"Reducing the portion sizes … would help reverse the obesity epidemic, say researchers," BBC News reports.
The researchers, who pooled the results of more than 70 previous studies, found a link between portion size and overeating.
Researchers found that increased portion size, packaging and the size of a plate led to people choosing larger amounts of food and eating more. It may be that the old saying "you have eyes bigger than your belly" rings true for some people. They eat what they are given, not what they need.
People also drank more when non-alcoholic drinks were provided in shorter, wider glasses and bottles than tall, thin ones. The researchers say that although the results were not surprising, they lend weight to the argument for portion sizes to be decreased to help reduce the UK's obesity epidemic.
It should be noted that the quality of the individual studies was rated as poor by the researchers, and most of the studies were conducted in the US, where portion sizes are infamously large.
The studies also did not look at whether people were able to reduce their intake over the long term through smaller portion sizes.
These limitations aside, it would seem a sensible option to choose a smaller portion if you are trying to achieve or maintain a healthy weight. Making sure you get your five portions of fruit and vegetables a day and increasing physical activity levels will also help.
Where did the story come from?
The study was carried out by researchers from the University of Cambridge, the University of Oxford, MRC Human Nutrition Research, the University of Plymouth and the University of Bristol. It was funded by the UK Department of Health Policy Research Programme.
The study was published in the peer-reviewed online medical resource The Cochrane Database of Systematic Reviews. As with all Cochrane studies, the research has been made available on an open-access basis, so it is free to read online.
The UK media reported the findings accurately and supported the notion that portion sizes have been increasing, which may be contributing to increasing obesity levels.
The Independent provided helpful expert commentary from one of the lead authors, Dr Gareth Hollands, that "helping people to avoid 'overserving' themselves or others with larger portions of food or drink by reducing their size, availability and appeal in shops, restaurants and in the home, is likely to be a good way of helping lots of people to reduce their risk of overeating".
What kind of research was this?
This was a systematic review of studies that have looked at the effect of different portion sizes on the consumption of food, alcohol or tobacco. The researchers pooled the results together in a meta-analysis.
Although this type of research brings together all of the evidence available for a topic, the results are reliant on the quality of the individual trials.
In this case, only randomised controlled trials were included, either comparing consumption between two groups or in individuals in crossover studies. However, despite this type of study design being the "gold standard", the researchers judged the studies to be at high or unclear risk of bias, so they say the overall evidence is of moderate to very low quality.
What did the research involve?
The study searched 12 medical databases and trial registries for relevant studies up to July 2013. Randomised controlled trials were included in the analysis if they compared the amount of food, alcohol or tobacco consumed or chosen, according to different portion:
- crockery dimensions
Standard Cochrane techniques were used for the search strategy in applying inclusion and exclusion criteria consistently across the identified search results, and when performing the statistical analyses.
What were the basic results?
There were 72 studies that met the inclusion criteria; 69 assessed food portion size and three looked at cigarette size. No studies were identified that assessed alcohol portion size.
Exposure to larger food portions, packaging or crockery size was associated with moderately increased food consumption for adults and children (standardised mean difference (SMD) 0.38, 95% confidence interval (CI) 0.29 to 0.46).
The researchers estimated that if smaller portion sizes were used consistently across meals, the average daily calorie consumption could reduce by 144 to 228 calories per day. This would be equivalent to 4,032 to 6,384 less calories per month, which would equal a weight loss of one to two pounds (0.45kg to 0.9kg) if everything else stayed the same.
A meta-analyses of 13 studies found that increased portion or crockery size led to adults selecting a greater amount of food (SMD 0.55, 95% CI 0.35 to 0.75). This was not found in studies on children.
There was low-quality evidence from three studies that shorter, wider glasses or bottles compared to thin, tall glasses increased the amount of non-alcoholic drinks selection (SMD 1.47, 95% CI 0.52 to 2.43).
Only one study looked at consumption of non-alcoholic drinks, which found that young adults drank more water if using shorter, wider bottles, but this was judged as very low-quality evidence (SMD 1.17, 95% CI 0.57 to 1.78).
Meta-analyses of the three studies on cigarette size found low-quality evidence that the length of cigarette did not influence the amount consumed. No studies were identified that looked at the effect of differently sized packs, such as packs of 10 cigarettes compared to packs of 20.
How did the researchers interpret the results?
The researchers concluded that, "people consistently consume more food and drink when offered larger-sized portions, packages or tableware than when offered smaller-sized versions".
They say this "suggests that policies and practices that successfully reduce the size, availability and appeal of larger-sized portions, packages, individual units and tableware can contribute to meaningful reductions in the quantities of food (including non-alcoholic beverages) people select and consume in the immediate and short term".
There was insufficient evidence for them to make recommendations for tobacco or alcohol portion sizes.
This systematic review and meta-analysis suggests that increased portion sizes, packaging and crockery influences the amount people choose to eat and actually consume.
The methods used to produce this review are robust; however, all 72 identified studies were assessed as being at high risk of bias or of unclear risk. This reduces confidence in the results. Other limitations include:
- the majority of studies were conducted in the US, so the results may not be directly applicable to the UK, because of the potential differences in portion sizes
- most studies were not conducted on people who were trying to lose weight, so it is not clear how effective this strategy would be for weight loss
- the studies included only assessed food consumption or selection at one time point, or over short time periods. This means that the studies did not look at whether eating more at one meal was compensated for at subsequent meals that day
- the studies were performed in controlled environments such as a laboratory, so it remains unclear what effect portion size may have in "normal" environments over the long term
Overall, common sense tells us that people are likely to eat more if the portion size is bigger for a variety of potential reasons, such as:
- social norms – someone has decided the portion size is appropriate, which may challenge internal perceptions.
- there is a delay in the time it takes to feel full (satiety) than the time it takes to consume the food in front of you
- people may not want to waste food and are taught from an early age to "finish your plate"
Reducing portion size or the size of the plate the food is presented on is not a new concept for weight loss – it is a strategy employed by many diet regimes. Other strategies to help maintain a healthy diet can be found in the healthy eating pages.
Links To The Headlines
Portion size key in tackling obesity, says study. BBC News, September 15 2015
Serving food on a larger plate 'makes people eat more'. The Independent, September 15 2015
End to supersizing could reverse obesity trend. The Daily Telegraph, September 15 2015
Links To Science
Hollands GJ, Shemilt I, Marteau TM, et al. Portion, package or tableware size for changing selection and consumption of food, alcohol and tobacco. Cochrane Database of Systematic Reviews. Published online September 14 2015
"Trans fat ban could save 7,200 lives by 2020, says study," The Guardian reports. This is the conclusion of a new modelling study looking at whether banning trans fatty acids – associated with "bad" cholesterol and heart disease – would improve public health outcomes.
Trans fats make up around 0.8% of the estimated energy consumption of the average UK diet. There are two types of trans fat: naturally occurring trans fatty acids found at low levels in meat and dairy products, and artificially made trans fatty acids labelled as hydrogenated fats or oils in some processed foods.
The artificial type became a popular ingredient for the food industry as they help prolong shelf-life while also improving taste. But research has shown a link between trans fats and heart disease. This led to several countries banning the use of artificial trans fats in food products.
In the UK there is no ban, but in 2012 most supermarkets and the bigger fast food chains agreed to sign up to a voluntary agreement not to use artificial trans fats. It is unclear how many products still contain trans fats.
The researchers calculated how many deaths they think could be avoided if a total ban was imposed, and what savings could be made in health and other costs.
While the figures are interesting, they are all based on assumptions fed into a mathematical model. It's hard to know how accurate these predictions are.Where did the story come from?
The study was carried out by researchers from the University of Lancaster, the University of Liverpool and the University of Oxford, and was funded by the National Institute for Health Research.
Most of the UK media covered the study accurately, although few questions were asked about how the figure of 7,200 prevented deaths had been reached.
Oddly, the Daily Mirror claimed a ban on trans fats "could prevent at least 10,000 deaths". They appear to have added a calculated 3,000 reduction in unequal deaths to the total 7,200 deaths prevented, when actually the 3,000 figure is part of the 7,200.What kind of research was this?
This was an epidemiological modelling study, which means it used data gathered about populations to create mathematical models to estimate the effect of possible changes in policy.
This type of study is a useful way to calculate the possible future effect of change, but it cannot be seen as a precise prediction of exactly what will happen.What did the research involve?
Researchers used several big data sets and the results of previous studies to construct mathematical models about the possible effects of three policies over the next five years:
- banning trans fats
- improving labelling of food containing trans fats
- banning trans fats only from restaurant and fast food outlets
They then calculated the effects in terms of deaths avoided or delayed, healthcare costs, costs to the economy, and the effect on health inequalities.
The researchers used the findings of a 2006 meta-analysis, which estimated the effect of how many trans fats we eat as a proportion of total energy intake. The meta-analysis found there are 23% more new cases of heart disease for every 2% of total energy that comes from trans fats.
The researchers then combined this figure with information from questionnaires from the National Diet and Nutrition Survey (an ongoing government project to monitor dietary trends) to find out what proportion of people's diets consisted of trans fats.
They also used data about the socioeconomic status of people in England, which assigned people into five groups depending on their wealth and levels of deprivation.
They used a mathematical model to calculate the different effect various policies might have on these groups – for example, people in the lowest socioeconomic group eat the most trans fats as percentage of diet, so any policy that affected this group more would have a bigger effect on health overall.
The researchers made assumptions for their models. For example, they assumed changing labelling would have a bigger effect on people in higher socioeconomic groups than on lower groups, and people from lower socioeconomic groups were more likely to eat at fast food outlets and less likely to eat at restaurants.
They did multiple calculations using this data to work out the possible reduction in deaths from heart disease, the savings to the taxpayer, the effect on health inequalities, and the savings to the economy overall.What were the basic results?
The researchers calculated an outright ban on the use of trans fats in food products would cut the amount of trans fats eaten by half, from 0.8% to 0.4% of total energy – the remainder would be the amount still consumed from naturally occurring trans fats in meat and dairy.
Their models found improved labelling or bans in restaurants and fast food outlets would, at best, achieve half that reduction, lowering trans fat consumption to around 0.6% of total energy.
They say most of the benefit from improved labelling or restaurant bans in terms of trans fat reduction would be seen among higher socioeconomic groups, so the policies would widen health inequalities.
In contrast, they say a total ban would affect lower socioeconomic groups more because they eat more trans fats, so it would narrow health inequalities. The researchers suggest the "gap" between the numbers of people from upper and lower groups who died of heart disease would narrow by about 3,000 people with a total ban.
They used the figures from the previous analysis to calculate the effect of this reduction in trans fat in the diet. They assumed deaths from heart disease would fall at the same rate as numbers of new cases of heart disease, giving a total figure of 7,200 deaths delayed or avoided over five years from a total ban (95% confidence interval [CI] 3,200 to 12,500).
They said improved labelling or restaurant bans might delay or avoid 1,800 to 3,500 deaths, depending on the model used. They claim a total ban would save £297 million (95% CI £131 to £466 million). These savings mainly represent savings in "informal care" – the care given to people with heart disease by friends and family.
They also included productivity at work and healthcare costs. Estimated direct healthcare savings are relatively small, at around £42 million, while estimated informal care savings are £196 million.How did the researchers interpret the results?
The researchers say their findings show that, "elimination of trans fatty acids from processed foods is an achievable target" and "would lead to health benefits at least twice as large as other policy options".
They warn trans fats "could creep back into processed foods" if action is not taken now to ban them completely.Conclusion
Trans fats are already at low levels in the UK diet compared with 10 or 20 years ago. However, this study suggests lowering them even further could reduce the number of people getting and dying from heart disease over the next five years.
This study does have limitations, however, which means we cannot rely on the findings to be precise. Any study that uses a mathematical model relies on the researchers making correct assumptions when they feed in the data.
The researchers say they have had to make assumptions based on little data in some cases. For example, there is no information about what proportion of the diet is made up of trans fats for those in the top socioeconomic class. We also don't know what proportion of trans fats are consumed in restaurants or fast food outlets.
More importantly, it is possible reducing consumption of trans fats will not have the effect on heart disease the researchers think it will. They used a study from 2006 that combined the results of previous trials to come up with their figure. But this study's finding that trans fats are linked to an increased chance of heart disease does not automatically mean reducing trans fats will reduce the chance of heart disease by the same amount.
However, it does seem likely reducing trans fats will reduce the numbers of people getting heart disease and dying from it. Whether or not banning trans fats will have exactly the effect the researchers predict is less certain.
Links To The Headlines
Trans fat ban could save 7,200 lives by 2020, says study. The Guardian, September 15 2015
Ban on trans fats in processed food could save 7,000 lives over the next five years. Daily Mail, September 16 2015
Banning trans fats in Britain would save lives, research suggests. The Daily Telegraph, September 16 2015
Banning trans fats could prevent 7,000 deaths from heart disease over next five years, claim experts. The Independent, September 15 2015
Banning trans fats could prevent at least 10,000 deaths in the UK over 5 years. Daily Mirror, September 16 2015
Links To Science
Allen K, Pearson-Stuttard J, Hooton W, et al. Potential of trans fats policies to reduce socioeconomic inequalities in mortality from coronary heart disease in England: cost effectiveness modelling study. BMJ. Published online September 15 2015
"England's richest people 'live eight years longer than the country's poorest'," The Independent reports.
A major new study has found a significant difference in life expectancy of the richer South East England compared to the poorer North.
The researchers found that overall life expectancy increased by more than five years from 1990 to 2013, from 75.9 to 81.3 years. The gap in mortality between men and women has also decreased, which is encouraging.
However, more deprived areas have failed to catch up with less deprived areas, with a difference of more than eight years. Areas of deprivation were mainly located in the North, the Midlands and some areas of London.
There is also evidence that, while there has been an overall decline in mortality, there has been less of a reduction in the length of time people are living in poor health with chronic illness or disability.
The study has shown where improvements have been made and areas that would benefit from more attention. Many of the leading causes of death are preventable through an active and healthy lifestyle and a good diet.Where did the story come from?
The study was carried out by researchers from a number of institutions, including Public Health England and the London School of Hygiene and Tropical Medicine.
Funding was primarily provided by the Bill & Melinda Gates Foundation. Additional funding for the study was provided by Public Health England.
The study has been widely reported in the UK media. Reporting of the study was accurate for all sources.
What kind of research was this?
This study used data from the Global Burden of Disease (GBD) 2013 study to analyse the burden of diseases and injuries in England, by region and within each region by level of deprivation. GBD is an ongoing global collaboration looking at trends in diseases that can cause death or disability.
Researchers compared this data with earlier years, going back to 1990. This method is able to look at large amounts of data for a long period to draw overall patterns and conclusions. However, it cannot provide definite answers as to why mortality or illness rates are as they currently stand, or why they have changed.
What did the research involve?
This study used data from the GBD 2013 study on causes of death, disease, and injury incidence and prevalence, as well as years lived with disability (YLDs) and disability-adjusted life-years (DALYs). DALYs is a term used by epidemiologists to measure the number of "healthy years" lost due to ill health, disability or early death.
Researchers looked at the following countries:
- The first 15 EU members (excluding the UK)
The GBD 2013 study also provides independent and overlapping attributable risk for five tiers of risk factors:
- All GBD risks combined.
- Three large categories of metabolic, behavioural, and environmental and occupational risks.
- Single risks, such as high blood pressure, and risk clusters, such as child and maternal under-nutrition or air pollution.
- Single risks within such clusters, such as vitamin A deficiency or household air pollution.
- Individual occupational exposure to cancer-causing substances or the division of childhood underweight into stunting, underweight and wasting.
The Index of Multiple Deprivation (IMD-2010) was used to measure deprivation. This is a government study that aimed to assess levels of deprivation in areas of the UK.
Mortality data for the period 1990 to 2012 was obtained from the Office for National Statistics and split into regional and deprivations groups based on postcode.
What were the basic results?
The study found that from 1990 to 2013, life expectancy from birth in England increased by 5.4 years (95% confidence interval [CI] 5.0 to 5.8) from 75.9 years (95% CI 75.9 to 76.0) to 81.3 years (95% CI 80.9 to 81.7). A greater improvement in life expectancy gains was seen for men than for women.
Rates of age-standardised years of life lost (YLLs) reduced by 41.1%, which indicates a greater reduction in premature mortality compared with overall mortality. A small decrease was seen for age-standardised YLDs. DALYs were reduced by 23.8%.
The range in life expectancy across deprivation areas has stayed the same for men since 1990 – an 8.2 year difference between the least and most deprived areas. However, for women, the deprivation differences decreased from 7.2 years in 1990 to 6.9 years in 2013. In 2013, the leading cause of YLLs was heart disease, and the leading cause of DALYs was low back and neck pain. Leading behavioural risk factors were suboptimal diet and tobacco.
Overall, England ranked better than the other UK countries and was found to be the EU country with one of the largest gains in life expectancy among men (6.4 years). This is less than Luxembourg, but the same as Finland.
All English regions except for South West England, gained at least six years, which is equal to or greater than all comparator countries except Austria, Finland, Ireland, Germany and Luxembourg.
Among women, the increase in life expectancy in England overall was 4.4 years, which is equal to or in excess of all countries except Finland, Germany, Ireland, Luxembourg and Portugal.
How did the researchers interpret the results?
The researchers conclude that, "Health in England is improving, although substantial opportunities exist for further reductions in the burden of preventable disease. The gap in mortality rates between men and women has reduced, but marked health inequalities between the least deprived and most deprived areas remain".
They go on to say that policies must address the causes of ill health and premature mortality. Action is needed to reduce risk exposures, support healthy behaviours, alleviate the severity of chronic disabling disorders, and mitigate the effects of socioeconomic deprivation.
This study used data to analyse the burden of disease and injury in England, and within each English region by level of deprivation. This was compared with the remaining constituent countries of the UK and with other comparable countries.
The researchers found an overall increase in life expectancy from 1990 to 2013. The decreased mortality gap between men and women is also encouraging. However, the inequality of life expectancy across regions of England has not improved. Those in more deprived areas have not yet reached the life expectancy of the less deprived in 1990.
Despite the overall decline in mortality, this has not been matched by a similar decline in the number of years people are living in poor health or with chronic illness.
The authors suggest the main reasons for improvement in life expectancy are reductions in:
- cardiovascular disease
- cancer mortality
- chronic respiratory disease
- road injuries
However, they report that conditions still having a negative impact on life expectancy include:
- cirrhosis of the liver (related to alcoholic liver disease)
- mental disorders
- substance use
Strengths of this study are the large amount of population data used and the long follow-up period. Some limitations are that data was not available for some diseases or by specific deprivation level. The relative level of deprivation of an area may also have changed since the measurement tool was created, and the cross-country comparisons may not be as straightforward as presented.
The findings have indicated areas where improvement has been made and possible areas that would benefit from more attention.
Though not all diseases are preventable, poor health can be caused by risk factors such as poor diet, low levels of physical activity, smoking and alcohol consumption.
Links To The Headlines
Life Expectancy in the UK: England's richest people 'live eight years longer than the country's poorest'. The Independent, September 15 2015
English life expectancy catches up with the west but poorest lag behind. The Guardian, September 15 2015
Huge increase in life expectancy: Britons now live average of 5.4 years longer than in 1990 - but only if they are wealthy. Mail Online, September 15 2015
Average life expectancy in England rises to 81 years but north-south divide remains. ITV News, September 15 2015
Where In England Do People Live The Longest? Sky News, September 15 2015
Links To Science
Newton JN, Briggs ADM, Murray CJL, et al. Changes in health in England, with analysis by English regions and areas of deprivation, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013. The Lancet. Published online September 14 2015
"People who use marijuana may be more likely to develop pre-diabetes than those who have never smoked it," The Independent reports, after a US study found a link between long-term cannabis use and pre-diabetes.
Pre-diabetes is defined as having abnormally high blood sugar levels, but not high enough to meet criteria for diagnosis of type 2 diabetes.
The study enrolled around 3,000 healthy young US adults in the mid-1980s. Over the following years, researchers carried out regular medical assessments and questioned participants about their use of cannabis and other substances.
Cannabis use at the 25-year assessment, when the person was now in middle age, was associated with an increased risk of having pre-diabetes. However, there were no significant links between cannabis use and "full-blown" diabetes.
The main difficulty with this research is that the study design cannot prove direct cause and effect. Many other health and lifestyle factors could be linked to both cannabis use and diabetes risk, such as diet.
Cannabis is a notorious appetite stimulant – know as "the munchies", which often leads users to eat energy-rich, nutritiously poor snacks, such as crisps and sweets. If there is a link, it's possible that diet could be having an effect on diabetes risk, rather than cannabis itself.
The study was carried out by researchers from the University of Minnesota and the University of California, San Francisco. It received various sources of financial support, including from the US National Institutes of Health.
The Independent and the Mail Online's reporting of the study is accurate, although both articles could benefit from highlighting that this study cannot prove direct cause and effect.What kind of research was this?
This cohort study aimed to see whether cannabis use is associated with the presence or development of diabetes or pre-diabetes.
Pre-diabetes is when the person has blood glucose levels just below the threshold for meeting the criteria for diabetes. If the person doesn't make lifestyle changes, such as changing their diet, upping their physical activity and trying to lose weight, it can progress to type 2 diabetes.
Cannabis, or marijuana, has uncertain effects on a person's physical or mental health. In the US, where this study was based, it is the most frequently used illegal drug, with 18.9 million people over the age of 12 reportedly having used cannabis in 2012.
Recent studies have suggested that cannabis use may be associated with reduced odds of diabetes and other metabolic risk factors, such as a high body mass index (BMI) and waist circumference. The researchers report the possibility of bias with these studies, and the need for prospective studies to better examine these links.
In this study, researchers aimed to look at the link between self-reported cannabis use and the presence of diabetes or pre-diabetes (cross-sectional link) or the development of these conditions (prospective link).
The main limitation with this type of study is not being able to prove cannabis use has caused the diabetic conditions, as other factors may have had an influence – particularly with the cross-sectional association.What did the research involve?
This study involved participants of the Coronary Artery Risk Development in Young Adults (CARDIA) study. They were recruited from four urban areas in the US and aged 18 to 30 years at the time of enrolment in 1985-86.
At enrolment and each follow-up, the participants completed questionnaires and had clinical examinations, including blood tests and measurements of blood pressure and BMI. Questionnaires involved assessments of their health and lifestyle, including physical activity, alcohol, smoking and use of illegal substances.
The substance assessment asked specifically about the use of cannabis, crack or other cocaine, amphetamines or opiates in the person's lifetime or past 30 days, with frequency of once or twice, 3 to 9 times, 10 to 99 times, more than 100, or more than 500 times.
Pre-diabetes and diabetes were defined by blood glucose levels using American Diabetes Association criteria. For example, pre-diabetes was a fasting blood glucose of 5.6 to 6.9 millimole (mmol) per litre, and diabetes was a level of 7.0mmol per litre or greater.
The cross-sectional link between lifetime cannabis use and pre-diabetes or diabetes was assessed at the last follow-up assessment, around 25 years after enrolment.
The prospective link was examined between cannabis use seven years after enrolment and the later development of pre-diabetes or diabetes by year 25. The assessments included around 3,000 people.
When looking at the links between cannabis use and diabetes, the researchers took into account potential confounders – the use of other substances, smoking and alcohol, educational attainment, and examination findings, including BMI, blood pressure and cholesterol.What were the basic results?
Factors associated with cannabis use were being male, of white ethnicity, greater reported smoking, alcohol and other substance use, and greater physical activity.
Higher educational attainment and higher BMI were factors associated with less cannabis use. By the age of 24, 45% of the participants (1,193) had pre-diabetes and 357 had diabetes.
With full adjustment for all confounders, current use of cannabis was associated with about a two-thirds increased odds of pre-diabetes compared with never using the drug (hazard ratio [HR] 1.66, 95% confidence interval [CI] 1.15 to 2.38).
There were no significant links between pre-diabetes and former cannabis use. When broken down into frequency of use, there was a trend for increased lifetime use to be associated with an increased risk of pre-diabetes.
However, the only significant link was found for a lifetime use of 100 or more times being associated with a 40% increased risk of pre-diabetes (HR 1.40, 95% CI 1.13 to 1.72). There were no convincing links for a lower frequency use than this.
There was no statistically significant link between former, current or any lifetime use of cannabis and actual diabetes.How did the researchers interpret the results?
The researchers concluded that, "Marijuana [cannabis] use in young adulthood is associated with an increased risk of pre-diabetes by middle adulthood, but not with the development of diabetes by this age."Conclusion
This long-term study of healthy US adults found current cannabis use at the 25-year assessment – when the person had reached middle age – was associated with an increased likelihood of the person having pre-diabetes at this time.
Higher lifetime use of more than 100 times was also associated with an increased likelihood of pre-diabetes. However, there were no significant links between cannabis use and actual diabetes.
The main limitation of this study comes from the possibility of confounding. The researchers have attempted to take several confounders into account, including smoking and the use of alcohol and other substances.
However, various physical and mental health, lifestyle, personal and socioeconomic characteristics may be associated with both cannabis use and diabetes risk. For example, one possible factor that could be linked to both cannabis use and diabetes risk is poor diet.
Cannabis use can cause sudden and intense hunger pangs, nicknamed "the munchies". This can lead users to snack on foods with a high calorie and sugar content, but with little in the way of nutritional value. If maintained on a long-term basis, this type of diet can lead to obesity, which is a risk factor for type 2 diabetes.
This study is not able to account for the influence of all these factors, particularly as the main link was for the current use of cannabis at the 25-year assessment and pre-diabetes at the same time. This cannot prove that one thing has caused the other.
There was no link with type 2 diabetes itself. Pre-diabetes suggests the person may be on the border of developing diabetes, but they don't yet have the condition.
Another – admittedly unavoidable – limitation is that cannabis use was self-reported. This may be inaccurate, particularly when it comes to estimating the lifetime frequency of use. There is also the possibility when questioning people about their use of illegal substances that they may report never using them, when in fact they have.
This urban sample of US citizens may not be representative of everyone, particularly given they were enrolled 30 years ago. Patterns of cannabis use during the 80s and 90s may differ from use of the substance today. In particular, the strength of cannabis in terms of one of the active ingredients, tetrahydrocannabinol (THC), is thought to be much stronger than in the past.
The various possible effects of cannabis on physical and mental health – both in the immediate and longer term – are often debated. However, this study alone provides no proof that cannabis use will increase your risk of diabetes.
Cannabis remains a class B drug that is illegal to possess or distribute.
Links To The Headlines
Marijuana users may be more likely to develop diabetes, research finds. The Independent, September 13 2015
Cannabis smokers are far more likely to develop early stages of diabetes, research finds. Mail Online, September 14 2015
Links To Science
Bancks MP, Pletcher MJ, Keresz SG, et al. Marijuana use and risk of prediabetes and diabetes by middle adulthood: the Coronary Artery Risk Development in Young Adults (CARDIA) study (PDF, 384kb). Published online September 12 2015
"Older people could reduce risk of osteoporosis by hopping for two minutes a day," the Daily Mirror reports. A UK study found regular hopping increased bone density in older men.
The study assigned more than 30 healthy older men to exercises on one leg and compared the change in bone density with the other leg.
It found five sets of 10 hops, with a 15-second rest between each set, every day increased the density of some parts of the hip. The men, aged 65 to 80 years old, were followed up with a second scan after 12 months.
Some of the media claim this has major implications for the prevention and management of osteoporosis. But these findings were from a group of healthy older males without osteoporosis and no other health conditions. It is unclear whether hopping would be effective, and safe, for people who actually have osteoporosis.
The follow-up time was also relatively modest – just 12 months – so it is uncertain whether this exercise regime would prevent bone fractures in the long term. Women feature in many of the newspaper pictures, but were not participants in this study.
The study was carried out by researchers from Loughborough University, the University of Cambridge, University Hospitals Leicester, and Derby Hospitals NHS foundation Trust.
It was funded by the National Osteoporosis Innovative Award, a Medical Research Council UK Interdisciplinary Bridging Award, and a Loughborough University Scholarship.
The study was published in the peer-reviewed Journal of Bone and Mineral Research.
This study has been widely reported in the UK media, with many sources suggesting hopping reduces the risk of a fracture. This was not reported in the paper and it is not yet known whether the bone density improvements demonstrated led to reduced numbers of fractures.What kind of research was this?
This randomised controlled trial aimed to evaluate the effects of these exercises on cortical and trabecular bone (found in the hip) and its 3D distribution across the hip.
This study design is the best way to assess such an effect, but as it was only the participants' legs that were randomised in this instance, both legs may have benefited from changes to other behaviours.What did the research involve?
Researchers recruited 50 healthy men of European origin who were aged 65 to 80. The men had no involvement in exercises of a strength, power or weightlifting nature for more than one hour a week, and had no health conditions likely to influence bone, neuromuscular function or their ability to perform exercises.
The "exercise leg" of each participant was randomly assigned (left or right) using sealed opaque envelopes. Limb dominance had no effect on allocation.
All participants were to perform hopping exercises on their exercise leg only and avoid any other changes to their physical activity or dietary habits during the trial.
The hopping exercise involved around 10 minutes of activity and consisted of five sets of 10 hops, with a 15-second rest between each set. This was performed in a variety of directions. Exercises were to be performed as high and fast as they could on a hard, even surface, while barefoot and when another person was nearby.
Measurements of bone mineral content were taken by CT scan before and after the study period. This was performed by a radiographer who was unaware (blinded) to leg allocation and efforts were made to standardise leg placement. Researchers were interested in how the exercise affects different parts of the hip.
Participants were to complete a seven-day food diary and health and physical activity questionnaire before the trial began. Anthropometric measurements (height, weight and BMI) and body composition were taken by DEXA (DXA) scan before and after the trial period. The men were followed up after 12 months.What were the basic results?
Of the 50 men who started the trial, only 34 remained for analysis. The withdrawal rate was 32% (16 men). This was mainly because of either health problems unrelated to the intervention, time commitments or discomfort during exercise.
The study found bone mineral density in the outer and spongy layers significantly increased over time in each leg. The density of the outer layer increased significantly more in the exercise leg, compared with the control leg.
There was a greater increase in density in the exercise leg than the control leg in terms of where the femur connects to the hip bone. Instability of the hip was reduced more in the exercise leg.How did the researchers interpret the results?
The researchers state short bursts of regular hopping exercises increased hip bone density, and exercise that targets localised regions of the proximal femur (the section of bone that connects the upper thigh bone to the hip) could produce greater increases in bone strength and resistance to fracture.Conclusion
This was a randomised controlled trial assessing the effect on hip bone density of hopping as a form of weight-bearing exercise in older men. The study found the hopping exercise to be of significant benefit to certain parts of the hip. But this study was performed in healthy men with no health concerns.
The study had a number of strengths and limitations. Strengths are that it was randomised in design, and the fact there was concealed allocation to the intervention group and blinded assessors, reducing the risk of bias. The researchers also performed calculations to estimate the number of participants needed for their study.
Limitations are that the study may have benefited from having a control group who did not take part in the hopping exercise, rather than just a randomly assigned leg. In addition, the sample size was quite small, the study did not assess physical activity or dietary habits after the intervention, and it was conducted in a group of healthy older men.
This means the findings may not be generalisable to other groups, especially those with osteoporosis, where boosting bone density would be of great benefit.
While this study has presented some significant findings, it is not possible to say whether this intervention would be of use to other older people who have health issues or are perhaps unsteady on their feet. The high drop-out rate of 32% suggests it may not be a suitable exercise for many men.
If you do have osteoporosis, hopping may not be the ideal exercise plan for you as there is a risk of falling, which could result in fracture. Your GP or the doctor in charge of your care should be able to recommend a suitable exercise plan.
Links To The Headlines
Older people could reduce risk of osteoporosis by HOPPING for two minutes a day. Daily Mirror, September 10 2015
Older people urged to 'hop more' to reduce fracture risk. ITV News, September 11 2015
Just two minutes of HOPPING a day can strengthen bones and reduce the risk of suffering a fracture, scientists find. Daily Mail, September 11 2015
Experts say hopping for two minutes a day could reduce osteoporosis risk. The Daily Telegraph, September 11 2015
Links To Science
Allison SJ, Poole KES, Treece GM, et al. The Influence of High-Impact Exercise on Cortical and Trabecular Bone Mineral Content and 3D Distribution Across the Proximal Femur in Older Men: A Randomized Controlled Unilateral Intervention. Journal of Bone and Mineral Research. Published online August 17 2015
Secondhand smoke is dangerous, especially for children. The best way to protect loved ones is to quit smoking. At the very least, make sure you have a smokefree home and car.
When you smoke a cigarette (or roll-up, pipe or cigar), most of the smoke doesn't go into your lungs, it goes into the air around you where anyone nearby can breathe it in.
Secondhand smoke is the smoke that you exhale plus the 'sidestream' smoke created by the lit end of your cigarette.
When friends and family breathe in your secondhand smoke – what we call passive smoking – it isn't just unpleasant for them, it can damage their health too.
Pregnant women exposed to passive smoke are more prone to premature birth and their baby is more at risk of low birthweight and cot death.
The only surefire way to protect your friends and family from secondhand smoke is to keep the environment around them smoke free.
The best way to do that is to quit smoking completely. If you're not ready to quit, make every effort to keep your cigarette smoke away from other people and never smoke indoors or in the car.
- Always smoke outside
- Ask your visitors to smoke outside
- Don't smoke in the car or allow anyone else to
Secondhand smoke is a lethal cocktail of more than 4,000 irritants, toxins and cancer-causing substances.
Most secondhand smoke is invisible and odourless, so no matter how careful you think you're being, people around you still breathe in the harmful poisons.
Opening windows and doors or smoking in another room in the house doesn't protect people. Smoke can linger in the air for two to three hours after you've finished a cigarette, even with a window open. And even if you limit smoking to one room, the smoke will spread to the rest of the house where people can inhale it.
Passive smoking is especially harmful for children as they have less well-developed airways, lungs and immune systems.
It's estimated that more than one in five children in the UK live in a household where at least one person smokes and, as a result, they're more likely to develop:
Children are particularly vulnerable in the family car where secondhand smoke can reach hazardous levels even with the windows open.
It's estimated that smoking in cars produces concentrations of toxins up to 11 times higher than you used to find in the average smoky pub.
To protect children, there is a new ban on smoking in cars and other vehicles carrying children. From October 1 2015 it is against the law to smoke in a private vehicle if there’s a young person under-18 present.
Read about the new law on smoking in private vehicles.How safe is e-cig vapour?
E-cigarettes don't produce tobacco smoke so the risks of passive smoking with conventional cigarettes don't apply to e-cigs.
Research into this area is ongoing, but it seems that e-cigs release negligible amounts of nicotine into the atmosphere and the limited evidence available suggests that any risk from passive vaping to bystanders is small relative to tobacco cigarettes.
In England, the Government has no plans to ban vaping indoors (although some employers have banned them in the workplace) but some health professionals recommend avoiding using them around pregnant women, babies and children.
Read about the safety of e-cigarettes.
Your GP can give you advice about quitting smoking.
The results of a study that reported finding markers for Alzheimer's disease in the brains of some people who died of Creutzfeldt-Jakob disease (CJD) has led to many inaccurate headlines in the press.
The Daily Mirror claims "You can catch Alzheimer's", while the Mail Online claims that an "explosive new study suggests the disease is spread like CJD and could be passed on through blood transfusions, operations and dental work".
Neither claim adds up to much scrutiny, as the "explosive" study itself concludes: "There is no suggestion that Alzheimer's disease is a contagious disease and no supportive evidence … that Alzheimer's disease is transmissible, notably by blood transfusion".
The eight people involved in the study were infected with brain-damaging proteins called prions, which cause CJD, through injections of human growth hormone taken from the brains of people who had died. All the infections happened before 1985, when this type of treatment was stopped.
None of the eight people studied actually had Alzheimer's – they all died of CJD. During their autopsies, researchers were surprised to find evidence of amyloid beta protein deposits (abnormal clumps of protein), which can be a precursor of Alzheimer's, in seven people's brains.
These people were aged 36 to 51 years – too young for most people to develop Alzheimer's. The researchers suggest they may have been infected with amyloid proteins – dubbed Alzheimer's "seeds" – in the same way they had been infected with prions: through human growth hormone treatment.
But nobody should worry that they have "caught" Alzheimer's from routine medical treatment using the information this study has gathered.
Where did the story come from?
The study was carried out by researchers from the National Hospital for Neurology and Neurosurgery, the Medical Research Council Prion Unit, and University College London, and was funded by the UK Medical Research Council and the National Institute of Health Research.
Two of the study authors are shareholders in a company called D-Gen, which makes products to decontaminate surgical instruments.
This might be seen as a conflict of interest – if this study was borne out by other research, there might be an increased demand for this type of product to ensure amyloid proteins were not passed on through surgery. This fact was not reported in the media.
The quality of the UK's media reporting was decidedly mixed. The actual reporting of the study was generally accurate and contained useful words of reassurance from independent experts.
For example, Dr Eric Karran, director of research at Alzheimer's Research UK, was quoted as saying: "There is currently no evidence to suggest that the amyloid protein could be passed through dental surgery or blood transfusions." Indeed, a study in 1997 found that Alzheimer's disease was more common in people who had not had blood transfusions.
But the headline writers had a field day, generating a range of needlessly alarmist and inaccurate headlines, from the Mirror's "You can catch Alzheimer's" and the Mail's "Alzheimer's links to blood transfusions", to the Daily Express' "Alzheimer's bombshell".What kind of research was this?
This autopsy study was part of a larger ongoing study looking into what happened to people in the UK who received human growth hormone therapy.
Researchers are trying to follow all the people who get CJD in the UK in a study called the National Prion Monitoring Cohort study and – where possible – perform autopsies after their death.
The aim is to advance our understanding of prion disease in the brain. The researchers were not expecting to find signs of Alzheimer's disease.What did the research involve?
Eight patients were given autopsies after they died of CJD following infection from human growth hormone. The researchers used standard techniques to look for prions in the brain and the damage they had done. They also looked for any other abnormalities.
The researchers reviewed autopsy results of 116 patients who had died from other types of prion disease so they could compare their initial results with groups of people with prion disease not caused by human growth hormone.
They also looked at the genetic profile of the eight people in their study to see if they had genetic mutations for early Alzheimer's.
Amyloid protein deposits are not common in the brains of younger people, unless they have a genetic mutation that means they are more likely to get early onset Alzheimer's.What were the basic results?
During the eight autopsies, the researchers found some evidence of amyloid protein deposits in seven of the patients. This was "substantial" in four patients.
They also found a build-up of amyloid protein in the brain arteries of four of the patients. Amyloid deposits in brain arteries can cause bleeding, strokes and dementia. None of the eight patients had genetic markers for early Alzheimer's.
The autopsy results of people who died from prion diseases not caught through medical treatment found none of them had similar results. Their results were in line with what you would expect to see in people across a similar age range.How did the researchers interpret the results?
The researchers concluded their findings were "consistent with the hypothesis that amyloid beta seeds have been iatrogenically [caused by medical treatment] transmitted to these patients with CJD". In other words, the patients were infected with amyloid proteins from the brain tissue used to make human growth hormone, in the same way they had been infected with prions.
They warned that, "amyloid beta seeds are known, like prions, to adhere to metal surfaces and to resist formaldehyde inactivation and conventional hospital sterilisation", and say scientists should consider whether amyloid protein could be transmitted through surgical instruments and blood products.Conclusion
This small study raises questions about how a group of relatively young people with CJD came to have amyloid protein deposits in their brains when they died. But it doesn't answer those questions.
The theory that amyloid proteins were transferred, along with prions, through growth hormone therapy is still just that: a theory. There are other possibilities – for example, the prions could have somehow encouraged the growth of amyloid protein. That would mean people who are already infected with prions are at an increased risk of early-onset Alzheimer's disease.
However, it's also important to remember no-one in the study actually developed Alzheimer's. They may have done so had they lived longer, but we don't know. As the cause of Alzheimer's remains unknown, it is also feasible that another process or risk factor could have accounted for the results seen.
Other studies that looked at people who received human growth hormone treatment found they were not at any increased risk of getting Alzheimer's disease. But that study only looked at death certificates, not autopsy results. We don't know if these people had amyloid protein deposits in their brains.
The implications if amyloid protein could be passed on through blood products and surgery are that many more people may be at risk of Alzheimer's than previously thought. Yet there is no evidence from this study to suggest this is the case. Previous studies looking at people who have had blood transfusions have not found they are more likely to get Alzheimer's disease.
This is just one small, exploratory study that made a surprising finding. Researchers will now need to look at other data – for example, any additional autopsy data from people who have died of CJD caused by medical treatment over the past few decades – to see whether these findings stand up.
NHS procedures have improved significantly since the 1970s, when the patients in this study contracted CJD. Modern surgical equipment used in the UK is very safe and the NHS has extremely stringent procedures to make sure of this. There has so far been no evidence of Alzheimer's disease being transmitted through surgery, blood transfusion or dental treatment.
Links To The Headlines
Alzheimer's disease may be caught through medical accidents. The Telegraph, September 9 2015
Study finds seed of Alzheimer's may have spread in medical procedure. Mail Online, September 9 2015
'Transmittable Alzheimer's' concept raised. BBC News, September 9 2015
Alzheimer's 'Could Be Passed On In Surgery'. Sky News, September 10 2015
Alzheimer's disease may be infectious, study claims. The Independent, September 10 2015
Alzheimer's Q&A: Does this mean that we can 'catch' the disease? Is this a health scare? The Independent, September 9 2015
Alzheimer's can be spread from human to human, explosive research claims. Daily Mirror, September 9 2015
Can people catch Alzheimer's? Possibility cannot be ruled out. The Guardian, September 10 2015
Alzheimer's 'could be spread during surgery'. ITV News, September 10 2015
Can you CATCH Alzheimer's? British experts find disease can be PASSED between humans. Daily Express, September 10 2015
Links To Science
Jaunmuktane Z, Mead S, Ellis M, et al. Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy. Nature. Published online September 9 2015