SSRIs compared with women taking common stomach ulcer drugs.

SSRIs are primarily used to treat symptoms such as depression and anxiety, but they are also used when treating the hot flushes that can come with the menopause. While not licensed for this use in the UK, consultants can prescribe them at their own discretion for women unable or unwilling to use hormone replacement therapy (HRT)

Researchers found that risk difference was statistically significant only after the second year. This suggests SSRIs may need several months to produce clinically meaningful effects on bone mineral density.

Importantly, the study results may not be directly applicable to women taking SSRIs for mental health reasons. So while it is possible that use may be associated with a small increase in fracture risk for menopausal women, this small risk must be balanced against the benefit of taking them for the prescribed reason.  

 

Where did the story come from?

The study was done by researchers from Harvard University, University of North Carolina at Chapel Hill, and Northeastern University. It was funded by the US National Institute of Mental Health and the National Institute on Aging at the National Institutes of Health.

One study author declared they receive: "salary support from the Center for Pharmacoepidemiology and from unrestricted research grants from pharmaceutical companies (GlaxoSmithKline, Merck, Sanofi) to the Department of Epidemiology, University of North Carolina at Chapel Hill".

The study was published in the peer-reviewed medical journal Injury Prevention.

Generally the Mail reported the story accurately although its headline was inaccurate for a number of reasons. The use of Prozac in the headline was inappropriate (if understandable as it is the one SSRI that most people have heard of). Another SSRI, paroxetine, is usually the first-line option for hot flushes (and is licensed for this use in the United States).

Also the headline says that SSRIs were being used to "counter mood change". This may be incorrect. The study excluded any women who were using SSRIs for mental health reasons, which may have covered this.

 

What kind of research was this?

The study used data from US medical databases to analyse a cohort of women taking SSRI drugs to treat symptoms of menopause. They wanted to see if it weakened their bones, leading to more reports of bone fractures.

In the UK SSRIs are prescribed to treat depression and various other mental health problems, though some consultants do use them off-licence for menopausal symptoms in certain cases.

In the US, an SSRI drug (paroxetine) has been approved to treat hot flushes and night sweats linked to the menopause. Due to changes in hormones associated with the menopause women’s bones can begin to thin, increasing the risk of bone fractures. So the researchers wanted to find out whether SSRI drugs might make this worse.

They used an existing data set of drug prescriptions to investigate the issue, which was like a large cohort study. However, the research team would have been limited by the information available in the database, so might not have been able to collect all the information they desired.

 

What did the research involve?

Women without mental illness, aged 40-64 years, who started taking SSRI drugs were compared with a cohort of women who started taking drugs to treat stomach ulcers and stomach irritation (H2 antagonists or proton pump inhibitors, H2As/PPIs) from 1998-2010, using data from a US database of prescriptions. The researchers were looking for differences in the rate of bone fractures in each group.

The research team says it chose the comparison group of drugs as H2As have a trivial or no association with risk of fractures, but PPIs are associated with a slightly increased risk of fractures.

They used the "PharMetrics Claims Database", which contains medical and pharmaceutical claims for over 61 million unique patients. In the US medical and drugs costs are "claimed" through a person’s health insurance. This gave them information on the amount of drugs prescribed and for how long. Age, gender and where they lived was also available, as were diagnosed medical conditions.

Fractures of the hip or arm bones (humerus, radius or ulna) at least one day after starting SSRI or H2A/PPI were analysed.

Women with mental health conditions were excluded.

Starting SSRIs or H2A/PPI was defined as filling a prescription without evidence of having filled a prescription for any kind of antidepressants or anti-ulcer drugs in the preceding 12 months.

As it was a US health insurance based database, it won't include all medical insurance schemes and definitely won’t include those without medical insurance. 

The analysis adjusted for a very large list of confounders. Some of the more important ones were:

  • age
  • history of previous fractures
  • osteoporosis
  • previous bone mineral density scans
  • use of medications that are known to affect risk of fractures

The groups were "weighted" for many different characteristics and potential confounders. A statistical technique to ensure the two comparison groups were reasonably balanced before comparison.

 

What were the basic results?

Fracture rates were higher in the 137,031 women starting SSRI compared with the 236,294 starting H2A/PPI.

Hazard ratios comparing the risk of fracture of SSRI compared with H2A/PPI at different time points were:

  • 1.76 (95% confidence interval (CI) 1.33 to 2.32) over one year
  • 1.73 (95% CI 1.33 to 2.24) at two years
  • 1.67 (95% CI 1.30 to 2.14) at five years

The research team thought that there might be a delay between taking SSRIs and them having a clinically meaningful effect on bone mineral density. As such they factored in a six-month lag period in their main analysis.

 

How did the researchers interpret the results?

The researchers concluded: "SSRIs appear to increase fracture risk among middle-aged women without psychiatric disorders, an effect sustained over time, suggesting that shorter duration of treatment may decrease fracture risk. Future efforts should examine whether this association pertains at lower doses."

 

Conclusion

This study found women aged 40-64 years without mental health illness who started taking SSRI medications had significantly higher fracture risk up to five years after starting, compared with women taking other drugs prescribed for stomach ulcers or irritation (H2A or PPIs).

Risk difference was statistically significant only after the second year, suggesting SSRIs may need several months to produce clinically meaningful effects on bone mineral density.

Importantly, and acknowledged by the study authors, this study can't prove cause and effect. There may be other confounding factors mediating the link between the drugs and fracture risk. There are a number of reasons why certain women cannot safely use hormone replacement therapy, so these may contribute towards fracture risk.

Another limitation was the fact the cohort included women prescribed SSRIs for many non-mental health related reasons. So the risk profile across different disease categories may vary, grouping them may hide more nuanced results. The study team was not able to analyse the relationship between different doses of SSRIs and the risk of fractures. So we don’t know if there are any dose thresholds at which the fracture risk starts to increase significantly.

Proton pump inhibitors can increase the risk of fractures, particularly when used at high doses for over a year in the elderly. The fact SSRIs increased the risk still further, relative to this group, suggests the risk associated with SSRI compared with no drugs may be slightly higher. However, shorter courses of SSRIs, maybe less than six months, might not be associated with fracture risk.

Importantly, SSRIs are not currently licensed for the treatment of menopausal-related symptoms in the UK – though they are occasionally prescribed off-licence. So their use would mainly be in the treatment of depression and other mental health conditions. This study does not tell us much about the effect of SSRIs upon fracture risk in women with mental health conditions as they were excluded from the analysis.

Therefore while it is possible that SSRIs taken for mental health conditions may also be associated with a small increase in the risk of fracture, any possible increase must be balanced against the benefits of taking SSRIs for the reasons originally prescribed. This risk benefit balance should be discussed with your GP or other medical professional. Take all medicines as prescribed and do not change them without discussing your treatment options with a medical profession.

Links To The Headlines

Taking anti-depressants like Prozac to counter mood changes in menopause 'raises risk of broken bones'. Daily Mail, June 26 2015

Links To Science

Sheu Y, Lanteigne A, Stürmer T, et al. SSRI use and risk of fractures among perimenopausal women without mental disorders. Injury Prevention. Published online June 25 2015

Categories: NHS Choices

Women with history of stillbirth at 'high risk of another'

NHS Choices - Behind the Headlines - Fri, 26/06/2015 - 14:00

“Women who suffer stillbirths are four times more likely to suffer the tragedy again,” the Daily Mirror reports. Researchers who have analysed previous data warn that women with a history of stillbirth should be regarded as being at high risk of another.

stillbirth is when a baby is born dead after 24 completed weeks of pregnancy, and is more common than many people think. There are more than 3,600 stillbirths every year in the UK, and 1 in every 200 births ends in a stillbirth.

Researchers pooled the results of 13 previous studies. The results suggested that women who had had a previous stillbirth were more than four times more likely to have another, compared with women without a previous stillbirth. This risk reduced a little to just over three times more likely after potential contributory factors (confounders) were taken into account.

While the result appears reliable, there are small limitations to consider. The studies included in the review had very variable definitions of stillbirth and adjustment for confounders, resulting in a diverse group of studies being pooled.

Stillbirths happen for many different reasons and not all can be prevented. However, there are some things you can do to reduce your risk, such as stopping smoking and avoiding alcohol or drugs during pregnancy. Read more about preventing a stillbirth

 

Where did the story come from?

The study was carried out by researchers from The University of Aberdeen and was also funded by The University of Aberdeen.

The study was published in the peer-reviewed British Medical Journal (BMJ). The study was published open-access, meaning it can be viewed online or downloaded as a PDF for free.

The Daily Mirror’s reporting of the story was accurate and contained some useful additional commentary from the lead author of the study.

 

What kind of research was this?

This was a systematic review and meta-analysis aiming to work out the risk of having repeated stillbirths.

A stillbirth is when a baby is born dead after 24 completed weeks of pregnancy.

If the baby dies before 24 completed weeks, it's known as a miscarriage or late foetal loss.

Stillbirth is more common than many people think. There are more than 3,600 stillbirths every year in the UK, and 1 in every 200 births ends in a stillbirth. 11 babies are stillborn every day in the UK, making it 15 times more common than sudden infant death syndrome – also known as cot death.

A systematic review and meta-analysis is one of the best ways to identify and summarise all the available evidence on a topic such as stillbirths. However, the conclusions of systematic reviews are only as good as the evidence that informs them.

 

What did the research involve?

The study team systematically searched the science literature for published and unpublished studies looking at links between stillbirth in an initial pregnancy and risk of stillbirth in a subsequent pregnancy. The results of included studies were combined in a meta-analysis.

Only cohort studies or case-control studies from high-income countries were included.

For the purposes of this review, and somewhat oddly, the researchers used a definition of stillbirth as foetal death occurring at more than 20 weeks’ gestation or a birth weight of at least 400g. This is not the standard definition in the UK, where stillbirth means a baby born dead after 24 completed weeks of pregnancy (notably the World Health Organization set the definition much later, at 28 weeks).

Two reviewers independently screened search results against pre-defined inclusion and exclusion criteria, and scored the studies for methodological quality.

Some of the meta-analysis made adjustment for confounders identified in the primary studies. Most primary studies adjusted for maternal age, smoking and socioeconomic status. Adjustment for other potential confounders, such as living with a partner or marital status, education, race or ethnicity, and interval between pregnancies, varied among the studies. Two studies adjusted for body mass index, six adjusted for pregnancy complications such as pre-eclampsia, placental abruption (when the placenta prematurely breaks away from the wall of the womb), or risk factors for preterm birth.

 

What were the basic results?

13 cohort studies and three case-control studies were included in the meta-analysis.

This included information on 3,412,079 women with pregnancies beyond 20 weeks. Of these, most (99.3%) had had a previous live birth and 24,541 (0.7%) a stillbirth.

A total of 14,283 stillbirths occurred in subsequent pregnancies; 606 out of 24,541 (2.5%) in women with a history of stillbirth and 13,677 out of 3,387,538 (0.4%) among women with no such history. This meant that women with a history of stillbirth were almost 4.8 times more likely to have a subsequent stillbirth, compared with women without (pooled odds ratio (OR) 4.83, 95% confidence interval (CI) 3.77 to 6.18). Meta-analyses are most effective when they pool the results of studies measuring the same thing in a similar way. However, this wasn’t the case in this meta-analysis. The studies varied a lot, so the pooled result represents a mixed bag of methods and measures, lessening its precision.

12 studies specifically examined the risk of stillbirth in second pregnancies. The pooled risk increase for this sub-analysis (OR 4.77, 95% CI 3.70 to 6.15) was very similar to the risk increase found in those with any history.

The pooled odds ratio using the confounder-adjusted effect measures from the primary studies was 3.38 (95% CI 2.61 to 4.38).

Four studies examined the risk of recurrent unexplained stillbirth. Methodological differences between these studies meant it wasn’t sensible to pool the results.

 

How did the researchers interpret the results?

The study team say they: “… have shown that women who experience a stillbirth in their initial pregnancy have a higher risk of stillbirth in a subsequent pregnancy. Even after adjusting for potential confounding factors, the increased risk remains. Risk of recurrent unexplained stillbirth is largely unstudied, and therefore evidence about this remains controversial.”

In considering the implications of their research, the team say: “Smoking and obesity are independently associated with an increased risk of stillbirth, and modification of these lifestyle factors may make a small, but important, reduction in the risk of recurrence. Current management of pregnancies should take account of pregnancy history and make use of pre-pregnancy counselling services.”

 

Conclusion

This systematic review and meta-analysis of 13 cohort studies and three case-control studies showed that women who had had a previous stillbirth were more than four times more likely to have another, compared to women without a previous stillbirth. The research team wanted to look at the combined risk associated with unexplained stillbirths, but were unable to do so due to lack of suitable evidence.

The review and associated BMJ editorial say that current guidance from the UK’s Royal College of Obstetricians and Gynaecologists recommend that women with a previous stillbirth are managed as high risk during a subsequent pregnancy. The results of this systematic review and meta-analysis seem consistent with this advice.

While the review conclusions can be considered reliable, there are a number of limitations to bear in mind. For example, the meta-analysis was limited by large variations in the definition of stillbirth and the extent of adjustments for confounding factors. This meant the pooled results were a bit of a mixed bag of studies, lessening confidence in the overall result a little. The researchers called for international standardisation of definitions of stillbirth, to help conduct more accurate research in the future.

The meta-analysis taking account of confounders produced a lower relative risk increase (OR 3.38) compared with the unadjusted result (OR 4.83), suggesting confounders were influencing the results.

The team were unable to explore the contribution of specific causes of stillbirth to risk in a subsequent pregnancy. The implication of this, as the BMJ Editorial pointed out, is that “if heightened surveillance is recommended for pregnant women with a history of stillbirth, it should be offered to all affected women, not just those with an identifiable and potentially recurring cause.”

Not all stillbirths can be prevented. However, there are some things you can do to reduce your risk.

These include:

  • stopping smoking if you smoke
  • avoiding alcohol and drugs during pregnancy – these can seriously affect your baby's development, as well as increasing the risk of miscarriage and stillbirth
  • attending all your antenatal appointments, so that midwives can monitor the growth and wellbeing of your baby
  • making sure you're a healthy weight before trying to get pregnant
  • protecting yourself against infections (see causes of stillbirth) and avoiding certain foods
  • reporting any tummy pain or vaginal bleeding that you have to your midwife on the same day
  • being aware of your baby's movements and reporting any concerns you have to your midwife straight away
  • reporting any itching to your midwife

Links To The Headlines

Women who suffer stillbirths are FOUR TIMES more likely to suffer the tragedy again. Daily Mirror, June 25 2015

Links To Science

Lamont K, Scott NW, Jones GT, Bhattacharya S. Risk of recurrent stillbirth: systematic review and meta-analysis. BMJ. Published online June 24 2015

Categories: NHS Choices

Some health food brands may 'do more harm than good' claim

NHS Choices - Behind the Headlines - Thu, 25/06/2015 - 13:30

"'Healthy' snacks could do more harm than good," claims the Mail Online, as it reports on a series of experiments investigating the effects of fitness branding in food marketing on food consumption and physical activity. 

Researchers came to the conclusion that fitness branding increases consumption for people concerned with body weight (restrained eaters) unless the food is viewed as forbidden. So, while they may have restrained from eating, say, 500 calories in the shape of crisps, they could then end up consuming a similar amount in muesli.

Restrained eaters were also found to be less active after eating fitness-branded food.

The authors conclude that branding food with "fitness" may have undesirable effects on the weight control behaviours of restrained eaters because it discourages physical activity despite an increase in consumption.

People often underestimate how many calories are in certain foods, while also overestimating how many calories they burn off during exercise – for example an hour of vigorous cycling will burn off around 800 calories, which is roughly equivalent to a takeaway burger and chips.

If you want to lose weight then check out the NHS Choices weight loss plan, which provides information on both diet and exercise.

 

Where did the story come from?

The study was carried out by researchers from the Technical University of Munich in Germany and Pennsylvania State University in the US. It was supported by a fellowship within the postdoc programme of the German Academic Exchange Service (DAAD).

The study was published in the peer-reviewed Journal of Marketing Research.

This study has been reported accurately by the Mail, with a useful number of examples of the amount of energy expenditure needed to burn the calories in various food items.

 

What kind of research was this?

The researchers performed three single-blinded randomised controlled trials to investigate a series of research questions to do with the effect of fitness branding on restrained eaters' food consumption and post-consumption exercise. This type of study design is the gold standard for investigating such relationships, but is more robust when the researchers are also blinded to the intervention.

 

What did the research involve?

This US-based research reports on three studies in which participants were told that the purpose was to investigate consumers' opinion about a new food product that was going to be introduced into the market. After tasting and rating the products a survey was performed that covered confounding variables, sociodemographics, and dietary restrained eating behaviour. Participants then completed a test to measure whether they had guessed the true purpose of the study in an attempt to reduce bias of results.

Participants were university students with a mean age of 19.2 (study 1), 22 (study 2) and 23.5 years (study 3). Mean body mass index (BMI) levels were within the healthy range (19 to 25).

The three studies were performed as follows:

Study 1

This study investigated whether restrained eaters consume more food when it is fitness branded compared with non-fitness branded.

It involved 163 university students who completed the study in exchange for course credit.

Participants were randomly assigned to either the 'Fitness' (fitness label) (n = 80) or the 'Trail Mix' (no fitness label) conditions (n = 82). Product packaging was similar for both.

Participants were told to behave as if they were at home, helping themselves to an afternoon snack.  They were given eight minutes to taste and rate the product, after which a written survey was administered.

Study 2 

The second study assessed the effect of fitness branding on consumption for restrained eaters when the food is framed as dietary permitted.

The study was completed by 231 university students in exchange for a small monetary reward. Participants were randomly assigned to the experimental conditions regarding framing of the food (dietary permitted/forbidden) and product labelling (fitness/no fitness).

Participants were told that the dietary permitted food was high in vitamins and minerals and contained many nutrients that support the monitoring of body weight. Dietary forbidden foods were manipulated to be perceived as high in fat and sugar and containing many nutrients that do not support the monitoring of body weight, such as fatty acids, fructose and oils.

As in study 1, after tasting, participants answered a written survey in a different room.

Study 3 

The final study considered whether restrained eaters are less physically active after consuming fitness-branded food.

This study was completed by 145 university students in exchange for a small monetary reward. Participants were randomly assigned to the fitness label (n = 49), the no label (n = 49), or the diet label conditions (n = 46). The first two labelling manipulations were identical to the manipulations used in the previous studies, the third manipulation was implemented by labelling the product 'Diet'.

The study was conducted in a university laboratory and only one person participated per session. When the tasting had ended, participants were led to another room where they answered a written survey as in the previous studies.

After the survey, participants were given a 30-second warm-up on an exercise bicycle and told they could decide how much effort to put into cycling. The bicycle adjusted according to exertion and participants were asked to keep a constant cycling rate of 65 rotations per minute for a period of approximately five minutes or longer/shorter as they prefer.

 

What were the basic results?

The study found that the effect of gender was significant when considering whether food branded with fitness increases consumption. Males consumed more trail mix than females. Results for food consumption indicate that a 'Fitness' label on food makes restrained eaters consume more, relative to when the food is not associated with fitness.

When trail mix was framed as 'dietary prohibited', males ate more than females. Restrained eaters were found to eat more fitness-branded food when the food is framed as dietary permitted, but this effect disappears when the food is framed as dietary forbidden.

The study showed that both a fitness label and a diet label increased food consumption for restrained eaters, however this did not have a positive effect on physical exertion. Restrained eaters expended less energy in physical activity after consuming fitness-branded food.

 

How did the researchers interpret the results?

The researchers conclude: "Restrained eaters want to manage their weight, but their weight control behaviours are not always successful. Fitness branding in food marketing can exacerbate this problem because fitness cues make eating dietary permitted food compatible with weight control, and increased consumption of fitness-branded food may even serve as a substitute for actual physical activity."

 

Conclusion

This research was a series of randomised controlled trials to investigate the effect of fitness branding on restrained eaters’ food consumption and post-consumption exercise.

It demonstrated that fitness branding increases consumption for people concerned with body weight, unless the food is viewed as forbidden. Restrained eaters were also found to be less active after eating fitness-branded food.

Limitations of this study are that only a single type of product was assessed and only used food packaging for branding. The study was also performed in a small number of participants representing one age group (young adults) and location, reducing the generalisability of these findings. The participants were on average within the healthy BMI range and so findings may have been different for people who are outside of the healthy range. The researchers were not blinded to which condition the participants were allocated to, which could also have influenced the results.

A larger-scale study with a more varied population, especially in those with an 'unhealthy' BMI, would be useful in drawing firmer conclusions on the use of such products in those concerned with body weight.

These findings are interesting as they highlight the importance of being aware of 'fitness'- and 'diet'-related products and tries to explain why the idea of 'reward' post exercise can have negative effects on weight loss.

It can be tempting to indulge yourself if you have spent an hour in the gym or have spent your working day eating "healthy" low-calorie snacks, but such behaviour can be self-defeating.

The bad news is losing weight on a sustainable long-term basis does take discipline. The good news is that NHS Choices provides a range of free resources that can help you achieve your goal. 

Links To The Headlines

How so-called 'healthy' snacks could do more harm than good: People who eat them are more likely to overindulge and avoid exercise. Mail Online, June 24 2015

Links To Science

Koenigstorfer J, Baumgartner H. The Effect of Fitness Branding on Restrained Eaters' Food Consumption and Post-Consumption Physical Activity. Journal of Marketing Research. Published online June 24 2015

Categories: NHS Choices

No evidence 'cocktail of everyday chemicals' causes cancer

NHS Choices - Behind the Headlines - Thu, 25/06/2015 - 13:00

“Fifty everyday chemicals…could be combining to increase our risk of cancer,” is the alarmist headline in the Mail Online.

A major review into chemicals commonly found in the environment, such as those found in suncream and handwash, found no conclusive proof that they were definitely increasing cancer risk.

Researchers identified 85 chemicals that have the potential to cause cells to switch into “cancer mode” – that is, replicate at a dangerous rate inside the body. 50 of them could have this effect at the low-dose level that we are exposed to in the environment. However, the researchers also found that over half of them also had protective effects against the development of cancer.

Currently, the safety of a chemical is looked at on its own. The researchers are calling for chemicals such as those in this list to be looked at in combination when assessing their safety. This is because they think exposure to a combination of chemicals acting on different characteristics could be important in the development of cancer.

The risk associated with these “everyday chemicals” should be put into context. There is little point in worrying about handcream if you are smoking 20 cigarettes a day, or avoiding suncream so you get exposed to high levels of cancer-causing ultraviolet radiation.

 

Where did the story come from?

The study was carried out by an international panel of experts and was funded by a large number of foundations and government medical programmes across the globe. It was called The Halifax Project and the initial kick-off meeting was held in Halifax, Nova Scotia.

The study was published in the peer-reviewed medical journal Carcinogenesis on an open-access basis, so it is free to read online or download as a PDF.

The Mail confusingly tried to reassure the public by saying “the 50 chemicals were safe in low doses”, while having large headlines such as “From chips to perfume, the danger list”.

They also didn't make it clear that the researchers don't know what effect combinations of the chemicals would have. The media failed to point out that over half of the chemicals identified also had preventative properties.

 

What kind of research was this?

This was a series of systematic reviews aimed at collating evidence of chemicals in the environment that can affect different stages in the development of cancer.

The World Health Organization (WHO) and the International Agency for Research on Cancer (IARC) estimate that 7% to 19% of cancers are due to exposure to toxic substances in the environment. For example, it is estimated that the naturally occurring radioactive gas radon is responsible for 3% of all lung cancer cases in England.

Here they wanted to explore their hypothesis that exposure to low doses of multiple chemicals may combine to cause cancer.

Chemicals are usually tested individually in animal studies to determine what dose is harmful. This is then used to estimate the level at which the chemical is likely to be harmful to humans. Safety margins for low-dose exposure are then worked out. The researchers say that this approach could miss chemicals that do not individually cause cancer, but do when combined with others. They wanted to create a list of chemicals that affect each stage of cancer development, so that future research could look at the effect of combining some of these chemicals at low doses.

 

What did the research involve?

An international collaboration was established, including an initial 703 experts. They had different backgrounds, including cancer biologists, environmental health experts, toxicologists (specialists who look at the effects of chemicals on living organisms) and endocrinologists (clinicians who look at hormonal disorders).

11 teams were created from this large international pool of researchers. One team looked at the development of cancer as a whole, while each of the other teams looked at one of the following 10 characteristics (or hallmarks) of cancer:

  • unlimited cell growth
  • insensitivity to signals to stop growing
  • resisting internal signals for cell death
  • cell death no longer occurring after a certain number of cell divisions
  • ability to make new blood vessels form to feed the tumour
  • invasion of tissues and spread to other organs
  • spread of the mutation in the DNA
  • creation of inflammation, which helps the tumour to grow
  • resisting destruction by the immune system
  • disturbance in metabolism, which provides more energy for the cancer

The teams were asked to describe their allocated characteristic and up to 10 biological targets that could cause the characteristic. Each team then drew up a list of up to 10 chemicals (so 110 in total) that are commonly found in the environment, which have been shown to cause disruption to these 10 biological targets. They excluded any chemicals that are known to directly cause cancer. They also excluded any chemicals that are linked to cancer through “lifestyle”, such as tobacco, red meat and lack of fruit and vegetables.

A separate team of researchers then looked at whether these chemicals had an effect on more than one characteristic.

 

What were the basic results?

In total, the researchers reviewed the evidence of 85 chemicals that have the potential to cause the characteristics of cancer without being known to cause cancer. 50 of them were found to be able to cause these changes at the type of low doses that might be encountered in the environment. Information was not available on the dosage required for 22 chemicals, and 13 chemicals only caused the changes at a higher dose. Over half the chemicals also had protective effects against the cancer characteristics.

The chemicals identified as potentially harmful in several areas included:

  • sulphur dioxide
  • paraquat (weedkiller)
  • phthalates (substances that soften plastic and are in some cosmetics)
    titanium dioxide (used in sunscreen and
  • as a whitener)
  • copper
  • iron
  • nickel

 

How did the researchers interpret the results?

The researchers concluded that further research is needed to investigate the effect of a combination of low doses of chemicals. They say this is a new way of looking at the causes of cancer and should be incorporated into the WHO International Programme on Chemical Safety, rather than looking at exposure to chemicals individually. The researchers say their results have been compiled as a starting point for future research into mixtures of chemical exposure.

 

Conclusion

This systematic review has identified 85 chemicals found in the environment that have the potential to affect different stages in the development of cancer. The researchers say this is intended as a starting point, so that future research can look at what effect these chemicals may have when there is exposure to more than one. This is a new approach to understanding the risk that various chemicals may have.

The study did not find that these chemicals cause cancer, but that they have the potential to make changes to cells, which would then create particular characteristics of cancer, such as increased uncontrolled cell growth.

The researchers acknowledge that the development of cancer is complex and that it is caused by a combination of genetic susceptibility, environmental factors and exposures to toxins, such as through smoking. They hope this research can pave the way for further understanding of how these factors combine.

A limitation of this study is that it was reliant on previous research and available literature. Many of the studies only provided short-term toxicity data and not long-term exposure to the chemicals. The study types were also of varying quality.

This study will be of importance to regulators when considering how to assess the toxicity of chemicals and whether this needs to be done in combination, rather than just individually.

From what we know, the most effective methods of reducing your risk of cancer are regular exercise, a healthy diet with no more than 70g of red meat a day, quitting smoking if you smokeprotecting your skin from the sun and drinking too much alcohol.

Read more about cancer prevention

Links To The Headlines

50 everyday chemicals that can mix to raise cancer risk: Substances found in fried potatoes, handwash and suncream could lead to cancer if combined. Mail Online, June 23 2015

Cancer risk from chemical cocktail. The Times, June 23 2015

Links To Science

Goodsoon WH, Lowe L, Carpenter DO, et al. Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead. Carcinogenesis. Published online July 22 2015

Categories: NHS Choices

Mushroom supplement could be one way to tackle obesity

NHS Choices - Behind the Headlines - Wed, 24/06/2015 - 15:30

"A mushroom used for centuries in Chinese medicine reduces weight gain in animals," BBC News reports.

A supplement from the Ganoderma lucidum mushroom (more commonly known as "reishi") slowed the pace of weight gain by apparently altering bacteria inside the digestive system of mice.

In this study, the researchers aimed to see if reishi was effective in preventing obesity. They gave mice different amounts of reishi or placebo and either a normal diet or a high-fat diet for eight weeks. All mice on the high-fat diet gained a lot of weight and body fat, but those given reishi did not gain as much weight or body fat. The reishi supplement did not have an effect on mice fed a normal diet. The supplement appeared to work by improving the number of "good" bacteria in the gut and through reducing inflammation. Some studies have suggested that chronic inflammation and an increased number of "bad" bacteria in the gut are linked to obesity in humans.

Randomised controlled trials in humans would be required to see if it is safe and effective.

Even if it is, it is unlikely to be useful in tackling obesity by itself; you would still need to eat a balanced diet and take plenty of exercise. Sadly, as far as we know, there is no such thing as a single superfood that will magically enable you to lose weight.

 

Where did the story come from?

The study was carried out by researchers from Chang Gung University and other institutes in Taiwan, and the University of the Pacific and Rockefeller University in the US. It was funded by the Ministry of Science and Technology of Taiwan and Chang Gung Memorial Hospital in Taiwan. Two of the authors have financial interests in Chang Gung Biotechnology, a company that produces Ganoderma lucidum products. The other authors declared no conflict of interest.

The study was published in the peer-reviewed scientific journal Nature Communications.

The BBC and Mail Online reported the study accurately and included expert commentary from microbiologist Professor Colin Hill.

 

What kind of research was this?

This was a laboratory study on mice. The researchers aimed to see if reishi has any effect on body weight and obesity.

Chinese medicine has used a number of different mushrooms to treat a variety of conditions over thousands of years. One of these is called reishi, or Ganoderma lucidum, which is believed to improve health and lifespan. It has also been tested as a possible cancer treatment as some research has suggested it is beneficial to the immune system. However, the effect against cancer remains uncertain, as a recent Cochrane systematic review highlighted the lack of large and high-quality randomised controlled trials in this area.

A similar lack of robust studies was found in a Cochrane review of Ganoderma lucidum to improve cardiovascular risk factors such as blood pressure or cholesterol in people with type 2 diabetes.

Some studies have suggested that obesity is linked to chronic inflammation, and Ganoderma lucidum is linked to an improvement in the immune system, so the researchers wanted to assess whether Ganoderma lucidum has an effect on obesity in mice.

This type of animal study is useful in determining whether a particular treatment shows promise and investigates its biological effects, as there can be several different groups whose diets and living conditions are strictly controlled, allowing them to be directly compared. If a treatment does show promise at this stage and appears safe then it would usually progress to trials in primates, which would indicate whether a treatment is more likely to work in humans, as they are more similar to us than mice. Human clinical trials would then follow if the treatment appeared to be sufficiently safe and effective in the animal trials.

 

What did the research involve?

The researchers split mice into six groups and fed them either a high-fat diet or a normal "chow" diet for eight weeks. Each group either had a supplement of different amounts of Ganoderma lucidum extract in water or just water alone (as a control). They then compared their weight, body fat and insulin resistance.

The amount of food each mouse ate was measured, as was the amount of energy they extracted from the food, by measuring the energy left in the faeces.

Finally, as the researchers thought the effects might be related to bacteria in the gut, they transplanted faeces from mice given Ganoderma lucidum supplement into mice without the supplement to work out if the effects could be passed on this way (!horizontally transmitted").

 

What were the basic results?

The Ganoderma lucidum supplement reduced the amount of weight gain and fat deposits in mice fed a high-fat diet. The most weight gain was seen in mice given the control (about 18g), and the least weight gain in mice given the highest dose of Ganoderma lucidum (about 12g). This was despite each group eating the same amount of food and extracting the same amount of energy from it (by measuring the energy left in the faeces).

The Ganoderma lucidum supplement did not have any effect on mice fed a normal diet, with both groups gaining around 4g.

Markers of inflammation were increased in the mice fed a high-fat diet, but this was reduced by Ganoderma lucidum.

Ganoderma lucidum also reduced insulin resistance in mice fed a high-fat diet.

Ganoderma lucidum reversed an imbalance in gut bacteria in the mice fed a high-fat diet, increasing the number of "good" bacteria. This effect was also achieved by transferring the faeces of mice fed Ganoderma lucidum to mice not given the supplement. This supported the possibility that the effect could be due to gut bacteria.

 

How did the researchers interpret the results?

The researchers concluded that the water extract of Ganoderma lucidum reduces obesity and inflammation in mice fed a high-fat diet. They say that this may be due to changes in the gut bacteria, evidenced by the fact that the effects were replicated when they transplanted these gut bacteria (through faeces samples) into other mice.

 

Conclusion

This study of Ganoderma lucidum in mice eating a high-fat diet found that it may help to reduce weight and fat gain, reduce inflammation and improve the levels of "good" gut bacteria in the gut. It also appeared to reduce the risk of insulin resistance. Ganoderma lucidum was not seen to have a significant effect for mice fed a normal diet.

The results of this study suggest a possible use for the extract, but randomised controlled trials in humans are required to determine safety and effectiveness for preventing weight gain. The same is true for any other conditions that Ganoderma lucidum is currently believed to improve.

Either way, it is clear that eating a high-fat diet was the cause of the increased weight gain and body fat in these mice. Even if the mushroom extract is found to help prevent weight gain in humans, it is likely to be healthier to avoid a diet very high in fat. Eating a balanced diet including plenty of fruit and vegetables and taking regular exercise based on your ability is the best way to combat obesity.

Ganoderma lucidum supplements are available to buy online but we wouldn’t recommend doing so. Just because something is “natural” doesn’t mean it is safe. The supplements can cause thinning of the blood, which could be very dangerous for people with high blood pressure. They are also known to interact in adverse ways with certain medications.

Always check with your GP before taking any kind of herbal or plant-based supplement. 

Links To The Headlines

Mushroom used in Chinese medicine 'slows weight gain'. BBC News, June 24 2015

Could MUSHROOMS be the key to losing weight? Fungi used in Chinese medicine 'alters gut bacteria' and could be used to treat obesity. Mail Online, June 24 2015

Links To Science

Chang C, Lin C, Lu C, et al. Ganoderma lucidum reduces obesity in mice by modulating the composition of the gut microbiota. Nature Communications. Published online June 23 2015

Categories: NHS Choices

Elderly living near noisy roads have 'increased stroke risk'

NHS Choices - Behind the Headlines - Wed, 24/06/2015 - 14:00

“Living in a neighbourhood with noisy road traffic may ... increase the risk of stroke,” The Guardian reports. Researchers looked at noise levels across London and found a link between high levels of noise and increased risk of hospital admission for stroke, with the risk slightly higher in older people.

This ecological study included the 8.6 million inhabitants of London and assessed day and night-time exposure to levels of road traffic noise in excess of 55 decibels (dB), which is roughly equivalent to the sort of background conversation you would hear in a restaurant.

55dB is the threshold set by the World Health Organization beyond which health problems are possible in relation to cardiovascular diseases, such as stroke and heart disease.

This study is now complete and has found some small associations, mainly in terms of increased stroke risk. The population level findings observed were small and could not account for all possible confounders. They may also not represent findings on an individual level. 

There are steps you can take to compensate for any small increased risk of stroke, such as eating a healthy diet, taking regular exercise, stopping smoking if you smoke and sticking to the recommended guidelines for alcohol consumption

Read more about stroke prevention.

 

Where did the story come from?

The study was carried out by researchers from the London School of Hygiene and Tropical Medicine, Imperial College London, Imperial College Healthcare Trust, and Kings College London. Funding was provided by the UK Natural Environment Research Council; Medical Research Council; Economic and Social Research Council; Department of Environment, Food and Rural Affairs; and the Department of Health.

The study was published in the peer-reviewed European Heart Journal on an open-access basis, so it is free to read online or download as a PDF.

Generally, the UK media reported the story accurately, with most sources making clear that a cause and effect relationship had not been proven, and that more research is needed.  

 

What kind of research was this?

This was an ecological study designed to assess whether higher noise levels are associated with greater risk of cardiovascular disease and death at a population level. This study design is suitable for assessing this kind of research question, but will not provide conclusive answers.

 

What did the research involve?

The study included the 8.61 million inhabitants of London (within the M25) from 2003 to 2010. It examined the effects of their exposure to road traffic noise, independent of air pollution, on all-cause cardiovascular death, as well as on cardiovascular hospital admissions in adult and elderly populations.

Associations of day (7:00 to 22:59) and night-time (23:00 to 06:59) road traffic noise with cardiovascular hospital admissions and all-cause and cardiovascular death in all adults (≥25 years) and elderly (≥75 years) were assessed through modelling. The researchers made adjustments for the possible confounding effects of:

  • age
  • sex
  • area-level socioeconomic deprivation
  • ethnicity
  • smoking
  • air pollution
  • “neighbourhood spatial structure” – the actual physical environment of the region being studied

Traffic noise exposure was categorised in five-decibel increments:

  • less than 55 (reference)
  • 55 to 60
  • more than 60

Hospital admission data was taken from Hospital Episode Statistics and are held by the UK Small Area Health Statistics Unit (SAHSU). Death and population data was supplied by the Office for National Statistics, derived from the national mortality registrations and the Census, and are held by SAHSU.

For assessing outcomes, the first registered emergency hospital episode of each year for all cardiovascular causes, coronary heart disease and stroke were used.

Deaths were classified according to the underlying cause on the death certificate; causes included in this analysis were from all natural causes, all cardiovascular causes, coronary heart disease and stroke.

Data was also collected of the person’s age, sex and postcode of residential address at the time of admission or death.

 

What were the basic results?

The total number of hospital admissions from cardiovascular causes was 400,494 among adults, and 179,163 among the elderly. There were 442,560 adult and 291,139 elderly deaths.

The average (median) daytime exposure to road traffic noise was 55.6dB.

Daytime road traffic noise increased the risk of hospital admission for stroke by 5% in adults, and 9% in the elderly in areas >60 compared with <55dB (baseline). Similar levels were observed when comparing 55 to 60dB to baseline; this was 4% in adults and 6% in the elderly. A small increased risk of hospital admissions for all cardiovascular diseases was seen in the elderly group exposed to daytime road traffic noise of 55 to 60dB when compared to the lower level group, but not for above 60dB.

Night-time road traffic noise of between 55 and 60dB was associated with a 5% increased risk of stroke among the elderly. Levels above this were not significant.

Daytime road traffic noise was associated with a 3-4% increased risk of death from any cause in adults and the elderly in areas exposed to more than 55dB.

 

How did the researchers interpret the results?

The researchers conclude: “Results suggested small increased population risks of all-cause mortality and cardiovascular mortality and morbidity, particularly of stroke in the elderly, at moderate levels of road noise exposure”.

 

Conclusion

This modelling study has examined the associations of exposure to traffic noise, independent of air pollution, on all-cause and cardiovascular mortality, as well as on cardiovascular hospital admissions in adult and elderly populations.

It has shown a link between increased noise from traffic pollution and risk of hospital admission for stroke and death. Possible reasons for deaths were most likely to be linked to heart or blood vessel disease, which could be due to increased blood pressure, sleep problems and stress from the noise.

The limitations of this study are that the exposure model used is likely to overestimate noise at low exposure levels and underestimate noise in areas with heavy traffic on minor roads. This may result in bias when analysing dose-response relationships.

The model did not take into account population activities, such as working and commuting outside residential areas, or residence characteristics, such as windows towards roads or building materials. The researchers did not have data on residential histories, which may have introduced further exposure misclassification.

Associations found in this study are in agreement with some, but not all, other previous work in this area, so caution should be taken with interpreting this small increased risk. There was often a lack of dose-response relationship, which requires further investigation. The whole populations study used London inhabitants as their population, which may reduce the ability to generalise the findings to other populations and also on an individual level.

If this association was found to be true, changes would have to be made by legislation; however, to reduce your own risk of cardiovascular disease, it is important to make the right lifestyle choices which protect against both heart disease and stroke.

These include eating a healthy diet, taking regular exercisestopping smoking if you smoke and sticking to the recommended guidelines for alcohol consumption.

Read more about cardiovascular disease prevention

Links To The Headlines

Noisy roads linked to higher stroke risk. The Guardian, June 24 2015

Long-term exposure to traffic noise 'increases risk of death or strokes', study finds. ITV News, June 24 2015

Traffic noise 'link' to increased strokes. Mail Online, June 24 2015

Living next to a busy road could raise your risk of stroke. Daily Express, June 24 2015

Links To Science

Halonen JI, Hansell AL, Gulliver J, et al. Road traffic noise is associated with increased cardiovascular morbidity and mortality and all-cause mortality in London. European Heart Journal. Published online June 23 2015

Categories: NHS Choices

Could a smart insulin patch mean no more diabetic injections?

NHS Choices - Behind the Headlines - Tue, 23/06/2015 - 14:00

“A 'smart' insulin patch could replace painful injections to help millions of people with diabetes keep their blood sugar levels in check,” the Daily Mirror reports; though the technology has only been tested on mice.

Insulin is a hormone that plays a vital role in regulating blood glucose levels. People with type 1 diabetes, as well as advanced type 2 diabetes, require regular insulin injections, as their body either doesn’t produce enough insulin or reacts to it in the wrong way.

Researchers have developed a new type of glucose-sensing patch, which is worn on the skin and delivers insulin in response to sensing high levels of glucose.

The study showed that the patch was capable of reducing blood glucose levels to normal in mice with chemically induced diabetes over about four hours.

This research is at an early stage, so we therefore don't know if it will be both safe and effective in humans. Before any human testing can occur, researchers will need to study the longer-term effects on animals. Researchers will also need to work out whether they can deliver enough insulin to regulate blood glucose levels in humans, and how often the patches need to be changed.

All in all, we wouldn’t expect to see these patches at your local chemist in the near future.

 

Where did the story come from?

The study was carried out by researchers from the University of North Carolina and North Carolina State University. It was funded by the American Diabetes Association, and the North Carolina Translational and Clinical Sciences Institute, which is supported by the National Institutes of Health.

The study was published in the peer-reviewed scientific journal Proceedings of the National Academy of Sciences (PNAS).

The UK media’s reporting of the study was patchy. The Mirror fails to mention that the study involved mice, rather than humans. This fact was acknowledged by The Daily Telegraph, though its headline “End in sight for diabetes injections as scientists develop smart patch” is premature, considering the early stage of the research.

 

What kind of research was this?

This was laboratory and animal research testing a new “smart insulin patch”. It is placed on the skin, and aims to sense blood glucose levels and release insulin accordingly. It could eventually be used to control blood sugar levels in people with diabetes who normally inject insulin, and potentially give better glucose control than the injections. It could enable glucose levels to be monitored constantly, avoiding the need for people to inject themselves, and reduce the chance of errors in the amount of insulin delivered.

Currently, there are mechanical devices that can sense blood glucose and inject insulin into the bloodstream in response. The new system relies on different (chemical) methods to detect glucose levels and deliver insulin, and is smaller than the mechanical devices.

Animal research is an important part of early testing, to make sure things are safe and effective enough to undergo human testing.

 

What did the research involve?

The researchers first developed and tested their “smart insulin patch” technology in the lab. They then used the patch on mice with a chemically induced form of diabetes. They looked at how well the patch was able to control blood glucose levels in these mice.

The patches were in silicone molds, and had many tiny “micro-needles” on one surface, to project into the skin. The needles contain even smaller packets, called “glucose responsive vesicles” (GRVs). These GRVs contain insulin, and burst and release this insulin into the skin when a high concentration of glucose is detected.

The GRVs contain a protein that binds to glucose and attaches it to oxygen molecules. This causes levels of oxygen in the area around the vesicle to reduce. The molecules that make up the outer surface of the vesicles are sensitive to low oxygen levels, and break down, causing release of the insulin. This all happens rapidly, allowing the insulin to act swiftly to increase the uptake of glucose from the blood by cells.

The researchers developed these GRVs and tested them in the lab first to make sure they did not just release insulin spontaneously. They also tested what happened when they were exposed to solutions with different concentrations of glucose in the lab. They then made micro-needle patches containing the GRVs. The patch itself was made out of a material called hyaluronic acid, which is naturally found in the human body, and the GRVs were chemically attached to it. They researchers tested the response of the patch to solutions with different concentrations of glucose in the lab.

Finally, they tested the patches on mice with chemically induced diabetes. They tested patches with and without GRVs. They also tested GRVs with and without the glucose-sensing protein. The patches were designed to deliver 10 milligrams of insulin per kilogram in body weight.

 

What were the basic results?

The researchers were able to make GRVs successfully. These GRVs released insulin in response to high glucose concentrations in the lab, even once they were placed in the micro-needles.

The micro-needles on the patches successfully entered the skin of mice with diabetes. The tiny holes left in the skin by the micro-needles closed up within six hours of the patch being removed. The blood glucose levels in mice with the GRV-loaded patches reduced to normal levels after about 30 minutes. They stayed this way for four hours, and then gradually increased again. If the GRVs were missing the glucose-sensing protein, blood glucose levels did not change noticeably.

If the mice were injected with glucose, the mice with the patches showed better “glucose tolerance” than those without the patches. This meant that their blood glucose levels rose more slowly and returned to normal within 30 minutes.

The mice did not show any adverse reactions to the patches or the GRVs.

 

How did the researchers interpret the results?

The researchers concluded that this was the first demonstration of a man-made glucose-responsive device using low levels of oxygen as a trigger for regulating insulin release. They say that if this technology is developed for human use, its fast responsiveness could help to avoid blood glucose levels getting too high (hyperglycaemia) or too low (hypoglycaemia).

 

Conclusion

This laboratory and animal study has developed a new type of glucose-sensing patch. This patch is worn on the skin and delivers insulin in response to sensing high levels of glucose. The study showed that the patch was capable of reducing blood glucose levels in mice with chemically induced diabetes.

This research is at an early stage and as yet, we don’t know how well it works in humans. For example, humans are much bigger than mice, and researchers will need to work out whether they can deliver enough insulin to regulate blood glucose levels in humans. They will also need to see how long such patches could regulate blood glucose levels for. Although people might prefer patches to injections, they might not want to change them frequently. Researchers will need to look at the long-term effects of wearing these patches in animals, to make sure they are safe and effective enough before testing them on humans.

There is a lot of work going on in the field of diabetes research, looking at developing alternatives to insulin injections. This study has developed another possible approach, and research will likely continue on these patches and other alternatives.

Links To The Headlines

Diabetes sufferers could say goodbye to painful injections as insulin patch is devised. Daily Mirror, June 22 2015

The end of injections for diabetics? Smart patch can automatically release insulin into the bloodstream. Mail Online, June 23 2015

Insulin patch could free diabetics from pain of daily jabs. Daily Express, June 22 2015

End in sight for diabetes injections as scientists develop smart patch. The Daily Telegraph, June 22 2015

Links To Science

Yu J, Zhang Y, Ye Y, et al. Microneedle-array patches loaded with hypoxia-sensitive vesicles provide fast glucose-responsive insulin delivery. PNAS. Published online June 22 2015

Categories: NHS Choices

A case report about skinny jeans sparks media frenzy

NHS Choices - Behind the Headlines - Tue, 23/06/2015 - 13:00

The UK media have had a field day with the suggestion that "Skinny Jeans Could Be Bad for Health".

They have taken the opportunity to indulge in some shameless clickbaiting by showing photos of various skinny-jean-wearing celebs such as Russell Brand, Kate Moss, Harry Styles and the Duchess of Cambridge.

By the tone of the reporting you could assume that hordes of hipsters are having skinny-jean-related health problems. In fact the furore has been sparked by just a single case report.

A woman in Australia who, after squatting for a long time while wearing skinny jeans, had severe ankle weakness. She fell over and could not get back up by herself, and ended up having her jeans cut off and staying in hospital for four days until she recovered.

It is thought that she developed a condition called compartment syndrome, where pressure in an enclosed bundle of muscles can adversely affect muscle and nerve function. This can sometimes occur, for example, as a result of a crush injury, or in people who are wearing a plastic cast, which constricts swelling tissue.

Given the fact that many people wear skinny jeans and this is the first report of this kind of severe problem, it is likely to be a rare occurrence. If you know you’re going to be squatting for long periods, even if it’s just for your comfort and the safety of your jeans, commonsense dictates that it’s probably better to wear looser trousers. Also make sure you take regular breaks to stretch your legs.

 

Where did the story come from?

The case study was written up by researchers at the Royal Adelaide Hospital in Australia. No specific funding was reported for the study and the researchers reported no conflicts of interest.

The case was published in the peer-reviewed Journal of Neurology, Neurosurgery and Psychiatry.

Many news sources covered this story. We suspect that this was because it gave them an excuse to carry photos of skinny-jean-wearing celebrities such as the Duchess of Cambridge. Call us cynical, but we doubt a case report involving anoraks or thermal underwear would generate the same level of coverage.

BBC News and The Guardian make it clear that the squatting was a major factor, and the jeans made the effect worse. The Daily Mail focuses on the jeans, suggesting that they "drastically reduced the blood supply to her leg muscles, causing swelling of the muscles and compression of the adjacent nerves". This is not quite true, as the blood supply to her feet was normal and doctors believed it was the prolonged squatting that started the problem, and her jeans made it worse. The Mail does not mention the squatting until later in the article.

 

What kind of research was this?

This was a case report describing a woman who presented with severe weakness in her ankles, what the doctors found and how she recovered.

Doctors will often publish reports of unusual cases they have seen, or phenomena that have not yet been described in medical literature. These reports can be useful for describing unusual conditions, or rare side effects of treatments or combinations of circumstances that have never been seen before. As they describe only one person, it can be difficult to be absolutely certain of what causes these events, and also to know how frequently they occur.

 

What did the research involve?

The researchers describe the woman’s symptoms and the results of their investigations.

 

What were the basic results?

The 35-year-old woman came to hospital after experiencing severe ankle weakness, which led to her falling over and not being able to get up by herself.

The doctors found out that the day before she had been helping a relative move house, and had been squatting for many hours cleaning cupboards. She was wearing skinny jeans while doing this, and felt that they were becoming tighter during the day. When she was walking home she realised her feet were feeling numb and she was not able to pick them up off the floor properly. This resulted in her tripping and falling. She then spent several hours on the floor until she was found.

When the doctors examined her, her lower legs were swollen and her jeans had to be cut off. Her ankles showed weakness and she had poor toe movement, she also had reduced feeling in her feet and the sides of her lower legs. Her hips and knees showed normal muscle strength.

One of the nerves travelling down her legs was found to not be transmitting electrical signals to her feet properly. Testing also showed that there had been some muscle damage, a part of something called "compartment syndrome", which occurs when too much pressure builds up in the muscle. There were also problems with the nerves lower down in her leg.

The woman was given intravenous fluids and her legs gradually improved. After four days she was discharged from hospital and could walk unaided.

 

How did the researchers interpret the results?

The researchers say that the sort of nerve problem the woman had has been known to be caused by the nerve being squashed at around the knee, for example through prolonged squatting. They suggest that the woman’s squatting probably started the problem off, and caused her calves to start to swell. This swelling caused problems with other nerves in the calf, and the skinny jeans were "likely" to have made this worse by causing even more pressure as her legs swelled. They say that while there have been reports of compression of nerves in the thigh with skinny jeans, this case of nerve problems in the lower leg is a "new neurological complication of wearing tight jeans".

 

Conclusion

This study describes a case where the combination of squatting for a prolonged period while wearing skinny jeans seems to have led to severe ankle weakness.

With this kind of one-off event, it is difficult to be absolutely certain what causes it, but doctors look at the circumstances around the event and see what might explain it. They concluded that it was the extensive squatting that probably started the problem off, but once the woman's legs started to swell the jeans probably made it worse.

Given the fact that many people wear skinny jeans and this is the first report of this kind of severe problem, it is likely to be a rare occurrence. If you know you’re going to be squatting for long periods it is important to take breaks and stretch your legs, and even if it’s just for comfort and the safety of your jeans, it’s probably better to wear looser trousers. You don’t want to end up as a "fashion victim". 

Links To The Headlines

Russell Brand and Kate Moss take note – skinny jeans are bad for your health. The Guardian, June 22 2015

Skinny jeans given health warning. BBC News, June 23 2015

Health warning issued over skinny jeans. The Independent, June 23 2015

Why squatting in skinny jeans could lead to nerve damage. The Daily Telegraph, June 22 2015

Careful, girls, those skinny jeans can be a health hazard: Doctors' warning after woman, 35, spent four days in hospital after trousers were so tight they cut off circulation to her feet. Daily Mail, June 23 2015

Warning: Skinny Jeans Could Be Bad For Health. Sky News, June 23 2015

Careful Kate! Doctors say skinny jeans are a SERIOUS health hazard. Daily Express, June 23 2015

Links To Science

Wai K, Thompson PD, Kimber TE. Fashion victim: rhabdomyolysis and bilateral peroneal and tibial neuropathies as a result of squatting in ‘skinny jeans’. Journal of Neurology, Neurosurgery and Psychiatry. Published online June 23 2015

Categories: NHS Choices

Being a 'couch potato' linked to increased anxiety risk

NHS Choices - Behind the Headlines - Mon, 22/06/2015 - 14:30

“Being a couch potato is bad for your mental health,” the Mail Online reports. However, the evidence gathered by a new review is not as clear-cut as the headline would lead you to believe.

The review summarised the results of nine studies on the link between anxiety symptoms and sedentary behaviour, such as using a computer or watching TV. 

Overall, five of the nine studies found a positive link – that as time spent sitting went up, so did the risk of anxiety symptoms.

However, the results of a review are only as reliable as the studies it includes, and in this case they weren’t very good. The majority of studies looked at sitting and anxiety at one time.

This can’t prove cause and effect, as we are faced with the classic “chicken and egg” dilemma: does sedentary behaviour cause anxiety symptoms, or are anxious people likely to spend more time sitting?

Importantly, we don’t know whether the studies took account of other factors that could be influencing the results, and most looked only at anxiety symptoms, not a diagnosis of anxiety.

Overall, this review doesn’t provide conclusive proof of a definitive link. The occasional boxset binge is probably not going to trigger general anxiety disorder by itself, but it is important to balance this out with regular exercise. Aside from the physical health benefits of exercise, it can also often reduce feelings of depression and anxiety.

Where did the story come from?

The study was carried out by researchers from the School of Exercise and Nutrition Sciences at Deakin University in Burwood, Australia. No sources of funding are reported and the authors declare no conflicts of interest.

The study was published in the peer-reviewed medical journal BioMed Central Public Health. BioMed Central (BMC) publishes all its articles on an open-access basis. This means you can read the original research for free online, or download the PDF.

In concluding that being a couch potato is bad for your mental health and can cause anxiety, the Mail does not consider the important limitations of the studies on which this review is based. This includes that they cannot prove causation, and the majority have not looked at diagnoses of mental health illnesses.

 

What kind of research was this?

This was a systematic review aiming to look at the links between sedentary behaviour and anxiety levels.

Sedentary behaviour encompasses activities that require limited or no body movement, such as sitting (e.g. for work, travel), and screen-based activities, such as computer use, computer gaming and watching TV.

The researchers discuss how time spent sedentary has been associated with worse health in adults, irrespective of whether people do the recommended level of physical activity. Research has linked it to various chronic diseases, such as cardiovascular disease, diabetes and cancer. Studies have also looked into links with depression, but have not looked into other mental health illnesses, such as anxiety. Therefore, the research team decided to explore the potential effect of sedentary behaviour on anxiety.

A systematic review is one of the best ways of identifying and summarising all the available research on a particular issue. However, the review findings are only as good as the quality of the evidence they include. If the evidence is shaky, the review findings may be similarly unreliable.

 

What did the research involve?

The researchers searched literature databases for studies published from 1990 to end-2014. They looked for studies reporting keywords such as mental health or anxiety linked to sedentary behaviour, or computer or TV viewing. Eligible studies could be observational, including cross-sectional studies or prospective cohorts, or experimental study designs. The study populations could be children or adult, provided they only had anxiety or anxiety symptoms and did not have chronic medical conditions that could be affecting mental health.

The researchers assessed quality of the included studies and extracted the relevant data.

A total of nine relevant studies were eligible for inclusion in the review, seven of which were cross-sectional studies and two had a prospective (follow-up) design.

The studies varied in their included populations, measures and assessments. Seven studies included adults and two included children. Study sample sizes ranged from 189 to 13,470. Two of the studies came from Australia, two from the Netherlands, and the remaining came individually from the UK, US, Spain, China and Singapore.

Seven of the studies assessed sedentary behaviour by self-reporting questionnaires, asking people questions such as how much time they spent sitting, watching TV or viewing a computer screen. One of the studies in children had used parent reporting of the time the child spent in front of a screen. Four of the studies had looked specifically at leisure viewing, one looked at occupational viewing, and the others measured total daily time spent sedentary.

Only one of the studies used an accelerometer to objectively measure sedentary time and activity. When looking at anxiety, only one of the studies actually used a diagnostic interview to look for the presence of an anxiety disorder; the others all looked at symptoms. One of the studies used parent reporting of their child’s emotional symptoms on the Strengths and Difficulties Question; the other studies all assessed self-reported anxiety symptoms on a range of questionnaires.

 

What were the basic results?

Of the nine included studies, five – four cross-sectional and one prospective – found a positive link between sedentary behaviour and risk of anxiety. The other prospective study found no link, and the remaining three cross-sectional studies found either no link or the opposite link.

The researchers considered that, overall, there was moderate evidence for a link between sedentary behaviour and anxiety risk. Moderate evidence was defined as consistent results in one high-quality study and at least one weak-quality study; or consistent results in two or more weak-quality studies.

Looking more specifically into the results, four of five studies examining sitting times had found positive links. Two of four studies had found positive links with screen time (TV, gaming or computer). Two of three studies had found positive links with TV viewing, and one of two with computer use.

 

How did the researchers interpret the results?

The researchers conclude: “Limited evidence is available on the association between sedentary behaviour and risk of anxiety. However, our findings suggest a positive association (i.e. anxiety risk increases as sedentary behaviour time increases) may exist (particularly between sitting time and risk of anxiety). Further high-quality longitudinal/interventional research is needed to confirm findings and determine the direction of these relationships.”

 

Conclusion

This systematic review suggests that the more time people are sedentary (not moving much), the higher the risk of anxiety symptoms.

It has strengths in its systematic review methods, searching the literature for studies published over 25 years that examined the association, and assessing the quality of these studies. However, the results are only as reliable as the studies it includes. There are also important limitations to consider:

  • The majority of studies in this review – seven of nine – were cross sectional. This means they questioned sedentary time and anxiety symptoms at once. These studies can show associations, but they cannot prove cause and effect. It is possible that sedentary time caused the anxiety symptoms, but just as possible that anxiety symptoms could have led to more sedentary behaviour.
  • The possibility of confounding is another important limitation – both in the cross-sectional studies and the cohorts. From the information in the review, we have no idea whether the studies have taken into account the range of other factors that could be influencing any links between sedentary behaviour and anxiety symptoms. This could include physical and mental health illnesses, lifestyle (including diet and physical activity), environment and life events.
  • The studies varied in their study methods, but most of them relied on self-reporting questionnaires, both for sedentary time and for the assessment of anxiety symptoms. For assessments of sedentary time, this could be inaccurate. For anxiety symptoms, this means the person doesn’t necessarily have anxiety. It is important to note that only one of the nine studies actually diagnosed anxiety; the other studies were looking at symptoms of anxiety. Without being an actual diagnosis of anxiety, is not known how many symptoms there were, or whether it would have actually be having an influence on the person’s daily life and wellbeing.
  • The variations across the nine studies, including differences in age, nationality and type of sedentary time examined, mean the review conclusions aren’t particularly reliable. As the researchers say, further high-quality evidence is needed to confirm the links.

Despite the limitations, it is known that taking regular exercise has many health benefits, so reducing the time you spend sitting at work, while travelling or at home is a good thing.

Read more about why sitting too much is bad for your health

Links To The Headlines

Sitting comfortably? Then your anxiety levels may be mounting: Being a couch potato is bad for your mental health. Mail Online, June 19 2015

Links To Science

Teychenne M, Costigan SA, Parker K. The association between sedentary behaviour and risk of anxiety: a systematic review. BMC Public Health. Published online June 19 2015

Categories: NHS Choices

Drinking 'plenty of red wine' won’t help you lose weight

NHS Choices - Behind the Headlines - Mon, 22/06/2015 - 14:00

Sorry to be party poopers, but The Daily Telegraph’s headline "How to lose weight – drink plenty of red wine," is simply nonsense. First, the study it reports on did not involve red wine. Second, it was carried out on mice, not humans.

The mistaken headline was triggered by a study in mice looking into whether resveratrol, a plant polyphenol chemical found in the skin of red grapes, can stimulate the development of brown fat deposits within white fat tissue.

Human adults have very little brown fat, but we did as babies, where it helped us regulate our body temperature. Build-ups of white fat cause obesity, so finding a way to turn it into calorie-burning brown fat is thought to be one way to try to tackle the obesity problem.

This study found that higher doses of resveratrol caused the development of brown-fat-like cells within the white fat tissue of mice. The researchers hoped something like this might be possible in people. Importantly, based on mice studies only, we don't know whether resveratrol will have the same effect in people. 

And drinking "plenty of red wine" will not lead you to lose weight – if anything the opposite will occur. A standard 750cl bottle of red wine contains around 570 calories, which is more than is found in two McDonald’s hamburgers.

Read more about how alcohol can make you fat 

Where did the story come from?

The study was carried out by researchers from South China Agricultural University and Washington State University in the US. Funding was provided by the National Institutes of Health, National Natural Science Foundation of China, Muscular Dystrophy Association, and the National Science Foundation. The study was published in the peer-reviewed medical journal International Journal of Obesity.

The Daily Telegraph was one of the few UK media outlets to run the story. Its headline was poor, which is frustrating as the actual reporting in the study is accurate and responsible.

The body of the article made clear that the study was in mice, advised readers to drink responsibly and even pointed out that "red wines such as merlot or cabinet sauvignon are known to contain resveratrol, but at a fraction of the levels found in grapes".

 

What kind of research was this?

This was an animal study looking into how to stimulate the development of brown fat deposits within white fat tissue in an effort to reduce obesity.

Mammals have two types of fat tissue involved in energy balance in the body – brown and white. In humans, brown fat is mostly found in babies where it is needed to keep the baby warm when they are unable to shiver. As we grow, most of our brown fat is replaced by white. Excessive accumulation of white fat causes obesity, which is linked to a range of diseases.

Though adults have little brown fat, it is said to have been recently discovered that white fat contains brown-fat-like cells called "beige" fat cells. Therefore it was thought that stimulating the development of these beige cells – so called "browning" - could reverse the harmful effects of excess white fat and improve health. How to stimulate the browning was the goal of this study.

Resveratrol, a natural chemical present in the skin of grapes and other berries, is one possibility. Research has suggested it can have beneficial effects upon metabolism in mammals and protect against high-fat-diet-induced obesity in mice. It has also been demonstrated to prevent fat development and enhance fat breakdown. However, whether it can stimulate brown fat cell development is unknown, so that’s what this research aimed to look into.

 

What did the research involve?

The study investigated whether resveratrol helped brown fat cells develop into white fat tissue or beige fat, and to look into the biology underlying the process.

The study included 12 female mice that were divided into two groups – one fed a high-fat diet, the other the same high-fat diet supplemented with resveratrol. Before and during the weeks on the diets the researchers took regular body measurements and examined respiratory function. At the end of the four weeks they examined samples of the mice’s fat tissue.

In the laboratory they specifically looked into how resveratrol influences activity of stromal vascular cells, which are a type of fat stem cell that can develop into different types of cells. They also further looked into the specific biochemical pathways behind any changes.

 

What were the basic results?

Overall the researchers found that resveratrol has a dose-dependent influence on the development of brown or beige fat cells from fat stem cells (stromal vascular cells) present in white fat tissue. Higher concentrations of resveratrol caused the development of brown or beige cells within white fat tissue, changes that could prevent the accumulation of further white fat.

When looking into the biochemical process, they found that activation of AMP-activated protein kinase – a key regulator of energy metabolism – was essential to the process. Specifically the alpha 1 form – AMPKα1.

 

How did the researchers interpret the results?

The researchers conclude that resveratrol induces brown-like (beige) fat cell formation in white fat tissue via AMPKα1 activation, suggesting its possible beneficial anti-obesity effects.

 

Conclusion

This animal and laboratory research has demonstrated that resveratrol can stimulate the development of brown-fat-like cells in white fat tissue. Adults have very little brown fat, though these cells are found and it is proposed that increasing their numbers could prevent the accumulation of more white fat and so tackle obesity.

The researchers here looked at the potential of resveratrol, a polyphenol chemical found in red grapes, and found that it can stimulate more of these brown-fat-like cells to develop in the white fat tissue of mice. However, it’s difficult to draw much more meaning from this.

Mouse studies can give an indication of biological processes that may also work in humans, but we are not identical. We don’t know that if we were to be given daily resveratrol we would also start developing more brown-fat-like cells in our fat tissue. Even if we did, we don’t know whether this would cause weight loss, or reverse obesity and its associated health risks.

Also, of course, though resveratrol may be found in red wine, the mice were not drinking red wine on a daily basis. As one of the lead researchers is quoted in the media, the amount of resveratrol found in wine is a fraction of that present in grapes and berries, as much of the chemical is filtered out during the wine production process. You would gain more resveratrol from eating the grapes and berries themselves than drinking wine – but that makes a much less exciting headline.

Wine is also high in calories, which may cancel out any slight theoretical benefit you may gain from trying to convert white fat to brown. A high alcohol intake is also known to be associated with many health risks both in the immediate and long term. The proven risks of drinking too much red wine probably outweigh any possible benefits from trying to convert white fat to brown fat.

Overall the study provides no evidence that drinking red wine will help you lose weight.  

Links To The Headlines

Revealed: How to lose weight - drink plenty of red wine. The Daily Telegraph, June 21 2015

Want to lose weight? Drink red wine. The Independent, June 22 2015

Links To Science

Wang S, Liang X, Yang Q, et al. Resveratrol induces brown-like adipocyte formation in white fat through activation of AMP-activated protein kinase (AMPK) α. US National Library of Medicine. Published online March 12 2015

Categories: NHS Choices

Meningitis B vaccine 'available from September'

NHS Choices - Behind the Headlines - Mon, 22/06/2015 - 12:45

"All newborn babies in England and Scotland are to be offered a vaccine to combat meningitis B from September," BBC News reports. This will be the world’s first publicly funded vaccination programme for the potentially fatal disease.

 

What is meningitis B?

Meningitis B is a highly aggressive strain of bacterial meningitis that infects the protective membranes surrounding the brain and spinal cord. It is very serious and should be treated as a medical emergency. If the infection is left untreated, it can cause severe brain damage and infect the blood (septicaemia). In some cases, bacterial meningitis can be fatal.

 

How common is meningitis B?

The charity Meningitis Now estimates that there are 1,870 cases of meningitis B each year in the UK. Meningitis B is most common in children under five years old, particularly in babies under the age of one.

Initial signs and symptoms of meningitis B in babies include:

  • a high temperature with cold hands and feet
  • they may feel agitated, but not want to be touched
  • they may cry continuously
  • some children are very sleepy and it may be difficult to wake them up
  • they may appear confused and unresponsive
  • they may develop a blotchy red rash that does not fade when you roll a glass over it

For more information, read about the signs and symptoms of serious illness in babies.

 

Why is this meningitis B vaccine in the news?

The development of a safe and effective meningitis B vaccine is the culmination of more than 20 years of research and represents a significant breakthrough in disease prevention.

While the vaccine has been available for some time on a private basis, this is the first time it has been made available free of charge.

 

What do we know about the vaccine?

The vaccine, Bexsero, is thought to provide 73% protection against meningitis B, which should significantly reduce the number of cases. The vaccine can be administered to infants aged two months or older either by itself, or in combination with other childhood vaccines.

The vaccine has been tested in clinical trials involving more than 8,000 people.

In infants, it was found to have similar levels of safety and tolerability as other routine childhood vaccines. The most commonly reported side effects were:

  • redness and swelling at the site of the injection
  • irritability
  • fever

Edited by NHS Choices. Follow Behind the Headlines on TwitterJoin the Healthy Evidence forum.

Links To The Headlines

Meningitis B vaccine offered to all babies from September. BBC News, June 21 2015

Links To Science

 

Categories: NHS Choices

Weighing yourself every day may help with weight loss

NHS Choices - Behind the Headlines - Fri, 19/06/2015 - 13:30

"Stepping on the scales every day could be the key to weight loss, a study has found," the Mail Online reports. This report was based on a US study which suggested daily weighing can lead to a small, though sustainable, loss in weight.

The study involved 162 overweight and obese adults trying to lose weight, who were allocated to either weighing themselves daily and tracking their weight on a graph, or a control group. Both groups were given an educational session about other evidence-based strategies they could use to lose weight.

After a year, those weighing themselves lost more weight – about two kilos more on average – than those who didn’t. This difference seen in the averages between the two groups seemed largely to be due to an effect in men. The results in women in both of the groups were similar.

There are limitations to this study. For example, participants in the weighing group may have felt more pressure to lose weight than the control group as they were receiving the intervention.

Also, the fact that the weight loss was mainly found in a small group of men (just 40) is a preliminary finding, and needs to be confirmed in a larger sample.

Weight monitoring is already a part of many weight loss strategies. For some people, weighing themselves regularly may not be helpful and could actually be discouraging. Different people often find different ways to motivate themselves and a one-size fits all solution may not be effective.

Where did the story come from?

The study was carried out by researchers from the University of Minnesota and Cornell University in the US. No specific funding for the study itself was reported, but the first author was funded by a National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases-Ruth L. Kirschstein National Research Service Award.

The study was published in the peer-reviewed Journal of Obesity. This is an open-access journal, meaning that its content is available for free online.

The Mail Online’s story incorrectly reports the amount of weight lost in the study. It says that “Eventually, each participant lost a total of 10 per cent of their body weight.” While losing 10% of weight was the target for those taking part, only about 9% of those who weighed themselves and 5% of the control group achieved this. On average they only lost 2.5% of their weight.

 

What kind of research was this?

This was a randomised controlled trial (RCT) which looked at whether daily weighing and recording weight helped overweight adults to lose weight and keep it off.

Many trials have tested weighing yourself combined with other activities aimed at weight loss, but the researchers in this study wanted to look at the effect of just weighing yourself. They report that previous studies have had conflicting findings about whether weighing yourself helps you to lose weight, and many of the studies have been observational, meaning drawing conclusions about its effects is difficult.

An RCT is the best way to identify the effects of a particular intervention or treatment.

 

What did the research involve?

The researchers recruited 162 overweight or obese adults and allocated them at random to either weighing themselves daily or not doing this. After a year, the non-weighing group also started weighing themselves daily. The researchers compared how much weight each group lost in the first year, and whether they kept the weight off in the second year.

The researchers recruited participants through advertisements asking for volunteers who wanted to lose weight. Only adults aged 18 or over, who had a body mass index (BMI) of 27 or more, who did not have diabetes, and had never had an eating disorder were eligible to take part.

All participants had an educational session about evidence-based ways to lose weight, and a target of 10% reduction in weight over the year was recommended. These sessions emphasised that people should chose a weight loss strategy to suit their own needs. They also encouraged small changes to reduce intake by about 100 kilocalories a day, such as:

  • skipping dessert a few times per week
  • using a meal replacement for lunch three times a week
  • abstaining from snacking most days of the week

At the end of the sessions for people in the self-weighing group, the intervention was explained to them. The researchers called their weighing intervention the "Caloric Titration Method" (CTM). They gave each member of the group a standard bathroom weighing scale and asked them to weigh themselves at the same time and way every day. Ideally, they were asked to do this first thing in the morning immediately after getting up. They were also asked to enter their weight on a website each day. (The site is still, at time of writing, accepting free registrations for people who want to try CTM.)

The website plotted a graph of weight to show whether it was changing, and also highlight the next weight loss target on the graph. The targets were each set at 1% of body weight, and once a target was achieved and the person stayed at this weight for eight days, the next target was set at 1% lower, and so on. This continued up to a maximum of 10% weight loss, after which they were asked to maintain the weight loss. If the participants did not enter at least three weights a week, they were sent an email reminder. In the second year, the group were asked to continue to use self-weighing to maintain their weight loss or lose more weight if they wished.

The idea is to allow people to see the effect of small changes to diet through weighing themselves, to see quickly whether the changes are working or whether they need to make more changes. The method promotes slow weight loss with the idea that this might be maintained better than rapid weight loss.

The control (no weighing) group were not asked to weigh themselves, but were told they would receive the intervention after a year. After a year they were given the scales and a session on CTM.

The researchers weighed participants four times during the study, and compared weight changes between the groups.

 

What were the basic results?

The participants were aged about 46 years old on average, and had an average BMI of 33.5 and average weight of 93.8kg. Most of the participants were female (82%), and of white ethnicity (89%).

The researchers found that over the first year, those who were weighing themselves daily lost significantly more weight than those who were not. People in the self-weighing group who completed the year lost an average of 2.6kg while the non-weighing group lost an average of 0.5kg. The results were similar if the last measurement available for people who did not complete the year were included in the analysis.

When looking at the results by gender, women in the two groups did not differ very much in their weight loss, but men who weighed themselves lost more weight than those who didn’t. However, this difference did not reach statistical significance, probably due to the small number of men in the study.

In the second year of the study, the weighing group kept off the weight they had lost (average change in weight 0.1kg). Once the control group started weighing themselves daily in the second year, they also lost 1.9kg on average.

Most of the participants did not reach their target 10% weight loss; on average they lost 2.5%.

 

How did the researchers interpret the results?

The researchers concluded that "the use of frequent weighing accompanied by visual feedback of weight, without a prescribed diet or exercise plan, was effective in producing a small but sustainable weight loss in overweight males". They suggest this strategy may be useful when combined with other approaches to achieve healthy weight loss.

 

Conclusion

This RCT suggested that weighing yourself daily and tracking your weight on a graph might help some people to lose weight.

The strength of this study was its RCT design, but there are some limitations:

  • Participants could not be blinded to what intervention they were receiving, and this might have affected their attempts to lose weight. Those in the weighing group may have felt more pressure to lose weight than the control group as they were receiving the intervention, rather than the weighing having an effect itself.
  • While the difference between the groups appeared to be due to an effect in men only, the study only included a small number of men (40) and results need to be confirmed in a larger sample.
  • Participants were all volunteers who wanted to lose weight, and may be more motivated to do so than people in the general population.
  • Most participants were adults of white ethnicity and results may not be representative of other groups.
  • The average amount of weight lost was relatively small – 2.6kg or 5.7lbs over a year. As the authors suggest, it may need to be combined with other techniques to improve these results.

Overall, these results suggest that weighing yourself and keeping track of your progress on a chart might be useful, possibly more so for men. Weight monitoring is already a part of many weight loss strategies. NICE guidance recommends that lifestyle weight management services should include monitoring weight and participants' personal goals throughout these programmes. What helps people to lose weight may differ for each person, and the main thing is to find something that works for you.

The average effects seen in this study were relatively small so daily weighing is likely to need to be combined with other approaches to a calorie controlled diet and regular exercise to achieving greater weight loss. For more information join up with the NHS weight loss plan

Links To The Headlines

Desperate to shed the pounds? Weigh yourself EVERY DAY and you'll be more conscious of what you eat, scientists say. Mail Online, June 19 2015

Links To Science

Pacanowski CR, Levitsky DA. Frequent Self-Weighing and Visual Feedback for Weight Loss in Overweight Adults. Journal of Obesity. Published online June 18 2015

Categories: NHS Choices

New chlamydia vaccine shows promise after being tested on mice

NHS Choices - Behind the Headlines - Fri, 19/06/2015 - 01:00

“Researchers in the United States say they have developed a vaccine that can protect against chlamydia,” The Independent reports. Initial results in mice have shown promise in protecting against this common sexually transmitted infection (STI).

Chlamydia is one of the most common STIs in the UK, and can lead to female infertility. It can also cause blindness in babies if their mother has a chlamydia infection and babies are exposed to the bacteria when they are born.

Researchers tested a new vaccine that contains ultraviolet (UV) light, which killed chlamydia bacteria when attached to tiny man-made nanoparticles – these contained chemicals that tried to enhance the immune response. When given as a spray into the nose, or directly onto the internal surface of the womb, the vaccine protected the mice against chlamydia infection. If the mice were just given UV light that killed chlamydia bacteria without attachment to the nanoparticles, this actually made them more susceptible to infection.

This is early stage research, and more animal testing is needed before the vaccine could be tested on humans. Until human studies are carried out, we won’t know whether the vaccine is safe or effective.

Currently, the most effective way to prevent catching chlamydia is considerably more low-tech than nanoparticles; always use a condom during sex, including oral and anal sex.

 

Where did the story come from?

The study was carried out by researchers from Harvard Medical School and other research centres in the US and Saudi Arabia, and from the pharmaceutical company Sanofi Pasteur. It was funded by the National Institutes of Health, Sanofi Pasteur, the Ragon Institute, the David Koch Prostate Cancer Foundation, and Harvard University. Some of the researchers are inventors on patent applications relating to the vaccine technology tested in the study. Some had financial interests in biotechnology companies developing this type of technology.

The study was published in the peer-reviewed medical journal Science.

The Independent covered this study well. The headline does not over-state the impact of the research; the article says the research was carried out on mice, and also includes an expert comment highlighting the early stage of the research.

The Mail Online’s subheads suggest that the vaccine is a “jab” but the vaccine actually didn't work if injected; it only worked if given via the mucous membranes, such as into the nose or womb. The Mail's headline also suggests that chlamydia is the most common cause of infertility, but this may not be correct. There are many potential causes of infertility, and in about a quarter of cases no cause can be found.

 

What kind of research was this?

This was animal research that aimed to test a new vaccine against chlamydia.

Chlamydia is an STI caused by the bacteria Chlamydia trachomatis. Chlamydia is one of the most common STIs in the UK, and about two-thirds of those infected are aged under 25.

In around 70-80% of women, and half of all men, chlamydia does not cause noticeable symptoms. This has resulted in widespread infection, as people do not realise they are infected, so do not seek treatment.

While symptoms of chlamydia tend to be mild (if annoying), such as pain when urinating, complications of chlamydia can be very serious, such as infertility in women.

In the developing world, it is also a common cause of blindness in babies born to women with an active infection.

There is currently no vaccine against the disease. A chlamydia vaccine was last tested in the 1960s, and although it seemed to offer some protection initially, some people who had the vaccine had more symptoms when they were exposed to chlamydia than those who were given placebo (dummy treatment). Because of this, development of the vaccine stopped.

The chlamydia bacteria infect the mucus-producing (mucosal) surfaces of the body, such as the linings of the reproductive tract. Injecting vaccines against this type of infection often does not offer much protection, because the immune response does not easily reach the mucosal surfaces. Delivering vaccines directly onto the mucosal surface has not always worked well in the past for a variety of reasons, such as not producing a strong immune response or causing side effects. The current study wanted to test a new vaccine made by attaching killed chlamydia bacteria to tiny particles called nanoparticles, given directly onto the mucosal surfaces.

This type of animal research is essential for the early testing of vaccines and drugs, to test their effects and make sure they are safe for testing on humans. While they can give an early indication of whether a vaccine may work in humans, there's no certainty until they reach human trials.

 

What did the research involve?

The researchers developed a new vaccine by attaching UV light-killed chlamydia bacteria to tiny man-made nanoparticles. These nanoparticles acted as biodegradable “carriers” for the vaccine and also contained chemicals that enhance immune responses, called “adjuvants”.

They compared the effect of this vaccine in mice to an infection using live chlamydia or the UV light-killed chlamydia bacteria alone. They looked at what immune response these different approaches produced, and what happened when they exposed the mice to live chlamydia bacteria four weeks later. They also compared the effects of giving the vaccine through different routes – under the skin, directly onto the mucosal surface lining the womb (uterus) or the mucosal surface lining the inside of the nose.

 

What were the basic results?

The researchers found that vaccinating the mice with UV light-killed chlamydia bacteria into the uterus produced a different kind of immune response to infecting them with live chlamydia. When the mice were exposed to live chlamydia bacteria four weeks later, the ones which had been vaccinated with UV light-killed chlamydia bacteria actually had worse infections (more chlamydia bacteria) than those which had been previously exposed to the live chlamydia.

However, when the researchers vaccinated the mice with UV light-killed chlamydia bacteria attached to the nanoparticles, this prompted a different immune response to UV light-killed chlamydia bacteria alone. Giving this nanoparticle vaccination through the mucosal membranes of the nose or the uterus protected the mice when they were exposed to live chlamydia bacteria four weeks later. However, giving the nanoparticle vaccination by injecting it under the skin did not work.

The researchers identified that the reason mice experienced protection when the vaccine was given onto mucous membranes was the interaction between two different types of immune system cells called memory T cells. One set of these cells remained in the mucosal tissue of the uterus, and prompted a response from the other type when exposed to chlamydia infection.

 

How did the researchers interpret the results?

The researchers concluded that combining UV light-killed chlamydia bacteria with nanoparticle carriers changed the immune response compared to the UV light-killed bacteria alone, and “achieved long-lived protection” against chlamydia infection.

They suggest that their nanoparticle system is an efficient way of getting vaccines onto mucosal surfaces, and might also be useful for developing vaccines against other harmful infections that target these surfaces.

 

Conclusion

This animal research has tested out a potential new vaccine against chlamydia, which utilises UV light-killed chlamydia bacteria linked to tiny nanoparticles. The vaccine did protect against chlamydia infection in mice, if it was given directly onto the mucous-producing surfaces of the nose or uterus.

Previous attempts to make a chlamydia vaccine have not been successful, and the current research also identified that this may have been due to the type of immune response produced. This new approach prompts a different immune response, including “memory” cells, which remain in the mucosal tissue. These cells prompt an immune response if they are exposed to chlamydia infection again, allowing the mice to fight the infection off more successfully.

This type of animal research is essential for the early testing of vaccines and drugs, to make sure they are safe enough for testing on humans. Humans and animals are similar enough for these studies to give an early indication of whether a vaccine may work on humans. However, it will not be possible to say for certain whether this new vaccine is effective and safe until it does reach human trials.

Chlamydia is one of the most common STIs in the UK. Although there is no vaccine currently, you can protect yourself by:

  • using a condom every time you have vaginal or anal sex
  • using a condom to cover the penis during oral sex
  • using a dam (a piece of thin, soft plastic or latex) to cover the female genitals during oral sex or when rubbing female genitals together
  • not sharing sex toys

Read more about chlamydia prevention and sexual health in general

Links To The Headlines

Chlamydia: US researchers claim to have developed vaccine against the disease. The Independent, June 18 2015

New chlamydia vaccine 'roots out and destroys the STI, the most common cause of infertility'. Mail Online, June 18 2015

Links To Science

Stary G, Olive A, Radovic-Moreno AF, et al. A mucosal vaccine against Chlamydia trachomatis generates two waves of protective memory T cells. Science. Published online June 19 2015

Categories: NHS Choices

Too soon to say if breastfeeding problems could be genetic

NHS Choices - Behind the Headlines - Thu, 18/06/2015 - 15:15

"Is your inability to breastfeed written in your genes?" the Mail Online asks. The question is prompted by animal research that discovered that problems with a protein called ZnT2 may restrict milk production after pregnancy.

The protein in question helps move zinc into breast tissue cells (so it is known as a zinc transporter). ZnT2 was found to play an important role in the structure and function of normal mammary (breast) tissue in mice.

When the mice had babies, those that were genetically engineered to have a missing or malfunction version of ZnT2 did not produce as much milk as normal mice, and their milk did not have as many nutrients in it. This meant that fewer of their offspring survived.

Animal studies such as this can give a good insight into the role that individual proteins play in the biology and function of tissues. While it is likely that these proteins play a similar role in humans, there may be important differences.

We also can't say to what extent abnormalities of this zinc transporter might be responsible for the difference in the quantity and quality of milk production in women, as this has not been assessed.

Many women have initial problems with breastfeeding, as it does not necessarily come naturally. Though with patience, perseverance and if need be, professional advice, these problems can usually be overcome.

Read more about common breastfeeding problems

Where did the story come from?

The study was carried out by researchers from The Pennsylvania State University and Penn State Hershey College of Medicine in the US, and RIKEN Center for Integrative Medical Sciences and Suzuka University of Medical Science in Japan. The study was funded by the National Institutes of Health and Penn State Hershey College of Medicine Department of Surgery. It was published in the peer-reviewed scientific journal The Journal of Biological Chemistry.

Only quite a way into the Mail Online’s coverage does it report that the study was in mice.

It also does not acknowledge the uncertain applicability of these findings to breastfeeding problems in humans, or that breastfeeding decisions in women have many different influences.

 

What kind of research was this?

This was an animal study that aimed to look at the role of a particular gene, and the protein it codes for, in the function of mammary (breast) tissue in mice.

The research centres on the zinc transporter (ZnT2) protein, which transports zinc into the mammary cells in the breast that produce milk. ZnT2 also transports zinc into the energy powerhouses of the cells (mitochondria), and is found in the non-milk-producing mammary cells. This suggested that ZnT2 might be important in the biology of mammary tissue. This is what this study aimed to look into further.

Animal studies such as this can give a good insight into biology that may be applicable to humans, but there may be differences. Also, even if the protein is important in the development of breast tissue, it does not necessarily mean it is a significant cause of breastfeeding problems. Additional research looking at this gene in women with and without problems with milk production would be needed to assess this.

 

What did the research involve?

This animal study looked into the role of ZnT2 using different types of mice:

  • normal mice that could produce ZnT2, or genetically engineered so that they could not produce a working zinc transporter
  • the above types of mice who either hadn’t had babies, or those currently producing milk (lactating)

Under anaesthetic they took samples of mammary tissue from the different groups of mice. They examined it in the laboratory using fluorescent antibodies that would attach to and highlight ZnT2 so they could look at its workings.

In the lactating mice they also looked at the weight and survival of the offspring as an indicator of how much milk they were receiving, and took milk samples to examine its composition.

 

What were the basic results?

The researchers found that mice without a working zinc transporter who had not yet had any babies had overall reduced growth and development of the mammary tissue compared with normal mice.

When they looked at mice without a working zinc transporter who had had babies and were lactating, they found that they have tended to build up zinc in the mammary tissue. In both normal and genetically engineered mice, zinc concentration in the mammary gland was higher in lactating than non-lactating mice. However, accumulation in the mammary gland was a third higher in the mice without a functioning zinc transporter than the normal lactating mice.

When their mammary tissue was examined, lactating mice without the working zinc transporter did not demonstrate the same structure and function of the tissue as the normal mice. This included problems with the milk secreting cells. 

Milk production was reduced by up to a third in these mice without a working zinc transporter. As a result the survival rate of the offspring was lower. The milk they produced also contained a third less zinc, as well as having reduced concentration of other milk components, such as fat, lactose (a sugar normally found in milk) and beta-casein (a protein normally found in milk).

 

How did the researchers interpret the results?

The researchers conclude "ZnT2-mediated zinc transport is critical for mammary development and function during lactation" and say this is "crucial for sustaining infant health".

 

Conclusion

This animal study demonstrates how the zinc transporter ZnT2 plays an important role in the development of normal, functioning mammary (breast) tissue in mice and allowing them to produce sufficient quality milk to feed their offspring.

Animal studies such as this can give a good insight into the biology and function of tissues that may be applicable to humans. However, there are many important cautions to bear in mind when drawing any conclusions about humans from this study. 

It is likely that this protein does play a role in breast tissue development in humans, and therefore not having it might be a problem for breastfeeding. However, we don’t know how common problems with this protein are in humans, and what effects this might have. There will also be many other genes and associated proteins that are vital for the healthy composition of mammary tissue and milk production in humans. Therefore a single gene or protein is unlikely to provide the whole answer to insufficient milk production.

What is most important to recognise is that decisions about breastfeeding in women usually involve a multitude of factors. Having insufficient milk production, or a baby not gaining enough weight from breast milk alone, are only one possible influence. Many women chose not to start, or continue with, breastfeeding for many different reasons. These may include for example:

  • culture
  • views and support of close family, friends or society in general
  • previous experiences of breastfeeding herself, or hearing those of other women
  • health of the mother and baby (e.g. if the baby is premature or the mother has had health complications around birth)
  • if she experiences difficulties breastfeeding
  • the availability of support from health professionals

This animal study is of interest into the biology of breastfeeding, but cannot say that whether you breastfeed or not all comes down to genetics. 

Breastfeeding is associated with many benefits both to mother and baby, but if you are unable to breastfeed then you shouldn’t feel guilty or ashamed. There is much more to bonding with your baby, such as regular physical contact and playing with them, than just providing them with breast milk.

Links To The Headlines

Is your inability to breastfeed written in your genes? Mutation 'stops mammary glands producing enough milk', say experts. Mail Online, June 17 2015

Links To Science

Lee S, Hennigar SR, Alam S, et al. Essential Role for Zinc Transporter 2 (ZnT2)-mediated Zinc Transport in Mammary Gland Development and Function during Lactation. The Journal of Biological Chemistry. Published online April 7 2015

Categories: NHS Choices

Smoking causes half of all deaths in 12 different cancers

NHS Choices - Behind the Headlines - Thu, 18/06/2015 - 13:00

"Roughly half of deaths from 12 smoking-related cancers may be linked directly to cigarette use, a US study estimates," the Mail Online reports. Due to similar smoking rates in the UK (19% of adults) and USA (17% of adults) there may be a similar pattern.

Researchers used data from previous studies to estimate the proportion of deaths from 12 cancers associated with smoking.

The researchers estimated that smoking may account for half of these cancer deaths overall.

Unsurprisingly, lung cancer was most strongly associated with smoking (accounting for 80% of deaths), followed by cancers of the mouth and throat.

It is important to note, however, that these are just estimates based on data taken from previous studies, which may have various limitations. Therefore, we cannot be certain that these figures on the proportion of cancers caused by smoking are 100% accurate – or directly applicable to the UK.

The results still make for sobering reading, with the World Health Organization (WHO) estimating that smoking kills nearly 6 million people a year worldwide, due to cancer and other diseases, such as heart disease.

If you are a smoker, the best thing you can do for your health is to stop smoking.

Where did the story come from?

This study was by researchers from the American Cancer Society in Atlanta; Harvard Medical School in Boston; National Cancer Institute in Bethesda, Maryland; and Fred Hutchison Cancer Research Center in Seattle. The analysis part of this work was funded by the American Cancer Society.

The study was published in the peer-reviewed medical journal JAMA Internal Medicine.

The Mail Online’s reporting of the study was accurate. However, one of the background quotes from the lead author – “e-cigarettes are now the most common form of tobacco use among high school students” – is open to criticism, as e-cigarettes do not contain any tobacco.

 

What kind of research was this?

This study was titled as a research letter, and the researchers used data from previous studies to estimate the proportion of deaths from 12 different cancers in the US in 2011 that could be attributed to smoking. 

The researchers say that the 2014 US Surgeon General’s Report estimated the number of cancer deaths overall and lung cancer deaths specifically that were caused by smoking. However, they missed out the other 11 that are reported to be caused by smoking. Previous data on smoking deaths due to these cancers is said to come from 10 or more years ago. Since then, smoking prevalence has decreased, but risk of cancer among smokers can increase over time. Because of this, the study aimed to look at more up-to-date information on specific cancer deaths in 2011.

The research used data from various previous studies and surveys. Specific methods on how these studies were identified and selected is not reported in this brief publication; therefore, it is not possible to comment on whether all relevant evidence will have been considered.

systematic review would probably have provided more detailed information. However, these types of reviews can be both expensive and time-consuming, and some research teams just don’t have the resources to carry them out.

 

What did the research involve?

The researchers obtained information on smoking prevalence from the 2011 National Health Interview Survey. This was based on interviews from a nationally representative sample.

Age- and sex-specific cancer risk for former and current smokers came from cohort studies that had assessed smoking in questionnaires, and then followed the people up looking for risk of cancer and cancer deaths. One data source was the Cancer Prevention Study II, which included people aged 35 to 54 years (covering the follow-up period 1982-88), and the source for other age groups was the Pooled Contemporary Cohort (follow-up period 2000-11) which has pooled data from five cohorts.

Using information from these data sources, the researchers calculated the population attributable fraction (PAF) of smoking for different cancer deaths. The PAF is the proportion of the number of deaths that are caused by smoking, or by what proportion the number of deaths would be reduced if there was no smoking. 

 

What were the basic results?

In 2011, there were 345,962 cancer deaths in adults aged 35 or over with the 12 different cancer sites examined. The researchers estimated that 167,805, or 48.5% (95% confidence interval (CI) 46.2 to 51.2%), of these overall cancer deaths were caused by cigarette smoking. Smoking accounted for 51.5% of cancer deaths in men and 44.5% of cancer deaths in women.

By far the largest proportions of smoking-attributable deaths were cancers of the lungs and airways. 80% of these cancer deaths – broken down as 83% for men and 76% for women – were estimated to be caused by smoking. The second highest proportion was for cancers of the larynx (vocal cords), where smoking accounted for 77% (72% in men and 93% in women).

Smoking accounted for around half of all deaths of the mouth, throat and oesophagus (food pipe), and just under half of bladder cancers.

Smoking was attributable to around a quarter of cervical and liver cancers.

The remaining cancers examined where the PAF of smoking was less than 20% were those of the kidney, pancreas, stomach, bowel, and a type of leukaemia.

 

How did the researchers interpret the results?

The researchers conclude, “Cigarette smoking continues to cause numerous deaths from multiple cancers, despite half a century of decreasing prevalence. The smoking downturn is likely reflected in the generally lower proportions of deaths caused by smoking in 2011 than in 2000 to 2004”.

 

Conclusion

This study has used data from previously published cohort studies and national surveys to estimate the proportion of cancer deaths that can be attributed to smoking in men and women. They examined 12 cancers that are already known to be associated with smoking and estimated that smoking may account for half of them overall. The vast majority of cancers of the lungs and airways were estimated to be caused by smoking.

It is important to note that these are only estimates. The study has used data from cohort studies to inform the risk of different cancers in former and current smokers, and those who have never smoked. However, these cohort studies may have various inherent limitations and potential biases in their designs, which cannot be analysed here. For example:

  • the populations studied may not be representative of everyone
  • the follow-up period may be too short to capture all newly developed cancers and cancer deaths caused by smoking
  • they may not have taken into account other confounders (e.g. alcohol intake, diet and physical activity)
  • there may be inaccuracies around assessments of lifetime smoking habits
  • they may not have been able to assess the effects of passive smoking from environmental exposure

Specific methods on how the cohorts and national survey were identified and selected are not reported in this brief publication. It is likely that the researchers will have selected the best available and most nationally representative evidence on which to form estimates. However, this cannot be assumed, and it is not possible to comment on whether all relevant evidence will have been considered.

Another point to bear in mind is that the cancers studied were selected as they are known to be linked to be smoking. It is possible that other cancers may be associated with smoking that are currently less well recognised. It is worth again highlighting that these are estimates for the US population – not the UK.

Despite limitations in terms of whether this study provides accurate estimates on the proportion of these cancer deaths that are caused by smoking, it nevertheless reinforces the health message. Smoking is known to have many detrimental effects on health, not only on risk of cancer, but for many other chronic diseases.

As the researchers conclude, “more comprehensive tobacco control, including targeted cessation support” seem to be an important way forward.

Even if you have been a smoker for many years, quitting will still provide a tremendous health benefit. For example, 10 years after you've stopped smoking, your lung cancer risk is half that of someone who has continued to smoke.

Read more methods you can use to quit smoking

Links To The Headlines

Half of all deaths from 12 different cancers are caused by smoking, study finds. Mail Online, June 17 2015

Links To Science

Siegel RL, Jacobs EJ, Newton CC, et al. Deaths Due to Cigarette Smoking for 12 Smoking-Related Cancers in the United States. JAMA Internal Medicine. Published online June 15 2015

Categories: NHS Choices

Knee surgery 'waste of time', researchers argue

NHS Choices - Behind the Headlines - Wed, 17/06/2015 - 12:50

"Knee surgery is 'pointless and potentially harmful' for thousands of patients," the Daily Mirror reports.

Researchers have looked at previous studies that had compared arthroscopic (keyhole) knee surgery with exercise or sham surgery (placebo) for middle-aged people with knee pain – specifically, knee pain caused by osteoarthritis or a tear in the cartilage, but not those with a ligament condition.

They found that both exercise and arthroscopy improved knee pain. Arthroscopy was slightly better, improving pain by a small amount, which was described as the equivalent to using a painkiller such as paracetamol or ibuprofen. There was no difference between the interventions for function of the knee.

Current UK guidelines recommend arthroscopy for people with knee osteoarthritis and a clear history of "mechanical locking", where a person is unable to bend or straighten the knee. People with this symptom were not analysed separately in this research, so it remains unclear whether this recommendation would change on the basis of this study.

Patient satisfaction reported after surgery appears to be positive.

Whether surgery is an option for you or not, UK guidelines recommend that all people with osteoarthritis should do exercise for local muscle strengthening and general aerobic fitness purposes.

 

Where did the story come from?

The study was carried out by researchers from the University of Southern Denmark, Copenhagen University Hospital, Odense University Hospital in Denmark and the University of Lund in Sweden. It was funded by the Swedish Research Council.

The study was published in the peer-reviewed British Medical Journal on an open-access basis, so the study is free to read online or download as a PDF.

The UK media’s reporting of the story was possibly a little over-dramatic and gave the impression that these results would lead to a change in clinical guidelines. The Daily Telegraph said keyhole knee surgery "does little good and could kill patients". The Mail Online reported that experts were saying: "Surgeons should stop carrying out keyhole knee operations on middle-aged and elderly people."

The review concluded that the evidence did not support keyhole knee surgery for middle-aged or older patients with knee pain, with or without signs of arthritis, but this is not official advice.

This study is new, and while it may stimulate discussion about whether current advice is appropriate, it will not change it overnight. This research needs to be considered in light of all other evidence.

 

What kind of research was this?

This was a systematic review of randomised controlled trials (RCTs) on the benefits of arthroscopy for knee pain in middle-aged and older people. It included a meta-analysis, which pooled the results of the studies. This type of study can provide a clearer picture of clinical effectiveness than individual studies. It involves systematically identifying all the available evidence, assessing the quality and summarising the findings.

Arthroscopy is a type of keyhole surgery for the knee. It can be used to remove a damaged section of the cartilage (partial meniscectomy) or for removing any dead tissue that might be floating in the fluid of the knee joint and causing the knee to lock (debridement).

 

What did the research involve?

The researchers searched five medical databases, including Medline and Embase, for RCTs on the benefits of arthroscopy for people with or without osteoarthritis. The reference list of any relevant study was also reviewed, in an attempt to capture all available trials. They looked for any studies published up to 2014.

When looking at the potential harm of arthroscopy, they limited the time period to after the year 2000, due to surgical and anaesthetic advances in technique. They also opened up the search criteria to include adverse events reported in observational studies, as well as RCTs.

Two researchers independently sifted all of the results, which is important for reducing any potential bias.

Studies were excluded if the person had a ligament injury.

 

What were the basic results?

Nine trials were identified in which arthroscopy was compared to sham surgery or exercise. Sham surgery, sometimes called "placebo surgery", is the surgical equivalent of using a placebo pill to test a new drug. Sham surgery is thought to offer no benefit to the patient, but typically contains the same pre- and post-surgery elements of real surgery. These included a total of 1,270 people aged 49.7 to 62.8 years.

Both arthroscopy and exercise were shown to substantially improve symptoms. Arthroscopy was slightly better than control conditions for pain 3 to 24 months post-op. This difference was 2.4mm on a 0 to 100mm visual analogue scale for pain – essentially, a sliding scale of reported pain ranging from entirely pain-free to intolerable pain (95% confidence interval (CI) 0.4 to 4.3). There was no difference in physical function between arthroscopy or control conditions.

Arthroscopy was associated with side effects that included:

  • deep vein thrombosis (4.13 occurrences per 1,000 procedures) – a blood clot that usually develops in the blood vessels of the legs
  • pulmonary embolism (1.45 occurrences per 1,000 procedures) – a blood clot that develops inside the lungs
  • infection (2.11 occurrences per 1,000 procedures)
  • death (0.96 occurrences per 1,000 procedures)

 

How did the researchers interpret the results?

The researchers concluded that: "The small inconsequential benefit seen from interventions that include arthroscopy for the degenerative knee is limited in time and absent at one to two years after surgery. Knee arthroscopy is associated with harms. Taken together, these findings do not support the practise of arthroscopic surgery for middle-aged or older patients with knee pain with or without signs of osteoarthritis."

 

Conclusion

This systematic review has found there is little difference between arthroscopy and exercise in the treatment of knee pain, excluding people with damage to their ligaments. Both arthroscopy and exercise improved symptoms for people with and without osteoarthritis. However, there were rare but serious risks associated with the arthroscopy procedure.

In 2008, the National Institute for Health and Care Excellence (NICE) produced a guideline on the treatment of osteoarthritis and recommended that "referral for arthroscopic lavage and debridement should not be offered as part of treatment for osteoarthritis, unless the person has knee osteoarthritis with a clear history of mechanical locking". This systematic review did not separately analyse results for people with a history of mechanical locking – where a person is unable to bend or straighten the knee, which can occur when the cartilage is torn. Therefore, it is unclear whether this recommendation would change following this piece of research.

Before consenting to any type of surgery, it is recommended that you ask your surgeon or clinical in charge of your care for an explanation of both the potential benefits and risks of surgery, so you can make an informed decision.

The NHS Choices Health A-Z section contains details of the most widely used types of surgery. 

Links To The Headlines

Knee surgery is 'pointless and potentially harmful' for thousands of patients says study. Daily Mirror, June 16 2015

Common knee surgery only has 'inconsequential benefits', experts say. The Independent, June 17 2015

Is keyhole knee surgery HARMFUL? Negative consequences of operations in middle-aged or older patients said to outweigh long-term benefits. Mail Online, June 17 2015

Keyhole knee surgery 'does little good and could kill patients’. The Daily Telegraph, June 16 2015

Links To Science

Thorlund JB, Juhl CB, Roos EM, Lohmander LS. Arthroscopic surgery for degenerative knee: systematic review and meta-analysis of benefits and harms. BMJ. Published online June 16 2015

Categories: NHS Choices

Could avocados hold the key to treating leukaemia?

NHS Choices - Behind the Headlines - Wed, 17/06/2015 - 12:22

"Avocados could hold the key to helping beat rare form of leukaemia," The Independent reports; specifically acute myeloid leukaemia, which is an uncommon and aggressive cancer of the white blood cells.

The headline may give readers the impression that eating avocados may help fight leukaemia, which is not the case. Researchers were actually looking at a compound found in avocado seeds that is not eaten, called avocatin B, which appears to be effective against leukaemia cells in the laboratory.

The researchers tested 800 compounds against human leukaemia cells. Avocatin B was the most effective compound to cause the leukaemia cells to die. It did not have an effect on normal blood cells.

This is an exciting discovery and there are now plans to use this compound to begin development of a new drug, though of course this will be a long road.

Current treatments for leukaemias involve chemotherapy and, in some cases, stem cell transplants (previously, and somewhat inaccurately, known as bone marrow transplants). Stem cell transplants offer the chance of a cure. People aged between 16 and 30 can join the stem cell register, and if you are a match for a patient, you could save their life. The register is managed by the Anthony Nolan charity and you can find out how to register here.

 

Where did the story come from?

The study was carried out by researchers from the University of Waterloo and Mount Sinai Hospital in Canada and the University of Perugia in Italy. It was funded by the Leukemia & Lymphoma Society of Canada, the Natural Sciences and Engineering Research Council of Canada and the Canadian Institutes of Health Research.

The study was published in the peer-reviewed medical journal Cancer Research.

The media in general have reported on the study accurately though have not pointed out that the compound avocatin B was obtained from the seed of the avocado and not from the flesh that is eaten.

So headlines such as "An avocado a day keeps leukaemia away" are inaccurate and misleading.

 

What kind of research was this?

This was a laboratory study looking at the effect of an avocado extract on acute myeloid leukaemia.

Acute myeloid leukaemia is an aggressive cancer of the blood. Blood cells are made in the bone marrow from stem cells – the type of cells that are not specialised and can divide and produce a wide range of specialised cells. In acute myeloid leukaemia, there is an overproduction of myeloid white blood cells, which are usually involved in fighting infections.

When this system goes into overdrive, the bone marrow releases large numbers of immature myeloid blood cells into the circulation. They do not continue to develop into normal myeloid blood cells. The production of large numbers of these cells causes a reduction in the production of normal blood cells, which leads to the symptoms of leukaemia.

 

What did the research involve?

The researchers tested 800 natural health products against human acute myeloid leukaemia cells in the laboratory.

Human acute myeloid leukaemia cells were obtained and grown in dishes. They were then exposed to each of the products.

The most effective compound at causing leukaemia cell death was then tested on normal blood stem cells. These samples of peripheral blood stem cells were collected from healthy volunteers. They had been given a drug called G-CSF, which stimulates the body to produce increased numbers of these stem cells from the bone marrow and release them into the circulation.

The researchers then injected acute myeloid cells exposed to avocatin B into mice. They compared their ability to grow and develop in the bone marrow with acute myeloid cells that had not been exposed.

 

What were the basic results?

The compound avocatin B was effective in causing leukaemia cells to die. It was particularly effective against immature myeloid blood cells. It did not affect normal peripheral blood stem cells. When the researchers treated immature myeloid cells with avocatin B, their ability to develop in the bone marrow of mice was reduced.

The study authors say that previous research has found that the immature myeloid blood cells found in leukaemia contain more mitochondria than normal blood cells. Mitochondria are the specialised compartments in cells that generate energy. The experiments seemed to indicate that it was this difference that caused avocatin B to be effective against the leukaemia cells rather than normal blood cells.

Avocatin B is a compound made of two 17-carbon lipids that was extracted from avocado pear seeds.

How did the researchers interpret the results?

The researchers concluded that their laboratory studies demonstrated that avocation B "induced selective toxicity toward leukaemia and LSCs [leukaemia stem cells] with no toxicity toward normal cells".

 

Conclusion

This study has identified a compound that may lead to a new drug for treating acute myeloid leukaemia. As the research has only so far been conducted in a laboratory setting, it should be stressed that this is the beginning of a long road in drug development and may not necessarily lead to a successful treatment.

It is also important to note that the compound was extracted from the seed of the avocado and not from the flesh.

Current treatments for leukaemias involve chemotherapy and in some cases stem cell transplants.

Stem cell transplants offer the chance of a cure. People aged between 16 and 30 can join the stem cell register, managed by the Anthony Nolan charity, and if you are a match for a patient, you could save their life. Most people can donate stem cells via their blood, a process similar to donating blood itself. This is known as peripheral blood stem cell collection and is both painless and extremely safe.  

Links To The Headlines

Avocados could hold the key to helping beat rare form of leukaemia. The Independent, June 16 2015

How avocado could help fight CANCER: Fat from the fruit 'targets leukaemia cells and stops them growing' - raising hopes for a new drug. Mail Online, June 16 2015

Links To Science

Lee EA, Angka L, Rota SG, et al. Targeting Mitochondria with Avocatin B Induces Selective Leukemia Cell Death. Cancer Research. Published online June 15 2015

Categories: NHS Choices

Four out of ten Brits may naturally show fewer flu symptoms

NHS Choices - Behind the Headlines - Tue, 16/06/2015 - 14:00

Thinking of throwing a sicky? Your usual alibi might be a little less convincing after today’s report by The Independent that "Four in 10 Britons immune to flu symptoms, leading to hopes of a new vaccine".

A survey of 1,414 people found that 43% of them had a type of immune cell – T cells – that partially protects against the symptoms of a flu infection.

Researchers found that T cells target specific parts of the flu virus machinery, called nucleoprotein. So the lucky 43% had less flu symptoms after becoming infected.

The logic is that if people have fewer symptoms, they are less likely to spread the virus through coughs and sneezes, and this may slow the spread of both seasonal and pandemic flu strains, such as swine flu. The logic is plausible, but was not directly tested in this study.

The research team suggested vaccines that boost T cell numbers might be worth exploring as an alternative to those that try to stop flu virus infection altogether.

An added potential benefit of their finding was that protection from symptoms of one virus strain showed similar signs in another. That said, only two virus types were tested, so we don’t know whether this "cross-reactivity" is widespread.

We know coughs and sneezes spread diseases, but do you know what to do about it? Read how to prevent flu

 

Where did the story come from?

The study was led by researchers from University College London and was funded by a large range of charity, government and university sources, including the Medical Research Council, the British Heart Foundation and Cancer Research UK. 

The study was published in the peer-reviewed American Journal of Respiratory and Critical Care Medicine.

Generally, the UK media reported the story accurately. Hope of a new vaccine was widely discussed by the media. This was not investigated in the study, so remains speculative at this stage.

 

What kind of research was this?

This was a cohort study looking to understand naturally existing resistance to the symptoms of flu in the hope the knowledge might one day be useful in lessening the spread of seasonal and pandemic flu.

The study authors say that a high proportion of flu (influenza) infections do not cause flu symptoms like coughing and sneezing – which is the main way the virus spreads from person to person.

Animal, human and observational studies suggest T cells, part of the immune system, are involved in lessening flu symptoms in some people, but the impact of this at a population level is not known.

The T cells are thought to target an important part of the flu virus machinery called nucleoprotein. Nucleoprotein exists across many strains of flu virus, so T cell-linked immunity against this key part of the virus may help to confer protection from symptoms for a wide range of different strains. If true, the hope is this might be harnessed to form a more effective vaccine and limit the spread of both seasonal and pandemic flu through coughs and sneezes.

 

What did the research involve?

The researchers measured flu-specific T-cells in an English population cohort during seasonal and pandemic periods between 2006 and 2010.

A total of 1,414 unvaccinated individuals had T cell measurements. They were part of a "Flu Watch Study". The study recruited successive groups each year via random selection of households from general practice registers across England.

Blood samples were taken prior to the natural circulation of flu virus to measure baseline antibody and T cell responses. Participants were then followed up intensively over the flu season to determine who got ill with flu. This involved weekly follow-up from late autumn to late spring, using automated telephone calls or emails.

Nasal swabs were also taken and analysed in the laboratory to confirm flu infection.

 

What were the basic results?

The study found people with T cells targeting flu virus nucleoprotein before exposure to the virus generally had less symptomatic disease (odds ratio, 0.27; 95% confidence interval, 0.11 to 0.68) during pandemic and seasonal periods.

They found T cells reacting to a specific flu virus (H3N2) also reacted to a different one (H1N1).

Influenza-specific T cell responses were detected in 43% of people, indicating a lot of people carried some level of immunity that showed lesser symptoms.

This link was independent of baseline antibodies. The antibodies actually help prevent flu infection, whereas the T cells are involved in lessening symptoms. So this confirmed people were still getting infected, but symptoms were varying in line with T cell characteristics.

 

How did the researchers interpret the results?

"Naturally occurring cross-protective T cell immunity protects against symptomatic PCR-confirmed disease in those with evidence of infection and helps to explain why many infections do not cause symptoms. Vaccines stimulating T cells may provide important cross-protective immunity."

 

Conclusion

A study of 1,414 unvaccinated people showed those with T cells targeting virus nucleoprotein still got infected by flu, but had fewer symptoms. The logic is that people with fewer symptoms are less likely to spread the virus through coughs and sneezes, which may slow the spread of both seasonal and pandemic flu strains.

This is plausible, but was not directly tested in this study, so we don't know if it's true in real life. The research team suggested vaccines that boost T cell numbers might be worth exploring, as an alternative to those that try to stop virus infection altogether. An added potential benefit of their finding was that lessened symptoms in one virus strain showed similar signs in another.

That said, only two virus types were tested, so we don't know whether this "cross-reactivity" is more widespread.

The findings suggest around 43% of people had some form of this natural immunity, but it's not clear if this is across a broad range of flu viruses or just a couple.

The study is encouraging, but is in its early stages of understanding, raising as many questions as it answers. For example:

  • Is it possible to boost this natural symptom immunity in those that have it?
  • How common is this natural immunity in the public?
  • Is it possible to transfer this symptom immunity to those that don’t have it?
  • How useful is this at preventing new cases of flu or deaths from flu?

If you are particularly vulnerable to the effects of a flu infection due to factors such as having a chronic disease or being aged 65 or over, then you should take advantage of the seasonal flu vaccine. Read more about who should get the “flu jab”

Links To The Headlines

Four in 10 Britons immune to flu symptoms, leading to hopes of a new vaccine. The Independent, June 16 2015

Half 'have natural flu protection'. BBC News, June 15 2015

Never had flu? That's because half of us are immune to its symptoms: Findings raise prospect of jab to reduce severity of all types of the illness. Mail Online, June 16 2015

New flu jab could prevent future pandemics. The Times, June 16 2015

Four in 10 Brits immune to flu symptoms raising hopes of new vaccine. The Daily Telegraph, June 15 2015

Links To Science

Hayward AC, Wang L, Goonetilleke N, et al. Natural T Cell-mediated Protection against Seasonal and Pandemic Influenza. Results of the Flu Watch Cohort Study. American Journal of Respiratory and Critical Care Medicine. Published online June 15 2015

Categories: NHS Choices

Eating chocolate may slightly lower your risk of stroke

NHS Choices - Behind the Headlines - Tue, 16/06/2015 - 12:00

“Two chocolate bars a day can SLASH the risk of heart disease and stroke,” the Daily Mirror reports.

The headline is prompted by the results from a large study involving Norfolk residents, investigating how chocolate is linked to cardiovascular diseases. These are diseases that affect the heart and blood vessels, such as coronary heart disease and stroke.

By comparing the highest chocolate consumers with complete chocolate abstainers, they found that chocolate was linked to a lower risk of stroke and cardiovascular disease. However, the risk for coronary heart disease was not statistically significant, so the aforementioned results could have been down to chance.

The biggest caution in taking these results at face value is the possibility that some of the benefits linked to chocolate are actually linked to the person being generally healthier overall.

There were signs of this in the study. For example, the researchers found that higher chocolate consumption was linked to some healthy qualities and behaviours, such as being more physically active.

It is also important not to overlook the large amounts of fat and sugar in chocolate that can contribute to weight gain. If you are overweight or obese, by definition, your weight is probably damaging your health and eating lots of chocolate will make the problem worse.

Read more about how to maintain a healthy weight

 

Where did the story come from?

The study was carried out by researchers from the University of Aberdeen and was funded by the Medical Research Council and Cancer Research UK.

The study was published in the peer-reviewed medical journal Heart.

The story was very widely reported by the UK media. Generally, the study facts were reported accurately, but the wider implications and inherent limitations of the study were not fully explained. For example, most coverage correctly said that study participants reporting higher chocolate consumption were generally healthier in many other ways, but did not explain how this makes it particularly hard to attribute any health benefits to chocolate on its own.

BBC News provided a useful quote from an independent expert, Dr Tim Chico: "The message I take from this study is that if you are a healthy weight, then eating chocolate (in moderation) does not detectably increase risk of heart disease and may even have some benefit. I would not advise my patients to increase their chocolate intake based on this research, particularly if they are overweight."

 

What kind of research was this?

This was a prospective cohort study looking at the effect of eating chocolate on cardiovascular disease.

Cardiovascular disease is a general term that describes a disease of the heart or blood vessels, and is one of the UK's largest causes of death.

There are four main types of cardiovascular disease. They are:

  • coronary heart disease – when the flow of oxygen-rich blood to the heart is blocked
  • stroke – when blood supply to the brain is blocked
  • peripheral arterial disease – when bloodflow to your limbs, usually your legs, are blocked
  • aortic disease – problems with the aorta, the largest blood vessel in the body, which takes blood from your heart to the rest of your body, which may need to be treated with an aortic valve replacement

Chocolate, more so the dark variety, contains flavonoids. These are plant chemicals that have antioxidant properties, that many speculate give it health-promoting properties, including keeping hearts and blood vessels healthy.

Small experimental and observational studies, the Aberdeen researchers report, indicate that chocolate might be good for heart and blood vessel health, but the picture is not clear, as these studies have design limitations. This research group wanted to use a large group of people, tracked over a long period of time, to improve the evidence base and better understand if chocolate might be affecting cardiovascular disease risk in real life.

 

What did the research involve?

The researchers analysed data from a cohort study, which assessed chocolate consumption at baseline and then followed people over an average of 11 years to see who developed cardiovascular disease. They then supplemented this research with a systematic review and meta-analysis of literature.

Researchers analysed data from 20,951 adult men and women taking part in the EPIC-Norfolk study, a large UK-based cohort study started in the 1990s to look at the connection between diet, lifestyle factors and disease. Average chocolate intake was measured once at the start of the study, before people were tracked over decades, to see if they developed or died from cardiovascular disease. The main analysis looked at how chocolate consumption affected the risk of developing or dying from cardiovascular disease, taking into account a range of other known risk factors, like smoking and alcohol consumption.

EPIC-Norfolk cohort participants are men and women who were aged between 40 and 79 when they joined the study, and who lived in Norwich and the surrounding towns and rural areas. They have been contributing information about their diet, lifestyle and health through questionnaires and health checks over two decades.

Chocolate consumption was measured at a single point in time at the start of the study (1993 to 1997). They were asked to indicate which foods they ate from a large list and how often.

Three questions from the food questionnaire related to chocolate consumption:

  • “Chocolates singles or squares” (average portion size of 8g)
  • “Chocolate snack bars – for example, Mars, Crunchie” (average portion size of 50g)
  • “Cocoa, hot chocolate (cup)” (average portion size of 12g powder weight; the liquid to make up the beverage was not included)

Frequency categories were multiplied by the portion size to get the amount of chocolate eaten daily (g/day). The sum of the weights of these food items consumed, rather than their flavonoid or cocoa content, were the important measure in this study. 

This average daily chocolate consumption was divided into five equal groups, from highest consumption to lowest. The lowest group didn’t eat or drink any chocolate at all and acted as the comparison group.

After the food questionnaire, participants were tracked for a mean average of 11.3 years to see if they developed or died from cardiovascular disease, coronary heart disease or stroke.

Both admission to hospital and deaths due to these conditions were included in the analysis.

After some people were excluded because of missing data, extreme chocolate intake (thought to be an error), or pre-existing cardiovascular disease, it left 20,951 people for the analysis.

The analysis adjusted for a range of common confounders associated with cardiovascular disease, including:

  • gender
  • age
  • smoking
  • physical activity
  • energy intake
  • alcohol
  • body mass index (BMI)
  • systolic blood pressure
  • LDL cholesterol (bad cholesterol)
  • HDL cholesterol (good cholesterol)
  • having diabetes
  • C-reactive protein – a protein associated with inflammation inside the body

To supplement the EPIC-Norfolk-derived results, the researchers also carried out a systematic review and meta-analysis of research related to chocolate and cardiovascular disease.

 

What were the basic results?EPIC

Higher chocolate consumption was associated with lower age, more physical activity and lower prevalence of diabetes mellitus.

Higher chocolate consumption was more common in men and among smokers. Higher chocolate intake was associated with a higher energy intake, with lower contributions from protein and alcohol sources, and higher contribution from fat and carbohydrates.

The percentage of participants with coronary heart disease in the highest and lowest fifth of chocolate consumption was 9.7% and 13.8%, and the respective rates for stroke were 3.1% and 5.4%.

The confounder-adjusted risk of coronary heart disease was 9% less for those in the top quintile of chocolate consumption (16 to 99g/ day) compared with those not consuming chocolate (hazard ratio (HR) 0.91, 95% confidence interval (CI) 0.80 to 1.04). The confidence interval spans 1, meaning this result could be due to chance alone.

By contrast, chocolate consumption in the highest consuming group was associated with significantly less risk for stroke (HR 0.78, 95% CI 0.63 to 0.98) and cardiovascular disease (defined as the sum of coronary heart disease and stroke, HR 0.89, 95% CI 0.79 to 1.00) compared with chocolate abstainers.

Systematic review

The systematic review and meta-analysis included eight studies (seven cohort studies, one randomised control trial). These were combined with results from the EPIC-Norfolk study to get pooled results (total 157,809 participants).

The studies measured chocolate consumption in different ways, adjusted for different confounders, and measured different health outcomes related to cardiovascular disease. Consequently, only similar studies were combined in meta-analyses.

Overall, the different meta-analysis showed that:

  • chocolate consumption was linked with significantly lower risk of coronary heart disease across five studies (pooled relative risk (RR) 0.71, 95% CI 0.56 to 0.92)
  • the risk of coronary heart disease mortality from one study showed no significant difference with and without chocolate consumption (RR 0.98, 95% CI 0.88 to 1.10).
  • for risk of stroke with chocolate consumption, there was significantly lower risk of both stroke incidence (pooled RR 0.79, 95% CI 0.70 to 0.87; five studies) and mortality (RR 0.85, 95% CI 0.74 to 0.98; one study)
  • there was a lower risk of any cardiovascular event (pooled RR 0.75, 95% CI 0.54 to 1.05, two studies, not statistically significant) and cardiovascular mortality (pooled RR 0.55, 95% CI 0.36 to 0.83; three studies, statistically significant)

 

How did the researchers interpret the results?

The research authors said: “Cumulative evidence suggests that higher chocolate intake is associated with a lower risk of future cardiovascular events, although residual confounding cannot be excluded. There does not appear to be any evidence to say that chocolate should be avoided in those who are concerned about cardiovascular risk”.

 

Conclusion

This study used a large prospective cohort of English residents to estimate the risk chocolate poses to cardiovascular death and disease. In addition, they systematically combed the research literature for other similar studies, combining their results with that of other researchers.

By comparing the highest chocolate consumers with chocolate abstainers, they found that chocolate was linked to a lower risk of stroke and cardiovascular disease. The risk for coronary heart disease was not statistically significant.

Results from the meta-analysis of eight additional studies showed higher chocolate consumption was linked with lower risk of cardiovascular disease, stroke and death from cardiovascular disease. Two studies showed cardiovascular events were not statistically linked with chocolate consumption.

The biggest reservation for believing these results is the possible role of residual confounding, rightly highlighted by the study authors themselves. In the cohort study part, chocolate consumption was linked to a range of healthy qualities and behaviours, such as lower blood pressure and more physical activity. There is a real possibility that some of the benefits linked to chocolate are actually linked to the person being generally healthier in other ways.

The researchers did their best to account for this using standard statistical techniques, but the possibility remains.

This is just one explanation. Another is that the flavonoids in chocolate do benefit heart and blood vessel health. Although plausible, this study cannot prove this. There are far too many other elements in the mix to pinpoint the risk reduction observed for chocolate.

The study has a number of other smaller limitations that make its results a little less reliable. Chocolate consumption was measured at a single point in time at the start of the study. This does not take account of changes in chocolate consumption over the following decades. Chocolate consumption was measured without consideration of the flavonoid content. Not all chocolate contains the same amount of flavonoids – thought to be the potential disease-preventing ingredient – so lumping them together could have clouded the picture.

Overall, though the message seems to be that if you are generally healthy, eating a little chocolate probably won’t do any harm, and may in fact do some good, this is not actually proven in this study.

The issue arises when chocolate affects your weight. We know that chocolate is high in sugar and fat, both of which can contribute to weight gain. Being overweight or obese is bad for your health, including your heart and blood vessels. 

Links To The Headlines

Two chocolate bars a day can SLASH the risk of heart disease and stroke. Daily Mirror, June 16 2015

More evidence that chocolate may be good for the heart, say researchers. The Guardian, June 16 2015

Eating two chocolate bars A DAY 'cuts your risk of heart attack and stroke by up to 25%' - and milk is just as good as dark. Mail Online, June 16 2015

Study Links Chocolate To Lower Risk Of Stroke. Sky News, June 16 2015

Two bars of chocolate a day 'lowers risk of stroke and heart disease'. The Daily Telegraph, June 16 2015

Link between eating chocolate and lowered stroke risk. ITV News, June 16 2015

Links To Science

Kwok CS, Boekholdt SM, Lentjes MAH, et al. Habitual chocolate consumption and risk of cardiovascular disease among healthy men and women. Heart. Published online June 15 2015

Categories: NHS Choices

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